gebhart/patrepeval huggingface dataset:
Haplotype and Cell Proliferation Analyses of Candidate Lung Cancer Susceptibility Genes on Chromosome 15q24-25.1 (2009)

Recent genome-wide association studies have linked the chromosome 15q24-25.1 locus to nicotine addiction and lung cancer susceptibility. To refine the 15q24-25.1 locus, we performed a haplotype-based association analysis of 194 familial lung cases and 219 cancer-free controls from the Genetic Epidemiology of Lung Cancer Consortium (GELCC) collection, and used proliferation and apoptosis analyses to determine which gene(s) in the 15q24-25.1 locus mediates effects on lung cancer cell growth in vitro. We identified two distinct subregions, hapL (P = 3.20 x 10(-6)) and hapN (P = 1.51 x 10(-6)), which were significantly associated with familial lung cancer. hapL encompasses IREB2, LOC123688, and PSMA4, and hapN encompasses the three nicotinic acetylcholine receptor subunit genes CHRNA5, CHRNA3, and CHRNB4. Examination of the genes around hapL revealed that PSMA4 plays a role in promoting cancer cell proliferation. PSMA4 mRNA levels were increased in lung tumors compared with normal lung tissues. Down-regulation of PSMA4 expression decreased proteasome activity and induced apoptosis. Proteasome dysfunction leads to many diseases including cancer, and drugs that inhibit proteasome activity show promise as a form of cancer treatment. Genes around hapN were also investigated, but did not show any direct effect on lung cancer cell proliferation. We concluded that PSMA4 is a strong candidate mediator of lung cancer cell growth, and may directly affect lung cancer susceptibility through its modulation of cell proliferation and apoptosis.
Theory of Alternating Current Polarography (1961)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTTheory of Alternating Current PolarographyW. H. Reinmuth and D. E. SmithCite this: Anal. Chem. 1961, 33, 7, 964–966Publication Date (Print):June 1, 1961Publication History Published online1 May 2002Published inissue 1 June 1961https://pubs.acs.org/doi/10.1021/ac60175a047https://doi.org/10.1021/ac60175a047research-articleACS PublicationsRequest reuse permissionsArticle Views54Altmetric-Citations8LEARN 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
Antioncogenes and human cancer. (1993)

The antioncogenes, or tumor suppressor genes, as negative regulators of cell division, stand in contrast to oncogenes. For most human cancers, the more frequently mutated genes are the antioncogenes, the principal exception being the leukemias and lymphomas. Persons heterozygous for germ-line mutations in antioncogenes are strongly predisposed to one or more kinds of cancer, and most dominantly inherited cancer is attributable to such heterozygosity. Seven antioncogenes have been cloned through the study of these persons, and several others have been mapped. An eighth one was mapped and cloned through the investigation of tumors and is not yet known in hereditary form. Three dominantly inherited forms of cancer are not attributable to mutations in antioncogenes. The corresponding nonhereditary forms of most cancers generally reveal abnormalities of the same antioncogenes that are found in the hereditary forms but may also show additional ones. Some cancers, especially the embryonal tumors of children, have a small number of antioncogene mutations; some others, such as most sarcomas, have more, and the common carcinomas have the most, reflecting a hierarchy of controls over growth of stem cell populations. Still more members of this gene category remain to be mapped and cloned through the study of cancer families and of tumors. The genes that have been cloned act at diverse points in the signal transduction pathway in cells, from the outer cell membranes to sites of gene transcription, in some cases as negative regulators of oncogene expression.
Nucleotide Sequence and Regulation of a Human 90-kDa Heat Shock Protein Gene (1989)

In order to define the mechanisms responsible for the regulated expression of a human 90-kDa heat shock protein (HSP90) gene, we have determined the complete genomic sequence of the gene encoding HSP90 beta, including 1102 base pairs upstream of the transcription initiation site. This gene consists of 12 exons and 11 introns. The exons range in size from 99 to 396 base pairs and the introns range from 91 to 1433 base pairs. Analysis of the 5' promoter region revealed TATA and CAAT consensus sequences. Additionally, Sp1 factor binding sites and presumptive heat shock element consensus sequences were found surrounding the transcription initiation site. Three out of the six identified potential heat shock elements reside within the first intron. The ability of the promoter region to respond to heat shock was examined by constructing a plasmid containing the 5' end of the HSP90 beta gene driving a neomycin phosphotransferase reporter gene. This plasmid was used to stably transform human K562 erythroleukemia cells. With heat shock, the abundance of HSP-neo transcripts increased, demonstrating that the promoter region of this gene contains the cis-acting DNA elements required for the heat shock response.
Digital Breast Imaging: Tomosynthesis and Digital Subtraction Mammography (1998)

