gebhart/patrepeval huggingface dataset:
Power conversion architecture for grid interface at high switching frequency (2014)

This paper presents a new power conversion architecture for single-phase grid interface. The proposed architecture is suitable for realizing miniaturized ac-dc converters operating at high frequencies (HF, above 3 MHz) and high power factor, without the need for electrolytic capacitors. It comprises of a line-frequency rectifier, a stack of capacitors, a set of regulating converters, and a power combining converter (or set of power combining converters). The regulating converters have inputs connected to capacitors on the capacitor stack, and provide regulated outputs while also achieving high power factor, with twice-line-frequency energy buffered on the capacitor stack. The power combining converter combines power from the individual regulated outputs to a single output, and may also provide isolation. While this architecture can be utilized with a variety of circuit topologies, it is especially suited for systems operating at HF (above 3 MHz), and we introduce circuit implementations that enable efficient operation in this range. The proposed approach is demonstrated for an LED driver operating from 120 V <sub xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">ac</sub> , and supplying a 35 V, 30 W output. The prototype converter operates at a (variable) switching frequency of 5-10 MHz and an efficiency of > 93%. The converter achieves a displacement power density of 130 W/in <sup xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">3</sup> , while providing a 0.89 power factor, without the use of electrolytic capacitors.
The Use of Congenitally Immunodeficient Mice to Study Human Tumor Metastases and Immunotherapy (1992)

Congenitally immunodeficient strains of mice have proven valuable in the development of relevant models to study human tumor biology, metastases, and immunotherapy. Local invasion and extensive multiorgan metastases in athymic mice have been obtained following orthotopic implantation or onplantation of histologically intact fragments of human tumors. In C.B-17 severe combined immunodeficient (SCID) mice or in triple immunodeficient, beige/nude/xid (BNX) mice, the development and spread of inoculated human leukemia/lymphoma and/or melanoma have mimicked, in some cases, those observed in patients. Reports of reconstitution of SCID and BNX mice with human myeloid or lymphoid cells have suggested that these models might be useful for the study of human immune responses to autologous tumors in vivo. The severe immunocompromised status of these mice have also led to evaluations of the therapeutic efficacy of adoptively transferred, tumor-reactive human T cells. In this report, we review the pertinent information currently available on the use of congenitally immunodeficient mice in studies of human cancer biology and treatment.
MMR gene expression pattern in sporadic colorectal cancer. (2010)

ANKRD17 mRNA appears to be the most sensitive target and may have a potential value as an additional marker for the existing multitarget assay panel for colorectal cancer detection.
The Effect of Tetrandrine and Extracts of Centella asiatica on Acute Radiation Dermatitis in Rats. (1999)

Radiation injury to the skin is one of the major limiting factors in radiotherapy. We designed this study using Sprague-Dawley rats to evaluate the reduction in skin injury achieved using natural products from plant extracts as protection. The acute skin reaction in tetrandrine- and Madecassol-treated animals appeared earlier, but was significantly less severe, than in the control group. The peak skin reactions in the tetrandrine group were less serious than those of the control group at three different radiation doses. At a high dose irradiation, the healing effect of tetrandrine is better than Madecassol and vaseline. The histologic findings indicate that tetrandrine and Madecassol are able to reduce acute radiation reactions by their anti-inflammatory activity.
Direct interaction of hematopoietic transcription factors PU.1 and GATA-1: functional antagonism in erythroid cells (1999)

Malignant transformation usually inhibits terminal cell differentiation but the precise mechanisms involved are not understood. PU.1 is a hematopoietic-specific Ets family transcription factor that is required for development of some lymphoid and myeloid lineages. PU.1 can also act as an oncoprotein as activation of its expression in erythroid precursors by proviral insertion or transgenesis causes erythroleukemias in mice. Restoration of terminal differentiation in the mouse erythroleukemia (MEL) cells requires a decline in the level of PU.1, indicating that PU.1 can block erythroid differentiation. Here we investigate the mechanism by which PU.1 interferes with erythroid differentiation. We find that PU.1 interacts directly with GATA-1, a zinc finger transcription factor required for erythroid differentiation. Interaction between PU.1 and GATA-1 requires intact DNA-binding domains in both proteins. PU.1 represses GATA-1-mediated transcriptional activation. Both the DNA binding and transactivation domains of PU.1 are required for repression and both domains are also needed to block terminal differentiation in MEL cells. We also show that ectopic expression of PU.1 in Xenopus embryos is sufficient to block erythropoiesis during normal development. Furthermore, introduction of exogenous GATA-1 in both MEL cells and Xenopus embryos and explants relieves the block to erythroid differentiation imposed by PU.1. Our results indicate that the stoichiometry of directly interacting but opposing transcription factors may be a crucial determinant governing processes of normal differentiation and malignant transformation.
Gap detection deficits in rats with tinnitus: A potential novel screening tool. (2006)

