[Cinedensitometry of blood flow in lower extremity (author's transl)].
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Biomedical subjects
Publications and source records attributed to H Akagi.
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An attempt was made to identify the immunoreactive substance P (SP) released from isolated rat spinal cords using reversed-phase high-performance liquid chromatography (HPLC) combined with radioimmunoassay (RIA) for SP. Soaking the spinal cords of newborn rats in Krebs solution containing 90 mM K+ evoked a release of immunoreactive SP as well as of GABA and glycine in a calcium-dependent manner. Capsaicin also evoked a release of immunoreactive SP but not of GABA and glycine. The immunoreactive SP released from rat spinal cords by high K+ or capsaicin was analyzed by HPLC. A single peak was detected by RIA whose elution position coincided with that of synthetic SP.
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Hematological and clinical biochemistry values of two species of monkeys (Macaca mulatta and Macaca fascicularis) were measured by using auto-analyzers. WBC and RBC counts of M. fascicularis were high and Hb, MCV, MCH and MCHC values of M. fascicularis were low in comparison with those of M. mulatta. Albumin and creatinine levels of M. fascicularis were lower than those of M. mulatta. Total protein and A1P values of female M. fascicularis were higher than those of female M. mulatta. Differences between the sexes were observed in MCV, inorganic phosphorus, total protein, albumin and creatinine in M. mulatta, whereas in M. fascicularis, such differences were demonostrated as to creatinine, phospholipids and triglycerides.
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The biological activities of benzo(a)pyrene, cyclopenta(c,d)pyrene, and 12 other structurally related compounds were assessed by mutagenicity studies with bacterial and mammalian cells and/or skin tumorigenicity studies with mice. The ability of the parent hydrocarbons to be metabolically activated to mutagenic products was examined in strains TA98 and TA100 of Salmonella typhimurium, using 3 experimental protocols. In each case, cyclopenta(c,d)pyrene was metabolically activated to products mutagenic to the bacteria to a greater extent than was benzo(a)pyrene. However, 7,8-dihydrobenzo(a)pyrene and 0,10-dihydrobenzo(e)pyrene were the best substrates for metabolic activation to bacterial mutagens. Highly purified epoxide hydrase added to a purified and reconstituted monooxygenase system readily abolished the mutagenic activity observed in strain TA100 of S. typhimurium when cyclopenta(c,d)pyrene was the substrate, but not when benzo(a)pyrene was the substrate. Inherent mutagenicity of several epoxides of the hydrocarbons generally paralleled the ability of their potential metabolic precursors to be activated to mutagens. 1-Pyrenyloxirane and 10,11-dihydrocycloheptapyrene 8,9-oxide were highly mutagenic in strains TA98 and TA100 of S. typhimurium, and in the former strain these activities were comparable to that observed with 9,10-epoxy-7,8,9,10-tetrahydrobenzo(a)pyrene, 4-Pyrenyloxirane was significantly less mutagenic than was 1-pyrenyloxirane in both strains of bacteria and in mammalian cells. Benzo(a)pyrene was over 20 times more tumorigenic than was cyclopenta-(c,d)pyrene, and it was the most potent of the 11 compounds tested for tumor-initiating activity in 2-stage initiation-promotion experiments on the skin of mice. Cyclopenta(c,d)pyrene had tumor-initiating activity comparable to that of benzo-(a)anthracene, but it was significantly less active than chrysene. Thus, contrary to inferences made from its high mutagenic activity, cyclopenta(c,d)pyrene is a weak tumor initiator on mouse skin.
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