gebhart/patrepeval huggingface dataset:
Inhibiting the Complement System Does Not Reduce Injury in Renal Ischemia Reperfusion (2001)

The complex pathogenesis of ischemia reperfusion injury (IRI) includes endothelial expression of adhesion molecules, leukocyte recruitment and activation, reactive oxygen species production, and apoptotic and necrotic cell death. A role for complement in IRI of different organs, including kidney, has been proposed on the basis of results of experiments that used pharmacologic inhibitors as well as animals that were deficient in individual complement proteins. Here, renal IRI in mice was examined. Animals that were deficient in C3 had partial protection from IRI induced by 27.5 min of bilateral renal ischemia, followed by 20 h of reperfusion (blood urea nitrogen [BUN] values, 46.6 +/- 6.9 and 68.4 +/- 7.9 mg/dl in C3 -/- and C3 +/+ mice; n = 7 and 8, respectively; P = 0.033). Given the reduction in IRI in C3 -/- mice, it was investigated, by use of the rodent C3 convertase inhibitor CR1-related gene/protein y-Ig (Crry-Ig), whether exogenous administration of a complement inhibitor could lessen renal injury. Despite the use of Crry-Ig in high doses, there was no significant reduction of injury induced by 20 to 30 min of ischemia followed by up to 30 h of reperfusion. Histologic examination revealed acute tubular necrosis and neutrophilic infiltration, both of which correlated significantly with BUN values (P < 0.001). Of interest, C3 deposition around renal tubules was significantly less in animals with IRI, compared with that in unmanipulated controls (P < 0.001). In Crry-Ig-treated animals, C3 deposition was inversely proportional to BUN values (r = -0.63; P < 0.001), which presumably indicates that severe vascular IRI allowed access of the 160 kD Crry-Ig to the interstitium. Thus, renal IRI in mice may have a partial complement dependence, yet pharmacologic inhibition of the complement system does not seem to be effective, likely because of the presence of other mediator systems that operate in parallel.
Klebsiella pneumoniae genes for citrate lyase and citrate lyase ligase: localization, sequencing, and expression (1994)

In the course of studies on anaerobic citrate metabolism in Klebsiella pneumoniae, the DNA region upstream of the gene for the sodium-dependent citrate carrier (citS) was investigated. Nucleotide sequence analysis revealed a cluster of five new genes that were oriented inversely to citS and probably form an operon. The genes were named citCDEFG. Based on known protein sequence data, the gene products derived from citD, citE and citF could be identified as the gamma-, beta-, and alpha-subunits of citrate lyase, respectively. This enzyme catalyses the cleavage of citrate to oxaloacetate and acetate. The gene product derived from citC (calculated M(r) 38,476) exhibited no obvious similarity to other proteins. In the presence of acetate and ATP, cell extracts from a citC-expressing Escherichia coli strain were able to reactivate purified citrate lyase from K. pneumoniae that had been inactivated by chemical deacetylation of the prosthetic group. This represents 5-phosphoribosyl-dephospho-acetyl-coenzyme A which is covalently bound to serine-14 of the acyl carrier protein (gamma-subunit). CitC was thus identified as acetate:SH-citrate lyase ligase. The function of the gene product derived from citG (M(r) 32,645) has not yet been identified. Expression of the citCDEFG gene cluster in E. coli led to the formation of citrate lyase which was active only in the presence of acetyl-coenzyme A, a compound known to substitute for the prosthetic group. These and other data strongly indicated that the enzyme synthesized in E. coli lacked its prosthetic group. Thus, additional genes besides citCDEFG appear to be required for the formation of holo-citrate lyase.
Co-Expression of Yeast Amber Suppressor tRNATyr and Tyrosyl-tRNA Synthetase in Escherichia coli: Possibility to Expand the Genetic Code (1998)

