gebhart/patrepeval huggingface dataset:
Next-generation genome sequencing : towards personalized medicine (2008)

SANGER DNA SEQUENCING Sanger DNA sequencing (Men) NEXT GENERATION SEQUENCING - TOWARDS PERSONALIZED MEDICINE Illumina Genome Analyzer II System (Lakdawalla) Applied Biosystems SOLiD? System - Ligation-based Sequencing (Prediger) The next Generation Genome Sequencing: 454/Roche GS FLX (Egholm) Polony Sequencing - History, technology, and Applications (Edwards) THE BOTTLENECK: SEQUENCE DATA ANALYSIS Next Generation Sequence Data Analysis (Bloksberg) DNASTARs Next Generation Software (Durfee) EMERGING SEQUENCING TECHNOLOGIES Real-time DNA sequencing (Hardin) Direct Sequencing by TEM of Z-substituted DNA Molecules (Glover) A Single DNA Molecule Barcoding Method with Applications in DNA Mapping and Molecular Haplotyping (Xao) Optical Sequencing - Acquisition from Mapped Single Molecule Templates (Schwartz) Microchip-based Sanger Sequencing of DNA (Barron) NEXT GENERATION SEQUENCING - TRULY INTEGRATED GENOME ANALYSIS Multiplex Sequencing of Paired End diTags for Transcriptome and Genome Analysis (Ruan) Palaeogenomics using the 454 Sequencing Platform (Gilbert) ChIPSeq: Mapping of Protein-DNA Interactions (Fejes) MicroRNA Discovery and Expression Profiling using Next-generation Sequencing (Cuppen) DeepSAGE - Tag-based Transcriptome Analysis beyond Microarrays (Nielsen) The new Genomics and Personal Genome Information: Ethical Issues (Lunshof)
Syntheses of Analgesics. XIV (1958)

Ethyl cyclohexylidenecyanoacetates (VI), obtained by the Cope condensation of cyclohexanone derivatives (V), was reacted with the Grignard reagent of phenyl bromide to form ethyl α-cyano-1-phenylcyclohexaneacetates (VII) and their decarboxylation afforded the 1-phenylcyclohexaneacetonitriles (VIII). Hydrolysis of (VIII) gave 1-phenylcyclohexaneacetic acids (XI), while the reduction of (VIII) followed by dimethylation, or the condensation of (XI) and dimethylamine followed by reduction, afforded N, N-dimethyl-1-phenylcyclohexaneethylamines (X and III). 1-(1-phenylcyclohexyl) trimethylamine (IV) was prepared by the Curtius degradation of (XI) and subsequent dimethylation.
Races of Phytophthora sojae on Soybean in Illinois (2000)

Phytophthora root rot of soybean (Glycine max (L.) Merr.), caused by Phytophthora sojae M. J. Kauffmann & J. W. Gerdemann, has been isolated throughout the soybean-producing regions of the United States. There are more than 39 identified races of P. sojae pathogenic on soybean, and 13 host resistance alleles have been identified at 7 loci (1). None of these alleles confers resistance to all races of P. sojae. The most commonly used resistance allele, Rps1k, confers resistance to the greatest number of races (2). The objective of this study was to identify races of P. sojae in Illinois soybean fields to determine whether the currently used resistance alleles are effective against the P. sojae races found in Illinois. Soybean breeders must be aware of the existence and distribution of races to incorporate appropriate sources of genetic resistance into cultivars. From 192 soil samples collected throughout Illinois in 1997, 33 isolates were obtained and identified to race by inoculating Rps isolines of soybean cv. Williams. A new race with virulence to the Rps1d and Rps7 alleles, designated as race 54, accounted for 48% of the isolates. Another new race with virulence to Rps1d, Rps3a, Rps3c, Rps4, Rps5, Rps6, and Rps7 alleles, designated race 55, was identified in one sample. One isolate, identified as race 41, was obtained from a diseased plant with the Rps1k allele. Another isolate, identified as race 43, was obtained from a diseased plant with the Rps1c allele. Based on virulence patterns of P. sojae, most of the isolates obtained from Illinois soils were races 1, 3, and 4 or variants of these races, such as race 54, with added virulence to the Rps1d allele. References: (1) A. F. Schmitthenner. 1999. Compendium of Soybean Diseases. 4th ed. G. L. Hartman, J. B. Sinclair, and J. C. Rupe, eds. The American Phytopathological Society, St. Paul, MN. pp. 39-42. (2) A. F. Schmitthenner, M. Hobe, and R. G. Bhat. Plant Dis. 78:269, 1994.
The ligase chain reaction in a PCR world. (1991)

