gebhart/patrepeval huggingface dataset:
vic-DICARBOXYLIC ACID DERIVATIVES OF PYRAZOLE, ISOXAZOLE, AND PYRIMIDINE (1955)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTvic-DICARBOXYLIC ACID DERIVATIVES OF PYRAZOLE, ISOXAZOLE, AND PYRIMIDINER. G. JONES and C. W. WHITEHEADCite this: J. Org. Chem. 1955, 20, 10, 1342–1347Publication Date (Print):October 1, 1955Publication History Published online1 May 2002Published inissue 1 October 1955https://pubs.acs.org/doi/10.1021/jo01127a008https://doi.org/10.1021/jo01127a008research-articleACS PublicationsRequest reuse permissionsArticle Views457Altmetric-Citations30LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InRedditEmail Other access optionsGet e-Alertsclose Get e-Alerts
Fusion properties of cells persistently infected with human parainfluenza virus type 3: participation of hemagglutinin-neuraminidase in membrane fusion (1991)

Cells persistently infected with human parainfluenza virus type 3 (HPF3) exhibit a novel phenotype. They are completely resistant to fusion with each other but readily fuse with uninfected cells. We demonstrate that the inability of these cells to fuse with each other is due to a lack of cell surface neuraminic acid. Neuraminic acid is the receptor for the HPF3 hemagglutinin-neuraminidase (HN) glycoprotein, the molecule responsible for binding of the virus to cell surfaces. Uninfected CV-1 cells were treated with neuraminidase and then tested for their ability to fuse with the persistently infected (pi) cells. Neuraminidase treatment totally abolished cell fusion. To extend this result, we used a cell line deficient in sialic acid and demonstrated that these cells, like the neuraminidase-treated CV-1 cells, were unable to fuse with pi cells. We then tested whether mimicking the agglutinating function of the HN molecule with lectins would result in cell fusion. We added a panel of five lectins to the neuraminic acid-deficient cells and showed that binding of these cells to the pi cells did not result in fusion; the lectins could not substitute for interaction of neuraminic acid with the HN molecule in promoting membrane fusion. These results provide compelling evidence that the HN molecule of HPF3 and its interaction with neuraminic acid participate in membrane fusion and that cell fusion is mediated by an interaction more complex than mere juxtaposition of the cell membranes.
Genomic Analysis of Transgenic Animals: Southern Blotting (2003)

Although subsequent generations can be rapidly screened using slot blotting (Chapter 35) or the polymerase chain reaction (PCR; Chapter 36), founder transgenic animals should initially be analyzed by Southern blotting for two reasons. First, low copy number transgenics or mosaic transgenics (where only a small number of the cells in a biopsy may be transgenic, and hence the effective copy number of the transgene in the DNA preparation is less than one) may not be clearly identifiable using slot blots because of high background. Such animals can, however, be unambiguously identified by the presence of bands of predicted sizes on Southern blot filters. Note that PCR can also clearly detect low copy-number transgenes. Second, both slot blot and PCR are unable to give direct information on transgene copy number, transgene integrity (i.e., the presence or absence of gross deletions, insertions, and so forth), and the number of independent transgene integration sites. Careful choice of restriction enzymes used to cleave the DNA, followed by Southern blotting, can reveal information about all of these features of a transgenic animal.
Glucagon-Like Peptide-1 (2001)

