408 research outputs found
The role of qualitative research in adding value to a randomised controlled trial: lessons from a pilot study of a guided e-learning intervention for managers to improve employee wellbeing and reduce sickness absence
The GEM study was funded by the National Institute for Health Research
Public Health Research Programme (project number 10/3007/06)
Quantification of particle-induced inflammatory stress response: a novel approach for toxicity testing of earth materials
Intra-articular temperatures of the knee in sports – An in-vivo study of jogging and alpine skiing
<p>Abstract</p> <p>Background</p> <p>Up to date, no information exists about the intra-articular temperature changes of the knee related to activity and ambient temperature.</p> <p>Methods</p> <p>In 6 healthy males, a probe for intra-articular measurement was inserted into the notch of the right knee. Each subject was jogging on a treadmill in a closed room at 19°C room temperature and skiing in a ski resort at -3°C outside temperature for 60 minutes. In both conditions, temperatures were measured every fifteen minutes intra-articulary and at the skin surface of the knee. A possible influence on joint function and laxity was evaluated before and after activity. Statistical analysis of intra-articular and skin temperatures was done using nonparametric Wilcoxon's sign rank sum test and Mann-Whitney's-U-Test.</p> <p>Results</p> <p>Median intra-articular temperatures increased from 31.4°C before activity by 2.1°C, 4°C, 5.8°C and 6.1°C after 15, 30, 45 and 60 min of jogging (all p ≤ 0.05). Median intra-articular temperatures dropped from 32.2°C before activity by 0.5°C, 1.9°C, 3.6°C and 1.1°C after 15, 30, 45 and 60 min of skiing (all n.s.). After 60 minutes of skiing (jogging), the median intra-articular temperature was 19.6% (8.7%) higher than the skin surface temperature at the knee. Joint function and laxity appeared not to be different before and after activity within both groups.</p> <p>Conclusion</p> <p>This study demonstrates different changes of intra-articular and skin temperatures during sports in jogging and alpine skiing and suggests that changes are related to activity and ambient temperature.</p
Modulation of Tcf7l2 Expression Alters Behavior in Mice
The comorbidity of type 2 diabetes (T2D) with several psychiatric diseases is well established. While environmental factors may partially account for these co-occurrences, common genetic susceptibilities could also be implicated in the confluence of these diseases. In support of shared genetic burdens, TCF7L2, the strongest genetic determinant for T2D risk in the human population, has been recently implicated in schizophrenia (SCZ) risk, suggesting that this may be one of many loci that pleiotropically influence both diseases. To investigate whether Tcf7l2 is involved in behavioral phenotypes in addition to its roles in glucose metabolism, we conducted several behavioral tests in mice with null alleles of Tcf7l2 or overexpressing Tcf7l2. We identified a role for Tcf7l2 in anxiety-like behavior and a dose-dependent effect of Tcf7l2 alleles on fear learning. None of the mutant mice showed differences in prepulse inhibition (PPI), which is a well-established endophenotype for SCZ. These results show that Tcf7l2 alters behavior in mice. Importantly, these differences are observed prior to the onset of detectable glucose metabolism abnormalities. Whether these differences are related to human anxiety-disorders or schizophrenia remains to be determined. These animal models have the potential to elucidate the molecular basis of psychiatric comorbidities in diabetes and should therefore be studied further
Overexpression of endothelial nitric oxide synthase suppresses features of allergic asthma in mice
BACKGROUND: Asthma is associated with airway hyperresponsiveness and enhanced T-cell number/activity on one hand and increased levels of exhaled nitric oxide (NO) with expression of inducible NO synthase (iNOS) on the other hand. These findings are in paradox, as NO also relaxes airway smooth muscle and has immunosuppressive properties. The exact role of the endothelial NOS (eNOS) isoform in asthma is still unknown. We hypothezised that a delicate regulation in the production of NO and its bioactive forms by eNOS might be the key to the pathogenesis of asthma. METHODS: The contribution of eNOS on the development of asthmatic features was examined. We used transgenic mice that overexpress eNOS and measured