Advances in the computer technology and the introduction of new digital imaging detectors offer the potential for digital image acquisition and several new mammography techniques, such as tomosynthesis and digital subtraction mammography. Tomosynthesis is a method of obtaining tomographic images of a breast. In tomosynthesis, any number of tomographic planes may be reconstructed from a set of images obtained as the X-ray source is moved in an arc above the breast. By shifting and adding the information obtained at different source positions, any plane of the breast can be brought into a sharp focus, while structures outside this selected plane are blurred. This may lead to improved lesion detection, especially in dense breast tissue. Thus, tomosynthesis may play a role in improving breast cancer screening and lesion characterization. Digital subtraction mammography is a method of breast angiography. It is performed by obtaining a digital radiographic image before, and one or more digital radiographic images after the injection of a contrast agent such as iodine. The pre- and post-contrast images are subtracted, resulting in an image of the vascular structures in the breast. Because breast cancer lesions have increased vascularity, digital subtraction mammography may play an important role in improving lesion detection, characterizing lesions, monitoring response to therapy, and determining lesion extent.Thus, both of these new digital techniques have the potential to address the major limitation of conventional mammography, namely the difficulty in detecting cancer in radiographically dense breasts.
Site-directed mutagenesis of the SH2- and SH3-coding domains of c-src produces varied phenotypes, including oncogenic activation of p60c-src. (1990)

The products of the viral and cellular src genes, p60v-src and p60c-src, appear to be composed of multiple functional domains. Highly conserved regions called src homology 2 and 3 (SH2 and SH3), comprising amino acid residues 88 to 250, are believed to modulate the protein-tyrosine kinase activity present in the carboxy-terminal halves of the src proteins. To explore the functions of these regions more fully, we have made 34 site-directed mutations in a transformation-competent c-src gene encoding phenylalanine in place of tyrosine 527 (Y527F c-src). Twenty of the new mutations change only one or two amino acids, and the remainder delete small or large portions of the SH2-SH3 region. These mutant alleles have been incorporated into a replication-competent Rous sarcoma virus vector to examine the biochemical and biological properties of the mutant proteins after infection of chicken embryo fibroblasts. Four classes of mutant proteins were observed: class 1, mutants with only slight differences from the parental gene products; class 2, mutant proteins with diminished transforming and specific kinase activities; class 3, mutant proteins with normal or enhanced specific kinase activity but impaired biological activity, often as a consequence of instability; and class 4, mutant proteins with augmented biological and catalytic activities. In general, there was a strong correlation between total kinase activity (or amounts of intracellular phosphotyrosine-containing proteins) and transforming activity. Deletion mutations and some point mutations affecting residues 109 to 156 inhibited kinase and transforming functions, whereas deletions affecting residues 187 to 226 generally had positive effects on one or both of those functions, confirming that SH2-SH3 has complex regulatory properties. Five mutations that augmented the transforming and kinase activities of Y527F c-src [F172P, R175L, delta(198-205), delta(206-226), and delta(176-226)] conferred transformation competence on an otherwise normal c-src gene, indicating that mutations in SH2 (like previously described lesions in SH3, the kinase domain, and a carboxy-terminal inhibitory domain) can activate c-src.
Recombination mediated by vaccinia virus DNA topoisomerase I in Escherichia coli is sequence specific. (1991)

Specialized type I topoisomerases catalyze DNA strand transfer during site-specific recombination in prokaryotes and fungi. As a rule, the site specificity of these systems is determined by the DNA binding and cleavage preference of the topoisomerase per se. The Mr 32,000 topoisomerase I encoded by vaccinia virus (a member of the eukaryotic family of "general" type I enzymes) is also selective in its interaction with DNA; binding and cleavage occur in vitro at a pentameric motif 5'-(C or T)CCTT in duplex DNA. Expression of vaccinia virus DNA topoisomerase I in a lambda lysogen of Escherichia coli promotes int-independent excisive recombination of the prophage. To address whether the topoisomerase directly catalyzes DNA strand transfer in vivo, the recombination junctions of plaque-purified progeny phage were cloned and sequenced. In five of six distinct excision events examined, a topoisomerase cleavage sequence is present in one strand of the DNA duplex of both recombining partners. Recombination entails no duplication, insertion, or deletion of nucleotides at the crossover points, consistent with excision via conservative strand exchange at sites of topoisomerase cleavage. Three of these five recombination events are distinguished by the presence of direct repeats at the parental half-sites that extend beyond the pentameric cleavage motif, suggesting that sequence homology may facilitate excision. The data are consistent with a model in which vaccinia topoisomerase catalyzes reciprocal strand transfer, leading to the formation of a nonmigrating Holliday junction, the resolution of which can lead to excisive recombination.
Inhibition of [3H]-MK801 binding and protection against NMDA-induced lethality in mice by a series of imipramine analogs. (1992)

