gebhart/patrepeval huggingface dataset:
Expansion of unusual CD4+ T cells in severe rheumatoid arthritis (1997)

The bimodality of distribution of CD4+ CD28- T cell frequencies is compatible with genetic control of the generation of these unusual T cells. In RA patients, CD4+ CD28- T cells are not an epiphenomenon of the disease process, but predispose patients to developing inflammatory lesions in extraarticular tissues.
Calcimimetic R-568 Decreases Extraosseous Calcifications in Uremic Rats Treated with Calcitriol (2006)

Calcimimetics decrease parathyroid hormone (PTH) levels in uremic patients with secondary hyperparathyroidism without increasing serum calcium (Ca). The aim of this study was to evaluate the effect of calcimimetic R-568 alone or in combination with calcitriol on vascular and other soft tissue calcifications in uremic rats with secondary hyperparathyroidism. Sham-operated and 5/6 nephrectomized Wistar rats were studied. 5/6 Nephrectomized rats were treated with vehicle, calcitriol (80 ng/kg every other day), R-568 (1.5 and 3 mg/kg per d), and both calcitriol and R-568 1.5 mg/kg, as above. Rats were killed after 14 or 56 d of treatment. Blood was drawn for biochemical measurements. Aortic, heart, kidney, lung, and stomach tissue samples were processed for histopathology and measurement of tissue Ca and phosphorus content. PTH concentrations were significantly reduced by all treatments. Treatment with calcitriol induced significant vascular calcification (aortic Ca increased to 4.2+/-1.2 mg/g at day 14 and to 11.4+/-0.7 mg/g at day 56; P<0.05 versus vehicle). Treatment with R-568 did not induce vascular calcification. Concurrent administration of R-568 with calcitriol reduced the aortic Ca (1.9+/-0.2 mg/g at day 14 and 7.5+/-1.4 mg/g at day 56) in relation to calcitriol alone. Soft tissue calcifications mirrored aortic mineralizations. Survival was significantly (P<0.001) reduced in calcitriol-treated rats, and mortality was attenuated (P=0.01) by concurrent treatment with R-568. In uremic rats, R-568 reduces elevated PTH levels without inducing vascular calcification, prevents calcitriol-induced vascular calcification, and decreases mortality.
Isolation pattern and clinical outcome of genital mycoplasma in neonates from a tertiary care neonatal unit (1999)

The role of genital mycoplasma in perinatal mortality and morbidity has been debated. This study was undertaken to determine the frequency of isolation of genital mycoplasma and evaluate its association with clinical outcome. Sixty-six cerebrospinal fluid (CSF) and 49 tracheal aspirates taken from 100 low birthweight infants who had suspected meningitis and/or respiratory distress respectively were cultured for genital mycoplasma. Ureaplasma urealyticum was isolated from 9 per cent of CSF and 14 per cent of tracheal aspirates. Mycoplasma hominis was isolated from CSF in one case and none at the tracheal aspirates. Three out of seven mycoplasma-infected CNS cases showed CSF pleocytosis while three out of seven patients whose tracheal aspirates grew mycoplasma had congenital pneumonia. None of the patients were treated with antimycoplasmal therapy and none developed chronic lung disease.
Xylitol production by Petromyces albertensis grown on medium containing D-xylose (1991)

Petromyces albertensis produced xylitol and D-xylulose when cultivated on a medium containing D-xylose. These fermentative products were identified by high-performance liquid chromatography. A large amount of xylitol was obtained from a D-xylose medium containing ammonium acetate and yeast extract at an initial pH of 7.0. Maximum production of xylitol and of the enzymes concerned with its production was observed after 10 days of cultivation. A D-xylose (100 g/L) medium supplemented with 1% (v/v) methanol gave the highest yields of xylitol (39.8 g/L) and D-xylulose (2.8 g/L). Key words: Petromyces albertensis, D-xylulose, xylitol.
Antibody-DerivedIn VivoImaging of Tau Pathology (2014)

