gebhart/patrepeval huggingface dataset:
Influence of Retarding Hydrogen Diffusion in Boron Phosphosilicate Glass on Annealing Damage of Metal‐Oxide Semiconductor Transistors (1999)

This paper reports results on an investigation of the influence of titanium film in interconnects on incomplete transistor annealing. Annealing damage may be impeded when titanium directly overlays transistors. This may be due to not only gettering of hydrogen by titanium films but also to retarding hydrogen diffusion of the interlayer between the gate electrode of transistors and the titanium‐containing interconnects in boron phosphosilicate glass. The hydrogen diffusion coefficient in the boron phosphosilicate glass film was approximately at 400°C, which is three orders of magnitude smaller than that in the thermal oxide. © 1999 The Electrochemical Society. All rights reserved.
Changes in plasma levels of complement in patients with acute ischemic stroke. (2008)

Inflammatory processes are involved in cerebral ischemia. Patients with ischemic stroke may be predisposed to marked activation of the inflammatory system. The objective was to analyze the association between the level of complement at different stages after stroke and outcome. We collected blood samples from 179 patients (81 men and 98 women, mean age 73 +/- 5.6 years) within 24 hours after ischemic stroke, within 48 to 72 hours and at hospital discharge (16 +/- 7 days) as compared to 156 healthy controls, matching ischemic stroke patients with regard to sex and age. We measured levels of total hemolytic activity of serum complement (EIA method) and of C3, C4 (nephelometric measurements). The data were evaluated using chi 2 test. Within 24 hours after ischemic stroke in 38% patients mean value of CH50 was 148.4 +/- 57 CH50 U Eq/mL (p<0.05), of C3 was 1.49 +/- 0.24 mg/L (p<0.05) and of C4 was 0.32 +/- 0.08 mg/L (p<0.05). Within 48-72 hours after ischemic stroke in 34% patients mean value of CH50 was 167 +/- 5.9 CH50 U Eq/mL (p<0.01), of C3 was 1.58 +/- 0.27 mg/L (p<0.01) and of C4 was 0.38 +/- 0.08 mg/L (p<0.01). At hospital discharge in 31% patients mean value of CH50 was 192.8 +/- 64 CH50 U Eq/mL (p<0.001), of C3 was 1.66 +/- 0.28 mg/L (p<0.001) and of C4 was 0.49 +/- 0.07 mg/L (p<0.001). Patients with ischemic stroke who had elevated complement levels (inflammatory marker) at discharge had a worse neurological disability; complement might directly contribute to vascular damage.
Product of the steel locus suppresses apoptosis in hemopoietic cells. Comparison with pathways activated by granulocyte macrophage colony-stimulating factor. (1994)

Steel factor (SF), also referred to as Kit ligand, stem cell factor, or mast cell growth factor, is essential for the development of hematopoietic stem cells in vivo.It is shown here that SF is mainly a survival factor for hemopoietic cells with little if any proliferative effect.In contrast, granulocyte macrophage colony-stimulating factor (GM-CSF) acts both as a survival factor and as a potent growth factor.We have probed the pathways activated by SF and GM-CSF in suppression of active cell death (apoptosis) using two classes of inhibitors: Tyrphostins that are specific inhibitors of protein tyrosine kinase, and amiloride derivatives (5-(N-ethyl-n-isopro-py1)amiloride and 5-(N,N-hexamethylene)amiloride) that have been designed as specific inhibitors of the Na+/H+ antiporter.Both SF-dependent and GM-CSF-dependent pathways are sensitive to inhibition by Tyrphostins with, nonetheless, a quantitative difference.All Tyrphostins tested are more potent inhibitors of c-Kit than of GM-CSF receptor triggered pathways, the most striking being Tyrphostin B42 that is 10 times more potent.In contrast to the discrepancy in Tyrphostin doseresponse curves, titration curves for 5-(N-ethyl-n-iso-propy1)amiloride and 5-(N,N-hexamethylene)amiloride are comparable in SF-or GM-CSF-stimulated cells.Furthermore, SF induces a rapid and sustained alkalinization of the intracellular pH, as assessed with the pHsensitive probe 2',7'-bis(2-carboxyethyl)-5-carboxyfluorescein.Taken together, our data indicate that input from two distinct pathways with discrepancy in immediate early events, that of c-Kit and GM-CSF receptor, results in a common output, activation of the Na+/€I+ antiporter and suppression of apoptosis by the two ligands.Mutations in both the Steel locus (Sl) and the "dominant white spotting" locus result in developmental defects in three
Mild Hemophilia A Caused by Increased Rate of Factor VIII A2 Subunit Dissociation: Evidence for Nonproteolytic Inactivation of Factor VIIIa In Vivo (1999)