S i n c e its discovery in 1985, the polymerase chain reaction (PCR) has had a profound impact on detecting genetic and infectious diseases, identifying new genes, and unraveling the mysteries of protein-ligand recognition.(1-s) Its universal utility is due to the exquisite specificity of amplification and ease of cycling made possible by the cloning and careful characterization of a thermostable polymerase from Thermus aquaticus. (6,7) Likewise, cloning of a thermostable ligase enabled a new amplification method, termed ligase chain reaction (LCR), to both amplify DNA and discriminate a single base mutation. (8-1~ Although these DNA amplification techniques are new, they bring to fruition the enzymes as reagents philosophy expounded by A. Kornberg and I.R. Lehman a quarter of a century ago. Allele-specific LCR employs four oligonucleotides, two adjacent oligonucleotides which uniquely hybridize to one strand of target DNA and a complementary set of adjacent oligonucleotides, which hybridize to the opposite strand (see Fig. 1, top left). Thermostable DNA ligase will covalently link each set, provided that there is complete complementarity at the junc~ tion. (8) Because the oligonucleotide products from one round may serve as substrates during the next round, the signal is amplified exponentially, analogous to PCR amplification. A single-base mismatch at the oligonucleotide junction will not be amplified and is therefore distinguished (Fig. 1, top right). A second set of mutantspecific oligonucleotides is used in a separate reaction to detect the mutant allele. This review will give a brief introduction to (1) determinants of specificity in amplification reactions; (2) differences between thermostable and thermophilic enzymes; (3) detection of single-base substitutions in DNA diagnostics; (4) characterization of DNA ligases; (5) cloning of DNA ligases; (6) use of ligases in DNA detection; (7) other methods that use ligase, such as ligase-mediated PCR and the branch capture reaction; and (8) potential new uses of ligase in PLCR and nested LCR amplification reactions. It will close with speculations on future prospects.
In Vivo Role of Complement-Interacting Domains of Herpes Simplex Virus Type 1 Glycoprotein Gc (1999)

Immune evasion is critical for survival of viruses that establish persistent or recurrent infections. However, at the molecular level, little is known about how viruses evade immune attack in vivo. Herpes simplex virus (HSV)-1 glycoprotein gC has two domains that are involved in modulating complement activation; one binds C3, and the other is required for blocking C5 and properdin (P) binding to C3. To evaluate the importance of these regions in vivo, HSV-1 gC mutant viruses were constructed that lacked one or both gC domains and studied in a murine model of infection. Each gC region of complement regulation contributed to virulence; however, the C3 binding domain was far more important, as virus lacking this domain was much less virulent than virus lacking the C5/P inhibitory domain and was as attenuated as virus lacking both domains. Studies in C3 knockout mice and mice reconstituted with C3 confirmed that the gC domains are inhibitors of complement activation, accounting for a 50-fold difference in virulence between mutant and wild-type viruses. We conclude that the C3 binding domain on gC is a major contributor to immune evasion and that this site explains at a molecular level why wild-type virus resists complement attack.
Upregulation of MMPs by soluble E‐cadherin in human lung tumor cells (2003)

Loss of E-cadherin/catenin mediated cell-cell adhesion and overexpression of matrix metalloproteinases (MMPs) are largely involved in tumor invasion. It has been recently shown that high levels of a soluble 80 kDa fragment of E-cadherin, resulting from a cleavage by MMPs, are found in serum and in urine from cancer patients. Additionally, this soluble E-cadherin (sE-CAD) promotes cell invasion into chick heart and into collagen type I gels. The aim of our study was to examine the mechanism of sE-CAD-induced cell invasion. Since MMPs play a crucial role in invasion, we looked for induction of MMPs by sE-CAD in noninvasive human lung tumor cells 16HBE. An induction of MMP-2, MMP-9 and MT1-MMP expression was observed both at the mRNA and at the protein level in the presence of sE-CAD (in conditioned medium form or in E-cadherin HAV peptide form). No induction of MMP-1, -3 and -7 or variation of the levels of their inhibitors, TIMP-1 and TIMP-2, were detected. The biologic relevance of the sE-CAD-induced MMP upregulation was tested by demonstrating that sE-CAD promotes in vitro cell invasion in a modified Boyden chamber assay. These data provide new insight into mechanisms of tumor invasion by ectodomain shedding of the cell-cell adhesion molecule E-cadherin.
Photodynamic Biologic Tissue Glue (1994)

