tbuckley/cabot-search huggingface dataset:
Individual responses to short-term heat acclimatisation as predictors of football performance in a hot, dry environment
Authors: Sebastien Racinais, Magni Mohr, Martin Buchheit, Sven Christian Voss, Nadia Gaoua, Justin Grantham, Lars Nybo
Journal: British Journal of Sports Medicine (2012)

To identify the relationship between field performance in a hot environment and individual heat acclimatisation responses in football players.Nineteen semiprofessional football players completed a match in 21°C followed by 6 days of acclimatisation in dry heat (38-43°C, 12-30% relative humidity) and a match in ~43°C. A heat-response test (30 min walk+30 min seated; 44°C) was performed at the beginning and end of the acclimatisation period.The acclimatisation period increased sweat rate by 34% during a standard heat-exposure test and reduced sweat sodium concentration by 18% (both p≤0.005). Plasma volume changes showed large interindividual differences (-10 to +20%). Match-running performance was impaired in hot ambient condition and demonstrated marked interindividual differences (total distance -6.0±5.8%, high-intensity running -16.4±21.5%, both p≤0.002). Only haematological markers investigated during the heat-response test correlated with the ability of the player to cope with heat stress in a competitive situation; that is, changes in haematocrit between the heat-response tests were correlated to changes in total running during the game, r=-0.75; 90%CI [-0.88 to -0.51].Heat acclimatisation responses and in turn, match-running performance in the heat, are highly individual. The players displaying the largest haematological adaptations were able to maintain the same activity when playing in the heat as when playing in temperate conditions. As such, team doctors might use acclimatisation indicators obtained from a heat-response test to predict the ability of individual players to cope with heat in competitive situations and individualise their preparation accordingly.
Coffee drinking and hepatocellular carcinoma risk: A meta-analysis
Authors: Francesca Bravi, Cristina Bosetti, Alessandra Tavani, Vincenzo Bagnardi, Silvano Gallus, Eva Negri, Silvia Franceschi, Carlo La Vecchia
Journal: Hepatology (2007)

Several studies suggest an inverse relation between coffee drinking and risk of hepatocellular carcinoma (HCC). We conducted a meta-analysis of published studies on HCC that included quantitative information on coffee consumption. Ten studies were retrieved (2,260 HCC cases), including 6 case–control studies from southern Europe and Japan (1551 cases) and 4 cohort studies from Japan (709 cases). The summary relative risk (RR) for coffee drinkers versus non-drinkers was 0.54 (95% confidence interval [CI] 0.38-0.76) for case–control studies and 0.64 (95% CI 0.56-0.74) for cohort studies. The overall RR was 0.59 (95% CI 0.49-0.72), with significant heterogeneity between studies. The overall summary RR for low or moderate coffee drinkers was 0.70 (95% CI 0.57-0.85), and that for high drinkers was 0.45 (95% CI 0.38-0.53). The summary RR for an increase of 1 cup of coffee per day was 0.77 (95% CI 0.72-0.83) from case–control studies, 0.75 (95% CI 0.65-0.85) from cohort studies, and 0.77 (95% CI 0.72-0.82) overall. The consistency of an inverse relation between coffee drinking and HCC across study design and geographic areas weighs against a major role of bias or confounding. Coffee drinking has also been related to reduced risk of other liver diseases, thus suggesting a continuum of the favorable effect of coffee on liver function. However, subjects with liver conditions may selectively reduce their coffee consumption. Conclusion: The present analysis provides evidence that the inverse relation between coffee and HCC is real, though inference on causality remains open to discussion. (HEPATOLOGY 2007.)
Predictors of HBeAg loss after lamivudine treatment for chronic hepatitis B
Authors: Robert P. Perrillo, Ching-Lung Lai, Yun-Fan Liaw, Jules L. Dienstag, Eugene R. Schiff, Solko W. Schalm, Jenny E. Heathcote, Nathaniel A. Brown, Mark Atkins, Mary Woessner, Stephen D. Gardner
Journal: Hepatology (2002)

