Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A control series of 105 patients in hospital with non-malignant diseases was used in a limited clinical assessment of the MOD-MEM test. Twenty-seven positive results could be explained on the basis of destruction of nervous parenchyma, tissue necrosis, tuberculosis, malignant disease, etc. The remaining 13 unexplained positives showed a sex and age distribution in agreement with that predicted from cancer registration statistics if the MOD-MEM test detects cancer about 16 years before the clinical appearance of the disease.
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PMID:Clinical assessment of the MOD-MEM cancer test in controls with non-malignant diseases. 6 Jan 18

Maturity onset diabetes (MOD) is characterized by the fact that the response of insulin secretion to glucose loading is either completely missing or is reduced if compared with that of persons whose metabolism is intact. But insulin secretion can be provoked by other specific stimuli. However, the quantitative IRI response can provide no information as to which of the MO diabetics must be treated by dietetic measures only and which of them are liable to treatment with sulfonylurea. It was, therefore, investigated whether in 109 patients suffering from recently developed overt MOD a differentiation from a therapeutical point of view can be attained by joint evaluation of stimulated IRI secretion, of glucose tolerance, of the dynamics of free fatty acids, of the fasting values of triglycerides and cholesterol and of the body weight. The findings suggest that no better differentiation for the two methods of treatment of MOD stated above is possible by simultaneous evaluation of the parameters of fat metabolism, glucose level and IRI secretion than by IRI secretion and carbohydrate tolerance alone.
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PMID:Insulin secretion, carbohydrate tolerance, fat metabolism and body weight in maturity onset diabetics requiring various methods of therapy. 9 78

The mixed lymphocyte reaction (MLR) between donor and recipient lymphocytes has been measured by the macrophage electrophoretic mobility (MEM) test and the modified (MOD-MEM) test. Its value as a measure of compatibility has been assessed by comparison with conventional HL-A serotyping and with the outcome of renal transplantation. Thirty-six living donor/recipient pairs and 59 cadaver donor/recipient pairs for transplantation have been studied. Whilst uniovular twins gave lymphocyte interactions, measured as macrophage slowings of about 1%, the slowing produced by paired allogeneic lymphocytes ranged from 2% to 26% depending on the number of HL-A matches. The test measurement of lymphocytic interaction was significantly correlated with histocompatibility measured by HL-A serotyping, in both living and cadaver donors. One way MEM-MLR showed the dominant role of the second HL-A sublocus in mixed lymphocyte reactivity. The long term success of the renal graft correlated with the pre-transplant initial reaction between donor and recipient lymphocytes. The test has advantages in the field of human histocompatibility assessment since no particular reference to individual antigens is made and it may be performed in a matter of hours.
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PMID:The assessment of histocompatibility by mixed lymphocyte reaction as measured by the macrophage electrophoretic mobility (MEM) test. 12 69

Hyperglycemia induced in animals by beta cell toxins or by pancreatectomy can be reversed by pancreatic islet transplantation. Abnormal carbohydrate metabolism in juvenile onset human diabetics has also been corrected, albeit temporarily because of graft rejection, by pancreatic transplantation. It does not necessarily follow that naturally occurring diabetes in animals or adult onset diabetes in man would respond to similar treatment. Islet transplantation was studied in mice with chemically induced or genetically determined diabetes. Streptozotocin-induced diabetic mice were permanently cured by syngeneic islets and, when immunosuppressed, were rendered normoglycemic for six weeks after receiving xenogeneic rat islets. In contrast, histocompatible islets from normoglycemic coisogenic donors were ineffective in hyperglycemic db/db recipients as were xenogeneic rat islets in immunosuppressed db/db hosts. However, when islets were isolated from db/db donors and transplated to genetically normal coisogenic mice, which had been rendered hyperglycemic with streptozotocin, they became normoglycemic. Apparently the metabolic defect in the db/db mice, which is similar in some ways to human maturity onset diabetes, does not reside in their islets as these cells can function normally if transplanted to genetically nondiabetic hosts. In two other types of genetic diabetes (ob/ob and NZO) islet transplantation was more effective. Pancreatic transplantation is unlikely to be the proper treatment for all types of diabetes even if technical and immunological problems are overcome.
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PMID:Islet transplantation in genetically determined diabetes. 14 16

Nonketotic hyperosmolar diabetic coma is a rare manifestation of juvenile diabetes, in contrast to adult onset diabetes. To date only 20 cases have been published, the majority of them infants and toddlers. This type of diabetic coma is seen with unusual frequency in children with Down's syndrome and psychomotor retardation. The clinical picture is characterised by severe dehydration, hyperglycemia with often extremely high blood sugar levels, hyperosmolarity and glucosuria without ketonuria. Mortality in children has been high (24%). This paper reports the case of a 14-month-old girl with Down's syndrome. Clinical and therapeutic as well as pathogenetic aspects are discussed.
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PMID:[Hyperosmolar nonketotic diabetic coma in children]. 15 87

