gebhart/patrepeval huggingface dataset:
Manipulation of independent synthesis and degradation of polyphosphate in Escherichia coli for investigation of phosphate secretion from the cell (1997)

The genes involved in polyphosphate metabolism in Escherichia coli were cloned behind different inducible promoters on separate plasmids. The gene coding for polyphosphate kinase (PPK), the enzyme responsible for polyphosphate synthesis, was placed behind the Ptac promoter. Polyphosphatase, a polyphosphate depolymerase, was similarly expressed by using the arabinose-inducible PBAD promoter. The ability of cells containing these constructs to produce active enzymes only when induced was confirmed by polyphosphate extraction, enzyme assays, and RNA analysis. The inducer concentrations giving optimal expression of each enzyme were determined. Experiments were performed in which ppk was induced early in growth, overproducing PPK and allowing large amounts of polyphosphate to accumulate (80 mumol in phosphate monomer units per g of dry cell weight). The ppx gene was subsequently induced, and polyphosphate was degraded to inorganic phosphate. Approximately half of this polyphosphate was depleted in 210 min. The phosphate released from polyphosphate allowed the growth of phosphate-starved cells and was secreted into the medium, leading to a down-regulation of the phosphate-starvation response. In addition, the steady-state polyphosphate level was precisely controlled by manipulating the degree of ppx induction. The polyphosphate content varied from 98 to 12 mumol in phosphate monomer units per g of dry cell weight as the arabinose concentration was increased from 0 to 0.02% by weight.
Primary structure analysis of the major internal protein p24 of human type C T-cell leukemia virus (1982)

A human type C retrovirus [human T-cell leukemia (lymphoma) virus; HTLV], recently isolated from young adult patients with cutaneous T-cell lymphoma or leukemia, was not detectably related to other known animal retroviruses in molecular hybridization studies, by comparison of reverse transcriptase and the major core protein p24. The p24 core protein was purified to homogeneity. The amino acid composition, the COOH-terminal amino acid, and the NH(2)-terminal amino acid sequence of the first 25 residues of this major internal structural protein were determined. These results were then compared to the known structure of the internal core protein of other retroviruses. The compositional data reveal that HTLV p24 is chemically distinct from p30-p24 of other animal retroviruses, in agreement with the earlier immunological analyses. However, HTLV p24 shares the common NH(2)-terminal proline and COOH-terminal leucine of all mammalian type C viral p30s. In addition, like bovine leukemia virus (BLV), HTLV lacks the common prolylleucylarginine tripeptide and the larger conserved region found near the NH(2) terminus of the other mammalian type C viral p30s. Alignment of the amino acid sequence of HTLV p24 with previously determined sequences of other retrovirus proteins, including BLV p24, reveals statistically significant sequence homology only to BLV. The results reported here demonstrate that HTLV p24 is related to but chemically distinct from the major core protein of other retroviruses. Similarly, previous results showed that there was no immunological crossreactivity of the p24 protein and reverse transcriptase of HTLV with other retroviruses, including BLV, and no nucleic acid sequence homology. However, the present results, combined with the common size of the p24 and reverse transcriptase, suggest that HTLV may be closer to BLV than any other known retrovirus.
Inosamycin, a complex of new aminoglycoside antibiotics. II. Structure determination. (1985)

Structures of the new aminocyclitol antibiotics, inosamycins A, B, C, D and E, have been determined by a combination of chemical degradation and spectroscopic studies. They are structurally related to neomycin, paromomycin and ribostamycin but differ in that all the inosamycin components contain 2-deoxy-scyllo-inosamine in place of 2-deoxystreptamine in the known aminoglycoside antibiotics.
Increased amount of nitric oxide in exhaled air of asthmatics (1993)

