gebhart/patrepeval huggingface dataset:
Overexpression of the Cell Death Suppressor Bcl-w in Ischemic Brain: Implications for a Neuroprotective Role via the Mitochondrial Pathway (2000)

Bcl-w is a newly described cell death suppressor member of the Bcl-2 gene family. As these genes may have a role in the outcome of ischemic brain injury, the regional expression of Bcl-w protein in rat brain was examined at 6 to 72 hours after 90 minutes of transient middle cerebral artery occlusion. Bcl-w protein, although constitutively expressed at low levels in nonischemic brain, was found to be overexpressed in ischemic brain at all time points studied. Up-regulation of Bcl-w protein was particularly abundant in the penumbral region of the cortex and mainly in cells lacking DNA fragmentation. In the cortical penumbra, Bcl-w protein was detected predominantly in neurons and showed mitochondrial localization, as determined using double-label immunohistochemistry. Bcl-w expression was also detectable, to a lesser extent, in reactive astrocytes in the infarct border zone and in microvessel walls in the infarct regions. At the mechanistic level, incubation of isolated brain mitochondria with the addition of recombinant Bax or high concentration of calcium resulted in release of cytochrome c from the mitochondria. In the presence of recombinant Bcl-w protein, however, the release of cytochrome c induced by Bax or calcium was largely inhibited. Further, recombinant Bcl-w protein inhibited calcium-induced loss of mitochondrial transmembrane potential, indicative of permeability transition, in a dose-dependent manner. These results suggest that Bcl-w may be an endogenous neuroprotectant against ischemic neuronal death and that, like its analogues such as Bcl-2 and Bcl-x-long, Bcl-w may achieve this protection via the mitochondrial death-regulatory pathway.
Adiposity of the Heart*, Revisited (2006)

Obesity is a major risk factor for heart disease. In the face of obesity's growing prevalence, it is important for physicians to be aware of emerging research of novel mechanisms through which adiposity adversely affects the heart. Conventional wisdom suggests that either hemodynamic (that is, increased cardiac output and hypertension) or metabolic (that is, dyslipidemic) derangements associated with obesity may predispose individuals to coronary artery disease and heart failure. The purpose of this review is to highlight a novel mechanism for heart disease in obesity whereby excessive lipid accumulation within the myocardium is directly cardiotoxic and causes left ventricular remodeling and dilated cardiomyopathy. Studies in animal models of obesity reveal that intracellular accumulation of triglyceride renders organs dysfunctional, which leads to several well-recognized clinical syndromes related to obesity (including type 2 diabetes). In these rodent models, excessive lipid accumulation in the myocardium causes left ventricular hypertrophy and nonischemic, dilated cardiomyopathy. Novel magnetic resonance spectroscopy techniques are now available to quantify intracellular lipid content in the myocardium and various other human tissues, which has made it possible to translate these studies into a clinical setting. By using this technology, we have recently begun to study the role of myocardial steatosis in the development of obesity-specific cardiomyopathy in humans. Recent studies in healthy individuals and patients with heart failure reveal that myocardial lipid content increases with the degree of adiposity and may contribute to the adverse structural and functional cardiac adaptations seen in obese persons. These studies parallel the observations in obese animals and provide evidence that myocardial lipid content may be a biomarker and putative therapeutic target for cardiac disease in obese patients.
The microbicidal agent C31G inhibits Chlamydia trachomatis infectivity in vitro (1997)

