tbuckley/cabot-search huggingface dataset:
Effects of long chain fatty acids on solute absorption: perfusion studies in the human jejunum.
Authors: H V Ammon, P J Thomas, S F Phillips
Journal: Gut (1977)

Perfusion studies were performed in healthy volunteers to test the hypothesis that net fluid secretion induced by fatty acids is accompanied by parallel reduction in solute transport. Ricinoleic acid provoked a marked net secretion of fluid and concomitantly inhibited the absorption of all solutes tested; these included glucose, xylose, L-leucine, L-lysine, Folic acid, and 2-mono-olein. Oleic acid also reduced net fluid and solute transport, but was less potent in reducing solute absorption than was ricinoleic acid. When fluid secretion was induced osmotically with mannitol, glucose and xylose absorption was not affected. The mechanism for this generalised effect of fatty acids on solute absorption is uncertain, possibly nonspecific, and might be related to mucosal damage and altered mucosal permeability induced by these agents.
Greater Clinical Benefit of More Intensive Oral Antiplatelet Therapy With Prasugrel in Patients With Diabetes Mellitus in the Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition With Prasugrel–Thrombolysis in Myocardial Infarction 38
Authors: Stephen D. Wiviott, Eugene Braunwald, Dominick J. Angiolillo, Simha Meisel, Anthony J. Dalby, Freek W.A. Verheugt, Shaun G. Goodman, Ramon Corbalan, Drew A. Purdy, Sabina A. Murphy, Carolyn H. McCabe, Elliott M. Antman
Journal: Circulation (2008)

Patients with diabetes mellitus (DM) are at high risk for recurrent cardiovascular events after acute coronary syndromes, in part because of increased platelet reactivity. The Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition With Prasugrel-Thrombolysis in Myocardial Infarction 38 (TRITON-TIMI 38) showed an overall reduction in ischemic events with more intensive antiplatelet therapy with prasugrel than with clopidogrel but with more bleeding. We compared prasugrel with clopidogrel among subjects with DM in TRITON-TIMI 38.We classified 13 608 subjects on the basis of preexisting history of DM and further according to insulin use. Prespecified analyses of the primary (cardiovascular death, nonfatal myocardial infarction, or nonfatal stroke) and key secondary end points, including net clinical benefit (death, nonfatal myocardial infarction, nonfatal stroke, and nonfatal TIMI major bleeding) were compared by use of the log-rank test. We found that 3146 subjects had a preexisting history of DM, including 776 receiving insulin. The primary end point was reduced significantly with prasugrel among subjects without DM (9.2% versus 10.6%; hazard ratio [HR], 0.86; P=0.02) and with DM (12.2% versus 17.0%; HR, 0.70; P<0.001, P(interaction)=0.09). A benefit for prasugrel was observed among DM subjects on insulin (14.3% versus 22.2%; HR, 0.63; P=0.009) and those not on insulin (11.5% versus 15.3%; HR, 0.74; P=0.009). Myocardial infarction was reduced with prasugrel by 18% among subjects without DM (7.2% versus 8.7%; HR, 0.82; P=0.006) and by 40% among subjects with DM (8.2% versus 13.2%; HR, 0.60; P<0.001, P(interaction)=0.02). Although TIMI major hemorrhage was increased among subjects without DM on prasugrel (1.6% versus 2.4%; HR, 1.43; P=0.02), the rates were similar among subjects with DM for clopidogrel and prasugrel (2.6% versus 2.5%; HR, 1.06; P=0.81, P(interaction)=0.29). Net clinical benefit with prasugrel was greater for subjects with DM (14.6% versus 19.2%; HR, 0.74; P=0.001) than for subjects without DM (11.5% versus 12.3%; HR, 0.92; P=0.16, P(interaction)=0.05).Subjects with DM tended to have a greater reduction in ischemic events without an observed increase in TIMI major bleeding and therefore a greater net treatment benefit with prasugrel compared with clopidogrel. These data demonstrate that the more intensive oral antiplatelet therapy provided with prasugrel is of particular benefit to patients with DM.
Diabetes Prevention: How Important Is Geographic Divergence Regarding the Role of Fish Intake?
Authors: Judith Wylie-Rosett, Karin B. Aebersold, Beth A. Conlon
Journal: Diabetes Care (2012)

