Datasets:

medarc

/

clinical_pile_v1_minhash_deduped

like 1

/index.php/XIAP

# XIAP X-linked Inhibitor of Apoptosis Protein (XIAP) is a member of the Inhibitor of apoptosis family of proteins (IAP). IAPs were initially identified in baculoviruses, but XIAP is one of the homologous proteins found in mammals. It is so called because it was first discovered by a 273 base pair site on the X chromosome. The protein is also called human IAP-like Protein (hILP), because it is not as well conserved as the human IAPS: hIAP-1 and hIAP-2. XIAP is the most potent human IAP protein currently identified. Neuronal apoptosis inhibitor protein (NAIP) was the first homolog to baculoviral IAPs that was identified in humans. With the sequencing data of NIAP, the gene sequence for a RING zinc-finger domain was discovered at site Xq24-25. Using PCR and cloning, three BIR domains and a RING finger were found on the protein, which became known as X-linked Inhibitor of Apoptosis Protein. The transcript size of Xiap is 9.0kb, with an open reading frame of 1.8kb. Xiap mRNA has been observed in all human adult and fetal tissues "except peripheral blood leukocytes". The XIAP sequences led to the discovery of other members of the IAP family. XIAP, like the rest of the IAP family, has two major structural elements. Firstly, there is the baculoviral IAP repeat (BIR) domain consisting of approximately 70 amino acids. Secondly, there is a zinc-binding domain, or a "carboxy-terminal RING Finger". XIAP has been characterized with three amino-terminal BIR domains and one RING domain. Between the BIR-1 and BIR-2 domains, there is a linker-BIR-2 region that is thought to contain the only element that comes into contact with the caspase molecule to form the XIAP/Caspase-7 complex. XIAP stops apoptotic cell death induced either by viral infection or by overproduction of caspases, the enzymes primarily responsible for cell death . XIAP binds to and inhibits caspase 3, 7 and 9. Recent studies have pinpointed the structural location of these inhibiting properties: the region immediately following the terminal end of BIR2 inhibits caspase 3 and 7, while BIR3 binds to and inhibits caspase 9. The RING domain utilizes E3 ubiquitin ligase activity and enables IAPs to catalyze ubiquination of self, caspase-3, or caspase-7 by degradation via proteasome activity. However, mutations affecting the RING Finger do not significantly affect apoptosis, indicating that the BIR domain is sufficient for the protein's function. When inhibiting caspase-3 and caspase-7 activity, the BIR2 domain of XIAP binds to the active-site substrate groove, blocking access of the normal protein substrate that would result in apoptosis. Caspases are activated by cytochrome c, which is released into the cytosol by dysfunctioning mitochondria. Studies show that XIAP does not directly affect cytochrome c. XIAP distinguishes itself from the other human IAPs because it is able to effectively prevent cell death due to "TNF-α, Fas, UV light, and genotoxic agents". The second BIR domain of XIAP can be shown binding to caspase 3 where a protein substrate would normally bind during aptosis. By blocking this binding, XIAP inhibits apoptosis. XIAP is inhibited by Smac/DIABLO and Omi/HtrA2, two death-signaling proteins released into the cytoplasm by the mitochondria. Smac/ DIABLO, a mitochondrial protein and negative regulator of XIAP, can enhance apoptosis by binding to XIAP and preventing it from binding to caspases. This allows normal caspase activity to proceed. The binding process of Smac/DIABLO to XIAP and caspase release requires a conserved tetrapeptide motif. Deregulation of XIAP can result in "cancer, neurodegenerative disorders, and autoimmunity". High proportions of XIAP may function as a tumor marker. In the development of lung cancer NCI-H460, the overexpression of XIAP not only inhibits caspase, but also stops the activity of cytochrome c (Apoptosis). In developing prostate cancer, XIAP is one of four IAPs overexpressed in the prostatic epithelium, indicating that a molecule that inhibits all IAPs may be necessary for effective treatment. Apoptotic regulation is an extremely important biological function, as evidenced by "the conservation of the IAPs from humans to Drosophila".

wikidoc

/index.php/XIST

# XIST Xist (X-inactive specific transcript) is an RNA gene on the X chromosome of the placental mammals that acts as a major effector of the X inactivation process. It is a component of the Xic – X-chromosome inactivation centre – along with two other RNA genes (Jpx and Ftx) and two protein genes (Tsx and Cnbp2). The Xist RNA, a large (17 kb in humans) transcript, is expressed on the inactive chromosome and not on the active one. It is processed in a similar way to mRNAs, through splicing and polyadenylation. However, it remains untranslated. It has been suggested that this RNA gene evolved at least partly from a protein coding gene that became a pseudogene. The inactive X chromosome is coated with this transcript, which is essential for the inactivation. X chromosomes lacking Xist will not be inactivated, while duplication of the Xist gene on another chromosome causes inactivation of that chromosome. X inactivation is an early developmental process in mammalian females that transcriptionally silences one of the pair of X chromosomes, thus providing dosage equivalence between males and females (see dosage compensation). The process is regulated by several factors, including a region of chromosome X called the X inactivation center (XIC). The XIST gene is expressed exclusively from the XIC of the inactive X chromosome. The transcript is spliced but apparently does not encode a protein. The transcript remains in the nucleus where it coats the inactive X chromosome. Alternatively spliced transcript variants have been identified, but their full length sequences have not been determined. The functional role of the Xist transcript was definitively demonstrated in mouse female ES cells using a novel antisense technology, called peptide nucleic acid (PNA) interference mapping. In the reported experiments, a single 19-bp antisense cell-permeating PNA targeted against a particular region of Xist RNA prevented the formation of Xi and inhibited cis-silencing of X-linked genes. The association of the Xi with macro-histone H2A is also disturbed by PNA interference mapping. The human Xist RNA gene is located on the long (q) arm of the X chromosome. The Xist RNA gene consists of conserved repeats within its structure and is also largely localized in the nucleus. The Xist RNA gene consists of an A region, which contains 8 repeats separated by U-rich spacers. The A region appears to contain two long stem-loop structures that each include four repeats. An ortholog of the Xist RNA gene in humans has been identified in mice. This ortholog is a 15 kb Xist RNA gene that is also localized in the nucleus. However, the ortholog does not consist of conserved repeats. The gene also consists of an Xist Inactivation Center (XIC), which plays a major role in X inactivation. The Xist RNA contains a region of conservation called the repeat A (repA) region that contains up to nine repeated elements. It was initially suggested that repA repeats could fold back on themselves to form local intra-repeat stem-loop structures. Later work using in vitro biochemical structure probing proposed several inter-repeat stem-loop structures. A recent study using in vivo biochemical probing and comparative sequence analysis proposed a revision of the repA structure model that includes both intra-repeat and inter-repeat folding found in previous models as well as novel features (see Figure). In addition to its agreement with the in vivo data, this revised model is highly conserved in rodents and mammals (including humans) suggesting functional importance for repA structure. Although the exact function of the repA region is uncertain, it was shown that the entire region is needed for efficient binding to the Suz12 protein. The Xist RNA directly binds to the inactive X-chromosome through a chromatin binding region of the RNA transcript. The Xist chromatin binding region was first elucidated in female mouse fibroblastic cells. The primary chromatin binding region was shown to localize to the C-repeat region. The chromatin-binding region was functionally mapped and evaluated by using an approach for studying noncoding RNA function in living cells called peptide nucleic acid (PNA) interference mapping. In the reported experiments, a single 19-bp antisense cell-permeating PNA targeted against a particular region of Xist RNA caused the disruption of the Xi. The association of the Xi with macro-histone H2A is also disturbed by PNA interference mapping. The Xist RNA gene lies within the X-Inactivation Centre (XIC), which plays a major role in Xist expression and X inactivation. The XIC is located on the q arm of the X chromosome (Xq13). XIC regulates Xist in cis X inactivation, where Tsix, an antisense of Xist, downregulates the expression of Xist. The Xist promoter of XIC is the master regulator of X inactivation. X inactivation plays a key role in dosage compensation. The Tsix antisense gene is a transcript of the Xist gene at the XIC center. The Tsix antisense transcript acts in cis to repress the transcription of Xist, which negatively regulates its expression. The mechanism behind how Tsix modulates Xist activity in cis is poorly understood; however, there are a few theories on its mechanism. One theory is that Tsix is involved in chromatin modification at the Xist locus and another is that transcription factors of pluripotent cells play a role in Xist repression. The Tsix antisense is believed to activate DNA methyl transferases that methylate the Xist promoter, in return resulting in inhibition of the Xist promoter and thus the expression of the Xist gene. Methylation of histone 3 lysine 4 (H3K4) produces an active chromatin structure, which recruits transcription factors and thus allows for transcription to occur, therefore in this case the transcription of Xist. A dsRNA and RNAi pathway have been also proposed to play a role in regulation of the Xist Promoter. Dicer is an RNAi enzyme and it is believed to cleave the duplex of Xist and Tsix at the beginning of X inactivation, to small ~30 nucleotide RNAs, which have been termed xiRNAs, These xiRNAs are believed to be involved in repressing Xist on the probable active X chromosome based upon studies. A study was conducted where normal endogenous Dicer levels were decreased to 5%, which led to an increase in Xist expression in undifferentiated cells, thus supporting the role of xiRNAs in Xist repression. The role and mechanism of xiRNAs is still under examination and debate.[citation needed] Pluripotent stem cells express transcription factors Nanog, Oct4 and Sox2 that seem to play a role in repressing Xist. In the absence of Tsix in pluripotent cells, Xist is repressed, where a mechanism has been proposed that these transcription factors cause splicing to occur at intron 1 at the binding site of these factors on the Xist gene, which inhibits Xist expression A study was conducted where Nanog or Oct4 transcription factors were depleted in pluripotent cells, which resulted in the upregulation of Xist. From this study, it is proposed that Nanog and Oct4 are involved in the repression of Xist expression. Polycomb repressive complex 2 (PRC2) consist of a class of polycomb group proteins that are involved in catalyzing the trimethylation of histone H3 on lysine 27 (K27), which results in chromatin repression, and thus leads to transcriptional silencing. Xist RNA recruits polycomb complexes to the inactive X chromosome at the onset of XCI. SUZ12 is a component of the PRC2 and contains a zinc finger domain. The zinc finger domain is believed to bind to the RNA molecule. The PRC2 has been observed to repress Xist expression independent of the Tsix antisense transcript, although the definite mechanism is still not known. X inactivation plays a key role in dosage compensation mechanisms that allow for equal expression of the X and autosomal chromosomes. Different species have different dosage compensation methods, with all of the methods involving the regulation of an X chromosome from one of the either sexes. Some methods involved in dosage compensation to inactivate one of the X chromosomes from one of the sexes are Tsix antisense gene, DNA methylation and DNA acetylation; however, the definite mechanism of X inactivation is still poorly understood. If one of the X chromosomes is not inactivated or is partially expressed, it could lead to over expression of the X chromosome and it could be lethal in some cases. Turner's Syndrome is one example of where dosage compensation does not equally express the X chromosome, and in females one of the X chromosomes is missing or has abnormalities, which leads to physical abnormalities and also gonadal dysfunction in females due to the one missing or abnormal X chromosome. Turner's syndrome is also referred to as a monosomy X condition. Xist expression and X inactivation change throughout embryonic development. In early embryogenesis, the oocyte and sperm do not express Xist and the X chromosome remains active. After fertilization, when the cells are in the 2 to 4 cell stage, Xist transcripts are expressed from parent X chromosome(Xp) in every cell, causing that X chromosome to become imprinted and inactivated. Some cells develop into pluripotent cells (the inner cell mass) when the blastocyte forms. There, the imprint is removed, leading to the downregulation of Xist and thus reactivation of the inactive X chromosome. Recent data suggests that Xist activity is regulated by an anti-sense transcript. The epiblast cells are then formed and they begin to be differentiated, and the Xist is upregulated from either of the two X chromosomes and at random in ICM, but the Xist is maintained in epiblast, an X is inactivated and the Xist allele is turned off in the active X chromosome. In maturing XX primordial germ cells, Xist is downregulated and X reactivation occurs once again.

wikidoc

/index.php/XK_(protein)

# XK (protein) XK (also known as Kell blood group precursor) is a protein found on human red blood cells and other tissues which is responsible for the Kx antigen which helps determine a person's blood type.

wikidoc

/index.php/XLD_agar

# XLD agar Xylose lysine deoxycholate agar (XLD agar) is a selective growth medium used in the isolation of Salmonella and Shigella species from clinical samples and from food. It has a pH of approximately 7.4, leaving it with a bright pink or red appearance due to the indicator phenol red. Sugar fermentation lowers the pH and the phenol red indicator registers this by changing to yellow. Most gut bacteria, including Salmonella, can ferment the sugar xylose to produce acid; Shigella colonies cannot do this and therefore remain red. After exhausting the xylose supply Salmonella colonies will decarboxylate lysine, increasing the pH once again to alkaline and mimicking the red Shigella colonies. Salmonellae metabolise thiosulfate to produce hydrogen sulfide, which leads to the formation of colonies with black centers and allows them to be differentiated from the similarly coloured Shigella colonies.

wikidoc

/index.php/XPB

# XPB ## Structure The 3D-structure of the archaeal homolog of XPB has been solved by X-ray crystallography by Dr. John Tainer and his group at The Scripps Research Institute. ## Function XPB plays a significant role in normal basal transcription, transcription coupled repair (TCR), and nucleotide excision repair (NER). Purified XPB has been shown to unwind DNA with 3'-5' polarity. ## Disorders The function of the XPB(ERCC3) protein in NER is to assist in unwinding the DNA double helix after damage is initially recognized. NER is a multi-step pathway that removes a wide range of different DNA damages that distort normal base pairing. Such damages include bulky chemical adducts, UV-induced pyrimidine dimers, and several forms of oxidative damage. Mutations in the XPB(ERCC3) gene can lead, in humans, to xeroderma pigmentosum (XP) or XP combined with Cockayne syndrome (XPCS). Mutant XPB cells from individuals with the XPCS phenotype are sensitive to UV irradiation and acute oxidative stress.

wikidoc

/index.php/XPC_(gene)

# XPC (gene) Xeroderma pigmentosum, complementation group C, also known as XPC, is a human gene involved in the recognition of bulky DNA adducts in Nucleotide Excision Repair.

wikidoc

/index.php/XPO5

# XPO5 Exportin-5 (XPO5) is a protein that, in humans, is encoded by the XPO5 gene. In eukaryotic cells, the primary purpose of XPO5 is to export pre-microRNA (also known as pre-miRNA) out of the nucleus and into the cytoplasm, for further processing by the Dicer enzyme. Once in the cytoplasm, the microRNA (also known as miRNA) can act as a gene silencer by regulating translation of mRNA. Although XPO5 is primarily involved in the transport of pre-miRNA, it has also been reported to transport tRNA. Much research on XPO5 is ongoing. miRNA is a prominent research topic due to its potential use as a therapeutic, with several miRNA-based drugs already in use. After RanGTP binds to XPO5, the XPO5-RanGTP complex forms a U-like structure to hold the pre-miRNA. The XPO5-RanGTP complex recognizes pre-miRNA by its two-nucleotide 3' overhang—a sequence consisting of two bases at the 3' end of the pre-miRNA that are not paired with other bases. This motif is unique to pre-miRNA, and by recognizing it XPO5 ensures specificity for transporting only pre-miRNA. On its own, pre-miRNA is in a "closed" conformation, with the 3' overhang flipped up toward the RNA minor groove. However, upon binding to XPO5, the 3' overhang is flipped downwards away from the rest of the pre-miRNA molecule into an "open" conformation. This helps the backbone phosphates of these two nucleotides form hydrogen bonds with many XPO5 residues, allowing XPO5 to recognize the RNA as pre-miRNA. Because these interactions involve only the RNA phosphate backbone, they are nonspecific and allow XPO5 to recognize and transport any pre-miRNA. The rest of the pre-miRNA stem binds to XPO5 via interactions between the negatively-charged phosphate backbone and several positively-charged interior XPO5 residues. The combined structure of XPO5, RanGTP, and pre-miRNA is known as the ternary complex. Once the ternary complex is formed, it diffuses through a nuclear pore complex into the cytoplasm, transporting pre-miRNA into the cytoplasm in the process. Once in the cytoplasm, RanGAP hydrolyzes GTP to GDP, causing a conformational change that releases the pre-miRNA into the cytoplasm. It has been suggested, through evidence provided by contour maps of water density, that the interior of XPO5 is hydrophilic, while the exterior of XPO5 is hydrophobic. Therefore, this enhances the binding capabilities of XPO5 to the nuclear pore complex, allowing for transport of the ternary complex out of the nucleus. Recent evidence has shown higher levels of XPO5 in prostate cancer cell lines in-vitro, suggesting that altered XPO5 expression levels may have a role in cancer development. Suppressing XPO5 has also been found to be therapeutic in-vitro.

wikidoc

/index.php/XRCC1

# XRCC1 DNA repair protein XRCC1 also known as X-ray repair cross-complementing protein 1 is a protein that in humans is encoded by the XRCC1 gene. XRCC1 is involved in DNA repair where it complexes with DNA ligase III. XRCC1 is involved in the efficient repair of DNA single-strand breaks formed by exposure to ionizing radiation and alkylating agents. This protein interacts with DNA ligase III, polymerase beta and poly (ADP-ribose) polymerase to participate in the base excision repair pathway. It may play a role in DNA processing during meiogenesis and recombination in germ cells. A rare microsatellite polymorphism in this gene is associated with cancer in patients of varying radiosensitivity. The XRCC1 protein does not have enzymatic activity, but acts as a scaffolding protein that interacts with multiple repair enzymes. The scaffolding allows these repair enzymes to then carry out their enzymatic steps in repairing DNA. XRCC1 is involved in single-strand break repair, base excision repair and nucleotide excision repair. As reviewed by London, XRCC1 protein has three globular domains connected by two linker segments of ~150 and 120 residues. The XRCC1 N-terminal domain binds to DNA polymerase beta, the C-terminal BRCT domain interacts with DNA ligase III alpha and the central domain contains a poly(ADP-ribose) binding motif. This central domain allows recruitment of XRCC1 to polymeric ADP-ribose that forms on PARP1 after PARP1 binds to single strand breaks. The first linker contains a nuclear localization sequence and also has a region that interacts with DNA repair protein REV1, and REV1 recruits translesion polymerases. The second linker interacts with polynucleotide kinase phosphatase ( PNKP) (that processes DNA broken ends during base excision repair), aprataxin (active in single-strand DNA repair and non-homologous end joining) and a third protein designated aprataxin- and PNKP-like factor. XRCC1 has an essential role in microhomology-mediated end joining (MMEJ) repair of double strand breaks. MMEJ is a highly error-prone DNA repair pathway that results in deletion mutations. XRCC1 is one of 6 proteins required for this pathway. Deficiency in XRCC1, due to being heterozygous for a mutated XRCC1 gene coding for a truncated XRCC1 protein, suppresses tumor growth in mice. Under three experimental conditions for inducing three types of cancer (colon cancer, melanoma or breast cancer), mice heterozygous for this XRCC1 mutation had substantially lower tumor volume or number than wild type mice undergoing the same carcinogenic treatments. Cancers are very often deficient in expression of one or more DNA repair genes, but over-expression of a DNA repair gene is less usual in cancer. For instance, at least 36 DNA repair proteins, when mutationally defective in germ line cells, cause increased risk of cancer (hereditary cancer syndromes). (Also see DNA repair-deficiency disorder.) Similarly, at least 12 DNA repair genes have frequently been found to be epigenetically repressed in one or more cancers. (See also Epigenetically reduced DNA repair and cancer.) Ordinarily, deficient expression of a DNA repair enzyme results in increased un-repaired DNA damages which, through replication errors (translesion synthesis), lead to mutations and cancer. However, XRCC1 mediated MMEJ repair is directly mutagenic, so in this case, over-expression, rather than under-expression, apparently leads to cancer. Reduction of mutagenic XRCC1 mediated MMEJ repair leads to reduced progression of cancer. The NMR solution structure of the Xrcc1 N-terminal domain (Xrcc1 NTD) shows that the structural core is a beta-sandwich with beta-strands connected by loops, three helices and two short two-stranded beta-sheets at each connection side. The Xrcc1 NTD specifically binds single-strand break DNA (gapped and nicked) and a gapped DNA-beta-Pol complex.

wikidoc

/index.php/X_chromosome

# X chromosome The X chromosome is one of the two sex-determining chromosomes (allosomes) in many organisms, including mammals (the other is the Y chromosome), and is found in both males and females. It is a part of the XY sex-determination system and X0 sex-determination system. The X chromosome was named for its unique properties by early researchers, which resulted in the naming of its counterpart Y chromosome, for the next letter in the alphabet, following its subsequent discovery. It was first noted that the X chromosome was special in 1890 by Hermann Henking in Leipzig. Henking was studying the testicles of Pyrrhocoris and noticed that one chromosome did not take part in meiosis. Chromosomes are so named because of their ability to take up staining (chroma in Greek means color). Although the X chromosome could be stained just as well as the others, Henking was unsure whether it was a different class of object and consequently named it X element, which later became X chromosome after it was established that it was indeed a chromosome. The idea that the X chromosome was named after its similarity to the letter "X" is mistaken. All chromosomes normally appear as an amorphous blob under the microscope and only take on a well defined shape during mitosis. This shape is vaguely X-shaped for all chromosomes. It is entirely coincidental that the Y chromosome, during mitosis, has two very short branches which can look merged under the microscope and appear as the descender of a Y-shape. It was first suggested that the X chromosome was involved in sex determination by Clarence Erwin McClung in 1901. After comparing his work on locusts with Henking's and others, McClung noted that only half the sperm received an X chromosome. He called this chromosome an accessory chromosome, and insisted (correctly) that it was a proper chromosome, and theorized (incorrectly) that it was the male-determining chromosome. Luke Hutchison noticed that a number of possible ancestors on the X chromosome inheritance line at a given ancestral generation follows the Fibonacci sequence. A male individual has an X chromosome, which he received from his mother, and a Y chromosome, which he received from his father. The male counts as the "origin" of his own X chromosome (<math>F_1=1</math>), and at his parents' generation, his X chromosome came from a single parent (<math>F_2=1</math>). The male's mother received one X chromosome from her mother (the son's maternal grandmother), and one from her father (the son's maternal grandfather), so two grandparents contributed to the male descendant's X chromosome (<math>F_3=2</math>). The maternal grandfather received his X chromosome from his mother, and the maternal grandmother received X chromosomes from both of her parents, so three great-grandparents contributed to the male descendant's X chromosome (<math>F_4=3</math>). Five great-great-grandparents contributed to the male descendant's X chromosome (<math>F_5=5</math>), etc. (Note that this assumes that all ancestors of a given descendant are independent, but if any genealogy is traced far enough back in time, ancestors begin to appear on multiple lines of the genealogy, until eventually, a population founder appears on all lines of the genealogy.) The X chromosome in humans spans more than 153 million base pairs (the building material of DNA). It represents about 800 protein-coding genes compared to the Y chromosome containing about 70 genes, out of 20,000–25,000 total genes in the human genome. Each person usually has one pair of sex chromosomes in each cell. Females have two X chromosomes, whereas males have one X and one Y chromosome. Both males and females retain one of their mother's X chromosomes, and females retain their second X chromosome from their father. Since the father retains his X chromosome from his mother, a human female has one X chromosome from her paternal grandmother (father's side), and one X chromosome from her mother. This inheritance pattern follows the Fibonacci numbers at a given ancestral depth. The X chromosome carries hundreds of genes but few, if any, of these have anything to do directly with sex determination. Early in embryonic development in females, one of the two X chromosomes is randomly and permanently inactivated in nearly all somatic cells (cells other than egg and sperm cells). This phenomenon is called X-inactivation or Lyonization, and creates a Barr body. If X-inactivation in the somatic cell meant a complete de-functionalizing of one of the X-chromosomes, it would ensure that females, like males, had only one functional copy of the X chromosome in each somatic cell. This was previously assumed to be the case. However, recent research suggests that the Barr body may be more biologically active than was previously supposed. The following are some of the gene count estimates of human X chromosome. Because researchers use different approaches to genome annotation their predictions of the number of genes on each chromosome varies (for technical details, see gene prediction). Among various projects, the collaborative consensus coding sequence project (CCDS) takes an extremely conservative strategy. So CCDS's gene number prediction represents a lower bound on the total number of human protein-coding genes. It is theorized by Ross et al. 2005 and Ohno 1967 that the X chromosome is at least partially derived from the autosomal (non-sex-related) genome of other mammals, evidenced from interspecies genomic sequence alignments. The X chromosome is notably larger and has a more active euchromatin region than its Y chromosome counterpart. Further comparison of the X and Y reveal regions of homology between the two. However, the corresponding region in the Y appears far shorter and lacks regions that are conserved in the X throughout primate species, implying a genetic degeneration for Y in that region. Because males have only one X chromosome, they are more likely to have an X chromosome-related disease. It is estimated that about 10% of the genes encoded by the X chromosome are associated with a family of "CT" genes, so named because they encode for markers found in both tumor cells (in cancer patients) as well as in the human testis (in healthy patients). Sex linkage was first discovered in insects, e.g., T. H. Morgan's 1910 discovery of the pattern of inheritance of the white eyes mutation in Drosophila melanogaster. Such discoveries helped to explain x-linked disorders in humans, e.g., haemophilia A and B, adrenoleukodystrophy, and red-green color blindness. XX male syndrome is a rare disorder, where the SRY region of the Y chromosome has recombined to be located on one of the X chromosomes. As a result, the XX combination after fertilization has the same effect as a XY combination, resulting in a male. However, the other genes of the X chromosome cause feminization as well. Adrenoleukodystrophy, a rare and fatal disorder that is carried by the mother on the x-cell. It affects only boys between the ages of 5 and 10 and destroys the protective cell surrounding the nerves, myelin, in the brain. The female carrier hardly shows any symptoms because females have a copy of the x-cell. This disorder causes a once healthy boy to lose all abilities to walk, talk, see, hear, and even swallow. Within 2 years after diagnosis, most boys with Adrenoleukodystrophy die. The X-chromosome has played a crucial role in the development of sexually selected characteristics for over 300 million years. During that time it has accumulated a disproportionate number of genes concerned with mental functions. For reasons that are not yet understood, there is an excess proportion of genes on the X-chromosome that are associated with the development of intelligence, with no obvious links to other significant biological functions. . In other words, a significant proportion of genes associated with intelligence is passed on to the male offspring from the maternal side and to the female offspring from either/both maternal and paternal side.There has also been interest in the possibility that haploinsufficiency for one or more X-linked genes has a specific impact on development of the Amygdala and its connections with cortical centres involved in social–cognition processing or the 'social brain'. [clarification needed]

wikidoc

/index.php/Xaliproden

# Xaliproden Xaliproden (codenamed SR57746) is a drug which acts as a 5HT1A agonist. It has neurotrophic and neuroprotective effects in vitro, and has been proposed for use in the treatment of several neurodegenerative conditions including amyotrophic lateral sclerosis (ALS) and Alzheimer's disease. Development of xaliproden for these two indications was discontinued in 2007 following analysis of Phase III data. While the drug did show an effect on hippocampal volume (suggesting perhaps a slowing of cell loss), there was insufficient evidence for efficacy in counteracting Alzheimer's related cognitive decline. Similarly while there were some indicators of efficacy in ALS, including a small but clinically noteworthy effect on some functional parameters, the overall benefit did not reach statistical significance when results across several Phase III trials were averaged. Xaliproden remains under investigation for treatment of chemotherapy-induced peripheral neuropathy.

wikidoc

/index.php/Xamoterol

# Xamoterol Xamoterol is a cardiac stimulant. It works by binding to the β1 adrenergic receptor. It is a 3rd generation adrenergic beta receptor partial agonist. It provides cardiac stimulation at rest but it acts as a blocker during exercise.

wikidoc

/index.php/Xanthelasma

# Xanthelasma Xanthelasma (or xanthelasma palpebrarum) is a sharply demarcated yellowish collection of cholesterol underneath the skin, usually on or around the eyelids. The plural is "xanthelasmata". The root of the word is from Greek xanthos, ξανθος, "yellow". In a prospective population based cohort study (The Copenhagen City Heart Study), a total of 12,745 participants who were free of ischemic heart disease and aged 20-93 years were followed for a mean of 22 years . The mulivariate adjusted risk (hazard/odds ratios adjusted for confounders including cholesterol and triglyceride concentrations) of an adverse outcome associated with the presence of xanthelasmata were as follows: Thus, independent of other cardiac risk factors, the presence of a xanthelasma appers to be an independent risk factor for atherosclerotic heart disease. In the same study, arcus senilis was not identified as an independent risk factor . These minor growths may be disfiguring and can be removed. Xanthelasmata can be removed with trichloroacetic acid peel, surgery, lasers or cryotherapy. Removal can cause scarring and pigment changes, but it is unusual after treatment with trichloroacetic acid.

