Gene/Protein Disease Symptom Drug Enzyme Compound
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 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

M-mode echocardiography was performed 18 to 22 hours after a haemodialysis session in 16 patients under chronic dialysis. The patients (12 men and 4 women, mean age 21 years, haematocrit 24 +/- 5%) were normotensive and had no clinical or radiological sign of heart failure. Patients with renal hypertension, diabetes or amyloidosis had been excluded from the study. Eight healthy subjects of similar age, heart rate and blood pressure were used as controls. In all 24 individuals the following parameters were calculated: end diastolic time diameter index (DTDI), end systolic time diameter index (STDI), ejection time (ET), mean velocity of circumferential fiber shortening (VCF) and ejection fraction (EF). DTDI was greater in haemodialyzed patients (31 +/- 2 mm/m2) than in controls, but STDI and ET were the same in both groups. This would explain the increase of VCF (1.68 +/- 0.1 c/sec) and EF (0.78 +/- 0.05) observed in dialyzed patients. After compression of the fistula for 3 min the differences disappeared. These results suggest that the echocardiographic measurements listed above give a better idea of the true contractile state of the left ventricle in haemodialyzed patients, disregarding load changes due to the fistula, to anaemia and to intermittent volume expansion.
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PMID:[Echocardiographic measurement of true left ventricular inotropism in patients under haemodialysis (author's transl)]. 731 3

Approximately 40% of the US population report using complementary and alternative medicine, including Maharishi Vedic Medicine (MVM), a traditional, comprehensive system of natural medicine, for relief from chronic and other disorders. Although many reports suggest health benefits from individual MVM techniques, reports on integrated holistic approaches are rare. This case series, designed to investigate the effectiveness of an integrated, multimodality MVM program in an ideal clinical setting, describes the outcomes in four patients: one with sarcoidosis; one with Parkinson's disease; a third with renal hypertension; and a fourth with diabetes/essential hypertension/anxiety disorder. Standard symptom reports and objective markers of disease were evaluated before, during, and after the treatment period. Results suggested substantial improvements as indicated by reductions in major signs, symptoms, and use of conventional medications in the four patients during the 3-week in-residence treatment phase and continuing through the home follow-up program.
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PMID:Improvements in chronic diseases with a comprehensive natural medicine approach: a review and case series. 1097 82

Appropriate nephron function is dependent on the detailed spatial interrelationship of blood vessels with the tubular components. However, because of methodological limitations,the three-dimensional anatomical complexity of the renal vasculature and its geometrical relationship with specific tubular segments along the nephron has been difficult to study in a quantitative manner. Three-dimensional microcomputed tomography (3D micro CT) offers the unique opportunity to image kidney sample volumes with a high spatial resolution (of up to 5 microm cubic voxel size) without physically sectioning them, thereby allowing accurate calculations of vessel tortuosity and density, as indices of neovascularization, as well as volume and distribution of various kidney structures. In conjunction with molecular biology techniques, valuable associations between renal microstructures and activation of local molecular pathways can be drawn to elucidate mechanisms of renal disease and design therapeutic approaches. For example, recent studies in animal models of renal hypertension, hypercholesterolemia, and diabetes mellitus have shown that medical intervention to decrease oxidative stress and micro-inflammation may preserve renal microstructures as well as renal function in these chronic renal diseases. Future developments will be needed to establish the place of 3D micro CT in developing, directing, and monitoring the treatment of chronic kidney diseases.
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PMID:Review--3D micro CT imaging of renal micro-structural changes. 1654 58

Atherosclerosis is a systemic disease responsible for strokes, myocardial infarction, renal hypertension, and intermittent claudication. Acute coronary syndromes (unstable angina, acute myocardial infarction, and sudden cardiac death) are the major causes of morbidity and mortality in developed countries. These acute manifestations of heart disease share a common pathophysiologic phenomenon: coronary thrombosis. Two principal mechanisms are responsible for coronary thrombosis: plaque disruption (75%) and plaque erosion (25%). Disrupted plaques exhibit a large lipid content, increased macrophages, and a thin fibrous cap. Hypercholesterolemia and diabetes are associated with plaque disruption. Eroded plaques are smooth muscle-cell rich with an intact fibrous cap. Cigarette smoking is associated with plaque erosion, most frequently in women with sudden death when they are younger than 50 years of age. Systemic inflammation is a novel, robust marker for future cardiovascular events, not only in patients with established atherosclerotic disease but also in apparently healthy individuals. Local inflammation at the plaque disruption site is documented by increased macrophage infiltration. Macrophages are responsible for plaque disruption, neovascularization, smooth muscle cell apoptosis, and plaque thrombogenicity. Experimental studies have identified the lipid core as the most thrombogenic substrate of the atherosclerotic plaque. Tissue factor, a cell membrane-bound protein, is crucial in thrombus formation. Tissue factor is expressed in apoptotic macrophages, suggesting that macrophages are not only responsible for plaque disruption but also pivotal in thrombus generation, the most important mechanism of acute coronary syndromes.
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PMID:Pathophysiology of plaque disruption and thrombosis in acute ischemic syndromes. 1790 43

