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"Targeting Human Telomerase in Cancer Therapy\nTelomerase is a specialized RNA template-containing reverse transcriptase that mediates telomere repeat synthesis at chromosome ends. The maintenance of telomere length and integrity is essential for cell survival. Telomerase is active in most immortal and tumor cells, whereas the majority of normal human cells demonstrate no detectable activity and undergo telomere shortening. The identification of a possible role for telomerase in cellular aging and cancer has led to numerous studies designed to characterize this ribonucleoprotein enzyme. Inhibiting telomerase activity in immortal human cells reduces cellular proliferative capacity and can lead to cell death. Identifying mechanisms to specifically inhibit telomerase activity in malignant cells could thus be of great therapeutic value in the treatment of cancer. In this review, we summarize the current understanding of the mechanism of action of human telomerase. The biochemical characterization of telomerase is necessary for the design and evaluation of antitelomerase therapies. Different strategies are currently under investigation to design inhibitors that target the reverse transcriptase and RNA components of the telomerase complex. Recent advances in the design of these inhibitors and their properties are discussed.\nKeywords: Human Telomerase, Cancer Therapy, Proteins, hTERT and hTR, Antisense, Ribozymes\nRights & PermissionsPrintExport"

"The linear ends of chromosome are protected by specialized ribonucleoprotein (RNP) termed as telomere. These specialized terminal elements with tandem repeated sequence are the protective cap that alleviate end replication problem and cell senescence. The telomere length maintenance is essential to avoid cell death and apoptosis. Telomere shortening has been related to chronic stress due to several factors, which include not only psychological stress but also diseases such as cardiovascular diseases and cancer. Telomerase enzyme which maintains telomere length is the major factor responsible for evading cell death. Telomere length maintenance and telomerase expression put together are the prerequisite for immortality, an essential character for cancer cells. Understanding the mechanism of telomere and telomerase functions paves way for eradicating the diseases such as cancer.\n- telomere length\n- tumor progression\n- tumor immortality\nTelomeres are specialized DNA structures consisting of tandem arrays of hexa-nucleotide (TTAGGG) DNA sequences that cap the end of chromosomes. These structures residing near the ends of chromosomes play a very vital role in maintaining the integrity of the whole genome and prevent the loss of genetic material. As a consequence of cell division, short stretches of DNA will be lost from telomeric region and eventually lead to cellular senescence and death. There are a lot of evidences to suggest that telomere length is a better biomarker for overall health status, compared to the currently used biomarkers for the same. Few of the phenomena regarding the telomere length are unanswered till now. Till date it is unclear about the mechanistic correlation between telomere size and life span of various species. To prevent senescence of cell, the preservation of telomere length is essential, which is maintained by telomerase enzyme. Telomerase is a reverse transcriptase enzyme which has recently emerged as an attractive target for cancer as it is a crucial factor required for the tumor immortalization of a subset of cells, including cancer stem cells. Studies have proved that 80–85% of the tumor cells express telomerase whereas somatic cells lack the expression of telomerase . The important paradox is that telomerase-negative normal cells have lengthier telomeres than telomerase-positive cancer cells . Thus difference in telomere length and cell kinetics between normal and cancerous cells shows that targeting telomerase is a more effective way to target cancer cells. Owing to the significant role of telomere and telomerase in tumor immortalization understanding their amassed influence on cancer is crucial for cancer therapy. In this context, this book chapter is focused on disseminating the integrated impact of telomere and telomerase on cancer progression.\n2. Telomere construction\nThe basic structure of telomere is conserved among eukaryotes and consists of short tandem DNA repeats, with G-rich sequence at the three-end referred to as the G-strand and the complementary strand is called the C-strand at the five-end (Figure 1) . The length of telomeric DNA varies from 2 to 20 kilobase pairs, depending on factors such as tissue type and human age . The telomere is conspicuous owing to the presence of G-overhang which extends beyond its complementary C-rich strand to form a single-stranded overhang, termed the G-tail. It has been proposed that the 3′ G-overhang can be sequestered into a lasso-like structure known as the T-loop (Figure 2) [5, 6]. The single-stranded G-overhang invades the double-stranded telomeric DNA, which displaces the bound G-strand base-pairing with the C-strand. As this displaced binding takes place at a distance from the physical end of the telomere, it generates a large duplex structure called the T-loop (Figure 2) [3, 5].\nTelomeres can also fold into G-quadruplex DNA, an unusual DNA conformation that is based on a guanine quartet . The repetitive and GC-rich nature of telomeric DNA endows it with the capability to form the higher-order DNA conformation, G-quadruplexes [8, 9]. To maintain such unusual structure of telomeres, a set of telomeric protein complex has evolved, termed shelterin. The shelterin complex consists of six individual proteins, telomeric repeat binding factor 1 (TRF1), TRF2, repressor/activator protein 1 (RAP1), TIN2 (TRF1 interacting protein 2), TPP1 (TINT1/PIP1/PTOP 1), and protection of telomeres 1 (POT1) [6, 10]. The proteins TRF1 and TRF2 attach to double-stranded telomeric repeats facilitating the anchoring of the complex along the length of telomeres [11–14], whereas POT1 binds to the single-stranded overhang. TPP1 and TIN2 act as bridging proteins between the above DNA-binding modules and are crucial for chromosome end protection and telomere length regulation. TRF1 and TRF2 with the help of TIN2 bind with POT1 via TPP1 [16–19]. TIN2 also connects TRF1 to TRF2, and this interaction contributes to the stabilization of TRF2 on telomeres [17–19]. Besides this shelterin complex, other proteins like TEN1 and Pinx1, which are not telomere specific, are also present at telomeres and carry out important functions in recruitment of telomerase .\n3. Telomere: a knight cap\nDuring the evolvement of linear genome, the natural ends of linear chromosomes resemble DNA breaks and tend to induce DNA damage response (DDR). These natural linear ends are protected by the sequestration of the ribonucleoprotein (RNP) sequence, telomeres which mask the ends from continuous exposure to the DNA damage response (DDR). Telomeres serve as protective caps, preventing the chromosomal ends from being recognized as double-strand breaks by the DNA damage repair system and the activation of the p53 or p16INK4a pathway and the start of senescence or apoptosis. If the telomere cap is removed, genome instability is induced. Telomeres with its tightly regulated complexes consisting of repetitive G-rich DNA and specialized proteins accomplish the task of not only concealing the linear chromosome ends from detection and undesired repair, but also protect from checkpoints, homologous recombination, end-to-end fusions, or other events that normally promote repair of intra-chromosomal DNA breaks acts . Telomeric proteins and their interacting factors create an environment at chromosome ends that inhibits DNA repair at that point; however, the repair machinery is also essential for proper telomere function.\nThe closed configuration of the T-loop of telomeric region provides a protective cap that defines the natural end of the chromosome and masks the telomere from the DDR machinery (Figure 2) . In particular, T-loops could provide an architectural solution to the repression of the ataxia telangiectasia mutated (ATM) kinase pathway, which relies on a sensor (the MRN (Mre11/Rad50/Nbs1) complex) with DNA end-binding activity. In addition, T-loops could prevent the Ku70/80 heterodimer, a DNA repair factor that binds to DNA ends, from loading onto the telomere terminus, thereby blocking the initiation of the non-homologous end-joining (NHEJ) pathway (Figure 4).\nAmong the DNA-binding proteins, TRF1 has DNA remodeling activity [5, 22] and also shown to promote efficient replication of telomeres [23, 24]. On the contrary, TRF2 engages in chromosome end protection by inducing topological changes in telomeric DNA , T-loop assembly [26, 27] and by suppression of ATM dependent DDR and NHEJ (Figure 4) [28, 29]. Besides that, TRF2 plays a critical role in chromatin assembly, which was demonstrated by the observation that overexpression of TRF2 resulted in aberrant nucleosome spacing and decreased abundance of the core histones H3 and H4 at chromosome ends . TRF2 lacking cells are reported to be growth arrested because of up-regulation of p53 and also show other hallmarks of ATM signaling, including the phosphorylation of ATM and Chk2 [31, 32]. Among the two DDR, the ATM kinase pathway at telomeres is repressed by TRF2 subunit, whereas POT1 is responsible for protection of telomere by suppression of ATR (ATM Rad3-related protein)-dependant DDR pathways [28, 33].\nThe high affinity of POT1 for single-stranded telomeric DNA makes it a G-strand binding component displaced from the T-loop and forms a closed configuration locking in the structure (Figure 2). Earlier report models suggest that POT1 and TPP1 compete with telomerase for access to the overhang . Contrarily, direct interaction between TPP1 and telomerase bolsters telomerase processivity [34, 35] whereas increased loading of POT1 along the overhang block telomerase accessibility to the 3′-OH substrate. The role of RAP1 is obscure and its function has recently been elucidated. The presence of RAP1 at telomeres appears as a backup mechanism to prevent NHEJ when topology-mediated telomere protection is impaired . In case of mutation in TRF2 which wraps the DNA, RAP1 has been implicated in the inhibition of NHEJ [37, 38].\nThus physically taken together, the shelterin complex and G-overhang of telomere are the protective cap that have an immensely complex role in convergence of end protection and telomere length maintenance mechanisms.\n4. Telomerase activity\nWith each cell division, telomere length is reduced by ~50 to 200 bp primarily because the lagging strand of DNA synthesis is unable to replicate the extreme 3′ end of the chromosome which is denoted as end replication problem [40, 41]. When telomeres become sufficiently short, cells enter an irreversible growth arrest called cellular senescence. In most eukaryotes, telomeres are stabilized, and the shortening telomeric DNA is replenished, by the action of the RNP reverse transcriptase telomerase. Progressive telomere loss has been experimentally demonstrated using non-immortalized cells in culture that lack detectable telomerase [42, 43].\nIn cells with active telomerase, such as cancer cells, the telomere length is continually being built up and shortened in a regulated way that maintains telomere length homeostasis and retains telomere functionality. Shortening of telomeres occur due to nucleolytic degradation and incomplete DNA replication. On the contrary, lengthening is primarily accomplished by the action of a specialized reverse transcriptase called telomerase and occasionally by homologous recombination (HR) . Telomerase uses the 3′ G-rich strand of a chromosome as primer to elongate chromosome end by reverse-transcribing the template region of its tightly associated RNA moiety and coordinative action with the DNA replication machinery [44, 46]. For lengthening activity, telomerase requires not only hTERT catalytic subunit and RNA template (hTR) but also other factors [47, 48].\nThe 3′ half of the hTR resembling the box H/ACA family of small nucleolar RNAs (snoRNAs) [49, 50] is essential for proper 3′-end processing, stability and nucleolar targeting in vivo . The 5′ end of hTR not only acts as template for the telomere extension at chromosome ends [5, 51] but also serves as a pseudoknot that is likely to be important for telomerase function (5, 49). A 6 bp U-rich sequence at the 5′ end of hTR also interacts directly with hnRNPs C1 and C2 (Figure 3) . Even though hTR is highly expressed in all tissues regardless of telomerase activity , in cancer cells hTR is generally expressed fivefold higher than normal cells . However, the expression (mRNA) of the telomeric catalytic component hTERT which is closely associated with telomerase activity is estimated to be less than one to five copies per cell . hTERT is generally repressed in normal cells and up-regulated in immortal cells, suggesting that hTERT is the primary determinant for the enzyme activity.\nIt has been suggested that in addition to telomere elongation another aspect of telomerase RNP function is to allow even short telomeres to remain functional, which in the absence of telomerase would have caused cells to stop dividing or led to telomere–telomere fusions . In other words, telomerase permits cell proliferation by stabilizing short telomeres that would be unstable in the absence of functional telomerase. In recent years, evidence has accumulated that telomerase, and in particular its catalytic subunit TERT, is involved in various non-telomere-related functions such as regulation of gene expression, growth factors and cell proliferation [56–61]. It has been reported that the telomerase has a role in modulation of Wnt/β-catenin pathway . TERT has been demonstrated to bind to TBE-containing promoter elements, the specific chromatin sites of Wnt/β-catenin target genes, forming a part of the β-catenin transcriptional complex, which was facilitated by interaction with BRG1. These data endorsed the precipitous role for telomerase as a transcriptional modulator of Wnt/β-catenin signaling pathway involved in progenitor cell regulation.\nIn addition, various groups have shown that TERT shuttles from the nucleus and translocates to mitochondria upon exogenous stress [62–67]. Singhapol and his coworkers have demonstrated that mitochondrial telomerase localization specifically decreases mitochondrial ROS generation and cellular oxidative stress after induction of exogenous stress generated by H2O2 or irradiation in cancer cells and might thereby prevent damage to nuclear DNA . Thus the presence of telomerase not only maintains telomere length imparting immortality but also play multifarious role in tumorigenesis via non-telomere-dependent mechanism which demonstrated the imperative ubiquity of telomerase in cancer cells.\n5. Skewed expression of telomerase\nTelomerase, the RNA-dependent DNA polymerase by preventing the shortening of telomeric DNA sequences, accouters unlimited proliferation. As per the telomere hypothesis of cancer cell immortalization, telomere shortening limits the life span of telomerase-negative normal cells, whereas telomerase activation in cancer cells extends their life span . In normal human cells, telomerase activity is quenched during embryonic differentiation . On the contrary in some tissues, like male germ cells, activated lymphocytes, and certain types of stem cell populations, the telomerase activity is induced [15, 70]. Owing to its diverse activity, the telomerase which was established to be absent in most of the normal human somatic cells is recorded to be expressed in more than 90% of cancerous cells and in vitro-immortalized cells [15, 70]. A study showed that while most of the glioma tissues possess increased telomerase activity, only few (10%) anaplastic astrocytomas are reported to be telomerase positive [72–74]. In contrast to most cancerous cells, the telomerase expression is present in only 50% of glioblastoma and retinoblastoma samples, and activity is even rarely found in meningiomas and astrocytomas [75, 76].\nInduction of telomerase activity in primary human keratinocytes and mammary epithelial cells has been attributed to the effect of human papillomavirus 16 E6 protein . Similarly, during the menstrual cycle involving the proliferation of endometrial cells, telomerase activity is detected in normal human endometrium [78, 79]. These reports emphasis that telomerase might be the reason for tumorigenesis in hormone-dependent cancers.\nIt has been suggested that up-regulated expression of telomerase is contributed by the increased copy number of hTERT which was demonstrated by the report that while hTERT protein expression was strongly positive in tumor cells, the expression of hTERT in non-neoplastic mucosal cells as well as stromal elements (except lymphocytes) was weak or negative . In most cases, hTERT expression is closely correlated not only with telomerase activity but also with cancer initiation and progression. In head and neck squamous cell carcinoma and human glioma cell lines, there was decrease in telomerase activity which has been correlated with overexpression of p53, E2F, p16, p21, and p15 individually [81, 82]. In malignant and nonmalignant human hematopoietic cell lines, primary leukemic cells, and normal T lymphocytes, IFN-α is reported to inhibit telomerase activity by suppressing hTERT transcription . In addition to growth and differentiation-related regulation, telomerase activity is subject to regulation by other external and intracellular factors such as UV irradiation . The telomerase having influence over several signaling pathways that determine cell proliferative or death responses when overexpressed might abrogate anti-proliferative or cell death signals. Thus cancer cells with high levels of telomerase might gain a selective growth advantage.\n6. Telomerase as biomarker of cancer\nAdvent of latest cancer biomarkers has increased opportunities for improving cancer diagnostics by enhancing the quickness of detection and efficacy of treatment. In relation to the practice of new therapeutic interventions, proficient biomarkers are helpful in detection and prediction of remission or relapse of cancer at both gross and molecular levels. Telomerase activity is a hallmark of most cancer biopsies, but not generally detected in premalignant lesions and in normal tissue samples except germ cells and hematopoietic stem cells. Thus telomerase activity can be a promising biomarker for diagnosis of malignancies and a target for chemotherapy or gene therapy. Extent of telomerase activity in tumor tissues may be prognostic indicators of patient outcome. Thus, at the present time telomerase is being studied in anticipation of clinical usage. Many clinical trials for telomerase assay in cancer diagnosis are under trial. Fresh or fresh-frozen biopsies, fluids, and secretions are subject for these trials.\nOther components of telomerase enzyme complex have also been utilized as biomarkers for telomerase activity. The expression of the RNA subunit of the telomerase complex (hTR) is also regarded as a diagnostic marker . But the expression of hTR does not always correlate with telomerase protein expression in that particular cell type. hTR can be constitutively expressed in certain cell types in which even telomerase activity is not present . Apart from this, mutation in genes of telomerase and associated proteins are considered as a diagnostic and prognostic marker for many genetic abnormalities collectively termed as telomeropathies. Early-onset melanoma tumor syndrome with multiple co-morbid cancers can be predicted from telomerase gene promoter mutation analysis. In this disorder, the mutation in promoter of telomerase gene introduces an erythroblast transformation-specific transcription factor-binding site, resulting in approximately twofold up-regulation of telomerase .\nIntroduction of telomeric repeat amplification protocol (TRAP) assay has facilitated the detection of telomerase activity in tumor biopsy samples as well as cell lines . Specificity of telomerase activity in malignant phenotype further enforces the reliability of this assay. The most important advantage of TRAP assay is its low detectable limit. TRAP assay has allowed the analysis of minimal tissue samples, such as fine-needle aspirates of the breast and thyroid, cervical smears, oral washings, and urine [89, 90]. Telomerase also has been used to detect circulating tumor cells also . Newly emerged technique, droplet digital TRAP assay can detect telomerase activity even in a single cell . However, the positive ratios of detection of telomerase vary in sedimented cells obtained from secretion, washing, brushing samples, etc. Electrochemical telomerase assay (ECTA) is another newly emerged technique to detect telomerase activity in biological samples . It is comparatively simple and rapid PCR-free method. ECTA consists of a TS primer-immobilized electrode and ferrocenyl naphthalene diimide derivative as a tetraplex binder. This method has shown a high efficiency of telomerase detection in oral cancer biopsies . Taken in account of all these reports, telomerase and its functionality can be utilized as a promising diagnostic and prognostic method in cancer.\n7. Telomeres in prognosis\nBetter understanding of telomere structure and its dynamics focused the research on telomeres as biomarkers for several diseases especially in early detection and prognosis of cancers. A reduced telomere length in human hematopoietic tumors predicts a reduced survival time in patients suffering from myeloid leucaemia , chronic lymphocytic leucaemia , and myelodysplastic syndromes . Although telomere length in solid tumors is suggested as a potential prognostic marker, patient survival rates vary with different cancer types. For example, a short telomere length in prostate cancer correlates with short disease-free interval and shorter overall survival time . Analysis of telomere length of blood cells is also considered as predictive markers for pulmonary and esophageal neoplasia as well as of lymphoma in humans . It has been suggested that the reduced TL in these patients reflects the effects of increased oxidative stress which correlates with cancer risk. Advent of latest technologies to measure relative and absolute telomere lengths has paved the way to use telomere length as diagnostic and prognostic markers. Telomere restriction fragment assay, qFISH, flow FISH, qPCR assay, single telomere length analysis (STELA), and dot-blot telomere assay are the currently available assay methods for telomere length .\n8. Telomerase as drug target\nTelomerase enzyme has recently emerged as an attractive target for cancer as it is a crucial factor required for the tumor immortalization of a subset of cells, including cancer stem cells. Studies have shown that 80–85% of the tumor cells express telomerase, whereas somatic cells lack the expression of telomerase . In the present scenario, the major concern about the chemotherapeutic approaches is the specificity of action and side effects of drugs on normal cells. Difference in telomere length and cell kinetics between normal and cancerous cells shows that targeting telomerase is an effective system to target cancer cells specifically . Although telomerase is not considered as an oncogene, the expression of telomerase is the major reason for the transformation of a normal cell to cancer cell . Compared to most other cancer targets, telomerase antagonists are advantageous due to the wide expression of this enzyme in cancer types . Telomerase also possesses extra telomeric functions which are very crucial for tumor survival and homeostasis . Studies have shown that telomerase-based cancer therapies are less likely to develop resistance against the drugs compared to drugs which target growth factor receptors or signal-transducing enzymes in cancer cells . This ensures that cancer drugs based on telomerase inhibition are non-cytotoxic anticancer approach and have a broad therapeutic value.\nMaintenance of telomere length in cancer cells is a critical factor in imparting the ability to undergo uncontrolled multiplication and thus immortality to the cells. It is imperative to discern the factors involved in telomere length preservation. Understanding the influence of telomerase and other factors in sustaining telomere length in cancer cells paves way for perceiving the theranostic role of telomere and telomerase in cancer treatment. Besides the theranostic effect, the possible side effects could be determined leading to precautionary methods to nullify the negative impact."

"|Hallmarks of Aging Brochure: Tools and Solutions for your research\nRequest Yours Today\n*Limited quantities available.\nHallmarks of Aging Miniseries No. 2 Telomere Attrition\nAs cells divide, the telomere ends of chromosomes get shorter. Eventually, the enzyme that adds telomeric repeat sequences, telomerase, gets silenced and the telomeres are too short for cells to divide. Shortened telomeres are associated with aging cells that are senescent.\nTelomeres at the ends of chromosomes, like all other sections of DNA, are prone to DNA damage, including double-strand breaks (DSBs). And unlike the rest of the chromosome, telomere DSBs aren’t fixed by the DNA repair pathway, as this would frequently lead to fused chromosomes and genomic instability. That’s why we have telomerase. However, telomerase expression is silenced in many adult cells, to curb rampant cell proliferation and tumorigenesis, and so telomeres get progressively shorter with age.\nFeatured Solution for Studying Telomere Attrition\nTRAPeze® Telomerase Detection Kit\nTelomerase activity has been detected in over 85% of all tumors. The TRAPeze® Telomerase Detection Kit is a highly sensitive in vitro\nassay system for detecting telomerase activity.\nThe TRAPeze® Telomerase Detection Kit contains a modified reverse primer sequence which:\nOrder Now Download Application Note\n- eliminates the need for a wax barrier hot start\n- reduces amplification artifacts\n- permits better estimation of telomerase processivity"

"Telomeres, the natural termini of linear chromosomes, are crucial for genome stability and cell proliferation. Telomere length reservoirs which are inadequate to sustain organ function in humans can be a substantial contributing factor to degenerative organ failure, referred to as \"\"\"\"\"\"\"\"syndromes of telomere shortening\"\"\"\"\"\"\"\". Recent evidence indicates that defects in three telomere-related complexes - telomerase, shelterin and a heterotrimeric RPA-like complex - can each give rise to the same detrimental consequences in humans. This third activity was first identified in budding yeast as a telomere-dedicated version of the canonical RPA complex (referred to as the t-RPA complex);it has long been assumed to function as an end protection factor, by protecting chromosome termini from unregulated resection while bound to the terminal G-strand overhang of fully replicated telomeres. This application proposes instead that the t-RPA complex performs its functions at telomeres during DNA replication by promoting passage of the replisome through telomeric duplex DNA. In this model, the essential function of the t-RPA complex is to prevent stalling and subsequent collapse of the replication fork, by modifying the DNA replication machinery to form a telomere- specific replisome. When fork collapse does occur, this model further proposes that telomerase is recruited to the site of fork collapse, to prevent the accumulation of prematurely truncated termini. This will be tested by the following three approaches. First, the mechanism by which the t-RPA complex promotes duplex telomeric DNA replication will be elucidated by constructing a comprehensive genetic map of the functional surface of the t-RPA complex, identification of protein interactions that mediate t-RPA-specific activities and construction of at-RPA-specific epistasis network. Second, the functional interplay between the t-RPA and RPA complexes at telomeres will be examined by asking whether the t-RPA complex replaces RPA as the replisome encounters repetitive telomeric DNA, or whether t-RPA becomes an additional component of the replisome. Third, a novel assay designed to capture replication errors that occur during a single cell cycle will be used to determine whether collapsed replication forks are elongated by telomerase;in addition, proteins previously thought to regulate recruitment of telomerase to fully replicated ends will be examined for whether they instead impact telomere length through effects on replication fork stalling/collapse. All three of these approaches will be aided by an assay that monitors sequence changes that arise in response to replication errors in duplex telomeric DNA at single-nucleotide resolution, which provides a level of analysis not previously possible with conventional protocols. This integrated approach will elucidate how the t-RPA complex interfaces with the DNA replication machinery to ensure faithful progression of the replisome through duplex telomeric DNA and thereby ensure telomere homeostasis.\nTelomeres, specialized termini that cap the ends of chromosomes, need to be maintained in order to promote cell proliferation. Inadequate telomere function accounts for a wide range of pathophysiologies among a broad segment of the human population, referred to as syndromes of telomere shortening. The goal of this application is to provide a mechanistic basis for understanding how a crucial telomere complex helps promote fully functional chromosome ends."

"Category — telomerase activation\nIlaria Chiodi and Chiara Mondello*\nIstituto di Genetica Molecolare, Consiglio Nazionale delle Ricerche, Pavia, Italy\nTelomerase canonical activity at telomeres prevents telomere shortening, allowing chromosome stability and cellular proliferation. To perform this task, the catalytic subunit (telomerase reverse transcriptase, TERT) of the enzyme works as a reverse transcriptase together with the telomerase RNA component (TERC), adding telomeric repeats to DNA molecule ends. Growing evidence indicates that, besides the telomeric-DNA synthesis activity, TERT has additional functions in tumor development and is involved in many different biological processes, among which cellular proliferation, gene expression regulation, and mitochondrial functionality. TERT has been shown to act independently of TERC in the Wnt-β-catenin signaling pathway, regulating the expression of Wnt target genes, which play a role in development and tumorigenesis. Moreover, TERT RNA-dependent RNA polymerase activity has been found, leading to the genesis of double-stranded RNAs that act as precursor of silencing RNAs. In mitochondria, a TERT TERC-independent reverse transcriptase activity has been described that could play a role in the protection of mitochondrial integrity. In this review, we will discuss some of the extra-telomeric functions of telomerase.\nKeywords: telomerase, TERT, telomere, transformation, cancer, apoptosis, mitochondria, RNA interference\nCitation: Chiodi I and Mondello C (2012) Telomere-independent functions of telomerase in nuclei, cytoplasm, and mitochondria. Front. Oncol. 2:133. doi: 10.3389/fonc.2012.00133\nReceived: 31 July 2012; Accepted: 18 September 2012;\nPublished online: 28 September 2012.\nClaus M. Azzalin, Eidgenössische Technische Hochschule Zürich, Switzerland\nSusan M. Bailey, Colorado State University, USA\nXu-Dong Zhu, McMaster University, Canada\nYongmei Song, Chinese Academy of Medical Sciences and Peking Union Medical College, China\nCopyright: © 2012 Chiodi and Mondello. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and subject to any copyright notices concerning any third-party graphics etc.\n*Correspondence: Chiara Mondello, Istituto di Genetica Molecolare, Consiglio Nazionale delle Ricerche, Via Abbiategrasso 207, 27100 Pavia, Italy. e-mail: email@example.com\nOctober 3, 2012 No Comments\nMouse lifespan extended up to 24 percent with a single treatment.\nA number of studies have shown that it is possible to lengthen the average life of individuals of many species, including mammals, by acting on specific genes. To date, however, this has meant altering the animals’ genes permanently from the embryonic stage – an approach impracticable in humans. Researchers at the Spanish National Cancer Research Centre (CNIO), led by its director María Blasco, have proved that mouse lifespan can be extended by the application in adult life of a single treatment acting directly on the animal’s genes. And they have done so using gene therapy, a strategy never before employed to combat ageing. The therapy has been found to be safe and effective in mice.\nRead more by downloading the .pdf\nMay 15, 2012 No Comments\nGeron and TA Therapeutics Announce Presentation of New Data Supporting Utility of Their Small Molecule Telomerase Activator TAT0002; TAT0002 Selected as Lead Compound for HIV/AIDS Indication\nMENLO PARK, Calif. — Geron Corporation (Nasdaq:GERN) and TA Therapeutics, Ltd., a joint venture between Geron Corporation and the Biotechnology Research Corporation of Hong Kong (BRC), announced today the presentation of studies demonstrating that their small molecule telomerase activator, TAT0002, enhances the anti-viral activity of CD8 T-cells from HIV/AIDS donors against infected CD4 cells from the same donors. TA Therapeutics is exploring multiple applications for telomerase activators in chronic degenerative and infectious diseases. The company’s most advanced program is HIV/AIDS, and it has selected TAT0002 as the lead development candidate for this indication.\nThe new research was presented at the annual meeting of the American Association of Immunologists in Boston by Steve Fauce, from the laboratory of Rita Effros, Ph.D., professor of pathology and laboratory medicine and a member of the AIDS Institute at the David Geffen School of Medicine at UCLA. The studies are the product of a collaboration between Geron scientists, Dr. Effros and colleagues at UCLA.\nAs HIV disease progresses, certain immune cells called CD8 cytotoxic T-cells undergo accelerated replicative senescence (cellular aging) and lose their ability to proliferate and kill HIV-infected CD4 T-cells. Previously, Dr. Effros and colleagues demonstrated that introducing the telomerase gene into CD8 cells from HIV/AIDS donors increased: 1) their proliferative capacity, 2) their ability to produce IFN-gamma, and 3) their ability to inhibit virus production and kill HIV-infected T-cells. Dr. Effros’ team also showed that Geron’s small molecule telomerase activators had similar activity enhancing the ability of certain HIV-specific CD8 T-cells to inhibit virus production when co-cultured with an HLA-matched HIV-infected CD4 T-cell line.\nMarch 18, 2010 No Comments\nResearcher who Discovered Telomerase’s Role in Aging and Cell Mutation among Five Women Scientists Awarded in Paris\nNEW YORK, NY – December 6, 2007 – For her pioneering work with telomeres, the protective caps at the ends of chromosomes, and their relation to cell aging and disease, Dr. Elizabeth Blackburn was presented the prestigious L’ORÉAL -UNESCO For Women in Science Award. An expert in the area of telomere and telomerase research, Dr. Blackburn, Morris Herzstein Professor of Biology and Physiology in the Department of Biochemistry and Biophysics at the University of California, San Francisco, has worked to create a better understanding of stress as a cause leading to cell aging and the diseases of old age, including cancer.\nSelected as the North American Laureate for her discovery of the ribonucleoprotein enzyme telomerase, Dr. Blackburn’s research examines the function of the enzyme as it relates to cell aging and mutations that can cause cancer. During DNA synthesis, telomerase restores the ends of eukaryotic chromosomes, called telomeres, and Dr. Blackburn’s research has found that mutant variations of telomerase impair cell division, which can contribute to aging and cancer.\n“I would like to see our research be useful in furthering human well-being,” said Dr. Blackburn. “Perhaps it will be useful in understanding what happens to our cells’ telomere maintenance that can cause common diseases to progress. Perhaps this understanding will prompt and guide interventions to try to improve health.”\nDecember 6, 2007 No Comments\nJoseph M. Raffaele MD gave a very well-received presentation November 11 2007 to the Age Management Medical Group (AMMG) Annual Meeting titled: “Report on Clinical Trials Involving Telomerase Activation, and the Impact on Aging.”. Topics covered include: h-tert, senescence, telomere length as biomarker for aging and survival, telomerase is not an oncogene.\nNovember 18, 2007 No Comments\nTelomerase reverses epidermal hair follicle stem cell defects and loss of long-term survival associated with critically short telomeres\nSiegl-Cachedenier I, Flores I, Klatt P, Blasco MA. J Cell Biol. ;179(2):277-90.\nOrgan homeostasis and organismal survival are related to the ability of stem cells to sustain tissue regeneration. As a consequence of accelerated telomere shortening, telomerase-deficient mice show defective tissue regeneration and premature death. This suggests a direct impact of telomere length and telomerase activity on stem cell biology. We recently found that short telomeres impair the ability of epidermal stem cells to mobilize out of the hair follicle (HF) niche, resulting in impaired skin and hair growth and in the suppression of epidermal stem cell proliferative capacity in vitro. Here, we demonstrate that telomerase reintroduction in mice with critically short telomeres is sufficient to correct epidermal HF stem cell defects. Additionally, telomerase reintroduction into these mice results in a normal life span by preventing degenerative pathologies in the absence of increased tumorigenesis.\nOctober 22, 2007 No Comments\nRita Effros Presentation Summary for SENS (Aubrey de Grey) Conference 6 Sept 2007\nR.B. Effros David Geffen School of Medicine at UCLA, Department of Pathology and Laboratory Medicine, 10833 Le Conte Avenue, Los Angeles, CA 90095-1732, USA\nThe immune system plays a role not only in controlling infections, but also in certain age-related pathologies, such as atherosclerosis, osteoporosis, cancer and Alzheimer’s disease. In humans, ageing is associated with the accumulation of high proportions of CD8 (cytotoxic) T lymphocytes with markers of replicative senescence, including inability to proliferate, altered cytokine profiles, absence of the critical co-stimulatory receptor, CD28, reduced anti-viral function, shortened telomeres and loss of telomerase inducibility. Most of these senescent CD8 T lymphocytes are specific for latent viruses acquired early in life, and thus, reflect the constant “work” required over many decades to keep these infections from re-emerging. Since high proportions of senescent CD8 T lymphocytes are correlated with such deleterious outcomes as early mortality in the very old, reduced responses to vaccines, immune suppression, and, in persons infected with HIV, accelerated progression to AIDS, our research has focused on strategies to prevent or retard the process of replicative senescence. In earlier work, we documented that gene transduction with the human telomerase catalytic component (hTERT) leads to enhanced proliferation, telomere length stabilization, and increased anti-viral immunity. Current experiments are testing small molecule telomerase activators, which would be more suitable for clinical use, for their effects on CD8 T lymphocyte biology. Our data demonstrate that exposure to TAT2, one of these activators, significantly enhances telomerase activity, increases the ability of T lymphocytes to control viral production, enhances proliferation, increases production of anti-viral cytokines/chemokines, and retards telomere loss. The enhanced telomerase activity is associated with increased hTERT gene transcription. These studies support the notion that therapeutic manipulation of telomerase in human T lymphocytes may provide novel clinical avenues to enhancing viral immunity and retarding the immune exhaustion associated with ageing. (These studies were supported by the National Institutes of Health, TA Therapeutics, Ltd, and Geron Corporation).\nSeptember 6, 2007 No Comments\nGeron Corporation (Nasdaq: GERN) and the Biotechnology Research Corporation (BRC) of Hong Kong today announced that Geron has increased its stake in their joint venture entity, TA Therapeutics Limited (TAT), from 50% ownership to 75% ownership.\nTAT is a Hong Kong company that conducts research and develops therapeutics based on telomerase activator drugs to restore the functional and regenerative capacity of cells. BRC, a company established by The Hong Kong University of Science and Technology (HKUST), continues to hold the remaining 25% of the shares of TAT.\n“TAT has made great progress in its development of telomerase activator compounds for therapeutic applications,” said David J. Earp, J.D., Ph.D., Geron’s senior vice president of business development and a director of TAT. “The company is now expanding its efforts in pre-clinical development and working toward the filing of an Investigational New Drug (IND) Application with the U.S. Food and Drug Administration for a small molecule compound for the treatment of HIV/AIDS. This is an opportune time for Geron, the development and commercial partner in the joint venture, to negotiate for a larger interest in the company.”\nJune 18, 2007 No Comments\nRita B. Effros, Experimental Gerontology, Volume 42, Issue 5, 416-420.\nClinical studies have shown that high proportions of CD8 T cells with the senescent phenotype correlate with several deleterious physiologic outcomes, including poor vaccine responses, bone loss, and increased proinflammatory cytokines. CD8(+)CD28(-) T cells have also been shown to exert suppressive activity on other immune cells. Based on the central role of telomere shortening in the replicative senescence program, we are developing several telomerase-based approaches as potential immunoenhancing treatments for aging and HIV disease. Gene therapy of HIV-specific CD8 T cells with the telomerase catalytic component (hTERT) results in enhanced proliferative capacity, increased anti-viral functions, and a delay in the loss of CD28 expression, with no changes in karyotype or growth kinetics. These proof-of-principle studies have led to screening for pharmacological approaches that might mimic the gene therapy effects, in a more clinically suitable formulation.”\nMay 1, 2007 No Comments\nE Hiyama and K Hiyama, British Journal of Cancer 96, 1020-1024.\nTelomeres, guanine-rich tandem DNA repeats of the chromosomal end, provide chromosomal stability, and cellular replication causes their loss. In somatic cells, the activity of telomerase, a reverse transcriptase that can elongate telomeric repeats, is usually diminished after birth so that the telomere length is gradually shortened with cell divisions, and triggers cellular senescence. In embryonic stem cells, telomerase is activated and maintains telomere length and cellular immortality; however, the level of telomerase activity is low or absent in the majority of stem cells regardless of their proliferative capacity. Thus, even in stem cells, except for embryonal stem cells and cancer stem cells, telomere shortening occurs during replicative ageing, possibly at a slower rate than that in normal somatic cells. Recently, the importance of telomere maintenance in human stem cells has been highlighted by studies on dyskeratosis congenital, which is a genetic disorder in the human telomerase component. The regulation of telomere length and telomerase activity is a complex and dynamic process that is tightly linked to cell cycle regulation in human stem cells. Here we review the role of telomeres and telomerase in the function and capacity of the human stem cells.\nApril 10, 2007 No Comments"

"Nucleic acids research\nTelomerase is the ribonucleoprotein (RNP) enzyme that elongates telomeric DNA to compensate for the attrition occurring during each cycle of DNA replication. Knowing the levels of telomerase in continuously dividing cells is important for understanding how much telomerase is required for cell immortality. In this study, we measured the endogenous levels of the human telomerase RNP and its two key components, human telomerase RNA (hTR) and human telomerase reverse transcriptase (hTERT). We estimate ∼ 240 telomerase monomers per cell for HEK 293T and HeLa, a number similar to that of telomeres in late S phase. The subunits were in excess of RNPs (e.g. ∼ 1150 hTR and ∼ 500 hTERT molecules per HeLa cell), suggesting the existence of unassembled components. This hypothesis was tested by overexpressing individual subunits, which increased total telomerase activity as measured by the direct enzyme assay. Thus, there are subpopulations of both hTR and hTERT not assembled into telomerase but capable of being recruited. We also determined the specific activity of endogenous telomerase and of overexpressed super-telomerase both to be ∼ 60 nt incorporated per telomerase per minute, with Km(dGTP) ∼ 17 μM, indicating super-telomerase is as catalytically active as endogenous telomerase and is thus a good model for biochemical studies.\nXi, Linghe and Cech, Thomas R, \"Inventory of telomerase components in human cells reveals multiple subpopulations of hTR and hTERT.\" (2014). University Libraries Open Access Fund Supported Publications. 72."

"Telomerase gene expression in adult sockeye salmon\nResearch for the following capstone project is to be performed by Jason G. Tayag, under the guidance of Professor Steven Roberts and Graduate Student Caroline Storer. The project is an assay measuring telomerase gene expression in adult sockeye salmon. The results of the study can hopefully help to explain how quickly or how slowly telomeres are shortening in adult sockeye salmon.\nAccurate and complete DNA replication is important for cell division. Mutations in genetic information can result in deleterious phenotypic changes in an organism (Geserick and Blasco 2006). Cells utilize a number of ways to protect against deletions and changes to DNA. One such way to protect against deletion of genetic information is with telomeres. Telomeres are 6-base-pair repeat sequences at the ends of chromosomes that haven’t been known to code for anything Geserick and Blasco 2006). During DNA replication, DNA is packaged into chromosomes. When chromosomes replicate, genetic material on the ends of the chromosomes is deleted (Geserick and Blasco 2006). Telomeres protect genomic DNA from being deleted. Over time, however, telomeres shorten with every cell division – cells divide many times throughout an organism’s life. Telomere shortening may ultimately have links to aging and senescence (Geserick and Blasco 2006).\nSalmon are a very interesting organism we can use to study senescence because salmon health declines rapidly after releasing gametes. Studies have been done looking at post- and pre-spawning adults arriving at their natal stream, as well as juvenile telomere lengths. I want to focus on telomere lengths of adults in the ocean that may be getting ready to return to their natal stream to spawn. My hypothesis is that salmon at sea undergo rapid telomere shortening because that is where growth is occurring most rapidly. Before they even reach their natal stream, it is likely that telomere lengths have already shortened past critical length. This means that sockeye would already be going through a decline in health before they reach their natal stream. Though looking at actual telomere lengths can be difficult, there is a proximate way to measure telomeres by looking at the expression of the telomerase gene. Telomerase is an enzyme that restores telomeres. High telomerase activity allows us to know that at one particular point in time, telomerase is rapidly restoring telomeres – likely because telomeres are rapidly shortening.\nAt what life stage/stages does telomere shortening occur most rapidly?\nIs telomerase gene expression high in adult sockeye salmon in the ocean?\n-Find a salmon fishery where we can obtain flash-frozen adult sockeye salmon tissue samples from 8-10 individuals.\n-Research and design primers that will target telomerase gene sequence.\n-Extract RNA from tissues, reverse-transcribe RNA to DNA.\n-Measure telomerase gene expression by qPCR.\n-qPCR a normalizing gene so that we have a standard or a baseline to compare telomerase.\nTRI Reagent, Chloroform, Isopropanol, 75% Ethanol, DNA Free DNase kit, 0.1% DEPC-H2O, Oligo dT, Nuclease-free water, M-MLV 5X Reaction Buffer, dNTPs, M-MLV RT, GoTaq Master Mix Forward and Reverse Primers (need to be designed), Pipets, pipet tips, Microcentrifuge tubes, qPCR tubes, Thermocycler, -80°C freezer, -20° freezer, centrifuge, microcentrifuge, plastic plungers, spectrophotometer.\n-Transform C(t) values into relative gene expression values.\nAt the end of my research, my goal is to be able to write a scientific paper on my findings.\n-January 20, 2011 (2:00 PM): Next meeting with Professor Roberts.\n-Before January 20: try to come up with primer design for sockeye salmon telomerase gene.\n-The limiting step is finding adult sockeye salmon samples and getting them frozen and shipped. My goal is to obtain all of my samples by February 4, 2011.\n-qPCR would take 2-3 weeks to complete and analyze. I need to design and order primers, which takes a few days. Most of the reagents for qPCR are easy to obtain.\n-End of quarter: qPCR should be complete (data collection complete)\nWe have read and discussed the above proposal thoroughly and we believe this is an achievable yet challenging project for the student named. We have also discussed how the student will get any needed supplies, etc. for this project.\n(Faculty Sponsor’s Signature) ______________________\n(Printed name of Faculty Sponsor)"

"Hematology / Oncology (Paediatrics)\nTelomere Lengths in Pediatric Acute Lymphblastic Leukamia (ALL)\nShortened telomeres and high levels of telomerase activity are found in different cancers, as compared to normal cells.\nTelomeres are repetitive non-coding nucleotide sequences capping the termini of linear chromosomes. They play a pivotal role in normal cell replication during which they get shorter and shorter.\nA ribonucleoprotein complex, the so-called telomerase, protects telomeres from shortening by promoting their regeneration after cell division. Thus, cell proliferation capacity is greatly dependent on telomere length and telomerase function. High levels of telomerase activity probably allow leukemic cells to continuously replicate despite marked telomeric shortening. For childhood (ALL) and other pediatric malignancies, only very limited data on telomere lengths in different cell subsets is available. Telomere maintenance has become an important target of new therapies and recent studies show antiproliferative effects of genetic and pharmacological telomerase inhibition. In particular, Baerlocher and colleagues have shown that the telomerase inhibitor Imetelstat induces complete hematological remission in the majority of patients with Essential Thrombocythemia (ET).\nIn our study, the pilot phase of which is supported by “Grants-in-Aid” of the DBMR, we are planning to systematically determine telomere lengths from peripheral blood of pediatric patients with ALL at the Division of Paediatric Haematology / Oncology, Department of Paediatrics, Inselspital, Bern University Hospital. Measurements will be performed using multicolor flow-FISH system, a differentiated and sensitive method combining flow cytometry with fluorescence in situ hybridization, allowing analyses of distinct cell subpopulations. This method is established and, as part of a collaboration in this project, accessible in the laboratory of Professor Gabriela Baerlocher at the Inselspital, Bern University Hospital. In addition to measurements at time of diagnosis, we are going to determine telomere lengths and telomerase activity during therapy. This will give us the opportunity to correlate telomere lengths and telomerase activity with other laboratory and clinical parameters, i.e. response to therapy. A long-term goal of this study is to assess the in vitro antiproliferative effects of telomerase inhibition, to develop more targeted therapeutic approaches for pediatric ALL.\nNew therapeutic targets and innovative drug deliveries for pediatric solid tumors\nOur aim is to improve existing therapies and devise novel therapies for pediatric solid tumors, with particular focus on rhabdomyosarcoma.\nThe treatment of tumors in children must meet specific needs, as chemotherapeutic agents can lead to significant long-term consequences. It is therefore the aim of our research to optimize existing therapies by targeting them to the tumor, sparing normal tissues.\nOne strategy is to decorate drug-loaded nanoparticles with molecules that promote tumor accumulation. We are developing approaches based on two well established technologies: liposomes and silica nanotubes. Liposomes are small lipid vesicles, approximately 100 nm in size. Silica nanotubes, are hollow tubes, 30 to 300 nm in length, with an inner diameter of 10-20 nm. Both liposomes and silica nanotubes can be loaded with chemotherapeutic agents.\nOne way to achieve tumor accumulation, is the identification of molecules which bind specifically to tumor cells and thus can concentrate therapeutic agents in the tumor tissue. Peptides or nanobodies that bind specifically to tumors, are a promising possibility. We will develop peptides or nanobodies that bind specifically to rhabdomyosarcoma, the most common soft tissue sarcoma in children. We have optimized the technology to decorate liposomes with these molecules. We are now selecting for the best molecules and will be establishing the optimal conditions to deliver chemotherapeutic drugs in pre-clinical models.\n- +41 31 632 93 37\n- +41 31 63 2 95 21\n- +41 44 63 4 88 06\n- +41 31 632 11 84\n- +41 31 632 93 07\n- Name / Titel\n- Dr. med. Mutlu Kartal-Kaess\n- Deputy Senior Physician\n- +41 31 632 95 23\n- +41 31 632 90 46\n- +41 31 632 55 33"

"Shortened telomere length is associated with increased risk of\nThe powerful and complex impact of telomere dynamics in model organisms and humans reflects the crucial role of telomere function in processes of genomic instability, organ homeostasis, chronic diseases, aging, and tumorigenesis. Telomeres, Telomerase and Cancer An Endless Search to Target the Ends ABSTRACT Maintenance of functional telomeres, the highly complex nucleo-protein structures, at the end of linear eukaryotic chromosomes, appears to be essential for growth and survival of the cells. 2019-10-03 Telomerase therapy is not only unlikely to result in an increased risk of cancer but is likely to lower the risk of cancer compared to age-matched patients not treated with telomerase therapy. Review of available data suggests that cancer should not be considered a significant risk to patients undergoing telomerase therapy, but the actual outcome will require human trials. 2019-06-21 2020-05-31 A video overview of what telomerase is, its function in normal cells and how telomerase activating mutations can lead to cancer.By The Immortal Instruments: Telomerase, an enzyme responsible for the synthesis of telomeres, is activated in many cancer cells and is involved in the maintenance of telomeres. The activity of telomerase allows cancer cells to replicate and proliferate in an uncontrolled manner, to infiltrate tissue, and to metastasize to distant organs. Because these genes coding for telomerase turn off after birth, normal cells do not have this abundance of telomerase in them.This makes it easier for radioactive micro complexes to be used for diagnosing purposes, since these biomarkers will attach to where there is an abundance of telomerase, which is also the likely site of the cancer cells.\n- Goteborgs stadsmission lediga jobb\n- Statistik integrationskurs\n- Visa bulletin\n- Brännskada grad 1 2 3\n- Photoelectron spectroscopy and electron configuration\n- Arbetsträning landstinget\n- Norge ekonomi olja\n- Amal india\n5. Telomerase and Radiosensiticity of Human Tumors; T.K. Pandita. 7. Amplification of hTERT, the Telomerase Reverse Transcriptase Gene in Human Cancers; D. Xu, et al. 8. Telomerase Activity as a Marker of Tumor Cell Survival to Evaluate Sensitivity of Neoplastic Cells to Cancer Treatment; I. Faraoni, E. Bonmassar.\nShortened telomere length is associated with increased risk of\n5 okt. 2009 — En viktig pusselbit – människans åldrande, cancer och stamceller A telomeric sequence in the RNA of Tetrahymena telomerase required for 15 maj 2019 — response against the universal cancer antigen telomerase.\nNya Umeårön om telomerer och åldrande Umeå universitet\nTelomere length was similar in school-age children with bronchopulmonary dysplasia and allergic asthma.\nFOLLOW ON INSTAGRAM :- https://www.instagram.com/drgbhanuprakash/Channel Memberships : https://www.youtube.com/channel/UCG5TBPANNSiKf1Dp-R5Dibg/joinTelomeras\nTelomerase and cancer: revisiting the telomere hypothesis Chantal Autexier and Carol W. Greider Telomerase is a ribonucleoprotein DNA polymerase that elongates telo- meres in eukaryotes. The telomere hypothesis implicates short telomere length and telomerase activation as critical players in cellular immortaliz-\nBecause these genes coding for telomerase turn off after birth, normal cells do not have this abundance of telomerase in them.This makes it easier for radioactive micro complexes to be used for diagnosing purposes, since these biomarkers will attach to where there is an abundance of telomerase, which is also the likely site of the cancer cells. 70%-90% of all cancers have lengthened telomeres\nThe pancreas is an organ that releases enzymes involved with digestion, and hormones to regular blood sugar levels. The pancreas is located behind the stomach, so having pancreatic cancer doesn't involve a palpable mass that you can feel. I\nGlioblastoma is an aggressive cancer of the brain. It is a very fast-growing cancer that spreads quickly. Glioblastoma is the most common type of malignant brain tumor in adults.\nRättsmedicinalverket göteborg jobb\nStuart Wolpert | June 6, 2018. Cancer, aging-related diseases and other illnesses are closely tied to an important Telomerase as a Diagnostic Tool in Clinical Oncology. The near universal expression of telomerase in cancer cells has made this enzyme the most prevalent Apr 25, 2018 In cancer cells, telomerase is turned back on and replenishes telomeres, allowing them to maintain a stable telomere length and live forever. Feb 20, 2012 In cancer, telomerase becomes active during telomere crisis and rescues the genomically abnormal cells by lengthening telomeres.\n2 dec. 2019 — Ändarna av kromosomerna utgörs av en specifik repetitiv DNA-sekvens som kallas för telomerer vilka är viktiga vid cancerutveckling. Sofia\nCancer Epidemiol Biomarkers Prev, 9 dec. 37. Verde, Z. m.\nMona eliasson mans vald mot kvinnor\nAccording to the American Cancer Society, a When cancerous tumors form on connective tissues, it is a sarcoma. Sarcomas can either be bone or soft tissue, with additional sub-classifications depending on the origin of the cells (according to The Sarcoma Alliance). Sarcoma is rare and If breast cancer is diagnosed at an early enough stage, it's treatable. There are a number of different treatments doctors recommend.\nThe recently discovered relationships identified among telomeres, telomerase, aging, and cancer have opened a new avenue in tumor biology research that may revolutionize anticancer therapy. This review summarizes the critical aspects of\n(A) Survival curve summarizing data from mouse models examining the role of telomerase and telomere length in cancer-related survival. It shows a survival advantage for short-telomere mice in a model of Myc-induced lymphoma, according to Feldser et al. (adapted with permission from Cancer Cell ; ref. 91 ). In cancer, telomerase becomes active during telomere crisis and rescues the genomically abnormal cells by lengthening telomeres. In a series of experiments in a lymphoma mouse model, the team found:\nphp mysql insert\njensen gymnasium örebro schema\nmaskiningenjör utbildning skåne\n- 25000 5g phone\n- Statsskuld sverige per invånare\n- Södertörns simskola huddinge\n- Auto records warehouse\n- Ge några exempel på vilka fördelar en konsument har av marknadsekonomi\nKommande avhandlingar - Svensk Förening för Hematologi\n Se hela listan på en.wikipedia.org Telomerase activity, cell proliferation, and cancer Carol W. Greider* Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, 617 Hunterian Building, 725 N. Wolfe Street, Baltimore, MD 21205 Telomerase and telomere length have received a lot of recent attention from the biomedical research community. The can- [Telomerase and cancer]. [Article in Japanese] Oshimura M(1). Author information: (1)Department of Molecular & Cell Genetics, School of Life Sciences, Tottori University. Telomeres progressively shorten with age in somatic cells in culture and in vivo because DNA replication results the loss of sequence at the 5' ends of double-stranded DNA. Telomerase, a eukaryotic ribonucleoprotein (RNP) complex (26– 33), helps to stabilize telomere length in human stem cells, reproductive cells and cancer cells (35, 36) by adding TTAGGG repeats onto the telomeres using its intrinsic RNA as a template for reverse transcription . Recent work has confirmed these observations in both solid and hematopoietic cancers , leading to the proposal that telomerase expression may prove to be an important diagnostic tool as well as a novel target for cancer therapy. Although active telomerase requires the coexpression of both hTR and hTERT components, the RNA component is ubiquitously expressed , and expression of hTERT correlates most closely with telomerase activity in most tumor cell lines, which suggests that it is the 2019-03-08 · Telomerase, the enzyme that reduces telomere shortening in certain cells, is reactivated or increased in more than 90 percent of cancers, found a 2016 study."

