gebhart/patrepeval huggingface dataset:
Application of circulation control to advanced subsonic transport aircraft. Part II - Transport application (1994)

An experimental/ analytical research program was undertaken to develop advanced versions of circulation control wing (CCW) airfoils and to address specific issues related to the application of these blown high-lift devices to subsonic transport aircraft. The primary goal was to determine the feasibility and potential of these pneumatic configurations to increase high-lift system performance in the terminal area while reducing system complexity and aircraft noise. A four-phase program was completed, including 1) experimental development and evaluation of advanced CCW high-lift configurations; 2) development of effective pneumatic leading-edge devices; 3) computational evaluation of CCW airfoil designs plus high-lift and cruise capabilities; and 4) the investigation of the terminal-area performance of transport aircraft employing these airfoils. The first three phases were presented in Part I of this article. This segment, Part II, describes the fourth phase of the program. Experimental lift coefficient values approaching 8.0 at zero incidence were demonstrated by two-dimension al CCW configurations and were reported in Part I. These were used to predict 70-80% reductions in takeoff and landing distances for a three-dimensional advanced subsonic transport configuration employing a simplified pneumatic high-lift system. These results and the methodology used to obtain them will be presented in greater detail in the following discussions.
Cannabinoid receptors and pain (2013)

Abstract Activation of both cannabinoid 1 (CB1) and cannabinoid 2 (CB2) receptors reduces nociceptive processing in acute and chronic animal models of pain. In addition, nociceptive processing is tonically modulated by endogenous cannabinoids (endocannabinoids, ECs). This review examines the role of cannabinoids and ECs in the brain stem–spinal pathway of pain inhibition. Preclinical studies evaluating cannabinoids in neuropathic pain management are also reviewed. Pharmacological tools modulating the interaction of cannabinoids with its receptors and the treatment of pain by the augmentation of EC levels, specifically anandamide, are discussed. Particular attention is attributed to neuropathic pain in which pharmacological manipulation resulting in EC accumulation can be protective and produce antinociception, thereby making the system an attractive therapeutic target. Finally, the therapeutic value of cannabinoids in clinical research is summarized. WIREs Membr Transp Signal 2013, 2:121–132. doi: 10.1002/wmts.83 For further resources related to this article, please visit the WIREs website . The authors have declared no conflicts of interest for this article.
Gas Sensor Array Based on Metal-Decorated Carbon Nanotubes (2006)

Here we demonstrate design, fabrication, and testing of electronic sensor array based on single-walled carbon nanotubes (SWNTs). Multiple sensor elements consisting of isolated networks of SWNTs were integrated into Si chips by chemical vapor deposition (CVD) and photolithography processes. For chemical selectivity, SWNTs were decorated with metal nanoparticles. The differences in catalytic activity of 18 catalytic metals for detection of H(2), CH(4), CO, and H(2)S gases were observed. Furthermore, a sensor array was fabricated by site-selective electroplating of Pd, Pt, Rh, and Au metals on isolated SWNT networks located on a single chip. The resulting electronic sensor array, which was comprised of several functional SWNT network sensors, was exposed to a randomized series of toxic/combustible gases. Electronic responses of all sensor elements were recorded and the sensor array data was analyzed using pattern-recognition analysis tools. Applications of these small-size, low-power, electronic sensor arrays are in the detection and identification of toxic/combustible gases for personal safety and air pollution monitoring.
High sensitivity image intensifier-TV detector for x-ray diffraction studies (1978)

A sensitive, efficient image intensifier-TV x-ray detector is described that has been optimized for a large class of diffraction studies of biological structures. All of the major components are commercially available. The system is well suited to measuring the intensity of diffraction patterns that are weak, or changing with time. Because there is no count rate limitation, it is particularly well suited for studies utilizing the high fluxes of synchrotron sources.
Liver sinusoidal endothelial cells induce immunosuppressive IL‐10‐producing Th1 cells via the Notch pathway (2015)

