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)

Previously, DNA polymorphisms in the HLA gene cluster have been analyzed using radioactive probes in Southern blot experiments; the restriction fragment length polymorphisms (RFLPs) revealed by this analysis are capable of subdividing HLA serological types. Here, we report the use of DNA probes labeled with biotinylated psoralen to provide nonisotopic detection of HLA class II RFLP patterns. These biotinylated probes contain cDNA sequences encoding the alpha and beta chains of DP, DQ, and DR HLA class II genes as inserts in M13 vectors. The recombinant M13 molecules are partially double-stranded with single-stranded HLA cDNA regions and contain biotinylated psoralen covalently linked to duplex DNA by UV irradiation. Following hybridization, the presence of biotinylated probe bound to target DNA is detected using a streptavidin-horseradish peroxidase conjugate, which converts the colorless substrate 3,3',5,5'-tetramethylbenzidine to a blue precipitate in less than 1 hr. The probe and detection system described here can detect single-copy genes in less than 0.5 microgram of total human DNA on Southern blots and generates the same specific RFLP patterns as do probes labeled with 32P by nick-translation. These biotinylated HLA class II probes have been applied to tissue typing for bone marrow transplantation and the study of insulin-dependent diabetes susceptibility, revealing in each case relevant polymorphisms not detected by serologic typing.
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PMID:Use of nonisotopic M13 probes for genetic analysis: application to HLA class II loci. 287 31

Forty patients with cystic fibrosis (CF), including 34 who died above age 10 years without having developed clinical diabetes mellitus and 6 who died with both cystic fibrosis and diabetes mellitus, were studied. The mean age of the female patients with CF but not diabetes was 15.8 +/- 5.6 years; of males without diabetes, 17.2 +/- 6.4 years; of female patients with CF and diabetes mellitus, 20.2 +/- 6.9 years; and of males with CF and diabetes, 21.3 +/- 6.6 years. The mean number of pancreatic islets in microscopic sections for patients with cystic fibrosis but not diabetes was 4.18 +/- 2.76/mm2, and the value for patients with both cystic fibrosis and diabetes mellitus was 2.61 +/- 2.07/mm2. The lowest density of pancreatic islets (1.69 +/- 0.48/mm2) for cystic fibrosis was found in patients with the latest-stage pathologic lesion. Nesidioblastosis (presence of ductuloinsular complexes) was identified in 14 of 38 cystic fibrosis patients, both with and without diabetes mellitus. The pancreatic islets of both diabetic and nondiabetic patients with CF showed hypertrophy; the mean volume of the three largest pancreatic islets for CF only was 0.0117 +/- 0.00657 mm3 and that for cystic fibrosis and diabetes was 0.00795 +/- 0.00599 mm3, both values being larger than normal. Ratios of the amounts of islet endocrine cells, A cells, B cells, and D cells, were determined by peroxidase--anti-peroxidase labeled antibody staining. The B cells composed 43.0% of endocrine cell mass in cystic fibrosis alone and 30.1% in cystic fibrosis with diabetes mellitus, which were lower than normal proportions. The D cell values, 11.9% in cystic fibrosis and 15.1% in cystic fibrosis with diabetes mellitus, on the other hand, were greater than normal ratios.
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PMID:Pancreatic islets in older patients with cystic fibrosis with and without diabetes mellitus: morphometric and immunocytologic studies. 288 Dec 83

Whether the increased capillary permeability characteristic of diabetes extends to the blood-brain barrier is presently unclear. We have examined in streptozotocin-diabetic rats the permeability of the blood-brain barrier at the level of 12 discrete brain regions employing 3 intravenous tracers of different molecular weight: sucrose, insulin and horseradish peroxidase. In animals killed 5 min after tracer injection both the sucrose and the inulin spaces were similar to controls. In order to assess whether more prolonged circulation of tracers would uncover leakage, we studied brain spaces at longer intervals after tracer injections. When inulin was allowed to circulate for 15 min prior to killing, animals with 4 weeks of diabetes (but not 2 weeks) exhibited larger inulin spaces at the level of the medio-basal hypothalamus (p less than 0.01), medio-dorsal hypothalamus (p less than 0.05) and periaqueductal gray (p less than 0.01). Horseradish peroxidase, even after 75 min of perfusion, remained confined in both diabetic and control animals to central nervous system areas devoid of blood-brain barrier. Thus, after a relatively short duration of diabetes the blood-brain barrier manifests an increased permeability. It is subtle, limited to some brain regions and selective for low molecular weight tracers.
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PMID:Studies on the permeability of the blood-brain barrier in experimental diabetes. 293 77

