gebhart/patrepeval huggingface dataset:
Research Papers: Effect of Ethoprop, Carbofuran and Aldicarb on Flue-Cured Tobacco Infected with Three Species of Meloidogyne (1982)

Ethoprop, carbofuran and aldicarb were applied at 6.7 kg a.i./ha broadcast to field microplots (76 cm diam) separately infested with Meloidogyne javanica, M. incognita or M. arenaria. Initial population densities of the three species averaged 70, 120 and 170 nematodes per 250 cm of soil, respectively. Two flue-cured tobacco seedlings ('McNair 944') were transplanted into each microplot, and each treatment was replicated six times. Aldicarb significantly increased yields of tobacco infected with all nematode species, whereas ethoprop failed to increase yields of tobacco infected with M. javanica. Carbofuran did not significantly increase yields. Numbers of nematodes of the three species taken at 11 and 15 weeks after planting were reduced by aldicarb and ethoprop, but not by carbofuran. All three nematicides increased plant heights up to 70 days after planting with the exception of carbofuran for plants infected with M. javanica. Gall index ratings at final harvest were high and did n
Review Article: Genetics of Alzheimer Disease (2010)

Alzheimer disease (AD) is the most common causes of neurodegenerative disorder in the elderly individuals. Clinically, patients initially present with short-term memory loss, subsequently followed by executive dysfunction, confusion, agitation, and behavioral disturbances. Three causative genes have been associated with autosomal dominant familial AD (APP, PSEN1, and PSEN2) and 1 genetic risk factor (APOEε4 allele). Identification of these genes has led to a number of animal models that have been useful to study the pathogenesis underlying AD. In this article, we provide an overview of the clinical and genetic features of AD.
Neutrophil Involvement in Cross-Priming CD8+ T Cell Responses to Bacterial Antigens (2004)

Substantial CD8(+) T cell responses are generated after infection of mice with recombinant Listeria monocytogenes strains expressing a model epitope (lymphocytic choriomeningitis virus NP(118-126)) in secreted and nonsecreted forms. L. monocytogenes gains access to the cytosol of infected cells, where secreted Ags can be accessed by the endogenous MHC class I presentation pathway. However, the route of presentation of the nonsecreted Ag in vivo remains undefined. In this study we show that neutrophil-enriched peritoneal exudate cells from L. monocytogenes-infected mice can serve as substrates for in vitro cross-presentation of both nonsecreted and secreted Ag by dendritic cells as well as for in vivo cross-priming of CD8(+) T cells. In addition, specific neutrophil depletion in vivo by low dose treatment with either of two Ly6G-specific mAb substantially decreased the relative CD8(+) T cell response against the nonsecreted, but not the secreted, Ag compared with control Ab-treated mice. Thus, neutrophils not only provide rapid innate defense against infection, but also contribute to shaping the specificity and breadth of the CD8(+) T cell response. In addition, cross-presentation of bacterial Ags from neutrophils may explain how CD8(+) T cell responses are generated against Ags from extracellular bacterial pathogens.
Kinetic basis for selective inhibition of cyclo-oxygenases (1999)

Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit the formation of prostaglandins by cyclo-oxygenases (COX). The discovery of a second COX isoform (COX-2) associated with inflammation led to agents that selectively inhibit COX-2, e.g. celecoxib. We evaluated the kinetics of inhibition of celecoxib and several NSAIDs. Celecoxib displays classic competitive kinetics on COX-1 (Ki=10-16 microM). An initial competitive interaction with COX-2 can also be discerned with celecoxib (Ki=11-15 microM), followed by a time-dependent interaction leading to potent inhibition, characterized as inactivation (Kinact=0.03-0.5 s-1). Half-maximal inhibition (IC50) using end-point assays reflects the competitive component on COX-1 (IC50=4-19 microM) and the inactivation component on COX-2 (IC50=0.003-0.006 microM). NSAIDs exhibit four distinct modes of COX inhibition based on kinetic behaviour: (1) competitive, e.g. ibuprofen; (2) weak binding, time-dependent, e.g. naproxen, oxicams; (3) tight binding, time-dependent, e.g. indomethacin; (4) covalent, e.g. aspirin. In addition, most NSAIDs display different kinetic behaviour for each isoform. Weakly binding inhibitors show variable behaviour in enzyme assays, with apparent inhibitory activity being markedly influenced by experimental conditions; determination of kinetic constants with this class is unreliable and IC50 values are strongly dependent on assay conditions. Although IC50 determinations are useful for structure/activity analyses, the complex and distinct mechanisms of enzyme inhibition of each COX isoform by the NSAIDs renders comparison of inhibitory activity on COX-1 and COX-2 using IC50 ratios of questionable validity.
Characterization of an Immunoglobulin Binding Protein Homolog in the Maize floury-2 Endosperm Mutant (1991)