Approximately 5% of hemophilia A patients have normal amounts of a dysfunctional factor VIII (FVIII) protein and are termed cross-reacting material (CRM)-positive. FVIII is a heterodimer (domain structure A1-A2-B/A3-C1-C2) that requires thrombin cleavage to elicit procoagulant activity. Thrombin-activated FVIII is a heterotrimer with the A2 subunit (amino acid residues 373 to 740) in a weak ionic interaction with the A1 and A3-C1-C2 subunits. Dissociation of the A2 subunit correlates with inactivation of FVIII. Recently, a phenotype of CRM-positive hemophilia A patients has been characterized whose plasma displays a discrepancy between their FVIII activities, where the one-stage clotting assay displays greater activity than the two-stage clotting assay. One example is a missense mutation whereARG531 has been substituted by HIS531. An FVIII cDNA construct was prepared containing theARG531HIS mutation and the protein was expressed in COS-1 monkey cells by transient DNA transfection. Metabolic labeling with [35S]-methionine demonstrated that ARG531HIS was synthesized at an equal rate compared with FVIII wild-type (WT) but had slightly reduced antigen in the conditioned medium, suggesting a modest secretion defect. A time course of structural cleavage of ARG531HISdemonstrated identical thrombin cleavage sites and rates of proteolysis as FVIII WT. Similar to the patient phenotypes,ARG531HIS had discrepant activity as measured by a one-stage activated partial thromboplastin time (aPTT) clotting assay (36% ± 9.6% of FVIII WT) and a variation of the two-stage assay using a chromogenic substrate (COAMATIC; 19% ± 6.9% of FVIII WT). Partially purified FVIII WT and ARG531HISproteins were subjected to functional activation by incubation with thrombin. ARG531HIS demonstrated significantly reduced peak activity and was completely inactivated after 30 seconds, whereas FVIII WT retained activity until 2.5 minutes after activation. Because the ARG531HIS missense mutation predicts a charge change to the A2 subunit, we hypothesized that theARG531HIS A2 subunit could be subject to more rapid dissociation from the heterotrimer. The rate of A2 dissociation, using an optical biosensor, was determined to be fourfold faster forARG531HIS compared with FVIII WT. Because the two-stage assay involves a preincubation phase before assay measurement, an increased rate of A2 dissociation would result in an increased rate of inactivation and reduced specific activity.
Increased uncoupling proteins and decreased efficiency in palmitate-perfused hyperthyroid rat heart (2001)

The physiological role of mitochondrial uncoupling proteins (UCPs) in heart and skeletal muscle is unknown, as is whether mitochondrial uncoupling of oxidative phosphorylation by fatty acids occurs in vivo. In this study, we found that UCP2 and UCP3 protein content, determined using Western blotting, was increased by 32 and 48%, respectively, in hyperthyroid rat heart mitochondria. Oligomycin-insensitive respiration rate, a measure of mitochondrial uncoupling, was increased in all mitochondria in the presence of palmitate: 36% in controls and 71 and 100% with 0.8 and 0.9 mM palmitate, respectively, in hyperthyroid rat heart mitochondria. In the isolated working heart, 0.4 mM palmitate significantly lowered cardiac output by 36% and cardiac efficiency by 38% in the hyperthyroid rat heart. Thus increased mitochondrial UCPs in the hyperthyroid rat heart were associated with increased uncoupling and decreased myocardial efficiency in the presence of palmitate. In conclusion, a physiological effect of UCPs on fatty acid oxidation has been found in heart at the mitochondrial and whole organ level.
During a corticotropin-releasing hormone test in healthy subjects, administration of a beta-adrenergic antagonist induced secretion of cortisol and dehydroepiandrosterone sulfate and inhibited secretion of ACTH (2003)

A beta-adrenergic influence seems to decrease CRH-stimulated cortisol in relation to ACTH and 17OHP, and decreases DHEAS in relation to DHEA. Although other workers have found beta-adrenergic stimulation of steroid secretion in cultured adrenocortical cells, the overall systemic influence of the SNS via beta-adrenoceptors seems to inhibit adrenal steroids under unstimulated and stimulated conditions. Sympathetic hyperactivity may be a common denominator for low levels of DHEAS in inflammatory and non-inflammatory diseases.
Specific tolerance to neural allografts induced with an antibody to the interleukin 2 receptor. (1993)