A series of imipramine analogs were tested for inhibition of [3H]-MK801 binding and for their ability to protect against NMDA-induced lethality in mice. The structure-activity relationship (SAR) for the inhibition of [3H]-MK801 binding found primary amines on short linkers to be optimum. For protection against NMDA lethality, compounds containing an unsaturated link to a cyclic amine were the most potent analogs tested. Possible explanations for the lack of correlation observed are briefly discussed.
Equilibrium, Kinetic, and UV-Spectral Characteristics of Aqueous Bromine Chloride, Bromine, and Chlorine Species (1994)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTEquilibrium, Kinetic, and UV-Spectral Characteristics of Aqueous Bromine Chloride, Bromine, and Chlorine SpeciesTian Xiang Wang, Mark D. Kelley, John N. Cooper, Richard C. Beckwith, and Dale W. MargerumCite this: Inorg. Chem. 1994, 33, 25, 5872–5878Publication Date (Print):December 1, 1994Publication History Published online1 May 2002Published inissue 1 December 1994https://pubs.acs.org/doi/10.1021/ic00103a040https://doi.org/10.1021/ic00103a040research-articleACS PublicationsRequest reuse permissionsArticle Views1578Altmetric-Citations151LEARN 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
Aryl hydrocarbon receptor pathway activation enhances gastric cancer cell invasiveness likely through a c-Jun-dependent induction of matrix metalloproteinase-9 (2009)

AhR pathway activation enhances gastric cancer cell invasiveness likely through a c-Jun-dependent induction of MMP-9. Our results provide insight into the mechanism and function of the AhR pathway and its impact on gastric cancer progression.
Preterm labor and bacterial vaginosis-associated bacteria among urban women (2008)

Further identification of the individual attributable risk for separate BV-associated bacteria may be most useful in developing successful treatments to prevent SPTB among BV positive women.
Acute Myocardial Infarction (1995)

Dramatic changes in the management of acute myocardial infarction (AMI) have occurred in the past decade. While previous management strategies were primarily supportive, current strategies focus on achieving and maintaining patency of the infarct-related artery restoring blood flow to jeopardized myocytes, preserving left ventricular function, and preventing recurrences and complications in addition to promoting healing. Restoration of blood flow can be achieved pharmacologically with thrombolytic agents or mechanically with percutaneous transluminal coronary angioplasty (PTCA). Early use of antiplatelet agents and anticoagulants helps maintain patency of the infarct-related arteries and prevents thromboembolic complications. Administration of beta-blockers and angiotensin enzyme inhibitors are more specific means of conserving myocardium and preserving ventricular function. Additionally, several strategies for preventing arrhythmias such as prophylactic lidocaine use and routine long-term suppression of premature ventricular contractions with antiarrhythmic drugs are no longer routinely advocated. Basically, in the era prior to the eighth decade of this century, the primary direction of the therapeutic strategy for AMI was to reduce the oxygen demands in the infarcted myocardium; whereas in the subsequent years, the emphasis shifts to improvement in oxygen delivery, via thrombolysis, PTCA, and coronary artery bypass graft surgery. These interventional changes, when added to greater sophistication in the use of drugs to reduce oxygen demands, resulted in significant lowering of myocardial mortality.
Spirodioxolanonarenones. II.1 Synthesis of a Halogenated 1,4-Dioxaspiro[4,5]deca-7,9-diene-2,6-dione (1965)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTSpirodioxolanonarenones. II.1 Synthesis of a Halogenated 1,4-Dioxaspiro[4,5]deca-7,9-diene-2,6-dioneGian Gualberto Gallo, Carmine Renato Pasqualucci, and Alberto DienaCite this: J. Org. Chem. 1965, 30, 5, 1657–1658Publication Date (Print):May 1, 1965Publication History Published online1 May 2002Published inissue 1 May 1965https://pubs.acs.org/doi/10.1021/jo01016a510https://doi.org/10.1021/jo01016a510research-articleACS PublicationsRequest reuse permissionsArticle Views57Altmetric-Citations1LEARN 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
Amino acid sequence and entomocidal activity of the P2 crystal protein. An insect toxin from Bacillus thuringiensis var. kurstaki. (1988)