The presence of nitric oxide (NO) in the exhaled air of humans has recently been described. We wanted to assess at what level exhaled NO originates in normal airways, and to determine whether airway inflammation induces changes in the levels of exhaled NO. Exhaled NO was continuously measured by chemiluminescence technique during normal tidal breathing through the nose or mouth, with a detection limit of 1 part per billion (ppb). Twelve control subjects were compared to eight patients with mild atopic asthma and rhinitis caused by occupational allergen. In control subjects, the major part of NO in exhaled air (up to 30 ppb) seemed to originate in the nasal airways, with only minor contribution from the lower airways and the oral cavity. However, in mild asthmatics, the level of exhaled NO during oral breathing, indicating the involvement of the lower airways, was increased 2-3 fold. Since increased production of NO in the lower airways may involve activated macrophages or neutrophils, we suggest that exhaled NO may be used to instantly monitor ongoing bronchial inflammation, at least when involving inducible NO synthase.
Channel profile optimization and device design for low-power high-performance dynamic-threshold MOSFET (2002)

In this work device design of DTMOS and its parasitic components are studied by experiments and simulations. The gate and the body are tied at the side of the device. Similar gate-body tie can also be accomplished in bulk substrate using multiple-well technology. For a circuit whose speed is predominately determined by wiring capacitances, DTMOS can greatly enhance performance by engineering the vertical doping profiles to scale the depletion width. When the circuit speed is dominated by device capacitances, lateral doping engineering is important to reduce Cbs and Cbd in order to obtain performance improvements, especially in certain logic circuits where Miller effect is important.
Integration of human papillomavirus type 16 DNA into the human genome leads to increased stability of E6 and E7 mRNAs: implications for cervical carcinogenesis. (1995)

In many cervical cancers, human papillomavirus type 16 (HPV-16) DNA genomes are found to be integrated into the host chromosome. In this study, we demonstrate that integration of HPV-16 DNA leads to increased steady-state levels of mRNAs encoding the viral oncogenes E6 and E7. This increase is shown to result, at least in part, from an increased stability of E6 and E7 mRNAs that arise specifically from those integrated viral genomes disrupted in the 3' untranslated region of the viral early region. Further, we demonstrate that the A+U-rich element within this viral early 3' untranslated region confers instability on a heterologous mRNA. We conclude that integration of HPV-16 DNA, as occurs in cervical cancers, can result in the increased expression of the viral E6 and E7 oncogenes through altered mRNA stability.
Cytokine production by peripheral blood monocytes/macrophages in multiple sclerosis patients (1993)

To determine the function of monocytes/macrophages in the acute phase of multiple sclerosis (MS), we investigated the production of tumor necrosis factor alpha (TNF alpha), interleukin-1 alpha (IL-1 alpha), IL-1 beta and IL-6 by peripheral blood monocytes/macrophages (PBM) in patients with MS, other autoimmune neurological disease (OAND), other neurological disease (OND) and normal controls was assessed using enzyme-linked immunosorbent assay (ELISA). When stimulated with lipopolysaccharide or phorbol ester, PBM obtained during acute phase of MS relapse patients produced significantly higher amounts of all these cytokines than did PBM from patients with chronic stable MS or OAND or OND or from normal controls. The results suggest a possible role of activated monocytes/macrophages in the acute exacerbation of MS.
The structure of tumor necrosis factor-alpha at 2.6 A resolution. Implications for receptor binding. (1989)

The three-dimensional structure of tumor necrosis factor (TNF-alpha), a protein hormone secreted by macrophages, has been determined at 2.6 A resolution by x-ray crystallography. Phases were determined by multiple isomorphous replacement using data collected from five heavy atom derivatives. The multiple isomorphous replacement phases were further improved by real space symmetry averaging, exploiting the noncrystallographic 3-fold symmetry of the TNF-alpha trimer. An atomic model corresponding to the known amino acid sequence of TNF-alpha was readily built into the electron density map calculated with these improved phases. The 17,350-dalton monomer forms an elongated, antiparallel beta-pleated sheet sandwich with a "jelly-roll" topology. Three monomers associate intimately about a 3-fold axis of symmetry to form a compact bell-shaped trimer. Examination of the model and comparison to known protein structures reveals striking structural homology to several viral coat proteins, particularly satellite tobacco necrosis virus. Locations of residues conserved between TNF-alpha and lymphotoxin (TNF-beta, a related cytokine known to bind to the same receptors as TNF-alpha) suggest that lymphotoxin, like TNF-alpha, binds to the receptor as a trimer and that the general site of interaction with the receptor is at the "base" of the trimer.
Endocrine patterns in patients with benign and malignant prostatic diseases (2000)

