gebhart/patrepeval huggingface dataset:
Prospective study of systemic and mucosal immune responses in dysenteric patients to specific Shigella invasion plasmid antigens and lipopolysaccharides (1991)

Shigellosis is a major cause of infant morbidity and mortality in developing countries. To find immunological correlates of specific protection against shigellosis, we examined chronological samples of sera, stool extracts, duodenal aspirates, and saliva samples from 39 adults and 22 children with shigellosis from Peru for the presence of specific antibody to invasion plasmid antigens (Ipa) common to all virulent Shigella strains, by using both a whole-organism enzyme-linked immunosorbent assay (ELISA) and a Western blot (immunoblot) assay. Antibody responses to lipopolysaccharide (LPS) from Shigella serotypes both homologous and heterologous to the infecting strain were also determined by ELISA. ELISAs showed that the highest serum immunoglobulin G (IgG) antibody titers to Shigella whole organisms both with and without surface Ipa were found in adults and malnourished children, the two groups with the shortest and longest durations of disease, respectively. Mucosal IgA antibody titers to Shigella strains decreased over time to a much greater extent than serum IgG titers, and IgA to Ipa in mucosal secretions was found in adults and well-nourished children but not in malnourished children. The presence of mucosal antibody to Ipa may limit the spread and severity of the infection, as indicated by the prolonged illness observed in malnourished children who have no significant mucosal antibody to Shigella Ipa. Serum antibody titers to the Ipa antigens were high relative to anti-Shigella LPS antibody titers, especially in pediatric patients. In contrast to the anti-Ipa responses observed, no differences in antibody responses to LPS in children compared by nutritional status were found. High levels of serum and mucosal cross-reacting antibody to heterologous serotype LPS were found between Shigella flexneri serotypes 1a and 2a. Different patterns of immune response to Ipa proteins and LPS that may aid in the definition of Shigella antigens important in host protection were observed in adults, well-nourished children, and malnourished children.
Myocardial ischemia-reperfusion injury is exacerbated in absence of endothelial cell nitric oxide synthase (1999)

Myocardial ischemia and reperfusion (MI/R) initiates a cascade of polymorphonuclear neutrophil (PMN)-mediated injury, the magnitude of which may be influenced by the bioavailability of nitric oxide (NO). We investigated the role of endothelial cell nitric oxide synthase (ecNOS) in MI/R injury by subjecting wild-type and ecNOS-deficient (-/-) mice to 20 min of coronary artery occlusion and 120 min of reperfusion. Myocardial infarct size represented 20.9 +/- 2.9% of the ischemic zone in wild-type mice, whereas the ecNOS -/- mice had significantly (P < 0.01) larger infarcts measuring 46.0 +/- 3.8% of the ischemic zone. Because P-selectin is thought to be involved with the pathogenesis of neutrophil-mediated I/R injury, we assessed the effects of MI/R on P-selectin expression in the myocardium of wild-type and ecNOS -/- mice. P-selectin expression measured with a radiolabeled monoclonal antibody (MAb) technique after MI/R in wild-type mice was 0.037 +/- 0.009 microgram MAb/g tissue, whereas ecNOS -/- coronary vasculature was characterized by significantly (P < 0.05) higher P-selectin expression (0.080 +/- 0.013 microgram MAb/g tissue). Histological examination of the postischemic myocardium revealed significantly (P < 0.01) more neutrophils in the ecNOS -/- (29.5 +/- 2.5 PMN/field) compared with wild-type (5.0 +/- 0.9 PMN/field) mice. A similar trend in infarct size and neutrophil accumulation was observed when wild-type and ecNOS -/- mice were subjected to 30 min of ischemia and 120 min of reperfusion. These novel in vivo findings demonstrate a cardioprotective role for ecNOS-derived NO in the ischemic-reperfused mouse heart.
Novel strategy for identification of candidate cytotoxic T‐cell epitopes from human preproinsulin (2003)