Elizabeth B. P. Fontes, Brain B. Shank, Russell L. Wrobel, Stephen P. Moose, Gregory R. OBrian, Eleanore T. Wurtzel, Rebecca S. Boston, Characterization of an Immunoglobulin Binding Protein Homolog in the Maize floury-2 Endosperm Mutant, The Plant Cell, Vol. 3, No. 5 (May, 1991), pp. 483-496
Carcinosarcoma of the ovary (2004)

Ovarian carcinosarcoma is a distinct entity with a poor prognosis. Patients with carcinosarcoma differ from those with SAC with regard to having an older mean age of onset, an inferior response to platinum-based chemotherapy, and worse progression-free and cause-specific survival. The extent of benefit from chemotherapy is unclear.
Positively charged side chains in the insulin-like growth factor-1 C- and D-regions determine receptor binding specificity. (1994)

Human insulin-like growth factor-1 (hIGF-1) contains seven positively charged residues in the A-, C-, and D-regions that are not present in similar positions in insulin. To determine whether these residues contribute to receptor binding specificity for the insulin-like growth factor-1 receptor (IGF-1R) relative to the insulin receptor (IR) we examined the binding of hIGF-1 analogs in which these residues have been replaced with either alanine or the corresponding residue of insulin. To improve expression and facilitate purification we employed insulin-like growth factor (IGF-1) analogs modified with an N-terminal 8-amino acid epitope. This additional epitope did not alter receptor binding specificity. Alanine substitution for the positively charged residues in the C- and D-regions of IGF-1 led to 15- and 10-fold losses, respectively, in binding potency for the human IGF-1R, but they increased the potency of binding to the human IR 29- and 6-fold, respectively. In contrast, substitution of the positively charged side chains in the A-region with the corresponding uncharged residues of insulin had little effect on binding to either receptor. These data suggest that the positive charges in the C- and D-regions of IGF-1 contribute significantly to the binding preference of the IGF-1R for IGF-1. In complementary experiments using chimeric receptors we have also shown that the IGF-1 receptor elements required to discriminate in favor of the positive charges in the C- and D-regions are contained in the N-terminal 283 amino acids of the alpha-subunit. Insulin receptor elements that discriminate against these charges are within the N-terminal 225 amino acids of its alpha-subunit.
Insulin-induced Activation of Atypical Protein Kinase C, but Not Protein Kinase B, Is Maintained in Diabetic (ob/ob and Goto-Kakazaki) Liver (2004)

Insulin resistance in type 2 diabetes is characterized by defects in muscle glucose uptake and hepatic overproduction of both glucose and lipids. These hepatic defects are perplexing because insulin normally suppresses glucose production and increases lipid synthesis in the liver. To understand the mechanisms for these seemingly paradoxical defects, we examined the activation of atypical protein kinase C (aPKC) and protein kinase B (PKB), two key signaling factors that operate downstream of phosphatidylinositol 3-kinase and regulate various insulin-sensitive metabolic processes. Livers and muscles of three insulin-resistant rodent models were studied. In livers of type 2 diabetic non-obese Goto-Kakazaki rats and ob/ob-diabetic mice, the activation of PKB was impaired, whereas activation of aPKC was surprisingly maintained. In livers of non-diabetic high fatfed mice, the activation of both aPKC and PKB was maintained. In contrast to the maintenance of aPKC activation in the liver, insulin activation of aPKC was impaired in muscles of Goto-Kakazaki-diabetic rats and ob/ob-diabetic and non-diabetic high fat-fed mice. These findings suggest that, at least in these rodent models, (a) defects in aPKC activation contribute importantly to skeletal muscle insulin resistance observed in both high fat feeding and type 2 diabetes; (b) insulin signaling defects in muscle are not necessarily accompanied by similar defects in liver; (c) defects in hepatic PKB activation occur in association with, and probably contribute importantly to, the development of overt diabetes; and (d) maintenance of hepatic aPKC activation may explain the continued effectiveness of insulin for stimulating certain metabolic actions in the liver.
Molecular Genetics of Human Blood Pressure Variation (1996)