BACKGROUND The known importance of the endocrine system, particularly of steroid hormones, for development of the prostate gland and the fact that steroid hormones act as immunmodulators prompted us to compare hypophyseal, adrenal, and gonadal hormones, including cortisol, in patients with benign and malignant prostatic diseases. METHODS Patients with newly diagnosed, untreated prostate cancer (PC) (n = 75) and, as a control population, those with untreated lower urinary tract symptoms (LUTS) due to benign prostatic hyperplasia (BPH) (n = 159) entered this prospective study. In all patients, the following parameters were obtained by serum analysis: prostate-specific antigen (PSA), human luteinizing hormone (hLH), human follicle-stimulating hormone (hFSH), testosterone, estradiol (E2), cortisol, and dehydroepiandrosterone-sulphate (DHEA-S). Serum samples were collected of fasting patients between 7.30–10.00 AM. RESULTS Age was comparable in both groups (PC: 65.6 ± 7.6 years (mean ± standard deviation) vs. controls: 64.9 ± 8.1 years; P = 0.56). HFSH (PC: 6.6 ± 3.9 mIU/ml; controls: 8.4 ± 6.4 mIU/ml; P = 0.04), hLH (PC: 5.3 ± 4.8mIU/ml; controls: 7.6 ± 6.2 mIU/ml; P = 0.009), and estradiol (PC: 25.8 ± 12.7 pg/ml; controls: 32.6 ± 12.6 pg/ml; P = 0.0003) were significantly lower in PC patients than controls. Cortisol (PC: 16.7 ± 4.2 μg/dl; controls: 13.5 ± 4.3 μg/dl; P < 0.0001) was significantly higher in cases. The difference for cortisol and estradiol concentrations between PC patients and controls held true in all life-decades. Serum concentrations for DHEA-S and testosterone were comparable between PC and control patients. In PC patients, none of the endocrine parameters correlated to serum PSA or clinical/pathological stage. CONCLUSIONS Patients with newly diagnosed, untreated PC yielded significantly higher cortisol and lower estradiol serum concentrations than controls. The known effect of cortisol on the immune status warrants further studies. Prostate 44:219–224, 2000. © 2000 Wiley-Liss, Inc.
Genes, Assisted Reproductive Technology and Trans -illumination (2013)

Genomic imprinting is a parent-of-origin allele-specific epigenetic process that is critical for normal development and health. The establishment and maintenance of normal imprinting is dependent on both cis-acting imprinting control centers, which are marked by differentially (parental allele specific) methylated marks, and trans mechanisms, which regulate the establishment and/or maintenance of the correct methylation epigenotype at the imprinting control centers. Studies of rare human imprinting disorders such as familial hydatidiform mole, Beckwith-Wiedemann syndrome and familial transient neonatal diabetes mellitus have enabled the identification of genetic (e.g., mutations in KHDC3L [C6ORF221], NLRP2 [NALP2], NLRP7 [NALP7] and ZFP57) and environmental (assisted reproductive technologies) factors that can disturb the normal trans mechanisms for imprinting establishment and/or maintenance. Here we review the clinical and molecular aspects of these imprinting disorders in order to demonstrate how the study of rare inherited disorders can illuminate the molecular characteristics of fundamental epigenetic processes, such as genomic imprinting.
Complement Factor H Variant Increases the Risk of Age-Related Macular Degeneration (2005)

