gebhart/patrepeval huggingface dataset:
Detection of Radiation-Induced Hydrocarbons in Irradiated Fish and Prawns by Means of On-Line Coupled Liquid Chromatography−Gas Chromatography (1997)

Radiation-induced hydrocarbons were analyzed in a fatty (halibut) and a lean fish (cod) as well as in a prawn species by on-line coupled liquid chromatography (LC)−gas chromatography (GC) combined with mass spectrometry. In irradiated halibut which is known to contain mainly saturated and monounsaturated fatty acids, all expected radiolytic alkanes, alkenes, and alkadienes could be detected. The yields of the Cn-1 and Cn-2:1 hydrocarbons were comparable to those found in irradiated lipids of terrestrial animals and plants. However, in cod and prawns which contain high levels of polyunsaturated fatty acids (PUFA), the Cn-1 hydrocarbons were found in concentrations which were up to 10 times higher whereas the Cn-2:1 products were again comparable to those of terrestrial animals and plants. The identification of radiation-induced hydrocarbons in fish lipids was achieved by transfer of the hydrocarbons from the LC column to the gas chromatographic column in fractions differing in their degree of unsaturation. For the first time, radiation-induced hydrocarbons with more than four double bonds generated from polyunsaturated fatty acids (20:4ω6 and 20:5ω3) could be identified. Keywords: Food irradiation; detection; hydrocarbons; fish; liquid chromatography; gas chromatography; mass spectrometry
Decision Tree-Based Methodology for High Impedance Fault Detection (2004)

This paper presents a high impedance fault (HIF) detection method based on decision trees (DTs). The features of HIF, which are the inputs of DTs, are those well-known ones, including current [in root mean square (rms)], magnitudes of the second, third, and fifth harmonics, and the phase of the third harmonics. The only measurements needed in the proposed method are the current signals sampled at 1920 Hz. It will reduce the cost of hardware compared with methods that use high sampling rates. A new HIF model is also used. The data of current signals are from the simulation of Electromagnetic Transients Program (EMTP). The DT algorithm trained can successfully distinguish the HIFs from most normal operations on simulation data, including switching loads, switching shunt capacitors, and load transformer inrush currents. Testing on experimental data is recommended for future work.
Induction of interleukin 3 and tumor resistance by SSM, a cancer immunotherapeutic agent extracted from Mycobacterium tuberculosis. (1990)

Interleukin 3 (IL-3) activity was demonstrated when inguinal lymph node cells obtained from Bacillus Calmette-Guérin-sensitized mice (BCG-ILNC) were stimulated in vitro with SSM, an immunomodulator extracted from Mycobacterium tuberculosis. The IL-3 activity was first detected on Day 1 in culture fluids of BCG-ILNC stimulated with SSM, reached a peak on Day 3, and then gradually decreased. The activity was completely neutralized by treatment with anti-murine IL-3 monoclonal antibody (mAb). When BCG-ILNC were treated with anti-Thy 1.2 or anti-Lyt 1.2 mAb followed by complement, IL-3 was not produced in the culture fluids. However, IL-3 in the culture fluids was detected when BCG-ILNC were treated with anti-Lyt 2.2 mAb, anti-asialo-GM1, or anti-mouse immunoglobulin antiserum followed by complement. These results suggested that Lyt 1+ T-cells appeared to be required for the production of IL-3 from BCG-ILNC stimulated with SSM. In addition, low but significant IL-3 activity was also observed in sera of mice treated with SSM. However, serum IL-3 activity was not detected in mice treated with both SSM and Thy 1.2 or Lyt 1.2 mAb, whereas the activity was induced by SSM in mice treated with anti-Lyt 2.2 mAb or anti-asialo-GM1 antiserum. On the other hand, the in vivo growth of IMC tumors inoculated in BALB/c x DBA/2 F1 mice was significantly decreased by intralesional injection of culture fluids containing IL-3, as well as by SSM itself. This antitumor activity of the culture fluids was not altered when it was treated with mAbs for interleukin 1, interleukin 2, or anti-mouse gamma-interferon antiserum. The antitumor activity of the fluid was only eliminated when it was treated with anti-mouse IL-3 mAb. Since nonspecific resistance to tumors in mice stimulated with SSM appears to require Lyt 1+ T-cells, these results suggest that, in part, nonspecific resistance to tumors of mice stimulated with SSM may be developed through IL-3, which was produced by Lyt 1+ T-cells after SSM stimulation.
Isolation and structural characterization of a potent inhibitor of coagulation factor Xa from the leech Haementeria ghilianii. (1989)