Evidence-based health recommendations are founded on the assumption that quality of research and findings are largely reproducible (1). Prospective cohort studies that have examined how fish and omega-3 fatty acid intake are related to the risk of developing diabetes have yielded inconsistent findings. This issue of Diabetes Care includes articles from two research teams that each conducted a meta-analysis of fish intake and incident diabetes (Table 1) (2,3). Independently both teams found the same explanation for the lack of consistent findings and no overall association between fish intake and incident diabetes. Separating the studies based on geography yielded two distinctly opposing associations. Analysis of studies conducted in Western countries (U.S. and Europe) found that a higher intake of fish was associated with a higher incidence of diabetes, whereas analysis of studies conducted in Eastern countries (Asia and Australia) found that eating more fish was associated with a lower incidence of diabetes (2,3).

View this table:

Table 1 
Meta-analysis criteria and overview of findings reported by Xun and He (2) and by Wallin et al. (3)



These divergent associations raise a number of questions regarding variables that may account for the inconsistencies. Considerations should be given to environmental factors, e.g., wild versus farm raised, mercury content, differences in preparation methods, e.g., frying, and demographic and health characteristic confounding or interaction. A recent study of restaurant food intake and incident diabetes found the relationship between fried fish and diabetes was attenuated by BMI (4). The use of objective biomarkers for omega-3 fatty acid intake in the Cardiovascular Health …
Influence of Fv-1 alleles on cellular expression of gp70.
Authors: J S Tung, E A Boyse, F W Shen
Journal: The Journal of Experimental Medicine (1980)

Type-variants of gp70 (glycoprotein-70), which is the major envelope protein of C-type mouse virus and is also found in plasma membranes, are identified immunogenetically by the antigens Gix and Ec. Cellular expression of Gix+ gp70 does not depend on production of virus, but expression of Ec+ gp70 (formerly X-gp70) has been observed only in AKR and other strains of mice that produce large amounts of virus throughout life. To test the inference that cellular expression of Ec+ gp70 is secondary to production of virus we examined the effect of Fv-1 alleles, which govern the replicability of N-tropic and B-tropic C-type virus, on the expression of Ec+ gp70 on thymocytes. By typing thymocytes of Fv-1-congenic mice for Ec+ gp70 was found that manifestation of the Ec+ gp70 phenotype requires the Fv-1n allele, which is permissive for replication of N-tropic virus produced by AKR and other virus-producing mouse strains. Substitution of the Fv-1b allele for the Fv-1n allele abolishes demonstrable expression of Ec+ gp70 by AKR thymocytes at ages up to 9 mo, the oldest AKR mice tested.
Protein Kinase Cε Interacts with Signal Transducers and Activators of Transcription 3 (Stat3), Phosphorylates Stat3Ser727, and Regulates Its Constitutive Activation in Prostate Cancer
Authors: Moammir H. Aziz, Herbert T. Manoharan, Dawn R. Church, Nancy E. Dreckschmidt, Weixiong Zhong, Terry D. Oberley, George Wilding, Ajit K. Verma
Journal: Cancer Research (2007)

