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

Alterations in Relative Plasma Viscosity (RPV) and Plasma Fibrinogen Concentration (PFC) were compared in 24 insulin-dependent (IDDM) and 33 non-insulin-dependent (NIDDM) black Nigerian diabetics, during the course of treatment. Both PFC and RPV were significantly (p less than 0.001) increased in the diabetics, as a group, compared to a non-diabetic control group. PFC and RPV showed consistently marginal, though insignificant, increases in the IDDM vs NIDDM. Hypertensive diabetics, as a group, had significantly greater PFC (p less than 0.025), and RPV (p less than 0.025) than normotensive diabetics. Although PFC was significantly (p less than 0.05) raised in hypertensive IDDM, there was no marked change in RPV, compared to normotensive IDDM. Neither PFC nor RPV revealed a significant change between hypertensive and normotensive NIDDM. The implication of the present findings is that insulin-dependent diabetics may be more prone than non-insulin-dependent diabetics to develop haemorheological and hence circulatory disorders.
West Indian Med J 1990 Sep
PMID:Comparison of plasma viscosity and fibrinogen concentration in African insulin-dependent and non-insulin-dependent diabetics with and without hypertension. 226 27

The paper describes two individuals presenting with acute insulin dependent diabetes mellitus for a brief and transient period. Both had had chicken pox infection in the immediate past. After establishing good diabetic control, insulin was withdrawn over a few weeks. Follow-up for the next two years did not reveal recurrence of diabetes. A causal relation between varicella zoster virus and the onset of diabetes is suggested.
J Assoc Physicians India 1990 Sep
PMID:Transient diabetes following chicken pox. 226 90

The NOD mouse is a model of human juvenile type I diabetes mellitus. As in humans and in the BB rat model, the development of diabetes in NOD mice is accompanied by evident manifestations of cell-mediated and humoral autoimmunity. Beside autoantibodies directed at putative islet cell antigens, NOD sera contain antibodies with specificity for lymphocyte cell-surface determinants. Here we demonstrate that these anti-lymphocyte antibodies have the same characteristics of target cell specificity, of isotype, and of temperature reactivity, as do natural thymocytotoxic autoantibodies (NTA) from lupic NZB mice, or from mice undergoing polyclonal B cell activation. We also demonstrate that the thymocytotoxic activity of NOD sera is not due to cross-reactive anti-insulin antibodies. Biochemical characterization of the determinants recognized by these anti-lymphocyte antibodies reveals two membrane-associated proteins of 28 and 33 kD, partially similar to the two peptides recognized by NTA from NZB mice (30 and 33 kD). Altogether, these results suggest that NOD mice develop manifestations of polyclonal B cell activation similar to those observed in lupus-prone mice. The relationship of these anomalies with the organ-specific pancreatic disease remains to be properly evaluated.
Clin Exp Immunol 1990 Sep
PMID:Natural thymocytotoxic autoantibodies in non-obese diabetic (NOD) mice: characterization and fine specificity. 239 10

Minimal vascular resistance (MVR) was determined in a paralysed cutaneous vascular bed at the dorsum of the foot in diabetic patients. Twelve long-term insulin-dependent diabetic (IDDM) patients with and nine short-term IDDM patients without nephropathy and retinopathy and eight control subjects were investigated. The vascular bed was paralysed by local injection of histamine. Skin perfusion pressure was varied by applying graded external counter pressure over the investigated area. Skin blood flow was measured by the local 99mTc wash-out technique before, during and after three to five step-wise increases of external counter pressure. The MVR was calculated from the reciprocal of the slope of the relationship between blood flow and applied pressure. The MVR was significantly increased in diabetic patients with (mean: 9.3 mmHg ml-1.100 g.min) and without nephropathy and retinopathy (8.5 mmHg ml-1.100 g.min) compared with non-diabetic subjects (5.2 mmHg ml-1.100 g.min) (p less than 0.001 and p less than 0.005, respectively). Diabetic microangiopathy (increased hyalinosis of the basement membranes in the terminal arterioles) was found in skin biopsies in nine of the 12 long-term IDDM patients and in four of the nine short-term IDDM patients, but not in the control subjects. Multiple regression analysis demonstrated a highly significant direct association between MVR and degree of diabetic microangiopathy in the same skin area (p less than 0.0002). A less significant direct association between MVR and arm diastolic blood pressure (p less than 0.05) and blood glucose concentration (p less than 0.05) was also found.(ABSTRACT TRUNCATED AT 250 WORDS)
Scand J Clin Lab Invest 1987 Sep
PMID:Increased minimal vascular resistance and arteriolar hyalinosis in skin on the leg in insulin-dependent diabetic patients. 244 58

