gebhart/patrepeval huggingface dataset:
B7, a new member of the Ig superfamily with unique expression on activated and neoplastic B cells. (1989)

The human B cell restricted activation antigen B7 identifies an in vivo primed subpopulation of B cells that demonstrate an accelerated response to triggers of B cell activation and proliferation. The cDNA encoding B7 was molecularly cloned by cDNA expression. The identity of the B7 cDNA was confirmed by indirect immunofluorescence and immunoprecipitation of a 44/54-kDa protein from B7 transfected COS cells. The sequence of the B7 polypeptide predicts a type I membrane protein of 262 amino acids with eight potential N-linked glycosylation sites in the extracellular region and a short, highly positively charged cytoplasmic tail. The extracellular region is homologous to the Ig gene superfamily and consists of two contiguous Ig-like domains. The first Ig domain has the characteristics of a variable domain and the second that of a constant region domain. B7 mRNA was detected only on anti-Ig activated B lymphocytes and not in other hematopoietic cells. After in vitro activation of B cells with anti-Ig, B7 mRNA was maximally expressed between 4 and 12 h with four RNA transcripts of 1.7, 2.9, 4.2, and 10 kb. The 2.9-kb mRNA predominated in in vitro-activated B cells whereas the 1.7-kb mRNA was most abundant in tumor cells of B cell origin. B7 expression was confined to several histologically defined subgroups of B cell malignancies. The majority of non-Hodgkin's lymphomas were B7+ whereas the B cell leukemias and circulating non-Hodgkin's lymphomas were generally negative. These results demonstrate that the B7 gene encodes a unique molecule belonging to the Ig superfamily and that B7 expression is limited to normal activated B cells and noncirculating B cell malignancies.
Expression of 15-Lipoxygenase by Human Colorectal Carcinoma Caco-2 Cells during Apoptosis and Cell Differentiation (1998)

We studied arachidonic acid metabolism and the expression of cyclooxygenase (Cox) and 15-lipoxygenase (15-LO) in the human colorectal carcinoma cell line, Caco-2, which undergo apoptosis and cell differentiation in the presence of sodium butyrate (NaBT). Caco-2 cells expressed very low levels of Cox-1 but highly expressed Cox-2. NaBT treatment shifted the arachidonic acid metabolites by cell lysates from prostaglandins to 15-hydroxyeicosatetraenoic acid, indicating the presence of a 15-LO. Linoleic acid, an excellent substrate for 15-LO, was metabolized poorly by the Caco-2 cells, but NaBT treatment shifted metabolism to 15-LO metabolite, 13(S)-hydroxyoctadecadienoic acid. Caco-2 cells expressed a 15-LO but only after treatment with NaBT, as determined by Northern blotting. Immunoblotting with anti-human 15-LO antibody detected a 72-kDa band in NaBT-treated Caco-2 cells. Expression of 15-LO mRNA was dependent on the duration of NaBT treatment, with the highest expression observed between 10 and 24 h. Results from expression and metabolism studies with arachidonic and linoleic acid cells indicated Cox-2 was responsible for the lipid metabolism in control cells, whereas 15-LO was the major enzyme responsible after NaBT induction of apoptosis and cell differentiation. The 15-LO in Caco-2 cells was characterized as human reticulocyte 15-LO by reverse transcription-polymerase chain reaction and restriction enzyme analysis. The expression of 15-LO and 15-hydroxyeicosatetraenoic acid or 13(S)-hydroxyoctadecadienoic acid formation correlates with cell differentiation or apoptosis in Caco-2 cells induced by NaBT. The addition of nordihydroguaiaretic acid, a lipoxygenase inhibitor, significantly increased NaBT-induced apoptosis, whereas the addition of indomethacin did not alter NaBT-induced apoptosis in the Caco-2 cells. However, indomethacin treatment decreased the expression of Cox-2 in NaBT-treated cells and significantly increased the expression of 15-LO during NaBT treatment. These studies suggest a role for 15-LO, in addition to Cox-2, in modulating NaBT-induced apoptosis and cell differentiation in human colorectal carcinoma cells.
Effects of 6-diazo-5-oxol-norleucine and other tumor inhibitors on the biosynthesis of nicotinamide adenine dinucleotide in mice. (1966)

