441 research outputs found

    Nachtlärminduzierte Schlafstörungen und Herz-Kreislauf-Risiko

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    Impairment of sleep in the sense of insomnias, i.e. difficulties falling asleep and staying asleep, early morning awakening and chronical unrestful sleep is widespread in the population and are associated with a variety of physical and mental health disorders. The environmental causes of insomnia include a number of factors, with nighttime noise being an important cause. Recent data from the European Environment Agency shows that environmental noise (road traffic, railway, aircraft and industrial noise) causes severe sleep disorders among 6.5 million people in Europe. New epidemiological and mechanistic field studies show that in particular night traffic noise can lead, among other things, to impaired vascular function, thrombo-inflammatory changes, an increase in stress hormones and increased blood pressure, representing significant risk factors for cardiovascular diseases. According to the European Environment Agency, environmental noise causes 48000 additional cases of ischemic heart disease and 12000 premature deaths each year

    Lärm und Herz-Kreislauf-Erkrankungen

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    Environmental noise is a significant environmental risk factor for public health. The European Environment Agency states that at least 20% of the European population are exposed to harmful day-evening-night noise levels of 55 decibels (dB), whereas the World Health Organization recommends up to 10 dB lower limit values, depending on the noise source, for the protection of the population. Chronic noise can interfere with daily activities and sleep and trigger mental and physiological stress reactions that can increase the risk of cardiovascular disease in the long term. Therefore, preventive measures at the source including noise-reducing structural changes are essential to ensure compliance with noise limits and to protect the population from the negative health effects of noise

    Gesundheitsrisiko Mobilfunkstrahlung? Was ändert sich mit 5G?

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    Exposure of the population to radiofrequency electromagnetic fields (RF-EMF) is dominated by the use of wireless communication devices close to the body. Exposure from transmitters far from the body is on average several orders of magnitude below the international guideline values. With increasing mobile data usage and the associated use of higher frequencies for 5G, a densification of the mobile network is to be expected. However, this will not necessarily increase the overall RF-EMF exposure of the population, as mobile phones emit less with better signal quality. 5G is a technological advancement of the previous mobile radio technology with the same biophysical properties. So far, no health effects below the guideline limits have been consistently demonstrated for RF-EMF. Biological effects such as changes of the electrical activity of the brain or the oxidative balance were observed for high local exposure in the range of the exposure guideline limits. According to current knowledge, they do not represent a health risk

    Mitochondrial oxidative stress and nitrate tolerance – comparison of nitroglycerin and pentaerithrityl tetranitrate in Mn-SOD(+/- )mice

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    BACKGROUND: Chronic therapy with nitroglycerin (GTN) results in a rapid development of nitrate tolerance which is associated with an increased production of reactive oxygen species (ROS). According to recent studies, mitochondrial ROS formation and oxidative inactivation of the organic nitrate bioactivating enzyme mitochondrial aldehyde dehydrogenase (ALDH-2) play an important role for the development of nitrate and cross-tolerance. METHODS: Tolerance was induced by infusion of wild type (WT) and heterozygous manganese superoxide dismutase mice (Mn-SOD(+/-)) with ethanolic solution of GTN (12.5 μg/min/kg for 4 d). For comparison, the tolerance-free pentaerithrityl tetranitrate (PETN, 17.5 μg/min/kg for 4 d) was infused in DMSO. Vascular reactivity was measured by isometric tension studies of isolated aortic rings. ROS formation and aldehyde dehydrogenase (ALDH-2) activity was measured in isolated heart mitochondria. RESULTS: Chronic GTN infusion lead to impaired vascular responses to GTN and acetylcholine (ACh), increased the ROS formation in mitochondria and decreased ALDH-2 activity in Mn-SOD(+/- )mice. In contrast, PETN infusion did not increase mitochondrial ROS formation, did not decrease ALDH-2 activity and accordingly did not lead to tolerance and cross-tolerance in Mn-SOD(+/- )mice. PETN but not GTN increased heme oxygenase-1 mRNA in EA.hy 926 cells and bilirubin efficiently scavenged GTN-derived ROS. CONCLUSION: Chronic GTN infusion stimulates mitochondrial ROS production which is an important mechanism leading to tolerance and cross-tolerance. The tetranitrate PETN is devoid of mitochondrial oxidative stress induction and according to the present animal study as well as numerous previous clinical studies can be used without limitations due to tolerance and cross-tolerance

    Myeloperoxidase Serum Levels Predict Risk in Patients With Acute Coronary Syndromes

