The ability of the SCORE high-risk model to predict 10-year cardiovascular disease mortality in Norway.

AIMS: To evaluate the predictive accuracy of the Systematic Coronary Risk Evaluation (SCORE) project high-risk function in Norway. METHODS AND RESULTS: We included 57 229 individuals screened in 1985-1992 from two population-based surveys in Norway (age groups 40-49, 50-59, and 60-69 years). The data have been linked to the Norwegian Cause of Death Registry. The SCORE high-risk algorithm for the prediction of 10-year cardiovascular disease (CVD) mortality was applied, and the risk factors entered into the model were age, sex, total cholesterol, systolic blood pressure, and smoking (yes/no). The number of expected events estimated by the SCORE model (E) was compared with the observed numbers (O). The SCORE low-risk algorithm was studied for comparison. In men, the observed number of CVD deaths was 718, compared with 1464 estimated by the SCORE high-risk function (O/E ratios 0.53, 0.53 and 0.45, for age groups 40-49, 50-59 and 60-69, respectively). In women, the observed and expected numbers were 226 and 547. The O/E ratios decreased with age (ratios 0.60, 0.45 and 0.37, respectively), i.e. the overestimation increased with age. The low-risk function predicted reasonably well for men (ratios 0.85, 0.92 and 0.79, respectively), whereas an overestimation was found for women aged 50-59 and 60-69 years (ratios 0.69 and 0.56, respectively). CONCLUSION: The SCORE high-risk model overestimated the number of CVD deaths in Norway. Before implementation in clinical practice, proper adjustments to national levels are required.     

Effects of the angiotensin II type 1 receptor antagonist telmisartan on monocyte adhesion and activation in patients with essential hypertension.

Circulating monocytes from hypertensive patients show elevated secretion patterns of pro-inflammatory cytokines, an increased expression of adhesion molecules, and an increased adhesion to vascular endothelial cells. We tested the hypothesis that telmisartan, an angiotensin II type 1 (AT(1)) receptor antagonist, reduces the activation of circulating monocytes from hypertensive patients and diminishes the monocyte-endothelial cell adhesion. Monocytes of 20 hypertensive patients and 20 normotensive controls were isolated by density gradient centrifugation and Dynabeads, and the monocyte adhesion to human aortic endothelial cell monolayers was measured by adhesion assays. To characterize monocyte activation we assessed the expression of activity-related cell surface markers that are also involved in monocyte adhesion to endothelial cells, such as CD11a/b and CD54, as well as the chemokine receptors CCR1, CCR2 and CCR5 before and after telmisartan therapy using flow cytometry. Spontaneous adhesion of monocytes from hypertensive patients and the adhesion after stimulation with angiotensin II were significantly increased compared with those in normotensive controls (p<0.05). Treatment of hypertensive patients with the AT(1) receptor antagonist telmisartan significantly diminished the adhesion of circulating monocytes to human endothelial cells (p=0.02) despite the increase in the expressions of CD11b, CD54 and CCR5 after telmisartan therapy. Reducing monocyte adhesion may be a novel beneficial effect of the AT(1) receptor antagonist telmisartan helping to prevent vascular alterations in hypertension. The mechanism of action remains to be elucidated, since reduction in monocyte adhesion was not attributable to changes in adhesion molecule expression.     

Management respiratorischer Störungen bei Polytrauma

Trauma und Berufskrankheit - Respiratorische Störungen im Rahmen einer Polytraumatisierung sind nicht selten. Sie können sich bereits in der präklinischen Phase entwickeln und damit...     

New aspects of the etiology of tendon rupture

Summary Native collagen fibers were exposed to different dynamic loads to simulate damage to tendons and ligaments relevant clinically and for sports medicine. The results suggest that the rupture of a tendon is caused at the submicroscopic fibrillar level. Not only slow or very fast elongation, but also very fast unloading of stretched fibers seems to be responsible for disseminated damage, which reduces the stability of a fiber. This damage is induced by intrafibrillar sliding processes, which occur only a few seconds before macroscopic slippage takes place. The significance of these events for the beginning and progress of repair in vivo is discussed. The conclusions are supported by simultaneous mechanical and radiological measurements, as well as by light- and electron-microscopic results.

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Zusammenfassung Zur Simulierung klinisch bzw. sportmedizinisch relevanter Schäden an Sehnen und Bändern wurden native Kollagenfasern unterschiedlichen dynamischen Belastungen ausgesetzt. Die erzielten Ergebnisse sprechen dafür, die Ursachen einer Sehnenruptur im submikroskopischen fibrillären Bereich zu suchen. Sowohl eine langsame oder ruckartige Dehnung als auch eine ruckartige Entlastung zugbelasteter Fasern scheinen für das Auftreten disseminierter, die Faserstabilität reduzierender Gefügestörungen verantwortlich zu sein. Diese Gefügestörungen werden durch intrafibrilläre Gleitvorgänge eingeleitet, die an den noch voll belastbaren Fasern nur wenige Sekunden vor dem Einsetzen eines makroskopischen Faserfließens auftreten. Die Bedeutung dieser Ereignisse für den Beginn und Verlauf einer in vivo stattfindenden Reparationsphase wird erörtert. Die Aussagen werden gestützt durch simultane mechanische und röntgenographische Messungen sowie durch makroskopische, licht- und elektronenmikroskopische Befunde.

     

Role of cytokines and chemokines in prion infections of the central nervous system

Prion infections of the central nervous system (CNS) are characterised by a reactive gliosis and the subsequent degeneration of neuronal tissue. The activation of glial cells, which precedes neuronal death, is likely to be initially caused by the deposition of misfolded, proteinase K-resistant, isoforms (termed PrP(res)) of the prion protein (PrP) in the brain. Cytokines and chemokines released by PrP(res)-activated glia cells may contribute directly or indirectly to the disease development by enhancement and generalisation of the gliosis and via cytotoxicity for neurons. However, the actual role of prion-induced glia activation and subsequent cytokine/chemokine secretion in disease development is still far from clear. In the present work, we review our present knowledge concerning the functional biology of cytokines and chemokines in prion infections of the CNS.     

Akromegalie und generalisierte Lipodystrophie

The rare autosomal-recessive Berardinelli-Seip congenital lipodystrophy syndrome (BSCL) is characterized by general lipodystrophy, acromegalic appearance, hypertriglyceridemia, insulin resistance and hepatomegaly. Here, we present the case of an 11 month old female infant of consanguineous parents from Libya, who was brought to us for diagnosis because of her unusual appearance since birth. Additionally to the above mentioned symptoms, we found an accelerated bone age, myopathy without muscle weakness, but no signs of mental retardation or cardiomyopathy. This constellation of symptoms is typical for the BSCL1 mutation phenotype, which was confirmed by molecular genetics. The girl will undergo frequent clinical and laboratory controls and follow a fibre- and medium chain fatty acid rich diet. This case demonstrates a genetic extreme of“metabolic syndrome X” and thus could provide new knowledge about diabetes mellitus type 2 and its prophylaxis.