There is a progressive impairment in beta-cell function with age. As a result, 19 percent of the U.S. population over the age of 65 is diagnosed with type 2 diabetes mellitus (DM). Glucagon-like peptide-1 (GLP-1) is a potent insulin secretagogue that has multiple synergetic effects on the glucose-dependent insulin secretion pathways of the beta-cell. This peptide and its longer-acting analog exendin-4 are currently under review as treatments for type 2 DM. In our work on the rodent model of glucose intolerance in aging, we found that GLP-1 is capable of rescuing the age-related decline in beta-cell function. We have shown that this is due to the ability of GLP-1 to 1) recruit beta-cells into a secretory mode; 2) upregulate the genes of the beta-cell glucose-sensing machinery; and 3) cause beta-cell differentiation and neogenesis. Our investigations into the mechanisms of action of GLP-1 began by using the reverse hemolytic plaque assay to quantify insulin secretion from individual cells of the RIN 1046-38 insulinoma cell line in response to acute treatment with the peptide. GLP-1 increases both the number of cells secreting insulin and the amount secreted per cell. This response to GLP-1 is retained even in the beta cell of the old (i.e., 22-month), glucose-intolerant Wistar rat, which exhibits a normal, first-phase insulin response to glucose following an acute bolus of GLP-1. Preincubation with GLP-1 (24 hours) potentiates glucose- and GLP-1-dependent insulin secretion and increases insulin content in the insulinoma cells. Treatment of old Wistar rats for 48 hours with GLP-1 leads to normalization of the insulin response and an increase in islet insulin content and mRNA levels of GLUT 2 and glucokinase. PDX-1, a transcriptional factor activator of these three genes, also is upregulated in the insulinoma cell line in aged rats and diabetic mice following treatment with GLP-1. Administration of GLP-1 to old rats leads to pancreatic cell proliferation, insulin-positive clusters, and an increase in beta-cell mass. This evidence led us to believe that GLP-1 is an endocrinotrophic factor. We used an acinar cell line to show that GLP-1 can directly cause the conversion of a putative pro-endocrine cell into an endocrine one. Thus, the actions of GLP-1 on the beta-cell are complex, with possible benefits to the diabetic patient that extend beyond a simple glucose-dependent increase in insulin secretion. The major limitation to GLP-1 as a clinical treatment is its short biological half-life. We have shown that the peptide exendin-4, originating in the saliva of the Gila monster, exhibits the same insulinotropic and endocrinotrophic properties as GLP-1 but is more potent and longer acting in rodents and humans.
Fire Protection of LPG Storage Tanks - Reduction of Project Risks (1996)

There are inherent risks in the application of passive fire protection materials. The reduction of these risks in the scoping phase of such a project ensured a successful outcome at the ESSO Long Island Point fractionation plant. The upgrade of the 19 LPG pressurised storage started in 1992 and completed in 1994 was one of the largest such upgrades undertaken in Australia. The project itself was the result of an internal audit and risk assessment performed by the company. The presentation deals with two aspects of risk; risks associated with the storage of LPG and with the implementation of the project. An intensive research programme was undertaken to reduce project risks and to formulate an optimal specification for the application of material. There are a number of crucial lessons to be learned. Risks and risk reduction steps were analysed using risk concepts and tools of risk assessment.
Proton nuclear magnetic resonance studies of hemoglobins M Boston (.alpha.58E7 His .fwdarw. Tyr) and M Milwaukee (.beta.67E11 Val .fwdarw. Glu): spectral assignments of hyperfine-shifted proton resonances and of proximal histidine (E7) NH resonances to the .alpha. and .beta. chains of normal human adult hemoglobin (1980)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTProton nuclear magnetic resonance studies of hemoglobins M Boston (.alpha.58E7 His .fwdarw. Tyr) and M Milwaukee (.beta.67E11 Val .fwdarw. Glu): spectral assignments of hyperfine-shifted proton resonances and of proximal histidine (E7) NH resonances to the .alpha. and .beta. chains of normal human adult hemoglobinSeizo Takahashi, Allison Lin, K. L. C., and Chien HoCite this: Biochemistry 1980, 19, 23, 5196–5202Publication Date (Print):November 11, 1980Publication History Published online1 May 2002Published inissue 11 November 1980https://pubs.acs.org/doi/10.1021/bi00564a007https://doi.org/10.1021/bi00564a007research-articleACS PublicationsRequest reuse permissionsArticle Views79Altmetric-Citations55LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InRedditEmail Other access optionsGet e-Alertsclose Get e-Alerts
Deimination of Myelin Basic Protein. 2. Effect of Methylation of MBP on Its Deimination by Peptidylarginine Deiminase (2000)

