gebhart/patrepeval huggingface dataset:
Human leukocyte activation antigen M6, a member of the Ig superfamily, is the species homologue of rat OX-47, mouse basigin, and chicken HT7 molecule (1992)

Peripheral granulocytes from rheumatoid arthritis and reactive arthritis patients were recently found to express higher levels of a newly defined Ag, termed M6, in comparison to granulocytes from healthy subjects. We present here the molecular characterization of M6 Ag and show that it is a novel human leukocyte activation-associated cell surface glycoprotein. Peripheral lymphocytes do not significantly express M6 Ag, however, it appears upon 3-day PHA-activated T blasts. On monocytes, which constitutively express M6 Ag, it is down-regulated on day 1 but re-induced on day 3 of granulocyte-macrophage CSF stimulation. SDS-PAGE analysis of M6 immunoprecipitates shows a single band of 54 kDa under nonreducing conditions that shifts to 65 kDa under reducing conditions. Endoglycosidase F treatment of M6 immunoprecipitate reveals that 50% of the M6 molecule is composed of N-linked carbohydrates. By modifying the COS cell cloning strategy, we have isolated cDNA clones encoding M6 Ag. M6 cDNA hybridizes with a single mRNA transcript of approximately 1.7 kb in Northern blotting. Comparison analysis of the M6 sequence indicates that M6 Ag is a member of the Ig superfamily and the species homologue of rat OX-47 Ag, mouse basigin (gp42), and chicken HT7 molecule. The highly conserved remarkable transmembrane domain suggests that the M6 Ag may be a component of a multichain complex in the plasma membrane.
Cysteine protease inhibitors as chemotherapy: Lessons from a parasite target (1999)

Papain family cysteine proteases are key factors in the pathogenesis of cancer invasion, arthritis, osteoporosis, and microbial infections. Targeting this enzyme family is therefore one strategy in the development of new chemotherapy for a number of diseases. Little is known, however, about the efficacy, selectivity, and safety of cysteine protease inhibitors in cell culture or in vivo. We now report that specific cysteine protease inhibitors kill Leishmania parasites in vitro, at concentrations that do not overtly affect mammalian host cells. Inhibition of Leishmania cysteine protease activity was accompanied by defects in the parasite's lysosome/endosome compartment resembling those seen in lysosomal storage diseases. Colocalization of anti-protease antibodies with biotinylated surface proteins and accumulation of undigested debris and protease in the flagellar pocket of treated parasites were consistent with a pathway of protease trafficking from flagellar pocket to the lysosome/endosome compartment. The inhibitors were sufficiently absorbed and stable in vivo to ameliorate the pathology associated with a mouse model of Leishmania infection.
Identification of Upper Airway Anatomic Risk Factors for Obstructive Sleep Apnea with Volumetric Magnetic Resonance Imaging (2003)

We used sophisticated volumetric analysis techniques with magnetic resonance imaging in a case-control design to study the upper airway soft tissue structures in 48 control subjects (apnea-hypopnea index, 2.0 +/- 1.6 events/hour) and 48 patients with sleep apnea (apnea-hypopnea index, 43.8 +/- 25.4 events/hour). Our design used exact matching on sex and ethnicity, frequency matching on age, and statistical control for craniofacial size and visceral neck fat. The data support our a priori hypotheses that the volume of the soft tissue structures surrounding the upper airway is enlarged in patients with sleep apnea and that this enlargement is a significant risk factor for sleep apnea. After covariate adjustments the volume of the lateral pharyngeal walls (p < 0.0001), tongue (p < 0.0001), and total soft tissue (p < 0.0001) was significantly larger in subjects with sleep apnea than in normal subjects. These data also demonstrated, after covariate adjustments, significantly increased risk of sleep apnea the larger the volume of the tongue, lateral pharyngeal walls, and total soft tissue: (1) total lateral pharyngeal wall (odds ratio [OR], 6.01; 95% confidence interval [CI], 2.62-17.14); (2) total tongue (OR, 4.66; 95% CI, 2.31-10.95); and (3) total soft tissue (OR, 6.95; 95% CI, 3.08-19.11). In a multivariable logistic regression analysis the volume of the tongue and lateral walls was shown to independently increase the risk of sleep apnea.
Enabling an Energy-Efficient Future Internet Through Selectively Connected End Systems (2007)