characteristic features of allergic asthma after sensitisation and challenge of these mice with the allergen ovalbumin. RESULTS: eNOS overexpression resulted in both increased eNOS activity and NO production in the lungs. Isolated thoracic lymph nodes cells from eNOS overexpressing mice that have been sensitized and challenged with ovalbumin produced significantly less of the cytokines IFN-γ, IL-5 and IL-10. No difference in serum IgE levels could be found. Further, there was a 50% reduction in the number of lymphocytes and eosinophils in the lung lavage fluid of these animals. Finally, airway hyperresponsiveness to methacholine was abolished in eNOS overexpressing mice. CONCLUSION: These findings demonstrate that eNOS overexpression attenuates both airway inflammation and airway hyperresponsiveness in a model of allergic asthma. We suggest that a delicate balance in the production of bioactive forms of NO derived from eNOS might be essential in the pathophysiology of asthma
Robotic neurorehabilitation: a computational motor learning perspective
Conventional neurorehabilitation appears to have little impact on impairment over and above that of spontaneous biological recovery. Robotic neurorehabilitation has the potential for a greater impact on impairment due to easy deployment, its applicability across of a wide range of motor impairment, its high measurement reliability, and the capacity to deliver high dosage and high intensity training protocols
Significance of vascular endothelial growth factor in growth and peritoneal dissemination of ovarian cancer
Vascular endothelial growth factor (VEGF) is a key regulator of angiogenesis which drives endothelial cell survival, proliferation, and migration while increasing vascular permeability. Playing an important role in the physiology of normal ovaries, VEGF has also been implicated in the pathogenesis of ovarian cancer. Essentially by promoting tumor angiogenesis and enhancing vascular permeability, VEGF contributes to the development of peritoneal carcinomatosis associated with malignant ascites formation, the characteristic feature of advanced ovarian cancer at diagnosis. In both experimental and clinical studies, VEGF levels have been inversely correlated with survival. Moreover, VEGF inhibition has been shown to inhibit tumor growth and ascites production and to suppress tumor invasion and metastasis. These findings have laid the basis for the clinical evaluation of agents targeting VEGF signaling pathway in patients with ovarian cancer. In this review, we will focus on VEGF involvement in the pathophysiology of ovarian cancer and its contribution to the disease progression and dissemination
Diffractive Dijet Production at s = 630 and 1800 GeV at the Fermilab Tevatron
We report a measurement of the diffractive structure function F-jj(D) of the antiproton obtained from a study of dijet events produced in association with a leading antiproton in (p) over barp collisions at roots = 630 GeV at the Fermilab Tevatron. The ratio of F-jj(D) at roots = 630 GeV to F-jj(D) obtained from a similar measurement at roots = 1800 GeV is compared with expectations from QCD factorization and other theoretical predictions. We also report a measurement of the xi (x-Pomeron) and beta (x of parton in Pomeron) dependence of F-jj(D) at roots = 1800 GeV . In the region 0.035 < ξ < 0.095 , \t\ < 1 GeV2 , and β < 0.5 , F-jj(D)(beta, xi) is found to be of the form beta(-1.0+/-0.1) xi(-0.9+/-0. 1) , which obeys beta-xi factorization
Direct CP violation searches in charmless hadronic B meson decays
This is the pre-print version of the Article. The official published version can be accessed from the links below. Copyright @ 2002 APSWe search for direct CP violation in charmless hadronic B decays observed in a sample of about 22.7 million BB̅ pairs collected with the BABAR detector at the SLAC PEP-II asymmetric-energy e+e- collider. We measure the following charge asymmetries: ACP(B±→η′K±)=-0.11±0.11±0.02, ACP(B±→ωπ±)=-0.01 - 0.31 + 0.29±0.03, ACP(B±→φK±)=-0.05±0.20±0.03, ACP(B±→φK*±)=-0.43 - 0.30 + 0.36±0.06, and ACP(B0→φK*0)=0.00±0.27±0.03.This work was supported by DOE and NSF (USA), NSERC (Canada), IHEP (China), CEA and CNRS-IN2P3 (France), BMBF (Germany), INFN (Italy), NFR (Norway), MIST (Russia), and PPARC (United Kingdom). Individuals have received support from the Swiss NSF, A. P. Sloan Foundation, Research Corporation, and Alexander von Humboldt Foundation
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