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Traffic-related air pollution and the onset of myocardial infarction: disclosing benzene as a trigger? A small-area case-crossover study.
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OBJECTIVE
Exposure to traffic is an established risk factor for the triggering of myocardial infarction (MI). Particulate matter, mainly emitted by diesel vehicles, appears to be the most important stressor. However, the possible influence of benzene from gasoline-fueled cars has not been explored
The effect of 17-methoxyl-7-hydroxy-benzene-furanchalcone on NF-κB and the inflammatory response during myocardial ischemia reperfusion injury in rats.
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The aim of this study was to investigate the effect of 17-methoxyl-7-hydroxy-benzene-furanchalcone (MHBFC) on nuclear factor-kappa-binding (NF-κB) and the inflammatory response in rats with myocardial ischemia reperfusion injury (MI/RI). Sprague-Dawley rats were randomly divided into 7 groups, and
A randomized, double-blind, placebo-controlled study of the safety and efficacy of intravenous MCC-135 as an adjunct to primary percutaneous coronary intervention in patients with acute myocardial infarction: Evaluation of MCC-135 for left ventricular salvage in acute myocardial infarction (EVOLVE).
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OBJECTIVE
The objective of the study was to test the hypothesis that intracellular calcium modulation by 5-methyl-2-[piperazin-1-yl] benzene sulfonic acid monohydrate (MCC-135 [Caldaret]; Mitsubishi Pharma Corporation, Osaka, Japan) would preserve left ventricular function and reduce infarct size in
Effects of the spin trap agent disodium- [tert-butylimino)methyl]benzene-1,3-disulfonate N-oxide (generic NXY-059) on intracerebral hemorrhage in a rabbit Large clot embolic stroke model: combination studies with tissue plasminogen activator.
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OBJECTIVE
It has been proposed that the novel spin trap agent disodium-[(tert-butylimino)methyl]benzene-1,3-disulfonate N-oxide (NXY-059) may be useful in the treatment of ischemia and stroke. To date, there is little information concerning the safety of NXY-059 when administered in combination with
Neuroprotective effects of water-soluble Ganoderma lucidum polysaccharides on cerebral ischemic injury in rats.
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OBJECTIVE
To investigate the neuroprotective effects of water-soluble Ganoderma lucidum polysaccharides (GLPS) on cerebral ischemic injury in rats, and to explore the involved mechanisms.
METHODS
Two models [middle cerebral artery occlusion (MCAO) in Sprague-Dawley (SD) rats and oxygen and glucose
Adipose tissue levels of organochlorine pesticides and polychlorinated biphenyls and risk of non-Hodgkin's lymphoma.
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In this nested case-control study we examined the relationship between non-Hodgkin's lymphoma (NHL) and organochlorine pesticide exposure. We used a data set originally collected between 1969 and 1983 in the U.S. Environmental Protection Agency National Human Adipose Tissue Survey. Adipose samples
[IR and Raman spectroscopic studies on the derivatives of butylphthalide].
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dl-NBP is a potentially beneficial and promising drug for treatment of ischemic stroke with multiple actions that affect different pathophysiologic processes, such as improving microcirculation, decreasing brain infarct volume, regulating energy metabolism, and especially inhibiting platelet
Synthesis of novel ligustrazine derivatives as NA+/H+ exchange inhibitors.
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A novel series of 3,5,6-trimethylpyrazine-2-methoxy (or methylamino) substituted benzoyl-guanidine derivatives were designed and synthesized as Na(+)/H(+) exchange (NHE) inhibitors. In this study, compounds with electron-withdrawing substituents on the benzene ring seemed to improve NHE-1 inhibitory
[Breathing: Ambient Air Pollution and Health - Part II].
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The second part of the DGP-statement on adverse health effects of ambient air pollution provides an overview of the current ambient air quality in Germany and its development in the past 20 years. Further, effects of air pollution on the cardiovascular system und underlying pathophysiological
Comparison of two indices of exposure to polycyclic aromatic hydrocarbons in a retrospective aluminium smelter cohort.
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BACKGROUND
The association between coal tar-derived substances, a complex mixture of polycyclic aromatic hydrocarbons, and cancer is well established. However, the specific aetiological agents are unknown.
OBJECTIVE
To compare the dose-response relationships for two common measures of coal
Subchronic oral toxicity and metabolite profiling of the p53 stabilizing agent, CP-31398, in rats and dogs.
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CP-31398 (N'-[2-[2-(4-methoxyphenyl)ethenyl]-4-quinazolinyl]-N,N-dimethyl-1,3-propanediamine dihydrochloride) is a styrylquinazoline that stabilizes the DNA binding conformation of p53, thereby maintaining the activity of p53 as a transcription factor and tumor suppressor. In consideration of the
Long term effects of traffic noise on mortality in the city of Barcelona, 2004-2007.
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Numerous studies showing statistically significant associations between environmental noise and adverse health effects already exist for short-term (over one day at most) and long-term (over a year or more) noise exposure, both for morbidity and (albeit to a lesser extent) mortality. Recently,
Why do neuroprotective drugs that are so promising in animals fail in the clinic? An industry perspective.
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1. No neuroprotective drug has yet been shown to be effective in treating acute ischaemic stroke in the clinic, despite evidence of efficacy in animal models. 2. An academic/industry round-table group recently published guidelines to be met if a drug was to be progressed to clinical trial. 3. Major
Impact of temporary traffic bans on the risk of acute coronary syndromes in a large metropolitan area
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Background: Strong epidemiologic evidence has highlighted the role of pollution, on top of adverse climate features, as a novel cardiovascular risk factor. However, mechanistic proof that reducing pollution may be beneficial to prevent
NXY-059 maintains Akt activation and inhibits release of cytochrome C after focal cerebral ischemia.
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Stroke is the third leading cause of death in the US, with a prevalence of 750,000 patients per year, and a social cost estimated at $50 billion. Current therapeutics are targeted at restoring blood flow rather than on preventing the actual mechanisms associated with neuronal cell death. Here, we
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