gebhart/patrepeval huggingface dataset:
DNA-Based Diagnostic Approaches for Identification of Burkholderia cepacia Complex, Burkholderia vietnamiensis, Burkholderia multivorans,Burkholderia stabilis, and Burkholderia cepacia Genomovars I and III (2000)

Bacteria of the Burkholderia cepacia complex consist of five discrete genomic species, including genomovars I and III and three new species: Burkholderia multivorans (formerly genomovar II), Burkholderia stabilis (formerly genomovar IV), and Burkholderia vietnamiensis (formerly genomovar V). Strains of all five genomovars are capable of causing opportunistic human infection, and microbiological identification of these closely related species is difficult. The 16S rRNA gene (16S rDNA) and recA gene of these bacteria were examined in order to develop rapid tests for genomovar identification. Restriction fragment length polymorphism (RFLP) analysis of PCR-amplified 16S rDNA revealed sequence polymorphisms capable of identifying B. multivorans and B. vietnamiensis but insufficient to discriminate strains of B. cepacia genomovars I and III and B. stabilis. RFLP analysis of PCR-amplified recA demonstrated sufficient nucleotide sequence variation to enable separation of strains of all five B. cepacia complex genomovars. Complete recA nucleotide sequences were obtained for 20 strains representative of the diversity of the B. cepacia complex. Construction of a recA phylogenetic tree identified six distinct clusters (recA groups): B. multivorans, B. vietnamiensis, B. stabilis, genomovar I, and the subdivision of genomovar III isolates into two recA groups, III-A and III-B. Alignment of recA sequences enabled the design of PCR primers for the specific detection of each of the six latter recA groups. The recA gene was found on the largest chromosome within the genome of B. cepacia complex strains and, in contrast to the findings of a previous study, only a single copy of the gene was present. In conclusion, analysis of the recA gene of the B. cepacia complex provides a rapid and robust nucleotide sequence-based approach to identify and classify this taxonomically complex group of opportunistic pathogens.
Visibility enhancement for silicon debug (2006)

Several emerging design-for-debug (DFD) methodologies are addressing silicon debug by making internal signal values and other data observable. Most of these methodologies require the instrumentation of on-chip logic for extracting the internal register data from in situ silicon. Unfortunately, lack of visibility of the combinational network values impedes the ability to functionally debug the silicon part. Visibility enhancement techniques enable the virtual observation of combinational nodes with minimal computational overhead. These techniques also cover the register selection analysis for DFD and multi-level design abstraction correlation for viewing values at the register transfer level (RTL). Experimental results show that visibility enhancement techniques can leverage a small amount of extracted data to provide a high amount of computed combinational signal data. Visibility enhancement provides the needed connection between data obtained from the DFD logic and HDL simulation-related debug systems.
Native mRNA antisense-accessible sites library for the selection of antisense oligonucleotides, PNAs, and siRNAs (2010)

A procedure for rapidly generating a library of antisense-accessible sites on native mRNAs (mRNA antisense-accessible sites library [MASL]) is described that involves reverse transcription of whole cell mRNA extracts with a random oligodeoxynucleotide primer followed by mRNA-specific polymerase chain reaction (PCR). Antisense phosphorothioate oligodeoxynucleotides (ODNs), peptide nucleic acids (PNAs), and small interfering RNAs (siRNAs) can then be identified by screening against the antisense-accessible sites. The utility of this methodology is demonstrated for the identification of more effective inhibitors of inducible nitric oxide synthase (iNOS) induction than have previously been reported. This method may also be useful for constraining folding calculations of native mRNAs and for designing mRNA imaging probes.
The Use of N,N-Dimethylformamide–Sulfonyl Chloride Complex for the Preparation of Thiophenesulfonyl Chlorides (1985)

Abstract A 1:1 N,N-dimethylformamide–SO2Cl2 complex was found to be a useful agent for the one-step preparation of thiophenesulfonyl chlorides.
Botulinum toxin: Influence on respiratory heart rate variation (1995)