"The telomeres at the end of human chromosomes are responsible for safeguarding DNA termini while chromosome replication is taking place. They represent unique structures characterized by a pattern of short tandem repeats rich in guanine that shorten with each cell division.\nShortening of telomeres can also occur as a part of the general stress response that can take place in different pathological states; therefore, measuring telomere length represents an important approach to study the stressed and aging cell, as well as to gain insights into the different mechanisms.\nMethods of measurement\nSouthern blotting and terminal restriction fragment analysis have traditionally been regarded as the gold standard for measuring telomere length. In this technique, a cocktail of common cutting restriction enzymes without recognition sites in the telomeric and subtelomeric regions is used to digest genomic DNA.\nNevertheless, due to its labor-intensive and time-consuming nature, reproducibility problems, as well as the requirement for large amounts of genomic DNA, newer analysis methods based on polymerase chain reaction have been developed. Real-time PCR (qPCR) is the most widely used among them, and the ensuing results show a high degree of correlation with results from Southern blot analyses.\nOriginally developed by Cawton, qPCR technology entails separate polymerase chain reactions to measure telomeres, which are normalized to a single copy gene, yielding a telomere/gene ration as a measure of telomere length. Still, even when performed by experts, there can be a significant variability across laboratories, reflecting measurement variation between aliquots and differential amplification efficiency.\nOther measurement methods use cytometry hybridization techniques, which are designed to measure the shortest telomeres, as well as telomeres from specific chromosomes. The length of the shortest telomere represents a much better indicator of cellular aging than the average telomere length, since cells either die or become senescent once the shortest telomeres are depleted.\nApproaches and challenges in studies of telomere length\nWhen a research study wants to include telomere length in the analysis, the most important steps are thorough evaluation of the research question, sample types, population, timing of analysis, as well as resources that are available in order to choose the most suitable measurement method available.\nOne of the major drawbacks in using telomere length as a clinical measure is its high variability between different individuals, which is determined at birth. Furthermore, shortening with age is more rapid in males than females, and the rates can also differ between various ethnic groups.\nAll these factor limits the usefulness of telomere measurement in cross-sectional studies; thus longitudinal studies measuring actual telomere erosion rates in individuals over times represent more powerful study designs for demonstrating causal effects.\nIn any case, telomere measurement can be used as a tool that, either alone or together with other biomedical and biobehavioral attributes, may have significant implications for preventative efforts, disease monitoring, development of different interventions and, of course, further improvement of our knowledge.\n- Ridout SJ, Ridout KK, Kao HT, Carpenter LL, Philip NS, Tyrka AR, Price LH. Telomeres, Early-Life Stress and Mental Illness. In: Balon R, Wise TN, editors. Clinical Challenges in the Biopsychosocial Interface: Update on Psychosomatics for the 21st Century. Karger Medical and Scientific Publishers, 2015; pp. 92-108."

"New technique detects telomere length for research into cancer and aging.\nTelomeres are the ends of chromosomes, which package genetic information to pass from parents to children. As the cell divides, these endcaps help keep the genetic information stable and prevent the chromosomes from fusing together. But as cells divide, the telomeres shorten and, eventually, trigger DNA damage that in conjunction with other factors can lead to progression of aging and an increased chance of cancer emerging. Now, a study from researchers at the UT Southwestern Medical Center identifies a new method for determining the length of telomeres, the endcaps of chromosomes, which can influence cancer progression and aging. The opensource study is published in the journal BioTechniques.\nPrevious studies show that telomeres help determine whether a cell reproduces accurately. As the cell divides, these endcaps degrade, causing the cell to age, and it is believed this degradation may lead to some aspects of aging in humans. Finding the best and most sensitive methods for measuring telomeres is an important initial step that could eventually enable scientists to encourage healthy cell growth or, in the case of cancer, limit or halt the cell growth. The standard method to measure telomere length relies on Southern blot analysis with radioactively or non-radioactively labeled probes containing several telomeric DNA repeats. However, this approach requires relatively large amounts of genomic DNA, making it difficult to measure telomere length when a limited amount of sample is available. A popular nonradioactive alternative called DIG (digoxigenin) probes requires relatively large amounts of genomic DNA and is less sensitive. The current study generates DIG-based probes to detect both C- and G-rich telomeric DNA strands, which significantly enhance the sensitivity of telomere length measurements.\nThe current study develops a nonradioactive method which uses multiple DIG molecules to increases both the sensitivity and stability of telomere detection. The lab, after applying 3′ fill-in reactions, applied T4 DNA polymerase for DNA blunting in order to remove the additional nucleotide at the 3′ end from the template DNA generated by 3′ fill-in reactions. Results show that this reaction greatly improved the specificity of DIG-labeled telomere probes.\nThe team surmise that they hope to use knowledge of telomeres to slow or stop cells from aging, or to potentially help stop the uncontrolled growth of cancer cells that maintain their telomeres. For the future, the researchers state that they are interested in understanding this cellular aging process to create an ‘immortal cell,’ which could continue to create new cells without degrading and that could have important implications for diseases related to aging, which, in reverse, could accelerate the mortality of cancer cells."

"Researchers from the University of California, San Francisco, and Bio-Rad Laboratories, Inc. are using Bio-Rad’s ddPCR technology with intercalating dye chemistry to provide absolute quantification of telomerase activity.\nTelomeres, the protective structures at the ends of chromosomes, naturally degrade with each cell division. Once they are below a critical length, the cells arrest and become senescent before dying or passing through crisis, incurring additional genomic mutations, and becoming immortalized cancer cells.\nOne of the mechanisms of immortality is the activation of the telomerase enzyme. This enzyme adds a specific sequence of nucleotide repeats to telomeres, thus rewinding the clock and enabling a cell to divide continuously. Researchers are investigating telomerase activity as a biomarker for cancer diagnosis and as a target for anticancer drugs. Measuring telomerase activity more sensitively may enhance our understanding of its role in oncogenesis and other cellular and physiological phenotypes.\nddPCR Technology Enhances the Telomerase Activity Assay\nTraditionally, the telomerase repeat amplification protocol (TRAP) assay measures the presence of active telomerase by measuring the activity of the enzyme on a starting DNA template, which is then amplified by PCR. For samples with abundant telomerase activity, SYBR® Green qPCR assays deliver high throughput and sufficient sensitivity. However, the most sensitive detection method still requires radioactive labeling, laborious polyacrylamide sequencing gels, and densitometry.\nIn the cited study, single-molecule counting of telomerase-extended templates was accomplished by partitioning the sample into droplets followed by PCR amplification and detection by fluorescence droplet reading using Bio-Rad’s ddPCR technology. The study results indicate that ddPCR is significantly more sensitive than traditional TRAP radiography and is also more amenable to high-throughput analysis.\n“This new (ddPCR TRAP) telomerase activity assay demonstrates the ability to quantify telomerase enzymatic activity in droplets,” said George Karlin-Neumann, director of scientific affairs at Bio-Rad’s Digital Biology Center. “The sensitivity of ddPCR technology enables the measurement of telomerase activity in samples below the detection limit of traditional radiographic methods, while also providing a quick and facile method of measurement in cells where telomerase is more highly expressed."

"Polymerase chain reaction (PCR) is a technique used in molecular biology to make millions of copies of DNA.\nPCR is now a common and used in clinical and research laboratories for a broad variety of applications.\nReal- time PCR monitors the process of amplification in real time using fluorescence; not only at the end of\nthe reaction as occurs in conventional PCR Digital PCR is a quantitative method that provides a sensitive\nway of measuring the amount of DNA in a sample. Photomultiplier tube (PMT),\nSiPM(MPPC) and CMOS camera are mainly considered for the fluorescence detection system.\nYOU MIGHT BE INTERESTED IN\nEnter a person’s email to send them a link to this page\nIn order to download the PDF please fill in your details"

"The polymerase chain reaction (PCR) has found wide application in biochemistry and molecular biology such as gene expression studies, mutation detection, forensic analysis and pathogen detection. Increasingly, quantitative real time PCR is used to assess copy numbers from overall yield. In this study the yield is analyzed as a function of several processes: (1) thermal damage of the template and polymerase occurring during the denaturing step, (2) competition existing between primers and templates to either anneal or form dsDNA, (3) polymerase binding to annealed products (primer/ssDNA) to form ternary complexes and (4) extension of ternary complexes. Explicit expressions are provided for the efficiency of each process, therefore reaction conditions can be directly linked to the overall yield. Examples are provided where different processes play the yield-limiting role. The analysis will give researchers a unique understanding of the factors that control the reaction and will aid in the interpretation of experimental results.\n- Biological and biomolecular engineering\n- Mathematical modeling\n- Molecular biology\n- PCR efficiency\nASJC Scopus subject areas\n- Chemical Engineering(all)\n- Industrial and Manufacturing Engineering"

"Polymerase chain reaction (PCR) is a technique used to amplify specific DNA sequences in vitro. The PCR technique, developed in the early 80’s by Kary Mullis, is a highly efficient method of DNA amplification that has numerous applications and has revolutionised molecular biology. The procedure relies on the use of a thermostable enzyme, DNA polymerase, which can function at temperatures more than 90oC. It also depends on the use of oligonucleotides primers that are designed to bind to the 5’ and 3’ sequences on opposite strands of DNA, flanking specific sites of interest. The basic process of PCR amplification involves a cycle of 1) DNA denaturation, 2) annealing of primers to complementary sequences on the denatured DNA strands and 3) extension of the primers along the DNA fragment, by DNA polymerase, to form two new double strands of DNA. This cycle of denaturation, annealing and extension can be repeated many times resulting in selective enrichment of a DNA sequence in a short time. By amplifying the DNA fragment of interest, PCR enables scientists to study DNA that would otherwise be present in amounts that are undetectable. RNA can also be amplified using PCR.\nThe PCR technique has been used widely in clinical diagnostics, forensic science and biomedical research. Since the invention of PCR, the technique has been developed further to enable researchers to quantitatively measure PCR product accumulation as it happens in ‘real-time’. The various methods of real-time PCR all rely on the use of fluorescent reporters which can be automatically detected as the DNA is amplified. Real-time methods of PCR provide a more accurate and reliable measurement of the amplified PCR product."

"- Polymerase Chain Reaction (PCR) is a technique to amplify specific DNA fragments from their DNA template into multiple copies. Kary Mullis first invented the Polymerase Chain Reaction (PCR) technique in 1983. This technique aims to amplify a DNA fragment from its template to produce a large number of copies.\n- The DNA template is obtained from different serological samples present on various substrates, for instance, saliva from a cigarette butt.\nClose-up of white DNA helix\n- Saliva in the cigarette butt consists of proteins, DNA, lipids, and other enzymes. From handling the sample to isolating the DNA template from the sample, different handling protocols and isolation kits are used to extract high-quality DNA yield. The extracted DNA is then amplified using PCR to generate a higher yield of that DNA template.\n- Since the PCR technique is very precise and sensitive, any contamination in the extracted DNA can lead to undesired copies of the expected DNA sample. Hence, care must be taken during the extraction stage to avoid any contamination during the handling and isolation stage.\n- PCR technique has a wide range of applications used across various sectors of medical and biological research laboratories. These applications include paternity testing, DNA profiling in forensic investigations, detecting diseases, biotechnology, species identifications, cloning, etc.\nSteps in Polymerase Chain Reaction\n- Ingredients added in a PCR tube required for PCR reaction are DNA template (target DNA to amplify), two primers (short complementary sequences that attach at the ends of DNA template), Taq polymerase (DNA polymerase to synthesize DNA strands), dNTPs (nucleotides that build to the complementary DNA strand), buffer solution (provides optimum stability to DNA polymerase), and divalent cations (Mg2+ or Mn2+).\n- Taq polymerase is a heat-stable enzyme extracted from the bacterium Thermus aquaticus. The role of this DNA polymerase is to attach the dNTPs (nucleotides) to the single-stranded DNA template to create complementary strands to double-stranded DNA fragments.\n- Primers for a DNA template can be designed with the help of software that assists in determining suitable primers for that DNA sequence. The two primers are specially designed to complement the targeted DNA fragment to make copies. These primers begin to bind from 3’ to 5’ of the DNA template.\n- The primers are designed based on the GC (Guanine and Cytosine) content in the template from the 3’ region. The G and C bases have three H-bonds; therefore, this strong bonding will help the primers to stabilize when binding.\n- dNTPs consists of adenine (A), guanine (G), thymine (T), and cytosine (C). These nucleotides continue to bind to the primary single-stranded DNA after primer annealing. Additionally, ddNTPs (dideoxynucleotide triphosphates) are added for chain termination for DNA Sanger sequencing.\n- When a DNA polymerase anneals a ddNTP at random, the elongation step ceases. This method is utilised for DNA barcoding, majorly used in species identification.\n- Divalent cations, especially Mg2+ from Magnesium Chloride (MgCl2) required to improve the enzymatic activity of DNA polymerase to increase the PCR’s amplification.\nStepwise procedure of PCR’s process\nDenaturation is the first step involving two strands of DNA template being separated or denatured at a high temperature (94-98°C) for 20-30 seconds. This causes the DNA melting to yield a single-stranded DNA template.\nAnnealing is the process of attaching primers complementary to the single-stranded DNA template at low temperatures (50-70°C) for 20-40 seconds.\nFinally, a new DNA strand complementary to the single-stranded DNA template is produced in a 5’ to 3’ direction. The elongation step is also called an extension; upon increasing the temperature (75-80°C), with the help of heat-stable Taq polymerase (a DNA polymerase), it synthesises new DNA strands using dNTPs (deoxynucleoside triphosphates). dNTPs are the building blocks from which DNA polymerase synthesizes new DNA strands.\n- Final elongation\nThis is the last step of PCR’s, where the remaining single-stranded DNA is fully extended for 5-15 minutes at 70-74°C.\n- Final hold\nThis step is optional, where the PCR’s product is kept at 4-15°C for an infinite period as short-term storage of the DNA template.\nClose-up of Transferring pink liquid into tubes,\n- The PCR’s cycle is repeated 25-35 times to produce billions of DNA copies. After the PCRs process, the amplified DNA template (called an amplimer or amplicon), the concentration and quality of the DNA yield are determined via the gel electrophoresis method. The DNA size is identified against the standard size ladder of known DNA fragment size is run alongside the DNA yield in gel electrophoresis.\n- Sometimes, if the primers’ concentration is high, these primers would self-anneal forming primer dimer bands affecting the DNA sequencing. Therefore, a PCR’s clean-up is performed using ExoSAP (Exonuclease I and Shrimp Alkaline Phosphatase) to hydrolyse excess nucleotides and primers.\nTypes of PCR’s\n- There are more than 20 types of PCRs; Real-time PCRs, Multiplex PCRs, Hot Start PCRs, and Reverse Transcriptase PCRs (RT-PCR), to name a few. Real-time PCR is also known as Quantitative PCR. Multiplex PCR is frequently used in molecular biology to amplify multiple targets of the DNA in a single PCR run.\n- The amplified DNA is directly proportional to the concentration of DNA in the reaction, hence providing real-time detection of the analysed PCR products. Hot Start PCRs is a new technique aimed at reducing the number of unwanted PCRs products that occurred due to primer-dimer (two primers bind with\n- each other to create complementary strands) formation at room temperatures. Reverse Transcriptase PCRs is carried out by converting RNA into complementary DNA, which PCRs then amplifies."

"Polymerase chain reaction (PCR) is a robust and familiar technique for genotyping in laboratories around the world for over thirty years. The PCR method is used to create millions of copies of a specific, targeted, fragment of DNA which can then be studied in closer detail. Since 2009, this tried and true technology has been at the core of the genotypic screening process of transgenic organisms created here at InVivo Biosystems.\nWhen used as part of the screening method to detect precise deletions (knockout: KO) or insertions (knock-in: KI) in the genome of C. elegans, the PCR method provides consistent and reliable results. The DNA products created from PCR are frequently analyzed using gel electrophoresis. When these products are run on an agarose gel, the differences in fragment size between mutant and wildtype organisms (as typically seen in KO/KI builds) can be easily visualized. This allows laboratory technicians to quickly and confidently identify potential transgenic candidates for sequencing confirmation of the desired edit.\nUnfortunately, using some of these traditional methods to screen for smaller genomic changes, such as point mutations, can be labor intensive, time consuming, and fraught with inconclusive results (such as false positives and/or negatives). When screening point mutation builds, the resulting PCR product may be the same size for both mutant and wildtype strains. It is no longer possible to differentiate between two different animals by comparison of PCR product size with gel electrophoresis. It is often necessary to employ other, less robust, screening techniques to identify the desired genotypic edit. Allele specific PCR and restriction enzyme digestion are two common alternative screening methods. And while they are proven to work, these tests are often unreliable with difficult to interpret results. This has the potential to cause unnecessary rework, and can delay completion and increase delivery time of the desired transgenic.\nIs there a better way to screen transgenic builds involving small genomic mutations? Perhaps something faster, more robust, and that provides more reliable results?\nHigh Resolution Melt Analysis (HRMA), in contrast, excels at genotypic screening processes for transgenic builds involving point mutations. HRMA is a powerful screening tool that allows for the differentiation between mutant and wildtype PCR products based on their own unique and distinct melting profiles. To perform these assays, we use a real-time PCR detection system and dedicated HRMA data collection software. This allows laboratory staff to monitor the results in real-time as the assay is being performed. This is just one of the many advantages to this screening method.\nFigure 1: HRMA melt curve and melt peak traces as shown using BioRad CFX Maestro software. Homozygous mutant candidates (green trace) with a predicted melting point of 82.5°C as compared to wildtype control samples (blue trace) with a predicted melting point of 86.5°C. Candidates of interest are easily differentiated and identified in real time.\nSimilar to traditional screening, PCR amplification is the first step of the process. However, a fluorescent dye is added to the reaction mix that binds to the DNA product created by the PCR reaction. The resulting PCR product is then precisely heated in small increments, causing dissociation of the DNA fragments. The HRMA software monitors the dissociation and subsequent release of the fluorescent molecules. Variations in the nucleic acid sequences (such as point mutations) between mutant (homozygous/heterozygous) and wildtype fragments will result in distinct melt curves displayed by the software (Figure 1). This allows for easy identification of potential transgenic candidates without the need for time consuming and less reliable screening methods. Additionally, because the HRMA process is not damaging to the DNA product, it is also possible to use the resulting product for sequencing purposes without the need to run another PCR reaction!\nWith all of these advantages over traditional screen methods, HRMA screening allows us to quickly and confidently detect and identify the desired point mutations in our transgenic animal builds. Use of this cutting edge genotyping technology and user friendly analysis allows InVivo to consistently build and deliver accurate transgenic animals to clients for all of their research purposes.\nInVivo Biosystems offers a variety of C. elegans services packages to fit the needs and budget of every lab. Learn more.\nAbout the Author: Preston Kendrick\nPreston joined InVivo Biosystems in 2016 and currently acts as the operations supervisor of the C. elegans transgenic team at the Salt Lake City, Utah location. He received his degree in Marine Science from the University of South Carolina. Preston has over fifteen years of lab experience, working in academia, federal government, and private industry. Most recently he investigated the behavioral and physiological effects of chronic exposure to marine algal toxins using vertebrate models (zebrafish and mice) at NOAA’s Northwest Fisheries Science Center in Seattle, Washington. The work at NOAA also involved an extensive monitoring program for measuring and mapping the spatial and temporal occurrence of algal toxins in over 20 marine mammal species (and sharks!) along the US West Coast and Alaska. Outside of the laboratory environment, Preston enjoys exploring and photographing nature whether by motorcycle, mountain bike, or kayak."

"The polymerase chain reaction, or PCR, is a widely used technique for copying segments of DNA. Due to exponential amplification, PCR can produce millions or billions of DNA copies within just a few hours. In a PCR reaction, a heat-resistant DNA polymerase enzyme amplifies the original DNA through a series of temperature changes inside an automated machine called a thermocycler.\nPCR is a Versatile Method that Revolutionized Molecular Biology\nKary Mullis developed PCR in 1983, for which he was awarded the 1993 Nobel Prize in Chemistry. Being a relatively fast, inexpensive, and precise way of copying a DNA sequence, PCR became an invaluable tool for numerous applications, including molecular cloning, gene mutagenesis, pathogen detection, gene expression analysis, DNA quantitation and sequencing, and genetic disease diagnosis.\nThe PCR Reaction Cycle\nPCR mimics the natural DNA replication process that occurs in cells. The reaction mixture includes a template DNA sequence to be copied, a pair of short DNA molecules called primers, free DNA building blocks called deoxynucleotide triphosphates (dNTPs), and a specialized DNA polymerase enzyme.\nPCR involves a series of steps at high temperatures, requiring a DNA polymerase enzyme that is functional at such temperatures. The most commonly used DNA polymerase is Taq polymerase, named after Thermus aquaticus, the bacterium from which the polymerase was initially isolated. DNA polymerase is unable to synthesize a DNA molecule from scratch, or de novo. Instead, DNA polymerase adds to short DNA molecules, called primers, which bind to the DNA template through complementary base pairing. The primers provide a free 3’ hydroxyl group to which DNA polymerase can attach new dNTPs. There are four types of dNTPs in a PCR, one for each nucleotide in the DNA molecule: dATP, dCTP, dGTP, and dTTP.\nEach PCR cycle consists of three steps: Denaturation, Annealing, and DNA Synthesis.\n- Denaturation. The PCR cycle is initiated by heating the reaction mixture to a high temperature, causing separation of the DNA double helix into two strands. This “melting” process usually occurs at a temperature of 90°C–100°C.\n- Annealing. The reaction mixture is quickly cooled (usually to 50°C–65°C), allowing the two primers to bind to their complementary sequences on the template DNA strands.\n- DNA Synthesis (Primer Extension). The reaction mixture is heated again, this time to a temperature (usually 60°C–75°C) that allows DNA polymerase to extend the primers by adding dNTPs that pair with the bases in the template strand.\nA typical PCR involves 20-40 repeated cycles of these three steps, occurring in the thermocycler. Since the number of DNA molecules is doubled in each cycle, the DNA is amplified exponentially.\nLimitations of PCR\nIf the scientist wants to amplify a specific stretch of the genome, the scientist must know at least part of the target DNA sequence to design appropriate primers. Another potential issue is the nonspecific annealing of primers to partially similar DNA sequences, leading to amplification of non-target DNA. This issue can be controlled by optimizing the reaction conditions. Being a highly sensitive detection method, PCR is also vulnerable to contamination, and even trace amounts of contaminating DNA can cause misleading results. The DNA polymerases used in PCR can be prone to errors. If a mutation happens within the first few cycles, most of the amplified DNA will carry the mutation."

"Polymerase Chain Reaction (PCR) is a biotechnological technique which amplifies a particular sequence of DNA and produces millions of copies of specific gene sequence. Kary Mullis developed this technique in 1938.\nThe basic principle of this technique is that the DNA replicates itself with the help of polymerase enzyme using its bases and the primer sequence. Most of the PCR reactions can amplify the genetic sequence of 0.1 to 10 kbs and this range can be up to 40 kbs. The repeated replication of one particular sequence of DNA provides millions of its copies that can be used in microbiological and molecular researches and in field of forensic science also.\nBasic steps of Polymerase chain reaction (PCR)\nThe basic steps in all the types of polymerase chain reaction are almost the same. These are:\nThese three steps constitute one cycle of replication. This cycle repeats itself for about 35 times to get millions of copy of the initial DNA sequence.\nThe requirements of this process are:\n- Primer sequence to bind to 3’ end of DNA strand from where the replication will start\n- Taq polymerase enzyme that adds DNA bases to the growing strand of DNA and can withstand the high temperature of reaction mixture required to unwind DNA\n- DNA bases & PCR machine that amplifies the gene number\nTypes of Polymerase chain reaction\nHere are some types of PCR that are based upon their type of genetic sequence they amplify and their specificity as well:\n- Reverse Transcribed PCR\n- Multiplex PCR\n- Touchdown PCR\n- Nested and Semi-nested PCR\n- Inverse PCR\n- Quantitative PCR\n1.Reverse Transcribed PCR\nThis type is based upon the principle of reverse transcription of gene that is amplified. So it is basically used to amplify and identify the genomic sequence of viruses and retroviruses that become incorporated in the host genome.\nThe enzyme used in this PCR reaction is RNA dependent polymerase obtained from thermus themophillus bacterial species. Depending upon the type of transcriptase enzyme it can amplify genomic sequences ranging from 1-12 kbs.\nOne of modified form is anchored PCR. In this type both the strands of DNA are amplified using two separate poly dT primers for each of them. In this way a small quantity of DNA template can be amplified.\n2. Multiplex PCR\nThis type is useful for simultaneous amplification of multiple sequences within the same sample. It also has applications for identification of exonic and the intronic sequences in DNA strand.\nDepending upon the number and the type of primer required in the process, it can be classified as:\n- Single Template PCR\nIf a single strand is to be amplified, primers are added both for forward and reverse transcriptions to amplify a specific region within the same template strand.\n- Multiple Templates PCR\nAs indicated by its name, it can amplify multiple template strands by application of multiple primers but in the same reaction mixture.\n3. Touchdown PCR\nIn this type of PCR reaction, the initial or the annealing temperature is kept higher as compared to the standard temperature and this temperature is lowered systematically in each cycle. Moreover, each cycle is repeated twice and the number of repeating cycles is controlled.\n4. Nested PCR\nThis type is based upon the principle of double amplification that is accomplished using two different sets of primers. The principle is that the amplified product of the first primer is subjected to second amplification cycle that applies second set of primer in a separate tube. This second primer basically amplifies a specific region inside the genomic sequence that was amplified.\nBut this process has a disadvantage that it causes contamination of sample when transferred to separate tube for second phase of amplification. Maintaining a high annealing temperature in second phase prevents this contamination.\nSemi-Nested PCR is similar to the nested type but the difference is that three primers are required to complete the process. Two primers are similar as in nested technique and one separate internal polymerase chain reaction is required before the second amplification cycle. This technique is helpful for the detection and amplification of six different genotypes of some viruses like rabies virus.\n5. Inverse PCR\nMainly the polymerase chain reaction needs the identification of the 5’ end of the DNA sequence that is amplified by the enzymes and the primer used in the process. The inverse PCR has the advantage that the enzyme itself can create the known 5’ and 3’ ends of the genetic sequence.\nThis occurs by using restriction endonuclease enzyme that digests the targeted DNA strand at specific restriction sites. Later, by mean of self-ligation, it creates a circular ring of DNA sequence. Cutting the circle by restriction enzyme develops a strand of DNA that has known sequence at both ends and from where the amplification of DNA sequence is done successfully.\n6. Quantitative / Real-Time PCR\nThis type is useful for approximate quantification of the transcripts being amplified by the PCR process, present within the sample. The copies of DNA or c-DNA are quantified and are controlled by this technique.\nAfter the amplification, the researchers observe the results with the help of some fluorescent dye. Also, they may use some labeled probes for this purpose.\nDyes are actually fluorochromes like SYBR Green that upon attachment to amplified DNA sequences cause fluorescence. If the emitted fluorescence increases, it indicated more copies of the genetic sequence in sample.\nSimilarly the genetic probes hybridize with the double stranded DNA and create fluorescence that is directly proportional to the number of transcripts or the copies of DNA that are amplified.\nIn addition to these types, there are many other advanced modifications of PCR techniques and devices as well to enhance the efficiency of this process. Each type has its specificity, efficiency and limitations.\nApplications of PCR\nPolymerase chain reaction is a wonderful technique of biotechnology for research purposes and many others. A few applications are:\n1. Diagnosis of genetic disorders\nGenetic disorders are those which occur due to sudden change in structure of genetic material. These diseases pass on to next generations. PCR is helpful tool to find out the chances of genetic disorders. For instance, screening of genetic disorder is done by using the cells form chorionic villus. This is membrane barrier between mother and the baby. The DNA of fetus when amplifies by this technique helps in detailed analysis and identification of gene mutation.\n2. Genetic fingerprinting\nThis is also named as DNA fingerprinting or DNA profiling. The researchers isolate DNA from cells such as blood, hair or semen samples. DNA fingerprinting basically compares and analyze certain stretches of DNA that are unique in every person. This helps the crime investigation agencies to have a record of DNA fingerprints of the criminals. Similarly, mitochondrial DNA fingerprinting is also a technique to identify the blood relations to maternal side of a person because the only the maternal mitochondria passes on to next offspring.\n3. Diagnostic tests\nPCR can detect various infectious diseases before the serological lab tests. For instance, PCR detects the typhoid fever. Moreover, this is helpful to detect any possible infection in donated blood or a person. Here comes the example of tuberculosis. PCR has its application to find out the compatibility of donor and recipient before the organ transplantation.\n4. Personalized medicine\nThis is a new revolution in medicine and therapeutics that drugs for treatment of disease should design according to his/her genome. Depending on the genome of each person, this medicine will be customized and personalized and so will be its dose.\n5. Detection of environmental pathogens\nPCR helps in detection of various pathogenic particles not only in body of organism but also outside of it. Therefore, this can help in detection of pathogenic bacteria or viruses in water supplies.\n6. A research tool\nThe most significant role of PCR is in research and analytics. This amplifies the minor amount of DNA which the researchers may insert into other organism’s genome. For instance, in genetic engineering experiments of E.coli genome, Human Genome Project. This helps is studying the gene expression in relation to various factors and environmental conditions.\nThis technique is also helpful for archaeological studies. The DNA of dead and extinct organisms is obtained from their fossils and bones and is amplified with the help of PCR for further studies and analysis."

"Polymerase chain reaction, (PCR), a technique used to make numerous copies of a specific segment of DNA quickly and accurately. The polymerase chain reaction enables investigators to obtain the large quantities of DNA that are required for various experiments and procedures in molecular biology, forensic analysis, evolutionary biology, and medical diagnostics.\nPCR was developed in 1983 by Kary B. Mullis, an American biochemist who won the Nobel Prize for Chemistry in 1993 for his invention. Before the development of PCR, the methods used to amplify, or generate copies of, recombinant DNA fragments were time-consuming and labour-intensive. In contrast, a machine designed to carry out PCR reactions can complete many rounds of replication, producing billions of copies of a DNA fragment, in only a few hours.\nThe PCR technique is based on the natural processes a cell uses to replicate a new DNA strand. Only a few biological ingredients are needed for PCR. The integral component is the template DNA—i.e., the DNA that contains the region to be copied, such as a gene. As little as one DNA molecule can serve as a template. The only information needed for this fragment to be replicated is the sequence of two short regions of nucleotides (the subunits of DNA) at either end of the region of interest. These two short template sequences must be known so that two primers—short stretches of nucleotides that correspond to the template sequences—can be synthesized. The primers bind, or anneal, to the template at their complementary sites and serve as the starting point for copying. DNA synthesis at one primer is directed toward the other, resulting in replication of the desired intervening sequence. Also needed are free nucleotides used to build the new DNA strands and a DNA polymerase, an enzyme that does the building by sequentially adding on free nucleotides according to the instructions of the template.\nPCR is a three-step process that is carried out in repeated cycles. The initial step is the denaturation, or separation, of the two strands of the DNA molecule. This is accomplished by heating the starting material to temperatures of about 95° C (203° F). Each strand is a template on which a new strand is built. In the second step the temperature is reduced to about 55° C (131° F) so that the primers can anneal to the template. In the third step the temperature is raised to about 72° C (162° F), and the DNA polymerase begins adding nucleotides onto the ends of the annealed primers. At the end of the cycle, which lasts about five minutes, the temperature is raised and the process begins again. The number of copies doubles after each cycle. Usually 25 to 30 cycles produce a sufficient amount of DNA.\nIn the original PCR procedure, one problem was that the DNA polymerase had to be replenished after every cycle because it is not stable at the high temperatures needed for denaturation. This problem was solved in 1987 with the discovery of a heat-stable DNA polymerase called Taq, an enzyme isolated from the thermophilic bacterium Thermus aquaticus, which inhabits hot springs. Taq polymerase also led to the invention of the PCR machine.\nBecause DNA from a wide range of sources can be amplified, the technique has been applied to many fields. PCR is used to diagnose genetic disease and to detect low levels of viral infection. In forensic medicine it is used to analyze minute traces of blood and other tissues in order to identify the donor by his genetic “fingerprint.” The technique has also been used to amplify DNA fragments found in preserved tissues, such as those of a 40,000-year-old frozen woolly mammoth or of a 7,500-year-old human found in a peat bog."

"Laser PCR®: Lighting the way for Innovation\nLaser PCR® is a patented molecular technology, based on Pulse Controlled Amplification, developed by GNA Biosolutions and designed for time-sensitive molecular applications.\nLimitations of conventional PCR\nConventional Polymerase Chain Reaction (PCR) requires time-consuming, repetitive heating and cooling cycles, typically achieved by a heating block or a stream of air. The poor thermal conductivity of the bulk solution and reaction vessel severely limits heating and cooling rates in conventional PCR, and increases time to result.\nLaser heating of nanoparticles\nIn Laser PCR®, gold nanoparticles are conjugated with nucleic acids and added to a PCR reaction containing a potential target. A laser beam is pulsed through the solution, causing the nanoparticles to absorb light and emit heat within a short range, creating cycles of denaturation, annealing, and elongation.\n1.000.000x shorter PCR temperature ramps\nHeating is localized to the nanoparticles while the bulk solution is held at constant temperature. This allows heating and cooling ramps a million times faster than conventional PCR and accelerates time to results.\nUltrafast time to results\nRealizing the potential of PCR-based molecular applications requires time-sensitive approaches. By achieving ultrafast time to results, Laser PCR® creates new possibilities for molecular applications in point of care testing, infectious diseases, biosecurity and food safety. Laser PCR® accelerates time to results, which can accelerate time to decisions and help deliver the power of molecular technology to multiple industries and environments.\nA variety of detection options are possible with Laser PCR®, including real-time fluorescence detection of hydrolysis probes within 10 minutes."

"The pcr technique can also be used to detect breast cancer, follicular lymphoma, stomach cancer, prostate cancer, wlings sarcoma. Principles and technical aspects of pcr amplification. This document type is operating system independent. Currently, molecular beacons are extensively used to detect the pcr products in digital pcr assays 3. Explain and describe basic features of dna and how it functions in a eukaryotic cell. Pcr and rt pcr description polymerase chain reaction pcr pcr is the enzymatic amplification of a specific dna sequence in vitro9. Make sure to keep the enzymes and dntp stocks on ice when taken outside the freezer. The validation protocol for legionella pcr methods detection.\nPolimerasa, pcr en tiempo real, sybr green, taqman. As mentioned earlier, the exponential phase is the optimal point for analyzing data. This process uses multiple cycles of template denaturation, primer annealing, and primer. Further, many important technical issues have been addressed, including types of pcr template material, pcr optimization, the analysis of pcr products, quality control and quality assurance, variants and adaptations of the standard pcr protocol, quantitative pcr and in situ pcr. Polymerase chain reaction, 122004 5 mgcl 2 the concentration of mgcl 2 influences the stringency of the interaction between the primers and the template dna.\nDigital pcr works by partitioning a sample of dna or cdna into many individual, parallel pcr reactions. If theres time in class, well also mention the sdsproteinase k method. Realtime rtpcr is a multistep protocol that requires. Our goal is to help you understand what a file with a.\nOct 22, 2015 digital pcr is emerging as gold standard method for cnv biogazelle is reference lab for biorads qx100200 droplet digital pcr technology scalable precision and relative sensitivity needle in the haystack more is better high accuracy without calibration excels in quantification of small differences and rare events. Altair feko is a comprehensive computational electromagnetics cem code used widely in the telecommunications, automobile, space and defense industries. Digital pcr and its role in gmo analysis david dobnik department for biotechnology and systems biology national institute of biology ljubljana, slovenia david. It is technically difficult to amplify targets 5000 bp long. Specific synthesis of dna in vitro via a polymerasecatalyzed chain reaction. Pcr file is an altair feko exported ilu preconditioner data. Downloads files from nimagen nimagen innovators in dna tech. See the list of programs recommended by our users below.\nIt can be viewed in web browsers if the pdf plugin is installed on the browser. Pdf converter pdf pdf is a document file format that contains text, images, data etc. Polymerase chain reaction pcr thermo fisher scientific es. Prc to pdf convert your prc to pdf for free online. Acropdf a quality pdf writer and pdf converter to create pdf files. Quantstudio 3d digital pcr system thermo fisher scientific. Pcr or the polymerase chain reaction has become the cornerstone of modern. Powledge it is hard to exaggerate the impact of the polymerase chain reaction. Both cdna synthesis and pcr are performed in a single tube using genespeci. Droplet digital pcr system need for improved methods to validate, diagnose, and monitor copy number variations given the high incidence and clinical impact of cnvs, a precise, rapid, and costeffective method is needed for highthroughput validation of candidate cnv associations and for subsequent routine deployment in diagnostic settings. Polymerase chain reaction, 122004 7 melting temperature of primertemplate dna duplex. Realtime rt pcr is a multistep protocol that requires. In the open with dialog box, click the program whith which you want the file to open, or click browse to locate the program that you want. We strive for 100% accuracy and only publish information about file formats that we have tested and validated.\nThe diagnosis of the tomato variant of pepino mosaic virus. However, if nonspecific pcr products are obtained in addition to the expected product, the annealing temperature should be optimized by increasing it stepwise by 12o c. Pcr, the quick, easy method for generating unlimited copies of any fragment of dna, is one of those scientific developments that actually deserves timeworn superlatives like revolutionary and breakthrough. Kary mullis was awarded a nobel prize for inventing the pcr technique more than 15 years ago in 1993. Polymerase chain reaction pcr university of toledo. At the conclusion of this training, participants should be able to. Colony pcr is a method for rapidly screening colonies of yeast or bacteria that have grown up on selective media following a transformation step, to verify that the desired genetic construct is present, or to amplify a portion of the construct. For mutational analysis, a pair of molecular beacons is designed with one hybridizing to the wild type.\nThis uitlity is portable, hence no need to install. It being a very standard procedure often embedded in kits. Pcr pdf download we would like to thank all contributors and editors for their diligent efforts. Rtpcr reverse transcription pcr, real time pcr used to reversetranscribe and amplify rna to cdna. These one step qrtpcr kits have been formulated for use with. Reacao em cadeia da polimerase pcr artigo khan academy. Generally, pcr amplifies small dna targets 100 base pairs bp long. Pcr is preceded by a reaction using reverse transcriptase, an enzyme that converts rna into cdna.\nIt is used in laboratories around the world in a wide array of applications such as cloning, gene expression analysis, genotyping, sequencing, and mutagenesis. Methods for the detectionquantification of legionella or legionella pneumophila by pcr. It is an open standard that compresses a document and vector graphics. Eef1a1, y b actina sequence accession number e m33581, nm010106 location of amplicon d. Pcr generated the expected dna fragment, 12% agarose or 6% acrylamide gel electrophoresisis employed for size separation of the pcr products. Pcr and rtpcr description polymerase chain reaction pcr pcr is the enzymatic amplification of a specific dna sequence in vitro9. Pcr fundamentals introduction the polymerase chain reaction pcr is arguably the most important technique in the molecular biologists repertoire important enough to win its inventors the nobel prize. In our pcr experiment, we performed a simple boiling step to get the job done. Traditional pcr methods use agarose gels or other post pcr detection methods, which are not as precise.\nKary mullis developed a biochemical technology called polymerase chain reaction pcr which can be used to amplify a single copy or a few copies of a piece of dna across several orders of. Select the always use the selected program to open this kind of file check box. Realtime pcr makes quantitation of dna and rna easier and more precise than past methods. The polymerase chain reaction can be used to amplify both double and single stranded dna. Without their work, this project would not have been possible. Human identification and sample tracking, brochure. Pcr polymerase chain reaction is an invaluable tool for molecular biology research. Digital pcr is emerging as gold standard method for cnv biogazelle is reference lab for biorads qx100200 droplet digital pcr technology scalable precision and relative sensitivity needle in the haystack more is better high accuracy without calibration excels in quantification of small differences and rare events. Digital pcr is a new approach to nucleic acid detection and quantification that offers an alternate method to conventional realtime quantitative pcr for absolute quantification and rare allele detection. Definition and developer the polymerase chainreaction pcr is a molecular biology technique to amplify a single. While we do not yet have a description of the pcr file format and what it is normally used for, we do know which programs are known to open these files. Rightclick a file with the extension whose association you want to change, and then click open with. Since its discovery, multiple adaptations and variations of the standard pcr technique have been described, with many of these adaptations and variations currently being used in clinical, diagnostic and academic laboratories across the world.\nEvery day thousands of users submit information to us about which programs they use to open specific types of files. In order to perform pcr, one must know at least a portion of the sequence of the target dna molecule that has to be copied. Pcr pdf download pcr pdf download pcr pdf download download. Our lab dntp stocks contain 10 mm each of datp, dttp, dctp, and dgtp. In this exercise, you will become familiar with the technique, some of the parameters. In carcinoma of head and neck, pcr technique is used to detect ebv virus in nasopharynx cancer and squamous cell carcinoma in lymph nodes. Colony pcr is a method for rapidly screening colonies of yeast or bacteria that have grown up on selective media following a transformation step, to verify that. Convert prc to pdf online and free this page also contains information on the prc and pdf file extensions.859 701 891 1418 1263 558 713 559 416 502 1232 746 1031 752 372 1224 1416 828 417 1073 1159 1339 1241 1218 1026 1481 735 86 826 1202"

"RT-PCR is one of the most widely used target amplification techniques for detection of HIV nucleic acid. The method entails an initial step of transcribing a portion of the RNA genome into complementary DNA (cDNA) which is then amplified through PCR.\nPCR depends on the Taq Polymerase enzyme. RNA is not an efficient substrate for this enzyme. Therefore, the target of interest (if present) is first transcribed into complementary DNA (cDNA), which can then be amplified.\n- After RNA is released from cellular material through extraction, an aliquot of the extracted sample is added to a reaction mixture which contains reverse transcriptase enzyme, primers specific for the target of interest (in this case, HIV RNA), and nucleotides.\n- If the target is present, primers anneal to the RNA strand.\n- Reverse transcriptase enzyme synthesizes a complementary DNA strand, extending from the primer.\n- The temperature is raised to 95o C, and the RNA/DNA strands are denatured.\n- The temperatures are lowered, allowing primers to anneal to the newly formed cDNA.\n- Polymerase enzyme synthesizes a new DNA strand, extending from the primer.\n- Multiple cycles geometrically increase the number of copies of DNA.\nRT-PCR can be performed as a one- or two-step procedure. In a one-step procedure, the reverse transcriptase is performed in the same reaction tube as the polymerase chain reaction. In a two-step procedure, transcription of the RNA to cDNA is performed first. Transcription occurs between 40o C and 50o C, depending on the properties of the reverse transcriptase enzyme utilized. Products of that reaction are then amplified in a separate reaction."

"Extraction of DNA before its amplification is an essential step for the measurement of any DNA target. It releases the DNA and removes substances inhibitory to PCR that are initially present in the matrix.\nSince we live in the digital era, why shouldn’t a popular method like PCR go digital as well? What is digital PCR (dPCR) and how it is different in comparison to PCR and qPCR, has been explained in the webinar “Why go Digital in qPCR”.\nWill ddPCR replace qPCR technology?"

"Polymerase chain reaction (PCR) is a process extensively applied in molecular biology for generating multiple copies of a particular DNA segment. It was developed in 1985 and has since played a substantial role in molecular diagnostics for forensic identification, genetic diseases, pathogens, and oncogenes. In the past few decades, PCR has progressed from end-point PCR and real-time PCR to its present, advanced version - the accurate quantitative digital PCR (dPCR). Due to the increasing need for a precise, and highly sensitive target quantification, there is a rising interest building towards digital PCR. This can be attributed to the technological advancements in the field, which has made it one of the most accurate, practical, and importantly, affordable technology.\nDigital PCR (dPCR) is the latest biotechnological approach towards the detection of DNA and RNA in samples. Digital PCR is not dependent on a calibration curve, reference standards, or endogenous controls for sample target quantification. It is also an accurate viewpoint for nucleic acid detection and quantification that provides an alternative, reproducible, and a highly sensitive method for traditional real-time quantitative PCR (qPCR), with the use of fluorescent probe-based detection techniques.\nThe functioning of Digital PCR\nDigital PCR functions by segregating samples of DNA and cDNA into separate, parallel PCR reaction wells in such a way that there is one or zero target molecule in each reaction. This is the primary method for conducting digital PCR measurements and is the most crucial step of the process. This method relies on the hypothesis that the sample segregation will follow the Poisson distribution and cause zero or one target molecule in each reaction well. The reaction wells with fluorescent signals contain one target molecules and are considered positive, while the reaction wells with the absence of fluorescence consist of zero target molecule, and are noted as negative. Poisson statistical evaluation is then applied to determine the precise aggregation of the target molecules present in the primary sample.\nThese integrations are especially favorable for micro-fluidic based digital PCR. These methods also provide a broader scope of potential applications for digital PCR, such as early diagnosis and prognosis monitoring, among others.\nAdvantages of Digital PCR\nThere are numerous advantages of digital PCR, including the lessened need to rely on references and standards, and the acquired ability to increase accuracy with the usage of multiple PCR replicates. Digital PCR also allows a higher tolerance to inhibitors. Additionally, digital PCR enables the analysis of complex mixtures, along with the ability of linear detection of small-fold changes. Digital PCR offers augmented sensitivity for the detection of target molecules in limited clinical samples and enhanced multiplexing abilities.\nApplications of Digital PCR\nDigital PCR is employed in several fields of biology and medical sciences, such as molecular medical diagnostics, biology research, including a few branches of ecology. One of the increasingly widespread applications of digital PCR is testing prospective parents testing for genetic carriers for diseases that can get transmitted to children. Digital PCR analysis is similarly crucial to preimplantation genetic diagnosis, where distinct cells of an evolving embryo are tested for transmutations. Digital PCR is also getting adopted for oncological diagnosis for the early diagnosis or detection of possible cancer. Therefore, it is one of the most significant technological break-throughs in the field of medical science.\nFor instance, multiplexed digital PCR was recently deployed by Chinese researchers from the NHC Key Laboratory of Systems Biology of Pathogens, to clinically detect sexually transmitted pathogens, to identify the several agents resulting in sexually transmitted infections (STIs). They succeeded in distinguishing eleven STI-causing agents. This ground-breaking discovery will now help create remedies for STIs, which are a major global health issue.\nCheck Our Research Report for Reference: https://www.wiseguyreports.com/reports/3792077-global-digital-pcr-market-2019-2026\nGet in touch quickly. We are keen to help !"

"Digital PCR detects single molecule amplifications. This is done by splitting the sample into micro-droplets in which single target reactions are monitored. A labeled probe incorporated into each amplification product allows the reactions to be detected and monitored. The number of droplets with amplification is counted to give the total target number of the sample. Small differences in copy numbers can be determined because quantitation is performed on a linear scale. This differs from conventional PCR where amplification is detected on a log scale and small differences target numbers can’t be differentiated. The ability to detect small differences in target number between samples makes this technique valuable in the detection of single nucleotide polymorphisms, gene expression and copy number variations."

"Digital PCR: the most accurate PCR method for assessing the genetic integrity of Stem Cells\nDigital PCR is the most accurate PCR method for assessing the genetic integrity of stem cells through the detection of Copy Number Variants (CNVs).\nAt Stem Genomics, we help you assess the genetic integrity of your stem cell lines with digital PCR-based tests designed to suit your organization and the specific features of your cell lines.\nDigital PCR - A key tool for genomic integrity testing\nDigital PCR (dPCR) is the most accurate PCR method for assessing the genetic integrity of stem cells through the detection of Copy Number Variants (CNVs).\nUsing specific primer sets and fluorescent probes, dPCR amplifies targeted genomic fragments in thousands of individual reactions, thus allowing nucleic acid quantification and detection with high precision.\nThe power of dPCR relies on the random distribution of the sample and assay mixture into a very large number of distinct sub-reactions. Such partition allows multiple simultaneous endpoint PCR amplifications through the measurement and counting of positive (i.e. containing the amplified target) and negative (i.e. without the amplified target) partitions. The term ‘digital’ defines this binary result counting method. Positive reactions, which contain at least one copy of the target DNA fragment, are identified by their fluorescence signal. Comparison of the number of positive and negative reactions allows the target quantification using the Poisson distribution method. Then, the absolute number of molecules present in the sample is calculated by comparison with the results obtained for a reference gene.\nThese features make of dPCR an ideal tool for CNV detection with high sensitivity and precision.\nComparison with quantitative PCR\nAlthough it uses the same amplification reagents as dPCR, quantitative PCR (qPCR) is based on the analysis of a single homogeneous reaction mixture. Therefore, the number of template DNA copies is measured by real-time monitoring of the amplification at the exponential phase of the reaction, providing only a relative CNV quantification.\nMain advantages of dPCR\nThe main advantages of dPCR compared with conventional qPCR methods are:\n• Absolute quantification of nucleic acids without relying on external references (e.g. standard calibration curves);\n• Robustness to variations (thus, dramatic reduction of inter- and intra-assay variability) and tolerance to PCR inhibitors;\n• High precision in CNV detection thanks to reaction partitioning (i.e. small fold differences can be revealed and this can be interesting for the detection of low-frequency mosaic abnormalities)."

"(This webinar was delivered and produced by Bio-Rad)\nDroplet Digital PCR is being used to identify cancer subtypes, optimize drug treatment plans, monitor residual disease, and study tumor evolution. ddPCR offers advantages in the field of liquid biopsies, enabling circulating nucleic acids (cfDNA) and circulating tumor cells (CTCs) to be measured in blood. ddPCR can detect rare tumorigenic mutations in a high background of \"normal\" DNA, routinely down to 0.01% and often further. We will discuss the technique and methods that will enable you to begin your own investigations."

"Overview of Droplet Digital™ PCR Technology\nDroplet Digital PCR (ddPCR™) enables precise, reliable, and highly sensitive quantification of nucleic acids. The technology is based on water-oil emulsion droplet chemistry which fractionates a DNA sample into about 20,000 droplets within a single well. PCR amplification of the template DNA occurs within the individual droplets via specific primers and fluorescent probes, causing the droplets to fluoresce if the target DNA is present. Each droplet is then read in a droplet reader to determine the number of fluorescent and non-fluorescent droplets. These data are analyzed using Poisson statistics to determine the target DNA template concentration in the original sample with extremely high accuracy and precision.\nDroplet Digital PCR for Gene Edit Detection\nGenome editing has become a widely used tool and allows for specific modification of almost any cell’s genome. However, the often low (<5%) frequency of gene edits, in particular for primary or induced pluripotent stem cells, hinders simple and reliable detection by gel- or sequencing-based methods, or requires laborious clonal isolation of edited cells. Droplet Digital PCR is a powerful technology for ultrasensitive detection and quantification of NHEJ- and HDR-edited alleles in heterogeneous cell pools. This rapid, cost-effective method is amenable to high throughput and provides a convenient readout for the detection of edited alleles and optimization of editing protocols."

"Recent events have proven that the world of medicine continues to require reliable testing solutions that can be implemented quickly and on a large scale. Digital PCR provides scientists with the means to carry out high precision genetic analyses, thus improving their testing protocols significantly. It can be used to calculate the abundance of a target molecule based on a dilution factor.\nWhat Is Digital PCR?\nDigital Polymerase Chain Reaction, also known as Digital PCR or DPCR, is the clonal amplification and quantification process of nucleic acid strands using biotechnological refinement. This breakthrough technology consists in the partitioning of samples into microscopic droplets and the induction of a reaction in each droplet through amplification. This technique possesses various advantages over real-time or traditional endpoint methods. Digital PCR, by providing absolute quantification, improves the accuracy of an assay that no longer relies on a standard curve.\nStilla Technologies has developed a unique integrated solution that uses a 3-color detection technique to offer a fast time to result: The naica® system workflow.\nWhat Makes DPCR So Innovative?\nDigital PCR is quite different from other protocols in that it does away with standard curves and delivers sensitive results through a user-friendly, easy-to-interpret panel. DPCR uses an inhibitor-resistant process which is particularly suitable for complex environments where it quantifies nucleic acids reliably by providing an absolute count of DNA or RNA molecules.\nTo achieve this, the constituting elements of a sample are isolated in droplet form and an amplifying reaction is initiated. This process – reveals the presence of the molecule being tested for inside a droplet by emitting a fluorescent signal.\nThis can now all be done digitally thanks to Stilla®’s Crystal Digital PCR™ technology. It utilises microfluidic innovations to integrate PCR in a convenient consumable. By having the sample flow through a network of microchannels and partitioning it into a droplet crystal – a 30,000-droplet array – the procedure can be carried out digitally. The droplets containing amplified targets are then revealed on the imaged crystal. Finally, positive droplets are counted, allowing for the extraction of the absolute quantity of nucleic acids. This PCR solution produces trustworthy data for an unmatched level of confidence.\nWhat Are the Most Prominent Digital PCR Applications?\nDigital PCR assays can be used for a wide variety of testing applications and brings a concrete answer to measurement sensitivity issues. Single cell analysis, sequencing, clinical microbiology, pathogen detection, gene expression analysis … without the reliance on a standard curve, PCR can even be reliably used by non-specialists.\nIn the current context, Digital PCR can be an invaluable tool as it has the ability to detect even low viral loads. In the case of the SARS-CoV-2 pathogen (which is responsible for COVID-19), for instance, the risk of false negative is greatly mitigated even when testing mildly infected patients. Virology is far from being the only field where the sensitivity of PCR solutions is relevant. It can also provide immediately useable information in serology, toxicology, parasitology, haematology, and more.\nAs the PCR technology can be used to monitor the evolution of cancerous cells very effectively, it constitutes a reliable means of utilising liquid biopsy to assess the efficacy of chemotherapy treatments. Highly dependable, PCR allows medical professionals to employ non-invasive testing methods without lowering the quality of the results. Naturally, Digital PCR is not limited to cancer applications and is also indicated to observe the progression of various medical conditions.\nBeing able to identify the presence of pathogens as well as the risks they pose gives scientists the advantage when it comes to developing measures to contain their spread. As previously noted, digital PCR assays, through absolute quantification, can participate in the early detection of a wide array of issues without implying invasive testing. Prenatal screenings or transplant rejection monitoring, for instance, greatly benefit from the implementation of PCR techniques.\nThe applications of Digital PCR are not restricted to the medical field. The advanced detection capabilities of PCR mean that DNA contaminants, water pollutants, genetically modified organisms, and other elements potentially present in environmental samples can be quantified reliably.\nThe food industry is not without its fair share of health concerns. These can derive from poor transparency or a lack of reliable testing. Requirements surrounding genetically modified organisms, drinking water supplies, or organic foodstuff, for instance, demand the precise and quantitative assessment of potential contaminants. Digital PCR provides easily-implementable tools to obtain trustworthy, real-time information on these highly sensitive matters.\nStilla Technologies innovates by making multiplexing technology available to specialist and non-specialist actors in a variety of fields where sensitive DNA detection is of the essence. Their products are paving the way towards the generalisation of genome amplification, gene expression, rare event detection and absolute quantification in areas where they could become instrumental."

