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)

The extent of microleakage under MOD composites was studied when an aluminum oxalate dentin bonding agent (Tenure), a phosphonated resin bonding agent (Bondlite), and a glass-ionomer cement (Ketac Silver) were used. Three groups of 10 extracted molars were prepared with MOD cavities; one box ended on enamel, the other on cementum. In Group 1, Bondlite was applied to dentin and etched enamel before the sample was restored with a light-cured hybrid composite. In Group 2, a 2-mm increment of Ketac Silver was placed in each box before Bondlite and composite. In Group 3, Tenure was applied to dentin before being restored. Teeth were thermal-cycled, stained in silver nitrate, sectioned, and scored for microleakage. Microleakage along the gingival floor was significantly less at enamel margins than at cementum margins in all three groups. All groups showed severe marginal microleakage on cementum.
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PMID:Microleakage in MOD resin composite with three dentin bonding agents. 270 Sep 71

The purpose of this in vitro study was to evaluate the microleakage of indirect composite inlays and to compare leakage of inlays with directly placed composite restorations. Standardized MOD preparations were cut in 50 extracted human molars. One gingival margin was placed in enamel above the CEJ, and the other was placed in dentin below the CEJ. Two groups of teeth were directly filled with composites (P-30 and Heliomolar) after being etched, and dentin bonding agents were applied. Two groups of teeth were restored with composite inlays that were fabricated on stone dies. The inlays were made and luted with the same two composites. The last group of teeth was restored with Heliomolar inlays luted with Dual cement. The specimens were thermocycled 300 times between 5 and 50 degrees C. Microleakage was evaluated by use of the silver-nitrate staining technique. The depth of leakage was measured microscopically after the teeth were sectioned. Both direct restorations and inlays showed substantial leakage at gingival-dentin margins; however, there was only superficial leakage at enamel margins. P-30 inlays and Heliomolar inlays cemented with Dual leaked less than direct restorations at the gingival-dentin margins. There was no difference in leakage of enamel margins of inlays and direct restorations, except that direct Heliomolar restorations leaked more than the others. There was no difference in leakage between Heliomolar restorations luted with light-cured or dual-cured cement.
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PMID:Microleakage of indirect composite inlays. 270 Sep 73

The aim of this study was to evaluate the variations in microleakage of large Class II (MOD) restorations over time. Three different combinations of dentine bonding agents and posterior resin composites which had previously shown promise were used: Vitrebond/Scotchbond 2 plus P50, Tripton plus Occlusin and Clearfil Photo Bond plus Clearfil Photo Posterior. Conventional Class II cavities were prepared in freshly extracted third molars. All gingival margins were terminated at the cemento-enamel junction. A fluid-under-pressure apparatus connected with the pulp chamber of each tooth was used to evaluate the permeability and marginal leakage of the restorations at 0.069 MPa. Microleakage was tested after insertion of restorations at 2, 15, 45, 150 min, after 1, 2, 7, 14 days, after 1, 2, 3 months, after thermal cycling and 10 months later, after occlusal loading. Finally, all specimens were exposed to silver nitrate solution to measure microleakage as dye penetration. Immediately after insertion of the restorations, all the materials showed a higher microleakage than after 1-2 days. After 4-8 weeks, all the restorations exhibited an increased permeability suggesting that hygroscopic expansion was not sufficient to keep pace with hydrolytic degradation of the restorations. Neither thermocycling or occlusal stresses increased the microleakage of the restorations.
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PMID:Permeability and microleakage of Class II resin composite restorations. 815 12