The study describes a novel method for tinnitus screening in rats by use of gap detection reflex procedures. The authors hypothesized that if a background acoustic signal was qualitatively similar to the rat's tinnitus, poorer detection of a silent gap in the background would be expected. Rats with prior evidence of tinnitus at 10 kHz (n = 14) exhibited significantly worse gap detection than controls (n = 13) when the gap was embedded in a background similar to their tinnitus. No differences between tinnitus and control rats were found with 16 kHz or broadband noise backgrounds, which helped to rule out explanations related to hearing loss or general performance deficits. The results suggest that gap detection reflex procedures might be effective for rapid tinnitus screening in rats.
Leptin Acts on Human Marrow Stromal Cells to Enhance Differentiation to Osteoblasts and to Inhibit Differentiation to Adipocytes (1999)

Both bone mass and serum leptin levels are increased in obesity. Because osteoblasts and adipocytes arise from a common precursor in bone marrow, we assessed the effects of human recombinant leptin on a conditionally immortalized human marrow stromal cell line, hMS2–12, with the potential to differentiate to either the osteoblast or adipocyte phenotypes. By RT-PCR and Western immunoblot analysis, the hMS2–12 cells expressed messenger RNA (mRNA) and protein for the leptin receptor. Leptin did not affect hMS2–12 cell proliferation, but resulted in dose- and time-dependent increases in mRNA and protein levels of alkaline phosphatase, type I collagen, and osteocalcin, and in a 59% increase in mineralized matrix. Leptin increased mRNA levels of lipoprotein lipase at 3 days, but decreased mRNA levels of adipsin and leptin at 9 days and decreased lipid droplet formation by 50%. Leptin did not affect the expression of Cbfa1 or peroxisome proliferator-activated receptor-γ2, transcription factors involved in commitment to the osteoblast and adipocyte pathways, respectively. Thus, leptin acts on human marrow stromal cells to enhance osteoblast differentiation and to inhibit adipocyte differentiation. Our data support the hypothesis that leptin is a previously unrecognized, physiological regulator of these two differentiation pathways, acting primarily on maturation of stromal cells into both lineages.
Inhibition of enterotoxigenic Escherichia coli K88, K99 and 987P by the Lactobacillus isolates from porcine intestine (2000)

Thirty-six Lactobacillus strains were isolated from the small intestine of piglets and 14 of them were chosen as they had a good ability (>5 bacteria per cell) to attach to the epithelial cells of the small intestine. They were selected to investigate the antagonistic effects against enterotoxigenic Escherichia coli (ETEC) including K88ab, K88ac, K88+MB (a local strain of haemolytic (H) ETEC K88+ bacterium from Manitoba, Canada), K99 and 987P. Their effects on the adhesion of E coli K88+MB and K88ac to the intestinal mucus of piglets were also studied. The results indicated that six out of the 14 Lactobacillus isolates were able to moderately or strongly inhibit the growth of eight strains of ETEC through the production of organic acids, but not by bacteriocin or hydrogen peroxide. Well diffusion assays of the major organic acids of the Lactobacillus culture supernatants showed that both acetic acid and lactic acid inhibited the growth of E coli. Lactobacillus isolates did not affect the attachment of E coli K88+MB and K88ac to the small intestinal mucus of piglet. © 2000 Society of Chemical Industry
2′F-Arabinonucleic acids (2′F-ANA) — History, properties, and new frontiers (2008)