Abstract Prostate cancer is the most common type of cancer in men and ranks second only to lung cancer in cancer-related deaths. The management of locally advanced prostate cancer is difficult because the cancer often becomes hormone insensitive and unresponsive to current chemotherapeutic agents. Knowledge about the regulatory molecules involved in the transformation to androgen-independent prostate cancer is essential for the rational design of agents to prevent and treat prostate cancer. Protein kinase Cε (PKCε), a member of the novel PKC subfamily, is linked to the development of androgen-independent prostate cancer. PKCε expression levels, as determined by immunohistochemistry of human prostate cancer tissue microarrays, correlated with the aggressiveness of prostate cancer. The mechanism by which PKCε mediates progression to prostate cancer remains elusive. We present here for the first time that signal transducers and activators of transcription 3 (Stat3), which is constitutively activated in a wide variety of human cancers, including prostate cancer, interacts with PKCε. The interaction of PKCε with Stat3 was observed in human prostate cancer, human prostate cancer cell lines (LNCaP, DU145, PC3, and CW22rv1), and prostate cancer that developed in transgenic adenocarcinoma of mouse prostate mice. In reciprocal immunoprecipitation/blotting experiments, prostatic Stat3 coimmunoprecipitated with PKCε. Localization of PKCε with Stat3 was confirmed by double immunofluorescence staining. The interaction of PKCε with Stat3 was PKCε isoform specific. Inhibition of PKCε protein expression in DU145 cells using specific PKCε small interfering RNA (a) inhibited Stat3Ser727 phosphorylation, (b) decreased both Stat3 DNA-binding and transcriptional activity, and (c) decreased DU145 cell invasion. These results indicate that PKCε activation is essential for constitutive activation of Stat3 and prostate cancer progression. [Cancer Res 2007;67(18):8828–38]
Gene Delivery to the Corneal Endothelium
Authors: ANDREW J. T. GEORGE, CAROLINA V. ARANCIBIA-CÁRCAMO, HANNA M. AWAD, RICHARD M. COMER, ZOLTAN FEHEVARI, WILLIAM J. KING, MOHAMMED KADIFACHI, TOBIAS HUDDE, CHRISTELLE KEROUEDAN-LEBOSSÉ, FAREED MIRZA, H. BARBAROS ORAL, SANDRA A. RAYNER, PENG H. TAN, EUGENE TAY, D. FRANK P. LARKIN
Journal: American Journal of Respiratory and Critical Care Medicine (2000)

Section:ChooseTop of pageAbstract <<INTRODUCTIONGENE TRANSFER TO THE CORN...CONCLUSIONReferencesCITING ARTICLES
Internal surface area and other measurements in emphysema
Authors: W. M. Thurlbeck
Journal: Thorax (1967)

Some measurements of emphysema were made on 29 pairs of non-emphysematous lungs and 44 pairs of emphysematous lungs inflated at a standard transpulmonary pressure of 25 cm. of formalin. These were: a subjective visual assessment (units); an assessment of the volume of the lung parenchyma involved by emphysema (point count); an average subjective visual grading by eight pathologists (Co-op score); mean linear intercept or average distance between alveolar walls at a transpulmonary pressure of 25 cm. of formalin (Lm); mean linear intercept corrected to total lung capacity (Lm<sub>C</sub>); internal (alveolar) surface area at 25 cm. transpulmonary pressure (ISA); internal surface area at total lung capacity (ISA<sub>C</sub>); internal surface area corrected to an arbitrary lung volume of 5 litres (ISA<sub>5</sub>). Internal surface area measurements were generally decreased in severe emphysema. Because of the wide range of ISA and ISA<sub>C</sub> in non-emphysematous lungs, most emphysematous lungs fell within the normal range. The range of ISA<sub>5</sub> was smaller in non-emphysematous lungs and most emphysematous lungs fell outside this range. ISA<sub>5</sub> in `mild9 emphysema was not distinguishable from non-emphysematous lungs. Most emphysematous lungs in which the surface area was decreased less than expected from subjective assessment were examples of centrilobular emphysema. Lm and Lm<sub>C</sub> were increased in emphysema. ISA<sub>5</sub>, Lm, and Lm<sub>C</sub> paralleled the subjective assessments of emphysema rather better than ISA or ISA<sub>C</sub>, even when the latter were expressed as a percentage of predicted. Lm and Lm<sub>C</sub> in lungs with mild emphysema fell within the ranges found in non-emphysematous lungs, but the mean value of Lm in lungs with `mild9 emphysema was different from the mean Lm of non-emphysematous lungs, at conventional levels of significance. Since objective methods did not recognize adequately examples of `mild9 emphysema, a subjective visual grading system (with its limitations) may have a definite place.
Use of short-term culture for identification of Mycobacterium avium subsp. paratuberculosis in tissue from Crohn's disease patients
Authors: D. Schwartz, I. Shafran, C. Romero, C. Piromalli, J. Biggerstaff, N. Naser, W. Chamberlin, S.A. Naser
Journal: Clinical Microbiology and Infection (2000)
Behcet's syndrome with ulcerative oesophagitis: report of the first case
Authors: T. E. Brodie, J. L. Ochsner
Journal: Thorax (1973)

