gebhart/patrepeval huggingface dataset:
Hash Functions for Rapid Storage and Retrieval of Chemical Structures (1978)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTHash Functions for Rapid Storage and Retrieval of Chemical StructuresW. T. Wipke, S. Krishnan, and G. I. OuchiCite this: J. Chem. Inf. Comput. Sci. 1978, 18, 1, 32–37Publication Date (Print):February 1, 1978Publication History Published online1 May 2002Published inissue 1 February 1978https://pubs.acs.org/doi/10.1021/ci60013a008https://doi.org/10.1021/ci60013a008research-articleACS PublicationsRequest reuse permissionsArticle Views153Altmetric-Citations22LEARN 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 options Get e-Alerts
Mice lacking fatty acid amide hydrolase exhibit a cannabinoid receptor-mediated phenotypic hypoalgesia (2004)

Although the N-arachidonoyl ethanolamine (anandamide) binds to cannabinoid receptors and has been implicated in the suppression of pain, its rapid catabolism in vivo by fatty acid amide hydrolase (FAAH) has presented a challenge in investigating the physiological functions of this endogenous cannabinoid. In order to test whether anandamide and other non-cannabinoid fatty amides modulate nociception, we compared FAAH (+/+) and (-/-) mice in the tail immersion, hot plate, and formalin tests, as well as for thermal hyperalgesia in the carrageenan and the chronic constriction injury (CCI) models. FAAH (-/-) mice exhibited a CB1 receptor-mediated phenotypic hypoalgesia in thermal nociceptive tests. These mice also exhibited CB1 receptor-mediated hypoalgesia in both phases of the formalin test accompanied with a phenotypic anti-edema effect, which was not blocked by either CB1 or CB2 antagonists. Additionally, FAAH (-/-) mice displayed thermal anti-hyperalgesic and anti-inflammatory effects in the carrageenan model that were mediated, in part, by CB2, but not CB1 receptors. In contrast, no genotype differences in pain behavior were evident following CCI, which was instead found to obliterate the phenotypic hypoalgesia displayed by FAAH (-/-) mice in the tail immersion and hot plate tests, suggesting that nerve injury may promote adaptive changes in these animals. Collectively, these findings demonstrate a cannabinoid receptor-mediated analgesic phenotype in FAAH (-/-) mice. In more general terms, these findings suggest that selective inhibitors of FAAH might represent a viable pharmacological approach for the clinical treatment of pain disorders.
The t(5;14) chromosomal translocation in a case of acute lymphocytic leukemia joins the interleukin-3 gene to the immunoglobulin heavy chain gene (1989)

Chromosomal translocations have proven to be important markers of the genetic abnormalities central to the pathogenesis of cancer. By cloning chromosomal breakpoints one can identify activated proto-oncogenes. We have studied a case of B-lineage acute lymphocytic leukemia (ALL) that was associated with peripheral blood eosinophilia. The chromosomal translocation t(5;14) (q31;q32) from this sample was cloned and studied at the molecular level. This translocation joined the immunoglobulin heavy chain joining (Jh) region to the promotor region of the interleukin-3 (IL-3) gene in opposite transcriptional orientations. The data suggest that activation of the IL-3 gene by the enhancer of the immunoglobulin heavy chain gene may play a central role in the pathogenesis of this leukemia and the associated eosinophilia.
NF-κB-Inducing Kinase (NIK) Mediates Skeletal Muscle Insulin Resistance: Blockade by Adiponectin (2011)