Hypertension is a common multifactorial vascular disorder of largely unknown cause. Recognition that hypertension is in part genetically determined has motivated studies to identify mutations that confer susceptibility. Thus far, mutations in at least 10 genes have been shown to alter blood pressure; most of these are rare mutations imparting large quantitative effects that either raise or lower blood pressure. These mutations alter blood pressure through a common pathway, changing salt and water reabsorption in the kidney. These findings demonstrate the utility of molecular genetic approaches to the understanding of blood pressure variation and may provide insight into the physiologic mechanisms underlying common forms of hypertension.
Inheritance of a genetic factor from the Copenhagen rat and the suppression of chemically induced mammary adenocarcinogenesis. (1988)

Female rats of ten different inbred strains were tested for their susceptibility to 7, 12-dimethylbenz[a]anthracene (DMBA)-induced mammary adenocarcinogenesis. Five of these strains (OM, NSD, WF, LEWIS, BUFF) were demonstrated to be highly susceptible to DMBA exposure developing greater than 2 continuously growing, macroscopically detectable mammary adenocarcinomas/rat following gastric intubation with DMBA. In contrast, the COP female rat is completely resistant. Cross-breeding COP to any of the highly susceptible strains produced F1 hybrids which are resistant to DMBA-induced mammary adenocarcinogenesis. Cross-breeding the same highly susceptible strains to the Fischer strain (i.e., a strain only intermediately susceptible to DMBA) produced F1 hybrids which were just as highly inducible as their highly susceptible non-Fischer parental strain. The resistance of the F1 hybrids produced by cross-breeding these highly susceptible strains to the COP strain therefore is not due to a recessive lack of susceptibility but to an active process of suppression of the high susceptibility of these F1 hybrids to DMBA-induced mammary adenocarcinogenesis. To determine if the site of action of the COP gene responsible for this suppression is in the mammary gland itself or at the host systemic level, a series of factors (i.e., host growth rate, mammary gland growth rate, systemic hormone level during the estrus cycle, serum and tissue levels of DMBA and its metabolites) were compared between female rats of the highly susceptible NSD versus the resistant COP strain. These results suggested that host systemic factors are not involved. To test this directly, donor mammary glands from the highly susceptible NSD and the resistant COP strains were transplanted into F1 hybrids produced by cross-breeding these two strains. The resultant donor glands were then directly exposed to DMBA, the animals were followed, and the incidence of mammary adenocarcinomas was determined. Seventy % of the NSD donor glands developed continuously growing cancers while only 10% of COP donor glands did the same. These results are clearly incompatible with host systemic factors being the major determinant in the resistance of NSD X COP F1 hybrids to DMBA-induced mammary adenocarcinogenesis. Instead, these results directly demonstrate that it is the genetic makeup of the donor mammary gland itself which determines its response to DMBA exposure.
Novel illumination system of synchrotron radiation stepper with full field exposure method (1997)

We estimate the pattern distortion and the critical dimension (CD) variation due to the thermal distortion under a large exposure field for the full field exposure method. We verify that the effect of the thermal distortion of the mask and wafer on the pattern distortion and the CD variation is small enough under the condition of mass production of devices of 0.1 μm design rule. We present a design of the novel two mirror illumination system which can improve the throughput both by exposing a field as large as 50 mm square and by condensing synchrotron radiation (SR) spread in the horizontal plane. The effects of the variation of the position of the SR source and the mirrors and the size of the SR source on the performance of the stepper are investigated.
Effect of preservative, antioxidant and viscolizing agents on in vitro transcorneal permeation of ketorolac tromethamine. (2002)