Using I131 VLDL selectively labelled in the B-apoprotein and I125 LDL injected simultaneously into the patient we have derived some quantitative measures of VLDL and LDL metabolism in man. The effects of insulin resistance, associated with idiopathic hypertriglyceridaemia, adult onset diabetes and diabetic lipodystrophy on the metabolic behaviour of these molecules were also assessed. In the normal subjects 72-83% of the total daily plasma VLDL B-apoprotein flux was metabolised via a pathway which involved its ultimate conversion to plasma LDL, while 21-28% was degraded without such conversion. The amount of B-apoprotein metabolised by either of these routes was proportionate to the flux rate and the two pathways accounted for the total VLDL B-apoprotein removed from the plasma. In patients with idiopathic hypertriglyceridaemia and in the adult onset diabetics the total plasma VLDL B-apoprotein flux was higher than normal, indicating increased production of this apoprotein. On the other hand, the flux rate of plasma VLDL B-apoprotein in the patients with diabetic lipodystrophy was normal, suggesting that the increase in the circulating mass of these molecules was due to impaired clearance. In all the patients, however, the fractions of the total flux either converted to LDL or degraded were lower than normal, suggesting that insulin resistance limited the removal of this apoprotein by these pathways. The results also indicate that a fraction of the total VLDL removed from the plasma has been retained in an extravascular compartment, possibly representing VLDL molecules trapped in the vascular structures. In the control and the insulin resistant subjects the quantity of LDL apoprotein catabolised per day agreed closely with the amount derived from VLDL B-apoprotein conversion, suggesting that VLDL-B-apoprotein serves as the main source of LDL apoprotein. In patients with idiopathic hypertriglyceridaemia and in adult onset diabetics the absolute turnover rate of plasma LDL apoprotein was higher than normal, while in the lipodystrophic patients it was reduced. It is suggested that the increase in LDL turnover seen in the former groups could be an additive factor in the deposition of lipid rich material in arterial walls.
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PMID:The metabolic fate of plasma lipoproteins in normal subjects and in patients with insulin resistance and endogenous hypertriglyceridaemia. 18 13

In a dye penetration test and a scanning electron microscopic evaluation MOD-restorations made of a thixotropic material (ZKP-A-5(2)) and of two syringe system composites (Concise-Capsule-Composite3, Compocap-S4) were investigated with respect to microleakage and marginal adaptation. These materials did not reveal better marginal micromorphology than a comparable two-paste composite system (Concise3); Compocap-S showed markedly less microleakage. The quality of marginal adaptation, however, was improved to 52% when a low viscosity sealant (ZKP-A-2(2), Concise Enamel Bond3) was applied before insertion of the restorative. A sealant pretreatment is therefore compulsory in thixotropic and syringe packed composites as well. The perfection reached with these composite brands is equal to that of adhesive restorations made of Concise or Adaptic5 [6,7]. Restorations performed with new, complete composite systems (Nimetic6, GC's Epolite 100/Epobond7) revealed moderate results when compared to standard materials like Concise or Adaptic [6,7].
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PMID:[Adpatation and marginal fit of thixotropic composites and syringe system composites. In vitro findings]. 27 43

Microleakage and marginal adaptation of different composite brands (Epoxydent, Restodent, Cosmic) in conventional and adhesive MOD-cavities have been investigated in an in vitro dye-penetration and scanning electron microscope study. The results were compared to those of a standard composite brand (Adaptic). Unrelated to the type of cavity and enamel etching procedures Epoxydent and Restodent revealed moderate results only. When the use of a sealant was omitted prior to bulk placement Cosmic showed the best adaptation. Priming (Cosmic Bond) was found to impede microleakage but not to influence marginal adaptation. The superiority of the adhesive restorations that had been performed with the Adaptic and the Concise system [4] is a result of the combination of these composite materials with a sealant and the new cavity design.
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PMID:[In vitro evaluation of the adaptation and quality of the margins in various composite systems]. 27 47

The marginal integrity of MOD adhesive restorations of a thixotropic test composite (ZKP-A-5) and of two injection-capsule composites (Concise -capsule composite and Compocap-S) was examined. Dy penetration tests measured microleakage and scanning electron microscope evaluated marginal adaptation. The test restorations showed no improved micromorphological marginal adaptation when compared to those of a standard paste-paste composite (Concise). Compocap-S demonstrated better prevention of microleakage than did the other test preparations. The marginal quality of these thixotropic and injection-capsule composite restorations was improved from 34% to 52% with utilization of a sealer application (ZKP-A-2), (Concise-Enamel Bond). The application of a sealer prior to insertion of thixotropic and injection-capsule composites is, therefore, definitely indicated when these materials are used. The resultant restorations obtained with these test materials plus sealer correspond qualitatively to those of standard composites Concise or Adaptic [6,7]. The newly developed, complete composite systems (Nimetic, GC's Epolite 100/Epobond) demonstrated in comparison to Concise and Adaptic [6,7] inferior results.
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PMID:Marginal adaptation and microleakage of thixotropic and injection-capsule composites, an in vitro study. 27 18

A technique involving 5-bromodeoxyuridine, 33258 Hoechst, and fluorescence microscopy has been used to analyze replication kinetics in cells from embryonic and adult mice bearing the Cattanach [T(X;7)ICt] translocation in a balanced or an unbalanced form. In balanced 9- and 13-day female embryos, the translocated X was late replicating in 28 and 22% of the cells, respectively, whereas it was late replicating in only 13% of adult cells. In contrast, in unbalanced females, the translocated X was late replicating in 62 and 70% of 9- and 13-day embryos and in 70% of adult cells. Such divergent late replication frequencies suggest the operation, during development, of selection against cells with extreme genetic imbalance. Within a late-replicating translocated X chromosome, the autosomal segment itself replicated late approximately half of the time, regardless of karyotypic balance. The late replication data are consistent with the measurements of levels of mitochondrial malic enzyme (MOD-2, whose locus is on the autosomal segment) activity in these mice [Eicher E. & Coleman, D. (1977) Genetics 85, 647-658]. The present study also shows a dissociation between the replication timing in X chromatin distal and proximal to the autosomal segment, supporting the hypothesis of at least two inactivation centers in the X chromosome.
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PMID:Late replication in an X-autosome translocation in the mouse: correlation with genetic inactivation and evidence for selective effects during embryogenesis. 29 40


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