Despite considerable evidence documenting the central nervous system as a site of immunological privilege, immune responses do occur within the brain and neural allografts between major histocompatibility complexes (MHC) and minor antigen incompatible rat strains may be rejected. The survival of completely MHC incompatible neural allografts has been found to be prolonged indefinitely after administration of a monoclonal antibody (mAb) to the interleukin 2 receptor (IL-2R) for 10 d after transplantation. Here we present evidence that rats with long-term surviving lateral ventricular neural allografts, after anti-IL-2R treatment, accept subsequent neural allografts from the same donor strain, placed in a peripheral nonprivileged site, but rapidly reject third-party grafts. Thus, treatment with a mAb to the p55 chain of the IL-2R has resulted in the specific acceptance of second grafts of fully allogeneic neural tissue. These results suggest that ongoing interaction between elements of the host immune system and alloantigen within the brain maintains the tolerant state and furthermore, that interruption of signaling through the IL-2R may be important in allospecific tolerance induction.
Proppant Flowback Control in High Temperature Wells (1998)

Abstract The control of proppant flowback following fracturing operations can be obtained by several different methods such as resin coated proppant, inorganic fibres or polymer strips. However, each one of the presently available technologies has its limitations, e.g. resin coated proppant cannot generally be used above 190 C (374 F) and requires an activator below about 70 C (158 F), and thermoplastic strips cannot be used above their melting point. Current fibre technology is normally limited to reservoir temperatures below 150 C (302 F), provides only short term control in carbonate reservoirs and cannot be used in situations where the fibres may be exposed to HF. A new high performance fibre for proppant flowback control has been developed to overcome these limitations. Laboratory testing has shown that these fibres are resistant to steam, diesel, xylene, Hcl, and mud acid at temperatures up to 250 C (482 F) for periods up to 7 months. In addition, proppant flowback control measurements at high temperatures have confirmed that the fibres retain excellent proppant flowback control properties. Results of field testing in deep, hot (177 C (350 F) carbonate reservoirs have confirmed the performance of the new fibre. P. 523
Thirty years of hemophilia treatment in the Netherlands, 1972-2001 (2004)

Since the introduction of replacement therapy in the early 1960s by the infusion of plasma-derived factor VIII and IX preparations, important changes have occurred for hemophilia patients. We studied the medical and social developments over 30 years of hemophilia treatment. Since 1972, 5 cross-sectional national postal surveys among all hemophilia patients in the Netherlands were performed, the latest in 2001. The prestructured questionnaires included items on treatment, the presence of inhibitory antibodies against factor VIII or IX, the annual number of bleeding episodes, use of inpatient hospital care, and hepatitis C and HIV infections. Response rate in 2001 was 70%. Young patients (<16 years) with severe hemophilia showed the largest increase in use of prophylaxis, from 34% in 1972 to 86% in 2001. The occurrence of hemorrhages has gradually decreased. Hospital admissions decreased from 47% of all patients in 1972 to 18% in 2001. Our study shows that the treatment of patients with severe hemophilia in the Netherlands has focused on the use of prophylactic treatment, especially in children. This has resulted in a decrease in bleeding frequency and an improvement of the medical and social circumstances of patients.
Theophylline inhibits early and late asthmatic reactions induced by allergens in asthmatic subjects. (1991)

To determine whether oral slow-release theophylline inhibits asthmatic reactions and the associated increase of airway responsiveness to methacholine induced by allergens, we examined six asthmatic subjects who developed a dual asthmatic reactions after allergen bronchoprovocation with Dermatophagoides pteronyssinus or with grass pollen. We gave oral slow-release theophylline and placebo to each subject for seven days in two series of experiments in a double-blind, randomized, crossover study. The individual daily dose of theophylline (4.7 to 16.6 mg/kg/day, divided into two doses) was calculated for each subject by measuring individual theophylline clearance and optimal daily dosage. During treatment with placebo, the subjects developed dual asthmatic reactions, ie, FEV1 decreased from 4.1 +/- 0.17 L before bronchoprovocation to 3.2 +/- 0.14 L at 15 minutes and to 3.2 +/- 0.19 L at seven hours after allergen bronchoprovocation. By contrast, during active treatment FEV1 decreased from 4.2 +/- 0.28 L to 3.9 +/- 0.26 L at 15 minutes, and to 3.8 +/- 0.13 L at seven hours (both cases, P less than .03 compared with placebo). Mean serum theophylline concentration was 13.2 +/- 0.6 mg/L. Although 1 week's treatment with slow-release theophylline did not modify significantly either prechallenge airway responsiveness to methacholine or its increase after allergen inhalation challenge, in five out of six subjects theophylline significantly inhibited the increase of airway responsiveness to methacholine induced by allergens compared to placebo and control day (P less than .05). These results suggest that slow-release theophylline may inhibit allergen-induced asthmatic reactions and the associated increase of airway responsiveness, suggesting some antiinflammatory effects for this drug.
Knowledge acquisition planning for inference from large databases (2002)