Under homeostasis, liver sinusoidal endothelial cells (LSECs) shift intrahepatic T-cell responses towards tolerance. However, the role of LSECs in the regulation of T-cell-induced liver inflammation is less clear. Here, we studied the capacity of LSECs to modulate pro-inflammatory Th1-cell differentiation in mice. Using in vitro co-culture systems and subsequent cytokine analysis, we showed that LSECs induced high amounts of the anti-inflammatory cytokine IL-10 in developing Th1 cells. These LSEC-stimulated Th1 cells had no pro-inflammatory capacity in vivo but instead actively suppressed an inflammatory Th1-cell-induced delayed-type hypersensitivity reaction. Blockage of IL-10 signaling in vivo inhibited immunosuppressive activity of LSEC-stimulated Th1 cells. We identified the Notch pathway as a mechanism how LSECs trigger IL-10 expression in Th1 cells. LSECs expressed high levels of the Delta-like and Jagged family of Notch ligands and induced expression of the Notch target genes hes-1 and deltex-1 in Th1 cells. Blockade of Notch signaling selectively inhibited IL-10 induction in Th1 cells by LSECs. Our findings suggest that LSEC-induced IL-10 expression in Th1 cells via the Notch pathway may contribute to the control of hepatic inflammatory immune responses by induction of a self-regulatory mechanism in pro-inflammatory Th1 cells.
d - and l -Isoleucine Metabolism and Regulation of Their Pathways in Pseudomonas putida (1974)

Pseudomonas putida oxidized isoleucine to acetyl-coenzyme A (CoA) and propionyl-CoA by a pathway which involved deamination of d-isoleucine by oxidation and l-isoleucine by transamination, oxidative decarboxylation, and beta oxidation at the ethyl side chain. At least three separate inductive events were required to form all of the enzymes of the pathway: d-amino acid dehydrogenase was induced during growth in the presence of d-isoleucine; branched-chain keto dehydrogenase was induced during growth on 2-keto-3-methylvalerate and enzymes specific for isoleucine metabolism; tiglyl-CoA hydrase and 2-methyl-3-hydroxybutyryl-CoA dehydrogenase were induced by growth on isoleucine, 2-keto-3-methylvalerate, 2-methylbutyrate, or tiglate. Tiglyl-CoA hydrase and 2-methyl-3-hydroxybutyryl-CoA dehydrogenase were purified simultaneously by several enzyme concentration procedures, but were separated by isoelectric focusing. Isoelectric points, pH optima, substrate specificity, and requirements for enzyme action were determined for both enzymes. Evidence was obtained that the dehydrogenase catalyzed the oxidation of 2-methyl-3-hydroxybutyryl-CoA to 2-methylacetoacetyl-CoA. 2-Methyl-3-hydroxybutyryl-CoA dehydrogenase catalyzed the oxidation of 3-hydroxybutyryl-CoA, but l-3-hydroxyacyl-CoA dehydrogenase from pig heart did not catalyze the oxidation of 2-methyl-3-hydroxybutyryl-CoA; therefore, they appeared to be different dehydrogenases. Furthermore, growth on tiglate resulted in the induction of tiglyl-CoA hydrase and 2-methyl-3-hydroxybutyryl-CoA dehydrogenase, but these two enzymes were not induced during growth on crotonate or 3-hydroxybutyrate.
NEUROELECTRIC PROCESSES IN INDIVIDUALS AT RISK FOR ALCOHOLISM (1990)

The literature dealing with electrophysiologic research in alcoholics and individuals at risk for alcoholism is reviewed. Event-related potential (ERP) differences between family history positive (FHP) and family history negative (FHN) males have been reported both prior to the ingestion of alcohol and following alcohol challenge doses. At present, the most robust of these electrophysiological findings is the lower P3 amplitude of the ERP, which has now been replicated in several laboratories. This perhaps provides a phenotypic marker, distinguishing those at risk for alcoholism.
Xanthines Inhibit 3T3 Fibroblast Proliferation (1991)

It is believed that xanthines can inhibit cell proliferation by elevating intracellular cAMP. Therefore, these compounds can be useful in hyperproliferative disorders. Our aim was to assess the efficacy of theophylline, caffeine and dyphylline on 3T3 fibroblast proliferation. 3T3 subconfluent cultures were incubated for 3 days with the xanthine derivatives (1 mM-1 microM). At 1 and 0.1 mM the three derivatives exhibited marked inhibition of fibroblast proliferation. Theophylline and caffeine were more potent than dyphylline. At a concentration of 1 mM, the three xanthine derivatives also inhibited proliferation of psoriatic dermal fibroblast, albeit to a lower extent. Caffeine was the most active compound followed by theophylline and dyphylline. We conclude that xanthine derivatives are good candidates for use as fibroblast antiproliferative drugs. We also conclude that 3T3 fibroblasts appear to be a valid system for the pharmacological screening of fibroblast antiproliferative drugs.
Reduced expression of syndecan‐1 in human hepatocellular carcinoma with high metastatic potential (1997)