"Digital PCR (dPCR) as an enumeration-based quantification method is capable of quantifying the DNA copy number without the help of standards. prepared the unknown samples and quantified them by flow cytometry. In this study, several factors like selection of the PCR master mix, the fluorescent label, and the position of the primers were evaluated for quantifying supercoiled DNA by dPCR. This work confirmed a 16S PCR get better at blend prevented poor amplification from the supercoiled DNA, whereas HEX labels on dPCR probe resulted in robust amplification curves. Optimizing the dPCR assay based on these two observations resulted in accurate quantification AI-10-49 supplier of supercoiled DNA without preanalytical linearization. This result was validated in close agreement (101~113%) with the result from flow cytometry. Accurate DNA concentration measurement that is traceable to AI-10-49 supplier the International System of Units (SI) is very important for producing reproducible measurements in many applications involving DNA analysis. Like many other analytical measurements, accuracy of DNA quantification requires application of high quality reference materials that are certified for its DNA concentration. So far, only a few certified DNA reference materials are available. Enumeration-based quantification does not require such calibration standards, which is of great importance when reliable DNA reference materials are not readily available. In addition, enumeration-based quantification can be utilized to quantify DNA reference materials due to its high precision and theoretical accuracy1,2,3,4. One method of enumeration-based DNA quantification is counting the individual DNA molecule by flow cytometry directly, where in fact the DNA substances are tagged and separately counted inside a standard movement stream4 fluorescently,5. The movement cytometric keeping track of of specific DNA fragments for bacterial recognition was initially reported by a study group at Los Alamos Country wide Lab6,7. Thereafter, many research groups reported the usage of movement cytometric keeping track of for DNA quantification8,9. In ’09 2009, Korea Study Institute of Specifications and Technology (KRISS) was the first ever to report a research method for organized investigation from the analytical efficiency of DNA count-based quantification. Lately, Yoo (15 U/L) limitation enzyme, 10 L of plasmid DNA, and 7 L of ddH2O. Non-enzyme and Non-DNA controls were made by updating the DNA and enzyme with 10 L of just one 1??TE0.1 (10 mM Tris-HCl, 0.1 mM EDTA, pH?=?8.0) and 1 L of just one 1??TE0.1 in the get better at blend, respectively. The enzymatic response was completed for 1 h at 37?C, and inactivated for 15 min at 65?C. After the enzymatic reaction, the DNA was analyzed around the qPCR or dPCR instrument. Agarose gel analysis with fluorescent staining was used to check if the restriction digestion was completed, the electrophoresis image was in Fig. S1 (in supplemental material). Comparison of the PCR grasp mix for the PCR performance To assess the impact of the PCR grasp mix selection on PCR performance of plasmid DNA with different conformations, 3 different plasmid DNA (pBR322, pNIM-001, and pNIM-002) with linearized or supercoiled conformation were analyzed on Roche480 real-time quantitative PCR machine (Roche, Sweden). Three PCR grasp mixes (abbreviations underlined): Gene Expression grasp mix (GE; Life Technologies), 16S DNA Free grasp mix (DF; Molzym) and Environmental grasp mix (EN, Life Technologies) were used. The reaction mixture preparation for each plasmid with 3 different grasp mixes is described in the supplemental material (Table S3). The PCR thermal profiles include a 10 min activation period at 95?C, accompanied by 45 cycles of the 2 measures account of 15 s at 95 thermal?C denaturation and 60 s at 60?C for combined annealing-extension. Quantification of unidentified test by dPCR Digital PCR was quantified in the BioMark Program (Fluidigm, SAN FRANCISCO BAY AREA, CA) using 37 K qdPCR (48??770) integrated IFC controller (Fluidigm, SAN FRANCISCO BAY AREA, Rabbit Polyclonal to VPS72 CA). Three different vials from each AI-10-49 supplier known degree of unknown test, called A1, B1, and C1 were selected for optimizing the DNA focus on the 48 first??770 chip as well as for assay comparison. The response volume was prepared in 5 L made up of 2??DF grasp mix, forward and reverse primer, probe, ROX, and 20??GE loading (see Table S4 in the product material). To minimize the uncertainty from pipetting, the PCR reagents other than DNA template were premixed, and the final reaction mix was prepared gravimetrically by combining the DNA and PCR reagents. The PCR thermal profile was the same as that for the qPCR except for 50 cycles instead of 45 cycles. After marketing from the DNA focus, the rest of the 9 vials (three vials from each level) had been after that quantified by dPCR through the use of Assay I with HEX labeling. Each vial was examined in 5 replicates. The ultimate stock focus for each degree of the test was computed by averaging the 15 measurements of 3 vials altogether. Data Evaluation The stock focus (may be the variety of copies per."

"Advancing Molecular Diagnostics with dPCR\nArticle May 03, 2017\nDigital PCR (dPCR) is an increasingly popular manifestation of PCR that offers a number of unique advantages when applied to preclinical research, particularly when used to detect rare mutations and in the precise quantification of nucleic acids. As is common with many new research methods, the application of dPCR to potential clinical scenarios is also being increasingly described.1\nA recently published study in Analytical Chemistry set out to explore the clinical utility of dPCR. Twenty-one independent laboratories quantified a rare single nucleotide variant using digital PCR with high reproducibility between labs, demonstrating the method’s potential for routine clinical testing. The study was the first to ever look at the reproducibility and highlights several potential advantages of the technique in measuring clinically important mutations.\nTo find out more about dPCR and what this study means we spoke to Jim Huggett, Principal Scientist, LGC, Senior Lecturer, The University of Surrey.\nWhat prompted LGC to conduct this study and what did you find?\nThis study was performed as part of the European Metrology Research Progamme funded project, BioSITrace, which was focused on developing (SI) traceable quantification of biological entities through the concept of enumeration. dPCR has the potential to be a highly reproducible method for the quantification of DNA and this study investigated this reproducibility by comparing the performance of 21 laboratories when quantifying DNA materials containing mutations associated with cancer. The study demonstrated that dPCR was indeed highly reproducible in the absence of a calibrator when measuring these sequences; the vast majority of laboratories got the same result. For the three that did not, this was clearly due to analysis of the results rather than the instrument.\nWhat implications does this study have for the adoption of digital PCR in clinical testing?\nThese findings demonstrate that quantification using dPCR can be reproducible without calibration in this example. This makes it much simpler for laboratories to obtain similar results which are crucial for a clinical test to be applied across different laboratories on large numbers of patients; a major challenge when performing quantitative analysis using qPCR is calibration to ensure harmonisation between laboratories. This study demonstrates that dPCR could have an important role in advancing molecular diagnostics either by supporting qPCR calibration or as a diagnostic method in its own right. I suspect more advanced diagnostic methods demanding improved sensitivity or quantitative performance are going to be needed if the promise of precision medicine is to be maximised.\nDoes it provide all the evidence decision makers need?\nWhile I am not a clinician it is my understanding that clinical decisions are rarely made on a single result. However, for such a methodology to be clinically useful in contributing to such a decision it must ideally be accurate, robust and reproducible. These findings contribute to a growing body of evidence from our group, and others, that suggest dPCR is a robust and reproducible approach that could lend itself to supporting accurate diagnostics in the future.\nLooking into the future can you see any applications that digital PCR may be able to support in a way that qPCR has not been able to?\nYes, areas, where qPCR cannot currently compete, is in the detection of rare genetic variants in cell-free DNA, such as those analysed in this study. Another important question is whether next generation sequencing will eclipse other methods including dPCR. NGS allows you to measure many more mutations than PCR-based approaches and is already the method of choice for genotyping in many clinical laboratories. However, NGS is still under development when it comes to the need for quantification or for more sensitive analyses. Our study demonstrates that dPCR may be a robust alternative. dPCR is also likely to be a valuable tool for ensuring quantitative measurements associated with NGS are accurate even if the later becomes more established in this context.\nAre there any domains that you believe will remain firmly entrenched with qPCR?\nGiven that changes in clinical testing can be compared to an oil tanker altering direction then in the short to medium term qPCR is certainly here to stay. It is relatively cheap, fast, has been developed in high throughput formats as well as point of care and, crucially, is automated, which was a major advantage when it came along. While qPCR and dPCR were invented at a similar time, it was qPCR that was extensively developed whereas dPCR had to wait over 10 years for the advances in microfluidics and emulsions chemistries that make it a practical approach. Had this not been the case then I suspect dPCR would be used far more routinely due to the characteristics demonstrated by our study; so I think dPCR has a lot to offer in advancing molecular diagnostics in the coming years.\nJim Huggett was speaking to Jack Rudd, Senior Editor for Technology Networks.\n1. Huggett, J. F., Cowen, S., & Foy, C. A. (2015). Considerations for digital PCR as an accurate molecular diagnostic tool. Clinical chemistry, 61(1), 79-88.\nWill Microfluidic Cell Culture Fulfill its Long-awaited Potential?Article\nThe first paper ever published on microfluidic cell culture is 19 years old. Microfluidic cell culture has now outgrown its infancy and is about to survive its teenage years. It has matured considerably but still needs to transition from academia into clinics and industry. Will it come of age?READ MORE\nTracking the Heritability of Cell StressArticle\nAs part of work recently published in Science Advances, a team of researchers from the Institute of Systems Biology at Yale University has built a microfluidic device to demonstrate that single cells preserve a memory of their mother's dynamic response to glucose limitation stress for multiple generations.READ MORE\nThe 3D Structure of Telomerase: Uncovering Its Role in Human DiseaseArticle\nResearchers have published the first detailed picture and description of the 3-dimensional molecular structure of telomerase – a discovery that could enable better targeted drug screening and could result in more successful telomerase-related clinical therapeutics.READ MORE"

"Study Demonstrates Potential Importance of Digital PCR in a Clinical Setting\nHERCULES, Calif. — March 14, 2017 — Twenty-one independent laboratories quantified a rare single nucleotide variant using digital PCR (dPCR) with high reproducibility between labs, demonstrating the method’s potential for routine clinical testing, according to a study published in Analytical Chemistry.\nThe study is the first to examine the reproducibility of digital PCR, an approach to quantifying nucleic acids that partitions samples into thousands of smaller reactions, between such a large number of laboratories at different geographic locations. The findings illustrate the inherent potential advantages of dPCR in measuring clinically important mutations, including greater reproducibility and less variability than real-time quantitative PCR (qPCR). In addition, the findings highlight the ability of dPCR to detect relevant rare sequence variants, according to the authors.\n“Digital PCR lends itself to clinical testing where precise and reproducible results are critical not only for interlab data comparability, but also for dynamic testing in the same lab to track disease progression,” said George Karlin-Neumann, co-author and Director of Scientific Affairs at Bio-Rad’s Digital Biology Group.\nThe method permits precise and accurate quantification of nucleic acid concentration by minimizing the variability from common sources of error that can influence qPCR results. These sources include PCR inhibitors that can alter assay efficiency and skew standard curves. Digital PCR also provides absolute quantification of target nucleic acids without the need to establish standard curves, a major source of variability in qPCR.\nThe blinded study was part of the BioSITrace project, coordinated by the Laboratory of the Government Chemist (LGC), a private life sciences measurement and testing company and the UK’s designated National Measurement Laboratory for chemical and biomeasurement. Researchers in 21 laboratories across North America and Europe were asked to use dPCR to quantify copy number concentrations and fractional abundance of a KRAS mutant DNA with a single nucleotide variation (G12D) in the presence of excess wild-type DNA (down to ~0.2% minor allele frequency). The laboratories performed the experiments using Bio-Rad’s Droplet Digital™ PCR (ddPCR™) technology, on either a QX100™ or a QX200™ Droplet Digital PCR System from Bio-Rad. Droplet Digital PCR is Bio-Rad’s proprietary method for performing digital PCR in which a sample is divided into 20,000 water-oil emulsion droplets.\nCancer-derived mutations that differ only slightly from a wild-type sequence present in a sample in large excess are particularly difficult to detect and quantify using qPCR, especially when fractional abundance of the mutant is less than 5%.\nThe results of all 21 laboratories agreed with each other within a rigorously defined margin of error. Though three laboratories initially reported differing results, further analysis revealed methodological error attributed to misclassification of positive and negative droplets rather than measurement error. When the data were reanalyzed according to the recommended guidelines, they generated results consistent with the other 18 labs, validating the potential of dPCR for clinical testing applications.\n“The ability to detect and quantify rare single nucleotide variants is another strength of dPCR and a measurement that is difficult to make at all with conventional qPCR,” said Karlin-Neumann. “So, similar to the Olympics, the inter-lab study attempted a very difficult ‘routine’ that, when done well, scores higher marks than a simpler, safer routine.”\nToward Clinical Adoption of dPCR\nThe study supports a new and more robust approach to nucleic acid analysis to address the reproducibility challenges that have plagued the clinical adoption of other PCR-based platforms.\n“In the short term, I would anticipate digital PCR will be increasingly used as a reference method to improve the harmonization across laboratories,” said Jim Huggett, corresponding author of the article and a Principal Scientist at LGC. “As digital PCR is increasingly used for clinical diagnostics and preclinical research, people will find that they are more easily able to obtain comparable results.”\nFor more information about Bio-Rad’s Droplet Digital PCR technology, please visit bio-rad.com/digital-pcr.\nBio-Rad Laboratories, Inc. (NYSE: BIO and BIOb) develops, manufactures, and markets a broad range of innovative products and solutions for the life science research and clinical diagnostic markets. The company is renowned for its commitment to quality and customer service among university and research institutions, hospitals, public health and commercial laboratories, as well as the biotechnology, pharmaceutical, and food safety industries. Founded in 1952, Bio-Rad is based in Hercules, California, and serves more than 100,000 research and healthcare industry customers through its global network of operations. The company employs more than 8,250 people worldwide and had revenues exceeding $2 billion in 2016. For more information, please visit www.bio-rad.com.\nBio-Rad Forward-Looking Statements\nThis release may be deemed to contain certain forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. These forward-looking statements include, without limitation, statements we make regarding our development and launch of new products. Forward-looking statements generally can be identified by the use of forward-looking terminology such as “plan”, “believe,” “expect,” “anticipate,” “may,” “will,” “intend,” “estimate,” “continue,” or similar expressions or the negative of those terms or expressions, although not all forward-looking statements contain these words. Such statements involve risks and uncertainties, which could cause actual results to vary materially from those expressed in or indicated by the forward-looking statements. These risks and uncertainties include our ability to develop and market new or improved products, our ability to compete effectively, international legal and regulatory risks, and product quality and liability issues. For further information regarding our risks and uncertainties, please refer to the “Risk Factors” and “Management’s Discussion and Analysis of Financial Condition and Results of Operation” in Bio-Rad’s public reports filed with the Securities and Exchange Commission, including our most recent Annual Report on Form 10-K and our Quarterly Reports on Form 10-Q. Bio-Rad cautions you not to place undue reliance on forward-looking statements, which reflect an analysis only and speak only as of the date hereof. We disclaim any obligation to update these forward-looking statements.\nFor more information contact:\nBio-Rad Laboratories, Inc."

"|Send to printer »|\nTutorials : Jun 15, 2008 ( )\nCounting Chromosome Copy Numbers Efficiently\nDigC Is Designed to Analyze CNV in a Single Cell!--h2>\nThe analysis of copy numbers of genetic sequences is of fundamental importance in biology and medicine, and Digital Counting (DigC) is a new method to determine copy numbers at the single-cell level. Researchers at Olympus’ (www.advalytix.com) Advalytix division have applied DigC to detect Trisomy 21 (Down syndrome) from single human fibroblasts.\nDigC, a PCR-based method, is an alternative to FISH-based testing. It integrates with a molecular approach to creating single-cell populations from imperfectly enriched samples. This method has broad applications for noninvasive prenatal testing and other clinical tests that require the determination of copy numbers from single cells such as the detection of deletions or insertions that occur in tumors like retinoblastoma and lung cancer.\nDigC counts the number of genetic copies contained in single cells, especially in the clinically important 0–5 range. The method is related to digital PCR in that the DNA sample is diluted and aliquoted into compartments such that, on average, there is less than one copy per compartment before PCRs are run in each compartment. That way, the traditional qPCR approach of quantifying the copy number of a genetic sequence from an analog amount of amplified material is converted into adding up the number of positive, digital PCR results from each compartment.\nThe key difference between DigC and digital PCR is that DigC starts with a single cell, while digital PCR starts with extracted DNA from a larger, unknown number of cells. This means that DigC requires few parallel reactions and results in a plain copy number, not a ratio from which a copy number can be inferred. A key requirement for the accuracy and efficiency of DigC is a sensitive amplification directly from single cells with a low drop-out rate. The platform used in this experiment to deliver the requisite low drop-out rate consists of Advalytix’ AmpliGrid, a surface-structured glass slide with 48 individual 1 µl reaction sites, and AmpliSpeed, the thermal cycler for AmpliGrid slides.\nPrenatal genetic testing (PGT) refers to all the techniques that screen or diagnose fetal genetic defects. PGTs fall into two groups: invasive tests such as amniocentesis and chorionic villus sampling and noninvasive tests based either on cell-free DNA or RNA or the direct analysis of fetal cells in maternal circulation (CFC). Given the medical risks associated with invasive PGTs, a lot of attention is focused on the development of noninvasive tests.\nThe challenges that have to be resolved to bring a noninvasive PGT to market fall into two categories: the enrichment of fetal cells in maternal samples and the genetic analysis of a small number of fetal cells available in enriched samples that may also contain maternal background cells.\nWhile recent advances have improved enrichment purity, consistently achieving 100% pure fetal cell samples remains a challenge. In order to produce 100% pure fetal cell samples from enriched samples that may contain up to 95% maternal cells, the Advalytix team is developing a “molecular last mile” that uses a variation of standard forensic identification techniques to precisely identify fetal cells. Using this method, 100% pure fetal samples will be available for DigC analysis.\nHow DigC Works\nUsing flow sorting or micromanipulation, cells are placed one-by-one on the AmpliGrid slide’s reaction sites and analyzed by DigC. Figure 1 depicts a stable (nondividing) haploid cell such as a sperm cell that contains one set of chromosomes with one chromatid each. Restriction enzymes are pipetted onto the single cell to fragment its chromosomes. Then the AmpliSpeed thermocycler heats up the AmpliGrid slide to denature the DNA. This produces two single-stranded DNA templates from each sequence, depicted as red, yellow, blue, and green fragments. A 4-plex PCR reaction mix is added and the entire volume is aliquoted into four subreactions across the AmpliGrid.\nThe 4-plex PCR, specific for the red, yellow, blue, and green fragments, is run and then the products are analyzed by gel or capillary electrophoresis. Since the chromatid of the haploid cell has been denatured into two strands, studying the illustrative gel bands in Figure 1 should show 0, 1, or 2 bands of each color:\n• 0 if none of the fragments were amplified correctly (they were drop-outs)\n• 1 band, if either there was a drop-out or both colors happened to end up in the same reaction site\n• 2 bands, if both reactions worked and the fragments took part in separate reactions.\nNote, then, that if all of the bands corresponding to a color across all four sub-reactions are added up and more than two bands are obtained, there has to be more than one chromosome present in the cell. The chromosome corresponding to the surplus color must have been aneuploid. The inverse, however, is not true; observing two or fewer bands does not rule out aneuploidy. A drop-out of a surplus fragment would cause a false declaration of the corresponding cell as normal. This explains why an extremely low drop-out rate is required for accurate tests based on DigC.\nFigure 2 shows actual results from analyzing stable (i.e., nondividing) diploid and triploid fibroblasts from a human cell line. An 8-plex reaction was used; that is eight independent sequences located on chromosome 21 were redundantly amplified and the reaction mix across eight subreactions was divided (one gel band per reaction).\nA stable diploid cell has two copies of chromosome 21 with one chromatid each, that means that after denaturing researchers expect to see a maximum sum of four copies of each genetic fragment across all eight reaction sites (Figure 2, upper gel image). If more are seen, then the cell must have been triploid. This is exactly what is observed in Figure 2 (lower gel image); the second to last band occurs five times. Thus the corresponding chromosome is diagnosed triploid.\nThe stochastic probability of a false negative such as not finding five or six bands for a triploid cell is 20% for this 8-plex/8 sub-PCR setup. In an analysis of 40 triploid human fibroblast cells, a false negative rate of 23% was observed, very close to the stochastic prediction.\nExperimental false negative rates are expected to be slightly higher than stochastic predictions due to a small amount of drop-outs. Increasing the degree of multiplex and/or number of subreactions quickly reduces the expected false negative rate. The same 8-plex reaction spread across 12 sub-PCRs theoretically achieves <2% false negatives; increasing the multiplex degree to 24 and spreading across eight sub-reactions predicts a false negative rate <1%.\nDigC has been successfully applied to Trisomy 21 detection and can be extended to diagnose other genetic disorders. By varying the multiplex grade and the number of reaction sites, test accuracy can be engineered to a wide range of specifications.\n© 2013 Genetic Engineering & Biotechnology News, All Rights Reserved"

"|Send to printer »|\nTutorials : May 1, 2012 ( )\nDigital PCR: Improving Nucleic Acid Quantification\nPrecision, Accuracy, and Sensitivity Are Among the Benefits Reported by Researchers!--h2>\nResearchers at Harvard Medical School are studying the differences in human genomes to identify the genes underlying biological processes and human disease. One of the researchers, professor Steve McCarroll, is analyzing the copy number variations (CNV) of genome segments from tens to hundreds of thousands of base pairs long. This requires the ability to measure the precise copy number of these segments in thousands of individuals.\nUsing technologies such as real-time PCR (qPCR) and comparative genomic hybridization arrays, the McCarroll lab could measure simple deletions and duplications—changes in copy number from two to one or zero, or from two to three or four. But what they lacked was the ability to precisely and reproducibly measure copy numbers greater than four.\nBio-Rad Laboratories’ QX100 Droplet Digital PCR (ddPCR) system provides an absolute measure of target DNA and RNA molecules. It can be used to discriminate small-fold differences in copy number, enabling researchers to measure 1, 2, 3, 4, 5, 6, or more copies.\nWhereas qPCR quantifies nucleic acids by comparing the number of amplification cycles and amount of PCR end-product to those of a reference sample, ddPCR enables researchers to directly quantify nucleic acids. In other words, ddPCR does not require the use of a standard curve.\nAlthough qPCR is a viable detection strategy when mutant and wild-type sequences are mixed, its effectiveness declines when the mutated sequence is relatively rare, such as in myleoplastic syndromes (<20–25%).\nDroplet Digital PCR separates samples into 20,000 droplets, and reactions are carried out individually in each. This reduces background interference for more reliable and sensitive measurement of low concentrations of nucleic acid that may not have been detectable using qPCR.\nHow ddPCR Works\nDroplet Digital PCR takes advantage of simple microfluidic circuits and surfactant chemistries to divide a 20 µL mixture of sample and reagents into 20,000 droplets with target and background DNA randomly distributed among them. These droplets support PCR amplification of single template molecules using assay chemistries and workflows similar to those for qPCR applications (i.e., TaqMan).\nAfter PCR amplification occurs, a reader determines which droplets contain a target and which do not. Software calculates the concentration of target DNA as copies per microliter from the fraction of positive reactions using Poisson statistics.\nIn digital PCR, having more partitions provides greater precision and resolution for detecting small concentration differences. Sample partitioning to levels above 10,000 allows for extremely accurate Poisson correlations and substantial enrichment effects when screening for rare events. The QX100 is the only digital PCR system that generates uniform droplets to partition a target sample. Others use microfluidic chips, which are challenging to scale to higher partition numbers per sample while maintaining low costs.\nThe arrival of qPCR revolutionized the field of gene expression, becoming the predominant technology for this type of research. With improved instrumentation and high-quality reagents, researchers are now able to report gene-expression levels varying at very fine amounts.\nUnfortunately, resolution at levels below 50% are difficult to achieve due to the compounding of errors derived from each step in the quantification process. From a qPCR perspective, these include the dependence on a standard curve for amplification efficiency determination, standard error of this curve, technical replicate variation, normalization to reference genes (each of which carries previous errors), and comparisons between samples (e.g., normal and treated) that carry all these errors. Low expression targets tend to demonstrate greater variability between replicates due to the larger number of cycles required for amplification.\nDroplet Digital PCR alleviates the compounding error effect, as readings are absolute; quantification is precise due to the digital nature of the assay and the fact that no standard curve is required. Normalization to multiple reference genes should still be performed (according to the MIQE guidelines) but here again, all values for these are standalone and not dependent on other samples or references, minimizing carried errors. Additionally, as a result of this independence, when quantifying samples on different plates, different dates, or in different labs, the use of normalizing reference samples is no longer required.\nCopy Number Variation Determination\nCNVs include deletions, insertions, duplications, and complex amplifications. The accelerated discovery of CNVs has increased the need for high-throughput, low-cost options for validation and follow-up studies.\nTraditional high-throughput technologies such as comparative genomic hybridization and single nucleotide polymorphism (SNP) arrays lack resolution and the ability to discriminate copy number differences of less than 50%. Quantitative PCR experiments require dozens of technical replicates for each target and reference gene in order to statistically discriminate between higher order variations.\nThe high resolution made possible by sample partitioning and digital analysis in ddPCR provides the precision necessary to resolve higher-order copy number states, making the QX100 ddPCR system the ideal solution for CNV validation while delivering the necessary throughput and cost efficiency.\nEmploying ddPCR, researchers have been able to completely resolve CNVs, distinguish less than 50% differences in gene copy, and accurately count genes that differ by only one nucleotide. For the HapMap MRGPRX1 sample, copy number states from 1 up to 6 were completely resolved (Figure 1).\nRare Event Detection\nRare events include single nucleotide mutation, alteration of copy number, and deletion or insertion of nucleotides. These genetic variant molecules are difficult to detect due to their dilution by normal cells from either tissues or bodily fluids such as blood. Early detection of rare events can make all the difference in the outcome of cancer patients, as well as lead to more sensitive and less invasive diagnostics.\nDuring qPCR, rare and normal variants of DNA molecules are amplified at an equivalent rate. If the normal gene is initially present in 100-fold abundance over the mutated gene, at the end of the reaction, 1% of the total amplification product will be the mutated gene amplicon. Its detection will be extremely difficult as the total signal generated will be 1% of that generated by the wild-type gene amplicon.\nFor rare event detection, sample partitioning increases sensitivity by distributing both mutant and normal genes into a large number of isolated reaction compartments. In each one of these isolated droplets, the rare mutant molecules are now at a more favorable ratio compared to the wild-type, and thus become detectable within that individual droplet. The QX100 can detect amplifications even in highly heterogeneous matrices where only a fraction of the cells are affected. This precision enables the detection of somatic copy number alteration—the hallmark of many cancers.\nThe detection of point mutations requires a high degree of sensitivity. Droplet Digital PCR allows the detection of 0.001% mutation fractions, as demonstrated in a duplex PCR reaction using TaqMan probes targeting the BRAF 600E mutation (Figure 2). This detection limit is more than 1,000 times lower than qPCR.\nLooking Ahead with the McCarroll Lab\nWhen McCarroll’s lab acquired the QX100 ddPCR system, they immediately began using the instrument to study structurally complex regions of the genome—regions that have historically been influenced by many different structural mutations. In such regions, ddPCR has allowed them to quantitate copy numbers in large populations, which is important in both population genetic analysis and disease analysis. Now they can analyze these regions in the same high-quality, high-precision way that is the standard for genetic analysis of simpler kinds of variation such as SNPs.\n© 2016 Genetic Engineering & Biotechnology News, All Rights Reserved"

"Definition of Waardenburg syndrome\nWaardenburg syndrome: A genetic disorder that causes deafness, white forelock (a frontal white blaze of hair), a difference of color between the iris of one eye and the other (heterochromia iridis), white eye lashes, and wide-set inner corners of the eyes.\nThe deafness is typically congenital (present at birth), bilateral, profound sensorineural (nerve) deafness. The severity of Waardenburg syndrome (WS) varies and about 40 percent of affected persons escape the deafness. The white forelock may be present at birth. The majority of individuals with WS have the white forelock or early graying of the scalp hair before age 30.\nWS is inherited in an autosomal dominant manner in which the heterozygous state (with one copy of the gene) is sufficient to cause the syndrome. The homozygous form of WS with two copies of the gene is a very severe (and fortunately rare) disorder with very severe upper-limb defects that has been called the Klein-Waardenburg syndrome.\nThe gene for classic WS, symbolized WS1, is on chromosome 2 (in band q35) and is the PAX3 gene which encodes a DNA-binding transcription factor that is expressed in the early embryo. The syndrome is named for a Dutch eye doctor named Petrus Johannes Waardenburg (1886-1979) who first noticed that people with differently colored eyes often had a hearing impairment.\nLast Editorial Review: 8/28/2013\nBack to MedTerms online medical dictionary A-Z List\nNeed help identifying pills and medications?"

"Waardenburg syndrome is a genetic condition which affects the color of a person’s eyes, skin, and hair.\nIt is most often inherited as an autosomal dominant trait. This actually means that only 1 parent has to pass on the faulty gene for a child to have WS.\nThe syndrome is named after Petrus Johannes Waardenburg, a Dutch ophthalmologist, who first described a patient with dystopia canthorum, hearing loss, and retinal pigmentary differences.\nWS causes 1 to 3% of cases of congenital deafness and affects approximately 1 in 42,000 people.\n- type 1 – it causes someone to have a wide space between their eyes;\n- type 2 – the symptoms are similar to type 1, including changes in the pigment of the skin, hair, and eyes, but hearing loss is more frequent in type 2 WS than type 1, with around fifty percent of suferrers losing their hearing;\n- type 3 – it is characterized by facial, eye, and hearing abnormalities;\n- type 4 – it is the association of WS with congenital aganglionic megacolon which affects 1 neonates per 5000 births.\nNote – types 1 and 2 are the most common forms of WS, while types 3 and 4 are rare.\nCommon signs and symptoms of WS include:\n- cleft lip, mostly associated with Type I;\n- eyes with one iris having two different colors;\n- eyes of two different colors;\n- brilliantly blue eyes;\n- very pale;\n- neurologic manifestations, linked with Type IV;\n- premature graying of the hair;\n- a forelock of white hair (poliosis);\n- abnormalities of the arms, linked with Type III;\n- a low hairline and eyebrows which meet in the middle;\n- moderate to profound hearing loss (linked with Type II);\n- the appearance of wide-set eyes due to a prominent, broad nasal root (linked with Type I).\nPossible complications of WS can include:\n- cognitive problems;\n- problems with self-esteem due to abnormal facial appearance;\n- severe constipation requiring removal of a portion of the large bowel;\n- severe hearing loss.\nIn most cases, WS type I and type II are inherited as autosomal dominant traits with variable expressivity and penetrance.\nWS type I and type III are caused by mutations in the PAX3 gene. Mutations in the EDN3, SOX10, or EDNRB gene can cause WS type IV.\nIn order to diagnose WS, the treating health care professional may order the following tests:\n- genetic testing;\n- colon biopsy;\n- bowel transit time;\n- audiometry testing to look for hearing loss.\nThere is no cure for the syndrome, but it can be managed. The hearing should be checked closely. In addition, special medicines and diets to keep the bowel moving are prescribed to patients who have constipation.\nList With 4 Famous People With Waardenburg Syndrome:\n1) Camren Bicondova (Catwoman)\nShe is an American dancer and actress who is best known for her role in the television show Gotham, where she plays a young Catwoman (Selina Kyle).\nCamren was discovered by Chris Stokes, a film director who put her in his musical ”Battlefield America.”\nIn September 2015, Bicondova was listed in Variety’s annual Youth Impact Report, as a female artist who “represents the next wave of Hollywood talent and savvy.” She also earned a Saturn Award nomination for best performance by a young actor in her impressive role in the Gotham.\nCamren Bicondova has Waardenburg’s Syndrome. Due to this syndrome, she has some unique facial features.\n2) Stef Sanjati\nStef Sanjati is a transgender woman who lives with WS. His birth name is Stefan, and, according to ”GoFundMe,” his current legal name is Stephanie Luciana Peloza.\nIn December 2016, he underwent facial feminization surgery. However, Stef Sanjati did not allow her surgeon to alter any of her WS facial characteristics. Interestingly, Stef vlogged the whole healing process on his YouTube channel.\nCurrently, his YouTube channel has more than 590,000 subscribers, who are collectively known as the Bread Squad due to Stef’s love of bread.\nSanjati also responded with a video called ”My face: Waardenburg syndrome,” that went viral and has over 8.9 million views.\n3) Mila Kunis\nShe is an American actress who appeared in a few television commercials and series, before acquiring her first important role at age 14, playing series That ’70s Show as Jackie Burkhart.\nIn 2012, Kunis co-starred with Mark Wahlberg in a comedy called ”Ted,” that was directed by Seth MacFarlane. In 2010, Mila starred alongside Natalie Portman in the thriller ”Black Swan.”\nKunis is presently married to actor Ashton Kutcher. Some sources claimed that she also has Waardenburg syndrome.\n4) Paris Jackson\nShen is the second child and only daughter of pop superstar Michael Jackson. She was born on April 3, 1998, in Beverly Hills, California and was named after the French city in which she was conceived.\nIn 1999, Debbie Rowe, her mother, signed custody of the children over to Michael after their divorce.\nIn 2009, Jackson attended the function Michael Jackson Memorial, a tribute to her father. In May 2012, Paris made People Magazine’s Most Beautiful list.\nIn June 2012, she also made a guest appearance on the Oprah Winfrey Show, where she discussed her experience as a victim of cyberbullying.\nParis Jackson’s blue eyes are due to a rare eye condition, however, the specific condition has not been confirmed; there is a chance it is the Waardenburg syndrome.\nSources https://jmg.bmj.com/content/jmedgenet/34/8/656.full.pdf https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4575665/ http://www.ovpjournal.org/uploads/2/3/8/9/23898265/ovp1-6_article_khanal https://journals.lww.com/plasreconsurg/Citation/1976/07000/Waardenburg_syndrome"

"Waardenburg syndrome (WS) is a group of genetic conditions characterized by varying degrees of hearing loss and differences in the coloring (pigmentation) of the eyes, hair, and skin. Signs and symptoms can vary both within and between families. Common features include congenitalsensorineural deafness; pale blue eyes, different colored eyes, or two colors within one eye; a white forelock (hair just above the forehead); or early graying of scalp hair before age 30. Various other features may also be present. WS is classified into 4 subtypes (types 1, 2, 3 and 4) based on whether certain features are present and the genetic cause. Mutations in at least 6 different genes are known to cause WS, and it may be inherited in an autosomal dominant (most commonly) or autosomal recessive manner. Treatment depends on the specific symptoms present.\nLast updated: 2/10/2016\nWhat is Waardenburg syndrome type 2?\nWaardenburg syndrome type 2 (WS2) is a type of Waardenburg syndrome characterized by varying degrees of deafness and pigmentation (coloring) abnormalities of the eyes, hair and/or skin. WS2 differs from WS1 and some other types of WS by the absence of dystopia canthorum (lateral displacement of the inner canthi of the eyes).Sensorineural hearing loss occurs in the majority of people with WS2, and heterochromia iridis (differences in eye coloring) occurs in about half. WS2 may be caused by changes (mutations) in any of several genes, but in many cases the genetic cause is unknown. While inheritance is usually autosomal dominant, sometimes WS2 is not inherited, occurring for the first time in someone with no family history of the condition. Treatment may include the use of hearing aids and/or cosmetic products (if desired) for skin hypopigmentation.\nWaardenburg syndrome type 2 can be further divided into subtypes based on the genetic cause, when it can be identified.\nLast updated: 6/28/2016\nWhat are the signs and symptoms of Waardenburg syndrome type 2?\nWaardenburg syndrome type 2 (WS2) is characterized by varying degrees of deafness and pigmentation (coloring) anomalies of the eyes, hair and skin, but without dystopia canthorum (lateral displacement of the inner canthi of the eyes). Sensorineural hearing loss is present in the majority of people with WS2 (almost 80%), and heterochromia iridum (differences in eye coloring) is present in almost half. In some people, particularly those with WS type 2E, signs of Kallmann syndrome are present.\nLast updated: 6/28/2016\nIs the hearing loss in individuals with Waardenburg syndrome type 2 likely to be progressive?\nAfter an extensive search of the medical literature, we were only able to find one journal articlet hat directly addresses this topic. According to this article, it appears as if, in contrast to Waardenburg syndrome type 1 in which the hearing loss is typically non-progressive, there is some evidence that the hearing loss in Waardenburg syndrome type 2 is progressive. Since the information on this topic is quite limited and somewhat dated, we strongly recommend that you discuss your concerns with your healthcare provider.\nLast updated: 10/19/2011\nWe hope this information is helpful. We strongly recommend you discuss this information with your doctor. If you still have questions, please\nHildesheimer M, Maayan Z, Muchnik C, Rubinstein M, Goodman RM. Auditory and vestibular findings in Waardenburg's type II syndrome. J Laryngol Otol. December 1989; http://www.ncbi.nlm.nih.gov/pubmed/2614228. Accessed 10/19/2011."

"Among the numerous problems that today afflict the African continent, it is possible to note that Albinism is particularly relevant and heavily affects the lives of many people, particularly in Sub-Saharan African countries.\nAs shown in this article several measures have been taken in order to preserve the lives of people with Albinism; in order to better understand this situation, firstly we will focus on the analysis of albinism; secondly we will analyze the conditions of albinos in Africa, with a focus on Tanzania and finally we will verify the measures taken in favor of this category of people.\n1. What is Albinism?\nAlbinism is a rare, non-contagious, genetic condition that limits the body’s ability to process melanin, reducing or eliminating pigmentation in the skin, eyes and hair; it’s a lifelong condition and does not cause intellectual disabilities. This condition occurs if both parents carry the albinism gene, in which case the probability of having an affected baby is 1 in 4 (25%); this possibility is the same in every pregnancy, having no relation to other births.\nMany children with Albinism have blue or brown eyes, occasionally the eyes might appear pink or reddish, because of very little color in the iris; because of these conditions and due of poor health and poor vision many children usually abandon schools. People with this condition are considered legally blind because their photoreceptors are unable to appropriately convert light into clear signals to the brain, leading to a condition called nystagmus, having also problems with reduced depth perception and with tracking an object with their eyes. Albinism occurs globally, in all gender, racial and ethnic groups affecting 1 person in 18,000; estimations of affected people as part of the local population vary from region to region, even though the highest rate is in Sub-Saharan Africa with an estimated 1 person in 1,400 people in Tanzania\n2. The condition of people with albinism in Africa\nDiscriminations and attacks on people with albinism are particularly frequent in sub-Saharan Africa because of superstitious myths surrounding their nature. Albinos in these regions are often avoided by their communities and viewed as non-human spirits or ghosts; some believe that minerals contained within albino body parts bring wealth and luck, leading to dismember and kills of many albinos, including infants and children.\n“In some communities, erroneous beliefs and myths, heavily influenced by superstition, put the security and lives of persons with albinism at constant risk,” states the United Nations website. “These beliefs and myths are centuries old and are present in cultural attitudes and practices around the world.”\nAlbino body parts such as teeth, bones, genitals, and thumbs have been used in rituals by traditional healers and witchdoctor, who say they promote health, riches and success; these body parts, consumed as “medicine” or carried around for good luck, are dried up, ground, and packaged for illegal trade. According to a 2013 UN Report, some believe albino body parts are more potent if the victims scream intensely during amputation.Moreover, there are superstitions in some parts of Africa that albino body parts bring power, wealth or sexual conquest, that having sex with a person with albinism cures HIV and AIDS. Furthermore, some believe that albinism is contagious and can be spread through touching, that their mothers were impregnated by a white man, that people with albinism have a low IQ and that they are housed by the ghosts of the European colonists\nThe Office of the UN High Commissioner for Human Rights stated in 2016 that albino hunters sell an entire human corpse for up to $75,000, while an arm or a leg could fetch about $2,000; related to that is also common that Albino graves are dug up and desecrated to procure body parts. There are very few health services in Africa focused on people with albinism, and many of those people cannot afford neither sunscreen nor protective clothing.Identified areas requiring both governmental and societal intervention include healthcare, advocacy and social awareness education, social inclusion, academic education, economic empowerment and socio-political protection from various forms of societal abuse and discrimination.\n3. The Tanzanian case\nAs we have already seen, Tanzania has a high albinism rate (1 person in 1,400 people) that related to the high poverty of the country, (in which 80% of the population lives with less than $1.50 a day) makes life very difficult to people with Albinism, especially because of the cost of sunscreen, that is around $10, $15; furthermore, a very high number of Albinos murders have been recorded in this country, reaching 80 people since 2000, becoming one of the most dangerous countries for people suffering from this pathology.\nFollowing increased international inquiry at the end of the 2000s, Tanzania began to utilize resources to cope with traffickers and protect people with albinism; in order to do so since 2007 hundreds of children were removed from their families, sometimes without any consultation or consent, and placed in shelters where they were isolated from society; according to activists who spoke to Human Rights Watch, orders from the government to protect people with albinism were enforced by district commissioners, who oversee security in their respective districts being also responsible for their safety. The Tanzanian government also tackled impunity for ritual crimes, notably by investigating, arresting and prosecuting those who attack or sponsor attacks against people with albinism; in 2015, it announced a ban on witchdoctors, leading to over 200 suspects who were reportedly arrested by the authorities. After ten years from the begin of the wave of killings and attacks these appear to have decreased, because of Tanzania’s stronger response to ritual crimes and attacks and protective measures, although these holding shelters are a temporary solution: “The shelters were emergency, temporary solutions. But 10 years is not temporary anymore,” an activist for the rights of people with albinism told Human Rights Watch.\n4. Measures in favor of people with albinism\nIn 2017 the European parliament (EP) stated a resolution on situation of people with albinism in Malawi and other African countries:\n1. ” The EP remains deeply concerned about the continuing systematic attacks and killings suffered by persons with albinism in Africa, in particular in Malawi, and strongly condemns any violence, discrimination and persecution directed at persons with albinism, as well as the trafficking of their body parts;\n2. Urges the Malawi’s government, and the authorities of all countries affected, to take all necessary measures to ensure the effective protection of persons with albinism, as well as their families, and to eliminate all forms of discrimination against them;\n3. Recalls the Malawi’s government of its obligation to protect the rights, dignity and physical integrity of their citizens in all circumstances and to put an end to the impunity enjoyed by their perpetrators by conducting the necessary investigations into these crimes and bringing those responsible to justice;\n4. Acknowledges the efforts made by the Malawi’s authorities to tackle the phenomena; stresses however that progress is still lacking, in particular on improving the legal protection and action for victims, and ensuring adequate redress and rehabilitation mechanisms;\n5. Calls on the Malawi’s authorities to adopt concrete strategies and policies to address the root causes of the phenomenon, notably by developing education and awareness-raising activities and campaigns on albinism; insists in this regard on the crucial role of local authorities and civil society organisations in promoting the rights of persons with albinism;\n6. Recalls that access to healthcare and education remains a great challenge for persons with albinism which needs to be tackled; calls for greater investment in creating adequate social, care and counselling structures for victims, in particular for women and children, as well as a better response to their medical and psychological needs; insists that policies should be put in place to facilitate their reintegration in their communities;\n7. Stresses the need to combat the marginalization of persons with albinism by ensuring their free and equal participation in society and the enjoyment of their civil and economic rights;\n8. Calls on the authorities of the countries affected, in cooperation with their international and regional partners, to commit to taking all necessary measures to prevent and tackle the illegal trade of albinos’ body parts, track down traffickers and dismantle their networks;\n9. Recalls that violence against albinos is often of a cross-border nature and insists on the need to strengthen regional cooperation on the matter; welcomes, therefore, all initiatives taken at the regional and international levels to fight violence against persons with albinism and in particular the recent adoption of the Regional Action Plan 2017-2021, jointly by the African Union and the UN which is a positive and concrete signal of commitment by African leaders; calls for its immediate and effective implementation;\n10. Calls on the EU to closely monitor the human rights situation of PWA in Africa, particularly through regular reporting by its delegations in the countries most affected;\n11. Reiterates its full support to the work of the Independent Expert on the human rights of people with albinism;\n12. Calls on the EU and its Member States to continue to support the countries affected in fighting violence on grounds of albinism and improving the social integration of persons with albinism, notably through its development programmes and political dialogue and by sharing best practices and providing the necessary technical assistance;\n13. Instructs its President to forward this resolution to the Council, the Commission, Vice-President of the Commission / High Representative of the Union for Foreign Affairs and Security Policy, the African Union and the Secretary-General of the United Nations”.\nAs stated by international human rights law, children with albinism have the right to live in a family environment. This is why local NGOs are making efforts to reunite children and families; among these Advantage Africa in the Busoga sub-region of Uganda is supporting more than 1,000 people with albinism to improve all aspects of their lives, helping children and adults with albinism to feel safe, accepted and included within their schools and communities. In doing so these organizations operates improving livelihoods, access to hats, high-factor sun screen, dermatology, vision and other health care services; moreover, it has introduced cryosurgery, a product that use liquid nitrogen to remove pre-cancerous lesions from the skin of people with albinism.\nAnother important activity conducted by NGO is advocate in favor of people with Albinism, informing common people about this disease, thus eliminating prejudices and beliefs and conducting awareness-raising lessons in schools, achieving greater understanding among children, as Tulime Onlus is currently doing in the Iringa region in Tanzania.\nThe United Nations (UN) has stressed the extreme discrimination faced by people with albinism; in 2013 the UN Human Rights Council called for the prevention of attacks and discrimination against PWA and in December 2014, the UN General Assembly adopted a resolution declaring the 13th of June each year as International Albinism Awareness Day.\nMoreover, as person with albinism are identified as disabled people they have guaranteed human rights as set out by the United Nations Convention on the Rights of Persons with Disabilities (UNCRPD); these rights include a right to life, adequate standards of living and social protection, equality and non-discrimination, freedom from exploitation, violence and abuse, and a right to education, health, work and employment.\nDespite the huge work that is currently carried on in Africa, especially from NGOs, people with albinism are still exposed to different risks and threats from both their relatives and community; in countering this situation is important to consider the important role played by several international organization, which play an important part in sensitizing and informing people, although old beliefs and rites are hardly abandoned by the poorest and less educated people, who think they can solve their problems by turning to sorcerers and wizards.\nIn order to cope to this situation, the government’s response should be guided on one hand by the best interests of the children involved, balancing the child’s protection and safety with the preservation of the family environment and the pleasure of other rights and on the other hand on the education of the population of the poorest countries of Sub-Saharan Africa through the development of new educational policies at national level, a policy which is unfortunately often not pursued by governments.\n Melanin is a natural skin pigment produced by melanocytes that determines hair, skin, and eye color in people and animals. Source: Webmd.com, https://www.webmd.com/a-to-z-guides/what-is-melanin#1\n cells in the retina that detect light\n Nystagmus is a vision condition in which the eyes make repetitive, uncontrolled movements. Source: Aoa.org, https://www.aoa.org/patients-and-public/eye-and-vision-problems/glossary-of-eye-and-vision-conditions/nystagmus\n Source Aljazeera.com, https://www.aljazeera.com/indepth/interactive/2017/04/albinism-170424053209871.html\n Source: Insideover.com, https://www.insideover.com/society/the-albinos-born-with-targets-on-their-heads.html\n Source: Aljazeera.com, https://www.aljazeera.com/indepth/interactive/2017/04/albinism-170424053209871.html\n the UN agency that deals with human rights issues\n Source: Europarl.europa.eu, https://www.europarl.europa.eu/doceo/document/B-8-2017-0547_EN.html\n International days are occasions to educate the public on issues of concern, to mobilize political will and resources to address global problems, and to celebrate and reinforce achievements of humanity https://www.un.org/en/events/albinismday/\n Disability specifically refers to negative interactions between people with deficiency and the internal and external environment; it’s the umbrella term for impairments, activity limitations and participation restrictions, referring to the negative aspects of the interaction between an individual (with a health condition) and that individual’s contextual factors (environmental and personal factors)https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5767025/\nFor further information:"

"2 Segregation of chromosomes during meiosis causes predictable patterns of inheritance. REVIEW: During Meiosis, segregation of maternal and paternal chromosomes is random.Because segregation of chromosomes is random, inheritance of single genes follows the rules of probability.\n3 Simple Example: Single celled eukaryote with diploid number 2. One homologous pair of chromosomesGene for Protein X.There are two variants of protein X (small differences in the DNA coding for protein X)One variant is functional (X+)The other variant is non-functional (X-)If an individual has both alleles it will express the functional protein.X-X+\n4 Crossing individuals with different genotypes: Parent one is homozygous for the functional alleleThis is how we denote the genotype of parent one :X+X+Parent two is homozygous for the non-functional allele: X-X-\n5 First: predict the possible gametes that each individual will produce Meiosis produces haploid gametes.Parent One Parent TwoX-X-X+X+X+X-\n6 What are the possible genotypes of the offspring produced by parent one and two? Fertilization:Genotype of offspring: X+X-Phenotype of offspring: All will express functional protein X\n7 What if two heterozygotes are crossed? What are the possible gametes that can be produced by a heterozygous individual?X+ or X- X+ or X-\n8 Fertilization Possible offspring genotypes: X+X+, X+X-, X+X-, X-X- Parent 1 gametesParent 2 gametesX+X-X+X-Possible offspring genotypes: X+X+, X+X-, X+X-, X-X-What are the proportions of each phenotype?¾ or 75% will express the functional protein¼ or 25% will express the non-functional protein\n9 Gregor Mendel observed these patterns when he performed test crosses with Pea Plants. Mendel was able to discover some important features of inheritance- not knowing about DNA, chromosomes, or meiosisHOW?He used mathematical analysis to show that inheritance patterns followed rules of probability.He deduced features of chromosomal and genetic inheritance using the proportions he observed\n10 Lived from 1822 to 1884“In this generation, along with the dominating traits, the recessive ones also reappear, their individuality fully revealed, and they do so in the decisively expressed average proportion of 3:1, so that among each four plants of this generation three receive the dominating one and one the recessive characteristic.”\n11 Significant and enduring understanding from Mendel’s work Traits are inherited as discrete units “genes”Traits are not blended; genes remain distinct unitsMendel's Law of SegregationMendel’s Law of Independent Assortment\n12 Mendel’s Law of Segregation: Individuals have two of each geneIndividuals pass only version of each gene to their offspringWhat is the basis for this law in terms of chromosomes and the process of Meiosis?Most Eukaryotes are Diploid; they have a pair of homologous chromosomes with the same genes on them.Meiosis produces haploid gametes with one of each type of chromosome.\n13 Mendel discovered the Law of Independent assortment by studying inheritance patterns of dihybrid crosses. -Patterns of inheritance of two separate single gene traits.\n14 Mendel’s Law of Independent Assortment: Genes assort independentlyFor genes located on different chromosomes: the inheritance of one gene does not influence the inheritance of another gene.What is the basis for this law in terms of chromosomes and the process of meiosis?\n15 Basic Rules of Probability For two independent events (a and b), the probability that two events will occur at the same time is:The and rule:Probability of a and b= P(a) x P (b)The probability of a or b (exclusive) occurring is:The or ruleProbability of a or b = P(a) + P(b)\n16 Rules of probability can be applied to analyze the passage of single genes traits from parent to offspringWhat is the probability of a heterozygous individual (genotype Aa) producing a gamete with the A allele?What is the probability of a heterozygous individual (Aa) producing a gamete with A or a alleles?\n17 More application of probability What is the probability of two heterozygous individuals (Aa) producing offspring with the genotype aa?\n18 What is the probability of a homozygous recessive and heterozygote producing offspring with the dominant phenotype\n19 Two gene inheritance and probability Use the probability rules to predict the outcome of inheritance of two genes located on different chromosomes.Parents: YyGg x YyGgWhat are the possible offspring genotypes and phenotypesWhat will be the proportion of each genotype and phenotype?\n20 What were the genotypes of the parents? A scientist crossed two parents with unknown genotypes and observed the following phenotypes in the offspring:75 white flowers225 Purple flowersWhich trait is dominant, which trait is recessive?What were the genotypes of the parents?\n21 What was the genotype and phenotype of the parents? Two parents of unknown genotype were crossed. The following phenotypes were observed:30 Yellow and Wrinkled seed coat10 Green and Wrinkled seed coat90 Yellow and Round seed coat30 Green and Round seed coat\n22 Sex linked traits are traits that are inherited via the X or Y chromosome. Sexual dimorphism: characteristic that differ between genders.Example: In placental mammals and marsupials the SRY gene determines development of testes.SRY is located on the Y chromosomeThe SRY gene codes for a transcription factor that binds Regulatory DNA and influences what proteins the cells will makeIf SRY gene is non functional, XY Female develops (Swyer Syndrome)Translocation of the SRY gene to the X chromosome (due to incorrect crossing over event between X and Y) causes XX male to develop.\n23 Sex-linked inheritance patters Example: hemophilia is an X linked recessive disorderConventions:XH (normal functional allele)Xh (non functional allele –causes hemophilia)The following parents are expecting a daughter: XHXh and XHY. What is the probability that she will have hemophilia?If the same couple is expecting a son, what is the probability he will have hemophilia?\n24 Gene linkageGenes on different chromosomes follow the rules of segregation and independent assortment.Genes located on the same chromosome tend to assort together to a certain extent.The closer two genes are on the same chromosome, the more likely they will be inherited together.This is called gene linkage\n25 Data of parent and offspring inheritance can be used to predict whether genes are linked. Possibilities: monohybrid cross, dihybrid cross, sex-linked trait, genes linked on same homolgous chromosome.\n26 Monohybrid crossDihybrid crossSex-linked traitsLinked genesGenetic diseasesPredict the pattern of inheritance based on parent and offspring genotype and phenotype"

