gebhart/patrepeval huggingface dataset:
A solid state modulator using energy recovery to delivery 20 kVA to an inductive load from a 2.5 kJ/s power source (2002)

A modulator using an energy recovery scheme has been developed which is capable of delivering 20 kW to an inductive load from a 2.5 kJ/s power supply. The modulator delivers peak current pulses of 390 A to 27 mu H load at a repetition rate of 10 kHz with a current regulation of 0.1%. The modulator uses arrays of MOSFETs as the switching elements and a Maxwell capacitor charging power supply, model CCDS-2.502. The modulator can be conveniently reconfigured to vary the load current and energy/pulse delivered to the load. For applications requiring peak output currents greater than approximately=400 A, the modulator efficiency will decrease. As a result, the maximum power which can be delivered to the load will be limited by the capacitor charging power supply. The efficiency of the modulator can be tailored to the specific application requirements by properly choosing the number of MOSFETs which comprise the FET arrays and paying close attention to the high-frequency characteristics of the energy storage capacitor.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>
Cancer Immunoediting: Integrating Immunity’s Roles in Cancer Suppression and Promotion (2011)

Understanding how the immune system affects cancer development and progression has been one of the most challenging questions in immunology. Research over the past two decades has helped explain why the answer to this question has evaded us for so long. We now appreciate that the immune system plays a dual role in cancer: It can not only suppress tumor growth by destroying cancer cells or inhibiting their outgrowth but also promote tumor progression either by selecting for tumor cells that are more fit to survive in an immunocompetent host or by establishing conditions within the tumor microenvironment that facilitate tumor outgrowth. Here, we discuss a unifying conceptual framework called "cancer immunoediting," which integrates the immune system's dual host-protective and tumor-promoting roles.
Optimization of Antitumor Modulators of Pre-mRNA Splicing (2013)

The spliceosome regulates pre-mRNA splicing, which is a critical process in normal mammalian cells. Recently, recurrent mutations in numerous spliceosomal proteins have been associated with a number of cancers. Previously, natural product antitumor agents have been shown to interact with one of the proteins that is subject to recurrent mutations (SF3B1). We report the optimization of a class of tumor-selective spliceosome modulators that demonstrate significant in vivo antitumor activity. This optimization culminated in the discovery of sudemycin D6, which shows potent cytotoxic activity in the melanoma line SK-MEL-2 (IC50 = 39 nM) and other tumor cell lines, including JeKo-1 (IC50 = 22 nM), HeLa (IC50 = 50 nM), and SK-N-AS (IC50 = 81 nM). We also report improved processes for the synthesis of these compounds. Our work supports the idea that sudemycin D6 is worthy of further investigation as a novel preclinical anticancer agent with application in the treatment of numerous human cancers.
Two distinctly regulated events, priming and triggering, during retinoid-induced maturation and resistance of NB4 promyelocytic leukemia cell line. (1994)

In t(15;17) acute promyelocytic leukemia, all-trans retinoic acid (RA) induces leukemic cell maturation in vitro and remission in acute promyelocytic leukemia patients, but in vivo treatments invariably lead to relapse with resistance to RA. NB4, a maturation-inducible cell line, and NB4-RAr sublines (R1 and R2) displaying no maturation in the presence of RA have been isolated from a patient in relapse. We show that resistance to maturation is not a mere unresponsiveness to RA: rather, R1 "resistant" cells do respond to RA (1 microM) by sustained growth, become competent to undergo terminal maturation, and up-regulate CD11c/CD18 integrins. Interestingly, maturation of "resistant" cells, rendered competent by RA, can be achieved by cAMP-elevating agents (prostaglandin E, isoproterenol, cholera toxin, or phosphodiesterase inhibitor) or stable agonistic cAMP analogs such as (SP)-8-chloroadenosine cyclic 3',5'-phosphorothioate. This shows that activation of cAMP-dependent protein kinase (cA kinase) can override the RA resistance and suggests interdependent RA and cAMP signaling pathways in acute promyelocytic leukemia maturation. No such cooperation was observed in the R2 resistant cells, though their cA-kinase was functional. (RP)-8-Chloroadenosine cyclic 3',5'-phosphorothioate, which by displacing endogenous cAMP inhibits the basal cA-kinase activity, decreased the response of sensitive cells to RA. This raises the possibility that cA-kinase plays a key role in the maturation also of RA-sensitive cells. Our results define two discrete steps in the maturation process: an RA-dependent priming step that maintains proliferation while cells become competent to undergo maturation in response to retinoids and a cAMP-dependent step that triggers RA-primed cells to undergo terminal maturation. Uncoupling RA and cAMP action might cause the so-called "resistance."
Object-oriented design of an expandable hardware description language analyzer for a high-level synthesis system (1992)

