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 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The incidence and prevalence of diabetes have reached epidemic proportions worldwide. The reasons for the pandemic are the sharp rise in obesity, decline in physical activity and the increase in life expectancy. There are some 400,000 people with diagnosed diabetes in Israel and they are at a markedly increased risk for cardiovascular disease, blindness, end-stage renal disease and lower limb amputation. To effectively lower this significantly increased burden of disease, a comprehensive multidisciplinary approach to chronic disease management is required. To facilitate such an approach, the Israel Diabetes Association published a guideline for the diagnosis, prevention and treatment of diabetes. The guideline, based on the ADA (American Diabetes Association) and IDF (International Diabetes Federation) guidelines, was approved by other national professional societies including hypertension, family practice, obesity, nephrology, atherosclerosis and internal medicine. The guidelines highlight the metabolic syndrome and prediabetic states, interventions for the prevention of diabetes, the new definitions of diabetes and impaired glucose metabolism and the newly defined targets for glucose, lipid, cholesterol and blood pressure control. In addition, the recommendations for periodic review and screening for complications are summarized. The need for patient education and empowerment are emphasized as is the need for the development and implementation of unique tools including computerized treatment flow-charts, prompts and quality measures, for the long term management of a complex metabolic disease.
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PMID:[The guidelines for the diagnosis prevention and treatment of type 2 diabetes mellitus--2005]. 1698 42

Up-to-date therapy has in recent years substantially modified the clinical course of HIV infections and AIDS. The progress of the disorder has changed-today it is a chronic disease of many years. Already in 1997 and 1998 it transpired that long-term HAART, highly active antiretroviral therapy, produced adverse metabolic changes, which significantly affect the subsequent progress of the disease. The mechanism responsible for these metabolic changes has not, as yet, been fully clarified-in all probability its etiology is multifactorial. Even prior to the introduction of HAART, some metabolic changes were observed in HIV-infected subjects. These changes are, however, not specific for the pathogen concerned, they are generally seen in acute inflammatory reactions. Since the introduction of HAART in 1996 the range of metabolic changes has expanded. Gradually we detect more and more anthropometric, metabolic and coagulation changes, closely resembling changes seen in the metabolic syndrome (SIR, syndrome of insulin resistance), well known from cardiology and internal medicine-dyslipoproteinaemia, insulin resistance, abdominal obesity. A combination of these disorders is clinically significant due to their role in the development of atherosclerosis and their by no means negligible involvement in the onset of ischaemic heart disease. In view of the much lower mean age of HIV-positive subjects the earlier mentioned complications should be expected in much lower age categories than with HIV-negative individuals. The paper discusses the possible pathogenesis and potential mechanisms of metabolic complications related to HAART, its impact on the cardiovascular risk and the possibilities of hypolipidaemic therapy in HIV-positive patients.
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PMID:[Metabolic syndrome and HIV/AIDS disorder]. 1705 72

Diabetes is a chronic disease secondary to the interaction of the hereditary and environmental factors and is characterized by an abnormal secretion of insulin or by an ineffective use of this hormone. The result is the elevation of glycemia rate (N < 126 mg/dl). Untreated hyperglycemia can lead to serious complications like retinopathy, nephropathy, neuropathy, atherosclerosis, foot lesions (ulcer, infections, Charcot's arthropathy), even to amputations. The diabetes is a worldwide pandemic: 150 million people in the world, which will double in the next twenty-five years. The diabetes foots have a tremendous social and economic impact. The mechanisms which are implicated in development of the diabetic foot are the neuropathy and the arteriopathy. Lesions appear in the presence of the triggering factors. Diabetes is a disease in which several specialities are implicated. They should work together when treating these patients. Prevention is essential. The patient must be educated, then the complications of diabetes can be avoided.
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PMID:[Diabetic foot]. 1709 96

