gebhart/patrepeval huggingface dataset:
Menjugate (Chiron). (2001)

Chiron has developed and launched Menjugate, a vaccine for the treatment for meningococcus C infections caused by the pathogen Neisseria meningitidis [177064]. In August 1999, Chiron filed with the UK MCA for a license to market Menjugate. The licence was granted in March 2000 [339082], [344773], [357897] and as of April 2000, a vaccination program was underway in the UK [362152]. Menjugate is indicated for children of 12 months and older, but Chiron was expecting approval in the US for infants younger than 12 months by the end of 2000. The company will also pursue mutual recognition in Europe [376204]. In August 2000, Chiron received marketing clearance for Menjugate from the Irish Medicines Board as a conjugate against meningococcal C disease [378353]. The vaccine employs CRM-conjugate technology, whereby a diphtheria toxoid is used as a carrier protein for the meningitis C-specific antigens. The vaccine is being developed for its potential to provide protection against meningitis in both adults and infants. In July 2000, Chiron entered into a comarketing and co-promotion agreement with Aventis Pasteur under which Aventis will assist Chiron in marketing and sales efforts for Menjugate in the UK [374760].
Induction of Silencing in Plants by High-Pressure Spraying of In vitro-Synthesized Small RNAs (2016)

In this report, we describe a method for the delivery of small interfering RNAs (siRNAs) into plant cells. In vitro synthesized siRNAs that were designed to target the coding region of a GREEN FLUORESCENT PROTEIN (GFP) transgene were applied by various methods onto GFP-expressing transgenic Nicotiana benthamiana plants to trigger RNA silencing. In contrast to mere siRNA applications, including spraying, syringe injection, and infiltration of siRNAs that all failed to induce RNA silencing, high pressure spraying of siRNAs resulted in efficient local and systemic silencing of the GFP transgene, with comparable efficiency as was achieved with biolistic siRNA introduction. High-pressure spraying of siRNAs with sizes of 21, 22, and 24 nucleotides (nt) led to local GFP silencing. Small RNA deep sequencing revealed that no shearing of siRNAs was detectable by high-pressure spraying. Systemic silencing was basically detected upon spraying of 22 nt siRNAs. Local and systemic silencing developed faster and more extensively upon targeting the apical meristem than spraying of mature leaves.
Tolerance towards resident intestinal flora in mice is abrogated in experimental colitis and restored by treatment with interleukin‐10 or antibodies to interleukin‐12 (1996)

There is now increasing evidence that hyperresponsiveness towards intestinal flora is a crucial event in the pathogenesis of inflammatory bowel disease (IBD). In support of this hypothesis, we recently described in humans that tolerance exists towards indigenous intestinal flora but is broken in active IBD lesions. In the present study, we have attempted to transfer this model into mice from different genetic backgrounds (BALB/c, SJL/J, C3H/HeJ). We found that mononuclear cells from spleen, small bowel and large bowel of mice do not proliferate, i.e. are tolerant when exposed to bacterial sonicates derived from autologous intestine (BsA) but do proliferate, i.e. are immune when exposed to bacterial sonicates derived from the heterologous intestine of syngenic littermates (BsH). Furthermore, we demonstrate that both local and systemic tolerance to BsA is broken in a murine model of chronic intestinal inflammation induced by the hapten reagent 2, 4, 6-trinitrobenzene sulfonic acid (TNBS), which mimics several important characteristics of Crohn's disease. Tolerance to BsA was restored and TNBS-induced colitis was abrogated in mice systemically treated with interleukin (IL)-10 or antibodies to IL-12. Treatment specifically restored tolerance to BsA, but did not suppress proliferation to BsH. In summary, we here report a new model for the study of immunity and tolerance towards bacterial products. Our data suggest that tolerance to BsA is an important protective mechanism and that restoration of tolerance intestinal flora by IL-10 and antibodies to IL-12 may be of potential therapeutic utility in patients with inflammatory bowel disease.
Analysis and Mitigation of Tropospheric Error Effect on GPS Positioning Using Real GPS Data (2014)

The GPS (Global Positioning System) is used for navigation and positioning purposes by a diverse set of users. The navigation solution provided by a commercial GPS receiver is subject to errors contributed by various sources. These sources of errors in GPS navigation (e.g. satellite clock, receiver clock, atmospheric and multipath errors etc.) induce biases in the measurement of pseudo range and degrade system accuracy. In the current research endeavor the atmospheric and troposphere error sources and its impact on GPS position accuracy is critically analyzed. In this regard a tropospheric error correction model is simulated on real captured GPS data and results are analyzed. 
Optimal therapy of hepatitis C (2002)