Antibodies or their derivatives as imaging probes for pathological tau protein have great potential, but have not been well studied. In particular, smaller, single-chain-variable antibody fragments (scFv's) are attractive for detecting tau lesions in live subjects. Here, we generated libraries of scFv's and identified numerous phospho-tau-selective scFv's. Peripheral injection of one of these scFv's consistently resulted in a strong in vivo brain signal in transgenic tauopathy mice, but not in wild-type or amyloid-β plaque mice. The parent tau antibody provided similar results, albeit with a weaker signal intensity. The imaging signal correlated very well with colocalization of the probe with intraneuronal tau aggregates. Both were associated with markers of endosomes, autophagosomes, and lysosomes, suggesting their interaction in these degradation pathways. Such specific antibody-derived imaging probes have great potential as diagnostic markers for Alzheimer's disease and related tauopathies.
Human adhalin is alternatively spliced and the gene is located on chromosome 17q21. (1994)

Mutations in the dystrophin gene cause the X chromosome-linked, recessive Duchenne and Becker muscular dystrophies. Dystrophin, a large cytoskeletal protein, copurifies with a complex of dystrophin-associated proteins which serve to anchor dystrophin to the sarcolemma. One of these associated proteins, adhalin, has been implicated as a candidate for severe childhood autosomal recessive muscular dystrophy (SCARMD) due to absence of anti-adhalin staining in muscle biopsy samples taken from SCARMD patients. Furthermore, the Duchenne-like dystrophic phenotype seen in the SCARMD families was shown to be tightly linked to chromosome 13 markers. To determine the genetic mutation responsible for autosomal dystrophy, we characterized the human adhalin gene. Contrary to our expectation, human adhalin was mapped to chromosome 17q21, excluding adhalin as the gene causing chromosome 13-associated SCARMD. Additionally, a splice form of adhalin message was found that predicts a 35-kDa nontransmembrane adhalin. The expression of both adhalin splice forms is exclusively restricted to striated muscle, unlike other components of the dystrophin-glycoprotein complex.
MicroRNA Profiling in Mucosal Biopsies of Eosinophilic Esophagitis Patients Pre and Post Treatment with Steroids and Relationship with mRNA Targets (2012)

Our findings add to the accumulating body of data defining a regulatory role for miRNA in immune and allergic processes.
Absence of Apparent Phenotype in Mice Lacking Cdc25C Protein Phosphatase (2001)

The Cdc25 family of protein phosphatases positively regulate the cell division cycle by activating cyclin-dependent protein kinases. In humans and rodents, three Cdc25 family members denoted Cdc25A, -B, and -C have been identified. The murine forms of Cdc25 exhibit distinct patterns of expression both during development and in adult mouse tissues. In order to determine unique contributions made by the Cdc25C protein phosphatase to embryonic and adult cell cycles, mice lacking Cdc25C were generated. We report that Cdc25C(-/-) mice are viable and do not display any obvious abnormalities. Among adult tissues in which Cdc25C is detected, its transcripts are most abundant in testis, followed by thymus, ovary, spleen, and intestine. Mice lacking Cdc25C were fertile, indicating that Cdc25C does not contribute an essential function during spermatogenesis or oogenesis in the mouse. T- and B-cell development was also found to be normal in Cdc25C(-/-) mice, and Cdc25C(-/-) mouse splenic T and B cells exhibited normal proliferative responses in vitro. Finally, the phosphorylation status of Cdc2, the timing of entry into mitosis, and the cellular response to DNA damage were unperturbed in mouse embryo fibroblasts lacking Cdc25C. These findings indicate that Cdc25A and/or Cdc25B may compensate for loss of Cdc25C in the mouse.
Radiation Pneumonitis: A Possible Lymphocyte-mediated Hypersensitivity Reaction (1993)

In most patients, a lymphocytic alveolitis develops in both lung fields after strictly unilateral thoracic irradiation; this is more pronounced in patients developing clinical pneumonitis. These findings suggest that radiotherapy may cause a generalized lymphocyte-mediated hypersensitivity reaction.
Demonstration of a functional apical sodium hydrogen exchanger in isolated rat gastric glands (2003)