"Biology Archive: Questions from February 13, 2012\nAbsurdWizard8237 askeda. The number...Which would lead one to expect linkage of genes if we assume genes are on chromosomes ?\na. The number of hereditary traits always exceeds the number of chromosomes.\nb. Multiple alleles sometimes occur.\nc. The most complex organism does not always have the most chromosomes.\nd. Chromosomes physically cross over during nuclear divisions.\nRebelPlanet4401 askedend diastole volume, end systolic volume, stroke volume and how ventricular depolarization works &qu...1 answer\nRebelPlanet4401 asked2 answers\nRebelPlanet4401 asked3 answers\nAmbitiousClock8592 askedSuppose that a \"fabulouse \" phenotype is controlled by two genes A and B.allele A peoduces enough en...Suppose that a \"fabulouse \" phenotype is controlled by two genes A and B.allele A peoduces enough enzyme 1 to convert plain to smashing.Allelel B produces enough enzyme 2 to convert smashing to fbulouse.Allale b produces no enzyme 2. A and B are both autosomal and asoourt independantly.( please explain )\nPlain........ >enzyme 1>........ smashing....... > enzyme 2........> fabulous\na)15 fabulouse :1 smashing\nb)9 fabulouse : 1 plain\nc)9 fabulouse : 3 smashing : 4 plain\nd)12 plain :3 fabulouse : 1 smashing\nc)13 fabulose :3 plain •3 answers\nAmbitiousClock8592 askeda)at least one...two parents affected with a genetic disease have 5 chidren. all of whom are affected.\na)at least one parent must be homozygouse for a dominant recessive.\nb)both parents must be homozybouse for recessiv trait.\nc)both parents must have at least 1 mutant allele.the trait might be recessive or dominant.\nd) at least 1 parent must be homozygous. •2 answers\nAmbitiousClock8592 asked5 answers\nAmbitiousClock8592 askedexplain and differentiate among the molecular bases codominance,incomplete dominance, complete domin...1 answer\nAmbitiousClock8592 askedRed- Green blindness is X-linked recessive.a woman with normal color vision has father with color bl...Red- Green blindness is X-linked recessive.a woman with normal color vision has father with color blind vision.the woman has a child with a man who is normal color vision.which phenotype is not expected?\na)a noncolor blind male\nb) color blind male\nc) noncolor blind female\nd) color blind female •5 answers\nAmbitiousClock8592 askedIn human blood type A and b are codominat to eachother and dominant to O.what type of blood is possi...In human blood type A and b are codominat to eachother and dominant to O.what type of blood is possible among offspring of couple with blood type AB and A.( please explain)\na)A and B only\nb)A, b, AB and O\nc)A, B, and AB only\nd)A and B only\ne) A , B and O only •1 answer\nAnonymous asked1. Which is FALSE about enzyme catalysis? A. Enzymes are highly specific for their substrates B. Enz1 answer\nAnonymous asked1. What is the primary result of the proximity effect in enzyme catlysis? A. Reduction in entropy an0 answers\nRebelPlanet4401 asked3 answers\nHillzguy23 asked1 answer\nAnonymous asked5 answers\nAnonymous asked1 answer\nAnonymous asked4 answers\nAnonymous asked1 answer\nAnonymous asked0 answers\nWackyShoes4252 asked1. In Drosophila, a kidney-shaped eye is produced by a recessive gene k on the third chromosome. Rec0 answers\nWackyShoes4252 asked2. In corn (Zea mays), a dominant gene c+ produces colored kernels and its recessive allele (c) prod0 answers\nWackyShoes4252 asked3. Consider three characteristics in the hypothetical animal, the zeebog from Madagascar. In the pop1 answer\nWackyShoes4252 asked4. A true breeding wild-type strain of flies was crossed to another strain homozygous for the recess0 answers\nWackyShoes4252 asked5. The following alleles exist in a population: A and a; B and b; and C and c. All three loci are on0 answers\nPreciseBandana6566 askedhow do i draw this graph with the date below . i dont know how to have to data on the same axis help...\nhow do i draw this graph with the date below . i dont know how to have to data on the same axis help.•\nMake a graph of the physiological responses of your exercising subject (Only one subject). Show the\nchanges in SBP, DBP and HR from rest to the final stage of exercise. On the vertical axis use mmHg and bpm. On the horizontal axis, use resistance of bike (kg).\nSBP DBP KG BP(mmHg) Heart rate (bpm)\n130 60 0 130/60 68\n130 80 0.5 130/80 78\n160 80 1 160/80 80\n185 80 1.5 185/80 1002 answers\nWackyShoes4252 asked6. You have two true-breeding lines of fruit flies. One is gray (eb+), red eyed (w+), and dwarf (d).0 answers\nAnonymous asked4 answers\nAnonymous askedPlease explain the concept of semi-permeable membrane. Provide an example of what can and cannot g...3 answers\nAnonymous asked4 answers\nAnonymous askedDuring exercise does the sympathetic nerve activity increase or decrease. What does the parasympathe...4 answers\nWackyShoes4252 asked7. You are studying a new species of wild flower which can have white (W) or red (w) flowers; long (1 answer\nRaynorsss askedlist three types of particle morphology possible in viruses of any kind. Indicate parenthetically if...list three types of particle morphology possible in viruses of any kind. Indicate parenthetically if the virus morphology us known to infect at least one of the following host:algae, human/animal, bacteria, fungi, insect, or plant.\nPLZ help me!!!!! thx •1 answer\nRaynorsss askedHow do animals differ from plants, in relation to viral entry and exit of the cell?\nPLZ help me !!!!t...How do animals differ from plants, in relation to viral entry and exit of the cell?\nPLZ help me !!!!thx a lot:) •2 answers\nRaynorsss asked1 answer\nRaynorsss asked2 answers\nAnonymous askedWhat are the prop...Study Guide for Quiz\n• What are the fundamental properties of life? (only names)\n• What are the properties of water?\n• Solutions with pH less than 7 are _______________\n• Solutions with pH greater than 7 are ________________________\n• _____________________solution contains components that enable\nthe solution to resist large changes in pH when either acids or bases are added.\n• Biological macromolecules are\n• Examples of monosaccharides are\n• Examples of polysaccharides are\n• _________________________fatty acids have all the hydrogen that the carbon atoms can hold.\n• ________________________fatty acids have only one double bond.\n• ____________________________ fatty acids have more than one double bond.\n• Functions of proteins are _____________________________, _______________________, ___________________________, ______________________________, _______________________, ________________________________.\n• What are the (full) names of nucleic acids?\n• What are the names of organelles of the animal cells?\n• What is the foundation of the cell membrane?\n• The structure of the cell membrane (with all of the components) is called __________________________ model.\n• Classes of membrane proteins are __________________, ___________________.\n• The substances cross the cell membrane by ______________________ or ________________ transport.\n• __________________carries the genetic material.\n• The proteins are synthesized by ___________________.\n• ER with ribosome is called _____________________________________________\n• The functions of Golgi are ____________________________, _________________________, ___________________________________\n• _______________________ are the sites of cellular respiration.\n• ______________________________is the maintenance of a stable internal environment.\n• An example of negative feedback mechanism is __________________________________\n• An example of positive feedback mechanisms is ___________________________________\n• What are the names of primary tissues?\n• What are the types of epithelial tissue?\n• __________connect muscle to bone.\n• _____________ attach one bone to another.\n• What are the types of bones?\n• What are the types of muscle tissue?\n• A typical neuron consists of ______________, ________________, _______________.\n• The tips of axons meet other neurons at junctions called ____________________.\n• The tips of axons meet muscles at junctions called _____________________________.\n• Schwann cells produce the myelin sheath that surrounds axons in _________________\n• Oligodendrocytes produce the myelin sheath that surrounds axons in ____________________\n• Please write the names of the body cavities.\n• What are the names of chambers of the heart?\n• What are the types of valves of the heart?\n• What are the names of valves of the heart?\n• What is the name of the blood vessel that carries oxygenated blood from lungs to the heart?\n• What is the name of the blood vessel that carries deoxygenated blood from heart to lungs?\n• What is systole?\n• What is diastole?\n• What are the names of nodes that regulate the rhythmic heart rate, and cardiac output?\n• What is tachycardia?\n• What is bradycardia?\n• What are the types of blood vessels?\n• What is average blood pressure (healthy adults)?\n• What are the names of cardio-vascular system disorders?\n• What are names of formed elements of blood?\n• What is the main function of red blood cells?\n• What are the names of white blood cells?\n• What are the causes of anemia?\n• What are the names of agranular leucocytes?\n• What are the names of granular leucocytes?\n• What is the main function of platelets?\n• What are the blood types in humans?\n• What are the functions of lymphatic system?\n• What are the names of primary lymphatic organs?\n• What are the names of secondary lymphatic organs?\nAnonymous askedConsider a reaction where 27.0 g of mercuric oxide (a red solid compound) is heated and completely d...Consider a reaction where 27.0 g of mercuric oxide (a red solid compound) is heated and completely decomposes to give the elements oxygen and mercury. If 2.0 g of oxygen is produced by this reaction, what mass of mercury is produced?\nI know this is a lot simpler than I'm making it but I just can't even think about where to start. I'm pretty sure the equation is HgO. Anyways, help is greatly appreciated! •1 answer\nAnonymous askedIf the membrane between these two compartments is permeable to just B+, how much B+ will be on the l...\nIf the membrane between these two compartments is permeable to just B+, how much B+ will be on the left side at equilibrium?•0 answers\nAnonymous askedList the tissues found in a segment of a three year old stem starting from the outside and moving to...List the tissues found in a segment of a three year old stem starting from the outside and moving to its center. Include both primary and secondary xylem/phloem, pith, cortex, vascular and cork cambiums, epidermis, periderm. Explain how “ray (parenchyma) cells” are formed through these tissues\nAnonymous askedImagine that you briefly heat 84.0 g of a red powder known to be mercuric oxide. After the sample ha...0 answers\nAnonymous askedFor simplicity, assume that the resting potential of a nerve membrane is -60 mV and the peak of the...\nFor simplicity, assume that the resting potential of a nerve membrane is -60 mV and the peak of the NAP is +40 mV. Calculate the number of Na+ ions that are transferred to create the voltage seen at the peak of the NAP. You need the fact that the capacitance of the nerve membrane is about 1 uF/cm2•0 answers\nAnonymous askedC, of 58.5 grams of NaCl in 1 liter of solution against pure w...Calculate the osmotic pressure, at 30°C, of 58.5 grams of NaCl in 1 liter of solution against pure water with a membrane that separates the pure water and salt solution and is impermeable to NaCl but permeable to water.\n(Assume 100% dissolution of NaCl)\nHappyKoala8469 askedIf a woman who is red-green color-blind, an X-linked trait, married a man with normal vision, what p...1 answer\nAmbitiousBandana1850 askedLimit resp...\nWhich group is more closely related to mammals: Frogs/toads/salamanders or Lizards/snakes?•\nLimit response to one answers.\nLizards/snakes—they share a more recent common ancestor with mammals.\nSame—they are both the same distance from mammals on the tree.\nLizards/snakes—they are closer on the tree.\nFrogs/toads/salamanders—they are the more ancient group.2 answers\nHappyKoala8469 askedDMD is inherited as a sex-linked recessive trait. A couple was surprised to learn that their first c...1 answer\nRaynorsss askedsome viruses have fusion protein, decribe their function and specifically how they participate in ce...2 answers\nAnonymous asked2 answers\nHappyKoala8469 askedMr. and Mrs. Jackson have three children. Each of the three is found to have a different blood type....1 answer\nRaynorsss askedThe ionomial system of nomenclature confers three kinds of information about the organism:(three thi...The ionomial system of nomenclature confers three kinds of information about the organism:(three things)\nPLZ help me, thx a lot •0 answers\nAnonymous asked2 answers\nAnonymous askedDescribe in 3 sentences the three lines of evidence that suggest that the diversity of genes coding ...1 answer\nHappyKoala8469 askedA sex-linked recessive gene in humans produced color-blind men when hemizygous and color-blind women...2 answers"

"The recessive gene s produces shrunken endosperm in corn kernals and\nits dominant allele S produces full, plump kernals. The recessive gene c\nproduces colorless endosperm and its dominant allele C produces\ncolored endosperm. Two homozygous plants are crossed, producing an\nF1 which are all phenotypically plump and colored. The F1 plants are\na) What were the phenotypes and genotypes of the original parents?\nb) How are the genes linked in the F\nc) Calculate the map distance between the two gene loci.\nIn corn, the gene R for red color is dominant over the gene r for green\ncolor. The gene N for normal seeds is dominant over the gene n for\ntassel seed. A fully heterozygous red plant with normal seeds was\ncrossed with a green plant with tassel seeds, and the following ratios\nwere obtained in the offspring:\n124 red, normal\n77 red, tassel\n126 green, tassel\n72 green, normal.\nDoes this indicate linkage? If so, what is the map distance between the\nSuppose genes A and B are 14.5 map units apart. Another gene, C,\nlinked to these, is found to cross with gene B, 7 percent of the time. Are\nthese data sufficient to determine the exact order of the three genes? If\nnot, what other information is needed to order the genes?\nThe cross-over percentage between linked genes J and M is 20%, J and\nL 35%, J and N 70%, L and K 15%. M and N 50%, M and K 30%, and\nM and L 15%. Thus , the sequence of genes on this chromosome is\nOne of your unicorns gives birth after you and she toured the Ukraine.\ndoes not look like its parents or your other\nunicorns. While your animals have a straight horn and a green coat; this\none has a twisted horn and a blue coat. You mate “Old Blue” and keep\nonly the blue offspring, after successive generations you have pure-\nbreeding progeny of “Old Blue.\" Now when you mate animals from\nyour two populations: all the progeny have straight horns and green\ncoats. These hybrid offspring are then crossed to unicorns with twisted\nhorns—blue coats. This cross produces offspring in the following"

"Gregor Johann Mendel was a Silesian monk that in 1822 set the main principles of the genetics. His theories are, still today, the basis for developing inheritances laws and theories. His “laws of genetics” are still learned in high schools and colleges.\nMendel’s First Law\nThe meanings of DOMINANT AND RECESSIVE we seen are essential for the good understanding of Mendel’s theories. Let us make the things easier working with “pure” bloodlines.\n“bloodline is the group of direct descendants from a common ancestor.”\nThat means the sons, grandsons, grand grands, etc from a determined bird. Nowadays it is very difficult to get pure bloodlines due to the enormous number of mating done. So a single bird carries several mutant genes that were added from generations of previous mating.\nThis does not mean we have hybrids, or mestizos. We just have carries of several pairs of mutant genes; i.e., heterozygotes, or splits, for several mutations. The term split is commonly used in aviculture as a synonym for heterozygote. (D’Angieri, A. –“The Colored Atlas of Lovebirds” – TFH-1997)\n“PURE line is one that carries just one pair of mutant genes”\nSo first we will work just with pure lines: Pastels will transmit just pastel, the dilutes just dilute and so on. The generations of descendants are designated as F1 (first generation), F2 (second generation), F3 (third generation), etc.\n|100% GREEN /RECESSIVE PIED (split for recessive pied).|\nWe have seen above that the genes are given by each one of the parents which originates “Paupau” birds: green split recessive pied.\nThe green color is a schizochroic interaction of several genes. The gene “Pau” IS NOT responsible for the green color, but just ONE OF THEM. Here it shows just the absence of the mutant factor.\n|GREEN/RECESSIVE PIED||×||GREEN/RECESSIVE PIED|\n|Green||green / recessive pied||recessive pied|\n|75% green phenotype||25% recessive pied phenotype|\n|green||0.5Pau × 0.5Pau||0.25=25%|\n|green / recessive pied||2 ( 0.5Pau × 0.5pau )||0.25=25%|\n|recessive pied||0.5pau × 0.5pau||0.25=25%|\nHere we observe a 3 to 1 rate (non-pied : pied). This rate occurs in pure bloodlines due to the chromosome segregation. This is Mendel’s First Law.\n“The gametes are transmitted to their descendants in a 50% rate”\n|GREEN/RECESSIVE PIED||×||RECESSIVE PIED|\n|2 (0.5P × 0.5p) = 50%||green / recessive pied|\n|2 (0.5p × 0.5p) = 50%||recessive pied|\nMendel’s Second Law\nMendel’s First Law is very restricted to be used in Agapornis breeding as gene interaction is not involved.\nThe schizochroic nature of Agapornis coloration is such that all characters are the result of genic interaction. Therefore, the second Mendelian law, which considers two or more allele pairs at the same time, is more pertinent. (D’Angieri, A. –“The Colored Atlas of Lovebirds” – TFH-1997)\nLet us better illustrate the phenomenon of the independent segregation of gene pairs: each pair of parental genes will produce gametes that carry just one its allele like in first law!\n|american dilute edged o (gaga)||×||aqua (pp)|\n|N.B: The genes “Ga” and “P” show the absence of the (ga) e aqua (p) respectively.|\nThe double split GagaPp is GREEN. Both genes are in heterozygosis so we have a NON-DILUTE EDGED NON-AQUA green bird which does not show any mutant color as both involved genes are recessive.\nThe Mendel’s Second Law proportionate a 1/16 (6,25%.) frequency in each square above.\n|GagaPp||25.00||green/dilute edged, aqua|\n|gagaPp||12.50||dilute edged./ aqua,dilute edged aqua|\n|gagapp||6.25||dilute edged aqua (former silver cherry)|\nThe double homozygosis gagapp is an interaction producing a third phenotype inexistent so far: the former silver cherry. There will be four different color is this pair: green, aqua, dilute edged green and dilute edged aqua.\nThis is a typical example of the way of action of mutant genes of the Agapornis and very good illustrates the genetics and its DOMINANCE, RECESSIVE AND GENE INTERACTION PHENOMENA.\n|aqua / dilute edged||×||aqua / dilute edged|\nPay attention to aqua factor in homozygosis from both parents which leads the frequencies to the Mendel’s first law.\n|blue personatus||×||pastel green personatus|\n|100% personatus green/blue, pastel|\n|Aaidid||green pastel /blue|\nLet us try three pairs of genes together:\n|pastel blue personatus||×||DD green personatus (olive)|\n|100% medium green (D)|\nTwelve different phenotypes were produced:\n|medium green||(D)I_ A_D_A_dd|\n|green||I_ A_ dd|\n|DD green||I_ AaDD|\n|DD pastel||idid A _ DD|\n|pastel medium green||idid A _ DD|\n|D blue||I_ aa D_|\n|pastel D blue||ididiaaD_|\n|DD blue (dark blue)||I_aaDD|\n|pastel DD blue (dark blue)||ididaaDD|\nCrossing Over And Linkage\nThe tendencies of the genes to keep together in chromosomes is called “linkage” that will show us the Mendel’s second Law is related only to different chromosomes (non-homologous). Indeed, a chromosome consists of a chain of genes. They are lined up, and, when they are duplicated, identical genes should result. However, the practical results show us that gene recombination can nevertheless occur, as a result of another phenomenon: crossing over .Crossing over is an occasional exchange, without preset rules and at no particular point, of parts of the filaments (chromatids) of homologous chromosomes, in a tetrad (the group of four chromatids formed in the course of duplication of the homologous chromosomes).\nAfter an initial intertwine, the filaments repel one another, allowing an exchange of fragments bearing several genes. This mechanism accounts for just one aspect of the impossibility of recombination predicted by Mendel’s second law.\nThe crossing-over rate between two genes is directly proportional to the distance along the chromosome between them: the farther apart, the greater the crossing rate, up to a maximum of 50%.(D’Angieri,A – The Colored Atlas of Lovebirds – TFH -1997).\nIn Agapornis, the linkage phenomenon together with crossing-over occurs clearly in roseicollis: Let us consider the turquoise Dark factor (D) and the Aqua factor (p). When there is a complete linkage between them, each gamete shall carry ether DP or dp and there will be no recombination. In this case there will be just two kinds of gametes: DP (50%) and dp (50%). However, we know that Dark Pastels (Mauves) do occur; this is genetically Dp, indicating that crossing have occurred.\nExample 8: Dark Green (DDPP) x AQUA (ddpp) yields 100% Medium Green (DdPp). These are next paired among themselves: DdPp x DdPp.\n|F1:||DdPp||100% D green (medium green)|\nTheoretically, we expect Dark Pastels (DDpp) at a rate of 1/16, or 6.25%. We have observed that their real frequency is 1/93, or 1.07%. A crossing rate of 1.07% means that approximately 1.10% was crossed over. So we have Dp = 0.55% and dP = 0.55%, yielding a sum of 1.10%. Thus 98.90% experienced no crossing over. (D’Angieri – “The colored Atlas of Lovebirds”):\nThere are two types of splits for aqua, just the type II will produce DD aquas:\n|type I||type II|\nIt is the occurrence of genes that are linked to sex chromosomes which must me designated by Z and W letters although the majority of the authors insists to use X and Y.\nThis should no be done as the use of X and Y indicates automatically that males do express the heterogametic sex (XY). This does not occur in birds. The Z and W system was first observed in genus Abraxas of insects, later in fishes and birds. There insects and fishes X and Y typed but so far no bird was observed. (D’Angieri,A, The Colored Atlas of Lovebirds-TFH -1997)\n“The use of XY with birds is complety wrong, because once it is applied, it is assumed that the heterogametic sex is represented by the males, which isn’t the case with birds” (D’Angieri,A, The Colored Atlas of Lovebirds-TFH -1997)\nFemales determine the sex in birds; it is done by W chromossome.\nThat means MALES are ZZ and FEMALES ZW. That explains there are more females than males of sex-linked characters, they occur just in roseicollis and are the opaline, lutino, pallid and cinnamon factors.\nYou must keep in mind that birds have a chromosome map with diploid chains 40-80, that means linkage phenomenon is a rule not exception in birds (Bucley, 1987)\n|100% green/opaline, aqua males|\n|100% opaline green/aqua females|\nPolyallelia is quite representative in lovebirds. Recently the pastel factor in personatus and its transgenics have been proven to be polyalleles of ino factor.\nA typical case of multiple alleles, which means there are more than one pair of genes in the same locus. The ino factor in roseicollis is allele to pallid .It is also said by some authors that turquoise and aqua might be alleles. In our experience they are not as we are going to discuss further.\nThe roseicollis’ ino factor and the pallid (former Australian cinnamon) are the first example known between two multiple alleles that occurred apart in the world.\nU.S.A in 1973 and Australia in1957 respectively.\nPallid is indeed a partial ino factor, schizochroic color of lutinism.-(D’Angieri, A – The Colored atlas of Lovebirds-TFH-1997)\n|100% pallid (par-ino)|\n|males:||ZIZia||green / pallid (par-ino)|\n|ZIZi||green / ino|\nEpistasis (Non Visual Birds)\nEpistasis is a genetic phenomenon that occurs when a certain character dominates over another non-allelic gene.\nOne good example involves the Violet and Ino factor, which are found on different chromosomes. When together in the same bird, the ino trait dominates. We cannot detect the Dark factor, although the bird in question is genetically a Violet Lutino .\nWe can say that the Ino factor is epistatic to the Violet factor, or that the Violet is hypostatic to the Ino. It is important to note that only the Ino factor’s American allele is epistatic to the Violet factor. The Pallid factor interacts with Violet factor to produce a violet ramped dull yellow bird.\nLet us have a better idea with its genetic formulas:\nIt is important to say that Violet inos are non-visual violets.\n“Epistasis is the phenomenum that turns one expected visual bird to a non-visual bird. It may be either dominant or recessive”.\nThere are factors that are known as deleterious genes, or better say they provides such a kind of immune deficiency that increases lethality or diseases. They might be the pale fallow roseicollis and bronze fallow personatus. There is also the Japanese dilute that is quite deleterious to female birds. In fact they are so few in numbers that should be better studied.\nSo far there is no proven lethal gene described in lovebirds."

"2015-4-17EECS 7304 Chromosome structure Short arm: p long arm: q\n2015-4-17EECS 7305 A few terms A chromosome contains two (almost) identical copies of DNA molecules. Each copy is called a chromatid and two chromatids are joined at their centromeres. Chromosomes and regions in a chromosome are named. For example by notation 6p21.3, we mean 6 : chromosome number p : short arm (from petit in French), q for long arm 21.3 : band 21, sub-band 3 (microscope)\n2015-4-17EECS 7309 Mendelian Genetics Mendel started genetics research before we know chromosome and gene Phenotype-- observable difference among members in a population For example: hair color, eye color, blood type What controls a phenotype? This is the question that Mendel tried to answer Is still the central question of modern genetics He used pea, a simple organism, and quantitative method to study phenotypes. We call a quantitative study of biology computational biology now.\n2015-4-17EECS 73012 Mendel’s Experiments He bred green peas with yellow peas In genetics, we call this practice cross (or mating) -- sexual reproduction between 2 organisms Parental strains (denoted by P0 or F0)-- originally crossed organisms X F0\n2015-4-17EECS 73013 Mendel’s Results Mendel collected results for F1 and F2 generations F1 generation-- offspring of the F0 generation (parents) F 1 generation2270 greenyellowratio\n2015-4-17EECS 73014 Mendel’s Explanation: Gene Model Model postulated that there are something called “genes” that controls the phenotype For the time being, let’s assumes that each organism always have two copies of the same gene. One from “father” and the other from “mother”. Some genes are dominant: the associated phenotype is visible in the F1 generation, e.g. green seed color Some genes are recessive: the associated phenotype is invisible in the F1 generation, e.g. yellow seed color How could we tell whether the gene model is correct or not?\n2015-4-17EECS 73015 Mendel’s New Experiments F2 generation-- offspring of F1 generation crossed to itself What should we expect to see in F2? Green seed: ¾ Yellow seed: ¼ His experimental results: F 1 generation2270 F 2 generation5931933.07 greenyellowratio\n2015-4-17EECS 73016 Continuing the experiments If we pick up yellow seed from the F2 generation and breed from them, what should we expect: All yellow (since yellow are recessive and hence we have both genes that contribute to yellow)\n2015-4-17EECS 73017 Continuing the experiments If we pick up green seed from the F2 generation and cross these organisms, what should we expect: Green seeds: 8/9 Yellow seeds: 1/9 If we pick up green seed from the F2 generation and cross an organism with itself, what should we expect: Some produce only green seeds: 1/3 Some produces both green seeds and yellow seeds: 2/3\n2015-4-17EECS 73018 Mendelian Genetics Importantly, Mendel went another step further looking at F 3 plants 193 crosses 193 yellow offspring only 0 green pea pods 593 crosses 201 green offspring only 392 green and yellow F 3 2:1 ratio green: yellow overall 1/4 F 2 matings green, 1/2 F 2 matings mixed, 1/4 F 2 matings yellow 1:2:1 ratio for all F 2 crosses\n2015-4-17EECS 73019 Genetics by Diagram More terminology: Gamete -- reproductive cell Zygote-- fertilized egg Adult F0: gamete Zygote F1: X X gamete Zygote F2: Mendel's Principle of Segregation: In the formation of gametes, the paired gene separate such that each gamete is equally likely to contain either one.\n2015-4-17EECS 73020 Another Rule Principle of Independent Assortment: segregation of any pair of alleles is independent of other pairs in the formation of gametes adult gametes\n2015-4-17EECS 73021 Our Explanation of Mendelian Genetics The two chromatids belong to the same chromosome separated randomly during a cell division\n2015-4-17EECS 73022 Gene linkage Experiments: white eyed female flies cross with wild type males (red eye, dominant) What should we expect: All red eyed flies in F1 No! We have 50% red eyed and 50% white eyed Why? A further study show that all red eyed are female and all white eyed are male\n2015-4-17EECS 73023 Gene Linkage: Morgan’s explanation: wwww +Y+Y X w+w+ Female, red eye wYwY Male, while eye\n2015-4-17EECS 73024 Recombination F1 generation: white eyed, miniature wing female crossed to wild type male F2 generation (ie. heterozygous female crossed to a wm male. We know that white eye gene and the miniature gene are in the same chromosome What should we expect: female: 50% wm, 50% normal male: 50% wm, 50% normal\n2015-4-17EECS 73025 Recombination What we have: F2 generation (ie. heterozygous female crossed to a wm male: white eyes, normal wings 223 red eyes, miniature wings 247 red eyes, normal wings 395 white eyes, miniature wings 382 We have some combination that does not appear in parents!\n2015-4-17EECS 73026 Recombination chromtides exchange their DNA components.\n2015-4-17EECS 73027 Modern Genetics Forward genetics: given a phenotype, how do we identify the genes that contribute to the phenotype? Cancer, Parkinson's Disease,… Reverse genetics: given a gene, how could we know what are the phenotype that the gene might control? Diagnostics\n2015-4-17EECS 73028 How are Phenotypes Caused? Through a biochemical pathways: Genes, mRNA, and proteins A B C D E W X Y Z\n2015-4-17EECS 73030 Chromosome Structure Chromosomes are made up of a single continuous DNA molecule can’t be straight-- would be many times length of the cell Chromatin: ordered aggregate of DNA and proteins visible in the cell cycle\n2015-4-17EECS 73031 heterochromatin: dense, compact structure during interphase generally near the centromere and telomeres (chromosome ends) composed of long tracks of fairly short base pair repeats few genes compared to euchromatin euchromatin: less dense DNA that only becomes visible after condensing typically has genes being actively transcribed Chromosome Structure\n2015-4-17EECS 73032 } Gene Expression genes are located at specific places on the chromosome (loci) regions corresponding to genes are transcribed sequences flanking the coding sequence control the start and stop of transcription not all genes are expressed at the same rates or at the same times\n2015-4-17EECS 73033 Regulation of Expression gene expression is regulated by proteins binding to promoter and regulatory regions regulatory proteins (eg., hormones) can 'turn on' or 'turn off' genes according to other factors\n2015-4-17EECS 73034 Steroid Hormone Action nuclear receptors are transcription factors hormone binding exposes DNA binding domain binding to promoter region turns genes 'on' or 'off' tend to have a longer lasting effect"

"PCB 3063 Spring 2012 Problem Set 1 ANSWERS 1.\nDetermine the types of gametes produced by each of the following individuals: a. Aa1/2 A, 1/2 a b. AaBb1/4 AB, 1/4 Ab, 1/4 aB, 1/4 ab c. AABb1/2 AB, 1/ Ab d.\nAaBBCc1/4 ABC, 1/4 aBC, 1/4 ABc, 1/4 aBc 2. Use the Punnett square to determine the genotypes in the progeny of each of the following crosses: a. Dd x Dd b.\nAaBB x AaBB c. CcEE x CCEe Notice: in every case, each parent produces only two types of gametes. [pic] 3. In guinea pigs, rough coat (R) is dominant over smooth coat (r).A rough coated guinea pig is bred to a smooth one, giving eight rough and seven smooth progeny in the F1 generation. a. What are the genotypes of the parents and their offspring? The recessive trait is observed in the progeny, so the rough-coated parent must be heterozygous. P: Rr (rough) x rr (smooth) F1: 1/2 Rr, 1/2 rr b.\nIf one of the rough F1 animals is mated to its rough parent, what progeny would you expect? This would be a monohybrid cross: Rr x Rr => 1/4 RR, 1/2 Rr, 1/4 rr. 4. In maize, a dominant allele A is necessary for seed color, as opposed to colorless (a).Another gene has a recessive allele w that results in waxy starch, as opposed to normal starch (W). The two genes segregate independently. What are the phenotypes and relative frequencies of offspring from each of the following crosses? Notice: The question specifies phenotypic ratios.\na. AaWw x AaWw This is a dihybrid cross: 9/16 A_W_ (normal) 3/16 A_ww (waxy) 3/16 aaW_ (colorless) 1/16 aaww (waxy, colorless) b. AaWW x AaWW This works like a monohybrid cross because both parents are homozygotic for WW. 3/4 A_WW (normal), 1/4 aaWW (colorless) 5.In humans, alkaptonuria is a metabolic disorder in which affected persons produce black urine. Alkaptonuria results from an autosomal allele (a) that is recessive to the allele for normal metabolism (A).\nSally has normal metabolism, but her brother has alkaptonuria. Sally’s father has alkaptonuria, and her mother has normal metabolism. a. Construct a pedigree of this family and indicate the genotypes of Sally, her mother, her father, and her brother. Sally’s mother must be a carrier. Sally is also a carrier because she received one alkaptonuria allele from her father. [pic]Caution: this is not X-linked inheritance. b.\nIf Sally’s parents have another child, what is the probability that this child will have alkaptonuria? aa (father) x Aa (mother) 1/2 Aa (normal metabolism) 1/2 aa (alkaptonuria) 6. Both John and Cathy have normal vision. After 10 years of marriage to John, Cathy gave birth to a color-blind daughter (color blindness is an X-linked recessive trait). John filed for divorce, claiming that he is not the father of the child. Is John justified in his claim of non-paternity? Explain your answer. Give the genotypes of John, Cathy and the child.\nSince color blindness is an X-linked recessive trait, the color-blind daughter must be homozygous for the color blindness allele. That means that she inherited a color blindness allele from each parent. John can not be the father, because he has no color blindness alleles (he has normal vision, so he is hemizygous for the normal vision allele). Cathy is a carrier. She is also a big cheater! John: CY Cathy: Cc Daughter: cc Whoever the father of the girl is must be cY and color blind.\n[pic] 7. If the pedigree above illustrates an autosomal dominant trait, then individual I-1: (Note: the “carrier” symbol was not used in the above pedigree. a.\nmust be homozygous dominant b. must be heterozygous c. must be homozygous recessive d. could be either homozygous dominant or heterozygous e.\ncould be either homozygous recessive or heterozygous This is a dominant trait and I-1 is affected, but he had unaffected children. Therefore he must be heterozygous. 8. The following pedigree is for an X-linked trait: (Note: the “carrier” symbol was not used in this pedigree. ) [pic] a. Is this trait dominant or recessive? Recessive: unaffected females III-4 and IV-1have affected sons.\nb. Indicate the genotypes of all the individuals in the pedigree. Affected males are hemizygous for the recessive allele • Affected females are homozygous for the recessive allele • Unaffected males are hemizygous for the dominant allele • Heterozygotes are carrier females Pedigree with the carrier symbols: [pic] Notice: the exact genotype of individual IV-4 is uncertain.9. The following pedigree illustrates the inheritance of Nance-Horan syndrome, a rare X-linked genetic condition in which affected persons have cataracts and abnormally shaped teeth. (Note: the “carrier” symbol was not used in this pedigree. [pic] If III-2 and III-7 mated, what would be the expected genotypic and phenotypic ratios in their progeny? Draw a Punnett square.\nThe trait is recessive because some unaffected mothers have affected sons (and males get their X from their mothers). III-2 is an affected male, so he must be hemizygous for the condition. III-7 is a carrier female because her father is affected. [pic] 10.\nIf traits R1 and R2 exhibit incomplete dominance over each other, what will be the phenotypic ratio in the progeny of the cross R1R1 x R1R2 ? :1 (individual R1R1 produces only one type of gamete) 1/2 R1R1, 1/2 R1R2 11. In shorthorn cattle, coat color may be red, white, or roan. Roan is an intermediate phenotype. The following data were obtained from various crosses: red x red-> all red white x white-> all white red x white-> all roan roan x roan-> 1/4 red: 1/2 roan: 1/4 white a. How is coat color inherited? Incomplete dominance: heterozygotes have an intermediate color (roan) b. What are the genotypes of parents and offspring in each cross? RR x RR => all RR rr x rr => all rrRR x rr => all Rr Rr x Rr => 1/4 RR, 2/4 Rr, 1/4 rr [pic] 12. Bar is an X-linked mutation in Drosophila that exhibits incomplete dominance. Flies that are homozygous for Bar have bar-shaped eyes.\nHeterozygous flies have bean-shaped eyes (an intermediate phenotype). a. What will be the outcome of a cross between a normal female and a bar-eyed male? Normal females must be homozygous for the normal allele because Bar is an incomplete dominant. Bar-eyed males are hemyzygous Bar. [pic] b. Use the Punnett square to determine the genotypes and phenotypes of the F2 generation [pic]Note: always indicate sex along with the phenotypes for X-linked inheritance.\n13. If traits LM and LN exhibit codominance relative to each other, what will be the phenotypic ratio in the progeny of the cross LMLN x LMLN ? 1:2:1 (monohybrid ratio): 1/4 LMLM (M), 2/4 LMLN(MN), 1/4 LNLN (N) 14. In a rare species of frog, red color (Y) is dominant over yellow color (y, a null allele). The character is autosomal. The cross YY x Yy produced over 100 frogs: 96% red and 4% yellow.\nWhich complication of Mendelian genetics can explain this outcome? a. recessive lethality of the y allele . codominance c. incomplete dominance d. incomplete penetrance e. variable expressivity All the frogs in F1 are Y_ so they should all be red, but a small percentage is not. There are no yy individuals, so recessive lethality can not explain this. It is not incomplete dominance or codominance, because those would yield 1:1 ratios.\nIt is not variable expressivity because yellow is a recessive phenotype, not a variation of the dominant phenotype. 15. In foxes, two alleles of a single gene, P and p, may result in lethality (PP), platinum coat (Pp), or silver coat (pp).Notice: this is an autosomal trait because nothing is indicated otherwise. a. Is the P allele behaving dominantly or recessively in causing lethality? Recessive: heterozygotes survive. b.\nIs the P allele behaving dominantly or recessively in causing platinum coat color? Dominant: heterozygotes are platinum, while the pp homozygotes are silver (two p alleles are necessary for the silver coat, therefore silver is recessive). c. What ratios are obtained when platinum foxes are interbred? Pp x Pp => 1/4 PP (dead), 1/2 Pp (platinum), 1/4 pp (silver) Apparent ratio: 2/3 platinum: 1/3 silver [pic] 16.\nIn a rare species of duck there is an X-linked allele (E1) that results in animals with only one eye (pictured above). The normal phenotype results from the wild-type allele (E), which is also necessary for survival. Use the Punnet square to determine the genotypic and phenotypic ratios in the progeny of a cross between a one-eyed female and a normal male. Since E is necessary for survival, the E’ allele is recessive in causing lethality (because homozygous E’E’ would die) but dominant in causing the one-eye condition (since only heterozygotes would be able to carry the E’ allele, and they would be one-eyed).Notice: the one-eyed male (pictured above) cannot occur! [pic] 17. The g allele in the Chupacabra is X-linked recessive lethal. Heterozygous individuals have gray hair instead of the normal black hair. Use the Punnett square to determine the outcome of a cross between a normal male and a gray female.\nI made this up! The gray female must be heterozygous because she needs at least one copy of the normal allele to survive. Since she’s also gray, the g allele is recessive in causing lethality but dominant in causing color. [pic] Important: always indicate sex along with the phenotypes for X-linked inheritance."

"Also found in: Dictionary, Thesaurus, Legal, Encyclopedia, Wikipedia.\ntwins derived from two zygotes.\ntwo offspring born of the same pregnancy and developed from two ova that were released from the ovary simultaneously and fertilized at the same time. They may be of the same or opposite sex, differ both physically and genetically, and have two separate and distinct placentas and membranes, both amnion and chorion. The frequency of dizygotic twinning varies according to ethnic origin (the highest incidence occurs in African-Americans, the lowest in Asian-Americans, with Caucasians intermediate), maternal age (the highest rate occurs when the mother is 35 to 39 years of age), and heredity (showing an increase in the female genetic line rather than the male, although fathers may transmit the disposition to double ovulation to their daughters). In general the overall ratio is two thirds dizygotic twinning to one third monozygotic. Also called binovular twins, dissimilar twins, false twins, fraternal twins, heterologous twins."

"Dizygotic 5-day-old male and female twins came to clinic for their health maintenance visit after discharge from the newborn nursery. They were born to a 24 year old, G2P1 now 3, female at 36 5/7 week gestation by vaginal birth without complications. The mother was attempting to breastfeed each infant every other feed every 2-3 hours. They used formula supplementation after the feeding as needed and used formula for the other infant at each feeding. Her milk was starting to come in at this time. They seemed slightly jaundiced to the parents, but otherwise were doing well. The family history was positive for the mother being a twin herself and her twin sister also had 2 year old twins. There were also maternal cousins who were twins. The father’s family did not have twins in the family.\nThe pertinent physical exam showed twin infants with weights that were 4% and 6% down from birth weight. The male infant had jaundice to his abdomen and the female had jaundice to the nipple line, but were otherwise well. The laboratory evaluation showed a bilirubin of 12.3 mg/dl for the male and 8.4 mg/dl for the female, both of which were low-risk. The diagnosis of healthy twins was made and the family was to follow up in 5 days or sooner as needed.\nTwinning is the conception and development of more than one zygote during one pregnancy. Monozygotic (MZ) twins arise from one zygote that then splits to form two embryos so that the twins are necessarily of the same gender (male-male or female-female). Dizygotic (DZ) twinning arises from the development of two independent zygotes and therefore the genders may be the same or different (male-male, female-female or male-female).\nIncreased risks of spontaneous DZ twinning includes increased maternal age, parity and gravity, family history including familial clustering, maternal obesity and overweight and smoking. Nutrition itself may or may not play a role. Other factors also cited that are associated with increased rates of twinning are race (e.g. black), ethnicity (e.g. non-Hispanic) and socioeconomic status (e.g. higher). Recently two SNPs were identified which appear to contribute to familial reproductive capacity and DZ twinning (FSHB and SMAD3) in a multi-country, genome-wide association study.\nWhile overall, twins that survive do well with normal outcomes, there can be problems. Maternal complications of twinning include increased stillbirth, neonatal death, premature birth, preeclampsia, post-partum hemorrhage and related problems. Neonatal complications of twinning include preterm birth, intrauterine growth restriction, and discordant growth. Societal costs are also increased for twins. Twins use more health care resources with increased costs than singletons. Some cite information that the cost of raising twins is more than two separate singletons.\nWhile humans have a dominant ovarian follicle selection which usually causes singleton births, twinning is common in humans. Overall in the US, 1 in 30 people is a twin.\nUntil ~1970 the US rate of overall twin birth was ~1.9% and was constant. The rate has increased to 3.3% in 2009. This appears to be because more DZ twins (particularly opposite sex twins) are being born. Currently, for MZ twins the rate continues to be relatively constant at 3-4 births/1000 around the world. For DZ twins the rate is different with worldwide regional differences. Low rates are found in Asia and Latin America (~1%), but in Africa the rate is much higher at 40 twin births/1000 live births. The Yoruba in Nigeria have a rate of 5%.\nThe increased rates of DZ are felt to be multifactorial with pharmacological control of fertility, assisted reproductive technologies and increased maternal age being important factors. Note that assisted reproductive technologies also allows options for sperm and egg donations and therefore the DZ twins may be genetic half-siblings.\nQuestions for Further Discussion\n1. Twin studies are common in research, so how would increased DZ twinning possibly affect participant selection for the research studies?\n2. Are there differences in congenital anomalies for twins versus singleton deliveries?\n- Disease: Twins, Triplets, Multiple Births\n- Age: Newborn\nTo Learn More\nTo view pediatric review articles on this topic from the past year check PubMed.\nInformation prescriptions for patients can be found at MedlinePlus for this topic: Twins, Triples and Multiple Births\nTo view current news articles on this topic check Google News.\nTo view images related to this topic check Google Images.\nTo view videos related to this topic check YouTube Videos.\nDawson AL, Tinker SC, Jamieson DJ, Hobbs CA, Rasmussen SA, Reefhuis J; National Birth Defects Prevention Study. Epidemiology of twinning in the National Birth Defects Prevention Study, 1997 to 2007. Birth Defects Res A Clin Mol Teratol. 2015 Feb;103(2):85-99.\nBoothroyd C. Twinning: Double, double, toil and trouble? Aust N Z J Obstet Gynaecol. 2016 Oct;56(5):445-446.\nMbarek H, Steinberg S, Nyholt DR, et.al. Identification of Common Genetic Variants Influencing Spontaneous Dizygotic Twinning and Female Fertility. Am J Hum Genet. 2016 May 5;98(5):898-908.\nRhea SA, Corley RP, Heath AC, Iacono WG, Neale MC, Hewitt JK.\nHigher Rates of DZ Twinning in a Twenty-First Century Birth Cohort.\nBehav Genet. 2017 Jul 15. (ePub ahead of publication).\nDonna M. D’Alessandro, MD\nProfessor of Pediatrics, University of Iowa"

"Dizygotic 5-day-old male and female twins came to clinic for their health maintenance visit after discharge from the newborn nursery. They were born to a 24 year old, G2P1 now 3, female at 36 5/7 week gestation by vaginal birth without complications. The mother was attempting to breastfeed each infant every other feed every 2-3 hours. They used formula supplementation after the feeding as needed and used formula for the other infant at each feeding. Her milk was starting to come in at this time. They seemed slightly jaundiced to the parents, but otherwise were doing well. The family history was positive for the mother being a twin herself and her twin sister also had 2 year old twins. There were also maternal cousins who were twins. The father’s family did not have twins in the family.\nThe pertinent physical exam showed twin infants with weights that were 4% and 6% down from birth weight. The male infant had jaundice to his abdomen and the female had jaundice to the nipple line, but were otherwise well. The laboratory evaluation showed a bilirubin of 12.3 mg/dl for the male and 8.4 mg/dl for the female, both of which were low-risk. The diagnosis of healthy twins was made and the family was to follow up in 5 days or sooner as needed.\nTwinning is the conception and development of more than one zygote during one pregnancy. Monozygotic (MZ) twins arise from one zygote that then splits to form two embryos so that the twins are necessarily of the same gender (male-male or female-female). Dizygotic (DZ) twinning arises from the development of two independent zygotes and therefore the genders may be the same or different (male-male, female-female or male-female).\nIncreased risks of spontaneous DZ twinning includes increased maternal age, parity and gravity, family history including familial clustering, maternal obesity and overweight and smoking. Nutrition itself may or may not play a role. Other factors also cited that are associated with increased rates of twinning are race (e.g. black), ethnicity (e.g. non-Hispanic) and socioeconomic status (e.g. higher). Recently two SNPs were identified which appear to contribute to familial reproductive capacity and DZ twinning (FSHB and SMAD3) in a multi-country, genome-wide association study.\nWhile overall, twins that survive do well with normal outcomes, there can be problems. Maternal complications of twinning include increased stillbirth, neonatal death, premature birth, preeclampsia, post-partum hemorrhage and related problems. Neonatal complications of twinning include preterm birth, intrauterine growth restriction, and discordant growth. Societal costs are also increased for twins. Twins use more health care resources with increased costs than singletons. Some cite information that the cost of raising twins is more than two separate singletons.\nWhile humans have a dominant ovarian follicle selection which usually causes singleton births, twinning is common in humans. Overall in the US, 1 in 30 people is a twin.\nUntil ~1970 the US rate of overall twin birth was ~1.9% and was constant. The rate has increased to 3.3% in 2009. This appears to be because more DZ twins (particularly opposite sex twins) are being born. Currently, for MZ twins the rate continues to be relatively constant at 3-4 births/1000 around the world. For DZ twins the rate is different with worldwide regional differences. Low rates are found in Asia and Latin America (~1%), but in Africa the rate is much higher at 40 twin births/1000 live births. The Yoruba in Nigeria have a rate of 5%.\nThe increased rates of DZ are felt to be multifactorial with pharmacological control of fertility, assisted reproductive technologies and increased maternal age being important factors. Note that assisted reproductive technologies also allows options for sperm and egg donations and therefore the DZ twins may be genetic half-siblings.\nQuestions for Further Discussion\n1. Twin studies are common in research, so how would increased DZ twinning possibly affect participant selection for the research studies?\n2. Are there differences in congenital anomalies for twins versus singleton deliveries?\n- Disease: Twins, Triplets, Multiple Births\n- Age: Newborn\nTo Learn More\nTo view pediatric review articles on this topic from the past year check PubMed.\nInformation prescriptions for patients can be found at MedlinePlus for this topic: Twins, Triples and Multiple Births\nTo view current news articles on this topic check Google News.\nTo view images related to this topic check Google Images.\nTo view videos related to this topic check YouTube Videos.\nDawson AL, Tinker SC, Jamieson DJ, Hobbs CA, Rasmussen SA, Reefhuis J; National Birth Defects Prevention Study. Epidemiology of twinning in the National Birth Defects Prevention Study, 1997 to 2007. Birth Defects Res A Clin Mol Teratol. 2015 Feb;103(2):85-99.\nBoothroyd C. Twinning: Double, double, toil and trouble? Aust N Z J Obstet Gynaecol. 2016 Oct;56(5):445-446.\nMbarek H, Steinberg S, Nyholt DR, et.al. Identification of Common Genetic Variants Influencing Spontaneous Dizygotic Twinning and Female Fertility. Am J Hum Genet. 2016 May 5;98(5):898-908.\nRhea SA, Corley RP, Heath AC, Iacono WG, Neale MC, Hewitt JK.\nHigher Rates of DZ Twinning in a Twenty-First Century Birth Cohort.\nBehav Genet. 2017 Jul 15. (ePub ahead of publication).\nDonna M. D’Alessandro, MD\nProfessor of Pediatrics, University of Iowa"

"The Tgncog mutation causes the development of goiters due to failed processing of thyroglobulin. Homozygotes are smaller in overall size by 15 days of age. They have an increase in growth rate at the time of weaning but generally do not attain comparable size with their wildtype littermates. Increased thyroidal volume is apparent at embryonic day 18 and continues enlarging to an average of 5 fold higher than normal at 8 weeks of age and 20 fold normal at 10 months of age. In addition to decreased serum T3 and T4 levels, homozygotes have increased serum thyroid stimulating hormone levels, reduced levels of serum IGFBP-3, IGFBP-4, and IGFBP-2, mild anemia, and hypomyelination restricted to the cerebrum. Tgncog is an outwardly recessive mutation but microdissection reveals a heterozygous phenotype as well. Thyrofollicular cells of heterozygotes have swollen protein-containing vesicles similar to but more moderate than those found in homozygotes. Thyroid extracts from homozygotes have an increased percent of protein and heterozygotes have an intermediate percent of protein relative to wild type siblings. (Beamer et al., 1987; Adkison et al., 1990; Sugisaki et al., 1991, 1992, and 1993; Kim et al., 1996 and1998.)\nThe congenital goiter mutation arose spontaneously in the AKR/J strain (then at generation F131) at The Jackson Laboratory. The mutation was maintained via sibling mating for 9 generations then backcrossed once to AKR/J then sibling mated for 4 generations before being backcrossed to BALB/cBy. A single male at N1F4 was bred to a BALB/cBy female, their heterozygous offspring sibling mated to generate a homozygous N1F1 female that was backcrossed to a BALB/cBy male. Their heterozygous N2 offspring were sibling mated to generate a homozygous male that was backcrossed to a BALB/cBy female. The backcross-intercross breeding scheme was continued from this point on using female BALB/cBy and male homozygotes in the backcross generations until the congenic strain reached N10. This strain was then maintained via sibling mating and in 1995 homozygous males at generation N10F21 were bred with C57BL/6J females to generate embryos for cryopreservation.\n|Allele Name||congenital goiter|\n|Allele Synonym(s)||cog; Tgncog|\n|Gene Symbol and Name||Tg, thyroglobulin|\n|Strain of Origin||AKR/J|\n|Molecular Note||The mutation is a T-to-C transition at coding nucleotide 6848 (c.6848T>C) yielding a leucine to proline change at positionn 2283 (p.L2283P). This falls within the acetylcholinesterase domain and impacts protein conformation. This conformational mutation is temperature sensitive; there is an increase in the level of TGN secreted from mutant thyrocytes at 31 degrees relative to the level secreted at 37 degrees, which is below the threshold of detection by PAGE. A small amount of functional TGN is processed in homozygous mice and serum triiodothyroinine and tetraiodothyroinine are found, albeit at vastly reduced levels.|"

"If we mate two individuals that are heterozygous (e.g., Bb) for a trait, we find that\n- 25% of their offspring are homozygous for the dominant allele (BB)\n- 50% are heterozygous like their parents (Bb)\n- 25% are homozygous for the recessive allele (bb) and thus, unlike their parents, express the recessive phenotype.\nThis is what Mendel found when he crossed monohybrids. It occurs because meiosis separates the two alleles of each heterozygous parent so that 50% of the gametes will carry one allele and 50% the other and when the gametes are brought together at random, each B (or b)-carrying egg will have a 1 in 2 probability of being fertilized by a sperm carrying B (or b). (Left table)\n|Results of random union of the two gametes produced by two individuals, each heterozygous for a given trait. As a result of meiosis, half the gametes produced by each parent with carry allele B; the other half allele b.||Results of random union of the gametes produced by an entire population with a gene pool containing 80% B and 20% b.|\n|0.5 B||0.5 b||0.8 B||0.2 b|\n|0.5 B||0.25 BB||0.25 Bb||0.8 B||0.64 BB||0.16 Bb|\n|0.5 b||0.25 Bb||0.25 bb||0.2 b||0.16 Bb||0.04 bb|\nHowever, the frequency of two alleles in an entire population of organisms is unlikely to be exactly the same. Let us take as a hypothetical case, a population of hamsters in which 80% of all the gametes in the population carry a dominant allele for black coat (B) and 20% carry the recessive allele for gray coat (b).\nRandom union of these gametes (right table) will produce a generation:\n- 64% homozygous for BB (0.8 x 0.8 = 0.64)\n- 32% Bb heterozygotes (0.8 x 0.2 x 2 = 0.32)\n- 4% homozygous (bb) for gray coat (0.2 x 0.2 = 0.04)\nSo 96% of this generation will have black coats; only 4% gray coats.\nWill gray coated hamsters eventually disappear? No. Let's see why not.\n- All the gametes formed by BB hamsters will contain allele B as will one-half the gametes formed by heterozygous (Bb) hamsters.\n- So, 80% (0.64 + .5*0.32) of the pool of gametes formed by this generation with contain B.\n- All the gametes of the gray (bb) hamsters (4%) will contain b but one-half of the gametes of the heterozygous hamsters will as well.\n- So 20% (0.04 + .5*0.32) of the gametes will contain b.\nSo we have duplicated the initial situation exactly. The proportion of allele b in the population has remained the same. The heterozygous hamsters ensure that each generation will contain 4% gray hamsters. Now let us look at an algebraic analysis of the same problem using the expansion of the binomial (p+q)2.\n\\[(p+q)^2 = p^2 + 2pq + q^2\\]\nThe total number of genes in a population is its gene pool.\n- Let \\(p\\) represent the frequency of one gene in the pool and \\(q\\) the frequency of its single allele.\n- So, \\(p + q = 1\\)\n- \\(p^2\\) = the fraction of the population homozygous for \\(p\\)\n- \\(q^2\\) = the fraction homozygous for \\(q\\)\n- \\(2pq\\) = the fraction of heterozygotes\n- In our example, p = 0.8, q = 0.2, and thus\n(0.8 + 0.2)2 = (0.8)2 + 2(0.8)(0.2) + (0.2)2 = 064 + 0.32 + 0.04\nThe algebraic method enables us to work backward as well as forward. In fact, because we chose to make B fully dominant, the only way that the frequency of B and b in the gene pool could be known is by determining the frequency of the recessive phenotype (gray) and computing from it the value of q.\nq2 = 0.04, so q = 0.2, the frequency of the b allele in the gene pool. Since p + q = 1, p = 0.8 and allele B makes up 80% of the gene pool. Because B is completely dominant over b, we cannot distinguish the Bb hamsters from the BB ones by their phenotype. But substituting in the middle term (2pq) of the expansion gives the percentage of heterozygous hamsters. 2pq = (2)(0.8)(0.2) = 0.32\nSo, recessive genes do not tend to be lost from a population no matter how small their representation. So long as certain conditions are met (to be discussed next),\ngene frequencies and genotype ratios in a randomly-breeding population remain constant from generation to generation.\nThis is known as the Hardy-Weinberg law in honor of the two men who first realized the significance of the binomial expansion to population genetics and hence to evolution.\nEvolution involves changes in the gene pool. A population in Hardy-Weinberg equilibrium shows no change. What the law tells us is that populations are able to maintain a reservoir of variability so that if future conditions require it, the gene pool can change. If recessive alleles were continually tending to disappear, the population would soon become homozygous. Under Hardy-Weinberg conditions, genes that have no present selective value will nonetheless be retained.\nWhen the Hardy-Weinberg Law Fails to Apply\nTo see what forces lead to evolutionary change, we must examine the circumstances in which the Hardy-Weinberg law may fail to apply. There are five:\n- gene flow\n- genetic drift\n- nonrandom mating\n- natural selection\nThe frequency of gene B and its allele b will not remain in Hardy-Weinberg equilibrium if the rate of mutation of B -> b (or vice versa) changes. By itself, this type of mutation probably plays only a minor role in evolution; the rates are simply too low. However, gene (and whole genome) duplication - a form of mutation - probably has played a major role in evolution. In any case, evolution absolutely depends on mutations because this is the only way that new alleles are created. After being shuffled in various combinations with the rest of the gene pool, these provide the raw material on which natural selection can act.\nMany species are made up of local populations whose members tend to breed within the group. Each local population can develop a gene pool distinct from that of other local populations. However, members of one population may breed with occasional immigrants from an adjacent population of the same species. This can introduce new genes or alter existing gene frequencies in the residents.\nIn many plants and some animals, gene flow can occur not only between subpopulations of the same species but also between different (but still related) species. This is called hybridization. If the hybrids later breed with one of the parental types, new genes are passed into the gene pool of that parent population. This process is called introgression. It is simply gene flow between species rather than within them.\nComparison of the genomes of contemporary humans with the genome recovered from Neanderthal remains shows that from 1–3% of our genes were acquired by introgression following mating between members of the two populations tens of thousands of years ago.\nWhether within a species or between species, gene flow increases the variability of the gene pool.\nAs we have seen, interbreeding often is limited to the members of local populations. If the population is small, Hardy-Weinberg may be violated. Chance alone may eliminate certain members out of proportion to their numbers in the population. In such cases, the frequency of an allele may begin to drift toward higher or lower values. Ultimately, the allele may represent 100% of the gene pool or, just as likely, disappear from it.\nDrift produces evolutionary change, but there is no guarantee that the new population will be more fit than the original one. Evolution by drift is aimless, not adaptive.\nOne of the cornerstones of the Hardy-Weinberg equilibrium is that mating in the population must be random. If individuals (usually females) are choosy in their selection of mates, the gene frequencies may become altered. Darwin called this sexual selection.\nNonrandom mating seems to be quite common. Breeding territories, courtship displays, \"pecking orders\" can all lead to it. In each case certain individuals do not get to make their proportionate contribution to the next generation.\nHumans seldom mate at random preferring phenotypes like themselves (e.g., size, age, ethnicity). This is called assortative mating. Marriage between close relatives is a special case of assortative mating. The closer the kinship, the more alleles shared and the greater the degree of inbreeding. Inbreeding can alter the gene pool. This is because it predisposes to homozygosity. Potentially harmful recessive alleles — invisible in the parents — become exposed to the forces of natural selection in the children.\nFig. 18.6.1 Assortative mating. (Drawing by Koren © 1977 The New Yorker Magazine, Inc.)\nIt turns out that many species - plants as well as animals - have mechanisms be which they avoid inbreeding. Examples:\n- Link to discussion of self-incompatibility in plants.\n- Male mice use olfactory cues to discriminate against close relatives when selecting mates. The preference is learned in infancy - an example of imprinting. The distinguishing odors are\n- controlled by the MHC alleles of the mice\n- detected by the vomeronasal organ (VNO)\nIf individuals having certain genes are better able to produce mature offspring than those without them, the frequency of those genes will increase. This is simply expressing Darwin's natural selection in terms of alterations in the gene pool. (Darwin knew nothing of genes.) Natural selection results from\n- differential mortality and/or\n- differential fecundity.\nCertain genotypes are less successful than others in surviving through to the end of their reproductive period.\nThe evolutionary impact of mortality selection can be felt anytime from the formation of a new zygote to the end (if there is one) of the organism's period of fertility. Mortality selection is simply another way of describing Darwin's criteria of fitness: survival.\nCertain phenotypes (thus genotypes) may make a disproportionate contribution to the gene pool of the next generation by producing a disproportionate number of young. Such fecundity selection is another way of describing another criterion of fitness described by Darwin: family size.\nIn each of these examples of natural selection, certain phenotypes are better able than others to contribute their genes to the next generation. Thus, by Darwin's standards, they are more fit. The outcome is a gradual change in the gene frequencies in that population.\nCalculating the Effect of Natural Selection on Gene Frequencies.\nThe effect of natural selection on gene frequencies can be quantified. Let us assume a population containing\n- 36% homozygous dominants (AA)\n- 48% heterozygotes (Aa) and\n- 16% homozygous recessives (aa)\nThe gene frequencies in this population are\np = 0.6 and q = 0.4\nThe heterozygotes are just as successful at reproducing themselves as the homozygous dominants, but the homozygous recessives are only 80% as successful. That is, for every 100 AA (or Aa) individuals that reproduce successfully only 80 of the aa individuals succeed in doing so. The fitness (w) of the recessive phenotype is thus 80% or 0.8.\nTheir relative disadvantage can also be expressed as a selection coefficient, s, where\ns = 1 − w\nIn this case, s = 1 − 0.8 = 0.2.\nThe change in frequency of the dominant allele (Δp) after one generation is expressed by the equation\n|s p0 q02|\n|1 - s q02|\nwhere p0 and q0 are the initial frequencies of the dominant and recessive alleles respectively. Substituting, we get\n|1 − (0.2)(0.4)2||0.968|\nSo, in one generation, the frequency of allele A rises from its initial value of 0.6 to 0.62 and that of allele a declines from 0.4 to 0.38 (q = 1 − p).\nThe new equilibrium produces a population of\n- 38.4% homozygous dominants (an increase of 2.4%) (p2 = 0.384)\n- 47.1% heterozygotes (a decline of 0.9%)(2pq = 0.471) and\n- 14.4% homozygous recessives (a decline of 1.6%)(q2 = 0.144)\nIf the fitness of the homozygous recessives continues unchanged, the calculations can be reiterated for any number of generations. If you do so, you will find that although the frequency of the recessive genotype declines, the rate at which a is removed from the gene pool declines; that is, the process becomes less efficient at purging allele a. This is because when present in the heterozygote, a is protected from the effects of selection."