Safe and effective vaginal microbicidal compounds are being sought to offer women an independent method for protection against transmission of sexually acquired pathogens. The purpose of this study was to examine the efficacy of two formulations of one such compound, C31G, against Chlamydia trachomatis serovar E alone, its host epithelial cell (HEC-1B) alone, and against chlamydiae-infected HEC-1B cells. Preexposure of isolated, purified infectious chlamydial elementary bodies (EB) to C31G, at pHs 7.2 and 5.7, for 1 h at 4 degrees C resulted in reduced infectivity of EB for HEC-1B cells. Examination of the C31G-exposed 35S-EB on sodium dodecyl sulfate-polyacrylamide gel electrophoresis autoradiographs and by Western blotting revealed a C31G concentration-dependent and pH-dependent destabilization of the chlamydial envelope, resulting in the release of chlamydial lipopolysaccharide and proteins. Interestingly, when the host human genital columnar epithelial cells were infected with chlamydiae and then exposed to dilute concentrations of C31G which did not alter epithelial cell viability, chlamydial infectivity was also markedly reduced. C31G gained access to the developing chlamydial inclusion causing damage to or destruction of metabolically active reticulate bodies as well as apparent alteration of the inclusion membrane, which resulted in premature escape of chlamydial antigen to the infected epithelial surface. These studies show that the broad-spectrum antiviral and antibacterial microbicide C31G also has antichlamydial activity.
Detection and classification of football players with automatic generation of models (2010)

We focus on the automatic detection and classification of players in a football match. Our approach is not based on any a priori knowledge of the outfits, but on the assumption that the two main uniforms detected correspond to the two football teams. The algorithm is designed to be able to operate in real time, once it has been trained, and is able to detect partially occluded players and update the color of the kits to cope with some gradual illumination changes through time. Our method, evaluated from real sequences, gave better detection and classification results than those obtained by a system using a manual selection of samples to compute a Gaussian mixture model.
Receptor-interacting Protein 140 Directly Recruits Histone Deacetylases for Gene Silencing (2000)

Receptor-interacting protein 140 (RIP140) encodes a histone deacetylase (HDAC) inhibitor-sensitive repressive activity. Direct interaction of RIP140 with HDAC1 and HDAC3 occurs in vitro and in vivo as demonstrated in co-immunoprecipitation and glutathione S-transferase pull-down experiments. The HDAC-interacting domain of RIP140 is mapped to its N-terminal domain, between amino acids 78 and 303 based upon glutathione S-transferase pull-down experiments. In chromatin immunoprecipitation assays, it is demonstrated that histone deacetylation occurs at the chromatin region of the Gal4 binding sites as a result of Gal4 DNA binding domain-tethered RIP expression. The immunocomplexes of RIP140 from cells transfected with RIP140 and HDAC are able to deacetylate histone proteins in vitro. This study presents the first evidence for RIP140 as a negative coregulator for nuclear receptor actions by directly recruiting histone deacetylases and categorizes RIP140 as a novel negative coregulator that is able to directly interact with HDACs.
Extracting the textual and temporal structure of supercomputing logs (2009)

Supercomputers are prone to frequent faults that adversely affect their performance, reliability and functionality. System logs collected on these systems are a valuable resource of information about their operational status and health. However, their massive size, complexity, and lack of standard format makes it difficult to automatically extract information that can be used to improve system management. In this work we propose a novel method to succinctly represent the contents of supercomputing logs, by using textual clustering to automatically find the syntactic structures of log messages. This information is used to automatically classify messages into semantic groups via an online clustering algorithm. Further, we describe a methodology for using the temporal proximity between groups of log messages to identify correlated events in the system. We apply our proposed methods to two large, publicly available supercomputing logs and show that our technique features nearly perfect accuracy for online log-classification and extracts meaningful structural and temporal message patterns that can be used to improve the accuracy of other log analysis techniques.
Image Completion Using Global Optimization (2006)

A new exemplar-based framework unifying image completion, texture synthesis and image inpainting is presented in this work. Contrary to existing greedy techniques, these tasks are posed in the form of a discrete global optimization problem with a well defined objective function. For solving this problem a novel optimization scheme, called Priority- BP, is proposed which carries two very important extensions over standard belief propagation (BP): "prioritybased message scheduling" and "dynamic label pruning". These two extensions work in cooperation to deal with the intolerable computational cost of BP caused by the huge number of existing labels. Moreover, both extensions are generic and can therefore be applied to any MRF energy function as well. The effectiveness of our method is demonstrated on a wide variety of image completion examples.
Evidence for at least two dominant neutralization antigens on human rhinovirus 14 (1985)