The paper presents a new approach to high-level synthesis system design in which object-oriented programming techniques are used to construct an expansible hardware description language (HDL) analyzer. There are several major advantages of this new methodology over the traditional top-down approaches. The object-oriented data model for high-level synthesis systems is shown to be a better way to model the high-level synthesis design entities. A formal object oriented programming(OOP) model of high-level synthesis and systematic ways of expanding the system are also described. This design style influences the construction of the entire high-level synthesis system. The system has been successfully implemented in C++ and has proven to be reliable, expansible, and sufficiently fast.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>
Streptococcus pneumoniae-induced p38 MAPK-dependent Phosphorylation of RelA at the Interleukin-8 Promotor (2004)

Streptococcus pneumoniae is the major cause of community-acquired pneumonia and one of the most common causes of death by infectious disease in industrialized countries. Little is known concerning the mechanisms of target cell activation in this disease. The present study shows that NF-kappaB and p38 MAPK signaling pathways contribute to chemokine synthesis by lung epithelial cells in response to pneumococci. In infected lungs of mice pneumococci stimulate expression of the interleukin (IL)-8 homolog keratinocyte-derived chemokine and granulocyte-macrophage colony-stimulating factor, as well as activate p38 MAPK. Human bronchial epithelium was chosen as a cellular model, because it establishes the first barrier against pathogens, and little is known about its function in innate immunity. Pneumococci infection induces expression of IL-8 and granulocyte-macrophage colony-stimulating factor as well as activation of p38 MAPK in human bronchial epithelial cells (BEAS-2B). Inhibition of p38 MAPK activity by SB202190 and SB203580 blocks pneumococci-induced cytokine release. In mouse lungs in vivo as well as in cultured cells, pneumococci activate NF-kappaBinanIkappaB kinase-dependent manner. Inhibition of p38 MAPK by chemical inhibitors or by RNA interference targeting p38alpha reduces pneumococci-induced NF-kappaB-dependent gene transcription. Blockade of p38 activity did not affect inducible nuclear translocation and recruitment of NF-kappaB/RelA to the IL-8 promotor but did reduce the level of phosphorylated RelA (serine 536) at IL-8 promotor and inhibited pneumococci-mediated recruitment of RNA polymerase II to IL-8 promotor. Thus, p38 MAPK contributes to pneumococci-induced chemokine transcription by modulating p65 NF-kappaB-mediated transactivation.
Modification of the binding site(s) of lectins by an affinity column carrying an activated galactose-terminated ligand (1987)

An affinity column approach is described, aimed at the modification of the galactose binding site(s) of ricin in an effort to block the binding of ricin to cells. The affinity column was prepared by linking N-(2'-mercaptoethyl)lactamine to pyridyldithio-activated polyacrylamide heads. The linker between the ligand and the solid support thus contained a disulfide bond and an unmodified terminal galactose moiety. The amino group of the ligand was allowed to react with the bifunctional cross-linking reagent 2,4-dichloro-6-methoxytriazine. The lectin was then allowed to bind to the galactose functions on the activated column at pH 7.0, prior to raising the pH to 8.6 to initiate the cross-linking reaction between the ligand and the lectin. Lectin that was not covalently linked to the functionalized galactose residues on the column was eluted with galactose or lactose. Finally, the covalent ligand-lectin complexes were released from the solid support by reducing the disulfide bond between the ligand and the support. The affinity column was used in this way to modify the galactose binding site(s) of ricin. Upon release from the affinity column, blocked ricin was purified from unmodified ricin by affinity chromatography on columns of immobilized asialofetuin (a ligand to which ricin binds very tightly). The sulfhydryl group formed by cleavage of the ligand-ricin complex from the column was labeled with [3H]-N-ethylmaleimide to provide evidence that one blocking ligand was linked per ricin molecule. The blocked ricin and a conjugate of the blocked ricin with the monoclonal antibody J5 were toxic for cultures of Namalwa cells in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)
β-Adrenergic Receptor Kinase: Primary Structure Delineates a Multigene Family (1989)

