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One Cause (one + cause)
Selected AbstractsInsulin resistance and endothelial dysfunction: the road map to cardiovascular diseasesDIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 6 2006Eugenio Cersosimo Abstract Cardiovascular disease affects approximately 60% of the adult population over the age of 65 and represents the number one cause of death in the United States. Coronary atherosclerosis is responsible for the vast majority of the cardiovascular events, and a number of cardiovascular risk factors have been identified. In recent years, it has become clear that insulin resistance and endothelial dysfunction play a central role in the pathogenesis of atherosclerosis. Much evidence supports the presence of insulin resistance as the fundamental pathophysiologic disturbance responsible for the cluster of metabolic and cardiovascular disorders, known collectively as the metabolic syndrome. Endothelial dysfunction is an important component of the metabolic or insulin resistance syndrome and this is demonstrated by inadequate vasodilation and/or paradoxical vasoconstriction in coronary and peripheral arteries in response to stimuli that release nitric oxide (NO). Deficiency of endothelial-derived NO is believed to be the primary defect that links insulin resistance and endothelial dysfunction. NO deficiency results from decreased synthesis and/or release, in combination with exaggerated consumption in tissues by high levels of reactive oxygen (ROS) and nitrogen (RNS) species, which are produced by cellular disturbances in glucose and lipid metabolism. Endothelial dysfunction contributes to impaired insulin action, by altering the transcapillary passage of insulin to target tissues. Reduced expansion of the capillary network, with attenuation of microcirculatory blood flow to metabolically active tissues, contributes to the impairment of insulin-stimulated glucose and lipid metabolism. This establishes a reverberating negative feedback cycle in which progressive endothelial dysfunction and disturbances in glucose and lipid metabolism develop secondary to the insulin resistance. Vascular damage, which results from lipid deposition and oxidative stress to the vessel wall, triggers an inflammatory reaction, and the release of chemoattractants and cytokines worsens the insulin resistance and endothelial dysfunction. From the clinical standpoint, much experimental evidence supports the concept that therapies that improve insulin resistance and endothelial dysfunction reduce cardiovascular morbidity and mortality. Moreover, interventional strategies that reduce insulin resistance ameliorate endothelial dysfunction, while interventions that improve tissue sensitivity to insulin enhance vascular endothelial function. There is general agreement that aggressive therapy aimed simultaneously at improving insulin-mediated glucose/lipid metabolism and endothelial dysfunction represents an important strategy in preventing/delaying the appearance of atherosclerosis. Interventions that 1 correct carbohydrate and lipid metabolism, 2 improve insulin resistance, 3 reduce blood pressure and restore vascular reactivity, and 4 attenuate procoagulant and inflammatory responses in adults with a high risk of developing cardiovascular disease reduce cardiovascular morbidity and mortality. Whether these benefits hold when the same prevention strategies are applied to younger, high-risk individuals remains to be determined. Copyright © 2006 John Wiley & Sons, Ltd. [source] Are Anorexia nervosa and bulimia nervosa separate disorders?EUROPEAN EATING DISORDERS REVIEW, Issue 1 2009Challenging the, transdiagnostic' theory of eating disorders Abstract Background Anorexia nervosa (AN) and bulimia nervosa (BN) are classified as separate and distinct clinical disorders. Recently, there has been support for a transdiagnostic theory of eating disorders, which would reclassify them as one disorder. Objective To determine whether AN and BN are a single disorder with one cause or separate disorders with different causes. Method Hill's Criteria of Causation were used to test the hypothesis that AN and BN are one disorder with a single cause. Hill's Criteria of Causation demand that the minimal conditions are needed to establish a causal relationship between two items which include all of the following: strength of association, consistency, temporality, biological gradient, plausibility, coherence, experimental evidence and analogy. Results The hypothesis that AN and BN have a single cause did not meet all of Hill's Criteria of Causation. Strength of association, plausibility, analogy and some experimental evidence were met, but not consistency, specificity, temporality, biological gradient, coherence and most experimental evidence. Conclusions The hypothesis that AN and BN are a single disorder with a common cause is not supported by Hill's Criteria of Causation. This argues against the notion of a transdiagnostic theory of eating disorders. Copyright © 2008 John Wiley & Sons, Ltd and Eating Disorders Association. [source] Caffeine administration results in greater tension development in previously fatigued canine muscle in situEXPERIMENTAL PHYSIOLOGY, Issue 6 2005Richard A. Howlett In isolated single skeletal myocytes undergoing long-term fatiguing contractions, caffeine (CAF) can result in nearly immediate restoration of generated tension to near-prefatigue levels by increasing Ca2+ release via activation of sarcoplasmic reticulum release channels. This study tested whether arterial CAF infusion (>5 mm) would cause a similar rapid restoration of tetanic isometric tension during contractions to fatigue in perfused canine hindlimb muscle in situ. Tetanic contractions were elicited by electrical stimulation (200 ms trains, 50 Hz, 1 contraction