<b>Brodie, T. E., and Ochsner, J. L. (1973).</b><i>Thorax</i>, <b>28</b>, 637-640. <b>Behçet9s syndrome with ulcerative oesophagitis: report of the first case.</b> A patient is presented who has the typical manifestations of Behçet9s syndrome—oral, perianal, and skin ulcerations, arthritis, and thrombophlebitis. His presenting symptom, consisting of severe dysphagia caused by oesophageal ulceration, is unreported in connection with this disease. The ulceration became a perforation requiring surgical treatment. His malnourished state and long-term steroid therapy made him a poor surgical risk and preoperative and postoperative nutritional and respiratory support were necessary. Prophylaxis against thromboembolic phenomena is indicated postoperatively in these patients.
Chemoembolization of hepatocellular carcinoma with drug eluting beads: Efficacy and doxorubicin pharmacokinetics
Authors: María Varela, María Isabel Real, Marta Burrel, Alejandro Forner, Margarita Sala, Mercé Brunet, Carmen Ayuso, Lluis Castells, Xavier Montañá, Josep M. Llovet, Jordi Bruix
Journal: Journal of Hepatology (2006)
Participation of Central Noradrenergic Neurons in Arterial Baroreceptor Reflexes in the Rabbit
Authors: J. P. CHALMERS, R. J. WURTMAN
Journal: Circulation Research (1971)

Disappearance rates of intracisternally administered 3 H-norepinephrine and activities of tyrosine hydroxylase were examined in the rabbit in five brain regions (telencephalon, hypothalamus, midbrain, medulla-pons, and cerebellum) and in three cord regions (cervical, thoracolumbar, and lumbosacral) 2 weeks after section of the carotid sinus and aortic nerves. Mean blood pressure rose by 29% and heart rate by 17% in the animals with neurogenic hypertension. Endogenous catecholamine concentrations in the eight regions examined were not altered by denervation. In the thoracolumbar region of the spinal cord, 3 H-norepinephrine turnover and tyrosine hydroxylase activity were increased approximately twofold in hypertensive rabbits. We suggest that these changes reflect increased physiological activity of bulbospinal noradrenergic neurons and that this increase may mediate the rise in arterial pressure or heart rate that follows sinoaortic denervation. The turnover of 3 H-norepinephrine increased in the hypothalamus of denervated animals; tyrosine hydroxylase activity remained unchanged in this region.
The Langerhans' cells*
Authors: Luigi P. Ruco, Stefania Uccini, Carlo D. Baroni
Journal: Allergy (1989)