The influence of formulation additives, e.g. preservative, antioxidant and viscolizing agents on in vitro transcorneal permeation of ketorolac tromethamine from 0.5%(w/v) aqueous drop was studied using goat cornea. Permeation characteristics of drug, from selected formulations, through excised rabbit cornea were also evaluated. Aqueous solution of ketorolac tromethamine (0.5% w/v), pH 6.5 or 7.0 having ionic strength 0.2, was prepared. To this solution perservatives either alone or in combination with other additives were added to have drops of various composition. Permeation studies with goat cornea showed maximum permeation of ketorolac tromethamine from formulation containing benzalkonium chloride and disodium edetate. Increase in viscosity of drop resulted in decreased permeation of drug. Formulation containing benzalkonium chloride and disodium edetate also increased permeation of drug through rabbit cornea. Cumulative permeation of drug through rabbit cornea was found to be 2.3-2.4 fold higher than that observed with goat cornea.
Role of low-affinity Fc receptors in antibody-dependent tumor cell phagocytosis by human monocyte-derived macrophages. (1991)

Human monocyte-derived macrophages (MDM) mediate efficient antibody-dependent cellular cytotoxicity (ADCC) against a variety of human tumor cell types in the presence of an anti-tumor monoclonal antibody. We have recently shown that the mechanism of this ADCC in our in vitro system involves phagocytosis of intact tumor cells. Some forms of macrophage ADCC have been reported to be inhibited by serum immunoglobulin, which competes with monoclonal antibodies for binding to the high-affinity Fc receptor (FcRI). In this study we investigated the role of the three macrophage FcR-gamma in antibody-dependent tumor cell phagocytosis. Hybridoma cells bearing surface antibody directed against either of the two low-affinity Fc receptors (FcRII or FcRIII) were efficiently phagocytosed by MDM, compared to hybridomas bearing irrelevant antibody. Soluble anti-receptor antibodies against FcRII and FcRIII were able to inhibit ADCC but only when both antibodies were simultaneously present. These data suggest that either low-affinity Fc receptor is capable of functioning independently to mediate phagocytosis of tumor cells. Consistent with a mechanism involving the low-affinity receptors rather than FcRI, antibody-dependent phagocytosis occurred in the presence of human serum, purified human IgG, and irrelevant murine antibody. Greater than 75% of the MDM in our culture system were able to ingest tumor cells when a suitable target was available. Optimal phagocytosis occurred at monoclonal antibody concentrations of 10-100 ng/ml. Like other forms of macrophage phagocytosis, ingestion of tumor cells required the presence of divalent cations (either Ca2+ or Mg2+) and an intact actin cytoskeleton (as indicated by sensitivity to cytochalasin D). Because FcRI is normally occupied in vivo by serum immunoglobulin, the participation of low-affinity FcR in tumor cell phagocytosis is potentially important in establishing the in vivo applicability of this efficient form of cytotoxicity.
CD4 is retained in the endoplasmic reticulum by the human immunodeficiency virus type 1 glycoprotein precursor (1990)

We analyzed coexpression of the human immunodeficiency virus type 1 glycoprotein precursor, gp160, and its cellular receptor CD4 in HeLa cells to determine whether the two molecules can interact prior to transport to the cell surface. Results of studies employing coprecipitation, analysis of oligosaccharide processing, and immunocytochemistry showed that newly synthesized CD4 and gp160 form a complex prior to transport from the endoplasmic reticulum (ER). CD4 expressed by itself was transported efficiently from the ER to the cell surface, but the complex of CD4 and gp160 was retained in the ER. This retention of CD4 within the ER is probably a consequence of the very inefficient transport of gp160 itself (R. L. Willey, J. S. Bonifacino, B. J. Potts, M. A. Martin, and R. D. Klausner, Proc. Natl. Acad. Sci. USA 85:9580-9584, 1988). Retention of CD4 in the ER by gp160 may partially explain the down regulation of CD4 in human immunodeficiency virus type 1-infected T cells. Inhibition of CD4 transport appears to be a consequence of the interaction of two membrane-bound molecules, because a complex of CD4 and gp120 (the soluble extracellular domain of gp160) was transported rapidly and efficiently from the ER.
Green Fluorescent Protein in the sea urchin: new experimental approaches to transcriptional regulatory analysis in embryos and larvae (1997)

