Biomedical subjects
Publications and source records attributed to H Ishida.
The preoperative diagnosis of diffuse heterotopic submucosal cystic malformation of the stomach is very difficult to make with upper gastrointestinal (GI) series or endoscopy. We report a case of submucosal cysts associated with an early gastric carcinoma in which ultrasonography (US) and endoscopic ultrasonography (EUS) were very useful in the preoperative diagnosis.
Changes in glucagon, insulin and somatostatin secretion induced by electrical splanchnic nerve stimulation were examined in rats treated with streptozotocin as neonates and as adults. In order to study the direct neural effects we used the isolated perfused rat pancreas with intact left splanchnic nerve in vitro. In normal rats splanchnic nerve stimulation causes significant decreases in insulin (30-40%) and somatostatin (30-50%) secretion at both 16.7 mmol/l and 1 mmol/l glucose concentrations. In the neonatal streptozotocin-diabetic rat splanchnic nerve stimulation at 16.7 mmol/l glucose decreased insulin secretion (14%) further than in the control rats (30%), however, somatostatin secretion did not decrease to the same extent. Similar results were also observed at the low (1 mmol/l) glucose concentration. On the other hand, percent decreases of insulin and somatostatin secretion induced by splanchnic nerve stimulation in the streptozocin-diabetic rats were similar to the values observed in the normal control rats. The glucagon secretion in response to splanchnic nerve stimulation at 16.7 mmol/l glucose from pancreatic Alpha cells in both types of induced diabetes is exaggerated, and the degree of exaggeration seems to parallel the severity of the hyperglycaemia. However, the splanchnic nerve stimulation-induced glucagon secretion at 1 mmol/l glucose was impaired in the streptozotocin-diabetic rats, but not in the neonatal streptozotocin-diabetic rats. These data suggest that the sensitivity of diabetic Alpha and Delta cells to sympathetic neural activation are blunted, whereas the sensitivity of Beta cells is enhanced in the diabetic animal model.
Diurnal changes in the neurotransmitter receptors are important for studying the receptor function in neurophysiology. The purpose of this study is to gain an insight into the regulatory mechanisms of the diurnal variation of amylase secretion. Rat salivary amylase levels showed a diurnal variation with two peaks, a marked peak at 13 h and a lesser peak at 21 h. This increase in salivary amylase levels was completely inhibited by pretreatment of rats with the beta-adrenergic antagonist propranolol, but not by the alpha-adrenergic antagonist phentolamine. Amylase level in parotid tissue homogenate also showed a diurnal change, but there was only one peak, at 13 h. The number of maximal binding sites (Bmax) for [3H]dihydroalprenolol (DHA) in parotid membranes showed a diurnal variation with two marked peaks at 13 and 21 h, but the affinity of parotid beta-adrenoceptors for agonists or antagonists did not show any diurnal changes. Phosphorylation of nuclear non-histone proteins in the rat parotid gland showed diurnal variation with two marked peaks at 13 and 21 h. These results indicate that a diurnal variation in the number of rat parotid beta-adrenoceptors, which is presumably regulated by gene expression, is coupled with a change in salivary amylase secretion.
Castable apatite ceramic crowns are subjected to heat treatment during crystallizing and during coloring after casting. The dimensional accuracy of the heat-treated crowns was investigated with respect to its influence on dimensional changes in castable apatite ceramic crowns and on distortion of the interior of the crowns, using two investment techniques and a three-coordinate measuring machine. Dimensional changes were not influenced by the number of coloring firings. Distortion of the interior of crowns was slightly outward at the gingival plane. Shrinkage because of crystallizing was approximately 20 microns and the shrinkage of the gingival plane was equal to that of the occlusal plane.
