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Biomedical subjects

K Miyoshi

Publications and source records attributed to K Miyoshi.

At least 181 records · Page 10Linked to original sources
PubMed1987

Inhibitory effects of oxatomide on intracellular Ca mobilization, Ca uptake and histamine release, using rat peritoneal mast cells.

Oxatomide at concentrations of 0.01-10 microM inhibited not only an increase in 45Ca uptake but also the intracellular Ca2+ release induced by compound 48/80 in rat peritoneal mast cells. At higher concentrations, ketotifen or other calcium antagonists caused similar inhibitory effects. However, the inhibitory effect of oxatomide on the 45Ca uptake into rat neonatal heart cells was much weaker than that of verapamil. Through image processing of quin 2-stained mast cells, it was revealed that oxatomide inhibited Ca2+ release from the intracellular store. Although oxatomide alone did not affect cAMP and cGMP contents in sensitized guinea pig lung samples, the drug effectively prevented changes in the nucleotide contents evoked by antigen challenge. These results suggest that the inhibitory effect of oxatomide on histamine release may be caused by a combination of prevention of Ca uptake, which is highly selective toward mast cells; inhibition of Ca2+ release from the intracellular Ca store, and elevation of the cAMP content in mast cells.

Aminoquinolines↗
PubMed1987

Antiallergic effects of terfenadine on immediate type hypersensitivity reactions.

Terfenadine dose-dependently inhibited rat homologous PCA (2.5-10 mg/kg, p.o.) and experimentally-induced asthma in guinea pigs (0.5-5 mg/kg, p.o.). Similarly, metabolites I and II dose-dependently inhibited experimentally-induced asthma but their respective potencies were approximately 1/2 and 1/15th that of terfenadine. These results suggest that the metabolites contribute to the antiallergic effects of terfenadine. In ex vivo, terfenadine (5-20 mg/kg, p.o.) also inhibited the release of both antigen-induced histamine and SRS-A from sensitized guinea pig lung samples and that of histamine from rat peritoneal mast cells. Terfenadine dose-dependently increased the cAMP content in rat mast cells and in the lungs; in the latter, the augmented cAMP is associated with an increase in adenylate cyclase activity, but not with the inhibition of phosphodiesterase activity. The above evidence indicates that the inhibitory effects of terfenadine on mediator release from mast cells are in some way related to its antiallergic effects, and that an elevated cAMP content may be effective to enhance mediator release inhibition.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1987

Prothrombin Tokushima: characterization of dysfunctional thrombin derived from a variant of human prothrombin.

A mutant prothrombin, designated prothrombin Tokushima, was purified from plasma of a proband with 12% of normal plasma clotting activity and 42% of normal prothrombin antigen. The purified preparation gave a single band with the same mobility as that of "prothrombin" by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE). The factor Xa-catalyzed proteolysis of prothrombin Tokushima examined by SDS-PAGE was found to be identical to that of "prothrombin." Subsequently thrombin Tokushima was prepared by CM-Sepharose CL-6B column chromatography after prothrombin activation by factor Xa. The molecular weight of thrombin Tokushima estimated by SDS-PAGE was identical to that of "thrombin." Thrombin Tokushima exhibited less than 22% of normal clotting activity, and the value of kcat/Km (mumol/L-1 second-1) was less than one tenth of that of "thrombin" when Boc-Val-Pro-Arg-4-methylcoumaryl-7-amide was used as a substrate. However, active site titration using p-nitrophenyl-p'-guanidinobenzoate failed to detect any difference between the two. Thrombin Tokushima was 2.5% as effective as "thrombin" in inducing platelet aggregation. Interaction of thrombin Tokushima with antithrombin III was much slower than "thrombin" when followed by SDS-PAGE. Based on the residual thrombin activity, it was 33% as effective as "thrombin" in forming a complex with antithrombin III. These results indicate that the molecular defect resides in the thrombin portion of prothrombin Tokushima and that the binding sites for various substrates appear to be greatly impaired.

Blood Coagulation Disorders↗
PubMed1987

[Intracranial hemorrhage in infancy due to vitamin K deficiency: report of a case with multiple intracerebral hematomas with ring-like high density figures].