Enhanced levels of nuclear factor (NF)-κB-inducing kinase (NIK), an upstream kinase in the NF-κB pathway, have been implicated in the pathogenesis of chronic inflammation in diabetes. We investigated whether increased levels of NIK could induce skeletal muscle insulin resistance. Six obese subjects with metabolic syndrome underwent skeletal muscle biopsies before and six months after gastric bypass surgery to quantitate NIK protein levels. L6 skeletal myotubes, transfected with NIK wild-type or NIK kinase-dead dominant negative plasmids, were treated with insulin alone or with adiponectin and insulin. Effects of NIK overexpression on insulin-stimulated glucose uptake were estimated using tritiated 2-deoxyglucose uptake. NF-κB activation (EMSA), phosphatidylinositol 3 (PI3) kinase activity, and phosphorylation of inhibitor κB kinase β and serine-threonine kinase (Akt) were measured. After weight loss, skeletal muscle NIK protein was significantly reduced in association with increased plasma adiponectin and enhanced AMP kinase phosphorylation and insulin sensitivity in obese subjects. Enhanced NIK expression in cultured L6 myotubes induced a dose-dependent decrease in insulin-stimulated glucose uptake. The decrease in insulin-stimulated glucose uptake was associated with a significant decrease in PI3 kinase activity and protein kinase B/Akt phosphorylation. Overexpression of NIK kinase-dead dominant negative did not affect insulin-stimulated glucose uptake. Adiponectin treatment inhibited NIK-induced NF-κB activation and restored insulin sensitivity by restoring PI3 kinase activation and subsequent Akt phosphorylation. These results indicate that NIK induces insulin resistance and further indicate that adiponectin exerts its insulin-sensitizing effect by suppressing NIK-induced skeletal muscle inflammation. These observations suggest that NIK could be an important therapeutic target for the treatment of insulin resistance associated with inflammation in obesity and type 2 diabetes.
Slow cleavage at the proinsulin B-chain/connecting peptide junction associated with low levels of endoprotease PC1/3 in transformed beta cells (1993)

Conversion of rat proinsulins I and II was slower in transformed INS cells than in primary (islet) beta cells, with accumulation of des-64,65 but no detectable des-31,32-split proinsulin, indicating slow cleavage at the B-chain/connecting peptide (C-peptide) junction. Western blot analysis showed lower levels of the endoprotease PC1/3 in INS cells than in beta cells, as well as a 4-fold reduction in the ratio of PC1/3 to PC2, thus supporting the hypothesis that PC1/3 is the endoprotease responsible for cleavage at the B-chain/C-peptide junction.
Evidence for in vitro replication of hepatitis C virus genome in a human T-cell line. (1992)

A human T-cell line, MOLT-4, either uninfected or infected with murine retroviruses, was tested for its susceptibility to hepatitis C virus (HCV) infection. The cell cultures were inoculated with a serum containing HCV and then examined for the presence of viral sequences by cDNA/PCR. In murine retrovirus-infected MOLT-4 (MOLT-4 Ma) cells, intracellular minus-strand viral RNA, a putative replication intermediate, was first detected 3 days after inoculation, and the maximum signal was seen on day 7. When the cells were continuously subcultured in fresh medium, HCV sequences were intermittently detected in cells over a period of 3 weeks. In MOLT-4 cells free of retroviruses, replication of minus-strand HCV RNA appeared less efficient than in MOLT-4 Ma cells. The presence of minus-strand viral RNA in MOLT-4 Ma cells inoculated with HCV was confirmed by in situ hybridization with a strand-specific RNA probe. Immunofluorescence tests with antibodies specific for HCV core and NS4 antigens showed that MOLT-4 Ma cells were positive for viral antigen 7 days after inoculation. Thus, it appears likely that the HCV genome can replicate in the human T-cell line MOLT-4.
Fast-scanning THz medical imaging system for clinical application (2012)

Applications for terahertz (THz) medical imaging have proliferated over the past few years due to advancements in source/detector technology and vigorous application development. While considerable effort has been applied to improving source output power and detector sensitivity, significantly less work has been devoted to improving image acquisition method and time. The majority of THz medical imaging systems in the literature typically acquire pixels by translating the target of interest beneath a fixed illumination beam. While this single-pixel whiskbroom methodology is appropriate for in vitro models, it is unsuitable for in vivo large animal and patient imaging due to practical constraints. This paper presents a scanned beam imaging system based on prior work that enables for reduced image acquisition time while allowing the source, target and detector to remain stationary. The system employs a spinning polygonal mirror and a set of high-density polyethylene (HDPE) objective lenses, and operates at a center illumination frequency of 525GHz with ~125GHz of 3dB bandwidth. The system achieves a focused beam diameter of 1.66mm and a large depth of field of <25 mm. Images of characterization targets and ex vivo tissue samples are presented and compared to results obtained with conventional fixed beam scanning systems.
Immunoglobulin V region heavy and light chain gene sequences of the lymphoblastoid cell line GM 4672 (1993)