Industrial and technological revolutions have resulted in dramatic shifts in the diseases that are responsible for illness and death. In particular, cardiovascular disease (CVD) has emerged as the dominant chronic disease in many parts of the world. Diet, tobacco smoking, physical inactivity, obesity, lipid levels, hypertension and diabetes mellitus have contributed to their wide diffusion. Oxidative damage and the production of free radicals in the endothelium are two of the main factors involved in the pathogenesis of the atherosclerotic process that causes CVD. One of the more important results of basic research on dietetic regimes has shown that people who consume large amounts of fruits and vegetables have a lower incidence of CVD, stroke and tumours, but the specific mechanisms of these foods (which have an apparently protective effect) are still not completely clear. Possible reasons could include a greater consumption of fruit and vegetables, and an increased consumption of dietetic fibres. Recently, it been proposed that micronourishments with an antioxidant activity could be responsible for the reduction of chronic diseases. Research supplies a hypothetical mechanism by which antioxidant substances may be reducing the risk of atherosclerosis through the inhibition of oxidative damage. Appropriate nutritional practices are of central importance in managing risk and treatment of CVD; in fact, many current guidelines for a healthy general population contain nutritional recommendations to reduce the risk of these diseases. A large number of descriptive and case-control studies suggests that the consumption of many antioxidant vitamins (A, C and E) reduces the risk of CVD. Such data raises the following problem of whether supplementation of vitamins A, C and E emerges as being useful in the primary prevention of CVD. Many important studies involving a great number of participants have not confirmed this hypothesis and the results are often contradictory. This review examines the studies published in the literature that document the effect of supplementation with antioxidant vitamins (A, C and E) in the primary and secondary prevention of CVD due to an atherosclerosis process.
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PMID:The role of the antioxidant vitamin supplementation in the prevention of cardiovascular diseases. 1715 51

Diabetes mellitus is a chronic disease in its own right and is also regarded as a cardiovascular risk factor as well as a cardiovascular disease, due to its ability to progress to a stage of cardiovascular co-morbidity. The pathophysiology of cardiovascular complications in diabetes is reported to involve hyperglycaemia-induced oxidative stress. The erythrocyte has an array of endogenous antioxidants involved in quenching oxidant production and the exponential chain reactions in diabetes. When the erythrocyte is oxidatively stressed, as demonstrated by depleted reduced glutathione and/or increased malondialdehyde in its cell membrane, the risk of diabetes progression and its cardiovascular sequelae, including atherosclerosis and coronary artery disease, is increased. Virtually all studies that determined erythrocyte malondialdehyde and glutathione in diabetes show consistently increased and reduced levels, respectively. Furthermore, cardiovascular complications of diabetes are reported to commence at the prediabetes stage. Current coronary artery disease screening programmes based on the presence of two or more risk factors are failing to identify those with increased risk of diabetes and cardiovascular complications, thereby limiting early interventions. Screening that includes erythrocyte oxidative stress determination may provide an additional marker for both preclinical and advanced disease. In this review, a concise description of the involvement of erythrocyte oxidative stress in diabetes mellitus and its cardiovascular sequelae is presented. Antioxidant action and interaction in the erythrocyte are also described, with emphasis on why current coronary artery disease screening markers cannot be regarded as erythrocyte oxidative stress markers.
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PMID:Erythrocyte oxidative stress in clinical management of diabetes and its cardiovascular complications. 1744 18

Nitric oxide regulation of the cardiovascular system involves both cGMP-dependent and independent mechanisms. The former directly interacts with the family of catabolic phosphodiesterases (PDEs) that control cGMP levels and thus distal effects such as protein kinase G stimulation. Growing evidence supports an important role of several PDEs, including PDE1, PDE2, and PDE5, in the regulation of cGMP in both vascular smooth muscle and cardiac myocytes. These PDEs have relatively little impact on resting function, but they can potently modulate acute contractile tone in cells stimulated by external agonists such as angiotensin or catecholamines. Regulation by PDEs is compartmentalized, with selective interactions occurring between a given source of cGMP and PDE hydrolysis. PDE1 and/or PDE5 are also reportedly up-regulated in chronic disease conditions such as atherosclerosis or cardiac pressure-load stress and heart failure as well as in response to long-term exposure to nitrates. Such up-regulation is thought to contribute to vascular and cardiac pathophysiology and to drug tolerance. Recent studies utilizing selective PDE5 inhibitors support significant cross-signaling with NO-cGMP synthetic pathways that may be particularly helpful in treating certain disease states.
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PMID:Phosphodiesterase regulation of nitric oxide signaling. 1746 73

