gebhart/patrepeval huggingface dataset:
Identification of tumour rejection antigens recognized by T lymphocytes. (1992)

On the basis of the results reviewed here, there are two major mechanisms whereby tumour rejection antigens may arise. The first mechanism is mutational. Point mutations occurring in a large variety of genes may produce new antigenic peptides, either by providing them with the ability to bind to MHC class I molecules or by providing them with a new epitope (Fig. 2). The second mechanism is the activation of a gene that is silent in normal tissues and for which no strong natural tolerance has been established. Plausible candidates for the mutational mechanism are the "tumour specific transplantation antigens" observed on methylcholanthrene induced tumours and tumours induced by ultraviolet light. The diversity of these antigens appears to be very large, like that of the tum- antigens. Moreover, these tumours have been obtained with high doses of carcinogens, which are proven mutagens. On the other hand, a P815 tumour rejection antigen appears to arise through the activation of a silent gene, and it may turn out that this is the rule for most tumour rejection antigens. It is our hope that other genes coding for mouse and human tumour rejection antigens will soon be identified, so that it will become clear whether the activational mechanism is the rule or the exception. In our view, this is a crucial issue. Insofar as tumour rejection antigens result from mutations, they may be highly specific for every individual tumour. The tumour specific nature of these antigens would then be easily ascertained. However, active immunization of cancer patients would require that a tumour cell line be obtained from each patient, a most unpractical prospect. If, on the other hand, production of tumour rejection antigens results from the activation of a normal gene, then there is a good probability that the same gene may be activated in many different tumours, being perhaps preferentially shared by tumours of the same histological type. This would probably not result in the expression of the same antigen in all these tumours, because the patients would differ in their presenting molecules, which are determined by their HLA haplotype. However, a subset of the tumours expressing the same "tumour rejection" gene should share the same class I restricting element, so that all of these patients could be immunized with a cell that would express the gene and carry the appropriate HLA molecule.(ABSTRACT TRUNCATED AT 400 WORDS)
Complete nucleotide sequence of the murine gamma 3 switch region and analysis of switch recombination sites in two gamma 3-expressing hybridomas. (1985)

The heavy chain isotype switch is mediated by a DNA rearrangement between a donor switch region (usually mu) and a recipient switch region (gamma, epsilon, or alpha). Switch regions lie upstream of the appropriate heavy chain constant region gene and are composed of simple sequences repeated in tandem. It is not known to what extent the tandemly repeated sequences are important to the heavy chain switch recombination, and to what extent other features of switch region sequences might contribute to the switch process. We studied switches to the gamma 3 isotype by sequencing the entire gamma 3 switch region. This switch region is composed of forty-four 49 base pair units repeated in tandem. These repeated units share modest homology with the mu switch region repeated elements. Evolution of the gamma 3 switch region seems to involve insertions and deletions of the 49mer elements. We also molecularly cloned rearranged switch regions from two gamma 3-expressing hybridomas and determined the DNA sequences at the mu-gamma 3 recombination sites. We located these switch recombination sites within the germ-line gamma 3 switch region, as well as switch recombination sites from two myelomas. All four sites are found in the 5' one-third of the gamma 3 switch region. We discuss some additional trends in the sequence data near these four recombination sites.
Neurite guidance by non-neuronal cells in culture: preferential outgrowth of peripheral neurites on glial as compared to nonglial cell surfaces (1985)