GM 4672 is an IgG2 kappa-producing lymphoblastoid cell line derived from a patient with multiple myeloma. It has been used by many laboratories as a fusion partner for the production of human-human hybridoma monoclonal antibodies. GM 4672 immunoglobulin variable region heavy and light chain family usage was originally assigned to VH1 and VK1, respectively. This assignment was based on the positions of [3H]leucine of the heavy and light chain proteins using the Edman degradation method. Using the polymerase chain reaction and variable region leader primers and constant region primers, we report here the immunoglobulin variable region gene sequence expressed by GM 4672. The VH region belongs to the VH4 family and is most homologous with the V71-2 (87.9%), DK1, and JH4 germline genes. The entire heavy chain V region contained 41 mutations in 36 codons and included 11 N nucleotide additions flanking the D region. GM 4672 VK region contained a VK1 gene rearranged with a JK4 gene. The VK germline gene used by GM 4672 light chain was not identified but showed the most homology with Vb' germline gene (87.7%). When compared to Vb' and JK4 genes, there were 37 mutations in 30 codons with evidence of antigen selection as determined by the replacement to silent mutation ratio in the complementarity-determining regions. The high frequency of mutations in the V region genes of GM 4672 is comparable to the sequences of other myeloma proteins.
Iron transport: emerging roles in health and disease (2002)

In the theater of cellular life, iron plays an ambiguous and yet undoubted lead role. Iron is a ubiquitous core element of the earth and plays a central role in countless biochemical pathways. It is integral to the catalysis of the redox reactions of oxidative phosphorylation in the respiratory chain, and it provides a specific binding site for oxygen in the heme binding moiety of hemoglobin, which allows oxygen transport in the blood. Its biological utility depends upon its ability to readily accept or donate electrons, interconverting between its ferric (Fe3+) and ferrous (Fe2+) forms. In contrast to these beneficial features, free iron can assume a dangerous aspect catalyzing the formation of highly reactive compounds such as cytotoxic hydroxyl radicals that cause damage to the macromolecular components of cells, including DNA and proteins, and thereby cellular destruction. The handling of iron in the body must therefore be very carefully regulated. Most environmental iron is in the Fe3+ state, which is almost insoluble at neutral pH. To overcome the virtual insolubility and potential toxicity of iron, a myriad of specialized transport systems and associated proteins have evolved to mediate regulated acquisition, transport, and storage of iron in a soluble, biologically useful, non-toxic form. We are gradually beginning to understand how these proteins individually and in concert serve to maintain cellular and whole body homeostasis of this crucial yet potentially harmful metal ion. Furthermore, studies are increasingly implicating iron and its associated transport in specific pathologies of many organs. Investigation of the transport proteins and their functions is beginning to unravel the detailed mechanisms underlying the diseases associated with iron deficiency, iron overload, and other dysfunctions of iron metabolism.
Optimizing GPU energy efficiency with 3D die-stacking graphics memory and reconfigurable memory interface (2013)