NAD[2][1] in extracts of mouse liver and tumor was determined enzymically by ADH and chemically by reaction with cyanide. The presence of Sarcoma 180 caused a decrease in the level of NAD in the host liver. Of the 16 antitumor agents tested for inhibition of nicotinamide-induced biosynthesis of NAD, DON was the most effective. 6-Fluoronicotinamide, 5-fluoronicotinic acid, azaserine, and 6-mercaptopurine were inhibitory but less effective, and mitomycin, actinomycin, and amethopterin were ineffective. DON caused a slight decrease in the normal levels of liver and tumor NAD and completely prevented the increased synthesis of NAD induced by nicotinamide. Glutamine given before administration of DON and nicotinamide did not prevent the effect of DON. An accumulation of desamido-NAD in the livers of mice treated with nicotonamide plus DON was found approximately equal to the amounts of NAD synthesized in the absence of DON. It is suggested that DON inhibits the enzyme system that converts desamido-NAD to NAD—NAD synthetase.

 [1]: #fn-2
Thrombocytopenia found uncommonly during heparin therapy (1979)

In a prospective study to determine the frequency of thrombocytopenia in patients treated with intravenous heparin sodium of porcine gut origin, only four of 120 patients with suspected venous thromboembolism showed a depression of the platelet count to below 150×10<sup>9</sup>/L. In two of these patients, heparin was not considered to be the cause of thrombocytopenia because the platelet count, which fell transiently, rose again while heparin therapy was continued. These results indicate that thrombocytopenia is an uncommon complication of anticoagulant therapy with heparin derived from porcine gut mucosa. (<i>JAMA</i>241:2396-2397, 1979)
Low voltage analog circuit design techniques (2002)

Analog signal processing is fast and can address real world problems. The applications of battery powered analog and mixed mode electronic devices require designing analog circuits to operate at low voltage levels. In this paper, some of the issues facing analog designers in implementing low voltage circuits are discussed, and possible low voltage design techniques are examined. The authors describe briefly almost all low voltage design techniques suitable for analog circuit structures along with their merits and demerits.
Therapeutic Co-targeting of WEE1 and ATM Downregulates PD-L1 Expression in Pancreatic Cancer (2019)

Dual blockade of WEE1 and ATM might be a potential therapeutic strategy for PC. Taken toget.
Conservative synchronization in object-oriented parallel battlefield discrete event simulations (1997)

We present a conservative strategy for spatially decomposed parallel discrete event battlefield simulation. The traditional null message algorithm provides a foundation from which a mapping to generic simulation attributes can be made. We informally discuss preservation of logical correctness and freedom from deadlock. Experimental results demonstrate the potential execution time savings when load imbalance is not dominant; more importantly, they highlight improvement opportunities in spite of potential load imbalance. The net result is that a very reasonable performance gain can be delivered for little effort in a way that supports good simulation system design principles. The approach is straightforward and can be easily implemented as part of a more general sequential or parallel simulation support environment. While the approach is expressed in terms of battlefield simulation, its essence applies to many simulation applications.
The procedure of a camera calibration using Camera Calibration Toolbox for MATLAB (2012)

This paper describes the calibration procedure of a CCD digital camera based on the perspective projection method. The idea of this method is to calibrate the camera in order to extract precise three dimensional information from the images so that they can be used for the computer vision and similar applications which take the images acquired from the camera as an input. The image capturing process reduces the dimensions of data from three to two. The camera calibration procedure determines which light source is associated with each pixel on the resulting image. Since the camera used in the process is a complex CCD camera, errors resulting from the misaligned lenses and deformations in their structures result in more complex distortions in the acquired image. In order to associate the points in the cameras image space with the locations in a 3D world space the camera projection matrix consisting of the estimated intrinsic and extrinsic parametars is calculated. The calibration process is comprised of capturing calibration images and processing them in order to get the intrinsic and extrinsic camera parameters. The results of the calibration are tested using the test images captured with the same camera. The calibration process was implemented using a MATLAB software package.
Clinical predictors of central sleep apnea evoked by positive airway pressure titration (2016)

Clinical predictors of treatment-evoked central apnea spanned demographic, medical history, sleep physiology, and titration factors. Improved predictive models may be increasingly important as diagnostic and therapeutic modalities move away from the laboratory setting, even as PSG remains the gold standard for characterizing primary central apnea and TECSA.
Beta-caryophyllene is a dietary cannabinoid (2008)