Growing axons in the peripheral nervous system (PNS) encounter a variety of cellular and extracellular substrates. Since it is difficult to sort out the possible contributions of these diverse components of the extracellular environment to axonal guidance in vivo, I have developed an in vitro system to study neurite outgrowth on two classes of cells which may provide as substrates for growing axons during development or regeneration: glial cells, e.g., astrocytes and Schwann cells, and nonglial cells, e.g., fibroblasts. Although neurites from sympathetic and spinal sensory ganglia explants grew onto preformed monolayers of both glial and nonglial cells, glial cells were a markedly better substrate. On the glial cells the neurites extended at a rate of 25 to 30 micron/hr and traveled singly or in fine fascicles; their growth cones displayed long filopodia and migrated on the upper surface of the monolayer cells. Conditioned media experiments suggested that neurite outgrowth on glial cell monolayers was not mediated by soluble secreted factors. These results indicate that the glial cell surface is an attractive substrate for neurite outgrowth. In contrast, on nonglial cells the rate of outgrowth was only 10 to 15 micron/hr, large neurite fascicles were common, and the growth cones migrated beneath the monolayer cells in contact with the underlying artificial substrate. This location of the growth cone, coupled with the observation that conditioned medium from these cells promoted neurite outgrowth only when bound to artificial substrates, suggests that secreted substrate-associated components may be an important determinant of neurite outgrowth on nonglial cell monolayers.(ABSTRACT TRUNCATED AT 250 WORDS)
Protease-resistant PrP accumulation and scrapie agent replication: a role for sulphated glycosaminoglycans? (1994)

Conference Article| February 01 1994 Protease-resistant PrP accumulation and scrapie agent replication: a role for sulphated glycosaminoglycans? Byron Caughey Byron Caughey 1Laboratory of Persistant Viral Diseases, NIH Rocky Mountain Laboratories, National Institute for Allergy and Infectious Diseases, Hamilton, Montana 59840, U.S.A. Search for other works by this author on: This Site PubMed Google Scholar Author and article information Publisher: Portland Press Ltd Received: September 24 1993 Online ISSN: 1470-8752 Print ISSN: 0300-5127 © 1994 Biochemical Society1994 Biochem Soc Trans (1994) 22 (1): 163–167. https://doi.org/10.1042/bst0220163 Article history Received: September 24 1993 Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn Email Cite Icon Cite Get Permissions Citation Byron Caughey; Protease-resistant PrP accumulation and scrapie agent replication: a role for sulphated glycosaminoglycans?. Biochem Soc Trans 1 February 1994; 22 (1): 163–167. doi: https://doi.org/10.1042/bst0220163 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsBiochemical Society Transactions Search Advanced Search Keywords: f.t.i.r., Fourier transform infrared, GAG, glycosaminoglycan, MNB, mouse neuroblastoma, TSE, transmissible spongiform encephalopathies This content is only available as a PDF. © 1994 Biochemical Society1994 Article PDF first page preview Close Modal You do not currently have access to this content.
LC-MS/MS Quantification of Zn-α2 Glycoprotein: A Potential Serum Biomarker for Prostate Cancer (2007)

This LC-MS/MS assay is reproducible and can be used to evaluate the clinical utility of ZAG as a cancer biomarker.
Pituitary adenylate cyclase-activating polypeptide protects rat cerebellar granule neurons against ethanol-induced apoptotic cell death (2002)

Alcohol exposure during development can cause brain malformations and neurobehavioral abnormalities. In view of the teratogenicity of ethanol, identification of molecules that could counteract the neurotoxic effects of alcohol deserves high priority. Here, we report that pituitary adenylate cyclase-activating polypeptide (PACAP) can prevent the deleterious effect of ethanol on neuronal precursors. Exposure of cultured cerebellar granule cells to ethanol inhibited neurite outgrowth and provoked apoptotic cell death. Incubation of granule cells with PACAP prevented ethanol-induced apoptosis, and this effect was not mimicked by vasoactive intestinal polypeptide, suggesting that PAC1 receptors are involved in the neurotrophic activity of PACAP. Ethanol exposure induced a strong increase of caspase-2, -3, -6, -8, and -9 activities, DNA fragmentation, and mitochondrial permeability. Cotreatment of granule cells with PACAP provoked a significant inhibition of all of the apoptotic markers investigated although the neurotrophic activity of PACAP could only be ascribed to inhibition of caspase-3 and -6 activities. These data demonstrate that PACAP is a potent protective agent against ethanol-induced neuronal cell death. The fact that PACAP prevented ethanol toxicity even when added 2 h after alcohol exposure, suggests that selective PACAP agonists could have potential therapeutic value for the treatment of fetal alcohol syndrome.
Characterization of outer membranes isolated from Borrelia burgdorferi, the Lyme disease spirochete (1995)