"4.2: Females produce gametes of types A B, a b, A b, and a B in the proportions (1-0.08)/2 = 0.46 and (1-0.08)/2 = 0.46 for each of the nonrecombinant types. It is 0.08/2 = 0.04 and 0.08/2 = 0.04 for each of the recombinant types. Since there is no crossing over in male Drosophila, males produce only two gamete types (A B, a b) in equal (0.50, 0.50) proportions.\n4.7: The map distance between s and c is 18 cM, but there is only 16% recombination, and the map distance between p and c is 13 cM, but there is only 12% recombination. The fact that the frequency of recombination is smaller than the map distance results from double crossovers.\n4.8: The data include 108 progeny with either both mutations or neither, and 92 progeny with one mutation or the other. The first of these groups consists of parental chromosomes; the second consists of recombinant chromosomes. The chi-square test compares the observed ratio (108:92) to the expected (100:100) under the hypothesis of no linkage. The chi-square value equals 1.28 and there is one degree of freedom. P is approximately 0.26, so there is no evidence of linkage even though both loci are on the X.\n4.10: (a) the mutant genes are not alleles because they do not show segregation; if they were alleles, the progeny would show resistance to one insecticide or the other. (b) the genes are not linked. The chi-square of 177 parental:205 recombinants compared to 191:191 (expected) equals 2.05. With one degree of freedom, P is 0.15 (not significant). (c) The two genes must be far apart on the chromosome – too far to be ‘linked’.\n(a) The gene in the middle has the alleles D and d.\n(b) The triply heterozygous parent has genotype A d B / a D b or B d A / b D a.\n(c) The closest genes are B and D.\n(d) B−D distance equals (40 + 60 + 10)/1000 = 0.11 = 11 map units = 11 centimorgans (cM).\n4.12: (a) parental types = v+ pr bm and v pr+ bm+. Double recombinants = v+ pr+ bm+ and v pr bm. This means that gene v is in the middle. The pr-v recombination frequency is 20.7% and the v-bm frequency is 41.5%. The expected number of double crossovers = 85.9, so the coincidence is 0.90. The interference is thus 0.10. (b) The true map distances are larger than 20.7cM and 41.5 cM because the frequency of recombination between these genes is sufficiently large that there must have been some double crossover events that went undetected in the analysis.\n(a) To solve this type of problem, you should first deduce the genotype of the gamete contributed by the triply heterozygous parent to each class of progeny. In this case the gamete types are, from top to bottom, + + +, + + unc, + dor unc, dpy + +, dpy dor +, dpy dor unc. To determine the order of the genes, you must identify which gene is in the middle. You can do this by comparing the parental type gametes with the double crossovers. The two parental types are dpy dor + and + + unc, because these are the most frequent. In these data there are no observed double crossovers (which means that interference across the region is complete). The missing classes of progeny correspond to the double crossovers. The missing phenotypes of progeny are normal body, deep orange eye, coordinated, corresponding to the genotype + dor +, and dumpy body, red eye, uncoordinated, corresponding to the genotype dpy + unc. Comparing the parental types with the inferred double crossover types reveals that dpy+ and dpy are interchanged relative to the alleles of the other two genes. Hence, the genotype of the F1 heterozygous female is dor dpy unc+ / dor+ dpy+ unc or unc+ dpy dor/ unc dpy+ dor+.\n(b) Analysis of the single recombinants indicates (96 + 110)/1000 = 20.6% recombination between dor and dpy, and (75 + 65)/1000 = 14.0% recombination between dpy and unc.\n(c) Because there are no double recombinants observed, the interference is complete, which means interference = 1."

"Monday, February 25, 2013. Take a penny lab and staple it Take a “ How to Solve a Basic…. ” handout Turn in Meiosis Lab onto Computer cart. Genotype Phenotype Homozygous Heterozygous Allele. Gregor Mendel : ‘ father ’ of modern genetics.\nIf alleles for a trait are different (Rr) then 50% chance of gametes (1/2) receive one allele (R) & 50% receive the other allele (r)\nit can be assumed (unless otherwise stated) that each allele (letter) is on a separate chromosome\n-->So how many chromosomes are represented by the genotype above?\n-->How many possible gametes are created from the genotype above? (HINT: each trait is on a separate chromosome so apply law of independent assortment!)\n--> How many possible offspring genotypes exist if both parents have the genotype above?\nTrait = Seed shape\nPhenotypes: Round seeds or Wrinkled seeds\nGenotypes: = AA, Aa, aa\nHomozygous = AA or aa\nHomozygous Dominant = AA\nHomozygous Recessive = aa\nHeterozygous (hybrid) = Aa\nGenotypic Ratio: 1AA : 2 Aa : 1aa\nPhenotypic Ratio: 3 Round : 1 Wrinkled\nProbability = chance event will occur\ntotal # of possible events\n“AND” Rule: Rule of Multiplication\nFor two or more separate events occurring at the same time (or in succession), multiply the individual probabilities of events together\nEX 1: If parents are BB and Bb, what is chance of B gamete & b gamete combining to form zygote?\n1/1 B and 1/2 b = 1/1 * 1/2 = 1/2 chance of Bb zygote\nEX 2: Parent genotype is AaBBDdEe:\nWhat is probability of gamete with genotype of ABdE?\n1/2 * 1* 1/2 * 1/2 = 1/8 chance of ABdE\nA pedigree is a family history showing inheritance of a particular trait through familial generations\nKaryotypes are photographs of stained, human chromosomes present at metaphase of mitosis. Karyotypes are used to determine if chromosomes are defective and help to diagnose chromosomal disorders such as Down’s Syndrome.\nIs this a boy or girl’s karyotype?\nNon-disjunction of sister chromatids during meiosis II"

"Modified dihybrid ratios with codominant and lethal alleles\nThe classical phenotypic ratio resulting from the mating of dihybrid genotypes is 9:3:3:1. This ratio appears whenever the alleles at both loci display dominant and recessive relationships. The classical dihybrid ratio may be modified if one or both loci have codominant alleles or lethal alleles. A summary of these modified phenotypic ratios in adult progeny is shown below:\nThe genetic systems described so far have been limited to a single pair of alleles. The maximum number of alleles at a gene locus that any individual possesses is 2, with 1 on each of the homologous chromosomes. But since, a gene can be changed to alternative forms by the process of mutation, a large number of alleles is theoritically possible in a population of individuals. This is because the nucleic acid structure of a gene consists of many nucleotides and variations can arise at each of the nucleotide positions along its length. Thus there ar more than only two possible kinds of alleles in a gene; hundreds or perhaps thousands of possibilities exist and called multile alleleic series. i.e., A1, A2, A3,..An\nA capital letter is used to designate the allele that is dominant to all others in the series. The corresponding small letter designates the allele that is recessive to all others in the series. Other alleles, intermediate in their degree of dominance between these two extremes, are usually assigned the small letter with some suitable superscript.\nThe colour of drosophila eyes is governed by a series of alleles that cause the hue to vary from red or wild type (w+or W) through coral (wcc), blood (w bl), cherry (wch), apricot (wa), honey (wh), buff (wbf), tinged (wt ), pearl (wp), and ivory (wi) to white (w). Each allele in the system exvept w can be considered to produce pigment, but successfully less is produced by alleles as we proceed down the hirearchy: w+ > wcc >w bl> wch> wa> wh> wbf> wt > wp> wi> w. The wild type allele (w+) is completely dominant and w is copletely recessive to all other alleles in the series.\nA classical example of multiple alleles is found in the ABO blood group system of humans, where the allele IA for the antigen is codominant with the allele IB for the antigen. Both IA and IB are completely dominant to te allele i, which fails to specify any detectable antigenic structure. The hirearchy of dominance relationships is symbolized as (IA = IB) >1. (I stands for isohaemagglutinatinogen). Thus when paired with either IA or IB, its effect is masked. Since, three alleles of the gene exists in a population, it is considered a multiple allele system. The genotypes that produce the four blood groups are represented in the following table:\nIf the blood groups of the parents are known, the blood groups of the children can be determined (or vice versa) by using the"

"Assignments Read from Chapter 3, 3.6 (pp ), Master Problems…3.12, 3.15, 3.20, Chapter 4, Problems 1, 2, Questions , 4.6, 4.7, 4.9, , a,b,c,d. Exam Week from Friday… –One hour (you can use the entire 80 minutes, but no more). One 8” x 11”, one sided crib sheet.\nSex Determination Systems Different mechanisms of sex selection exist: » XX / XO (O = null), ZW / ZZ (female ZW, Male ZZ), haplo / diplo (males are haploid), XX / XY (most mammals).\nSex Chromosomes most mammals…... ‘X’ and ‘Y’ chromosomes that determine the sex of an individual in many organisms, Females: XX Males: XY\nDifferential Region Differential Region Paring Region XY: male XX: female aaA hemizygous: condition where gene is present in only one dose (one allele).\nX Linkage …the pattern of inheritance resulting from genes located on the X chromosome. X-Linked Genes… …refers specifically to genes on the X- chromosome, with no homologs on the Y chromosome.\nBlue Female Pink Male x P Gametes or Blue is dominant.\nGametes or F1 Blue FemaleBlue Male\nF1 Blue FemaleBlue Male x Gametes or\nGametes or F2 Blue FemaleBlue MaleBlue FemalePink Male\nF2 Blue FemaleBlue MaleBlue FemalePink Male 3 : 1 Blue to Pink 1 : 1 Female to Male\nPink Female Blue Male x P Gametes or\nF1 Blue FemalePink Male Gametes or\nF2 Pink FemalePink MaleBlue FemaleBlue Male Gametes or\nF2 Pink FemalePink MaleBlue FemaleBlue Male : 1 Female to Male 1 : 1 Pink to Blue\nSex Linkage to Ponder Female is homozygous recessive X-linked gene, –what percentage of male offspring will express? –what percentage of female offspring will express if, mate is hemizygous for the recessive allele? mate is hemizygous for the dominant allele? Repeat at home with female heterozygous X- linked gene!\nSex-Linked vs. Autosomal autosomal chromosome: non-sex linked chromosome, autosomal gene: a gene on an autosomal chromosome, autosomes segregate identically in reciprocal crosses.\nX-Linked Recessive Traits Characteristics Many more males than females show the phenotype, –female must have both parents carrying the allele, –male only needs a mother with the allele, Very few (or none) of the offspring of affected males show the disorder, –all of his daughters are carriers, roughly half of the sons born to these daughters are carriers.\nX-Linked Dominant Affected males married to unaffected females pass the phenotype to their daughters, but not to their sons, Heterozygous females married to unaffected males pass the phenotype to half their sons and daughters, Homozygous dominant females pass the phenotype on to all their sons and daughters.\nAutosomal Dominant Phenotypes appear in every generation, Affected males and females pass the phenotype to equal proportions of their sons and daughters.\nRecessive?---> Yes! Pedigree for Very Rare Trait ? = kid with trait Autosomal?X-Linked?---> Yes! 1/2 1/2 x 1/2 x ?1/2 = 1/8 ? x 1/2 = 1/16 (p)boy\nX-Linked Dominant examples (OMIM) HYPOPHOSPHATEMIA: “Vitamin-D resistant Rickett’s”, LISSENCEPHALY: “smooth brain”, FRAGILE SITE MENTAL RETARDATION : mild retardation, RETT Syndrome: neurological disorder, More on OMIM…\nGenetics: … in the News\nLinkage Genes linked on the same chromosome may segregate together.\nA b 2n = 4 Independent Assortment a A A B B b a B a b\nMeiosis No Cross Over Parent Cell Daughter Cells Have Parental Chromosomes Aa Bb A B a b a b A B 2n = 1\nMeiosis With Cross Over Parent Cell Daughter Cells Have Recombinant Chromosomes Aa Bb A B A b a b a B 2n = 1\nDihybrid Cross yellow/round green/wrinkled GGWW x ggww GW gw GgWw phenotype genotype gametes genotype P F1\nGamate Formation in F1 Dihybrids P: GGWW x ggww, Independent Assortment G g W w GWGwgWgw alleles gametes probability.25 F1 Genotype: GgWw\nHow do you test for assortment of alleles? GWGwgWgw.25 F1: GgWw Test Cross: phenotypes of the offspring indicate the genotype of the gametes produced by the parent in question.\nTest Cross GgWw x ggww GW (.25) Gw (.25) gW (.25) gw (.25) G gww (.25) GgWw (.25) ggWw (.25) ggww (.25) gw (1) x x x x\nTest Cross GgWw x ggww GW (.25) Gw (.25) gW (.25) gw (.25) gw (1) Ggww (.25) GgWw (.25) ggWw (.25) ggww (.25) P P F1 parental types GgWw and gwgw R R recombinant types Ggww and ggWw x x x x\nRecombination Frequency …or Linkage Ratio: the percentage of recombinant types, –if 50%, then the genes are not linked, –if less than 50%, then linkage is observed.\nLinkage Genes closely located on the same chromosome do not recombine, –unless crossing over occurs, The recombination frequency gives an estimate of the distance between the genes.\nRecombination Frequencies Genes that are adjacent have a recombination frequency near 0%, Genes that are very far apart on a chromosome have a recombination frequency of 50%, The relative distance between linked genes influences the amount of recombination observed.\nAB In this example, there is a 2/10 chance of recombination. ab AC In this example, there is a 4/10 chance of recombination. ac homologs\nLinkage Ratio P GGWW x ggww Testcross F1: GgWw x ggww # recombinant # total progeny GWGwgWgw ???? x 100 = Linkage Ratio Units: % = mu (map units) - or - % = cm (centimorgan) determine\nFly Crosses (simple 3-point mapping) (white eyes, minature, yellow body) In a white eyes x miniature cross, 900 of the 2,441 progeny were recombinant, yielding a map distance of 36.9 mu, In a separate white eyes x yellow body cross, 11 of 2,205 progeny were recombinant, yielding a map distance of 0.5 mu, When a miniature x yellow body cross was performed, 650 of 1706 flies were recombinant, yielding a map distance of 38 mu. Study Figs 4.2, 4.3, and 4.5\nSimple Mapping white eyes x miniature = 36.9 mu, white eyes x yellow body = 0.5 mu, miniature x yellow body = 38 mu, my 38 mu 36.9 mu w 0.5 mu\nDo We have to Learn More Mapping Techniques? Yes, –three point mapping, Why, –Certainty of Gene Order, –Double crossovers, –To answer Cyril Napp’s questions, –and, for example: over 4000 known human diseases have a genetic component, knowing the protein produced at specific loci facilitates the treatment and testing.\nClassical Mapping Cross an organism with a trait of interest to homozygous mutants of known mapped genes. Then, determine if segregation is random in the F2 generation, if not, then your gene is linked (close) to the known mapped gene. target What recombination frequency do you expect between the target and HY2? What recombination frequency do you expect between the target and TT2?\nGene Order It is often difficult to assign the order of genes based on two-point crosses due to uncertainty derived from sampling error. A x B = 37.8 mu, A x C = 0.5 mu, B x C = 37.6 mu,\nDouble Crossovers More than one crossover event can occur in a single tetrad between non-sister chromatids, –if recombination occurs between genes A and B 30% of the time (p = 0.3), then the probability of the event occurring twice is 0.3 x 0.3 = 0.09, or nearly one map unit. If there is a double cross over, does recombination occur? –how does it affect our estimation of distance between genes?\nClassical Mapping model organisms Cross an organism with a trait of interest to homozygous mutants of known mapped genes. Then, determine if segregation is random in the F2 generation, if not, then your gene is linked (close) to the known mapped gene. target What recombination frequency do you expect between the target and HY2? What recombination frequency do you expect between the target and TT2?\nClassical mapping in humans requires pedigrees…\nThree Point Testcross Triple Heterozygous (AaBbCc ) x Triple Homozygous Recessive (aabbcc)\nThree Point Mapping Requirements The genotype of the organism producing the gametes must be heterozygous at all three loci, You have to be able to deduce the genotype of the gamete by looking at the phenotype of the offspring, You must look at enough offspring so that all crossover classes are represented.\nw g d\nRepresenting linked genes w g d x w g d P Testcross = WwGgDd = wwggdd\nPhenotypic Classes tri-hybrid cross?\nW-G-D- W-G-dd W-gg-D W-gg-dd wwG-D- wwG-dd wwggD- # wwggdd173 Parentals Recombinants, double crossover Recombinants 1 crossover, Region I Recombinants 1 crossover, Region II\nW-G-D- W-G-dd W-gg-D W-gg-dd wwG-D- wwG-dd wwggD- # wwggdd173 Parentals Recombinants, double crossover Recombinants 1 crossover, Region I Recombinants 1 crossover, Region II W G D w g d I Total = 500 Region I: x 100 = 20.8 mu\nW-G-D- W-G-dd W-gg-D W-gg-dd wwG-D- wwG-dd wwggD- # wwggdd173 Parentals Recombinants, double crossover Recombinants 1 crossover, Region I Recombinants 1 crossover, Region II W G D w g d II Total = 500 Region II: x 100 = 10.0 mu 20.8 mu\nW G D w g d W-gg-D wwG-dd 4 2 Recombinants, double crossover Total = mu20.8 mu 0.1 x = /500 = NO GOOD! Coefficient of Coincidence = Observed Expected Interference = 1 - Coefficient of Coincidence\nInterference …the effect a crossing over event has on a second crossing over event in an adjacent region of the chromatid, –(positive) interference: decreases the probability of a second crossing over, most common in eukaryotes, –negative interference: increases the probability of a second crossing over.\nGene Order in Three Point Crosses Find - either - double cross-over phenotype…based on the recombination frequencies, Two parental alleles, and one cross over allele will be present, The cross over allele fits in the middle... –\n# Which one is the “odd” one? A C B a c b III A-B-C- A-B-cc A-bb-C- A-bb cc aaB-C- aaB-cc aabbC- aabbcc\nA-B-C- A-B-cc A-bb-C- A-bb cc aaB-C- aaB-cc aabbC- # aabbcc1786 Region I A C B a c b I x 100 = 28.4 mu\nA-B-C- A-B-cc A-bb-C- A-bb cc aaB-C- aaB-cc aabbC- # aabbcc1786 Region II A C B a c b 28.4 mu x 100 = 18.5 mu II 18.5 mu"

"*Please note: you may not see animations, interactions or images that are potentially on this page because you have not allowed Flash to run on S-cool. To do this, click here.*\nThere are several causes for variation being present within a population:\n- Each gene has different alleles. Therefore, different individuals may have different alleles.\n- During prophase I of meiosis, chiasmata (crossing over) occurs whereby sections of DNA are swapped between sister chromatids.\n- During metaphase I of meiosis, there is independent assortment of the homologous pairs of chromatids.\n- Mutation - gene and chromosome.\n- Random fertilisation.\nThis shows that there is variation of genotype and phenotype between individuals. The environment also exerts an effect and can cause variation.\nFor each characteristic, the population may show either continuous or discontinuous variation.\nThe genetic basis for discontinuous variation\nThis is where different alleles for one gene have a large effect on the phenotype.\nABO blood groups, there are no intermediates; you are either A, B, AB or O.\nThe genetic basis for continuous variation\nDifferent alleles for one gene have small effects.\nDifferent loci have the same or additive effects. (When a large number of loci produce a combined effect it is called polygeny.)\nImagine height is controlled just by two genes (though in reality, many genes will contribute to height). Each has two alleles; E and e, F and f.\nE and F contribute 2cm to height whereas e and f contribute just 1cm to height.\nEEFF = 8cm\neeff = 4cm\nIf EeFf is crossed with EeFf, the outcome will be...\n|Gametes:||All EF||x||All ef|\n|Gametes:||EF, Ef, eF, ef||x||EF, Ef, eF, ef|\n|F2 punnett square:||EF||Ef||eF||ef|\n|Phenotypes:||8 cm tall||7 cm tall||6 cm tall||5 cm tall||4 cm tall|\nThis crudely shows the continuous variation in a population with regard to height.\nDon't forget that environment also causes variation of the phenotype. This will not be passed on to offspring.\nIn any population, the total variety of genes and alleles present is called the gene pool.\nThis gene pool can change in content (new alleles arriving, existing alleles being lost) or the ratio of alleles altering due to the following:\n- Natural selection\n- Mate selection\nThe factors favouring stability of the gene pool are:\n- No mutation\n- No natural selection\n- The population being large\n- No gene flow (due to individuals emigrating or immigrating)\n- Random mating\nIf these factors favouring stability are fulfilled, the ratio of the alleles for a gene can be established using the Hardy-Weinberg Equilibrium.\nLog in here"

"This preview has intentionally blurred sections. Sign up to view the full version.View Full Document\nUnformatted text preview: Biological Sciences 101 -002\nDr. Mark Sanders\nWinter Quarter 2010 First Midterm Exam Answer Key — FORM C\n1A. 28 chromatids\n1B. 7 chromosomes\n,2 M4 1C. 28 chromatids\n1D. 10 picograms\n1B. 5 picogram ( 1 2A. The F1 are wild-type because the plants are heterozygous for the flower color\n[ mutation. The 3:1 F2 ratio is consistent with inherited variation of a single gene causing\nZ flower color mutation.\n3 4 2B. Genetic complementation\n(6 z 2C. Both mutant lines carry mutations of the same gene.\n< 2D. The F1 progeny are dihybrid and are expected to produce F2 progeny in the ratio 9/16\nyellow to 7/16 white. The F2 progeny will be r+_d+_ (yellow) 9/16, r+_dd (white) 3/ 16,\nL z rrd+_ (white) 3/16, rrdd (white) 1/16. I 6,4, 3A. Cross 1: T tAa x T tAa Both parent tall, axial\nCross 11: TTAa x T-Aa Both parents tall, axial\n3B. )8 = (92-90)2/9o + (28—30)2/30 + (29—30)2/30 + (11-10)2/10 = 0.310\n//M /- Df = 3; P value > 0.90, independent assortment between the gene is not rejected\non the basis of the P value bbing greater than 0.05. \\ l \\/ / 4A. Tall parent Short parent Tall F1 Lane 1 2 3 Kb z 4B. All three band patterns are possible. Homozygous tall will have a single band of 3.4\n:5 kb, homozygous short will have a single band of 2.2 kb and heterozygous (tall) will have z both bands. z 5A. The mutant allele is dominant. The heterozygous organism nor the mutant\nZ homozygote fall short of producing sufficient enzymatic activity to produce the wild-type\n1 z phenotype and both are phenotypic mutants. SB.\nUnaffected Unaffected Affected Affected\nFemale Male Heteroz ous Homo ous Heteroz ous Homoz ous 6A. Each prospective parent has a 2/3 chance of being a carrier (conditional probability).\nwait The chance the first child has galactosemia is (2/3)(2/3)(l/4) = 4/36 = 1/9 63. If the first child has galactosemia, then the parents are carriers. The second child is\nthe product of a heterozygous mating and has a 1A chance of having the disease. “,3” 6C. If the parents are carriers, there is a ‘A chance of disease in each subsequent child and\n<9- a 3A chance of being disease-free. The probability that child 2 and child 3 are disease-free\nis (3/4)(3/4) = 9/16.\n7A. The trait is most likely X-linked recessive. The preponderance of males, the\nl “l uniformity of affected males from an affected mother in generation 11, and the ease of X-\n‘pay/lb linked recessive explanation of affected males in generations III and IV all argue in favor\nl of this mode of inheritance. Q 4/ L 7B. Woman A is most likely GG. Her mate is gY. » 7C. The man C is GY. The woman B has a 1/: chance of being a carrier (Gg). Her\n; maternal grandmother was a carrier and there is a ‘/2 chance of passing the X-linked\naub recessive to Cs mother and another 1/2 chance her mother passes the allele to C. The son\n1 #3 cm and c has a (1/2)(1/4) = 1/8 chance of being affected. 8. The format of this answer is illustrated in Figure 3-8, page 104 of the text. ...\nView Full Document\n- Fall '09\n- Genetics, first child, galactosemia, Midterm Exam Answer, parent Tall F1"

"Assigning genotypes for a sex influenced female dominant trait can be challenging. The trait is dominant in females while at the same time it is recessive in males. It is difficult to use “R” to represent the dominant allele and “r” to represent the recessive allele because they behave differently as they pass from females to males. It is customary to use R’ to represent the allele for the unusual condition and R to represent the normal condition. If the shaded individuals in the tree were expressing the trait we call Herberden’s nodes (bony excrescences on fingers) which is sex influenced female dominant, then:\n- RR would be expressed as no Herberden’s nodes in both males and females (not shaded)\n- RR’ would be expressed as Herberden’s nodes in females (shaded) and no Herberden’s nodes in males (not shaded). This is the difficult one.\n- R’R’ would be expressed as Herberden’s nodes in both males and females (shaded)\nWhen completing this pedigree, begin with females with no Herberden’s nodes, these females would have to be RR (if they had an R’ allele they would have Herberden’s nodes because it is dominant in females) and males with Herberden’s nodes would have to be R’R’ (it takes two alleles for it to express in males because it is recessive in males).\nReal Examples: Heberden nodes or a variety of osteoarthritis.\nPatterns for Sex Influenced, Female Dominant Inheritance\nAfter filling in the genotypes for individuals in several family trees that exhibit this mode of inheritance, some patterns that can be noticed are:\n- If the father possesses the trait, all of his daughters will have it.\n- Two parents having the trait may have sons without it.\n- Parents without the trait may have a daughter with it.\n- Generally, more females than males show the trait.\n- Genes act in pairs, one from each parent.\n- Gene pairs separate during meiosis and the formation of the sex cells along with the chromosomes.\n- When the sperm fertilizes the egg, the father’s genes (and chromosomes) join the mother’s, or both contribute to the genetic makeup of the offspring.\n- One form of a gene may be dominant over another form which is recessive and the dominant form would be expressed."

"Mendel's First Law\nThe genes of an individual do not operate isolated from one another, but obviously are functioning in a common cellular environment. Thus, it is expected interactions between genes would occur. Bateson and Punnett performed a classical experiment that demonstrated genetic interactions. They analyzed the three comb types of chicken known to exist at that time:\nResult: The F1 differed from both parents and two new phenotypes not seen in the parents appeared in the F2. How can this result be explained? The first clue is the F2 ratio. We have seen this ratio before when the F1 from a dihybrid cross is selfed (or intermated). This observation suggests that two genes may control the phenotype of the comb. The gene interactions and genotypes were determined by performing the appropriate testcrosses.\nA series of experiments demonstrated that the genotypes controlling the various comb phenotypes are as follows.\nIt was later shown that the genotypes of the initial parents were:\nRose = RRpp\nPea = rrPP\nTherefore, genotypically the cross was:\nThe development of any individual is obviously the expression of all the genes that are a part of its genetic makeup. Therefore, it is not an unexpected conclusion that more than one gene could be responsible for the expression of a single phenotype. We will now discuss this situation. First let's give a definition.\nEpistasis - the interaction between two or more genes to control a single phenotype\nThe interactions of the two genes which control comb type was revealed because we could identify and recognize the 9:3:3:1. Other genetic interactions were identified because the results of crossing two dihybrids produced a modified Mendelian ratio. All of the results are modifications of the 9:3:3:1 ratio.\nExample 1: 15:1 Ratio\nFor this type of pathway a functional enzyme A or B can produce a product from a common precursor. The product gives color to the wheat kernel. Therefore, only one dominant allele at either of the two loci is required to generate the product.\nThus, if a pure line wheat plant with a colored kernel (genotype = AABB) is crossed to plant with white kernels (genotype = aabb) and the resulting F1 plants are selfed, a modification of the dihybrid 9:3:3:1 ratio will be produced. The following table provides a biochemical explanation for the 15:1 ratio.\nIf we sum the three different genotypes that will produce a colored kernel we can see that we can achieve a 15:1 ratio. Because either of the genes can provide the wild type phenotype, this interaction is called duplicate gene action.\nExample 2: 9:7 Ratio\nIf two genes are involved in a specific pathway and functional products from both are required for expression, then one recessive allelic pair at either allelic pair would result in the mutant phenotype. This is graphically shown in the following diagram.\nIf a pure line pea plant with colored flowers (genotype = CCPP) is crossed to pure line, homozygous recessive plant with white flowers, the F1 plant will have colored flowers and a CcPp genotype. The normal ratio from selfing dihybrid is 9:3:3:1, but epistatic interactions of the C and P genes will give a modified 9:7 ratio. The following table describes the interactions for each genotype and how the ratio occurs.\nBecause both genes are required for the correct phenotype, this epistatic interaction is called complementary gene action.\nExample 3: 12:3:1 Ratio\nWith this interaction, color is recessive to no color at one allelic pair. This recessive allele must be expressed before the specific color allele at a second locus is expressed. At the first gene white colored squash is dominant to colored squash, and the gene symbols are W=white and w=colored. At the second gene yellow is dominant to green, and the symbols used are G=yellow, g=green. If the dihybrid is selfed, three phenotypes are produced in a 12:3:1 ratio. The following table explains how this ratio is obtained.\nShapes of Squash Fruit\nBecause the presence of the dominant W allele masks the effects of either the G or g allele, this type of interaction is called dominant epistasis.\nExample 4: 13:3 ratio\nCertain genes have the ability to suppress the expression of a gene at a second locus. The production of the chemical malvidin in the plant Primula is an example. Both the synthesis of the chemical (controlled by the K gene) and the suppression of synthesis at the K gene (controlled by the D gene) are dominant traits. The F1 plant with the genotype KkDd will not produce malvidin because of the presence of the dominant D allele. What will be the distribution of the F2 phenotypes after the F1 was crossed?\nThe ratio from the above table is 13 no malvidin production to 3 malvidin production. Because the action of the dominant D allele masks the genes at the K locus, this interaction is termed dominant suppression epistasis.\nSuppressor - a genetic factor that prevents the expression of alleles at a second locus; this is an example of epistatic interaction\nRemember that epistasis is the interaction between different genes. If one allele or allelic pair masks the expression of an allele at the second gene, that allele or allelic pair is epistatic to the second gene. Therefore, the following table summarizes the four epistatic interactions discussed above.\nCopyright © 2000. Phillip McClean"

"This histogram shows the distribution of heights among a group of male secondary-school seniors. As you can see, the plot resembles a bell-shaped curve. Such distributions are typical of quantitative traits.\nSome of the variation can be explained by differences in diet and perhaps other factors in the environment. Environment alone is not, however, sufficient to explain the full range of heights or weights.\nAn understanding of how genes can control quantitative traits emerged in 1908 from the work of the Swedish geneticist Nilsson-Ehle who studied quantitative traits in wheat. Using Mendel's methods, he mated pure-breeding red-kernel strains with pure-breeding white-kernel strains. The offspring were all red, but the intensity of color was much less that in the red parent. It seemed as though the effect of the red allele in the F1 generation was being modified by the presence of the white allele.\nWhen Nilsson-Ehle mated two F1 plants, he produced an F2 generation in which red-kerneled plants outnumbered white-kerneled plants 15:1. But the red kernels were not all alike. They could quite easily be sorted into four categories. One sixteenth of them were deep red, like the P type. Four sixteenths were medium dark red, six sixteenths were medium red (like the F1 generation), and four sixteenths were light red.\nThe genetics of the two crosses is shown here. The alleles at one locus are indicated with prime marks; at the other, without.\nThese results could be explained by assuming that kernel color in wheat is controlled by not one, but two pairs of genes, the effects of which add up without distinct dominance. Each pair is located on a different chromosome or so far apart on the same chromosome that there is no linkage. Four alleles for red produce a deep red kernel. Four alleles for white produce a white kernel. Just one red allele out of four produces a light red kernel. Any two out of the four produce a medium red kernel. Any three of the four produce a medium dark red kernel.\nIf one plots the numbers of the different colored offspring in the F2 generation against color intensity, one gets a graph like the one below.\nIn other wheat varieties, Nilsson-Ehle found F2 generations with a ratio of red kernels to white of 63:1. These could be explained by assuming that three pairs of alleles were involved. In these cases, six different shades of red could be detected, but the color differences were very slight. Environmental influences also caused alterations in intensity so that in practice the collection of kernels displayed a continuous range of hues all the way from deep red to white.\nSo the occurrence of continuous variation of a trait in a population can be explained by assuming it is controlled by several pairs of genes — called quantitative trait loci (QTL) — the effects of which are added together. This is called polygenic inheritance or the multiple-factor hypothesis.At first the study of quantitative traits was mostly confined to animal husbandry and the breeding of agricultural crops. It was based on the premise that\nIn more recent times, the search for quantitative trait loci has turned to humans. A number of diseases, cancers for example, are thought to be caused by the additive effects of genes at different loci [view an example]. Pedigree analysis has provided some insights, but the use of microarrays promises to provide more."

"The Evidence of Creighton and McClintock\nIn 1932, the geneticists Harriet Creighton and Barbara McClintock provided an elegant demonstration that the recombination of genes linked on a chromosome requires the physical exchange of segments of the chromosome with its homologous partner.\nDuring their studies of linkage in corn, they developed a strain of corn that had one chromosome (number 9 of 10 pairs) with two unusual features:\n- a knob at one end of the chromosome and\n- an extra piece at the other. The extra piece of chromosome (shown in gray in the figure below) was the result of a translocation that had occurred at an earlier generation.\nHere was an organism with a rare chromosomal aberration that made it possible to distinguish two homologs from each other under the microscope. Furthermore, this unusual chromosome carried the dominant allele for colored kernels (C) and the recessive allele for waxy endosperm (wx). Its normal-appearing mate carried the recessive allele for colorless kernels (c) and the dominant allele for normal (starchy) endosperm (Wx).\nThus the plant was a dihybrid for these two linked traits and, in addition, one chromosome of the pair was visibly marked at each end.\nCreighton and McClintock reasoned that this plant would produce 4 kinds of gametes:\nFertilization of these gametes by gametes containing a chromosome of normal appearance and both recessive alleles cwx (a typical testcross) should produce 4 kinds of kernels:\n- the parental kinds\n- and the recombinant kinds\nproduced by crossing over.\nFurthermore, microscopic examination of each of the plants grown from these four kinds of kernels should reveal the following kinds of chromosomes.\n- colored waxy (Ccwxwx) kernels\n- colorless kernels with normal endosperm (ccWxwx)\n- colorless waxy (ccwxwx) and\n- colored kernels with normal endosperm (CcWxwx).\n- In the first case, there should be one normal chromosome and one extra-long chromosome with the knob at the end.\n- In the second case, both chromosomes should be of normal appearance. However,\n- in the third case (colorless, waxy), where crossing over had occurred, one would hope to find evidence that a physical exchange of parts between the homologous chromosomes of the dihybrid parent had occurred. Either a chromosome of normal length, but with a knob at one end, or an extra-long chromosome with no knob should be present. Creighton and McClintock found the latter, thus indicating that the gene locus for wx was associated with (and thus near) the end of the chromosome with the extra segment. The gene locus for kernel color must then be neared the end with the knob.\n- Examination of the plants in class 4 (colored kernels and normal endosperm) revealed a chromosome of normal length but with a knob at the end.\nThus, behavior of the genes as revealed by the study of the phenotypes produced was shown to be directly related to the behavior of chromosomes as seen under the microscope. The recombination of genes occurs when homologous chromosomes exchange parts.\n17 December 2009"

"A pink aleurone color, varying in intensity and giving a mottled appearance, was observed in stocks of corn homozygous a1a1 and heterozygous Dtdt. Crosses made in the summer of 1946, in the course of other studies with this stock, indicated an unusual mode of inheritance of this color factor called flush.\nIn general, of 105 ears examined, all were either 100% flush, 100% colorless, or segregating 1:1. Selfed plants from flush kernels of segregating ears had two classes of ears; some were altogether colored, and others segregated 1:1. Selfed plants fron colorless kernels of these same segregating ears also had two classes of ears; some colorless and some segregating 1:1.\nFurther crosses made in the summer of 1947 indicated the same pattern of inheritance and especially the total lack of effect of the male parent in determining the phenotype of the offspring.\nWhen the female parent is homozygous for flush, all offspring kernels will be colored regardless of the male constitution, provided only that it comes from the same stock. When the female parent is homozygous colorless, all offspring kernels are colorless. When the female parent is heterozygous, all ears segregate 1:1. However, let us consider the genotype of these kernels. When a heterozygous plant is selfed, half the colored kernels of the offspring ear will be homozygous flush and half heterozygous. Half the colorless kernels will also be heterozygous for flush and half homozygous colorless. All these cases have been observed.\nThe data indicate that the expression of flush depends upon the presence of the allele for color in at least two of the three loci present in each aleurone cell. There is no dominance. This mode of inheritance resembles that of floury.\nLinkage tests are in progress. Expression of flush is independent of Dt. It follows then that the aleurone color factors A2 C and R are all homozygous dominant. When homozygous flush plants were used as female times a1‑et tester stock, the offspring ears were all colorless, indicating the male carried some factor inhibiting expression of flush. However, when sib females were crossed to C.497 a1 tester, some of the kernels on the offspring ear were pigmented faintly.\nThe variability in intensity of color seems to be affected greatly by both environmental conditions and modifiers. Careful grading of color intensity of several ears individually gave in each case a fairly typical normal distribration range with no appearance of sharp discontinuities or classes. When a pale flush heterozygote female was crossed to a deep flush male, the colored kernels on the offspring ear were, on the average, deeper in color than were the colored kernels on ears from crosses of sib females to pale flush males. Thus it appears that the male parent carries modifiers that can affect the intensity of pigmentation, but the male cannot determine whether or not the color will be present.\nUnder controlled environmental conditions this factor may be useful for a quantitative study of modifiers, and further work is in progress."

"|For the mu allele:|\n|mu Allele (MGI)||Gene (MGI)||All Alleles (MGI)|\nAnother coat-color mutation affecting otolith development is muted ( mu) which arose spontaneously in a stock segregating for t-alleles ( Lyon and Meredith, 1965a). This autosomal recessive on chromosome 13 ( Lyon, 1966) slightly dilutes both eumelanin and phaeomelanin ( Lyon and Meredith, 1969). Accordingly black becomes dark grey, yellow and brown become a somewhat lighter shade, and many animals have white underfur. The color of the eyes also is diluted, so that the iris ring appears very light in newborns, and the adult eye is a dark red color. When combined with other genes affecting eye color the eyes may be colorless at birth and pink in the adult. In general, the color change produced by muted ( mu/mu) resembles that produces by ruby-eye ( ru/ru) and beige ( bg/bg) ( Chapter 6, Section I), and is much less severe than that produced by pallid ( pa/pa) ( Lyon and Meredith, 1969).\nAs well as affecting pigment, muted causes changes in postural reflexes very similar to those described above for pallid mice. \"Some muted homozygotes hold the head tilted to one side; some flex the spine and tuck the head under when held by the tail, and give no normal landing reaction when dropped head downwards towards a table\" ( Lyon and Meredith, 1969). As in the case of pallid these behavioral disorders are associated with the absence of otoliths from the sacculus and utriculus of one or both ears as well as by an absence of pigmentation in the membranous labyrinth ( Erway et al., 1966). According to Lyon and Meredith ( 1969) of 17 mu/mu animals examined \"12 lacked all otoliths, 3 had one otolith in each ear, one had two otoliths in the left ear and one in the right, and the remaining one had otoliths in both ears. The bony labyrinth appeared completely normal in all the animals, and none was deaf or showed circling behavior.\"\nAlthough the effect of muted parallels very closely that of pallid, especially insofar as otolith development is concerned, only future studies can reveal whether these two genes act similarly. Of particular interest will be whether supplementing the mother's diet during pregnancy with manganese can alleviate the otolith defect in muted offspring, as it does in pallid mice ( Erway et al., 1971)."

