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

Factors to be checked concerning local and systemic condition were studied statistically in order to clarify the methodology for clinical management of diabetic retinopathy. NIDDM (n = 1517) and IDDM (n = 30) persons participating in baseline and follow-up examinations were included. The vitreous fluorophotometric values were selected for local check factors. Glycosylated hemoglobin was selected for systemic check factors. To determine the retinopathy status at both the baseline and follow-up examinations, all fundus photographs were graded in a masked fashion, using the author's classification scheme (1983) which specified six levels of retinopathy for each excepted from the interrupted proliferative retinopathy. Level 0: no retinopathy, Level 1: microaneurysms only (AI), Level 2: microaneurysms and retinal hemorrhages (AII), Level 3: preproliferative retinopathy (soft exudates, increased capillary occlusion and intraretinal microvascular abnormalities) (BI), Level 4: neovascularization elsewhere (BII), Level 5: neovascularization of the disc (BIII), Level 6: vitreous hemorrhages or proliferative tissue (BIV, V). A positive correlation between the progression of retinopathy and glycosylated hemoglobin or vitreous fluorophotometric values were observed. The coefficient of correlation was 0.67 between posterior vitreous fluorophotometric values and levels (scores) of retinopathy. The coefficient of correlation was 0.41 between glycosylated hemoglobin and levels of retinopathy. These data suggest that these two factors can predict the progression of diabetic retinopathy.
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PMID:[Clinical management of diabetic retinopathy]. 261 Jan 68

Serum levels of total cholesterol, triglycerides, lipoproteins (VLDL, LDL, HDL) and apoproteins (apo-AI, apo-AII, apo-B) were measured in 112 children (70 boys, 42 girls) aged 6 to 13 with type I diabetes mellitus and healthy controls. Poorly controllable diabetes was associated with elevated concentrations of total cholesterol and low-density lipoproteins C and lowered levels of high-density lipoproteins C, apo AI and apo-AII, while differences in triglyceride, very low density lipoproteins, and apo-B were insignificant. Children with a good metabolic control (HbA1 8.8 +/- 1.2%) had a much more favorable lipid profile. The differences may be explained by lipid-reducing effects of diets and insulin therapy. Deficiency of HDL-C, apo-AI and apo-AII in type I diabetes in children indicates the importance of HDL subclasses and of lipolytic enzymes evaluation for an early detection of atherosclerosis risk.
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PMID:[Serum apoproteins and lipoproteins in diabetic children]. 841 18

Proinflammatory cytokine induction of NO synthesis may contribute to the destruction of pancreatic beta cells leading to type 1 diabetes. The NO synthase substrate arginine can also be metabolized to ornithine and urea in a reaction catalyzed by cytosolic (AI) or mitochondrial (AII) isoforms of arginase. Recent evidence suggests that the rate of NO generation is dependent on the relative activities of NO synthase and arginase. The objectives of this study were (i). to identify the arginase isoforms expressed in rat and human islets of Langerhans and a rat beta cell line, RINm5F and (ii). to investigate the competition for arginine between NO synthase and arginase in IL-1beta-treated rat islets. Arginase activity was detected in rat islets (fresh tissue, 346 mU/mg protein; cultured, 587 mU/mg), cultured human islets (56 mU/mg), RINm5F cells (376 mU/mg), rat kidney (238 mU/mg), and rat liver (6119 mU/mg). Using Western blots, AI was shown to be the predominant isoform expressed in rat islets and in RINm5F cells while human islets expressed far more AII than AI. Rat islets were cultured in medium containing 1.14, 0.1, and 0.01 mM arginine and treated with IL-1beta and the arginase inhibitor 2(S)-amino-6-boronohexanoic acid (ABH). IL-1beta-induced NO generation was unaffected by ABH at 1.14 mM arginine, but significantly increased at 0.1 and 0.01 mM arginine. These findings suggest that the level of islet arginase activity can regulate the rate of induced NO generation and this may be relevant to the insulitis process leading to beta cell destruction in type 1 diabetes.
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PMID:Arginase expression and modulation of IL-1beta-induced nitric oxide generation in rat and human islets of Langerhans. 1244 78