The lack of methods for isolating Borrelia burgdorferi outer membranes (OMs) has hindered efforts to characterize borrelial surface-exposed proteins. Here we isolated OMs by immersion of motile spirochetes in hypertonic sucrose followed by isopycnic ultracentrifugation of the plasmolyzed cells. The unilamellar vesicles thus obtained were shown to be OMs by the following criteria: (i) they contained OspA and OspB; (ii) they did not contain flagellin, NADH oxidase activity, or the 60-kDa heat shock protein; and (iii) their morphology by freeze-fracture electron microscopy was identical to that of OMs of intact organisms. Consistent with previous studies which employed immunoelectron microscopy and detergent-based solubilization of B. burgdorferi OMs, only small proportions of the total cellular content of OspA or OspB were OM associated. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) fluorography of OMs from spirochetes metabolically radiolabeled with [3H]palmitate or 35S-amino acids demonstrated that the OMs contained both nonlipidated and lipidated proteins. This fractionation procedure was also used to isolate OMs from virulent and avirulent isolates of the well-characterized B. burgdorferi N40 strain. SDS-PAGE fluorography revealed that OMs from the two isolates differed with respect to both nonlipoprotein and lipoprotein constituents. When whole cells, protoplasmic cylinders, and OMs were immunoblotted against sera from mice persistently infected with B. burgdorferi N40, the majority of antibody reactivity was directed against intracellular proteins. The availability of isolated OMs should facilitate efforts to elucidate the complex relationship(s) between B. burgdorferi membrane composition and Lyme disease pathogenesis.
Low-complexity occlusion handling for motion-compensated frame rate up-conversion (2009)

This paper presents a novel low-complexity pixel-based occlusion handling algorithm. A smooth dense motion field associated with the interpolated frame is derived from the result of block-based motion estimation. The occlusion type of each pixel is determined by the corresponding divergence value of the motion field. Experimental results show that the proposed method reliably yields high quality interpolated frames, especially at occlusion regions, with an extremely low computational complexity.
Regulation of Apoptosis by the Transforming Genes of the DNA Tumor Virus Adenovirus (1993)

The human DNA tumor virus adenovirus encodes two transforming genes, the E1A and E1B oncogenes, which cooperate to oncogenically transform primary rodent cells. The E1A products efficiently stimulate cell proliferation, but fail to transform cells due to the induction of programmed cell death (apoptosis). Expression of either the E1B oncogene, or the human bcl-2 proto-oncogene, blocks E1A-associated apoptosis to produce transformation with high frequency. Thus, induction of proliferation by E1A must be coupled to suppression of an intrinsic cell suicide pathway for the efficient transformation of primary cells.The E1B oncogene encodes the unique 19-kDa and 55-kDa proteins, both of which independently suppress apoptosis and greatly enhance transformation by E1A. Suppression of apoptosis by the E1B 19-kDa protein is required not only in transformation of rodent cells with E1A, but also in adenovirus-infected human cells, where it sustains cell viability to maximize virus production. The E1B 19-kDa protein has the additional ability to block apoptosis induced by tumor necrosis factor (TNF)-α, and anti-Fas antibodies, potentially contributing to escape from antiviral and anticancer immune surveillance.What E1A does to trigger apoptosis and the mechanism utilized by E1B 19-kDa and 55-kDa proteins and Bcl-2 to suppress apoptosis is of fundamental importance to understand how programmed cell death is regulated. It is now clear that the p53 tumor suppressor gene product mediates apoptosis by E1A, and that the E1B gene encodes independent, overlapping functions to disable p53-mediated apoptosis. The E1B 55-kDa protein binds to and inhibits p53 directly, but the mechanism by which the 19-kDa protein interferes with p53 function is not yet known.In this review, I will discuss the means by which these conclusions were derived and how the transforming genes of adenovirus can be utilized to ascertain the molecular basis by which apoptosis is regulated.
Sintokamides A to E, Chlorinated Peptides from the Sponge Dysidea sp. that Inhibit Transactivation of the N-Terminus of the Androgen Receptor in Prostate Cancer Cells (2008)