Abstract: We describe a strategy for identifying ligands of human leukocyte antigen (HLA) class I molecules based on a peptide library‐mediated in vitro assembly of recombinant class I molecules. We established a microscale class I assembly assay and used a capture ELISA to quantify the assembled HLA‐peptide complexes. The identity of the bound ligands was then deduced by mass spectrometry. In this method, HLA complexes assembled in vitro in the presence of components of a mixture of peptides were immunoprecipitated and the bound peptide(s) identified by matrix‐assisted laser desorption ionization‐time of flight (MALDI‐TOF) mass spectrometry. This process of epitope extraction is robust and can be used with complex mixtures containing in excess of 300 candidate ligands. A library of overlapping peptides representing all potential octamers, nonamers and decamers from human preproinsulin was synthesized using unique library chemistry. Peptides from the library were used to initiate assembly of recombinant HLA‐B8, HLA‐B15 and HLA‐A2, facilitating the identification of candidate T‐cell epitopes from preproinsulin.
Recruitment of mitochondrial cyclophilin to the mitochondrial inner membrane under conditions of oxidative stress that enhance the opening of a calcium-sensitive non-specific channel (1994)

Binding of mitochondrial matrix cyclophilin (CyP) to the rat liver mitochondrial membranes was detected by SDS/PAGE and Western blotting with suitable antipeptide antibodies. Binding was not affected by prior exposure of mitochondria to Ca2+, adenine nucleotides or inhibitors of the adenine nucleotide translocase, but was greatly increased by t-butyl hydroperoxide (tBH), phenylarsine oxide or diamide. These all sensitized the opening of the non-specific mitochondrial pore to [Ca2+], and the effect of tBH was shown to be maintained after washing away the tBH, consistent with it being caused by the enhanced CyP binding. The bound CyP did not demonstrate peptidyl-prolyl cis-trans isomerase activity. CyP-binding was prevented by 5 microM cyclosporin A, but not reversed by cyclosporin treatment of the membranes. The effect of tBH on binding was concentration-dependent and maximal within 30 s.
Electrochemical Impedance Study of Tl+ Reduction through Gramicidin Channels in Self-Assembled Gramicidin-Modified Dioleoylphosphatidylcholine Monolayers on Mercury Electrodes (1999)

Impedance measurements for the reduction of Tl+ on gramicidin-modified dioleoylphosphatidylcholine-coated mercury electrodes have been performed. The frequency dependence of the admittance data fits well to a Randles circuit, and the Warburg coefficient, σ, and the irreversibility coefficient, p‘, can be obtained at every dc potential from the frequency analysis conforming to this circuit. However, the potential dependence of the Warburg coefficient is different from the one expected for a simple electron transfer. Instead, the σ−E data can be analyzed conforming to a mechanism including preceding and following homogeneous chemical steps to the electron transfer (CEC mechanism). In addition, from the irreversibility coefficient, p‘, a value of the standard rate constant for the electron transfer of 0.035 cm s-1 and a potential independent value for the transfer coefficient, α, of close to 0.5 are obtained. The possibility that the CEC mechanism originates partly from nonlinear diffusion is considered, and the results are discussed in comparison with those given in the literature for Tl+ reduction on pure mercury.
Mechanisms of Hepatic Toxicity. III. Intracellular signaling in response to toxic liver injury (1998)

Toxin-induced liver injury was formerly considered a passive biochemical event, but recent evidence has demonstrated that signal transduction pathways actively modulate the hepatocyte's response to this form of injury. Investigations have examined the effects of a variety of toxins on the activation of receptor-coupled signal transduction, mitogen-activated protein kinases, and Fas signaling, as well as the generation of second messengers such as ceramide and nitric oxide. Many of these pathways culminate in the activation of transcription factors such as activator protein-1, c-Myc, or nuclear factor-KB. This Themes article discusses the effects of toxic injury on these signaling pathways and their known functions in regulating hepatocyte death and proliferation following injury.
Chromatin clearance in C57Bl/10 mice: interaction with heparan sulphate proteoglycans and receptors on Kupffer cells (1999)

