gebhart/patrepeval huggingface dataset:
Removal of anti-Galα1,3Gal xenoantibodies with an injectable polymer (2002)

Preformed and elicited Ab's against the Galα1,3Gal terminating carbohydrate chains (αGal Ab's) are the primary cause of hyperacute and acute vascular xenograft rejection in pig-to-primate transplantation. αGal Ab's are produced by long-lived Ab-producing cells that are not susceptible to pharmacological immunosuppression. We reasoned that antigen-specific elimination of αGal Ab's might be achieved in vivo by systemic administration of nonimmunogenic polyvalent αGal structures with high avidity for αGal Ab's. We devised GAS914, a soluble trisaccharide-polylysine conjugate of approximately 500 kDa that effectively competes for αGal binding by αGal IgM (IC50, 43 nM) and IgG (IC50, 28 nM) in vitro. Injections of GAS914 in cynomolgus monkeys, at the dose of 1 mg/kg, resulted in the immediate decrease of more than 90% of circulating αGal Ab's and serum anti-pig cytotoxicity. In baboons, repeated injections of GAS914 effectively reduced both circulating αGal Ab's and cytotoxicity over several months. Studies with [14C]GAS914 in rhesus monkeys and Gal–/– mice indicate that GAS914 binds to circulating αGal Ab's and that the complex is quickly metabolized by the liver and excreted by the kidney. Remarkably, posttreatment αGal Ab titers never exceeded pretreatment levels and no sensitization to either αGal or the polylysine backbone has been observed. Furthermore there was no apparent acute or chronic toxicity associated with GAS914 treatment in primates. We conclude that GAS914 may be used therapeutically for the specific removal of αGal Ab's.
Radiation-induced neoplastic transformation of human prostate epithelial cells. (1996)

We report the malignant transformation of human prostate epithelial cells (267B1) after multiple exposures to ionizing radiation. Carcinogenic progression of cells from immortal growth to anchorage-independent growth in soft agar to tumorigenicity in athymic mice resulted after a cumulative X-ray dose of 30 Gy. The tumors were characterized histologically as poorly differentiated adenocarcinomas, expressed prostate-specific antigen, and stained positive for keratin. No p53 or ras mutations were observed. Numerous chromosomal defects were noted on karyotypes after radiation exposure. However, chromosome 3 and 8 translocations were observed predominantly in the tumor outgrowths. These findings provide the first evidence of malignant transformation of human prostate epithelial cells exposed to ionizing radiation.
Phase II Randomized Study Comparing the Toxicity Profile of Gemcitabine plus Cisplatin with Gemcitabine plus Oral Etoposide in the Treatment of Advanced Non-Small Cell Lung Cancer (2005)

This toxicity profile of GE is similar to GP, but the apparent inferior efficacy may discourage further investigation.
Solid-Surface Characterization by Wetting (2009)

The current status of the theories that are required for characterization of solid surfaces by equilibrium contact angles is reviewed. Some important aspects, which are not yet completely understood, are explained and listed as future challenges. The theoretical conclusions are integrated into a methodology and technique for contact angle measurement and interpretation that avoid existing pitfalls.
Characterization of Clone 13, a Naturally Attenuated Avirulent Isolate of Rift Valley Fever Virus, which is Altered in the Small Segment (1995)

The 74HB59 strain of Rift Valley fever (RVF) virus, isolated from a human case in the Central African Republic, was shown to be composed of a heterogeneous population of viruses when plaque-purified clones were analyzed for their reactivity with monoclonal antibodies (MAbs) directed against the nucleocapsid (N) protein or the nonstructural (NSs) protein. One of these clones, C13, was of particular interest in that it proved to be avirulent in mice and hamsters, and highly immunogenic. Although C13 showed normal reactivity with a large panel of MAbs directed at the glycoproteins, it failed to react with specific MAbs or polyclonal antibodies directed at the NSs protein and with a specific MAb recognizing the N protein of the Egyptian strains. Consequently, the small RNA segment, which encodes the N and NSs proteins in an ambisense strategy, was sequenced and compared with the existing sequence of the attenuated MP-12 RVF virus strain. We found that the NSs gene contained, in addition to two conservative coding changes, a large internal deletion of 549 nucleotides that removes 69% of the open reading frame but conserves in-frame the N and C termini of the predicted translation product. In addition, the sequence revealed that the N protein of C13 contained a single amino acid change. Clone C13 replicated normally in certain cell types in vitro and in Culex pipiens mosquitoes after intrathoracic inoculation, but established abortive infections in MRC-5 human fibroblasts.
Lines of T Lymphocytes Induce or Vaccinate Against Autoimmune Arthritis (1983)