The highest response rates to antiviral therapy for the treatment of chronic hepatitis C have been achieved using the combination of peginterferon and ribavirin. Recently completed controlled trials have reported rates of sustained virological response (SVR) between 50% and 60% in patients treated with higher doses of peginterferon and ribavirin, which was 5% to 10% higher with standard doses of interferon alfa and ribavirin. The major determinant of outcome of therapy is hepatitis C virus (HCV) genotype. With the combination of peginterferon and ribavirin, patients with genotype 1 achieve response rates of 40% to 45%, compared with rates approaching 80% with genotypes 2 or 3. Importantly, patients with HCV genotype 1 achieve higher rates of response with 48 weeks than with 24 weeks of therapy, whereas patients with genotypes 2 and 3 are adequately treated with a 24-week course. Furthermore, patients with genotypes 2 and 3 require only 800 mg of ribavirin daily to achieve optimal response rates, whereas 1,000 to 1,200 mg daily is needed for patients with genotype 1. Future studies should focus on optimizing the dose of peginterferon and ribavirin by patient characteristics, particularly on resolving the issue of weight-based dosing. For patients with good prognostic factors, a lower dose and shorter course of peginterferon may be adequate for full effect. Importantly, research is needed to show how treatment regimens can best be applied to other patient groups with hepatitis C, such as patients with acute hepatitis, human immunodeficiency virus coinfection, renal disease, solid-organ transplant, neuropyschiatric disease, autoimmunity, and alcohol or substance abuse.
Megakaryocytic and erythrocytic cell lines share a common precursor cell. (1993)

Several recent studies show that production of platelets and red blood cells (RBC) are inversely related. For example, it is well established that hypoxia, a stimulator of erythropoiesis, causes thrombocytopenia in laboratory animals. The thrombocytopenia is most likely the result of a reduction in the production of platelets caused by a decrease in the number of colony-forming units-megakaryocyte (CFU-Meg), early precursor megakaryocytes (small acetylcholinesterase-positive cells, SAChE+), and recognizable megakaryocytes in the bone marrow. In all cases, active erythropoiesis was required for the thrombocytopenia. The hypoxia-induced thrombocytopenia was not caused by sequestration of platelets in an enlarged spleen or by expanding blood volumes. We speculate that this thrombocytopenia is caused by competition of a precursor cell of the erythrocytic and megakaryocytic cell lines; that is, marked stimulation of the erythroid cells by erythropoietin (Epo) causes a decrease in the number of immature megakaryocytes, leading to decreased thrombocytopoiesis. In support of this hypothesis, other recent work shows that thyroxine (a stimulator of erythropoiesis) and Epo (when given in large, chronic doses) elevate erythropoiesis and cause thrombocytopenia. Conversely, both endogenous and exogenous sources of thrombopoietin lead to elevated thrombocytopoiesis and anemia in mice. It should also be mentioned that megakaryocytes and erythrocytes have several biochemical similarities, and several clinical conditions point to an inverse relationship between RBC and platelet production. These in vivo, biochemical, and clinical data support the hypothesis that megakaryocytes and erythrocytes share a common precursor cell.
Anomalousg-Value of a Cr-Trimer Complex, Cr-Propionate {Cr3O(C2H5COO)6(H2O)3}NO32H2O (1985)

Origin of anomalous g -shift observed in a Cr-trimer complex {Cr 3 O(C 2 H 5 COO) 6 (H 2 O) 3 }NO 3 2H 2 O is discussed. It is found that the Dzyaloshinsky-Moriya interaction in the trimer produces the in-plane g -shift for the triangular trimer plane. The g -shift in magnetic field H 0 is negative with the magnitude of (8/3) D z 2 /{( Δ E ) 2 -( g ⊥ 0 µ B H 0 ) 2 } where D z is the Dzyaloshinsky-Moriya interaction perpendicular to the trimer plane. g ⊥ 0 is in-plane g -value of each Cr 3+ ion, µ B is Bohr magneton and Δ E is the energy gap between the ground and first excited Kramers doublets splitted by the intra-trimer exchange interaction. The observed in-plane g -value 1.89 is well explained by introducing D z of 0.9 K in the trimer.
N.epsilon.-(Carboxymethyl)lysine Is a Dominant Advanced Glycation End Product (AGE) Antigen in Tissue Proteins (1995)