An efficient system was developed for the co-expression of a yeast tRNATyr/tyrosyl-tRNA synthetase (TyrRS) pair in Escherichia coli. Analysis of suppression patterns using several sets of E. coli and lambda phage mutants indicated that the expressed yeast suppressor tRNATyr was aminoacylated only with tyrosine by its cognate yeast TyrRS and not by E. coli TyrRS or other aminoacyl-tRNA synthetases. This extra tRNA/TyrRS pair is expected to be a key bridgehead for developing an in vivo system for the site-directed incorporation of unnatural amino acids into proteins.
A novel approach: high resolution inspection with wafer plane defect detection (2008)

High Resolution reticle inspection is well-established as a proven, effective, and efficient means of detecting yield-limiting mask defects as well as defects which are not immediately yield-limiting yet can enable manufacturing process improvements. Historically, RAPID products have enabled detection of both classes of these defects. The newly-developed Wafer Plane Inspection (WPI) detector technology meets the needs of some advanced mask manufacturers to identify the lithographically-significant defects while ignoring the other non-lithographically-significant defects. Wafer Plane Inspection accomplishes this goal by performing defect detection based on a modeled image of how the mask features would actually print in the photoresist. This has the effect of reducing sensitivity to non-printing defects while enabling higher sensitivity focused in high MEEF areas where small reticle defects still yield significant printing defects on wafers. WPI is a new inspection mode that has been developed by KLA-Tencor and is currently under test with multiple customers. It employs the same transmitted and reflected-light high-resolution images as the industry-standard high-resolution inspections, but with much more sophisticated processing involved. A rigorous mask pattern recovery algorithm is used to convert the transmitted and reflected light images into a modeled representation of the reticle. Lithographic modeling of the scanner is then used to generate an aerial image of the mask. This is followed by resist modeling to determine the exposure of the photoresist. The defect detectors are then applied on this photoresist plane so that only printing defects are detected. Note that no hardware modifications to the inspection system are required to enable this detector. The same tool will be able to perform both our standard High Resolution inspections and the Wafer Plane Inspection detector. This approach has several important features. The ability to ignore non-printing defects and to apply additional effective sensitivity in high MEEF areas enables advanced node development. In addition, the modeling allows the inclusion of important polarization effects that occur in the resist for high NA operation. This allows for the results to better match wafer print results compared to alternate approaches. Finally, the simulation easily allows for the application of arbitrary illumination profiles. With this approach, users of WPI can make use of unique or custom scanner illumination profiles. This allows the more precise modeling of profiles without inspection system hardware modification or loss of company intellectual property. This paper examines WPI in Die:Die mode. Future work includes a review of Die:Database WPI capability.
Parenteral Amino Acid and Metabolic Acidosis in Premature Infants (2007)

Low-birth-weight infants develop metabolic acidosis between 2 and 5 days after birth, irrespective of dose and duration of parenteral amino acid administration. Careful management of parenteral fluids and comorbidities may lower the incidence of acidosis and promote protein accretion.
Combined two‐photon luminescence microscopy and OCT for macrophage detection in the hypercholesterolemic rabbit aorta using plasmonic gold nanorose (2012)

Results suggest that TPL microscopy combined with OCT can simultaneously reveal macrophage distribution with respect to aorta surface structure, which has the potential to detect vulnerable plaques and monitor plaque-based macrophages overtime during cardiovascular interventions.
Current Pharmacological Treatment of Nonalcoholic Fatty Liver (2006)

Nonalcoholic fatty liver disease (NAFLD) is a frequent and potentially progressive chronic liver disease that occurs in subjects who do not abuse alcohol. NAFLD is often associated with obesity, metabolic syndrome and insulin resistance and its more aggressive form, nonalcoholic steatohepatitis (NASH) is a major cause of cryptogenic cirrhosis. NAFLD/NASH are commonly detected because of elevated serum aminotransferase levels, ultrasonographic fatty liver and, at liver histology, steatosis, inflammation, and occasionally fibrosis that may progress to cirrhosis. No established treatment exists for this potentially serious disorder. Current management of NAFLD/NASH is largely conservative and includes diet regimen, aerobic exercise, and interventions towards the associated metabolic abnormalities. The main concern is therefore to decrease liver steatosis and its progression toward steatohepatitis and fibrosis, and the risk of "cryptogenic" cirrhosis. Among the most promising medications, weight reducing drugs, insulin sensitizers and lipid-lowering agents, antioxidants, bile salts, co-factors increasing the mitochondrial transport of fatty acids are being considered. Among them, thiazolidinediones are the most promising drug family that act by activating PPARgamma nuclear receptors and by regulating both microsomal and peroxisomal lipid oxidative pathways. Pharmacological treatment of obesity and probiotics should be considered as potential therapeutic options. In this review, after summarizing the general background on fatty liver, the most current and attractive pharmacological approaches to the problem of NAFLD/NASH are discussed.
Hormonal treatment for prostate cancer (2001)

