gebhart/patrepeval huggingface dataset:
N‐Acetylaspartylglutamate Inhibits Forskolin‐Stimulated Cyclic AMP Levels via a Metabotropic Glutamate Receptor in Cultured Cerebellar Granule Cells (1993)

The neuronal dipeptide N-acetylaspartylglutamate (NAAG) fulfills several of the criteria for classification as a neurotransmitter including localization in synaptic vesicles, calcium-dependent release after neuronal depolarization, and low potency activation of N-methyl-D-aspartate receptors. In the present study, the influence of NAAG on metabotropic receptor activation in cerebellar granule cells was examined in cell culture. Stimulation of granule cell adenylate cyclase with forskolin increased cyclic AMP (cAMP) several hundredfold above basal levels within 10 min in a concentration-dependent manner. Although glutamate, NAAG, and the metabotropic receptor agonist trans-1-amino-1,3-cyclopentanedicarboxylic acid did not alter the low basal cAMP levels, the application of 300 microM glutamate or NAAG or trans-1-amino-1,3-cyclopentanedicarboxylic acid reduced forskolin-stimulated cAMP in granule cells by 30-50% in the absence or presence of inhibitors of ionotropic acidic amino acid receptors, as well as 2-amino-4-phosphonobutyrate. No additivity in the inhibition of cAMP was found when 300 microM NAAG and trans-1-amino-1,3-cyclopentanedicarboxylic acid were coapplied. The beta-analogue of NAAG failed to reduce cAMP levels. Similar effects of NAAG and glutamate were obtained under conditions of inhibition of phosphodiesterase activity and were prevented by pretreatment of the cells with pertussis toxin. These data are consistent with the activation by NAAG of a metabotropic acidic amino acid receptor coupled to an inhibitory G protein. In contrast, the metabotropic acidic amino acid receptor coupled to phosphoinositol turnover in these cells was not activated by NAAG.(ABSTRACT TRUNCATED AT 250 WORDS)
Inhibition of Angiogenesis by Recombinant Human Platelet Factor-4 and Related Peptides (1990)

Recombinant human platelet factor-4 (rhPF4), purified from Escherichia coli, inhibited blood vessel proliferation in the chicken chorioallantoic membrane in a dose-dependent manner. Treatment of several cell types with rhPF4 in vitro suggested that the angiostatic effect was due to specific inhibition of growth factor-stimulated endothelial cell proliferation. The inhibitory activities were associated with the carboxyl-terminal, heparin-binding region of the molecule and could be abrogated by including heparin in the test samples, an indication that sulfated polysaccharides might modulate the angiostatic activity of platelet factor-4 in vivo. Understanding of the mechanisms of control of angiogenesis by endogenous proteins should facilitate the development of effective treatments for diseases of pathogenic neovascularization such as Kaposi's sarcoma, diabetic retinopathy, and malignant tumor growth.
Performance Tuning in Distributed Processing of ETL (2013)

Extract, transform, and load (ETL) is a very common and important technology for building data warehouse includes business intelligence. When people issue a very complex SQL query to acquit data from a transaction system into a data warehouse, it involves many procedures including table-joining, sort, and aggregation. Such procedures require significant retrieving step and huge data transferring from tables. The intensive querying very often causes performance issues to be concerned. Moreover, it commonly generates negative impacts on data instance resources. How to improve the performance for ETL becomes critical and challenging. This paper presents a parallel processing solution that splitting big and complex SQL query into small pieces in distributed computing manor. The proposed method aims at reducing cost of computation, while ensuring data integrity among joined tables. The innovative idea can be verified through selected test-beds of performance tuning.
Quantitative analysis of alkaline phosphatases in serum and amniotic fluid: comparison of biochemical and immunologic assays. (1985)

An immunoprecipitation method using monoclonal antibodies specific for the three categories of alkaline phosphatases, liver/bone/kidney, placental, and intestinal, is described and compared with the heat denaturation-chemical inhibition method for quantitating the contributions of the various isoenzymes to the total activity in biologic fluids. Activity values for the three categories of isoenzymes present in normal and pregnancy sera as well as in early gestation amniotic fluids were determined by both methods. There is very close correlation between the values obtained by both methods. Thus, two independent procedures are now available for quantitating the contributions of the various alkaline phosphatase isoenzymes in biologic fluids.
Motion adaptive deinterlacing of video data with texture detection (2006)