Although inherited forms of phagocyte defects affect a small proportion of the general population, their clinical course can be altered dramatically by a physician's awareness of these diseases and modifications of the approach to and treatment of affected patients. The most common syndromes are chronic granulomatous disease of childhood (CGD), the Chediak-Higashi syndrome (CHS), the hyperimmunoglobulin-E-recurrent infection (Job's) syndrome (HIE), and myeloperoxidase (MPO) deficiency. CGD patients have defects in the oxidative metabolism involved in killing catalase-positive organisms. CHS patients have giant granules defective in fusing with phagosomes and subsequent killing of ingested organisms. HIE patients have abnormal chemotaxis and elevated IgE levels and are susceptible to skin infections with Staphylococcus aureus and recurrent sinopulmonary infections. MPO-deficient patients often go undetected since they rarely have recurrent infections unless they have a concomitant disease such as diabetes mellitus. Patients with a recently described syndrome, C3bi receptor deficiency, have recurrent bacterial infections and persistent leukocytosis, and their neutrophils have abnormal adherence and phagocytosis. The absence of specific granules is a more rare entity but these patients also have recurrent infections thought to be secondary to a chemotactic defect and a minor abnormality of microbial killing exhibited by their neutrophils. This review will focus on the clinical presentation and management of these patients.
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PMID:Phagocyte defects. 294 Nov 93

The hypothalamic paraventricular and supraoptic nuclei and the neurohypophysis of rats were investigated 8 weeks after streptozotocin (STZ)-induction of type 1 diabetes. Vasopressin (VP)- and oxytocin (OT)-containing neuronal profiles were examined using the pre-embedding peroxidase-antiperoxidase technique for electron microscopy. Ultrastructural alterations were observed in the somata, dendrites and axons of VP- and OT-labelled profiles. There was no evidence, however, for alterations in the synapses associated with VP- or OT-labelled somata, dendrites and axons. The results indicate that both VP- and OT-containing neuronal profiles are involved in the ultrastructural reorganisation of the hypothalamo-neurohypophysial complex during diabetic conditions. Depletion of VP- and OT-containing axon profiles in the neurohypophysis may suggest increased release of both neurohypophysial hormones in STZ-induced diabetes.
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PMID:The hypothalamo-neurohypophysial system in streptozotocin-diabetic rats: ultrastructural and immunocytochemical evidence for alterations of oxytocin- and vasopressin-containing neuronal profiles. 296 36

Salivary gland striated duct cells play an important role in the modification of primary saliva by secretion and reabsorption of electrolytes, and secretion of glycoproteins. Recent observations have shown that in the rat parotid gland these cells are able to internalize exogenous proteins, e.g., horseradish peroxidase and ferritin, from the ductal lumen. In rats made diabetic by injection of streptozotocin, dense vacuoles and crystalloids are present in the apical cytoplasm of parotid striated duct cells. In this study we utilized electron microscopic immunocytochemistry to determine if these vacuoles and crystalloids contain acinar secretory proteins. At various times after induction of diabetes by streptozotocin (65 mg/kg), the parotid glands were fixed in a glutaraldehyde-formaldehyde mixture, postfixed in OsO4, and embedded in epoxy resin. Thin sections were immunolabeled with antibodies to protein B1 (Ball et al., 1988) and alpha-amylase (Baum et al., 1982) using a modification of the Protein A-gold technique (Bendayan and Duhr, 1986). With antibody to B1, label was localized in the secretory granules of acinar and intercalated duct cells of both normal and diabetic rats. In striated duct cells of diabetic rats, label was present over the electron-dense vacuoles but not over the crystalloids. Since crystalloids appear to form within the vacuoles, their lack of reactivity may indicate degradation of the internalized protein. The same distribution of label was found with antibody to amylase except for the intercalated duct granules, which were unlabeled in both control and diabetic animals. These results demonstrate that striated duct cells take up salivary proteins from the lumen and that the endocytosis of some secretory proteins from the saliva may be a significant function of these cells in certain pathological conditions.
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PMID:Endocytosis of parotid salivary proteins by striated duct cells in streptozotocin-diabetic rats. 297 65