The use of Green Fluorescent Protein (GFP) as a reporter for expression transgenes opens the way to several new experimental strategies for the study of gene regulation in sea urchin development. A GFP coding sequence was associated with three different previously studied cis-regulatory systems, viz those of the SM50 gene, expressed in skeletogenic mesenchyme, the CyIIa gene, expressed in archenteron, skeletogenic and secondary mesenchyme, and the Endo16 gene, expressed in vegetal plate, archenteron and midgut. We demonstrate that the sensitivity with which expression can be detected is equal to or greater than that of whole-mount in situ hybridization applied to detection of CAT mRNA synthesized under the control of the same cis-regulatory systems. However, in addition to the important feature that it can be visualized nondestructively in living embryos, GFP has other advantages. First, it freely diffuses even within fine cytoplasmic cables, and thus reveals connections between cells, which in sea urchin embryos is particularly useful for observations on regulatory systems that operate in the syncytial skeletogenic mesenchyme. Second, GFP expression can be dramatically visualized in postembryonic larval tissues. This brings postembryonic larval developmental processes for the first time within the easy range of gene transfer analyses. Third, GFP permits identification and segregation of embryos in which the clonal incorporation of injected DNA has occurred in any particular desired region of the embryo. Thus, we show explicitly that, as expected, GFP transgenes are incorporated in the same nuclei together with other transgenes with which they are co-injected.
Interaction between Deformation and Crack Initiation under Vickers Indentation in Na2O–TiO2–SiO2 Glasses (2017)

An observed minimum in the critical crack initiation load at Poisson's ratio (ν) of 0.21-0.22 in Na2O-TiO2-SiO2 glasses was investigated. Vickers indentation was used to examine hardness and average cracking length, fracture toughness was measured through the single-edge pre-cracked beam method (SEPB), and volumes of densification and shear flow around indents were measured using atomic force microscopy (AFM). Relations between the critical crack initiation load and hardness, average crack length, fracture toughness, and the volume fractions of densification and shear flow were studied. No correlations were observed between hardness, average crack length, or fracture toughness with the critical crack initiation load. A link between the minimum in crack initiation load and a change in deformation mechanisms (densification vs. shear flow) was observed.
Passatempo Virus, a Vaccinia Virus Strain, Brazil (2005)

Passatempo virus was isolated during a zoonotic outbreak. Biologic features and molecular characterization of hemagglutinin, thymidine kinase, and vaccinia growth factor genes suggested a vaccinia virus infection, which strengthens the idea of the reemergence and circulation of vaccinia virus in Brazil. Molecular polymorphisms indicated that Passatempo virus is a different isolate.
Immunohistological intensity measurements as a tool to assess sarcolemma‐associated protein expression (2009)

This comparative method adds value to techniques that are already part of the diagnostic process and can be used with minimal variation of the standardized protocols, without using extra amounts of valuable biopsy samples. Comparative quantification of sarcolemmal proteins on immunostained muscle sections will be of use to establish both the abundance and localization of the protein. Moreover, it can be applied to assess the efficacy of experimental therapies where only partial restoration or upregulation of the protein may occur.
Approximating age-based arbitration in on-chip networks (2010)

The on-chip network of emerging many-core CMPs enables the sharing of numerous on-chip components. This on-chip network needs to ensure fairness when accessing the shared resources. In this work, we propose providing equality of service (EoS) in future many-core CMPs on-chip networks by leveraging distance, or hop count, to approximate the age of packets in the network. We propose probabilistic arbitration combined with distance-based weights to achieve EoS and overcome the limitation of conventional round-robin arbiter. We describe how nonlinear weights need to be used with probabilistic arbiters and propose three different arbitration weight metrics - fixed weight, constantly increasing weight, and variably increasing weight. By only modifying the arbitration of an on-chip router, we do not require any additional buffers or virtual channels and create a complexity-effective mechanism for achieving EoS.
Development of Single Phase UPS having AC Chopper and Active Filter Ability (2006)

This paper describes about development of single phase uninterruptible power supply (UPS) having AC chopper and active filter ability. The proposed UPS consists of a single phase full bridge type active filter and the source and load side AC choppers using bidirectional IGBT switches. It realizes long life and maintenance free of the main circuit because it has no use of the bulky electrolytic capacitor. The proposed UPS has active filter ability between the source and load side choppers, which realizes unity input power factor operation. The AC chopper regulates the output voltage sinusoidaly. The fundamental source power supply to the load in direct without switching of the every AC choppers under the normal power condition, which achieves high efficient system and high system reliability. The simulation results point out that the proposed UPS has the desired input and output characteristics such as 99% power factor and under 3% voltage regulation.