In this paper, we propose a motion adaptive deinterlacing method with texture detection for scan-rate conversion of video data. The basic idea of this method is to classify the missing pixel to four different regions including motion smooth region, motion texture region, static smooth region, and static texture region based on the results of motion detection and texture detection, then four different interpolation methods are used to produce the missing pixel. Extensive simulations conducted for video sequences indicate that the performance of the proposed method is superior to the previous methods based on the direct merging method, bilinear interpolation, ELA, and vertical temporal median method. Moreover, our proposed method requires lower computational complexity and provides better object and subject performance
Cytomegalovirus immune globulin intravenous (human) administration modulates immune response to alloantigens in sensitized renal transplant candidates (2000)

One of the important parameters for prolonged waiting time for potential renal transplant recipients is the presence of preformed antibodies to human leucocyte antigen (HLA) antigens, which is often caused by previous transplants, pregnancy or transfusions. In vivo administration of specific and unselected polyclonal intravenous immunoglobulin (IVIGs) preparations have been shown to inhibit anti-HLA alloantibodies in highly sensitized patients. We sought to determine whether Cytogam (Medimmune Inc., Gaithersburg, MD, USA), a hyperimmune anticytomegalovirus immunoglobulin would (1) effect either in vitro or in vivo alloreactivity, and (2) whether Cytogam therapy could reduce the titre of preformed anti-HLA antibodies in highly sensitized patients. Alloreactivity was assessed by mixed lymphocyte reaction (MLR) and cytotoxic T lymphocyte (CTL) assay. A complement dependent microlymphocytotoxicity assay was done to assess for panel reactive antibody (PRA) status and the presence of anti-idiotypic antibodies in the Cytogam preparation. The MLR was inhibited by Cytogam in vitro in a dose-dependent fashion ranging from 31-92%. Significant inhibition of the MLR responses was not observed in recipients who received Cytogam in vivo (50 mg/kg). This could be a result of adminstration of a low dose of IVIG. However, CTL activity against the alloantigens in all individuals assessed was significantly inhibited after in vivo administration of Cytogam. Three of five individuals experienced a decrease of 5-32% in the PRA status at 4 weeks post administration of Cytogam. Cytogam also blocked the anti-HLA antibody titres in a microlymphocytotoxicity assay, suggesting the presence of anti-idiotypic antibodies. Our study was based on a single prophylactic dose of Cytogam (50 mg/kg), however, higher dose administration could be feasible by removing more fluid at dialysis, but should be given intradialytically to avoid volume overload. Overall, our results suggest that Cytogam can modulate the in vivo and in vitro T cell responses against the alloantigens.
Antibodies cross-reactive with E- and P-selectin block both E- and P- selectin functions (1995)

E- and P-selectin are inflammation-induced cell adhesion molecules that mediate leukocyte-endothelial cell and leukocyte-platelet interactions. Monoclonal antibodies (MoAbs) specific for either E-selectin or P-selectin are protective in several animal models of inflammatory disease. To generate an MoAb with broader therapeutic potential, MoAbs that bind to both E- and P-selectin were generated by immunization of mice with mouse pre-B cell lines transfected with human E- and P-selectin. Interestingly, although the only selection criterion was the ability to bind both E- and P-selectin, all three antibodies obtained efficiently block both E- and P-selectin-mediated functions. The inhibited functions include neutrophil or HL-60 cell binding to tumor necrosis factor-alpha-activated human umbilical vein endothelial cells, E- or P-selectin transfectant cell lines, and platelet-HL-60 rosetting. These antibodies, EP-5C7, EP-2C9, and EP-1D8, recognize the same or overlapping epitope within the lectin domains of E- and P-selectin. The data suggest that functionally important epitopes of homologous proteins can be targeted by selecting for antibodies with reactivity toward both proteins. Furthermore, a potent blocking antibody specific for both E- and P-selectin may provide a more effective and broadly useful reagent for treating acute and potentially certain chronic inflammatory conditions.
Transgenic Mice Overexpressing Presenilin cDNAs (2000)