Remote adverse effects of local intramuscular botulinum toxin were investigated in a prospective follow-up study. Twenty-six patients with spasmodic torticollis were examined (18 women, eight men, 45 +/- 13 years). Respiratory heart rate variation (HRV) was investigated by a computerized method. Different parameters were recorded (beats per minute, coefficient of variation, root mean square successive difference (RMSSD), spectral analysis, difference and quotient between maximum and minimum RR intervals, mean circular resultant). After one intramuscular injection of 12.5 ng botulinum toxin (Porton Products Ltd., England), no significant influence on HRV was seen. After the second injection, a significant attenuation was seen of four parameters (coefficient of variation, Rmax - Rmin, Rmax divided by Rmin, mean circular resultant) that lasted up to several months. No clinically manifest remote side effects and no cardiac arrhythmia were seen for several months of botulinum toxin treatment. Our investigation proves an effect of local intramuscular botulinum toxin on autonomic cardiac innervation.
Targeted Inhibition of the Complement Alternative Pathway with Complement Receptor 2 and Factor H Attenuates Collagen Antibody-Induced Arthritis in Mice (2009)

The alternative pathway (AP) of complement is required for the induction of collagen Ab-induced arthritis (CAIA) in mice. The objective of this study was to examine the effect of a recombinant AP inhibitor containing complement receptor 2 and factor H (CR2-fH) on CAIA in mice. CR2 binds to tissue-fixed activation fragments of C3, and the linked fH is a potent local inhibitor of the AP. CAIA was induced in C57BL/6 mice by i.p. injections of 4 mAb to type II collagen (CII) on day 0 and LPS on day 3. PBS or CR2-fH (250 or 500 microg) were injected i.p. 15 min after the mAb to CII on day 0 and 15 min after LPS on day 3; the mice were sacrificed on day 10. The disease activity score (DAS) was decreased significantly (p < 0.001) in both groups receiving CR2-fH compared with the PBS. Histology scores for inflammation, pannus, bone damage, and cartilage damage decreased in parallel with the DAS. C3 deposition in the synovium and cartilage was significantly reduced (p < 0.0001) in the mice treated with CR2-fH. In vitro studies with immune complexes containing type II collagen and mAb to CII showed that CR2-fH specifically inhibited the AP with minimal effect on the classical pathway (CP) and no effect on the lectin pathway (LP). The relative potency of CR2-fH in vitro was superior to mAbs to factor B and C5. Thus, CR2-fH specifically targets and inhibits the AP of complement in vitro and is effective in CAIA in vivo.
Detection of methicillin and mupirocin resistance in Staphylococcus aureus isolates using conventional and molecular methods: a descriptive study from a burns unit with high prevalence of MRSA (2002)

The specificity of routine laboratory tests for MRSA detection was variable. mecA gene detection, the "gold standard" to confirm ambiguous results, is difficult to perform in routine diagnostic laboratories. The Mastalex kit for the detection of PBP2a is an alternative that could be used in most laboratories. High level mupirocin resistance can be confirmed with genotypic methods.
Can the effects of vasoactivity of molecular hemoglobin-based plasma expanders be ignored?* (2006)

University of California, San Diego, La Jolla, CA, La Jolla Institute of Bioengineering, La Jolla, CA
Q1311X: a novel nonsense mutation of putative ancient origin in the von Willebrand factor gene (2000)

Type 3 von Willebrand disease, a recessive autosomally inherited bleeding disorder, refers to complete deficiency of von Willebrand factor (VWF). The novel Q1311X mutation was detected in the homozygous state in four Spanish patients from two apparently unrelated families of gypsy origin. The lack of specific amplification of platelet VWF cDNA from two of the patients indicates reduced levels of mutated gene expression. The similar haplotype linked to mutated alleles suggests a common origin. On the basis of the two instabilities observed and the estimated mutation rate of the microsatellites of intron 40 of the VWF gene, we can estimate that this mutation could have arisen about 2300 years ago.
Concurrent file reorganization for record clustering: a performance study (2003)