The Internet’s architecture largely and implicitly assumes full-time connectivity, a notion that is embodied in key networking principles including fate sharing, soft state, and the end-to-end principle. In contrast, efforts to allow for more graceful operation in the presence of forced disconnectedness have recently been undertaken that change the underlying style of networking used by applications to accommodate both host-level and hop-by-hop disconnectedness (e.g., for deep space networks where connectivity depends on orbital mechanics). In this paper, we offer an initial exploration of the architectural constructs required to support selective connectivity, whereby a host can choose whether to be “connected” or “disconnected”. While we keep our notion of selective connectivity general, the driver behind our thinking is to allow hosts to go to sleep to realize energy savings while not sacrificing their standing in the network. Studies show that enabling such sleeping offers large potential energy savings. Specifically, we explore ideas related to assistants, soft state, host-based control, and application primitives.
Enzyme Induction by L-Buthionine(S,R)-Sulfoximine in Cultured Mouse Hepatoma Cells (1995)

Induction of Phase II enzymes of the [Ah] gene battery by L-buthionine (S,R)-sulfoximine (BSO) and other agents was examined in mouse hepatoma Hepa-1c1c7 cells. BSO, a nonelectrophilic inhibitor of gamma-glutamylcysteine synthetase (GCS), is routinely used to examine the toxicological implications of GSH depletion. Exposure to BSO for 24 h produced a 75-85% depletion of GSH levels, proportional to the inhibition of GCS activity, as well as small increases in the UDP-glucuronosyltransferase (UGT, 60%) and glutathione transferase (GST, 30%) enzyme activities in Hepa-1 wild-type (wt) cells. However, for the NAD(P)H:menadione oxidoreductase (NMO1) and cytosolic aldehyde dehydrogenase class 3 (AHD4) enzyme activities, BSO produced larger increases (110% and 170%, respectively). The mechanisms of NMO1 and AHD4 induction were examined further. In Hepa-1 wt cells, NMO1 and AHD4 activities were increased by the aromatic hydrocarbon inducer 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and by the electrophile tert-butylhydroquinone (tBHQ), known inducing agents for these enzymes. However, NMO1 and AHD4 were induced in Ah receptor nuclear translocation-defective mutant (c4) cells by BSO and tBHQ, but not by TCDD, suggesting that the induction by BSO and tBHQ is not Ah receptor-mediated. In wt cells, N-acetylcysteine produced a concentration-dependent increase in intracellular cysteine levels, but not GSH levels, in the absence or presence of BSO. Furthermore, N-acetylcysteine had no effect on NMO1 activity under any conditions examined, suggesting that GSH levels per se, rather than change in overall thiol status, might be mediating increased NMO1 activity.(ABSTRACT TRUNCATED AT 250 WORDS)
Gene Transfer in Mammalian Cells Using Liposomes as Carriers (1994)

After understanding the molecular genetic cause(s) for human diseases, gene therapy is a method of treatment under active research. As the name implies, gene therapy involves treatment of diseases by product(s) of foreign gene which return(s) affected cells or tissues to normal status. The successful application of this approach begins with the development of a suitable carrier for the target specific delivery of genetic material followed by expression of DNA at that site. This carrier should also be able to protect the DNA from surrounding environment, e.g., from plasma for in vivo delivery. Under ideal conditions this expression should be controlled by using inducible or tissue specific promoters. Different kinds of systems are being used to effectively transfer and express the foreign DNA in various types of mammalian cells. These are classified below: (i) agents which deliver DNA by physical means: e.g. microinjection (Capecchi, 1980), electroporation (Paquereau and Cam, 1992), biobalistic or particle bombardment (Yang et al., 1990) and jet injection (Furth et al., 1992). (ii) agents which deliver DNA by chemical means: e.g. calcium phosphate (Wigler et al., 1977), DEAE dextran (Ishikawa and Homey, 1992), polylysine conjugates (Wu and Wu, 1987; Wagner et al., 1990), polybrene-dimethyl sulfoxide (Kawai and Nishizawa, 1984) and liposomes (Feigner et al., 1987; Gao and Huang, 1991) (iii) agents which deliver DNA by biological means: e.g. virus derived vectors (Ferry et al., 1991; Culver et al., 1992).
Advances in automatic meeting record creation and access (2002)