The morphological, enzymatical, immunocytochemical and functional properties of Langerhans' cells are briefly reviewed. Langerhans' cells are located mainly in the squamous stratified epithelia, but are also present in the thymus and in superficial lymphnodes. At the ultrastructural level, they are characterized by unique cytoplasmic organelles, the Birbeck granules, whose function is still unknown. Langerhans' cells possess strong ATPase activity and are weakly positive for alpha‐naphtyl acetate esterase and for acid phosphatase; they are immunoreactive for CD1a (T6), class II MHG antigens and S‐100 protein. In some pathological conditions, like dermatopathic lymphadenopathy and Langerhans' cell histocytosis, Langerhans' cells also are characterized by the expression of monocyte‐macrophage antigens. Langerhans' cells act as antigen‐presenting cells to T lymphocytes; their functional capacity is strictly dependent on the levels of expression of class II MHG antigens. Langerhans' cells are of bone marrow origin and are derived from a circulating precursor which is probably related to the monocyte.
‘Physical Activity 4 Everyone’ school-based intervention to prevent decline in adolescent physical activity levels: 12 month (mid-intervention) report on a cluster randomised trial
Authors: Rachel Sutherland, Elizabeth Campbell, David R Lubans, Philip J Morgan, Anthony D Okely, Nicole Nathan, Luke Wolfenden, Jarrod Wiese, Karen Gillham, Jenna Hollis, John Wiggers
Journal: British Journal of Sports Medicine (2015)

Background Adolescence is a recognised period of physical activity decline, particularly among low-income communities. We report the 12-month (midpoint) effects of a 2-year multicomponent physical activity intervention implemented in disadvantaged secondary schools. Methods A cluster randomised trial was undertaken in 10 secondary schools located in disadvantaged areas in New South Wales, Australia. Students in Grade 7 were recruited, with follow-up in Grade 8. The intervention was guided by socioecological theory and included seven physical activity strategies, and six implementation adoption strategies. The primary outcome was mean minutes of moderate-to-vigorous physical activity (MVPA) per day assessed using Actigraph GT3X accelerometers. Outcome data were analysed using repeated measures linear mixed models. Results At baseline, 1150 (93%) students participated in the data collection (mean age 12 years, 48% boys) and 1050 (79%) students participated at 12-month follow-up. By the 12-month follow-up, the six implementation adoption strategies had been used to support schools to deliver four of the seven physical activity elements. There was a significant group-by-time interaction for mean minutes of MVPA per day in favour of the intervention group (adjusted difference between groups at follow-up=3.85 min, 95% CI (0.79 to 6.91), p≤0.01), including significantly more vigorous physical activity (2.45 min, p≤0.01), equating to 27 min more MVPA per week. Summary At 12-month follow-up, the intervention had reduced the decline in physical activity among adolescents from disadvantaged schools. The intervention may assist students to meet physical activity guidelines.
Apolipoprotein CIII in Apolipoprotein B Lipoproteins Enhances the Adhesion of Human Monocytic Cells to Endothelial Cells
Authors: Akio Kawakami, Masanori Aikawa, Peter Libby, Pilar Alcaide, Francis W. Luscinskas, Frank M. Sacks
Journal: Circulation (2006)

Lipoproteins containing apolipoprotein (apo) CIII predict coronary heart disease and associate with components of the metabolic syndrome. ApoCIII inhibits lipoprotein catabolism in plasma. However, it is unknown whether apoCIII itself, or in association with VLDL, LDL, or HDL, directly affects atherogenic mechanisms in vascular cells. Thus, we investigated the direct effect of lipoproteins that do or do not have apoCIII, and apoCIII itself, on adhesion of THP-1 cells, a human monocytic cell line, to vascular endothelial cells (ECs).VLDL CIII+ and LDL CIII+ (100 microg apoB/mL) from fasting plasma of 18 normolipidemic volunteers increased THP-1 cell adhesion to ECs under static conditions by 2.4+/-0.3-fold and 1.8+/-0.7-fold, respectively (P<0.01), whereas VLDL or LDL without apoCIII did not affect THP-1 cell adhesion. ApoCIII (100 microg/mL), but not apoCI, apoCII or apoE, also increased THP-1 cell adhesion by 2.1+/-0.6-fold. Studies with human peripheral blood monocytes yielded similar results. ApoCIII also had strong proadhesive effects under shear flow conditions. VLDL CIII+, LDL CIII+, or apoCIII itself activated PKCalpha and RhoA in THP-1 cells, which resulted in beta1-integrin activation and enhancement of THP-1 cell adhesion. Interestingly, HDL CIII+ did not affect THP-1 cell adhesion, whereas HDL without apoCIII decreased their adhesion.ApoB lipoproteins that contain apoCIII increase THP-1 cell adhesion to ECs via PKCalpha and RhoA-mediated beta1-integrin activation. These results indicate that apoCIII not only modulates lipoprotein metabolism but also may directly contribute to the development of atherosclerosis.
Complex regional pain syndrome in thoracic outlet syndrome
Authors: B Kaymak, L Özçakar
Journal: British Journal of Sports Medicine (2004)