wikidoc

/index.php/Xanthine

# Xanthine Derivatives of xanthine, known collectively as xanthines, are a group of alkaloids commonly used for their effects as mild stimulants and as bronchodilators, notably in treating the symptoms of asthma. On the contrary, they really only eliminate the actions of adenosine to some extent, adenosine causing sleepiness, thus they are by far less in effectiveness as stimulants than sympathomimetic amines. Their effects, however, are widespread and their therapeutic range is narrow, so they are not the drug of choice in asthma treatment. Therapeutic level is 10-20 micrograms/mL blood. Signs of toxicity include tremor, nausea, nervousness, and tachycardia/arrhythmia. Methylated xanthine derivatives include caffeine, paraxanthine, theophylline, and theobromine (found mainly in chocolate). These drugs inhibit phosphodiesterase and antagonise adenosine. Xanthines are also found very rarely as constituents of nucleic acids.

wikidoc

/index.php/Xanthine_dehydrogenase

# Xanthine dehydrogenase Xanthine dehydrogenase belongs to the group of molybdenum-containing hydroxylases involved in the oxidative metabolism of purines. The enzyme is a homodimer. Xanthine dehydrogenase can be converted to xanthine oxidase by reversible sulfhydryl oxidation or by irreversible proteolytic modification. This enzyme belongs to the family of oxidoreductases, to be specific, those acting on CH or CH2 groups with NAD+ or NADP+ as acceptor. The systematic name of this enzyme class is xanthine:NAD+ oxidoreductase. Other names in common use include NAD+-xanthine dehydrogenase, xanthine-NAD+ oxidoreductase, xanthine/NAD+ oxidoreductase, and xanthine oxidoreductase.

wikidoc

/index.php/Xanthine_oxidase

# Xanthine oxidase Xanthine oxidase (XO, sometimes 'XAO') is a form of xanthine oxidoreductase, a type of enzyme that generates reactive oxygen species. These enzymes catalyze the oxidation of hypoxanthine to xanthine and can further catalyze the oxidation of xanthine to uric acid. These enzymes play an important role in the catabolism of purines in some species, including humans. Xanthine oxidase is defined as an enzyme activity (EC 1.17.3.2). The same protein, which in humans has the HGNC approved gene symbol XDH, can also have xanthine dehydrogenase activity (EC 1.17.1.4). Most of the protein in the liver exists in a form with xanthine dehydrogenase activity, but it can be converted to xanthine oxidase by reversible sulfhydryl oxidation or by irreversible proteolytic modification. Because XO is a superoxide-producing enzyme, with general low specificity, it can be combined with other compounds and enzymes and create reactive oxidants, as well as oxidize other substrates. Bovine xanthine oxidase (from milk) was originally thought to have a binding site to reduce cytochrome c with, but it has been found that the mechanism to reduce this protein is through XO's superoxide anion byproduct, with competitive inhibition by carbonic anhydrase. Another reaction catalyzed by xanthine oxidase is the decomposition of S-Nitrosothiols (RSNO), a reactive nitrogen species, to nitric oxide (NO), which reacts with a superoxide anion to form peroxynitrite under aerobic conditions. XO has also been found to produce the strong one-electron oxidant carbonate radical anion from oxidation with acetaldehyde in the presence of catalase and bicarbonate. It was suggested that the carbonate radical was likely produced in one of the enzyme's redox centers with a peroxymonocarbonate intermediate. The protein is large, having a molecular weight of 270 kDa, and has 2 flavin molecules (bound as FAD), 2 molybdenum atoms, and 8 iron atoms bound per enzymatic unit. The molybdenum atoms are contained as molybdopterin cofactors and are the active sites of the enzyme. The iron atoms are part of [2Fe-2S] ferredoxin iron-sulfur clusters and participate in electron transfer reactions. The active site of XO is composed of a molybdopterin unit with the molybdenum atom also coordinated by terminal oxygen (oxo), sulfur atoms and a terminal hydroxide. In the reaction with xanthine to form uric acid, an oxygen atom is transferred from molybdenum to xanthine, whereby several intermediates are assumed to be involved. The reformation of the active molybdenum center occurs by the addition of water. Like other known molybdenum-containing oxidoreductases, the oxygen atom introduced to the substrate by XO originates from water rather than from dioxygen (O2). During severe liver damage, xanthine oxidase is released into the blood, so a blood assay for XO is a way to determine if liver damage has happened. Because xanthine oxidase is a metabolic pathway for uric acid formation, the xanthine oxidase inhibitor allopurinol is used in the treatment of gout. Since xanthine oxidase is involved in the metabolism of 6-mercaptopurine, caution should be taken before administering allopurinol and 6-mercaptopurine, or its prodrug azathioprine, in conjunction. Xanthinuria is a rare genetic disorder where the lack of xanthine oxidase leads to high concentration of xanthine in blood and can cause health problems such as renal failure. There is no specific treatment, sufferers are advised by doctors to avoid foods high in purine and to maintain a high fluid intake. Type I xanthinuria has been traced directly to mutations of the XDH gene which mediates xanthine oxidase activity. Type II xanthinuria may result from a failure of the mechanism which inserts sulfur into the active sites of xanthine oxidase and aldehyde oxidase, a related enzyme with some overlapping activities (such as conversion of allopurinol to oxypurinol). Inhibition of xanthine oxidase has been proposed as a mechanism for improving cardiovascular health. A study found that patients with chronic obstructive pulmonary disease (COPD) had a decrease in oxidative stress, including glutathione oxidation and lipid peroxidation, when xanthine oxidase was inhibited using allopurinol. Oxidative stress can be caused by hydroxyl free radicals and hydrogen peroxide, both of which are byproducts of XO activity. Increased concentration of serum uric acid has been under research as an indicator for cardiovascular health factors, and has been used to strongly predict mortality, heart transplant, and more in patients. But it is not clear whether this could be a direct or casual association or link between serum uric acid concentration (and by proxy, xanthine oxidase activity) and cardiovascular health. States of high cell turnover and alcohol ingestion are some of the most prominent cases of high serum uric acid concentrations. Reactive nitrogen species, such as peroxynitrite that xanthine oxidase can form, have been found to react with DNA, proteins, and cells, causing cellular damage or even toxicity. Reactive nitrogen signaling, coupled with reactive oxygen species, have been found to be a central part of myocardial and vascular function, explaining why xanthine oxidase is being researched for links to cardiovascular health. Inhibitors of XO include allopurinol, oxypurinol, and phytic acid. It has also been found to be inhibited by flavonoids, including those found in Bougainvillea spectabilis Willd (Nyctaginaceae) leaves (with an IC50 of 7.23 μM), typically used in folk medicine.

wikidoc

/index.php/Xanthone

# Xanthone Xanthone is an organic compound with the molecular formula C13H8O2. It can be prepared by the heating of phenyl salicylate. In 1939, xanthone was introduced as an insecticide. Xanthone currently finds uses as ovicide for codling moth eggs and as a larvicide. It is also used in the preparation of xanthydrol, used in the determination of urea levels in the blood. The chemical structure of xanthone forms the central core of a variety of naturally occurring organic compounds, such as mangostin, which are sometimes collectively referred to as xanthones. Over 200 xanthones have been identified. Many of these xanthones are found in the pericarp of the mangosteen fruit (Garcinia mangostana), which can be found in the region of Southeast Asia.

wikidoc

/index.php/Xenin

# Xenin Xenin is a peptide hormone produced by a subpopulation of chromogranin A-positive endocrine cells in the mucous membrane of the duodenum. The peptide has been found in humans, dogs, pigs, rats, and rabbits. In humans, xenin circulates in the blood plasma. There is a relationship between peaks of xenin concentration in the plasma and the third phase of the Migrating Motor Complex. For example, infusion of synthetic xenin in fasting volunteers will cause phase III activity. After a meal (the 'postprandial state'), infusion of xenin increases both frequency and the percentage of aborally propagated contractions. In higher concentrations xenin stimulates exocrine pancreatic secretion and inhibits the gastrin-stimulated secretion of acid in dogs. Xenin is also produced in neuroendocrine tumors of the duodenal mucosa. Xenin is a 25-amino acid polypeptide. The amino acid sequence of xenin is identical to the N-terminal end of cytoplasmic coatomer subunit alpha, from which xenin can be cleaved by aspartic proteases. Xenin is structurally related to the amphibian peptide xenopsin and to the neuropeptide neurotensin. Proxenin is the precursor to xenin. It is a 35-amino acid polypeptide. Like xenin, its amino acid sequence exactly matches the N-terminus of coatomer subunit alpha. Xenin promotes beta-cell survival and xenin has been evaluated in animal models of obesity and diabetes where it has demonstrated an antidiabetic potential. In humans, co-administration of xenin-25 and gastric inhibitory polypeptide (GIP) reduces postprandial glycemia by delaying gastric emptying.

wikidoc

/index.php/Xenobiotic

# Xenobiotic ## Overview A xenobiotic is a chemical which is found in an organism but which is not normally produced or expected to be present in it. It can also cover substances which are present in much higher concentrations than are usual. Specifically, drugs such as antibiotics are xenobiotics in humans because the human body does not produce them itself nor would they be expected to be present as part of a normal diet. However, the term is also used in the context of pollutants such as dioxins and polychlorinated biphenyls and their effect on the biota. Natural compounds can also become xenobiotics if they are taken up by another organism (e.g., uptake of natural human hormones by fish found downstream of sewage treatment plant outfalls). ## Xenobiotic metabolism The body removes xenobiotics by xenobiotic metabolism. This consists of the deactivation and the secretion of xenobiotics, and happens mostly in the liver. Secretion routes are urine, feces, breath, and sweat. Hepatic enzymes are responsible for the metabolism of xenobiotics by first activating them (oxidation, reduction, hydrolysis and/or hydration of the xenobiotic), and then conjugating the active secondary metabolite with glucuronic or sulphuric acid, or glutathione, followed by excretion in bile or urine. An example of a group of enzymes involved in xenobiotic metabolism is hepatic microsomal cytochrome P450. These enzymes that metabolize xenobiotics are very important for the pharmaceutical industry, because they are responsible for the breakdown of medications. ## Xenobiotics in the environment Xenobiotic substances are becoming an increasingly large problem in Sewage Treatment systems, since they are relatively new substances and are very difficult to categorize. Antibiotics, for example, were derived from plants originally, and so mimic naturally occurring substances. This, along with the natural monopoly nature of municipal Waste Water Treatment Plants makes it nearly impossible to remove this new pollutant load. ## Inter-species organ transplantation Some xenobiotics are resistant to degradation. For example, they may be synthetic organochlorides such as plastics and pesticides, or naturally occurring organic chemicals such as polyaromatic hydrocarbons (PAHs) and some fractions of crude oil and coal. However, it is believed that microorganisms are capable of degrading all the different complex and resistant xenobiotics found on the earth. ## See also The term xenobiotic is also used to refer to organs transplanted from one species to another. For example, some researchers hope that hearts and other organs could be transplanted from pigs to humans. Many people die every year whose lives could have been saved if a critical organ had been available for transplant. Kidneys are currently the most commonly transplanted organ. Xenobiotic organs would need to be developed in such a way that they would not be rejected by the immune system. With the development of vitrification transplantable organs could be stored in organ banks for long periods.

wikidoc

/index.php/Xenoestrogen

# Xenoestrogen ## Contents Xenoestrogens are synthetic substances that differ from those produced by living organisms and imitate or enhance the effect of estrogens. The estrogenic stimulation is an unintended side-effect of these agents or their metabolites. ## Effects Xenoestrogens are part of a heterogeneous group of chemicals that are hormone or endocrine disruptors. They differ from phytoestrogens (estrogenic substances from plants), mycoestrogens (estrogenic substances from fungi), and pharmacological estrogens (estrogenic action is intended). External estrogens from a variety of sources may have a cumulative effect upon living organisms, and xenoestrogens may be part of a larger picture of a process of estrogenization of the environment. Xenoestrogens have only been recently (less than 70 years) introduced into the environment, as produced by industrial, agricultural, and chemical companies. ## Presence Xenoestrogens have been implicated in a variety of medical problems. Foremost is the concern that xenoestrogens as false messengers disrupt the process of reproduction. Studies have implicated observations of disturbances in wildlife with estrogenic exposure. Reproductive issues which are of concerns in humans are fetal exposure (perhaps leading to hypospadias) and decreased reproductive ability in men (i.e. decrease in sperm numbers). Another issue is the potential effect of xenoestrogens on oncogenes, specifically in relation to breast cancer. ## Research The ubiquitous presence of such estrogenic substances is a significant health concern, both individually and for a population. Life relies on the transmission of biochemical information to the next generation, and the presence of xenoestrogens may interfere with this transgenerational information process through "chemical confusion" (Vidaeff, Sever). Environmental protection laws and regulations are supposed to protect the environment from hormonal disruption. Agencies such as the United States Environmental Protection Agency and the World Health Organization International Program on Chemical Safety are charged to address these issues. ## Synthetic chemicals shown to have unintended estrogenic effects The study of the problem is difficult and complex. Transgenerational effects are difficult to prove, effects may be multifactorial, and the large variety of substances in question with the absence of unexposed controls do not lend themselves to easy interpretation. Believers that environmental estrogen disruption is a major health hazard are opposed by detractors who argue that observed effects are spurious and inconsistent, or that the quantities of the agents are too low to have any effect. ## See also A 2005 study by Belcher and coworkers demonstrated that even very low levels of a xenoestrogen, in this case Bisphenol A, could affect fetal neural development more than higher levels (PMID 16123166), indicating that classical models where dose equals response may not be applicable in susceptible tissue.

wikidoc

/index.php/Xenograft

# Xenotransplantation Xenotransplantation (xeno- from the Greek meaning "foreign") is the transplantation of living cells, tissues or organs from one species to another such as from pigs to humans (see Medical grafting). Such cells, tissues or organs are called xenografts or xenotransplants. The term allotransplantation refers to a same-species transplant. Human xenotransplantation offers a potential treatment for end-stage organ failure, a significant health problem in parts of the industrialized world. It also raises many novel medical, legal and ethical issues. A continuing concern is that pigs have different lifespans than humans and their tissues age at a different rate. Disease transmission (xenozoonosis) and permanent alteration to the genetic code of animals are also a cause for concern. Because there is a worldwide shortage of organs for clinical implantation, about 60% of patients awaiting replacement organs die on the waiting list. In many cases there is so little chance of a person actually receiving a transplant, doctors do not even add the person to the list, causing an underrepresentation of the shortage[citation needed]. Recent advances in understanding the mechanisms of transplant organ rejection have brought science to a stage where it is reasonable to consider that organs from other species, probably pigs, may soon be engineered to minimize the risk of serious rejection and used as an alternative to human tissues, possibly ending organ shortages. Other procedures, some of which are being investigated in early clinical trials, aim to use cells or tissues from other species to treat life-threatening and debilitating illnesses such as cancer, diabetes, liver failure and Parkinson's disease. If vitrification can be perfected it could allow for long-term storage of xenogenic cells, tissues and organs so they would be more readily available for transplant. There are only a few published successful xenotransplant procedures. Some patients who were in need of liver transplants were able to use pig livers that were on a trolley by their bedside successfully until a proper donor liver was available . Some recipients of pig neural cells with paralysis due to stroke (CVA) and Parkinson's disease have experienced dramatic improvements[citation needed]. Immune rejection remains the biggest challenge for xenotransplantation. The problem exists even for human to human transplants (known as allotransplantation), but is more serious for transplants between different species. Nearly all mammalian cells have markers which enable the immune system to recognise them as being foreign. The more different the genetic code between the donor organ and recipient, the greater the difference between a "self" marker and a "foreign" marker. Some companies are currently developing transgenic animals such as pigs, that produce human markers to try and lessen the chance of rejection.. Cross-species transplants are more likely to produce host-vs-graft or graft-vs-host reactions than same-species transplants, because of the lack of antigenic similarity. Organisms which have been genetically engineered to reduce this lack of similarity have been produced but are not yet used to any significant degree in medical care. A worrisome element of xenotransplantation is the potential for infectious disease to spread from the donor animal, which is called xenozoonosis. One example is porcine endogenous retroviruses (PERVs) which are viruses within pigs that pigs are immune to, but can infect humans. Some recipients of pig neural cell transplants have had to agree to never donate blood, take frequent blood tests and use safe sex methods for the rest of their lives due to the risk of spreading such viruses. However, the patients who have received these pig cell transplants have yet to show any PERV-type infection. The situation with other animals is currently unknown. Xenografts have been a controversial procedure since they were first attempted. Many, including animal rights groups, strongly oppose killing animals in order to harvest their organs for human use. Legitimate medical concerns exist about possible disease transfer between animals and humans, such as the porcine endogenous retrovirus found in pig tissues. Religious beliefs, such as the Jewish and Muslim prohibition against eating pork, may also present concerns for some. In general, however, the use of pig and cow tissue in humans has been met with little resistance. The tissue is harvested from agricultural animals that were already being butchered, which is less offensive to most people than the idea of raising a primate (which due to its genetic similarity would produce more suitable organs for transplants to humans) solely as an organ donor. Similarly, while some individual Jews may not wish to receive a pig valve based on their personal beliefs, the rabbinical view is that the use of pig valves in humans is not a violation of kashruth law. In fact, killing a pig in order to save a human life is a requirement in the Jewish faith, under the laws of pikuach nefesh. In 2005, the Australian National Health and Medical Research Council declared a five-year moratorium on all animal-to-human transplantation, concluding that the risks of transmission of animal viruses to patients and the wider community have not yet been resolved.

wikidoc

/index.php/Xenon

# Xenon Xenon (Template:PronEng in the UK, Template:IPA in the US) is a chemical element that has the symbol Xe and atomic number 54. A colorless, heavy, odorless noble gas, xenon occurs in the earth's atmosphere in trace amounts. Although generally unreactive, xenon can undergo a few chemical reactions such as the formation of xenon hexafluoroplatinate, the first noble gas compound to be synthesized. Naturally occurring xenon is made of nine stable isotopes, but there are also over 40 unstable isotopes that undergo radioactive decay. The isotope ratios of xenon are an important tool for studying the early history of the Solar System. Xenon-135 is produced as a result of nuclear fission and acts as a neutron absorber in nuclear reactors. Xenon is used in flash lamps and arc lamps, and as a general anesthetic. The first excimer laser design used a xenon dimer molecule (Xe2) as its lasing medium, and the earliest laser designs used xenon flash lamps as pumps. Xenon is also being used to search for hypothetical weakly interactive massive particles and as the propellant for ion thrusters in spacecraft. Xenon was discovered in England by William Ramsay and Morris Travers on July 12, 1898, shortly after their discovery of the elements krypton and neon. They found it in the residue left over from evaporating components of liquid air. Ramsay suggested the name xenon for this gas from the Greek word ξένον [xenon], neuter singular form of ξένος [xenos], meaning foreign, strange, or host. In 1902, Ramsay estimated the proportion of xenon in the Earth's atmosphere as one part in 20 million. During the 1930s, the engineer Harold Edgerton began exploring strobe light technology for high-speed photography. This led him to the invention of the xenon flash lamp, in which light is generated by sending a brief electrical current through a tube filled with xenon gas. In 1934, Edgerton was able to generate flashes as brief as one microsecond with this method. Albert R. Behnke Jr. began exploring the causes of "drunkenness" in deep-sea divers in 1939. He tested the effects of varying the breathing mixtures on his subjects, and discovered that this caused the divers to perceive a change in depth. From his results, he deduced that xenon gas could serve as an anesthetic. Although Lazharev, in Russia, apparently studied xenon anesthesia in 1941, the first published report confirming xenon anesthesia was in 1946 by J. H. Lawrence, who experimented on mice. Xenon was first used as a surgical anesthetic in 1951 by Stuart C. Cullen, who successfully operated on two patients. In 1960, the physicist John H. Reynolds discovered that certain meteorites contained an isotopic anomaly in the form of an overabundance of xenon-129. He inferred that this was a decay product of radioactive iodine-129. As the half-life of 129I is 16 million years, this demonstrated that the meteorites were formed during the early history of the Solar System, as the 129I isotope was likely generated before the Solar System was formed. Xenon and the other noble gases were for a long time considered to be completely chemically inert and not able to form compounds. However, while teaching at the University of British Columbia, Neil Bartlett discovered that the gas platinum hexafluoride (PtF6) was a powerful oxidizing agent that could oxidize oxygen (O2) to form dioxygenyl hexafluoroplatinate (O2+[PtF6]−). Since O2 and xenon have almost the same first ionization potential, Bartlett realized that platinum hexafluoride might also be able to oxidize xenon. On March 23, 1962, he mixed the two gases and produced the first known compound of a noble gas, xenon hexafluoroplatinate. Bartlett thought its composition to be Xe+[PtF6]−, although later work has revealed that it was probably a mixture of various xenon-containing salts. Since then, many other xenon compounds have been discovered, and some compounds of the noble gases argon, krypton, and radon have been identified, including argon fluorohydride (HArF), krypton difluoride (KrF2), and radon fluoride. Xenon is a trace gas in Earth's atmosphere, occurring at 0.087±0.001 parts per million (μL/L). It is also found in gases emitted from some mineral springs. Some radioactive species of xenon, for example, 133Xe and 135Xe, are produced by neutron irradiation of fissionable material within nuclear reactors. Xenon is obtained commercially as a byproduct of the separation of air into oxygen and nitrogen. After this separation, generally performed by fractional distillation in a double-column plant, the liquid oxygen produced will contain small quantities of krypton and xenon. By additional fractional distillation steps, the liquid oxygen may be enriched to contain 0.1–0.2% of a krypton/xenon mixture, which is extracted either via adsorption onto silica gel or by distillation. Finally, the krypton/xenon mixture may be separated into krypton and xenon via distillation. Extraction of a liter of xenon from the atmosphere requires 220 watt-hours of energy. Worldwide production of xenon in 1998 was estimated at 5,000–7,000 m3. Due to its low abundance, xenon is much more expensive than the lighter noble gases—approximate prices for the purchase of small quantities in Europe in 1999 were 10 €/L for xenon, 1 €/L for krypton, and 0.20 €/L for neon. Xenon is relatively rare in the Sun's atmosphere, on Earth, and in the asteroids and comets. The atmosphere of Mars shows a similar xenon abundance to that of Earth: 0.08 parts per million. However, Mars shows a higher proportion of 129Xe than the Earth or the Sun. As this isotope is generated by radioactive decay, the result may indicate that Mars lost most of its primordial atmosphere, possibly within the first 100 million years after the planet was formed. By contrast, the planet Jupiter has an unusually high abundance of xenon in its atmosphere; about 2.6 times as much as the Sun. This high abundance remains unexplained, but may have been caused by an early and rapid buildup of planetesimals—small, subplanetary bodies—before the presolar disk began to heat up. (Otherwise, xenon would not have been trapped in the planetesimal ices.) Within the Solar System, the nucleon fraction for all isotopes of xenon is 1.56 × 10-8, or one part in 64 million of the total mass. The problem of the low terrestrial xenon may potentially be explained by covalent bonding of xenon to oxygen within quartz, hence reducing the outgassing of xenon into the atmosphere. Unlike the lower mass noble gases, the normal stellar nucleosynthesis process inside a star does not form xenon. Elements more massive than iron-56 have a net energy cost to produce through fusion, so there is no energy gain for a star to create xenon. Instead, many isotopes of xenon are formed during supernova explosions. An atom of xenon is defined as having a nucleus with 54 protons. At standard temperature and pressure, pure xenon gas has a density of 5.761 kg/m3, about 4.5 times the surface density of the Earth's atmosphere, 1.217 kg/m3. As a liquid, xenon has a density of up to 3.100 g/mL, with the density maximum occurring at the triple point. Under the same conditions, the density of solid xenon, 3.640 g/cm3, is larger than the average density of granite, 2.75 g/cm3. Using gigapascals of pressure, xenon has been forced into a metallic phase. Xenon is a member of the zero-valence elements that are called noble or inert gases. It is inert to most common chemical reactions (such as combustion, for example) because the outer valence shell is completely filled with eight electrons. This produces a stable, minimum energy configuration in which the outer electrons are tightly bound. However, xenon can be oxidized by powerful oxidizing agents, and many xenon compounds have been synthesized. In a gas-filled tube, xenon emits a blue or lavenderish glow when the gas is excited by electrical discharge. Xenon emits a band of emission lines that span the visual spectrum, but the most intense lines occur in the region of blue light, which produces the coloration. Naturally occurring xenon is made of nine stable isotopes. The isotopes 124Xe, 134Xe and 136Xe are predicted to undergo double beta decay, but this has never been observed so they are considered to be stable. Besides these stable forms, there are over 40 unstable isotopes that have been studied. 129Xe is produced by beta decay of 129I, which has a half-life of 16 million years, while 131mXe, 133Xe, 133mXe, and 135Xe are some of the fission products of both 235U and 239Pu, and therefore used as indicators of nuclear explosions. The various isotopes of xenon are produced from supernova explosions, red giant stars that have exhausted the hydrogen at their cores and entered the asymptotic giant branch, classical novae explosions and the radioactive decay of elements such as iodine, uranium and plutonium. The artificial isotope 135Xe is of considerable significance in the operation of nuclear fission reactors. 135Xe has a huge cross section for thermal neutrons, 2.6×106 barns, so it acts as a neutron absorber or "poison" that can slow or stop the chain reaction after a period of operation. This was discovered in the earliest nuclear reactors built by the American Manhattan Project for plutonium production. Fortunately the designers had made provisions in the design to increase the reactor's reactivity (the number of neutrons per fission that go on to fission other atoms of nuclear fuel). Under adverse conditions, relatively high concentrations of radioactive xenon isotopes may be found emanating from nuclear reactors due to the release of fission products from cracked fuel rods, or fissioning of uranium in cooling water. Because xenon is a tracer for two parent isotopes, xenon isotope ratios in meteorites are a powerful tool for studying the formation of the solar system. The iodine-xenon method of dating gives the time elapsed between nucleosynthesis and the condensation of a solid object from the solar nebula. Xenon isotopic ratios such as 129Xe/130Xe and 136Xe/130Xe are also a powerful tool for understanding terrestrial differentiation and early outgassing. Excess 129Xe found in carbon dioxide well gases from New Mexico was believed to be from the decay of mantle-derived gases soon after Earth's formation. Xenon hexafluoroplatinate was the first chemical compound of xenon, synthesized in 1962. Following this, many additional compounds of xenon have been discovered. These include xenon difluoride (XeF2), xenon tetrafluoride (XeF4), xenon hexafluoride (XeF6), xenon tetroxide (XeO4), and sodium perxenate (Na4XeO6). A highly explosive compound, xenon trioxide (XeO3), has also been made. Most of the more than 80 xenon compounds found to date contain electro-negative fluorine or oxygen. When other atoms are bound (such as hydrogen or carbon), they are often part of a molecule containing fluorine or oxygen. Some compounds of xenon are colored but most are colorless. In 1995, a group of scientists at the University of Helsinki in Finland (M. Räsänen and co-workers) announced the preparation of xenon dihydride (HXeH), and later xenon hydride-hydroxide (HXeOH), hydroxenoacetylene (HXeCCH), and other Xe-containing molecules. Deuterated molecules, HXeOD and DXeOH, have also been produced. As well as compounds where xenon forms a chemical bond, xenon can form clathrates—substances where xenon atoms are trapped by the crystalline lattice of another compound. An example is xenon hydrate (Xe·5.75 H2O), where xenon atoms occupy vacancies in a lattice of water molecules. The deuterated version of this hydrate has also been produced. Such clathrate hydrates can occur naturally under conditions of high pressure, such as in Lake Vostok underneath the Antarctic ice sheet. Clathrate formation can be used to fractionally distill xenon, argon and krypton. Xenon can also form endohedral fullerene compounds, where a xenon atom is trapped inside a fullerene molecule. The xenon atom trapped in the fullerene can be monitored via 129Xe nuclear magnetic resonance spectroscopy. Using this technique, chemical reactions on the fullerene molecule can be analyzed, due to the sensitivity of the chemical shift of the xenon atom to its environment. However, the xenon atom also has an electronic influence on the reactivity of the fullerene. Xenon is used in light-emitting devices called xenon flash lamps, which are used in photographic flashes and stroboscopic lamps; to excite the active medium in lasers which then generate coherent light; and, occasionally, in bactericidal lamps. The first solid-state laser, invented in 1960, was pumped by a xenon flash lamp, and lasers used to power inertial confinement fusion are also pumped by xenon flash lamps. Continuous, short-arc, high pressure xenon arc lamps have a color temperature closely approximating noon sunlight and are used in solar simulators. That is, the chromaticity of these lamps closely approximates a heated black-body radiator that has a temperature close to that observed from the Sun. After they were first introduced during the 1940s, these lamps began replacing the shorter-lived carbon arc lamps in movie projectors. They are employed in typical 35mm and IMAX film projection systems, automotive HID headlights and other specialized uses. These arc lamps are an excellent source of short wavelength ultraviolet radiation and they have intense emissions in the near infrared, which is used in some night vision systems. The individual cells in a plasma display use a mixture of xenon and neon that is converted into a plasma using electrodes. The interaction of this plasma with the electrodes generates ultraviolet photons, which then excite the phosphor coating on the front of the display. Xenon is used as a "starter gas" in high pressure sodium lamps. It has the lowest thermal conductivity and lowest ionization potential of all the non-radioactive noble gases. As a noble gas, it does not interfere with the chemical reactions occurring in the operating lamp. The low thermal conductivity minimizes thermal losses in the lamp while in the operating state, and the low ionization potential causes the breakdown voltage of the gas to be relatively low in the cold state, which allows the lamp to be more easily started. In 1962, a group of researchers at Bell Laboratories discovered laser action in xenon, and later found that the laser gain was improved by adding helium to the lasing medium. The first excimer laser used a xenon dimer (Xe2) energized by a beam of electrons to produce stimulated emission at an ultraviolet wavelength of 176 nm. Xenon chloride and xenon fluoride have also been used in excimer (or, more accurately, exciplex) lasers. The xenon chloride excimer laser has been employed, for example, in certain dermatological uses. Xenon has been used as a general anesthetic, although it is expensive. Even so, anesthesia machines that can deliver xenon are about to appear on the European market. Two mechanisms for xenon anesthesia have been proposed. The first one involves the inhibition of the calcium ATPase pump—the mechanism cells use to remove calcium (Ca2+)—in the cell membrane of synapses. This results from a conformational change when xenon binds to nonpolar sites inside the protein. The second mechanism focuses on the non-specific interactions between the anesthetic and the lipid membrane. Xenon has a minimum alveolar concentration (MAC) of 0.63, making it 50% more potent than N2O as an anesthetic. Thus it can be used in concentrations with oxygen that have a lower risk of hypoxia. Unlike nitrous oxide (N2O), xenon is not a greenhouse gas and so it is also viewed as environmentally friendly. Because of the high cost of xenon, however, economic application will require a closed system so that the gas can be recycled, with the gas being appropriately filtered for contaminants between uses. Gamma emission from the radioisotope 133Xe of xenon can be used to image the heart, lungs, and brain, for example, by means of single photon emission computed tomography. 133Xe has also been used to measure blood flow. Nuclei of only two of the stable isotopes of xenon, 129Xe and 131Xe, have non-zero intrinsic angular momenta (nuclear spins). When mixed with alkali vapor and nitrogen, their nuclear spins can be aligned along the laser beam of circularly-polarized light that is tuned to an absorption line of the alkali atoms. Typically, pure rubidium metal, heated above 100 °C, is used to produce the alkali vapor. This alignment (spin polarization) of xenon nuclei can surpass 50% of its maximum possible value, greatly exceeding the equilibrium value dictated by the Boltzmann distribution (typically 0.001% of the maximum value at room temperature, even in the strongest magnets). Such non-equilibrium alignment of spins is a temporary condition, and is called hyperpolarization. Because the 129Xe isotope has a nuclear spin value of 1/2 (and therefore the electric quadrupole moment of 129Xe nucleus must be zero), 129Xe nucleus does not experience any quadrupolar interactions during collisions with other atoms, and thus its hyperpolarization can be maintained for long periods of time even after the laser beam has been turned off and the alcali vapor removed by condensation on a room-temperature surface. The time it takes for a collection of spins to return to their equilibrium (Boltzmann) polarization is called the T1 relaxation time. For 129Xe isotope it can range from several seconds for xenon atoms dissolved in blood to several hours in the gas phase and to several days in the deeply-frozen solid xenon. In contrast, the 131Xe isotope has a nuclear spin value of 3/2, does possess a non-zero quadrupole moment, and has T1 relaxation times in the millisecond and second ranges. The hyperpolarization process (such as Spin-Exchange optical pumping described above) renders the 129Xe isotope much more detectable via magnetic resonance imaging and has been used for studies of the lungs and other tissues. It can be used, for example, to trace the flow of gases within the lungs. In nuclear energy applications, xenon is used in bubble chambers, probes, and in other areas where a high molecular weight and inert nature is desirable. Liquid xenon is being used as a medium for detecting hypothetical weakly interactive massive particles, or WIMPs. When a WIMP collides with a xenon nucleus, it should, theoretically, strip an electron and create a primary scintillation. By using xenon, this burst of energy could then be readily distinguished from similar events caused by particles such as cosmic rays. However, the XENON experiment at the Gran Sasso National Laboratory in Italy has thus far failed to find any confirmed WIMPs. Even if no WIMPs are detected though, the experiment will serve to constrain the properties of dark matter and some physics models. The current detector at this facility is five times as sensitive as other instruments world-wide, and the sensitivity will be increased by an order of magnitude in 2008. Xenon is the preferred fuel for ion propulsion of spacecraft because of its low ionization potential per atomic weight, the ability to store it as a liquid at near room temperature (but at high pressure) yet easily converts back into a gas to fuel the engine. The inert nature of xenon makes it environmentally friendly and less corrosive to an ion engine than other fuels such as mercury or caesium. Xenon was first used for satellite ion engines during the 1970s. It was later employed as a propellant for Europe's SMART-1 spacecraft and for the three ion propulsion engines on NASA's Dawn Spacecraft. Chemically, the perxenate compounds are used as oxidizing agents in analytical chemistry. Xenon difluoride is used as an etchant for silicon, particularly in the production of microelectromechanical systems (MEMS). The anticancer drug 5-fluorouracil can be produced by reacting Xenon difluoride with Uracil. Xenon is also used in protein crystallography. Applied at pressures from 0.5 to 5 MPa (5 to 50 atm) to a protein crystal, xenon atoms bind in predominantly hydrophobic cavities, often creating a high quality, isomorphous, heavy-atom derivative, which can be used for solving the phase problem. Xenon gas can be safely kept in normal sealed glass or metal containers at standard temperature and pressure. However, it readily dissolves in most plastics and rubber, and will gradually escape from a container sealed with such materials. Xenon is non-toxic, although it does dissolve in blood and belongs to a select group of substances that penetrate the blood-brain barrier, causing mild anaesthesia when inhaled in very high concentrations (see anesthesia subsection above). Many of xenon compounds are explosive and toxic due to their strong oxidative properties. At 169 m/s, the speed of sound in xenon gas is slower than that in air (due to the slower average speed of the heavy xenon atoms compared to nitrogen and oxygen molecules), so xenon lowers the resonant frequencies of the vocal tract when inhaled. This produces a characteristic lowered voice pitch, opposite the high-pitched voice caused by inhalation of helium. Like helium, xenon does not satisfy the body's need for oxygen and is a simple asphyxiant; consequently, many universities no longer allow the voice stunt as a general chemistry demonstration. As xenon is expensive, the gas sulfur hexafluoride, which is similar to xenon in molecular weight (146 versus 131), is generally used in this stunt, although it too is an asphyxiant. It is possible to safely breathe heavy gases such as xenon or sulfur hexafluoride when they include a 20% mixture of oxygen. The lungs mix the gases very effectively and rapidly, so that the heavy gases are purged along with the oxygen and do not accumulate at the bottom of the lungs. There is, however, a danger associated with any heavy gas in large quantities: it may sit invisibly in a container, and if a person enters a container filled with an odorless, colorless gas, they may find themselves breathing it unknowingly. Xenon is rarely used in large enough quantities for this to be a concern, though the potential for danger exists any time a tank or container of xenon is kept in an unventilated space.