For nearly six decades the preferred primary treatment for advanced prostate cancer has been continuous suppression of testicular androgen production by medical or surgical castration. While androgen deprivation is effective in inducing tumour regression in the large majority of cases, essentially all patients will develop progressive disease. In addition androgen deprivation may be associated with a variety of side effects. Thus, strategies that minimise the use of these agents could potentially lower the morbidity and cost associated with the treatment of advanced prostate cancer. In the era of prostate-specific antigen (PSA) testing, hormonal therapy is being used earlier in the course of the disease when the only evidence of recurrent disease is an elevated PSA. These men may survive for many years and thus have the potential for long periods of exposure to hormonal therapy and its side effects. It has been hoped that the development of alternative hormonal interventions might lead to both enhanced antitumour efficacy as well as improvements in side effect profile.
Lutetium Texaphyrin (PCI‐0123): A Near‐Infrared, Water‐Soluble Photosensitizer (1996)

Lutetium texaphyrin, PCI-0123, is a pure, water-soluble photosensitizer with a large broad absorption band centered at 732 nm. The compound was tested for photodynamic therapy (PDT) effectiveness in a murine mammary cancer model. The texaphyrin macrocycle as illustrated by magnetic resonance imaging and 14C-radiolabeled texaphyrin studies was shown to be tumor selective; a tumor-to-muscle ratio of 10.55 was seen after 5 h. Lutetium texaphyrin, at a drug dose of 20 mumol/kg with irradiation 5 h postinjection at 150 J/cm2 and 150 mW/cm2, had significant efficacy (P < 0.0001) in treating neoplasms of moderate size (40 +/- 14 mm3) and also had significant efficacy (P < 0.0001) in treating larger neoplasms (147 +/- 68 mm3). The PDT efficacy was correlated with the time interval between PCI-0123 administration and light exposure. A 100% cure rate was achieved when photoirradiation took place 3 h postinjection compared to 50% for 5 h using 10 mumol/kg and 150 J/cm2 at 150 mW/cm2. The PDT efficacy was attributable to the selective uptake/retention of the texaphyrin photosensitizer in addition to the depth of light penetration achievable at the 732 nm laser irradiation.
Property-based software engineering measurement (1996)

Little theory exists in the field of software system measurement. Concepts such as complexity, coupling, cohesion or even size are very often subject to interpretation and appear to have inconsistent definitions in the literature. As a consequence, there is little guidance provided to the analyst attempting to define proper measures for specific problems. Many controversies in the literature are simply misunderstandings and stem from the fact that some people talk about different measurement concepts under the same label (complexity is the most common case). There is a need to define unambiguously the most important measurement concepts used in the measurement of software products. One way of doing so is to define precisely what mathematical properties characterize these concepts, regardless of the specific software artifacts to which these concepts are applied. Such a mathematical framework could generate a consensus in the software engineering community and provide a means for better communication among researchers, better guidelines for analysts, and better evaluation methods for commercial static analyzers for practitioners. We propose a mathematical framework which is generic, because it is not specific to any particular software artifact, and rigorous, because it is based on precise mathematical concepts. We use this framework to propose definitions of several important measurement concepts (size, length, complexity, cohesion, coupling). It does not intend to be complete or fully objective; other frameworks could have been proposed and different choices could have been made. However, we believe that the formalisms and properties we introduce are convenient and intuitive. This framework contributes constructively to a firmer theoretical ground of software measurement.
Parallel simulation environment for mobile wireless networks (1996)