Oral communication is transient, but many important decisions, social contracts and fact findings are first carried out in an oral setup, documented in written form and later retrieved. At Carnegie Mellon University's Interactive Systems Laboratories we have been experimenting with the documentation of meetings. The paper summarizes part of the progress that we have made in this test bed, specifically on the question of automatic transcription using large vocabulary continuous speech recognition, information access using non-keyword based methods, summarization and user interfaces. The system is capable of automatically constructing a searchable and browsable audio-visual database of meetings and provide access to these records.
Mucoadhesive DL-Lactide/Glycolide Copolymer Nanospheres Coated with Chitosan to Improve Oral Delivery of Elcatonin (2000)

The purpose of this work was to develop a novel mucoadhesive DL-lactide/glycolide copolymer (PLGA) nanosphere system to improve peptide absorption and prolong the physiological activity following oral administration. The desired PLGA nanospheres with elcatonin were prepared by the emulsion solvent diffusion method to coat the surface of the resultant nanospheres with a mucoadhesive polymer such as chitosan, poly(acrylic acid), and sodium alginate. Their mucoadhesive properties were evaluated by measuring the nanospheres adsorbed to a rat everted intestinal sac (in vitro). The chitosan-coated nanospheres showed higher mucoadhesion to the everted intestinal tract in saline than the other polymer-coated nanospheres. There was no mucoadhesion site-specificity of the chitosan-coated nanospheres between duodenal, jejunal, and ileal sacs. The payload of drug in the chitosan-coated nanospheres was successfully increased by using the solvent diffusion method in oil. The pattern of drug release of the resultant nanospheres did not differ markedly from that of uncoated nanospheres. The chitosan-coated nanospheres with elcatonin were administered intragastrically to fasted Wistar rats. The chitosan-coated nanosphere reduced significantly the blood calcium level compared with elcatonin solution and uncoated nanospheres, and the reduced calcium level was sustained for a period of 48 hr. Even under nonfasting conditions, the mucoadhesion of chitosan-coated nanospheres was unaltered and the reduction in blood Ca levels was maintained satisfactorily.
Chemiluminescence yields and detection limits of some isoluminol derivatives in various oxidation systems (1978)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTChemiluminescence yields and detection limits of some isoluminol derivatives in various oxidation systemsHartmut R. Schroeder and Frances M. YeagerCite this: Anal. Chem. 1978, 50, 8, 1114–1120Publication Date (Print):July 1, 1978Publication History Published online1 May 2002Published inissue 1 July 1978https://pubs.acs.org/doi/10.1021/ac50030a027https://doi.org/10.1021/ac50030a027research-articleACS PublicationsRequest reuse permissionsArticle Views599Altmetric-Citations120LEARN 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
Cellular models and therapies for age-related macular degeneration (2015)

Age-related macular degeneration (AMD) is a complex neurodegenerative visual disorder that causes profound physical and psychosocial effects. Visual impairment in AMD is caused by the loss of retinal pigmented epithelium (RPE) cells and the light-sensitive photoreceptor cells that they support. There is currently no effective treatment for the most common form of this disease (dry AMD). A new approach to treating AMD involves the transplantation of RPE cells derived from either human embryonic or induced pluripotent stem cells. Multiple clinical trials are being initiated using a variety of cell therapies. Although many animal models are available for AMD research, most do not recapitulate all aspects of the disease, hampering progress. However, the use of cultured RPE cells in AMD research is well established and, indeed, some of the more recently described RPE-based models show promise for investigating the molecular mechanisms of AMD and for screening drug candidates. Here, we discuss innovative cell-culture models of AMD and emerging stem-cell-based therapies for the treatment of this vision-robbing disease.
Influence of Diet on Basal and Growth Hormone-Stimulated Plasma Concentrations of IGF-I in Beef Cattle (1989)

