[Two cases of fusion of the musculocutaneous and median nerves].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to N Sakamoto.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Cellular localization of cholecystokinin-8-like immunoreactive (CCK-IR) structures in the pre- and post-central gyri of the human cerebral cortex was examined by indirect immunofluorescence. CCK-IR was localized mostly in perikarya of non-pyramidal cells such as multipolar, bitufted and bipolar cells, and to a lesser extent in medium and small pyramidal cells. CCK-IR fibers were also observed in these gyri, predominantly in layers I and III.
Intraventricular administration of insulin stimulates increases in the levels of thyrotropin-releasing hormone and thyrotropin in rats.
Oral administration of a calcium antagonist, nicardipine hydrochloride (simply designated as nicardipine), in doses of 10-100 mg/kg tended to decrease total serum cholesterol and to increase high density lipoprotein (HDL) cholesterol in the normal rat. These effects of nicardipine were much greater than those of clofibrate, a standard cholesterol-lowering drug. Neither nicardipine nor clofibrate caused significant alteration in serum triglyceride and phospholipid. In hypercholesterolemic rats, nicardipine increased significantly HDL cholesterol with a reduction of total serum cholesterol, whereas clofibrate did not change HDL cholesterol. Separation of serum lipoproteins either by ultracentrifugation in various densities of KBr-NaCl solution or by polyacrylamide gel electrophoresis demonstrated that nicardipine increased preferentially HDL2 (density: 1.063-1.125), with a reduction of the low density lipoprotein (LDL) (density: 1.006-1.063) level in hypercholesterolemic rats. Serum triglyceride and liver phospholipid were increased slightly by nicardipine with no clear dose-dependency. Clofibrate also increased serum triglyceride. In normal rats, neither nicardipine nor nicotinic acid inhibited sterol biosynthesis from [1-14C]acetate in the liver, whereas clofibrate inhibited sterol production. Oral administration of [4-14C]cholesterol to hypercholesterolemic rats indicated that nicardipine had no inhibitory effect on the intestinal absorption of cholesterol.
Fasting in normal rats produced a fall in hepatic triglyceride lipase (H-TGL) activity as well as lipoprotein lipase (LPL) activities of adipose tissue and psoas minor muscle. On the other hand, LPL activities of heart and diaphragm were not decreased by fasting; the former, in fact, was increased significantly. Changes in tissue specific lipase activity caused by withdrawal of insulin from insulin-treated diabetic animals paralleled in direction the changes induced by starvation of normal rats. Furthermore, it was shown in the present paper that the tissue specific lipase activity of diabetic rats became stuck in the starve phase of the starve-feed cycle regardless of dietary intake. The changes of the tissue specific lipase activities, especially of liver, adipose tissue and heart, appeared to coincide with those of plasma insulin levels. These results strongly suggest that the tissue specific lipase system is under hormonal regulation by insulin. Streptozotocin diabetes produced hypertriglyceridemia. The possible mechanism of the hypertriglyceridemia in diabetic animals was discussed in connection with the role of the tissue specific lipase system in the serum triglyceride metabolism.
A case of benign recurrent intrahepatic cholestasis was reported. A man had first experienced jaundice at the age of twenty-five, and suffered three subsequent attacks over the next five years. These attacks were characterized by prodromal severe pruritus. During the icteric phase, serum levels of total bile acids increased, most being conjugates of primary bile acids. Electron microscopy revealed that the bile canaliculi were filled with an increased volume of granular substances. Some bile canaliculi fused together resulting in the formation of abnormally elongated channels which abutted on the Disse space. These observations suggest bile regurgitation through the channel of altered canaliculi. In convalescence, these bile canaliculi disappeared. Every attack was followed by complete recovery of liver structure and function.
Explore the source record for details and available documents.
A quantitative method for the determination of coenzyme Q10 (CoQ10) in human blood has been devised which allows recovery of essentially 100% of the CoQ10. The use of whole blood rather than plasma includes the CoQ10 in white cells. The method utilizes TLC instead of saponification to fractionate lipid impurities, because CoQ10 is sensitive to saponification, and utilizes CoQ11 as an internal standard which is advantageous over CoQ9 and a synthetic quinone. The final step of HPLC frequently reveals a peak with a retention time like that of CoQ9 which, being less than that of CoQ10, can be near other peaks of impurities.
Tissue sensitivity to insulin was evaluated in 6 trained athletes and 9 untrained controls using the euglycemic insulin clamp technique. The amount of glucose metabolism is a measure of overall tissue sensitivity to insulin. During insulin clamp study comparable plasma glucose (80-90 mg/dl) and insulin (90-100 microU/ml) were achieved in both groups. The glucose infusion rate in the athletes (10.70 +/- 0.32 mg/kg/min) was significantly higher than in the controls (7.37 +/- 0.23 mg/kg/min). During euglycemic hyperinsulinemia plasma FFA decreased by 80% while glycerol showed only a 20% reduction in both groups. Urinary catecholamine concentrations in the athletes were similar to those in the controls, and these levels did not change during the insulin clamp period. From these results, it might be concluded that tissue sensitivity to exogenous insulin is 45% higher in trained athletes and that physical exercise can reduce the insulin requirements in insulin-dependent diabetic patients in addition to being beneficial to noninsulin-dependent diabetics.