Genetic analysis has implicated four genes in the etiology of Alzheimer’s disease (AD) : the amyloid precursor protein (APP) gene, the presenilin 1 and presenilin 2 (PS1 and PS2) genes, and the apolipoprotein E gene (reviewed in 1). Transgenic mice with mutations in these genes replicate some of the features of the disease (1–;8) and while molecular analysis of the effects of the mutations in these genes has implicated APP metabolism and the production of Aβ1–42(43) as important in the initiation of the pathogenesis of the disease (6–9), the relationship between the presenilins (PSs) and APP remains obscure, although a direct association seems probable (10).
Influence of charge on the rate of amide proton exchange (1982)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTInfluence of charge on the rate of amide proton exchangePeter S. Kim and Robert L. BaldwinCite this: Biochemistry 1982, 21, 1, 1–5Publication Date (Print):January 5, 1982Publication History Published online1 May 2002Published inissue 5 January 1982https://doi.org/10.1021/bi00530a001RIGHTS & PERMISSIONSArticle Views239Altmetric-Citations77LEARN 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 InReddit PDF (589 KB) Get e-Alerts Get e-Alerts
Geomaster - a Program for Interactive 3D Gravity Inversion and Forward Modelling (1995)

We have developed a program package, called GEOMASTER for interactive inversion and forward modeling of gravity data in three dimensions. In our application we combine the advantages of robust algorithms with the use of an advanced visualisation system, AVSTM, which provides the tools for interactive displaying and model manipulation.
Tardive Psychopathology (1995)

Tardive psychopathology (TP) corresponds to mental changes from chronic neuroleptic exposure, as tardive dyskinesia corresponds to induced movement disorders. TP was prospectively identified in 4 inpatients. Each took neuroleptics more than 3 years, showed good premorbid adjustment or initiative, and met criteria for chronic schizophrenia. Each also had obsessions or compulsions, and apathetic dysphoria, symptoms not previously attributed to TP. Following neuroleptic termination with introduction of lithium and sertraline, each showed atypically rapid disappearance of this psychopathology. The incidence of these features is over 47% (p < 0.05). Some cases of apparent neuroleptic-resistant schizophrenia may be TP.
Proliferative and degenerative changes in striatal spiny neurons in Huntington's disease: a combined study using the section-Golgi method and calbindin D28k immunocytochemistry (1991)

Dysmorphic alterations of dendritic arbors and spines in spiny striatal neurons were identified in section-Golgi impregnations of moderate and severe grades of Huntington's disease (HD). These alterations could be characterized as either proliferative or degenerative changes. Proliferative changes included prominent recurving of distal dendritic segments, short-segment branching along dendrites, and increased numbers and size of dendritic spines. Degenerative alterations consisted of truncated dendritic arborizations, occasional focal dendritic swellings, and marked spine loss. Proliferative changes were found primarily in moderate grades of HD, while degenerative changes were predominantly found in severe grades. Cytopathologic changes increased with neuropathologic severity. Similar morphologic alterations were observed in calbindin D28k (Calb) stained neurons in HD striatum. The immunoreactive intensity of Calb staining was increased in the distal dendrites of positive neurons in HD striatum. The present findings provide morphologic and quantitative evidence that confirms an early and marked involvement of spiny striatal neurons in HD and suggest that neuronal growth, rather than degeneration, may be the harbinger of cell death in this disorder.
A novel mechanism for aspirin-mediated growth inhibition of human colon cancer cells. (2003)

We conclude that aspirin acts through COX-independent mechanisms by resulting in an increase in MMR protein expression and subsequent apoptosis, which might serve as an additional means of growth inhibition in aspirin-treated human colon cancer cells.
Collagen-Based Biomimetic Nanofibrous Scaffolds: Preparation and Characterization of Collagen/Silk Fibroin Bicomponent Nanofibrous Structures (2008)

