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

Newton's laws of motion play a major role in blood flow. Inertia and conservation of momentum cause flow to separate at branches and curves in large blood vessels. Areas of separated flow in the arterial system are sites of atherogenesis. The place at which the separation ends, called the stagnation point, is the focus for plaque development. Pulsation of the arterial circulation causes the stagnation point to move downstream with each systole and upstream with each diastole. This movement generates forward and backward shearing force in the stagnation region as the separated flow migrates back and forth. Angular momentum, introduced into flowing blood with each heart beat and further enhanced by the asymmetry of origin of vessels branching from the aorta, generates a sidewise force component that is preserved during migration of the stagnation point. The sidewise force, added to the forward and backward shear stresses, creates an area of multidirectional shear stress under the migrating stagnation point that increases the permeability of the local endothelium. Blood is a complex fluid; it can generate greater shear stresses near the stagnation point than the simple fluids normally studied by fluid mechanicists. Blood is capable of retaining shear stress for short periods after it ceases to flow and extra work is required to establish its flow. In diabetes, reduced erythrocyte deformability further burdens flow onset. We are not yet able to establish whether the increase is only a few percent, or whether the burden is larger. Whatever its magnitude, diabetic modifications of the flow properties of blood, directly affect the size, location, and rate of development of atherosclerotic plaques.
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PMID:Effects of insulin on physical factors: atherosclerosis in diabetes mellitus. 390 64

Patients with insulin-dependent diabetes mellitus (IDDM) have autoantibodies that react with cells in the islets of Langerhans. To determine whether these patients suffer from a more generalized immunoregulatory disorder, the ratio of phenotypic helper to suppressor cells was evaluated by specific monoclonal antibodies. Our experiments showed that the helper/suppressor cell ratio was significantly increased in patients with IDDM of less of 2 mo duration and then gradually returned to normal. Despite the alteration in the helper/suppressor cell ratio, there was no evidence for polyclonal activation as measured by the number of immunoglobulin-secreting plaque-forming cells in the peripheral blood. There was, however, a significant increase in the number of spontaneous plaque-forming cells in patients suffering from both IDDM and Hashimoto's thyroiditis (HT). Nonetheless, immunoglobulin production after stimulation with pokeweed mitogen was not different in diabetics with or without HT when compared to normal controls. These findings suggest that subtle changes in the immunoregulatory system occur during the early stages of IDDM.
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PMID:Abnormalities of immunoregulatory T cell subsets in patients with insulin-dependent diabetes mellitus. 621 14

The peak plaque-forming-cell (PFC) and serum antibody responses of diabetic mice to type III pneumococcal capsular polysaccharide (S3) were delayed compared with normals. Proliferation of PFC precursors was not inhibited in an insulin-deficient environment. The delay in the PFC response to S3 did not occur in diabetic nude mice but was demonstrable in their thymus-bearing heterozygote littermates. Therefore, T-cells appear to mediate the delay in the response of diabetic mice to S3 probably by delaying their differentiation into PFC. Diabetic mice responded normally to the induction of low-dose tolerance to S3, indicating the presence of active suppressor T-cells (Ts) in these mice. However, inactivation of Ts by anti-lymphocyte serum (ALS) required a higher dose in the diabetic mice. Furthermore, inactivation of Ts by ALS totally abolished the delay in peak PFC response. These findings suggest that the delayed PFC response to S3 in diabetic mice was the result of excessive splenic Ts activity. In peripheral blood, diabetic mice appeared to have more amplifier T-cell activity or less suppressor T-cell activity than normals. This response was normalized by insulin treatment. DIABETES 32:156-164, February 1983.
Diabetes 1983 Feb
PMID:Impairment of T-cell regulation of the humoral immune response to type III pneumococcal polysaccharide in diabetic mice. 621 27