Advanced glycation end products (AGEs) and glycoxidation products are formed during Maillard or browning reactions between sugars and proteins and are implicated in the pathophysiology of aging and the complications of diabetes. To determine the structure of AGEs, antibodies were prepared to protein browned by incubation with glucose and used in ELISA assays to measure AGEs formed in model reactions between bovine serum albumin (BSA) or N alpha-acetyllysine and glucose, fructose, or glyoxal. AGEs were formed from glucose and fructose only under oxidative conditions, but from glyoxal under both oxidative and antioxidative conditions. Gel permeation chromatographic analysis indicated that a similar AGE was formed in reactions of N alpha-acetyllysine with glucose, fructose, and glyoxal and that this AGE co-eluted with authentic N alpha-acetyl-N epsilon-(carboxymethyl)lysine. Amino acid analysis of AGE proteins revealed a significant content of N epsilon-(carboxymethyl)lysine (CML). In ELISA assays using polyclonal antibodies against AGE proteins, CML-BSA (approximately 25 mol of CML/mol of BSA), prepared by chemical modification of BSA, was a potent inhibitor of the recognition of AGE proteins and of AGEs in human lens proteins. We conclude that AGEs are largely glycoxidation products and that CML is a major AGE recognized in tissue proteins by polyclonal antibodies to AGE proteins.
Characterizing errors on qubit operations via iterative randomized benchmarking (2016)

With improved gate calibrations reducing unitary errors, we achieve a benchmarked single-qubit gate fidelity of $0.9995\ifmmode\pm\else\textpm\fi{}0.0002$ with superconducting qubits in a circuit quantum electrodynamics system. We present a method for distinguishing between unitary and nonunitary errors in quantum gates by interleaving repetitions of a target gate within a randomized benchmarking sequence. The benchmarking fidelity decays quadratically with the number of interleaved gates for unitary errors but linearly for nonunitary errors, allowing us to separate systematic coherent errors from decoherent effects. With this protocol, we show that the fidelity of the gates is not limited by unitary errors.
Expression of human and mouse nonhistone chromosomal proteins in hybrid mouse erythroleukemia cells containing a single human chromosome. (1981)

The nonhistone chromosomal proteins of a series of hybrid mouse erythroleukemia cell lines containing human chromosome 16 were investigated by two-dimensional gel electrophoresis to determine if such cells contained nonhistone chromosomal proteins of both human and mouse origin. Comparison of the two-dimensional gel electrophoretograms of the nonhistone chromosomal proteins of mouse and human cell lines showed 400 and 280 chromosomal proteins, respectively, of which about 75% were electrophoretically identical. The two-dimensional gel electrophoretogram of a cloned hybrid mouse erythroleukemia cell line that retained a tetraploid complement of mouse chromosomes and human chromosome 16 (as the only human chromosome) displayed a nonhistone chromosomal protein of pI 6.2 and Mr 65,000. This protein, which comigrates with a nonhistone chromosomal protein present in the human cell line used to produce this hybrid cell and which is also present in two additional human cells lines studied, could not be detected in the mouse erythroleukemia parent before fusion. This polypeptide also was shown by similar techniques to be associated with the presence of human chromosome 16 in four out of five other independently derived hybrid mouse erythroleukemia cell lines that contained a near tetraploid complement of mouse erythroleukemia chromosomes.
Comamonas testosteronan synthase, a bifunctional glycosyltransferase that produces a unique heparosan polysaccharide analog (2011)

Glycosaminoglycans (GAGs) are linear hexosamine-containing polysaccharides. These polysaccharides are synthesized by some pathogenic bacteria to form an extracellular coating or capsule. This strategy forms the basis of molecular camouflage since vertebrates possess naturally occurring GAGs that are essential for life. A recent sequence database search identified a putative protein from the opportunistic pathogen Comamonas testosteroni that exhibits similarity with the Pasteurella multocida GAG synthase PmHS1, which is responsible for the synthesis of a heparosan polysaccharide capsule. Initial supportive evidence included glucuronic acid (GlcUA)-containing polysaccharides extracted from C. testosteroni KF-1. We describe here the cloning and analysis of a novel Comamonas GAG synthase, CtTS. The GAG produced by CtTS in vitro consists of the sugars d-GlcUA and N-acetyl-D-glucosamine, but is insensitive to digestion by GAG digesting enzymes, thus has distinct glycosidic linkages from vertebrate GAGs. The backbone structure of the polysaccharide product [-4-D-GlcUA-α1,4-D-GlcNAc-α1-](n) was confirmed by nuclear magnetic resonance. Therefore, this novel GAG, testosteronan, consists of the same sugars as the biomedically relevant GAGs heparosan (N-acetyl-heparosan) and hyaluronan but may have distinct properties useful for future medical applications.
Detection of high impedance arcing faults using a multi-layer perceptron (1992)