The authors presents performance analysis of a concurrent file reorganization algorithm. They examined the effect of buffer size, degree of reorganization, and write probability of transactions on system throughput. The problem of file reorganization considered involves altering the placement of records on pages on a secondary storage device. This reorganization must be done in-place. The approach is appropriate for a non-in-place reorganization. The motivation for such a physical change is to improve the database system's performance, by minimizing the number of page accesses made in answering a set of queries. It is shown through simulation that the algorithm, when run concurrently with user transactions, provides an acceptable level of overall database system performance. >
Budding and fission yeast casein kinase I isoforms have dual-specificity protein kinase activity. (1994)

We have examined the activity and substrate specificity of the Saccharomyces cerevisiae Hrr25p and the Schizosaccharomyces pombe Hhp1, Hhp2, and Cki1 protein kinase isoforms. These four gene products are isotypes of casein kinase I (CKI), and the sequence of these protein kinases predicts that they are protein serine/threonine kinases. However, each of these four protein kinases, when expressed in Escherichia coli in an active form, was recognized by anti-phosphotyrosine antibodies. Phosphoamino acid analysis of 32P-labeled proteins showed phosphorylation on serine, threonine, and tyrosine residues. The E. coli produced forms of Hhp1, Hhp2, and Cki1 were autophosphorylated on tyrosine, and both Hhp1 and Hhp2 were capable of phosphorylating the tyrosine-protein kinase synthetic peptide substrate polymer poly-E4Y1. Immune complex protein kinases assays from S. pombe cells showed that Hhp1-containing precipitates were associated with a protein-tyrosine kinase activity, and the Hhp1 present in these immunoprecipitates was phosphorylated on tyrosine residues. Although dephosphorylation of Hhp1 and Hhp2 by Ser/Thr phosphatase had little effect on the specific activity, tyrosine dephosphorylation of Hhp1 and Hhp2 caused a 1.8-to 3.1-fold increase in the Km for poly-E4Y1 and casein. These data demonstrate that four different CKI isoforms from two different yeasts are capable of protein-tyrosine kinase activity and encode dual-specificity protein kinases.
Effects of Reverse Transcriptase Inhibitors on Telomere Length and Telomerase Activity in Two Immortalized Human Cell Lines (1996)

The ribonucleoprotein telomerase, a specialized cellular reverse transcriptase, synthesizes one strand of the telomeric DNA of eukaryotes. We analyzed telomere maintenance in two immortalized human cell lines: the B-cell line JY616 and the T-cell line Jurkat E6-1, and determined whether known inhibitors of retroviral reverse transcriptases could perturb telomere lengths and growth rates of these cells in culture. Dideoxyguanosine (ddG) caused reproducible, progressive telomere shortening over several weeks of passaging, after which the telomeres stabilized and remained short. However, the prolonged passaging in ddG caused no observable effects on cell population doubling rates or morphology. Azidothymidine (AZT) caused progressive telomere shortening in some but not all T- and B-cell cultures. Telomerase activity was present in both cell lines and was inhibited in vitro by ddGTP and AZT triphosphate. Prolonged passaging in arabinofuranyl-guanosine, dideoxyinosine (ddI), dideoxyadenosine (ddA), didehydrothymidine (d4T), or phosphonoformic acid (foscarnet) did not cause reproducible telomere shortening or decreased cell growth rates or viabilities. Combining AZT, foscarnet, and/or arabinofuranyl-guanosine with ddG did not significantly augment the effects of ddG alone. Strikingly, with or without inhibitors, telomere lengths were often highly unstable in both cell lines and varied between parallel cell cultures. We propose that telomere lengths in these T- and B-cell lines are determined by both telomerase and telomerase-independent mechanisms.
Differential response to myocardial reperfusion injury in eNOS-deficient mice (2002)