Syndecans comprise a gene family of transmembrane proteoglycans that regulate cellular behavior through interactions with various effectors, including heparin-binding growth factors and insoluble matrix components. Syndecan-1, the most extensively studied, localizes in epithelial cells and has been shown to present in normal hepatocytes. However, little is known about the change of syndecan-1 expression in human hepatocellular carcinoma (HCC). We investigated syndecan-1-protein expression by immunohistochemistry in 57 HCC tissue samples. Syndecan-1 gene expression was also determined. Syndecan-1 protein was expressed in cytoplasm and cell membrane of the hepatocytes and in the bile duct epithelial cells of liver with underlying hepatitis and cirrhosis. Conversely, among 57 HCC tissues, 39 HCC (68.4%) showed negative staining; 50% of well-differentiated HCC showed positive staining, whereas 82.4% of poorly differentiated HCC were negative. Loss of syndecan-1-protein expression was more prevalent in HCC with intra-hepatic metastasis (85.2%) than those without metastasis (48.0%). Similarly, syndecan-1 expression was significantly reduced in HCC with extra-hepatic metastasis (91.7%) as compared with the HCC without extra-hepatic metastasis (62.2%). The gene expression of syndecan-1 was significantly lower in HCC tissue than that in non-tumoral liver tissue. In 2 human HCC cell lines with poorly differentiated phenotype, HLE and HLF, syndecan-1 expression was markedly decreased both at the mRNA and the protein levels. These results suggest that the loss of syndecan-1 expression is a characteristic feature of HCC with high metastatic potential.
Intramuscular pressure varies with depth: The tibialis anterior muscle studied in 12 volunteers (1993)

Pressures in the tibialis anterior muscle were recorded at rest and during exercise with transducer-tipped catheters in 12 volunteers while they were supine or standing. The recordings were repeated with venous stasis created by an inflated tourniquet cuff on the thigh. Catheters were placed at 3 different sites in the muscle: catheter I adjacent to the deep surface of the fascia over the anterior compartment; catheter II between the fascia and the central tendon; and catheter III deep in the muscle close to the interosseous membrane. In both the supine and standing positions the intramuscular pressure at rest and the muscle relaxation pressure during exercise, obtained by catheter II, were greater than the corresponding pressures measured by the superficially located catheter I in the normal as well as in the volume loaded limb. The same conditions for pressure measurement consistently revealed lower pressures recorded by catheter III compared to II, but the difference was not significant. Our results indicate that intramuscular pressure increases centripetally, as the centrally lying tendon is approached. We conclude that pressure measurements for diagnosis of acute and chronic compartment syndromes and in ergonomic studies should be based on recordings from a standard location of the catheter within the muscle and a standard posture of the subject.
Phenylarsine Oxide Blocks Interleukin-1β–Induced Activation of the Nuclear Transcription Factor NF-κB, Inhibits Proliferation, and Induces Apoptosis of Acute Myelogenous Leukemia Cells (1999)