Endothelium-dependent and -independent vascular responses were assessed in 10 NIDDM patients and 6 normal subjects with no evidence of atherosclerotic disease. Changes in forearm blood flow and arteriovenous (AV) serum nitrite/nitrate (NO2-/NO3-) concentrations were measured in response to intra-arterial infusion of acetylcholine (ACh) (7.5, 15, 30 microg/min, endothelium-dependent response) and sodium nitroprusside (SNP) (0.3, 3, 10 microg/min, endothelium-independent response). Insulin sensitivity (determined by minimal model intravenous glucose tolerance test) was lower in NIDDM patients (0.82 +/- 0.20 vs. 2.97 +/- 0.29 10(4) min x microU(-1) x ml(-1); P < 0.01). Baseline forearm blood flow (4.8 +/- 0.3 vs. 4.4 +/- 0.3 ml x 100 ml(-1) tissue x min(-1); NS), mean blood pressure (100 +/- 4 vs. 92 +/- 4 mmHg; NS), and vascular resistance (21 +/- 1 vs. 21 +/- 1 units; NS), as well as their increments during ACh and SNP, infusion were similar in both groups. No difference existed in baseline NO2-/NO3- concentrations (4.09 +/- 0.33 [NIDDM patients] vs. 5.00 +/- 0.48 micromol/l [control subjects]; NS), their forearm net balance (0.31 +/- 0.08 [NIDDM patients] vs. 0.26 +/- 0.08 micromol/l x 100 ml(-1) tissue x min(-1); NS), and baseline forearm glucose uptake. During ACh infusion, both NO2- and NO3- concentrations and net balance significantly increased in both groups, whereas glucose uptake increased only in control subjects. When data from NIDDM and control groups were pooled together, a correlation was found between the forearm AV NO2- and NO3- differences and blood flow (r = 0.494, P = 0.024). On the contrary, no correlation was evident between NO2- and NO3- concentrations or net balance and insulin sensitivity. In summary, 1) no difference existed in basal and ACh-stimulated NO generation and endothelium-dependent relaxation between uncomplicated NIDDM patients and control subjects; 2) in both NIDDM and control groups, forearm NO2- and NO3- net balance following ACh stimulation was related to changes in the forearm blood flow; and 3) ACh-induced increase in forearm blood flow was associated with an increase in glucose uptake only in control subjects but not in NIDDM patients. In conclusion, our results argue against a role of impaired NO generation and blood flow regulation in determining the insulin resistance of uncomplicated NIDDM patients; rather, it supports an independent insulin regulation of hemodynamic and metabolic effects.
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PMID:Forearm nitric oxide balance, vascular relaxation, and glucose metabolism in NIDDM patients. 916 77

The role of reduced endothelial production of EDRF-NO in the pathogenesis of diabetic angiopathy has received much attention, however, most of the rather conflicting data were gained from animal experiments. Limited human experience seems to be available in insulin dependent diabetes, calling attention to decreased EDRF-NO production. Hereby the clinical, as well as laboratory investigation (urinary and serum nitrate/nitrite, lipid peroxidation, glucometabolic parameters, endothelial and in vivo platelet activation markers, etc.) of 35 non-insulin dependent (NIDDM) and 15 insulin dependent diabetics (IDDM) patients are given. Urinary and serum nitrate/nitrite concentrations were proven to be reduced in both patients groups. This change was independent of diabetes duration, presence of macroangiopathy, coronary heart disease and the glucometabolic parameters, however, correlation was registered with lipid peroxidation (total antioxidant status). An inverse correlation of nitrate/nitrite excretion with endothelial markers (von Willebrand factor, soluble thrombomodulin) was documented in NIDDM, this correlation was much stronger in IDDM. Moreover, in IDDM patients reduced nitrate/nitrite excretion was strongly associated with elevated plasmatic beta-thromboglobulin levels. The data presented here support to the hypothesis, that EDRF-NO production is reduced in diabetes and this reduction seems to correlate with endothelial damage. In IDDM the decreased nitrate/nitrite excretion may also lead to increased in vivo platelet activation, which suggests that the reduced amount of EDRF-NO might play a role in the pathogenesis of angiopathy in IDDM.
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PMID:The association of reduced endothelium derived relaxing factor-NO production with endothelial damage and increased in vivo platelet activation in patients with diabetes mellitus. 917 38