The performance of graphics processing unit (GPU) systems is improving rapidly to accommodate the increasing demands of graphics and high-performance computing applications. With such a performance improvement, however, power consumption of GPU systems is dramatically increased. Up to 30% of the total power of a GPU system is consumed by the graphic memory itself. Therefore, reducing graphics memory power consumption is critical to mitigate the power challenge. In this article, we propose an energy-efficient reconfigurable 3D die-stacking graphics memory design that integrates wide-interface graphics DRAMs side-by-side with a GPU processor on a silicon interposer. The proposed architecture is a “3D+2.5D” system, where the DRAM memory itself is 3D stacked memory with through-silicon via (TSV), whereas the integration of DRAM and the GPU processor is through the interposer solution (2.5D). Since GPU computing units, memory controllers, and memory are all integrated in the same package, the number of memory I/Os is no longer constrained by the package’s pin count. We can reduce the memory power consumption by scaling down the supply voltage and frequency of memory interface while maintaining the same or even higher peak memory bandwidth. In addition, we design a reconfigurable memory interface that can dynamically adapt to the requirements of various applications. We propose two reconfiguration mechanisms to optimize the GPU system energy efficiency and throughput, respectively, and thus benefit both memory-intensive and compute-intensive applications. The experimental results show that the proposed GPU memory architecture can effectively improve GPU system energy efficiency by 21%, without reconfiguration. The reconfigurable memory interface can further improve the system energy efficiency by 26%, and system throughput by 31% under a capped system power budget of 240W.
Laboratory Techniques of Purification and Isolation (2012)

Purification is the main basis for synthesis of new molecules and drug discovery and sometimes we need to use proper techniques for isolation and purification so that we can get pure drug. This article describes about solution of problems which we have to face during laboratory experiments like selection of proper solvent for reaction, isolation procedures and purification techniques
A novel silicon texturization method based on etching through a silicon nitride mask (2005)

We present a new texturing technique applicable to silicon solar cells. The technique is based on the isotropic etching of silicon through a very thin layer of silicon nitride, deposited by low-pressure chemical vapor deposition. Spectrophotometry measurements show that the resulting surface texture displays low reflectivity after encapsulation behind glass, and nearly ideal light-trapping behaviour. The surfaces can also be well passivated using standard passivation techniques. Emitter dark saturation currents in the range 4–5 × 10−14 A/cm2 have been measured by quasi-steady-state photoconductance following the growth of a thermal oxide. Copyright © 2005 John Wiley & Sons, Ltd.
Temporally and spectrally resolved fluorescence spectroscopy for the detection of high grade dysplasia in Barrett's esophagus (2003)

In the diagnosis of HGD in BE, steady-state fluorescence was more effective than time-resolved data, and excitation at 400 nm excitation was more effective than 337 nm. While fluorescence-targeted biopsy is approaching clinical usefulness, increased sensitivity to dysplastic changes-possibly through modification of system parameters-is needed to improve accuracy levels.
The renal monoamine oxidases (1998)

The mitochondrial enzyme monoamine oxidases A and B are among the major metabolic agents for the degradation of the biogenic amines adrenaline, noradrenaline, dopamine and serotonin. The fact that the kidney contains a large amount of monoamine oxidase suggests that the renal effects of biogenic amines might depend in part on the activity of these enzymes.
Cloning, bacterial expression, purification, and characterization of the cytoplasmic domain of rat LAR, a receptor-like protein tyrosine phosphatase. (1991)

This report describes the cloning and characterization of rat leukocyte common antigen-related protein (rLAR), a receptor-like protein tyrosine phosphatase (PTPase). The recombinant cytoplasmic PTPase domain was expressed at high levels in bacteria and purified to homogeneity. Kinetic properties of the PTPase were examined along with potential modulators of PTPase activity. Several sulfhydryl-directed reagents were effective inhibitors, and a surprising distinction between iodoacetate and iodoacetamide was observed. The latter compound was an extremely poor inhibitor when compared to iodoacetate, suggesting that iodoacetate may interact selectively with a positive charge at or near the active site of the enzyme. Site-directed mutants were made at 4 highly conserved cysteine residues found at positions 1434, 1522, 1723, and 1813 within the protein. The Cys-1522/Ser mutation resulted in a 99% loss of enzymatic activity of the pure protein. This observation is consistent with greater than 99% of the PTPase activity being found in the first domain of the PTPase and demonstrates the critical importance of this cysteine residue in catalysis. The recombinant C1522S mutant phosphatase could also be phosphorylated in vitro by protein kinase C and p43v-abl tyrosine kinase. When pure recombinant PTPase was mixed with 32P-labeled tyrosine substrate and then rapidly denatured, a 32P-labeled enzyme intermediate could be trapped and visualized by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The catalytically inactive C1522S mutant did not form the phosphoenzyme intermediate.
Overproduction of l -Cysteine and l -Cystine by Escherichia coli Strains with a Genetically Altered Serine Acetyltransferase (1998)

