gebhart/patrepeval huggingface dataset:
Isolation, characterization, and identification of two methomyl-degrading bacteria from a pesticide-treated crop field in West Bengal, India (2017)

Two methomyl-degrading bacteria (initially named Disha A and Disha B) were isolated from a pesticide-treated crop field in Baruipur, 24 Parganas (South), West Bengal, India. Both strains could not grow in mineral salt (MS) medium but showed efficient growth in the presence of methomyl. The highest growth was observed in the MS medium containing 0.16% methomyl. When methomyl was supplemented with glucose, no further enhancement of growth was observed, whereas supplementation with yeast extract had a positive effect on growth of both strains, indicating that methomyl could be utilized as the sole source of carbon but not that of nitrogen. In Nutrient Broth and Luria Bertani medium, these strains could tolerate 0.4% methomyl. Optimum pH and temperature for growth of both bacteria in the methomyl-containing MS medium were 7.0 and 30°C, respectively. Protein concentration in the cell-free extracts of bacterial cultures was directly proportional to methomyl concentration in the medium. Disha A was more resistant to the antibiotics amoxicillin and penicillin, as indicated by minimum inhibitory concentration (600 and 500 μg/mL, respectively), which were higher than those obtained for Disha B (350 and 300 μg/mL, respectively). Both Disha A and Disha B were plasmid-bearing, gram-positive, endospore-producing, rod-shaped bacteria. Biochemical studies, 16S rDNA sequencing, and phylogenetic analysis indicated maximum similarity of Disha A to Bacillus cereus ATCC 14579, whereas Disha B showed maximum similarity to Bacillus safensis F0-36b ATCC BAA-1126. The HPLC analysis clearly indicated that B. cereus and B. safensis showed 88.25 and 77.5% of methomyl (Sigma) degradation, respectively within 96 h of growth. This is the first report of Bacillus species that can degrade the carbamate pesticide methomyl and thrive in presence of its high concentrations.
High‐Throughput Dip‐Pen‐Nanolithography‐Based Fabrication of Si Nanostructures (2006)

Si nanostructures: A new method for fabricating large-area Si nanostructures in a high-throughput fashion has been demonstrated. The procedure is based upon dip-pen nanolithography in combination with wet-chemical etching and reactive ion etching. Multipen techniques have been demonstrated for the fabrication of large-area Si nanostructure arrays (see AFM image; dot 1: diameter/height=1460/140 nm; dot 9: diameter/height=385/75 nm).
LR11/SorLA Expression Is Reduced in Sporadic Alzheimer Disease but not in Familial Alzheimer Disease (2006)

LR11 is an ApoE receptor that is enriched in the brain. We have shown that LR11 is markedly downregulated in patients with sporadic Alzheimer disease (AD). This finding led us to explore whether reduced LR11 expression reflects a primary mechanism of disease or merely a secondary consequence of other AD-associated changes. Therefore, LR11 expression was assessed in a transgenic mouse model of AD and familial AD (FAD) brains. Immunohistochemistry and immunoblotting of LR11 in PS1/APP transgenic and wild-type mice indicated that LR11 levels are not affected by genotype or accumulation of amyloid pathology. LR11 expression was also evaluated based on immunoblotting and LR11 immunostaining intensity in human frontal cortex in controls, sporadic AD, and FAD, including cases with presenilin-1 (PS1) and presenilin-2 (PS2) mutations. Although LR11 was reduced in sporadic AD, there was no difference in protein level or staining intensity between control and FAD cases. The finding that LR11 expression is unaffected in both a mouse model of AD and autosomal-dominant forms of AD suggests that LR11 is not regulated by amyloid accumulation or other AD neuropathologic changes. We hypothesize that LR11 loss may be specific to sporadic AD and influence amyloid pathology through mechanisms independent of substrate-enzyme interactions regulated by FAD mutations.
Effects of continuous positive airway pressure on lung function in patients with chronic obstructive pulmonary disease and sleep disordered breathing (1999)

Improvements in gas exchange, airflow obstruction and hospitalization rates were observed in patients with COPD and SDB treated with nasal CPAP during sleep.
[Use of "TVT" in surgery for female urinary incontinence]. (2000)