The importance of the hippocampus in declarative memory is limited to recently acquired memory, and remotely acquired memory is believed to be stored somewhere in the neocortex. However, it remains unknown how the memory network is reorganized from a hippocampus-dependent form into a neocortex-dependent one. We reported previously that the medial prefrontal cortex (mPFC) is important for this neocortex-dependent remote memory in rat trace eyeblink conditioning. Here, we investigate the involvement of NMDA receptors in the mPFC in this reorganization and determine the time window of their contribution using chronic infusion of an antagonist into the mPFC, specifically during the postlearning consolidation period. The rats with blockade of the mPFC NMDA receptors during the first 1 or 2 weeks after learning showed a marked impairment in memory retention measured 6 weeks after learning, but relearned normally with subsequent conditioning. In contrast, the same treatment had no effect if it was performed during the third to fourth weeks or during the first day just after learning. The specificity of NMDA receptor blockade was confirmed by the reduced long-term potentiation in the hippocampal-prefrontal pathway in these rats. These results suggest that successful establishment of remotely acquired memory requires activation of NMDA receptors in the mPFC during at least the initial week of the postlearning period. Such NMDA receptor-dependent processes may mediate the maturation of neocortical networks that underlies permanent memory storage and serve as a way to reorganize memory circuitry to the neocortex-dependent form.
Soluble PD-1 Facilitates 4-1BBL–Triggered Antitumor Immunity against Murine H22 Hepatocarcinoma <i>In vivo</i>
Authors: Han Xiao, Bo Huang, Ye Yuan, Dong Li, Ling-Fei Han, Yi Liu, Wei Gong, Feng-Hua Wu, Gui-Mei Zhang, Zuo-Hua Feng
Journal: Clinical Cancer Research (2007)

Abstract Purpose: The use of costimulatory molecules targeting distinct T-cell signaling pathways has provided a means for triggering and enhancing antitumor immunity; however, it is still not fully understood what types of costimulatory molecules are suitable for the combination in tumor therapy. Our purpose in this study is to establish an effective antitumor immune approach by using costimulatory molecule 4-1BBL in combination with soluble PD-1. Experimental Design: The murine H22 hepatocarcinoma served as an ectopic tumor model. Local gene transfer was done by injection with naked plasmid p4-1BBL and/or psPD-1. The synergistic mechanism of dual-gene therapy was elucidated by detecting the change of gene expression of immunoregulatory factors in tumor microenvironment. The effects of immunotherapy were evaluated by testing the function of tumor-specific T cells, measuring tumor weight or volume, survival of mice, and H&amp;E staining of tissues. Results: 4-1BBL expressed by normal nonimmune cells effectively enhanced antitumor immune response but up-regulated PD-L1 and did not reduce IL-10 and transforming growth factor-β (TGF-β). sPD-1 synergized with 4-1BBL to establish efficient antitumor immune environment, including down-regulation of IL-10 and TGF-β, further up-regulation of interleukin (IL)-2 and IFN-γ, and higher CD8+ T-cell infiltration. The combined treatment by 4-1BBL/sPD-1 eradicated tumors from mice with small amounts of preexistent tumor cells or tumors from ∼60% of individuals with larger amounts of preexistent tumor cells. Conclusions: Our findings in this report imply a great potential of 4-1BBL in combination with sPD-1 in tumor therapeutics with the in vivo existent tumor cells as antigens.