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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The isolation of pluripotent human embryonic stem (hES) cells having the capacity to differentiate in vitro to numerous cell types generated much excitement and promise in the field of regenerative medicine. However, along with great enthusiasm came hot controversy for stem cell research and researchers alike because available hES cell lines were isolated from "excess" embryos from in vitro fertilization clinics. Despite ethical and political debates, the methods and protocols to study diverse lineages are developing. Furthermore, strategies using specific growth factor combinations, cell-cell and cell-extracellular matrix induction systems are being explored for directed differentiation along a desired lineage. However, there is a great need to characterize the mechanisms that control self-renewal and differentiation and a necessity to improve methodologies and develop new purification protocols for the potential future clinical application of hES cells. After the scientific and political obstacles are overcome, it is anticipated that the hES cell field will make a tremendous difference in conditions, such as burn traumas and diabetic foot ulcers, as well a number of degenerative diseases such as Parkinson's disease, type 1 diabetes, rheumatoid arthritis, and myocardial infarction. In this introductory chapter, we will summarize and review recent progress in the field of hES cell differentiation protocols and discuss some of the current issues surrounding hES cell research.
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PMID:Human embryonic stem cells: isolation, maintenance, and differentiation. 1688 5

Autoimmune or type 1 diabetes mellitus (T1DM), accounts for 90-95% of all cases of diabetes, while type 2 diabetes mellitus (T2DM), characterized by impaired insulin sensitivity and production, accounts for the other 5-10%. Atherosclerotic process starts during childhood and recognize several mechanisms that are activated in response to NOXIUS STIMULI and participate in a complex state which is accepted to be a chronic inflammatory state. T1DM patients, especially those with a non-optimal metabolic control, have a higher risk of developing all macrovascular complications such as myocardial infarction, stroke and silent ischemia. Macrovascular disease is mainly associated with hyperglycemia, dyslipidemia, obesity, hypertension, hypercoagulable state, cigarette smoking, lack of exercise, endothelial dysfunction, hyperhomocysteinemia and vascular wall abnormalities. In this paper we review the importance of traditional and non-traditional risk factors for macrovascular complications in children with T1DM and discuss their role in the pathogenesis of the excess cardiovascular mortality in these patients.
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PMID:Macroangiopathy in adults and children with diabetes: risk factors (part 2). 1711 Dec 97

It is becoming increasingly clear that suboptimal blood glucose control results in adverse effects on large blood vessels, thereby accelerating atherosclerosis and cardiovascular disease, manifested as myocardial infarction, stroke, and peripheral vascular disease. Cardiovascular disease is accelerated by both type 1 and type 2 diabetes. In type 1 diabetes, hyperglycemia generally occurs in the absence of elevated blood lipid levels, whereas type 2 diabetes is frequently associated with dyslipidemia. In this review article, we discuss hyperglycemia versus hyperlipidemia as culprits in diabetes-accelerated atherosclerosis and cardiovascular disease, with emphasis on studies in mouse models and isolated vascular cells. Recent studies on LDL receptor-deficient mice that are hyperglycemic, but exhibit no marked dyslipidemia compared with nondiabetic controls, show that diabetes in the absence of diabetes-induced hyperlipidemia is associated with an accelerated formation of atherosclerotic lesions, similar to what is seen in fat-fed nondiabetic mice. These effects of diabetes are masked in severely dyslipidemic mice, suggesting that the effects of glucose and lipids on lesion initiation might be mediated by similar mechanisms. Recent evidence from isolated endothelial cells demonstrates that glucose and lipids can induce endothelial dysfunction through similar intracellular mechanisms. Analogous effects of glucose and lipids are also seen in macrophages. Furthermore, glucose exerts many of its cellular effects through lipid mediators. We propose that diabetes without associated dyslipidemia accelerates atherosclerosis by mechanisms that can also be activated by hyperlipidemia.
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PMID:Do glucose and lipids exert independent effects on atherosclerotic lesion initiation or progression to advanced plaques? 1752 72

Individuals with diabetes mellitus are at considerably higher risk for coronary artery disease compared with individuals without diabetes. In the United States, diabetes is the most prevalent factor putting patients at risk for coronary events. Intensive control of blood glucose has been demonstrated to reduce the risk for cardiovascular disease in patients with type 1 diabetes, but this has yet to be proved in patients with type 2 diabetes. Aggressive management of established cardiovascular risk factors using blood pressure-lowering and lipid-lowering therapies (particularly the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, or statins) has been conclusively shown to reduce cardiovascular risk in patients with type 2 diabetes. Patients with type 2 diabetes remain at residual excess risk compared with individuals without diabetes, such that there is still a need for novel therapeutic approaches. Thiazolidinediones (TZDs) may have beneficial effects on cardiovascular disease in diabetes beyond improving blood glucose control. Although the evidence regarding rosiglitazone is yet to mature, completed and ongoing clinical trials with pioglitazone suggest that this TZD may be a novel treatment for managing cardiovascular risk in patients with diabetes. Addition of pioglitazone to existing therapy in high-risk patients with diabetes and atherosclerotic disease improves cardiovascular outcomes, and may be particularly beneficial for patients with previous myocardial infarction or stroke.
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PMID:Prevention of macrovascular disease in patients with diabetes mellitus: opportunities for intervention. 1782 43

Diabetic ketoacidosis is a major cause of morbidity and mortality in patients with insulin dependent diabetes. Myocardial infarction is an uncommon but well-recognised precipitating cause of diabetic ketoacidosis, accounting for 1% of cases. Many diabetic patients with ketoacidosis initially present with hyperkelamia, which may affect the electrocardiographic morphology. We present a patient with diabetic ketoacidosis and hyperkalemia, whose initial electrocardiogram showed a sinoventricular rhythm and subsequently pseudoinfarction pattern. (Cardiol J 2007; 14: 497-499).
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PMID:ST segment elevation following sinoventricular rhythm in a patient with diabetic ketoacidosis. 1865 10