Age-related macular degeneration (AMD) is a leading cause of visual impairment and blindness in the elderly whose etiology remains largely unknown. Previous studies identified chromosome 1q32 as harboring a susceptibility locus for AMD. We used single-nucleotide polymorphisms to interrogate this region and identified a strongly associated haplotype in two independent data sets. DNA resequencing of the complement factor H gene within this haplotype revealed a common coding variant, Y402H, that significantly increases the risk for AMD with odds ratios between 2.45 and 5.57. This common variant likely explains approximately 43% of AMD in older adults.
Cellular pathology changes in rat skin following intradermal injection of nerve growth factor: neutrophil‐dependent and ‐independent events (2002)

Nerve growth factor (NGF) regulates the survival and development of specific populations of neurones and is involved in wound healing. A further area of study relating to the role of neurotrophins in the mature animal has concerned the possibility that NGF may be a pivotal mediator of inflammation and pain. It has previously been shown that injection of intradermal NGF can result in a neutrophil-dependent hyperalgesia in the rat. The purpose of the present study was to examine the pathological consequence of NGF injected intradermally into mature rat skin and to examine further the role of neutrophils. Standard histopathology techniques (H & E) were employed to determine inflammatory cell counts. Circulating neutrophils were depleted using an anti-rat neutrophil antiserum and results were compared to treatment with vehicle controls. Saline-pretreated rats exhibited normal circulating neutrophil numbers and the dorsal skin showed a significant increase of neutrophil and macrophages at 3 and 5 h and lymphocytes at 5 h after NGF treatment. By comparison, skin sites from neutrophil-depleted rats did not demonstrate a significant increase in neutrophil and macrophage accumulation after NGF administration. All NGF-treated sites, independent of pretreatment, demonstrated abnormal muscle fibre morphology and proliferation of the muscle sarcolemmal nuclei after NGF injection, indicative of tissue injury. In addition, oedema and some fibroplasia were also noted. Furthermore, fibrin production was increased at 3 and 5 h after NGF administration. It is suggested that NGF has a damaging effect on rat muscle which is independent of accumulating neutrophil and other inflammatory cells. In conclusion, the findings indicate a link between NGF-induced neutrophil and macrophage accumulation, as the increase in dermal macrophages was not observed in neutrophil-depleted rats. The results also suggest that NGF can have a profound effect on rat muscle and that this effect may be related to muscle regeneration.
Hemoglobin parameters from diffuse reflectance data (2014)

Tissue vasculature is altered when cancer develops. Consequently, noninvasive methods of monitoring blood vessel size, density, and oxygenation would be valuable. Simple spectroscopy employing fiber optic probes to measure backscattering can potentially determine hemoglobin parameters. However, heterogeneity of blood distribution, the dependence of the tissue-volume-sampled on scattering and absorption, and the potential compression of tissue all hinder the accurate determination of hemoglobin parameters. We address each of these issues. A simple derivation of a correction factor for the absorption coefficient, μa, is presented. This correction factor depends not only on the vessel size, as others have shown, but also on the density of blood vessels. Monte Carlo simulations were used to determine the dependence of an effective pathlength of light through tissue which is parameterized as a ninth-order polynomial function of μa. The hemoglobin bands of backscattering spectra of cervical tissue are fit using these expressions to obtain effective blood vessel size and density, tissue hemoglobin concentration, and oxygenation. Hemoglobin concentration and vessel density were found to depend on the pressure applied during in vivo acquisition of the spectra. It is also shown that determined vessel size depends on the blood hemoglobin concentration used.
Speech Signal Extraction Utilizing PCA-ICA Algorithm With a Non-Uniform Spacing Microphone Array (2006)

Speech signal extraction is becoming more and more important as evidently displayed by its numerous applications such as mobile phones, conference equipments and surveillance. This paper presents a blind method to enhance a speech source of interest in noisy environments. The proposed technique consists of the principal component analysis (PCA) and the independent component analysis (ICA) to extract the speech signal. In an effort to overcome the small phase resolution due to the constraint on the inter-element distance, a non-uniform spacing PCA-ICA algorithm is suggested. By utilizing a different inter-element distance processing on each pair of microphones in a multistage fashion, a better separation is achieved. Results show better separation performance for the proposed method compared to the uniformly spaced microphone array.
Overexpression, Purification, and Characterization of the SbcCD Protein from Escherichia coli (1997)