The objective of this study was to compare glycemic control and insulin dosage in children with type 1 diabetes treated by a modified intensified insulin therapy MII using insulin pens (and premixed and regular insulin) with those on conventional insulin therapy. This was a longitudinal, randomized controlled trial for 6 months or more. From a cohort of 125 children with previously diagnosed type-1 diabetes (more than a year after diagnosis) two groups were randomly selected Group AI (n=20) and Group B (n=20). Group AI children and 10 children with recently diagnosed type 1 diabetes (Group AII) were allocated to MII using regular insulin and premixed insulin (30/70 and 40/60 and 50/50). Group B patients continued their conventional insulin therapy for the whole period of the trial. The main outcome measures were glycemic control measured by mean blood glucose concentration and percentage of glycated haemoglobin and total daily insulin dose. Mean blood glucose concentrations before the three main meals, and at midnight, (148, 147, 179 and 127 mg/dl, respectively) were lower in children receiving intensified MII compared with those receiving conventional insulin therapy (192, 174, 194 and 179 mg/dl, respectively) (standardized mean difference 34+/-15 mg/dl), equivalent to a difference of 1.9+/-0.8 mmol/l. This improved control during MII was achieved with no change in the average daily insulin dose in group-AI. In group-AII insulin dose decreased significantly during their first 6 moths of treatment (honeymooning). Glycemic control is better during MII using insulin pens and premixed and regular insulin compared with conventional insulin therapy, without any significant change in insulin dose needed to achieve this level of control. The difference in glycemic control between the two methods is significant and could reduce the risk of micro-vascular complications.
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PMID:Glycaemic control with modified intensive insulin injections (MII) using insulin pens and premixed insulin in children with type-1 diabetes: a randomized controlled trial. 1641 Feb 76

Neonatal autoimmune diseases are distinctly rare. Most neonatal autoimmune diseases result from the transplacental transfer of maternal antibodies directed against fetal or neonatal antigens in various tissues. In neonatal lupus, the heart seems to be particularly susceptible. Primary autoimmunity in newborns, with the exception of familial autoinflammatory diseases, is virtually non-existent. The pathophysiologic basis for the development of neonatal autoimmunity is not entirely clear, but differences in the neonatal immune system compared with the adult immune system, as well as unique characteristics of target antigens in the newborn period may be important factors. Neonatal lupus is the most common presentation of autoimmunity in the newborn. But the characteristics defining neonatal lupus are not well defined and the presentation of neonatal lupus differs from that of classical lupus. Other neonatal autoimmune diseases involving the interaction between maternal antibodies and fetal/neonatal antigens include neonatal anti-phospholipid syndrome, Behcet's disease, neonatal autoimmune thyroid disease, neonatal polymyositis and dermatomyositis, neonatal scleroderma and neonatal type I diabetes mellitus. While autoantibodies have been detected in patients with neonatal autoimmune disease, the pathogenic role of autoantibodies has not been well defined. Other mechanisms may play a role in the development of neonatal autoimmunity, including fetal/maternal microchimerism and aberrant apoptosis of fetal cells. The autoinflammatory syndromes are a completely different category, but are also included in discussion of neonatal autoimmune diseases. The autoinflammatory syndromes include the cryopyrin associated periodic syndromes (CAPS) - familial cold autoinflammatory syndrome (FCAS), neonatal onset multisystem inflammatory disease (NOMID) and Muckle-Wells syndrome, which all share a common pathophysiologic mechanism.
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PMID:Neonatal autoimmune diseases: a critical review. 2240 39

The reduced levels of high-density lipoprotein (HDL) 2-cholesterol (C) in diabetes and other metabolic disorders associated with a high risk of cardiovascular disease are well established. Few studies, however, have compared the HDL subspecies in type 1 diabetes (T1D) with those in type 2 diabetes (T2D) with or without insulin. We examined HDL subspecies in 27 T1D with insulin, 33 T2D with insulin or insulin plus oral-anti-diabetic drugs (OADs), 36 T2D with OADs or diet/exercise, and 25 non-diabetic controls. Insulin was injected four times daily in a basal-bolus manner for both T1D and T2D. Plasma levels of C, apolipoprotein (apo) AI, and AII were determined in HDL2 and HDL3 by the single precipitation method. HDL-C levels were significantly higher in T1D and lower in T2D, compared with the controls. Insulin-treated T2D had higher HDL-C than non-insulin-treated T2D. T1D had higher HDL2-C and HDL2-apo AI levels than T2D. Insulin-treated T2D had higher HDL2-C and HDL2-apo AI levels than non-insulin-treated T2D. All of these differences were more pronounced for men than for women. HDL3 levels were comparable among controls,T1D and T2D. HDL2-C levels were inversely associated with BMI, HbA1c, triglyceride, small dense LDL-C, and LDL-C. Multiple regression analysis revealed that HDL2-C was independently associated with triglyceride, LDL-C, and intensive insulin therapy but not with HbA1c. In conclusion, these results suggest that intensive insulin therapy is associated with alterations of HDL subspecies, irrespective of the type of diabetes.
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PMID:High-density lipoprotein subspecies between patients with type 1 diabetes and type 2 diabetes without / with intensive insulin therapy. 2250 74