wikidoc

/index.php/Xenon_xe-133_gas

# Xenon xe-133 gas Xenon xe-133 gas is an odorless noble gas that is FDA approved for the diagnosis of pulmonary function and for imaging the lungs. Common adverse reactions include not reported. Pregnancy Category (FDA): There is no FDA guidance on usage of Xenon xe-133 gas in women who are pregnant. Pregnancy Category (AUS): There is no Australian Drug Evaluation Committee (ADEC) guidance on usage of Xenon xe-133 gas in women who are pregnant. There is limited information regarding Xenon xe-133 gas overdosage. If you suspect drug poisoning or overdose, please contact the National Poison Help hotline (1-800-222-1222) immediately. The Xenon Xe 133 gas is supplied as part of the Calidose™ system, consisting of 3ml unit dose vials and the Calidose™ dispenser for shielded dispensing.

wikidoc

/index.php/Xenotropic_MuLV-related_virus

# Xenotropic MuLV-related virus Xenotropic MuLV-related virus (XMRV) is a newly identified and provisionally named gammaretrovirus which may be involved in the pathology of familial prostate cancer. Its name refers to its similarity to xenotropic murine leukemia viruses, although it does show some substantial differences. It is though to be linked to prostate cancer by ribonuclease L, part of the cell's natural defense against viruses. When activated, RNase L destroys RNA in an effort to halt viral gene expression. R462Q is a mutation that results in a decreased level of RNase L function, and this mutation's presence in prostate tumors shows a strong correlation with the presence of XMRV. The virus was discovered in cancerous prostate tissues using a microarray containing samples of genetic material from over 1000 viruses. The screen revealed the presence of a gammaretrovirus in a substantial number of the homozygous R462Q cells, but very few of the heterozygous or wild type cells. An expanded screen showed the virus present in 40% of men homozygous for R462Q and only 1.5% of those not, and also demonstrated that each case showed the same virus. In another study, the viral genome was reconstructed from prostate mRNA and used to infect prostate tissues in vitro. The researchers were able to show that RNase L deficient lines were more susceptible to infection. These data do not necessarily show that XMRV causes prostate cancer, but they do show that RNase L deficiency makes prostate tissue more susceptible to the virus. This in turn suggests the possibility of a link between the virus and the disease.

wikidoc

/index.php/Xeroderma_pigmentosum

# Xeroderma pigmentosum Xeroderma pigmentosa, or XP, is an autosomal recessive genetic disorder of DNA repair in which the ability to repair damage caused by ultraviolet (UV) light is deficient. This disorder leads to multiple basaliomas and other skin malignancies at a young age. In severe cases, it is necessary to avoid sunlight completely. The two most common causes of death for XP victims are metastatic malignant melanoma and squamous cell carcinoma . XP is about six times more common in Japanese people than in other groups. File:Autorecessive.svg The most common defect in xeroderma pigmentosum is an autosomal recessive genetic defect whereby nucleotide excision repair (NER) enzymes are mutated, leading to a reduction in or elimination of NER. The most important part of managing the condition is reducing exposure to the sun. The number of keratoses can be reduced with Isotretinoin ( ) (though there are significant side-effects.) Existing keratoses can be treated using cryotherapy or fluorouracil. Christopher Snow, the protagonist and narrator of Dean Koontz' Moonlight Bay Trilogy of novels (Fear Nothing, Seize The Night and the to-be-completed Ride The Storm), has severe enough XP that he must avoid sunlight and as much artificial light as possible at all costs, living his life at night and then only by dim bulbs and candlelight, though always maintaining a positive and envigorated attitude about life, even authoring a best-selling autobiographical book on living with XP. In Jodi Picoult's novel 'Second Glance' nine year old character Ethan Wakeman suffers from XP so severe he can only leave the house after sunset. Alejandro Amenábar's Award-winning film, The Others, centers around a woman (Nicole Kidman) whose children suffer from XP and must be kept indoors, behind closed curtains, at all times. 'A Cool Moonlight', written by Angela Johnson, also deals with eight year old Lila who suffers from XP. Her XP is so bad that she is sometimes burned by streetlamps or certain lightbulbs. Yui stars in a romantic Japanese movie Taiyō no Uta, where she plays the lead character, a street musician named Kaoru Amane, who is diagnosed with Xeroderma Pigmentosum and only performs at night because of this disease. Even with this diagnosis, she chases her dreams of becoming a singer and meets Kōji Fujishiro (Takashi Tsukamoto), who also has a passion for music and whom Kaoru eventually falls in love with. This story was also the basis for a Japanese TV drama series, also called "Taiyō no Uta", starring Erika Sawajiri and Takayuki Yamada in the roles of Kaoru and Kōji.

wikidoc

/index.php/Xerophthalmia

# Xerophthalmia ## Overview Xerophthalmia (Greek for dry eyes) is a medical condition in which the eye fails to produce tears. It may be caused by a deficiency in vitamin A and is sometimes used to describe that lack, although there may be other causes. ## Epidemiology and Demographics Xerophthalmia is a term that usually implies a destructive dryness of the conjunctival epithelium due to dietary vitamin A deficiency — a rare condition in developed countries, but still causing much damage in developing countries. ## Causes Xerophthalmia can be associated with systemic diseases such as Sjögren's syndrome, systemic lupus erythematosus, rheumatoid arthritis, scleroderma, sarcoidosis, amyloidosis, and hypothyroidism; deficiency of vitamin A; and the use of some medications including antihistamines, nasal decongestants, tranquilizers, and anti-depressant drugs. When xerophthalmia is due to vitamin A deficiency, the condition begins with night blindness and conjunctival xerosis (dryness of the eye membranes) and progresses to corneal xerosis (dryness of the cornea), and, in the late stages, to keratomalacia (softening of the cornea). Other forms of dry eye are associated with aging, poor lid closure, scarring from previous injury, or autoimmune diseases such as rheumatoid arthritis, and these can all cause chronic conjunctivitis. ## Treatment The treatment depends on the cause. Artificial tears, which lubricate the eye, are the principal symptomatic treatment for dry eye. They are available over-the-counter as eye drops. Using humidifiers, wearing wrap-around glasses when outside, and avoiding outside windy and dry conditions may bring relief. For people with severe cases of dry eye, temporary or permanent closure of the tear drain (small openings at the inner corner of the eyelids where tears drain from the eye) may be helpful. Also known as conjunctivitis arida.

wikidoc

/index.php/Xg_antigen_system

# Xg antigen system The PBDX gene that encodes the antigen is located on the short arm of the X chromosome. Since males normally have one X chromosome they are considered hemizygotes. Since women have two copies of the gene and could be heterozygotic for the presence or absence of the functioning gene they could (through the process of lyonisation) express the functioning protein on just some of their red blood cells.

wikidoc

/index.php/Xipamide

# Xipamide Xipamide is a sulfonamide diuretic drug marketed by Eli Lilly under the trade names Aquaphor (in Germany) and Aquaphoril (in Austria). It is used for the treatment of oedema and hypertension. Like the structurally related thiazide diuretics, xipamide acts on the kidneys to reduce sodium reabsorption in the distal convoluted tubule. This increases the osmolarity in the lumen, causing less water to be reabsorbed by the collecting ducts. This leads to increased urinary output. Unlike the thiazides, xipamide reaches its target from the peritubular side (blood side). Additionally, it increases the secretion of potassium in the distal tubule and collecting ducts. In high doses it also inhibits the enzyme carbonic anhydrase which leads to increased secretion of bicarbonate and alkalizes the urine. After oral administration, 20 mg of xipamide are resorbed quickly and reach the peak plasma concentration of 3 mg/l within an hour. The diuretic effect starts about an hour after administration, reaches its peak between the third and sixth hour, and lasts for nearly 24 hours. One third of the dose is glucuronidized, the rest is excreted directly through the kidney (1/3) and the faeces (2/3). The total plasma clearance is 30-40 ml/min. Xipamide can be filtrated by haemodialysis but not by peritoneal dialysis. On 17 July 2012, cyclist Fränk Schleck was removed from the Tour de France by his team RadioShack-Nissan after his A-sample returned traces of xipamide.

wikidoc

/index.php/Xist

# Xist The Xist RNA, a large (18 kb) transcript, is expressed on the inactive chromosome and not on the active one. It is processed similarly to mRNAs, through splicing and polyadenylation, however, it remains untranslated. It has been suggested that this RNA gene evolved at least partly from a protein coding gene that became a pseudogene. The inactive X is coated with this transcript, which is essential for the inactivation. X lacking Xist will not be inactivated, while duplication of the Xist gene on another chromosome causes inactivation of that chromosome.

wikidoc

/index.php/Xlear_Nasal_Wash

# Xlear Nasal Wash Xlear Nasal Wash is the brand name of a saline-based nasal spray containing xylitol. Xlear claims to be effective in reducing bacteria in the nose and eustachian tubes, thus decreasing the risk of sinus infections, while improving such conditions as allergic rhinitis and asthma. Studies support this assertion by showing that the presence of xylitol prevents the growth of bacteria in the eustachian tubes which connect the nose and ear. Xylitol also interferes with the ability of bacteria to adhere to body tissues . The name "Xlear" is pronounced "clear" or Template:IPA. The inventor of the nasal spray, Dr. Alonzo "Lon" Jones, coined the term. The 'x' is intended to reference the xylitol, but is realized as a /k/ sound. This pronunciation is allegedly derived from that of the Russian alphabet character X .

wikidoc

/index.php/Xylazine

# Xylazine Xylazine is a drug that is used for sedation, anesthesia, muscle relaxation, and analgesia in animals such as horses, cattle and other large mammals {non-human}. An analogue of clonidine, it is an agonist at the α2 class of adrenergic receptor. As with other α2 agonists, adverse effects include bradycardia, conduction disturbances, and myocardial depression. Yohimbine (Yobine) can be used to reverse xylazine effects. In veterinary anesthesia, xylazine is often used in combination with ketamine. No formal information in humans available. Xylazine is sold by Bayer under the brand name Rompun.

wikidoc

/index.php/Xylene

# Xylene The term xylenes refers to a group of 3 benzene derivatives which encompasses ortho-, meta-, and para- isomers of dimethyl benzene. The o-, m- and p- isomers specify to which carbon atoms (of the main benzene ring) the two methyl groups are attached. Counting the carbon atoms from one of the ring carbons bonded to a methyl group, and counting towards the second ring carbon bonded to a methyl group, the o- isomer has the IUPAC name of 1,2-dimethylbenzene. The m- isomer has the IUPAC name of 1,3-dimethylbenzene. And p- isomer has the IUPAC name of 1,4-dimethylbenzene. It is a colorless, sweet-smelling liquid that is very flammable. It occurs naturally in petroleum and coal tar and is formed during forest fires. The chemical properties differ slightly from isomer to isomer. The melting point is between −47.87 °C (−54.17 °F) (m-xylene) and 13.26 °C (55.87 °F) (p-xylene). The boiling point is for each isomer at around 140 °C (284 °F). The density is at around 0.87 kg/L (7.26 lb/U.S. gallon or 8.72 lb/imp gallon) and thus is less dense than water. Xylene in air can be smelled at 0.08 to 3.7 parts of xylene per million parts of air (ppm) and can begin to be tasted in water at 0.53 to 1.8 ppm. Chemical industries produce xylene from petroleum. It is one of the top 30 chemicals produced in the United States in terms of volume. Xylene is used as a solvent and in the printing, rubber, and leather industries. p-Xylene is used as a feedstock in the production of terephthalic acid, which is a monomer used in the production of polymers. It is also used as a cleaning agent for steel and for silicon wafers and chips, a pesticide , a thinner for paint, and in paints and varnishes. It may be substituted for toluene to thin lacquers where slower drying is desired. It is found in small amounts in airplane fuel and gasoline. In animal studies it is often swabbed on the ears of rabbits to facilitate blood flow and collection, although the area must subsequently be cleansed with alcohol to prevent inflammation. Xylenes are a starting material for the production of other chemicals. For instance chlorination gives a xylylene dichlorides or 1,2-bis(chloromethyl)benzene (again three possible isomers). With oxidizing agents, such as potassium permanganate (KMnO4), the methyl group can be oxidized to a carboxylic acid. By oxidizing both methyl groups towards the acid, o-xylene forms phthalic acid, whereas p-xylene forms terephthalic acid. Xylene affects the brain. High levels from exposure for short periods (14 days or less) or long periods (more than 1 year) can cause headaches, lack of muscle coordination, dizziness, confusion, and changes in one's sense of balance. Exposure of people to high levels of xylene for short periods can also cause irritation of the skin, eyes, nose, and throat; difficulty in breathing; problems with the lungs; delayed reaction time; memory difficulties; stomach discomfort; and possibly changes in the liver and kidneys. It can cause unconsciousness and even death at very high levels (see inhalants). Studies of unborn animals indicate that high concentrations of xylene may cause increased numbers of deaths, and delayed growth and development. In many instances, these same concentrations also cause damage to the mothers. It is not yet known whether xylene harms the unborn fetus if the mother is exposed to low levels of xylene during pregnancy. Besides occupational exposure, the principal pathway of human contact is via soil contamination from leaking underground storage tanks containing petroleum products. Humans who come into contact with the soil or groundwater may become affected. Use of contaminated groundwater as a water supply could lead to adverse health effects. Another common form of human exposure to xylene is in the use of certain types of pens, writing and drawing instruments, bingo dabbers and art supplies.

wikidoc

/index.php/Xyloglucan

# Xyloglucan Xyloglucan is the main hemicellulose in the primary cell wall of dicotyledonous plants. Xyloglucan links cellulose microfibrils together, as well as avoid their adhesion and allow controlled creep. Xyloglucan has a cellulosic semirigid backbone of β1→4-linked glucose residues that are substituted with a variety of 1-6 flexibly linked glycosidic sidechains. The most common sidechain is a single xylose residue, but longer sidechains that include the sugars galactose and fucose are also common. Xyloglucan is synthesised in Golgi trans cisternae and in the trans Golgi network (TGN) and is transported to the cell membrane by vesicles, where it is expelled and adsorbs on nascent cellulosic microfibrils .

wikidoc

/index.php/Xylometazoline

# Xylometazoline Xylometazoline is a sympathomimetic, descongestant that is FDA approved for the treatment of nasal congestion due to cold, hay fever or other respiratory allergies. Common adverse reactions include rhinitis medicamentosa, atrophic rhinitis, sinusitis and otitis media. Pregnancy Category (FDA): Consult your physician before using. Pregnancy Category (AUS): There is no Australian Drug Evaluation Committee (ADEC) guidance on usage of Xylometazoline in women who are pregnant.

wikidoc

/index.php/Y-23684

# Y-23684 Y-23684 is an anxiolytic drug with a novel chemical structure, which is used in scientific research. It has similar effects to benzodiazepine drugs, but is structurally distinct and so is classed as a nonbenzodiazepine anxiolytic. Y-23684 is a nonselective partial agonist at GABAA receptors. It has primarily anxiolytic and anticonvulsant effects, with sedative and muscle relaxant effects only appearing at higher doses. It produces little ataxia or potentiation of other sedatives such as ethanol or barbiturates when compared to the benzodiazepines diazepam and clobazam in animal tests. Y-23684 has a favourable pharmacological profile, producing strong anxiolytic and moderate anticonvulsant effects at low doses that cause little or no sedative side effects. It has been proposed for development for human medical use, but has not yet gone beyond animal tests.