The sbcC and sbcD genes mediate palindrome inviability in Escherichia coli. The sbcCD operon has been cloned into the plasmid pTrc99A under the control of the strong trc promoter and introduced into a strain carrying a chromosomal deletion of sbcCD. The SbcC and SbcD polypeptides were overexpressed to 6% of total cell protein, and both polypeptides copurified in a four-step purification procedure. Purified SbcCD is a processive double-strand exonuclease that has an absolute requirement for Mn2+ and uses ATP as a preferred energy source. Gel filtration chromatography and sedimentation equilibrium analyses were used to show that the SbcC and SbcD polypeptides dissociate at some stage after purification and that this dissociation is reversed by the addition of Mn2+. We demonstrate that SbcD has the potential to form a secondary structural motif found in a number of protein phosphatases and suggest that it is a metalloprotein that contains the catalytic center of the SbcCD exonuclease.
Evaluation of a decision support system for pressure ulcer prevention and management: preliminary findings. (1997)

A decision support system for prevention and management of pressure ulcers was developed based on AHCPR guidelines and other sources. The system was implemented for 21 weeks on a 20-bed clinical care unit. Fifteen nurses on that unit volunteered as subjects of the intervention to see whether use of the system would have a positive effect on their knowledge about pressure ulcers and on their decision-making skills related to this topic. A similar care unit was used as a control. In addition, the system was evaluated by experts for its instructional adequacy, and by end users for their satisfaction with the system. Preliminary results show no effect on knowledge about pressure ulcers and no effect on clinical decision making skills. The system was rated positively for instructional adequacy, and positively for user satisfaction. User interviews related to satisfaction supplemented the quantitative findings. A discussion of the issues of conducting experiments like this in today's clinical environment is included.
Expression of Inhibin/Activin Subunit Messenger Ribonucleic Acids during Rat Embryogenesis* (1991)

Inhibin (alpha/beta) and activin (beta/beta) were first recognized as gonadal hormones that regulate the production and release of FSH from the anterior pituitary gland. Studies now show that these proteins, which are members of the transforming growth factor-beta (TGF beta) superfamily, and their corresponding messenger RNAs have a broad anatomical distribution and may regulate the growth and differentiation of a variety of cell types. To determine whether inhibin and activin may also play a role in embryonic development, in situ hybridization techniques were utilized to examine the localization of the mRNAs encoding the inhibin/activin subunits (alpha, beta A, beta B) in rat embryos from 12 days post coitum (p.c.) until birth. The beta A-subunit message was localized in the heart at 12 days p.c. and in the dermal layer of the skin starting at 13 days p.c. At 14 days p.c. this mRNA was first observed in the whisker follicles, in the developing skeleton of the snout, limbs, and in the intervertebral disks. At 16 days p.c. the beta A-message was found in the striatum of the brain, and at 18 days p.c. it was also detected in the cerebral cortex. The beta A-mRNA signal appeared in hair bulbs at 17 days p.c., in teeth at 18 days p.c., and in tendons and gonads just before birth. Expression of beta A-mRNA was no longer detected in the skin or intervertebral disks after 17 days p.c. The beta B-subunit message was found in the area of rapidly dividing cells surrounding the forebrain ventricle, starting at 14 days p.c., in the gonads from the time of gonadal sexual differentiation, at 14 days p.c., and in the salivary gland as early as 17 days p.c. The beta B-message continued to be expressed in these areas throughout embryogenesis. The inhibin-alpha subunit message was also detectable in the gonads from 14 days p.c. until birth. These data suggest that 1) inhibin and activin may be produced in the gonads and possibly play a hormonal role in the embryonic rat during the last trimester of pregnancy, and 2) activin may regulate aspects of the embryonic development of the heart, skin, hair and whiskers, cartilage, bone, tendons, teeth, salivary gland, brain, and gonads, possibly in coordination with other members of the TGF beta superfamily whose mRNAs are expressed in some of these same tissues during development.