It is shown that by combining techniques from machine learning and robot planning, knowledge acquisition (KA) planning provides a framework for automatically applying diverse and complex analytical tools to extremely large collections of data. KA planning is the process of automatically combining inferential tools such as induction, search, database lookup, and statistical analysis into methods for addressing complex query statements. This process depends on having both a domain model that supports subgoal decomposition and a library of KA actions annotated with the type and form of required input data, expected outcomes of the action, estimates of computational resources needed, and so on. When analytical tools are annotated in this way, it is possible to automatically select and deploy them and combine their results, even if they run on incompatible platforms. KA planning was implemented in a program that learned about diagnosing lung tumors. A larger project is underway in the domain of molecular biology.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>
ZmES genes encode peptides with structural homology to defensins and are specifically expressed in the female gametophyte of maize (2001)

All four members of a gene family, which are highly expressed in the cells of the female gametophyte (ZmES1--4: Zea mays embryo sac), were isolated from a cDNA library of maize egg cells. High expression of ZmES genes in the synergids around the micropylar region was detected in thin sections of maize ovaries. Single-cell RT--PCR analyses with the various cells of the female gametophyte confirmed the expression in synergids and also showed expression in the egg cell and central cell, and low expression in the antipodals. The expression of the whole gene family is suppressed after fertilization of the embryo sac, and expression in two-cell or later embryo stages or other tissues of maize could not be detected. In order to investigate ZmES mRNA gradients in the highly polarized and vacuolized cells of the maize embryo sac, a whole-mount in situ protocol with isolated single cells was developed: as for total RNA, ZmES transcripts are uniformly distributed in the cytoplasm of egg cell, synergids and central cell. ZmES genes encode small, cysteine-rich proteins with an N-terminal signal peptide, probably for translocation into the embryo sac cell wall. The four ZmES proteins display high sequence identity with each other, and the proposed tertiary structure of the mature peptides is similar to that of plant and animal defensins. The function of ZmES1-4 during the fertilization process is discussed.
CpG RNA: Identification of Novel Single-Stranded RNA That Stimulates Human CD14+CD11c+ Monocytes (2005)

Synthetic immunostimulatory nucleic acids such as CpG DNA are being harnessed therapeutically as vaccine adjuvants, anticancer or antiallergic agents. Efforts to identify nucleic acid-based agents capable of more specifically modulating the immune system are being developed. The current study identifies a novel class of single-stranded oligoribonucleotides (ORN) containing unmethylated CpG motifs and a poly(G) run at the 3' end (CpG ORN) that directly stimulate human CD14+CD11c+ monocytes but not dendritic cells or B cells. CpG ORN activate NF-kappaB and p38 MAPK, resulting in IL-6 and IL-12 production and costimulatory molecule up-regulation but not IFNalpha. Methylation of cytosine at the 5' portion in core CpG motif abrogates such activation. TLR3, 7, 8, or 9 alone did not confer response to CpG ORN, in contrast to previously reported respective nucleic acid ligands. These data suggest that CpG ORN represent a novel class of synthetic immunostimulatory nucleic acids with distinct target cells, receptors, and functions from that of previously known immunomodulatory nucleic acids.
Immunological and Infectious Diseases of the Peripheral Nerves (1998)