The ability of different strains of a single virus type to produce different pathogenic expressions is well documented within the picornavirus group. Coxsackievirus, group B, type 4 (CB4) has been associated with viral-induced diabetes in man, but expression of its potential to induce diabetes in experimental animals is variable. Evidence is presented here for one of the primary sources of this variability that could explain resulting contradictory reports offered in support or rejection of its diabetogenic potential. C57B1/6 and SWR mice were infected with the Edwards isolate of CB4 (CB4-Edw) and three of its plaque-purified virion "strains." These were designated Edwards isolate-1 (E1), E2, and E3. CB4-Edw, E1, E2, and E3 were serologically similar by infectivity neutralization tests, had identical plaque morphology, and replicated to a similar level in the pancreas. The most profound difference was the level of virus antigen accumulation in the islet cells as determined by immunoperoxidase localization. CB4-Edw had moderate antigen accumulation in most islet cells of SWR mice but was restricted to only a few specific cells within the periphery islets of C57B1/6 mice. Unlike CB4-Edw all three new isolates accumulated antigen in most islet cells of both mouse strains. Virus isolate (strain) E2 showed the most intense accumulation in islet cells. These observations suggest that the Edwards isolate of CB4, like other human isolates of CB4 virus, probably exists as a heterogeneous population of virion strains. The pathogenic consequences and expression of any diabetogenic potential is, therefore, dependent on virus strain selection. This diversity must be considered when evaluating the pathogenic nature of CB4 viruses in experimental animals and the possible role of the viruses in diabetes of man.
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PMID:Diversity within a human isolate of coxsackie B4: relationship to viral-induced diabetes. 630 Mar 15

Ultrastructural changes in heart muscle due to chronic diabetes subsequent to a single injection of streptozotocin (65 mg/kg body wt, i.v.) were studied in rats. Presence of diabetes was indicated by hyperglycaemia (plasma glucose, control, 120 +/- 7; diabetic, 448 +/- 21 mg/dl) as well as hypo-insulinaemia (plasma insulin, control, 25.6 +/- 5.2; diabetic, 11.2 +/- 0.5 microU/ml). After 8 weeks of diabetes, the hearts were processed for electron microscopic examination. Cardiac muscle cells in diabetic hearts showed condensation of nuclear chromatin and folding of nuclear membranes. Swelling of mitochondria, clearing of mitochondrial matrix and incorporation of lysosomal membranes into mitochondrial matrix was also noted. A marked increase in both lysosomes and lipid droplets was apparent. Focal areas in diabetic hearts showed contracted sarcomeres, myofibrillar degeneration and separation of the intercalated disc. Atherosclerotic plaque formation as well as structural changes in the smooth muscle or endothelial cells in the small arteries, arterioles or capillaries were not seen to accompany the structural changes in the cardiac muscle cells of the diabetic hearts. This study provides strong evidence for the occurrence of primary myocardial disease in streptozotocin-induced chronic diabetes.
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PMID:Cardiac cell damage: a primary myocardial disease in streptozotocin-induced chronic diabetes. 648 39

Observations are described in 12 massively obese patients (5 women, 7 men), aged 25 to 59 years (mean 37), who weighed 312 to more than 500 pounds (mean 381). Seven patients had had systemic hypertension, 4 hypersomnia or sleep apnea, 2 diabetes mellitus, and 1 patient symptomatic coronary artery disease. Five patients died suddenly from undetermined causes, 2 from right-sided congestive heart failure, 1 patient from acute myocardial infarction; 1 from aortic dissection; 1 from intracerebral hemorrhage; 1 from a drug overdose, and 1 soon after an ileal bypass. The heart weight was increased in all 12 patients. The heart weight to body weight ratio expressed as a percent ranged from 0.22 to 0.61 (mean 0.37) (normal for men 0.42 to 0.46 [mean 0.43], normal for women 0.38 to 0.46 [mean 0.40]). The left ventricular cavity was dilated in 11 patients and the right ventricular cavity in all 12. Only 2 patients (aged 42 and 59 years) had 1 or more major epicardial coronary arteries narrowed greater than 75% in cross-sectional area by atherosclerotic plaque, 1 of whom had no symptoms of myocardial ischemia. Of 664 five-millimeter segments from the 4 major epicardial coronary arteries from 11 patients (mean 60 per patient), 431 (65%) were narrowed 0 to 25% in XSA, 143 (21%) were narrowed 26 to 50%, 73 (11%) were narrowed 51 to 75%, and 17 (3%) were narrowed 76 to 100%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The heart in massive (more than 300 pounds or 136 kilograms) obesity: analysis of 12 patients studied at necropsy. 649 30