Patients with type 2 diabetes are at high risk of cardiovascular disease. Schramm et al. have published a study in which all residents of Denmark aged 30 years or older on 1 January 1997 (approximately 3.3 million individuals) were followed up for 5 years by individual-level linkage of nationwide registers. The study indicated that patients requiring glucose-lowering therapy (oral treatment, insulin, or combined insulin and oral therapy) exhibited a cardiovascular risk comparable to that of nondiabetic individuals with a prior myocardial infarction, irrespective of sex and type of diabetes. In recent AHA and American Diabetes Association guidelines for the primary prevention of cardiovascular disease, all treatment recommendations for patients with type 2 diabetes also apply to those with type 1 diabetes and to both sexes. Epidemiological evidence reported by Schramm et al. is in line with these recommendations.
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PMID:Diabetes as a 'cardiovascular disease equivalent': implications for treatment. 1879 31

The control of glycosylated hemoglobin (HbA(1c)) levels is crucial to the successful treatment of patients with diabetes mellitus (T2DM). Glycemic control is a cornerstone for reducing end-organ disease, and HbA(1c) is the benchmark for defining glucose control over long durations. The author reviews available information from published clinical trials regarding the benefits of tight glycemic control in type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM). He notes that published data support the use of tight glucose control for reducing risks of retinopathy, nephropathy, and neuropathy in both patients with T1DM and patients with T2DM. He also notes that early aggressive insulin management of younger individuals with T1DM led to reductions in the incidence of myocardial infarction (MI), stroke, and death. However, published data do not clearly support benefits of tight glucose control for the prevention of cardiovascular events in older patients with long-standing T2DM. The author also reviews recommended treatments for achieving and maintaining glycemic control in patients. He concludes that the most successful treatment requires that physicians encourage patients to actively participate in the management of their own disease, and that physicians provide patients with opportunities to learn the cornerstones of effective therapy.
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PMID:Achieving glycemic control: cornerstone in the treatment of patients with multiple metabolic risk factors. 1945 Dec 56

Diabetes increases cardiovascular (CV) risk to a similar extent as myocardial infarction. Epidemiologic data support the same concept for the presence of Stage 3 (ie, glomerular filtration rate of < 60 mL/min) or higher nephropathy without diabetes. The most common cause of end-stage kidney disease requiring dialysis is diabetes. Hence, CV risk is highest among those with kidney disease and diabetes. Glycemic control in the context of CV risk reduction among patients with kidney disease has not been the focus of any specific trial; however, secondary analyses of trials, primarily in type 1 diabetes, have looked at this issue. Nevertheless, the outcome data are sparse. What can be said, however, is that failure to achieve reasonable glycemic control (ie, glycated hemoglobin < 7.5%) is associated with a higher risk of CV events and hospitalizations for CV events and infections among those with advanced kidney disease. The impact of poor glycemic control on kidney disease progression has not been well studied and should be the focus of future studies.
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PMID:Glycemic control and cardiovascular disease in chronic kidney disease. 1949 Aug 27

The number and volume of cells in the blood affect a wide range of disorders including cancer and cardiovascular, metabolic, infectious and immune conditions. We consider here the genetic variation in eight clinically relevant hematological parameters, including hemoglobin levels, red and white blood cell counts and platelet counts and volume. We describe common variants within 22 genetic loci reproducibly associated with these hematological parameters in 13,943 samples from six European population-based studies, including 6 associated with red blood cell parameters, 15 associated with platelet parameters and 1 associated with total white blood cell count. We further identified a long-range haplotype at 12q24 associated with coronary artery disease and myocardial infarction in 9,479 cases and 10,527 controls. We show that this haplotype demonstrates extensive disease pleiotropy, as it contains known risk loci for type 1 diabetes, hypertension and celiac disease and has been spread by a selective sweep specific to European and geographically nearby populations.
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PMID:A genome-wide meta-analysis identifies 22 loci associated with eight hematological parameters in the HaemGen consortium. 1986 6

Several inflammatory cytokines are involved in vascular inflammation resulting in endothelial dysfunction which is the earliest event in the atherosclerotic process leading to manifest cardiovascular disease. YKL-40 is an inflammatory glycoprotein involved in endothelial dysfunction by promoting chemotaxis, cell attachment and migration, reorganization and tissue remodelling as a response to endothelial damage. YKL-40 protein expression is seen in macrophages and smooth muscle cells in atherosclerotic plaques with the highest expression seen in macrophages in the early lesion of atherosclerosis. Several studies demonstrate, that elevated serum YKL-levels are independently associated with the presence and extent of coronary artery disease and even higher YKL-40 levels are documented in patients with myocardial infarction. Moreover, elevated serum YKL-40 levels have also been found to be associated with all-cause as well as cardiovascular mortality. Finally, YKL-40 levels are elevated both in patients with type 1 and type 2 diabetes, known to be at high risk for the development of cardiovascular diseases, when compared to non-diabetic persons. A positive association between elevated circulating YKL-40 levels and increasing levels of albuminuria have been described in patients with type 1 diabetes indicating a role of YKL-40 in the progressing vascular damage resulting in microvascular disease. This review describes the present knowledge about YKL-40 and discusses its relation to endothelial dysfunction, atherosclerosis, cardiovascular disease and diabetes and look ahead on future perspectives of YKL-40 research.
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PMID:YKL-40--an emerging biomarker in cardiovascular disease and diabetes. 1993 Jun 30


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