The TVT procedure (tension-free vaginal tape) was described by U. Ulmsten (Sweden) in 1996. This new procedures questions the numerous procedures proposed for female stress urinary incontinence (SUI). The mesh is placed under the urethra (and not under the bladder neck) and cures SUI without important voiding difficulties. Use of this operation is growing fast in Europe and Australia and is beginning to be used in the USA. TTV is a minimally invasive technique using local or spinal anesthesia applicable as an ambulatory procedure. Peroperative complications are limited to bladder perforation (without detrimental consequences) and bleeding. Postoperative complications are very rare. Local tolerance of the prolene mesh is excellent. Failure rates have been very low, about 6% for SUI and more controversial for unstable bladder. Since January 1997, we have performed about 400 TVT either as single procedures or in association with prolapsus cure. After 1 to 3 years follow-up, cure rate in the first 156 SUI patients was 89.1%, almost the same with or without associated procedures. For the 36 patients with an urethral closure pressure less than 30 cm H(2)O, cure rate was 75%. In cases of mixed incontinence, the cure rate varied from 57.9% (associated procedures to 61.3% (single procedures). The rate of de novo instability was less than 4.6%. Induced and increased voiding difficulties (5.7% and 6% respectively) remained at a relatively low level provided the strict operative protocol was used. The TVT procedure is easy to perform, relatively harmless, reproducible and very efficient even for patients with risk factors, sphincteric weakness, previous operations or an associated prolapsus cure procedure.
Quo Vadis, Action Recognition? A New Model and the Kinetics Dataset (2017)

The paucity of videos in current action classification datasets (UCF-101 and HMDB-51) has made it difficult to identify good video architectures, as most methods obtain similar performance on existing small-scale benchmarks. This paper re-evaluates state-of-the-art architectures in light of the new Kinetics Human Action Video dataset. Kinetics has two orders of magnitude more data, with 400 human action classes and over 400 clips per class, and is collected from realistic, challenging YouTube videos. We provide an analysis on how current architectures fare on the task of action classification on this dataset and how much performance improves on the smaller benchmark datasets after pre-training on Kinetics. We also introduce a new Two-Stream Inflated 3D ConvNet (I3D) that is based on 2D ConvNet inflation: filters and pooling kernels of very deep image classification ConvNets are expanded into 3D, making it possible to learn seamless spatio-temporal feature extractors from video while leveraging successful ImageNet architecture designs and even their parameters. We show that, after pre-training on Kinetics, I3D models considerably improve upon the state-of-the-art in action classification, reaching 80.2% on HMDB-51 and 97.9% on UCF-101.
Myeloid-Derived Suppressor Cells Inhibit T-Cell Activation by Depleting Cystine and Cysteine (2009)

Myeloid-derived suppressor cells (MDSC) are present in most cancer patients and are potent inhibitors of T-cell-mediated antitumor immunity. Their inhibitory activity is attributed to production of arginase, reactive oxygen species, inducible nitric oxide synthase, and interleukin-10. Here we show that MDSCs also block T-cell activation by sequestering cystine and limiting the availability of cysteine. Cysteine is an essential amino acid for T-cell activation because T cells lack cystathionase, which converts methionine to cysteine, and because they do not have an intact xc- transporter and therefore cannot import cystine and reduce it intracellularly to cysteine. T cells depend on antigen-presenting cells (APC), such as macrophages and dendritic cells, to export cysteine, which is imported by T cells via their ASC neutral amino acid transporter. MDSCs express the xc- transporter and import cystine; however, they do not express the ASC transporter and do not export cysteine. MDSCs compete with APC for extracellular cystine, and in the presence of MDSCs, APC release of cysteine is reduced, thereby limiting the extracellular pool of cysteine. In summary, MDSCs consume cystine and do not return cysteine to their microenvironment, thereby depriving T cells of the cysteine they require for activation and function.
ChemInform Abstract: ADDITION REACTIONS OF HETEROCYCLIC COMPOUNDS. PART 79. REACTION OF DIMETHYL ACETYLENEDICARBOXYLATE WITH SOME CYCLOHEPT(B)INDOLES AND CYCLOOCT(B)INDOLES (1983)

Abstract Umsetzung der Heterocyclen (I) mit dem Titel‐Diester (II) führt zu einer Reihe neuartiger Addukte, z.B. (III)+(IV) bzw. (V) + (VI) bzw. (VII) [in wäßriger Essigsäure entstehen aus (Ic), (Id) zusätzlich die (IV)‐Analogen (VIII); in Acetonitril/HzO entstehen aus (Ic), (Id) zusätzlich (Vc) bzw. (Vd)] bzw. (IX), (X) und (XI).
Location of the epidermal growth factor binding site on the EGF receptor. A resonance energy transfer study (1990)