The function of the local nervous veno-arteriolar reflex regulation of blood flow in subcutaneous tissue of the lower leg was studied in diabetic patients. The material comprised 11 long-term insulin-dependent diabetic (IDDM) patients with retinopathy and nephropathy and eight short-term IDDM patients without retinopathy or nephropathy and 11 non-diabetic subjects. The diabetic patients had no or a slight to moderate degree of peripheral autonomic and sensoric neuropathy. Blood flow was measured by the local 133Xe wash-out technique. Blood flow was determined before, during and after an approximately 40 mmHg increase in venous transmural pressure, induced by lowering the lower leg 50 cm below heart level. During lowering of the leg, the subcutaneous blood flow decreased to the same level in long-term IDDM patients (mean: 46%), short-term IDDM patients (53%) and control subjects (53%). There was no association between the relative local blood flow during lowering and the degree of terminal arteriolar hyalinosis studied in skin biopsies from the same tissue area. Our results suggest that terminal arteriolar hyalinosis does not interfere with the local sympathetic-mediated veno-arteriolar reflex regulation of blood flow. Moreover, the vasoconstriction mediated by the veno-arteriolar reflex probably occurs in the larger arterioles (greater than 50-100 micron) or small arteries.
Scand J Clin Lab Invest 1987 Sep
PMID:Arteriolar hyalinosis does not interfere with the local veno-arteriolar reflex regulation of subcutaneous blood flow in insulin-dependent diabetic patients. 244 59

The serum levels of the low molecular form of insulin-like growth factor binding protein (IGFBP) was determined in 56 outpatients with diabetes mellitus by a radioimmunoassay developed for amniotic 35 kDa IGFBP. The mean level of 35 kDa IGFBP was found to be threefold higher in insulin dependent diabetes mellitus (IDDM), 112 +/- 13 ng/ml, than in age matched controls, 37 +/- 2 ng/ml, while the mean level in non-insulin dependent diabetes mellitus (NIDDM), 16 +/- 2 ng/ml, was decreased. In hospitalized IDDM patients there was a significant correlation (r = 0.91, p less than 0.01) between fasting blood-glucose and 35 kDa IGFBP levels, not found in NIDDM patients. During insulin infusion the 35 kDa IGFBP levels declined with a half-life of 60-120 min. The decline in IGFBP continued even after the establishment of steady state B-glucose at 4.7 mmol/l. In conclusion, the elevated 35 kDa IGFBP levels in IDDM can be attributed to insulin deficiency and may reflect a reduced bioavailability of the IGFs at the target cells.
J Endocrinol Invest 1988 Sep
PMID:Insulin regulates the 35 kDa IGF binding protein in patients with diabetes mellitus. 246 6

Circulating insulin-like growth factor binding protein (IGF BP) activity is increased in animals with streptozotocin-induced diabetes. Separation of BPs by SDS/PAGE for ligand and immunoblot analysis revealed that a 32,000 molecular weight BP is present and increased in diabetic serum. This BP is immunologically distinct from the low molecular weight fetal rat BP (rBP2) and is related to the human amniotic fluid BP (hBP1) that is increased in patients with insulin dependent diabetes mellitus.
Biochem Biophys Res Commun 1989 Sep 15
PMID:Identification of a type 1 insulin-like growth factor binding protein (IGF BP) in serum from rats with diabetes mellitus. 247 84