"Genes/Colors and their location:\nBody colors (all autosomal) are:\n– grey – dominant over all over body colors\n– gold/tiger/bronze – recessive\n– blond/gold – recessive\n– albino/rrea – recessive\nthere are two different genes which cause the albino phenotype and which can’t be differentiated.\n– lutino/wrea – recessive\n– there are three types of blau:\none blau –gene shows no red and no yellow\nanother blau gene could show reduced red but no yellow\nand the other blau gene (this one is called “hellblau”, this is a German word which means light blue) could show yellow e.g. snake skin\nis something special because of its peculiarities, it has a reduced number of the big black colour cells (melanophores) and it looks like tiger in its pure manifestation (without the hb). In the combination with the Nigrocaudatus 2 gene (it’s the gene for half black/tuxedo) the back becomes pink, that was the reason for the name “pink”, because the first guppies with this body colour where pink half blacks. It is suspected that they have also an increased number of iridophores. – cream – double recessive, gold + tiger\n– white – double recessive, blau + gold\n– silver – double recessive, blau + tiger\n– “super white” – triple recessive, blau + gold + albino\nyou can breed more combinations but only for these double and triple recessive body colours exists a specific name.\nSome (not all!) colors:\n1. colors for the fore-body (the belly, until the beginning of dorsal in their original appearance):\n– Coral is a metallic red which is in most cases y-linked but there should be one x-linked strain in Germany too.\nIn Germany we call it “neon” . In the combination with one of the blau genes it becomes light blue.\n– Moscow is a y-linked gene in most cases but there are some x-linked strains too.\nIt is a metallic silver until dark blue colour. The intensity depends of the mood of the male. You can find this gene in metal heads (y-linked moscow + y-linked snake skin) or moscow blues (y-linked moscow + y-linked blue + x-linked blue) or in moscow greens and moscow purples\n– Schimmelpfennig Metall (this is the original German name)\nor platinum is a metallic white/yellow/bright purple/bright blue. It is y-linked in most cases but there are some x-linked strains e.g. in Japan too.\n– Lazuli is a light blue which is y-linked (I don’t know it for sure,\nbecause only the Japanese breed it and in Europe there are no lines of this strain, so I had to use a online-translation which could be wrong)\n2. colors for the lower-back:\n– half black (it is the Nigrocaudatus 2 gene)\nis a x-linked gene in most cases but there are some y-linked strains too. It is a more or less black colour. It could become dark blue too after some selective breeding ( you have to increase the number of iridophores which lay above the melanophores) . In combination with the platinum it seems to be greenish.\n– japan blue/aquamarine\nis a light blue which is a y-linked gene in most cases but there are some x-linked strains too.\n– Störzbach (Stoerzbach) metal is a recessive and autosomal metallic blue,\nbut in combination with other colour-genes it makes them a metallic colour e.g. Mikarif (Stoerzbach metal + snake skin)\nThere a lot of colours which consists of several different genes for example full reds. There are 6 (perhaps more) different genes for red and they can be y-linked, x-linked and autosomal, some are dominant and others are recessive, so it’s very difficult to talk about reds and full reds. Some colours are shown on the whole body e.g. snake skin. And some colors are shown on the body and the fins e.g. blues (in blue delta IFGA strains), parrish and hutter greens, snake skins, reds, purples, 3/4 blacks etc.\nThe problem is that some body-colours or normal colours also effect the form of the caudal e.g. you cannot create a half black double sword. There are some genes which are not really a colour like red, but the effect the caudal form too. The x-linked gene “cp” is such a gene. It causes a dark pigmentation of the caudal and together with the “double sword-gene” it causes a delta tail. The delta tail always consists of two or more genes. There has to be the “double sword-gene” (which can be y- or x-linked) and a colour gene for the caudal. Sometimes the male has both necessary genes or the female has both genes or each sex has only one of these genes, but in all these case you got a delta tail.\nI hope you can see that the genetic of the guppy is very complex and to create a new strain is a lot of hard work and a great challenge.\nwhen your cross a grey guppy (GG) with a gold guppy(gg),\nyour will get guppy of these four different genotype (GG), (Gg), (gG) & (gg).\nAll 3 fish with genotype (GG), (Gg), (gG) will turn out to be a grey guppy,\nin this case gene (G) is considered dominant over other gene (g).\nRecessive – A gene in which the trait it represent will not show\nbecause its dominanted by another gene it pair with is considered recessive.\nRefer to the example above,\nthose guppy with genotype(Gg) will turn out to be grey instead of gold\nbecause the gold gene (g) is recessive.\nOnly instance when you can have a gold body guppy\nis when the guppy have this genotype (gg).\nHomozygous – Paired genes that are the same at the same locus(location). Using the above example we can say that a gold body guppy have homozygous gold body trait.\nWe commonly refer a heterozygous guppy as one that does not breed true.\nHeterozygous – Paired genes that are different. Referring to the example above, the grey guppy with (Gg) & (gG) genotype are heterozygous.\nWe commonly refer a homozygous guppy as one that breed true.\nOnly the male can show y-linked traits.\nBut they can also show x-linked taits or a mix of y- and of x-linked traits.\nY-linked means that the gene(s) for this trait are on the Y-chromosome.\nIt’s the same with x-linked. Females can’t show all traits because there is a lack of some special colorcells in their skin. They have all kinds of colorcells but they have less cells of certain kinds than the males.\nIf a y-linked gene becomes x-linked because of a crossing-over the appearance of the phenotype of this trait on the females could be the same as on the males. But sometimes there are some changes in the appearance e.g. japan blue. Females with x-linked japan blue don’t show any blue on the body, they only show sometimes some blue on the caudal. Don’t ask me why they don’t show it. Full gold females show that females have enough iridophores to show metalic colors. You see the same genotype (same genes) doesn’t mean the same phenotype (this what you can see with your eyes if you look on the fsih) at both sexes.\nIt’s like every science: there are more questions than answers and even if got the answer to one question there two new questions in this one answer.\nWhen making outcrosses you want to cross with lines that you are pretty sure are going to give the desired results. Somewhere around 80% to 90% of outcrosses produce fish that are inferior to both parents. When you are selecting which strains of fish you would like to work with, it is advantageous to select lines that can be used to improve each other. Over the years I nave Kept a mental catalog of the crosses that have worked well. Today, these crosses are the backbone of my breeding program. Below are some of the crosses that have worked well in my fish room using my lines. These are pretty well tested crosses so they should work for most lines of these colors.\nReds and H/B Reds: I will use the gold bodied red males into the gray bodied h/b red females to improve the h/b reds. First generation will give 100% h/b reds. These are show stoppers. I then discard all the females from the cross and breed the males back to the pure gray bodied h/b red females. The downside of this cross is losing the deep h/b body color in the males. Always select the females with the darkest body color. (Note: you can create an excellent gray red line by saving some of the F1 females and crossing them back to the pure gold red males. The resultant offspring will be 25% gray reds.)\nReds and Albinos: I will cross the gold red males into the albino females to improve the albino line. The F1 is 100% gray reds. I then take these gray red males back to the pure albino females. Theoretically you should get 30% albinos, but I usually end up with 25-30%. You can then brother/sister these again for about three generations without much loss in vigor or fertility.\nPurples and Greens: One of the best kept secrets in the hobby! This cross works both ways and will produce some excellent blues as well. The purple is dominant and will darken the greens considerably. With this in mind, use the lightest green colored male into the purple females to produce bigger and better greens. To improve the purples, cross the purple males into the green females. To select the grown females from the hybrid cross, shine a flashlight on them at night with the lights turned off. The green females will have a green crescent at the base of the peduncle and the purple females will have a purple crescent.\nVariegated Yellow Snakeskin and H/B AOC (leopard): To improve the pattern in the h/b Aocs, cross the snake males into h/b females. In my lines the h/b is X linked and dominant. This means that the resulting offspring will all be h/b. Take the best male from the cross and breed them back to the pure h/b females. I use this cross about every 5 or 6 generations in my h/b aoc line.\nH/B Pastel and Pastels: To improve the size and finnage of the pastels, cross a gold bodied white pastel into a gray bodied h/b pastel female. The offspring from this cross will be washed out gray bodied h/b pastels. Take the best of these males and breed them back to the pure gold bodied pastel females. The offspring will be 50% gold bodied pastels. These will be bigger and more vigorous than the original pastel line.\nBlue/Green Bicolors and Yellow Variegated Snakeskins: Take the largest blue/green male (don’t worry too much about the color pattern) and cross this fish with the snake females. Take the males from this cross and breed them back to the bl/gr females. I have some excellent bl/gr bis coming up from this exact cross.\nSource; Fish Forums"

"||This article may be too technical for most readers to understand. (June 2009)|\n|Classification and external resources|\nFacial morphology of Waardenburg syndrome, not type IV\nABCD syndrome is the acronym for albinism, black lock, cell migration disorder of the neurocytes of the gut and sensorineural deafness. It has been found to be caused by mutation in the endothelin B receptor gene (EDNRB).\nABCD syndrome is defined as albinism, black lock, cell migration disorder of the neurocytes of the gut, and deafness. It was initially misdiagnosed and later discovered that a homozygous mutation in the EDNRB gene causes ABCD syndrome. This helped scientists discover that it is the same as type IV Waardenburg syndrome, also known as Shah-Waardenburg Syndrome.\nIn the beginning, medical officials defined ABCD syndrome by the four key characteristics of the syndrome. In the first case study of the Kurdish girl, researches described her as having “albinism and a black lock at the right temporo-occiptital region along Blaschko lines, her eyelashes and brows were white, the irises in her eyes appeared to be blue, she had spots of retinal depigmentation, and she did not react to noise.” The albinism is interesting in this diagnosis because the skin of an affected individual is albino pale besides the brown patches of mispigmented skin. The “black locks” described and seen in clinical pictures of the infants are thick patches of black hair above the ears that form a half circle reaching to the other ear to make a crest shape.\nAs identified in this first case study and stated in a dictionary of dermatologic syndromes, ABCD syndrome has many notable features, including “snow white hair in patches, distinct black locks of hair, skin white except brown macules, deafness, irises gray to blue, nystagmus, photophobia, poor visual activity, normal melanocytes in pigmented hair and skin, and absent melanocytes in areas of leukoderma.” Individuals have the blue/gray irises typical of people affected by blindness. The C of ABCD syndrome is what distinguishes this genetic disorder from BADS and it involves cell migration disorder of the neurocytes of the gut. This characteristic occurs when nerve cells do not function correctly in the gut, which results in aganglionosis: The intestines’ failure to move food along the digestive tract. Deafness or being unresponsive to noise due to very low quality of hearing was reported in every case of ABCD syndrome. The characteristics of ABCD syndrome are clearly evident in an inflicted individual.\nNo longer considered a separate syndrome, ABCD syndrome is today considered to be a variation of Shah-Waardenburg type IV. Waardenburg syndrome (WS) is described as “the combination of sensorinerual hearing loss, hypopigmentation of skin and hair, and pigmentary disturbances of the irides.” Hearing loss and deafness, skin mispigmentation and albinism, and pigmentary changes in irises are the similarities between WS and ABCD. According to a dictionary of dermatologic syndromes, Waardenburg syndrome has many notable features, including “depigmentaion of hair and skin - white forelock and prematuring graying of hair, confluent thick eyebrows, heterochromic irides or hypopigmentation of iris, laterally displacy inner canthi, congenital sensorinerual deafness, broad nasal root, autosomal dominant disorder, and other associated findings, including black forelocks.”\nCauses and DNA testing\nResearchers in the past 20 years have determined that a gene mutation, specifically a homozygous mutation in the EDNRB gene, is the cause of ABCD syndrome. The advancement of technology led to new DNA material testing methods and this discovery changed the view of ABCD syndrome completely. A homozygous mutation means that there was an identical mutation on both the maternal and paternal genes. The identifying clinical report stated the test was done by scanning the Kurdish family for mutations in the EDNRB gene and the EDN3 gene by using a test called denaturing gradient gel electrophoresis. The electrophoresis test takes advantage of electrical currents and differences in melting points of fragments of DNA or RNA to move them based on their molecular weight; the differences in mobility of the fragments then can be analyzed to determine different sequences and to detect individual alleles. Different nucleotides in DNA are codes for certain proteins, which are formed by different patterns of the base pairs adenine, thymine, guanine, and cytosine. The combination of adenine and thymine and guanine and cytosine align on the double strands of DNA. The test results found “an aberrant DGGE pattern of exon 3 of the EDNRB gene. The mutation was determined to be a homozygous C to T base pair transition at the amino acid level, causing a premature stop in gene translation.” This specialized testing enables geneticists to recognize the gene mutation that is the cause of ABCD syndrome.\nNew findings introduced an important break in the beliefs about ABCD syndrome because the endotherlin B gene is a gene involved in Shah-Waardenburg syndrome. The endothelin receptor B produces Waardenburg syndrome type IV. Researchers began discussing the possibility that ABCD syndrome was in fact not a syndrome; rather it was a type of another syndrome known as Waardenburg. Discovering that the same gene is involved in ABCD and Waardenburg syndrome is important because researchers can now look further into ways to fix this crucial gene.\nScreening generally only takes place among those displaying several of the symptoms of ABCD, but a study on a large group of institutionalized deaf people in Columbia revealed that 5.38% of them were Waardenburg patients. Because of its rarity, none of the patients were diagnosed with ABCD (Waardenburg Type IV). Nothing can be done to prevent the disease.\nThe occurrence of WS has been reported to be one in 45,000 in Europe. The diagnosis can be made prenatally by ultrasound due to the phenotype displaying pigmentary disturbances, facial abnormalities, and other developmental defects. After birth, the diagnosis is initially made symptomatically and can be confirmed through genetic testing. If the diagnosis is not made early enough, complications can arise from Hirschsprung's disease.\nTreatment for the disease itself is nonexistent, but there are options for most of the symptoms. For example, one suffering from hearing loss would be given hearing aids, and those with Hirschsprung’s disorder can be treated with a colostomy.\nIf the Hirschsprung's disease is treated in time, ABCD sufferers live otherwise healthy lives. If it is not found soon enough, death often occurs in infancy. For those suffering hearing loss, it is generally regressive and the damage to hearing increases over time. Digestive problems from the colostomy and reattachment may exist, but most cases can be treated with laxatives. The only other debilitating symptom is hearing loss, which is usually degenerative and can only be treated with surgery or hearing aids.\nDutch ophthalmologist Petrus Johannes Waardenburg (1886–1979) brought about the idea of Waardenburg syndrome when he examined two deaf twins. Waardenburg decided to define the syndrome with the six major symptoms that patients most commonly had.\n- He defined “lateral displacement of the medial canthi combined with dystopia of the lacrimal punctum and blepharophimosis” referring to people with broader and flatter nasal bridges, which in turn leads to folds in the skin that cover the inner corners of the eye.\n- Secondly, people who are born with a “prominent broad nasal root,” have a widened area between the eyes, causing them to have a flatter and wider face, along with eyes farther apart than normal.\n- Thirdly, “hypertrichosis of the medial part of the eyebrows” is present, meaning excessive hair growth in the patients’ eyebrow region, most likely leading to a unibrow.\n- The fourth symptom, “white forelock,” was commonly seen as depigmented strands of hair\n- “Heterochromia iridis” indicates that the patient has two different colored eyes or two colors in the same eyes.\n- “Deaf-mutism”: People with the disorder are both deaf and mute.\nWhen scientists further investigated the syndrome, they realized that patients exhibited a wider range of symptoms of this disease in different combinations. This helped them distinguish forms of Waardenburg syndrome. Their evaluation consisted of specifying Waardenburg syndrome type I (WS1), type II (WS2), type III (WS3), and type IV (WS4).\nIn 1995, a case study was performed of a Kurdish family. Scientists completed a molecular analysis with DNA strands of the patients diagnosed with ABCD syndrome. Their task was to scan the sequences to find a mutation in the EDNRB gene, one of the most important protein-coding genes. When they completed the scan they “found a homozygous C to T transition resulting, at the amino acid level, in a premature stop codon.” Then, they went back and defined that Shah-Waardenburg syndrome consisted majorly of “mutations in the ENDRB or END3 gene,” along “with [some] SOX10 mutations.” Therefore, the researchers confirmed that ABCD syndrome was a form of Shah-Waardenburg syndrome. The genetic tests that they performed on the patients DNA helped in identifying the appropriate diagnosis.\nIn 2002, Whitkop and other scientists examined patients born with white hair, some black locks, and depigmented skin; he diagnosed them as having black lock albinism deafness syndrome (BADS). Those who were closely working with this case suggested that it was an autoimmune disorder rather than a genetic defect. However, soon after, they had a patient who was one of fourteen children of Kurdish parents. The pedigree they examined revealed autosomal-recessive inheritance which led to cell migration of the neurocytes in the gut and, therefore, they redefined the syndrome as ABCD syndrome. This revealed “a homozygous nonsense mutation in the EDNRB gene” meaning that ABCD syndrome was not a separate entity but rather the same as Shah-Waardenburg syndrome.\n- Gross A, Kunze J, Maier RF, Stoltenburg-Didinger G, Grimmer I, Obladen M (1995). \"Autosomal-recessive neural crest syndrome with albinism, black lock, cell migration disorder of the neurocytes of the gut, and deafness: ABCD syndrome\". Am J Med Genet 56 (3): 322–6. doi:10.1002/ajmg.1320560322. PMID 7778600.\n- Mallory, Susan B. (2006). \"ABCD Syndrome\". An Illustrated Dictionary of Dermatologic Syndromes (2 ed.). Taylor & Francis.\n- Verheij, Joke B.G.M., Jurgen Kunze, Jan Osinga, Anthonie J. van Essen, and Robert M. W. Hofstra (January 2002). \"ABCD Syndrome is Caused by a Homozygous Mutation in the EDNRB Gene\". American Journal of Medical Genetics 108 (3): 223–225. doi:10.1002/ajmg.10172. PMID 11891690.\n- Sato-Jin, Kayo, et al. (April 2008). \"Epistatic connections between microphthalmia-associated transcription factor and endothelin signaling in Waardenburg syndrome and other pigmentary disorders\". FASEB Journal 22 (4): 1155–1168. doi:10.1096/fj.07-9080com. PMID 18039926.\n- Kujat, Annegret, et al (March 2007). \"Prenatal Diagnosis and Genetic Counseling in a Case of Spina Bifida in a Family with Waardenburg Syndrome Type I\". Fetal Diagnosis & Therapy 22 (2): 155–158. doi:10.1159/000097117. PMID 17139175.\n- Waardenburg, P. J. (September 1951). \"A new syndrome combining developmental anomalies of the eyelids, eyebrows and noseroot with pigmentary anomalies of the iris and head hair and with congenital deafness\". American Journal of Human Genetics (American Society of Human Genetics) 3 (3): 195–253. PMC 1716407. PMID 14902764.\n- Disease ID 335 at NIH's Office of Rare Diseases\n- GeneCard for EDNRB\n- OMIM Genetic disorder catalog - Waardenburg syndrome"

"National Organization for Rare Disorders, Inc.\nIt is possible that the main title of the report Waardenburg Syndrome is not the name you expected. Please check the synonyms listing to find the alternate name(s) and disorder subdivision(s) covered by this report.\nWaardenburg syndrome is a genetic disorder that may be evident at birth (congenital). The range and severity of associated symptoms and findings may vary greatly from case to case. However, primary features often include distinctive facial abnormalities; unusually diminished coloration (pigmentation) of the hair, the skin, and/or the iris of both eyes (irides); and/or congenital deafness. More specifically, some affected individuals may have an unusually wide nasal bridge due to sideways (lateral) displacement of the inner angles (canthi) of the eyes (dystopia canthorum). In addition, pigmentary abnormalities may include a white lock of hair growing above the forehead (white forelock); premature graying or whitening of the hair; differences in the coloration of the two irides or in different regions of the same iris (heterochromia irides); and/or patchy, abnormally light (depigmented) regions of skin (leukoderma). Some affected individuals may also have hearing impairment due to abnormalities of the inner ear (sensorineural deafness).\nResearchers have described different types of Waardenburg syndrome (WS), based upon associated symptoms and specific genetic findings. For example, Waardenburg syndrome type I (WS1) is characteristically associated with sideways displacement of the inner angles of the eyes (i.e., dystopia canthorum), yet type II (WS2) is not associated with this feature. In addition, WS1 and WS2 are known to be caused by alterations (mutations) of different genes. Another form, known as type III (WS3), has been described in which characteristic facial, eye (ocular), and hearing (auditory) abnormalities may be associated with distinctive malformations of the arms and hands (upper limbs). A fourth form, known as WS4 or Waardenburg-Hirschsprung disease, may be characterized by primary features of WS in association with Hirschsprung disease. The latter is a digestive (gastrointestinal) disorder in which there is absence of groups of specialized nerve cell bodies within a region of the smooth (involuntary) muscle wall of the large intestine.\nIn most cases, Waardenburg syndrome is transmitted as an autosomal dominant trait. A number of different disease genes have been identified that may cause Waardenburg syndrome in certain individuals or families (kindreds).\nNational Organization for Albinism and Hypopigmentation\nPO Box 959\nEast Hempstead, NH 03826-0959\nMarch of Dimes Birth Defects Foundation\n1275 Mamaroneck Avenue\nWhite Plains, NY 10605\nFACES: The National Craniofacial Association\nPO Box 11082\nChattanooga, TN 37401\n111 E 59th St\nNew York, NY 10022-1202\nNational Vitiligo Foundation\n11250 Cornell Park Drive\nCincinnati, OH 45242\nAlexander Graham Bell Association for the Deaf and Hard of Hearing\n3417 Volta Place NW\nWashington, DC 20007-2778\nAmerican Foundation for the Blind\n2 Penn Plaza\nNew York, NY 10121\nAmerican Council of the Blind\n2200 Wilson Boulevard\nArlington, VA 22201\nNational Association of the Deaf\n8630 Fenton Street\nSilver Springs, MD 20910\nNIH/National Eye Institute\n31 Center Dr\nBethesda, MD 20892-2510\nGenetic and Rare Diseases (GARD) Information Center\nPO Box 8126\nGaithersburg, MD 20898-8126\nPO Box 241956\nLos Angeles, CA 90024\nLet Them Hear Foundation\n1900 University Avenue, Suite 101\nEast Palo Alto, CA 94303\nAmerican Academy of Audiology\n11730 Plaza America Drive, Suite 300\nReston, VA 20190\nPerkins School for the Blind\n175 North Beacon Street\nWatertown, MA 02472\nNational Consortium on Deaf-Blindness\nThe Teaching Research Institute\n345 N. Monmouth Avenue\nMonmouth, OR 97361\nHearing Loss Association of America\n7910 Woodmont Avenue\nBethesda, MD 20814\nCleft Lip and Palate Foundation of Smiles\n2044 Michael Ave SW\nWyoming, MI 49509\nFor a Complete Report\nThis is an abstract of a report from the National Organization for Rare Disorders (NORD). A copy of the complete report can be downloaded free from the NORD website for registered users. The complete report contains additional information including symptoms, causes, affected population, related disorders, standard and investigational therapies (if available), and references from medical literature. For a full-text version of this topic, go to www.rarediseases.org and click on Rare Disease Database under \"Rare Disease Information\".\nThe information provided in this report is not intended for diagnostic purposes. It is provided for informational purposes only. NORD recommends that affected individuals seek the advice or counsel of their own personal physicians.\nIt is possible that the title of this topic is not the name you selected. Please check the Synonyms listing to find the alternate name(s) and Disorder Subdivision(s) covered by this report\nThis disease entry is based upon medical information available through the date at the end of the topic. Since NORD's resources are limited, it is not possible to keep every entry in the Rare Disease Database completely current and accurate. Please check with the agencies listed in the Resources section for the most current information about this disorder.\nFor additional information and assistance about rare disorders, please contact the National Organization for Rare Disorders at P.O. Box 1968, Danbury, CT 06813-1968; phone (203) 744-0100; web site www.rarediseases.org or email email@example.com\nLast Updated: 9/5/2012\nCopyright 1987, 1988, 1989, 1993, 2000, 2003, 2009, 2012 National Organization for Rare Disorders, Inc.\nHealthwise, Healthwise for every health decision, and the Healthwise logo are trademarks of Healthwise, Incorporated."

"South African Journal of Child Health\nversión On-line ISSN 1999-7671\nversión impresa ISSN 1994-3032\nNOUBIAP, J-J N et al. Waardenburg syndrome in childhood deafness in Cameroon. S. Afr. j. child health [online]. 2014, vol.8, n.1, pp.03-05. ISSN 1999-7671.\nBACKGROUND: Waardenburg syndrome (WS) is a rare hereditary disorder essentially characterised by deafness and pigment disorders of the eyes, hair and skin. METHODS: Between October 2010 and December 2011, we identified six patients with WS during an aetiological survey of 582 deaf participants recruited in schools for the deaf and ear, nose and throat outpatient clinics in seven of the ten regions of Cameroon. Two classic characteristics of WS were used as diagnostic criteria: deafness and pigmentation abnormalities (heterochromia iridis, white forelock and depigmented skin patches). In addition, to identify dystopia canthorum, a sign of WS type I, we calculated the W-index. RESULTS: WS comprised 1% of the whole sample, 7% of the genetic cases, and 50% of the genetic syndromic cases. All patients with WS had severe to profound congenital sensorineural and symmetrical hearing loss with flat audiograms. They also had pigment disorders of the eyes and the skin. In the absence of dystopia canthorum, they were all classified as having WS type II. The pedigree was suggestive of autosomal dominant inheritance in two cases, and the four others seemed to be de novo cases. CONCLUSION: The results suggest that WS type II is the most common syndromic form of hearing loss among Cameroonians. This has implications for retrospective genetic counselling and hearing tests for earlier management in affected families."

"2 Answers | Add Yours\nIn this line, Juliet laments Romeo's last name as a result of the feud between their families. She asserts that his name is not as vital as a body part (hand, foot, arm, face). This line is closely akin to \"A rose by any other name would smell as sweet,\" as both relate to the idea that one's name holds little importance in the affairs of affection.\nWhat's more, Juliet wishes Romeo's last name to be different in the last line: \"O, be some other name belonging to a man.\" The \"O\" here shows her dire discontent with the situation, and her request plays directly into the idea of her previous statement about the unimportance of title. Despite her argument that names don't matter, she still desires Romeo's name to be something other than what it is.\nJuliet's musings are a reflection of her love (or lust, depending on your take) for Romeo. Her family (the Capulets) have been feuding with Romeo's family (the Montagues) for decades. She knows the two families would be enraged to know that she and Romeo were in love, and they would do anything they could to prevent them being together.\nJuliet asks what it means to be a Montague--it's just a name. It's not an essential part of who Romeo is (like a hand or a face). As she states before, if was named anything else, he would still just him (and just as wonderful). She wishes for his name to be anything else, so she could be with him peacefully and not cause the trouble between their families.\nWe’ve answered 315,472 questions. We can answer yours, too.Ask a question"

"Scene 2 Act 2\nAnswers 1Add Yours\nThis takes place largely during the famous balcony scene. Juliet is concerned with Romeo's name. Montague is a sworn enemy to her (Capulet) family.\nWhat's in a name? That which we call a rose\nBy any other word would smell as sweet.\nSo Romeo would, were he not Romeo called,\nRetain that dear perfection which he owes\nWithout that title.\nJuliet justifies her love for her sworn enemy by saying that there is really nothing of substance in a name. She reasons that Romeo is good husband material despite his last name."

"It is not what a thing is called that matters, but what it is. The same applies to people\nThe quotation comes from Shakespeare’s tragedy, Romeo and Juliet. The two chief families in Verona, the Capulete and the Montagues, are long-standing enemies. Romoe who is a Montague, falls in love with Juliet, who is a Capulete, and she with him. Knowing that there can be no marriage between the two houses, Juliet laments that she was born a Capulete and he a Montague.\n‘Tis but thy name that is my enemy …\nWhat’s in a name? that which we call a rose\nBy any other name would smell as sweet."

"“What’s in a name?” Shakespeare has Juliet ask in Act II, Scene II of Romeo and Juliet. “That which we call a rose by any other name would smell as sweet,” she says – arguing that a name is merely a label, and a label does not change the essence of a thing.\nIt’s a lovely sentiment, but modern psychological science comes to a different conclusion.\nFor many in the UK, and indeed around the world, one name that matters a great deal is that of William and Kate’s newborn baby. On Monday afternoon, the Associated Press reported that the betting agency Ladbrokes had taken 50,000 bets as the Duchess of Cambridge went into labour. Favourite names were Alexandra for a girl – no longer relevant – and James or George for a boy.\nAnother study, published in the journal Psychological Science in 2011, found that American babies who were born in older parts of the country, such as New England, were more likely to be given popular names. Parents in regions that were once part of the American frontier, such as the Pacific Northwest or the Rocky Mountains, were somewhat less likely to have popular names.\nRead the whole story: The Guardian\nLeave a comment below and continue the conversation."

"What's in a Name?\nClick here to listen to this sermon.\n“Truly, truly, I say to you, whatever you ask of the Father in My name, He will give it to you” (John 16:23).\n“Truly, truly, I say to you, whatever you ask of the Father in My name, He will give it to you” (John 16:23).\nGrace and peace to you from God our Father and the Lord Jesus Christ!\n“What’s in a name? That which we call a rose by any other name would smell as sweet.” So says Juliet Capulet to Romeo Montague in William Shakespeare’s lyrical tale of star-crossed lovers. Juliet tells Romeo that a name is an artificial and meaningless convention, and that she loves the person who is called “Montague,” not the Montague name nor the Montague family. Romeo, out of his passion for Juliet, renounces his family name and vows, as Juliet asks, to “deny [his] father” and instead be “new baptized” as Juliet’s lover.\nBut that begs the question: Is a name simply an artificial and meaningless convention? Certainly, if you started calling roses “skunk blossoms,” they would be no less beautiful and smell just as fragrant. But when you start talking about personal names, then it starts getting personal! In the Old Testament, names were chosen carefully to reflect the character of the person or their relationship to God. Jacob was born “the cheater”; God later gave him the name Israel, “He strives with God.” Family names can carry a lot of weight or baggage. If you come from the Bush or Kennedy families, it’s just expected that you’ll one day seek political office. One current presidential candidate likes his name so much he has it put on almost everything he builds, buys, and sells. But how many people do you think kept the surname, Hitler, after Adolf departed from this world?\nSo, names can be important. But no name is more important than Jesus’ name. Jesus, the name given by the angel, which means “the Lord saves,” for “He will save His people from their sins” (Matthew 1:21). When called before the Council, St. Peter confesses, “Let it be known to all of you… that by the name of Jesus Christ of Nazareth, whom you crucified… this man is standing before you well…And there is salvation in no one else, for there is no other name under heaven given among men by which we must be saved” (Acts 4:10-12).\nSt. Paul tells us Jesus humbled Himself by dying on the cross. “Therefore God has highly exalted Him and bestowed on Him the name that is above every name, so that at the name of Jesus every knee should bow, in heaven and on earth and under the earth, and every tongue confess that Jesus Christ is Lord, to the glory of the Father” (Philippians 2:8–11). No wonder Jesus is able to promise: “Whatever you ask of the Father in My name, He will give it to you” (John 16:23).\nJohn Kleinig tells a story from World War 1 that illustrates the power of Jesus’ name in our prayers:\nTwo unrelated British soldiers, who looked like identical twins, served together in the same unit with the same rank. They came from the opposite ends of society. One came from a good family, was married with a young son, and had a share in his family’s business. The other came from a broken family. The two soldiers became the best of friends. The young man with a good family spent much of his time telling the other about his wife and family. He even told his friend that if he was killed, his friend should take his name and to use it to impersonate him. That is exactly what happened. The man without any family and prospects in life swapped places with his friend who died. The soldier who impersonated his friend gained much more than a new name. He also received membership in a family with loving parents and siblings, a loving wife and son, part ownership of the family’s business, and the social status that went with it. All this became his at the death of his friend by his friend’s word and the gift of his name.[i]\nJesus has done something far greater than that by His incarnation and sacrificial death. He involves us in what Luther calls the great exchange. In His Baptism, Jesus takes on our sin and guilt, our death and damnation; in our Baptism, Jesus gives us His place with God the Father and His status as the only Son of the Father. He takes our sin and disobedience, and credits us with His righteousness and obedience. He gives all that He is and has to us. We get a new self and life from Him.\nAs part of our new identity, Jesus gives us His name and the privilege of praying to God the Father in His name. Jesus explains what He means by this in John 16:23-24, 26-28:\nIn that day you will ask nothing of Me. Truly, truly, I say to you, whatever you ask of the Father in My name, He will give it to you. Until now you have asked nothing in My name. Ask, and you will receive, that your joy may be full… In that day you will ask in My name, and I do not say to you that I will ask the Father on your behalf; for the Father Himself loves you, because you have loved Me and have believed that I came from God. I came from the Father and have come into the world, and now I am leaving the world and going to the Father.\nHere, Jesus is speaking to His disciples on Maundy Thursday. There are two things that Jesus does for His disciples this night before His death. For one, He gives them His Supper, the new testament of His very body and blood, given and shed for the forgiveness of their sins. Although they will not see Him face to face, He will still be with them to the end of the age in His Word and Sacrament. As we speak of often, this is how Jesus is present with His people even today. This is how He comes to us with forgiveness, life, and salvation—in His means of grace.\nHere, in our text, Jesus reinforces another gift: the gift of prayer in His name. “Truly, truly, I say to you, whatever you ask of the Father in My name, He will give it to you.” Until He returns in glory, this is how we converse with our Lord. He comes to us in Word and Sacraments. We go to Him in prayer.\nJesus speaks about two different ways of praying. There was the old way of praying in which people had no direct access to God the Father and His grace. Since the disciples had no access to the Father, they asked Jesus to put their requests to Him. But after Jesus’ death and resurrection, the disciples will be able to pray in a new way that is symbolized at His death by the splitting of the curtain of the temple. Jesus says that after His resurrection, He won’t have to pray for them any longer. He won’t be a third party standing between His Father and the disciples because they will be so closely united with Him in faith that their prayers will be His prayers. Jesus’ disciples will use His name and faith in Him to approach the Father directly in prayer together with Jesus.\nThe most remarkable thing about this new way of praying is that it overcomes our fears about our performance and acceptability. God the Father hears our prayers as if they come from the mouth of Jesus; He is just as pleased with us and our prayers as He is with Jesus and His prayers. He listens to us as we are in Jesus, dressed up in Him and all His qualities. This means that we can now approach our heavenly Father as if we were Jesus Himself and claim all His blessings for ourselves. It also means that our heavenly Father regards and treats us just like His beloved Son. He loves us and hears us as He loves and hears His Son. We are, in fact, as inseparable from Jesus as the head is from the rest of the body. God the Father does not consider us as we are in ourselves, but only as we are in Jesus.\nLuther explains what praying in the name of Jesus means:\nI am justified in saying: “I know that my heavenly Father is heartily glad to hear all my prayers, inasmuch as I have Christ, this Savior, in my heart. Christ prayed for me, and for this reason my prayers are acceptable through His.” Accordingly, we must weave our praying into His. He is forever the Mediator for all men. Through Him we come to God. In Him we must incorporate and envelop all our prayers and all that we do. As St. Paul declares (Romans 13:14), we must put on Christ; and everything must be done in Him (1 Corinthians 10:31) if it is to be pleasing to God.\nBut all this is said to Christians for the purpose of giving them the boldness and the confidence to rely on this Man and to pray with complete assurance; for we hear that in this way He unites us with Himself, really puts us on a par with Him, and merges our praying into His and His into ours. Christians can glory in this great distinction. For if our prayers are included in His, then He says (Psalm 22:22): “I will tell of Thy name to My brethren” and (Romans 8:16–17) “It is the Spirit Himself bearing witness with our spirit that we are children of God, and if children, then heirs, heirs of God and fellow heirs with Christ.” What greater honor could be paid us than this, that our faith in Christ entitles us to be called His brethren and coheirs, that our prayer is to be like His, that there is really no difference except that our prayers must originate in Him and be spoken in His name if they are to be acceptable and if He is to bestow this inheritance and glory on us. Aside from this, He makes us equal to Himself in all things; His and our prayer must be one, just as His body is ours and His members are ours.[ii]\nIn keeping with this teaching of Jesus, we normally address our prayer to God the Father. We may, of course, also pray to Jesus and to the Holy Spirit. But that’s not the normal way. We commonly conclude our prayers to the First Person of the Trinity by saying that we pray “through Jesus Christ” or “in the name of Jesus.” We thereby acknowledge that we pray together with Jesus who intercedes for us and leads us in our prayers. We use the name of Jesus and our faith in Him to approach the Father with a good conscience without fear of condemnation or rejection by Him.\nThis teaching makes us bold and confident in prayer for two reasons. We need not be anxious about whether God is pleased with us or whether He will give us a favorable hearing (1 John 3:21-22; 4:13-15). We need not worry about what to pray for, or how, because Jesus covers us with His righteousness and perfects our prayers. Our performance does not matter; what matters is Jesus and our faith in Him as our intercessor. What matters is His name, His Word, His promises!\nWhat’s in a name? Everything, when it comes to prayer. The power of prayer is not found within us; it is found in Jesus’ name, according to His Word and according to His holy will. To pray in Jesus’ name is to trust that the prayer will be answered because Christ has died for you. To pray in Jesus’ name is to pray with Jesus. Even now, He prays for you until He comes again.\nTherefore, dear friends, rejoice: you can be sure that the Lord hears your prayers for Jesus’ sake… because Jesus brings them to His heavenly Father on your behalf… because you are God’s beloved child… because Jesus died and rose for you. You have forgiveness, salvation, and eternal life. Indeed, you are forgiven for all of your sins. In Jesus’ name. Amen.\n[i] Kleinig, John W. (2008). Grace upon Grace: Spirituality for Today. (p. 168-169). Saint Louis: Concordia Publishing House.\n[ii] Luther, M. (1999). Luther’s Works, vol. 24: Sermons on the Gospel of St. John: Chapters 14-16. (J. J. Pelikan, H. C. Oswald, & H. T. Lehmann, Eds.) (Vol. 24, p. 407). Saint Louis: Concordia Publishing House."

"The Baby Name Uniqueness Analyzer can determine how likely a person with a given name is to encounter another individual with the same name.With the latest trend of selecting unique and unusual names, popular names are not as popular as they once were. The probability that parents in 2021 name their child Liam or Olivia, the top boys' and girls' names, is only 1.04%. Twenty-five years ago the top boys' and girls' names were Michael or Emily. Back then, a baby had a 1.75% probability of being given either name. In other words, a child born twenty-five years ago is over twice as likely to be given the current year's top name than a child born today. While this trend away from the most popular names may be associated with the current generation of parents, it's been occurring for far longer. Only 4.2% of children born last year were given a name in the top ten. In comparison, twenty-five years ago 7.5% of children would be given a name in the top ten, and 50 years ago that number was 12%. A person born into our parents' generation is nearly three times as likely to be given a top ten name than a person born into our kids' generation. As someone who had two other 'Sara's (spelled differently) in her kindergarten class, I am fascinated that the probability of a kindergarten class of 35 in 2023 having any two children with the same name is only 41.9%. The probability of a kindergarten class having three children with the same name? Just 1.6%. That doesn't mean it never happens. With so many kindergarteners in the US, we estimate approximately 2,791 kindergarten classes across the country will have three kids with the same name.\nHow unique is a given name? You might be surprised\nWhere does your data come from?\nThe Social Security Administration (SSA) for baby name popularity and population size. The SSA publishes background information on how the data is collected and distributed for the interested. Average elementary school size comes from the National Center for Educational Statistics. Similar names are computed using a combination of string and phonetic edit distances.\nWere there really ten boys named Sarah in 2015?\nLooks like! Our data comes direct from the US Census Data, and that's what the Social Security Administration (SSA) reports. With a 3,961,981 babies born in 2015, there's bound to be at least a few reporting errors. There's also going to be a few really far out their names. There may have been 10 boys named Sarah, but there were also 16 girls named 'Abcde'.\nHey, my daughter's/brother's/neighbor's name isn't on the list! What gives?\nCongratulations on a super rare name! Your daughter/brother/neighbor is one of a kind! Or, more precisely, one of no more than 4. The Social Security Administration (SSA) does not include baby names when fewer than five babies were given the name.\nLove Baby Names? Try our other Baby Name Apps. The Baby Name Explorer lets you explore names based on gender ratio, substring, popularity, or the number of syllables. If you like more unusual names, you may enjoy the Unique Name Generator, Name Blender which merges two names into one or Alternate Spelling Suggester. Finally, the Nickname Finder can help you find that perfect nick name."

"Boy Names of Combination theme\nCombination names for baby boys, related also with compound, with 307 entries. The term ‘combination names’ is a loose description of either double names or blended names. Double names are two given names, sometimes held together with a dash: consider the English name John Paul, or its French version Jean-Paul. Double names may have been popularized by the Christian tradition of baptism, where a person who was being baptized would be given another name from a biblical figure or saint. Blended names consist of syllables found in two separate names, then put together to coin a new name. Deshawn, e.g., is a blend of the name component “De” and popular boys’ name “Shawn”.\nCombination names are fairly popular baby names for boys, and they are also considered trendy. In 1900, 5.120% of baby boys were given Combination names. There were 9 Combination names ranked within the top 1000 baby names then. Combination names have since experienced a decline in frequency. In 2018, 19 Combination names listed among the top 1000, with a combined usage of 1.377%, having regained their popularity somewhat in the recent decade. Within all Combination names, the English Lincoln was the most commonly used, with a ranking of #40 and a usage of 0.382%."

"Boy Names of Folk theme\nFolk names for baby boys, related also with tribal and clan, with 64 entries. Folk names are related to tribe, kinship, and an idea that clan relationships should stand the test of time.\nFolk names are popular baby names for boys. At the height of their usage in 1931, 8.318% of baby boys were given Folk names. There were 17 Folk names ranked within the top 1000 baby names then. Folk names have since experienced a decline in frequency, but are nonetheless used on a heavy scale now. In 2018, 14 Folk names listed among the top 1000, with a combined usage of 1.859%. Within all Folk names, the English and Dutch Jack was the most commonly used, with a ranking of #28 and a usage of 0.458%."

"Inspired by a recent visualization of the most popular baby names, Brian Rowe of computational design studio Zato Novo wanted to make his own. His take? Visualizing how individual baby names have risen and fallen in popularity across the U.S. since the 1900's.\nCreated from U.S. Census data, Rowe’s interactive map lights up based on prevalence of a particular name in each state. Just plug in a name and watch its popularity spread across the country. There are 29,000 names in the database, so there’s a good chance you can try it out with your own name.\nIn a blog post, Rowe shared some observations from creating the visualizations. He noticed the prevalence of names is sometimes geographically clustered. For example, Terrence was first popular in the Midwest in the 1940's but then became popular in the South by the 1980's. Rowe also thinks some names are clearly influenced by media and pop culture. He credits The Matrix (1999) for the sharp rise of “Trinity” and “Neo”. Here's a comparison of \"Trinity\" in 1998 versus 2000."

"Celebrities aren't the only ones giving their babies unusual names. Compared with decades ago, parents are choosing less common names for kids, which could suggest an emphasis on uniqueness and individualism, according to new research.\nEssentially, today's kids (and later adults) will stand out from classmates. For instance, in the 1950s, the average first-grade class of 30 children would have had at least one boy named James (top name in 1950), while in 2013, six classes will be necessary to find only one Jacob, even though that was the most common boys' name in 2007.\nThe researchers suspect the uptick of unusual baby names could be a sign of a change in culture from one that applauded fitting in to today's emphasis on being unique and standing out. When taken too far, however, this individualism could also lead to narcissism, according to study researcher Jean Twenge, of San Diego State University.\nBaby naming history\nThe results come from an analysis of 325 million baby names recorded by the Social Security Administration from 1880 to 2007. The research team figured out the percentage of babies given the most popular name or a name among the 10, 20, or 50 most popular for that year and sex. Since it wasn't required that people get a social security card until 1937, names before that time may not be random samples of the population, the researchers note.\nResults showed parents were less likely to choose those popular names as time went on. For instance, in the late 1800s and early 1900s, about 5 percent of babies were named the top common name, while more recently that dropped to 1 percent.\n- About 40 percent of boys received one of the 10 most common names in the 1880s, while now fewer than 10 percent do.\n- For girls, the percentage with a top-10 name dropped from 25 percent in about 1945 to 8 percent in 2007.\n- Similar results were seen for the top-50 names. About half of girls received one of the 50 most popular names until the mid-20th century. Now, just one in four have these names.\n(A list of top-10 baby names by year, and their popularity, can be found here.)\nThis trend in baby-naming didn't show a constant decrease. Between 1880 and 1919, fewer parents were giving their children common names, though from 1920 to the 1940s common names were used more often than before. Then, when baby boomers came on the scene, so did more unusual names.\nThe biggest decrease in usage of common names came in the 1990s, said Twenge, who is also an author of \"The Narcissism Epidemic: Living in the Age of Entitlement\" (Free Press, 2009) and \"Generation Me: Why Today's Young Americans Are More Confident, Assertive, Entitled – and More Miserable Than Ever Before\" (Free Press, 2007).\nThe results held even when the researchers accounted for immigration rates and increasing Latino populations, which could bring relatively less common names into the mix.\n\"The most compelling explanation left is this idea that parents are much more focused on their children standing out,\" Twenge told LiveScience. \"There's been this cultural shift toward focusing on the individual, toward standing out and being unique as opposed to fitting in with the group and following the rules.\"\nThe positive side of individualism, Twenge said, is that there is less prejudice and more tolerance for minority groups. But she warns that when individualism is taken too far, the result is narcissism.\n\"I think it is an indication of our culture becoming more narcissistic,\" Twenge said.\nPast research has shown that back in the 1950s parents placed a lot of importance on a child being obedient, which has gone way down. \"Parenting has become more permissive and more child-focused and [parents] are much more reluctant to be authority figures,\" Twenge said.\nAs for whether these unusually named kids will have personalities to match is not known.\n\"It remains to be seen whether having a unique name necessarily leads to narcissism later in life,\" Twenge said. \"If that unique name is part of a parent's overall philosophy that their child is special and needs to stand out and that fitting in is a bad thing, then that could lead to those personality traits.\"\nThe research, which is detailed in the January issue of the journal Social Psychological and Personality Science, also included Emodish M. Abebe of SDSU and W. Keith Campbell of the University of Georgia in Athens."

"Which is more dangerous: a gun or a swimming pool? How much does campaign spending really matter? What truly made crime fall in the 1990s? These are the sort of questions raised—and answered—in the new book Freakonomics: A Rogue Economist Explores the Hidden Side of Everything. In yesterday's excerpt, authors Steven D. Levitt and Stephen J. Dubner explored the impact of a child's first name, particularly a distinctively black name. Today's excerpt shows how names work their way down the socio-economic ladder.\nThe California names data tell a lot of stories in addition to the one about the segregation of white and black first names. Broadly speaking, the data tell us how parents see themselves—and, more significantly, what kinds of expectations they have for their children.\nThe actual source of a name is usually obvious: There's the Bible, there's the huge cluster of traditional English and Germanic and Italian and French names, there are princess names and hippie names, nostalgic names and place names. Increasingly, there are brand names (Lexus, Armani, Bacardi, Timberland) and what might be called aspirational names. The California data show eight Harvards born during the 1990s (all of them black), 15 Yales (all white), and 18 Princetons (all black). There were no Doctors but three Lawyers (all black), nine Judges (eight of them white), three Senators (all white), and two Presidents (both black).\nBut how does a name migrate through the population, and why? Is it purely a matter of zeitgeist, or is there a more discernible pattern to these movements?\nConsider the 10 most popular names given to white girls in California in 1980 and then in 2000. A single holdover: Sarah. So, where do these Emilys and Emmas and Laurens all come from? Where on earth did Madison come from? It's easy enough to see that new names become very popular very fast—but why?\nLet's take a look at the top five girls' names and top five boys' names given during the 1990s among high-income white families and low-income white families, ranked in order of their relative rarity in the opposite category. Now compare the \"high-end\" and \"low-end\" girls' names with the most popular ones overall from 1980 and 2000. Lauren and Madison, two of the most popular high-end names from the 1990s, made the overall top-10 list in 2000. Amber and Heather, meanwhile, two of the overall most popular names from 1980, are now among the low-end names.\nThere is a clear pattern at play: Once a name catches on among high-income, highly educated parents, it starts working its way down the socioeconomic ladder. Amber, Heather, and Stephanie started out as high-end names. For every high-end baby given those names, however, another five lower-income girls received those names within 10 years.\nMany people assume that naming trends are driven by celebrities. But how many Madonnas do you know? Or, considering all the Brittanys, Britneys, Brittanis, Brittanies, Brittneys, and Brittnis you encounter these days, you might think of Britney Spears; but she is in fact a symptom, not a cause, of the Brittany/Britney/Brittani/Brittanie/Brittney/Brittni explosion—and hers is a name that began on the high end and has since fallen to the low. Most families don't shop for baby names in Hollywood. They look to the family just a few blocks over, the one with the bigger house and newer car. The kind of families that were the first to call their daughters Amber or Heather, and are now calling them Alexandra or Katherine. The kind of families that used to name their sons Justin or Brandon and are now calling them Alexander or Benjamin. Parents are reluctant to poach a name from someone too near—family members or close friends—but many parents, whether they realize it or not, like the sound of names that sound \"successful.\"\nOnce a high-end name is adopted en masse, however, high-end parents begin to abandon it. Eventually, it will be considered so common that even lower-end parents may not want it, whereby it falls out of the rotation entirely. The lower-end parents, meanwhile, go looking for the next name that the upper-end parents have broken in.\nSo, the implication is clear: The parents of all those Alexandras and Katherines, Madisons and Rachels should not expect the cachet to last much longer. Those names are just now peaking and are already on their way to overexposure. Where, then, will the new high-end names come from? Considering the traditionally strong correlation between income and education, it probably makes sense to look at the most popular current names among parents with the most years of education. Here, drawn from a pair of databases that provide the years of parental education, is a sampling of such names. Some of them, as unlikely as it seems, may well become tomorrow's mainstream names. Before you scoff, ask yourself this: Do Aviva or Clementine seem any more ridiculous than Madison might have seemed 10 years ago?\nObviously, a variety of motives are at work when parents consider a name for their child. It would be an overstatement to suggest that all parents are looking—whether consciously or not—for a smart name or a high-end name. But they are all trying to signal something with a name, and an overwhelming number of parents are seemingly trying to signal their own expectations of how successful they hope their children will be. The name itself isn't likely to make a shred of difference. But the parents may feel better knowing that, from the very outset, they tried their best."

"The History of Virtue Names\nThoroughly Modern Melody\nAs a naming fashion, virtue names kept on burbling along for many years as a fairly minor tributary to the naming pool. The fashion ebbed and flowed a bit, but it stayed in place fairly well until the beginning of the twentieth century. At that time, most of these names were seen as outdated remnants of eras gone by, and they were discarded for names that were more fashionable and mainstream.\nIt took the social unrest and turmoil of the 1960s to bring virtue names back into at least some semblance of fashion, and it was the hippies who did it. They may not have trusted anyone over 30, but they did unknowingly embrace a naming fashion that even their parents thought was out of date. The rallying cry at the love-ins and peace marches was \"make love, not war,\" and many participants practiced what they preached. Lots of babies were conceived at this time, and some of them received classic virtue names, including Harmony, Freedom, Bliss, and Peace.\nThe use of abstract virtues as names has once again fallen from the spotlight in the world of popular name fashions, but it's by no means dead and buried. In 1997, such virtuous names as Destiny, Faith, Serena, Precious, Chastity, and Divine were given often enough to make it onto the 1,000 most popular names list for girls. Boys' names on the list included Justice, Blessing, and Peerless. What has fallen from favor, however, is the use of some of the most classic abstract virtues as names. Perhaps, unlike the Puritans and the hippies, we find that these names make too strong a statement in an age when being politically correct is of such great concern. However, many parents are still giving their children virtue names. They just don't realize it.\nThe first things most parents look for when they choose a name are the sound and the feel of that name, not what it means. That consideration comes later-if at all-and it's for this reason that almost every baby book (including this one) is formatted by name, not meaning. This doesn't enable an easy search for a virtuous name should you want to find one, but don't let this stop you. They can be relatively easy to find if you know how to look for them. Read Virtue Names and Their Meanings to get you started.\nMore on: Choosing a Name\nExcerpted from The Complete Idiot's Guide to Baby Names © 1999 by Sonia Weiss. All rights reserved including the right of reproduction in whole or in part in any form. Used by arrangement with Alpha Books, a member of Penguin Group (USA) Inc.\nTo order this book visit the Idiot's Guide web site or call 1-800-253-6476."

"Alacamli Surname History\nThe family history of the Alacamli last name is maintained by the AncientFaces community. Join the community by adding to to our knowldge of the Alacamli:\n- Alacamli family history\n- Alacamli country of origin, nationality, & ethnicity\n- Alacamli last name meaning & etymology\n- Alacamli spelling & pronunciation\nLatest photos on AncientFaces\nNo one from the alacamli community has shared photos. Here are new photos on AncientFaces:\nAlacamli Country of Origin, Nationality, & Ethnicity\nNo one has submitted information on alacamli country of origin, nationality, or ethnicity. Add to this section\nNo content has been submitted about the Alacamli country of origin. The following is speculative information about Alacamli. You can submit your information by clicking Edit.\nThe nationality of Alacamli may be complicated to determine because countries change over time, leaving the nation of origin indeterminate. The original ethnicity of Alacamli may be in dispute depending on whether the name came about naturally and independently in different locales; e.g. in the case of family names that come from a craft, which can appear in multiple places independently (such as the family name \"Carpenter\" which was given to woodworkers).\nAlacamli Meaning & Etymology\nNo one has submitted information on alacamli meaning and etymology. Add to this section\nNo content has been submitted about the meaning of Alacamli. The following is speculative information about Alacamli. You can submit your information by clicking Edit.\nThe meaning of Alacamli come may come from a profession, such as the name \"Bishop\" which may have been taken by church officials. Some of these trade-based surnames may be a profession in some other language. This is why it is good to know the ethnicity of a name, and the languages spoken by its progenitors. Many western names like Alacamli originate from religious texts like the Quran, the Bible, the Bhagavadgītā, and so forth. Commonly these family names relate to a religious expression such as \"Favored of God\".\nAlacamli Pronunciation & Spelling Variations\nNo one has added information on alacamli spellings or pronunciations. Add to this section\nNo content has been submitted about alternate spellings of Alacamli. The following is speculative information about Alacamli. You can submit your information by clicking Edit.\nKnowing misspellings and alternate spellings of the Alacamli last name are important to understanding the history of the name. Surnames like Alacamli transform in how they're spelled as they travel across tribes, family branches, and languages over time. In the past, when few people knew how to write, names such as Alacamli were transcribed based on how they were heard by a scribe when people's names were recorded in public records. This could have resulted in misspellings of Alacamli.\nLast names similar to AlacamliAlacan, Alacanagonzalez, Alacan-cappa, Alacander, Alacani, Alacano, Alacan-pumar, Alacan-saa, Alacaoglu, Alacapinar, Alacapunar, Alacar, Alacaras, Alacaraz, Alacardia, Alacardio, Alacaro, Alacata, Alacatag, Alacatei\nalacamli Family Tree\nNo one from the alacamli community have added family members to the alacamli family tree."

"Latest Thiel photos\nThese photos were uploaded by members of the Thiel community on AncientFaces.\nThiel Surname History\nThe family history of the Thiel last name is maintained by the AncientFaces community. Join the community by adding to to this genealogy of the Thiel:\n- Thiel family history\n- Thiel country of origin, nationality, & ethnicity\n- Thiel last name meaning & etymology\n- Thiel spelling & pronunciation\n- genealogy and family tree\nThiel Country of Origin, Nationality, & Ethnicity\nNo one has submitted information on Thiel country of origin, nationality, or ethnicity. Add to this section\nNo content has been submitted about the Thiel country of origin. The following is speculative information about Thiel. You can submit your information by clicking Edit.\nThe nationality of Thiel may be complicated to determine in cases which country boundaries change over time, making the nation of origin a mystery. The original ethnicity of Thiel may be in dispute depending on whether the family name originated naturally and independently in various locales; for example, in the case of surnames that come from professions, which can crop up in multiple regions independently (such as the last name \"Bishop\" which may have been taken by church officials).\nThiel Meaning & Etymology\nNo one has submitted information on Thiel meaning and etymology. Add to this section\nNo content has been submitted about the meaning of Thiel. The following is speculative information about Thiel. You can submit your information by clicking Edit.\nThe meaning of Thiel come may come from a trade, such as the name \"Carpenter\" which was given to woodworkers. Some of these profession-based surnames can be a profession in a different language. This is why it is important to research the ethnicity of a name, and the languages spoken by its family members. Many western names like Thiel are inspired by religious texts such as the Bhagavadgītā, the Quran, the Bible, and so forth. In many cases these names relate to a religious expression such as \"Grace of God\".\nThiel Pronunciation & Spelling Variations\nNo one has added information on Thiel spellings or pronunciations. Add to this section\nNo content has been submitted about alternate spellings of Thiel. The following is speculative information about Thiel. You can submit your information by clicking Edit.\nIn the past, when few people knew how to write, names such as Thiel were transliterated based on their pronunciation when people's names were recorded in government records. This could have led to misspellings of Thiel. Understanding misspellings and alternate spellings of the Thiel last name are important to understanding the history of the name. Last names like Thiel change in their spelling as they travel across villages, family branches, and languages across time.\nLast names similar to ThielThiela Thielaen Thielager Thiélain Thielake Thielamann Thielan Thieland Thiéland Thielant Thielas Thielaske Thielat Thielau Thielbaar Thielbahr Thielbalt Thielban Thielband Thielbar\nThiel Family Tree\nHere are a few of the Thiel genealogies shared by AncientFaces users. Click here to see more Thiels\n- Joseph Thiel 1912 - 1983\n- Helen Thiel 1917 - 1994\n- Catherine Thiel 1886 - 1968\n- Arthur Thiel 1897 - 1978\n- Elizabeth A Thiel 1917 - 2005\n- R Thiel 1976 - 1994\n- Elizabeth A Thiel 1920 - 1999\n- Lawrence Thiel 1936 - 2002\n- Clarence Thiel 1908 - 1980\n- Frank Thiel 1886 - 1962"

"In the spirit of mother's day, I'm answering a question from one of my family members.\nUnfortunately my mom did not get the chance to send me a question, but my Aunt did.\nSo Aunt Itzel from Crestview noticed that many people from ancient history are only known by their first names, so she asked me this:\nWhen did people start using last names?\nAunt Itzel, that's a good question.\nIt certainly helps when you have a common first name like John for instance, but when did last names come about?\nThe nice folks at searchforancestors.com gave us the answer.\nThe officials say the use of a last name is fairly new to human history, and was started to legally distinguish between two people with the same first name.\nThe Chinese were among the first cultures to adopt this practice nearly 5000 years ago.\nSearchforancestors.com says the use of last names first appeared in Venice, Italy somewhere around the 10th or 11th centuries, and it soon spread its way through Europe.\nBut your last name could actually tell you a lot about your ancestors.\nSurnames came from 4 different sources- the father's name, where the family is from, an occupation or social status, or a nickname that describes your looks or personality.\nHere are some examples-\n'Peterson' means son of Peter.\nThe last name 'Kirkpatrick' means from the Church of St. Patrick.\nThe surname 'Cooper' means Barrel Maker.\nAnd if your last name is 'Reid', then your ancestors had red hair.\nIt may be just a name, but a last name can unlock secrets to your family history.\nThanks for your question Aunt Itzel!\nIf any of you have a unique or interesting question, ask me!\nJust send it to:\n1801 Halstead Blvd\nTallahassee, FL 32309\nor email it to John.Rogers@wctv.tv\nBe sure to let me know your name and where you're from and if you're lucky, I'll answer your question LIVE next Sunday!"

"🔼The name Hathath in the Bible\nThe name Hathath occurs only one time in the Bible, although it's not wholly clear whether Hathath is supposed to be a name. If it is, then it belongs to a son of Othniel of Judah (1 Chronicles 4:13). The problem is that the Hebrew speaks of sons, not son, and this \"name\" is identical to a word meaning terror.\nIf the Chronicler would have wanted to submit that the many unnamed sons of Othniel were a terror, he or she would have written the exact same text. It means exactly that.\nBut from ancient times translators have endowed Othniel with one son named Hathath, and thus all modern translations do the same thing.\n🔼Etymology of the name Hathath\nThe name Hathath is identical to the masculine noun חתת (hatat), meaning terror:\nFor a meaning of the name Hathath, both NOBSE Study Bible Name List and Jones' Dictionary of Old Testament Proper Names read Terror. BDB Theological Dictionary does not interpret our name but does confirm that it is identical to the noun חתת (hatat), meaning terror."

