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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seventeen Type 1 (insulin-dependent) diabetic patients with a history of recurrent and severe hypoglycaemia and Type 1 diabetic patients with no severe hypoglycaemia were compared as regarded performances in tests of neuropsychological functioning. To test the hypothesis that recurrent severe hypoglycaemia gives rise to permanent cognitive impairment, the study group was selected among those patients who had met with repeated attacks over the last three years or more as identified by a questionnaire among almost 600 insulin-treated diabetic patients. The comparison group without known severe reactions were comparable to the study group with respect to type of diabetes, sex, age, age at onset, duration of diabetes, socio-economic parameters, and prevalence of neuropathy and retinopathy. The results indicate that Type 1 diabetic patients with recurrent severe hypoglycaemia scored lower than those without severe hypoglycaemia in tests of motor ability, short-term and associative memory and visuospatial tasks assessing ability in general problem-solving. Type 1 diabetic patients with severe hypoglycaemia also displayed a higher frequency of perspective reversals suggesting frontal-lobe involvement. These data can be interpreted in two ways. One interpretation implies that the cognitive impairment of Type 1 diabetic patients with severe hypoglycaemia reflects a selection factor, the other that recurrent episodes of severe hypoglycaemia result in permanent cognitive impairment.
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PMID:Permanent neuropsychological impairment after recurrent episodes of severe hypoglycaemia in man. 218 66

NOD mice develop spontaneous IDDM as a result of T-cell-mediated autoimmune destruction of pancreatic beta-cells. It is not known why these T-cells become autoreactive, nor is it clear whether the breakdown in self-tolerance reflects a general problem in T-cell development or a selective defect in an as yet undefined regulatory cell population. In this study, we showed that NOD mice, although relatively normal with regard to most thymocyte subsets, exhibit a marked deficiency in alphabetaTCR+CD4-CD8- (alphabeta+DN) T-cells in the thymus and, to a lesser extent, in the periphery. These T-cells have been termed NKT cells (NK1.1+-like T-cells) because they share some cell surface markers with conventional natural killer (NK) cells. To examine the role of these cells in the pathogenesis of IDDM, semiallogeneic or syngeneic double-negative (DN) thymocytes, enriched for NKT cells, were transferred into intact 4-week-old NOD recipients; the onset of diabetes was then monitored over the ensuing 30 weeks. Mice receiving NKT-enriched thymocytes did not develop diabetes, whereas mice receiving unfractionated thymocytes or phosphate-buffered saline developed diabetes at the normal rate. NKT cells represent a distinct T-cell lineage that has been shown to play a role in immunoregulation in vivo. The deficiency of these cells observed in NOD mice may therefore contribute to destruction of pancreatic islet cells by conventional T-cells.
Diabetes 1997 Apr
PMID:Association between alphabetaTCR+CD4-CD8- T-cell deficiency and IDDM in NOD/Lt mice. 907 96

A 2-week summer school program, combining problem-based learning with behavior therapy, was developed to help adolescents with insulin-dependent diabetes improve their ability to cope with obstacles to dietary management. Ten students participated in a first session, and 9 participated in a second session, serving as a waiting list control group. Outcomes were evaluated pre- and postsession and at a 4-month follow-up using 3-day food diaries, blood glucose data, and paper-and-pencil tests of diabetes-related knowledge, self-efficacy, coping strategies, and general problem solving. Improvements were observed in self-efficacy, problem-solving skills, and self-reported coping strategies. No significant changes were observed in daily intake of fat, cholesterol, calories, mean blood glucose levels or blood glucose variability, and diabetes knowledge. Comparisons between the first group and the waiting list control group do not allow the significant pre-post changes to be clearly attributed to the summer school program.
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PMID:Evaluation of a multicomponent, behaviorally oriented, problem-based "summer school" program for adolescents with diabetes. 992 23