Arsenic compounds have recently been shown to induce high rates of complete remission in patients with acute promyelocytic leukemia (APL). One of these compounds, As(2)O(3), induces apoptosis in APL cells via a mechanism independent of the retinoic acid pathway. To test the hypothesis that arsenic compounds may be effective against other forms of acute myelogenous leukemia (AML), we studied the membrane-permeable arsenic compound phenylarsine oxide (PAO). Because interleukin-1beta (IL-1beta) plays a key role in AML cell proliferation, we first tested the effect of PAO on OCIM2 and OCI/AML3 AML cell lines, both of which produce IL-1beta and proliferate in response to it. We found that PAO inhibited the proliferation of both OCIM2 and OCI/AML3 cells in a dose-dependent fashion (0.01 to 0.1 micromol/L) and that IL-1beta partially reversed this inhibitory effect. We then measured IL-1beta levels in these cells by using an enzyme-linked immunosorbent assay and Western immunoblotting and found that PAO almost completely abolished the production of IL-1beta in these AML cells, whereas it did not affect the production of IL-1 receptor antagonist. Because PAO inhibits activation of the transcription factor NF-kappaB and because NF-kappaB modulates an array of signals controlling cellular survival, proliferation, and cytokine production, we also studied the effect of PAO on NF-kappaB activation in AML cells and found that PAO suppressed the IL-1beta-induced activation of NF-kappaB. Because inhibition of NF-kappaB may result in cellular apoptosis, we also tested whether PAO may induce apoptotic cell death in AML cells. We found that PAO induced apoptosis in OCIM2 cells through activation of the cystein protease caspase 3 and subsequent cleavage of its substrate, the DNA repair enzyme poly (ADP-ribose) polymerase. The PAO-induced apoptosis was caspase dependent, because it was completely blocked by the caspase inhibitor Z-DEVD-FMK. Finally, we tested the effect of PAO on fresh AML marrow cells from 7 patients with newly diagnosed AML and found that PAO suppressed AML colony-forming cell proliferation in a dose-dependent fashion. Taken together, our data showing that PAO is an effective in vitro inhibitor of AML cells suggest that this compound may have a role in future therapies for AML.
Urinary Kallikrein Excretion in Hypertensive Man (1974)

Urinary kallikrein excretion was measured by a radiochemical esterolytic assay in patients with essential hypertension or primary aldosteronism. Patients with essential hypertension excreted significantly less ( P &lt; 0.001) kallikrein than did normal subjects when they were allowed an ad libitum sodium intake or given 259 mEq sodium/day. When sodium intake was changed from ad libitum to 9 mEq/day, kallikrein excretion increased in the majority of patients with essential hypertension, but it remained significantly less ( P &lt; 0.001) than that in normal subjects; however, aldosterone excretion was similar in both groups. Fludrocortisone, 0.5 mg/day for 10 days, increased kallikrein excretion in three patients with essential hypertension. In patients with primary aldosteronism, mean kallikrein excretion was sevenfold higher ( P &lt; 0.001) than that in patients with essential hypertension; kallikrein excretion remained unchanged when dietary sodium was altered, but it was decreased by treatment with spironolactone. Mean kallikrein excretion in patients with primary aldosteronism was also significantly higher ( P &lt; 0.001) than that in a normotensive control population. The results show that kallikrein excretion reflects the effective level of circulating sodium-retaining steroid in patients with primary aldosteronism but suggest that it is relatively unresponsive to endogenous sodium-retaining steroid in patients with essential hypertension. The data raise the possibility that the kallikrein-kinin system is of pathogenetic significance in human hypertensive disease.
Heat Shock Proteins and Amateur Chaperones in Amyloid-Beta Accumulation and Clearance in Alzheimer’s Disease (2007)

The pathologic lesions of Alzheimer’s disease (AD) are characterized by accumulation of protein aggregates consisting of intracellular or extracellular misfolded proteins. The amyloid-β (Aβ) protein accumulates extracellularly in senile plaques and cerebral amyloid angiopathy, whereas the hyperphosphorylated tau protein accumulates intracellularly as neurofibrillary tangles. “Professional chaperones”, such as the heat shock protein family, have a function in the prevention of protein misfolding and subsequent aggregation. “Amateur” chaperones, such as apolipoproteins and heparan sulfate proteoglycans, bind amyloidogenic proteins and may affect their aggregation process. Professional and amateur chaperones not only colocalize with the pathological lesions of AD, but may also be involved in conformational changes of Aβ, and in the clearance of Aβ from the brain via phagocytosis or active transport across the blood–brain barrier. Thus, both professional and amateur chaperones may be involved in the aggregation, accumulation, persistence, and clearance of Aβ and tau and in other Aβ-associated reactions such as inflammation associated with AD lesions, and may, therefore, serve as potential targets for therapeutic intervention.
Blast colonies containing hemopoietic progenitor cells can give rise to Abelson virus (A-MuLV)-transformed cell lines. (1988)