People suffer increasingly from arterial hypertension and/or diabetes mellitus. These two diseases represent the most frequent causes leading to chronic kidney disease. The assessment of renal function by means of formulas serves as a basis for further decision making regarding the management of patients with chronic kidney disease. On one hand, the therapy focuses on the treatment of the underlying illness as well as possible, acute and reversible causes of renal dysfunction. On the other hand, the therapy includes measures to decelerate the progression of chronic kidney disease (nephroprotection) and to correct its associated complications (renal hypertension, renal anemia, secondary hyperparathyroidism). If these therapeutic measures are applied timely (ideally as of CKD stage 3 with glomerular filtration rate <60 ml/min) and in close collaboration with a nephrologist, end stage renal disease can be delayed by several years.
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PMID:[Chronic kidney disease in the general practitioner's office]. 1964 65

Caveolae act as signalling platforms serving as concentrating points for numerous signalling molecules, as well as regulating flux through many distinct signalling cascades. RhoA proteins have been identified as potential actors in the pathophysiology of the cardiovascular system. We used sucrose gradient fractionation and immunoblotting to determine caveolin-1 and RhoA presence in the kidney cortex of streptozotocin-induced T1 diabetes rats (4-week duration), and of diabetic rats treated with angiotensin receptor blocker losartan (4 weeks, 20 mg/kg/day) to retard renal hypertension. Positive RhoA/caveolin-1 co-immunoprecipitation result was detected in the caveolar fraction that corresponded to the light-scattering band obtained from diabetic rats, compared to negative co-immunoprecipitation result in the caveolar fraction obtained from control rats. The detection of RhoA protein in the caveolar fractions and the prospective RhoA/caveolin-1 association can be used to examine the role of these signalling reactions in the pathophysiology of microvascular complications in type 1 diabetes.
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PMID:RhoA distribution in renal caveolar fractions in experimental type 1 diabetes. 2197 55

Many studies, both national and international, have shown that tea has protective effects on many chronic diseases and their risk factors. In cancer prevention, our studies indicated that tea drinking could inhibit the carcinogenicity of various chemical carcinogens, including oral tumors induced by 7,12-dimethylbenz[a]anthracene (DMBA) in Golden hamsters, esophageal tumors in rats by blocking in vivo synthesis of N-Nitroso-methylbenzylamine (NMBzA), esophageal cancer induced by NMBzA in rats, precancerous liver lesions (r-GT and GST-P) induced by diethylnitrosamine (DENA) in rats, intestinal preneoplastic lesion (ACF) and intestinal tumors induced by 1,2-dimethyl-hydrazine (DMH) in rats, lung carcinoma induced by nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone(NNK) in A/J mice. Our studies have also shown that the protective effects of tea against cancer is a combined effects of various tea ingredients, among which the major ones are polyphenols and tea pigments. Based on animal studies, antioxidant properties, protection against DNA damage and modulation of immune functions were found to be the main mechanisms of anticancer effects of tea. In human trials, tea drinking showed protective effects against oxidative damage and DNA damage caused by cigarette smoking. Mixed tea drinking significantly blocked lesion progress in patients with oral mucosa leukoplakia, therefore, demonstrated its protective effects on oral cancer. Our studies have also shown effects of tea on prevention of cardiovascular diseases (CVD). For example, tea pigments was found to significantly inhibit LDL oxidation induced by Cu2+, Fe2+ in in vitro studies. In vivo studies showed that tea could prevent blood coagulation, facilitate fibrinogen dissolution, inhibit platelet aggregation, lower endothelin levels, enhance GSH-Px activities, protect against oxidated LDL-induced damage in endothelium cells, and prevent atherosclerosis of coronary arteries. The mechanisms of these protective effects of tea are possibly related to its antioxidant properties or its inhibition of lipid oxidation. Green tea and pigments was also found to inhibit cardiac hypertrophy induced by renal hypertension in rat models, whose mechanisms might, at least partly, involve its modulation on nitric oxide, angiotensin II and endothelin-1. Clinical intervention trials have indicated that tea and tea extracts decreased blood lipid, improved blood flow of coronary artery, and played an important role in atherosis inhibition and prevention. Our studies also showed that tea drinking has protective effects on diabetes. White tea drinking could significantly relieve symptoms including polyuria, polydipsia, polyphagia and weight loss in diabetic mice, decrease fasting plasma glucose level and improve glucose tolerance. In human trial, continuous white tea drinking could significantly improve symptoms of diabetic patients, such as relieve polydipsia, decrease plasma glucose levels, both fasting and 2 hours after meal, and increase insulin secretion. The effective rate for glucose lowering is 48% in clinical study.
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PMID:[Studies on tea and health]. 2227 81