Electrospinning of collagen (COL)/silk fibroin (SF) blend solutions in 1,1,1,3,3,3-hexafluoro-2-propanol was investigated for fabrication of a biocompatible and biomimetic nanostructured scaffold for tissue engineering. The morphology of the electrospun COL/SF blend nanofibers was observed by scanning electron microscopy. The average diameters of COL/SF blend fibers ranged from 320 to 360 nm, irrespective of SF content in the blends. Both COL and SF components in the as-spun COL/SF blend matrices were stabilized by glutaraldehyde and water vapor, respectively, under the saturated glutaraldehyde aqueous solution at 25 degrees C. The glutaraldehyde vapor chemically stabilized the COL component via cross-linking, whereas the water vapor physically stabilized the SF component via crystallization to the beta-sheet structure. These structural changes of after-treated COL/SF blend matrices were examined using ATR-IR and CP/MAS (13)C NMR spectroscopy. To assay the cytocompatibility and cellular behavior of the COL/SF blend nanofibrous scaffolds, cell attachment and the spreading of normal human epidermal keratinocytes (NHEK) and fibroblasts (NHEF) seeded on the scaffolds were studied. In addition, both morphological changes and cellular responses of COL/SF blend nanofibrous matrices were also compared with COL/SF hybrid nanofibrous matrices. Generally similar levels of cell attachment and spreading of NHEF were shown in the COL/SF blend nanofibrous matrix compared with those of the pure COL and pure SF matrices; the cellular responses of NHEK were, however, markedly decreased in the COL/SF blend nanofibrous matrix as compared to the pure matrices. In contrast, cell attachment and spreading of NHEK on the COL/SF hybrid nanofibrous matrix were significantly higher than that of the COL/SF blend nanofibrous matrix. Our results indicate that a COL/SF hybrid nanofibrous matrix may be a better candidate than a COL/SF blend nanofibrous matrix for biomedical applications such as wound dressing and scaffolds for tissue engineering.
Inhibition of the replication of the DNA polymerase M550V mutation variant of human hepatitis B virus by adefovir, tenofovir, L‐FMAU, DAPD, penciclovir and lobucavir (2000)

Several nucleoside analogues (penciclovir, lobucavir, dioxalane guanine [DXG], 1-beta-2,6-diaminopurine dioxalane [DAPD], L-FMAU, lamivudine) and acyclic nucleoside phosphonate analogues (adefovir, tenofovir) that are in clinical use, in clinical trials or under preclinical development for the treatment of hepatitis B virus (HBV) infections, were evaluated for their inhibitory effect on the replication of a la- mivudine-resistant HBV variant containing the methionine --> valine substitution (M550V) in the polymerase nucleoside-binding domain. The antiviral activity was determined in the tetracycline-responsive HepAD38 and HepAD79 cells, which are stably transfected with either a cDNA copy of the wild-type pregenomic RNA or with cDNA containing the M550V mutation. As expected, lamivudine was much less ( approximately 200-fold) effective at inhibiting replication of the M550V mutant virus than the wild-type virus. In contrast, adefovir, tenofovir, lobucavir, L-FMAU, DXG and DAPD proved almost equally effective against both viruses. A second objective of this study was to directly compare the antiviral potency of the anti-HBV agents in HepG2 2.2.15 cells (which are routinely used for anti-HBV drug-screening purposes) with that in HepAD38 cells. HepAD38 cells produce much larger quantities of HBV than HepG2 2.2.15 cells, and thus allow drug screening in a multiwell plate format. All compounds were found to be almost equally effective at inhibiting HBV replication in HepAD38 cells (as in HepG2 2.2.15 cells), except for penciclovir, which was clearly less effective in HepAD38 cells.
Inhibition of Transcription by the Trimeric Cyclin-dependent Kinase 7 Complex (1999)

Cyclin-dependent kinase 7 (CDK7) can be isolated as a subunit of a trimeric kinase complex functional in activation of the mitotic promoting factor. In this study, we demonstrate that the trimeric cdk-activating kinase (CAK) acts as a transcriptional repressor of class II promoters and show that repression results from CAK impeding the entry of RNA polymerase II and basal transcription factor IIF into a competent preinitiation complex. This repression is independent of CDK7 kinase activity. We find that the p36/MAT1 subunit of CAK is required for transcriptional repression and the repression is independent of the promoter used. Our results demonstrate a central role for CAK in regulation of messenger RNA synthesis by either inhibition of RNA polymerase II-catalyzed transcription or stimulation of transcription through association with basal transcription repair factor IIH.
Multiuser OFDM with adaptive subcarrier, bit, and power allocation (1999)