The authors present an arcing fault detector, motivated by the advances in neurocomputing in pattern recognition, that uses a simple preprocessing algorithm. A feedforward three-layer perceptron was trained by high-impedance fault, fault-like load, and normal load current patterns, using the backpropagation training algorithm. The neural network parameters were embodied in a high-impedance arcing fault detection algorithm, which used a simple preprocessing technique to prepare the information input to the network. The algorithm was tested by traces of normal load current disturbed by fault currents on dry and wet soil, an arc welder, computers, and fluorescent lights. The algorithm showed good performance in identifying faults disrupted by arc noise as well as good discrimination between faults and fault-like loads.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>
Altered Urinary Kallikrein Excretion in Rats with Hypertension (1972)

The urinary excretion of kallikrein, an enzyme which cleaves a vasodilator kinin from kininogen substrate, was examined in three types of hypertensive rats. Enzyme activity was measured by both esterase activity (isotopic assay) and bioassay with purified rat urinary kallikrein as a standard. Excretion of kallikrein was found to increase with age in spontaneously hypertensive rats, but levels were lower and stable in normotensive Wistar control animals. Rats with desoxycorticosterone-salt hypertension excreted markedly more, whereas rats with renal hypertension excreted significantly less kallikrein than did control animals. The alterations in kallikrein excretion were unrelated to changes in urine volume and protein excretion. The findings indicate that the kallikrein-kinin system may be involved in different forms of hypertension in the rat.
Inhibition by acetaminophen of intestinal cancer in rats induced by an aromatic amine similar to food mutagens (1997)

The widely used analgesic acetaminophen (APAP) was studied in rats for its ability to inhibit intestinal carcinogenesis induced by 3,2'-dimethyl-4-aminobiphenyl (DMAB), which was selected as the carcinogen because of its similarity to the heterocyclic amines formed during cooking and which are postulated to be involved in colon cancer in humans. APAP was fed to male F344 rats at 250 ppm, which is about 1/4 the human therapeutic dose and at 5000 ppm, which is about fivefold the human dose. DMAB was injected subcutaneously at 50 mg/kg body weight weekly for 20 weeks, to assure identical exposures to all animals, followed by 22 weeks of maintenance. The DMAB was an effective inducer of tumours in the small and large intestines, producing an average of 1.3 tumours per animal. Feeding of APAP began 2 weeks before DMAB administration and continued for 44 weeks. A 9% reduction in the number of colon tumours per rat cancer at the low dose and an 86% reduction at the high dose were found. Small intestinal tumour incidence was reduced at both doses. The number of multiple intestinal tumours per rat was reduced by 27% and 49% for the low and high doses, respectively. The dimensions of these neoplasms, especially those in the colon, were also reduced in both dose groups. Thus, APAP, even at a sub-therapeutic dose, inhibited intestinal carcinogenesis induced by DMAB. This allows us to speculate that the effects of low exposures to dietary carcinogens of the heterocyclic amine type could be inhibited by therapeutic doses of APAP.
Bidirectional regulation of Ca2+ sparks by mitochondria-derived reactive oxygen species in cardiac myocytes (2007)

Mitochondrial ROS exert bidirectional regulation of Ca(2+) sparks in a dose- and time (history)-dependent manner, and basal ROS constitute a hitherto unappreciated determinant for the production of spontaneous Ca(2+) sparks. As such, ROS signalling may play an important role in Ca(2+) homeostasis as well as Ca(2+) dysregulation in oxidative stress-related diseases.
Ca2+ influx, phosphoinositide hydrolysis, and histamine release induced by lysophosphatidylserine in mast cells (1995)