The present work reports the discovery and characterization of an anticoagulant protein in the salivary gland of the giant bloodsucking leech, H. ghilianii, which is a specific and potent inhibitor of coagulation factor Xa. The inhibitor, purified to homogeneity, displayed subnanomolar inhibition of bovine factor Xa and had a molecular weight of approximately 15,000 as deduced by denaturing SDS-PAGE. The amino acid sequence of the first 43 residues of the H. ghilianii derived inhibitor displayed a striking homology to antistasin, the recently described subnanomolar inhibitor of factor Xa isolated from the Mexican leech, H. officinalis. Antisera prepared to antistasin cross-reacted with the H. ghilianii protein in Western Blot analysis. These data indicate that the giant Amazonian leech, H. ghilianii, and the smaller Mexican leech, H. officinalis, have similar proteins which disrupt the normal hemostatic clotting mechanisms in their mammalian host's blood.
Supramolecular Organization and Materials Design (2001)

Supramolecular Chemistry deals with the design, synthesis and study of molecular structures held together by non-covalent interactions. Structures of this type are ubiquitous in nature and are frequently used as blueprints for the design of synthetic equivalents. This book is intended to demonstrate the seminal importance of supramolecular chemistry and self-organization in the design and synthesis of novel organic materials, inorganic materials and biomaterials. With contributions from leading workers in the field, the book shows how the bottom-up approach of supramolecular chemistry can be used to synthesize not only new materials, but function specific molecular devices as well. This book will be of interest to researchers and graduate students in chemistry, materials science and physics who need a summary of the most recent developments in the field.
Concerted Regulation of Inhibitory Activity of α1-Antitrypsin by the Native Strain Distributed throughout the Molecule (2002)

The native forms of common globular proteins are in their most stable state but the native forms of plasma serpins (serine protease inhibitors) show high energy state interactions. The high energy state strain of alpha(1)-antitrypsin, a prototype serpin, is distributed throughout the whole molecule, but the strain that regulates the function directly appears to be localized in the region where the reactive site loop is inserted during complex formation with a target protease. To examine the functional role of the strain at other regions of alpha(1)-antitrypsin, we increased the stability of the molecule greatly via combining various stabilizing single amino acid substitutions that did not affect the activity individually. The results showed that a substantial increase of stability, over 13 kcal mol(-1), affected the inhibitory activity with a correlation of 11% activity loss per kcal mol(-1). Addition of an activity affecting single residue substitution in the loop insertion region to these very stable substitutions caused a further activity decrease. The results suggest that the native strain of alpha(1)-antitrypsin distributed throughout the molecule regulates the inhibitory function in a concerted manner.
Kinetics of RNA Degradation by Specific Base Catalysis of Transesterification Involving the 2‘-Hydroxyl Group (1999)

A detailed understanding of the susceptibility of RNA phosphodiesters to specific base-catalyzed cleavage is necessary to approximate the stability of RNA under various conditions. In addition, quantifying the rate enhancements that can be produced exclusively by this common cleavage mechanism is needed to fully interpret the mechanisms employed by ribonucleases and by RNA-cleaving ribozymes. Chimeric DNA/RNA oligonucleotides were used to examine the rates of hydroxide-dependent degradation of RNA phosphodiesters under reaction conditions that simulate those of biological systems. Under neutral or alkaline pH conditions, the dominant pathway for RNA degradation is an internal phosphoester transfer reaction that is promoted by specific base catalysis. As expected, increasing the concentration of hydroxide ion, increasing the concentration of divalent magnesium, or raising the temperature accelerates strand scission. In most instances, the identities of the nucleotide bases that flank the target RNA linkage have a negligible effect on the pKa of the nucleophilic 2‘-hydroxyl group, and only have a minor effect on the maximum rate constant for the transesterification reaction. Under representative physiological conditions, specific base catalysis of RNA cleavage generates a maximum rate enhancement of ∼100 000-fold over the background rate of RNA transesterification. The kinetic parameters reported herein provide theoretical limits for the stability of RNA polymers and for the proficiency of RNA-cleaving enzymes and enzyme mimics that exclusively employ a mechanism of general base catalysis.
Measurement of the Electrically Evoked Compound Action Potential via a Neural Response Telemetry System (2002)