The effects of nutrition on plasma concentrations of insulin-like growth factor-I (IGF-I) were characterized in steers under basal conditions and following single i.m. injection of bovine growth hormone (bGH, .1 mg/kg BW). Nutritional effects on IGF-I were studied in three trials. In all trials steers were individually fed and penned Angus or Hereford x Angus (280 kg). In the first trial, two diets (LPLE1: 8% CP and 1.96 Mcal ME/kg, 4.5 kg.hd-1.d-1; MPHE1: 11% CP, 2.67 Mcal ME/kg, 6.5 kg.hd-1.d-1) were fed (n = 5/diet). Plasma IGF-I concentrations averaged 74 (LPLE1) and 152 (MPHE1) ng/ml (P less than .02). Following bGH injection, IGF-I increased to peak concentrations between 12 and 24 h (averaging 105 and 208 ng/ml at peak for LPLE and MPLE, respectively, P less than .01). In the second trial, steers were fed diets composed of 8, 11 or 14% CP and 1.96 or 2.67 Mcal ME/kg dry matter (6.35 kg.hd-1.d-1 in a factorial arrangement for 84 d, n = 4/diet). Within the low ME diet groups, plasma IGF-I was similar in steers fed 11 and 14% CP but greater at these two CP levels than in steers fed 8% CP (P less than .05). Within the high ME diet groups, plasma IGF-I increased linearly with CP (P less than .01). In the third trial, steers were fed diets to result in a negative N status. Insulin-like growth factor-I was lower (P less than .02) during feed restriction than when steers were full-fed. The IGF-I response to bGH was diminished or absent in underfed steers (P less than .01). These data are interpreted to suggest that diet composition and intake affect plasma concentrations of IGF-I in steers. In cattle, CP may be the primary nutritional determinant of basal IGF-I, but the IGF-I response to CP may be affected by the available ME. Undernutrition can attenuate the IGF-I response to GH and uncouple the regulation of IGF-I normally ascribed to GH.
High-Resolution Views of Io's Emakong Patera: Latest Galileo Imaging Results (2002)

This presentation will discuss analyses of the latest Galileo SSI (solid state imaging) high-resolution images of the Emakong lava channels and flow field on Jupiter's moon Io. Additional information is contained in the original extended abstract.
In vitro translation of the citrus tristeza virus coat protein from a 0.8 kbp double-stranded RNA segment (1990)

Several dsRNA segments, ranging in size from 0·8 to 19·5 kbp, have been isolated from citrus plants infected with the VT and ST strains of citrus tristeza virus (CTV) and translated, after denaturation, in a reticulocyte lysate cell-free system. Only two small dsRNA segments of 0·8 and 1·7 kbp were efficiently translated and showed a consistent pattern of products. The major translation product of the 0·8 kbp dsRNA was a 27K polypeptide, immunoprecipitated by antiserum to the CTV coat protein. The major translation product of the 1·7 kbp dsRNA segment was a 21·5K peptide. The possibility that the CTV coat protein may be translated from a subgenomic viral messenger RNA is discussed.
High NaCl causes Mre11 to leave the nucleus, disrupting DNA damage signaling and repair (2003)