This cross-sectional study examined the gingivitis occurring at puberty in a population of insulin-dependent juvenile diabetics. Seventy-seven children between the ages of 6 and 15 years were examined for gingivitis levels, stages of pubertal maturation and blood levels of glucose and glycosylated hemoglobin. Bacterial plaque was sampled from one or more approximal tooth surfaces of every subject and cultured under anaerobic and aerobic conditions on nonselective and selective media. The total cultivable flora and percentage of certain presumptive periodontopathic bacteria were determined. Before puberty, children with "high" levels of glycosylated hemoglobin also had higher gingivitis levels than children with "normal" metabolic control of diabetes. During puberty, the level of gingivitis increased independently from both fasting blood glucose levels and per cent glycosylated hemoglobin. The microbiota of marginal plaque was predominantly composed of facultatively anaerobic bacteria. The percentages of Capnocytophaga sp and Actinomyces naeslundii were statistically higher at the onset of puberty, suggesting that a specific bacterial shift in the microbial composition of marginal plaque occurs in response to host changes in juvenile diabetic children at this age period.
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PMID:Puberty gingivitis in insulin-dependent diabetic children. I. Cross-sectional observations. 660 30

The following immunological functions were studied in a case of insulin dependent diabetes mellitus with Graves' disease: (1) Lymphocyte subpopulations, (2) mitogen response, (3) immunoglobulin producing cells by the plaque forming cell assay, (4) cell-mediated cytotoxicity, and (5) natural killer activity were normal. The patient lacked antibody-dependent cell-mediated cytotoxicity. No conclusion could be drawn as to whether effector cells mediating natural (NK cell) and antibody-dependent cell-mediated cytotoxicity (K cell) are identical or different. However, the existence of such a case strongly suggests that the K cell is distinct from the NK cell. To resolve the question of whether or not a loss of antibody-dependent cell-mediated cytotoxicity activity plays an important role in the development of diabetes mellitus and Graves' disease, further studies on a large number of cases are necessary.
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PMID:A case of K cell deficiency with diabetes mellitus and Graves' disease. 668 43

Since Kahn et al. reported in 1976 insulin resistant diabetes due to anti-insulin receptor antibodies, an unusual form of diabetes mellitus (type B) has been found in many countries. We had two diabetic patients with anti-insulin receptor antibodies, associated with either acanthosis nigricans or systemic lupus erythematosus. Remission occurred 15 months after the onset of insulin resistant diabetes. One patient unfortunately died of acute pneumonia and the other has been followed up. The anti-insulin receptor antibodies were measured according to the method of Omori and Hirata by using the pellet of human placental membrane. The anti-insulin receptor antibodies in both cases diminished as remission occurred. Reverse hemolytic plaque assay (PFG) detected immunoglobulin-producing cells. In Case 2, the plaque forming cells were twenty times as many as the normal value. Immunosuppressive therapy with cyclophosphamide reduced the immunoglobulin secreting cells as remission occurred. The patients with insulin resistance (type B) should be treated with enough insulin inspite of the presence of insulin resistance. Besides, cyclophosphamide, 6-mercaptopurine and prednisolone should be used with caution. Plasma exchange is a treatment to be tried. It is important to note that spontaneous remission may occur more than half a year after the onset of insulin resistant diabetes.
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PMID:Remission of insulin resistant diabetes in two patients with anti-insulin receptor antibodies. 675 1

Earlier studies indicate that diabetic children are less resistant to periodontal disease than healthy children. As the degree of metabolic control of the diabetes ranges widely in a juvenile population, the susceptibility to gingival inflammation may vary. The aim of the present study was to compare the gingival status in diabetic children, subgrouped for control of the disease, with that in non-diabetic children. All comparisons were performed under controlled plaque conditions. 43 diabetic children took part in the study. The controls consisted of age- and sex-matched healthy children. The degree of gingival inflammation and the amount of bacterial plaque were assessed in terms of the Gingival Index and the Plaque Index, respectively. The Plaque Index scores constituted the basis for all comparisons of gingival status. The metabolic control of the diabetics was assessed from the amount of glycosylated hemoglobin fraction HbA1c. For children with the highest Plaque Index scores, diabetics showed statistically significantly higher Gingival Index scores. Only minor differences were seen in the other Plaque Index classes. The diabetic children with poor metabolic control showed a clear tendency towards higher Gingival Index scores than the non-diabetics, while no such tendency was seen between the diabetics with good metabolic control and the non-diabetics.
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PMID:Gingival inflammation in diabetic children related to degree of metabolic control. 693 90


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