Deimination of myelin basic protein (MBP) has been implicated in the chemical pathogenesis of multiple sclerosis (MS). Degradation of bovine MBP by cathepsin D, a myelin-associated protease, was increased when 6 arginyl residues were deiminated and became very rapid when all 18 arginyl residues were deiminated. Since MBP contains a number of modifications, including methylation, phosphorylation, etc., we studied the effect of methylation, an irreversible modification, to determine how this modification affected deimination. Methylation of Arg 106 in bovine MBP (Arg 107 in human), a naturally occurring modification of MBP, has been shown to affect the deimination of arginyl residues in the present study. Since fractionation of MBP into unmethylated, monomethylated, and dimethylated species cannot be done readily on a preparative scale, mass spectrometry with the Q-TOF instrument resolved these species readily since each differed from the other by 14 atomic mass units (amu). Examination of five different hMBP samples, two from normal brain and three from MS brain, revealed that increased deimination of arginyl residues correlated with a decreased methylation of Arg 107 (human sequence). To study this process in vitro, bovine MBP (bMBP) was used. Component 1 (C-1) is the most cationic of the MBP "charge isomers" and the most unmodified, in which all arginyl residues are intact. It was deiminated to various extents with purified bovine brain peptidylarginine deiminase, generating a number of species containing 0-13.7 mol of citrulline/mol of bMBP. Mass spectrometry of each of these species permitted us to determine the influence of methylation of Arg 106 (bovine sequence) on deimination by this enzyme. We found that bMBP with unmethylated arginine was deiminated at a rate of 0.081 mol of citrulline/min, with monomethylarginine, 0.068 mol of citrulline/min, and with dimethylarginine, 0.036 mol of citrulline/min. We suggest that the methylated arginyl residue becomes sequestered in the hydrophobic beta-sheet structure and disrupts the three-dimensional structure of the protein so that other arginyl residues are less accessible to peptidylarginine deiminase.
HistoneHits: A database for histone mutations and their phenotypes (2009)

Histones are the basic protein components of nucleosomes. They are among the most conserved proteins and are subject to a plethora of post-translational modifications. Specific histone residues are important in establishing chromatin structure, regulating gene expression and silencing, and responding to DNA damage. Here we present HistoneHits, a database of phenotypes for systematic collections of histone mutants. This database combines assay results (phenotypes) with information about sequences, structures, post-translational modifications, and evolutionary conservation. The web interface presents the information through dynamic tables and figures. It calculates the availability of data for specific mutants and for nucleosome surfaces. The database currently includes 42 assays on 677 mutants multiply covering 405 of the 498 residues across yeast histones H3, H4, H2A, and H2B. We also provide an interface with an extensible controlled vocabulary for research groups to submit new data. Preliminary analyses confirm that mutations at highly conserved residues and modifiable residues are more likely to generate phenotypes. Buried residues and residues on the lateral surface tend to generate more phenotypes, while tail residues generate significantly fewer phenotypes than other residues. Yeast mutants are cross referenced with known human histone variants, identifying a position where a yeast mutant causes loss of ribosomal silencing and a human variant increases breast cancer susceptibility. All data sets are freely available for download.
TL1A–DR3 interaction regulates Th17 cell function and Th17-mediated autoimmune disease (2008)