A parallel simulator has been designed for the evaluation of wireless, multihop, mobile networks. This paper describes the process of porting the simulator from a sequential to a parallel environment. Parallelization is critical in large radio networks, where the complexity of radio propagation models, channel access schemes and interference patterns makes sequential simulation very time consuming - in the order of several hours for 100 nodes experiments. With parallel execution, speedups of up to tenfold have been observed on a 16 processor SP/2, making large net work simulations viable.
Prevention of Diabetic Vascular Dysfunction by Guanidines: Inhibition of Nitric Oxide Synthase Versus Advanced Glycation End-Product Formation (1993)

This study was undertaken to compare the ability of two guanidine compounds (aminoguanidine and methylguanidine), with different in vitro effects on NO synthase activity and AGE formation, to inhibit diabetic vascular dysfunction developing early after the onset of diabetes. In rats with STZ-induced diabetes of 5-wk duration, regional vascular [125I]albumin permeation was increased about two- to threefold in ocular tissues, sciatic nerve, and aorta; in general, both guanidine compounds normalized albumin permeation in diabetic rats without affecting it in controls. Methylguanidine was only approximately 7% as effective as aminoguanidine as an inhibitor of AGE formation from L-lysine and G6P; both compounds were poor inhibitors of AR. Methylguanidine was approximately 1-5% as potent as aminoguanidine and L-NMMA as an inhibitor of the cytokine- and endotoxin-inducible isoform of NO synthase. In contrast, the potency of methylguanidine as an inhibitor of the constitutive isoform of NO synthase was comparable to that of aminoguanidine, and both guanidine compounds were much less effective than L-NMMA. These observations suggest a role for a relative or absolute increase in NO production in the pathogenesis of early diabetic vascular dysfunction and raise the possibility that inhibition of diabetic vascular functional changes by aminoguanidine may reflect inhibition of NO synthase activity rather than, or in addition to, prevention of AGE formation.
Monte carlo inference and maximization for phrase-based translation (2009)

Recent advances in statistical machine translation have used beam search for approximate NP-complete inference within probabilistic translation models. We present an alternative approach of sampling from the posterior distribution defined by a translation model. We define a novel Gibbs sampler for sampling translations given a source sentence and show that it effectively explores this posterior distribution. In doing so we overcome the limitations of heuristic beam search and obtain theoretically sound solutions to inference problems such as finding the maximum probability translation and minimum expected risk training and decoding.
Analogs of Pteroylglutamic Acid. III. 4-Amino Derivatives (1949)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTAnalogs of Pteroylglutamic Acid. III. 4-Amino DerivativesDoris R. Seeger, Donna B. Cosulich, James M. Smith, and Martin E. HultquistCite this: J. Am. Chem. Soc. 1949, 71, 5, 1753–1758Publication Date (Print):May 1, 1949Publication History Published online1 May 2002Published inissue 1 May 1949https://pubs.acs.org/doi/10.1021/ja01173a061https://doi.org/10.1021/ja01173a061research-articleACS PublicationsRequest reuse permissionsArticle Views642Altmetric-Citations232LEARN 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
Large-Scale Functional Purification of Recombinant HIV-1 Capsid (2013)

During human immunodeficiency virus type-1 (HIV-1) virion maturation, capsid proteins undergo a major rearrangement to form a conical core that protects the viral nucleoprotein complexes. Mutations in the capsid sequence that alter the stability of the capsid core are deleterious to viral infectivity and replication. Recently, capsid assembly has become an attractive target for the development of a new generation of anti-retroviral agents. Drug screening efforts and subsequent structural and mechanistic studies require gram quantities of active, homogeneous and pure protein. Conventional means of laboratory purification of Escherichia coli expressed recombinant capsid protein rely on column chromatography steps that are not amenable to large-scale production. Here we present a function-based purification of wild-type and quadruple mutant capsid proteins, which relies on the inherent propensity of capsid protein to polymerize and depolymerize. This method does not require the packing of sizable chromatography columns and can generate double-digit gram quantities of functionally and biochemically well-behaved proteins with greater than 98% purity. We have used the purified capsid protein to characterize two known assembly inhibitors in our in-house developed polymerization assay and to measure their binding affinities. Our capsid purification procedure provides a robust method for purifying large quantities of a key protein in the HIV-1 life cycle, facilitating identification of the next generation anti-HIV agents.
Determination of frequency of T cells expressing the T cell‐specific serine proteinase 1 (TSP‐1) reveals two types of L3T4+ T lymphocytes (1988)