Nuclear matrix protein (NMP), an indicator of apoptosis, was analyzed in patients with multiple organ dysfunction syndrome (MODS). Blood levels of tumor necrosis factor-alpha (TNF-alpha) and nitrite/nitrate (NOx) were also measured in these patients to determine the involvement of these factors in the production of NMP. Forty-six patients with MODS were studied, 21 (45.7%) of whom died. NMP and TNF-alpha were measured by enzyme-linked immunosorbent assay (ELISA). NOx was measured by the Griess's method. Marshall's multiple organ dysfunction score (MOD score) was used as an indicator of organ failure. The severity of organ failure was assessed by use of the acute physiology and chronic health evaluation II score (APACHE II score). The number of organs that failed was found to be significantly correlated with the NMP level. The NMP level was also correlated significantly with MOD score and APACHE II score, as well as with TNF-alpha and NOx levels. NMP and NOx levels in the group that died significantly exceeded those in the surviving group. Results suggest that apoptosis can occur in the presence of MODS, and that its extent increases as the number of failing organs increases. The results also suggest that TNF-alpha and NO are involved in the induction of apoptosis.
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PMID:Nuclear matrix protein, tumor necrosis factor-alpha, and nitrite/nitrate levels in patients with multiple organ dysfunction syndrome. 964 23

In this study, we have compared resistance to insulin-mediated glucose disposal and plasma concentrations of nitric oxide (NO) and cyclic-GMP in healthy volunteers with (n = 35) or without (n = 27) at least one sibling and one parent with type 2 diabetes. The 62 volunteers were further divided into groups of those with normal glucose tolerance or impaired glucose tolerance. Insulin-mediated glucose disposal was quantified by determining the insulin sensitivity index (ISI) in response to a low-dose, constant infusion of insulin (25 mU/kg x h) and glucose (4 mg/kg x min) for 150 min. The mean (+/-SEM) ISI [(mL kg(-1) min(-1)/pmol/L) x 10(3)] was significantly greater in those without a family history (30.3 +/- 2.3) as compared with nondiabetic volunteers with a family history of type 2 diabetes, whether they had normal glucose tolerance (17.0 +/- 7.2) or impaired glucose tolerance (9.5 +/- 1.4). In addition, basal NO levels, evaluated by the measurement of its stable end products [i.e. nitrite and nitrate levels (NO2-/ NO3-)], were significantly higher, and cyclic-GMP levels, its effector messenger, were significantly lower in those with a family history, irrespective of their degree of glucose tolerance, when compared with healthy volunteers without a family history of type 2 diabetes. Furthermore, when the 62 volunteers were analyzed as one group, there was a negative correlation between ISI and NO2-/NO3- levels (r = -0.35; P < 0.005) and a positive correlation between ISI and cyclic-GMP levels (r = 0.30; P < 0.02). These results have shown that alterations of the NO/cyclic-GMP pathway seem to be an early event in nondiabetic individuals with a family history of type 2 diabetes and these changes are correlated with the degree of insulin resistance.
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PMID:Alterations in nitric oxide/cyclic-GMP pathway in nondiabetic siblings of patients with type 2 diabetes. 1090 87

