Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cytokines are pivotal mediators of the interaction between immunocompetent cells. Moreover, they mediate the interaction between the immune system and other physiological systems, including the CNS. It has been shown recently that the antipsychotic drug clozapine stimulates in vivo the release of cytokines and soluble cytokine receptors. This holds true for the tumor necrosis factor(TNF)-system, the interleukin(IL)-2-system, IL-6, and granulocyte colony-stimulating factor (G-CSF). The present paper discusses the clinical relevance of these findings for the pathophysiology of clozapine-induced side-effects. It is very probable that TNF-alpha plays an important role in clozapin-induced fever and in the hematopoetic side effects, including agranulocytosis. Moreover, it is likely that TNF-alpha and other cytokines are involved in metabolic (weight gain, diabetes), cardiac (myocarditis), CNS (sedation) and other rare side effects. The mechanisms underlying clozapine-induced immunomodulation are unknown. Hence, further studies are very important to enhance our understanding of clozapins's side effects and to develop strategies for prevention and treatment.
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PMID:[On the clinical relevance of clozapine-triggered release of cytokines and soluble cytokine-receptors]. 1153 53

Phaeochromocytomas are rare endocrine tumours that secrete excessive amounts of catecholamines and can lead to myocarditis and cardiomyopathy. We report a 63-year-old man with long-standing hypertension and diabetes who presented with dilated cardiomyopathy, which was initially thought to be secondary to ischaemic heart disease. Subsequent coronary angiography was normal. Carvedilol therapy unmasked the characteristic features of phaeochromocytoma. Surgical resection of a right adrenal tumour cured his symptoms, hypertension and diabetes, as well as causing a substantial improvement in cardiac function. Phaeochromocytoma should be considered as a rare cause of dilated cardiomyopathy of uncertain aetiology.
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PMID:Phaeochromocytoma presenting as dilated cardiomyopathy. 1291 98

Encephalomyocarditis (EMC) virus induces insulin-dependent diabetes and myocarditis in several strains of mice. The T-cell receptor (TCR) Vbeta genes of infiltrating T cells in the pancreas and myocardium of BALB/C mice infected with EMC virus D-variant (EMC-D virus) were analyzed. Using a nested two-step polymerase chain reaction (PCR), TCR Vbeta cDNAs were cloned and sequenced. Two and four kinds of TCR Vbeta clones were obtained from T cells infiltrating into the pancreas and myocardium of BALB/C mice infected with EMC-D virus, respectively. The infiltrating lymphocytes in the diabetic mice expressed Vbeta 8.1, 8.2, and 8.3 genes predominantly. Previously, the use of Vbeta 8.2 has been reported in autoimmune diseases such as murine experimental allergic encephalomyelitis (EAE) and non-obese diabetic (NOD) mouse. This study suggests that mice infected with EMC virus are a useful animal model for autoimmune diseases such as insulin-dependent diabetes.
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PMID:Analysis of T-cell receptor Vbeta gene from infiltrating T cells in insulitis and myocarditis in encephalomyocarditis virus-infected BALB/C mice. 1455 Feb 73

A line of nonobese diabetic (NOD) mice expressing the human diabetes-associated HLA-DQ8 transgene in the absence of mouse IAbeta failed to show spontaneous insulitis or diabetes, but rather developed dilated cardiomyopathy, leading to early death from heart failure. Pathology in these animals results from an organ- and cell-specific autoimmune response against normal cardiomyoctes in the atrial and ventricular walls, as well as against very similar myocytes present in the outermost muscle layer surrounding the pulmonary veins. Progression of the autoimmune process could be followed by serial ECG measurements; irradiation of young animals significantly delayed disease progression, and this effect could be reversed by adoptive transfer of splenocytes taken from older animals with complete heart block. Disease progression could also be blocked by cyclosporin A treatment, but was accelerated by injection of complete Fruend's adjuvant. The constellation of findings of spontaneously arising destructive focal lymphocytic infiltrates within the myocardium, rising titers of circulating anticardiac autoantibodies, dilation of the cardiac chambers, and gradual progression to end-stage heart failure bears a striking resemblance to what is seen in humans with idiopathic dilated cardiomyopathy, a serious and often life-threatening medical condition. This transgenic strain provides a highly relevant animal model for human autoimmune myocarditis and postinflammatory dilated cardiomyopathy.
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PMID:Autoimmune cardiomyopathy and heart block develop spontaneously in HLA-DQ8 transgenic IAbeta knockout NOD mice. 1457 Sep 80

CD1d-reactive natural killer T (NKT) cells can rapidly produce T helper type 1 (Th1) and/or Th2 cytokines, can activate antigen-presenting cell (APC) interleukin-12 (IL-12) production, and are implicated in the regulation of adaptive immune responses. The role of the CD1d system was assessed during infection with encephalomyocarditis virus (EMCV-D), a picornavirus that causes acute diabetes, paralysis and myocarditis. EMCV-D resistance depends on IL-12-mediated interferon-gamma (IFN-gamma) production. CD1d-deficient mice, which also lack CD1d-reactive NKT cells, were substantially more sensitive to infection with EMCV-D. Infected CD1d knockout mice had decreased IL-12 levels in vitro and in vivo, and indeed were protected by treatment with exogenous IL-12. IFN-gamma production in CD1d knockout mice was decreased compared with that in wild-type (WT) mice in response to EMCV-D in vitro, although differences were not detected in vivo. Treatment with anti-asialo-GM1 antibody, to deplete NK cells, caused a marked increase in susceptibility of WT mice to EMCV-D infection, whereas CD1d knockout mice were little affected, suggesting that NK-cell-mediated protection is CD1d-dependent. Therefore, these data indicate that CD1d is essential for optimal responses to acute picornaviral infection. We propose that CD1d-reactive T cells respond to early immune signals and function in the innate immune response to a physiological viral infection by rapidly augmenting APC IL-12 production and activating NK cells.
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PMID:Innate immune response to encephalomyocarditis virus infection mediated by CD1d. 1463 51