Organisms that overproduced L-cysteine and L-cystine from glucose were constructed by using Escherichia coli K-12 strains. cysE genes coding for altered serine acetyltransferase, which was genetically desensitized to feedback inhibition by L-cysteine, were constructed by replacing the methionine residue at position 256 of the serine acetyltransferase protein with 19 other amino acid residues or the termination codon to truncate the carboxy terminus from amino acid residues 256 to 273 through site-directed mutagenesis by using PCR. A cysteine auxotroph, strain JM39, was transformed with plasmids having these altered cysE genes. The serine acetyltransferase activities of most of the transformants, which were selected based on restored cysteine requirements and ampicillin resistance, were less sensitive than the serine acetyltransferase activity of the wild type to feedback inhibition by L-cysteine. At the same time, these transformants produced approximately 200 mg of L-cysteine plus L-cystine per liter, whereas these amino acids were not detected in the recombinant strain carrying the wild-type serine acetytransferase gene. However, the production of L-cysteine and L-cystine by the transformants was very unstable, presumably due to a cysteine-degrading enzyme of the host, such as cysteine desulfhydrase. Therefore, mutants that did not utilize cysteine were derived from host strain JM39 by mutagenesis with N-methyl-N'-nitro-N-nitrosoguanidine. When a newly derived host was transformed with plasmids having the altered cysE genes, we found that the production of L-cysteine plus L-cystine was markedly increased compared to production in JM39.
Oxygen‐sensing persistent sodium channels in rat hippocampus (2000)

1. Persistent sodium channel activity was recorded before and during hypoxia from cell-attached and inside-out patches obtained from cultured hippocampal neurons at a pipette potential (Vp) of +30 mV. Average mean current (IU) of these channels was very low under normoxic conditions and was similar in cell-attached and excised inside-out patches (-0.018 +/- 0.010 and -0.025 +/- 0.008 pA, respectively, n = 24). 2. Hypoxia increased the activity of persistent sodium channels in 10 cell-attached patches (IU increased from -0. 026 +/- 0.016 pA in control to -0.156 +/- 0.034 pA during hypoxia, n = 4, P = 0.013). The increased persistent sodium channel activity was most prominent at a VP between +70 and +30 mV (membrane potential, Vm = -70 to -30 mV) and could be blocked by lidocaine, TTX or R56865 (n = 5). Sodium cyanide (NaCN, 5 mM; 0.5-5 min) increased persistent sodium channel activity in cell-attached patches (n = 3) in a similar manner. 3. Hypoxia also increased sodium channel activity in inside-out patches from hippocampal neurons. Within 2-4 min of exposure to hypoxia, I had increased 9-fold to -0. 18 +/- 0.04 pA (n = 21, P = 0.001). Sodium channel activity increased further with longer exposures to hypoxia. 4. The hypoxia-induced sodium channel activity in inside-out patches could be inhibited by exposure to 10-100 microM lidocaine applied via the bath solution (I = -0.03 +/- 0.01 pA, n = 8) or by perfusion of the pipette tip with 1 microM TTX (I = -0.01 +/- 0.01 pA, n = 3). 5. The reducing agent dithiothreitol (DTT, 2-5 mM) rapidly abolished the increase in sodium channel activity caused by hypoxia in excised patches (I = -0.01 +/- 0.01 pA, n = 4). Similarly, reduced glutathione (GSH, 5-20 mM) also reversed the hypoxia-induced increase in sodium channel activity (IU = -0.02 +/- 0.02 pA, n = 5). 6. These results suggest that persistent sodium channels in neurons can sense O2 levels in excised patches of plasma membrane. Hypoxia triggers an increase in sodium channel activity. The redox reaction involved in increasing the sodium channel activity probably occurs in an auxiliary regulatory protein, co-localized in the plasma membrane.