The main aim of this study was to validate a new technique, neural response telemetry (NRT), for measuring the electrically evoked compound action potential in adult cochlear implant users via their Nucleus C124M implant. Thirty-eight adults were evaluated with a variety of measurement procedures with the NRT software. Electrically evoked compound action potentials were obtained in 31 of the 38 adults (81.6%) and in 132 of the 160 electrodes (82.5%) tested. In addition to validating this technique, we also established a set of default clinical test parameters.
The Ras-JNK Pathway Is Involved in Shear-Induced Gene Expression (1996)

Hemodynamic forces play a key role in inducing atherosclerosis-implicated gene expression in vascular endothelial cells. To elucidate the signal transduction pathway leading to such gene expression, we studied the effects of fluid shearing on the activities of upstream signaling molecules. Fluid shearing (shear stress, 12 dynes/cm2 [1 dyne = 10(-5)N]) induced a transient and rapid activation of p21ras and preferentially activated c-Jun NH2 terminal kinases (JNK1 and JNK2) over extracellular signal-regulated kinases (ERK-1 and ERK-2). Cotransfection of RasN17, a dominant negative mutant of Ha-Ras, attenuated the shear-activated JNK and luciferase reporters driven by 12-O-tetradecanoylphorbol-13-acetate-responsive elements. JNK(K-R) and MEKK(K-M), the respective catalytically inactive mutants of JNK1 and MEKK, also partially inhibited the shear-induced luciferase reporters. In contrast, Raf301, ERK(K71R), and ERK(K52R), the dominant negative mutants of Raf-1, ERK-1, and ERK-2, respectively, had little effect on the activities of these reporters. The activation of JNK was also correlated with increased c-Jun transcriptional activity, which was attenuated by a negative mutant of Son of sevenless. Thus, mechanical stimulation exerted by fluid shearing activates primarily the Ras-MEKK-JNK pathway in inducing endothelial gene expression.
评《什么是音乐?——音乐哲学导论》 (1990)

《什么是音乐?》一书围绕音乐本体论和意义,作曲、演奏和演唱的基本问题展开论述,全面探索了对音乐的评价问题,及音乐在历史和文化中的地位。本书从哲学、历史的角度思考了音乐,阐明了区别规范化音乐美学与更为重要的音乐哲学的必要性——前者置音乐于艺术传统之中,后者则以将音乐的全部内容与意义转化为人类体验为目的。
Estrogen Treatment Down-Regulates TNF-α Production and Reduces the Severity of Experimental Autoimmune Encephalomyelitis in Cytokine Knockout Mice (2001)

A shift toward Th2 cytokine production has been demonstrated during pregnancy and high dose estrogen therapy and is thought to be the primary mechanism by which estrogen suppresses the development of experimental autoimmune encephalomyelitis. However, low dose estrogen treatment is equally protective in the absence of a significant shift in cytokine production. In this study cytokine-deficient mice were treated with estrogen to determine whether a shift in Th2 cytokine production was required for the protective effects of hormone therapy. Estrogen effectively suppressed the development of experimental autoimmune encephalomyelitis in IL-4 and IL-10 knockout mice and in wild type littermate mice with a similar potency of protection. Significant disease suppression was also seen in IFN-gamma-deficient mice. The decrease in disease severity was accompanied by a concomitant reduction in the number of proinflammatory cytokine- and chemokine-producing cells in the CNS. Although there was no apparent increase in compensatory Th2 cytokine production in cytokine-deficient mice, there was a profound decrease in the frequency of TNF-alpha-producing cells in the CNS and the periphery. Therefore, we propose that one mechanism by which estrogen protects females from the development of cell-mediated autoimmunity is through a hormone-dependent regulation of TNF-alpha production.
Neuroprotective effects of PPAR‐γ agonist rosiglitazone in N171‐82Q mouse model of Huntington's disease (2013)

Huntington's disease (HD) is a devastating genetic neurodegenerative disease caused by CAG trinucleotide expansion in the exon-1 region of the huntingtin gene. Currently, no cure is available. It is becoming increasingly apparent that mutant Huntingtin (HTT) impairs metabolic homeostasis and causes transcriptional dysregulation. The peroxisome proliferator-activated receptor gamma (PPAR-γ) is a transcriptional factor that plays a key role in regulating genes involved in energy metabolism; recent studies demonstrated that PPAR-γ activation prevented mitochondrial depolarization in cells expressing mutant HTT and attenuated neurodegeneration in various models of neurodegenerative diseases. PPAR-γ-coactivator 1α (PGC-1 α) transcription activity is also impaired by mutant HTT. We now report that the PPAR-γ agonist, rosiglitazone (RSG), significantly attenuated mutant HTT-induced toxicity in striatal cells and that the protective effect of RSG is mediated by activation of PPAR-γ. Moreover, chronic administration of RSG (10 mg/kg/day, i.p) significantly improved motor function and attenuated hyperglycemia in N171-82Q HD mice. RSG administration rescued brain derived neurotrophic factor(BDNF) deficiency in the cerebral cortex, and prevented loss of orexin-A-immunopositive neurons in the hypothalamus of N171-82Q HD mice. RSG also prevented PGC-1α reduction and increased Sirt6 protein levels in HD mouse brain. Our results suggest that modifying the PPAR-γ pathway plays a beneficial role in rescuing motor function as well as glucose metabolic abnormalities in HD.
Ubiquitin-Editing Enzyme A20 Promotes Tolerance to Lipopolysaccharide in Enterocytes (2009)