The gene encoding the 66-kDa entomocidal protein (P2 protein or mosquito factor) from Bacillus thuringiensis var. kurstaki has been isolated by the use of a 62-mer oligonucleotide probe that encoded 21 amino acids of the P2 protein NH2 terminus. The DNA sequence of the gene, designated cryBI, was unique from the published sequences of other B. thuringiensis genes. However, the amino acid sequence of the P2 protein, as deduced from the DNA sequence of the cryBI gene, was found to contain a sequence of 100 amino acids having 37% homology to a group of B. thuringiensis entomocidal proteins, the P1 proteins. Late stationary phase Bacillus megaterium cells harboring the cloned B. thuringiensis cryBI gene contained large aggregates of the P2 protein, and the cells were highly toxic to both lepidopteran and dipteran larvae. In contrast, Escherichia coli cells harboring the cloned cryBI gene contained very low levels of the P2 protein. DNA blot hybridization experiments showed that certain B. thuringiensis strains contained at least one cryBI-related DNA sequence in addition to the cryBI gene itself.
Revised Recommendations of the International Working Group for Diagnosis, Standardization of Response Criteria, Treatment Outcomes, and Reporting Standards for Therapeutic Trials in Acute Myeloid Leukemia (2003)

An International Working Group met to revise the diagnostic and response criteria for acute myelogenous leukemia originally published in 1990, as well as to provide definitions of outcomes and reporting standards to improve interpretability of data and comparisons among trials. Since the original publication, there have been major advances in our understanding of the biology and molecular genetics of acute leukemia that are clinically relevant and warrant incorporation into response definitions. Differences from the 1990 recommendations included a category of leukemia-free state, new criteria for complete remission, including cytogenetic and molecular remissions and remission duration. Storage of viable blasts for correlative studies is important for future progress in the therapy of these disorders.
Natural Human Immunoglobulins in Cancer Immunotherapy (2009)

The natural or innate immunity is the first-line defense against transformed cells. It guarantees the recognition and removal of malignant cells at an early stage and makes manifest cancers an exceptional event. Natural antibodies, which are predominantly IgM molecules, play a major role in these defense mechanisms and they have some typical features in common. They are coded by specific germline families and equipped mainly with lambda-chains, in contrast to the majority of circulating antibodies. The targets that are recognized by these antibodies are not newly synthesized proteins, but instead post-translationally modified carbohydrate structures on membrane-bound glycoproteins and glycolipids. Another typical feature of these natural IgM antibodies is their ability to induce apoptosis in vitro and in vivo in a death domain-independent manner. These results show that natural IgM antibodies represent a huge reservoir of therapeutic antibodies.
10 Endonuclease Activity Associated with Reverse Transcriptase of Avian Sarcoma-Leukosis Viruses (1993)

The pol genes of retroviruses encode reverse transcriptase (RT) polymerase and ribonuclease H (RNase H) domains, integrase (IN), and sometimes the protease (PR) domain. These pol gene products are translated as part of the large gag-pol-encoded precursor polyprotein processed by PR. However, the proteolytic processing strategies differ among retroviruses. In some cases, incomplete processing occurs, forming RT subunits that contain additional domains or activities. For example, RT of Moloney murine leukemia virus (Mo-MLV) is a monomer of 80 kD, whereas the RTs of avian sarcoma-leukosis virus (ASLV) and human immunodeficiency virus (HIV) are heterodimers (see Fig. 1). With the HIV RT, the larger subunit (p66) contains both the polymerase and RNase H domains; the smaller subunit (p51) has only the polymerase, the RNase H domain having been removed by carboxy-terminal processing. The ASLV RT subunits also differ by a carboxy-terminal processing. However, in this case, both (α of 63 kD, and β of 95 kD) contain polymerase and RNase H domains, and the larger subunit includes sequences encoding IN at its carboxyl terminus. The endonuclease activity associated with IN presumably reflects the enzyme’s ability to make single-stranded breaks (nicks) in both host and viral DNAs during the integration reaction. It is the presence of IN sequences on the β subunit of ASLV RT that accounts for the DNA endonuclease activity of this RT. The functional consequences of these differences in pol precursor processing are unknown. The IN domain could, however, contribute to the function of RT αβ in several ways...