wikidoc

/index.php/Y-chromosomal_Aaron

# Y-chromosomal Aaron Y-chromosomal Aaron is the name given to the hypothesised most recent common ancestor of many of the patrilineal Jewish priestly caste known as Kohanim (singular "Kohen", "Cohen", or Kohane). In the Hebrew Bible this ancestor is identified as Aaron, the brother of Moses. Research published in 1997 and thereafter has indicated that a large proportion of contemporary Jewish Kohanim share a set of Y chromosomal genetic markers, known as the Cohen Modal Haplotype, which may well derive from this single common ancestor. Although membership in the Jewish community is traditionally passed maternally (see: Who is a Jew?), membership in the group that originally comprised the Jewish priesthood ("Kohens" or Kohanim), is patrilineal, and modern Kohens claim descent from Aaron, brother of Moses. For human beings the normal number of chromosomes is 46, of which 23 are inherited from each parent. Two chromosomes, the X chromosome and Y chromosome, determine gender. Women have two X chromosomes, one inherited from their mother, and one inherited from their father. Men have an X chromosome inherited from their mother, and a Y chromosome inherited from their father. Males who share a common patrilineal ancestor should also share a Y chromosome, diverging only with respect to accumulated mutations. Since Y-chromosomes are passed from father to son, all Kohanim men should theoretically have almost identical Y chromosomes; this can be tested with a genealogical DNA test. As the rate that mutations accumulate on the Y chromosome is relatively constant, scientists can estimate the elapsed time since two men had a common ancestor. (See molecular clock.) The Cohen hypothesis was first tested by Prof. Karl Skorecki and collaborators from Haifa, Israel, in 1997. In their study, "Y chromosomes of Jewish priests," published in the journal Nature, they found that the Kohanim appeared to share a different probability distribution compared to the rest of the Jewish population for the two Y-chromosome markers they tested (YAP and DYS 19); and that furthermore the probabilities appeared to be shared by both Sephardi and Ashkenazi Cohens, pointing to a common Cohen population origin before the Jewish diaspora at the time of the Roman empire. A subsequent study the next year (Thomas MG et al, 1998) increased the number of Y-STR markers tested to six, as well as testing more SNP markers. Again, they found that a clear difference was observable between the Cohanim population and the general Jewish population, with many of the Cohen STR results clustered around a single pattern they named the Cohen Modal Haplotype: Here, becoming increasingly specific, xDE is the proportion who were not in Haplogroups D or E (from the original paper); xDE,PR is the proportion who were not in haplogroups D, E, P, Q or R; Hg J is the proportion who were in Haplogroup J (from the slightly larger panel studied by Behar et al (2003) ); CMH.1 means "within one marker of the CMH-6"; and CMH is the proportion with a 6/6 match. The final two columns show the conditional proportions for CMH.1 and CMH, given membership of Haplogroup J. The data shows that the Cohanim were more than twice as likely to belong to Haplogroup J than the average non-Cohen Jew; and of those who did belong to Haplogroup J, the Cohanim were more than twice as likely to have an STR pattern close to the CMH-6, suggesting a much more recent common ancestry for most of them compared to an average non-Cohen Jew of Haplogroup J. Thomas et al dated the origin of the shared DNA to approximately 3,000 years ago (with variance arising from different generation lengths). The techniques used to find Y-chromosomal Aaron were first popularized in relation to the search for the patrilineal ancestor of all contemporary living humans, Y-chromosomal Adam. The finding led to excitement in religious circles, with some seeing it as providing some "proof" of the historical veracity of the Bible or other religious convictions, but there was also criticism that the paper's evidence was being overstated. The detailed breakdown by 6-marker haplotype (the paper's online-only table B) suggests that some at least even of these groups (eg E3b, R1b) contain more than one distinct Cohen lineage. It is possible that still further other lineages may also exist, but were not captured in the sample. One source of early confusion was a widespread popular notion that only Cohens or only Jews could have the Cohen Modal Haplotype. It is now clear that this is not the case. The Cohen Modal Haplotype, whilst notably frequent amongst Cohens, is also far from unusual in the general populations of haplogroups J1 and J2 with no particular link to the Cohen ancestry. These haplogroups occur widely throughout the Middle East and beyond , . So whilst many Cohens have haplotypes close to the CMH, a far larger number of such haplotypes worldwide belong to people with no likely Cohen connection at all. In words, this says that the odds in favour of Cohen ancestry C (ie the probability of having Cohen ancestry, divided by the probability of not having Cohen ancestry), having observed some piece of data D, is given by the odds one would assign given only one's initial information I, multiplied by the probability of having observed D if C is true, divided by the probability of having observed D if C is false. The proportion of the whole male Jewish population that has Cohen ancestry has been estimated at 5% . So if we take that 5% as our initial estimate of the probability of shared Cohen ancestry, then on the basis of the data above: Even a full 6/6 match for the 6 marker CMH thus cannot "prove" Cohen ancestry. It can only somewhat strengthen a previously existing belief. But for populations where the background probability assessment of shared Cohen ancestry must be vanishingly low, such as almost all non-Jews, even a full 6/6 match makes only a small difference. For individuals in such populations the CMH likely indicates Haplogroup J, but a completely different ancestry to the Cohanim. The discussion above applies to the so far published scientific papers. However, in principle some more resolution could be obtained by determining the Cohen haplogroup more narrowly, and/or testing more Y-STR markers to determine whether there is an extended characteristic Cohen haplotype. Individuals with the genetic Cohen Modal Haplotype can be found in subgroup J2 as well, and occasionally in more genealogically distant haplogroups too; however these are not closely related to the cluster in Haplogroup J1. The subdivision of J2 which most closely matches the genetic signature of the J1 Cohens is subclade J2a1b, a large fraction of members of which will also have a 6/6 match for the 6-marker CMH. However, this is an example of (re)convergence of haplotypes of different genetic lines, which it is believed have been not been closely related for at least the last 10,000 years; the group in J2a1b who have the 6-marker CMH are devoid of any Cohen traditions in their families. On the other hand, there are families in Haplogroup J2 who do have a Cohen religious tradition and are proud of it (as there are in several other haplogroups, including Haplogroup R1b). The haplotypes of these Haplotype J2 Kohanim cluster in a unique, small offshoot of J2a1*, close to haplotypes of the J2a1k clade, not the J2a1b clade. These J2 Kohanim typically have a 4/6 match for the 6-marker CMH (with DYS19=15 rather than 14, and DYS388=15 rather than 16). They do not match the 12-marker J1-extended CMH, and they do not share a common ancestor with the J1 Kohanim in a Biblical timeframe; but they are equal co-inheritors of a patrilineal tradition which appears to date back well before the Diaspora. As it happens, three of the four markers for which they do match the CMH-6 were the markers tested by Malaspina et al (2001) . This appears to explain the finding of that paper that "typing a limited number of Italian Cohanim (A. Novelletto unpublished obs.) for the STRs used here, we determined that the Cohen Modal Haplotype ('an important component in the sharing of Ashkenazic and Sephardic Israelite Y chromosomes', Thomas et al. 2000) does indeed belong to network 1.2" (ie the population having DYS413a,b<=18, which is the signature of the J2a1 subclades). In the table below, the first line gives the original 6 marker Cohen Modal Haplotype (CMH-6), which was the basis for the original published papers. The second gives an extended 12 marker haplotype (CMH-12) informally released by the private company FTDNA, based on further work by much of the same research team. It has not yet been peer group reviewed by other scientists or published in the open technical literature. The next sequence of rows identify other 6-marker haplotypes in haplogroup J found to occur more than once in the sample of 145 Cohanim tested in Behar et al (2003) (table B (web-only) in that paper). Probable extensions of these haplotypes to 12 markers are shown, where it has been possible to find corresponding clusters of Cohen-type names in publicly accessible DNA databases, together with the apparent sub-clade of haplogroup J. This is more possible for the apparently Ashkenazi clusters than for Sephardis, who are much less strongly represented in the databases. Finally, for comparison, the 12-marker modal haplotypes for the haplogroups J1 and J2 are also shown. It is apparent that in both cases, their haplotype clusters are also centred very close to the Cohen modal haplotype. However, because of the much greater time that has elapsed since the mutations occurred that define the haplogroups, there has been much more time for Y-STR mutations to build up; so, although they have almost the same centre as the Cohen cluster, the J1 and J2 haplotype clusters are much more diffusely spread out. Thus although the CMH-6 is also very near to the most probable haplotype for both J1 and J2, its occurrence frequency is only about 1 to 8% amongst arbitrary members of haplogroup J with no particular Cohen connection. Critics of the theory point out that the Cohen Modal Haplotype has also been found in significant numbers in groups of non-Jews, notably Italians. However proponents of the theory are quick to explain these anomalies. They state that history records the migration of large numbers of Jews to Italy who married and took part in building the Colosseum. However, the Cohen Haplotype has also been found among significant numbers of non-Jewish Arab and Kurdish populations. Although this too could be explained in part by miscegenation, assimilation, and conversions, there is an alternate possibility that the marker precedes all of these populations and is a precursor to some common ancestral group. The Cohen Modal Haplotype has also been found in the Lemba of Southern Africa, who have a tradition of Jewish ancestry (Thomas MG et al 2000) . A similar investigation was made with men who consider themselves Levites. Whereas the priestly Kohanim are considered descendants of Aaron, who in turn was a descendant of Levi, son of Jacob, the Levites (a lower rank of the Temple) are considered descendants of Levi through other lineages. Levites should also therefore share common Y-chromosomal DNA. The investigation of Levites found high frequencies of multiple distinct markers, suggestive of multiple origins for the majority of non-Aaronid Levite families. One marker, however, present in more than 50% of Eastern European (Ashkenazi) Jewish Levites points to a common male ancestor or very few male ancestors within the last 2000 years for many Levites of the Ashkenazi community. This common ancestor belonged to the haplogroup R1a1 which is typical of Eastern Europeans, rather than the haplogroup J of the Cohen modal haplotype, and most likely lived at the time of the Ashkenazi settlement in Eastern Europe. . The E3b1 haplogroup has been observed in all Jewish groups world wide. It is considered to be the second most prevalent haplogroup among the Jewish population. According to one major paper, http://www.familytreedna.com/pdf/Behar_contrasting.pdf. It has also been observed in moderate numbers among individuals from Ashkenazi, Sephardic and Samaritan backgrounds that contain the E3b1 haplogroup, having a tradition of descending from the tribe of Levi, suggesting that the E3b1 Levites may have existed in Israel before the Diaspora of 70 C.E. The Samaritan community is a small, isolated, and highly endogamous group today numbering some 650 members who have maintained extensive genealogical records for the past 13–15 generations. Since the Samaritans maintain extensive and detailed genealogical records, it is possible to construct accurate pedigrees and specific maternal and paternal lineages. The Samaritan community in the Middle East survives as a distinct religious and cultural sect and constitutes one of the oldest and smallest ethnic minorities in the world. Y-Chromosome studies have shown that the majority of Samaritans belong to haplogroups J1 and J2 while the Samaritan Cohanim belong to haplogroup E3b1a. . In 1623-1624 the last member of the high-priestly family, which claimed descent from the eldest son of Aaron, died. The office was then given to the junior branch, descended from Uzziel, the son of Kohath. Since that date the priest has called himself "ha-kohen ha-Lewi," (Heb. "The Levite Priest") instead of "ha-kohen ha-gadol" (Heb. "The High Priest") as in previous times. The approximately 650 individuals comprising the total group of present day Samaritans trace their ancestry over a period of more than 2,000 years to the Biblical Israelite tribes of Ephraim, Menashe and Levi. As a religious sect, the Samaritans broke away from the main stream of Judaism around the fifth century B.C.E.

wikidoc

/index.php/Y-chromosomal_Adam

# Y-chromosomal Adam In human genetics, Y-chromosomal Adam (Y-mrca) is the patrilineal human most recent common ancestor (mrca) from whom all Y chromosomes in living men are descended. Y-chromosomal Adam is thus the male counterpart of Mitochondrial Eve (the mt-mrca), the matrilineal human most recent common ancestor, from whom all mitochondrial DNA in living humans is descended. By analyzing DNA from people in all regions of the world, geneticist Spencer Wells has concluded that all humans alive today are descended from a single man who lived in Africa around 60,000 years ago. Y-chromosomal Adam probably lived between 60,000 and 90,000 years ago, judging from molecular clock and genetic marker studies.[citation needed] While their descendants certainly became close intimates, Y-chromosomal Adam and mitochondrial Eve are separated by at least 30,000 years, or possibly a thousand generations. This is due to the differences found in male and female reproductive strategies. The more recent age of the Y-mrca compared to the mt-mrca corresponds to a larger statistical dispersion of the probability distribution for a Paleolithic man to have living descendants compared to that of a Paleolithic woman.[citation needed] While fertile women had more or less equally distributed chances of giving birth to a certain number of fertile descendants, chances for fertile men varied more widely, with some fathering no children and others fathering many, with multiple women. Y-chromosomal Adam is not the same individual at all points in human history; the Y-mrca of all humans alive today is different from the one for humans alive at some point in the remote past or future: as male lines die out, a more recent individual becomes the new Y-mrca. In times of rapid population growth, patrilineal lines are less likely to die out than during a population bottleneck. Y-chromosomal Adam is named after the Adam of the Genesis account of creation as a metaphor only. The name may seem to imply that Y-chromosomal Adam was the only living male of his time; he was not. "Y-Adam" is not even a single fixed individual but a title that continually passes on to more recent individuals as time goes on.

wikidoc

/index.php/YES1

# YES1 This gene is the cellular homolog of the Yamaguchi sarcoma virus oncogene. The encoded protein has tyrosine kinase activity and belongs to the src family of proteins. This gene lies in close proximity to thymidylate synthase gene on chromosome 18, and a corresponding pseudogene has been found on chromosome 22.

wikidoc

/index.php/YWHAH

# YWHAH ## Function This gene product belongs to the 14-3-3 family of proteins which mediate signal transduction by binding to phosphoserine-containing proteins. This highly conserved protein family is found in both plants and mammals, and this protein is 99% identical to the mouse, rat and bovine orthologs. This gene contains a 7 bp repeat sequence in its 5' UTR, and changes in the number of this repeat has been associated with early-onset schizophrenia.

wikidoc

/index.php/Y_Chromosome_Consortium

# Y Chromosome Consortium ## See also The Y Chromosome Consortium (YCC) was a collection of scientists who worked toward the understanding of human Y chromosomal phylogenetics and evolution. The consortium had the following objectives: web resources that communicate information relating to the non-recombinant region of the Y-chromosome including new variants and changes in the nomenclature. The consortium sponsored literature regarding updates in the phylogenetics and nomenclature.

wikidoc

/index.php/Y_chromosome

# Y chromosome The Y chromosome is one of two sex chromosomes (allosomes) in mammals, including humans, and many other animals. The other is the X chromosome. Y is the sex-determining chromosome in many species, since it is the presence or absence of Y that determines the male or female sex of offspring produced in sexual reproduction. In mammals, the Y chromosome contains the gene SRY, which triggers testis development. The DNA in the human Y chromosome is composed of about 59 million base pairs. The Y chromosome is passed only from father to son. With a 30% difference between humans and chimpanzees, the Y chromosome is one of the fastest-evolving parts of the human genome. To date, over 200 Y-linked genes have been identified. All Y-linked genes are expressed and (apart from duplicated genes) hemizygous (present on only one chromosome) except in the cases of aneuploidy such as XYY syndrome or XXYY syndrome. The Y chromosome was identified as a sex-determining chromosome by Nettie Stevens at Bryn Mawr College in 1905 during a study of the mealworm Tenebrio molitor. Edmund Beecher Wilson independently discovered the same mechanisms the same year. Stevens proposed that chromosomes always existed in pairs and that the Y chromosome was the pair of the X chromosome discovered in 1890 by Hermann Henking. He realized that the previous idea of Clarence Erwin McClung, that the X chromosome determines sex, was wrong and that sex determination is, in fact, due to the presence or absence of the Y chromosome. Stevens named the chromosome "Y" simply to follow on from Henking's "X" alphabetically. The idea that the Y chromosome was named after its similarity in appearance to the letter "Y" is mistaken. All chromosomes normally appear as an amorphous blob under the microscope and only take on a well-defined shape during mitosis. This shape is vaguely X-shaped for all chromosomes. It is entirely coincidental that the Y chromosome, during mitosis, has two very short branches which can look merged under the microscope and appear as the descender of a Y-shape. Most therian mammals have only one pair of sex chromosomes in each cell. Males have one Y chromosome and one X chromosome, while females have two X chromosomes. In mammals, the Y chromosome contains a gene, SRY, which triggers embryonic development as a male. The Y chromosomes of humans and other mammals also contain other genes needed for normal sperm production. There are exceptions, however. For example, the platypus relies on an XY sex-determination system based on five pairs of chromosomes. Platypus sex chromosomes have strong sequence similarity with the avian Z chromosome, (indicating close homology), and the SRY gene so central to sex-determination in most other mammals is apparently not involved in platypus sex-determination. Among humans, some men have two Xs and a Y ("XXY", see Klinefelter syndrome), or one X and two Ys (see XYY syndrome), and some women have three Xs or a single X instead of a double X ("X0", see Turner syndrome). There are other exceptions in which SRY is damaged (leading to an XY female), or copied to the X (leading to an XX male). Many ectothermic vertebrates have no sex chromosomes. If they have different sexes, sex is determined environmentally rather than genetically. For some of them, especially reptiles, sex depends on the incubation temperature; others are hermaphroditic (meaning they contain both male and female gametes in the same individual). The X and Y chromosomes are thought to have evolved from a pair of identical chromosomes, termed autosomes, when an ancestral animal developed an allelic variation, a so-called "sex locus" – simply possessing this allele caused the organism to be male. The chromosome with this allele became the Y chromosome, while the other member of the pair became the X chromosome. Over time, genes that were beneficial for males and harmful to (or had no effect on) females either developed on the Y chromosome or were acquired through the process of translocation. Until recently, the X and Y chromosomes were thought to have diverged around 300 million years ago. However, research published in 2010, and particularly research published in 2008 documenting the sequencing of the platypus genome, has suggested that the XY sex-determination system would not have been present more than 166 million years ago, at the split of the monotremes from other mammals. This re-estimation of the age of the therian XY system is based on the finding that sequences that are on the X chromosomes of marsupials and eutherian mammals are present on the autosomes of platypus and birds. The older estimate was based on erroneous reports that the platypus X chromosomes contained these sequences. Recombination between the X and Y chromosomes proved harmful—it resulted in males without necessary genes formerly found on the Y chromosome, and females with unnecessary or even harmful genes previously only found on the Y chromosome. As a result, genes beneficial to males accumulated near the sex-determining genes, and recombination in this region was suppressed in order to preserve this male specific region. Over time, the Y chromosome changed in such a way as to inhibit the areas around the sex determining genes from recombining at all with the X chromosome. As a result of this process, 95% of the human Y chromosome is unable to recombine. Only the tips of the Y and X chromosomes recombine. The tips of the Y chromosome that could recombine with the X chromosome are referred to as the pseudoautosomal region. The rest of the Y chromosome is passed on to the next generation intact, allowing for its use in tracking human evolution.[citation needed] By one estimate, the human Y chromosome has lost 1,393 of its 1,438 original genes over the course of its existence, and linear extrapolation of this 1,393-gene loss over 300 million years gives a rate of genetic loss of 4.6 genes per million years. Continued loss of genes at the rate of 4.6 genes per million years would result in a Y chromosome with no functional genes – that is the Y chromosome would lose complete function – within the next 10 million years, or half that time with the current age estimate of 160 million years. Comparative genomic analysis reveals that many mammalian species are experiencing a similar loss of function in their heterozygous sex chromosome. Degeneration may simply be the fate of all non-recombining sex chromosomes, due to three common evolutionary forces: high mutation rate, inefficient selection, and genetic drift. However, comparisons of the human and chimpanzee Y chromosomes (first published in 2005) show that the human Y chromosome has not lost any genes since the divergence of humans and chimpanzees between 6–7 million years ago, and a scientific report in 2012 stated that only one gene had been lost since humans diverged from the rhesus macaque 25 million years ago. These facts provide direct evidence that the linear extrapolation model is flawed and suggest that the current human Y chromosome is either no longer shrinking or is shrinking at a much slower rate than the 4.6 genes per million years estimated by the linear extrapolation model. The human Y chromosome is particularly exposed to high mutation rates due to the environment in which it is housed. The Y chromosome is passed exclusively through sperm, which undergo multiple cell divisions during gametogenesis. Each cellular division provides further opportunity to accumulate base pair mutations. Additionally, sperm are stored in the highly oxidative environment of the testis, which encourages further mutation. These two conditions combined put the Y chromosome at a greater risk of mutation than the rest of the genome. The increased mutation risk for the Y chromosome is reported by Graves as a factor 4.8. However, her original reference obtains this number for the relative mutation rates in male and female germ lines for the lineage leading to humans. Without the ability to recombine during meiosis, the Y chromosome is unable to expose individual alleles to natural selection. Deleterious alleles are allowed to "hitchhike" with beneficial neighbors, thus propagating maladapted alleles in to the next generation. Conversely, advantageous alleles may be selected against if they are surrounded by harmful alleles (background selection). Due to this inability to sort through its gene content, the Y chromosome is particularly prone to the accumulation of "junk" DNA. Massive accumulations of retrotransposable elements are scattered throughout the Y. The random insertion of DNA segments often disrupts encoded gene sequences and renders them nonfunctional. However, the Y chromosome has no way of weeding out these "jumping genes". Without the ability to isolate alleles, selection cannot effectively act upon them.[citation needed] A clear, quantitative indication of this inefficiency is the entropy rate of the Y chromosome. Whereas all other chromosomes in the human genome have entropy rates of 1.5–1.9 bits per nucleotide (compared to the theoretical maximum of exactly 2 for no redundancy), the Y chromosome's entropy rate is only 0.84. This means the Y chromosome has a much lower information content relative to its overall length; it is more redundant. Even if a well adapted Y chromosome manages to maintain genetic activity by avoiding mutation accumulation, there is no guarantee it will be passed down to the next generation. The population size of the Y chromosome is inherently limited to 1/4 that of autosomes: diploid organisms contain two copies of autosomal chromosomes while only half the population contains 1 Y chromosome. Thus, genetic drift is an exceptionally strong force acting upon the Y chromosome. Through sheer random assortment, an adult male may never pass on his Y chromosome if he only has female offspring. Thus, although a male may have a well adapted Y chromosome free of excessive mutation, it may never make it in to the next gene pool. The repeat random loss of well-adapted Y chromosomes, coupled with the tendency of the Y chromosome to evolve to have more deleterious mutations rather than less for reasons described above, contributes to the species-wide degeneration of Y chromosomes through Muller's ratchet. As it has been already mentioned, the Y chromosome is unable to recombine during meiosis like the other human chromosomes; however, in 2003, researchers from MIT discovered a process which may slow down the process of degradation. They found that human Y chromosome is able to "recombine" with itself, using palindrome base pair sequences. Such a "recombination" is called gene conversion. In the case of the Y chromosomes, the palindromes are not noncoding DNA; these strings of bases contain functioning genes important for male fertility. Most of the sequence pairs are greater than 99.97% identical. The extensive use of gene conversion may play a role in the ability of the Y chromosome to edit out genetic mistakes and maintain the integrity of the relatively few genes it carries. In other words, since the Y chromosome is single, it has duplicates of its genes on itself instead of having a second, homologous, chromosome. When errors occur, it can use other parts of itself as a template to correct them.[citation needed] Findings were confirmed by comparing similar regions of the Y chromosome in humans to the Y chromosomes of chimpanzees, bonobos and gorillas. The comparison demonstrated that the same phenomenon of gene conversion appeared to be at work more than 5 million years ago, when humans and the non-human primates diverged from each other.[citation needed] In the terminal stages of the degeneration of the Y chromosome, other chromosomes increasingly take over genes and functions formerly associated with it. Finally, the Y chromosome disappears entirely, and a new sex-determining system arises. [neutrality is disputed][improper synthesis?] Several species of rodent in the sister families Muridae and Cricetidae have reached these stages, in the following ways: Fisher's principle outlines why almost all species using sexual reproduction have a sex ratio of 1:1. W. D. Hamilton gave the following basic explanation in his 1967 paper on "Extraordinary sex ratios", given the condition that males and females cost equal amounts to produce: Many groups of organisms in addition to mammals have Y chromosomes, but these Y chromosomes do not share common ancestry with mammalian Y chromosomes. Such groups include Drosophila, some other insects, some fish, some reptiles, and some plants. In Drosophila melanogaster, the Y chromosome does not trigger male development. Instead, sex is determined by the number of X chromosomes. The D. melanogaster Y chromosome does contain genes necessary for male fertility. So XXY D. melanogaster are female, and D. melanogaster with a single X (X0), are male but sterile. There are some species of Drosophila in which X0 males are both viable and fertile.[citation needed] Other organisms have mirror image sex chromosomes: where the homogeneous sex is the male, said to have two Z chromosomes, and the female is the heterogeneous sex, and said to have a Z chromosome and a W chromosome. For example, female birds, snakes, and butterflies have ZW sex chromosomes, and males have ZZ sex chromosomes.[citation needed] There are some species, such as the Japanese rice fish, the XY system is still developing and cross over between the X and Y is still possible. Because the male specific region is very small and contains no essential genes, it is even possible to artificially induce XX males and YY females to no ill effect. In humans, the Y chromosome spans about 58 million base pairs (the building blocks of DNA) and represents approximately 1% of the total DNA in a male cell. The human Y chromosome contains over 200 genes, at least 72 of which code for proteins. Traits that are inherited via the Y chromosome are called Y-linked, or holandric traits. Some cells, especially in older men and smokers, lack a Y chromosome. It has been found that men with a higher percentage of hematopoietic stem cells in blood lacking the Y chromosome (and perhaps a higher percentage of other cells lacking it) have a higher risk of certain cancers and have a shorter life expectancy. Men with "loss of Y" (which was defined as no Y in at least 18% of their hematopoietic cells) have been found to die 5.5 years earlier on average than others. This has been interpreted as a sign that the Y chromosome plays a role going beyond sex determination and reproduction (although the loss of Y may be an effect rather than a cause). And yet women, who have no Y chromosome, have lower rates of cancer. Male smokers have between 1.5 and 2 times the risk of non-respiratory cancers as female smokers. The human Y chromosome is normally unable to recombine with the X chromosome, except for small pieces of pseudoautosomal regions at the telomeres (which comprise about 5% of the chromosome's length). These regions are relics of ancient homology between the X and Y chromosomes. The bulk of the Y chromosome, which does not recombine, is called the "NRY", or non-recombining region of the Y chromosome. The single-nucleotide polymorphisms (SNPs) in this region are used to trace direct paternal ancestral lines. The following are some of the gene count estimates of human Y chromosome. Because researchers use different approaches to genome annotation their predictions of the number of genes on each chromosome varies (for technical details, see gene prediction). Among various projects, the collaborative consensus coding sequence project (CCDS) takes an extremely conservative strategy. So CCDS's gene number prediction represents a lower bound on the total number of human protein-coding genes. In general, the human Y chromosome is extremely gene poor—it is one of the largest gene deserts in the human genome. Disregarding pseudoautosomal genes, genes encoded on the human Y chromosome include: Y chromosome microdeletion (YCM) is a family of genetic disorders caused by missing genes in the Y chromosome. Many affected men exhibit no symptoms and lead normal lives. However, YCM is also known to be present in a significant number of men with reduced fertility or reduced sperm count.[citation needed] This results in the person presenting a female phenotype (i.e., is born with female-like genitalia) even though that person possesses an XY karyotype. The lack of the second X results in infertility. In other words, viewed from the opposite direction, the person goes through defeminization but fails to complete masculinization.[citation needed] The cause can be seen as an incomplete Y chromosome: the usual karyotype in these cases is 45X, plus a fragment of Y. This usually results in defective testicular development, such that the infant may or may not have fully formed male genitalia internally or externally. The full range of ambiguity of structure may occur, especially if mosaicism is present. When the Y fragment is minimal and nonfunctional, the child is usually a girl with the features of Turner syndrome or mixed gonadal dysgenesis.[citation needed] Klinefelter syndrome (47, XXY) is not an aneuploidy of the Y chromosome, but a condition of having an extra X chromosome, which usually results in defective postnatal testicular function. The mechanism is not fully understood; it does not seem to be due to direct interference by the extra X with expression of Y genes.[citation needed] 47, XYY syndrome (simply known as XYY syndrome) is caused by the presence of a single extra copy of the Y chromosome in each of a male's cells. 47, XYY males have one X chromosome and two Y chromosomes, for a total of 47 chromosomes per cell. Researchers have found that an extra copy of the Y chromosome is associated with increased stature and an increased incidence of learning problems in some boys and men, but the effects are variable, often minimal, and the vast majority do not know their karyotype. In 1965 and 1966 Patricia Jacobs and colleagues published a chromosome survey of 315 male patients at Scotland's only special security hospital for the developmentally disabled, finding a higher than expected number of patients to have an extra Y chromosome. The authors of this study wondered "whether an extra Y chromosome predisposes its carriers to unusually aggressive behaviour", and this conjecture "framed the next fifteen years of research on the human Y chromosome". Through studies over the next decade, this conjecture was shown to be incorrect: the elevated crime rate of XYY males is due to lower median intelligence and not increased aggression, and increased height was the only characteristic that could be reliably associated with XYY males. The "criminal karyotype" concept is therefore inaccurate. Greater degrees of Y chromosome polysomy (having more than one extra copy of the Y chromosome in every cell, e.g., XYYY) are rare. The extra genetic material in these cases can lead to skeletal abnormalities, decreased IQ, and delayed development, but the severity features of these conditions are variable.[citation needed] XX male syndrome occurs when there has been a recombination in the formation of the male gametes, causing the SRY portion of the Y chromosome to move to the X chromosome. When such an X chromosome contributes to the child, the development will lead to a male, because of the SRY gene.[citation needed] In human genetic genealogy (the application of genetics to traditional genealogy), use of the information contained in the Y chromosome is of particular interest because, unlike other chromosomes, the Y chromosome is passed exclusively from father to son, on the patrilineal line. Mitochondrial DNA, maternally inherited to both sons and daughters, is used in an analogous way to trace the matrilineal line.[citation needed] Research is currently investigating whether male-pattern neural development is a direct consequence of Y-chromosome-related gene expression or an indirect result of Y-chromosome-related androgenic hormone production. A 2004 study at the Fred Hutchinson Cancer Research Center, Seattle, investigated the origin of male chromosomes found in the peripheral blood of women who had not had male progeny. A total of 120 subjects (women who had never had sons) were investigated, and it was found that 21% of them had male DNA. The subjects were categorised into four groups based on their case histories: The study noted that 10% of the women had never been pregnant before, raising the question of where the Y chromosomes in their blood could have come from. The study suggests that possible reasons for occurrence of male chromosome microchimerism could be one of the following:

wikidoc

/index.php/Yale-New_Haven_Hospital

# Yale-New Haven Hospital The hospital is owned and operated by the Yale New Haven Health System, Inc. Yale-New Haven Hospital includes the 201-bed Yale-New Haven Children's Hospital and the 76-bed Yale-New Haven Psychiatric Hospital. Yale-New Haven is the primary teaching hospital for Yale University School of Medicine. Yale-New Haven Hospital regularly ranks among the best hospitals in the U.S. and is accredited by the Joint Commission on the Accreditation of Healthcare Organizations (JCAHO). In 2007, YNHH was ranked by U.S. News & World Report as the 15th-best hospital out of 5,462 medical centers in the United States. Yale-New Haven Hospital was ranked among the very best in 10 of the 16 medical specialties evaluated, including cancer; digestive disorders; ear nose and throat; endocrinology; gynecology; heart and heart surgery; kidney disease; psychiatry; respiratory disorders; and urology. Yale-New Haven Hospital's geriatrics and psychiatry departments are ranked among the nation's top 10, while gynecology, digestive disorders, endocrinology, kidney disorders, respiratory disorders, and oncology are ranked among the nation's top 25. The hospital provides services to more than 503,000 outpatients and emergency visits and 50,000 inpatient discharges per year. Yale-New Haven Hospital is the second largest employer in New Haven, Connecticut with about 6,000 employees and has a physician base of over 2,200 university-based and community physicians practicing more than 100 medical specialties. The history of Yale-New Haven Hospital extends back to 1826 when the General Hospital Society of Connecticut was chartered as the first hospital in Connecticut and the fourth voluntary hospital in the nation. The hospital rented temporary quarters and raised US$5,000 toward the purchase of land and construction. A new 13-bed hospital opened in 1833 on seven and a half acres of land bordered by Cedar Street and Howard, Davenport and Congress avenues. The original building, called the State Hospital, was designed by prominent New Haven architect Ithiel Town and cost US$13,000. In 1862, the State Hospital was converted to a military hospital to care for Union soldiers during the American Civil War. The hospital was renamed to the Knight United State Army General Hospital in honor of Jonathan Knight, the president of the board of trustees. Some attending physicians moved with the civilian patients to temporary quarters on Whitney Avenue. After the Civil War, the hospital was turned over to the General Society of Connecticut in 1865. The hospital converted back to its original name of State Hospital. The Connecticut Training School, the third training school for nurses in the United States, was opened by the hospital in 1873. In 1884, the hospital's name was changed to New Haven Hospital to reflect the name that was widely being used by the residents of New Haven. Yale School of Medicine and New Haven Hospital formalized their relationship in 1913. U.S. medical education, which had begun as a simple apprenticeship system, evolved to become a formal educational plan based on alliances between medical schools and hospitals. This was the start of what is now known as the Yale-New Haven Medical Center. 1914 saw the first motorized ambulance being purchased by New Haven Hospital. In 1945 the hospital changed its name to Grace-New Haven Hospital after it affiliated itself with nearby Grace Hospital. In 1951, the New Haven Dispensary formally merged with Grace-New Haven Hospital. The New Haven Dispensary had opened in 1871 as the city's first outpatient clinic. In 1965, a more formal agreement with the Yale School of Medicine resulted in another name change to Yale-New Haven Hospital. 1993 saw the opening of the Yale-New Haven Children's Hospital becoming the first full-service children's hospital in Connecticut, including the first children's emergency department. The Yale-New Haven Psychiatric Hospital was opened in 2000, after the purchase of the Yale Psychiatric Institute. Today, YNHH is a 944-bed private, nonprofit facility that ranks among the premier medical centers in the nation. Yale-New Haven is the largest acute care provider in southern Connecticut and one of the Northeast's major referral centers. The main patient campus of Yale-New Haven Hospital is comprised of three inpatient pavilions bounded by South Frontage Road, Park Street, Howard Avenue and York Street. The East Pavilion, originally called the Memorial Unit, was opened in 1950 (designed by Douglas Orr). The South Pavilion was opened in 1982 and followed by the Yale-New Haven Children's Hospital (West Pavilion) in 1993. All three pavilions are connected by a central atrium. In 2000, Yale-New Haven Hospital acquired the nearby Yale Psychiatric Institute (designed by architect Frank Gehry in 1989) and opened Yale-New Haven Psychiatric Hospital. In 2004, the Yale-New Haven Shoreline Medical Center in Guilford, Connecticut was opened. The New Haven Pavilion houses outpatient clinics, clinical laboratories and admininstration, among other departments. Located across the street from the inpatient pavilions, it occupies land that the original hospital was built on in 1833. The New Haven Pavilion connects directly to facilities of Yale School of Medicine. Taking into account nearby outpatient and primary care facilities, along with administrative offices, Yale-New Haven Hospital covers 1.9 million square feet and growing. In 2004, Yale-New Haven Hospital proposed building a new 430-million-dollar building for Yale Cancer Center,a Comprehensive Cancer Center. While construction was scheduled to begin in September 2005, the project was delayed by disputes with unions and the city. On March 22, 2006, the unions and the hospital reached an agreement. Construction on the new Yale-New Haven Cancer Hospital started on May 18, 2006 with the demolition of the Grace Building and site preparation. Groundbreaking occurred on Wednesday, September 6, 2006. This new Cancer Center building will also be known as the North Pavilion and will be connected to the other facilities via the atrium. The building is scheduled to open in 2009.