Multiuser orthogonal frequency division multiplexing (OFDM) with adaptive multiuser subcarrier allocation and adaptive modulation is considered. Assuming knowledge of the instantaneous channel gains for all users, we propose a multiuser OFDM subcarrier, bit, and power allocation algorithm to minimize the total transmit power. This is done by assigning each user a set of subcarriers and by determining the number of bits and the transmit power level for each subcarrier. We obtain the performance of our proposed algorithm in a multiuser frequency selective fading environment for various time delay spread values and various numbers of users. The results show that our proposed algorithm outperforms multiuser OFDM systems with static time-division multiple access (TDMA) or frequency-division multiple access (FDMA) techniques which employ fixed and predetermined time-slot or subcarrier allocation schemes. We have also quantified the improvement in terms of the overall required transmit power, the bit-error rate (BER), or the area of coverage for a given outage probability.
Cardiovascular Actions and Clinical Outcomes With Glucagon-Like Peptide-1 Receptor Agonists and Dipeptidyl Peptidase-4 Inhibitors (2017)

Potentiation of glucagon-like peptide-1 (GLP-1) action through selective GLP-1 receptor (GLP-1R) agonism or by prevention of enzymatic degradation by inhibition of dipeptidyl peptidase-4 (DPP-4) promotes glycemic reduction for the treatment of type 2 diabetes mellitus by glucose-dependent control of insulin and glucagon secretion. GLP-1R agonists also decelerate gastric emptying, reduce body weight by reduction of food intake and lower circulating lipoproteins, inflammation, and systolic blood pressure. Preclinical studies demonstrate that both GLP-1R agonists and DPP-4 inhibitors exhibit cardioprotective actions in animal models of myocardial ischemia and ventricular dysfunction through incompletely characterized mechanisms. The results of cardiovascular outcome trials in human subjects with type 2 diabetes mellitus and increased cardiovascular risk have demonstrated a cardiovascular benefit (significant reduction in time to first major adverse cardiovascular event) with the GLP-1R agonists liraglutide (LEADER trial [Liraglutide Effect and Action in Diabetes: Evaluation of Cardiovascular Ourcome Results], -13%) and semaglutide (SUSTAIN-6 trial [Trial to Evaluate Cardiovascular and Other Long-term Outcomes with Semaglutide], -24%). In contrast, cardiovascular outcome trials examining the safety of the shorter-acting GLP-1R agonist lixisenatide (ELIXA trial [Evaluation of Lixisenatide in Acute Coronary Syndrom]) and the DPP-4 inhibitors saxagliptin (SAVOR-TIMI 53 trial [Saxagliptin Assessment of Vascular Outcomes Recorded in Patients With Diabetes Mellitus-Thrombolysis in Myocardial Infarction 53]), alogliptin (EXAMINE trial [Examination of Cardiovascular Outcomes With Alogliptin Versus Standard of Care in Patients With Type 2 Diabetes Mellitus and Acute Coronary Syndrome]), and sitagliptin (TECOS [Trial Evaluating Cardiovascular Outcomes With Sitagliptin]) found that these agents neither increased nor decreased cardiovascular events. Here we review the cardiovascular actions of GLP-1R agonists and DPP-4 inhibitors, with a focus on the translation of mechanisms derived from preclinical studies to complementary findings in clinical studies. We highlight areas of uncertainty requiring more careful scrutiny in ongoing basic science and clinical studies. As newer more potent GLP-1R agonists and coagonists are being developed for the treatment of type 2 diabetes mellitus, obesity, and nonalcoholic steatohepatitis, the delineation of the potential mechanisms that underlie the cardiovascular benefit and safety of these agents have immediate relevance for the prevention and treatment of cardiovascular disease.
ATM concepts, architectures, and protocols (1995)

Asynchronous transfer mode (ATM) is often described as the future computer networking paradigm that will bring high-speed communications to the desktop. What is ATM? How is it different from today's networking technologies? This article is intended to acquaint readers with this emerging technology and describe some of the concepts embodied within it. In order to understand why ATM was created and how it works, we first need to review a bit of computer networking history.