The development of arabinonucleosides and oligoarabinonucleotides is described, focusing especially on 2′-deoxy-2′-fluoroarabinonucleosides (araF-N) and -oligonucleotides (2'F-ANA). In addition to their chemical and enzymatic synthesis, we discuss various properties of 2′F-ANA: hydrolytic stability (to nucleases, acids, and bases), binding affinity to complementary strands, structure and conformation, and optimization of RNase H activity. We also discuss the use of 2′F-ANA in gene-silencing approaches (antisense, siRNA), and in the stabilization of higher-order structures (such as triplexes and quadruplexes) including aptamers. Finally, we examine several other oligonucleotide derivatives based on 2′F-ANA and look ahead to the future of 2′-fluoroarabinonucleosides and -oligonucleotides.Key words: arabinonucleic acids, 2′F-ANA, antisense oligonucleotides, siRNA, modified oligonucleotides.
Selective immunotargeting of diabetogenic CD4 T cells by genetically redirected T cells (2014)

The key role played by islet-reactive CD8 and CD4 T cells in type 1 diabetes calls for new immunotherapies that target pathogenic T cells in a selective manner. We previously demonstrated that genetically linking the signalling portion of CD3-ζ onto the C-terminus of β2 -microglobulin and an autoantigenic peptide to its N-terminus converts MHC-I complexes into functional T-cell receptor-specific receptors. CD8 T cells expressing such receptors specifically killed diabetogenic CD8 T cells, blocked T-cell-induced diabetes in immunodeficient NOD.SCID mice and suppressed disease in wild-type NOD mice. Here we describe the immunotargeting of CD4 T cells by chimeric MHC-II receptors. To this end we chose the diabetogenic NOD CD4 T-cell clone BDC2.5, which recognizes the I-A(g7) -bound 1040-31 mimotope. We assembled several constructs encoding I-A(g7) α- and β-chains, the latter carrying mim or hen egg lysozyme peptide as control, each supplemented with CD3-ζ intracellular portion, either with or without its transmembrane domain. Following mRNA co-transfection of reporter B3Z T cells and mouse CD8 and CD4 T cells, these constructs triggered robust activation upon I-A(g7) cross-linking. A BDC2.5 T-cell hybridoma activated B3Z transfectants expressing the mimotope, but not the control peptide, in both configurations. Potent two-way activation was also evident with transgenic BDC2.5 CD4 T cells, but peptide-specific activation required the CD3-ζ transmembrane domain. Chimeric MHC-II/CD3-ζ complexes therefore allow the selective immunotargeting of islet-reactive CD4 T cells, which take part in the pathogenesis of type 1 diabetes.
Histone deacetylases and cancer (2012)

Reversible acetylation of histone and non-histone proteins is one of the most abundant post-translational modifications in eukaryotic cells. Protein acetylation and deacetylation are achieved by the antagonistic actions of two families of enzymes, histone acetyltransferases (HATs) and histone deacetylases (HDACs). Aberrant protein acetylation, particularly on histones, has been related to cancer while abnormal expression of HDACs has been found in a broad range of cancer types. Therefore, HDACs have emerged as promising targets in cancer therapeutics, and the development of HDAC inhibitors (HDIs), a rapidly evolving area of clinical research. However, the contributions of specific HDACs to a given cancer type remain incompletely understood. The aim of this review is to summarize the current knowledge concerning the role of HDACs in cancer with special emphasis on what we have learned from the analysis of patient samples.
Type and Crossmatch of the Trauma Patient (2001)

Trauma patients with no risk factors at presentation were less likely to require emergent blood transfusion, especially in the setting of the ED.
Epigenetic Modifiers in Myeloid Malignancies: The Role of Histone Deacetylase Inhibitors (2018)

Myeloid hematological malignancies are clonal bone marrow neoplasms, comprising of acute myeloid leukemia (AML), the myelodysplastic syndromes (MDS), chronic myelomonocytic leukemia (CMML), the myeloproliferative neoplasms (MPN) and systemic mastocytosis (SM). The field of epigenetic regulation of normal and malignant hematopoiesis is rapidly growing. In recent years, heterozygous somatic mutations in genes encoding epigenetic regulators have been found in all subtypes of myeloid malignancies, supporting the rationale for treatment with epigenetic modifiers. Histone deacetylase inhibitors (HDACi) are epigenetic modifiers that, in vitro, have been shown to induce growth arrest, apoptotic or autophagic cell death, and terminal differentiation of myeloid tumor cells. These effects were observed both at the bulk tumor level and in the most immature CD34⁺38<sup>-</sup> cell compartments containing the leukemic stem cells. Thus, there is a strong rationale supporting HDACi therapy in myeloid malignancies. However, despite initial promising results in phase I trials, HDACi in monotherapy as well as in combination with other drugs, have failed to improve responses or survival. This review provides an overview of the rationale for HDACi in myeloid malignancies, clinical results and speculations on why clinical trials have thus far not met the expectations, and how this may be improved in the future.
On bit error rate performance of polar codes in finite regime (2010)