The new chlorinated peptides sintokamides A to E (1-5) have been isolated from specimens of the marine sponge Dysidea sp. collected in Indonesia. Their structures were elucidated by a combination of spectroscopic and single-crystal X-ray diffraction analyses. Sintokamide A (1) is an inhibitor of N-terminus transactivation of the androgen receptor in prostate cancer cells.
Chloroplast DNA polymorphisms in lodgepole and jack pines and their hybrids. (1987)

Samples taken from throughout the ranges of distribution of lodgepole pine (Pinus contorta Dougl. ex. Loud.) and jack pine (Pinus banksiana Lamb.) were assayed for Sal I and Sst I chloroplast DNA restriction fragment variation. Although the chloroplast genome is often regarded as highly conserved, at least 2 distinct Sal I and 13 distinct Sst I restriction fragment banding patterns occur in these closely related species. None of the chloroplast DNA restriction fragment banding patterns observed in allopatric lodgepole pine was observed in allopatric populations of jack pine, and vice versa, even though the two species share an extensive zone of sympatry, and gene flow between the species has been reported for nuclear genes. However, several atypical Sst I restriction fragment banding patterns occur only in or near the zone of sympatry. Chloroplasts have been reported to be inherited maternally in the great majority of species studied; however, restriction fragment analyses indicated that chloroplasts are inherited paternally in controlled matings between lodgepole pine (female) and jack pine (male).
Reduction of 1,3-diimines. A new and general method of synthesis of .gamma.-diamines, .beta.-amino ketones, and derivatives with two and three chiral centers (1983)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTReduction of 1,3-diimines. A new and general method of synthesis of .gamma.-diamines, .beta.-amino ketones, and derivatives with two and three chiral centersJose Barluenga, Bernardo Olano, and Santos FusteroCite this: J. Org. Chem. 1983, 48, 13, 2255–2259Publication Date (Print):July 1, 1983Publication History Published online1 May 2002Published inissue 1 July 1983https://pubs.acs.org/doi/10.1021/jo00161a022https://doi.org/10.1021/jo00161a022research-articleACS PublicationsRequest reuse permissionsArticle Views314Altmetric-Citations22LEARN 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-AlertscloseSupporting Info (1)»Supporting Information Supporting Information Get e-Alerts
Effect of Glucocorticosteroid Treatment on β-Adrenoceptor Subtype Function in Adipocytes from Patients with Asthma (1993)

1. Adrenoceptor subtype function was studied in isolated adipocytes obtained by subcutaneous fat biopsies from nine patients with mild asthma. The biopsies were taken before and after 7 days treatment with 25 mg of prednisolone given orally. Lipolytic activity after stimulation with various adrenergic agent was measured, using glycerol release as an index of lipolysis. The number of beta 1- and beta 2-adrenoceptor binding sites was determined in radioligand binding experiments and beta 1- and beta 2-adrenoceptor mRNA levels were measured with a solution hybridization assay. 2. Lipolytic sensitivity (ED50) to isoprenaline, a non-selective beta-adrenoceptor agonist, increased 50-fold after treatment (P = 0.04). Sensitivity to terbutaline, a selective beta 2-adrenoceptor agonist, increased 25-fold (P = 0.01), whereas the ED50 values for dobutamine, a selective beta 1-adrenoceptor agonist, did not change significantly. Likewise, the sensitivity to the alpha 2-adrenoceptor agonist, clonidine, and to the drugs acting at post-receptor levels did not change significantly. Basal and maximum lipolytic rates on stimulation were not altered by the treatment. 3. The number of beta 2-adrenoceptor binding sites increased by 60% after treatment (P < 0.05), whereas the beta 1-adrenoceptor binding sites were not affected. The affinity of each receptor subtype for the displacing ligand, ICI 118.551, was not significantly altered by steroids. No significant changes were demonstrated in either beta 1- or beta 2-adrenoceptor mRNA levels. 4. Thus, glucocorticoids selectively increase beta 2-adrenoceptor density and function in patients with asthma, studied by using subcutaneous fat cells as an experimental model.
Transforming growth factor-beta in human platelets. Identification of a major storage site, purification, and characterization. (1983)