Chromatin is an important autoantigen in the pathogenesis of systemic lupus erythematosus (SLE) as an immunogen and as a part of nephritogenic immune complexes. Earlier studies focused on clearance of DNA. However, DNA released into the circulation from dying cells is found associated with histones in nucleosomes. The liver is the major organ involved in clearance of chromatin from the circulation of mice. Heparan sulphate proteoglycans (HSPG) have been implicated in the clearance of various charged molecules. Receptor-mediated clearance of ssDNA by the liver has also been reported. Because chromatin contains positively charged histones in addition to DNA, we wished to determine if HSPG and/or DNA receptors are involved in chromatin clearance. The rate of clearance of H1-stripped chromatin from the bloodstream of C57Bl/10 mice was markedly decreased by prior treatment of mice with Heparinase I. Clearance was also inhibited by heparin, heparan sulphate, and DNA, but not by colominic acid. DNA was the most effective inhibitor of clearance and released chromatin from sites of clearance. Depletion of Kupffer cells and splenic macrophages using liposome-encapsulated Clodronate (dichloromethylene bisphosphonate) markedly inhibited chromatin clearance. These data suggest that chromatin clearance is mediated by charge interactions with cell surface HSPG and by DNA receptors. Clearance and degradation of chromatin require functional macrophages in the liver and spleen.
Crystal Structure of a Prolonged-Acting Insulin with Albumin-Binding Properties (1997)

The fatty acid acylated insulin, Lys(B29)-tetradecanoyl, des-(B30) human insulin, has been crystallized and the structure determined by X-ray crystallography. The fatty acid substituent on residue B29 Lys binds reversibly to circulating albumin protein in vivo, and by this mechanism the hormone's action is prolonged. Crystals of the fatty acid insulin grow in space group R3, with two dimers in the asymmetric unit, and diffract to 1.8 A spacing. The structure has been solved by molecular replacement and refined using a maximum likelihood method. The crystal structure consists of R6 zinc insulin hexamers which contain phenol. The fatty acids can be seen bound between the hexamers, making specific interactions with the side chains of residue B1 Phe; however, the lysine side chains to which the fatty acids are covalently attached are mostly disordered. The mode of binding of the fatty acids appears to be determined by crystal packing, and whether or not they interact with the protein in this way in solution remains uncertain.
An adaptive information retrieval system based on associative networks (2004)

In this paper we present a multilingual information retrieval system that provides access to Tourism in-formation by exploiting the intuitiveness of natural language. In particular, we describe the knowledge representation model underlying the information re-trieval system. This knowledge representation ap-proach is based on associative networks and allows the definition of semantic relationships between domain-intrinsic information items. The network structure is used to define weighted associations between in-formation items and augments the system with a fuzzy search strategy. This particular search strat-egy is performed by a constrained spreading activa-tion algorithm that implements information retrieval on associative networks. Strictly speaking, we take the relatedness of terms into account and show, how this fuzzy search strategy yields beneficial results and, moreover, determines highly associated matches to users ’ queries. Thus, the combination of the associa-tive network and the constrained spreading activation approach constitutes a search algorithm that evalu-ates the relatedness of terms and, therefore, provides a means for implicit query expansion.
Perovskites decorated with oxygen vacancies and Fe–Ni alloy nanoparticles as high-efficiency electrocatalysts for the oxygen evolution reaction (2017)

Oxygen vacancies and Fe–Ni alloy nanoparticles decorated on a perovskite backbone can boost the oxygen evolution activity of perovskites.
KRAS Protein Stability Is Regulated through SMURF2: UBCH5 Complex-Mediated β-TrCP1 Degradation (2014)