Although enterocytes are capable of innate immune responses, the intestinal epithelium is normally tolerant to commensal bacteria. To elucidate the mechanisms of tolerance, we examined the effect of preexposure to LPS on activation of p38, c-Jun, and NF-kappaB in enterocytes by several inflammatory and stress stimuli. Shortly after the initial LPS challenge, enterocytes become tolerant to restimulation with LPS or CpG DNA, but not with IL-17 or UV. The state of tolerance, which lasts 20-26 h, temporally coincides with LPS-induced expression of the anti-inflammatory ubiquitin-editing enzyme A20. Small interfering RNA silencing of A20 prevents tolerance, whereas ectopic expression of A20 blocks responses to LPS and CpG DNA, but not to IL-17 or UV. A20 levels in the epithelium of the small intestine are low at birth and following gut decontamination with antibiotics, but high under conditions of bacterial colonization. In the small intestine of adult rodents, A20 prominently localizes to the luminal interface of villus enterocytes. Lower parts of the crypts display relatively low levels of A20, but relatively high levels of phospho-p38. Gut decontamination with antibiotics reduces the levels of both A20 and phospho-p38. Along with the fact that A20-deficient mice develop severe intestinal inflammation, our results indicate that induction of A20 plays a key role in the tolerance of the intestinal epithelium to TLR ligands and bacteria.
Existence of a p-glycoprotein drug efflux pump in cultured rabbit conjunctival epithelial cells. (1998)

There may exist a P-gp-mediated drug efflux pump on the apical aspect of the rabbit conjunctiva to restrict the absorption of cyclosporin A and other lipophilic drugs.
Glycogen-Synthase Kinase3β/β-Catenin Axis Promotes Angiogenesis Through Activation of Vascular Endothelial Growth Factor Signaling in Endothelial Cells (2005)

Glycogen-Synthase Kinase 3beta (GSK3beta) has been shown to function as a nodal point of converging signaling pathways in endothelial cells to regulate vessel growth, but the signaling mechanisms downstream from GSK3beta have not been identified. Here, we show that beta-catenin is an important downstream target for GSK3beta action in angiogenesis and dissect the signal transduction pathways involved in the angiogenic phenotype. Transduction of human umbilical vein endothelial cells (HUVECs) with a kinase-mutant form of the enzyme (KM-GSK3beta) increased cytosolic beta-catenin levels, whereas constitutively active GSK3beta (S9A-GSK3beta) reduced beta-catenin levels. Lymphoid enhancer factor/T-cell factor promoter activity was upregulated by KM-GSK3beta and diminished by S9A-GSK3beta, whereas manipulation of Akt signaling had no effect on this parameter. beta-Catenin transduction induced capillary formation in a Matrigel-plug assay in vivo and promoted endothelial cell differentiation into network structures on Matrigel-coated plates in vitro. beta-Catenin activated the expression of vascular endothelial growth factor (VEGF)-A and VEGF-C in endothelial cells, and these effects were mediated at the levels of protein, mRNA, and promoter activity. Consistent with these data, beta-catenin increased the phosphorylation of the VEGF receptor 2 (VEGF-R2) and promoted its association with PI3-kinase, leading to a dose-dependent activation of the serine-threonine kinase Akt. Inhibition of PI3-kinase or Akt signaling led to a significant reduction in the pro-angiogenic activity of beta-catenin. Collectively, these data show that the growth factor-PI3-kinase-Akt axis functions downstream of GSK3beta/beta-catenin signaling in endothelial cells to promote angiogenesis.
T cells accumulating in the inflamed joints of a spontaneous murine model of rheumatoid arthritis become restricted to common clonotypes during disease progression (2003)