We studied both heat- and light-activated tissue glues, and while a heat-activated mixture such as albumin and fluorescein isothiocyanate was effective, we believed that a light-activated substance would have less of an effect on adjacent tissue. Our glue uses a photosensitive singlet oxygen generator to cross-link a protein solder with corneal stromal collagen. The mixture consists of 18% fibrinogen and 2.6 mg/ml of riboflavin-5-phosphate activated with a blue-green (488-514 nm) Argon laser. We tested our glue by soldering 5-mm penetrating central corneal incisions made in human cadaver eyes. The strength of the closure was measured by cannulating the vitreous cavity with an 18-gauge needle connected to a saline reservoir. The pressure in the reservoir was elevated by connecting it to a sphygmomanometer. Immediately following tissue closure, the intraocular pressure was increased until the wound burst. We soldered and measured 10 eyes and found a mean bursting pressure of 154 mm Hg, with a range of 80-260 mm Hg. Our laser-activated tissue glue is an effective adhesive for corneal tissue, and we now plan to carry out toxicity studies in living animals.
Multiplex digital PCR: breaking the one target per color barrier of quantitative PCR (2011)

Quantitative polymerase chain reactions (qPCR) based on real-time PCR constitute a powerful and sensitive method for the analysis of nucleic acids. However, in qPCR, the ability to multiplex targets using differently colored fluorescent probes is typically limited to 4-fold by the spectral overlap of the fluorophores. Furthermore, multiplexing qPCR assays requires expensive instrumentation and most often lengthy assay development cycles. Digital PCR (dPCR), which is based on the amplification of single target DNA molecules in many separate reactions, is an attractive alternative to qPCR. Here we report a novel and easy method for multiplexing dPCR in picolitre droplets within emulsions-generated and read out in microfluidic devices-that takes advantage of both the very high numbers of reactions possible within emulsions (>10(6)) as well as the high likelihood that the amplification of only a single target DNA molecule will initiate within each droplet. By varying the concentration of different fluorogenic probes of the same color, it is possible to identify the different probes on the basis of fluorescence intensity. Adding multiple colors increases the number of possible reactions geometrically, rather than linearly as with qPCR. Accurate and precise copy numbers of up to sixteen per cell were measured using a model system. A 5-plex assay for spinal muscular atrophy was demonstrated with just two fluorophores to simultaneously measure the copy number of two genes (SMN1 and SMN2) and to genotype a single nucleotide polymorphism (c.815A>G, SMN1). Results of a pilot study with SMA patients are presented.
Proton fourier transform NMR studies of insulin: coordination of calcium to the Glu(B13) site drives hexamer assembly and induces a conformation change (1988)

1H Fourier transform NMR investigations of metal ion binding to insulin in 2H2O were undertaken as a function of pH* to determine the effects of metal ion coordination to the Glu(B13) site on the assembly and structure of the insulin hexamer. The C-2 histidyl regions of the 1H NMR spectra of insulin species containing respectively one Ca2+ and two Zn2+/hexamer and three Cd2+/hexamer have been assigned. Both the Cd2+ derivative (In)6(Cd2+)2Cd2+, where two of the Cd2+ ions are coordinated to the His(B10) sites and the remaining Cd2+ ion is coordinated to the Glu(B13) site [Sudmeier, J.L., Bell, S.J., Storm, M. C., & Dunn, M.F. (1981) Science (Washington, D.C.) 212, 560], and the Zn2+-Ca2+ derivative (In)6-(Zn2+)2Ca2+, where the two Zn2+ ions are coordinated to the His(B10) sites and Ca2+ ion is coordinated to the Glu(B13) site, give spectra in which the C-2 proton resonances of His(B10) are shifted upfield relative to metal-free insulin. Spectra of insulin solutions (3-20 mg/mL) containing a ratio of In:Zn2+ = 6:2 in the pH* region from 8.6 to 10 were found to contain signals both from metal-free insulin species and from the 2Zn-insulin hexamer, (In)6(Zn2+)2. The addition of either Ca2+ (in the ratio In:Zn2+:Ca2+ = 6:2:1) or 40 mM NaSCN was found to provide sufficient additional thermodynamic drive to bring about the nearly complete assembly of insulin hexamers. Cd2+ in the ratio In:Cd2+ = 6:3 also drives hexamer assembly to completion. We postulate that the additional thermodynamic drive provide by Ca2+ and CD2+ is due to coordination of these metal ions to the Glu(B13) carboxylates of the hexamer. At high pH*, this coordination neutralizes the repulsive Coulombic interactions between the six Glu(B13) carboxylates and forms metal ion "cross-links" across the dimer-dimer interfaces. Comparison of the aromatic regions of the 1H NMR spectra for (In)6(Zn2+)2 with (In)6(Zn2+)2Ca2+, (In)6(Cd2+)2Cd2+, and (In)6(Cd2+)2Ca2+ indicates that binding of either Ca2+ or Cd2+ to the Glu(B13) site induces a conformation change that perturbs the environments of the side chains of several of the aromatic residues in the insulin structure. Since these residues lie on the monomer-monomer and dimer-dimer subunit interfaces, we conclude that the conformation change includes small changes in the subunit interfaces that alter the microenvironments of the aromatic rings.
Textile Finishing Chemicals: An Industrial Guide (1991)