Attempts to target mutant KRAS have been unsuccessful. Here, we report the identification of Smad ubiquitination regulatory factor 2 (SMURF2) and UBCH5 as a critical E3:E2 complex maintaining KRAS protein stability. Loss of SMURF2 either by small interfering RNA/short hairpin RNA (siRNA/shRNA) or by overexpression of a catalytically inactive mutant causes KRAS degradation, whereas overexpression of wild-type SMURF2 enhances KRAS stability. Importantly, mutant KRAS is more susceptible to SMURF2 loss where protein half-life decreases from >12 hours in control siRNA-treated cells to <3 hours on Smurf2 silencing, whereas only marginal differences were noted for wild-type protein. This loss of mutant KRAS could be rescued by overexpressing a siRNA-resistant wild-type SMURF2. Our data further show that SMURF2 monoubiquitinates UBCH5 at lysine 144 to form an active complex required for efficient degradation of a RAS-family E3, β-transducing repeat containing protein 1 (β-TrCP1). Conversely, β-TrCP1 is accumulated on SMURF2 loss, leading to increased KRAS degradation. Therefore, as expected, β-TrCP1 knockdown following Smurf2 siRNA treatment rescues mutant KRAS loss. Further, we identify two conserved proline (P) residues in UBCH5 critical for SMURF2 interaction; mutation of either of these P to alanine also destabilizes KRAS. As a proof of principle, we demonstrate that Smurf2 silencing reduces the clonogenic survival in vitro and prolongs tumor latency in vivo in cancer cells including mutant KRAS-driven tumors. Taken together, we show that SMURF2:UBCH5 complex is critical in maintaining KRAS protein stability and propose that targeting such complex may be a unique strategy to degrade mutant KRAS to kill cancer cells.
Leukocyte–Endothelial Cell–Cell Interactions in Vitro : Static Assays and Adhesion under Shear Stress (2005)

This chapter contains sections titled: Introduction Adhesion of Leukocytes to High Endothelial Venules: The HEV Assay Materials Procedure Preparation of Frozen Lymphatic Tissue Blocks HEV Assay Expected Results Troubleshooting References Adhesion of Leukocytes to Cultured Endothelium, With or Without Shear Materials Procedure Expected Results Troubleshooting Additional Comments and Hints Bibliography Relevant Webpages Adhesion Assay under Static Conditions in Microtiter Plates Materials Procedure Coating of the 96-Well Plate with Adhesion Molecules Cell Preparation and CFDA-SE Labeling Adhesion Assay Additional Comments Reference
Vitronectin Receptor (α v β 3 ) Mediates Platelet Adhesion to the Luminal Aspect of Endothelial Cells (1997)

The expression of vitronectin receptor exposed on the luminal aspect of activated endothelium is enhanced and mediates platelet/endothelium adhesion. Vitronectin receptor-mediated platelet attachment to activated endothelium during reperfusion may contribute to reperfusion injury and could be a target for antiadhesive therapy.
Robotic graphics: a new approach to force feedback for virtual reality (2002)

A new conceptual solution is presented for the problem of providing force feedback for virtual reality, concentrating on potential CAD/CAM applications. The essential concept is that force feedback is provided by interactions between the human operator and specialized external (as opposed to worn) robots. This is called "robotic graphics" to express the analogy between robots simulating the feel of an object, and graphics displays simulating its appearance. This is illustrated by introducing the derivative concepts of "robotic shape displays" and "roboxels.".< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>
Efficiency of recombinant human TNF in human cancer therapy. (2006)

Recombinant human tumour necrosis factor (TNF) has a selective effect on angiogenic vessels in tumours. Given that it induces vasoplegia, its clinical use has been limited to administration through isolated limb perfusion (ILP) for regionally advanced melanomas and soft tissue sarcomas of the limbs. When combined with the alkylating agent melphalan, a single ILP produces a very high objective response rate. In melanoma, the complete response (CR) rate is around 80% and the overall objective response rate greater than 90%. In soft tissue sarcomas that are inextirpable, ILP is a neoadjuvant treatment resulting in limb salvage in 80% of the cases. The CR rate averages 20% and the objective response rate is around 80%. The mode of action of TNF-based ILP involves two distinct and successive effects on the tumour-associated vasculature: first, an increase in endothelium permeability leading to improved chemotherapy penetration within the tumour tissue, and second, a selective killing of angiogenic endothelial cells resulting in tumour vessel destruction. The mechanism whereby these events occur involves rapid (of the order of minutes) perturbation of cell-cell adhesive junctions and inhibition of alphavbeta3 integrin signalling in tumour-associated vessels, followed by massive death of endothelial cells and tumour vascular collapse 24 hours later. New, promising approaches for the systemic use of TNF in cancer therapy include TNF targeting by means of single chain antibodies or endothelial cell ligands, or combined administration with drugs perturbing integrin-dependent signalling and sensitizing angiogenic endothelial cells to TNF-induced death.
Oxygen Isotopes in Mantle and Crustal Magmas as Revealed by Single Crystal Analysis (2008)