As a first step toward developing a structural map of key sites on the epidermal growth factor (EGF) receptor, we have used resonance energy transfer to measure the distance of closest approach between the receptor-bound growth factor molecule and lipid molecules at the surface of the plasma membrane. EGF, specifically labeled at its amino terminus with fluorescein 5-isothiocyanate, was used as an energy donor in these experiments, while either octadecylrhodamine B or octadecylrhodamine 101, inserted into plasma membranes isolated from human epidermoid carcinoma (A431) cells, served as the energy acceptors. The energy transfer measurements indicate that the amino terminus of the bound growth factor is about 67 A away from the plasma membrane. On the basis of the dimensions of the EGF molecule, this suggests that EGF binds to a site on its receptor that is a considerable distance (52-82 A) from the surface of these cells. Identical results were obtained under conditions where the receptor functions as an active tyrosine kinase, suggesting that the relative juxtaposition of the EGF binding domain to the membrane surface does not change with receptor autophosphorylation or with the activation of the receptor tyrosine kinase activity.
Hepatocyte Immobilization on Phema Microcarriers and its Biologically Modified Forms (1992)

Polyhydroxyethylmethacrylate (PHEMA) based microcarriers with different bulk structures were prepared by a phase inversion polymerization technique. PHEMA surfaces were further modified chemically by glow-discharge treatment, and biologically by covalent attachment of fibrinogen and collagen. Hepatocytes were isolated from young male Wistar rats using an in situ portal vein collagenase perfusion technique. Freshly isolated hepatocytes were seeded at 6 x 10(5) cells/mL and microcarrier concentration was 10 g/L. Stationary microcarrier cultures were carried out in standard (nontissue culture) polystyrene petri dishes in a humidified 5% CO2 incubator at 37 +/- 0.5 degrees C. Cell attachment was followed by light microscopy by taking samples from the culture medium every 30 min. Urea and protein syntheses by microcarrier-attached hepatocytes were determined by standard techniques. Nonswellable (highly cross-linked) hydrophilic PHEMA microcarriers did not support cell attachment and viability. However, swellable (low cross-linked) PHEMA microcarriers (pretreated in FBS) allowed high attachment and cell spreading. PHEMA microcarriers treated in dimethylaminoethylmethacrylate (DMAEMA) glow-discharge plasma also improved the cell attachment characteristics of the PHEMA microcarriers. The highest attachment efficiencies (immobilization yields) were observed with the biologically modified PHEMA microcarriers, especially modified with fibronectin. Metabolic activity, as estimated by urea and protein syntheses, was also higher in these microcarriers.
Diagnosis of Chlamydia trachomatis cervical infection by detection of amplified DNA with an enzyme immunoassay (1990)

A sensitive and specific system for detection of amplified Chlamydia trachomatis DNA from cervical specimens by fluorometric quantitation in an enzyme immunoassay (EIA) format (polymerase chain reaction [PCR]-EIA) is described. The primers selected for PCR-amplified DNA were from the 15 serovars of C. trachomatis and two strains of Chlamydia pneumoniae (TWAR). One strain of Chlamydia psittaci (Borg) was not amplified. One hundred four previously cultured cervical specimens were evaluated. Forty-six culture-positive specimens containing from 1+ to 4+ inclusion bodies were all positive by PCR-EIA. Of 58 culture-negative specimens, 2 were repeatedly positive and were nonreactive with control probes. This assay system represents a sensitive and specific combination of technologies for the quantitative detection of C. trachomatis DNA directly from a body fluid.
Noninvasive measurement of anatomic structure and intraluminal oxygenation in the gastrointestinal tract of living mice with spatial and spectral EPR imaging (1999)