The assay system of chondroitin sulfate iron colloid (CSFe) was established to evaluate the reticuloendothelial system (RES) function in individual rabbits. In the multi-dose study of CSFe, CSFe was repeatedly administered to each individual rabbit with increasing doses (0.6, 1.2, 2.4, 6.0 mg/kg) at set intervals. Blood samples were serially collected after injection of CSFe and the concentration of CSFe in serum was directly measured as an iron concentration by modifying the previously described assay method [1] to minimize the sample volume. The clearance rate of CSFe at each injected dose was computed by the least-squares method and the double-reciprocal plotting of the doses against the phagocytic velocities by the Lineweaver-Burk method was obtained in each rabbit. The maximum phagocytic velocity (Vmax) and the CSFe concentration producing 1/2 Vmax (Kp) obtained in ten rabbits were 0.129 +/- 0.025 mg/kg per min and 0.417 +/- 0.121 mg/kg (mean +/- S.D.), respectively. The results obtained from this multi-dose study were comparable to our previous results obtained from the mean values of five groups given different doses [1]. The clearance rates of CSFe (0.6, 1.2, 6 mg/kg) decreased after the co-injection of 80 mg/kg of carbon colloid. The calculated Vmax and Kp in 29 rabbits were 0.125 mg/kg per min and 1.167 mg/kg. The Kp was apparently greater than that of the control (Vmax = 0.128 mg/kg per min, Kp = 0.421 mg/kg). Carbon colloid (80 mg/kg) was injected to six rabbits after the completion of the first multi-dose study of CSFe and then the second multi-dose study of CSFe was repeated after 24 h. No differences were found in Vmax and Kp between the two studies as were in the control group (10 rabbits) where saline was injected instead of carbon colloid. These results indicated that carbon colloid (80 mg/kg) gives a competitive and reversible inhibition on the RES. This multi-dose study of CSFe may be applicable for a bed-side analysis of the RES function in a patient.
The responsiveness of human dental pulp (HDP) cells to parathyroid hormone (PTH) was investigated by measuring their cyclic AMP (cAMP) content, DNA synthesis, alkaline phosphatase activity, collagen synthesis, and glycosaminoglycan (GAG) synthesis. PTH dose-dependently increased the intracellular cAMP 1 min after the addition of PTH. Confluent HDP cells on day 14 expressed a high level of cAMP production after addition of 3 units/ml PTH. The hormone did not affect DNA synthesis by HDP cells. Alkaline phosphatase activity was suppressed by PTH to 81% of control (p < 0.01), and addition of dibutyryl cAMP to the medium mimicked the effect of PTH (79% of control, p < 0.01). The hormone inhibited collagen synthesis (15% decrease of [3H] proline incorporation, p < 0.01), and stimulated non-collagen protein synthesis (10% increase, p < 0.05). The increase of non-collagen protein by PTH was in accordance with the enhancement of GAG synthesis (17% increase of [35S]sulfate incorporation, p < 0.01). Dibutyryl cAMP caused further increase of GAG synthesis, to 155% of control (p < 0.01). Observations of the radiolabeled proteins on 10% sodium dodecyl sulfate-polyacrylamide gel electrophoresis after metabolic labeling with [14C]proline and [35S]sulfate revealed a similar tendency to the quantitative determinations in which PTH inhibited collagen synthesis and stimulated GAG synthesis. These findings suggest that HDP cells have some osteoblastic characteristics in terms of PTH responsiveness, and that this culture system is a useful model for studies of human dental pulp.
Phospholipase A2 (PLA2) is a proinflammatory enzyme in the synovial fluids of all--and sera of some--patients with rheumatoid arthritis. Due to the similarities in pathogenesis between rheumatoid arthritis and periodontitis, we sought to study the enzymatic properties of PLA2 in periodontal tissue. In this study, we demonstrated PLA2 activity in rat gingival tissue, about 80% of which was present in the cytosolic fraction. We characterized the cytosolic PLA2 enzyme with respect to substrate specificity, sensitivity to detergent, Ca2+ ion dependency and optimum pH. We found that phosphatidylethanolamine, rather than phosphatidylcholine, was the preferred substrate, the Ca2+ ion was essential for the expression of PLA2 activity, the enzyme was active over a broad pH range, with the optimum at pH 9.0, and sodium-deoxycholate inhibited the enzyme activity strongly in a concentration-dependent manner. These results are consistent with those which have been obtained with synovial fluid PLA2 and suggest that gingival PLA2 may be involved in the pathogenic processes of gingivitis and periodontitis.