Elevated alanine transaminase (ALT) levels and low serum hepatitis B virus (HBV) DNA predict a higher likelihood of hepatitis B e antigen (HBeAg) loss in patients with chronic hepatitis B treated with interferon. Predictors of HBeAg loss in patients treated with lamivudine are not known. The objective of this analysis of 4 lamivudine-controlled Phase III trials was to determine patient-dependent or laboratory variables that predict HBeAg loss. Predictors of HBeAg loss in patients treated with interferon, lamivudine plus interferon, or placebo are also described. A total of 805 adults with chronic hepatitis B were treated either with lamivudine (n = 406), matching placebo (n = 196), interferon (n = 68), or the combination of lamivudine plus interferon (n = 135). Demographic and baseline disease characteristics were used in stepwise multivariate analyses to identify features that were predictive of lamivudine-induced HBeAg loss. HBeAg loss correlated with increased pretreatment ALT levels in all groups. The rate of HBeAg loss was highest among patients with pretreatment ALT levels greater than 5 times the upper limit of normal (ULN) and was most pronounced in the lamivudine group (56%). Multivariate modeling indicated that elevated baseline ALT levels ( P &lt; .001) and histologic activity index (HAI) score ( P &lt; .001) were important predictors of HBeAg loss in response to lamivudine. The effect of pretreatment ALT levels on HBeAg loss was similar for Asians and Caucasians. In conclusion, elevated pretreatment ALT levels and/or active histologic disease were the most important predictors of lamivudine-induced HBeAg loss. Asians and Caucasians had similar rates of response to lamivudine at comparable ALT levels.
Oral Prednisolone for Preschool Children with Acute Virus-Induced Wheezing
Authors: Jayachandran Panickar, Monica Lakhanpaul, Paul C. Lambert, Priti Kenia, Terence Stephenson, Alan Smyth, Jonathan Grigg
Journal: New England Journal of Medicine (2009)

Attacks of wheezing induced by upper respiratory viral infections are common in preschool children between the ages of 10 months and 6 years. A short course of oral prednisolone is widely used to treat preschool children with wheezing who present to a hospital, but there is conflicting evidence regarding its efficacy in this age group.We conducted a randomized, double-blind, placebo-controlled trial comparing a 5-day course of oral prednisolone (10 mg once a day for children 10 to 24 months of age and 20 mg once a day for older children) with placebo in 700 children between the ages of 10 months and 60 months. The children presented to three hospitals in England with an attack of wheezing associated with a viral infection; 687 children were included in the intention-to-treat analysis (343 in the prednisolone group and 344 in the placebo group). The primary outcome was the duration of hospitalization. Secondary outcomes were the score on the Preschool Respiratory Assessment Measure, albuterol use, and a 7-day symptom score.There was no significant difference in the duration of hospitalization between the placebo group and the prednisolone group (13.9 hours vs. 11.0 hours; ratio of geometric means, 0.90; 95% confidence interval, 0.77 to 1.05) or in the interval between hospital admission and signoff for discharge by a physician. In addition, there was no significant difference between the two study groups for any of the secondary outcomes or for the number of adverse events.In preschool children presenting to a hospital with mild-to-moderate wheezing associated with a viral infection, oral prednisolone was not superior to placebo. (Current Controlled Trials number, ISRCTN58363576.)
Negative impact of bone metastasis on outcome in clear-cell renal cell carcinoma treated with sunitinib
Authors: B. Beuselinck, S. Oudard, O. Rixe, P. Wolter, A. Blesius, J. Ayllon, R. Elaidi, P. Schöffski, E. Barrascout, A. Morel, B. Escudier, H. Lang, J. Zucman-Rossi, J. Medioni
Journal: Annals of Oncology (2010)
Abstract 3754: A prospective imaging biomarker trial for early identification of GBM patients resistant to first line therapy
Authors: Craig J. Galban, Thomals L. Chenevert, Charles R. Meyer, Christina Tsien, Theodore S. Lawrence, Daniel A. Hamstra, Larry Junck, Pia C. Sundgren, Timothy D. Johnson, Alnawaz Rehemtulla, Brian D. Ross
Journal: Cancer Research (2010)

Abstract We assessed whether quantification of therapeutic-associated tumor cellularity and hemodynamic alterations may help in the early assessment of treatment resistance in patients with high grade glioma. Patients with high grade glioma (n=45) received concurrent chemoradiation. Apparent diffusion coefficient (ADC) and relative cerebral blood volume (rCBV) maps were acquired prior to chemoradiation and at week 3 during treatment on a prospective IRB-approved study. Clinical and conventional MR parameters, including average baseline ADC and rCBV and radiological response, were evaluated as prognostic indicators of one-year survival. Parametric response map (PRM), an innovative, voxel-by-voxel method of image analysis, was also performed. Of 45 patients, median survival was found to be 14.9 months with 44% of patients living shorter than one year (median survival of 6.6 months). Baseline ADC was the only single model not found to be predictive of survival at one year, whereas in a multivariate analysis PRMADC+ and PRMrCBV- had a stronger correlation to survival than baseline rCBV. Overall, a composite model of PRMADC+ and PRMrCBV- was found to have the strongest correlation with one-year survival. This study demonstrates the potential of a composite parametric model sensitive to both tumor cellularity and hemodynamic alterations following first line therapy for providing an early assessment of patient resistant to chemoradiation. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3754.
Original article: Prevalence and cumulative incidence of food hypersensitivity in the first 3 years of life
Authors: C. Venter, B. Pereira, K. Voigt, J. Grundy, C. B. Clayton, B. Higgins, S. H. Arshad, T. Dean
Journal: Allergy (2008)