wikidoc

/index.php/Yale_School_of_Medicine

# Yale School of Medicine The Yale School of Medicine at Yale University is a private medical school located in New Haven, Connecticut, U.S. It was founded in 1810 as The Medical Institution of Yale College, and formally opened in 1813. The primary teaching hospital for the school is Yale-New Haven Hospital. The school is home to the Harvey Cushing/John Hay Whitney Medical Library, one of the largest modern medical libraries, also known for its historical collections. The faculty includes 25 National Academy of Sciences members and 24 Institute of Medicine investigators. The School of Medicine offers a medical degree (M.D.) and a physician associate (PA) degree (M.M.S.). Public Health degrees are administered through the Yale School of Public Health. There are also joint degree programs with other disciplines at Yale including law (M.D/J.D.), business (M.D./M.B.A.), public health (M.D/M.P.H.) and science/engineering (M.D./Ph.D.). Students pursuing a tuition-free fifth year of research are eligible for the Master of Health Science degree. There is even a joint program in divinity (M.D./M.Div). The M.D. program is notable for its assessment of student achievement. In particular, the school employs the so-called "Yale System", established by Dean Winternitz in the 1920s, wherein first- and second-year students are not graded or ranked among their classmates. In addition, course examinations are anonymous, and are intended only for students' self-evaluation. Student performance is thus based on seminar participation, clinical clerkship evaluations, and the USMLE. Prior to graduation, students are required to submit a thesis based on original research. In 18th century America, credentials were not needed to practice medicine. Prior to the founding of the medical school, Yale graduates would train through an apprenticeship in order to become physicians. Yale president Ezra Stiles conceived the idea of training physicians at Yale and ultimately, his successor Timothy Dwight IV helped to found the medical school. The school was chartered in 1810 and opened in New Haven in 1813. Nathan Smith (medicine and surgery) and Benjamin Silliman (pharmacology) were the first faculty members. Silliman was a professor of chemistry and taught at both Yale College and the Medical School. The other two founding faculty were Jonathan Knight, anatomy, physiology and surgery and Eli Ives, pediatrics. The original building (at Grove and Prospect) later became Sheffield Hall, part of the Sheffield Scientific School (razed in 1931). In 1860, the school moved to Medical Hall on York Street, near Chapel (this building was razed in 1957). In 1925, the school moved to its current campus, neighboring the hospital.

wikidoc

/index.php/Yarrow_oil

# Yarrow oil The dark blue essential oil, extracted by steam distillation of the flowers, is generally used as an anti-inflammatory or in chest rubs for colds and influenza. Massage oil for inflamed joints, dilute 5-10 drops yarrow oil in 25ml infused St. John's wort oil. A chest rub can be made for chesty colds and influenza, combine with eucalyptus, peppermint, hyssop, or thyme oils, diluting a total of 20 drops of oil in 25ml almond or sunflower oil.

wikidoc

/index.php/Yaupon_Holly

# Yaupon Holly Yaupon Holly (Ilex vomitoria), also called Yaupon or Cassina (the latter shared with the Dahoon Holly), is an evergreen holly found in the southeast United States. It is a shrub or small tree reaching 5-8 m tall. The leaves are alternate, ovate to elliptical with an acute apex and crenate or finely serrated margin, 2-4.5 cm long and 1-2 cm broad, glossy dark green above, slightly paler below. Yaupon flowers are white, with a four-lobed corolla. The fruit is a small round or red (occasionally yellow) berry 5-6 mm diameter containing four seeds. Native Americans used the leaves and stems to brew a tea called Asi or Black drink for male-only purification and unity rituals. The ceremony included vomiting, and Europeans incorrectly believed that it was the drink itself that caused it (hence the Latin name). The active ingredient is actually caffeine, and the vomiting was either learned or as a result of the great quantities in which they drank the beverage (Hudson, The Southeastern Indians, ISBN 0-87049-248-9).

wikidoc

/index.php/Yawn

# Yawn A yawn (synonyms chasma, pandiculation , oscitation from the Latin verb oscitare, to open the mouth wide ) is a reflex of deep inhalation and exhalation associated with tiredness, stress, over-work, lack of stimulation, or boredom. Pandiculation is the term for the act of stretching and yawning. Yawning is a powerful non-verbal message with several possible meanings, depending on the circumstances. Another speculated reason for yawning is nervousness and is also claimed to help increase the state of alertness of a person - paratroopers were noted yawning right before their first jump.[citation needed] The exact causes of yawning are still undetermined. Some claim that yawning is not caused by lack of oxygen, for the reason that yawning allegedly reduces oxygen intake compared to normal respiration. However, both of these are as controversial as a debate over yawning can be. The word "yawn" has evolved from the Middle English word yanen, an alteration of yonen or yenen, which in turn comes from the Old English geonian. A recent(2007) hypothesis by Andrew C. Gallup and Gordon Gallup of the University of Albany states that yawning may be a means to keep the brain cool. Mammalian brains operate best when they are cool. In an experiment, he showed several groups of people videos of other people yawning. When the subjects held heat packs up to their foreheads while viewing the videos, they yawned often. But when they held cold packs up to their foreheads or breathed through their noses (another means of brain cooling), they did not yawn at all. Another recent hypothesis is that yawning is used for regulation of body temperature. Another hypothesis is that yawns are caused by the same chemicals (neurotransmitters) in the brain that affect emotions, mood, appetite and other phenomena. These chemicals include serotonin, dopamine, glutamic acid and nitric oxide. As more (or less) of these compounds are activated in the brain, the frequency of yawning increases. Conversely, a greater presence in the brain of opiate neurotransmitters such as endorphins reduces the frequency of yawning. Patients taking the serotonin reuptake inhibitor Paxil (Paroxetine HCl) or Citalopram, another SSRI, have been observed yawning abnormally often. Anecdotal reports by users of psilocybin mushrooms often describe a marked stimulation of yawning while intoxicated, often associated with excess lacrimation and nasal mucosal stimulation, especially while "peaking" (i.e. undergoing the most intense portion of the psilocybin experience). While opioids have been demonstrated to reduce this yawning and lacrimation provoked by psilocybin, it is not clear that the same pathways that induce yawning as a symptom of opioid abstinence in habituated users are the mode of action in psilocybin induced yawning. While even opioid dependent users of psilocybin on stable opioid therapy often report yawning and excess lacrimation while undergoing this entheogenic mushroom experience, there are no known reports in the literature that suggest psilocybin acts as any sort of general opioid antagonist. Psilocybin induced yawning in opioid habituated users does not appear to produce other typical opioid withdrawal symptoms such as cramping, physical pain, anxiety, gooseflesh etc. Recent research carried out at by Catriona Morrison, a lecturer in psychology at the University of Leeds, involving monitoring the yawning behaviour of students kept waiting in a reception area, indicates a connection (supported by neuro-imaging research) between empathic ability and yawning. "We believe that contagious yawning indicates empathy. It indicates an appreciation of other people's behavioural and physiological state," said Morrison. Another theory is that yawning is similar to stretching. Stretching, like yawning, increases blood pressure and heart rate while also flexing many muscles and joints. It is also theorized that yawning helps redistribute surfactant, an oil-like substance which coats the lungs and aids breathing. Some have observed that if one tries to stifle or prevent a yawn by clenching one's jaws shut, the yawn is unsatisfying. As such, the stretching of jaw and face muscles seems to be necessary for a satisfactory yawn. Yet another theory is that yawning occurs to stabilize pressure on either side of the ear drums. The deep intake of air can sometimes cause a popping sound that only the yawner can hear; this is the pressure on the inner ear stabilizing. This commonly occurs in environments where pressure is changing relatively rapidly, such as inside an airplane and when travelling up and down hills, which cause the eardrums to be bent instead of flat. Some people yawn when storms approach, which is a sure sign that changes in pressure affect them. Some movements in psychotherapy, such as Re-evaluation Counseling or co-counselling treatments, believe that yawning, along with laughter and crying, are means of "discharging" painful emotion, and therefore can be encouraged in order to promote physical and emotional healing. The yawn reflex is often described as contagious: if one person yawns, this will cause another person to "sympathetically" yawn. Observing another person's yawning face (especially his/her eyes), or even reading about or thinking about yawning, can cause a person to yawn. However, only about 55% of people in a given audience will respond to such a stimulus; fewer if only the mouth is shown in a visual stimulus. The proximate cause for contagious yawning may lie with mirror neurons, i.e. neurons in the frontal cortex of certain vertebrates, which upon being exposed to a stimulus from conspecific (same species) and occasionally interspecific organisms, activates the same regions in the brain. Mirror neurons have been proposed as a driving force for imitation which lies at the root of much human learning, e.g. language acquisition. Yawning may be an offshoot of the same imitative impulse. A 2007 study found that children with autism spectrum disorders, unlike typical children, did not yawn after seeing videos of other people yawning; this supports the claim that contagious yawning is based on the capacity for empathy. To look at the issue in terms of evolutionary advantage, if there is one at all, yawning might be a herd instinct. Other theories suggest that the yawn serves to synchronize mood behavior among gregarious animals, similar to the howling of the wolf pack. It signals tiredness to other members of the group in order to synchronize sleeping patterns and periods of activity. This phenomenon has been observed among various primates. The threat gesture is a way of maintaining order in the primates' social structure. Specific studies were conducted on chimpanzees and stumptail macaques . A group of these animals was shown a video of other conspecifics yawning, and both chimpanzees and stumptail macaques yawned also. This helps to partly confirm a yawn's "contagiousness". Gordon Gallup, who hypothesizes that yawning may be a means of keeping the brain cool, also hypothesizes that "contagious" yawning may be a survival instinct inherited from our evolutionary past. "During human evolutionary history when we were subject to predation and attacks by other groups, if everybody yawns in response to seeing someone yawn, the whole group becomes much more vigilant, and much better at being able to detect danger." In non-human animals, yawning can serve as a warning signal. For example, Charles Darwin, in his book The Expression of the Emotions in Man and Animals, mentioned that baboons use yawn to threaten their enemies, possibly by displaying large, canine teeth. Similarly, Siamese Fighting Fish yawn only when they see a conspecific (same species) or their own mirror-image, and their yawn often accompanies aggressive attack. Adelie Penguins employ yawning as part of their courtship ritual. Penguin couples face off and the males engage in what is described as an "ecstatic display," their beaks open wide and their faces pointed skyward. This trait has also been seen among Emperor Penguins. Researchers have been attempting to discover why these two different species share this trait, despite not sharing a habitat.[citation needed]. Certain superstitions surround the act of yawning. The most common of these is the belief that it is necessary to cover one's mouth when one is yawning in order to prevent one's soul from escaping the body. The Ancient Greeks believed that yawning was not a sign of boredom, but that a person's soul was trying to escape from its body, so that it may rest with the gods in the skies. This belief was also shared by the Maya.[citation needed] These superstitions may not only have arisen to prevent people from committing the faux pas of yawning loudly in another's presence — one of Mason Cooley's aphorisms is "A yawn is more disconcerting than a contradiction" — but may also have arisen from concerns over public health. Polydore Vergil (c. 1470–1555), in his De Rerum Inventoribus, writes that it was customary to make the sign of the cross over one's mouth, since "alike deadly plague was sometime in yawning, wherefore men used to fence themselves with the sign of the cross...which custom we retain at this day."

wikidoc

/index.php/Yeast

# Yeast Yeasts are a growth form of eukaryotic micro organisms classified in the kingdom Fungi, with about 1,500 species described; they dominate fungal diversity in the oceans. Most reproduce asexually by budding, although a few do by binary fission. Yeasts are unicellular, although some species with yeast forms may become multicellular through the formation of a string of connected budding cells known as pseudohyphae, or false hyphae as seen in most molds. Yeast size can vary greatly depending on the species, typically measuring 3–4 µm in diameter, although some yeasts can reach over 40 µm. The yeast species Saccharomyces cerevisiae has been used in baking and fermenting alcoholic beverages for thousands of years. It is also extremely important as a model organism in modern cell biology research, and is the most thoroughly researched eukaryotic microorganism. Researchers have used it to gather information into the biology of the eukaryotic cell and ultimately human biology. Other species of yeast, such as Candida albicans, are opportunistic pathogens and can cause infection in humans. Yeasts have recently been used to generate electricity in microbial fuel cells, and produce ethanol for the biofuel industry. Yeasts do not form a specific taxonomic or phylogenetic grouping. At present it is estimated that only 1% of all yeast species have been described. The term "yeast" is often taken as a synonym for S. cerevisiae, however the phylogenetic diversity of yeasts is shown by their placement in both divisions Ascomycota and Basidiomycota. The budding yeasts ("true yeasts") are classified in the order Saccharomycetales. The word "yeast" comes from the Old English language "gist", "gyst", and ultimately from the Indo-European root "yes-", meaning boil, foam, or bubble. Yeast microbes are probably one of the earliest domesticated organisms. People have used yeast for fermentation and baking throughout history. Archaeologists digging in Egyptian ruins found early grinding stones and baking chambers for yeasted bread, as well as drawings of 4,000-year-old bakeries and breweries. In 1680 the Dutch naturalist Antoine van Leeuwenhoek first microscopically observed yeast, but at the time did not consider them to be living organisms but rather globular structures. In 1857 French microbiologist Louis Pasteur proved in the paper "Mémoire sur la fermentation alcoolique" that alcoholic fermentation was conducted by living yeasts and not by a chemical catalyst. Pasteur showed that by bubbling oxygen into the yeast broth, cell growth could be increased, but the fermentation inhibited - an observation later called the Pasteur effect. The commercial use of yeast for baking bread and similar dough-based products did not become popular in the United States until after the Centennial Exposition in 1876 in Philadelphia, where Charles L. Fleischmann exibited the product and a process to use it, as well as serving the resultant baked bread. Yeasts are chemoorganotrophs as they use organic compounds as a source of energy and do not require sunlight to grow. The main source of carbon is obtained by hexose sugars such as glucose and fructose, or disaccharides such as sucrose and maltose. Some species can metabolize pentose sugars, alcohols, and organic acids. Yeast species either require oxygen for aerobic cellular respiration (obligate aerobes), or are anaerobic but also have aerobic methods of energy production (facultative anaerobes). Unlike bacteria, there are no known yeast species that grow only anaerobically (obligate anaerobes). Also, because they are adapted to them, yeasts grow best in a neutral pH environment. Yeasts will grow over a temperature range of 10°-37°C (50°-98.6°F), with an optimal temperature range of 30°-37°C (86°-98.6°F), depending on the type of species. S. cerevisiae works best at about 30°C. There is little activity in the range of 0°-10°C. Above 37°C yeast cells become stressed and will not divide properly. Most yeast cells die above 50°C (122°F). The cells can survive freezing under certain conditions, with viability decreasing over time. Yeasts are ubiquitous in the environment, but are most frequently isolated from sugar-rich samples. Some good examples include fruits and berries (such as grapes, apples or peaches), and exudates from plants (such as plant saps or cacti). Some yeasts are found in association with soil and insects. Yeast are generally grown in the laboratory on solid growth media or liquid broths. Common media used for the cultivation of yeasts include; potato dextrose agar (PDA) or potato dextrose broth, Wallerstien Laboratories Nutrient agar (WLN), Yeast Peptone Dextrose agar (YPD), and Yeast Mould agar or broth (YM). The antibiotic cycloheximide is sometimes added to yeast growth media to inhibit the growth of Saccharomyces yeasts and select for wild/indigenous yeast species. Yeasts have asexual and sexual reproductive cycles; however the most common mode of vegetative growth in yeast is asexual reproduction by budding or fission. Here a small bud, or daughter cell, is formed on the parent cell. The nucleus of the parent cell splits into a daughter nucleus and migrates into the daughter cell. The bud continues to grow until it separates from the parent cell, forming a new cell. The bud can develop on different parts of the parent cell depending on the genus of the yeast.Yeast needs the exact chemical form of sugar and cannot reproduce with sugar substitutes. However if the sugar substitute's chemical form is similar to sugar, yeast will reproduce a bit compared with many sugar substitutes where yeast will not reproduce at all. Under high stress conditions haploid cells will generally die, however under the same conditions diploid cells can undergo sporulation, entering sexual reproduction (meiosis) and producing a variety of haploid spores, which can go on to mate (conjugate), reforming the diploid. The useful physiological properties of yeast have led to their use in the field of biotechnology. Fermentation of sugars by yeast is the oldest and largest application of this technology. Many types of yeasts are used for making many foods: Baker's yeast in bread production, brewer's yeast in beer fermentation, yeast in wine fermentation and for xylitol production. Yeasts are also one of the most widely used model organisms for genetics and cell biology. Alcoholic beverages are loosely defined as a beverage that contains ethanol (C2H5OH). This ethanol is almost always produced by fermentation - the metabolism of carbohydrates by certain species of yeast. Beverages such as wine, beer, or distilled spirits all use yeast at some stage of their production. Beer brewers classify yeasts as top-fermenting and bottom-fermenting. This distinction was introduced by the Dane Emil Christian Hansen. Top-fermenting yeasts are so called because they form a foam at the top of the wort during fermentation. They can produce higher alcohol concentrations and prefer higher temperatures, producing fruitier ale-type beers. An example of a top-fermenting yeast is Saccharomyces cerevisiae, known to brewers as ale yeast. Bottom-fermenting yeasts are used to produce lager-type beers. These yeasts ferment more sugars, leaving a crisper taste, and grow well at low temperatures. An example of a bottom-fermenting yeast is Saccharomyces pastorianus. For both types, yeast is fully distributed through the beer while it is fermenting, and both equally flocculate (clump together and precipitate to the bottom of the vessel) when it is finished. By no means do all top-fermenting yeasts demonstrate this behaviour, but it features strongly in many English ale yeasts which may also exhibit chain forming (the failure of budded cells to break from the mother cell) which is technically different from true flocculation. In industrial brewing, to ensure purity of strain, a 'clean' sample of the yeast is stored refrigerated in a laboratory. After a certain number of fermentation cycles, a full scale propagation is produced from this laboratory sample. Typically, it is grown up in about three or four stages using sterile brewing wort and oxygen. Root beer and other sweet carbonated beverages can be produced using the same methods as beer, except that fermentation is stopped sooner, producing carbon dioxide, but only trace amounts of alcohol, and a significant amount of sugar is left in the drink. A distilled beverage is a beverage that contains ethanol that has been purified by distillation. Carbohydrate-containing plant material is fermented by yeast, producing a dilute solution of ethanol in the process. Spirits such as whiskey and rum are prepared by distilling these dilute solutions of ethanol. Components other than ethanol are collected in the condensate, including water, esters, and other alcohols which account for the flavor of the beverage. Yeast is used in winemaking where it converts the sugars present in grape juice or must into alcohol. Yeast is normally already invisibly present on the grapes. The fermentation can be done with this endogenous (or wild) yeast; however, this may give unpredictable results depending on the exact types of yeast species that are present. For this reason a pure yeast culture is generally added to the must, which rapidly predominates the fermentation as it proceeds. This represses the wild yeasts and ensures a reliable and predictable fermentation. Most added wine yeasts are strains of Saccharomyces cerevisiae, however not all strains of the species are suitable. Different S. cerevisiae yeast strains have differing physiological and fermentative properties, therefore the actual strain of yeast selected can have a direct impact on the finished wine. Significant research has been undertaken into the development of novel wine yeast strains that produce atypical flavour profiles or increased complexity in wines. The growth of some yeasts such as Zygosaccharomyces and Brettanomyces in wine can result in wine faults and subsequent spoilage. Brettanomyces produces an array of metabolites when growing in wine, some of which are volatile phenolic compounds. Together these compounds are often referred to as "Brettanomyces character", and are often described as antiseptic or "barnyard" type aromas. Brettanomyces is a significant contributor to wine faults within the wine industry. Yeast, most commonly Saccharomyces cerevisiae, is used in baking as a leavening agent, where it converts the fermentable sugars present in the dough into carbon dioxide. This causes the dough to expand or rise as the carbon dioxide forms pockets or bubbles. When the dough is baked it "sets" and the pockets remain, giving the baked product a soft and spongy texture. The use of potatoes, water from potato boiling, eggs, or sugar in a bread dough accelerates the growth of yeasts. Salt and fats such as butter slow down yeast growth. The majority of the yeast used in baking is of the same species common in alcoholic fermentation. Additionally, Saccharomyces exiguus (also known as S. minor) is a wild yeast found on plants, fruits, and grains that is occasionally used for baking. Sugar and vinegar are the best conditions for yeast to ferment. It is not known when yeast was first used to bake bread. The first records that show this use came from Ancient Egypt. Researchers speculate that a mixture of flour meal and water was left longer than usual on a warm day and the yeasts that occur in natural contaminants of the flour caused it to ferment before baking. The resulting bread would have been lighter and more tasty than the normal flat, hard cake. Today there are several retailers of baker's yeast; one of the best-known is Fleischmann's Yeast, which was developed in 1868. During World War II Fleischmann's developed a granulated active dry yeast, which did not require refrigeration and had a longer shelf life than fresh yeast. The company created yeast that would rise twice as fast, cutting down on baking time. Baker's yeast is also sold as a fresh yeast compressed into a square "cake". This form perishes quickly, and must be used soon after production in order to maintain viability. A weak solution of water and sugar can be used to determine if yeast is expired. When dissolved in the solution, active yeast will foam and bubble as it ferments the sugar into ethanol and carbon dioxide. Some recipes refer to this as proofing the yeast as it gives proof of the viability of the yeast before the other ingredients are added. When using a sourdough starter, flour and water are added instead of sugar and this is referred to as proofing the sponge. When yeast is used for making bread, it is mixed with flour, salt, and warm water (or milk). The dough is kneaded until it is smooth, and then left to rise, sometimes until it has doubled in size. Some bread doughs are knocked back after one rising and left to rise again. A longer rising time gives a better flavour, but the yeast can fail to raise the bread in the final stages if it is left for too long initially. The dough is then shaped into loaves, left to rise until it is the correct size, and then baked. Dried yeast is usually specified for use in a bread machine, however a (wet) sourdough starter can also work. Some yeasts can find potential application in the field of bioremediation. One such yeast Yarrowia lipolytica is known to degrade palm oil mill effluent, TNT (an explosive material), and other hydrocarbons such as alkanes, fatty acids, fats and oils. The ability of yeast to convert sugar into ethanol has been harnessed by the biotechnology industry, which has various uses including ethanol fuel. The process starts by milling a feedstock, such as sugar cane, sweetcorn, or cheap cereal grains, and then adding dilute sulfuric acid, or fungal alpha amylase enzymes, to break down the starches into complex sugars. A gluco amylase is then added to break the complex sugars down into simple sugars. After this, yeasts are added to convert the simple sugars to ethanol, which is then distilled off to obtain ethanol up to 96% in concentration. Saccharomyces yeasts have been genetically engineered to ferment xylose, one of the major fermentable sugars present in cellulosic biomasses, such as agriculture residues, paper wastes, and wood chips. Such a development means that ethanol can be efficiently produced from more inexpensive feedstocks, making cellulosic ethanol fuel a more competitively priced alternative to gasoline fuels. Yeast in symbiosis with acetic acid bacteria is used in the preparation of Kombucha, a fermented sweetened tea. Species of yeast found in the tea can vary, and may include: Brettanomyces bruxellensis, Candida stellata, Schizosaccharomyces pombe, Torulaspora delbrueckii and Zygosaccharomyces bailii. Yeast is used in nutritional supplements popular with vegans and the health conscious, where it is often referred to as "nutritional yeast". It is a deactivated yeast, usually Saccharomyces cerevisiae. It is an excellent source of protein and vitamins, especially the B-complex vitamins, whose functions are related to metabolism as well as other minerals and cofactors required for growth. It is also naturally low in fat and sodium. Some brands of nutritional yeast, though not all, are fortified with vitamin B12, which is produced separately from bacteria. Nutritional yeast, though it has a similar appearance to brewer's yeast, is very different and has a very different taste. Nutritional yeast has a nutty, cheesy, creamy flavor which makes it popular as an ingredient in cheese substitutes. It is often used by vegans in place of parmesan cheese. Another popular use is as a topping for popcorn. Some movie theaters are beginning to offer it along with salt or cayenne pepper as a popcorn condiment. It comes in the form of flakes, or as a yellow powder similar in texture to cornmeal, and can be found in the bulk aisle of most natural food stores. In Australia it is sometimes sold as "savory yeast flakes". Though "nutritional yeast" usually refers to commercial products, inadequately fed prisoners have used "home-grown" yeast to prevent vitamin deficiency. Some probiotic supplements use the yeast Saccharomyces boulardii to maintain and restore the natural flora in the large and small gastrointestinal tract. S. boulardii has been shown to reduce the symptoms of acute diarrhea in children, prevent reinfection of Clostridium difficile, reduce bowel movements in diarrhea predominant IBS patients, and reduce the incidence of antibiotic, traveler's, and HIV/AIDS associated diarrheas. Several yeasts, particularly Saccharomyces cerevisiae, have been widely used in genetics and cell biology. This is largely because the cell cycle in a yeast cell is very similar to the cell cycle in humans, and therefore the basic cellular mechanics of DNA replication, recombination, cell division and metabolism are comparable. Also many proteins important in human biology were first discovered by studying their homologs in yeast; these proteins include cell cycle proteins, signaling proteins, and protein-processing enzymes. On 24 April 1996 S. cerevisiae was announced to be the first eukaryote to have its genome, consisting of 12 million base pairs, fully sequenced as part of the Genome project. At the time it was the most complex organism to have its full genome sequenced and took 7 years and the involvement of more than 100 laboratories to accomplish. The second yeast species to have its genome sequenced was Schizosaccharomyces pombe, which was completed in 2002. It was the 6th eukaryotic genome sequenced and consists of 13.8 million base pairs. Yeast extract is the common name for various forms of processed yeast products that are used as food additives or flavours. They are often used in the same way that monosodium glutamate (MSG) is used, and like MSG, often contain free glutamic acids. The general method for making yeast extract for food products such as Vegemite and Marmite on a commercial scale is to add salt to a suspension of yeast making the solution hypertonic, which leads to the cells shrivelling up. This triggers autolysis, where the yeast's digestive enzymes break their own proteins down into simpler compounds, a process of self-destruction. The dying yeast cells are then heated to complete their breakdown, after which the husks (yeast with thick cell walls which would give poor texture) are separated. Yeast autolysates are used in Vegemite and Promite (Australia); Marmite, Bovril and Oxo (the United Kingdom, Republic of Ireland and South Africa); and Cenovis (Switzerland). Cryptococcus neoformans is a significant pathogen of immunocompromised people causing the disease termed Cryptococcosis. This disease occurs in about 7–8% of AIDS patients in the USA, and a slightly smaller percentage (3–6%) in western Europe. The cells of the yeast are surrounded by a rigid polysaccharide capsule, which helps to prevent them from being recognised and engulfed by white blood cells in the human body. Yeasts of the Candida genus are another group of opportunistic pathogens which causes oral and vaginal infections in humans, known as Candidiasis. Candida is commonly found as a commensal yeast in the mucus membranes of humans and other warm-blooded animals. However, sometimes these same strains can become pathogenic. Here the yeast cells sprout a hyphal outgrowth, which locally penetrates the mucosal membrane, causing irritation and shedding of the tissues. The pathogenic yeasts of candidiasis in probable descending order of virulence for humans are: C. albicans, C. tropicalis, C. stellatoidea, C. glabrata, C. krusei, C. parapsilosis, C. guilliermondii, C. viswanathii, C. lusitaniae and Rhodotorula mucilaginosa. Candida glabrata is the second most common Candida pathogen after C. albicans, causing infections of the urogenital tract, and of the bloodstream (Candidemia). Non-pathogenic yeast such as S. cerevisiae are also implicated in disease; anti saccharomyces cerevisiae antibodies (ASCA) have been found at relatively high frequencies in familial crohn's disease and at higher frequencies in other forms of colitis. Yeasts are able to grow in foods with a low pH, (5.0 or lower) and in the presence of sugars, organic acids and other easily metabolized carbon sources. During their growth, yeasts metabolize some food components and produce metabolic end products. This causes the physical, chemical, and sensory properties of a food to change, and the food is spoiled. The growth of yeast within food products is often seen on their surface, as in cheeses or meats, or by the fermentation of sugars in beverages, such as juices, and semi-liquid products, such as syrups and jams. The yeast of the Zygosaccharomyces genus have had a long history as a spoilage yeast within the food industry. This is mainly due to the fact that these species can grow in the presence of high sucrose, ethanol, acetic acid, sorbic acid, benzoic acid, and sulfur dioxide concentrations, representing some of the commonly used food preservation methods. Methylene Blue is used to test for the presence of live yeast cells.