Two strains of endothelial nitric oxide synthase (eNOS)-deficient (-/-) mice have been developed that respond differently to myocardial ischemia-reperfusion (MI/R). We evaluated both strains of eNOS(-/-) mice in an in vivo model of MI/R. Harvard (Har) eNOS(-/-) mice (n = 12) experienced an 84% increase in myocardial necrosis compared with wild-type controls (P < 0.05). University of North Carolina (UNC) eNOS(-/-) (n = 10) exhibited a 52% reduction in myocardial injury versus wild-type controls (P < 0.05). PCR analysis of myocardial inducible NO synthase (iNOS) mRNA levels revealed a significant (P < 0.05) increase in the UNC eNOS(-/-) mice compared with wild-type mice, and there was no significant difference between the Har eNOS(-/-) and wild-type mice. UNC eNOS(-/-) mice treated with an iNOS inhibitor (1400W) exacerbated the extent of myocardial necrosis. When treated with 1400W, Har eNOS(-/-) did not exhibit a significant increase in myocardial necrosis. These data demonstrate that two distinct strains of eNOS(-/-) mice display opposite responses to MI/R. Although the protection seen in the UNC eNOS(-/-) mouse may result from compensatory increases in iNOS, other genes may be involved.
Engineering of a Single Conserved Amino Acid Residue of Herpes Simplex Virus Type 1 Thymidine Kinase Allows a Predominant Shift from Pyrimidine to Purine Nucleoside Phosphorylation (2006)

Studies of herpes simplex virus type 1 (HSV-1) thymidine (dThd) kinase (TK) crystal structures show that purine and pyrimidine bases occupy distinct positions in the active site but approximately the same geometric plane. The presence of a bulky side chain, such as tyrosine at position 167, would not be sterically favorable for pyrimidine or pyrimidine nucleoside analogue binding, whereas purine nucleoside analogues would be less affected because they are located further away from the phenylalanine side chain. Site-directed mutagenesis of the conserved Ala-167 and Ala-168 residues in HSV-1 TK resulted in a wide variety of differential affinities and catalytic activities in the presence of the natural substrate dThd and the purine nucleoside analogue drug ganciclovir (GCV), depending on the nature of the amino acid mutation. A168H- and A167F-mutated HSV-1 TK enzymes turned out to have a virtually complete knock-out of dThd kinase activity (at least approximately 4-5 orders of magnitude lower) presumably due to a steric clash between the mutated amino acid and the dThd ring. In contrast, a full preservation of the GCV (and other purine nucleoside analogues) kinase activity was achieved for A168H TK. The enzyme mutants also markedly lost their binding capacity for dThd and showed a substantially diminished feedback inhibition by thymidine 5'-triphosphate. The side chain size at position 168 seems to play a less important role regarding GCV or dThd selectivity than at position 167. Instead, the nitrogen-containing side chains from A168H and A168K seem necessary for efficient ligand discrimination. This explains why A168H-mutated HSV-1 TK fully preserves its GCV kinase activity (Vmax/Km 4-fold higher than wild-type HSV-1 TK), although still showing a severely compromised dThd kinase activity (Vmax/Km 3-4 orders of magnitude lower than wild-type HSV-1 TK).
Detection of Salmonella typhi by polymerase chain reaction (1996)

A rapid and sensitive method for detection of Salmonella typhi would help in preventing the spread of outbreaks and in clinical diagnosis. In order to develop unique PCR primers to detect Salm. typhi, ribosomal RNA genes from Salm. typhi (Rawlings) were cloned in pUC18. The resulting clone was confirmed by sequencing. The cloned DNA fragment contained the 5S, part of the 23S rRNA genes and the 5S-23S spacer region (EMBL/GenBank accession No. U04734). It was expected that the 5S-23S spacer region is divergent unlike the highly conserved 23S + 5S genes. This was confirmed by comparison with the rRNA gene sequences in the EMBL/GenBank database. A pair of PCR primers specific for Salm. typhi was obtained, based on this spacer region sequence. The specificity of this pair of primers was tested with 54 Salm. typhi strains (of 27 different phage types). All these Salm. typhi strains showed the positive 300 bp PCR product with this pair of primers. Six other Salmonella species as well as six other non-Salmonella bacteria were tested and none showed the 300 bp PCR product. The sensitivity of the detection level was 0.1 pg of pure Salm. typhi genomic DNA, or approximately 40 Salm. typhi cells in a spiked food sample. This pair of primers therefore has the potential for development into a diagnostic tool for the rapid diagnosis of typhoid fever.
Genetic Factors in Type 2 Diabetes (2007)