Background: Prevalence and incidence of food hypersensitivity (FHS) and its trends in early childhood are unclear. Methods: A birth cohort born on the Isle of Wight (UK) between 2001 and 2002 was followed‐up prospectively. Children were clinically examined and skin prick tested at set times and invited for food challenges when indicated. Results: Nine hundred and sixty‐nine children were recruited and 92.9%, 88.5% and 91.9% of them respectively were assessed at 1, 2 and 3 years of age. Prevalence of sensitization to foods was 2.2%, 3.8% and 4.5% respectively at these ages. Cumulatively, 5.3% [95% confidence interval (CI): 3.9–7.1] children were sensitized to a food. Using open food challenge and a good clinical history, the cumulative incidence of FHS was 6.0% (58/969, 95% CI: 4.6–7.7). Based on double‐blinded, placebo‐controlled, food challenge (DBPCFC) and a good clinical history, the cumulative incidence was 5.0% (48/969, 95% CI: 3.7–6.5). There is no evidence to suggest that the incidence of FHS has increased, comparing these results with previous studies. Overall, 33.7% of parents reported a food‐related problem and of these, 16.1% were diagnosed with FHS by open challenge and history and 12.9% by DBPCFC and history. Main foods implicated were milk, egg and peanut. Conclusions: By the age of 3 years, 5–6% of children suffer from FHS based on food challenges and a good clinical history. There were large discrepancies between reported and diagnosed FHS. Comparing our data with a study performed in the USA more than 20 years ago, there were no significant differences in the cumulative incidence of FHS.
The Role of Hepatocyte Enlargement in Hepatic Pressure in Cirrhotic and Noncirrhotic Alcoholic Liver Disease
Authors: Laurence M. Blendis, Hector Orrego, Ian R. Crossley, Joan E. Blake, Alan Medline, Yedy Israel
Journal: Hepatology (1982)

The relationship between hepatocyte enlargement and intrahepatic and portal pressures was studied in a group of 163 patients with alcoholic liver disease presenting liver biopsy abnormalities, including 91 cirrhotics. For the complete group, hepatocyte surface areas were significantly correlated (r = 0.73, p &lt; 0.0001) with pressure. Cirrhotics as a group had a mean average pressure of 20.4 ± 0.9 mm Hg, while that for noncirrhotics was 11.7 ± 0.8 mm Hg (p &lt; 0.0001). The corresponding values for mean hepatocyte surface areas were 2,308 ± 76 μm 2 and 1,692 ± 63 /μm 2 . In cirrhotics with corrected sinusoidal pressures (wedged hepatic vein pressure–free pressure), or intrahepatic pressures below 10 mm Hg, mean hepatocyte surface area 1,405 ± 51 μm 2 was in the same area range as that of the group of noncirrhotics with similar pressures (1,410 ± 46 μm 2 ). It is postulated that higher pressures often seen in cirrhotics are due to the existence of larger cells in these patients, rather than the existence of “regenerative” nodules. Cirrhosis per se was not a good indicator of portal hypertension and 23% of cirrhotics were shown to have pressures below 10 mm Hg. On the other hand, when hepatocyte enlargement was used as an indicator of portal pressure, it was found that pressures below 10 mm Hg occurred in only 6.8% of individuals with cell surface areas exceeding 1,700 μm 2 . In patients with or without cirrhosis in whom two pressure determinations were carried out simultaneously with the biopsies, it was observed that changes in pressures were followed remarkably closely by changes in cell surface areas in the same direction (91% of cases, p &lt; 0.001). Elevated portal pressure could also be found in a group of 43 chronic alcoholics in whom 50 liver biopsies were reported as “normal.” In these, correlation between hepatocyte area and intrahepatic pressure was also highly significant (r = 0.88, p &lt; 0.0001) with an abrupt increase in intrahepatic pressure above 10 mm Hg, for hepatocyte areas greater than 1,500 μm 2 . Collagen accumulation in the space of Disse has been proposed as a cause of portal hypertension. While we have confirmed that a correlation exists between Disse collagen scores and intrahepatic or corrected sinusoidal pressures, when measured at a single point in time, (r = 0.63, p &lt; 0.0001), collagen did not follow the changes in pressure in 65% of the cases. While these observations firmly support our earlier postulation of a strong correlation between hepatocyte enlargement and the production of intrahepatic or portal hypertension, further studies should be conducted to establish causality in the association between these two factors.
Enhanced Apoptotic Activity of a p53 Variant in Tumors Resistant to Wild-Type p53 Treatment
Authors: Isabella A. Atencio, Jenny B. Avanzini, Duane Johnson, Saskia Neuteboom, Mei-Ting Vaillancourt, Loretta L. Nielsen, Gerry Hajian, Suganto Sutjipto, Barry J. Sugarman, Jennifer Philopena, Diane L. McAllister, Josefina C. Beltran, Margarita Nodelman, Murali Ramachandra, Ken N. Wills
Journal: Molecular Therapy (2001)