Preface The way things were: the discovery of experimental 'allergic' neuritis B. Waksman Part I. Biology and Epidemiology: 1. Immune interactions in the peripheral nervous system C. L. Koski 2. Epidemiology of autoimmune polyneuropathies J. J. Kelly Part II. Patient Evaluation: 3. Clinical evaluation and differential diagnosis J. H. J. Wokke, and N. C. Notermans 4. Electrophysiological studies H. Franssen 5. Immunopathological studies in immune-mediated neuropathies M. Corbo, and A. P. Hays Part III. Clinical Syndromes: 6. Guillain-Barre syndrome and variants F. G. A. Van der Meche 7. Chronic inflammatory demyelinating polyneuropathy M. Vermeulen 8. Acute and chronic sensory neuronopathy G. Sobue 9. Acute and chronic autonomic neuropathies G. A. Suarez, and P. A. Low 10. Vasculitic neuropathies G. Said 11. Neuropathies associated with anti-MAG antibodies and IgM monoclonal gammopathies E. Nobile-Orazio 12. Motor neuropathies associated with anti-GM1 ganglioside antibodies T. Kuntzer, and A. J. Steck 13. Neuropathies associated with anti-sulfatide and other glycoconjugate antibodies L. H. van der Berg 14. Paraneoplastic peripheral neuropathy P. Sillevis Smitt, and Jerome Posner 15. Polyneuropathies associated with myeloma, POEMS, and non-malignant IgG and IgA monoclonal gammopathies J. J. Kelly 16. Neuromyotonia and the Lambert-Eaton myasthenic syndrome J. Newsom-Davis 17. The Post-Polio syndrome M. Dalakas 18. Peripheral neuropathy in HIV-1 infection T. H. Brannagan, T. McAlarney, and N. Latov 19. Lyme neuropathy P. Coyle, and M. Kaufman 20. Neuropathy in leprosy F. G. I. Jennekens, and W. H. van Brakel 21. Neuropathies associated with herpes virus infections Israel Steiner, and Dana Wolf 22. Toxin-induced immune neuropathies N. L. Rosenberg 23. Immune-mediated experimental neuropathies J. D. Pollard Part IV. Therapy and Management: 24. Immunosuppression and immunomodulation A. Brand 25. Management of paralytic neuropathy in the intensive care unit C. F. Bolton 26. Diagnosis and symptomatic therapy of nerve pain Ch. J. Vecht, and P. L. I. Dellemijn 27. Medical rehabilitation G. Van Dijk, N. C. Notermans, and J. Gerritsen.
Reporter genes and highly regulated promoters as tools for transformation experiments in Volvox carteri. (1994)

The multicellular alga Volvox is an attractive model for the study of developmental processes. With the recent report of successful transformation, regulated promoters as well as reporter genes working in this organism are now required. The Volvox genes encoding arylsulfatase and the extracellular glycoprotein ISG are strictly regulated. The former is transcribed only under conditions of sulfur starvation, whereas the latter operates under extreme developmental control--i.e., it is transcribed for only a few minutes in Volvox embryos at the stage of embryonic inversion. The gene encoding the sexual pheromone of Volvox carteri was placed under the control of the arylsulfatase promoter. In response to sulfur deprivation, V. carteri transformed by this construct synthesized and secreted biologically active pheromone. In addition, the gene encoding Volvox arylsulfatase was placed under the control of the ISG promoter. Transformed algae synthesized arylsulfatase mRNA only during embryonic inversion. These experiments demonstrate the usefulness of both the arylsulfatase and the sexual pheromone reporter genes. In addition, the highly regulated arylsulfatase promoter allows the construction of inducible expression vectors for cloned genes.
Stabilization and Enhancement of the Antiapoptotic Activity of Mcl-1 by TCTP (2005)

Mcl-1 is one Bcl-2 family member that plays a pivotal role in animal development. The extremely labile nature of the Mcl-1 protein itself and the fact that the Mcl-1 level is a critical determinant in various cell survival pathways suggest that cellular processes that regulate Mcl-1 stability are as important as those that regulate Mcl-1 synthesis. Although transcriptional stimulation of Mcl-1 synthesis in response to various stimuli has been well documented, regulation of Mcl-1 stability has been hardly explored. In this study, we identified that the translationally controlled tumor protein (TCTP) was one cellular factor that interacted with Mcl-1 and modulated Mcl-1 stability. While overexpression of TCTP augmented the protein stability of Mcl-1, knockdown expression of TCTP by RNA interference destabilized Mcl-1. Furthermore, TCTP stabilized Mcl-1 through interfering with Mcl-1's degradation by the ubiquitin-dependent proteasome degradation pathway, and the TCTP binding-defective mutant of Mcl-1 (K257V) was much more susceptible to degradation and manifested a compromised antiapoptotic activity. Taken together, these results suggest that TCTP modulates Mcl-1's antiapoptotic activity by modulating its protein stability. The possible mechanism(s) involved in TCTP's modulation process is discussed.