More than 3,150 textile finishing chemicals currently available for industrial use are described. The information, taken from manufacturers' descriptions, includes company name, product category, trade name, product number, and product descriptions. Product descriptions include properties and applications. The table of contents is organized to serve as a subject index. Also included are a chemical name index, a trade name index, and a section containing suppliers' addresses.
Inflammasome Activation of IL-18 Results in Endothelial Progenitor Cell Dysfunction in Systemic Lupus Erythematosus (2011)

Systemic lupus erythematosus (SLE) is an autoimmune disease with heterogeneous manifestations including severe organ damage and vascular dysfunction leading to premature atherosclerosis. IFN-α has been proposed to have an important role in the development of lupus and lupus-related cardiovascular disease, partly by repression of IL-1 pathways leading to impairments in vascular repair induced by endothelial progenitor cells (EPCs) and circulating angiogenic cells (CACs). Counterintuitively, SLE patients also display transcriptional upregulation of the IL-1β/IL-18 processing machinery, the inflammasome. To understand this dichotomy and its impact on SLE-related cardiovascular disease, we examined cultures of human and murine control or lupus EPC/CACs to determine the role of the inflammasome in endothelial differentiation. We show that caspase-1 inhibition improves dysfunctional SLE EPC/CAC differentiation into mature endothelial cells and blocks IFN-α-mediated repression of this differentiation, implicating inflammasome activation as a crucial downstream pathway leading to aberrant vasculogenesis. Furthermore, serum IL-18 levels are elevated in SLE and correlate with EPC/CAC dysfunction. Exogenous IL-18 inhibits endothelial differentiation in control EPC/CACs and neutralization of IL-18 in SLE EPC/CAC cultures restores their capacity to differentiate into mature endothelial cells, supporting a deleterious effect of IL-18 on vascular repair in vivo. Upregulation of the inflammasome machinery was operational in vivo, as evidenced by gene array analysis of lupus nephritis biopsies. Thus, the effects of IFN-α are complex and contribute to an elevated risk of cardiovascular disease by suppression of IL-1β pathways and by upregulation of the inflammasome machinery and potentiation of IL-18 activation.
Recent Advances in Matrix Metalloproteinase Inhibitors Research (1999)

Excess MMP proteolytic activity has been associated with a wide variety of pathological conditions such as arthritis, cancer and heart failure. The potential utility of MMP inhibitors as therapeutic interventions in these diverse and important disease states has led to an intense effort toward the development of such inhibitors. The first generation of compounds were peptide-like broad spectrum inhibitors, active against a broad range of MMPs. However, the induction of musculoskeletal side effects seen in clinical trials with these agents has emphasized the need for a better understanding of the role that each of the MMPs plays in normal tissue turnover and disease progression. Advances in our ability to engineer and synthesize selective inhibitors as well as the discovery of small molecule, non-peptidic inhibitors has spurred an intense effort to identify potent and bioavailable second generation compounds. There are now several such compounds targeted against various subsets of the MMPs in clinical development. This review will focus on the design and structure activity relationships of these second generation compounds.
Statistical Theory and Modeling for Turbulent Flows (2010)