It is well known that vitamin K deficiency is an important cause of the spontaneous intracranial hemorrhage in infancy. A 60-day-old male infant with spontaneous intracerebral hematomas due to vitamin K deficiency was presented. He was breast-fed. He had been medicated oral antibiotic agent for diarrhea and fever. Three days later he developed petechien, vomiting and twitching, and became drowsy. The blood studies showed anemia, and advance of ESR. He was administered of vitamin K immediately. CT scan was showed four intracerebral hematomas with niveau, which were surrounded by high-density rings. The ring-like figures were unique for this case. The reason may be next, we think. Under the states in which blood can separate easily with advance of ESR, blood clot would adhere to the wall of the hematomas. So these hematomas showed ring-like figures and had niveau in them. CT scan of this case was also interesting because there was little deviation in spite of the big hematomas. The reason of this may be that the brain of infancy is incomplete in myelination and contains much water, and that the possibility of bleeding due to vitamin K occurs slowly. We examined 84 cases of intracranial hemorrhage due to vitamin K deficiency from literatures, and they were all identified for the hemorrhage sites by CT scan. Subarachnoidal hemorrhage was in 72 cases (85.7%), subdural hemorrhage was in 41 cases (48.8%), intracerebral hematomas was in 36 cases (42.9%) and intraventricular hemorrhage was in 9 cases (10.7%). In 52 cases the CT findings were described.(ABSTRACT TRUNCATED AT 250 WORDS)

Brain↗
PubMed1986

Plasma fibronectin deficiency in eight members of one family.

The proband, a 31-year-old female, had keloids at the sites of surgery and burns. Her plasma fibronectin level measured by Laurell's method was only 10 mg/dl (mean +/- SD in 101 healthy controls 32.2 +/- 5.6 mg/dl) but the electrophoretic mobility was normal. Low levels of plasma fibronectin (range 11-17 mg/dl) were found in the proband's mother, two uncles, two brothers, one daughter, and one nephew. Levels in her father and other family members examined were normal (range 32-51 mg/dl). The proband has been quite healthy, an haematological and haemostatic tests showed no abnormality except reduced phagocytosis by neutrophils. Other family members with low plasma fibronectin levels had no abnormalities on examination and no keloids.

Adolescent↗
PubMed1986

Distribution of actin filaments in rat mast cells and its role in histamine release.

The distribution of actin filaments was confirmed by immunofluorescence microscopy and immuno-electron microscopy in nonsecreting and secreting rat peritoneal mast cells. In a resting cell, immunofluorescence of the actin showed up as a net-like formation surrounding each granule. After stimulation with compound 48/80 or A-23187, the distribution of the actin filaments became very irregular and disordered, disappearing completely in some areas within the cell and expanding in conjunction with the swelling of the granules. Similar changes are seen in a passively sensitized mast cell exposed to antigen. When cells were pretreated with cytochalasin B or colchicine, the distribution of actin filaments was not greatly affected by stimulation. The results clearly show that actin filaments exist in mast cells.

Actins↗
PubMed1986

Autosomal recessive distal muscular dystrophy as a new type of progressive muscular dystrophy. Seventeen cases in eight families including an autopsied case.

A new type of progressive muscular dystrophy, autosomal recessive distal muscular dystrophy, is described, based on observations on 17 cases (8 males and 9 females) in 8 families, including an autopsied case. The disease developed in young adults. Muscle weakness and atrophy were most marked in the distal parts of the legs, especially in the gastrocnemius and soleus muscles, and then spread to the thighs and gluteal muscles. Early impairment of standing on tip-toe with retention of the ability to stand on the heels was conspicuous. Difficulty in climbing stairs, standing up and walking subsequently appeared, but rarely progressed to confinement to bed. The forearms became mildly atrophic, with decrease in grip strength, but the small hand muscles were spared. The EMG showed myopathic changes and nerve conduction was normal. Serum creatine kinase activity was characteristically increased up to 100-fold in the early stages of the disease. It was also markedly increased in subjects in the preclinical stage and mildly in some heterozygotes. Muscle biopsies revealed myopathic changes with severe segmental necrosis accompanied by regeneration. The changes were similar to those of Duchenne muscular dystrophy. An autopsied case, aged 68 years, showed generalized muscle abnormalities with a distal predominance. The muscles in the lower legs, especially those of the calves, were severely affected. No lesions were found in the brain, spinal cord or peripheral nerves.

Adolescent↗
PubMed1986

Experimental striatal degeneration induced by kainic acid administration: relevance to morphological changes in Huntington's disease.

In an attempt to reproduce the characteristic neuronal degeneration pattern in the striatum of human patients with Huntington's disease, the histological and ultrastructural features of the degeneration of medium-sized nerve cells in the striatum and its processes are described in young rats induced by a direct injection of a small amount of kainic acid into the striatum. A light microscopic examination revealed initial edema and necrotic changes at the site of injection. The area surrounding the needle track showed neuronal and dendritic swelling and eosinophilic neurons without the apparent involvement of the passing axons. Later changes consisted of a marked neuronal loss particularly of the small cells with consequent severe astrocytosis. Electron microscopy showed specific neuronal alterations in the form of ballooned Golgi apparatuses, swelling of the endoplasmic reticulum, dendritic swelling, proliferated neurofilaments and aggregation of polysomes together with a marked disruption of neuropil. Neuronal debris and small dense bodies appeared. The majority of neuronal loss consisted of medium-sized nerve cells: Type I. Some spheroid bodies and lipid droplets were also observed.