A collection of 28 mutants of human rhinovirus 14, selected for resistance to 10 individual neutralizing monoclonal antibodies, was used to identify two major neutralization antigens, N-Ag I and N-Ag II. Isoelectric analysis showed that all 16 of the N-Ag I mutants analyzed were charge altered in VP1;8 of 12 N-Ag II mutants were altered in VP3. These results suggest that N-Ag I resides on VP1, whereas N-Ag II lies on VP3. The frequency of charge alterations was much higher than predicted by the genetic code, suggesting that charged amino acids on the antigenic sites play an important role in interaction with neutralizing antibody. Antibodies against N-Ag I and N-Ag II neutralize with widely different efficiencies.
Essential Amino Acid and Carbohydrate Supplementation Ameliorates Muscle Protein Loss in Humans during 28 Days Bedrest (2004)

We determined whether essential amino acid and carbohydrate supplementation could offset the catabolic response to prolonged inactivity. Major outcome measures included mixed muscle fractional synthetic rate (FSR), phenylalanine net balance, lean leg mass, and leg extension strength. On d 1 and 28, vastus lateralis muscle biopsies and femoral arterio-venous blood samples were obtained during a primed constant infusion of l-[ring-(2)H(5)]phenylalanine. Net balance and FSR were calculated over 16 h, during which the control group (CON) received a nutritionally mixed meal every 5 h (0830, 1330, and 1830 h). The experimental group (EXP) also consumed 16.5 g essential amino acids and 30 g carbohydrate (1100, 1600, and 2100 h). The dietary regimen was maintained during bedrest. FSR was higher in the EXP group on d 1 (EXP, 0.099 +/- 0.008%/h; CON: 0.075 +/- 0.005%/h) and d 28 (EXP, 0.093 +/- 0.006%/h; CON, 0.055 +/- 0.007%/h). Lean leg mass was maintained throughout bedrest in the EXP group (+0.2 +/- 0.3 kg), but fell in the CON group (-0.4 +/- 0.1 kg). Strength loss was more pronounced in the CON group (EXP, -8.8 +/- 1.4 kg; CON, -17.8 +/- 4.4 kg). Essential amino acid and carbohydrate supplementation may represent a viable intervention for individuals at risk of sarcopenia due to immobility or prolonged bedrest.
Cortisol is not the primary mediator for augmented CXCR4 expression on natural killer cells after acute exercise (2014)

CXC-chemokine receptor 4 (CXCR4) and its ligand, stromal-derived factor 1α (SDF-1α; also known as CXCL12), are crucial for the redistribution of immune cells after acute exercise. We investigated the relationships between acute exercise and CXCR4 expression on natural killer (NK) cells. Peripheral blood mononuclear cells (PBMCs) were cultured with cortisol and analyzed for CXCR4 expression on CD3(-)/CD56(+) NK cells and NK cell migration activity. To determine the effect of exercise, we isolated PBMCs from subjects before and after a 90-min exercise at 70% peak O2 uptake (V̇o2peak) and determined the changes in CXCR4 expression on NK cells after exercise. We cultured PBMCs with plasma obtained before and after exercise and with the glucocorticoid antagonist RU-486 to determine NK cell migration activity and the effects of cortisol on CXCR4 expression in vitro. Cortisol treatment increased CXCR4 expression (P < 0.05) and migration activity (P < 0.05) of NK cells. Exercise did not affect CXCR4 expression on NK cells, whereas incubating them with postexercise plasma significantly increased CXCR4 expression (P < 0.05) and migration activity (P < 0.05). RU-486 blocked cortisol-induced CXCR4 upregulation on NK cells, but only partially blocked (7%) CXCR4 upregulation when PMBCs were incubated with postexercise plasma. Thus acute exercise increases CXCR4 expression on NK cells and their migration activity and may contribute to NK cell redistribution after acute exercise; however, cortisol did not appear to be the primary mediator of augmented CXCR4 expression.
Direct and Differential Suppression of Myeloid-Derived Suppressor Cell Subsets by Sunitinib Is Compartmentally Constrained (2010)