The pathophysiology of autoimmune arthritis was studied by selecting and isolating lines of effector T lymphocytes from rats administered an arthritogenic dose of Mycobacterium tuberculosis in complete Freund's adjuvant to induce adjuvant arthritis. Irradiated rats were intravenously inoculated with a cell line characterized by proliferative reactivity to Mycobacterium tuberculosis and, to a lesser degree, to rat collagen type II. This produced arthritis in all the irradiated rats. Nonirradiated recipients failed to develop arthritis. However, such rats, and those recovering from cell-mediated arthritis, were resistant to subsequent attempts to induce adjuvant arthritis. Lines of T lymphocytes selected for responsiveness to other antigens had no effect. Therefore, a line of T lymphocytes responsive to bacteria or to collagen type II could either induce autoimmune arthritis or serve as an agent of vaccination against it.
Neuroprotective Properties of Statins in Cerebral Ischemia and Stroke (1999)

In addition to reducing stroke, the statin class of drugs exhibits a number of important neuroprotective properties that likely attenuate the effects of ischemia on the brain vasculature and parenchyma. Further investigation of the role of statins in human neuroprotection by use of neuroimaging and cognitive studies is warranted to explore these preliminary observations. In addition to reducing ischemic stroke, early evidence indicates that statins may also be neuroprotective.
Characterization of Aδ- and C-Fibers Innervating the Plantar Rat Hindpaw One Day After an Incision (2002)

Primary hyperalgesia after tissue injury is suggested to result from sensitization of primary afferent fibers, but sensitization to mechanical stimuli has been difficult to demonstrate. In the companion study, sensitization of mechano-responsive Adelta- and C-fibers did not explain pain behaviors 45 min after an incision in the rat hindpaw. In the present study, we examined mechanical response properties of Adelta- and C-fibers innervating the glabrous skin of the plantar hindpaw in rats 1 day after an incision or sham procedure. In behavioral experiments, median withdrawal thresholds to von Frey filaments were reduced from 522 mN before to 61 mN 2 and 20 h after incision; median withdrawal thresholds after sham procedure were stable (522 mN). Responses to a nonpunctate mechanical stimulus were increased after incision. In neurophysiological experiments in these same rats, 67 single afferent fibers were characterized from the left tibial nerve 1 day after sham procedure (n = 39) or incision (n = 28); electrical stimulation was used as the search stimulus to identify a representative population of Adelta- and C-fibers. In the incision group, 11 fibers (39%) had spontaneous activity with frequencies ranging from 0.03 to 39.3 imp/s; none were present in the sham group. The median response threshold of Adelta-fibers was less in the incision (56 mN, n = 13) compared with sham (251 mN, n = 26) group, mainly because the proportion of mechanically insensitive afferents (MIAs) was less (8 vs. 54% after sham procedure). Median C-fiber response thresholds were similar in incised (28 mN, n = 15) and sham rats (56 mN, n = 13). Responsiveness to monofilaments was significantly enhanced in Adelta-fibers 1 day after incision; stimulus response functions of C-fibers after incision and after sham procedure did not differ significantly. Only Adelta-fibers but not C-fibers sensitized to the nonpunctate mechanical stimulus. The size of receptive fields was increased in Adelta- and C-fibers 1 day after incision. The results indicate that sensitization of Adelta- and C-fibers is apparent 1 day after incision. Because sensitization of afferent fibers to mechanical stimuli correlated with behavioral results, sensitization may contribute to the reduced withdrawal threshold after incision. Spontaneous activity in Adelta- and C-fibers may account for nonevoked pain behavior and may also contribute to mechanical hyperalgesia by amplifying responses centrally.
TRANCE Is a Novel Ligand of the Tumor Necrosis Factor Receptor Family That Activates c-Jun N-terminal Kinase in T Cells (1997)