The psychoactive cannabinoids from Cannabis sativa L. and the arachidonic acid-derived endocannabinoids are nonselective natural ligands for cannabinoid receptor type 1 (CB(1)) and CB(2) receptors. Although the CB(1) receptor is responsible for the psychomodulatory effects, activation of the CB(2) receptor is a potential therapeutic strategy for the treatment of inflammation, pain, atherosclerosis, and osteoporosis. Here, we report that the widespread plant volatile (E)-beta-caryophyllene [(E)-BCP] selectively binds to the CB(2) receptor (K(i) = 155 +/- 4 nM) and that it is a functional CB(2) agonist. Intriguingly, (E)-BCP is a common constituent of the essential oils of numerous spice and food plants and a major component in Cannabis. Molecular docking simulations have identified a putative binding site of (E)-BCP in the CB(2) receptor, showing ligand pi-pi stacking interactions with residues F117 and W258. Upon binding to the CB(2) receptor, (E)-BCP inhibits adenylate cylcase, leads to intracellular calcium transients and weakly activates the mitogen-activated kinases Erk1/2 and p38 in primary human monocytes. (E)-BCP (500 nM) inhibits lipopolysaccharide (LPS)-induced proinflammatory cytokine expression in peripheral blood and attenuates LPS-stimulated Erk1/2 and JNK1/2 phosphorylation in monocytes. Furthermore, peroral (E)-BCP at 5 mg/kg strongly reduces the carrageenan-induced inflammatory response in wild-type mice but not in mice lacking CB(2) receptors, providing evidence that this natural product exerts cannabimimetic effects in vivo. These results identify (E)-BCP as a functional nonpsychoactive CB(2) receptor ligand in foodstuff and as a macrocyclic antiinflammatory cannabinoid in Cannabis.
Isolation of a Degeneration-Resistant Mutant of Clostridium acetobutylicum NCIMB 8052 (1993)

Unless periodically grown from germinated spores, Clostridium acetobutylicum tends to degenerate (that is, to spontaneously lose the capacity both to produce solvents and to develop into spores). To obtain mutants that are deficient in degeneration, C. acetobutylicum NCIMB 8052 was mated with Enterococcus faecalis BM4110 harboring transposon Tn1545. We developed a degeneration resistance assay based on a secondary effect of degeneration, the production of toxic levels of acetic and butyric acids. Erythromycin-resistant transconjugant clones were tested individually for longevity by repeated and timely subculturing. One long-lived mutant, A10, survived 18 +/- 3 transfers (mean +/- standard deviation; n = 20) before extinction, while the wild type (parental cells) survived 6.6 +/- 1.5 transfers (n = 11). The three-fold difference in longevity is statistically significant. In a batch culture in a rich medium, the wild-type cells degenerated within 24 h after inoculation with 1% of an overnight culture derived from germinated spores. In contrast, A10 cells were able to switch to solventogenesis and to sporulate. In a minimal medium with greater buffering capacity, both cell types produced solvents and spores. Southern blots of EcoRI and HindIII restriction digests of A10 chromosomal DNA (but not parental DNA) showed that only one copy of Tn1545 was inserted into the clostridial chromosome. Our findings are consistent with the hypothesis that there was an alteration at a regulatory locus that was effected by the insertion of the transposon.
A Novel Family of Cyclic Peptide Antagonists Suggests That N-cadherin Specificity Is Determined by Amino Acids That Flank the HAV Motif (2000)

The classical cadherins (e.g. N-, E-, and P- cadherin) are well established homophilic adhesion molecules; however, the mechanism that governs cadherin specificity remains contentious. The classical cadherins contain an evolutionarily conserved His-Ala-Val (HAV) sequence, and linear peptides harboring this motif are capable of inhibiting a variety of cadherin-dependent processes. We now demonstrate that short cyclic HAV peptides can inhibit N-cadherin function. Interestingly, the nature of the amino acids that flank the HAV motif determine both the activity and specificity of the peptides. For example, when the HAV motif is flanked by a single aspartic acid, which mimics the natural HAVD sequence of N-cadherin, the peptide becomes a much more effective inhibitor of N-cadherin function. In contrast, when the HAV motif is flanked by a single serine, which mimics the natural HAVS sequence of E-cadherin, it loses its ability to inhibit the N-cadherin response. Our results demonstrate that subtle changes in the amino acids that flank the HAV motif can account for cadherin specificity and that small cyclic peptides can inhibit cadherin function. An emerging role for cadherins in a number of pathological processes suggests that the cyclic peptides reported in this study might be developed as therapeutic agents.
Cholinergic receptor up-regulates COX-2 expression and prostaglandin E2 production in colon cancer cells (2000)