Although a number of studies have revealed that T cells expand clonally in the joints of patients suffering from rheumatoid arthritis (RA), the kinetics of T cell clonality in multiple joints of an individual throughout progression of the disease is not known. By employing a TCR beta chain gene-specific RT-PCR and subsequent single-strand conformation polymorphism, which enables us to monitor T cell clonality, we analyzed transgenic mice (Tg) carrying the human T cell leukemia virus type I env-pX region. These mice spontaneously develop destructive progressive arthritis similar to RA as they age. In the early stage, the majority of accumulating T cell clones differed in each of four affected feet analyzed. However, in the advanced stage, many of the clones were common to all four feet. The total number of distinct clones gradually decreased as the disease progressed. When splenocytes from arthritic elder Tg were adoptively transferred into either nude mice or young Tg, the clones common to all four feet of the donor were detected again in four feet of the recipients. These findings suggest that, as arthritis progresses, the T cell clones accumulating in the arthritic joints are gradually restricted to certain common clonotypes, some of which are arthrotropic.
Bacillus anthracisSpores Stimulate Cytokine and Chemokine Innate Immune Responses in Human Alveolar Macrophages through Multiple Mitogen-Activated Protein Kinase Pathways (2006)

Contact with the human alveolar macrophage plays a key role in the innate immune response to Bacillus anthracis spores. Because there is a significant delay between the initial contact of the spore with the host and clinical evidence of disease, there appears to be temporary containment of the pathogen by the innate immune system. Therefore, the early macrophage response to Bacillus anthracis exposure is important in understanding the pathogenesis of this disease. In this paper, we studied the initial events after exposure to spores, beginning with the rapid internalization of spores by the macrophages. Spore exposure rapidly activated the mitogen-activated protein kinase signaling pathways extracellular signal-regulated kinase, c-Jun-NH2-terminal kinase, and p38. This was followed by the transcriptional activation of cytokine and primarily monocyte chemokine genes as determined by RNase protection assays. Transcriptional induction is reflected at the translational level, as interleukin-1alpha (IL-1alpha), IL-1beta, IL-6, and tumor necrosis factor alpha (TNF-alpha) cytokine protein levels were markedly elevated as determined by enzyme-linked immunosorbent assay. Induction of IL-6 and TNF-alpha, and, to a lesser extent, IL-1alpha and IL-1beta, was partially inhibited by the blockade of individual mitogen-activated protein kinases, while the complete inhibition of cytokine induction was achieved when multiple signaling pathway inhibitors were used. Taken together, these data clearly show activation of the innate immune system in human alveolar macrophages by Bacillus anthracis spores. The data also show that multiple signaling pathways are involved in this cytokine response. This report is the first comprehensive examination of this process in primary human alveolar macrophages.
Activity of the Osteocalcin Promoter in Skeletal Sites of Transgenic Mice and during Osteoblast Differentiation in Bone Marrow-Derived Stromal Cell Cultures: Effects of Age and Sex* (1997)

The bone-specific osteocalcin gene is a well established marker of osteoblast activity. We have studied osteocalcin transcription in transgenic mice carrying rat osteocalcin promoter-chloramphenicol acetyltransferase (CAT) reporter constructs. Transgenic lines carrying each of the 1.7-, 1.1-, 0.72-, or 0.35-kilobase promoter constructs expressed the reporter gene in a tissue-specific manner. However, each of these constructs was sensitive to site of integration effects, reflected by a high frequency of nonexpressing transgenic lines. High expression of the 1.7-kilobase promoter in osseous tissues was accompanied by low ectopic expression in the brain. Analysis of CAT expression in femurs, calvariae, and lumbar vertebrae of this line indicated considerable variability in promoter activity among individual transgenic animals. Analysis of the variance in CAT activity demonstrated a linkage between promoter activities in these distant skeletal sites. Promoter activity was inversely correlated with age, and females exhibited severalfold higher activity than age-matched males. Bone marrow stromal cells from these animals, cultured under conditions that support osteoblast differentiation, exhibited the expected postproliferative onset of osteocalcin promoter activity, as assessed by CAT assay. The ex vivo CAT activity was not dependent on the sex or the age of the donor transgenic mouse. Taken together, our results are consistent with the hypothesis that a common, probably humoral, factor(s) regulates osteocalcin transcription in distant skeletal sites. We suggest that the abundance of this factor(s) is different between males and females and among individual mice at a given time point, and that ex vivo culturing of osteoblasts reduces the variation in osteocalcin promoter activity by eliminating the physiological contribution of this factor.