Providing a comprehensive grounding in the subject of turbulence, â€œStatistical Theory and Modeling for Turbulent Flowsâ€ develops both the physical insight and the mathematical framework needed to understand turbulent flow. Its scope enables the reader to become a knowledgeable user of turbulence models; it develops analytical tools for developers of predictive tools. Thoroughly revised and updated, this second edition includes a new fourth section covering DNS (direct numerical simulation), LES (large eddy simulation), DES (detached eddy simulation) and numerical aspects of eddy resolving
Prevention of Angiotensin II–Mediated Renal Oxidative Stress, Inflammation, and Fibrosis by Angiotensin-Converting Enzyme 2 (2010)

Angiotensin-converting enzyme 2 (ACE2) is a monocarboxypeptidase capable of metabolizing angiotensin (Ang) II into Ang 1 to 7. We hypothesized that ACE2 is a negative regulator of Ang II signaling and its adverse effects on the kidneys. Ang II infusion (1.5 mg/kg⁻¹/d⁻¹) for 4 days resulted in higher renal Ang II levels and increased nicotinamide adenine dinucleotide phosphate oxidase activity in ACE2 knockout (Ace2(-/y)) mice compared to wild-type mice. Expression of proinflammatory cytokines, interleukin-1β and chemokine (C-C motif) ligand 5, were increased in association with greater activation of extracellular-regulated kinase 1/2 and increase of protein kinase C-α levels. These changes were associated with increased expression of fibrosis-associated genes (α-smooth muscle actin, transforming growth factor-β, procollagen type Iα1) and increased protein levels of collagen I with histological evidence of increased tubulointerstitial fibrosis. Ang II-infused wild-type mice were then treated with recombinant human ACE2 (2 mg/kg⁻¹/d⁻¹, intraperitoneal). Daily treatment with recombinant human ACE2 reduced Ang II-induced pressor response and normalized renal Ang II levels and oxidative stress. These changes were associated with a suppression of Ang II-mediated activation of extracellular-regulated kinase 1/2 and protein kinase C pathway and Ang II-mediated renal fibrosis and T-lymphocyte-mediated inflammation. We conclude that loss of ACE2 enhances renal Ang II levels and Ang II-induced renal oxidative stress, resulting in greater renal injury, whereas recombinant human ACE2 prevents Ang II-induced hypertension, renal oxidative stress, and tubulointerstitial fibrosis. ACE2 is an important negative regulator of Ang II-induced renal disease and enhancing ACE2 action may have therapeutic potential for patients with kidney disease.
Constructing, organizing, and visualizing collections of topically related Web resources (1999)

For many purposes, the Web page is too small a unit of interaction and analysis. Web sites are structured multimedia documents consisting of many pages, and users often are interested in obtaining and evaluating entire collections of topically related sites. Once such a collection is obtained, users face the challenge of exploring, comprehending and organizing the items. We report four innovations that address these user needs: (1) we replaced the Web page with the Web site as the basic unit of interaction and analysis;(2) we defined a new informationstructure, the clan graph , that groups together sets of related sites; (3) we augment the representation of a site with a site profile , information about site structure and content that helps inform user evaluation of a site; and (4) we invented a new graph visualization, the auditorium visualization , that reveals important structural and content properties of sites within a clan graph. Detailed analysis and user studies document the utility of this approach. The clan graph construction algorithm tends to filter out irrelevant sites and discover additional relevant items. The auditorium visualization, augmented with drill-down capabilities to explore site profile data, helps users to find high-quality sites as well as sites that serve a particular function.
HRTF selection for binaural synthesis from a database using morphological parameters. (2010)

International audience
The Synthesis of the Three Isomeric dl-β-Pyridylalanines (1942)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTThe Synthesis of the Three Isomeric dl-β-PyridylalaninesCarl Niemann, Richard N. Lewis, and John T. HaysCite this: J. Am. Chem. Soc. 1942, 64, 7, 1678–1682Publication Date (Print):July 1, 1942Publication History Published online1 May 2002Published inissue 1 July 1942https://pubs.acs.org/doi/10.1021/ja01259a059https://doi.org/10.1021/ja01259a059research-articleACS PublicationsRequest reuse permissionsArticle Views238Altmetric-Citations30LEARN 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
Effect of brain edema on infarct volume in a focal cerebral ischemia model in rats. (1993)

Traditional direct measurement of infarct volume is associated with an overestimation of infarct volume during the development of brain edema in the first 3 days after ischemia. This artifact can be reduced with indirect measurement, which is based on noninfarcted cortex volume.