"Names Mean Things\nIn our last teaching we covered the name YHVH. Names are nouns, and although virtually every Hebrew noun comes from a verb, when it becomes a noun it will be spelled differently. As a matter of fact, people's names are really not subject to rigid rules. Although it is traditional for eastern cultures to pass family names down from one generation to the next, there are plenty of variant spellings of those names. Names are also given to express an action or event that was taking place at the time of a child's birth. Most of the names in the scriptures come forth from this tradition.\nNouns come in two fundamental forms. A proper noun and a common noun. Nouns are people, places, and things. Proper nouns are those words that can be understood without an article. A few examples of proper nouns are YHVH, Moses, Jerusalem, Mt. Sinai, Kleenex, Coca-cola, Miss America, and O.J. These are words that do not require an 'a' or 'the' in front of them. We do not have to say the Kleenex or a Miss America or the O.J. Common nouns are king, mountain, office, car, husband, wife or pencil. YHVH is a proper noun. Names of people are proper nouns. They require no articles to preceed them. Proper nouns, with few exceptions, are to be transliterated. Take for instance the Hebrew word Mattityahu (Divre HaYamim Aleph 15:18). This name is a proper noun, it should be transliterated. So this name in Greek is Maththaion. In English it is Matthew. In Spanish and Italian it is Mateo. In Dutch it is Matteus. In Czech it is Matous. In Vietnamese it is Mathio. This is the rule of linguistics with few exceptions. For some reason, most western cultures do not have a problem turning the Hebrew common noun satan into a proper noun. In Greek, it is satana. In Russian and Spanish it is satanas. In Vietnamese it is satan. In Latin it is satanae, and in Italian it is satana. Yet for some reason western cultures take the PROPER noun YHVH and make it the common noun Lord. So the enemy's name we turn from common to proper and our Father's name we turn from proper to common. Hmmmmm.\nWhen you see LORD spelled out in all capital letters in your King James Bible, you are looking at a translation of a proper noun. YHVH is our Creator's name. You DO NOT translate it. You transliterate it into the available sounds in other alphabets. The English word LORD, in this case, is neither a translation or a transliteration. Remember that translation is closest in meaning and transliteration is closest in sound. The word LORD is in no way the meaning or the sound of YHVH. So why did they replace YHVH with LORD? - out of deference to Rabbinical thought that no one is to pronounce the ineffable name of the Creator. So at best, they bowed to political pressure.\nThere are hundreds of occurrences of the word Lord in our English Bibles as well. If you will, a capital L and small case 'ord'. When you see this in the text it is a translation of the Hebrew word adonay. In this form the word should have been transliterated, once again, and not translated. It is a proper noun. The King James text should read Adonay, or Adonai and not Lord. The ancient or pictographic meaning of adonay is the hand or work of the first judge. The aleph is the first letter with the meaning of power and strength. The dalet and nun are the letters for judge and the yod is, of course, the letter for the closed hand or the hand that works, makes, forms, and creates. So, instead of properly transliterating this word, they translated it into the Greek word kurios and into the English word Lord. We must keep in mind that the King James translators had the Hebrew and Greek text of the Old Testament to draw from. The words LORD, Lord, and lord in our Old Testaments are all translations of the Greek word kurios. This is the word used in the Septuagint to replace YHVH, 'Adonay and 'adon. The Greek word kurios is a common noun. It was originally only an adjective in Greek. No where is it used as an adjective in the scriptures, for it is used only as a noun (see Kittel's Theological Dictionary of the New Testament pg. 1041). In ancient Greek, this word was used as the lawful owner of a slave. It means having power over something. Since the Greek uses the same word to express YHVH, 'Adonay and 'adon, it is the Hebrew manuscripts and the context that must be sought in order to distingiush who is being addressed, for Hebrew makes a distinction between them. When referring to the Creator, Master and King of the universe, the word YHVH or 'Adonay should be used.\nWhen you see the word lord all in small case letters used in your English Bible, this is a correct translation of the common noun 'adon. This word still means master or superior, but is used to express earthy masters and a respectful term for the leader of a household, a business or governing authority. The word in Hebrew still means a 'first judge', but with respect to those outside of the Creator. Hebrew makes this distinction, Greek and English do not. The Greek kurios is used to express YHVH, a child's father, a wife's husband, a nasty boss, a political leader, Zeus, Tammuz, Ishtar, Mithras or any other number of gods and deities.\nMany of you have probably been told that when using the English word LORD, Lord or lord, that you are actually calling on baal, and that ba'al means lord. Well, not exactly. The Hebrew word ba'al refers to one who rules or masters. So you can see that the meaning is akin to the word 'adonay. It is a perfectly good Hebrew word that generally is used to refer to a husband or a married man. It is made up of the letters bet, ayin and lamed. These letters mean the leader of the house who watches. This is why it is used to refer to a husband in a marriage. It is used twice of the Creator Himself.\n\"For thy Maker is thine husband; the LORD of hosts is his name; and thy Redeemer the Holy One of Israel; The God of the whole earth shall he be called.\"\n\"Turn, O backsliding children, saith the LORD; for I am married unto you: and I will take you one of a city, and two of a family, and I will bring you to Zion:\"\nIf you look this word up in one of our americanized Hebrew lexicons, you will find that one of the main definitions is lord. This is because the editors of the lexicon chose the English word 'lord' to have the closest meaning to this Hebrew word. Because ba'al is a common noun, it must be translated. But this does not mean that ba'al means lord. Ba'al means what it means. Because some culture chose to use this word to refer to their gods or lords, does not mean that in Hebrew ba'al means lord. Assuming a belief in Hebrew being the best modern representation of the first proto-semitic language, it is easily understandable how the first languages to break off and separate in the beginning would have common syllabary's and alphabets. In turning away from the one God of creation, the scattered people after the tower of Babel would begin to worship other beings or predominantly inanimate objects. The names of these objects of worship would naturally be similar to many names and words of the original tongue. Because a group of people called the name of their pagan god ba'al, does not make the Hebrew word ba'al a pagan word. There are many gods in various cultures scattered throughout the world who have names very familiar in Hebrew. Jah, Yaw, Amun, Set, Sobek, Shiva, Allah, Adonis, Ashur, Shamash, Gaal, Pah, Dagon and Yam are but a few.\nFrom a strictly linguistic (how language works) point of view, the words YHVH and Adonay are proper nouns and should be transliterated and pronounced as such. The common nouns 'adon and 'elohiym should be translated. The translation of 'elohiym to 'God' will be covered in our next time together. I have also chosen to write the rest of this series based upon the questions I will get on what I have written so far. Please be patient with me concerning keeping up with the postings on the web site. I am not whining mind you, for I am a most fortunate and blessed man. But through the multiple mediums we are working with right now, I am dancing as fast as I can. Blessings to you."

"What exactly is a wealthy spear? Well, Edgar’s meaning is most likely associated with a prosperous and skilled spearman during the Middle Ages. Especially popular today with Latino parents, Edgar was the name of kings and a famous poet (Edgar Allan Poe) and has been a mainstay on the baby-name charts since the 19th century. Like the prefix for Edwin, its meaning is based on the Old English “ead,” meaning “wealthy”; the second half, “gar,” means “spear.”\nRoyal Baby Names\nKnown as Edgar the Peaceful, this royal ruled England from 959 until his death in 975. He became king at age 16, after the death of his older brother, Eadwig, who had become king when their father, Edmund, died. Edgar's coronation in Bath was so well received that it became the template for future coronations and is still followed today. The young king was called “peaceful” for good reason: Rather than encourage political rivalry among the kings throughout England, Edgar sought to unify all the kingdoms and stabilize the country.\nWondering who else shares this baby name? Check out these well known icons that made this baby name famous.\nEdgar Allan Poe\nEdgar: Baby Name Popularity\nPER MILLION BIRTHS\nU.S. POPULARITY RANKING\nRelated baby name lists\nCheck out these related baby name lists to discover more baby boy and baby girl names and meanings.\nCheck out these popular pages to discover more baby boy and baby girl names and meanings.\nBABY GIRL NAMES A-Z\nClick on a letter to search for more baby girl names and meanings.\nWatch These Videos Next:"

"he who supplants\nThis popular, traditional name has been found in the Bible, among British royalty and in the White House. No fewer than six US presidents—and six Scottish kings—have been named James. Its pop-culture cool is a direct descendant of James Bond and James Dean. It’s also in vogue as a fashionably trendy middle name for girls, less frequently as a first name. That didn’t stop Ryan Reynolds and Blake Lively from naming their eldest daughter James. Non-English takes are fresh and plentiful, from the Irish Seamus and the French Jacques to the Italian Giacomo and the Scottish Hamish.\nRoyal Baby Names\nJames was king of Scotland, and when he became king of England and Ireland, the kingdom of Great Britain was born. His mother was Mary, Queen of Scots; his father was Henry Stuart, or Lord Darnley. When his mother was forced to abdicate the throne, James—who was born on June 19, 1566—became king, even though he was only 13 months old. He formally became king in 1581. Though he was a teen, he was also a clever and shrewd ruler who controlled Scotland’s religious and political factors. When Queen Elizabeth I died, James took over as King of England and Ireland too.\nWondering who else shares this baby name? Check out these well known icons that made this baby name famous.\nJames: Baby Name Popularity\nPER MILLION BIRTHS\nU.S. POPULARITY RANKING\nRelated baby name lists\nCheck out these related baby name lists to discover more baby boy and baby girl names and meanings.\nCheck out these popular pages to discover more baby boy and baby girl names and meanings.\nBABY GIRL NAMES A-Z\nClick on a letter to search for more baby girl names and meanings.\nWatch These Videos Next:"

"When Prince Harry and Meghan Markle named their daughter Lilibet, it was the first time that the Queen’s childhood nickname had been used by any of her descendants. However, little Lili (as she will be known) is by no means the first baby in the royal family to be named after her world famous great-grandmother. We take a look at who is named after the Queen—as well as who she is named after:\nYou only have to look at the numerals after Queen Elizabeth II to know that Elizabeth is a well-established royal name. Queen Elizabeth I reigned from 1558 until 1603 and, while she had no children, the name Elizabeth has continued to feature widely in the royal family since. However, the current Queen was actually named after her mother, Elizabeth Bowes-Lyon, who was the Duchess of York when she gave birth to her first child in 1926. The Queen's middle names are Alexandra (her great-grandmother and wife of King Edward VII) and Mary (her grandmother and wife of King George V). When the Queen ascended to the throne in 1952, she was asked which name she wanted to use as sovereign. Some monarchs, including her father, had not used their given names; he was christened Albert but took the name George VI as sovereign. But when faced with the choice, Elizabeth famously replied, “My own, of course.”\nThe Queen gave her only daughter Princess Anne the name Elizabeth as her first middle name when she was born in 1950, christening her Anne Elizabeth Alice Louise. And the tradition of using Elizabeth as a middle name continues to be popular within the royal family. Three of the Queen’s four granddaughters have the moniker; Zara Anne Elizabeth Tindall, Princess Beatrice Elizabeth Mary, and Lady Louise Alice Elizabeth Mary Mountbatten-Windsor. Having already given Beatrice the middle name Elizabeth, her younger sister Princess Eugenie was christened Eugenie Victoria Helena.\nAmongst the Queen’s great-granddaughters, the picture is similar, with five out of her seven great-granddaughters bearing her name: Isla Elizabeth Phillips, Princess Charlotte Elizabeth Diana, Lena Elizabeth Tindall, Lilibet Diana Mountbatten-Windsor, and now Sienna Elizabeth Mapelli Mozzi."

"When did middle names start in your family?\nThe oldest one of mine is Robert Porten Beachcroft who was born in 1744. I thought 1744 was pretty early, because the majority of middle names in my tree start in the early 19th century, becoming more frequent as that century goes on. I would like to find out more about when it first became fashionable to give children a middle name, and when common-place. The entry in Wikipedia is not very helpful, saying:\nIt is debatable how long middle names have existed in English speaking countries, but it is certain that among royalty and aristocracy the practice existed by the late 17th century (and possibly much earlier), as exemplified in the name of the Stuart pretender James Francis Edward Stuart (1688–1766).\nI consulted Alison Weir’s Britain’s Royal Families and discovered that the first Stuart with two Christian names was born in 1594; Henry Frederick, eldest son of James VI of Scotland and I of England, and his wife Anne. Anne was the daughter of the King of Denmark and Norway and she seems to have brought the practice of middle names into the Scottish Stuarts. When the House of Hanover took over the English throne in 1714 they too added a Continental preference for second and third Christian names. George I was baptized George Louis, and his father was Ernest Augustus, (born in 1629). Perhaps it was George II and his family who made the practice of two names fashionable in London from the 1720s onwards. George III’s descendants had three or even four Christian names and from then on, many of the Royal children have had four names.\nBut the English had, and sometimes still have, a liking for giving a middle name to a child that comes from the surname of a grandparent or great-grandparent (or perhaps a godparent?), whereas the evidence is that our Royal family gave their children grand middle names such as Augustus (meaning ‘great’), not surnames from connected families. Thus Robert Porten Beachcroft is the first in my tree, not only to have a middle name but also one that provides an extra clue to his ancestors, Porten being his mother’s maiden name. His younger brother Joseph Mathews Beachcroft takes the Mathews not from a slip in any spelling of Mathew, but from his paternal grandmother’s maiden name of Mathews.\nThe Beachcrofts were a family ‘made good’ in Georgian London and they were probably only too conscious of status and the fact that they had no real gentry connections, so they were aping the aristocracy, where it was more common to take a female name into the male line when a wife was an heiress in her own right. I would be very interested to know more about when this practice started in families who were not landed gentry and without aristocratic connections, and whether it is confined to London or occurs country-wide. I wonder too whether such names were a way of expressing trading relationships in the City of London. My research has shown that City men married into those families they did business with. Good connections were vital in a world where personal recommendation was key, so a middle name that reminded your associates of connections to well-known business families would be important to help you advance.\nThe first female in my tree to have two Christian names, is Ann Juliana Taunton born in Devon in about 1748. Why did her parents give her such a European sounding middle name? I am glad they did, because with plain Ann as a name, I might not have found her family. The difference between Ann Taunton and the Beachcroft boys, is that her name does not come from a parental snobbery (or business good sense?) that wishes to emphasize valuable connections, but it is nevertheless a fancy sounding name. Perhaps it signifies a different kind of ‘otherness’; one that wishes to distinguish a female child from the run of the mill. Interestingly either Ann or her name was thought to be important enough for the name combination of Ann(a) and Juliana to pass down three generations in her tree. There is certainly room for some more investigation there. Was it fashion or something else entirely?\nWhat are the earliest middle names in your tree? Can you beat 1744? Are they female surnames or normal Christian first names and when did your female ancestors start being given middle names?"

"For me, O reminds me of another quirky mystery associated with my family's surnames.\nAlthough her maiden name appears to be RILEY in most documentation I have found about her so far, my great-grandmother's youngest son, Leo NORTHCOTE, always explained how his mother would sign her name with the \"biggest O she could find\" as Margaret O' RILEY or O'REILLY.\nTwo mysteries ....\n- Why was she signing her name using her maiden name instead of her married surname, NORTHCOTE after she was married? Perhaps Leo was referring to the time before she was married.\n- Why was she signing her maiden name with an O when most records I can find about her family record the surname as RILEY, REILLY or RIELY.\nHowever, there were three records I have found where the O is used but all of these were informed by her son, Leo, or his wife or son, whom he had presumably told the story about her signing her name with \"the biggest O she could find\".\nLeo’s mother was recorded as “Margaret O’Reilly” on his marriage certificate in 1930 and on his death certificate in 1970 she was also recorded with an O at the beginning of her maiden name. Also, on Margaret's death certificate, completed by her son Leo, her father is recorded as Thomas O’Riley."

"Societies and cultures, at least as far back as the Romans, have used conventions when naming their children. In searching my Scottish ancestry, this comes in handy as the Scots for many generations followed a naming convention. The first son was named after the father’s father; the second son after the mother’s father; and, the third son after the father. Girls in Scotland were similarly named: the first daughter after the mother’s mother; the second daughter after the father’s mother; and, the third daughter after the mother, and so on with subsequent children being named, in order, after aunts and uncles.\nKnowing the naming convention can often help direct your family history research. For example, if your great grandparents named their first son John, you would know that John was quite probably the name of the father’s father. Today, these naming conventions are not as frequently used, having given way to pop culture. Miley, for example, did not appear in the top 1000 girl’s names until Miley Cyrus became a pop star and the name surged up to be the 127th most popular name in 2008. My own name of Ian was the 948th most popular boy’s name in 1935 and today it is the 80th most popular name (based on U. S. statistics).\nAs I have suggested in earlier posts, finding ancestors can also be difficult because the name they were commonly known by might not have been their formal or registered name. My grandfather John Graham O’Neill used his middle name as his common name throughout his life. His brother-in-law Gerald Foley, from whom I receive my middle name, was not a Gerald at all which caused me many long hours of frustrating research before I discovered that he was born Louis Fitzgerald Foley. His name appears to be from his mother’s father, Lewis Fitzgerald. Researching Uncle “Gerald’s” brother Clarence Foley was even harder for Clarence was born William Dorsey Foley. Where he or his family derived Clarence I still don’t know but he used that name rather than his given names throughout his life and is listed on many official documents, including his marriage registration, as Clarence.\nGiven names are important in researching family members as they point to your ancestral culture or the honouring of family members through namesakes but you need to be prepared for the mysteries as well. “A rose by any other name…”"

"from The American Heritage® Dictionary of the English Language, 4th Edition\n- adj. Variant of matronymic.\nfrom Wiktionary, Creative Commons Attribution/Share-Alike License\n- adj. Alternative form of matronymic.\n- n. Alternative form of matronymic.\nfrom the GNU version of the Collaborative International Dictionary of English\n- adj. Derived from the name of one's mother, or other female ancestor.\nfrom The Century Dictionary and Cyclopedia\n- Derived from the name of a mother or other female ancestor: correlative to patronymic: as, a metronymic name.\n- n. A maternal name; a name derived from the mother or a maternal ancestor.\n- In anthropology, relating to that form of society in which the child takes its name from the mother's family, or in which the child is reckoned as a member of the maternal family.\nfrom WordNet 3.0 Copyright 2006 by Princeton University. All rights reserved.\n- n. a name derived from the name of your mother or a maternal ancestor\nSorry, no etymologies found.\nThe frozen smile has to go too, along with the metronymic nodding, which sometimes goes on long enough to suggest a placement within the autism spectrum.\nSome writers speak of it as a matriarchal period, but it does not appear that women governed; it is more proper to speak of the family as metronymic, for the children bore the mother's name and maternity outweighed paternity in social estimate.\nDescent henceforth was reckoned in the paternal line, and society had become patronymic instead of metronymic.\nAs we have said before, it is now fairly well established that in the transition from metronymic to patronymic forms, authority did not pass from women to men but from the brothers and maternal uncles of the women of the group to husbands and sons.\nIt is fairly well established that, in the transition from metronymic to patronymic forms, authority did not pass from women to men, but from the brothers and maternal uncles of the women of the group to the husbands and sons.\nIroquois Indians, among whom Morgan lived, were a typical maternal or metronymic people.\nStrictly speaking, therefore, there has never been a matriarchal stage of social evolution, but rather a maternal or metronymic stage.\nAmong many tribes of the North American Indians this metronymic or maternal system was peculiarly well-developed.\nEthnologists and sociologists have practically concluded, from the amount of evidence now collected, that this maternal or metronymic system was the primitive system of tracing relationships, and that it was succeeded among the European peoples by the paternal system so long ago that the transition from the one to the other has been forgotten, except as some trace of it has been preserved in customs, legends, and the like.\nThe following are unique -- Carteret, Doll [Footnote: This may also be a metronymic, from"

"A matronymic is a personal name based on the name of one's mother, grandmother, or any female ancestor. It is the female equivalent of a patronymic. In patriarchal societies, matronymic surnames are far less common than patronyms. In the past, matronymic last names were often given to children of unwed mothers. Other times when a woman was especially well known or powerful, her descendants would adopt a matronym based on her name.\nThe matrilineal communities in South India and Nepal, namely the Bunts and Newars, have family names which are inherited from their mother. Matronymic names are common in Kerala. Daughters take the names of their mothers as the second part of their name.\nPhilippine names legally have the maiden name of the child's mother as a middle name following Spanish and Portuguese custom (as opposed to Anglo-American use of secondary or tertiary given names). Filipino children born to unwed mothers, if not claimed by the father nor adopted by anyone else, automatically bear their mother's maiden name and sometimes middle name.\nSome Vietnamese names also function this way, as less of a \"tradition\" than a style or trend, in which the mother's maiden name is the child's middle name.\nAlthough many English matronyms were given to children of unwed mothers, it was not unusual for children of married women to also use a matronymic surname. For instance, it was traditional during the Middle Ages for children whose fathers died before their births to use a matronym, and it was not unheard of for children to be given a matronym if the father's name was foreign, difficult to pronounce, or had an unfortunate meaning. A child of a strong-minded woman might also take a matronym, as might a child whose name would otherwise be confused with that of a cousin or neighbour. Common English matronyms include Beaton, Custer, Tiffany, Parnell, Hilliard, Marriott, Ibbetson, Babbs, and Megson.\nIn the old Finnish system, women were standardly given matronyms, while men were given patronyms, for example, Ainontytär (female) or Pekanpoika (male). Since the 19th century the system of inherited family names has been used, however, and today nearly all Finns have inherited surnames.\nFamily names derived from matronyms are found in France, especially in Normandy: Catherine, Marie, Jeanne, Adeline. In medieval Normandy (Duchy of Normandy), a matronym might be used when the mother was of greater prominence than the father or the basis for a claim of inheritance, such as in the cases of Henry FitzEmpress and Robert FitzWimarc.\nIreland and Wales (Cymru)\nMatronymics are accepted in the Netherlands but are generally written as given names on identity cards.\nDue to the diversity of family structures in the United States, a considerable variation in naming patterns has emerged, despite the fact that traditional, patrilineal naming practices still constitute the majority. Part of the relatively new variation is due to second-wave feminism, which influenced many women to seek ways of preserving their natal names, family histories, and individual identities as distinct from that of their partners’.\nIt has become more common and accepted for parents to give their children two last names, with or without a hyphen. Also, it is becoming more common to merge surnames to create an entirely new surname, or to invent a new surname from \"whole cloth.\" These options have the advantage of allowing for one, shared nuclear family name.\nAdditionally, it is common for women in professional fields to keep their maiden name after they get married, often without pronounced feminist influences. In these cases, children typically are given the father’s surname.\nAn example of an Arabic matronymic is the name of Jesus in the Qur'an, ‘Īsá ibn Maryam, which means Jesus the son of Mary. The book Kitāb man nusiba ilá ummihi min al-shu‘arā’ (The book of poets who are named with the lineage of their mothers) by the 9th-century author Muḥammad ibn Ḥabīb is a study of the matronymics of Arabic poets. There exist other examples of matronymics in historical Arabic names.\nMost characters in the Bible are referred to with a patronymic. However, Abishai, Joab, and Asahel – the sons of Zeruiah, sister or stepsister of King David – are invariably referred to as \"Sons of Zeruiah\" and the name of their father remains unknown. Also the Biblical Judge Shamgar is referred to with the matronymic \"Son of Anat\".\nThere are indications of a Jewish history of matronymic names. Specifically, in East European Jewish society, there appeared various matronymic family names such as Rivlin (from Rivka/Rebecca), Sorkin (from Sarah), Zeitlin (from Zeitl), Rochlin (from Rachel), Feiglin (from Feige), Havkin (from Hava/Eve) and others.\nIn certain Jewish prayers and blessings, matronyms are used, e.g., \"Joseph ben (son of) Miriam\".\n- Page 201 mentions Mother's name becoming common in naming conventions in Kerala http://shodhganga.inflibnet.ac.in/bitstream/10603/2594/12/12_chapter%203.pdf\n- Bowman, William Dodgson. The Story of Surnames. London, George Routledge & Sons, Ltd., 1932. No ISBN.\n- Levi della Vida, Giorgio; Ḥabīb, MuḥAmmad Ibn; Habib, Muhammad Ibn (1942). \"Muḥammad Ibn Ḥabīb's \"Matronymics of Poets\"\". Journal of the American Oriental Society (JSTOR: Journal of the American Oriental Society, Vol. 62, No. 3 (Sep., 1942), pp. 156-171) 62 (3): 156–171. doi:10.2307/594132. JSTOR 594132.\n- Cross, Earle Bennett (1910). \"Traces of the Matronymic Family in the Hebrew Social Organization\". The Biblical World (JSTOR: The Biblical World, Vol. 36, No. 6 (Dec., 1910 ), pp. 407-414) 36 (6): 407–414. doi:10.1086/474406. JSTOR 3141456."

"What is a name? Way back when, people were given a first name and the last name was typically noted as the son or daugther of the father. For example, John nee Harris, Mary nee Harris, Bertha Marie Pedersdautter or Neils Pederson. All these names have a word that indicate they are the son/daughter of Harris or Peder. The customs of surnames is variable depending upon your heritage; for example, the hispanic culture has in the past included the father and mother's surname in the child's last name.\nWe have all been given surnames (last names). Have you ever thought about what/where your last name came from? Surnames could reflect a person's occupation, locality, or origin. You probably are asking, so what is the big deal? We all have last names. How is understanding my surname (last name) going to be of any assistance in researching my family history? The answer is knowing and understanding your surname (last name) can give you clues into where your family may have lived and their occupations. Additionally, you can possibly discover new relatives.\nOne mistake almost every new genealogist makes, is to assume that the way your last name is presently spelled is the only correct spelling. So for example, if your last name was Harris, the spelling of Haris, Harries, Harris, or any other name, could not be related to you. It is possible the person with the different spelling is not related, but don't write them off to quickly, as they could be related to you and they just spelled their last name differently. Family Search has a brief and to the point article about the spelling of surnames here.\nI came across a website titled Forebears. This site provide a search engine for names where you can type in the surname, see a meaning behind the name, origin and distribution map for the name, and possible alternate spellings of the name. If you would like to research the meaning of a surname, click Forebears Surname. Have fun!"

"Does any of these sentences entail the other one?\nMy last name is Jones.\nMy father's last name was Jones.\nLinguistics Stack Exchange is a question and answer site for professional linguists and others with an interest in linguistic research and theory. It only takes a minute to sign up.Sign up to join this community\nNo. Consider the case of a married woman who took her husband's name (as is still commonplace), her last name is Jones, but her father's last name was Smith\nTraditionally in Western society, the first statement would only entail the second for men or unmarried women, and then only if born within wedlock. Nowadays it's much more complicated as men might change their surname for various reasons, women might not, children born out of wedlock might take their father's surname anyway, and children born within wedlock might take a double-barrelled surname instead of their father's\nIt also definitely fails to hold in many other cultures as the last name is frequently not inherited, at least not in a simple patrilineal fashion\nFor example, the father of a Spanish person whose last name is Diaz might not have the name Diaz at all, instead Diaz will be the mother's paternal surname. Each person in the family has a given name followed by their paternal surname then their maternal surname (although these two surnames are sometimes reversed, with the reverse order being the norm in the related Portuguese) and each parent passes their paternal surname down to their child in their respective surname. I.e. using the example on wikipedia, the son of Ángela López Sáenz and Tomás Portillo Blanco would be Pedro Portillo López\nLikewise, in East Asia (or Hungary) family names appear before the given name, and so the last name is actually the given name so there would be no reason to expect anyone's last name to be the same as their father's\nThere are also a few cultures where patronymics are the norm such as Iceland where ones last name is the name of the father with a suffix meaning son or daughter so, whilst my last name being Jónsson wouldn't tell you anything about my father's last name, it would tell you that his given name is Jón\nLastly, there are a few cultures around the world that don't use surnames at all (especially in Indonesia) and only use a single given name. Obviously in this case, the notion of a last name is not very meaningful at all\nNames are surprisingly complicated, and it's very easy to make incorrect assumptions about them based on your own cultural context (in this case, that someone has a last name, and that it is inherited from the father). There is a good (and surprisingly short) video by Tom Scott summarising some of these issues from the point of view of designing web forms which can be found here\nThat said, in a Bayesian sense, taking the first statement as a prior does increase the likelihood of the latter (especially if speaking to someone who is culturally Western European), although certainly not to certainty (as would be required for entailment)"

"Let’s return to the Soo Hoo family for a bit! So far in this blog I have profiled Nam Art Soo Hoo, the patriarch of the Soo Hoo clan, his oldest son Peter, his oldest daughter Clara, his son Andrew, his daughter Lily, and his two children who died young, Pauline and Lincoln. Impressively, this represents only half of his 11 children, with 5 more children with distinguished careers left to profile. So today we will continue with the family by profiling Miss Antoinette Yut Yan Soo Hoo (司徒月蘭, pinyin Sītú Yuèlán, Cantonese Jyutping Si1tou4 Jyut6laan4).\nTag: Exit – 1932\nToday’s post is about the twin sons of Z. S. Bien and his wife Guojin Li: George Sung-Nian Bien (卞松年, pinyin Biàn Sōngnián) and Paul Bai-Nian Bien (卞柏年, pinyin Biǎn Bǎinián). Before I get into that, however, this seems like a good time to get into traditional naming conventions in Chinese and the way I write the students’ names in this blog.\nSince I am writing (mostly) in English and discussing students in an American context, in this blog I write out the students’ names in Western fashion: given names (first and middle) first, and family name second. You may have noticed that I often refer to students by their first initials and family names, which was the media style of the time used in newspapers and primary sources. Around the turn of the 20th century it was common practice in these sources to refer to men by the initials of their given names, followed by their family name. Unmarried women were referred to as “Miss”, followed by their full given names and family names, or “Mrs.”, followed by the full given names or initials of their husbands and then their husbands’ family names.\nChinese names are, of course, written “backwards” from the Western perspective, with the family name coming first and the given names second. However, because most Chinese given names are two characters long, this means that their names are easily adaptable to the early 20th century Western media style of naming. Z. S. Bien is a great example of this: his given name was “Zue Sun” (currently romanized to Shou Sun), and in Chinese his name was written 卞夀孫, or Biàn Shòusūn. However, since the given name was two characters, it stood in quite well for the American first name-middle name system of given names, making 卞夀孫’s name in America “Z. S. Bien”.\nYou may have also noticed that the three of Z. S. Bien’s children that I have mentioned so far have the name “Nian” (年 in Chinese) as the second character of their given names: Richard Peng-Nian Bien (卞彭年), George Sung-Nian Bien (卞松年), and Paul Bai-Nian Bien (卞柏年). As a matter of fact, Z. S. Bien also shares a bit of his name with his brother, F. S. or Fu Sun (福孫) Bien, the second character of their given names being 孫. This shared character is what is known as a generational name, which is shared by all the members of a current generation in a family, siblings and cousins alike. Since 年 is the generational name of Richard, Paul, and George’s generation, all of Z. S. Bien’s children have it as the second character of their given names, as do F. S. Bien’s daughters, although I have only been able to find documentation of one of them using it: his oldest daughter, whose Chinese given name was Li-Nian."