wikidoc

/index.php/Yeast_display

# Yeast display Yeast display (or yeast surface display) is a technique used in the field of protein engineering. The yeast display technique was first published by the laboratory of Professor K. Dane Wittrup. The technology was sold to Abbott Laboratories in 2001. A protein of interest is displayed as a fusion to the Aga2p protein on the surface of yeast. The Aga2p protein is naturally used by yeast to mediate cell-cell contacts during yeast cell mating. As such, display of a protein via Aga2p projects the protein away from the cell surface, minimizing potential interactions with other molecules on the yeast cell wall. The use of magnetic separation and flow cytometry in conjunction with a yeast display library is a highly effective method to isolate high affinity protein ligands against nearly any receptor through directed evolution. Advantages of yeast display over other in vitro evolution methods include eukaryotic expression and processing, quality control mechanisms of the eukaryotic secretory pathway, minimal avidity effects, and quantitative library screening through magnetic separation combined with fluorescent-activated cell sorting (FACS). Disadvantages include smaller mutagenic library sizes compared to alternative methods and differential glycosylation in yeast compared to mammalian cells. It should be noted that these disadvantages have not limited the success of yeast display for a number of applications, including engineering the highest monovalent ligand-binding affinity reported to date for an engineered protein (Boder, E.T. 2000)

wikidoc

/index.php/Yellow_fever_(patient_information)

# Yellow fever (patient information) ## Who is at highest risk? Anyone can get yellow fever, but the elderly have a higher risk of severe infection. It is common in South America and in sub-Saharan Africa. If a person is bitten by an infected mosquito, symptoms usually develop 3 - 6 days later. ## When to seek urgent medical care? A person with advanced yellow fever may show signs of liver failure, renal failure, and shock. Tell your health care provider right away if you or your child develop fever, headache, muscle aches, vomiting, or jaundice, especially if you have traveled to an area where yellow fever is known to occur. Blood tests can confirm the diagnosis. ## What to expect (Outlook/Prognosis)? There is an effective vaccine against yellow fever. Get medical attention at least 10 - 14 days before traveling to an endemic area for yellow fever to find out whether you should be vaccinated against the disease.

wikidoc

/index.php/Yellow_fever_differential_diagnosis

# Yellow fever differential diagnosis Yellow fever must be differentiated from other diseases that cause fever, diarrhea, dehydration and tachycardia, such as ebola, typhoid fever, malaria, Zika virus, and lassa fever.

wikidoc

/index.php/Yellow_fever_epidemiology_and_demographics

# Yellow fever epidemiology and demographics ## Epidemiology and Demographics Yellow fever occurs in sub-Saharan Africa and tropical South America, where it is endemic and intermittently epidemic. Urban yellow fever occurs periodically in Africa and sporadically in the Americas. In Africa, natural immunity accumulates with age, and thus, infants and children are at highest risk for disease. In South America, yellow fever occurs most frequently in unimmunized young men who are exposed to mosquito vectors through their work in forested areas.

wikidoc

/index.php/Yellow_fever_future_or_investigational_therapies

# Yellow fever future or investigational therapies In the hamster model of yellow fever, early administration of the antiviral ribavirin is an effective early treatment of many pathological features of the disease. Ribavirin treatment during the first five days after virus infection improved survival rates, reduced tissue damage in target organs (liver and spleen), prevented hepatocellular steatosis, and normalized alanine aminotransferase (a liver damage marker) levels. The results of this study suggest that ribavirin may be effective in the early treatment of yellow fever, and that its mechanism of action in reducing liver pathology in yellow fever virus infection may be similar to that observed with ribavirin in the treatment of hepatitis C, a virus related to yellow fever. Because ribavirin had failed to improve survival in a virulent primate (rhesus) model of yellow fever infection, it had been previously discounted as a possible therapy. In 2007 the World Community Grid launched a project where by computer modeling of the Yellow Fever Virus (and related viruses) thousands of small molecules are screened for their potential anti-viral properties in fighting Yellow Fever. This is the first project to utilize computer simulations in seeking out medicines to directly attack the virus once a person is infected. This is a distributed process project similar to SETI@Home where the general public downloads the World Community Grid agent and the program (along with thousands of other users) screens thousands of molecules while their computer would be otherwise idle. If the user needs to use the computer the program sleeps. There are several different projects running, including a similar one screening for anti-AIDS drugs. The project covering Yellow Fever is called "Discovering Dengue Drugs – Together." The software and information about the project can be found at:

wikidoc

/index.php/Yellow_fever_historical_perspective

# Yellow fever historical perspective Yellow fever has had an important role in the history of Africa, the Americas, Europe, and the Caribbean. Scientists believe that yellow fever evolved in Africa around 3,000 years ago. In 1937 Max Theiler working at the Rockefeller Foundation developed a vaccine for yellow fever that gives a ten-year or more immunity from the disease and effectively protects people traveling to affected areas, while at the same time being a means to control the disease.

wikidoc

/index.php/Yellow_fever_history_and_symptoms

# Yellow fever history and symptoms ## History and Symptoms Patients infected may have no symptoms; if they develop the disease, they can develop symptoms such as fever, muscle pain (with prominent backache), headache, shivers, loss of appetite, and nausea or vomiting. After three or four days most patients improve and their symptoms disappear. Fifteen percent of patients, however, enter a toxic phase within 24 hours. Fever reappears, the patient rapidly develops jaundice and abdominal pain with vomiting. Bleeding occurs and kidney function deteriorates.

wikidoc

/index.php/Yellow_fever_laboratory_tests

# Yellow fever laboratory tests ## Laboratory Findings Multiple laboratory abnormalities can be observed in patients with yellow fever, including leukopenia or leukocytosis, bleeding dyscrasias, thrombocytopenia, increased bilirubin and transaminases. Laboratory diagnosis of yellow fever is generally accomplished by testing of serum to detect virus-specific IgM and neutralizing antibodies. Sometimes the virus can be found in blood samples taken early in the disease.

wikidoc

/index.php/Yellow_fever_medical_therapy

# Yellow fever medical therapy ## Medical Therapy There is no antivirals approved for the treatment of for yellow fever, therefore vaccination is important. Treatment is symptomatic and supportive only. Fluid replacement, managing hypotension and transfusion of blood derivates is generally needed only in severe cases. In cases that result in acute renal failure, dialysis may be necessary.

wikidoc

/index.php/Yellow_fever_natural_history

# Yellow fever natural history Initial symptoms of yellow fever start 3-6 days after the mosquito bite, these include sudden onset of fever, chills, severe headache, back pain, general body aches, nausea and vomiting, fatigue, and weakness. Most people improve after these initial symptoms. However, roughly 15% of people will have a brief period of hours to a day without symptoms and will then develop a more , severe form of yellow fever disease. Possible complications include coma, disseminated intravascular coagulation (DIC), kidney failure, liver failure and shock. The prognosis is good in the majority of patients, infected persons will be asymptomatic or have mild disease with complete recovery.

wikidoc

/index.php/Yellow_fever_overview

# Yellow fever overview Yellow fever is an acute viral disease. It is an important cause of hemorrhagic illness in many African and South American countries despite existence of an effective vaccine. The yellow refers to the jaundice symptoms that affect some patients. Yellow fever has been a source of several devastating epidemics. French soldiers were attacked by yellow fever during the 1802 Haitian Revolution; more than half of the army perished due to the disease. Outbreaks followed by thousands of deaths occurred periodically in other Western Hemisphere locations until research, which included human volunteers (some of whom died), led to an understanding of the method of transmission to humans (primarily by mosquitos) and development of a vaccine and other preventative efforts in the early 20th century. Despite the costly and sacrificial breakthrough research by Cuban physician Carlos Finlay, American physician Walter Reed, and many others over 100 years ago, unvaccinated populations in many developing nations in Africa and Central and South America continue to be at risk. As of 2001, the World Health Organization (WHO) estimates that yellow fever causes 200,000 illnesses and 30,000 deaths every year in unvaccinated populations. Yellow fever has had an important role in the history of Africa, the Americas, Europe, and the Caribbean. Scientists believe that yellow fever evolved in Africa around 3,000 years ago. In 1937 Max Theiler working at the Rockefeller Foundation developed a vaccine for yellow fever that gives a ten-year or more immunity from the disease and effectively protects people traveling to affected areas, while at the same time being a means to control the disease. Yellow fever is caused by a single-stranded RNA virus that belongs to the genus Flavivirus. Vectorborne transmission occurs via the bite of an infected mosquito, primarily Aedes or Haemagogusspp. Nonhuman and human primates are the main reservoirs of the virus, with anthroponotic (human-to-vector-to-human) transmission occurring. Humans infected with YFV experience the highest levels of viremia and can transmit the virus to mosquitoes shortly before onset of fever and for the first 3–5 days of illness. Given the high level of viremia, bloodborne transmission theoretically can occur via transfusion or needlesticks. Yellow fever virus is caused by an arthropodborne virus of the Flaviviridae family in the genus Flavivirus. Flaviviruses are single stranded ribonucleic acid (RNA) viruses that replicate in the cytoplasm of infected cells. Seven genotypes of yellow fever virus have been identified, two in South America and five in Africa. A traveler's risk of acquiring yellow fever is determined by various factors, including immunization status, location of travel, season, duration of exposure, occupational and recreational activities while traveling, and the local rate of virus transmission at the time of travel. The two methods to prevent yellow fever are vaccination and vector control. Yellow fever vaccine is recommended for persons aged ≥9 months who are traveling to or living in areas at risk for yellow fever virus transmission in South America and Africa. Yellow fever vaccine may be required for entry into certain countries. The best way to prevent mosquitoborne diseases, including yellow fever, is to avoid mosquito bites.

wikidoc

/index.php/Yellow_fever_primary_prevention

# Yellow fever primary prevention Yellow fever vaccine is a live-virus vaccine which has been used for several decades. A single dose protects against disease for 10 years or more. If a person is at continued risk of infection, a booster dose is recommended every 10 years. Insecticides, protective clothing, and screening of houses are helpful but not always sufficient for mosquito control; people should always use an insecticide spray while in certain areas. In affected areas mosquito control methods have proven effective in decreasing the number of cases.

wikidoc

/index.php/Yellow_nail_syndrome

# Yellow nail syndrome Yellow nail syndrome is a medical syndrome that includes pleural effusions, lymphedema and yellow dystrophic nails. Sometimes yellow nails are referred to as smoker's fingers. Normal treatment for swelling and any respiratory problems is appropriate. Nutritional supplementation with Vitamin E in some studies has been shown to be effective in controlling nail changes.

wikidoc

/index.php/Yerba_mate

# Yerba mate Yerba mate / Erva-mate*, Ilex paraguariensis, is a species of holly (family Aquifoliaceae) native to subtropical South America in Argentina, eastern Paraguay, western Uruguay and southern Brazil. The yerba mate plant is a shrub or small tree growing up to 15 meters tall. The leaves are evergreen, 7–11 cm long and 3–5.5 cm wide, with a serrated margin. The flowers are small, greenish-white, with four petals. The fruit is a red berry 4–6 mm diameter. The infusion called mate is prepared by steeping dry leaves (and twigs) of yerba mate in hot water, rather than boiling water like black tea or coffee. It is a slightly less potent stimulant than coffee and much gentler on the stomach. Drinking mate with friends from a shared hollow gourd (also called a mate in Spanish, or cabaça or cuia in Portuguese) with a metal straw (a bombilla in Spanish, bomba or canudo in Portuguese) is an extremely common social practice in Argentina, Uruguay, Paraguay, southern Chile, eastern Bolivia and Brazil and also Syria and Lebanon. The flavor of brewed yerba mate is strongly vegetal, herbal, and grassy, reminiscent of some varieties of green tea. Many consider the flavor to be very agreeable, but it is generally bitter if steeped in boiling water, so it is made using hot but not boiling water. Unlike most teas, it does not become bitter and astringent when steeped for extended periods, and the leaves may be infused several times. Additionally, one can purchase flavored mate in many varieties. In Brazil, a toasted version of mate, known as chá mate or "mate tea", is sold in teabag and loose form, and served, sweetened, in specialized shops, either hot or iced with fruit juice or milk. An iced, sweetened version of toasted mate is sold as an uncarbonated soft drink, with or without fruit flavoring. The toasted variety of mate has less of a bitter flavor and more of a spicy fragrance. It is more popular in the coastal cities of Brazil, as opposed to the far southern states where it is consumed in the traditional way (green, drunk with a silver straw from a shared gourd). Similarly, a form of mate is sold in Argentina, Uruguay and Paraguay in tea bags to be drunk in a similar way to tea. This is known in Spanish as mate cocido or cocido. In Argentina this is commonly drunk with breakfast or as part of merienda (roughly, afternoon tea), often with a selection of facturas (sweet pastries). It is also made by heating yerba in water and straining it as it cools. In Paraguay, yerba mate is also drunk as a cold beverage. Usually drunk out of a cows horn in the countryside, terrerre as it is known in the guaraní language, is served with cold or iced water. Medicinal herbs mixed in a mortar and pestle are added to the water for taste or medicinal reasons. The pronunciation of yerba mate in standard Spanish is Template:IPA. The Rioplatense dialect spoken in most of Argentina turns the first sound in yerba into a postalveolar fricative consonant, giving Template:IPA in regions closer to Buenos Aires, gradually blending into Template:IPA as one goes farther from the city, and eventually to Template:IPA around Mendoza. The word hierba is Spanish for grass or herb; yerba is a variant spelling of it which is quite common in Argentina. Mate is from the Quechua mati, meaning "cup". Yerba mate is therefore literally the "cup herb". The (Brazilian) Portuguese name is erva-mate Template:IPA (also pronounced as Template:IPA in some regions) and is also used to prepare the drinks chimarrão (hot) or tereré (cold). While the tea is made with the toasted leaves, these drinks are made with green ones, and are very popular in the south of the country. The name given to the plant in Guaraní (Guarani, in Portuguese), language of the indigenous people who first cultivated and enjoyed erva-mate / yerba mate, is ka'a, which has the same meaning as erva/yerba. In English-speaking countries, the spelling used is yerba maté (with an accented é) —where the acute accent indicates that the e is not silent, and thus that the word should not be pronounced as the English word mate. The plant is grown mainly in South America, more specifically in Northern Argentina (Corrientes, Misiones), Paraguay, Uruguay and southern Brazil (Rio Grande do Sul, Santa Catarina and Paraná). The Guaraní are reputed to be the first people who cultivated the plant; the first Europeans to do this were Jesuit missionaries, who spread the drinking habit as far as Ecuador. When the yerba is harvested, the branches are dried sometimes with a wood fire, imparting a smoky flavor. Then the leaves and sometimes the twigs are broken up. There are many brands and types of yerba, with and without twigs, some with low powder content. Some types are less strong in flavor (suave, "soft") and there are blends flavored with mint, orange and grapefruit skin, etc. Mate contains xanthines, which are alkaloids in the same family as caffeine, theophylline, and theobromine, well-known stimulants also found in coffee and chocolate. Mate also contains elements such as potassium, magnesium and manganese. Caffeine content varies between 0.3% and 1.7% of dry weight (compare this to 2.5–4.5% for tea leaves, and 1.5% for ground coffee). Mate products are sometimes marketed as "caffeine-free" alternatives to coffee and tea, and said to have fewer negative effects. This is often based on a claim that the primary active xanthine in mate is "mateine", erroneously said to be a stereoisomer of caffeine (as it is not chemically possible for caffeine to have a stereoisomer). "Mateine" is an official synonym of caffeine in the chemical databases. Researchers at Florida International University in Miami have found that yerba mate does contain caffeine, but some people seem to tolerate a mate drink better than coffee or tea. This is expected since mate contains different chemicals (other than caffeine) from tea or coffee. From reports of personal experience with mate, its physiological effects are similar to (yet distinct from) more widespread caffeinated beverages like coffee, tea, or guarana drinks. Users report a mental state of wakefulness, focus and alertness reminiscent of most stimulants, but often remark on mate's unique lack of the negative effects typically created by other such compounds, such as anxiety, diarrhea, "jitteriness", and heart palpitations. (The laxative effect of coffee derives from a substance that surrounds the raw bean, not the caffeine itself.) Reasons for mate's unique physiological attributes are beginning to emerge in scientific research. Studies of mate, though very limited, have shown preliminary evidence that the mate xanthine cocktail is different from other plants containing caffeine most significantly in its effects on muscle tissue, as opposed to those on the central nervous system, which are similar to those of other natural stimulants. Mate has been shown to have a relaxing effect on smooth muscle tissue, and a stimulating effect on myocardial (heart) tissue. Mate's negative effects are anecdotally claimed to be of a lesser degree than those of coffee, though no explanation for this is offered or even credibly postulated, except for its potential as a placebo effect. Many users report that drinking yerba mate does not prevent them from being able to fall asleep, as is often the case with some more common stimulating beverages, while still enhancing their energy and ability to remain awake at will. However, the net amount of caffeine in one preparation of yerba mate is typically quite high, in large part because the repeated filling of the mate with hot water is able to extract the highly-soluble xanthines extremely effectively. It is for this reason that one mate may be shared among several people and yet produce the desired stimulating effect in all of them. In vivo and in vitro studies are showing yerba mate to exhibit significant cancer-fighting activity. Researchers at the University of Illinois (2005) found yerba mate to be "rich in phenolic constituents" and to "inhibit oral cancer cell proliferation". On the other hand, a study by the International Agency for Research on Cancer showed a limited correlation between oral cancer and the drinking of hot mate (no data were collected on drinkers of cold mate). Given the influence of the temperature of water, as well as the lack of complete adjustment for age, alcohol consumption and smoking, the study concludes that mate is "not classifiable as to its carcinogenicity to humans". Yerba mate consumption has been associated with increased incidence of bladder, esophageal, oral, squamous cell of the head and neck, and lung cancer. It should be noted that the consumption of hot beverages itself is a risk factor for several kinds of cancer. An August 11, 2005, United States patent application (documents #20050176777, #20030185908, and #20020054926) cites yerba mate extract as an inhibitor of MAO activity; the maximal inhibition observed in vitro was 40–50%. A monoamine oxidase inhibitor is a type of antidepressant, so there is some data to suggest that yerba mate has a calming effect in this regard. In addition, it has been noted by the U.S. Army Center for Health Promotion and Preventive Medicine that yerba mate can cause high blood pressure when used in conjunction with other MAO inhibitors (such as Nardil and Parnate). Emerging research also shows that Yerba Mate preparations can alter the concentration of members of the ecto-nucleoside triphosphate diphosphohydrolase (E-NTPDase) family, resulting in an elevated level of extracellular ATP,ADP, and AMP. This was found with chronic ingestion (15 days)of an aqueous Yerba extract, and can lead to a novel mechanism for manipulation of vascular regenerative factors, i.e., treating heart disease. . Mate contains both caffeine and theobromine (which antagonize adenosine receptors) and reduces the bodies production of adenosine in the blood (prolongs half life of ATP, ADP, and AMP). These two processes will synergize to provide a much cleaner stimulation than a simple dose of caffeine (only blocking adenosine receptors).

wikidoc

/index.php/Yersinia

# Yersinia Yersinia is a genus of bacteria in the family Enterobacteriaceae. Yersinia are Gram-negative rod shaped bacteria, a few micrometers long and fractions of a micrometer in diameter, and are facultative anaerobes. Some members of Yersinia are pathogenic in humans. Rodents are the natural reservoirs of Yersinia; less frequently other mammals serve as the host. Infection may occur either through blood (in the case of Y. pestis) or in an alimentary fashion, through occasionally via consumption of food products (especially vegetables, milk-derived products and meat) contaminated with infected urine or feces. Speculations exist as to whether or not certain Yersinia can also be spread via protozoonotic mechanisms, since Yersinia are known to be facultative intracellular parasites; studies and discussions of the possibility of amoeba-vectored (through the cyst form of the protozoan) Yersinia propagation and proliferation are now in progress. The genus is named for A.E.J. Yersin, a Swiss bacteriologist, who discovered the Yersinia pestis bacterium - the causative agent of the bubonic plague. The special genus Yersinia has been recognized since 1971, mainly for taxonomic reasons. The disease caused by Y. enterocolitica is called Yersiniosis. Another pathogen is Y. pseudotuberculosis, which is the least common species of Yersinia causing disease in humans. Yersinia is implicated as one of the pathogenic causes of reactive arthritis worldwide. An interesting feature peculiar to some of the Yersinia bacteria is the ability not only to survive, but also to proliferate at temperatures as low as 1-4 degrees Celsius (e.g., on cut salads and other food products in a refrigerator). Yersinia representatives also reveal relatively high heat resistantance, some of them being able to survive 50-60 degrees Celsius temperature for up to 20-30 minutes and (arguably, might be due to misreading of information like the first external link below) surviving standard pasteurization process (15 seconds at 72 degrees Celsius) in milk. Yersinia bacteria are relatively quickly inactivated by oxidizing agents such as hydrogen peroxide and potassium permanganate solutions.

wikidoc

/index.php/Yersinia_enterocolitica

# Yersinia enterocolitica Yersinia enterocolitica is a species of gram-negative coccobacillus-shaped bacterium, belonging to the family Enterobacteriaceae. Primarily a zoonotic disease (cattle, deer, pigs, and birds), animals which recover frequently become asymptomatic carriers of the disease. Acute Y. enterocolitica infections produce severe diarrhea in humans, along with Peyer's patch necrosis, chronic lymphadenopathy, and hepatic or splenic abscesses. Additional symptoms may include entero-colitis, fever, mesenteric adenitis, erythema nodosum and acute terminal ileitis, which may be confused with appendicitis or Crohn's disease. See yersiniosis for further details. Y. enterocolitica seems to be associated with autoimmune Graves-Basedow thyroiditis. Whilst indirect evidence exists, direct causative evidence is limited, and Y. enterocolitica is probably not a major cause of this disease, but may contribute to the development of thyroid autoimmunity arising for other reasons in genetically susceptible individuals. It has also been suggested that Y. enterocolitica infection is not the cause of auto-immune thyroid disease, but rather is only an associated condition; with both having a shared inherited susceptibility. More recently the role for Y. enterocolitica has been disputed.

wikidoc

/index.php/Yersinia_pestis_infection_chest_x_ray

# Yersinia pestis infection chest x ray A chest x-ray is required in patients suspected to have plague, especially those with pneumonic plague. Findings on chest x-ray may reveal the true burden of pulmonary disease when there are minimal findings on auscultation during physical examination. Chest x-rays can be variable but may show diffuse interstitial or unilateral lobar infiltrates or consolidation. A chest x-ray is indicated in patients suspected to have the plague, especially pneumonic plague, because findings on auscultation during physical exam are frequently deceiving and may underestimate the true burden of the infection. Chest x-ray of a plague patient revealing bilateral infection, greater on the patient's left side, which was diagnosed as a case of pneumonic plague, caused by Yersinia pestis. From Public Health Image Library (PHIL).

wikidoc

/index.php/Yizhi_Jane_Tao

# Yizhi Jane Tao Yizhi Jane Tao, Ph.D., is a Chinese biochemist, structural biologist, and Assistant Professor of Biochemistry and Cell Biology at Rice University in Houston, Texas. Professor Tao led a team of researchers to be the first to map the structure of the influenza A virus nucleoprotein to an atomic level, a feat which circulated widely in the popular press. She was named among the top ten most influential Chinese of 2006 by a consortium of China's leading media outlets including Phoenix Satellite Television, China News Service, Asia Newsweek, and World Journal. Born in China, Yizhi Jane Tao received a B.Sc. degree in biology from Peking University in Beijing, China, in 1992. She later moved to West Lafayette, Indiana, where she received her Ph.D. in biological science while studying under the German-American biophysicist Michael Rossmann. She completed a postdoctoral fellowship under Stephen C. Harrison at Harvard University in 2002. Upon completing her postdoctoral studies, Tao joined the faculty of Rice University, where she has made important contributions to the study of influenza and birnaviruses.

wikidoc

/index.php/Ylang-ylang

# Ylang-ylang Ylang-ylang (Template:IPA2) (ee-lahng ee-lahng) Cananga odorata, is a small flower of the cananga tree. It is a fast-growing tree that exceeds 5 meters per year and attains an average height of 12 meters. It grows in full or partial sun, and prefers the acidic soils of its native rainforest habitat. The leaves are long, smooth and glossy. The flower is greenish yellow (rarely pink), curly like a starfish, and yields a highly fragrant essential oil. A related species is Cananga fruticosa, which is a dwarf ylang-ylang that grows as small tree or compact shrub with highly scented flowers. Ylang-ylang has been cultivated in temperate climates under conservatory conditions. Its fruit are an important food item for birds, such as the Collared Imperial-pigeon, Purple-tailed Imperial-pigeon, Zoe's Imperial-pigeon, Superb Fruit-dove, Pink-spotted Fruit-dove, Coroneted Fruit-dove, Orange-bellied Fruit-dove, and Wompoo Fruit-dove (Frith et al. 1976). The name ylang-ylang is derived from Tagalog, either from the word ilang, meaning "wilderness", alluding to its natural habitat, or the word ilang-ilan, meaning "rare", suggestive of its exceptionally delicate scent. The plant is native to the Philippines and Indonesia and is commonly grown in Polynesia, Melanesia and Micronesia. The fragrance of ylang-ylang is rich and deep with notes of rubber and custard, and bright with hints of jasmine and neroli. The essential oil of the flower is obtained through steam distillation of the flowers and separated into different grades (extra; 1; 2; 3) according to when the distillates are obtained. The main aromatic component of ylang-ylang is methyl anthranilate. The essential oil of ylang-ylang is used in aromatherapy. It is believed to relieve high blood pressure, normalize sebum secretion for skin problems, and is considered to be an aphrodisiac. According to Margaret Mead, it was used as such by South Pacific natives such as the Solomons where she did much of her research. The oil from ylang-ylang is widely used in perfumery for oriental or floral themed perfumes. Ylang-ylang blends well with most floral, fruit and wood smells. In Indonesia, ylang-ylang flowers are spread on the bed of newlywed couples. In the Philippines, its flowers, together with the flowers of the sampaguita, are strung into a necklace and worn by women and used to adorn religious images.