A novel member of the tumor necrosis factor (TNF) cytokine family, designated TRANCE, was cloned during a search for apoptosis-regulatory genes using a somatic cell genetic approach in T cell hybridomas. The TRANCE gene encodes a type II membrane protein of 316 amino acids with a predicted molecular mass of 35 kDa. Its extracellular domain is most closely related to TRAIL, FasL, and TNF. TRANCE is an immediate early gene up-regulated by TCR stimulation and is controlled by calcineurin-regulated transcription factors. TRANCE is most highly expressed in thymus and lymph nodes but not in nonlymphoid tissues and is abundantly expressed in T cells but not in B cells. Cross-hybridization of the mouse cDNA to a human thymus library yielded the human homolog, which encodes a protein 83% identical to the mouse ectodomain. Human TRANCE was mapped to chromosome 13q14 while mouse TRANCE was located to the portion of mouse chromosome 14 syntenic with human chromosome 13q14. A recombinant soluble form of TRANCE composed of the entire ectodomain induced c-Jun N-terminal kinase (JNK) activation in T cells but not in splenic B cells or in bone marrow-derived dendritic cells. These results suggest a role for this TNF-related ligand in the regulation of the T cell-dependent immune response.
HBT before CMOS, a new modular SiGe BiCMOS integration scheme (2002)

Demonstrates a novel HBT-before-CMOS integration scheme to integrate SiGe:C HBTs with a 130 nm gate length CMOS frontend. This scheme entirely eliminates the impact of the HBT thermal steps on CMOS characteristics, opening the way for easy, modular integration of high-performance HBTs into highly scaled CMOS technologies. C doping of the SiGe layer prevents the degradation of HBT parameters by critical CMOS thermal steps. This is demonstrated for SiGe:C HBTs with f/sub T//f/sub max/ values of 80/90 GHz fabricated in the HBT-before-CMOS scheme and in a benchmark HBT-only process.
New APHA book a resource for creating healthy, safe homes (2010)

From radon to mold to lead-based paint, unhealthy housing conditions can take a significant and sometimes irreversible toll on the health and safety of a home’s occupants. Asthma, lead poisoning, injuries and cancer are some of the health and safety hazards associated with unhealthy housing, and few Americans are free from risk.
Cell death: Current difficulties in discriminating apoptosis from necrosis in the context of pathological processes in vivo (1995)

The term apoptosis was proposed to define a type of cell death morphologically, biochemically, and molecularly distinct from necrosis, which plays a fundamental regulatory function in the control of the overall size of cell populations, being complementary but opposite to cell proliferation [Kerr et al. (1972): Br J Cancer 26:239-257]. This view has led to the appreciation that apoptosis is an integral part of normal biological processes and may impact on disease states. Introduction of the concept of apoptosis has raised great interest and many studies have been aimed to the identification of genes responsible for the induction of cell death. Indeed, over the past few years, many genes whose expression is associated with cell death have been described, and the molecular mechanisms underlying cell death have been, in some circumstances, clearly established. However, it is now evident that extension of the conclusions achieved by studies performed with highly selected in vitro systems (simple systems), to in vivo conditions (complex systems), has generated a certain degree of confusion. This is in part due to the indiscriminate use of the term apoptosis and to the uncertainty whether apoptosis is always different from necrosis, and, if this is the case, to the lack of well established criteria to discriminate the two processes; in addition, it still remains to be established whether both types of cell death, although different, could be induced simultaneously by the same agent, depending on the cell type and the experimental condition used. The distinction between apoptosis and necrosis, is not simply a problem of terminology; if necrosis and apoptosis are different from a mechanistic point of view, and if necrosis is merely the passive result of cellular injury (still to be shown), it becomes critical to discriminate between the two processes, in order to understand how to modulate apoptosis in view of its potential therapeutic use. This review will summarize existing informations and discuss some of the conflicting issues related to cell death in the liver.
The bacterial periplasmic histidine-binding protein. structure/function analysis of the ligand-binding site and comparison with related proteins. (1994)

