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Biomedical subjects

S Gotoh

Publications and source records attributed to S Gotoh.

At least 127 records · Page 7Linked to original sources
PubMed1987

Revascularization surgery for 28 patients with moyamoya disease--operative methods, outcome and postoperative angiography.

51 times (sides) of reconstructive surgery using 28 patients with moyamoya diseases were evaluated concerning operative methods, outcome and postoperative angiographic findings. Twenty patients (72%) showed excellent results, 7 patients (25%) good and 1 patient (3%) poor. Development of collaterals shown on postoperative angiograms was excellent on 20 sides, good on 9 sides, and fair on 8. Abundant neovascularization was most commonly noted on angiogram in superficial temporal artery-middle cerebral artery bypass with encephalo-myo-synangiosis. Encephalo-myo-arterio-synangiosis, devised by the authors, or encephalo-myo-synangiosis alone also produced preferable development of collaterals shown on angiogram. Superficial temporal artery-middle cerebral artery bypass alone was insufficient for development of neovascularization.

Adolescent↗
PubMed1986

Enhancement of the expression of a rat neutrophil-specific cell surface antigen by activation with phorbol myristate acetate and concanavalin A.

A monoclonal antibody against rat neutrophils, RP-1, was produced by hybridizing a mouse myeloma (P3-X63-Ag8.653) with BALB/c mouse spleen cells sensitized with peritoneal neutrophils from Wistar-King-Aptakeman/Hok rats. RP-1 specifically reacted to neutrophils and bone marrow cells from rats of various strains. The expression of an antigen reactive to RP-1 on rat peritoneal neutrophils was enhanced by stimulation with phorbol myristate acetate and concanavalin A. The experimental result that the expression of an antigen reactive with another anti-neutrophil monoclonal antibody was not enhanced by stimulation with phorbol myristate acetate indicates that the antibody-binding capacity of stimulated neutrophils was not nonspecifically enhanced. The enhancement of antigen expression was temperature dependent. A glycolytic inhibitor, 2-deoxy-D-glucose, and an inhibitor of intracellular calcium mobilization, 3,4,5-trimethoxybenzoic acid 8-(diethylamino)-octyl ester hydrochloride, which inhibited hydrogen peroxide release from stimulated neutrophils, did not inhibit enhancement of the expression of an antigen reactive with RP-1.

Animals↗
PubMed1985

Heme metabolism and turnover of cytochrome P-450 in tumor-bearing mouse livers.

Hepatic heme metabolism and in vitro translation of poly(A) + RNA from livers were studied to elucidate the mechanism of the reduction of microsomal cytochrome P-450 in tumor-bearing mouse livers. Hepatic delta-aminolevulinic acid synthase activity in male C57BL/6N mice (0.203 nmol/mg protein/h) at 8 days after the transplantation of Ehrlich ascites tumor cells was the same level as that of normal livers (0.206 nmol/mg protein/h). On the other hand, hepatic heme oxygenase activity of tumor-bearing mice (0.482 nmol/mg protein/10 min) had increased 8 days following i. p. transplantation of tumor cells when compared with that of normal mouse livers (0.296 nmol/mg protein/10 min). SDS-gel electrophoresis of in vitro translation products of poly(A) + RNA extracted from membrane-bound polysomes of the livers from tumor-bearing mice showed no significant differences from that of normal controls in the region of cytochrome P-450, that is, the molecular weight region of Mr = 47,000-60,000, although microsomal protein content in this region estimated by Coomassie-blue staining was reduced. These results suggest that the decrease of heme biosynthesis or the translation of cytochrome P-450 mRNA played a very small part in the reduction of microsomal cytochrome P-450 in tumor-bearing mice.

5-Aminolevulinate Synthetase↗
PubMed1985

Acute predominantly sensory neuropathy.

An account is given of an unusual patient with acute sensory neuropathy, leading within a few weeks to almost generalized sensory loss. Generalized sensory deficits were involved in the face, tongue, and palate. He had a drug allergy from chemotherapy during an early stage of illness. An albuminocytological dissociation of the cerebrospinal fluid was noted in a few months. A sural nerve biopsy after 2 months showed a marked reduction of fibers, and extensive invasion of phagocytes throughout the endoneurium. This patient recovered poorly with profound sensory ataxia of the limbs and tongue. A possible explanation for the clinico-pathological findings may be that acute idiopathic polyradiculoneuritis (Guillain-Barré syndrome) and toxic neuropathy exert an etiological role in the extramedullary sensory system.

Acute Disease↗
PubMed1985

Thymocyte activating factors from SV40-transformed human embryo fibroblasts.