We have established an in vitro system with which to examine the ability of Abelson murine leukemia virus (A-MuLV) to infect early hemopoietic progenitor cells. Blast cell colonies containing less than 100 cells were shown to contain up to 85% of cells with secondary hemopoietic colony-forming ability. Infection of cells from these blast colonies resulted in generation of transformed mast cell lines when a feeder was provided. Morphological examination of cells taken from infected cultures at various times postinfection indicated a progression of cellular differentiation to the mast cell lineage. Southern analysis on early subclones of transformed cells from two wells, using a v-abl specific probe, indicated a unique pattern of viral integration amongst subclones, suggesting that all subclones had derived from a single cell in each well. Similar results were observed with helper-free Abelson virus obtained by transfecting psi 2 cells with P160 A-MuLV proviral DNA. These data indicate that hemopoietic progenitor cells can be infected by A-MuLV and subsequently in our in vitro culture condition give rise to transformed mast cell lines.
Pharmacokinetics and Steady-State Bioequivalence of Treprostinil Sodium (Remodulin®) Administered by the Intravenous and Subcutaneous Route to Normal Volunteers (2004)

Treprostinil sodium is a chemically stable analogue of prostacyclin administered as a chronic, continuous subcutaneous infusion for the treatment of pulmonary arterial hypertension (PAH). There has been significant clinical interest in determining the feasibility of delivering treprostinil by intravenous infusion. Therefore, a bioequivalence and comparative pharmacokinetics study of the two routes of administration was conducted in normal volunteers. A randomized, two-period, crossover study design was employed. Each subject was dosed at 10 ng/kg/min for 72 hours by each route, with the infusions separated by a 4-day wash-out period. In the 51 subjects who received at least 24 hours of treprostinil administered subcutaneously and intravenously, the steady-state ratios of the geometric means (i.v./s.c.) and 90% confidence intervals for AUCss and Cmaxss were 92.9% (89.8-96.1%) and 106% (99.4-113%), respectively. Secondary pharmacokinetic assessments confirmed the comparability of the two routes of administration at steady state, and also demonstrated that the elimination half-life of treprostinil was 4.4 and 4.6 hours following intravenous and subcutaneous administration, respectively. Based on these findings it was concluded that intravenously and subcutaneously administered treprostinil are bioequivalent at steady state.
Breakpoint Analysis of Transcriptional and Genomic Profiles Uncovers Novel Gene Fusions Spanning Multiple Human Cancer Types (2013)

Gene fusions, like BCR/ABL1 in chronic myelogenous leukemia, have long been recognized in hematologic and mesenchymal malignancies. The recent finding of gene fusions in prostate and lung cancers has motivated the search for pathogenic gene fusions in other malignancies. Here, we developed a "breakpoint analysis" pipeline to discover candidate gene fusions by tell-tale transcript level or genomic DNA copy number transitions occurring within genes. Mining data from 974 diverse cancer samples, we identified 198 candidate fusions involving annotated cancer genes. From these, we validated and further characterized novel gene fusions involving ROS1 tyrosine kinase in angiosarcoma (CEP85L/ROS1), SLC1A2 glutamate transporter in colon cancer (APIP/SLC1A2), RAF1 kinase in pancreatic cancer (ATG7/RAF1) and anaplastic astrocytoma (BCL6/RAF1), EWSR1 in melanoma (EWSR1/CREM), CDK6 kinase in T-cell acute lymphoblastic leukemia (FAM133B/CDK6), and CLTC in breast cancer (CLTC/VMP1). Notably, while these fusions involved known cancer genes, all occurred with novel fusion partners and in previously unreported cancer types. Moreover, several constituted druggable targets (including kinases), with therapeutic implications for their respective malignancies. Lastly, breakpoint analysis identified new cell line models for known rearrangements, including EGFRvIII and FIP1L1/PDGFRA. Taken together, we provide a robust approach for gene fusion discovery, and our results highlight a more widespread role of fusion genes in cancer pathogenesis.
Vapor-liquid equilibria below 0.degree.C of hydrogen chloride solutions saturated with calcium chloride (1990)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTVapor-liquid equilibria below 0.degree.C of hydrogen chloride solutions saturated with calcium chlorideEugene MillerCite this: J. Chem. Eng. Data 1990, 35, 4, 436–440Publication Date (Print):October 1, 1990Publication History Published online1 May 2002Published inissue 1 October 1990https://pubs.acs.org/doi/10.1021/je00062a019https://doi.org/10.1021/je00062a019research-articleACS PublicationsRequest reuse permissionsArticle Views42Altmetric-Citations-LEARN 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