The antiangiogenic drug sunitinib is a receptor tyrosine kinase inhibitor with significant, yet not curative, therapeutic effects in metastatic renal cell carcinoma (RCC). Sunitinib is also an immunomodulator, potently reversing myeloid-derived suppressor cell (MDSC) accumulation and T-cell inhibition in the blood even of nonresponder RCC patients. We observed that sunitinib similarly prevented MDSC accumulation and restored normal T-cell function to the spleens of tumor-bearing mice, independent of the capacity of sunitinib to inhibit tumor progression (RENCA>CT26>4T1). Both monocytic and neutrophilic splenic MDSC were highly repressible by sunitinib. In contrast, MDSC within the microenvironment of 4T1 tumors or human RCC tumors proved highly resistant to sunitinib and ambient T-cell function remained suppressed. Proteomic analyses comparing tumor to peripheral compartments showed that granulocyte macrophage colony-stimulating factor (GM-CSF) predicted sunitinib resistance and recombinant GM-CSF conferred sunitinib resistance to MDSC in vivo and in vitro. MDSC conditioning with GM-CSF uniquely inhibited signal transducers and activators of transcription (STAT3) and promoted STAT5 activation. STAT5ab(null/null) MDSC were rendered sensitive to sunitinib in the presence of GM-CSF in vitro. We conclude that compartment-dependent GM-CSF exposure in resistant tumors may account for the regionalized effect of sunitinib upon host MDSC modulation and hypothesize that ancillary strategies to decrease such regionalized escape will enhance the potency of sunitinib as an immunomodulator and a cancer therapy.
Rhodococcus equi (2004)

Rhodococcus equi is an important cause of subacute or chronic abscessating bronchopneumonia of foals up to 3-5 months of age. It shares the lipid-rich cell wall envelope characteristic of the mycolata, including Mycobacterium tuberculosis, as well as the ability of pathogenic members of this group to survive within macrophages. The possession of a large virulence plasmid in isolates recovered from pneumonic foals is crucial for virulence. The plasmid contains an 27 kb pathogenicity island (PI) that encodes seven related virulence-associated proteins (Vaps), including the immunodominant surface-expressed protein, VapA. Only PI genes are differentially expressed when the organism is grown in macrophages in vitro. Ten of the PI genes, including six Vap genes, have signal sequences, suggesting that they are exported from the cell to interact with the macrophage. Different PI genes are regulated by temperature, pH, iron, oxidative stress and probably also by magnesium, all environmental changes encountered after environmental R. equi are inhaled in dust and are ingested into macrophages in the lung. The basis of pathogenicity of R. equi is its ability to multiply in and eventually to destroy alveolar macrophages. Infectivity is largely or exclusively limited to cells of the monocyte-macrophage lineage. Current evidence suggests that infection of foals with virulent R. equi results in some foals in subversion of cell-mediated immunity and development of an ineffective and sometimes lethal Th2-based immune response. Significant progress has been made recently in the development of R. equi-E. coli shuttle vectors, transformation and random and site specific mutagenesis procedures, all of which will be important in molecular dissection of the mechanisms by which R. equi subverts normal macrophage killing mechanisms and cell-mediated immunity.
Effects of Alpha1-adrenoceptor (?1-AR) antagonists on cell proliferation and apoptosis in the prostate: Therapeutic implications in prostatic disease (2000)

Taken together, our findings demonstrate the ability of the quinazoline alpha-blockers, terazosin and doxazosin, but not the sulphonamide, tamsulosin, to suppress prostate growth by inducing apoptosis among the epithelial cells in the benign and malignant prostate. These studies underwrite the durability of the response seen in long-term studies with terazosin, and suggest the potential of this drug in the treatment of prostate carcinoma.
Viruses Recovered from Laboratory Dogs with Respiratory Disease (1967)

SummaryViruses were recovered from throat specimens of 21 of 53 dogs with respiratory disease and from the post-mortem tissues of 7 of 10 dogs. Many of these dogs were infected with more than one agent. The agents were 2 canine adenoviruses, a canine herpes virus and a SV-5-like virus. Rises in antibody titer to the isolated viruses were demonstrated in dogs which survived. The antibody response to the SV-5-like virus was specific to the isolated virus and SV-5 and not to other members of the parainfluenza group.
Total body hyperthermia and preliminary results in human neoplasms. (1976)