In order to examine a possible diabetic disturbance in the buffer mechanism in the liver for the caloric supply, different amounts of glucose (30 and 100 g) were given orally and the plasma glucose and IRI were compared between type 2 diabetics without retinopathy and those with retinopathy. In the diabetics without retinopathy, the time course change in the plasma glucose levels were not significantly different between the 100 g and 30 g OGTT, while in those with retinopathy the increments of plasma glucose levels were influenced by the variation of glucose load. The additional insulin secretions were similar after 30 g and 100 g OGTT in the diabetics with retinopathy, while in those without retinopathy the amounts of insulin secretions on the 100 g OGTT were larger than those observed after 30 g OGTT. These facts suggest that the liver of diabetics with retinopathy, in contrast to that in diabetics without retinopathy, cannot buffer the fuel supply against varying amounts ingested.
The influence of neuropeptides on hypothalamic regulation of plasma glucose and pancreatic hormone secretion was studied in anesthetized rats. Neuropeptides were injected directly into the ventromedial hypothalamus (VMH) and the lateral hypothalamic area (LHA) and changes in hepatic venous plasma glucose, insulin, and glucagon concentrations were studied. Injection of bombesin into the VMH resulted in a marked and sustained hyperglycemia in the hepatic venous plasma, which was also observed after injection into the LHA. Microinjection of SRIF into the VMH or LHA caused a decrease in hepatic venous plasma glucose concentration. Injection of neurotensin into the VMH or LHA resulted in a transient release of insulin in the 10-min postinjection samples. In 30- and 60-min postinjection samples, significant increases in glucagon concentrations were observed after substance P injection into the VMH or LHA. No major difference in the plasma glucose, insulin, or glucagon concentrations was observed when VMH and LHA stimulation was compared. These data suggest that glucoregulatory neuropeptides may act on the VMH and LHA, which do not necessarily follow the currently recognized anatomical boundaries.
This study was undertaken to determine the relationships between myocardial mitochondrial function, regional myocardial blood flow (MBF), and tissue ATP content in acute ischemia. Fifty-one anesthetized dogs were used in the tests. MBF was measured by the H2 gas clearance method in order to define the ischemic area, during periods of coronary occlusion of 10, 20, 60, and 90 min. The correlation between MBF and myocardial ATP content in the ischemic area was positive and significant in each group (r = 0.54-0.82). The ATP content in the true ischemic area (where MBF was less than 20 ml/min/100 Gm) decreased significantly even after 10 min of occlusion, but mitochondrial function decreased only after 20 min of coronary occlusion when compared to the nonischemic area. Although ischemia induces mitochondrial dysfunction, a very short period of ischemia did not cause significant disturbance of mitochondrial function. Moreover, in the areas with MBF of 20-40 ml/min/100 Gm, the ATP content began to decrease 60 min after occlusion, whereas 10 or 20 min of occlusion did not reduce the ATP content. These results suggest that normal maintenance of ATP levels depends not only on MBF itself but also on the duration of ischemia plus the degree of damage to mitochondrial function, and that critical blood flow, defined as the minimum flow necessary to maintain the level of myocardial ATP, varies with the duration of ischemia.
Explore the source record for details and available documents.
We measured Ia antigen bearing peripheral blood T cells, as an index of immunological stimulation, of patients with chronic active liver diseases (CALD) by the rosette assay method. We also examined the role of Ia antigen which represents the products of the genes of the major histocompatibility complex on the autologous mixed lymphocyte reaction (AMLR) since this reaction may reflect self regulation of immune responses. The percentages of Ia positive T cells of 29 patients with CALD (17.1 +/- 4.3%, P less than 0.001) and of 12 patients with other liver diseases (12.9 +/- 2.4%, P less than 0.05) were increased when compared with that of normal individuals (10.7 +/- 2.0%). However, levels of Ia positive T cells activated by phytohaemagglutinin-P in patients with CALD and other liver diseases did not differ from normal subjects. Ia positive cells in OKT8 positive cells were markedly elevated (P less than 0.001), whereas those in OKT4 positive cells were decreased (P less than 0.01) in CALD. The impaired values for the AMLR correlated inversely (P less than 0.01) with the increased percentages of Ia positive T cells in patients with CALD. Further analysis showed that there was no suppression of the proliferation of Ia and OKT4 positive cells by Ia and OKT8 positive cells although the culture of increasing numbers of Ia and OKT8 positive cells and decreasing numbers of Ia and OKT4 positive cells gave a lesser AMLR value. These data suggest that the increase in Ia positive T cells and the alteration of Ia positive cells in the T cell subsets reflect an activation of immune system and provide further evidence in favour of an abnormality of the immunoregulatory system in CALD.
Explore the source record for details and available documents.