Acidic ethanol extracts of human platelets induced non-neoplastic normal rat kidney fibroblasts to undergo anchorage-independent growth. Less than 100 ng/ml of the crude extract elicits 50% of the maximal biological response when assayed in the presence of epidermal growth factor (2.5 ng/ml). In the absence of epidermal growth factor, the potency of the extract decreased 1,000-fold. These results show that platelets contain a type beta transforming growth factor. The specific activity of the platelet extract is 100-fold greater than that of other non-neoplastic tissues. The growth factor was purified to homogeneity by sequential gel filtration on Bio-Gel P-60 columns, first in the absence and then in the presence of urea. As determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, this transforming growth factor-beta is a protein of 25,000 daltons. It is composed of two 12,500-dalton subunits held together by disulfide bonds. These results, as well as its amino acid composition and its lack of strong mitogenic activity, show that this protein is distinct from platelet-derived growth factor. When completely purified, transforming growth factor-beta elicits 50% of its maximal biological response at concentrations less than 5 x 10(-12) M.
Anticancer Activity of Sodium Stibogluconate in Synergy with IFNs (2002)

Cancer cell resistance limits the efficacy of IFNs. In this study, we show that sodium stibogluconate (SSG) and IFN-alpha synergized to overcome IFN-alpha resistance in various human cancer cell lines in culture and eradicated IFN-alpha-refractory WM9 human melanoma tumors in nude mice with no obvious toxicity. SSG enhanced IFN-alpha-induced Stat1 tyrosine phosphorylation, inactivated intracellular SHP-1 and SHP-2 that negatively regulate IFN signaling, and induced cellular protein tyrosine phosphorylation in cancer cell lines. These effects are consistent with inactivation of phosphatases as the basis of SSG anticancer activity. Characterization of SSG by chromatography revealed that only selective compounds in SSG were effective protein tyrosine phosphatase inhibitors. These observations suggest the potential of SSG as a clinically usable protein tyrosine phosphatase inhibitor in cancer treatment and provide insights for developing phosphatase-targeted therapeutics.
Evaluation of airway inflammation by quantitative Th1/Th2 cytokine mRNA measurement in sputum of asthma patients (2006)

Real time RT-PCR analysis of mRNA in induced sputum confirms a predominance of Th2 cytokines in both allergic and non-allergic asthma. IL-5 levels reflect eosinophil infiltration as well as eNO levels and hyperreactivity, and levels of the Th1 cytokine IFN-gamma indicate asthma severity. The technique is a promising tool for use in further studies of asthma severity and disease activity.
Insulin-like growth factor I and insulin rapidly increase casein kinase II activity in BALB/c 3T3 fibroblasts. (1988)

We have tested whether growth factors added to serum-deprived BALB/c 3T3 fibroblasts alter the casein kinase II activity measured in cell extracts. A rapid phosphocellulose chromatography method was developed that provides a 40-fold partial purification of casein kinase II activity assayed with the specific substrate peptide Arg-Arg-Glu-Glu-Glu-Thr-Glu-Glu-Glu. Using this technique, kinase activity is stimulated 1.6-2.5-fold when isolated from fibroblasts treated with insulin or insulin-like growth factor I (IGF-I). The activated kinase activity exhibits the specific properties of casein kinase II such as the ability to utilize [gamma-32P]GTP as phosphate donor and marked inhibition by low concentrations of heparin. Activation of casein kinase II appears specific for these hormones because epidermal growth factor and platelet-derived growth factor have no effect on the kinase activity when added to fibroblasts under conditions where they markedly stimulate [3H]thymidine incorporation into DNA. Increases of casein kinase II activity by insulin and IGF-I were detected within 1 min of their addition to cell cultures. IGF-I is more potent in stimulating casein kinase II than insulin in mouse fibroblasts. These results demonstrate that casein kinase II is a selective target for insulin and IGF-I action in BALB/c fibroblasts, consistent with the hypothesis that this kinase plays a role in cellular signaling by these hormones.