T helper type 17 (Th17) cells play an important pathogenic function in autoimmune diseases; their regulation, however, is not well understood. We show that the expression of a tumor necrosis factor receptor family member, death receptor 3 (DR3; also known as TNFRSF25), is selectively elevated in Th17 cells, and that TL1A, its cognate ligand, can promote the proliferation of effector Th17 cells. To further investigate the role of the TL1A-DR3 pathway in Th17 regulation, we generated a TL1A-deficient mouse and found that TL1A(-/-) dendritic cells exhibited a reduced capacity in supporting Th17 differentiation and proliferation. Consistent with these data, TL1A(-/-) animals displayed decreased clinical severity in experimental autoimmune encephalomyelitis (EAE). Finally, we demonstrated that during EAE disease progression, TL1A was required for the optimal differentiation as well as effector function of Th17 cells. These observations thus establish an important role of the TL1A-DR3 pathway in promoting Th17 cell function and Th17-mediated autoimmune disease.
Canonical Möbius subdivision (2018)

We present a novel framework for creating Möbius-invariant subdivision operators with a simple conversion of existing linear subdivision operators. By doing so, we create a wide variety of subdivision surfaces that have properties derived from Möbius geometry; namely, reproducing spheres, circular arcs, and Möbius regularity. Our method is based on establishing a canonical form for each 1-ring in the mesh, representing the class of all 1-rings that are Möbius equivalent to that 1-ring. We perform a chosen linear subdivision operation on these canonical forms, and blend the positions contributed from adjacent 1-rings, using two novel Möbius-invariant operators, into new face and edge points. The generality of the method allows for easy coarse-to-fine mesh editing with diverse polygonal patterns, and with exact reproduction of circular and spherical features. Our operators are in closed-form and their computation is as local as the computation of the linear operators they correspond to, allowing for efficient subdivision mesh editing and optimization.
Serologic Markers in Inflammatory Bowel Disease (2005)

Inflammatory bowel disease (IBD) is an enduring disease involving mostly young people, with symptoms of bloody diarrhea and abdominal cramps. Several antibodies have been associated with IBD, the 2 most comprehensively studied being autoantibodies to neutrophils (atypical perinuclear anti-neutrophil cytoplasmic antibodies) and anti-Saccharomyces cerevisiae antibodies. This review focuses on the value of these antibodies for diagnosing IBD, differentiating Crohn disease from ulcerative colitis, indeterminate colitis, monitoring disease, defining clinical phenotypes, predicting response to therapy, and as subclinical markers. Pancreatic antibodies and newly identified anti-microbial antibodies (anti-outer membrane porin C, anti-I2, and anti-flagellin) are also reviewed.
Effects of sodium citrate, potassium citrate, and citric acid in preventing experimental calcium oxalate urolithiasis in rats. (1987)

Male Wistar-strain rats which had been fed a glycolic-acid diet developed severe nephrocalcinosis with urinary calculi within 4 weeks. Rats fed the same diet with citrate salts added had, however, either slight or no nephrocalcinosis without any stones in the urinary system. Nephrocalcinosis intermediate between those in the citrate groups and the glycolic-acid group, with some urinary calculi, was observed in the citric-acid group. During the experiment, the urinary oxalate concentration increased markedly and was higher in the citrate and citric-acid than in the glycolic-acid group. The urinary citrate concentration was significantly higher in the citrate groups and lower in the citric acid and glycolic-acid groups. Therefore, citrate salts can be concluded to inhibit nephrocalcinosis and calculi formation as a result of decreased urinary saturation by means of increase in urinary citrate, in spite of a slight increase in the urinary oxalate.
Molecular alterations in sarcomas (2001)

Within the last decade, advances in tumor cytogenetics and molecular biology have led to an explosion of information related to the underlying molecular alterations in sarcomas. Many sarcomas have characteristic genetic findings that shed light on mechanisms of tumorigenesis, serve as diagnostic and/or prognostic markers, give clues to relationships between different sarcomas, and reveal targets for biologically rational therapies. This review summarizes recent progress in this fast-moving field, with particular emphasis on newly characterized genetic alterations present in inflammatory myofibroblastic tumor, alveolar soft part sarcoma, lipoblastoma, and angiomatoid fibrous histiocytoma. Also emphasized are developments in “genetic” diagnostics, new insights into the relationships between different entities, prognostic implications of genetic alterations, the development of an animal model for liposarcoma, and the validation of a rational therapy for gastrointestinal stromal tumors.
Lumbar discography: A comprehensive review of outcome studies, diagnostic accuracy, and principles (2005)

