gebhart/patrepeval huggingface dataset:
Transmission ofAnaplasma marginalewith adultBoophilus microplusticks fed as nymphs on calves with different levels of rickettsaemia (1994)

Nine splenectomised calves were infested with dissimilar numbers of adult Boophilus microplus ticks 72 h after collection as engorged nymphs from three non splenectomised calves with different levels of Anaplasma marginale rickettsaemia. Successful transmission of A. marginale appeared to be more dependent on the level of rickettsaemia of the donor calves than on the number of ticks attaching to the splenectomised calves, since infection was transmitted only when the rickettsaemia was 0.3% or greater. Field transmission would thus depend on the rate of tick migration amongst susceptible hosts and the rickettsaemia level of cattle on which the ticks fed previously.
A universal technique for fast and flexible instruction-set architecture simulation (2002)

In the last decade, instruction-set simulators have become an essential development tool for the design of new programmable architectures. Consequently, the simulator performance is a key factor for the overall design efficiency. Based on the extremely poor performance of commonly used interpretive simulators, research work on fast compiled instruction-set simulation was started ten years ago. However, due to the restrictiveness of the compiled technique, it has not been able to push through in commercial products. This paper presents a new retargetable simulation technique which combines the performance of traditional compiled simulators with the flexibility of interpretive simulation. This technique is not limited to any class of architectures or applications and can be utilized from architecture exploration up to end-user software development. The work-flow and the applicability of the so-called just-in-time cache compiled simulation (JIT-CCS) technique will be demonstrated by means of state of the art real world architectures.
Exploration of the directed self-assembly based nano-fabrication design space using computational simulations (2013)

Properly designed geometries of directing pre-patterns broaden the set of lattice symmetries and the local arrangements of patterns achievable by directed self-assembly (DSA) of block copolymers (BCP), compared to the ones achievable in un-directed, bulk systems. We present the results of parametric computational simulation studies, concentrating on exploring the chemoepitaxy or graphoepitaxy directing geometries yielding the DSA structures needed for typical integrated circuits, but not achievable in bulk, undirected annealing of BCP. The examples include the parametric studies of chemoepitaxy and graphoepitaxy DSA patterns etch-transferrable, respectively, into isolated lines and contact hole arrays. The results of the DSA defect simulations are also presented and discussed.
Akt substrate TBC1D1 regulates GLUT1 expression through the mTOR pathway in 3T3-L1 adipocytes (2008)

Multiple studies have suggested that the protein kinase Akt/PKB (protein kinase B) is required for insulin-stimulated glucose transport in skeletal muscle and adipose cells. In an attempt to understand links between Akt activation and glucose transport regulation, we applied mass spectrometry-based proteomics and bioinformatics approaches to identify potential Akt substrates containing the phospho-Akt substrate motif RXRXXpS/T. The present study describes the identification of the Rab GAP (GTPase-activating protein)-domain containing protein TBC1D1 [TBC (Tre-2/Bub2/Cdc16) domain family, member 1], which is closely related to TBC1D4 [TBC domain family, member 4, also denoted AS160 (Akt substrate of 160 kDa)], as an Akt substrate that is phosphorylated at Thr(590). RNAi (RNA interference)-mediated silencing of TBC1D1 elevated basal deoxyglucose uptake by approx. 61% in 3T3-L1 mouse embryo adipocytes, while the suppression of TBC1D4 and RapGAP220 under the same conditions had little effect on basal and insulin-stimulated deoxyglucose uptake. Silencing of TBC1D1 strongly increased expression of the GLUT1 glucose transporter but not GLUT4 in cultured adipocytes, whereas the decrease in TBC1D4 had no effect. Remarkably, loss of TBC1D1 in 3T3-L1 adipocytes activated the mTOR (mammalian target of rapamycin)-p70 S6 protein kinase pathway, and the increase in GLUT1 expression in the cells treated with TBC1D1 siRNA (small interfering RNA) was blocked by the mTOR inhibitor rapamycin. Furthermore, overexpression of the mutant TBC1D1-T590A, lacking the putative Akt/PKB phosphorylation site, inhibited insulin stimulation of p70 S6 kinase phosphorylation at Thr(389), a phosphorylation induced by mTOR. Taken together, our data suggest that TBC1D1 may be involved in controlling GLUT1 glucose transporter expression through the mTOR-p70 S6 kinase pathway.
Multiple metal carbon bonds. Part 29. Facile conversion of tungsten(VI) neopentylidyne complexes into oxo and imido neopentylidene complexes and the crystal structure of W(CCMe3)(PHPh)(PEt3)2Cl2 (1982)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTMultiple metal carbon bonds. Part 29. Facile conversion of tungsten(VI) neopentylidyne complexes into oxo and imido neopentylidene complexes and the crystal structure of W(CCMe3)(PHPh)(PEt3)2Cl2Scott M. Rocklage, Richard R. Schrock, Melvyn Rowen Churchill, and Harvey J. WassermanCite this: Organometallics 1982, 1, 10, 1332–1338Publication Date (Print):October 1, 1982Publication History Published online1 May 2002Published inissue 1 October 1982https://pubs.acs.org/doi/10.1021/om00070a015https://doi.org/10.1021/om00070a015research-articleACS PublicationsRequest reuse permissionsArticle Views380Altmetric-Citations70LEARN 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
The Structure of the MHC Class I Molecule of Bony Fishes Provides Insights into the Conserved Nature of the Antigen-Presenting System (2017)