High NaCl causes DNA double-strand breaks and cell cycle arrest, but the mechanism of its genotoxicity has been unclear. In this study, we describe a novel mechanism that contributes to this genotoxicity. The Mre11 exonuclease complex is a central component of DNA damage response. This complex assembles at sites of DNA damage, where it processes DNA ends for subsequent activation of repair and initiates cell cycle checkpoints. However, this does not occur with DNA damage caused by high NaCl. Rather, following high NaCl, Mre11 exits from the nucleus, DNA double-strand breaks accumulate in the S and G2 phases of the cell cycle, and DNA repair is inhibited. Furthermore, the exclusion of Mre11 from the nucleus by high NaCl persists following UV or ionizing radiation, also preventing DNA repair in response to those stresses, as evidenced by absence of H2AX phosphorylation at places of DNA damage and by impaired repair of damaged reporter plasmids. Activation of chk1 by phosphorylation on Ser345 generally is required for DNA damage-induced cell cycle arrest. However, chk1 does not become phosphorylated during high NaCl-induced cell cycle arrest. Also, high NaCl prevents ionizing and UV radiation-induced phosphorylation of chk1, but cell cycle arrest still occurs, indicating the existence of alternative mechanisms for the S and G2/M delays. DNA breaks that occur normally during processes such as DNA replication and transcription, as well as damages to DNA induced by genotoxic stresses, ordinarily are rapidly repaired. We propose that inhibition of this repair by high NaCl results in accumulation of DNA damage, accounting for the genotoxicity of high NaCl, and that cell cycle delay induced by high NaCl slows accumulation of DNA damage until the DNA damage-response network can be reactivated.
Embryonic stem cells and transgenic mice in the study of hematopoiesis (1998)

Blood formation (hematopoiesis) entails the generation of hematopoietic stem cells (HSCs) within the embryo and subsequent commitment of multipotential progenitors to differentiation along single lineages. These processes are controlled in large part by cell-restricted transcription factors which cooperate with more widely expressed factors to direct lineage-specific gene expression. Candidate hematopoietic transcriptional regulators have been identified by characterizing factors mediating cell-specific gene transcription and by defining genes involved in chromosomal rearrangements in leukemia. The application of transgenic and embryonic stem cell methods have provided insights into their in vivo functions and suggested mechanisms by which lineage selection may be achieved. One of the first, and best, characterized hematopoietic transcription factors is GATA-1. Herein studies of GATA-1 are reviewed to illustrate how manipulations of its locus in the mouse have contributed to current understanding in unique and unexpected ways.
The cell-binding domains of plasminogen and their function in plasma. (1988)

Plasminogen binding sites are expressed by a wide variety of cell types and serve to promote fibrinolysis and local proteolysis. In this study, the recognition specificity of cells for plasminogen has been examined, primarily using platelets as models. Analyses with plasminogen fragments implicated residues 79-337 (or 353), comprising the first three kringles of plasminogen, as a primary recognition site for plasminogen binding to both thrombin-stimulated and nonstimulated platelets. Other regions of plasminogen, namely residues 354-439 and 442-790, can also participate in the interaction, and these other regions contribute differentially to the binding of the ligand to stimulated and nonstimulated platelets. Binding to nucleated cells, with U937 cells serving as the prototype, is dependent upon a recognition specificity similar to that of unstimulated platelets. Binding of Glu-plasminogen, the native form of the molecule, to thrombin-stimulated platelets has been shown previously to require platelet fibrin. By comparing the interaction of Glu-plasminogen and its degradation product, Lys-plasminogen, with thrombin-stimulated platelets, it is concluded that the cell surface uniquely enhances the affinity of Glu-, but not Lys-plasminogen, for fibrin. Finally, we have demonstrated that cellular receptors and interactive sites within plasminogen are available in the plasma environment. Thus, the functions ascribed to cellular plasminogen receptors can occur within a physiologic setting.
Analysis of discharge techniques for multiple battery systems (2003)

We consider the problem of scheduling multiple identical batteries for discharge in portable electronic systems. Unlike previous work reporting some experimental data to suggest which scheduling schemes are better than others, we arrive at our general conclusions formally, based on the analysis of an accurate high-level model of battery behavior. Our analytical results show that: (1) the lifetime of a parallel discharge schedule is equal to that of an equivalent monolithic battery, (2) the lifetime of a parallel discharge schedule is no less than that of a sequential discharge schedule, and (3) the lifetime of a switched discharge schedule approaches that of an equivalent monolithic battery as the switching frequency increases. We also derive bounds on the lifetime of a single battery under a constant-rate load, and then extend them to multiple battery systems. Using a low-level battery simulator, we verify our analytical findings with numerical data. For the simulated cases, the parallel discharge schedule resulted in up to 72% higher lifetimes than the sequential discharge schedule but fell short of the lifetime upper bound by up to 29%.