Bacterial periplasmic binding proteins are initial receptors in the process of active transport across cell membranes and/or chemotaxis. Among them, the histidine-binding protein (HisJ) has been extensively studied from the biochemical, physiological, and genetic points of view. The three-dimensional crystal structure of the histidine-binding protein complexed with histidine has been determined at 2.5-A resolution by the molecular replacement method using a probe structure the previously solved lysine-liganded structure of the lysine-, arginine-, ornithine-binding protein (LAO), which shares 70% sequence identity with HisJ. The structure is bi-lobate; the two lobes, one bigger than the other, are connected by two short strands and are in contact with each other (closed) enclosing the histidine. Charged, polar, and non-polar side chains, as well as the peptide backbone, are involved in tight binding of the histidine. The bound histidine is involved in eight direct hydrogen bonds, six with the bigger lobe and two with the smaller lobe, in one potential water-mediated hydrogen bond with the bigger lobe, as well as in ionic interactions. The HisJ residues surrounding the ligand are the same as the LAO residues interacting with lysine, except for residue 52 which is leucine in HisJ and phenylalanine in LAO. The Leu-52 in HisJ makes a hydrophobic interaction with the imidazole ring of histidine. Of seven mutations affecting the ligand-binding site, five are located in the ligand-binding site, one in a connecting strand, and one at the domains interface. Based on comparisons among related binding proteins, the specific interactions between the ligands and the respective binding protein residues are predicted for the glutamine-binding protein and the opines-binding protein.
Neointimal coverage of sirolimus-eluting stents at 6-month follow-up: evaluated by optical coherence tomography (2006)

At 6 months, most of the SES were covered with thin neointima, but few showed full coverage.
Anti-CD81 antibodies can prevent a hepatitis C virus infection in vivo (2008)

Our experiments provide evidence for the critical role of CD81 in a genuine HCV infection in vivo and open new perspectives for the prevention of allograft reinfection after orthotopic liver transplantation in chronically infected HCV patients.
Consensus Statement on Concussion in Sport – the 3rd International Conference on Concussion in Sport held in Zurich, November 2008 (2009)

No Abstract.
Identification of the low density lipoprotein receptor-related protein (LRP) as an endocytic receptor for thrombospondin-1. (1995)

Thrombospondin-1 (TSP1) has potent biological effects on vasculature smooth muscle cells (SMCs) and endothelial cells. The regulation of extracellular accumulation of TSP1 is mediated by a previously obscure process of endocytosis which leads to its lysosomal degradation. Since members of the low density lipoprotein receptor (LDLR) family have been found to mediate endocytosis which leads to degradation of a diverse array of ligands, we evaluated their possible role in the uptake and degradation of TSP1 by vascular SMCs, endothelial-cells and fibroblasts. 125I-TSP1 was found to be internalized and degraded lysosomally by all these cell types. Both the internalization and degradation of 125I-TSP1 could be inhibited by a specific antagonist of the LDLR family, the 39-kD receptor-associated protein (RAP). Antibodies to the LDLR-related protein (LRP) completely blocked the uptake and degradation of 125I-TSP1 in SMCs and fibroblasts but not endothelial cells. Solid-phase binding assays confirmed that LRP bound to TSP1 and that the interaction was of high affinity (Kd = 5 nM). Neither RAP nor LRP antibodies inhibited the binding of 125I-TSP1 to surfaces of SMCs. However, cell surface binding, as well as, endocytosis and degradation could be blocked by heparin or by pre-treatment of the cells with either heparitinase, chondroitinase or beta-D-xyloside. The data indicates that cell surface proteoglycans are involved in the LRP-mediated clearance of TSP1. A model for the clearance of TSP1 by these cells is that TSP1 bound to proteoglycans is presented to LRP for endocytosis. In endothelial cells, however, the internalization of TSP1 was not mediated by LRP but since RAP inhibited TSP1 uptake and degradation, we postulate that another member of the LDLR family is likely to be involved.
Nonlinearity compensation of linear power amplifier for mobile communication (2002)