Previous studies have shown that gastric glands express at least sodium-hydrogen exchanger (NHE) isoforms 1-4. Our aim was to study NHE-3 localization in rat parietal cells and to investigate the functional activity of an apical membrane NHE-3 isoform in parietal cells of rats. Western blot analysis and immunohistochemistry showed expression of NHE-3 in rat stomach colocalizing the protein in parietal cells together with the beta-subunit of the H(+)-K(+)-ATPase. Functional studies in luminally perfused gastric glands demonstrated the presence of an apical NHE isoform sensitive to low concentrations of 5-ethylisopropyl amiloride (EIPA). Intracellular pH measurements in parietal cells conducted in omeprazole-pretreated superfused gastric glands showed an Na+-dependent proton extrusion pathway that was inhibited both by low concentrations of EIPA and by the NHE-3 specific inhibitor S3226. This pathway for proton extrusion had a higher activity in resting glands and was inhibited on stimulation of histamine-induced H(+)-K(+)-ATPase proton extrusion. We conclude that the NHE-3 isoform located on the apical membrane of parietal cells offers an additional pathway for proton secretion under resting conditions. Furthermore, the gastric NHE-3 appears to work under resting conditions and inactivates during periods of H(+)-K(+)-ATPase activity.
Nucleotide sequences of the genes for two distinct cephalosporin acylases from a Pseudomonas strain (1987)

Two genes, acyI and acyII, for distinct cephalosporin acylases from Pseudomonas sp. strain SE83 (A. Matsuda, K. Matsuyama, K. Yamamoto, S. Ichikawa, and K.I. Komatsu, J. Bacteriol. 169:5815-5820, 1987) were sequenced. Each sequence contained a single open reading frame for two nonidentical subunits, predicting a common precursor. Some homologies at the amino acid level were found between the acyII-encoded enzyme, but not the acyI-encoded one, and other related acylases.
Long chain acyl coenzyme A and signaling in neutrophils. An inhibitor of acyl coenzyme A synthetase, triacsin C, inhibits superoxide anion generation and degranulation by human neutrophils. (1994)

Ligand-initiated activation of neutrophils triggers O2- generation, degranulation, phospholipid remodeling, and release of fatty acids such as arachidonate, oleate, and palmitate. Long chain acyl-CoA synthetase converts free fatty acids to acyl-CoA esters; a role for acyl-CoA esters as positive modulators of neutrophil functions is proposed. Physiologically relevant concentrations (1-10 microM) of acyl-CoA esters such as palmitoyl-CoA, enhanced O2- generation triggered by fMet-Leu-Phe or guanosine 5'-O-(thiotriphosphate) (GTP gamma S) but did not act as a trigger per se. Triacsin C, an inhibitor of acyl-CoA synthetase, inhibited fMet-Leu-Phe-elicited O2- generation and degranulation in a concentration-dependent manner. Triacsin C inhibited O2- generation elicited by fMet-Leu-Phe and GTP gamma S in electroporated neutrophils, indicating that acyl-CoA acted downstream from the receptor. Palmitoyl-CoA reversed the Triacsin C-induced inhibition of O2- generation. fMet-Leu-Phe elicited a prompt increase in total long chain acyl-CoA esters. Arachidonoyl-CoA and oleoyl-CoA were elevated 5 s after addition of fMet-Leu-Phe, while palmitoyl-CoA was not elevated until 60 s. Triacsin C inhibited fMet-Leu-Phe-initiated increases in arachidonoyl-CoA, oleoyl-CoA, and palmitoyl-CoA. These results suggest a role for acyl-CoA esters in regulating activation of O2- generation and degranulation at the G protein or subsequent step(s).
Adsorption and surface-enhanced Raman of dyes on silver and gold sols (1982)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTAdsorption and surface-enhanced Raman of dyes on silver and gold solsP. C. Lee and D. MeiselCite this: J. Phys. Chem. 1982, 86, 17, 3391–3395Publication Date (Print):August 1, 1982Publication History Published online1 May 2002Published inissue 1 August 1982https://pubs.acs.org/doi/10.1021/j100214a025https://doi.org/10.1021/j100214a025research-articleACS PublicationsRequest reuse permissionsArticle Views25315Altmetric-Citations4092LEARN 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 options Get e-Alerts
Mutation of the myelin Po gene in Charcot — Marie — Tooth neuropathy type 1B (1993)

We have previously reported that the mutations of the myelin P0 gene were completely linked with Charcot-Marie-Tooth neuropathy type 1B (CMT1B) in two families. In this study we found a different mutation in another family with CMT1B. The mutation, a methionine substitution for isoleucine at amino acid position 30, is located in the extracellular domain, which constitutes an immunoglobulin domain responsible for the function of P0 as an adhesion molecule. The results confirmed that P0 is a gene responsible for CMT1B.
Networked UAV Command, Control and Communication (2006)