Although discography, especially combined with CT scanning, may be more accurate than other radiologic studies in detecting degenerative disc disease, its ability to improve surgical outcomes has yet to be proven. In the United States and Europe, there are inconsistencies in the use of lumbar discography such that it is routinely used before IDET, yet only occasionally used before spinal fusion.
Percutaneous drainage of postoperative intraabdominal abscesses (1982)

Twenty-two major intraabdominal abscesses in 19 postoperative patients were drained percutaneously using cross-sectional imaging techniques (computed tomography and sonography) for localization. Sixteen lesions were cured in 14 patients without reexploration. All patients were palliated by the percutaneous drainage procedure. All 22 abscess cavities were entered without complication or compromise of adjacent normal organs. Percutaneous abscess drainage is recommended as a safe, effective method of treating a major intraabdominal abscess in the postoperative patient.
Identification and Characterization of the Potential Promoter Regions of 1031 Kinds of Human Genes (2001)

To understand the mechanism of transcriptional regulation, it is essential to identify and characterize the promoter, which is located proximal to the mRNA start site. To identify the promoters from the large volumes of genomic sequences, we used mRNA start sites determined by a large-scale sequencing of the cDNA libraries constructed by the "oligo-capping" method. We aligned the mRNA start sites with the genomic sequences and retrieved adjacent sequences as potential promoter regions (PPRs) for 1031 genes. The PPR sequences were searched to determine the frequencies of major promoter elements. Among 1031 PPRs, 329 (32%) contained TATA boxes, 872 (85%) contained initiators, 999 (97%) contained GC box, and 663 (64%) contained CAAT box. Furthermore, 493 (48%) PPRs were located in CpG islands. This frequency of CpG islands was reduced in TATA(+)/Inr(+) PPRs and in the PPRs of ubiquitously expressed genes. In the PPRs of the CGM2 gene, the DRA gene, and the TM30pl genes, which showed highly colon specific expression patterns, the consensus sequences of E boxes were commonly observed. The PPRs were also useful for exploring promoter SNPs.
The Innate Mononuclear Phagocyte Network Depletes B Lymphocytes through Fc Receptor–dependent Mechanisms during Anti-CD20 Antibody Immunotherapy (2004)

Anti-CD20 antibody immunotherapy effectively treats non-Hodgkin's lymphoma and autoimmune disease. However, the cellular and molecular pathways for B cell depletion remain undefined because human mechanistic studies are limited. Proposed mechanisms include antibody-, effector cell-, and complement-dependent cytotoxicity, the disruption of CD20 signaling pathways, and the induction of apoptosis. To identify the mechanisms for B cell depletion in vivo, a new mouse model for anti-CD20 immunotherapy was developed using a panel of twelve mouse anti-mouse CD20 monoclonal antibodies representing all four immunoglobulin G isotypes. Anti-CD20 antibodies rapidly depleted the vast majority of circulating and tissue B cells in an isotype-restricted manner that was completely dependent on effector cell Fc receptor expression. B cell depletion used both FcgammaRI- and FcgammaRIII-dependent pathways, whereas B cells were not eliminated in FcR common gamma chain-deficient mice. Monocytes were the dominant effector cells for B cell depletion, with no demonstrable role for T or natural killer cells. Although most anti-CD20 antibodies activated complement in vitro, B cell depletion was completely effective in mice with genetic deficiencies in C3, C4, or C1q complement components. That the innate monocyte network depletes B cells through FcgammaR-dependent pathways during anti-CD20 immunotherapy has important clinical implications for anti-CD20 and other antibody-based therapies.
No. V. November 29 (2012)

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