A novel factor was found in the medium conditioned by SV40-transformed human embryo fibroblasts, which stimulate concanavalin A-induced thymocyte DNA synthetic response. This activity was estimated to be 10-15 kD and divided into two activities by ion exchange chromatography. One of them is a protein molecule and the other is a glycoprotein. In addition, these activities are not derived from the growth factors reported previously such as interleukin 2 (Morgan, R., Ruscetti, F. and Gallo, R. C. (1976) Science 193, 1007-1008) and transforming growth factor (De Larco, J. E. and Todaro, G. J. (1978) Proc. Natl. Acad. Sci. U.S.A. 75, 4001-4005).

Animals↗
PubMed1985

Monocyte thromboplastin (tissue factor): complementary effect of lymphocytes upon its generation by endotoxin-stimulated monkey (Macaca fuscata) cells.

Monkey (Macaca fuscata) mononuclear leukocytes were stimulated to produce thromboplastin (tissue factor) upon exposure to lipopolysaccharide, LPS. The stimulation was dose-related in the concentration range of 10(-5) to 10(-1) micrograms/ml of LPS. Lipid A portion of the LPS molecule was essential to induce the leukocyte ability for tissue factor generation. Thus, a lipid-lipid interaction between LPS and the cells is a plausible trigger for eliciting the ability. Approximately 50% of the tissue factor thus produced appeared to be located on the cell surface, at which the coagulation cascade is probably initiated via the activation of factor VII. Among monkey mononuclear cell populations, monocytes were responsible for LPS-induced tissue factor production. Lymphocytes amplified the basal ability of monocytes to produce the factor by two-fold at physiological lymphocyte-monocyte ratios of 8:1 to 10:1. This indicates a complementary effect of lymphocytes upon the LPS-mediated monocyte ability. The medium supernatant from LPS-stimulated lymphocytes affected the monocyte competence while the stimulated lymphocytes did not. This result suggests that a soluble product of lymphocytes, i.e., lymphokine-like mediator, but not the cellular entity, participates in LPS-induced tissue factor production of monocytes.

Animals↗
PubMed1985

Involvement of endogenous prostaglandins in salt-induced hypertension.

Insufficient production of prostaglandins, which are possible antihypertensive agents, may be a pathogenetic factor in hypertensive patients on salt loading. We compared the levels of plasma PGE2, plasma renin activity (PRA) and urinary 6-keto-PGF1 alpha (6-O-PGF1 alpha), a major stable metabolite of PGI2, on day 5 of salt deprivation and also on day 5 of subsequent salt loading in 17 patients with essential hypertension. Salt loading decreased plasma PGE2, and slightly increased urinary 6-O-PGF1 alpha. On salt loading, a positive correlation was found between the levels of plasma PGE2 and urinary sodium excretion. On salt deprivation, PRA was significantly correlated with plasma PGE2. The per cent change in mean blood pressure on changing from salt restriction to salt loading was inversely correlated with the per cent change in PGE2, and positively correlated with the per cent change in 6-O-PGF1 alpha excretion. These findings suggest that on salt restriction, PGE2 is involved in the renin-angiotension system and that on salt loading, PGE2 is produced to compensate for the excessive sodium. The finding that PGE2 production was attenuated progressively as the mean blood pressure increased on salt loading in patients with essential hypertension suggests that insufficient compensatory PGE2 production is a pathogenetic factor in salt-induced hypertensive patients. In contrast, PGI2 may be produced adaptively to regulate blood pressure during changes in salt balance.

Adult↗
PubMed1985

Hypotensive mechanism of potassium supplementation in salt-loaded patients with essential hypertension.

To investigate the hypotensive mechanism of potassium supplementation, blood pressure responses and hormonal changes were measured during KCl supplementation in salt-loaded patients with essential hypertension. Ten patients with essential hypertension were placed on low sodium intake, high sodium intake, and high sodium intake with KCl supplementation. Blood pressure increased during NaCl loading and decreased during KCl supplementation. The levels of urinary sodium and fractional sodium excretion increased after KCl supplementation. Reduction in blood pressure after KCl supplementation was correlated with an increase in blood pressure after NaCl supplementation, i.e., potassium sensitivity and sodium sensitivity were correlated. Plasma PGE2 and norepinephrine increased after KCl loading. Increases in plasma PGE2 were correlated with a reduction of blood pressure by KCl. These results indicate that natriuresis and hypotensive action of KCl are associated with increased PGE2 production, and the sympathetic nerve activity suggests a compensatory increase for the decrease in blood pressure.