MHC molecules evolved with the descent of jawed fishes some 350-400 million years ago. However, very little is known about the structural features of primitive MHC molecules. To gain insight into these features, we focused on the MHC class I <i>Ctid</i>-UAA of the evolutionarily distant grass carp (<i>Ctenopharyngodon idella</i>). The <i>Ctid</i>-UAA H chain and β2-microglobulin (<i>Ctid</i>-β2m) were refolded in vitro in the presence of peptides from viruses that infect carp. The resulting peptide-<i>Ctid</i>-UAA (p/<i>Ctid</i>-UAA) structures revealed the classical MHC class I topology with structural variations. In comparison with known mammalian and chicken peptide-MHC class I (p/MHC I) complexes, p/<i>Ctid</i>-UAA structure revealed several distinct features. Notably, 1) although the peptide ligand conventionally occupied all six pockets (A-F) of the Ag-binding site, the binding mode of the P3 side chain to pocket D was not observed in other p/MHC I structures; 2) the AB loop between β strands of the α1 domain of p/<i>Ctid</i>-UAA complex comes into contact with <i>Ctid</i>-β2m, an interaction observed only in chicken p/BF2*2101-β2m complex; and 3) the CD loop of the α3 domain, which in mammals forms a contact with CD8, has a unique position in p/<i>Ctid</i>-UAA that does not superimpose with the structures of any known p/MHC I complexes, suggesting that the p/<i>Ctid</i>-UAA to <i>Ctid</i>-CD8 binding mode may be distinct. This demonstration of the structure of a bony fish MHC class I molecule provides a foundation for understanding the evolution of primitive class I molecules, how they present peptide Ags, and how they might control T cell responses.
Deletion of TLR5 results in spontaneous colitis in mice (2007)

Activation of TLRs by bacterial products results in rapid activation of genes encoding products designed to protect the host from perturbing microbes. In the intestine, which is colonized by a large and diverse population of commensal bacteria, TLR signaling may not function in a simple on/off mode. Here, we show that the flagellin receptor TLR5 has an essential and nonredundant role in protecting the gut from enteric microbes. Mice lacking TLR5 (TLR5KO mice) developed spontaneous colitis, as assessed by well-defined clinical, serologic, and histopathologic indicators of this disorder. Compared with WT littermates, TLR5KO mice that had not yet developed robust colitis exhibited decreased intestinal expression of TLR5-regulated host defense genes despite having an increased bacterial burden in the colon. In contrast, such TLR5KO mice displayed markedly increased colonic expression of hematopoietic-derived proinflammatory cytokines, suggesting that elevated levels of bacterial products may result in activation of other TLRs that drive colitis in TLR5KO mice. In accordance, deletion of TLR4 rescued the colitis of TLR5KO mice in that mice lacking both TLR4 and TLR5 also had elevated bacterial loads in the colon but lacked immunological, histopathological, and clinical evidence of colitis. That an engineered innate immune deficiency ultimately results in spontaneous intestinal inflammation supports the notion that an innate immune deficiency might underlie some instances of inflammatory bowel disease.
Structural Determinants of the Factor IX Molecule Mediating Interaction with the Endothelial Cell Binding Site Are Distinct from Those Involved in Phospholipid Binding (1989)