We examines nonlinearity compensation with a 836.5 MHz high efficiency power amplifier. We use the high frequency negative feedback method, which is robust against changes in the amplifier characteristics and whose circuit implementation is easy. The maximum feedback gain of the amplifier is 9 dB. Thus, in the unsaturated region, the distortion is reduced by 9 dB. In the saturated region, an improvement is not obtained due to the reduction of the feedback gain. Computer simulation of the saturated region shows that the feedback amplifier provides a distortion improvement of 10 dB if a feedback gain of 20 dB is achieved. Computer aided design of a feedback amplifier shows an encouraging result for achieving a feedback gain of 20 dB.
Complete amino acid sequence of β2-microglobulin (1973)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTComplete amino acid sequence of β2-microglobulinBruce A. Cunningham, John L. Wang, Ingemar Berggard, and Per A. PetersonCite this: Biochemistry 1973, 12, 24, 4811–4822Publication Date (Print):November 1, 1973Publication History Published online1 May 2002Published inissue 1 November 1973https://pubs.acs.org/doi/10.1021/bi00748a001https://doi.org/10.1021/bi00748a001research-articleACS PublicationsRequest reuse permissionsArticle Views310Altmetric-Citations220LEARN 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
Comparative Evaluation of Three Commercial Systems for Nucleic Acid Extraction from Urine Specimens (2005)

A nucleic acid extraction system that can handle small numbers of specimens with a short test turnaround time and short hands-on time is desirable for emergent testing. We performed a comparative validation on three systems: the MagNA Pure compact system (Compact), the NucliSens miniMAG extraction instrument (miniMAG), and the BioRobot EZ1 system (EZ1). A total of 75 urine specimens submitted for polyomavirus BK virus detection were used. The human beta-actin gene was detected on 75 (100%), 75 (100%), and 72 (96%) nucleic acid extracts prepared by the miniMAG, EZ1, and Compact, respectively. The miniMAG produced the highest quantity of nucleic acids and the best precision among the three systems. The agreement rate was 100% for BKV detection on nucleic acid extracts prepared by the three extraction systems. When a full panel of specimens was run, the hands-on time and test turnaround time were 105.7 and 121.1 min for miniMAG, 6.1 and 22.6 min for EZ1, and 7.4 and 33.7 min for Compact, respectively. The EZ1 and Compact systems processed automatic nucleic acid extraction properly, providing a good solution to the need for sporadic but emergent specimen detection. The miniMAG yielded the highest quantity of nucleic acids, suggesting that this system would be the best for specimens containing a low number of microorganisms of interest.
Recent Progress in Understanding the Hormonal Regulation of Phosphodiesterases (1995)

LAYER after layer of novel regulatory circuits have been added to the map charting the signal transduction pathways that transport information throughout the cell. New components of these pathways are found at a breathtaking pace, and new functions for old components are continuously uncovered. It is now recognized that the complexity of these pathways resembles the intricacy and integration of the pathways of intermediate metabolism. This is especially true for the cyclic nucleotide-dependent signal transduction and its components, including cyclic nucleotide phosphodiesterases (PDEs).These are the enzymes that with cyclases control the intracellular concentration of cyclic nucleotides. With the development of new molecular tools, a wealth of new information has accumulated on the structure and function of these enzymes. Four years ago we reviewed the current knowledge on the mechanisms of hormonal regulation of PDEs (1). Here, we update this survey, reporting the most recent developments of this field. Since our previous review, many primary structures of the human and mammalian PDEs have been elucidated. This has brought about a better understanding of the structure/function relationship of these proteins. Furthermore, PDE gene structure is being actively investigated, adding a further dimension to the regulation of these enzymes and opening new avenues of investigation. Novel mechanisms of regulation have been uncovered, linking these enzymes to new hormone-dependent functions. As we will discuss in detail, the overall picture derived from these findings reinforces the concept that PDEs may serve three major functions in the cell target for hormones and neurotransmitters: 1) They are effectors in signal transduction, 2) they play a role in integrating different signal transduction pathways, and 3) they may also serve as a dampening device to decrease or terminate hormonal stimulation.