Polar codes have been recently proposed as the first low complexity class of codes that can provably achieve the capacity of symmetric binary-input memoryless channels. Here, we study the bit error rate performance of finite-length polar codes under Belief Propagation (BP) decoding. We analyze the stopping sets of polar codes and the size of the minimal stopping set, called “stopping distance”. Stopping sets, as they contribute to the decoding failure, play an important role in bit error rate and error floor performance of the code. We show that the stopping distance for binary polar codes, if carefully designed, grows as O(√N) where N is the code-length. We provide bit error rate (BER) simulations for polar codes over binary erasure and gaussian channels, showing no sign of error floor down to the BERs of 10 <sup xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">-11</sup> . Our simulations asserts that while finite-length polar codes do not perform as good as LDPC codes in terms of bit error rate, they show superior error floor performance. Motivated by good error floor performance, we introduce a modified version of BP decoding employing a guessing algorithm to improve the BER performance of polar codes. Our simulations for this guessing algorithm show two orders of magnitude improvement over simple BP decoding for the binary erasure channel (BEC), and up to 0.3 dB improvement for the gaussian channel at BERs of 10 <sup xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">-6</sup> .
Refractory Epilepsy: Clinical Overview (2007)

The incidence of refractory epilepsy remains high despite the influx of many new antiepileptic drugs (AEDs) over the past 10 years. Epidemiological data indicate that 20-40% of the patients with newly diagnosed epilepsy will become refractory to treatment. Factors that may be used to predict whether or not a patient will respond favorably to AED therapy include the type of epilepsy, underlying syndrome, etiology, and the patient's history of seizure frequency, density, and clustering. Environmental factors, such as trauma and prior drug exposure, and genetic factors that predetermine the rate of absorption, metabolism, and uptake of a drug by target tissue may also uniquely impact an individual and influence their response to AED therapy. Treatment resistance is, therefore, a multifaceted phenomenon. Since individuals with refractory epilepsy do not share a common reason for their treatment resistance, the use of targeted drug therapies may be our best option for improving treatment outcomes in this patient population. Pharmacogeneticists are currently attempting to understand the genetic basis of refractory epilepsy so that they can identify subgroups of patients who share a common genetic background and then target drug therapies to meet their specific needs.
Recombinant Human TSH–Assisted Radioactive Iodine Remnant Ablation Achieves Short-Term Clinical Recurrence Rates Similar to Those of Traditional Thyroid Hormone Withdrawal (2008)

rhTSH-assisted RRA is associated with rates of clinically evident disease recurrence and persistent uptake in the thyroid bed that are similar to those for traditional THW.
GAD Treatment and Insulin Secretion in Recent-Onset Type 1 Diabetes (2008)

GAD-alum may contribute to the preservation of residual insulin secretion in patients with recent-onset type 1 diabetes, although it did not change the insulin requirement. (ClinicalTrials.gov number, NCT00435981.)
Human Pancreatic Islet Isolation: Part I: Digestion and Collection of Pancreatic Tissue (2009)