EPR imaging has emerged as an important tool for noninvasive three-dimensional (3D) spatial mapping of free radicals in biological tissues. Spectral-spatial EPR imaging enables mapping of the spectral information at each spatial position, and, from the observed line width, the localized tissue oxygenation can be mapped. We report the development of EPR imaging instrumentation enabling 3D spatial and spectral-spatial EPR imaging of small animals. This instrumentation, along with the use of a biocompatible charcoal oximetry-probe suspension, enabled 3D spatial imaging of the gastrointestinal (GI) tract, along with mapping of oxygenation in living mice. By using these techniques, the oxygen tension was mapped at different levels of the GI tract from the stomach to the rectum. The results clearly show the presence of a marked oxygen gradient from the proximal to the distal GI tract, which decreases after respiratory arrest. This technique for in vivo mapping of oxygenation is a promising method, enabling the noninvasive imaging of oxygen within the normal GI tract. This method should be useful in determining the alterations in oxygenation associated with disease.
Galectin-3 Marks Activated Macrophages in Failure-Prone Hypertrophied Hearts and Contributes to Cardiac Dysfunction (2004)

This study shows that an early increase in galectin-3 expression identifies failure-prone hypertrophied hearts. Galectin-3, a macrophage-derived mediator, induces cardiac fibroblast proliferation, collagen deposition, and ventricular dysfunction. This implies that HF therapy aimed at inflammatory responses may need to be targeted at the early stages of HF and probably needs to antagonize multiple inflammatory mediators, including galectin-3.
Tolerance induction using the Malmö treatment model 1982–1995 (1999)

The ultimate goal in the treatment of haemophilia patients with inhibitors is to eradicate permanently the inhibitor and induce tolerance. Here we summarize our experience at the Malmö centre regarding tolerance induction according to the Malmö Treatment Model. The protocol includes immunoadsorption if needed, neutralization of inhibitor and replacement with factor concentrates, cyclophosphamide intravenously for 2 days (12-15 mg kg-1 bw) and then orally (2-3 mg kg-1 bw) for an additional 8-10 days and intravenous gammaglobulin daily at dosages of 0.4 g kg-1 bw for 5 days. This protocol has been applied in 23 haemophilia patients with inhibitors, 16 haemophilia A patients and seven haemophilia B patients. Altogether 36 attempts have been made to induce tolerance. Ten of the 16 haemophilia A (62.5%) and 6/7 patients with haemophilia B (86%) became tolerant after the treatment. The chances of success or failure are roughly equal, if the series is considered in a historical perspective. The data showed that the chances of success in tolerance induction with the Malmö protocol were best in those patients with low inhibitor titres, with relatively low historical inhibitory peak and with a long interval since the previous replacement therapy. This was especially true where no inflammatory state was present at the start or during tolerance induction. The advantage with this method compared to the high-dose regimen is that in the successful cases tolerance can be achieved within 3-4 weeks.
Control of PKR Protein Kinase by Hepatitis C Virus Nonstructural 5A Protein: Molecular Mechanisms of Kinase Regulation (1998)

The PKR protein kinase is a critical component of the cellular antiviral and antiproliferative responses induced by interferons. Recent evidence indicates that the nonstructural 5A (NS5A) protein of hepatitis C virus (HCV) can repress PKR function in vivo, possibly allowing HCV to escape the antiviral effects of interferon. NS5A presents a unique tool by which to study the molecular mechanisms of PKR regulation in that mutations within a region of NS5A, termed the interferon sensitivity-determining region (ISDR), are associated with sensitivity of HCV to the antiviral effects of interferon. In this study, we investigated the mechanisms of NS5A-mediated PKR regulation and the effect of ISDR mutations on this regulatory process. We observed that the NS5A ISDR, though necessary, was not sufficient for PKR interactions; we found that an additional 26 amino acids (aa) carboxyl to the ISDR were required for NS5A-PKR complex formation. Conversely, we localized NS5A binding to within PKR aa 244 to 296, recently recognized as a PKR dimerization domain. Consistent with this observation, we found that NS5A from interferon-resistant HCV genotype 1b disrupted kinase dimerization in vivo. NS5A-mediated disruption of PKR dimerization resulted in repression of PKR function and inhibition of PKR-mediated eIF-2alpha phosphorylation. Introduction of multiple ISDR mutations abrogated the ability of NS5A to bind to PKR in mammalian cells and to inhibit PKR in a yeast functional assay. These results indicate that mutations within the PKR-binding region of NS5A, including those within the ISDR, can disrupt the NS5A-PKR interaction, possibly rendering HCV sensitive to the antiviral effects of interferon. We propose a model of PKR regulation by NS5A which may have implications for therapeutic strategies against HCV.
The effective advertiser (1993)