All blood capillaries consist of endothelial tubes surrounded by mural cells referred to as pericytes. The origin, recruitment, and function of the pericytes is poorly understood, but the importance of these cells is underscored by the severe cardiovascular defects in mice genetically devoid of factors regulating pericyte recruitment to embryonic vessels, and by the association between pericyte loss and microangiopathy in diabetes mellitus. A general problem in the study of pericytes is the shortage of markers for these cells. To identify new markers for pericytes, we have taken advantage of the platelet-derived growth factor (PDGF)-B knockout mouse model, in which developing blood vessels in the central nervous system are almost completely devoid of pericytes. Using cDNA microarrays, we analyzed the gene expression in PDGF-B null embryos in comparison with corresponding wild-type embryos and searched for down-regulated genes. The most down-regulated gene present on our microarray was RGS5, a member of the RGS family of GTPase-activating proteins for G proteins. In situ hybridization identified RGS5 expression in brain pericytes, and in pericytes and vascular smooth muscle cells in certain other, but not all, locations. Absence of RGS5 expression in PDGF-B and PDGFR beta-null embryos correlated with pericyte loss in these mice. Residual RGS5 expression in rare pericytes suggested that RGS5 is a pericyte marker expressed independently of PDGF-B/R beta signaling. With RGS5 as a proof-of-principle, our data demonstrate the usefulness of microarray analysis of mouse models for abnormal pericyte development in the identification of new pericyte-specific markers.
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PMID:Transcription profiling of platelet-derived growth factor-B-deficient mouse embryos identifies RGS5 as a novel marker for pericytes and vascular smooth muscle cells. 1259 6

Redox regulatory system controls normal cellular functions. Controlled changes in redox couples potential serve as components for signal transduction, similarly to the phosphorylation cascade. Cellular redox biology requires both compartimentalisation and communication of redox systems: the thermodynamic disequilibrium of the major redox switches allows rapid and sensitive responses to perturbations in redox environments. The many oxidation states of sulphur are found in numerous sulphur species with distinct functional groups (thiols, disulphides, polysulphides, sulphenic, sulphinic and sulphonic acids, etc.), which participate in a complicated network of sulphur-based redox events. Human diseases such as diabetes mellitus and its cardiovascular complications have been associated with increased production of reactive oxygen species and perturbations of thiol redox homeostasis. The review surveys literature related to some etiopathogenic aspects and therapeutic perspectives. The dual toxic-protective property of sulphydryl-donor molecules in experimental settings proposes the general problem of designing antioxidants for therapeutic use.
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PMID:Thiol signalling network with an eye to diabetes. 2113 1

This analysis of the Portuguese health system reviews recent developments in organization and governance, health financing, health care provision, health reforms and health system performance. Overall health indicators such as life expectancy at birth and at age 65 years have shown a notable improvement over the last decades. However, these improvements have not been followed at the same pace by other important dimensions of health: child poverty and its consequences, mental health and quality of life after 65. Health inequalities remain a general problem in the country. All residents in Portugal have access to health care provided by the National Health Service (NHS), financed mainly through taxation. Out-of-pocket payments have been increasing over time, not only co-payments, but particularly direct payments for private outpatient consultations, examinations and pharmaceuticals. The level of cost-sharing is highest for pharmaceutical products. Between one-fifth and one-quarter of the population has a second (or more) layer of health insurance coverage through health subsystems (for specific sectors or occupations) and voluntary health insurance (VHI). VHI coverage varies between schemes, with basic schemes covering a basic package of services, whereas more expensive schemes cover a broader set of services, including higher ceilings of health care expenses. Health care delivery is by both public and private providers. Public provision is predominant in primary care and hospital care, with a gate-keeping system in place for access to hospital care. Pharmaceutical products, diagnostic technologies and private practice by physicians constitute the bulk of private health care provision. In May 2011, the economic crisis led Portugal to sign a Memorandum of Understanding with the International Monetary Fund, the European Commission and the European Central Bank, in exchange for a loan of 78 billion euros. The agreed Economic and Financial Adjustment Programme included 34 measures aimed at increasing cost-containment, improving efficiency and increasing regulation in the health sector. Reforms implemented since 2011 by the Ministry of Health include: improving regulation and governance, health promotion (launch of priority health programmes such as for diabetes and mental health), rebalancing the pharmaceutical market (new rules for price setting, reduction in the prices of pharmaceuticals, increasing use of generic drugs), expanding and coordinating long-term and palliative care, and strengthening primary and hospital care.
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PMID:Portugal: Health System Review. 2848 14