The high affinity calcium-binding protein calbindin-D28K is one of the known proteins transcriptionally up-regulated by the hormonally active form of vitamin D3, 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3]. This regulation is tissue specific, since in the absence of 1,25-(OH)2D3, the expression of calbindin-D28K is virtually abolished in intestine, whereas it is decreased, but clearly detectable, in kidney, and it remains present at its highest level in cerebellum. Several studies have shown that there is a strong correlation between an increase in the sensitivity to nuclease digestion of a given gene locus and its potential for transcription. Furthermore, hypersensitive sites have often been mapped to regions of DNA including or surrounding sequences known to be important for the regulation of gene transcription. In this study we have scanned the 5'-end and flanking DNA of the calbindin-D28K gene for the presence of DNase-I-hypersensitive (DH) sites in order to localize possible regulatory regions involved in the tissue-specific and hormone-dependent regulation of this gene. We have found that in tissues where calbindin is not expressed, such as liver, no DH sites could be detected. In cerebellum, the same set of DH sites was observed in the presence or absence of 1,25-(OH)2D3 treatment, reflecting the vitamin D-independent expression of the calbindin gene in this tissue. A more complex pattern of DH sites was found in intestine, independently of the vitamin D status of the animal.(ABSTRACT TRUNCATED AT 250 WORDS)
This study was designed to clarify the state of beta-adrenergic signal transduction and the disordered level of its transduction in hypertensive hearts, using myocardium from spontaneously hypertensive rats (SHR) as a generic model of essential hypertension. Beta-adrenergic receptor binding sites and dissociation constants in the extracted membranes of adult (70-100 days of age) SHR heart were not significantly different from those of Wistar-Kyoto (WKY) rats, the non-hypertensive control. The adenylate cyclase activities stimulated by isoproterenol with GTP, NaF and forskolin were significantly higher in SHR compared to those in WKY. To determine whether differences in signal transduction are natural or are a result of hypertension, we evaluated chronotropic responses in cultured cells of fetal hearts which had not been exposed to hypertension. Fetal cardiac muscle cells of SHR were more sensitive than WKY to isoproterenol stimulation over a wide concentration range. However, there were no statistically significant differences between these two strains with respect to the density of binding sites. These results suggest that in the transduction of adrenergic signals, alterations distal to the beta-receptors are present in the adult hearts of hypertensive rats, and, that the adrenergic signal transduction is already exaggerated in the pre-hypertensive fetal stage.
The kinetics of bradykinin derived from localized thermal injury on vascular-permeability were investigated in mice with experimental ear burn. The leakage of plasma into the ear tissue by accelerated vascular-permeability reached the maximum at 3 hr and decreased gradually until 6 hr after the thermal injury. The contents of bradykinin increased by the thermal injury and the increment continued up to 24 hr. Although the bradykinin contents in the burned ear decreased by using a protease inhibitor, the hyperpermeability of injured ear vessels was unchanged by protease inhibitors. These results suggest that bradykinin is concerned with the pain reaction rather than vascular-permeability.
Diabetic osteopenia has been known as one of the chronic complications of diabetes mellitus, and a decrease in bone turnover has been thought to be one of the pathophysiological characteristics of this complication. In order to investigate the effect of long-term insulin therapy on low bone turnover in diabetes, pancreas transplantation was performed on streptozotocin-induced diabetic rats. Plasma levels of bone gamma-carboxyglutamic acid-containing protein(osteocalcin) in untreated diabetic rats were 0.9 +/- 0.1 (mean +/- SEM) nmol/l, significantly lower than the value of 4.2 +/- 0.6 nmol/l in control rats (p less than 0.01). Pancreas transplantation reversed this decrease to 6.3 +/- 1.1 nmol/l, which was not significantly different from the value in control rats. The circulating levels of calcitriol were significantly decreased in the untreated diabetic group (p less than 0.01), and the decrease was fully reversed by pancreas transplantation. In addition, the decreases in bone length, strength and weight were also improved by the transplantation. This evidence clearly shows that the improvement of metabolic derangements in diabetes by insulin is essential for the prevention of deterioration in diabetic osteopenia. It is possible, therefore, that insulin exerts an indirect beneficial influence through the metabolic amelioration on the decreases in bone turnover and circulating osteocalcin in diabetes mellitus, or has a direct stimulatory effect on the osteoblasts via the insulin receptor since its presence has been shown recently in osteoblastic cells.