The beta-adrenergic receptor kinase (beta-ARK), which specifically phosphorylates only the agonist-occupied form of the beta-adrenergic and closely related receptors, appears to be important in mediating rapid agonist-specific (homologous) desensitization. The structure of this enzyme was elucidated by isolating clones from a bovine brain complementary DNA library through the use of oligonucleotide probes derived from partial amino acid sequence. The beta-ARK cDNA codes for a protein of 689 amino acids (79.7 kilodaltons) with a protein kinase catalytic domain that bears greatest sequence similarity to protein kinase C and the cyclic adenosine monophosphate (cyclic AMP)--dependent protein kinase. When this clone was inserted into a mammalian expression vector and transfected into COS-7 cells, a protein that specifically phosphorylated the agonist-occupied form of the beta 2-adrenergic receptor and phosphorylated, much more weakly, the light-bleached form of rhodopsin was expressed. RNA blot analysis revealed a messenger RNA of four kilobases with highest amounts in brain and spleen. Genomic DNA blot analysis also suggests that beta-ARK may be the first sequenced member of a multigene family of receptor kinases.
Genetic Heterogeneity in HER2 Testing in Breast Cancer: Panel Summary and Guidelines (2009)

Standardized methods for analysis will improve the accuracy and consistency of interpretation of HER2 gene amplification status in breast cancer.
Effects of sodium ascorbate (vitamin C) and 2-methyl-1,4-naphthoquinone (vitamin K3) treatment on human tumor cell growth in vitro. II. Synergism with combined chemotherapy action. (1993)

The growth inhibitory effects of a combined application of sodium ascorbate (Vitamin C) and 2-methyl-1,4-naphthoquinone (Vitamin K3) together with various chemotherapeutic agents has been examined on in vitro cultured human endometrial adenocarcinoma (AN3CA) cells. Combined vitamin treatment and chemotherapy in well defined conditions of cell confluence and at the dose levels applied result in a synergistic effect on growth inhibition. The combined vitamins when reaching their own synergistic cytotoxicity levels frequently obscure the additional synergistic effects attributable to the chemotherapeutic agents. Apart from the specific cytotoxic characteristics of the chemotherapeutic drugs examined, the formation of reactive oxygen radicals during treatment, possibly accentuated by less defined secondary mechanisms, appears essentially responsible for the observed stimulated cytotoxicity.
Current use of injectable agents for female stress urinary incontinence. (2005)

Injectable materials of various types have been used for decades as an alternative to surgery for the treatment of stress urinary incontinence. Their success stems from their ability to improve intrinsic sphincter function, and patients with hypermobility may benefit as well. Nevertheless, the ideal agent has yet to be discovered, and surgery still may be necessary after treatment in some patients. Results vary among the different materials used, and safety, durability, and cost-effectiveness are important areas of concern in which more research is needed.
Triple analysis of the cancer epigenome: an integrated microarray system for assessing gene expression, DNA methylation, and histone acetylation. (2003)