s,1), and biopsies were taken from the muscle at rest and during contractions: (1) following the onset of fatigue (tension ,60% of initial value); and (2) following CAF administration. Resting muscle ATP, PCr and lactate contents were 25.2 ± 0.4, 76.9 ± 3.3 and 14.4 ± 3.3 mmol (kg dry weight),1, respectively. At fatigue, generated tetanic tension was 61.1 ± 6.9% of initial contractions. There was a small but statistically significant recovery of tetanic tension (64.9 ± 6.6% of initial value) with CAF infusion, after which the muscle showed incomplete relaxation. At fatigue, muscle ATP and PCr contents had fallen significantly (P < 0.05) to 18.1 ± 1.1 and 18.9 ± 2.1 mmol (kg dry weight),1, respectively, and lactate content had increased significantly to 27.7 ± 5.4 mmol (kg dry weight),1. Following CAF, skeletal muscle ATP and PCr contents were significantly lower than corresponding fatigue values (15.0 ± 1.3 and 10.9 ± 2.2 mmol (kg dry weight),1, respectively), while lactate was unchanged (22.2 ± 3.9 mmol (kg dry weight),1). These results demonstrate that caffeine can result in a small, but statistically significant, recovery of isometric tension in fatigued canine hindlimb muscle in situ, although not nearly to the same degree as seen in isolated single muscle fibres. This suggests that, in this in situ isolated whole muscle model, alteration of Ca2+ metabolism is probably only one cause of fatigue. [source] Paraquat-induced Fanconi syndromeNEPHROLOGY, Issue 5 2005HYO W GIL SUMMARY: The ingestion of paraquat, a non-selective herbicide, can be fatal in humans. Paraquat is toxic to multiple organs, including the kidney, heart, gastrointestinal tract and central nervous system. Although paraquat has been established as one cause of acute tubular necrosis, Fanconi syndrome presenting as severe hypophosphataemia after paraquat intoxication has not been reported. Here, we report the case of a 44-year-old Korean woman who presented with generalized proximal tubular dysfunction including aminoaciduria, phosphaturia and glycosuria after paraquat intoxication. We found that severe hypophosphataemia induces deep drowsiness. Renal biopsy findings indicated the presence of acute tubular necrosis that may be reversible. [source] Ectopic pregnancy: Challenging accepted management strategiesAUSTRALIAN AND NEW ZEALAND JOURNAL OF OBSTETRICS AND GYNAECOLOGY, Issue 4 2009George CONDOUS Ectopic pregnancy is still the number one cause of maternal deaths in early pregnancy. The diagnostic capabilities of transvaginal ultrasound to confirm an EP are well founded. In fact, ultrasound technology, particularly the introduction of high-resolution transvaginal probes, has been the driving force behind the revolutionary change towards conservative management strategies in ectopic pregnancy care. Clinically stable women, however, with a scan diagnosis of a tubal ectopic pregnancy still routinely undergo surgery or are given methotrexate (MTX) at presentation. Conservative management for ectopic pregnancy may be considered in the context of clinical stability. Reassessment at 48 h allows evaluation of the trophoblast activity or ,trophoblastic load'. Falling serum hCG levels at 48 h suggest that the ectopic trophoblast is resolving spontaneously and it may be possible to avoid methotrexate administration in this sub-group. Women with increasing serum hCG levels at 48 h, indicating the trophoblast is still active, should be targeted for methotrexate. By calculating the pre-treatment hCG ratio (hCG 48 h/hCG 0 h), it is possible to triage women with an ectopic pregnancy for conservative management. There are, however, no randomised data to support the use of MTX over expectant management. In this review, some of the current management strategies in ectopic pregnancy management will be challenged. [source] Rise in maternal mortality in the NetherlandsBJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 4 2010JM Schutte Please cite this paper as: Schutte J, Steegers E, Schuitemaker N, Santema J, de Boer K, Pel M, Vermeulen G, Visser W, van Roosmalen J, the Netherlands Maternal Mortality Committee. Rise in maternal mortality in the Netherlands. BJOG 2009;117:399,406. Objective, To assess causes, trends and substandard care factors in maternal mortality in the Netherlands. Design, Confidential enquiry into the causes of maternal mortality. Setting, Nationwide in the Netherlands. Population, 2,557,208 live births. Methods, Data analysis of all maternal deaths in the period 1993,2005. Main outcome measures, Maternal mortality. Results, The overall maternal mortality ratio was 12.1 per 100 000 live births, which was a statistically significant rise compared with the maternal mortality ratio of 9.7 in the period 1983,1992 (OR 1.2, 95% CI 1.0,1.5). The most frequent direct causes were (pre-)eclampsia, thromboembolism, sudden death in pregnancy, sepsis, obstetric haemorrhage and amniotic fluid embolism. The number of indirect deaths also increased, mainly caused by an increase in cardiovascular disorders (OR 2.5, 95% CI 1.4,4.6). Women younger than 20 years and older than 45 years, those with high parity or from nonwestern immigrant populations were at higher risk. Most substandard care was found in women with pre-eclampsia (91%) and in immigrant populations (62%). Conclusions, Maternal mortality in the Netherlands has increased since 1983,1992. Pre-eclampsia remains the number one cause. Groups at higher risk for complications during pregnancy should be better identified early in pregnancy or before conception, in order to receive preconception advice and more frequent antenatal visits. There is an urgent need for the better education of women and professionals concerning the danger signs, and for the training of professionals in order to improve maternal health care. [source] | ||||||||||