Research Article| January 01, 2008 Oxygen Isotopes in Mantle and Crustal Magmas as Revealed by Single Crystal Analysis Ilya Bindeman Ilya Bindeman Department of Geological Sciences, University of Oregon, Eugene, Oregon, 97403-1272, U.S.A., bindeman@uoregon.edu Search for other works by this author on: GSW Google Scholar Reviews in Mineralogy and Geochemistry (2008) 69 (1): 445–478. https://doi.org/10.2138/rmg.2008.69.12 Article history first online: 13 Jul 2017 Cite View This Citation Add to Citation Manager Share Icon Share MailTo Twitter LinkedIn Tools Icon Tools Get Permissions Search Site Citation Ilya Bindeman; Oxygen Isotopes in Mantle and Crustal Magmas as Revealed by Single Crystal Analysis. Reviews in Mineralogy and Geochemistry 2008;; 69 (1): 445–478. doi: https://doi.org/10.2138/rmg.2008.69.12 Download citation file: Ris (Zotero) Refmanager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentBy SocietyReviews in Mineralogy and Geochemistry Search Advanced Search Oxygen is the most abundant element in the Earth’s crust, mantle, and fluids and therefore its isotopic composition provides robust constraints on magma genesis. Application of oxygen isotope geochemistry to volcanology and igneous petrology provides a much needed foundation for radiogenic isotope and trace element approaches. Since isotope fractionations at high temperature are small, there is a demand for high analytical precision in order to recognize and interpret small (tenths of permil) variations in isotopic composition. Recently improved analytical techniques involving lasers and ion microprobes, and reduction in sample and spot size, has painted a picture of isotope complexity on... You do not have access to this content, please speak to your institutional administrator if you feel you should have access.
Isolation and characterization of luteoskyrin and rugulosin, two hepatotoxic anthraquinonoids from Penicillium islandicum Sopp. and Penicillium rugulosum Thom. (1976)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTIsolation and characterization of luteoskyrin and rugulosin, two hepatotoxic anthraquinonoids from Penicillium islandicum Sopp. and Penicillium rugulosum Thom.Jean C. Bouhet, Paul Pham Van Chuong, Flavio Toma, Marek Kirszenbaum, and Pierre FromageotCite this: J. Agric. Food Chem. 1976, 24, 5, 964–972Publication Date (Print):May 1, 1976Publication History Published online1 May 2002Published inissue 1 May 1976https://pubs.acs.org/doi/10.1021/jf60207a028https://doi.org/10.1021/jf60207a028research-articleACS PublicationsRequest reuse permissionsArticle Views288Altmetric-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-Alertsclose Get e-Alerts
Defective regulation of complement by the sickle erythrocyte: evidence for a defect in control of membrane attack complex formation (1994)

A prominent clinical manifestation of sickle cell disease (SCD) is hemolytic anemia. Although complement activation can lead to intravascular hemolysis, its role in the hemolysis of SCD is not known. Because normal red blood cells induced to vesiculate by treatment with calcium and ionophore become sensitive to damage by activated complement and because sickle cells release microvesicles as they circulate, we postulated that sickle cells might also be unusually sensitive to complement-dependent hemolysis. Complement activation is tightly regulated on the membrane of the normal erythrocyte; therefore, defective complement regulation by the sickle cell would be necessary for complement-dependent hemolysis to occur. These studies show a defect in the regulation of membrane attack complex (C5b-9) formation in sickle erythrocytes, particularly in the most dense cells. The defect is characterized by increased binding of C5b-7 and of C9 to denser sickle cells and results in increased susceptibility of sickle cells to C5b-9-mediated (reactive) lysis initiated by either C5b6 or activated cobra venom factor. Among the densest sickle cells, irreversibly sickled cells are especially sensitive to reactive lysis. The similarity of this defect to that previously described in a patient with paroxysmal nocturnal hemoglobinuria suggests that complement-mediated hemolysis could play a role in the anemia of SCD.