Worldwide, infection with the human immunodeficiency virus (HIV) is increasing. At the same time, new treatments allow patients to live longer. Consequently, cardiovascular manifestations, most of which occur relatively late in the course of the infection, are becoming more frequent. Pericardial effusion, the most common cardiovascular manifestation of HIV infection, usually is small and causes no hemodynamic compromise or symptoms. It does, however, augur a grim prognosis, as do other cardiovascular conditions associated with the infection: myocarditis, dilated cardiomyopathy, pulmonary arterial hypertension, cardiac lymphoma, and Kaposi's sarcoma of the heart. Highly active antiretroviral therapy (HAART), especially when incorporating protease inhibitors, greatly improves overall outlook in these patients, but appears not only to cause a lipodystrophic syndrome, but to accelerate atherosclerotic cardiovascular disease by inducing glucose intolerance, frank diabetes mellitus, hypertriglyceridemia, hypercholesterolemia, increased lipoprotein (a), and decreased HDL cholesterol. Recent ongoing prospective trials also are showing an association of HAART with increased coronary artery disease and myocardial infarction.
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PMID:Cardiovascular disease in patients infected with the human immunodeficiency virus. 1475 Jul 51

Drinking water is a major source of microbial pathogens in developing regions, although poor sanitation and food sources are integral to enteric pathogen exposure. Gastrointestinal disease outcomes are also more severe, due to under-nutrition and lack of intervention strategies in these regions. Poor water quality, sanitation and hygiene account for some 1.7 million deaths a year world-wide (3.1% of all deaths and 3.7% of all DALY's), mainly through infectious diarrhoea. Nine out of 10 such deaths are in children and virtually all of the deaths are in developing countries. Major enteric pathogens in these children include: rotavirus, Campylobacter jejuni, enterotoxigenic Escherichia coli, Shigella spp. and Vibrio cholerae O1, and possibly enteropathogenic E. coli, Aeromonas spp. V. cholerae O139, enterotoxigenic Bacteroides fragilis, Clostridium difficile and Cryptosporidium parvum. All except the latter are easily control by chlorination of water, but recontamination of treated water is a huge problem. Emerging environmental pathogens, such as Helicobacter pylori and Burkholderia pseudomallei, may well be of significance in some regions. In adults, much less is understood of various sequellae such as myocarditis, diabetes, reactive arthritis and cancers some months-years after initial infections. So in addition to the traditional pathogens (helminths, Entamoeba histolytica, Giardia lamblia hepatitis A and E) various enteroviruses, C. jejuni and H. pylori are emerging issues in adults.
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PMID:Microbial contamination of drinking water and disease outcomes in developing regions. 1513 46

Managing the provision of safe drinking water has a renewed focus in light of the new World Health Organization (WHO) water safety plans. Risk analysis is a necessary component to assist in selecting priority hazards and identifying hazardous scenarios, be they qualitative to quantitative assessments. For any approach, acute diarrhoeal pathogens are often the higher risk issue for municipal water supplies, no matter how health burden is assessed. Furthermore, potential sequellae (myocarditis, diabetes, reactive arthritis and cancers) only further increase the potential health burden of pathogens; despite the enormous uncertainties in determining pathogen exposures and chemical dose-responses within respective microbial and chemical analyses. These interpretations are currently being improved by Bayesian and bootstrapping approaches to estimate parameters for stochastic assessments. A case example, covering the health benefits of ozonation for Cryptosporidium inactivation versus potential cancers from bromate exposures, illustrated the higher risks from a pathogen than one of the most likely disinfection by-products (DBPs). Such analyses help justify the industries long-held view of the benefits of multiple barriers to hazards and that microbial contamination of water supplies pose a clear public health risk when treatment is inadequate. Therefore, efforts to reduce potential health risks from DBP must not compromise pathogen control, despite socio-political issues.
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PMID:Risk analysis of drinking water microbial contamination versus disinfection by-products (DBPs). 1513 49

We report a case of diabetic ketoacidosis complicated by acute myocarditis which was confirmed by necroscopy. A 14 year boy was hospitalised with severe ketoacidosis. The patient levels of creatinine, transaminases were elevated, symptoms of hearth disease were complicated by dehydration and high temperature. An episode of upper respiratory viral infection before the onset of acute diabetes suggested that the patient died from viral myocarditis.
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PMID:[Sudden death caused by myocarditis in a 14-year old boy with type I diabetes]. 1535 39

The pathogenesis of immune-mediated myocarditis depends on genetic and environmental factors. To study the genetic mechanisms, we have developed a model of experimental autoimmune myocarditis in the A.SW mouse. Here we provide evidence that loci on murine chromosome 6, and possibly chromosome 1, are involved in regulating susceptibility. Moreover, these loci overlap with loci implicated in other autoimmune diseases including diabetes in the NOD mouse. These two loci also regulate apoptosis in thymocytes as well as peripheral T cells in the NOD mouse, and we report further that A.SW mice demonstrate the same characteristics in apoptosis. These results suggest that common pathogenetic mechanisms involving apoptosis of both thymic and peripheral T cells are shared by multiple autoimmune diseases.
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PMID:Two autoimmune diabetes loci influencing T cell apoptosis control susceptibility to experimental autoimmune myocarditis. 1569 48


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