Reduced bacterial killing by polymorphonuclear leucocytes has been reported in patients with diabetes mellitus. Whether this is due to reduced content of bactericidal granular proteins has not been determined. We therefore immunochemically measured the content of myeloperoxidase, lactoferrin, lysozyme, cathepsin G and elastase in polymorphonuclear leucocytes from 50 insulin-treated diabetic patients. The peroxidase activity was also measured. Normal contents of myeloperoxidase and lactoferrin as well as normal peroxidase activity were found. The average contents of cathepsin G, elastase and lysozyme were 2.5, 3.2 and 2.6 micrograms/10(6) polymorphonuclear leucocytes, respectively, and thus 14, 45 and 18% higher than the contents of normal polymorphonuclear leucocytes. The results indicate that reduced intracellular killing of bacteria demonstrated in previous studies in diabetic patients does not appear to be related to a reduction in the content of bactericidal proteins.
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PMID:Bactericidal proteins and neutral proteases in diabetes neutrophils. 301 98

The rates of basal pinocytosis and internalization of Fc receptor-bound model immune complexes by macrophages from control (Group 1, n = 9), insulin-treated non-diabetic (2, n = 9), insulin-deficient diabetic (3, n = 8) and insulin-treated diabetic (4, n = 8) rats were measured. Pinocytic rates, as determined by uptake of horseradish peroxidase (HRP), were comparable for all experimental groups (1, 19.6 +/- 5.3; 2, 18.6 +/- 6.0; 3, 18.7 +/- 5.5; 4, 24.5 +/- 9.1; mean +/- 1 SD, pg per min per 10(6) cells, analysis of variance P greater than 0.05). The rates of internalization of Fc receptor-bound model immune complexes were decreased in insulin-treated non-diabetic rats (2, 41.7 +/- 10) and both groups of diabetic rats (3, 39 +/- 5.6; 4, 44.6 +/- 6.9) compared with control animals (1, 54.4 +/- 7.2; mean +/- 1 SD, percentage internalized per 10 min per 10(6) cells, analysis of variance P less than 0.01). Under the conditions of study, comparable amounts of model immune complexes were bound by macrophages from each of the groups; thus, the amount of internalized material was decreased in all three experimental groups (2, 3 and 4). These data suggest that insulin treatment, as well as the diabetic environment, can contribute to a decreased rate of internalization of Fc receptor-bound immune complexes, and may thereby contribute to impaired phagocytosis that has been demonstrated to occur in diabetes. These changes appear to be specific to Fc receptor-mediated internalization, as no differences in the rates of basal pinocytosis were observed.
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PMID:Measurement of the rates of basal pinocytosis of horseradish peroxidase and internalization of heat-aggregated IgG by macrophages from normal and streptozotocin-induced diabetic rats. 306 33

The analytical reliability of the immunoenzyme methods for determination of the thyroid hormones thyroxin, triiodothyronine, thyroid-binding globulin, thyrotropic hormone and the thyroid-binding capacity was examined by the peroxidase activity of the marker enzyme of "Specol-11" 28 healthy controls, 28 patients with subcompensated insulin-dependent diabetes with mean duration of 8.4 years and 11 patients with hypogonadism were examined. In the diabetic patients were found changes in their thyroid state characteristic for hypothyroidism--increased thyroxin and a decrease of the thyroid-stimulating hormone with a lowered level of the binding proteins. The patients with hypogonadism showed changes mainly in the binding proteins level, a decrease of the thyroid-binding capacity with 70%. The results reveal interrelations between the thyroid gland hormonal state and other hormonal disorders.
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PMID:[Immunoenzyme methods for determining thyroid hormones]. 306 96

Permeability-surface-area products (PA) for sucrose at the blood-retinal barrier (BRB) were determined with quantitative in vivo techniques and compared in control rats, rats fed a 50% galactosemic diet, and rats fed a diet containing both galactose and the aldose reductase inhibitor sorbinil. The mean PA +/- SE for controls was 0.656 x 10(-5) +/- 0.13 ml.g-1.s-1 and increased by approximately 500% in galactose-fed animals to 3.13 x 10(-5) +/- 0.32 ml.g-1.s-1. Animals fed both galactose and sorbinil showed no significant difference from control animals (P greater than .05), with a PA of 0.91 x 10(-5) +/- 0.22 ml.g-1.s-1. No breach in the BRB to horseradish peroxidase was detected in any of the groups. These results demonstrate an increased permeability at the BRB to small molecules in galactosemic rats that is prevented by an aldose reductase inhibitor. This suggests that the retinal capillary basement membrane thickening seen in galactosemic rats is associated with an increased permeability of the BRB and that aldose reductase is implicated in its pathogenesis.
Diabetes 1987 Nov
PMID:Permeability changes in blood-retinal barrier of galactosemic rats are prevented by aldose reductase inhibitors. 311 6


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