Type 2 diabetes was once referred to as a “genet-icist’s nightmare ” (1) due to difficulties stemmingfrom the nature of the disease and the strategiesavailable for genetic analysis. Two key genetic approaches previously utilized—linkage analysis and can-didate gene association studies—each have limitations that have been difficult to overcome in the study of type 2 diabetes. Linkage studies have been hampered by difficul-ties in obtaining well-defined pedigrees because of the late onset of the disease, imprecise diagnostic criteria, and genetic heterogeneity. Association studies are limited in scope to the consideration of known genes that have an established biological link to diabetes. One approach to overcome some of these difficulties is to couple genome-wide linkage analysis in genetically isolated populations with high-resolution typing of ge-netic variations across the linkage region. This was shown to be a viable approach for the identification of novel diabetes genes with the discovery of variants in TCF7L2, a gene encoding a ubiquitous transcription factor with no previous functional connection to diabe-tes (2). Importantly, subsequent studies have revealed a previously unknown role for TCF7L2 in pancreatic -cells, with the risk allele leading to altered TCF7L2 expression levels and reduced insulin secretion (3), although the mechanism by which the intronic polymorphism functions is not clear. In this issue of Diabetes, a similar combined genetic linkage–association strategy has identified an association between LPIN2 and insulin sensitivity and BMI (4). Previ-ous genome-wide linkage studies identified a region of chromosome 18p11 linked to type 2 diabetes in popula-
Evolution of Glyphosate-Resistant Crop Technology (2009)

New and improved glyphosate-resistant (GR) crops continue to be rapidly developed. These crops confer greater crop safety to multiple glyphosate applications, higher rates, and wider application timings. Many of these crops will also have glyphosate resistance stacked with traits that confer resistance to herbicides with other modes of actions to expand the utility of existing herbicides and to increase the number of mixture options that can delay the evolution of GR weeds. Some breeding stacks of herbicide resistance traits are currently available, but the trend in the future will be to combine resistance genes in molecular stacks. The first example of such a molecular stack has a new metabolically based mechanism to inactivate glyphosate combined with an active site-based resistance for herbicides that inhibit acetolactate synthase (ALS). This stack confers resistance to glyphosate and all five classes of ALS-inhibiting herbicides. Other molecular stacks will include glyphosate resistance with resistance to auxin herbicides and herbicides that inhibit acetyl coenzyme A carboxylase (ACCase) and 4-hydroxyphenyl pyruvate dioxygenase (HPPD). Scientists are also studying a number of other herbicide resistance transgenes. Some of these new transgenes will be used to make new multiple herbicide-resistant crops that offer growers more herbicide options to meet their changing weed management needs and to help sustain the efficacy of glyphosate.
Macular Edema: Definition and Basic Concepts (2017)

Macular edema is the result of an accumulation of fluid in the retinal layers around the fovea. It contributes to vision loss by altering the functional cell relationship in the retina and promoting an inflammatory reparative response. Macular edema may be intracellular or extracellular. Intracellular accumulation of fluid, also called cytotoxic edema, is an alteration of the cellular ionic distribution. Extracellular accumulation of fluid, which is more frequent and clinically more relevant, is directly associated with an alteration of the blood-retinal barrier (BRB). The following parameters are relevant for clinical evaluation of macular edema: extent of the macular edema (i.e., the area that shows increased retinal thickness); distribution of the edema in the macular area (i.e., focal versus diffuse macular edema); central foveal involvement (central area 500 μm); fluorescein leakage (evidence of alteration of the BRB or ‘open barrier') and intraretinal cysts; signs of ischemia (broken perifoveolar capillary arcade and/or areas of capillary closure); presence or absence of vitreous traction; increase in retinal thickness and cysts in the retina (inner or outer), and chronicity of the edema (i.e., time elapsed since initial diagnosis and response to therapy). It is essential to establish associations and correlations of all the different images obtained, regardless of whether the same or different modalities are used.