The M(3) muscarinic cholinergic receptor has important physiological functions on normal colonic cells. It is frequently expressed on human colon cancer cells and is biologically active. Although it is mitogenic in certain cell models, the importance of this receptor on colon carcinogenesis is unknown. In the present study we have determined expression of the M(3) receptor on human colon cancer tissue compared with matched normal tissue and examined the downstream effect of receptor activation in the HT-29 human colon carcinoma cell line. Using reverse transcription-PCR, M(3) receptor RNA expression was detected in all matched colon carcinoma and normal specimens from eight patients. Five of the eight (62%) patients showed an up to 8-fold greater level of M(3) receptor expression in cancer compared with the matched normal tissue. Exposure of HT-29 cells to carbachol, a stable receptor agonist, results in a 10-fold increase in cyclooxygenase-2 (COX-2) protein. This induction of COX-2 protein was dose dependent and was inhibited by the cholinergic receptor antagonist N-methylscopolamine (NMS). Carbachol caused a dose-dependent increase in prostaglandin E(2) (PGE(2)), the main product of cyclooxygenase activity. The maximum stimulatory effect (40-fold increase) was noted with 1mM carbachol. The increase in PGE(2) was completely abolished by NMS and by the COX-2 selective inhibitor NS398. This suggests that the M(3) receptor mediates PGE(2) production by a mechanism involving COX-2. As COX-2 and PGE(2) are known promoters of gastrointestinal cancer, these data suggest that M(3) receptor activation may facilitate progression of colon carcinoma, in part by a COX-2-mediated cellular mechanism.
Irritable Bowel Syndrome (2003)

Irritable bowel syndrome, characterized by disordered bowel habits associated with abdominal pain or discomfort, affects roughly one in eight adults. This review discusses therapeutic options for patients with this disorder. Nonpharmacologic therapies alone are adequate for many patients. Nonspecific pharmacotherapy to treat constipation or diarrhea, as well as more specific therapy with antispasmodic agents, antidepressants, serotonin-receptor antagonists, and other agents are discussed. A doctor–patient alliance is important in treating the disorder.
Studies on the constituents of Xanthoceras sorbifolia Bunge. V. Major saponins from the fruits of Xanthoceras sorbifolia Bunge. (1985)

Four new saponins were isolated from the fruits of Xanthoceras sorbifolia BUNGE. The structures of these saponins were deduced on the basis of chemical and spectral evidence as 22-O-acetyl-21-O-(4-O-acetyl-3-O-angeloyl)-β-D-fucopyranosyl-3-O-[β-D-glucopyranosyl- (1→2)-β-D-glucuronopyranosyl] protoaescigenin (7), 22-O-acetyl-21-O- (3, 4-di-O-angeloyl) -β-D-fucopyranosyl-3-O- [β-D-glucopyranosyl- (1→2)-β-D-glucuronopyranosyl] protoaescigenin (8), 28-O-acetyl21-O- (4-O-acetyl-3-O-angeloyl) -β-D-fucopyranosyl-3-O- [β-D-glucopyranosyl- (1→2) -β-D-glucuronopyranosyl] protoaescigenin (9) and 28-O-acetyl-21-O-(3, 4-di-O-angeloyl) -D-fucopyranosyl-3-O- [β-D-glucopyranosyl-(1→2)-β-D-glucuronopyranosyl] protoaescigenin (10). The names "bunkankasaponins A, B, C and D"are proposed for 7, 8, 9 and 10, respectively.
Insulin-like Growth Factor Binding Protein-4 Differentially Inhibits Growth Factor-induced Angiogenesis (2011)

An in-depth understanding of the molecular and cellular complexity of angiogenesis continues to advance as new stimulators and inhibitors of blood vessel formation are uncovered. Gaining a more complete understanding of the response of blood vessels to both stimulatory and inhibitory molecules will likely contribute to more effective strategies to control pathological angiogenesis. Here, we provide evidence that endothelial cell interactions with structurally altered collagen type IV may suppress the expression of insulin-like growth factor binding protein-4 (IGFBP-4), a well documented inhibitor of the IGF-1/IGF-1R signaling axis. We report for the first time that IGFBP-4 differentially inhibits angiogenesis induced by distinct growth factor signaling pathways as IGFBP-4 inhibited FGF-2- and IGF-1-stimulated angiogenesis but failed to inhibit VEGF-induced angiogenesis. The resistance of VEGF-stimulated angiogenesis to IGFBP-4 inhibition appears to depend on sustained activation of p38 MAPK as blocking its activity restored the anti-angiogenic effects of IGFBP-4 on VEGF-induced blood vessel growth in vivo. These novel findings provide new insight into how blood vessels respond to endogenous inhibitors during angiogenesis stimulated by distinct growth factor signaling pathways.
Screening for prostate cancer. (1994)

