Dr. Imagawa's group proposed the concept of non-autoimmune fulminant type 1 diabetes citing cases which developed through ketoacidosis, and in which the patient's HbA1c was normal or increased only ...slightly at the time of outbreak, the auto-antibodies of the pancreatic beta cells were negative and the ability of insulin secretion was markedly lower. At our hospital, over several years, we studied the clinical picture and insulin secretion ability of 7 cases, which met this screening outline of non-autoimmune fulminant type 1 diabetes using glucagon loading tests In 5 cases in whom glucagon loading tests given during outbreak were examined, the serum CPR of glucagon loading after 6 minutes was below 0.1ng/ml and suggested the complete destruction of pancreatic beta cells at the time of outbreak. Furthermore, glucagon loading tests were administered about every six months after onset and the insulin secretion ability was examined over several years, the longest case being 7 years. In all 6 cases the serum CPR of glucagon loading after 6 minutes was below 0.1ng/ml, and in no case was recognizable recovery of insulin secretion ability seen.
This study investigated the physiologic and sedative parameters associated with a low-dose infusion of dexmedetomidine (Dex). Thirteen healthy volunteers were sedated with Dex at a loading dose of 6 ...mcg/kg/h for 5 minutes and a continuous infusion dose of 0.2 mcg/kg/h for 25 minutes. The recovery process was observed for 60 minutes post infusion. The tidal volume decreased significantly despite nonsignificant changes in respiratory rate, minute ventilation, oxygen saturation, and end-tidal carbon dioxide. The mean arterial pressure and heart rate also decreased significantly but within clinically acceptable levels. Amnesia to pin prick was present in 69% of subjects. A Trieger dot test plot error ratio did not show a significant change at 30 minutes post infusion despite a continued significant decrease in bispectral index. We conclude that sedation with a low dose of Dex appears to be safe and potentially efficacious for young healthy patients undergoing dental procedures.
We have reported that blood interleukin-6 (IL 6) and interleukin-8 (IL 8) are increased in diabetes ketoacidosis. Recently, hepatocyte growth factor (HGF) has been structurally analyzed as a factor ...in promoting regeneration of the liver. HGF was also resolved to be cytokine with various functions. We considered the potential of blood HGF increase in diabetic ketoacidosis and blood HGF for ketoacidosis patients. HGF of hyperglycemia patients not presenting ketosis in their serum was measured as a control. HGF of 12 hospitalized diabetic ketoacidosis patients and 8 hyperglycemia patients was measured from frozen stored serum 6, 12, 24, and 48 hours after insulin treatment using enzyme immunoassay (EIA). HGF of 12 hospitalized diabetic ketoacidosis patients, was 1.29±0.99ng/ml on admission, significantly higher (p<0.05) than HGF of hyperglycemia patients at 0.35±0.15ng/ml. HGF in the serum of ketoacidosis patients 6, 12, and 24 hours after insulin treatment was also significantly higher (p<0.05) than HGF of hyperglycemia patients. HGF gradually decreased after ketoacidosis treatment, compared to HGF from the serum of hyperglycemia patients where there was no significant difference between admission and 6, 12, 24, and 48 hours after treatment. High HGF was detected in the serum of 12 diabetes ketoacidosis patients on admission. Considering that HGF of hyperglycemia patients was 0.39 or under, which is normal, we suppose that ketoacidosis increased blood HGF. Although the mechanism of this increase HGF is not clear, acute failure of metabolism produces HGF from endothelial cells.
To clarify the relationship between arteriosclerosis of carotid artery and DC 36 antigen activation in peripheral blood monocytes in type 2 diabetes, we analyzed the activation of CD 36 by histogram ...using flow cytometry for 106 cases of type 2 diabetes divided into 3 groups: Group I, low activation; Group II, intermediate activation; and Group III, high activation. A comparison of intimamediathickness (IMT) in carotid arteries for the 3 groups should no significant difference between them. The frequency of atheromatous plaque formation for Group I was 43%, for Group II 63%, and for Group III 92%, indicating that the frequency of plaque formation significantly higher (p<0.05) with increasingly activate CD 36 in peripheral blood monocytes. CD 36 activation of peripheral blood monocytes thus appears to be correlated with plaque formation in carotid arteries in type 2 diabetic patients.
PDF