We believe the hyperthermia is an effective adjunct to current modes of cancer therapy and warrants further study. The method described is safe and effective in achieving controlled total body hyperthermia. Monitoring techniques and life support measure are discussed. Limits of tolerance in humans are defined in this series as 41.8 C for 5 hr and 42 C (108F) for 2 hr, with the heart and liver as the limiting organs.
Vertical device architecture by molding of organic-based thin film transistor (1998)

An organic thin film transistor (TFT) of circular geometry is constructed by the use of polymer-based substrate, insulator, and semiconductor. Owing to the plasticity of organic materials, this device is mechanically molded by pressing the central circular drain electrode. A shallow well is created, resulting in the localization of the transistor channel onto the wall of the well. The electrical characteristics of the transistor remain almost unchanged after this molding. The obtained vertical device architecture allows the use of a very large channel width over length ratio, while preserving a maximum drain electrode area to be devoted to the further deposition of liquid crystal or an electroluminescent film. Current output of the order of some milliamperes per square centimeter can be delivered, which makes these molded TFTs well adapted for the construction of display pixels.
The Pathology of Vitreous Hemorrhage (1979)

We undertook an ultrastructural study of the dual processes of hemolysis and vitreous membrane formation during the resolution of vitreous blood clots in rabbits. Red blood cell degradation began within 24 hours before the onset of the inflammatory response and occurred mainly in the extracellular matrix. Macrophage activity was directed at clearing lysed RBC debris, rather than engulfing whole RBCs. Hemolysis in the vitreous may have been initiated by the unfavorable microenvironment. Two types of vitreous membranes occurred during vitreous clot lysis. Cellular membranes were composed of aggregates of giant macrophages enclosed within a thin collagen sheet. Acellular membranes developed from coaggregated vitreous collagen fibers. A prominent acellular membrane surrounded the blood clot as a pseudocapsule. No fibroblasts or fresh collagen deposition were observed.
Stress and open-office noise. (2000)

Forty female clerical workers were randomly assigned to a control condition or to 3-hr exposure to low-intensity noise designed to simulate typical open-office noise levels. The simulated open-office noise elevated workers' urinary epinephrine levels, but not their norepinephrine or cortisol levels, and it produced behavioral aftereffects (fewer attempts at unsolvable puzzles) indicative of motivational deficits. Participants were also less likely to make ergonomic, postural adjustments in their computer work station while working under noisy, relative to quiet, conditions. Postural invariance is a risk factor for musculoskeletal disorder. Although participants in the noise condition perceived their work setting as significantly noisier than those working under quiet conditions did, the groups did not differ in perceived stress. Potential health consequences of long-term exposure to low-intensity office noise are discussed.
Heat shock stimulates the release of arachidonic acid and the synthesis of prostaglandins and leukotriene B4 in mammalian cells (1989)

Heat shock has a profound influence on the metabolism and behavior of eukaryotic cells. We have examined the effects of heat shock on the release from cells of arachidonic acid and its bioactive eicosanoid metabolites, the prostaglandins and leukotrienes. Heat shock (42-45 degrees) increased the rate of arachidonic acid release from human, rat, murine, and hamster cells. Arachidonate accumulation appeared to be due, at least partially, to stimulation of a phospholipase A2 activity by heat shock and was accompanied by the accumulation of lysophosphatidyl-inositol and lysophosphatidylcholine in membranes. Induction of arachidonate release by heat did not appear to be mediated by an increase in cell Ca++. Stimulation of arachidonate release by heat shock in hamster fibroblasts was quantitatively similar to the receptor-mediated effects of alpha thrombin and bradykinin. The effects of heat shock and alpha thrombin on arachidonate release were inhibited by glucocorticoids. Increased arachidonate release in heat-shocked cells was accompanied by the accelerated accumulation of cyclooxygenase products prostaglandin E2 and prostaglandin F2 alpha and by 5-lipoxygenase metabolite leukotriene B4. Elevated concentrations of arachidonic acid and metabolites may be involved in the cytotoxic effects of hyperthermia, in homeostatic responses to heat shock, and in vascular and inflammatory reactions to stress.