We have previously demonstrated that snake venom phospholipases A2 (PLA2s) and mammalian PLA2s induced inflammatory processes. This effect was correlated with the activity of the enzymes and the release of lipid mediators. We have now determined the role of lysophosphatidylserine (LysoPS) as an inflammatory lipid mediator. Thus, we have studied the possibility that intracellular calcium concentration, phosphoinositide hydrolysis, and the subsequent histamine release in mast cells is due to the action of lysophosphatidylserine. Lysophosphatidylserine-stimulated release of histamine was significantly higher than release by other lysophospholipids. The contribution of increased phospholipase C activity and the intracellular Ca2+ influx were therefore examined. LysoPS increased mast cell calcium concentration, and this increment was associated with phospholipase C activation and release of inositol phosphates. The increase in intracellular calcium and histamine degranulation induced by LysoPS were inhibited by apomorphine. Pretreatment of mast cells with pertussis toxin decreased the secretagogic effect of LysoPS and compound 48/80 without modifying the effect of the ionophore A23187. These results suggest that pertussis toxin-sensitive G-protein might be involved in the mast cell degranulation produced by lysophosphatidylserine and allow the increase in phospholipase C activity, thus enhancing intracellular calcium concentration, which then induces exocytosis of histamine.
AMP‐activated protein kinase phosphorylation of endothelial NO synthase (1999)

The AMP-activated protein kinase (AMPK) in rat skeletal and cardiac muscle is activated by vigorous exercise and ischaemic stress. Under these conditions AMPK phosphorylates and inhibits acetyl-coenzyme A carboxylase causing increased oxidation of fatty acids. Here we show that AMPK co-immunoprecipitates with cardiac endothelial NO synthase (eNOS) and phosphorylates Ser-1177 in the presence of Ca2+-calmodulin (CaM) to activate eNOS both in vitro and during ischaemia in rat hearts. In the absence of Ca2+-calmodulin, AMPK also phosphorylates eNOS at Thr-495 in the CaM-binding sequence, resulting in inhibition of eNOS activity but Thr-495 phosphorylation is unchanged during ischaemia. Phosphorylation of eNOS by the AMPK in endothelial cells and myocytes provides a further regulatory link between metabolic stress and cardiovascular function.
Antitumor Effects of Chimeric Receptor Engineered Human T Cells Directed to Tumor Stroma (2013)

Cancer-associated fibroblasts (CAFs), the principle component of the tumor-associated stroma, form a highly protumorigenic and immunosuppressive microenvironment that mediates therapeutic resistance. Co-targeting CAFs in addition to cancer cells may therefore augment the antitumor response. Fibroblast activation protein-α (FAP), a type 2 dipeptidyl peptidase, is expressed on CAFs in a majority of solid tumors making it an attractive immunotherapeutic target. To target FAP-positive CAFs in the tumor-associated stroma, we genetically modified T cells to express a FAP-specific chimeric antigen receptor (CAR). The resulting FAP-specific T cells recognized and killed FAP-positive target cells as determined by proinflammatory cytokine release and target cell lysis. In an established A549 lung cancer model, adoptive transfer of FAP-specific T cells significantly reduced FAP-positive stromal cells, with a concomitant decrease in tumor growth. Combining these FAP-specific T cells with T cells that targeted the EphA2 antigen on the A549 cancer cells themselves significantly enhanced overall antitumor activity and conferred a survival advantage compared to either alone. Our study underscores the value of co-targeting both CAFs and cancer cells to increase the benefits of T-cell immunotherapy for solid tumors.
Dual-Band Ultra-Wideband Bandpass Filter (2006)

This paper presented a dual-band ultra-wideband (UWB) bandpass filter. The filter is based on a novel UWB bandpass filter structure, proposed by authors recently, which consists of a broadside-coupled microstrip-coplanar waveguide and exhibited its excellent ultra-wideband property. The dual-band operation was implemented by integrating a stub in the broadside-coupled conductors. The resonance of the stub introduces a narrow rejection band in the UWB passband which then results in a dual-band filtering. Such a dual-band UWB bandpass filter is strongly required in practical systems in order to avoid the interference between the UWB radio system and existing radio systems. The rejection band can be easily designed to some specific frequency band(s) by tuning the length of the stub. Simulation, design, fabrication and measurement of dual-band UWB bandpass filters have been carried out mainly following FCC's spectrum mask. The proposed filters demonstrated both excellent ultra-wide bandwidth (from 2.8 GHz to 10.2 GHz) mid rejection performance (> 50 dB at rejection frequencies), as well as good out-band performance better than the requirement of FCC's mask