Previous studies have indicated that Factor IX/IXa interacts in a specific and high affinity manner with a binding site on the endothelial cell surface. In this study, the contributions of the gamma-carboxyglutamic acid-containing (GLA) and growth factor domains to the finding of Factor IX to the endothelium were assessed. While GLA-containing peptides from Factors IX, X, and prothrombin were inhibitors of 125I-Factor IX-endothelial cell binding, the GLA peptide from Factor IX was about 250-800-fold more effective than those from prothrombin and Factor X, respectively. In contrast to its relative efficacy as an inhibitor of Factor IX-cell surface interaction, the Factor IX-GLA peptide neither bound to lipid vesicles nor inhibited Factor IX-lipid interaction. A synthetic peptide comprising the entire first epidermal growth factor (EGF) exon was also an inhibitor of 125I-Factor IX-endothelial cell binding, although it did not interact with lipid vesicles. Experiments with synthetic peptides comprising each of the three loops of the first EGF domain or the entire first EGF region with specific substitutions indicated the importance of determinants in both the first and probably third loops for Factor IX-endothelial interaction. In contrast, the second loop of the first EGF domain and the first loop of the second EGF exon are probably not involved in Factor IX-endothelial interaction based on their inability to block 125I-Factor IX binding to cells. These results indicate that determinants in both the GLA and the first EGF domain contribute to the specific binding of Factor IX to the endothelial cell surface and that structural requirements for Factor IX-cell surface interaction are distinct from those for Factor IX binding to lipids.
Vacuum-Assisted Closure: State of Basic Research and Physiologic Foundation (2006)

A tremendous amount of research has been conducted in recent years investigating the mechanisms of action by which the application of subatmospheric pressure to wounds increases the rate of healing. Similarly, numerous studies have also been conducted examining the physiologic response of wounds to the applied subatmospheric pressure. However, many more need to be conducted. A series of basic studies examining the use of subatmospheric pressure to treat wounds is presented, including the original studies upon which the vacuum-assisted closure device was based (on blood flow, granulation tissue formation, bacterial clearance, and survival of random-pattern pedicle flaps). Subsequent studies analyzing removed fluids, envenomation/extravasation, burns, grafts, and in vitro tissue culture studies are also reviewed. Two broad mechanisms of action are proposed: removal of fluid and mechanical deformation. Fluid removal both decreases edema--thus decreasing interstitial pressure and shortening distances of diffusion--and removes soluble factors that may affect the healing process (both positively and negatively). The relationship of mechanical deformation to increased growth is well known to plastic surgeons, as it is the basis of tissue expansion. While much has been done, a great deal more needs to be done to elucidate the mechanisms of action responsible for the dramatic response seen clinically.
D-type cyclin-binding regions of proliferating cell nuclear antigen (1994)

Proliferating cell nuclear antigen (PCNA) is an auxiliary protein for DNA polymerase delta and is required for both DNA replication and DNA repair. PCNA forms complexes with D-type cyclins, candidate G1 cyclins in mammalian cells. To better understand the functions of the complexes, we examined interactions between PCNA and D-type cyclins, using in vitro-translated mouse PCNA and mouse cyclin D1 or D3 fused to glutathione S-transferase (GST). Analysis of a set of deletion mutants of PCNA revealed that either the N-terminal (residues 2-64) or the C-terminal (residues 197-228) region is necessary for association with D-type cyclins. The cyclin binding of the chimeric protein of the N-terminal (residues 1-68) or the C-terminal (residues 195-261) region of PCNA and rat DNA polymerase beta which does not bind to the cyclins by itself supports this notion. The purified recombinant mouse PCNA expressed in Escherichia coli bound to the D-type cyclin-GST fusion proteins, thereby suggesting that PCNA binds directly to D-type cyclins, without the requirement of other cellular factors. This is apparently the first report on the structure-function relationship of PCNA which may link DNA replication and DNA repair with cell cycle control.
New Strategies for the Synthesis of Hexahydropyrroloindole Alkaloids Inspired by Biosynthetic Hypotheses (2008)