Prostate cancer is a serious health care problem in the United States. Whether or not to screen for it has become a timely issue. Although a large number of men have clinically important, asymptomatic, undetected prostate cancer, an even larger number have clinically unimportant cancer. To justify screening programs, not only must we avoid detecting biologically unimportant cancers, we must also detect and effectively treat that subset of tumors that, if undiagnosed, would progress, produce symptoms, and reduce life expectancy. Serum prostate-specific antigen (PSA) assay, or its variations such as PSA density, PSA velocity, and age-specific reference ranges, and the digital rectal examination are the best tests for detecting clinically important, asymptomatic, curable tumors. Recent data suggest that using serum PSA levels does not result in an overdetection of unimportant tumors. Highly effective, curative treatment of localized prostate cancer is available. These factors promote optimism that screening for prostate cancer will ultimately prove beneficial. Nonetheless, men should be informed regarding the benefits and possible risks before being screened for prostate cancer.
Binding of Radioiodinated Parathyroid Hormone to Cloned Bone Cells* (1983)

We have investigated the binding of biologically active radioiodinated bovine PTH-(1-84) to cloned osteoblast-like rat osteosarcoma cells (ROS 17/2.8) and correlated binding with biological response assessed as cAMP production. The hormone was labeled with 125I on tyrosine-43 using a constant current microelectrolytic method which allows full retention of biological activity. At confluency, cells were removed from culture, and assays were carried out on intact cells in suspension. At 22 C, saturable binding reached equilibrium by 90 min. At that time, the apparent dissociation rate constant was 8 X 10(-8) min-1. At an earlier time, 10 min of incubation, the dissociation rate was twice that observed at equilibrium. Nonsaturable binding was 30-35% of the total binding. The dissociation constant derived from kinetic analysis was 41 nM and correlated with the half-maximal cAMP production at 36 nM. The results obtained suggest that cleavage amino-terminal to residue 43 is not required for binding to these bone-derived cells. Binding to receptors on the osteosarcoma cells was specific and reversible, and appeared biologically relevant, since it correlated closely with the biological response, cAMP production. The competitive inhibitor [Nle8,Nle18,Tyr34]bPTH-(3-34)amide showed the same apparent affinity in inhibiting receptor binding as in inhibiting cAMP production.
Role of macrophage inflammatory protein-1 alpha (MIP-1 alpha ) in acute lung injury in rats. (1995)

The role of macrophage inflammatory protein-1 alpha (MIP-1 alpha) in the pathogenesis of acute lung injury in rats after intrapulmonary deposition of IgG immune complexes or intratracheal administration of LPS has been assessed. Critical to these studies was the cloning and functional expression of rat MIP-1 alpha. The resulting product shared 92% and 90% homology with the known murine sequence at the cDNA level and protein level, respectively. Recombinant rat MIP-1 alpha exhibited dose-dependent chemotactic activity for both rat and human monocytes and neutrophils, which could be blocked by anti-murine MIP-1 alpha Ab. Rat MIP-1 alpha mRNA and protein expression were determined as a function of time in both injury models. A time-dependent increase in MIP-1 alpha mRNA in lung extracts was observed in both models. In the LPS model, MIP-1 alpha protein could also be detected in bronchoalveolar lavage (BAL) fluids by Western blot analysis. Anti-MIP-1 alpha administered at commencement of IgG immune complex- or LPS-induced injury resulted in significant reductions in BAL neutrophils as well as in injury as measured by pulmonary vascular permeability. Under such conditions, in both models TNF-alpha content in BAL fluids was substantially reduced as compared with BAL fluids from positive control animals. These findings suggest that rat MIP-1 alpha plays an important role in the development of lung injury in these neutrophil-dependent models. The role of MIP-1 alpha seems to be related to production of TNF-alpha, which in turn up-regulates vascular adhesion molecules required for neutrophil influx.
The Flood: New light on an old story. By Harold Peake, M.A., F.S.A. 8½ × 5½. Pp. x + 124. London: Kegan Paul. 1930. 5s. (1931)

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The Risk of Transfusion-Transmitted Viral Infections (1996)

The risk of transmitting HIV, HTLV, HCV, or HBV infection by the transfusion of screened blood is very small, and new screening tests will reduce the risk even further.