[Benzocycloheptathiazole. V. Syntheses of 2-mercapto-9,10-dihydro-8H-benzo(4,5)cyclohepta(d)thiazole and its derivatives].
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Biomedical subjects
Publications and source records attributed to K Fujimori.
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OBJECTIVE: The purpose of this study was to determine fetal endocrinological and biophysical responses to the further reduction in oxygenation following prolonged nonacidemic hypoxemia in fetal goats. METHODS: Seven further hypoxic experiments were performed after prolonged (24-h) nonacidemic hypoxemia, caused by an infusion of nitrogen into the maternal trachea and by reducing uterine arterial blood flow in four chronically instrumented goat fetuses at 123-131 days' gestation. We measured arginine vasopressin, adrenocorticotropic hormone, cortisol, and catecholamines as endocrinological parameters. Fetal heart rate, fetal blood pressure, and fetal breathing movement were observed as biophysical parameters. RESULTS: Fetal arterial pO2 was significantly decreased from 27.0 +/- 1.2 mmHg (control) to 18.0 +/- 0.7 mmHg and 11.3 +/- 1.3 mmHg at the end of the prolonged hypoxemia and the further hypoxia, respectively. The further hypoxia induced reductions in fetal heart rate, increases in fetal blood pressure, and a series of gasping. Arginine vasopressin and catecholamines were elevated significantly by the further hypoxia. Although adrenocorticotropic hormone and cortisol were increasingly elevated, they did not reach a significant level. CONCLUSIONS: Some specific fetal responses-excessive elevations of fetal catecholamines, arginine vasopressin, accompanied with fetal gasping-were observed during further severe hypoxia.
The chemiluminescence of the Cypridina luciferin analogue, 2-methyl-6-(p-methoxyphenyl)-3,7-dihydroimidazo[1,2-a]pyrazin++ +-3-one (MCLA) was observed at 462 nm in the presence of horseradish peroxidase (HRP) and the total spectrum of light emitted was found to depend linearly on HRP concentration. Methods for the determination of HRP concentration using the chemiluminescence was investigated. HRP could be detected in the range from 100 pmol/L to 100 nmol/L under the optimum condition, H2O2 (10 mmol/L) and MCLA (10 mumol/L) at pH 5.8.
Activation of Na(+)/H(+) exchanger (NHE) may have an important role in the ischemia/reperfusion injury by producing intracellular calcium overload. Recent studies have shown a beneficial effect of an NHE inhibitor on the ischemia/reperfusion injury in the heart. In this study, we examined the effect of FR183998, a potent NHE inhibitor, in porcine pancreas allotransplantation from non-heart-beating Landrace pig donors (NHBDs). The four experimental groups included: untreated with no preservation (group 1; n = 3), treated with no preservation (group 2; n = 5), untreated with preservation (group 3; n = 6), and treated with preservation (group 4; n = 4). The preservation was made in ice-cold University of Wisconsin (UW) solution for 24 hours. The groups treated received 1 mg/kg FR183998 before donor cardiac arrest and 10 mg in the UW solution flush in situ. Serum blood glucose, insulin, and amylase were measured daily. An intravenous glucose tolerance test (IVGTT) was performed on the postoperative day (POD) 7 when pigs were sacrificed for histological examination. Graft survival rates on that day in groups 1,2,3, and 4 were 3 of 3; 5 of 5; 3 of 6; and 4 of 4, respectively. The mean K values of IVGTT in groups 3 and 4 were 0.78 +/- 0.10 and 1.27 +/- 0.16, respectively, which were significantly different (P < .05). Upon histological examination, pancreatic tissue in group 3 showed more severe edema and necrosis than other groups. FR183998 may be considered beneficial for ischemia/reperfusion injury to pancreatic grafts from NHBDs.
Liposome-encapsulated dichloromethylene diphosphonate (clodronate) is known to deplete macrophages. We examined the effect of clodronate on xenoreactive antibody production and xenograft rejection. Hamster cardiac grafts were transplanted into Lewis rats. Clodronate (4 mL/kg) was injected intravenously on the day before transplantation. In some groups, cyclosporine A (CsA) at a dose of 15 mg/kg was given daily intramuscularly until the end of each experiment. Untreated Lewis rats rejected the grafts at 2 and 3 days after transplantation. Neither CsA treatment alone nor clodronate treatment alone prolonged graft survival. Five of 7 Lewis recipients treated with clodronate and CsA did not reject hamster hearts for 100 days. Antibody production in the CsA plus clodronate-treated group was suppressed compared with control groups.
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Plasma and brain levels of chlordecone in chlordecone-induced motor impairment, lethal levels of chlordecone, and cumulative LD50 of chlordecone in the mouse are presented. In terms of biochemical events, the possible contributory role of neurotransmitters in chlordecone-induced neurotoxicity is also discussed. On the basis of the data obtained so far, it is suggested that the dopaminergic pathway and its interaction with other neurotransmitter systems in the basal ganglia may be primarily involved in chlordecone-induced neurotoxicity.
A 73-year-old man with mild inactive interstitial pneumonitis and non-small cell bronchogenic carcinoma developed a cell-mediated hypersensitivity pneumonitis within 15 days following a second exposure to paclitaxel. Histological features of transbronchial lung biopsy were consistent with interstitial pneumonitis. Bronchoalveolar lavage showed increased lymphocytes and eosinophils, and decreased helper/suppressor T lymphocyte ratio. Leukocyte migration inhibitory test was positive for paclitaxel. These results support the possibility that paclitaxel-induced pneumonitis is due to delayed type hypersensitivity; they also support the hypothesis of a central role of T lymphocytes in drug-induced pneumonitis.