This account concerns synthetic studies of dimeric hexahydropyrroloindole alkaloids. 1 Introduction 2 A Biosynthetic Hypothesis for Calycanthaceous Alkaloids 3 Background 3.1 Prior Synthetic Studies of Calycanthaceous Alkaloids 3.2 Overman’s Enantioselective Syntheses of Chimonanthine 4 Our Work on the Syntheses of Hexahydropyrroloindole Alkaloids 4.1 Early Synthetic Studies of Chimonanthine 4.2 Development of a Cobalt(I)-Promoted Reductive Dimerization Strategy 4.3 New Directions and Our Biosynthetic Hypothesis for Dimeric Indole Alkaloids 5 Conclusion
Systemic expression of HIV-1 tat gene in transgenic mice induces endothelial proliferation and tumors of different histotypes. (1993)

The human immunodeficiency virus tat protein, a transactivator of viral and cellular genes, is suspected to be involved in the pathogenesis of acquired immunodeficiency syndrome-associated tumors. We report that transgenic mice carrying a recombinant DNA containing BK virus early region and the human immunodeficiency virus tat gene develop skin leiomyosarcomas, squamous cell papillomas and carcinomas, adenocarcinomas of skin adnexa, glands, and B-cell lymphomas. Although the incidence of hepatocellular carcinoma is low, most animals show a liver cell dysplasia of variable degree. These mice are also affected by skin lesions resembling the early stages of Kaposi's sarcoma. The transgene was detected intact in all the organs of transgenic mice, generally as multiple tandemly integrated copies. BK virus early region and tat were expressed in essentially all tissues and organs of BK virus/tat transgenic mice. This transgenic mouse model is representative of the systemic involvement of tat in human immunodeficiency virus natural infection and may be applied to investigate the role of tat in malignancies associated to acquired immunodeficiency syndrome, to study Kaposi's sarcoma pathogenesis and cell of origin, to characterize preneoplastic conditions established by tat in the skin and liver, and to assess in vivo the efficacy of antiangiogenic and anti-tat-specific drugs.
Age- and Light-Dependent Development of Localised Retinal Atrophy in CCL2−/−CX3CR1GFP/GFP Mice (2013)

Previous studies have shown that CCL2/CX3CR1 deficient mice on C57BL/6N background (with rd8 mutation) have an early onset (6 weeks) of spontaneous retinal degeneration. In this study, we generated CCL2(-/-)CX3CR1(GFP/GFP) mice on the C57BL/6J background. Retinal degeneration was not detected in CCL2(-/-)CX3CR1(GFP/GFP) mice younger than 6 months. Patches of whitish/yellowish fundus lesions were observed in 17∼60% of 12-month, and 30∼100% of 18-month CCL2(-/-)CX3CR1(GFP/GFP) mice. Fluorescein angiography revealed no choroidal neovascularisation in these mice. Patches of retinal pigment epithelium (RPE) and photoreceptor damage were detected in 30% and 50% of 12- and 18-month CCL2(-/-)CX3CR1(GFP/GFP) mice respectively, but not in wild-type mice. All CCL2(-/-)CX3CR1(GFP/GFP) mice exposed to extra-light (∼800lux, 6 h/day, 6 months) developed patches of retinal atrophy, and only 20-25% of WT mice which underwent the same light treatment developed atrophic lesions. In addition, synaptophysin expression was detected in the outer nucler layer (ONL) of area related to photoreceptor loss in CCL2(-/-)CX3CR1(GFP/GFP) mice. Markedly increased rhodopsin but reduced cone arrestin expression was observed in retinal outer layers in aged CCL2(-/-)CX3CR1(GFP/GFP) mice. GABA expression was reduced in the inner retina of aged CCL2(-/-)CX3CR1(GFP/GFP) mice. Significantly increased Müller glial and microglial activation was observed in CCL2(-/-)CX3CR1(GFP/GFP) mice compared to age-matched WT mice. Macrophages from CCL2(-/-)CX3CR1(GFP/GFP) mice were less phagocytic, but expressed higher levels of iNOS, IL-1β, IL-12 and TNF-α under hypoxia conditions. Our results suggest that the deletions of CCL2 and CX3CR1 predispose mice to age- and light-mediated retinal damage. The CCL2/CX3CR1 deficient mouse may thus serve as a model for age-related atrophic degeneration of the RPE, including the dry type of macular degeneration, geographic atrophy.
A Case for Regulatory B Cells (2006)