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    BACKGROUND: Polymorphonuclear neutrophils (PMNs) have gained attention as critical mediators of acute coronary syndromes (ACS). Myeloperoxidase (MPO), a hemoprotein abundantly expressed by PMNs and secreted during activation, possesses potent proinflammatory properties and may contribute directly to tissue injury. However, whether MPO also provides prognostic information in patients with ACS remains unknown. METHODS AND RESULTS: MPO serum levels were assessed in 1090 patients with ACS. We recorded death and myocardial infarctions during 6 months of follow-up. MPO levels did not correlate with troponin T, soluble CD40 ligand, or C-reactive protein levels or with ST-segment changes. However, patients with elevated MPO levels (>350 microg/L; 31.3%) experienced a markedly increased cardiac risk (adjusted hazard ratio [HR] 2.25 [1.32 to 3.82]; P=0.003). In particular, MPO serum levels identified patients at risk who had troponin T levels below 0.01 microg/L (adjusted HR 7.48 [95% CI 1.98 to 28.29]; P=0.001). In a multivariate model that included other biochemical markers, troponin T (HR 1.99; P=0.023), C-reactive protein (1.25; P=0.044), vascular endothelial growth factor (HR 1.87; P=0.041), soluble CD40 ligand (HR 2.78; P<0.001), and MPO (HR 2.11; P=0.008) were all independent predictors of the patient's 6-month outcome. CONCLUSIONS: In patients with ACS, MPO serum levels powerfully predict an increased risk for subsequent cardiovascular events and extend the prognostic information gained from traditional biochemical markers. Given its proinflammatory properties, MPO may serve as both a marker and mediator of vascular inflammation and further points toward the significance of PMN activation in the pathophysiology of ACS

    Mitochondrial genomes of giant deers suggest their late survival in Central Europe

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    The giant deer Megaloceros giganteus is among the most fascinating Late Pleistocene Eurasian megafauna that became extinct at the end of the last ice age. Important questions persist regarding its phylogenetic relationship to contemporary taxa and the reasons for its extinction. We analyzed two large ancient cervid bone fragments recovered from cave sites in the Swabian Jura (Baden-Württemberg, Germany) dated to 12,000 years ago. Using hybridization capture in combination with next generation sequencing, we were able to reconstruct nearly complete mitochondrial genomes from both specimens. Both mtDNAs cluster phylogenetically with fallow deer and show high similarity to previously studied partial Megaloceros giganteus DNA from Kamyshlov in western Siberia and Killavullen in Ireland. The unexpected presence of Megaloceros giganteus in Southern Germany after the Ice Age suggests a later survival in Central Europe than previously proposed. The complete mtDNAs provide strong phylogenetic support for a Dama-Megaloceros clade. Furthermore, isotope analyses support an increasing competition between giant deer, red deer, and reindeer after the Last Glacial Maximum, which might have contributed to the extinction of Megaloceros in Central Europe

    Monitoring changes in the position and boundaries of climate clusters at different time intervals

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    This article describes the development of a web application for the study of the correlation-regression analysis of meteorological data and search, the shift of the geographic center of clusters of different time intervals

    Coronary stent strut fractures: classification, prevalence and clinical associations

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    Introduction. The frequency, characteristics and clinical implications of Strut fractures (SFs) remain incompletely understood. Methods and results. A total of 185 (160 patients) newer-generation drug-eluting stents (DES) were imaged. SFs were found in 21 DES (11.4%) and were classified in four patterns: one single stacked strut (41%); two or more stacked struts (23%); deformation without gap (27%); transection (9%). In multivariable analysis, calcific and bifurcation lesions were associated with SF in DES (OR: 3.5 [1.1-11] and 4.0 [2.2-7.2], p < 0.05). Device eccentricity and asymmetry as well as optical coherence tomography (OCT) features of impaired strut healing were also associated with SF. The prevalence of fractures was similar in a set of 289 bioresorbable scaffolds (BRS). In a separate series of 20 device thromboses and 36 device restenoses, the prevalence of SF was higher (61.2% of DES and 66.7% of BRS, p < 0.001 for both), with a higher frequency of complex SF patterns (p < 0.0001). In logistic regression analysis, fractures were a correlate of device complications (p < 0.0001, OR = 24.9 [5.6-111] for DES and OR = 6.0 [1.8-20] for BRS). Discussion. The prevalence of OCT-diagnosed SF was unexpectedly high in the setting of elective controls and it increased by about three-fold in the setting of device failure. Fractures were associated with increased lesion complexity and device asymmetry/eccentricity and were more frequent in the setting of device failure such as restenosis and thrombosis.Cardiovascular Aspects of Radiolog
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