We developed a novel microarray system to assess gene expression, DNA methylation, and histone acetylation in parallel, and to dissect the complex hierarchy of epigenetic changes in cancer. An integrated microarray panel consisting of 1507 short CpG island tags located at the 5'-end regions (including the first exons) was used to assess effects of epigenetic treatments on a human epithelial ovarian cancer cell line. Treatment with methylation (5-aza-2'-deoxycytidine) or deacetylation (trichostatin A) inhibitors alone resulted in up-regulation of 1.9 or 1.1% of the genes analyzed; however, the combined treatment resulted in synergistic reactivation of more genes (10.4%; P < 0.001 versus either treatment alone). On the basis of either primary or secondary responses to the treatments, genes were identified as methylation-dependent or -independent. Synergistic reactivation of the methylation-dependent genes by 5-aza-2'-deoxycytidine plus trichostatin A revealed a functional interaction between methylated promoters and deacetylated histones. Increased expression of some methylation-independent genes was associated with enhanced histone acetylation, but up-regulation of most of the genes identified using this technology was because of events downstream of the epigenetic cascade. We demonstrate proof of principle for using the triple microarray system in analyzing the dynamic relationship between transcription factors and promoter targets in cancer genomes.
GPS 2.0, a Tool to Predict Kinase-specific Phosphorylation Sites in Hierarchy (2008)

Identification of protein phosphorylation sites with their cognate protein kinases (PKs) is a key step to delineate molecular dynamics and plasticity underlying a variety of cellular processes. Although nearly 10 kinase-specific prediction programs have been developed, numerous PKs have been casually classified into subgroups without a standard rule. For large scale predictions, the false positive rate has also never been addressed. In this work, we adopted a well established rule to classify PKs into a hierarchical structure with four levels, including group, family, subfamily, and single PK. In addition, we developed a simple approach to estimate the theoretically maximal false positive rates. The on-line service and local packages of the GPS (Group-based Prediction System) 2.0 were implemented in Java with the modified version of the Group-based Phosphorylation Scoring algorithm. As the first stand alone software for predicting phosphorylation, GPS 2.0 can predict kinase-specific phosphorylation sites for 408 human PKs in hierarchy. A large scale prediction of more than 13,000 mammalian phosphorylation sites by GPS 2.0 was exhibited with great performance and remarkable accuracy. Using Aurora-B as an example, we also conducted a proteome-wide search and provided systematic prediction of Aurora-B-specific substrates including protein-protein interaction information. Thus, the GPS 2.0 is a useful tool for predicting protein phosphorylation sites and their cognate kinases and is freely available on line.
Rheological properties of deacetylated xanthan in aqueous media. (1984)

Flow properties of aqueous deacetylated xanthan solutions could be approximated to pseudoplastic behavior at concentrations below 0.1% but to plastic behavior above 0.3%. The flow indices in the power law for the deacetylated xanthan were somewhat different at various concentrations. The apparent viscosity of deacetylated xanthan decreased with increasing temperature at relatively low concentrations from 0.1 to 0.5%, however, it increased with increasing temperature, showed a maximum value at 40°C and decreased gradually at 1.0%. Compared with native xanthan, deacetylated material showed higher dynamic viscoelasticity at high concentrations. The dynamic viscoelasticity of deacetylated xanthan decreased with increasing temperature at various concentrations. The dynamic viscoelasticity of deacetylated xanthan was decreased by addition of urea (4.0M). This suggests that acetate residues, which are attached to the inner mannose residues of the side chains, contribute to the intramolecular association, and that the side chains of xanthan become more flexible after deacetylation.
Chemistry of carbanions. XVIII. Preparation of trimethylsilyl enol ethers (1969)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTChemistry of carbanions. XVIII. Preparation of trimethylsilyl enol ethersHerbert O. House, Leonard J. Czuba, Martin Gall, and Hugh D. OlmsteadCite this: J. Org. Chem. 1969, 34, 8, 2324–2336Publication Date (Print):August 1, 1969Publication History Published online1 May 2002Published inissue 1 August 1969https://pubs.acs.org/doi/10.1021/jo01260a018https://doi.org/10.1021/jo01260a018research-articleACS PublicationsRequest reuse permissionsArticle Views7737Altmetric-Citations696LEARN 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
A Wideband On-Interposer Passive Equalizer Design for Chip-to-Chip 30-Gb/s Serial Data Transmission (2014)