Despite the high rate of occurrence of both diabetes and hypertension in humans, the cardiovascular effects of the two conditions have not been investigated when they occur simultaneously. Thus this study examined the vascular effects of simultaneous type 2 diabetes and renal hypertension on endothelial function. Serum malondialdehyde and systolic blood pressure (SBP) were measured, glucose tolerance test (GTT) was performed, and concentration-response to phenylephrine (PE) in the absence and presence of nitro-l-arginine methyl ester (l-NAME), acetylcholine and sodium nitroprusside were conducted on aortic rings from diabetic control, type 2 diabetes, sham-operated, renal hypertensive, and simultaneous type 2 diabetes plus hypertension rats respectively. Hypertension, diabetes, and simultaneous diabetes and hypertension were associated with either increased or decreased maximal responses (E(max)) of PE dependent on in the presence or absence of l-NAME. There was also increased serum malondialdehyde and decreased E(max) of acetylcholine. Thus simultaneous hypertension and diabetes caused a greater decrease in E(max) of acetylcholine compared to that seen with either diabetes or hypertension alone higher than that seen in hypertension. The blood glucose during GTT was lower than that seen in diabetes groups. Thus simultaneous type 2 diabetes and the SBP was renal hypertension is associated with improved glucose tolerance, but with further deterioration of endothelial dysfunction compared with either condition alone.
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PMID:Simultaneous renal hypertension and type 2 diabetes exacerbate vascular endothelial dysfunction in rats. 2245 8

While the lifespan of people with type 1 diabetes has increased progressively since the advent of insulin therapy, these patients still experience premature mortality, primarily from cardiovascular disease (CVD). However, a subgroup of those with type 1 diabetes survives well into old age without significant morbidity. It is the purpose of this review to explore the factors which may help in identifying these patients. It might be expected that hyperglycaemia plays a major role in explaining the increased incidence of CVD and mortality of these individuals. However, while a number of publications have associated poor long term glycaemic control with an increase in both all-cause mortality and CVD in those with type 1 diabetes, it is apparent that good glycaemic control alone cannot explain why some patients with type 1 diabetes avoid fatal CVD events. Lipid disorders may occur in those with type 1 diabetes, but the occurrence of elevated high-density lipoprotein-cholesterol is positively associated with longevity in this population. Non-renal hypertension, by itself is a significant risk factor for CVD but if adequately treated does not appear to mitigate against longevity. However, the presence of nephropathy is a major risk factor and its absence after 15-20 years of diabetes appears to be a marker of long-term survival. One of the major factors linked with long-term survival is the absence of features of the metabolic syndrome and more specifically the presence of insulin sensitivity. Genetic factors also play a role, with a family history of longevity and an absence of type 2 diabetes and hypertension in the family being important considerations. There is thus a complex interaction between multiple risk factors in determining which patients with type 1 diabetes are likely to live into older age. However, these patients can often be identified clinically based on a combination of factors as outlined above.
World J Diabetes 2014 Jun 15
PMID:Why do some patients with type 1 diabetes live so long? 2493 49

The mechanism of oleuropein's antihypertensive effects was examined in rat model of simultaneous type 2 diabetes and renal hypertension (diabetic hypertensive). Five groups of male Sprague-Dawley rats including a control, a diabetic-hypertensive group receiving vehicle, and three diabetic-hypertensive groups receiving oleuropein at 20, 40, or 60 mg/kg/day were used. The duration of diabetes was 10 weeks; during the last 4 weeks of which, animals were hypertensive and received vehicle or oleuropein. Systolic blood pressure, glucose and malondialdehyde, heart rate, and maximal response to phenylephrine (PE) in the absence of nitro-L-arginine methyl ester (L-NAME) of oleuropein-treated groups were significantly lower than those of vehicle-treated group. Erythrocyte superoxide dismutase, maximal response to PE in the presence of L-NAME, and maximal response to acetylcholine (Ach) of oleuropein-treated groups were significantly higher than those of vehicle-treated group. The findings indicate that antihypertensive effects of oleuropein might be partly mediated by improving the release of nitric oxide, and antioxidant and sympathoplegic activities.
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PMID:Effects of oleuropein in rats with simultaneous type 2 diabetes and renal hypertension: a study of antihypertensive mechanisms. 2495 37


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