Fun - a serious business Where advertising fits into business Why advertise? Why advertising? Identifying your market What does your market think? What's the message? Setting the objectives The right Investment Making the most of an agency Effective briefing Creative PITCHES Reaching the audience Assessing the proposals Research and advertising Approvals, production and control Your action plan.
Effects of hydrophobic surface on skin-friction drag (2004)

Effects of hydrophobic surface on skin-friction drag are investigated through direct numerical simulations of a turbulent channel flow. Hydrophobic surface is represented by a slip-boundary condition on the surface. When a slip-boundary condition is used in the streamwise direction, the skin-friction drag decreases and turbulence intensities and turbulence structures, near-wall streamwise vortices in particular, are significantly weakened. When a slip-boundary condition is used in the spanwise direction, on the other hand, the drag is increased. It is found that near-wall turbulence structures are modified differently, resulting in drag increase. It is also found that the slip length must be greater than a certain value in order to have a noticeable effect on turbulence. An important implication of the present finding is that drag reduction in turbulent boundary layers is unlikely with hydrophobic surface with its slip length on the order of a submicron scale.
Serotherapy of B-cell neoplasms with anti-B4-blocked ricin: a phase I trial of daily bolus infusion (1992)

Anti-B4-blocked Ricin (Anti-B4-bR) is an immunotoxin comprised of the anti-B4 monoclonal antibody (MoAb) and the protein toxin “blocked ricin.” The anti-B4 MoAb is directed against the B-lineage-restricted CD19 antigen expressed on more than 95% of normal and neoplastic B cells. Blocked ricin is an altered ricin derivative that has its nonspecific binding eliminated by chemically blocking the galactose binding domains of the B chain. In vitro cytotoxicity studies demonstrate that the IC37 of Anti-B4-bR is 2 x 10(-11) mol/L compared with 4 x 10(-12) mol/L for native ricin. A phase I dose escalation clinical trial was conducted in 25 patients with refractory B-cell malignancies. Anti-B4-bR was administered by daily 1-hour bolus infusion for 5 consecutive days at doses ranging from 1 microgram/kg/d to 60 micrograms/kg/d. Serum levels above 1 nmol/L were achieved transiently in the majority of patients treated at the maximum tolerated dose of 50 micrograms/kg/d for 5 days for a total dose of 250 micrograms/kg. The dose-limiting toxicity was defined by transient, reversible grade 3 elevations in hepatic transaminases, without impaired hepatic synthetic function. Minor toxicities included transient hypoalbuminemia, thrombocytopenia, and fevers. Human antimouse antibody and human anti-ricin antibody were detected in nine patients. One complete response, two partial responses, and eight mixed or transient responses were observed. These results show the in vitro and in vivo cytotoxicity of Anti-B4-bR and indicate that this immunotoxin can be administered as a daily bolus infusion for 5 days with tolerable, reversible toxicity.
Upregulation of caveolin‐1 and caveolae organelles in Taxol‐resistant A549 cells (1998)

Caveolin is a principal component of caveolae membranes. It has been demonstrated that the interaction of the caveolin scaffolding domain with signaling molecules can functionally inhibit the activity of these molecules. Taxol is an antitumor agent that suppresses microtubule dynamics and binds to microtubules thereby stabilizing them against depolymerization. The drug also has been implicated in the induction of apoptosis through activation of components in signal transduction cascades. Here we have investigated the role of caveolin in the development of drug resistance by examining the expression of caveolins in low- and high-level drug-resistant cell lines. Caveolin-1, but not caveolin-2, was upregulated in highly multidrug resistant SKVLBI cells that express high levels of P-glycoprotein, and in low-level Taxol-resistant A549 cell lines that express low amounts of P-glycoprotein. Two drug-resistant A549 cell lines (one 9-fold resistant to Taxol and the other 1.5-fold resistant to epothilone B), both of which express no P-glycoprotein, demonstrate a significant increase in the expression of caveolin-1. These results indicate that in low-level epothilone B- or Taxol-resistant A549 cells, increased caveolin-1 expression occurs independently of P-glycoprotein expression. Electron microscopic studies clearly demonstrate the upregulation of caveolae organelles in Taxol-resistant A549 cells. Upregulation of caveolin-1 expression in drug-sensitive A549 cells was observed acutely beginning 48 h after incubation with 10 nM Taxol. Thus, caveolin-1 may play a role in the development of Taxol resistance in A549 cells.