Immunoperoxidase techniques with a combined use of PAP and ABC procedures: application to immunohistochemical studies using monoclonal antibodies.
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Biomedical subjects
Publications and source records attributed to S Taniguchi.
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Pepleomycin ointment was developed to improve the antitumor activity afforded by endoscopic therapy for esophageal cancer. Through the esophagoscope we could observe this ointment specifically attacking the lesion. Furthermore we were able to recognize that peplomycin was acting directly on the lymph nodes as well as the tumor in a resected portion of the esophagus. It is hopefully anticipated that this method will be used as a combination therapy in pre-operative and inoperable esophageal cancer.
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It is a common experience that the facial nerve is affected in closed head injury. 781 patients with head injury were treated at Kobe Central Municipal Hospital over a period of 5 years from January 1977 to April 1982, and facial palsy occurred in 25 cases (3.2%). The male to female ratio was 22: 3 and age ranged from 9 to 78 (average 36). The patients were studied, using radiological, topognostic and electrodiagnostic methods. Facial nerve decompression was done in 5 cases and 20 cases were treated conservatively. Results were as follows. The overall rate of complete recovery was 64% (16 of 25 cases). In the conservative treatment group, all patients with incomplete paralysis and normal maximal stimulation test (MST) recovered completely. With complete paralysis, if the initial nerve excitability (MST) was normal, recovery could be expected by conservative treatment. Even if the patients had abnormal nerve excitability (MST) at first, complete recovery could be observed, when signs of recovery could be elicited and normalization of MST occurred within 3 weeks from the onset of the palsy. In severe cases, even with abnormal MST from the onset, complete or partial recovery can be expected after surgery. Therefore, microsurgical decompression of the facial nerve is indicated in the following cases: patients with complete paralysis and no response to MST from the onset. patients with complete paralysis and deteriorating response to MST 1 month after onset. Maximal stimulation test is a good guide for determining the necessity for surgical intervention.
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The patient was a 2-year-old boy, who was brought to our clinic with the chief symptom of urinary retention. We suspected retrovesical tumor by digital examination, intravenous pyelography and retrograde cystography. Surgery was performed and the bladder and prostate including the tumor were removed. Ureterocutaneostomy was constructed on both sides. The pathohistological diagnosis was rhabdomyosarcoma (embryonal type). Thereafter, chemotherapy and irradiation were applied, but the patient died of cachexia which was clinically caused by a local recurrence, fourteen months after the operation. Forty-six cases of retrovesical sarcoma were collected from the recent Japanese literature, and reviewed.
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Effects of Ca2+ on phospholipid methylation in rabbit platelet membranes were studied using S-adenosyl-L-[3H-methyl]methionine as a substrate. The methylation was inhibited to 30% of the basal activity with 100 microM Ca2+. The inhibition was completely counteracted by various calmodulin antagonists. Their concentrations, i.e., N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide, chlorpromazine and trifluoperazine, to be required for half maximal recovery were 32, 47 and 29 microM, respectively. In contrast, N-(6-aminohexyl)-1-naphthalenesulfonamide, a weaker calmodulin antagonist, did not lead to a sufficient recovery of the inhibition. Addition of exogenous phosphatidyl-N-monomethylethanolamine (PMME) and phosphatidyl-N,N-dimethylethanolamine, intermediates of phosphatidylcholine synthesis by successive methylation of phosphatidylethanolamine (PE), enhanced the formation of 3H-methylated products. However, the increased amount of 3H-methylated products by the addition of those intermediates was much the same either in the presence or absence of Ca2+. These results suggest that the Ca2+-induced inhibition of methylation in platelets is mediated either by calmodulin itself or by a site which has calmodulin antagonist binding properties similar to this protein and that Ca2+ seems to inhibit the first step of the methylation to form PMME from PE.
The enzymatic properties of phospholipid methylation in rabbit platelets were examined using S-adenosyl-L-[methyl-3H]methionine as a substrate. pH optimum for the methylation was around 10.5 under Tris-HCl and glycine-NaOH buffer systems. When Tris-HCl buffer was replaced by phosphate buffer, pH optimum shifted to around 8.0 and the methylation was increased approximately threefold, compared with that in the case of Tris-HCl buffer at pH 8.0. The formation of the 3H-methylated phospholipids was increased by addition of exogenous phosphatidyl-N-monomethylethanolamine or phosphatidyl-N,N-dimethylethanolamine, intermediates of the biosynthesis of phosphatidylcholine from phosphatidylethanolamine. However, the increase in product formations by addition of exogenous intermediates was all but equal under Tris-HCl and phosphate buffer systems at pH 8.0. These results suggest that phosphate ion stimulates the first step of the successive methylation to form phosphatidyl-N-monomethylethanolamine from phosphatidylethanolamine. The methylation in platelets was inhibited to 30% of the basal value with Ca2+ (0.2 mM). However, Ca2+ showed different effects on the methylation in various tissues (activation to 150% of the basal value in the adrenal gland and slight inhibition to 82-88% of corresponding basal values in the liver, lung, kidney and brain).
In epidermal cell cultures grown on type I collagen, the in vitro synthesis of basal lamina was studied by electron microscopy and indirect immunofluorescence with anti-type IV collagen antibody. The newly-formed basal lamina and type IV collagen were observed in a linear pattern beneath the epidermal cells. The observations strongly suggest that the basal lamina containing type IV collagen is newly synthesized by the epidermal cells.
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We studied the effects of combination chemotherapy of an antitumor drug cis-diamminedichloroplatinum (II) (DDP) and its potent antidote, sodium thiosulfate (STS) in rat liver tumor systems. This therapy was given to female WKA rats with metastatic liver tumors 13 days after inoculation of syngeneic hepatoma cells through the mesenteric vein. DDP and STS were administered via two different routes, hepatic artery and femoral vein, respectively (we call this treatment "two route infusion chemotherapy"). The antitumor effects were evaluated 21 days after the treatment by calculating the tumor weight from the total weight of the liver. Tumor weights of rats treated with 20 mg/kg of intra-arterial DDP plus 1,054 mg/kg of systemic STS (group A), 5 mg/kg of intra-arterial DDP alone (group B), and 5 mg/kg of systemic DDP alone (group C) were, about one fifth, two fifths and three fifths of the tumor weights in the untreated controls, respectively. In group A, no rats died despite administration of a 4-fold higher DDP dose than in the latter two groups B and C in which 14-18 per cent of the rats died, due to DDP-induced toxicity. The patterns of body weight gain in the three groups after the chemotherapy were much the same. Our results clearly indicate that the antitumor effect of DDP on metastatic liver tumors in rats can remarkably be enhanced by the "two route infusion chemotherapy" of DDP and STS.