Diabetic nephropathy is a leading cause of end-stage renal failure. Its incidence is higher and is increasing in persons of Indo-Asian and African-Caribbean (African-Asian) compared with those of white origin. Nitric oxide deficiency is associated with progressive renal disease. It was hypothesized that differences in the capacity to increase glomerular filtration (functional renal reserve) would exist between these racial groups in relation to nitric oxide availability. Patients with type 2 diabetes of African-Asian (n = 9) and white (n = 9) origin with microalbuminuria were studied under euglycemic conditions. Glomerular filtration, renal plasma flow, and clearance of the stable metabolites of nitric oxide, nitrite, and nitrate were measured before and after a renal vasodilatory stimulus of a mixed amino acid intravenous infusion. There were no significant differences in age, duration of diabetes, and baseline glomerular filtration (57.1 [14.1] versus 55.8 [10.1] yr; P = 0.82, 14.5 [10.2] versus 9.1 [7.0] yr; P = 0.19 and 125.9 [30.9] versus 127.2 [44.6] ml/min per 1.73 m(2); P = 0.94) between the African-Asian and white groups. Functional renal reserve, change in renal plasma flow, and percentage change in nitrate and nitrite clearance was significantly higher in the white compared with the African-Asian group (21.9 [45.7] versus -2.5 [28.2] ml/min per 1.73 m(2); P = 0.043, 155.8 [205.9] versus -90.1 [146.0]; P = 0.03 ml/min per 1.73 m(2) and 26.7 [85.1] versus -44.7 [16.9] %; P = 0.013, respectively). The differences in functional reserve were not confounded after adjustment for diabetes duration (P = 0.034). The data suggest that these patients with type 2 diabetes of African and Asian origin lose functional renal reserve earlier in the evolution of nephropathy than whites. The differences appear to be due to defective nitric oxide production or bioavailability and might explain some of the propensity to develop end-stage renal disease.
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PMID:Defective nitric oxide production and functional renal reserve in patients with type 2 diabetes who have microalbuminuria of African and Asian compared with white origin. 1156 11

Lysophosphatidylcholine (lysoPC), a component of oxidized low-density lipoprotein cholesterol (LDL-C), has been reported to impair nitric oxide production and endothelium-dependent vasorelaxation. The effects of troglitazone (CAS 97322-87-7), which is an antidiabetic agent with antioxidant properties, on serum levels of lysoPC and nitrite/nitrate (NOx) have been studied. Eight patients with Type 2 diabetes (non-insulin dependent diabetes mellitus, NIDDM) were studied (age: 61.5 +/- 2.8 years; diabetes duration: 10.2 +/- 1.6 years). They were additionally given troglitazone (200 mg once daily) since their fasting plasma glucose (FPG) and HbA1c levels had been increased in spite of conventional medications. Before and after 12 weeks of treatment with troglitazone their blood pressure, FPG, HbA1c, lipid profiles and NOx were measured. Troglitazone treatment had a slight depressor effect (decreasing the blood pressure from 133 +/- 5/72 +/- 3 to 127 +/- 4/68 +/- 1 mmHg; p < 0.05). FPG and HbA1c were significantly decreased with the therapy (181 +/- 10 to 160 +/- 10 mg/dl; p < 0.05 and 9.1 +/- 0.6 to 8.1 +/- 0.5%; p < 0.05, respectively). In contrast, total cholesterol, triglyceride, high-density lipoprotein cholesterol, and LDL-C were maintained within normal limits throughout the study. Although lysoPC and NOx levels were not altered, a negative correlation between lysoPC and NOx levels was observed. These results suggest that troglitazone is a beneficial agent improving FPG and HbA1c levels in NIDDM patients, while its effects on serum lysoPC and NOx levels, at least for 12 weeks, seem to be minimal.
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PMID:Effect of troglitazone on endothelial function in type 2 diabetic patients. 1183 72

L-arginine, a substrate of nitric oxide synthase, was infused (30 g/300 ml/30 min) to patients with or without type 2 diabetes to examine whether or not endothelial dysfunction expressed as attenuated depressor response to the substrate in diabetic patients may accompany attenuated plasma NOx (NO2- and NO3-; an index of NO formation) elevation. Decrease in blood pressure by L-arginine was significantly smaller in diabetic patients than that in non-diabetic patients, and increase in plasma cGMP level in diabetic patients tended to be smaller and retarded than non-diabetic patients. However, plasma NOx decreased in both groups in a similar degree without changes in urinary NOx excretion, implying that NOx in plasma moved to other compartments. These results indicate that plasma NOx could not be solely used as an index of NO formation by L-arginine load and that this paradoxical decrease in plasma NOx would require further examination extending to other NOx compartments.
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PMID:Paradoxical decrease in plasma NOx by L-arginine load in diabetic and non-diabetic subjects. 1188 90


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