Management of Type 1 diabetes is burdensome, both to the individual and society, costing over 100 billion dollars annually. Despite the widespread use of glucose monitoring and new insulin formulations, many individuals still develop devastating secondary complications. Pancreatic islet transplantation can restore near normal glucose control in diabetic patients, without the risk of serious hypoglycemic episodes that are associated with intensive insulin therapy. Providing sufficient islet mass is important for successful islet transplantation. However, donor characteristic, organ procurement and preservation affect the isolation outcome. At University of Illinois at Chicago (UIC) we have developed a successful isolation protocol with an improved purification gradient. The program started in January 2004, and more than 300 isolations were performed up to November 2008. The pancreata were sent in cold preservation solutions (UW, University of Wisconsin or HTK, Histidine-Tryptophan Ketoglutarate) to the Cell Isolation Laboratory at UIC for islet isolation. Pancreatic islets were isolated using the UIC method, which is a modified version of the method originally described by Ricordi et al. Briefly, after cleaning the pancreas from the surrounding tissue, it was perfused with enzyme solution (Serva Collagenase + Neutral Protease or Sigma V enzyme). The distended pancreas was then transferred to the Ricordi digestion chamber, connected to a modified, closed circulation tubing system, and warmed up to 37 degrees C. During the digestion, the chamber was shaken gently. Samples were taken continuously to monitor the digestion progress. Once free islets were detected under the microscope, the digestion was stopped by flushing cold (4 degrees C) RPMI dilution solution (Mediatech, Herndon, VA) into the circulation system to dilute the enzyme. After being collected and washed in M199 media supplemented with human albumin, the tissue was sampled for pre-purification count and incubated with UW solution before purification. Purification process will be described in Part II: Purification and Culture of Human Islets.
Dehydroquinate synthase in Bacillus subtilis. An enzyme associated with chorismate synthase and flavin reductase. (1978)

Dehydroquinate synthase, the enzyme which catalyzes the conversion of 3-deoxy-D-arabino-heptulosonic acid 7-phosphate (DAHP) to 5-dehydroquinate, has been purified from Bacillus subtilis in association with chorismate synthase and NADPH-dependent flavin reductase. The enzyme was only active when associated with chorismate synthase, whereas the flavin reductase could be separated from the complex with retention of dehydroquinate synthase activity. The enzyme requires NAD and either Co2+ or Mn2+ for maximal activity. The activity was completely inhibited by EDTA. The Km of the enzyme for DAHP, NAD, and Co2+ were estimated to be 1.3 X 10(-4), 5.5 X 10(-5), and 5.5 X 10(-5) M, respectively. Enzyme activity was completely inhibited by NADH and the inhibition was not reversed by the addition of NAD, NADPH and NADP were not inhibitory. The enzyme was unstable to heat and lost all activity at 55 degrees C. A protein fraction which did not adsorb to phosphocellulose was found to inhibit the enzyme.
HIV Vaccine Trial Justified (2004)

In this Policy Forum, the [authors][1] respond to [ Burton et al .][2] by asserting that the ongoing efficacy trial of ALVAC-HIV (vCP1521) and AIDSVAX B/E in Thailand is scientifically justified, morally correct, and strategically important. No laboratory assay or animal model has been validated as a predictor of the efficacy of HIV vaccines in humans, thus efficacy trials are essential to test bona fide vaccine hypotheses. Although there is a real chance that the prime-boost combination may not be efficacious, there is a very high probability that information gained will significantly advance HIV vaccine development. Established scientific principles and appropriate processes fully support the decision to proceed with this efficacy trial.

 [1]: http://www.sciencemag.org/cgi/content/full/303/5660/961
 [2]: http://www.sciencemag.org/cgi/content/short/303/5656/316
Structure of confined water (2001)

Water is essential for the stability and function of biological macromolecules. In living systems, essential water-related phenomena occur in restricted geometry in cells, and at active sites of proteins and membranes or at their surface. In this paper, we present the more recent results on the structure of confined water as compared with that of bulk supercooled water. In particular, the combined effects of the hydration level and the temperature on the change of the structure of water are discussed in the light of powerful techniques.
Protein synthesis in eukaryotic organisms: New insights into the function of translation initiation factor EIF‐3 (1995)

The pathway for initiation of protein synthesis in eukaryotic cells has been defined and refined over the last 25 years using purified components and in vitro reconstituted systems. More recently, powerful genetic analysis in yeast has proved useful in unraveling aspects of translation inherently more difficult to address by strictly biochemical approaches. One area in particular is the functional analysis of multi-subunit protein factors, termed eukaryotic initiation factors (eIFs), that play an essential role in translation initiation. eIF-3, the most structurally complex of the eIFs, has until recently eluded this approach. The identification of the yeast GCD10 gene as the structural gene for the zeta subunit of yeast eIF-3(1) and the analysis of mutant phenotypes has opened the door to the genetic dissection of the eIF-3 protein complex.