TP53 is the most commonly altered tumor-suppressor gene in cancer and is currently being tested in Phase II/III gene replacement trials. Many tumors contain wild-type TP53 sequence with elevated MDM2 protein levels, targeting p53 for degradation. These tumors are more refracto-ry to treatment with exogenous wild-type p53. Here we generate a recombinant adenovirus expressing a p53 variant, rAd-p53 (d 13–19), that is deleted for the amino acid sequence neces-sary for MDM2 binding (amino acids 13–19). We compared the apoptotic activity of rAd-p53 (d 13–19) with that of a recombinant adenovirus expressing wild-type p53 (rAd-p53) in cell lines that differ in endogenous p53 status. rAd-p53 (d 13–19) caused higher levels of apoptosis in p53 wild-type tumor lines compared with wild-type p53 treatment, as measured by annexin V-FITC staining. In p53-altered tumor lines, rAd-p53 (d 13–19) showed apoptotic activity similar to that seen with wild-type p53 treatment. In normal cells, no increase in cytopathicity was detected with rAd-p53 (d 13ndash;19) compared with wild-type p53 treatment. This variant protein displayed synergy with chemotherapeutic agents to inhibit proliferation of ovarian and breast cell lines. The p53 variant showed greater antitumor activity in an established p53 wild-type tumor com-pared with treatment with wild-type p53. The p53 variant represents a means of expanding TP53 gene therapy to tumors that are resistant to p53 treatment due to the cellular responses to wild-type p53.
Effects of Suramin on In Vitro Growth of Fresh Human Tumors
Authors: C. W. Taylor, R. Lui, P. Fanta, S. E. Salmon
Journal: JNCI Journal of the National Cancer Institute (1992)

Background: Suramin is a polysulfonated urea recently tested in clinical trials as an anticancer agent. Purpose: To define tumor types for further clinical testing of suramin, we assessed the in vitro activity of suramin against fresh human tumor specimens. Methods: Inhibition of tumor colony formation (human tumor clonogenic assay [HTCA] method) and inhibition of tritiated thymidine incorporation (TTI method) were used as indicators of drug sensitivity. Results: With the use of the HTCA method, 80% or more of carcinomas of the colon, endometrium, kidney, lung (non-small-cell), and ovary as well as malignant melanoma and mesothelioma were sensitive to 200/mL of suramin by continuous exposure. Suramin's antitumor activity was dose dependent, and it was less effective when tested at concentrations of 50μg/mL or less. With the TTI method, the more slowly growing tumors (breast cancer, colon cancer, multiple myeloma, non-Hodgkin's lymphoma, prostate cancer, and sarcoma) appeared to be less sensitive to suramin. However, when the two assay methods were directly compared in melanoma and ovarian cancer specimens, individual tumors were generally more sensitive to suramin (greater inhibition relative to control) using the HTCA method, whereas the TTI method appeared to underestimate suramin's antitumor activity. There was no significant difference in the activity of suramin when tested in the presence of 10% versus 50% serum. Conclusion: These results provide an experimental basis for clinical evaluations of suramin therapy in patients with colon, endometrial, kidney, non-small-cell lung, and ovarian cancers as well as malignant melanoma and mesothelioma. (J Natl Cancer Inst 84: 489–494, 1992].
Retinoic acid-induced gene expression in normal and leukemic myeloid cells.
Authors: M P Murtaugh, O Dennison, J P Stein, P J Davies
Journal: The Journal of Experimental Medicine (1986)

