44 research outputs found

    Diet as prophylaxis and treatment for venous thromboembolism?

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    <p>Abstract</p> <p>Background</p> <p>Both prophylaxis and treatment of venous thromboembolism (VTE: deep venous thrombosis (DVT) and pulmonary emboli (PE)) with anticoagulants are associated with significant risks of major and fatal hemorrhage. Anticoagulation treatment of VTE has been the standard of care in the USA since before 1962 when the U.S. Food and Drug Administration began requiring randomized controlled clinical trials (RCTs) showing efficacy, so efficacy trials were never required for FDA approval. In clinical trials of 'high VTE risk' surgical patients before the 1980s, anticoagulant prophylaxis was clearly beneficial (fatal pulmonary emboli (FPE) without anticoagulants = 0.99%, FPE with anticoagulants = 0.31%). However, observational studies and RCTs of 'high VTE risk' surgical patients from the 1980s until 2010 show that FPE deaths without anticoagulants are about one-fourth the rate that occurs during prophylaxis with anticoagulants (FPE without anticoagulants = 0.023%, FPE while receiving anticoagulant prophylaxis = 0.10%). Additionally, an FPE rate of about 0.012% (35/28,400) in patients receiving prophylactic anticoagulants can be attributed to 'rebound hypercoagulation' in the two months after stopping anticoagulants. Alternatives to anticoagulant prophylaxis should be explored.</p> <p>Methods and Findings</p> <p>The literature concerning dietary influences on VTE incidence was reviewed. Hypotheses concerning the etiology of VTE were critiqued in relationship to the rationale for dietary versus anticoagulant approaches to prophylaxis and treatment.</p> <p>Epidemiological evidence suggests that a diet with ample fruits and vegetables and little meat may substantially reduce the risk of VTE; vegetarian, vegan, or Mediterranean diets favorably affect serum markers of hemostasis and inflammation. The valve cusp hypoxia hypothesis of DVT/VTE etiology is consistent with the development of VTE being affected directly or indirectly by diet. However, it is less consistent with the rationale of using anticoagulants as VTE prophylaxis. For both prophylaxis and treatment of VTE, we propose RCTs comparing standard anticoagulation with low VTE risk diets, and we discuss the statistical considerations for an example of such a trial.</p> <p>Conclusions</p> <p>Because of (a) the risks of biochemical anticoagulation as anti-VTE prophylaxis or treatment, (b) the lack of placebo-controlled efficacy data supporting anticoagulant treatment of VTE, (c) dramatically reduced hospital-acquired FPE incidence in surgical patients without anticoagulant prophylaxis from 1980 - 2010 relative to the 1960s and 1970s, and (d) evidence that VTE incidence and outcomes may be influenced by diet, randomized controlled non-inferiority clinical trials are proposed to compare standard anticoagulant treatment with potentially low VTE risk diets. We call upon the U. S. National Institutes of Health and the U.K. National Institute for Health and Clinical Excellence to design and fund those trials.</p

    Chronic Nicotine Differentially Regulates ␣6-and ␤3- Containing Nicotinic Cholinergic Receptors in Rat Brain

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    ABSTRACT We investigated the effects of chronic nicotine on ␣6-and ␤3-containing nicotinic acetylcholine receptors (nAChRs) in two rat brain regions using three methodological approaches: radioligand binding, immunoprecipitation, and nicotine-stimulated synaptosomal release of dopamine. Nicotine was administered by osmotic minipumps for 2 weeks. Quantitative autoradiography with [ 125 I]␣-conotoxin MII to selectively label ␣6* nAChRs showed a 28% decrease in binding in the striatum but no change in the superior colliculus. Immunoprecipitation of nAChRs labeled by [ 3 H]epibatidine in these two regions showed that chronic nicotine increased ␣4-and ␤2-containing nAChRs by 39 to 67%. In contrast, chronic nicotine caused a 39% decrease in ␣6-containing nAChRs in striatum but no change in superior colliculus. No changes in ␤3-containing nAChRs were seen in either region after chronic nicotine. The decreased expression of ␣6-containing nAChRs persisted for at least 3 days, recovering to baseline by 7 days after removal of the pumps. There was a small but significant decrease in total nicotine-stimulated dopamine release in striatal synaptosomes after nicotine exposure. However, the component of dopamine release that was resistant to ␣-conotoxin MII blockade was unaffected, whereas dopamine release that was sensitive to blockade by ␣-conotoxin MII was decreased by 56%. These findings indicate that the ␣6* nAChR is regulated differently from other nAChR subtypes, and they suggest that the inclusion of a ␤3 subunit with ␣6 may serve to inhibit nicotineinduced down-regulation of these receptors

    Heat content of the Arabian Sea Mini Warm Pool is increasing

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    © The Author(s), 2015. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in Atmospheric Science Letters 17 (2016): 39-42, doi:10.1002/asl.596.Sea surface temperature in the Arabian Sea Mini Warm Pool has been suggested to be one of the factors that affects the Indian summer monsoon. In this paper, we analyze the annual ocean heat content (OHC) of this region during 1993–2010, using in situ data, satellite observations, and a model simulation. We find that OHC increases significantly in the region during this period relative to the north Indian Ocean, and propose that this increase could have caused the decrease in Indian Summer Monsoon Rainfall that occurred at the same time

    The ATLAS inner detector trigger performance in pp collisions at 13 TeV during LHC Run 2

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    The design and performance of the inner detector trigger for the high level trigger of the ATLAS experiment at the Large Hadron Collider during the 2016-18 data taking period is discussed. In 2016, 2017, and 2018 the ATLAS detector recorded 35.6 fb1^{-1}, 46.9 fb1^{-1}, and 60.6 fb1^{-1} respectively of proton-proton collision data at a centre-of-mass energy of 13 TeV. In order to deal with the very high interaction multiplicities per bunch crossing expected with the 13 TeV collisions the inner detector trigger was redesigned during the long shutdown of the Large Hadron Collider from 2013 until 2015. An overview of these developments is provided and the performance of the tracking in the trigger for the muon, electron, tau and bb-jet signatures is discussed. The high performance of the inner detector trigger with these extreme interaction multiplicities demonstrates how the inner detector tracking continues to lie at the heart of the trigger performance and is essential in enabling the ATLAS physics programme

    Biostatistics for dummies

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