The networked UAV command, control, and communication project has designed, implemented, and tested a network-centric, intelligent flight management system for UAVs. The system utilizes an existing ad-hoc network to demonstrate the ability of UAVs to make mission level decisions autonomously based upon network metrics and operator-specified parameters. Each UAV features a highly modular hardware architecture which provides a standardized interface to the onboard systems and enables system scaling. A high-level bus protocol is used on this interface to transport messages between the avionics package, network node, supervisory computer, and scientific payload. All decisions are made autonomously, but an operator maintains control of the mission parameters, and may modify them through the ad-hoc network using a mobile monitoring station. The station features a GUI to display feedback on node status as well as provide a visualization of any science data being collected. The collective system was tested and verified utilizing both a hardware-in-the-loop simulation, and an experiment at an outdoor range.
Identification of a Novel Lipopolysaccharide-Inducible Gene with Key Features of Both a Kinase Anchor Proteins and chs1/beige Proteins (2001)

Mutations in chs1/beige result in a deficiency in intracellular transport of vesicles that leads to a generalized immunodeficiency in mice and humans. The function of NK cells, CTL, and granulocytes is impaired by these mutations, indicating that polarized trafficking of vesicles is controlled by CHS1/beige proteins. However, a molecular explanation for this defect has not been identified. Here we describe a novel gene with orthologues in mice, humans, and flies that contains key features of both chs1/beige and A kinase anchor genes. We designate this novel gene lba for LPS-responsive, beige-like anchor gene. Expression of lba is induced after LPS stimulation of B cells and macrophages. In addition, lba is expressed in many other tissues in the body and has three distinct mRNA isoforms that are differentially expressed in various tissues. Strikingly, LBA-green-fluorescent protein (GFP) fusion proteins are localized to vesicles after LPS stimulation. Confocal microscopy indicates this protein is colocalized with the trans-Golgi complex and some lysosomes. Further analysis by immunoelectron microscopy demonstrates that LBA-GFP fusion protein can localize to endoplasmic reticulum, plasma membrane, and endocytosis vesicles in addition to the trans-Golgi complex and lysosomes. We hypothesize that LBA/CHS1/BG proteins function in polarized vesicle trafficking by guiding intracellular vesicles to activated receptor complexes and thus facilitate polarized secretion and/or membrane deposition of immune effector molecules.
Role of Insulin Resistance in Human M. REAVEN (1988)

Resistance to insulin-stimulated glucose uptake is present in the majority of patients with impaired glucose tolerance (IGT) or non-insulin-dependent diabetes mellitus (NIDDM) and in -25 % of nonobese individuals with normal oral glucose tolerance. In these conditions, deterioration of glucose tolerance can only be prevented if the p-cell is able to increase its insulin secretory response and maintain a state of chronic hyperinsulinemia. When this goal cannot be achieved, gross decompensation of glucose homeostasis occurs. The relationship between insulin resistance, plasma insulin level, and glucose intolerance is mediated to a significant degree by changes in ambient plasma free-fatty acid (FFA) concentration. Patients with NIDDM are also resistant to insulin suppression of plasma FFA concentration, but plasma FFA concentrations can be reduced by relatively small increments in insulin concentration. Consequently, elevations of circulating plasma FFA concentration can be prevented if large amounts of insulin can be secreted. If hyperinsulinemia cannot be maintained, plasma FFA concentration will not be suppressed normally, and the resulting increase in plasma FFA concentration will lead to increased hepatic glucose production. Because these events take place in individuals who are quite resistant to insulinstimulated glucose uptake, it is apparent that even small increases in hepatic glucose production are likely to lead to significant fasting hyperglycemia under these conditions. Although hyperinsulinemia may prevent frank decompensation of glucose homeostasis in insulin-resistant individuals, this compensatory response of the endocrine pancreas is not without its price. Patients with hypertension, treated or untreated, are insulin resistant,
The effect of exogenous glucagon-like peptide-1 on the glycaemic response to small intestinal nutrient in the critically ill: a randomised double-blind placebo-controlled cross over study (2009)