Insulin-dependent diabetes mellitus is widely believed to be an autoimmune disease. Recent onset diabetics show destruction of insulin-secreting pancreatic beta-cells associated with a lymphocytic infiltrate (insulitis), with autoantibodies to beta-cells being found even before the onset of symptoms. Susceptibility to the disease is strongly influenced by major histocompatibility complex (MHC) class II polymorphism in both man and experimental animal models such as the non-obese diabetic (NOD) mouse. As MHC class II molecules are usually associated with dominant immune responsiveness, it was surprising that introduction of a transgenic class II molecule, I-E, protected NOD mice from insulitis and diabetes. This could be explained by a change either in the target tissue or in the T cells presumed to be involved in beta-cell destruction. Recently, several studies have shown that I-E molecules are associated with ontogenetic deletion of T cells bearing antigen/MHC receptors encoded in part by certain T-cell receptor V beta gene segments. To determine the mechanism of the protective effect of I-E, we have produced cloned CD4+ and CD8+ T-cell lines from islets of recently diabetic NOD mice. These cloned lines are islet-specific and pathogenic in both I-E- and I-E+ mice. Both CD4+ and CD8+ cloned T cells bear receptors encoded by a V beta 5 gene segment, known to be deleted during development in I-E expressing mice. Our data provide, therefore, an explanation for the puzzling effect of I-E on susceptibility to diabetes in NOD mice.
Nature 1989 Sep 28
PMID:An explanation for the protective effect of the MHC class II I-E molecule in murine diabetes. 250 22

Over 80% of nonobese diabetic (NOD) mice develop lymphocytic infiltrates of their pancreatic islets (insulitis) by 6 wk of age and 50% of the females are diabetic by 6 mo of age. The incidence of insulitis in NOD mice injected once as neonates with 250 micrograms of the CD3 antibody, 145.2C11, was 8% at 10 wk of age, increasing to 25% at 32 wk of age. Fewer than 10% of these animals developed diabetes by 8 mo of age. Neonatal administration of 145.2C11 reduced the proliferative responses of spleen cells to mitogen stimulation 2 and 4 wk postinjection and expression of TCR was reduced 1 to 5 wk postinjection. The percentage of CD4 and CD8 cells in the spleen was transiently reduced after injection and the frequency of Pgp-1+-high cells (putative memory cells) was increased 2 to 4 wk postinjection, suggesting that in vivo administration of the antibody caused some T cells to divide as well as transiently reducing T cell numbers. IL-2R expression was not detected on spleen cells in the 4 wk after antibody injection. The phenotypic and functional changes after neonatal CD3 antibody injection resolved by 8 wk of age. The control and injected mice grew normally and made equivalent IgG antibody responses to injected human IgG. Neonatally injected 145.2C11 antibody was cleared from the circulation with a terminal half-life approximating to 21 days but greater than 90% of antigen binding activity was lost 6 days after injection. Protection from diabetes did not follow neonatal elimination of T cells with CD4 and CD8 antibodies, nor the injection of a TCR subset antibody, F23.1. Our data suggest that the neonatal T cell repertoire is open to modulation by a single injection of a CD3 antibody and they offer a new experimental approach to immunotherapy in an animal model of type 1 diabetes.
J Immunol 1989 Sep 01
PMID:Neonatal injection of CD3 antibody into nonobese diabetic mice reduces the incidence of insulitis and diabetes. 252 66

The prevalence of periodontitis was studied in a population of 157 insulin dependent diabetes mellitus patients aged 8-78 years attending the outpatients diabetic clinic of a large general hospital in Cork, Ireland. Every third diabetic patient attending the clinic was selected for examination. The dental parameters measured were plaque index (PI), gingivitis index (GI), periodontal pocket depth (PD) and periodontal attachment loss (PAL). Diabetic control was measured by estimating percentage haemoglobin glycolysation (% Hb Alc) known duration of diabetes (KDD) and insulin dependence. It was found that none of the diabetic measurements showed any consistent pattern in relation to any of the periodontal measurements. The findings are in agreement with other studies which suggest that no significant correlation between diabetic parameters and periodontal disease can be demonstrated. When the diabetic patient suffered periodontitis it was due to factors (such as genetic predisposition) other than impaired glucose metabolism.
J Periodontal Res 1989 Sep
PMID:Diabetes mellitus and periodontal disease in an Irish population. 253 53


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