In this paper, a novel on-interposer passive equalizer is proposed for chip-to-chip high-speed data transmission on the silicon-based on-interposer channel. The proposed equalizer uses the parasitic resistance and inductance of the on-interposer shunt metal lines to produce the high-pass filter. This filter enables the proposed equalizer to exhibit wideband channel equalization and low power-consumption. Based on the equivalent-circuit model of the proposed on-interposer passive equalizer, the physical dimensions of the equalizer are optimized for 30-Gb/s serial data transmission. The performance of the proposed equalizer with the optimized dimensions was successfully demonstrated by both frequency- and time-domain measurements at data rates of up to 30 Gb/s. In addition, a compact on-interposer passive equalizer was designed for the wide I/O interposer using the same mechanism. The improved quality of serial data transmission in the equalized wide I/O on-interposer channel was successfully verified by simulations at data rates of up to 10 Gb/s.
Genetic diversity and relationships among Streptococcus pyogenes strains expressing serotype M1 protein: recent intercontinental spread of a subclone causing episodes of invasive disease (1995)

Chromosomal diversity and relationships among 126 Streptococcus pyogenes strains expressing M1 protein from 13 countries on five continents were analyzed by multilocus enzyme electrophoresis and restriction fragment profiling by pulsed-field gel electrophoresis. All isolates were studied for the presence of the gene encoding streptococcal pyrogenic exotoxin A by PCR. Strain subsets were also examined by automated DNA sequencing for allelic polymorphism in genes encoding M protein (emm), streptococcal pyrogenic exotoxin A (speA), streptokinase (ska), pyrogenic exotoxin B (interleukin-1 beta convertase) (speB), and C5a peptidase (scp). Seven distinct emm1 alleles that encode M proteins differing at one or more amino acids in the N-terminal variable region were identified. Although substantial levels of genetic diversity exist among M1-expressing organisms, most invasive disease episodes are caused by two subclones marked by distinctive multilocus enzyme electrophoretic profiles and pulsed-field gel electrophoresis restriction fragment length polymorphism (RFLP) types. One of these subclones (ET 1/RFLP pattern 1a) has the speA gene and was recovered worldwide. Identity of speA, emm1, speB, and ska alleles in virtually all isolates of ET 1/RFLP type 1a means that these organisms share a common ancestor and that global dispersion of this M1-expressing subclone has occurred very recently. The occurrence of the same emm and ska alleles in strains that are well differentiated in overall chromosomal character demonstrates that horizontal transfer and recombination play a fundamental role in diversifying natural populations of S. pyogenes.
Effect of Elevated Left Atrial Pressure and Decreased Plasma Protein Concentration on the Development of Pulmonary Edema (1959)

In 97 dogs left atrial pressure was elevated to various levels up to 50 mm. Hg by partial constriction of the aorta. The effect of these pressures for from 30 min. to 3 hours on the accumulation of lung edema was then studied. Edema was estimated by determining the ratio of the weight of the wet lung to the weight of the same lung after drying. In animals with normal plasma protein concentrations fluid began to transude into the lungs when the left atrial pressure rose above an average of 24 mm. Hg. In another series of animals the plasma protein concentrations were reduced by plasmapheresis at the beginning of each experiment until the plasma protein concentration averaged 47 per cent of the control value. In these animals fluid began to transude into the lungs when the left atrial pressure rose above a critical value of 11 mm Hg. Furthermore, the rate at which fluid accumulated in the lungs, in all series of experiments, was directly proportional to the rise in left atrial pressure above the critical pressure at which fluid began to collect in the lungs.
Design, construction and use of a large-sample field-cycled PEDRI imager (1998)

The design, construction and use of a large-scale field-cycled proton-electron double-resonance imaging (FC-PEDRI) imager is described. The imager is based on a whole-body sized, vertical field, 59 mT permanent magnet. Field cycling is accomplished by the field compensation method, and uses a secondary, resistive magnet with an internal diameter of 52 cm. The magnetic field can be switched from zero to 59 mT or vice versa in 40 ms. It is used with a double-resonance coil assembly (NMR/EPR) comprising a solenoidal NMR transmit/receive coil and a coaxial, external birdcage resonator for EPR irradiation. Experiments to image the distribution of an exogenous nitroxide free radical in anaesthetized rabbits are described.