Blood Pressure↗
PubMed1984

Synergic effects of kallikrein-kinin and prostaglandins on renin release on infusion of isolated hog kidney with aldosterone.

The effects of infusion of a large amount of aldosterone into the renal artery of isolated perfused hog kidney on the release of renin, prostaglandins (PG) and kinin and the excretion of urinary kallikrein were investigated. Infusion of aldosterone at a rate of 100 ng/min (100 to 800 ng/ml of perfusate) resulted in significant releases of renin, PG (PGE2 , 6-0-PGF1 alpha), and kinin and increase in urinary kallikrein. Infusion of aldosterone and an inhibitor of kallikrein, aprotinin, decreased the releases of renin, PG and kinin and infusion of aldosterone with indomethacin decreased the release of PG but increased that of kinin and urinary kallikrein without significant change in renin releases. These findings suggest that the release of renin by aldosterone may result from synergic effects of renal PG and the kallikrein -kinin system.

Aldosterone↗
PubMed1984

PGE2, 6-O-PGF1 alpha and sodium balance in essential hypertensive patients.

Insufficient production of PGE2 has been thought to be a pathogenic factor in hypertensive patients on salt loading. However, the inter-relationship between PGE2 and sodium is still uncertain. Essential hypertensive patients participated in a salt balance study for two consecutive 5-day periods of restriction and repletion. Urinary PGE2 increased on the second or the third day of salt balance, but subsequently declined and remained stable. On the fifth day, PGE2 excretion on salt loading was lower than on salt deprivation. Changes in urinary PGE2 during salt loading paralleled those in urinary sodium excretion. Urinary 6-O-PGF1 alpha did not show any significant change. On salt deprivation PGE2 excretion was correlated with plasma renin activity (PRA). These results suggest the possibility that PGE2 is involved in sodium excretion on salt loading and that on salt depletion PGE2 excretion increases in association with activation of the renin-angiotensin axis.

6-Ketoprostaglandin F1 alpha↗
PubMed1984

[Bleomycin, vinca alkaloid and cis-diamminedichloroplatinum combination chemotherapy for advanced testicular tumors].

Thirteen patients with advanced testicular tumors (seminoma 2, non-seminoma 11) were treated with combination chemotherapy involving BLM, vinca alkaloid and CDDP (BVP) as induction therapy and followed with CPM, VCR and CDDP as maintenance therapy. BVP and COP administration was repeated every 3 and 4 to 8 weeks for 1 year, if there were no serious side effects. The overall response rate (CR + PR) was 92% with a 69% CR rate. At a mean follow-up of 30 months (7-52 month range), 54% of the patients were alive with no evidence of disease. Bulky metastases, failure to respond to prior chemotherapy and teratomatous metastases were considered to be poor prognostic factors. The toxicity of BVP was similar to that reported for CDDP, except that allergic reaction occurred in 3 patients after several courses of treatment. Two of the 3 went into anaphylactic shock.

Adult↗
PubMed1984

[HCG-positive cells in seminoma of the testis].

In a retrospective study of 38 patients with pure seminoma, serum and urine levels of human chorionic gonadotropin (HCG) were measured and the cellular origin of HCG-like substance was searched using the technique of indirect immunoperoxidase on step sections of the tumors. Eight of the patients had elevated HCG in serum or urine, and 5 had HCG-positive cells in the sections of tumor specimens. With this technique, two types of HCG-positive cells were identified, syncytiotrophoblastic giant cells (STGC) and mononuclear cells otherwise indistinguishable from seminoma cells. Patients in the present series responded well to conventional radiation therapy or cytotoxic chemotherapy and had a favorable outcome regardless of the presence of STGC or slightly elevated HCG levels.

Adult↗
PubMed1984

[A case of renal cell carcinoma in tuberous sclerosis followed by basic fetoprotein--a new carcinoembryonic protein].

There have been very few reports on renal malignancies in tuberous sclerosis and only 9 cases have been reported in the Japanese literature. A second case of renal cell carcinoma in tuberous sclerosis in Japan is reported. The present case is a 29-year-old male who visited our clinic with the chief complaint of right flank mass. The excretory urogram, and renal selective angiography suggested right benign renal tumor, possibly angiomyolipoma. But surgical exploration was performed because of the possibility of renal malignancy. The histological findings revealed renal cell carcinoma. At 18 months after operation, the patient died of multiple visceral metastasis, i.e., to lungs, left kidney and liver. In this case basic fetoprotein - a new carcinoembryonic protein - was measured and its level elevated gradually as the disease progressed. Judging from the measurement of basic fetoprotein in this patient it may be an efficient new tumor marker for renal cell carcinoma.

Adenocarcinoma↗