"Phillips Family Crest, Coat of Arms and Name History\nPhillips Coat of Arms Gallery\nDon’t know which Coat of Arms is yours?\nWe can do a genealogical research. Find out the exact history of your family!Learn More\nSurname Name Meaning, Origin, and Etymology\nThis is a baptismal or patronymic surname meaning “the son of Philip”, deriving from the personal (first) name Philip, an ancient Greek male given (originally Philippos) named meaning “horse-loving” deriving from the compounds philos (loved/dear) and hippos (horse). Given horses were only owned by the rich in classical times, the name was associated by nobility and royalty. It was popularized throughout Chistendom by the Kings of Macedonia (ex. Philip I born in 640 BC and Philip II born 359 BC, the latter being the father of Alexander The Great) as well as one of Christ’s Twelve Apostles (Philip the Apostle born in 80 AD from Antolia who preached in Greece, Syria, and Turkey). Notably, the name was born by five different kings of Spain and six kings of France.\nThe name made its way into medieval England after the Norman Conquest of 1066 AD, where it was spelled as Filippus in Danelaw documents in county Lincolnshire and as “Philipus in the Gilbertine Houses Charters of Lincolnshire, circa 1150 AD”. Another source asserts this last name was first found in Kent, England where legend states the family descended from Maximum, the Roman Emperor and King of Britain in the fourth century AD, and that the family was later pushed into Wales by invading Saxons where they claim descent from Tudwal (born 528 AD) who was a descendant of the First King of Wales, Rhodri Mawr (820-878 AD). The name was also present in Prussia and the Netherlands in early times.\nThis page serve as an excellent resource and authority not only on the over 80 Phillips coats of arms or “family crests” (an erroneous and slightly misleading term, see disclaimer at the very bottom of this page), but also the Phillips family history, Phillips family tree, genealogy, and ancestry, as it is fairly comprehensive compared to other pages on the internet on this heraldic and genealogical topic for this surname. This is a good resource for the Philips Coat of Arms, Philips Family Crest, Phillip Coat of Arms, Phillip Family Crest, Philip Coat of Arms, and Philip Family Crest.\nThe earliest known ancestor of this family (according to wikitree.com) was Artchorp mac Cairebe who was born in Ireland around 300 AD. The last section of this page contains one pedigree of the Phillips family tree from him.\nCommon spelling variants or names with similar etymologies include Phillip, Philip, Philipp, Philipps, Philippe, Phillipps, Philipp, Philip, Philipe, Philipe, Phelippe, Phillip, Philips, Fillups, Fulop, Pilip, Fillip, and others. The first name also has several variants such as Phill, Flip, Feli, Philly, Pip, Pep, or Pippo. The female version is Philippa or Philippine. As a font name, it became less popular after the reigns of Queen Mary and Elizabeth for patriotic reasons ( because Philip II of Spain was married to Queen Mary and both were Catholic). The French first name is Philippe. Foreign equivalent/similar surnames include Philippus (Norse), Philipp/Philipsen (Dutch), Phlups (Flemish), Philp (Swedish), Filippi (Italian), and Filipowicz (Poland).\nPopularity & Geographic Distribution\nThe last name Phillips ranks 47th in popularity in terms in the United Status as of the 2000 Census. The name ranks particularly high in the following eleven states: Tennessee, Alabama, Arkansas, North Carolina, Ohio, Michigan, Indiana, Oklahoma, West Virginia, Delaware, and Alaska.\nThe surname Phillips frequency/commonness ranks as follows in the British Isles: England (50th), Scotland (165th), Wales (17th), Ireland (454th) and Northern Ireland (205th). In England, it ranks highest in counties Cornwall and Hampshire. In Scotland, it ranks highest in Orkney. In Wales, the surname Phillips it ranks highest in counties Pembrokeshire and Carmarthenshire. In Ireland, it ranks highest in Mayo. In Northern Ireland, it ranks highest in county Londonderry.\nThe name is also present throughout the remainder English speaking world: Canada (99th), New Zealand (48th), Australia (56th), and South Africa (222nd).\nThe 1890 book Homes of Family Names by H.B. Guppy, states the following in regard to this surname: “Limiting our attention in the first place to the distribution of Phillips, the commonest form of Philip, we observe that it is confined to Wales and to the part of England south of a line drawn from the Humber to the Mersey, being by far the most numerous in the western half of this area, including Wales, and being much less frequent in the eastern part. Its great home is in South Wales and Monmouthshire, but it is also frequent in Herefordshire, Staffordshire, Cornwall, and Devonshire If we include the several other forms of the name, we find that Philip in its various shapes is still mainly confined south of the line above given, the Phillipsons of Northumberland being the only representatives of the name in the north of England. Philips is not an uncommon name in different parts of Scotland. It will also be remarked that the main features of the distribution are the same, its comparative scantiness in the eastern half of its area and its frequency in the western half, including Wales. In some counties the contractions and corruptions of Philip often take the place of Phillips, the commonest and least altered form, and are associated with it in others. Thus, the frequency of the name of Phelps gives Somerset a pre – eminence that it would not have obtained from Phillips alone. Phelps and Phipps similarly raise the counties of Gloucester and Worcester considerably in the scale. The absence or rarity of Phillips in Warwickshire and Northamptonshire is supplied, or compensated for, by Phipps; and Cornwall receives from Philp a further lift in position. Taking all the forms of the name of Philip together, we find that they distinguish different regions and counties in the following order: first comes South Wales and Monmouthshire, then Cornwall and Gloucestershire, then Herefordshire and Worcestershire, then Staffordshire, and after it Devon and Somerset There are a few distant derivatives of the names of Philip, which I think should be separately treated, to wit, Philpot and Philpots, which are chiefly south of England names. Phippen or Phippin is a Somerset form. However, I am now entering into debatable ground, and can only here remark that the more distant derivatives of Philip do not affect the main features of its distribution already discussed. The Philippos of Norfolk and Suffolk I have not included, there being something suspicious, indicating an independent origin, in the terminal o.”\nThe spelling variants rank as follows in the 2000 US Census: Philips (4,796th), Phillip (5,352nd), Philip (6,779th), Philipp (15,451st), Philipps (18,283rd), Philippe (20,036th), Phillipps (49,333th). The following variants do not rank in in the top 152,000 names: Philipp, Philip, Philipe, Philipe.\nHeritageregistry.net states the following in regard to the names roots in early colonial America: “The Wales Phillips family is the founding root family of the Massachusetts Phillips and New Jersey families. A branch later, via pathways through Somerset England, were signers of the First and Third Charters of Virginia, and thus founding the Phillips of Virginia, North Carolina, and beyond”. The same source also states “From the 15th to the 19th centuries the Philippses of Picton Castle were the most powerful family in Pembrokeshire, exercising tremendous political, social and economic influence over all aspects of local life”.\nEarly Bearers of the Surname\nThe Hundred Rolls of 1273 AD, a census of Wales and England, known in Latin as Rotuli Hundredorum lists four bearers of this surname: Simon filius Philippi (Kent), Henry Phelipe (Norfolk), Alicia Philippes (Huntingdonshire), and Ellis filius Philip (Huntingsonshire). The Poll Tax of Yorkshire in 1379 AD lists one bearer of this last name: Cecilia Philipp.\nHistory, Genealogy, and Ancestry\nThe famous genealogist Bernard Burke’s book “The Landed Gentry” and “Peerage and Knights” discusses several landed/noble branches of the Phillips and Philips family, which are summarized below. More details and Phillips pedigree can be obtained from his books.\nPhilipps of Mabws and Dale Castle\nJohn Philipps Allen Lloyd-Philipps Esquire of Dale Castle in Pembroke, Wales, and of Mabws in county Cardigan, was Justice of the Peace, Deputy Lieutenant, and High Sheriff in 1844. He was born in 1802 and he married Charlotte Caroline, daughter of Captain William Barlet, and had five issue her: John Allen (Justice of the Peace, Colonel Cardigan Militia, Captain in 82 Regiment, married Elizabeth Jones), Faulkonor Cecil, Charlotte Maria Carleton (married Henry Mathias of Haverford West), Elizabeth Mary (married Robert Dudley Ackland of Boulston), and Mary Frances (married Captain John Edwin Corner). He was born with the patronymic Lloyd and he assumed the surname Phillips upon the demise of Richard, Lord Milford, under the will of James Philipps, Esquire of Pent Park, brother of Mary Llyod, his great-great-grandmother. Burke traces the lineage/ancestry back to Tudwal Gloff, 4th son of Rhodri Mawr, King of Wales. The Philipps Coat of Arms (mistakenly called the Philipps Family Crest) is has the following heraldic blazon: Argent, a lion rampant sable ducally gorged and chair or. Crest: A lion as in the arms.\nPhilipps of Picton\nCharles Edward Gregg Philipps was an Esquire of Picton Castle in county Pembroke, Wales who was Justice of the Peace, Lord Lieutenant and Custos Rotulorum of Haverfordwest, as well as Captain of the Pembroke Yeomanry Cavalary. He was the son of Edward Fisher of Spring Dale in county York and Jane Gregg of Lisburn and Colerain in Ireland, who assumed the surname Philipps, in lieu of Fisher, by royal license in 1876 in compliance with the testamentary injunction of his father in law. He was born in 1840 and in 1868, he married Mary Philippa, daughter and co-heir of Reverend James Henry Alexander Philipps of Picton Castle and he had six children with her: Henry Erasmus Edward (born 1871), George William Fisher (born 1878), Ethel Philippa, Hilda Mary, Edith Catherine, and Mabel Gable. The branch of the Philipps family tree from Picton Castle in a line of great antiquity in the south of Wales, and descends from Cadifor ap Collwyn, Lord of Dyfed in county Pembroke, known as Cadifor Vawr (the Great) who died in 1089 AD. Thomas AP Philip of Hyslant in county Carmarthen, a descendant of Cadifor, who married Jane, daughter and co-heir of Sir Henry Donne, of Picton (who was the son of Owen Donne of Muddlescombe and Katherine Wogan of Picton Castle, lineally descended from the lords of Picton) and thus he acquired the estate of Picton. The great grandson of their marriage with Sir John Philipps, 1st Baron of Picton Castle, so created in 1621. He married Anne, daughter of Sir John Perrott, and he had issue with her: Sir Richard, Walter, Hugh (ancestor of Philipps, Bart of Picton), Dorothy (married France, 1st Viscount Valentia, ancestor of the Earls of Anglesey and Mount Norris), Lettice (married John Owen of Trecone), Jane (married James, 1st Viscount of Claneboy), Elizabeth, Mary (married John Scourfield), Olive (married Sampson Lort of Stackpole) and Francis (married Sir Hugh Owen, 1st Baronet of Orleton). The eldest son was Sir Richard Philipps, 2nd Baronet of Picton, married Elizabeth, daughter of Sir Erasmus Dryden, 1st Baronet on Canon Ashby, with whom he had two issue: Sir Erasmus and Frances (married James Philipps of Tregibbie in county Cardigan). The Philipps Coat of Arms (mistakenly called the Philipps Family Crest) is has the following heraldic blazon: Quarterly, 1st and 4th, argent, a lion rampant sable gorged with a ducal coronet, and therefrom a chain reflected over the back or, for distinguished in the centre chief point a cross crosslet of the second, for Philipp; 2nd and 3rd, argent, on a chevron gules three trefoils slipped of the field, in chief as many fleur-de-lis of the second, for Fisher. Crest—1st, Philipps: A lion rampant gorged and chained as in the arms, charged on the shoulder (for distinction) with a cross-crosslet or; 2nd, Fisher: in front of a bulrush erect a kingfisher proper resting the dexter claw on a fleur-de-lis or.\nPhilipps of Aberglasney\nJohn Walters-Phillips was an Esquire of Aberglasney in county Carmarthen, Justice of Peace and Deputy Lietuenant, as well as Hugh Sheriff in 1841. He was born in 1787 and in 1817 he married Ann, daughter of Thomas Bowen of Wann Ifor, and they had three issue: Bridget Jane (married Cecil Anson Harris), Mary Ann (married John Pugh Pryse), and Elizabeth Frances (married Frederick Lewis Lloyd Philipps). He succeeded his maternal uncle, Thomas Philipps, Esquire of Aberglasney in 1824 whereupon he acquired the manor and estate and surname of Philipps. His lineage is traces back to David Walters, Gentlemen of Perthygerant county Cardigan, son of John Walters. This branch of the Philipps family tree bore the following heraldic arms: Quarterly, 1st and 4th, or, a lion rampant sable, between two fleurs-de-lis in chief az. and a stag’s head erased in base gules, for Philipps; 2nd and 3rd, gules three snakes interlaced between two spears’ heads erect in chief, and a rose in base argent, barbed and seeded proper for Walters. Crests—1st, A lion rampant sable, holding between the fore paws an escutcheon or, thereon three snakes interlaced proper, the dexter hind-paw resting on a fleur-de-lis also or, for Philipps ; 2nd, An eagle displayed ermine the body entwined by two snakes respecting each other proper, and holding in each claw a rose, gules slipped and leaved, vert.\nPhilipps of Cwmgwilly\nGrismond Philipps was Esquire of Cwmgwilly in county Carmarthen and Justice of the Peace and Deputy Lieutenant, as well as Captain of the 23rd Regiment. He was born in 1824 and in 1854, he married Marianne, daughter of Major Thomas Bowen, of Pantyderi in Pembroke, and had children with her: Grismond (1867), John Picton (1870), and Catherine Elizabeth (1877). He was the son of Grismond Philipps, Esquire of Cwng, by Catherine his wife, daughter of Thomas Warlow of Castle Hall. The Philipps genealogy can be traced back to the year 1677. Several members of the family were High Sheriffs and Members of Parliament. Grismond Philipps was Esquire of Cwmgwilly, son of George, was a Member of Parliament, who married Anne, daughter of John Ball and had issuer with her: Grismond, John George (went to India), William, Cecil Eliza (married General Baillie), and Catherine Anne Prudence (married W.R.H. Powell) This branch of the Philipps family tree bore the following coat of arms (erroneously called a “family crest”): Argent, a lion rampant guardant sable ducally gorged and chained or. Crest: A lion rampant as in the arms.\nPhilips of the Heath House\nJohn Capel Philips was Esquire of The Heath House in county Stafford and Newlands, counties Gloucestershire who was Justice of the Peace and Deputy Lieutenant who was born in 1831 and in 1857 married Fanny Esther Flower, daughter of Henry Jeffrey, 5th Vissount of Ashbrook, and had five issue with her: Burton Henry (1858), John Augustus (1861), Montagu Capel (1875), Frances Margaret, and Bertha Mary. Burke traces the Philips genealogy or linceage back to Francis Phylyppe, Esquire of Neyther Teyne in the parish of Checkley, county Stafford, who died during the reign of King Edward VI of England and was the great grandfather of Anthony Philips, Esq. In 1617, Anthony married Elizabeth, daughter of Edward Rawlins of Tean. He died in 1648 and was succeeded by his son Richard Philips, Esq. who in 1649, married Christobel, daughter and co-heir of Robert Whetall, of Bignoll Hill, county Stafford. He died in 1685 and was succeeded by his son, Nathaniel Philips, Esquire Esq. of The Heath House, in Checkley, who was born in 1659, who married Elizabeth in 1690,daughter and co-heir of John Stubbs, Esquiore of The Shaw, county Stafford, by Ellen his wife, daughter of John Jervis, Esq. of Chatkill and Meaford, and had three issue with him: John, Richard (ancestor of Phillips-Jordell of Yeardsley Hall in county Chester, the seat of said family), and Nathaniel (ancestor of Philips of Bank Hall). He died in 1737 and was succeeded by his eldest son John. John Philips was Esquire of The Heath House, Lord of the Manors of Upper Teane, Nether Teyne, and Checkley who was born in 1695. In 1722, he married Susanna, daughter and co-heir of John Burton of Derby, and had three issue with her: John, Nathaniel (of Stand, married Elizabeth Hibbert), and Thomas (of Sedgley, ancestor of Philips Baronet of Weston in county Warwick). He died in 1777 and was succeeded by his son John Philips who was born in 1724 and married Catherine, daughter of William Turner of Upper Teane, but he died without issue and was succeeded by his newphew: John Philips. This branch of the Phillips family tree bore the following heraldic arms and crest: Per pale argent and sable within an orle of fleurs-de-lis arg. a lion rampant erminois, ducally crowned, and holding between the paws a mascle or, a canton arm. Crest: A demi-rampant erminois, collared sable ducally-crowned or, holding between the paws a fleur-de-lis arg. within a mascle gold.\nPhilips of Heybridge\nJohn William Philips was Esquire of Heybridge in county Stafford, England, as well as Justice of the Peace, Deputy Lieutenant, and High Sheriff in 1861. In 1852, he married Adelaide Louisa, daughter of Edward Buller of Dilhorn Hall, and had four issue with her: William Morton (1852), Robert Edward (1860), Evelyn Adelaide, and Nina Margaret. In 1867, he married Olivia, daughter of William Dodsworth and had four issue with her as well: John Cyril (1868), Arthur Dodsworth (1869), Lewis Francis (1870), and Maud Laetitia. This family is a branch of the family tree of Philips of Heath House. Robert Philips, Esquire of Hyebridge in county Stafford, was the fourth son of John Philips and Margaret Robinson and in 1825, he married Laetitia, the youngest son of William Hibbert of Hare Hill in county Chester, and he had five issue with her: John William, Edward (born 1832, married Emily Mather and had four children with her), Herbert Philips (born 1834, married Ellen Josephine Langton), Ellen Laetita, and Frances Elizabeth (married Reverend Thomas Wynter Blathwayt, Rector of Durham). This branch bore the same coat of arms as Philips of Heath House.\nPhilips of Welcombe\nRobert Needham Philips was an Esquire of Welcombe in county Warwick, and the Park Manchester who was Justice of the Peace, Deputy Lieutenant, and High Sheriff in 1857, and Member of Parliament for Bury who was born in 1815. His first wife was Anna Maria, daughter of Joseph Brooks Yates, and he had the following children with her: Caroline (married George Otto Trevelyan), and Margaret (married William Edward Price of Tibberton Court). His second wife was Mary Ellen, daughter of John Ashton Yates (a member of Parliament from Lindon) and had the following children with her: Anna Maria. Burke states this branch of the Philips family tree is part of the Heath House branch. Robert Philips, Esq. of the Park, Mancester, and Snittergeld in county Warwick was born in 1760 and in 1798 he married Anne, daughter of Matthew Needham of Nottingham, and had the following issue with her: Mark, Robert Needham, Mary (married Robert Hyde Gregg of Norcliffe Hall), Mary (married Robert Hyde Greg, Esq. of Norcliffe Hall) Sarah Jane (married J.W. Mylne, Barrister-at-Law), Anna Priscilla, Hester Emily (William Duckworth, of Pendleton), Isabella, Elizabeth Lucy, Jessy, Clara Octavia, and Caroline. The eldest son Mark was Esquire of Snitterfield and Welcome was a Member of Parliament for Manchester (from 1832-1847) who was born in 1800 and died in 1873, whereupon he was succeeded by his brother. This branch bore the same coat of arms as Philips of Heath House.\nPhilips of Bank Hall\nFrancis Philips, Esquire of Bank Hall in county Lancaster and Lee Priory, county Kent, was Justice of the Peace and Barrister-at-Law who was born in 1830 and in 1856 he married Caroline Mary, fourth daughter of Reverend Kenrick Prescot, Rector of Stockport. This family is a branch of the Philips family tree of Philips of Heath House. This branch bore the same coat of arms as Philips of Heath House. Nathaniel Philips, Esquire of Manchester, third son of Nathaniel Philips and Elizabeth Stubbs, who was born in 1693 and in 1729 married Elizabeth, daughter and co-heir of John Burton of Derby. They had the following issue: Narthaniel (born 1730, married Hannah Barrow of Salford) and John. He died in 1776 and was succeeded by his younger son John. John was born in 1734 and was an Esquire who purchased the estate of Bank Hall of Heaton Norris in county Lancaster in 1777. He married Sarah, daughter of George Leig of Oughtrington Hall in Chester), and had the following children with her: John Leigh (of Mayfield, Lieutenant Colonel Commandant 1st Regiment Manchester and Salford Volunteers who was born in 1761 and married April Penny and had issue with her), Henry (born 1792), = distinguished painter), Henry (of Philadelphia, born in 1767, married Sophia Chew, had daughter Sophia who married J.C. Montgomery of Eglinton, New York), Nathaniel George (born 1770), Francis, James (born 1777), Thomas (born 1781), Hardman (lived in Philipsburg, Pennsylvania, born 1784, married Sophia Lloyd), Ann (married John Potter and later Reverend George Hulme), Elizabeth (married Reverend George Leigh), and Sarah (married Sir Hungerford Hoskyns, 7th Baronet of Harewood). He died in 1824 and his heir was his fourth son, Francis Philips. Francis Philips was Esquire of Bank Hall, Justice of the Peace, and Deputy Lieutenant who was born in 1771 and in 1792 married Beatrice, daughter of James Aspinhall, a Merchant of Liverpool, with whom he had two sons: Francis Aspinall and Hindley Leight. The Philips genealogy continues for several more generations.\nPhelips of Montacute\nBurke states the following on the lineage of this family: “without dwelling on the tradition that the Phelips family originally migrated into Somerset from Wales, it is certain that it has been seated in cos. Somerset and Dorset for many centuries, and the muniments of title prove that Thomas Phelipp armiger; was a land-owner and resident at Montacute in 1480. He left two sous, Richard, his heir, and Thomas”. The list of ancestry and pedigree and Phelips family tree goes on for many generations and Burke concludes it with a mention of William Phelips, Esquire of Montacure in Somerset who was Justice of the Peace and Deputy Lieutenant, born in 1823. In 1845, he married Ellen Harriet, daughter of William Helyar and he had two issue with her: Edith Ellen and William Robert (Justice of the Peace, of the 6th Dragoon Guards, born in 1846, married Cicely Grace Augusta, daughter of Frederick Fane of Moles Court). The Phelips Coat of Arms (mistakenly called the Phelips Family Crest) is blazoned as follows in heraldry: Quarterly: 1st and 4th, arg., a chevron gules between three roses of the last seeded and leaved proper; 2nd and 3rd, or, on a chevron engrailed vert three eagles’ heads erased argent. Crest—A square beacon or chest on wheels or, filled with fire proper.\nPhelips of Briggins Park\nCharles James Phelips was an Esquire of Briggins Park in county Hertford, as well as Justice of the Peace for county Hertfordshire and Essex. He was born in 1821 and 1870 he married Emily Susannah Dunning, daughter of Charles James Dunning, a captain in the British Royal Navy. The lineage traces back to Reverend Charles Phelios who was born in 1765, the son of Edward Phelips of Montacure of Somerset. He married Mary, daughter of Thomas Blackmore of Briggins Park, and with her had ossue: Edward (Lieutnant in 13th Light Dragoons killed at Waterloo), Mary Anne (married her first cousin, John Phelips) and Charles Phelips. Charles was his son and heir, an Esquire of Briggins Park who was born in 1794 and was Justice of the Peace, Deputy Lieutenant, and High Sheriff in 1794. In 1820, he married Caroline Elizabeth, daughter of James Taylor of Wimpole Street, and had issue with her: Charles James, Edward Blatwayt, George Blackmore, Captain William Douglas, Captain Henry Plantagenet Prescott, Alfred Plumer Ward, Arthur Robert, Frances Emma (married William Philip Honywood of Marks Hall in county Essex), and Caroline Mary (in 1851, he married David Ward Chapman, son of David Barclay Chapman, and had issue with her). The Phelips Coat of Arms (mistakenly called the Phelips Family Crest) was the same arms as that of Phelips of Montacure discussed above.\nSir Robin Francis Phillips was born in 1940 and succeeded his father in 1944, becoming the 3rd Baronet. The lineage traces back to Sir Lionel Philips, 1st Baronet, who was created so in 1912, and was a Deputy Lieutenant and High Sheriff in 1903. He was the son of Philip Saunders Phillips of London, a merchant. Lionel was prominent in the Transvaal gold mining industry and was involved with the political development of South Africa. He was arrested in 1896 and condemned to death, but was released. He was born in 1855 and in 1885, he married Dorothea Sarah Florence Alexandra, daughter of Albert Frederick Ortlepp of Colesburg, Cape Colony. He had three children with her: Harold Lioned (born 1886, Captain in the Royal Airforece who married Hilda Wildman Hills and served in World War I), Francis Rudolph (Captain of the Surrey Yeomanry, born 1888, married Eileen Cicely Mander in 1920). The Phillips Coat of Arms (mistakenly called the Phillips Family Crest) for this branch is blazoned in heraldry as follows: Or on a pile azure, between two greyhounds courant in base sable, a lion rampant of the first, guttee de poix. Crest: A demi-lion azure, between two nuggets of gold and charged with two annulets interlaced palewise or. Motto: Veritas vincet.\nMacPhillips Family of Ireland\nThe book “A genealogical history of Irish families states the following: “MacPhillips family is of Norman origin, being a branch of the Burkes who took the name of MacPhillip from the founder of the family, Philip de Burgo. They possessed large estates in the barony of Ccstello, in the present County of Mayo, their principal seat being at Cloonmore. They had also a castle at Doon, a short distance east of Westport in the same county. Another branch of this family settled in the County of Monaghan. The McPhillips contributed many eminent men to the Irish hierarchy, among whom may be mentioned the Rev. Thomas McPhillip, formerly of Cleenish, Diocese of Clogher. He was educated in France, and was a man of varied learning and profound erudition. His brother, William McPhillips, was a man of much influence in his locality and exercised it on many occasions for the benefit of the people. He was gifted with great mechanical ingenuity, and had he a larger sphere of action would have left an enduring mark”. The name developed into MacPhilbin as well. One source asserts the name was first found in Connacht, where a man named MacPhilbin was one of the chiefs in that area, then named Sil Amachada (in East Galway).\nEarly American and New World Settlers\nElmer Phillips was recorded as living in Virginia (“Att West and Sherlow hundred”) in February 1623.\nThomas Phillips was recorded as living in Virginia (“At Chaplains choise”) in February 1623.\nHenry Phillips was recorded as living in Virginia (“At Warwick Squeake”) in February 1623.\nJohn Phillips was recorded among the dead in Virginia in February 1623.\nRichard Phillips, age 20, came to Virginia aboard the Speedwell of London in May 1635.\nElizabeth Phillips, age 22, came to Virginia aboard the America in June 1635.\nJames Phillips, age 26, came to Virginia aboard the Transport in June 1635.\nThomas Phillips, age 24, came to Virginia aboard the Assurance in July 1635.\nJoseph Phillips, age 28, came to Virginia aboard the Merchant’s Hope in July 1635.\nRichard Phillips, age 14, came to Virginia aboard the George in August 1635.\nEliazer Phillips came to Boston in 1679 aboard the Providence.\nWilliam Phillips, age 28, came to the Barbados aboard the Falcon in December 1635.\nWilliam Phillips, age 17, came to the Barbados aboard the Alexander in May 1635.\nJoseph Phillips, age 20, came to the Barbados aboard the Alexander in May 1635.\nMary, daughter of William and Mary Phillips was baptized in December of 1678 in the parish of Christchurch, Barbados.\nThomas Phillips, age 25, came to St. Christopher’s aboard the William & John in September 1635.\nWilliam Phillips was among a list of convicted rebels who came to the Caribbean in the late seventeenth century aboard the Jamaica Marchant.\nThe book Genealogical Guide to the Early Settlers, mentions 45 different bearers of the Phillips surname who lived in early colonial American (primarily in the 1600s). Several, but not all, will be discussed below:\n1) Andrew Phillips of Charlestown, married Elizabeth, had issue Andrew, Elizabeth (1657), and Ephraim (1659)\n2) Andrew Phillips, likely son of the above, who married Sarah, daughter of Michael Smith of Malden in 1683 and had the following issue with her: Andrew (1687), Ebenezer (1695), and Joanna (1697).\n3) Benjamin Phillips, Marshfield, who married Sarah Thomas, likely daughter of Nathaniel, in 1682.\n4) Caleb Phillips of Roxbury, who married Elizabeth and had issue Caleb (1682), John (1684), Elizabeth (1685), Mary (1688), and Ebenezer (1690)\n5) Charles Phillips of Lynn, had issue David (1656), Abigail, John, George, and John\n6) Daniel Phillips of Newtown, Long Island, 1686, brother of Theophilus, town clerk, may have served in Gallup’s company against Quebec, Canada in 1689\n7) David Phillips of Milford, around 1657\n8) George Phillips of Watertown, the first minister in said town who came aboard the Arabella with Governor Winthrop in 1630, bringing with him son Samuel and wife Elizabeth, and perhaps Abigail. He was the son of Christopher, born in 1593, at Rainham, St. Matins, bear Roughman. He had issue named Zarobabel, Jonathan, Theophilus, Amabel, Ephraim, Obadiah, and others.\n9) George Phillips of Dorchester, a freeman in 1631, perhaps came aboard the Mary and John and moved to Windsor. He had no children.\n10) Henry Phillips of Dedham, freeman in 1639, who was in an artillery company in 1640. He married Elizabeth Brock and later Ann Hunting and had issue named Eleazer, Hannah, and Abigail. His third wife was Mary, daughter of John Dwight, with whom he had the following issue: Nathaniel, Eleazur, Henry, Timothy, Mary, Samuel, Elisa, Jonathan, Mehitable, John, John, and Elizabeth.\n11) Henry Phillips of New London, listed on a tax record in 1667\nIn Canada, some of the earliest immigrants bearing this name include Diana and Eleonor Phillips who came to Nova Scotia in 1750. In Australia, one of the first bearers of this name was Bat Phillips, a convict from Middlesex, England who came to New South Wales (then a penal colony) aboard the Agamemnon in April of 1820. In New Zealand, several bearers of this name came in 1941 to Wellington aboard the Lord William Bentinck: William, Catherine, John, Fanny, and Henry Phillips.\nEarly Americans Bearing the Phillips Family Crest\nCharles Bolton’s American Armory (1927) contains three for this surname:\n1) Arg a lion sa ramp sa gorged [gu?] and chained [or?] Crest: a demi-lion ramp guard. Motto: Omnes benevolentia. Bookplate James Phillips.\n2) Or a lion ramp sa gorged and chained Crest: a lion sejant sa gorged and chained. Bookplate Phillips Academy, Andover, Mass. Another with azure field and a chief erm, the crest a demilion ramp guard.\n3) Or a lion ramp gorged sa. Impaling: Sa on a chev or [arg?] 3 sprigs of broom [vert]. On a canton or a spear head erect [az] embrued [gu] (Bromfield) Crest: a lion pass sejant. Engr. on flagon from Hen. William Phillips, 1804. Old South Ch., Boston. Old Sil. Am. Ch., p. 56.\nCrozier’s General Armory (1904) contains two entries for this name:\n1) Reverend George Phillips of Watertown, Massachusetts, 1630, from Boxford. Azure, a lion rampant sable, ducally gorged and chained or. Crest: A lion as in the arms. Motto: Ducit amor patriae.\n2) Mrs. William E. Phillips of Baltimore Maryland. Same Arms as Richard Gundry of Maryland: Argent two lions passant guardant, in pale azure. Crest: A demi lion holding in the dexter paw a sword all or.\nMatthew’s American Armoury (1907) and Bluebook contains one entry for this name: Henry Byron Phillips was born in Summit, Rhode Island in 1850. He married Henrietta, daughter of William F. Coper, Mayor of Santa Cruz and had three issue with her: Stanley Cooper, Alice Willetta, and Edith Henrietta. Arms: William: Azure, a lion rampant gules by nine pheons or. Lathame: Or, on a chief indented azure three plates. Arnold: Gules, a chevron ermine between three pheons or. He was the son of Albert Alexander Phillips of Scituate Rhode Island and Almira Rice. The author states he desends from Michel and Barbara Phelips (or Felipe) who descended from “ancient Irsaelitish stock of Spain, viara Portugal and Holland, of Newport, Rhode Island, 1668”.\nWe have identified 25 Phillips family mottoes (and mottos for its spelling variants such as Philips, Phillip and Phillip)\n1) Mens conscia recti (A mind conscious of rectitude)\n2) Cwell angau neu chivilydo or Gwell angau na Chywilydd (Better death than dishonor)**\n3) Animo et fide (By courage and faith)\n4) Spero meliora (I hope for better things)\n5) Ducit amor patriae (Patriotism leads me)**\n6) Pro Deo et rege (For God and King)\n7) Deus, patria, rex (God and the Fatherland)\n8) Quod justum non quod utile (What is just, not what is useful) (of Garedon Park)\n9) Ce m’est egal (It’s all the same to me)\n10) Nil nisi honestum (Nothing unless honorable)\n11) Simplex munditiis (Plain with neatness) (Philips of Somerset)\n12) Fy Nuw a Chymry (My God and Wales)\n13) Virtute et fide (By virtue and faith)\n14) Vivis sperandum (Where there is life there is hope)\n15) Sors omnia versat (Fate whirls everything about)\n16) Non dormit qui custodit (Who guards doesn’t sleep)\n17) Adjuvante Deo (God my helper)\n18) Arr dduw y Gyd (All depends on God)\n19) Auspice Deo extuli mari (God being my leader, I brought him out to sea)*\n20) Erectus non elatus (Exhalted, but not elated)\n21) Flecti non frangi (To be bent not to be broken)\n22) Quod tibi vis fieri facias (Do what you wish to be done to yourself) (Philipse)\n23) Per mutlos annos (Through many years)\n24) Omnes benevolentia (All goodwill)\n25) Pro aris et focis (For God and country or For altars and hearths)\n26) Veritas vincet (Truth prevails)\n*Upon a mount vert, in front of a Newfoundland dog. sejant, reguardant ppr. an Escutcheon ar. thereon, in base, waves of the sea, and floating therein a naked man, the sinister arm elevated also ppr. The crest and motto are borne in consequence of the life of William Phillips, Esq., of Cavendish Square, having been saved from drowning in Portsmouth harbour by a strange dog; this canine preserver was received into the family and passed the remainder of his days in ease and com fart. John William Phillips-Marshall, now deceased, was one of the Admirals of our Royal Navy ; he was a natural son of William Phillips. Esq., of Cavendish ppr (whose life was saved as stated above). His brother (Phillips) a clergyman, Vicar of Eling, Hants, also bore the same crest and motto.\n**A line from the ancient Roman poet Virgil (from the poem Aenied?)\n***Motto of the Welsh Regiment\nWe have 83 coats of arms for the Phillips surname depicted here. These 83 blazons are from Bernard Burke’s book The General Armory of England, Ireland, and Scotland, which was published in 1848. The bottom of this page contains the blazons, and in many instances contains some historical, geographical, and genealogical about where coat of arms was found and who bore it. People with this last name that bore a Phillips Coat of Arms (or its numerous spelling variants) include:\n1) Philip-Broade after Stanier, Francis, of co. Staff., \n2) Philipps to Lee, William, of co. York and Berks., \n3) Philipps, late Mansel, Richard, of Wales, \n4) late Grant [Sir Richard Bulkeley Philipps Phillips, Bart.], of Picton Castle, Wales [Roy. Lic, 10 Feb. 1824], \n5) Philipps, Sir Richard Bulkeley-Philipps, Bart., Baron Milfokd [21 Sept. 1847]. Supporters, [1847 ?]\n6) Philipps after Walters, . . . ., of Newcastle Emlvn and Aber Glasney, co. Carmarthen, and Bethgeraint, co. Cardigan, Wales, \n7) Philipps, late Lloyd, John Philipps Allen Lloyd Philipps, of Dale Castle, &c., Wales, \n8) late Lloyd, Col. James, of Dale Castle, &c., Wales, \n9) late Gwyther, . . . ., of Picton Castle, co. Pembroke, Wales, \n10) late Fisher , Charles E. Gregg, of Wales, and the Middle Temple, London (Gregg-Philipps. Bart.), 1876.\n11) Philipps to Scourfield, of Wales ; Williamston, The Mote, and Robeston Hall, co. Carab., \n12) to Maxnell, Maj. Courtenay, of Coedgaing, co. Carmarthen, Wales. Exemplification of Manx only. \n13) Dursley, co. Glouc. (See Phelps, or rather Purnell.) .\n14) Philips to Scott, (Spr.), of nr. Moreton-in-the-Marsh, co. Glouc, reputed dau. of Scott, of Bank Fee House, Vol\n15) Philips, John, of Heath House, co. Staff. Stubbs quartering, .\n16) Rev. Gilbert H., M.A., of co. York. Quartering Stubbs and Burton, \n17) Rev. Gilbert H., M.A., of co. York. Quartering Henderson, \n18) Phillipps after March, of co. Dorset. Quartering, \n19) Phillipps, late Winsloe, Thomas, of Collipriest, co. Devon, and Newport House, Camelford, co. Cornw. (Roy. Lie, 8 Nov. 1798), .\n20) Phillipps, James Orcbard Halliwell- (s. of Thomas, of Brixton Hill, deed.), F.R.S., of Jesus Coll., Camb., and Lincoln’s Inn, London, 1850, aged 30, 1872.\n21) of Lougworth, Lagwardine and Eaton Bishop, co. Hereford, \n22) Phillipps-Flamank, Rev. William [Phillipps], B.A., of Lanivet and Boscarne, CO. Cornw., and Glympton, co. Oxf., [1819 ?]\n23) Phillips-Treby, Col. Paul Winslow, R.A., of Goodarnor Plympton St. Mary, co. Devon, 1877,\n24) Phillips, Sir Thomas, Bart., of Middle Hill, co. Wore. First grant, \n25) Phillips after Spencer, of Riffhams, Langford Parsonage and Terling, co. Essex. Quarterly Arms, \n26) Phillips, Thomas, of Leeds, co. York.\n27) Phillips to Nicholson, William, B.A., of Roundhay, co. York, 1827,\n28) Phillips, John, of Hanbury Hall, co. Wore, [16 Feb.] 1825.\n29) Phillips, late Brown, Gov. of Penang, nat. s. of Maj.-Gen. Phillips, Gov. of Windsor Castle, and dau., wife of Bignell, 1825.\n30) late Brown, Maj.-Gen. Sir Charles, of Lyndhurst, Hampsh., 1825,\n31) Phillips, Edward, J.P., of Coventrv. co. Warw., and to the descendants of his father William, deed, 11 July 1835,\n32) Maj.-Gen. Sir Benjamin Travell, Knt. [18 Feb. 1858], of Hawldston, co. Pembroke, Wales (s. of Stephen Howell Phillips, Lieut, of Body Guard of Yeomen), 1858.\n33) Phillips-Jordell, Thomas, of county Chester and Lancashire, 1868\n34) Phillips to Church, Samuel, of Wales (name Church onlv). Church and Phillips quarterly, Vol.\n35) Phillips, Edward Clive Oldnall Long Phillijis, Vice-Consul at Kertch and of Rotherham, s. of Richard Augustus Long Phillips, of Rofherham, co. York, 1876,\n36) Phillips to Wolley, . . . ., of Kertch, and Rotherham, co. York, \n37) Phillips, Lionel, of Hohenheim, Braamfontein, South Africa, s. of Philip Saunders [Phillips], 1897,\nThere are hundreds of notable people with the Phillips surname. This page will mention a handful. Famous people with this last name include: 1) Stephen Clarendon Phillips (1801-1857) who was a merchant and member of the US House of Representatives from Massachusetts as a member of the Whig and Free Soil Party, 2) Sir Thomas Phillips, 1st Baronet (1792-1872) who was an English antiquary and book collector born in Manchester, 3) Thomas Warton Phillips (1835-1912) who was an Republican member of the US House of Representatives from Pennsylvania who was born near Mount Jackson and was a appointed a member of the US Industrial Commission by President McKinley, 4) Sir Thomas Phillips (1801-1867) who was a Welsh politician, lawyer, and businessmen who was of the Phillips of Llanella House who became the mayor of Newport in Monmouthshire, 5) Wendell Phillips (1811-1884) who was an American abolitionist, attorney, and advocate for Native American rights who was born in Boston, Massachusetts, 6) William Phillips Jr. (*1750-1827) who was born in Boston, MA and became the 10th Lieutenant Governor of Massachusetts, 7) William Phillips (1878-1968) who was a career diplomat from Beverly, MA who was United States Ambassador to Canada, Italy, and Belgium, as well as the Under Secretary of State, 8) General Samuel Cochrane Phillips (1921-1990) who was a United States Air Force General who was the Director of NASA’s Apollo program in the 1960s who was born in Springerville, AZ, 9) Ammi Phillips (1788-1865) who was an American portrait painter active primary in three states: New York, Connecticut, and Massachusetts, 10) Catherine Phillips (1727-1794) who was a Quaker Minister who was a Quaker minister who travel to the British Isles and Holland and was born in Dudely, Worcestershire, England, 11) Henry Frank Phillips (1889-1958) who was a businessman from Portland, Oregon who invented the phillips head (cross head) screw and screw driver, 12) Richard Phillips (1778-1851) who was a British chemist who was born on Lombard Street, London and became a member of the Royal Society, 13) Alban William Housego Phillips (1914-1975) who was an economist from New Zealand who became a professor at the London School of Economics and is best known for the idea of the Phillips curve (inverse relationship between unemployment and inflation), and 14) Keith Anthony Phillips (1959-2016) who was an American professional baseball player in the MLB who was born in Atlanta, Georgie and was a second baseman and shortstop who played for eight different MLB teams (ex. Oakland Athletics, Detroit Tigers).\nPhillips Family Tree, Pedigree, & Lineage\nThe first known ancestor of this family was Artchorp mac Cairebe who was born in Ireland around 300 AD. His son was named Echuid Allmuit mac Artchop who was born in Ireland around 330 AD. He in turn had a son named Corath mac Echuid who was born iaround 370 in Ireland. Below is the direct line of male descent from him (estimated):\nAled Brosc mac Corath (around 400 AD in Ireland)\nTryffin ap Aled Brosc (around 430 AD)\nAnonymous ap Tryffin ap Aled Tryffin (around 460 AD)\nAnonymous ap Tryffin ap Aled Tryffin (around 500 AD)\nCynan “Cylched” ap Tryffin (around 530 AD)\nCynan “Cylched” ap Tryffin (around 600 AD)\nCynan “Cylched” ap Tryffin (around 630 AD)\nCynan “Cylched” ap Tryffin (around 670 AD)\nCynan “Cylched” ap Tryffin (around 700 AD)\nLlywn “Cylched” ap Cynan (730)\nDei ap Llywri (770)\nIop Ap Dei (800)\nArthafad Ap Iop (830 in Dyfed, Camarthenshire, Wales)\nCynan ab Arthafad (870, Dyfed, Wales)\nElgan ap Cynan, Wefl-hwch, Thick Lips (900, Dyfed, Wales)\nRhydderch ab Elgan Wefi Hwch formerly Elgan (930 AD)\nGwyn Rhydderch formerly Ap Rhytherch (970, Dyfed, Wales)\nGollwyn Ap Gwyn (1000 AD, Balean Cuch, Carmarthenshire, Wales)\nLord Cydifor Fawr Fawr,ap Collwyn,ap Gollwyn formerly Fawr,ap Cloowyn,ap Gollwyn (1055 AD)\nBledri Latimer ap Cydifor (1057 AD, Cil Sant, Llanwinio, Wales)\nRhys ap Bledri (1115 AD)\nSir Aron ap Rhys (1165 AD)\nGwilym ap Aron (1200)\nMadog ap Gwilym formerly Gwilym\nEvan ap Madog formerly Madog\nPhilip Ap Evan formerly Evan\nMeredudd Ap Philip formerly Philip (1360)\nPhilip Phillips formerly Ap Meredudd (1415, Cilsant Castle, Wales)\nThomas Phillips (1465, Wales)\nSir Owen Phillips (1505 Kidwelly, Wales)\nSir Simon Phillips (1520 Llwyngwair, Pembroke, Wales)\nJohn Phillips (1539 Northamptonshire, Devon)\nThe aforementioned John married Johann Watters and later Margaret Porter and had the following issue: Nicholas, John Richard, Steven, Christopher, William, Richard, Margaret, John, and Florence.\nHis son Nicholas was born in 1560 in England. Here is the pedigree from him:\nNicholas Phillips Jr. was born in Dedham, Essex in 1586\nRichard Phillips (1635, Wendover, Buckinghamshire)\nCaleb Phillips Sr (1659, Wemouth, Suffolk, America)\nCaleb Phillips Jr (1682, Roxbury, Boston, MA)\nCaleb III (1705, Massachusetts)\nJoshua Phillips (born 1735 in MA, married Mary Heaton)\nBlazons & Genealogy Notes\n2) Phillips – (Newport House, co. Cornwall). Or, a lion ramp. sa. chained of the first. Crest—A lion, as in the arms.\n3) Phillips – (Tredrea, co. Cornwall). Az. on a cross engr. or, a torteau betw. fear crosses crosslet fitchee gu.\n4) Phillips – (Sir Thomas Phillips, Knt., Q.C.). Sa. a chev. betw. three spear heads ar. Crest—A dragon’s head erased. Motto—Cwell angau neu chivilydo.\n5) Phillips – (Winterdyne House, Bewdley, and Hanbury, co. Worcester, and Edstone, co. Warwick; granted, 1825, by Naylcr, Garter, to John Phillips, Esq., of Hanbury, High Sheriff of co. Worcester 1803). Erminois a lion ramp. sa. ducally gorged and chained or, betw. two cross crosslets fitchee in chief and an escallop in base gu. Crest—On a garb, lying fessways or, a lion ramp. sa. ducally gorged and chained of the first, holding betw. the forepaws a cross crosslet gold.\n6) Phillips – (Lawrenny, co. Pembroke). Ar. a lion ramp. sa. ducally gorged and chained or, quartering Lort. Crest—A lion, as in the arms. Motto—Animo et fide.\n7) Phillips – (Witston House, co. Monmouth). Quarterly, 1st and 4th, gu. three boars’ heads or; 2nd and 3rd, az. a cross betw. four pheons or. Crest—A boar’s head sa. langued gu. ringed or. Motto—Spero meliora.\n8) Phillips – (London, 1634). Ar. a lion ramp. sa. collared, chained, and ducally crowned or.\n9) Phillips – Az. a chev. or, betw. three falcons close ar. belled of the first.\n10) Phillips – (Chelmicke, co. Salop). Or, on a chev. gu. three cocks’ heads erased ar. combed and wattled of the first. Crest—An eagle’s head erased az.\n11) Phillips – (Netley, co. Salop). Ar. a lion ramp. sa. collared and chained or. Crest—A lion ramp. as in the arms.\n12) Phillips – (co. Salop). Ar. a cross engr. flory sa. betw. four Cornish choughs ppr. Crest—The trunk of a tree lying fesseways and sprouting at the dexter end vert, thereon a Cornish chough ppr.\n13) Phillips – (Yeovil, co. Somerset). Ar. a lion ramp. sa. collared and lined or. Crest—A lion sejant sa. collared and lined or.\n14) Phillips – Az. a lion ramp. sa. ducally gorged and chained or. Crest—A lion, as in the arms. Motto—Ducit amor patriae.\n15) Phillips – Az. a chev. ar. betw. three falcons ppr. ducally gorged, beaked, and membered or. Crest—Out of a ducal coronet or, an arm embowed in armour, the hand holding a broken spear ppr. powdered with fleurs-de-lis gold.\n16) Phillips – Sa. semee-de-lis or, a lion ramp. ar. ducally crowned of the second a canton erm. Crest—A demi lion crowned as in the arms, holding a fleur-de-lis or.\n17) Phillips – Vert three roses in pale ar. betw. two flaunches of the last. Crest—A horse pass. erm. gorged with a chaplet vert.\n18) Phillips – Ar. a chev. betw. three roses gu.\n19) Phillips – (Ireland; granted in 1600). Barry wavy of six. az. and ar. on a chief of the last a lion pass. sa. collared or. Crest—An arm embowed in armour ppr. charged with a fleur-de-lis gold, purlled or, grasping a broken spear also ppr.\n20) Phillips – (Mount Rivers, co. Tipperary; confirmed by Betham, Ulster, to Richard Edward Phillips, Esq.). Quarterly, 1st and 4th, ar. three bars wavy az. in chief a lion pass. sa., for Phillips; 2nd, ar. three fleurs-de-lis sa., for Stumbles; 3rd,, erm. three battleaxes sa., for Weekes. Crests—1st: An arm embowed in armour, garnished or, grasping a broken tilting spear ppr.; 2nd: A cock grouse rising ppr. Motto—Pro Deo et rege.\n21) Phillipps – (Eaton Bishop, co. Hereford; descended, according to tradition, from a junior branch of the family of Philipps, of Picton Castle; the first settler in co. Hereford, Owen Phillipps, younger brother of Johm Phillipps, of Kilgainvin in Disserth, co. Radnor, was living 1595). (Longworth, co. Hereford; descended from Phillipps, of Eaton). (Bryngwyn, co. Hereford; descended from Phillipps, of Eaton). Quarterly, 1st and 4th, or, a lion ramp. sa. collared and chained of the first, on a bordure of the second eight cross crosslets gold, for Phillipps; 2nd and 3rd, erm. three ravens ppr. each standing on a mount vert, for Ravenhill. Crest—A demi lion sa. collared and chained, holding betw. the paws a leopard’s face jessant- de-lis or.\n22) Phillipps – (Middle Hill, co. Worcester, bart., extinct). The Arms granted to Sir Thomas Phillipps, F.R.S. and F.S.A., on the creation of the baronetcy were: Sa. flory or, a lion ramp. ar. ducally crowned gold, and holding in dexter forepaw a sword erect ppr. all within a bordure wavy of the second. Crest—On a mount vert a lion ramp. sa. semée-de- lis or, charged with a bendlet wavy erm. and holding in dexter forepaw a sword, as in the arms. Sir Thomas Phillipps subsequently obtained a fresh grant, viz., Ar. a lion ramp. sa. flory and collared and chained or, in dexter paw a sword erect ppr. in a bordure wavy of the second. Motto—Deus, patria, rex.\n23) Phillipps – (exemplified to James Orchard Halliwell, Esq., now of Middle Hill, co. Worcester, on his assuming, by royal licence, 1872, the surname of Phillipps only, in right of his wife, Henrietta Elizabeth Molyneux, eldest dau. of the late Sir Thomas Phillipps, Bart., of Middle Hill). Ar. a lion ramp. sa. ducally gorged with chain reflexed over the back or, holding in the dexter paw a sword erect ppr. a canton (for distinction) of the second. Crest—On a mount vert a lion ramp. sa. ducally gorged and chain reflexed over the back or, holding in the dexter paw a sword erect ppr. charged on the shoulder (for distinction) with a cross crosslet gold.\n24) Phillipps – (Garendon Park and Grace Dieu Manor, co. Leicester; Charles March Phillipps, Esq., of Garendon Park, High Sheriff in 1825, and formerly M.P. co. Leicester, was son and heir of the late Thomas March, Esq., of More Critchell, co. Dorset, who took the surname and arms of Phillipps, and subsequently assumed the arms and crest of Lisle, in right of his mother, Susan Lisle, dau. and co-heiress of Charles Lisle, Esq., whose family Mr. March Phillipps represented. See De Lisle). Quarterly, 1st, az. a chev. betw. three mullets ar., for Phillipps; 2nd, quarterly, gu. and az. a cross erm. betw. four lions’ heads erased or, for March; 3rd, or, on a chief az. three lions ramp. of the field, for Lisle; 4th, ar. a chev. betw. three martlets sa., for Collumbers; 5th, gu. and az. a chev. betw. three roses or, Corormailles; 6th, or, three torteaux, for Courtenay. Crests—1st: A demi griffin ppr. gorged or, holding a shield az. charged with a lion ramp. gold, for Phillipps; 2nd: A demi lion ramp. ar. holding a Maltese cross or, for March; 3rd: A stag trippant ppr., for Lisle. Motto—Quod justum non quod utile.\n25) Phillipps – (Landue, co. Cornwall; exemplified to Thomas Winsloe, Esq., upon his assuming, by royal licence, dated 8 Nov. 1798, the surname and arms of Phillipps). Or, a lion ramp. sa. collared and chain reflexed over the back of the first and holding betw. the paws an escutcheon gu. charged with a stag’s head erased ar. Crest—A lion pass. tail extended sa. resting the dexter forepaw on an escutcheon ar. charged with a chev. also sa. Motto—Ce m’est egal.\n26) Phillip – (Donynton, co. Suffolk; Sir John Phillip was father of Sir William Phillip, elected K.G. 1418, m. Joan, dau., and co-heir of Thomas, fifth Lord Bardolf, and is said to have been created Lord Bardolf by patent, but was never summoned, d. 6 June, 1441, leaving an only dau. Elizabeth, m. John, first Viscount Beaumont). Quarterly, gu. and or, in the first quarter an eagle displ. of the second.\n27) Phillip – (Lord Mayor of London, 1463). Sa. semée-de-lis or, a lion ramp. erm. crowned of the second.\n28) Phillip – (Scotland). Az. a chev. betw. three talbots’ heads couped ar. Crest—A bear’s head erased sa.\n29) Phillip – Per bend or and ar. a lion ramp. sa. a bordure gobony of the second and purp. Crest—Out of a flower ar. stalked and leaved vert, a greyhound’s head issuing of the first, collared or.\n30) Phillip – Per fess indented or and ar. a lion ramp. sa. on a bordure gu. eight plates. Crest—A lion’s gamb sa. holding three branches of flowers az. leaved vert.\n31) Phillip – Quarterly, gu. and ar., in the 1st quarter an eagle displ. or. Crest—Out of a ducal coronet or, a pyramid ar.\n32) Phillip – Sa. a lion ramp. erm. crowned or, within an orle of fleurs-de-lis of the third.\n33) Phillip – Ar. on a chev. betw. three roses gu. a mullet of the field.\n34) Phillip – Paly of six or and gu. on a chief of the last a lion pass. ar.\n35) Philips – (Weston, co. Warwick, bart.). Per pale az. and sa. within an orle of fleurs-de-Iis ar. a lion ramp, ermoinois, ducally crowned and holding betw. the paws a mascle or, a canton erm. Crest—A demi Hon ramp, erminois, collared sa. ducally crowned or, holding between the paws a fleur-delis az. within a mascle gold. Motto—Nil nisi honestum.\n36) Philips – (Yarpole, co. Hereford; granted 14 June, 1579). Az. a fess betw. three falcons close ar. beaked and legged or.\n37) Philips – (Leominster, co. Hereford). Or, on a chev. gu. three falcons’ heads erased ar.\n38) Philips – (Tenterden, co. Kent). Per fess gu. and az. a lion ramp. or, within a bordure of the last. Crest—On a mount vert a stag sejant erm. attired or.\n39) Philips – (Inner Temple, London). Az. a chev. betw. three falcons ar.\n40) Philips – (co. Lancaster). Sa. a lion ramp. ar. (another, erm.) betw. ten fleurs-de-lis or.\n41) Philips – or Phillips – (Barnstaple, co. Devon). (London; descended out of co. Dorset; confirmed 10 Dec. 1633). Or, on a chev. engr. sa. three eagles’ heads erased ar. Crest—A rose branch vert, bearing three roses gu. betw. two wings ar.\n42) Philips – (co. Salop). Vert three cinquefoils betw. two flaunches ar.\n43) Philips – Same Arms. Crest—A horse pass. with a wreath of laurel encircling the neck.\n44) Philips – (Tamworth, co. Warwick). Or, a lion ramp. sa. a chief of the second. Crest—A leopard sejant or.\n45) Philips – (co. Worcester). Az. a lion ramp. ar. a chief erm. Crest—On a chapeau az. turned up erm. a demi lion ramp. guard. ar.\n46) Philips – Barry wavy of six az. and ar. on a chief or, a lion pass. sa.\n47) Philips – Ar. on a pile issuing out of the dexter chief of the escutcheon sa. a lion ramp. of the field.\n48) Philips – Sa. a bend erm.\n49) Philips – (Heath House, co. Stafford; descended from Francis Phylyppe, of Neyther Teyne, d. 6 Edward VI.; his great grandson, Richard Philips, Esq., m. Christobel, second dau. and co-heir of Robert Whetall, Esq., of Bignoll Hill, co. Stafford, and was father of Nathaniel Philips, Esq., of Heath House, b. 1650). (The Park, Prestwich, co. Lancaster, and Welcombe, co. Warwick; borne by Mark Philips, Esq., of The Park, grandson of Nathaniel Philips, Esq., of Stand, in Prestwich, who was second son of John Philips, Esq., of Heath House, by Susanna, youngest dau. and co-heir of John Burton, Esq., of Derby). Per pale az. and sa. within an orle of fleurs-de-lis ar. a lion ramp. erminois, ducally crowned and holding betw. the paws a mascle or, a canton erm Crest—A demi lion ramp. erminois, collared sa. ducally crowned or, holding betw. the paws a fleur-de-lis ar. within a mascle gold. Motto—Simplex munditiis.\n50) Philips – (Rev. Gilbert Henderson Philips, Vicar of Brodsworth, co. York, of the family of Philips, of Heath House). (Bank Hall, co. Lancaster, and Abbey Cwmhir, co. Radnor; descended from Nathaniel Philips, Esq., of Manchester, third son of Nathaniel Philips, Esq., of Heath House, by Elizabeth, his wife, dau. and co-heir of John Stubbs, Esq., of The Shaw, whose youngest son, John Philips, Esq., by Elizabeth, his wife, eldest dau. and co-heir of John Burton, Esq., of Derby, purchased, in 1777, the estate of Bank Hall, and which he devised at his death to his fourth son, Francis Philips). Quarterly, 1st, per pale az. and sa. within an orle of fleurs-de-lis ar. a lion ramp. erminois, ducally crowned and holding betw. the paws a mascle or, a canton erm., for Philips; 2nd, gu. on a bend ar. with cotises engr. erm. betw. two pheons of the second three stags’ heads caboshed of the field, for Stubbs; 3rd, ar. a crescent within an orle of estoiles gu. a bordure engr. of the last, for Burton; 4th, gu. three piles issuant from the sinister within a bordure or, on a chief erm. a crescent az., for Henderson. Crest—A demi lion ramp. erminois, collared sa. ducally crowned or, holding betw. the paws a fleur-de-lis az. within a mascle also or. Motto—Simplex munditiis.\n51) Philipps – (Picton Castle, co. Pembroke; Baron Milford, extinct 1823; derived from Cadivor Vawa; Sir John Philipps, of Picton Castle, was created a bart. 1621; Sir Richard Philipps, seventh bart., was elevated to the peerage of Ireland 1776, d. s. p. in 1823, when the estate of Picton Castle passed under his will to his cousin, Richard Bolkeley Philipps Grant, created a bart. in 1828; the ancient baronetcy devolved on the male heir of the family). Ar. a lion ramp. sa. ducally gorged and chained or. Crest—A lion, as in the arms. Supporters—Two horses ar.\n52) Philipps – (Picton Castle, co. Pembroke, bart.). Ar. a lion ramp. sa. ducally gorged and chained or. Crest—A lion, as in the arms. Motto—Ducit amor patriae.\n53) Philipps – (Baron Milford, extinct 1857; Richard Bulkekley Grant, Esq., who s. to the estates of the Philips family under the will of Lord Milford, assumed the surname of Philipps 1824, was created a bart. 1828, and a peer 1847, d.s.p.). Same Arms and Crest. Supporters—Two horses ar. Motto—Ducit amor patriæ.\n54) Philipps – (Aberglasney, co. Caermarthen). Quarterly, 1st and 4th, or, a lion ramp. sa. betw. two fleurs-de-lis in chief az. and a stag’s head erased in base gu., for Philipps: 2nd and 3rd, gu. three snakes interlaced betw. two spear heads erect in chief, and a rose in base ar. barbed and seeded ppr., for Walters. Crests—1st, Philipps: A lion ramp. sa. holding betw. the forepaws an escutheon or, thereon three snakes interlaced ppr. the dexter hind-paw on a fleur-de-lis also or; 2nd, Walters: An eagle displ. erm. the body entwined by two snakes respecting cach other ppr. and holding in each claw a rose gu. slipped and leaved vert. Motto—Fy Nuw a Chymry.\n55) Philipps – (Lloyd-Philipps, Penty Park, co. Pembroke, and Dale castle, co. Pembroke, and Mabws, co. Caermarthen; John Lloyd, of Foes-y-Bleiddiad, m. MABY, dau. of James Philipps Esq., of Penty Park, co. Pembroke, and was grandfather of John Lloyd, of Focs-y-Bleiddiad, who dying in 1820, was s. by his grandson, John Philipps-Allen-Lloyd, Esq., of Dale Castle, and Mabws, who assumed the name of Philipps, under the will of James Philipps. of Penty Park). Ar. a lion ramp. sa. ducally gorged gu. and chained or. Crest—A lion, as in the arms. Motto—Ducit amor patriae.\n56) Philipps – (Picton Castle, co. Pembroke; exemplified to Charles Edward Gregg Fisher, Esq., eldest son of Edward Fisher, Esq., of Spring Dale, co. York, upon his assuming by royal licence, dated 29 July, 1876, the surname of Philipps, in lieu of that of Fisher, in compliance with the testamentary injunction of his father-in-law, Rev. James Henry Alexander Philipps, M.A., of Picton Castle). Quarterly, 1st and 4th, ar. a lion ramp. sa. gorged with a ducal coronet, and therefrom a chain reflected over the back or, and for distinction in the centre chief point a cross crosslet of the second, for Philipps; 2nd and 3rd, ar. on a chev. gu. three trefoils slipped of the field in chief as many fleurs-de-lis of the second, for Fisher. Crests—1st, Philipps: A lion ramp. gorged and chained as in tbe arms charged on the shoulder for distinction with a cross crosslet or; 2nd, Fisher: in front o f a bulrush erect a kingfisher ppr. resting tbe dexter claw on a fleur-de-lis or. Mottoes—Ducit amor patriae; Virtute et fide.\n57) Philip – Per bend ar. and or, a lion ramp. sa. a bordure gobony of the first and gu.\n58) Philip – Per bend or and ar. a lion ramp. sa. within a bordure gobony of the second and purp.\n59) Philip – Sa. a lion ramp. crowned or, betw. eight fleurs-de-lis ar.\n60) Philip – (Ormistone, co. Haddington, 1685). Az. on a chev. betw. three talbots’ heads erased ar. two lozenges of the first. Crest—A talbot ppr. Motto—Vivis sperandum.\n61) Philip – (Over Carnbie, co. Fife, 1672). Az. a chev. invecked betw. three talbots’ heads erased or. Motto—Sors omnia versat.\n62) Philip – (Amrecloss, co. Forfar). Az. a chev. betw. three talbots’ heads couped ar. Motto—Non dormit qui custodit.\n63) Philip – Philip-ap-Uchdryd – Az. three cocks ar. armed, crested, and jelloped or.\n64) Philip – Philip-ap-Ivor – (Lordof Iscoed). At. an eagle displ. or.\n65) Philip – or Philips – (London, and co. Suffolk, late of Jamaica). Quarterly, gu. and ar. in the dexter chief quarter an eagle displ. or, armed of the field. Crest—Out of a ducal coronet az. three ostrich feathers ar.\n66) Philip – Provence – D’azur au chevron d’or acc en chef de deux étoiles d’argent et en pointe d’un pélican du même dans son aire de sable. English: Provence – azure a chevron or accompanied by in chief by two etoiles argent and in base a pelican of the same in its nest sable.\n67) Philip – Marseille – Règl. d’arm. du 29 octobre 1781 – D’argent à une tige de trois épis de sinople soutenue d’un croissant de gueules et surmontée de trois étoiles rangées du même Casque de deux tiers orné de lambrequins de gueules d’argent et de sinople. English: Marseille (regulation of Arms of 29th October 1781) Argent with a stem of three tufts vert supported by a crescent gules and surmounted by by three etoiles arranged of the same helmet of two layers decorated with mantling gules argent and vert.\n68) Philip – de Hoffnungswald – Transylvanie – (An., 7 avril 1716) – D’azur à une ancre au naturel Cimier un homme issant habillé d’azur tenant de sa main dextre une épée d’argent et de sa senestre une balance en équilibre Lambrequin d’or et d’azur. English: Of Hoffnungswald Transylvania ( 7th April 1716 ) Azure with an anchor proper Crest: a man issuant dressed azure holding in his dexter hand a sword argent and in his sinister a set of scales in equilibrium Mantling: or and azure.\n69) Philipe – de Beuville – Normandie – Règl. d’arm. du 20 juin 1696, donné en suite des Lettres d’Anob. de juin 1696, accordées à sieur Jacques Philippe, sieur de Beuville, lieutenant général en la vicomté du Perche. D’or à l’aigle de sable le vol étendu au chef de gueules chargé de deux croisettes d’argent Casque de profil avec lambrequins de sable d’or et de gueules. English: Beuville – Normandy – Regulations of Arms 20th june 1696, given in a set of letters referring to the enoblement of June 1696, according to Sir Jacques Philippe, Lord dof Beuville, lieutenant general and viscount of Perche. Or with an eagle sable the pair of wings extended a chief gules charged with two crosslets argent helmet in profile with Mantling: sable or and gules.\n70) Philipe – du Moncel – Normandie – Règl. d’arm. du 15 mars 1698, en conséquence des Lettres d’Anob. du mois de mars 1698, accordées à sieur Jacques Philipe, sieur du Moncel. Trésorier général de France à Alençon. D’argent au chevron de gueules acc de trois glands tigés et feuillés de sinople posés 2 en chef et 1 en pointe au chef d’azur chargé de trois étoiles d’or Casque de profil avec lambrequins d’azur d’or de sinople d’argent et de gueules. English: Moncel – Normandy – Regulation of Arms of 15th March 1698, in consequence of letters of enoblement of the month of March 1698, according to Sir Jacques Philipe, Lord of Moncel, treasurer general of France in Alencon. Argent a chevron gules accompanied by three acorns stemmed and leaved vert placed 2 in chief and 1 in base a chief azure charged with three etoiles or helmet in profile with Mantling: azure or vert argent and gules.\n71) Philippe – Normandie – Sieur de Glatigny, maintenu en 1666 – D’azur à trois flèches tombantes d’or. English: Normandy – Lord of Glatigny, maintained since 1666 – Azure three arrows hanging or.\n72) Philippe – Normandie – Sieur des Acres, Beaumont, etc. maintenu le 30 mars 1666. D’argent à la fasce crénelée de deux pièces de gueules acc en pointe d’une tête de lion vomissant des flammes du même. English: Normandy Lord of Acres, Beaumont etc, maintained since 30th March 1666. argent a fess embattled on the upper side of two pieces gules accompanied by in base a head of lion issuing with flames of the same.\n73) Philippe – Lorraine – Famille anoblie le 1er août 1584, qui succéda dans les armes de la famille de Bagadour – D’argent à un annelet de sable duquel pendent trois menottes ou carcans posés en pairle et acc en chef d’une étoile le tout de sable d’étoile est parfois remplacée par une molette) Casque avec lambrequins Cimier une des menottes en pal. English: Lorraine – Family enobled 1st August 1584, who inherited the arms from the family of Bagadour – Argent with a annulet sable from which hangs three handcuffs [shackles] placed in pall and accompanied by in chief a etoile all sable ( the etoile is sometimes replaced by a mullet ) helmet with Mantling: Crest: the shackles palewise.\n74) Philippe – Besançon, Genevois – (An., 25 avril 1646) – Écartelé aux 1 et 4 de gueules à la bande d’argent ch de trois têtes de cheval de sable aux 2 et 3 d’azur à un vautour d’argent le vol levé Cimier une tête de cheval de sable sommée de trois plumes d’autruche une d’argent entre deux de gueules Lambrequin d’argent et de gueules. English: Besancon, Geneva ( 25th April 1646 ) quarterly 1st and 4th gules a bend argent charged with three heads of horses sable 2nd and 3rd azure with a vulture argent the pair of wings upright Crest: a head of horse sable surmounted by three ostrich feathers one argent between two gules Mantling: argent and gules.\n75) Philippe – Lorraine – (An., 4 août 1584) – D’argent à trois menottes liées ensemble de celle du milieu en pend une autre de sable le tout acc en chef d’une étoile d’azur. English: Lorraine ( 4th August 1584 ) argent three shackles tied [banded] together with that of the middle hanging from the others sable all accompanied by in chief an etoile azure.\n76) Philippe – de Marigny – Normandie – D’azur au chevron d’or acc en chef à dextre d’un croissant d’argent à senestre d’une étoile du même et en pointe d’un cygne aussi d’argent. English: Marigny – Normandy – azure a chevron or accompanied by in chief to the dexter a crescent argent to the sinister a etoile of the same and in base a swan also argent.\n77) Philipp – Görlitz – (Conc. d’arm., 12 sept. 1617) – D’azur à deux colonnes accostées l’une d’argent et l’autre de gueules acc de trois étoiles d’argent 2 en chef et 1 en pointe Bourlet d’azur et d’argent Cimier une étoile d’argent entre un vol d’azur chaque aile ch d’une étoile d’argent Lambrequin d’argent et d’azur. English: Görlitz – (List of arms)., 12th Sept. 1617) – Azure two columns [pillars] side by side the one argent and the other gules accompanied by three etoiles argent 2 in chief and 1 in base the wreath on the helmet azure and argent Crest: an estoile argent between a pair of wings azure each wing charged with an etoile argent Mantling: argent and azure.\n78) Philipp – de Hoffnungswald – Transylvanie – (Nob. d’Autriche et du St-Empire, 18 sept. 1731) – D’argent à un sauvage de carnation ceint et couronné de lierre au milieu d’une forêt de sinople appuyant la main dextre sur une ancre d’argent accolée d’un rameau de laurier de sinople la senestre appuyée sur sa hanche et tenant un arbre arraché passé sous son bras soutenu d’une terrasse de sinople le champ chapé à dextre de sable et à senestre d’or avec un chevron de gueules brochant sur les lignes du chapé le sable chargé d’une étoile d’or et l’or d’un demi-vol de sable Cimier le sauvage issant avec son ancre et son arbre entre un vol coupé à dextre d’or sur sable et à senestre de gueules sur argent Lambrequin conformes aux émaux du vol. English: Hoffnungswald – Transylvanie – (Nobles of Autriche and of St-Empire, 18th Sept. 1731) -Argent with a savage carnation belted and crowned of ivy of of the type of the forest vert resting the dexter hand over an anchor argent side by side with a branch of laurel vert the sinister resting on his hip and holding a tree eradicated placed under his arm supported by a mount vert the field chape to the dexter sable and to the sinister or with a chevron gules covering over the edge of the chape the sable charged with an etoile or and the or a single wing sable Crest: the savage issuant with his anchor and his tree between a pair of wings per fess to the dexter or over sable and to the sinister gules over argent Mantling: conforming to the [same as] colours of pair of wings.\n79) Phillips – Wales – or, a lion, rampant, sa. collared and chained of the first.\n80) Phillips – Pembrike and Wales – sable, a lion rampant, sable, ducally gorged and chained, or\n81) Phelip – (Donnyton, co. Worcester). Quarterly, gu. and ar. in the 1st quarter an eagle displ. or, on the breast an annulet sa.\n82) Phelip – (Montacnte, co. Somerset, settled there for many centuries; descended from Sir Edward Phelips, Knt., Master of the Rolls, and Speaker of the House of Commons, temp. Queen Elizabeth, fourth son of Thomas Phelips Esq., of Barrington, who built the present mansion at Montacute, and d. 1588; Sir Edward’s son and heir, Robert Phelips, was M.P. co. Somerset in many Parliaments, temp. James I., and Charles I., and a distinguished and active member of the popular party). (Corfe Mullen, co. Dorset; the senior line of the Phelips, of Barrington and Corfe Mullen; the heiress, Jane Phelips, m. the Rev. Sir James Hanham, Bart.). (Briggins Park, co. Hertford; the Rev. Charles Phelips, fourth son of Edward Phelips, Esq., of Montacute, descended from Sir Edward Phelips, Knt., Master of the Rolls, temp. Elizabeth, m. in 1792, Mary, dau. of Thomas Blackmore, Esq., of Briggins Park, by Mary, his wife, sister of John Old Goodford, Esq.). Ar. a chev. gu. betw. three roses of the last, seeded and leaved ppr. Crest—A square beacon, or chest, on two wheels or, filled with fire ppr. Motto—Pro aris et focis.\n83) Phillips – Baronet – Or on a pile azure, between two greyhounds courant in base sable, a lion rampant of the first, guttee de poix. Crest: A demi-lion azure, between two nuggets of gold and charged with two annulets interlaced palewise or."

"Philip Had No Last Name Philip was mocked at prep school for having no surname.\nHowever this Maidan is not about the surname of this next president.\nLemieux is a French-Canadian surname which means “The Best.”\nMy surname is human, my middle name is Jewish and my private, given, name is Israeli.\nPhilip was mocked at prep school for having no surname, and only ever known as “Philip of Greece.”\nYes,” replied Ibarra absently, “we shortened the surname; it was too long.\nThe Alpe, or bullfinch, mentioned in the above lines, also survives as a surname.\nIn course of time, a distinction arose in the conception of Aphrodite, expressed by the surname applied to her.\nIn those olden days a man did not have a surname that belonged to everyone in his family.\nIf a widow is re-marrying, she uses the prefix \"Mrs.\" with her Christian names and the surname of her deceased husband.\nearly 14c., \"name, title, or epithet added to a person's name,\" from sur \"above\" (see sur-) + name (n.); modeled on Anglo-French surnoun \"surname\" (early 14c.), variant of Old French surnom, from sur \"over\" + nom \"name.\"\nAn Old English word for this was freonama, literally \"free name.\" Meaning \"family name\" is first found late 14c. Hereditary surnames existed among Norman nobility in England in early 12c., among common people began to be used 13c., increasingly frequent until near universal by end of 14c. The process was later in the north of England than the south. The verb is attested from 1540s."

"Seneca: Meaning, Popularity, Origin of Baby Name Seneca\nLooking for the perfect name? Try the Name MatchMaker to find the perfect baby name for you!\nSister & Brother Names\nKnow a Seneca? What are her siblings named?\nContribute your knowledge to the name Seneca\n- Comments and insights on the name Seneca: | Edit\nWe named our second daughter Seneca because my husband is from Elkins, West Virginia, and there is an Old Seneca Trail that runs through town.\n- Personal experiences with the name Seneca: | Edit\nWhen we wanted to name our second daughter Seneca, our family thought it was an awful name. But we stuck to our guns and we think it suits her perfectly. Everyone we meet thinks it's a great name. We've only had one person pronounce it wrong at a doctor's office, it is pronounced SEN-eh-ka, and on this one occasion they said Sen-NEEK-qua.\nMy daughter is 28 and we named her Seneca after Seneca Lake in the White Mountains in Arizona. She LOVES her name and it suits her perfectly as a free-spirit and artist and world traveler. We also pronounce it SEN-eh-ka. Her sister's name is Langley. Both are male names (traditional) but are exactly what we wanted\n- Nicknames for Seneca: | Edit\nwe call our Seneca \"sen\" the most, but when she was little \"sennie\" She still prefers Seneca after 28 yrs.\n- Meanings and history of the name Seneca: | Edit\nIt means \"from the Seneca tribe\". The Seneca Indians were part of the Iroquois five nations, and were known as the \"keepers of the western wall\". It is also the name of a Roman philosopher.\nSeneca is also one of the finger lakes in upper New York state, the local wine country.\nSeneca Falls was also the site of the historic Women's Rights convention in 1848 - a great namesake!\n- Famous real-life people named Seneca: | Edit\nThe Roman Philosopher, actually there were two. Seneca the elder and Seneca the younger. The younger Seneca was tutor to Nero.\n- Seneca in song, story & screen: | Edit\n- Share what you know!"

"A Semordnilap is a name designating a word or phrase that spells a different word or phrase backwards. “Semordnilap” is “palindromes” spelled backwards. My wife encountered interesting children’s names as she visited teenage mothers as part of her nursing career. One that I recall was Semaj [ pronounced see majz]. My wife asked, “Is that an old family name?” The young mother said, “No, it’s James- backwards.”\nRecently in the Toledo area, a young girl was murdered and had the odd name, Nevaeh. Later, I found out that it is a semordnilap of “Heaven.” Easy ones are Bob, Ada and Hannah. Then there is Werdan for Andrew and Harobed for Deborah. What’s yours?\nSometimes a palindrome of a name renders it ethnic such as Mike becoming Ekim– almost biblical. Or Rednaxela for Alexander. Ekardum [Egyptian?] for Mudrake. Ybbor [Yiddish?] for Robby and Ennazus [Greek?] for Suzanne. The Russian-sounding Assenav comes from Vanessa.\nFor a more thorough study of the effects of child-naming, see this link."

"What does Zephan mean?\nZephan /ze-phan/ [2 sylls.] as a boys' name is of Hebrew origin, and the meaning of Zephan is \"hidden by God\". Zephan is a version of Zephaniah (Hebrew). Biblical: a minor prophet. Zelman is a conventional last name.\nZephan has 1 relation via Zephaniah: Zeph.Kreatif forms: Zepha, Zephanniah, Zephanno. [more]\nHow popular is Zephan?\nZephan is a rare given name for men. Zephan is an equally rare surname for all people. (2000 U.S. Census)\nShown below is the birth name popularity of Zephan for boys. Zephan has not made it into the Top 1000 so far. (2014 Birth Statistics)"

"Alexzandre, Ayden, Braedyn, Kolten, Konner, Kaleb, Josef, and Kristopher are some different spellings of popular names for boys. Jazmyn, Rebekkah, Emilee, Katherin, Raechal, and Abigayle are unique twists of common names for girls.Continue Reading\nAlexzandre is a spin-off of the noble and kingly name of Alexander. Ayden, changed from the more common spelling of Aiden, has many different spelling options, including Aiiden, Aaden, Aeden and Aidan. Some parents choose to give a unique spin to a common name by changing the first letter of the popular name by dropping and substituted it with a similar sounding letter. For example, parents may opt to drop the \"c\" from Colten and add a \"k\" to come up with the unique spin, Kolten. Furthermore, parents can add other twists by changing vowels within the names, such as Kolton or Koltan. These changes and other like them do not change the pronunciation of the name typically.\nThe same kind of idea is used when substituting similar sounding letters at the end of names, as well. Such is the case with Joseph and Josef. Switching the order of letters or adding a silent or additional letter, such as from Rachel to Raechal, is another way to add unique spelling changes to names.Learn more about Education"