Sustained exposure to high concentrations of glucose selectively impairs the ability of pancreatic islets to secrete insulin in acute glucose stimulation. In order to evaluate the interrelationship between impaired insulin secretion and the dynamics of the cytosolic free Ca2+ level ([Ca2+]i), we have investigated the effect of high glucose exposure on both [Ca2+]i dynamics in single rat beta-cells and insulin release from rat pancreatic islets. Islets cultured at a high glucose concentration (16.7 mM) for 24 h showed significant reductions of the 16.7 mM GSIR compared with islets cultured at a normal glucose concentration (5.5 mM) (3.38 +/- 0.24 vs. 4.26 +/- 0.34%, respectively, P < 0.05). The capacity of glucose to raise the [Ca2+]i level also was significantly reduced in the beta-cells maintained for 24 h at 16.7 mM glucose (P < 0.001). An additional culture in the medium with 5.5 mM glucose for 16 h restored both the GSIR and the [Ca2+]i response of islets cultured at high glucose. On the other hand, insulin release and [Ca2+]i rise in response to 20 mM L-Arg were well preserved. These observations confirm that exposure of pancreatic beta-cells to high glucose concentrations induces a selective reduction of the GSIR and, further, shows that this impaired response is reversibly restored by an additional culture with normal glucose. We also suggest that the inability of glucose to provoke a [Ca2+]i rise, which is observed in the beta-cells exposed to high glucose, may be responsible for the selective impairment of the GSIR.
ATP-sensitive K+ channels (KATP channels) are known to play a key role in the cellular mechanism of insulin secretion from pancreatic beta cells. In order to examine the possible impairment of KATP channel function in non-insulin-dependent diabetes mellitus (NIDDM), we have studied the properties of the KATP channels in single beta cells of neonatally streptozotocin-induced diabetic rats (NSZ rats) using the patch-clamp technique. The unitary conductance of the channel in diabetic beta-cells was virtually identical to that in control beta cells and there was no difference in the sensitivity to ATP and glibenclamide of KATP channels between the NIDDM and control groups. In response to glucose, the activity of the KATP channels was diminished in a dose-dependent manner in both control and diabetic cells. However, the inhibition of the KATP channels in beta-cells of NSZ rats was significantly less than that in control cells. Even in the presence of 11.1 mM glucose, the openings of a few single KATP channels were consistently observed in cell-attached patch membranes of diabetic, but not control, beta-cells. Thus, it appears that the impaired insulinotropic action of glucose in beta-cells in NSZ rats is associated with a reduced sensitivity of the KATP channel to glucose, but not to ATP, presumably due to a deficiency in glucose metabolism.
Anthropometric data, nutrient intake data, and blood biochemical parameters were analyzed for 66 elementary school children living in Tokyo, Japan, and their nutritional status was evaluated focusing on three problems: (1) zinc nutriture and growth, (2) anemia with iron deficiency, and (3) lipid nutriture and obesity. The subjects' mean energy and protein intakes met the recommended levels for Japanese children. However, their zinc intake levels were inadequate at 7.2, 8.3, and 8.5 mg in grades 2 (mean age: 8 yr), 4 (10 yr), and 6 (12 yr), respectively. Mean serum zinc concentration was 0.82 +/- 0.15 microgram/ml; the percentages of subjects who showed serum zinc concentration lower than 0.68 microgram/ml, the lower limit of the normal serum zinc concentration, were 28.6, 15.4, and 5.0% in grades 2, 4, and 6, respectively. These serum zinc concentrations indicated the existence of marginal zinc deficiency in some children, particularly in grade 2, though it was not severe enough to retard growth. Their iron intake levels (8.2, 10.2, and 10.2 mg for grades 2, 4, and 6, respectively) in combination with the proportion of iron intake from animal foods (37%) were judged to be adequate because no children showed serum ferritin, serum iron, or transferrin saturation levels lower than the criteria levels recommended for iron deficiency. Moreover, no definitely anemic children were found. Daily lipid intakes were 65.7, 74.5, and 78.3 g in grades 2, 4, and 6, respectively, and the mean percentage of energy intake from lipid to total energy intake, 32%, exceeded the level recommended. Mean serum total cholesterol concentrations and the percentage of subjects with elevated cholesterol levels (greater than or equal to 200 mg/dl) were high compared with the reported values. Means of the body mass index (BMI) and Rohrer Index (RI) for the subjects were slightly higher than Japanese standards. With these parameters for obesity, triglycerides and atherogenic index were positively correlated and HDL cholesterol and HDL cholesterol percentage to total cholesterol were negatively correlated.