wikidoc

/index.php/Yo-yo_dieting

# Yo-yo dieting The term "yo-yo dieting" was coined by Kelly D. Brownell at Yale University, in reference to the cyclical up-down motion of a yo-yo. In this process, the dieter is initially successful in the pursuit of weight loss but is unsuccessful in maintaining the loss long-term and begins to gain the weight back. The dieter then seeks to lose the regained weight, and the cycle begins again. The reasons for yo-yo dieting are varied but often include embarking upon a hypocaloric diet that was initially too extreme. At first the dieter may experience elation at the thought of loss and pride of their rejection of food. Over time, however, the limits imposed by such extreme diets cause effects such as depression or fatigue that make the diet impossible to sustain. Ultimately, the dieter reverts to their old eating habits, now with the added emotional effects of failing to lose weight by restrictive diet. Such an emotional state leads many people to eating more than they would have before dieting, causing them to rapidly regain weight. This kind of diet is associated with extreme food deprivation as a substitute for good diet and exercise techniques. As a result, the dieter may experience loss of both muscle and body fat during the initial weight-loss phase (weight-bearing exercise is required to maintain muscle). After completing the diet, the dieter is likely to experience the body's starvation response, leading to rapid weight gain of only fat. This is a cycle that changes the body's fat-to-muscle ratio, one of the more important factors in health. One study in rats showed those made to yo-yo diet were more efficient at gaining weight. However, as of 1994, the research compiled by Atkinson et al. (1994) showed that there are "no adverse effects of weight cycling on body composition, resting metabolic rate, body fat distribution, or future successful weight loss", and that there is not enough evidence to show risk factors for cardiovascular disease being directly dependent on cyclical dieting patterns. Yo-yo dieting can have extreme emotional and physical ramifications due to the stress that someone puts on themselves to lose weight quickly. The instant gratification of losing the weight eventually gives way to old eating habits that cause weight gain and emotional distress. Since there is "no single definition of weight cycling [that] can be endorsed", it is almost impossible for research to draw specific conclusions about the actual effects of cyclical dieting, until it becomes more definitely defined.

wikidoc

/index.php/Yoga

# Yoga Yoga (Sanskrit: योग Yoga, Template:IPA2) is a group of ancient spiritual practices originating in India. According to Gavin Flood, Academic Director of the Oxford Centre for Hindu Studies it has been defined as referring to "technologies or disciplines of asceticism and meditation which are thought to lead to spiritual experience and profound understanding or insight into the nature of existence." Yoga is also intimately connected to the religious beliefs and practices of the other Indian religions. Outside India, Yoga is mostly associated with the practice of asanas (postures) of Hatha Yoga or as a form of exercise, although it has influenced the entire Indian religions family and other spiritual practices throughout the world. Hindu texts discussing different aspects of yoga include the Upanishads, the Bhagavad Gita, the Yoga Sutras of Patanjali, the Hatha Yoga Pradipika, the Shiva Samhita, and many others. Major branches of Yoga include: Hatha Yoga, Karma Yoga, Jnana Yoga, Bhakti Yoga, and Raja Yoga. Raja Yoga, established by the Yoga Sutras of Patanjali, and known simply as Yoga in the context of Hindu philosophy, is one of the six orthodox (āstika) schools of thought. The Sanskrit term yoga has a wide range of different meanings. It is derived from the Sanskrit root yuj, "to control", "to yoke", or "to unite". Common meanings include "joining" or "uniting", and related ideas such as "union" and "conjunction". Another conceptual definition is that of "mode, manner, means" or "expedient, means in general". Several seals discovered at Indus Valley Civilization (c. 3300–1700 BC) sites depict figures in a yoga or meditation like posture. There is considerable evidence to support the idea that the images show "a form of ritual discipline, suggesting a precursor of yoga" according to archaeologist Gregory Possehl. He points to sixteen other specific "yogi glyptics" in the corpus of Mature Harappan artifacts as pointing to Harappan devotion to "ritual discipline and concentration." These images show that the yoga pose "may have been used by deities and humans alike." Possehl suggests that yoga goes back to the Indus Valley Civilization. The most widely known of these images was named the "Pashupati seal" by its discoverer, John Marshall, who believed that it represented a "proto-Shiva" figure. Many modern authorities discount the idea that this "Pashupati" (Lord of Animals, Sanskrit Template:IAST) represents a Shiva or Rudra figure. Gavin Flood also characterizes these views as "speculative", saying that it is not clear from the 'Pashupati' seal that the figure is seated in a yoga posture, or that the shape is intended to represent a human figure. Authorities who support the idea that the 'Pashupati' figure shows a figure in a yoga or meditation posture include Archaeologist Jonathan Mark Kenoyer, current Co-director of the Harappa Archaeological Research Project in Pakistan and Indologist Heinrich Zimmer. In 2007, terracotta seals were discovered in the Cholistan Desert in Pakistan. Punjab University Archaeology Department Chairman Dr. Farzand Masih described one of the seals as similar to the previously discovered Mohenjodaro seals, with three pictographs on one side and a "yogi" on the other side. Ascetic practices (tapas) are referenced in the [[Brahmana|Template:IAST]] (900 BCE and 500 BCE), early commentaries on the vedas. In the Upanishads, an early reference to meditation is made in Brihadaranyaka Upanishad, one of the earliest Upanishads (approx. 900 BCE). The main textual sources for the evolving concept of Yoga are the middle Upanishads, (ca. 400 BCE), the Mahabharata (5th c. BCE) including the Bhagavad Gita (ca. 200 BCE), and the Yoga Sutras of Patanjali (200 BCE-300 CE). The Bhagavad Gita ('Song of the Lord'), uses the term yoga extensively in a variety of senses. Of many possible meanings given to the term in the Gita, most emphasis is given to these three: The influential commentator Madhusudana Sarasvati (b. circa 1490) divided the Gita's eighteen chapters into three sections, each of six chapters. According to his method of division the first six chapters deal with Karma yoga, the middle six deal with Bhakti yoga, and the last six deal with Jnana (knowledge). This interpretation has been adopted by some later commentators and rejected by others. In Indian philosophy, Yoga is the name of one of the six orthodox philosophical schools. The Yoga philosophical system is closely allied with the Samkhya school. The Yoga school as expounded by Patanjali accepts the Samkhya psychology and metaphysics, but is more theistic than the Samkhya, as evidenced by the addition of a divine entity to the Samkhya's twenty-five elements of reality. The parallels between Yoga and Samkhya were so close that Max Müller says that "the two philosophies were in popular parlance distinguished from each other as Samkhya with and Samkhya without a Lord...." The intimate relationship between Samkhya and Yoga is explained by Heinrich Zimmer: These two are regarded in India as twins, the two aspects of a single discipline. Template:IAST provides a basic theoretical exposition of human nature, enumerating and defining its elements, analyzing their manner of co-operation in a state of bondage (bandha), and describing their state of disentanglement or separation in release (Template:IAST), while Yoga treats specifically of the dynamics of the process for the disentanglement, and outlines practical techniques for the gaining of release, or 'isolation-integration' (kaivalya). The sage Patanjali is regarded as the founder of the formal Yoga philosophy. The Yoga Sutras of Patanjali are ascribed to Patanjali, who, may have been, as Max Müller explains, "the author or representative of the Yoga-philosophy without being necessarily the author of the Sutras." Indologist Axel Michaels is dismissive of claims that the work was written by Patanjali, characterizing it instead as a collection of fragments and traditions of texts stemming from the second or third century. Gavin Flood cites a wider period of uncertainty for the composition, between 100 BCE and 500 CE. Patanjali's yoga is known as Raja yoga, which is a system for control of the mind. Patanjali defines the word "yoga" in his second sutra, which is the definitional sutra for his entire work: This terse definition hinges on the meaning of three Sanskrit terms. I. K. Taimni translates it as "Yoga is the inhibition (Template:IAST) of the modifications (Template:IAST) of the mind (Template:IAST)". Swami Vivekananda translates the sutra as "Yoga is restraining the mind-stuff (Citta) from taking various forms (Vrittis)." Gavin Flood translates the sutra as "yoga is the cessation of mental fluctuations". Patanjali's writing also became the basis for a system referred to it as "Ashtanga Yoga" ("Eight-Limbed Yoga"). This eight-limbed concept derived from the 29th Sutra of the 2nd book became a feature of Raja yoga, and is a core characteristic of practically every Raja yoga variation taught today. The Eight Limbs of yoga practice are: They are sometimes divided into the lower and the upper four limbs, the lower ones being parallel to the lower limbs of Hatha Yoga, while the upper ones being specific for the Raja yoga. The upper three limbs practiced simultaneously constitute the Samyama. It details every aspect of the meditative process, and the preparation for it. The book is available in as many as 40 English translations, both in-print and on-line. The Primordial Yoga, more than 6.000 years old when only one form of Yoga was recognised - at the beginning Yoga was called Sámkhya – (without compromised power or modern simplifications), preserved over the last millennia in the Indian Himalayas and with older vestiges in the Indus Valley, taught by Manu/Rudra/Shiva, (it is assumed that it dates from between 9.500 and 11.500 years ago, according to the recent underwater discoveries in the Cambaia Gulf, the mythical city of Duarka, victim of the thaws and floods of the 2º phase of the last Ice Age). 2 – an Exceptional Development of the Human being in its all positive aspects, integrally and always in harmony, through the constant work, in each Class - Mahá Sádhaná (with 12 Anga or parts) with its 12 Technique Disciplines: 1 - Dhyána/Samyama - Meditation through the control of the frequency of brain waves; 2 - Pránáyáma - energetic and neuro-vegetative influence through respiratory Exercises; 3 - Ásana – psycho-bio-physical Positions; 4 - Yoganidrá - Physical, emotional and mental Relaxation Techniques; 5- Kriyá- Organic Cleaning and Strengthening; 6 - Mantra/Kírtana - Domain of external sounds and Harmony; 7 - Jápa - Concentrative Sounds; 8 - Bandha – Muscular enlivening and neuro-endocrinal; 9 - Yantra - concentrative Symbols for psychosomatic effect; 10 - Pujá - Energetic Repayments; 11 - Mudrá - Reflexive and energetic Gestures made with the hands; 12 - Mánasika - Mind process, will strengthening and projection of the Conscience. - and with its 6 secondary disciplines (total of 18) and complementary subjects (Sámkhya, Samskrta/Sanskrit, Chakra, Sat Sanga, Sat Chakra, Sháshtra, Great World Masters, Mauna, Nyása, Shákta, Nutrition, etc.), where the practical Philosopher will apply constantly in his daily life what he has learned in the Áshrama (place of practice), and where in the long run – the path – must be always in tune with the Grand goal, Hatha Yoga is a particular system of Yoga described by Yogi Swatmarama, a yogic sage of the 15th century in India, and compiler of the Hatha Yoga Pradipika. Hatha Yoga is a development of — but also differs substantially from — the Raja Yoga of Patanjali, in that it focuses on shatkarma, the purification of the physical as leading to the purification of the mind (ha), and prana, or vital energy (tha). In contrast, the Raja Yoga posited by Patanjali begins with a purification of the mind (yamas) and spirit (niyamas), then comes to the body via asana (body postures) and pranayama (breath). Hatha yoga contains substantial tantric influence, and marks the first point at which chakras and kundalini were introduced into the yogic canon. Compared to the seated asanas of Patanjali's Raja yoga which were seen largely as a means of preparing for meditation, it also marks the development of asanas as full body 'postures' in the modern sense. Hatha Yoga in its many modern variations is the style that most people actually associate with the word "Yoga" today. Because its emphasis is on the body through asana and pranayama practice, many western students are satisfied with the physical health and vitality it develops and are not interested in the other six limbs of the complete Hatha yoga teaching, or with the even older Raja Yoga tradition it is based on. Yoga is intimately connected to the religious beliefs and practices of the Indian religions. The influence of Yoga is also visible in Buddhism, which is distinguished by its austerities, spiritual exercises, and trance states. Yogacara (Sanskrit: "Practice of Yoga [Union]" ), also spelled yogāchāra, is a school of philosophy and psychology that developed in India during the 4th to 5th centuries. Yogacara received the name as it provided a yoga, a framework for engaging in the practices that lead to the path of the bodhisattva. The Yogacara sect teaches yoga in order to reach enlightenment. Zen (the name of which derives from the Sanskrit "dhyana" via the Chinese "ch'an" ) is a form of Mahayana Buddhism. The Mahayana school of Buddhism is noted for its proximity with Yoga. In the west, Zen is often set alongside Yoga; the two schools of meditation display obvious family resemblances. This phenomenon merits special attention since the Zen Buddhist school of meditation has some of its roots in yogic practices. Certain essential elements of Yoga are important both for Buddhism in general and for Zen in particular. Yoga is central to Tibetan Buddhism. In the Nyingma tradition, practitioners progress to increasingly profound levels of yoga, starting with Mahā yoga, continuing to Anu yoga and ultimately undertaking the highest practice, Ati yoga. In the Sarma traditions, the Anuttara yoga class is equivalent. Other tantra yoga practices include a system of 108 bodily postures practiced with breath and heart rhythm. Timing in movement exercises is known as Trul khor or union of moon and sun (channel) prajna energies. The body postures of Tibetan ancient yogis are depicted on the walls of the Dalai Lama's summer temple of Lukhang. Tantrism is a practice that is supposed to alter the relation of its practitioners to the ordinary social, religious, and logical reality in which they live. Through Tantric practice an individual perceives reality as maya, illusion, and the individual achieves liberation from it. This particular path to salvation among the several offered by Hinduism, links Tantrism to those practices of Indian religions, such as yoga, meditation, and social renunciation, which are based on temporary or permanent withdrawal from social relationships and modes. During tantric practices and studies, the student is instructed further in meditation technique, particularly chakra meditation. This is often in a limited form in comparison with the way this kind of meditation is known and used by Tantric practitioners and yogis elsewhere, but is more elaborate than the initiate's previous meditation. It is considered to be a kind of Kundalini Yoga for the purpose of moving the Goddess into the chakra located in the "heart," for meditation and worship. Within the monist schools of Advaita Vedanta and Shaivism this perfection takes the form of Moksha, which is a liberation from all worldly suffering and the cycle of birth and death (Samsara) at which point there is a realisation of identity with the Supreme Brahman. For the dualistic bhakti schools of Vaishnavism, bhakti itself is the ultimate goal of the yoga process , wherein perfection culminates in an eternal relationship with Vishnu or one of his associated avatars such as Krishna or Rama.

wikidoc

/index.php/Yohimbine

# Yohimbine The NIH states that Yohimbine hydrochloride is the standardized form of yohimbine that is available as a prescription medicine in the United States, and has been shown in human studies to be effective in the treatment of male impotence. Yohimbine chloride—a standardized form of yohimbine—is a prescription medicine that has been used to treat erectile dysfunction. Controlled studies suggest that it is not always an effective treatment for impotence, and evidence of increased sex drive (libido) is anecdotal only. It cannot be excluded that orally administered yohimbine can have a beneficial effect in some patients with ED. The conflicting results available may be attributed to differences in drug design, patient selection, and definitions of positive response. However, generally, available results of treatment are not impressive. Yohimbine hydrochloride has also been used for the treatment of sexual side effects caused by some antidepressants (SSRIs), female hyposexual disorder, as a blood pressure boosting agent in autonomic failure, xerostomia, and as a probe for noradrenergic activity. Yohimbine has been used to facilitate recall of traumatic memories in the treatment of post-traumatic stress disorder (PTSD). . Use of yohimbine outside therapeutic settings may not be appropriate for persons suffering from PTSD. Some internet shops sell expensive formulations of yohimbine for transdermal delivery to effect a local reduction of adipose tissue, although there is no evidence that it is effective. Demand for products of this kind is frequently found in the bodybuilding community. Yohimbine Hydrochloride is a selective competitive alpha2-adrenergic receptor antagonist. The alpha2 receptor is responsible for sensing adrenaline and noradrenaline and telling the body to decrease its production as part of a negative feedback loop. Yohimbine also antagonizes several serotonin receptor subtypes: 1A (inhibitory, behavioral control), 1B (inhibitory, vasoconstriction), 1D (inhibitory, vasoconstriction), and 2B (smooth muscle contraction). Since yohimbine is an antagonist, it will decrease the effects of these receptors, thus causing excitation, vasodilation, and smooth muscle relaxation. Yohimbine is also said to increase dopamine and have some actions as an MAOI, although these mechanisms are unknown. Yohimbine and Yohimbine bark may also cause vasodilation through endothelin B receptor stimulation and nitric oxide (NO) release. Yohimbine is the principal alkaloid of the bark of the West-African evergreen Pausinystalia yohimbe Pierre (formerly Corynanthe yohimbe), family Rubiaceae (Madder family). There are 31 other yohimbane alkaloids found in Yohimbe. In Africa, yohimbine has traditionally been used as an aphrodisiac. However it is very important to note that while the terms yohimbine, yohimbine hydrochloride, and yohimbe bark extract are related, they are not interchangeable. However, the levels of yohimbine that are present in yohimbe bark extract are variable and often very low. Therefore, although yohimbe bark has been used traditionally to reduce male erectile dysfunction, there is not enough scientific evidence to form a definitive conclusion in this area. Higher doses of oral yohimbine may create numerous side effects such as rapid heart rate, high blood pressure, and overstimulation. It causes insomnia and sleeplessness.

wikidoc

/index.php/Young_adult_(psychology)

# Young adult (psychology) According to Erik Erikson's stages of human development, first enumerated in Childhood and Society (1950) a young adult is a person between the ages of 18 and 40, whereas an adolescent is a person between the ages of 12 and 17. The young adult stage in human development precedes middle adulthood. A person in the middle adulthood stage is between the ages of 40 and 65. In maturity, a person is 65 years old or older. Biological function and physical performance reach their peak from 20-35 years of age, waning after 35. Strength peaks around 25 years of age, plateaus through 35 or 40 years of age, and then declines. Flexibility also decreases with age throughout adulthood. However, there are large individual differences and a fit 40-year-old may outcompete a sedentary 20-year-old. Women reach their peak fertility in their early 20s. Assuming unprotected intercourse with a man of the same age, women aged 19-26 have about a 50% chance of becoming pregnant during a given menstrual cycle, compared with 40% in the 27-34 age group and below 30% for women 35-39. In developed countries, mortality rates for the 20-40 age group are typically very low. Men are more likely to die at this age than women, particularly in the 18-25 group: reasons include car accidents and suicide. Mortality statistics among men and women level off during the late twenties and thirties, due in part to good health and less risk-taking behavior. In sub-Saharan Africa, HIV/AIDS has hit the early adult population particularly hard. According to a United Nations report, AIDS has significantly increased mortality of between ages 20 to 55 for African males and 20 to 45 for African females, reducing the life expectancy in South Africa by 18 years and in Botswana by 34 years. According to Erikson, the young adult stage involves the personal need for intimacy and sex. Failure to achieve this need results in isolation, which is avoided, and as a result the young adult strives for love and compassion. The young adult learns that love and compassion may get him what he wants. In modern societies, young adults in their late teens and early 20s encounter a number of issues as they finish school and begin to hold full-time jobs and take on other responsibilities of adulthood. In the late teens and early 20s, young adults become individuals and will set themselves apart. Self becomes the main reliance. Young adults will strive to become independent from parents, take responsibility for themselves and make their own decisions. During the young adult stage, mainly the majority think in a more mature manner and take issues more seriously. They focus on the construction of a better future. Adolescents are generally regarded as naïve and inexperienced, but are expected to grow into mature adults in their 20s. Young adults in this stage of human development learn value in both tangible and intangible objects. Their relationships with their parents and older adults change. However, in many cases, young adults and adolescents have enormous talent that can, in cases, outstrip some adults' talents. In many cases, problems such as lack of time (schooling and other commitments) and lack of money can arrest the adolescent's development in terms of intellectual and talent growth. After the upheaval of the early 30's, the middle to late 30's (roughly ages 34-39) are often characterized by settling down. People in their 30's may increase the financial and emotional investments they make in their lives. Many have been employed long enough to gain promotions and raises. They often become more focused on advancing their careers and gaining stability in their personal lives. They may have started a family.

wikidoc

/index.php/Youth_Tobacco_Cessation_Collaborative

# Youth Tobacco Cessation Collaborative The Youth Tobacco Cessation Collaborative (YTCC) was formed in 1998 to address the gap in knowledge about what cessation strategies are most effective in assisting youth to quit smoking. Collaborative members represent major organizations that fund research, program, and policy initiatives related to controlling youth tobacco use. The National Blueprint for Action for youth and young adult tobacco-use cessation was published in the Spring of 2000 by the Youth Tobacco Cessation Collaborative. The youth cessation blueprint was developed as a consensus document to guide decisions regarding funding research and programs related to youth tobacco-use cessation, to reflect common goals and objectives among national organizations that fund such efforts, to help ensure that funding plans and programs across organizations build the strongest possible national efforts to support youth cessation, and to coordinate funding efforts. The blueprint includes two-, five-, and 10-year objectives and funding strategies for research, implementation, and support and demand. Since publishing the blueprint, collaborative members have worked successfully to collectively address many of the needs identified in the blueprint, with a focus on its two-year objectives. Among the more significant and important developments are the relationships that have formed among the collaborative organizations, the increase in collaboration across organizations, the co-funding of research and other projects, and the increase in attention to the issue of cessation among youth. In addition, the blueprint approach has become a model for other activities such as the National Blueprint for Disseminating and Implementing Evidence-Based Clinical and Community Strategies to Promote Tobacco-Use Cessation and the National Partnership to Help Pregnant Smokers Quit's Action Plan (May 2002). The ten-year goal of the National Blueprint is to ensure that every young tobacco user (age 12–24) has access to appropriate and effective cessation interventions by the year 2010. The Collaborative recognizes that there is a need to explore and address the cessation needs and interests among different segments of the population of young tobacco users, defined by factors such as: In addition, it must be recognized that youth considering quitting do so within the context of other competing needs (e.g. family or living situation) and societal influences (e.g. accessibility to tobacco products). The Collaborative affirms the need to examine a broad range of possible interventions including individual, interpersonal, and organizational approaches. The Collaborative also encourages the involvement of youth in efforts to reach the objectives articulated in the National Blueprint for Action. In order to reach the ten year goal, a range of needs must be addressed in funding and conducting research, in developing and supporting proven interventions, in implementing and maintaining policy changes, in increasing public awareness of and support for youth tobacco-use cessation, and in raising young tobacco-users' interests in cessation. To provide an update on the accomplishments of its work, YTCC publishes a "highlights" document that outlines activity of the collaborative toward its short- and long-term goals. These activity highlights illustrate just some of the progress that has been made. Although progress is significant, more attention to this issue is needed.

wikidoc

/index.php/Youth_development

# Youth development Youth development or adolescent development is the process through which adolescents (alternately called youth or young adults) acquire the cognitive, social, and emotional skills and abilities required to navigate life. The experience of adolescence varies for every youth: culture, gender, and socioeconomic class are important influences on development. This development occurs throughout a young person's life, including formal and informal settings such as home, church, or school; and similar relationships, such as peer friendships, work, parenting, teaching, or mentoring. Youth is an important developmental period described in, most psychological theories of human development from Sigmund Freud's theory of psychosexual development, Carl Jung, and in particular Erik Erikson. Erikson's stages of psychosocial development identified adolescence is a time of identity formation). During each stage, behavior changes in response to biological maturation and changes in the social environment. The process of entering adulthood entails many decisions both conscious and not. The examination of this stage of life is rooted in the child development theories of John Dewey, Jean Piaget, and Erik Erikson. Anthropologist Margaret Mead also added a great deal of understanding to this field. Regarding the successive evolution of youth as a social phenomenon, Mead reportedly wrote, Youth development has been at the core of the mission of many youth organizations for almost 100 years. It is increasingly identified as an important component of school reform, led primarily by initiatives of the Carnegie Corporation and the Forum for Youth Investment. Other important international organizations include The European Knowledge Centre for Youth Policy and the Australian Clearinghouse for Youth Studies. The sociological field of study that examines youth development is separated into myriad political examinations of young people, including positive youth development, or PYD, and community youth development, or CYD. Each of these entails particular connotations of the particular relevance or importance of young people to their families, schools, and communities. Important factors in each of these theories include youth/adult partnerships and youth voice. CYD also places high value on youth leadership and civic engagement. PYD is the idea that all young people need support, guidance, and opportunities during adolescence. It also looks toward creating supportive communities for all young people and at the same time, engaging youth to contribute to the well-being of the larger community.

wikidoc

/index.php/Ypadu

# Ypadu Ypadú or ypadu is an unrefined, unconcentrated powder made from coca leaves and the ash of various other plants. Like coca teas consumed in Peru to adapt to sickness induced by high elevation, it has a long ethnobotanical history and cultural associations. "Ypadú would not be more than an element in Amazonian botanical and ethnographic folklore were it not for its use, which enshrines it as a precursor in the current trend in favour of the 'industrialisation' of coca. Because ypadú leaves are very fibrous and their alkaloid content is low, lowland cultures have developed a process for transformation of the leaf that produces a very fine powder [...]. The traditional technique consists of toasting the leaves in an earthenware pot, crushing them in a wooden mortar, mixing them with ash from the leaf of the yarumo plant (Cecropia spp.), and passing them through a sieve to eliminate the fibrous part. The resulting powder is easily handled and rapidly absorbed. Experiments done by Anthony Henman in Lima and São Paulo have shown that a modern ypadú, made with any variety of coca leaf and with ash made from quinoa straw, is well accepted by people who find the laborious process of chewing whole leaves to be tedious. Ypadú could become the much-desired bridge between the traditional use of coca and new industrialised products demanded by the 21st-century world. Although it probably would not replace the traditional chewing of coca leaves, or chacchado, in the Andean countries, it could become and alternative to refined cocaine, which – despite all efforts to suppress it – has become a mass-consumption commodity in large areas of the world. As a result, it could become an effective tool for public policies that seek 'harm reduction' and a way to absorb the properties of coca. In short, ypadú would help achieve what no government has managed to do: re-educate the demand for cocaine and, along the way, return coca to its deserved pre-eminence as an ancestral plant of wisdom." ("Coca yes, cocaine no?", p. 19) Foreign visitors to some Latin American countries have demonstrated an interest in commercial and cultural uses of the stimulant properties of the coca plant which are less harmful than cocaine, which is highly and unnaturally refined. ypadu. A few websites depict a mild modern preparation of the powdery ypadu mixture using plastic jars and coffee grinders or food processors rather than the traditional implements such as clay vessels and mortar-and-pestles fashioned from wood. Peruvian coca of the genus Erythroxilum coca var has reportedly been used in this adaptation to produce effective mixtures with pleasant taste. Protagonists of coca recommend mass production of ypadu as a harmless replacement for heavily refined and concentrated cocaine. They argue that a mild alternative to cocaine would cut into the illicit drug trade and the costs it imposes on societies. Antagonists of Coca claim that mild coca derivatives can serve as gateways to cocaine abuse. The also claim that economic rewards brought to coca producers would fuel illicit coca production and in turn the cocaine cartels.

wikidoc

/index.php/Yt_antigen_system

# Yt antigen system The Yt antigen system (also known as Cartwright) is present on the membrane of red blood cells and helps determine a person's blood type. The antigens are found on the protein acetylcholinesterase, an enzyme which helps break down acetylcholine. The Yt system features two alleles, Yt(a) and Yt(b). Antibodies against the Yt system can lead to transfusion reactions such as hemolytic anemia.

wikidoc

/index.php/Yttrium

# Yttrium Template:Elementbox header Template:Elementbox series Template:Elementbox groupperiodblock Template:Elementbox appearance img Template:Elementbox atomicmass gpm Template:Elementbox econfig Template:Elementbox epershell Template:Elementbox section physicalprop Template:Elementbox phase Template:Elementbox density gpcm3nrt Template:Elementbox densityliq gpcm3mp Template:Elementbox meltingpoint Template:Elementbox boilingpoint Template:Elementbox heatfusion kjpmol Template:Elementbox heatvaporiz kjpmol Template:Elementbox heatcapacity jpmolkat25 Template:Elementbox vaporpressure katpa Template:Elementbox section atomicprop Template:Elementbox crystalstruct Template:Elementbox oxistates Template:Elementbox electroneg pauling Template:Elementbox ionizationenergies4 Template:Elementbox atomicradius pm Template:Elementbox atomicradiuscalc pm Template:Elementbox covalentradius pm Template:Elementbox section miscellaneous Template:Elementbox magnetic Template:Elementbox eresist ohmm Template:Elementbox thermalcond wpmkat300k Template:Elementbox thermalexpansion umpmk Template:Elementbox speedofsound rodmpsat20 Template:Elementbox youngsmodulus gpa Template:Elementbox shearmodulus gpa Template:Elementbox bulkmodulus gpa Template:Elementbox poissonratio Template:Elementbox brinellhardness mpa Template:Elementbox cas number |- ! colspan="2" style="background:#ffc0c0; color:black" | Selected isotopes |- | colspan="2" |

wikidoc

/index.php/Yuremamine

# Yuremamine Yuremamine is a phytoindole chemical which was first isolated and identified from the plant material of Mimosa tenuiflora in 2005. It may explain the reason that the dimethyltryptamine in some ayahuasca preparations is orally active without the presence of any known MAOI.