Animals↗
PubMed1985

Survival of an extensively burned infant following purulent pericarditis.

This is a report of the treatment and survival of an extensively burned infant following purulent pericarditis with massive pericardial effusion due to Staphylococcus aureus. A 2-year-old boy fell into a bathtub and suffered scalds covering at least 70 per cent of the body surface area. Pericarditis with massive pericardial effusion was diagnosed on post-burn day 36. As conservative treatment was ineffective pericardiotomy and pericardial drainage were carried out. Whole body oedema disappeared promptly and entirely and the patient was discharged from hospital with healed burns and free of cardiac symptoms.

Burns↗
PubMed1985

Hepatic disorder in burn patients.

Changes in liver function were studied in 33 patients with burns. In 21 of these patients hepatic disorder developed relatively early after the injury (early hepatic disorder), with a relapse of hepatic disorder occurring later in 8 patients (late hepatic disorder). Our study demonstrated that these hepatic dysfunctions may largely be attributable to post-transfusion acute hepatitis (non-A, non-B or B types).

Biopsy↗
PubMed1985

Synthesis and secretion of human epidermal growth factor by Escherichia coli.

A synthetic gene for human epidermal growth factor (hEGF) was joined to a sequence encoding the signal peptide of Escherichia coli alkaline phosphatase. This hybrid gene was placed under the control of the alkaline phosphatase gene (phoA) promoter in a recombinant plasmid, which was used to transfect E. coli. The hybrid protein that was expressed in host cells under conditions of phosphate limitation was processed accurately during the secretion process, and mature hEGF was recovered in the periplasmic fraction. On the other hand, no EGF was detected in the periplasmic space when the synthetic hEGF gene was not accompanied by the phoA signal sequence.

Alkaline Phosphatase↗
PubMed1985

[A case of oral florid papillomatosis combined with gastroduodenal polyposis].

A 49-year-old man developing numerous papillary or partly cauliflower-like tumors over the lips, oral angles, gingiva and tongue starting 15 years earlier and associated with multiple gastroduodenal polyps of various sizes revealed by X-ray examination is presented. Histologically, the oral lesions consisted of marked proliferation of mature squamous cells without appreciable cellular atypism or submucosal invasion. Electron microscopic study failed to detect any virus-like particles, and negative reaction was obtained in immunohistological study for papilloma virus. The association of gastroduodenal polyposis with oral florid papillomatosis has appeared very rarely in the literature. Although the relationship between the two lesions remains unknown, it was assumed in the present case that all lesions would represent an entity of a hamartomatous nature.

Duodenal Neoplasms↗
PubMed1985

[A pharmacokinetic study of cefoperazone during percutaneous transhepatic cholangial catheterization].

The metabolic fate of cefoperazone (CPZ) was studied in 19 cases which underwent percutaneous transhepatic cholangial catheterization (PTC-catheterization, PTCC) and were under various conditions of the liver function. The peak of bile levels of CPZ immediately after PTCC differed greatly from one case to another at 12.6-7,260 micrograms/ml with 1 g intravenous injection and 23.0-5,800 micrograms/ml with 2 g intravenous injection. The ratio of the peak of bile level to the serum level immediately after PTCC showed the highest negative correlation with the serum total bilirubin level. It also showed a significant negative correlation with GOT, GPT, Al-P and LAP. The serum CPZ level and half-life showed no significant trend except half-life showed a significant correlation with LAP. The recovery rate in urine up to 12 hours was in the range of 14.8-93.6%, showing a significant correlation with the ratio of the peak of bile levels to the serum level and the date of liver function tests. The bile level, serum level and recovery rate in urine at the time the bile outflow from the catheter has become constant after PTCC (during the course of PTCC) showed a trend almost similar to that immediately after PTCC, there being no significant difference as to each parameter during the course of PTCC and immediately after PTCC. In the cases in which the sample was collected by the cross-over technique, the ratio of the peak of bile levels to the serum level from immediately after PTCC to during the course of PTCC increased in 2 cases and decreased in 6 cases. The 2 cases that showed the increase in the ratio were the case in which the serum total bilirubin level improved almost to normal. Findings above suggest that sufficient biliary decompression can improve the movement of CPZ into bile, despite the fact that the pharmacokinetics of CPZ is affected by the liver function, particularly serum total bilirubin level, that a decrease in the movement to bile and a compensatory increase in urinary excretion are observed in jaundice and disturbance of the liver function and that the ratio of the peak of bile level to the serum level decreases during the course of PTCC rather than immediately after PTCC in some cases.

Adult↗