Retinoic acid has been shown to induce large accumulations of tissue transglutaminase in cultured myeloid cells. Addition of retinoic acid to mouse resident peritoneal macrophages increased the level of tissue transglutaminase mRNA within 30-60 min. Retinoic acid also increased tissue transglutaminase mRNA levels in human promyelocytic leukemia (HL-60) cells. These studies show that retinoic acid can induce acute alterations in specific gene expression in both normal and leukemic myeloid cells.
Chronic Iron Administration Increases Vascular Oxidative Stress and Accelerates Arterial Thrombosis
Authors: Sharlene M. Day, Damon Duquaine, Lakshmi V. Mundada, Rekha G. Menon, Bobby V. Khan, Sanjay Rajagopalan, William P. Fay
Journal: Circulation (2003)

Iron overload has been implicated in the pathogenesis of ischemic cardiovascular events. However, the effects of iron excess on vascular function and the thrombotic response to vascular injury are not well understood.We examined the effects of chronic iron dextran administration (15 mg over 6 weeks) on thrombosis, systemic and vascular oxidative stress, and endothelium-dependent vascular reactivity in mice. Thrombus generation after photochemical carotid artery injury was accelerated in iron-loaded mice (mean time to occlusive thrombosis, 20.4+/-8.5 minutes; n=10) compared with control mice (54.5+/-35.5 minutes, n=10, P=0.009). Iron loading had no effect on plasma clotting, vessel wall tissue factor activity, or ADP-induced platelet aggregation. Acute administration of dl-cysteine, a reactive oxygen species scavenger, completely abrogated the effects of iron loading on thrombus formation, suggesting that iron accelerated thrombosis through a pro-oxidant mechanism. Iron loading enhanced both systemic and vascular reactive oxygen species production. Endothelium-dependent vasorelaxation was impaired in iron-loaded mice, indicating reduced NO bioavailability.Moderate iron loading markedly accelerates thrombus formation after arterial injury, increases vascular oxidative stress, and impairs vasoreactivity. Iron-induced vascular dysfunction may contribute to the increased incidence of ischemic cardiovascular events that have been associated with chronic iron overload.
Evaluation of the atopy patch test and the cutaneous late-phase reaction as relevant models for the study of allergic inflammation in patients with atopic eczema☆☆☆★
Authors: E LANGEVELDWILDSCHUT, T THEPEN, I BIHARIA, F VANREIJSEN, I DEVRIESA, P BRUIJNZEEL, C BRUIJNZEELKOOMEN
Journal: Journal of Allergy and Clinical Immunology (1996)
Cyclic Strain Inhibits Notch Receptor Signaling in Vascular Smooth Muscle Cells In Vitro
Authors: David Morrow, Catherine Sweeney, Yvonne A. Birney, Philip M. Cummins, Dermot Walls, Eileen M. Redmond, Paul A. Cahill
Journal: Circulation Research (2005)

Notch signaling has been shown recently to regulate vascular cell fate in adult cells. By applying a uniform equibiaxial cyclic strain to vascular smooth muscle cells (SMCs), we investigated the role of strain in modulating Notch-mediated growth of SMCs in vitro. Rat SMCs cultured under conditions of defined equibiaxial cyclic strain (0% to 15% stretch; 60 cycles/min; 0 to 24 hours) exhibited a significant temporal and force-dependent reduction in Notch 3 receptor expression, concomitant with a significant reduction in Epstein Barr virus latency C promoter-binding factor-1/recombination signal-binding protein of the Jkappa immunoglobulin gene-dependent Notch target gene promoter activity and mRNA levels when compared with unstrained controls. The decrease in Notch signaling was Gi-protein- and mitogen-activated protein kinase-dependent. In parallel cultures, cyclic strain inhibited SMC proliferation (cell number and proliferating cell nuclear antigen expression) while significantly promoting SMC apoptosis (annexin V binding, caspase-3 activity and bax/bcl-x(L) ratio). Notch 3 receptor overexpression significantly reversed the strain-induced changes in SMC proliferation and apoptosis to levels comparable to unstrained control cells, whereas Notch inhibition further potentiated the changes in SMC apoptosis and proliferation. These findings suggest that cyclic strain inhibits SMC growth while enhancing SMC apoptosis, in part, through regulation of Notch receptor and downstream target gene expression.