wikidoc

/index.php/Yuzpe_regimen

# Yuzpe regimen The Yuzpe Regimen is a method of emergency contraception using a combination of estrogen and progestogen hormones and started within 72 hours of sexual intercourse. It has subsequently been superseded by a progestogen-only hormonal regimen. The method was first developed by a Canadian Professor A. Albert Yuzpe who published the first studies demonstrating the method's safety and efficacy in 1974. This regimen allows a woman who has had unprotected sex to avoid pregnancy by taking 12 hours apart two sufficient doses of estrogen and progestogen hormones. The sooner this is started, the more effective it is and the effectiveness more than 72 hours after sexual intercourse is greatly reduced. The licensing for emergency Intrauterine device (IUD) insertion allows for up to 5 days and it is highly effective for up to five days after the time of ovulation, which may extend more than five days after the relevant risky intercourse. These hormones are administered as a number of combined oral contraceptive pills (COCPs). Each dose can vary from 2 to 5 pills depending on the brand of medication being used. Patients concurrently taking certain regular medications (e.g. rifamycin and many anticonvulsant drugs) that enhance the liver's break down of other drugs, must use an even higher hormone dose and may be better advised to use as an alternative the insertion of an IUD. The method is not guaranteed to prevent pregnancy and whilst the hormones may make the subsequent period come a few days early or late, a pregnancy test should be carried out if the period is more than 3 days late. The Yuzpe Regimen does not protect against sexually transmitted diseases. Subsequently, the World Health Organization (WHO) undertook an investigation into the use of progestogen-only tablets as an Emergency Hormonal Contraceptive (i.e. without any estrogen component). This showed greater efficacy with reduced side effects and has therefore superseded the Yuzpe method. A single dose of 100 mg mifepristone is also more effective than the Yuzpe regime . Should vomiting occur within 3 hours of taking a dose, then insufficient hormones may have been absorbed to provide the full contraceptive cover and an additional dose should be taken. Measures that may help to prevent nausea or vomiting include: Many common combined oral contraceptive pills could be used for the Yuzpe regimen , although their manufacturers did not label the pills for this use. Such off-label use of approved medications is legal and commonplace in American medicine. Further, in February 1997, the FDA declared emergency contraceptive use of certain birth control pills, following the Yuzpe regimen, as safe and effective. Yuzpe regimen dedicated products (Preven in US and Schering-PC4 in UK) were discontinued following the introduction of progestogen-only ECPs (Plan B in US and Levonelle in UK).

wikidoc

/index.php/Yves_Morin

# Yves Morin Born in Quebec City, Quebec, he received a Bachelor of Arts degree in 1948 and a Doctor of Medicine degree in 1953 from the Université Laval. In 2001, he was appointed to the Senate of Canada representing the senatorial division of Lauzon, Quebec. A Liberal, he served until his mandatory retirement on his 75th birthday in 2004. In 1990, he was made an Officer of the Order of Canada for having "a major influence on the training of a generation of doctors". In 1995, he was made an Officer of the National Order of Quebec.

wikidoc

/index.php/Z-plasty

# Z-plasty Z-plasty is a plastic surgery technique that is used to improve the functional and cosmetic appearance of scars. It can elongate a contracted scar or rotate the scar tension line. The middle line of the Z-shaped incision is made along the line of greatest tension or contraction, and triangular flaps are raised on opposite sides of the two ends and then transposed. The length and angle of each flap must be precisely the same to avoid mismatched flaps that may be difficult to close. Some possible complications of Z-plasty include flap necrosis, hematoma formation under the flaps, wound infection, trapdoor effect and sloughing of the flap caused by high wound tension.

wikidoc

/index.php/ZEB2-AS1

# ZEB2-AS1 ZEB2-AS1 (ZEB2 antisense RNA 1) is a long non-coding RNA, which is overlapping and antisense to the ZEB2 gene. It overlaps the 5' splice site of an intron within the 5'UTR of the ZEB2 gene. This intron contains an internal ribosome entry site (IRES), which is necessary for ZEB2 expression. ZEB2-AS1 prevents the splicing of this intron, and therefore activates ZEB2 expression.

wikidoc

/index.php/ZIC2

# ZIC2 Zinc finger protein ZIC2 is a protein that in humans is encoded by the ZIC2 gene. ZIC2 is a member of the Zinc finger of the cerebellum (ZIC) protein family. ZIC2 is classified as a ZIC protein due to conservation of the five C2H2 zinc fingers, which enables the protein to interact with DNA and proteins. Correct function of these proteins is critical for early development, and as such mutations of the genes encoding these proteins is known to result in various congenital defects. For example, mutation of ZIC2 is known to result in holoprosencephaly due to defect in the function of the organizer region (node), which leads to a defective anterior notochord (ANC). The ANC provides a maintenance signal to the Prechordal plate (PCP), thus a defective ANC results in degradation of the PCP, which is normally responsible for sending a shh signal to the developing forebrain resulting in the formation of the two hemispheres. Holoprosencephaly is the most common structural anomaly of the human forebrain. Recently ZIC2 has also been shown to be critical for establishment of the left-right axis, thus loss of ZIC2 function can result in defects in heart formation. Another member of the ZIC family, ZIC3, has previously been linked to establishment of the left-right axis. A polyhistidine tract polymorphism in this gene may be associated with increased risk of neural tube defects (spina bifida). This gene is closely linked to a gene encoding ZIC5, a related family member on chromosome 13. ZIC2 has recently been found to interact with TCF7L2, enabling it to act as a Wnt/β-catenin signalling inhibitor. Such a role is of critical importance, as not only is correct Wnt signalling critical for early development, Wnt signalling has also been found to be upregulated to several cancers. ZIC2 has also been shown to interact with GLI3.

wikidoc

/index.php/ZMA_(supplement)

# ZMA (supplement) ZMA (Zinc monomethionine aspartate and Magnesium Aspartate) is a supplement used by bodybuilders and athletes. It was developed by Victor Conte (founder of BALCO Laboratories in Burlingame, California) and is a combination of zinc, magnesium and vitamin B6. The formula is "patent pending" and the name "ZMA" trademarked by SNAC System Inc, also founded by Victor Conte. ZMA is claimed to raise testosterone and IGF-1 levels which may aid in gaining muscle size and strength. It is used as a bodybuilding supplement. ZMA is a combination of two minerals, zinc and magnesium, and Vitamin B-6 or pyridoxine. All three of these compounds are important in biological processes, and while studies have shown that most Americans get enough zinc and Vitamin B6, more than 50% are deficient in magnesium. An increase in exercise can lead to the loss of vitamins and minerals making it particularly important for bodybuilding due to the blood sugar level rises and urination increases, increasing the loss of magnesium, zinc, B12, B6, folic acid, and many other nutrients. Although drinking water re-hydrates an athlete, fruit juice, sports drinks or foods high in water such as vegetables are needed to replenish water-soluble nutrients. The proportion of ingredients generally used in products is 20-30 mg Zinc, 400-500 mg Magnesium and ~10mg B6. According to the label directions, ZMA should be taken before bed on an empty stomach (2 hours after eating your last meal and at least 30 minutes prior to any other supplements). The product should not be taken with calcium. A 1999 study was undertaken on NCAA Football players during an 8 week spring training program. Those who took the ZMA tablets showed greater increases in muscle strength, free testosterone levels, and IGF-1 levels. These ZMA study results were presented by Dr. Brilla (a sports performance researcher at Western Washington University) on June 2, 1999, at the 46th Annual Meeting of the American College of Sports Medicine in Seattle, Washington. This study was funded by SNAC Systems Inc. (the patent holders) and one of the study's authors (Victor Conte) has equity in this company. Another study in 2004 found that ZMA has no effect on strength or hormone levels, but did show a lower rate of muscle catabolism and cited further study was recommended.

wikidoc

/index.php/ZNF74

# ZNF74 ## Contents Zinc finger protein 74 is a protein that in humans is encoded by the ZNF74 gene. Schizophrenia susceptibility has been associated with a mutation in this protein.

wikidoc

/index.php/Zafirlukast

# Zafirlukast Zafirlukast is a anti-Inflammatory , leukotriene pathway inhibitor that is FDA approved for the prophylaxis of and chronic treatment of asthma. Common adverse reactions include headache, nausea, diarrhea, abdominal pain.

wikidoc

/index.php/Zalcitabine

# Zalcitabine (patient information) Zalcitabine can cause severe side effects, such as pancreatitis, severe liver damage or failure, lactic acidosis, and a serious nerve disorder called peripheral neuropathy. Some may even lead to death. Call your doctor immediately if you experience any of the following symptoms: unusual breathing, loss of appetite, upset stomach, vomiting, dark urine, yellowing of the skin, pale stools, stomach pain, or numbness, tingling, burning, or pain in the fingers or toes. Your doctor may have you stop taking your medicine. Zalcitabine is used alone or with other medications to treat human immunodeficiency virus (HIV) infection in patients with acquired immunodeficiency syndrome (AIDS). It will slow the spread of HIV infection in the body. Zalcitabine is not a cure and may not decrease the number of HIV-related illnesses. Zalcitabine does not prevent the spread of HIV to other people. Zalcitabine comes as a tablet to take by mouth. It is usually taken every 8 hours (three times a day). Follow the directions on your prescription label carefully, and ask your doctor or pharmacist to explain any part you do not understand. Take zalcitabine exactly as directed. Do not take more or less of it or take it more often than prescribed by your doctor.

wikidoc

/index.php/Zaldiar

# Zaldiar Zaldiar is a pain killer used to treat moderate to sever pain. It has proven good tolerability in chronic osteoarthritis, back pain and postoperative pain. It is not associated with prostaglandin-mediated side effects which have been reported with COX-2 inhibitors and NSAIDs, such as GI bleeding, renal insufficiency, cardiovascular disease and effect on platelet aggregation.

wikidoc

/index.php/Zanamivir

# Zanamivir Zanamivir is a antiviral agent that is FDA approved for the treatment of influenza and prophylaxis of influenza. Common adverse reactions include sinusitis, dizziness, fever and/or chills, arthralgia and articular rheumatism. Store at 25°C (77°F); excursions permitted to 15° to 30°C (59° to 86°F) (see USP Controlled Room Temperature). Keep out of reach of children. Do not puncture any RELENZA ROTADISK blister until taking a dose using the DISKHALER.

wikidoc

/index.php/Zantrex

# Zantrex ## Contents Zantrex-3 is a herbal supplement marketed by "Zoller Laboratories", a subsidiary of Basic Research of Salt Lake City, Utah. It is marketed towards people under 30 in fast paced television advertisements depicting athletic-looking people. A speaker loudly proclaims Zantrex as "America's number 1 selling weight loss pill!". ## Ingredients Its active ingredients include Yerba Mate, Guarana and regular caffeine. It's estimated that the pill contains as much caffeine as 3-4 cups of coffee . Additional ingredients include green tea extract, Damiana (a South American aphrodisiac), Schizonepeta, Ginseng, Maca root, Niacin and Kola nut. ## Criticism The marketing campaign of the pill has been criticized for its lack of evidence, in the form of scientific studies, listed supporting the claims. One reviewer said, "If you alter your diet accordingly, monitor your caloric intake, and implement a practical exercise program, Zantrex 3 may provide you with an extra edge." ## Pop Culture Near the end of the fifth season of VH1's Celebrity Fit Club, contestant Dustin Diamond gained a pathetic five pounds. At the next weigh-in, just two weeks later, he had lost five pounds. He revealed to the Fit Club panel that he had been taking Zantrex-3 and was pleased that he had undone the damage from the previous weigh-in. At the final weigh-in, another two weeks later, Diamond had lost an additional thirteen pounds. He was criticized extensively by both the panel as well as his fellow contestants for his use of Zantrex-3 as a dietary supplement.

wikidoc

/index.php/Zbigniew_Jaworowski

# Zbigniew Jaworowski Zbigniew Jaworowski is chairman of the Scientific Council of the Central Laboratory for Radiological Protection in Warsaw and former chair of the United Nations Scientific Committee on the Effects of Atomic Radiation. He was a principal investigator of three research projects of the U.S. Environmental Protection Agency and of four research projects of the International Atomic Energy Agency. The author of four books and 300 scientific papers, he has held posts with the Centre d'Etude Nucleaires near Paris; the Biophysical Group of the Institute of Physics, University of Oslo; the Norwegian Polar Research Institute and the National Institute for Polar Research in Tokyo In Jaworowski he (1992) suggested that the long-term CO2, record is an artifact caused by the structural changes of the ice with depth and by postcoring processes. However, increases in CO2, and CH4 concentrations in the Vostok core are similar for the last two glacial-interglacial transitions, even though only the most recent transition is located in the brittle zone. Such evidence argues that the atmospoheric trace-gas signal is not strongly affected by the presence of the brittle zone. Stephen Schneider said of him that "Jaworowski is perhaps even more contrarian than most, claiming that he can prove the climate is going to get colder through his work excavating glaciers on six different continents, which he says indicates what we should really be worrying about is 'The approaching new Ice Age...'." Jaworowski wrote The current sunspot cycle is weaker than the preceding cycles, and the next two cycles will be even weaker. Bashkirtsev and Mishnich (2003) expect that the minimum of the secular cycle of solar activity will occur between 2021 and 2026, which will result in the minimum global temperature of the surface air. The shift from warm to cool climate might have already started.. When approached to see if he would bet on future cooling, Jaworowski denied making any prediction, stating "I do not make my own detailed projections. In my paper I referred the reader to B&M paper, and that is all." Jaworowski has also written that the movement to remove lead from gasoline was based on a "stupid and fraudulent myth," and that lead levels in the human bloodstream are not significantly affected by the use of leaded gasoline.

wikidoc

/index.php/Zbigniew_Religa

# Zbigniew Religa Religa finished his studies at the Medical University of Warsaw in 1963. From 1966 to 1980 he worked in the Szpital Wolski in Warsaw, where he qualified in surgery. In 1973, he visited New York to train in vascular surgery, in 1975 he trained in cardiology in Detroit. In 1973, he obtained an MD degree (which in Poland, unlike most other countries, is a title reserved to physicians with particular academic achievement, similar to a Ph. D.); in 1981 he finished his habilitation, achieving academic recognition similar to an associate professor or senior lecturer. From 1980 to 1984, Religa lectured at the Warsaw Institute of Cardiology. In 1984 he obtained a chair in cardiology and directed the Cardiological Clinic in Zabrze, in 1990 he became full professor at the Silesian Medical University in Katowice, being its rector from 1997 to 1999. In 2001 he returned to Warsaw to become director of both the Cardiological Clinic No. 2 and the Institute of Cardiology. A pioneer in human heart transplantation in Poland, he led the team to prepare the first heart transplantation in the country, and in June 1995 he was the first surgeon to graft an artificial valve created from materials taken from human corpses. In 2004, a team led by Religa obtained a prestigious Brussels Eureka award at the World Exhibition of Innovation, Research and Technology for developing an implantable pump for a pneumatic heart assistance system. Parallel to his work as a physician, Religa has pursued a career in politics. In 1993, he became a member of the Polish senate and was re-elected in 1997 and 2001. As the center and right wing of the Polish political landscape has been in constant flux ever since democracy was reinstated, Religa was a member of several parties and organizations. In 1993, he co-founded the Non-Party Block for Supporting the Reforms (BBWR) which gathered behind president Lech Wałęsa and was its leader in 1994. In 1995, Religa became the chairman of the short-lived party "The Republicans" (Republikaninie) founded by renegade BBWR members who refused to back Wałęsa in the presidential elections of 1995. However, Religa refused to run for president himself, and the Republicans eventually disintegrated when they failed to enter the Sejm in 1997. Religa then joined the newly created Conservative-People's Party (SKL), which became part of the Solidarity Electoral Action (AWS) in 1997. In 2004, Religa was involved in founding the new Centrum Party and became its honorary chairman. Religa was considered a promising candidate in the 2005 Polish presidential elections. In his campaigning, Religa drove on his reputation and image as a successful physician, in January 2005, polls indicated support of more than 65%; in March 2005, with 17%, polls showed him ranking second behind Lech Kaczyński (19%) however as the elections neared he continued to lose support to professional politicians, ending up with only 6% votes in August. On September 2 in a move that gained him great respect in the Polish society, Religa pulled out of the presidential race urging his remaining supporters to vote for the conservative-liberal Donald Tusk from the Civic Platform.

wikidoc

/index.php/Zeaxanthin

# Zeaxanthin Lutein and zeaxanthin have identical chemical formulas and are isomers, but they are not stereoisomers. The main difference between them is in the location of a double bond in one of the end rings. This difference gives lutein three chiral centers whereas zeaxanthin has two. Because of symmetry, the (3R,3'S) and (3S,3'R) stereoisomers of zeaxanthin are identical. Therefore, zeaxanthin has only three stereoisomeric forms. The (3R,3'S) stereoisomer is called meso-zeaxanthin. There is epidemiological evidence of a relationship between low plasma concentrations of lutein and zeaxanthin on the one hand, and the risk of developing age-related macular degeneration (AMD) on the other. Some studies support the view that supplemental lutein and/or zeaxanthin help protect against AMD. Zeaxanthin is one of the most common carotenoid alcohols found in nature. It is the pigment that gives corn, saffron, and many other plants their characteristic color. Zeaxanthin breaks down to form picrocrocin and safranal, which are responsible for the taste and aroma of saffron.

wikidoc

/index.php/Zen_Shiatsu

# Zen Shiatsu Zen Shiatsu is a derivative form of the Japanese therapy Shiatsu, and is particularly popular in the United Kingdom and United States. It was developed by Shizuto Masunaga, a graduate of the Japan Shiatsu College who published a book entitled Shiatsu in 1974. This was translated into English in 1977 and retitled Zen Shiatsu. The name "Zen Shiatsu" was not coined by Masunaga himself but by Wataru Ohashi, the co-author of the English version. Zen Shiatsu, also known as Masunaga Therapy, is a form of Meridian Shiatsu. A difference between Masunaga's Zen Shiatsu and earlier forms of Shiatsu is that Zen Shiatsu uses not only thumbs and palms but also fists, elbows, and knees. Zen Shiatsu represents a return of the values of Traditional Chinese medicine, in comparison with anatomically or physiologically based Shiatsu (cf. Tsubo Shiatsu). While the Namikoshi school emphasizes Westernization at the expense of Chinese medical understanding, Masunaga advocated a return to Chinese Taoist practices such as Do-In and Ankyo within the context of Japanese Shiatsu. The meridian system represents the "crosstalk" between tsubos or acupoints of the human body. It also represents divisions of the complete function of the human organism into discrete spheres of influence. Masunaga advocated treating the whole meridian system through pressure and stretching to achieve systemic change for the entire body. Shizuto Masunaga founded a Japanese institute called the Iokai Center. "Io" means king/master of medicine, and "kai" means group/association. This center continues to the present day, propagating Masunaga's methods. Zen Shiatsu has proven to be widely influential throughout the US and UK. Students of Masunaga include Wataru Ohashi, Pauline Sasaki, Ryokyu Endo and Stephen Brown. The primary precept of Zen Shiatsu is the importance of remaining in a Zen-like, present state when practicing shiatsu; nourishing weak kyo areas and dispersing excess jitsu areas; using two-handed technique to better feel the flow of qi (life force); working from the hara (belly), which is the body's energy center; and using perpendicular pressure to access the qi. Masunaga moreover expanded the meridian system, discovering extensions of the classical Chinese meridians, and developed an effective new system of hara diagnosis predicated on his experience as a Western-trained psychologist.

wikidoc

/index.php/Zestoretic_detailed_information

# Zestoretic detailed information Zestoretic is the trade name of a combination of the drugs hydrochlorothiazide and lisinopril, respectively a diuretic and an ACE inhibitor, to control hypertension. It is a product of AstraZeneca.

wikidoc

/index.php/Zhang_Ji_(Chinese_physician)

# Zhang Ji (Chinese physician) Zhang Ji (Template:Zh-stp, 150 - 219), style name Zhang Zhongjing (Template:Zh-stpw), an Eastern Han (Template:Zh-tp) physician and author of the Shanghan Zabing Lun (Template:Zh-tp, lit. "Treatise on Cold Pathogenic and Miscellaneous Diseases"), was one of the most eminent Chinese physicians during the later years of the Eastern Han era. He lived in today's Nanyang in Henan Province. During his time, with warlords fighting for their own territories, many people were infected with febrile disease. Zhang's family was no exception. He learned medicine by studying from his townsfellow Zhang Bozu, assimilating from previous medicinal literature, and collecting many prescriptions elsewhere, finally writing the medical masterpiece Shanghan Zabing Lun. Unfortunately, shortly after its publication the book was lost during wartime. Due to Zhang's contribution to Traditional Chinese medicine he is often regarded as the sage of Chinese medicine. Zhang's masterpiece was collected by later people and compiled into two books, namely the Shanghan Lun (in full, Shanghan Zabing Lun or "Treatise on Febrile Diseases") which was a discourse on how to treat epidemic infectious diseases causing fevers prevalent during his era, and the other, highly influential doctrine Jingui yaolue (金匱要略, "Synoptic Essentials from the Golden Cabinet"), a compendium of his clinical experiences. He established medication principles and summed up the medicinal experience up until the Han Dynasty, thus making a great contribution to the development of Traditional Chinese Medicine. Though extremely well known in modern Chinese medicine and considered one of the finest Chinese physicians in history very little is known of his life. According to later sources he was born in Nie-Yang (Template:Zh-tp, modern day Nanyang), held an official position in Changsha and lived from approximately 150 to 219CE. Exact dates regarding his birth, death and works vary; an upper limit of 220CD is generally accepted. Revered for authoring the Shāng Hán Zá Bìng Lùn, Zhang Ji is considered to have founded the Cold Damage or "Cold Disease" school of Chinese medicine and is widely considered the seminal expert to this day. For more information on Zhong Ji it is best to refer directly to the Shang Han Lun.

wikidoc

/index.php/Zhang_Zhongjing

# Zhang Zhongjing Zhang Zhongjing (Template:Zh-stpw), formal name Zhang Ji (Template:Zh-stp, 150 - 219), was an Eastern Han physician and one of the most eminent Chinese physicians during the later years of the Eastern Han. He established medication principles and summed up the medicinal experience up until that time, thus making a great contribution to the development of Traditional Chinese Medicine. Though extremely well known in modern Chinese medicine and considered one of the finest Chinese physicians in history very little is known of his life. According to later sources he was born in Nanyang, held an official position in Changsha and lived from approximately 150 to 219CE. Exact dates regarding his birth, death and works vary; an upper limit of 220CD is generally accepted. During his time, with warlords fighting for their own territories, many people were infected with febrile disease. Zhang's family was no exception. He learned medicine by studying from his townsfellow Zhang Bozu, assimilating from previous medicinal literature, and collecting many prescriptions elsewhere, finally writing the medical masterpiece Shanghan Zabing Lun' (Template:Zh-tp, lit. "Treatise on Cold Pathogenic and Miscellaneous Diseases"). Shortly after its publication the book was lost during wartime. Due to Zhang's contribution to Traditional Chinese medicine he is often regarded as the sage of Chinese medicine. Zhang's masterpiece, Shanghan Zabing Lun, was collected by later people and compiled into two books, namely the Shang Han Lun (傷寒論, lit. "On Cold Damage"), which was a discourse on how to treat epidemic infectious diseases causing fevers prevalent during his era, and the other, highly influential doctrine Jinkui Yaolue (金櫃要略, lit. "Essential Prescriptions of the Golden Coffer"), a compendium of his clinical experiences. These two texts have been heavily reconstructed several times up to the modern era. Revered for authoring the Shāng Hán Zá Bìng Lùn, Zhang Zhongjing is considered to have founded the Cold Damage or "Cold Disease" school of Chinese medicine and is widely considered the seminal expert to this day.

wikidoc

/index.php/Ziconotide

# Ziconotide Ziconotide is an N-type calcium channel antagonist that is FDA approved for the {{{indicationType}}} of severe chronic pain in patients for whom intrathecal therapy is warranted, and who are intolerant of or refractory to other treatment, such as systemic analgesics, adjunctive therapies, or intrathecal morphine. There is a Black Box Warning for this drug as shown here. Common adverse reactions include dizziness, nausea, confusional state, nystagmus. Aphasia, areflexia, balance impaired, burning sensation, coordination abnormal, disturbance in attention, dizziness postural, dysarthria, dysgeusia, hypoaesthesia, mental impairment, paraesthesia, sedation, speech disorder, agitation, anxiety, cognitive disorder, confusional state, depression, depression aggravated, disorientation, hallucination, hallucination auditory, hallucination visual, insomnia, irritability, mood disorder, nervousness, paranoia

wikidoc

/index.php/Zidovudine

# Zidovudine Zidovudine is an anti-HIV agent, anti-infective agent that is FDA approved for the treatment of HIV-1, prevention of maternal-fetal HIV-1 transmission. There is a Black Box Warning for this drug as shown here. Common adverse reactions include headache, malaise, nausea, anorexia and vomiting, fever, cough, digestive disorders, anemia, and neutropenia.

wikidoc

/index.php/Ziehl-Neelsen_stain

# Ziehl-Neelsen stain The Ziehl-Neelsen stain, also known as the acid-fast stain, was first described by two German doctors; Franz Ziehl (1859 to 1926), a bacteriologist and Friedrich Neelsen (1854 to 1894), a pathologist. It is a special bacteriological stain used to identify acid-fast Mycobacteria. Mycobacterium tuberculosis is the most important of this group, as it is responsible for the disease called tuberculosis (TB). It can also be used to stain few other bacteria like Nocardia. The reagents used are Ziehl-Neelsen carbolfuchsin, acid alcohol and methylene blue. In 1877 the German pathologist Edwin Klebs (1834 to 1913) whilst at Zürich (Switzerland) published a paper describing an organism he had isolated from tuberculous material and with which he was able to reproduce tuberculosis. He named the organism 'Monas tuberculosum.' In 1880 Dr Max Schuller duplicated the results of Klebs but found that the ability of material to induce tuberculosis persisted only to the second generation. In 1881 Professor Jean Joseph Henri Toussaint of the Veterinary School at Toulouse described similar organisms isolated from the blood of tuberculosis patients. These organisms were from the descriptions undoubtedly micrococci and thus contaminants of the inocula. In 1881 the German physician Emanuel Aufrecht (1844 to 1933) physician-in-chief of the department of internal medicine at the Magdeburg City Hospital described the constant presence of rod shaped bacteria lying within the tubercules. His paper omitted to say how the organisms were demonstrated. In 1882 Robert Koch (1843 to 1910) published a paper in Berlin klin. Wochenschr. 15 wherein he described an unusual bacterium with which he was able to reproduce tuberculosis. The German pathologist Paul Clemens von Baumgarten (1848 to 1928) professor of pathological anatomy at Leipzig published a paper ten days later confirming Koch's findings. Koch's original method of staining the tubercule bacilli was to use an alkaline mixture of aniline dyes. This requires staining for 20 to 24 hours at room temperature or 30 to 60 minutes at 40 °C. On May 1, 1882 Professor Paul Ehrlich (1854-1915) published an improvement on Koch's method. Both methods held that the solution must be alkaline. Ziehl described a new method in a paper published on 12 August 1882 which showed that the solutions could be acidic rather than alkaline. The new stain was less damaging to tissue preparations of tubercules while still permitting the visualisation of the causative organisms. With minor modifications this is the stain in routine use today. These stains were enormously important in convincing doctors and scientists worldwide that the real cause of tuberculosis had been found in contrast to the false positives described earlier.

wikidoc

/index.php/Zika

# Zika virus infection For patient information, click here. Editor-In-Chief: C. Michael Gibson, M.S., M.D. ; Associate Editor(s)-in-Chief: Yazan Daaboul, M.D.; Nate Michalak, B.A.; Luke Rusowicz-Orazem, B.S.; Ilan Dock, B.S.; Serge Korjian M.D.; Yamuna Kondapally, M.B.B.S ; Tarek Nafee, M.D. History and Symptoms | Physical Examination | Laboratory Findings | Evaluation of Pregnant Women | Evaluation of Infants | Collection and Submission of Fetal Tissues | Other Diagnostic Studies

wikidoc

/index.php/Zika_virus

# Zika virus Zika virus infection is caused by Zika virus, an enveloped, single stranded positive sense RNA virus. Zika virus is a type of flavivirus. Mosquitoes are the primary disease vector of Zika virus.

wikidoc

/index.php/Zileuton

# Zileuton Zileuton is a leukotriene synthesis inhibitor that is FDA approved for the treatment of asthma in adults and children 12 years of age and older. Common adverse reactions include sinusitis, nausea, and pharyngolaryngeal pain.

wikidoc