A number of systems and devices have been developed to reduce peritonitis in CAPD patients. One of the newer developed systems in the UV-Flash. A retrospective study was conducted in five Japanese hospitals to measure the efficiency of the UV-Flash system in reducing the peritonitis rate for CAPD patients. This study took place between January 1983 to January 1992. The UV-Flash system had a significantly lower peritonitis rate (1/46.6 patient months) compared to the Standard system (1/27.5), but showed nominal significance when compared to the Disconnect system (1/47.6). Due to the lack of differentiation in peritonitis rates between the UV-Flash and Disconnect system, patient types for both systems were analyzed. The study found more impaired patients on UV-Flash (37.2%) as opposed to the Disconnect (9.8%). These impaired patients treated on the UV-Flash system showed a significantly lower peritonitis rate (1/27.5) when compared to the Disconnect (1/9.7) system. The UV-Flash system proved able to achieve sufficient prevention of peritonitis in CAPD patients. Thus, this system can be successfully applied to high risk CAPD patients.
Perioperative and anesthetic management of a patient with a diabetes insipidus is reported. A 33 year old man was followed by physical therapy after spinal cord injury. At that time polyuria (4300-8600 ml.day-1) and polydipsia developed. His urine output was controlled by DDAVP (desmopressin) preoperatively. As the result of water restriction test and Carter-Robbins test the diagnosis of complete central diabetes insipidus was doubted preoperatively. We investigated the changes of his perioperative body fluids and endocrine responses. The following conclusions are made: 1) The diagnosis of this case is not renal and true diabetes insipidus, but is probably partial or transient diabetes insipidus. 2) These results indicate that endocrine examinations related to AVP secretion are essential.
Thirty-four populations from Siberian and other circum-Pacific regions were compared in terms of facial flatness measurements of the cranium. While fundamentally having an extremely flat face, Siberian populations tend to be differentiated into two or three subgroups. On the other hand, other Mongoloid populations show greater variation in facial flatness. The less flat faces of the American Indians are almost equal to those of the Europeans. In Japan, the existence of two contrasting groups in terms of facial flatness have been found.
This study which was undertaken at several major hospitals in Ibaraki-ken revealed that, 1) the proportion of Staphylococcus aureus in all the isolates ranged from 5% to 17% and the prevalence of MRSA in isolates of Staphylococcus aureus varied from 51% to 82% depending upon each individual hospital. 2) the clinical response to FOM and CMZ combination therapy was 88.9% and, to FOM and CZON was 57.1% showing no statistical differences between the two regimens. 3) in vitro analyses assessed by the FIC index of 251 isolates revealed that FOM had an additive or synergistic effect with CMZ in 53.8%, with CZON in 66.9%, with minocycline (MINO) in 43.8%, with cefamandole (CMD) in 61.8%, with cefazolin (CEZ) in 62.9% and with imipenem/cliastatin sodium (IPM/CS) in 68.9% at all isolates. 4) the cumulative curve of susceptibility to single CMZ and the combination of CMZ and FOM revealed that the blood levels of CMZ at 3 hours after intravenous administration covered 57% of isolates when used alone and 82% of isolates when in combination with FOM. The blood levels of CZON at 3 hours covered 5% of isolates when used alone and 41% when in combination with FOM. The extent of the therapeutic effect increased from 6% to 42% by CMD, from 12% to 54% by CEZ, from 20% to 58% by IPM/CS and from 78% to 84% by MINO. The combination of CMZ and FOM was found to be the most effective for enhanced effects on MRSA in vitro.