TSP-1 is a murine T cell-specific serine proteinase which is exclusively expressed in activated but not in resting T lymphocytes. Among T lymphocyte clones tested so far the enzyme was found to be associated with all Ly-2+ but only with a fraction of L3T4+ lines. Here we have applied a limiting dilution system to determine the frequency of precursor cells of resting L3T4+ and Ly-2+ lymphocytes which can be induced in vitro by antigen/lectin to express TSP-1. T cell subsets were either positively enriched by flow cytofluorometry cell sorting or by negative selection using monoclonal antibodies and complement. Following stimulation of lymphocytes in vitro, individual microwells were tested for growth by visual examination and for the TSP-1 protein/enzyme by analyzing cell lysates using either a specific rabbit anti-TSP-1 antiserum and/or the chromogenic model peptide substrate H-D-Pro-Phe-Arg-p-nitroanilide. Moreover, a large panel of L3T4+ and Ly-2+ T lymphocyte clones generated from primary cultures were similarly investigated. In some cell cultures the presence of TSP-1 was also tested on the mRNA level using a TSP-1-specific oligonucleotide probe. The data show that the majority, if not all, of antigen/lectin-induced-Ly-2+ T cells expressed TSP-1. In contrast, only 12%-27% of the growing lectin or antigen-reactive L3T4+ lymphocytes were positive for the enzyme. Studies performed in parallel with L3T4+ and Ly-2+ lymphocyte populations sensitized in bulk culture showed that under these conditions similar levels of TSP-1-specific mRNA and enzyme activity are detected in both subsets. The finding of primary L3T4+ T lymphocyte clones with distinct patterns of TSP-1 production provides evidence for the existence of two types of L3T4+ effector cells with different functional capacities. The data also suggest a cooperation between distinct L3T4+ lymphocytes for induction of optimal TSP-1 activity in L3T4+ T cells.
DOCK7 interacts with TACC3 to regulate interkinetic nuclear migration and genesis of neurons from cortical neuronal progenitors (2012)

The six-layered mammalian neocortex derives from a pseudostratified neuroepithelium by a series of cell divisions of neuronal progenitors, neuroepithelial and radial glial cells. Neurogenesis, a major event in the developing neocortex, relies on the ability of radial glial cells (RGCs) to switch from proliferative self-expanding to differentiative neurongenerating/progenitor self-renewing divisions. However, the molecular mechanisms that control this switch in a correct temporal manner are not well understood. In this thesis, I demonstrated that the DOCK180 family member DOCK7, an activator of Rac GTPases, plays an important role in the regulation of RGC proliferation versus differentiation. Silencing of DOCK7 in RGCs of developing mouse embryos hampers neuronal differentiation and maintains cells as cycling progenitors. Conversely, DOCK7 overexpression promotes RGC differentiation into basal progenitors and neurons. Using different approaches, including live-cell imaging experiments, I obtained evidence that DOCK7 influences RGC fate and neurogenesis by controlling the apically directed interkinetic nuclear migration (INM) process of RGCs. Importantly, DOCK7 exerts its effects on INM and neurogenesis independently of its GEF activity towards Rac, but instead does so by antagonizing the microtubule growth-promoting function of the centrosome-associated protein TACC3. Taken together, DOCK7 interacts with TACC3 to control INM, as such governing RGC fate and genesis of neurons during cortical development. | 116 pages