The CXC chemokine receptor CXCR2 has been implicated in the pathogenesis of several chronic diseases including atherosclerosis. To enable animal studies towards understanding the role of human CXCR2 (hCXCR2) in disease development, we previously generated hCXCR2 knockin (hCXCR2(+/+)) mice. We have demonstrated that the phenotype and the acute immune response of the hCXCR2(+/+) mice was identical to that of wild-type mice, indicating that hCXCR2 indeed takes over the function of endogenous mouse CXCR2 (mCXCR2). In the present paper, we extend these findings by studying whether hCXCR2 functionally replaces the role of mCXCR2 in a chronic disease model for atherosclerosis. We first defined which of two well-described atherosclerosis models (ApoE(-/-) or LDLR(-/-) mice) is most suited for this purpose. When expression of mCXCR2 and that of its ligands in atherosclerotic lesions were compared in these mice, increased expression levels were observed only in LDLR(-/-) mice. Further, cultured atherosclerotic aortas from LDLR(-/-) mice did secrete significantly higher levels of CXCR2 ligands compared to aortas from healthy controls. Since these results support the role of CXCR2 in the atherogenesis in the LDLR(-/-) mice, double mutant hCXCR2(+/+)/LDLR(-/-) mice were generated and diet-induced atherosclerosis in these mice was compared to that in LDLR(-/-) mice. Upon an atherogenic diet, the hCXCR2(+/+)/LDLR(-/-) mice developed plaque lesions in a similar manner to those in LDLR(-/-) mice, indicating successful functional replacement of mCXCR2 by hCXCR2 in this disease model. We conclude that hCXCR2(+/+)/LDLR(-/-) mice present an attractive model to study the role of hCXCR2 in atherosclerosis development and for future testing of novel pharmaceuticals designed to antagonize hCXCR2.
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PMID:Functional replacement of murine CXCR2 by its human homologue in the development of atherosclerosis in LDLR knockout mice. 1760 59

An alteration in the character and function of platelets is manifested in patients with inflammatory diseases, and these alterations have been dissociated from the well-characterized involvement of platelets in thrombosis and haemostasis. Recent evidence reveals platelet activation is sometimes critical in the development of inflammation. The mechanisms by which platelets participate in inflammation are diverse, and offer numerous opportunities for future drug intervention. There is now acceptance that platelets act as innate inflammatory cells in immune responses, with roles as sentinel cells undergoing surveillance, responding to microbial invasion, orchestrating leukocyte recruitment, and migrating through tissue, causing damage and influencing repair processes in chronic disease. Some of these processes are targeted by drugs that are being developed to target platelet participation in atherosclerosis. The actions of platelets therefore influence the pathogenesis of diverse inflammatory diseases in various body compartments, encompassing parasitic and bacterial infection, allergic inflammation (especially asthma and rhinitis), and non-atopic inflammatory conditions, for example, chronic obstructive pulmonary disease (COPD), rheumatoid arthritis (RA), inflammatory bowel disease (IBD) and atherosclerosis. This review will first discuss the evidence for platelet activation in these various inflammatory diseases, and secondly discuss the mechanisms by which this pathogenesis occurs and the various anti-platelet agents which have been developed to combat platelet activation in atherosclerosis and their potential future use for the treatment of other inflammatory diseases.
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PMID:Novel uses for anti-platelet agents as anti-inflammatory drugs. 1760 47

The metabolic syndrome is a long-term process, explained by the interaction of genetic and environmental factors, that starts early in life and is involved in the pathophysiology of a large percentage of cases with type 2 diabetes and atherosclerosis. A number of clinical studies have demonstrated the importance of fat distribution and especially the contribution of visceral fat accumulation to the development of metabolic disorders. Visceral adipose tissue can be studied through different imaging techniques. The accumulation of visceral adipose tissue, as opposed to subcutaneous fat, increases the risk of developing metabolic disease and cardiovascular diseases (CVD). Visceral adipocytes secrete a variety of cytokines known as adipocytokines suggesting that adipose tissue is an endocrine organ that may affect the function of other organs. Weight loss, particularly a reduction in waist circumference, improves insulin sensitivity, lipid profile, and serum adipocytokines, reducing the risk of developing chronic disease and CVD. Waist circumference is a required component of metabolic syndrome under the International Diabetes Federation (IDF) criteria, rather than an optional component as used by other previous classifications. Studies have shown that using a lower waist circumference threshold within the context of metabolic syndrome increases the prevalence, but decreases the risk of mortality and type 2 diabetes. It is possible that waist circumference acts as a marker for other risk factors. These findings reinforce the notion that reductions in visceral adipose tissue should be a primary aim of strategies designed to reduce health risks associated with metabolic syndrome.
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PMID:Metabolic syndrome and adipose tissue: new clinical aspects and therapeutic targets. 1762 47

Atherosclerosis is a chronic disease associated with accumulation of lipids in lesions along blood vessels, leading to the occlusion of blood flow. Much of the focus has been on the role of low-density lipoprotein (LDL), and of oxidatively modified LDL, in the initiation and progression of this disease. LDL is in fact a metabolic end-product of the triglyceride-rich lipoproteins (ie, very-low density lipoproteins). Over the years, univariate analyses have implicated triglycerides as a contributor in atherosclerosis. However, depending on the studies, the significance of this relationship is either reduced or nullified when other co-variates are taken into account. This review summarizes more recent data that support the role of triglyceride-rich lipoproteins in the atherosclerotic process, both in the fasted as well as in the postprandial state.
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PMID:The role of hypertriglyceridemia in atherosclerosis. 1787 19


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