Australian New Zealand Clinical Trials Registry number: ACTRN12609000093280.
Designing secure intranets (1998)

A secure intranet can now be built with existing technology, and replicated and scaled throughout an organisation to provide a set of managed information services. The author looks at the main security issues which are in the policy and procedural areas, rather than in technological ones.
Robotic Devices for Movement Therapy After Stroke: Current Status and Challenges to Clinical Acceptance (2002)

Robotic devices for movement therapy are moving closer to becoming commercially available tools for aiding in stroke rehabilitation. Robotic technology offers a range of functions that will augment current clinical practice by leveraging therapists' time, cost effectively extending therapy programs, providing new measures of impairment, and offering new therapy protocols. In this article, we review work from several research laboratories that supports the clinical value of stroke therapy systems. A commercialization effort based on these results is described. We also discuss challenges to achieving clinical acceptance and practical implementation of these devices.
NovelN-methyl-d-aspartate receptor antagonists: a review of compounds patented since 2006 (2010)

The most important recent strategies aiming for inhibition of NMDA receptor-mediated neurotransmission avoid for safety reasons full receptor blockade but allow a low degree of normal receptor function. Approaches pursued by the latest patents comprise blocking the channel with compounds of low affinity, antagonizing receptor activity by highly potent NR2B ligands, partial agonism at the glutamate or glycine-binding site and improvement of pharmacokinetic properties of well established, safe antagonists by deuteration.
The Annealing Time and Temperature Dependence of Electrical Dopant Activation in High‐Dose  BF 2 Ion Implanted Silicon (1994)

The electrical dopant activation of high‐dose ion implanted layers was investigated as a function of annealing time and temperature using rapid thermal annealing (RTA) and furnace annealing (FA). Fast recrystallization using RTA produces low sheet resistance, and prolonged annealing at low temperatures causes electrical dopant deactivation. The deactivation was controlled by a diffusion limited process with an activation energy value of 3.46 eV, which is equal to the value of boron diffusion in the amorphous region that regrows to a single crystal. RTA yields low sheet resistances compared with FA, because RTA minimizes not only the redistribution of fluorine atoms in the amorphous region during the recrystallization, but also the electrical dopant deactivation during the time the wafer is cooling.
Two types of complementary DNAs of rat brain protein kinase C (1986)

Two types of complementary DNA clones for rat brain protein kinase C were isolated. These clones encode 671 and 673 amino acid sequences, which differ from each other only in the carboxyl-terminal regions of approx. 50 amino acid residues. This difference seems to result from alternative splicing. Elucidation of the sequences of these cDNA clones as well as some peptides from the purified rat brain enzyme suggests the existence of an additional species of protein kinase C in this tissue. It is attractive to imagine that the heterogeneity of protein kinase C may reflect diverse pathways of signal transduction into the cell.
RNA Interference Directed against Viral and Cellular Targets Inhibits Human Immunodeficiency Virus Type 1 Replication (2002)

Human immunodeficiency virus type 1 (HIV-1) gene expression is regulated by both cellular transcription factors and Tat. The ability of Tat to stimulate transcriptional elongation is dependent on its binding to TAR RNA in conjunction with cyclin T1 and CDK9. A variety of other cellular factors that bind to the HIV-1 long terminal repeat, including NF-kappaB, SP1, LBP, and LEF, are also important in the control of HIV-1 gene expression. Although these factors have been demonstrated to regulate HIV-1 gene expression by both genetic and biochemical analysis, in most cases a direct in vivo demonstration of their role on HIV-1 replication has not been established. Recently, the efficacy of RNA interference in mammalian cells has been shown utilizing small interfering RNAs (siRNAs) to result in the specific degradation of host mRNAs and decreases the levels of their corresponding proteins. In this study, we addressed whether siRNAs directed against either HIV-1 tat or reverse transcriptase or the NF-kappaB p65 subunit could specifically decrease the levels of these proteins and thus alter HIV-1 replication. Our results demonstrate the specificity of siRNAs for decreasing the expression of these viral and cellular proteins and inhibiting HIV-1 replication. These studies suggest that RNA interference is useful in exploring the biological role of cellular and viral regulatory factors involved in the control of HIV-1 gene expression.