B cells are typically characterized by their ability to produce Abs, including autoantibodies. However, B cells possess additional immune functions, including the production of cytokines and the ability to function as a secondary APC. As with T cells, the B cell population contains functionally distinct subsets capable of performing both pathogenic and regulatory functions. Recent studies indicate that regulatory B cells develop in several murine models of chronic inflammation, including inflammatory bowel disease, rheumatoid arthritis, and experimental autoimmune encephalomyelitis. The regulatory function may be directly accomplished by the production of regulatory cytokines IL-10 and TGF-beta and/or by the ability of B cells to interact with pathogenic T cells to dampen harmful immune responses. In this review, we make a case for the existence of regulatory B cells and discuss the possible developmental pathways and functional mechanisms of these B cells.
Cardiovascular and pulmonary response to oral administration of ATP in rabbits (2000)

Extracellular purines such as ATP and adenosine participate in the regulation of cardiovascular and respiratory functions through specific P1 and P2 purine receptors. These properties have mainly been described after intravenous infusion. Experiments reported herein were designed to explore the possible effect of oral ATP administration (3 or 20 mg. kg(-1). day(-1)) on vascular, cardiac, and pulmonary functions in rabbits. Whereas a unique oral dose of ATP has no effect, chronic supplementation during 14 days reduces peripheral vascular resistance, pulmonary resistance, and respiratory frequency and increases arterial PO(2). No effect on central blood pressure and heart rate is observed, but an increase of the left ventricular work index is noticed subsequent to the diminution of vascular resistance. Rather similar cardiovascular modifications are observed in rabbits given 20 mg. kg(-1). day(-1) adenosine for 14 days but without variation of respiratory parameters. These original effects of repeated oral treatment with ATP may result from an adaptive metabolic response to nucleoside supplementation that might affect the turnover of extracellular purines leading to P1- and/or P2-receptor activation.
Structural Relationship of Sperm Soluble Hyaluronidase to the Sperm Membrane Protein PH-201 (1996)

The sperm plasma membrane protein PH-20 has a hyaluronidase activity that enables acrosome-intact sperm to pass through the cumulus cell layer of the egg. In this study we analyzed the relationship of guinea pig PH-20 and the "classical" soluble hyaluronidase released at the time of the acrosome reaction of guinea pig sperm. PH-20 is a membrane protein, anchored in the plasma and inner acrosomal membranes by a glycosyl phosphatidyl inositol anchor. Several types of experiments indicate a structural relationship of PH-20 and the soluble hyaluronidase released during the acrosome reaction. First, an antiserum raised against purified PH-20 is positive in an immunoblot of the soluble protein fraction released during the acrosome reaction. In the released, soluble protein fraction, the anti-PH-20 antiserum recognizes a protein of approximately 64 kDa, i.e., identical in molecular mass to PH-20 (approximately 64 kDa). Second, the enzymatic activity of the released hyaluronidase is completely inhibited (100%) by the anti-PH-20 antiserum. Third, almost all (97%) of the soluble hyaluronidase is removed from the released protein fraction by a single pass through an affinity column made with an anti-PH-20 monoclonal antibody. These findings suggest that the released, soluble hyaluronidase is a soluble form of PH-20 (sPH-20). During the acrosome reaction, PH-20 undergoes endoproteolytic cleavage into two disulfide-linked fragments whereas the released sPH-20 is not cleaved, suggesting the possible activity of a membrane-bound endoprotease on PH-20. We searched for a cDNA encoding sPH-20 but none was found. This result suggests that sPH-20 may arise from the enzymatic release of PH-20 from its membrane anchor, possibly at the time of acrosome reaction.
The PacketStar6400 IP switch - An IP switch for the converged network (1998)

With the transformation of the Internet into a commercial infrastructure, the ability to provide customer-specific and differentiated services has become as important as the ability to meet the massive increases in bandwidth demand. Internet service providers would also like to provide Internet protocol (IP)-based virtual private network (VPN) services that satisfy customer-specific service level agreements using the same shared infrastructure. To meet these demands, it is necessary that routers and switches, in addition to being fast enough to meet ever increasing bandwidth demands, also be capable of providing quality of service (QoS) in a customer-specific manner. This paper describes the architecture, features, and technology innovations of Lucent Technologies' PacketStar 6400-Series IP switch - the first IP switch designed specifically to meet the rising bandwidth demand and the rising need for differentiated services of the evolving, multiservice QoS-capable Internet.