Biomedical subjects
Publications and source records attributed to Y Baba.
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Effects of enzyme inhibitors and membrane-active drugs on the binding of 125I-labelled thyroid-stimulating hormone (TSH) to human thyroid membranes and membrane adenylate cyclase (AC) activity were studied. FOY, a synthetic polyvalent proteolytic enzyme inhibitor, Trasylol, alpha- and beta-adrenergic blocking agents, tranquilizers, anti-histamines and polyene antibiotics enchanced TSH binding in a dose-dependent manner, whereas selective enzyme inhibitors and adrenergic stimulating agents had no effect. Both propranolol and FOY inhibited basal and TSH stimulated AC activity of thyroid membranes. FOY, as well as propranolol was found to have protective effects on hypotonic erythrocyte lysis. These results suggest that propranolol and FOY increased TSH binding by the same mechanism, probably the so-called membrane-stabilizing effects. Although the detailed mechanisms underlying the increased TSH binding by these drugs remain unknown, they may change the membrane structure, thereby enhancing the TSH receptor affinity.
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Cefmetazole (CMZ) is an antibiotic agent belonging to the cephamycin group, which is resistant to beta-lactamase and has a broad antibacterial spectrum covering from Gram-negative to -positive organisms. Although this agent has been proved to have an antibacterial activity against Staphylococcus spp., it has not been used for treatment of the infections caused by the organism. Thus, 62 strains of S. aureus isolated clinically were compared for their sensitivity to CMZ, cefoxitin (CFX), cefuroxime (CXM), cefazolin (CEZ), and ampicillin (ABPC). In addition, 5 children suffering from septicemia due to S. aureus were treated with CMZ 158 mg/kg at a mean daily dose for a mean period of 14 days. The dose was used after dividing into 3 and 4 equal parts in 1 and 4 children, respectively. One old patient with septicemia was given 2,000 mg of CMZ twice daily for 4 days and once daily for subsequent 3 days. Another child with bacterial meningitis was treated with 50 mg/kg of CMZ 4 times daily for 63 days. The drug was given intravenous injection by one-shot or drip infusion in all cases under observation of clinical effects, bacteriological effects and side effects. The MIC of CMZ against S. aureus at inoculum sizes of 10(6) and 10(8) cells/ml was 1.56 mcg/ml in 72.6 and 56.5% of the strains, respectively. When 5 drugs were compared on the basis of the MIC to which the largest number of strains were sensitive, CEZ was most active, and CMZ was ranked in the next place and similar to CXM in activity. However, when the whole range of the MIC was considered, CMZ was more excellent than CXM, its MIC was lower than those of CEZ, CFX and ABPC in a greater number of strains. It was considered from the results that the serum level of CMZ was effective against 100 and 93.5% of strains at an inoculum size of 10(6) cells/ml and against 100 and 83.9% of strains at an inoculum size of 10(8) cells/ml until 4 and 6 hours after a one-shot intravenous injection of 50 mg/kg of Moni-trol I standard, respectively in the children. Thus, CMZ is expected to manifest a sufficient effect on septicemia caused by S. aureus in children who receive a one-shot intravenous injection of 50 mg/kg of it 4 times daily. Treatment with CMZ was clinically evaluated to be excellent in 3, good in 3 and poor in none of 6 patients with septicemia due to S. aureus, and fair in the 1 with Staphylococcal meningitis. The bacteriological result was excellent, since the causal organisms were eradicated in all cases. With regard to side effects, abnormal eosinophilia was found in 2 cases, but it was no ascribable to this drug in 1 of them. GOT showed an abnormal rise in 1 case and both GOT and GPT in 1, although they were considered not to be related to this drug in either case. It is considered from these results that CMZ is a valuable drug in treatment of septicemia due to S. aureus.
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To clarify whether TSH binding inhibitor immunoglobulins (TBII) are antibodies to the membrane site associated with the TSH receptor itself or its neighboring sites, the interactions of TSH and TBII with soluble TSH receptor were investigated with a TSH radioreceptor assay using labeled highly purified bovine TSH (bTSH) and Triton extracts from guinea pig crude fat cell membranes (800-10,000 x g fraction). Treatment of the crude fat cell membranes with 0.5% (vol/vol) Triton X-100 resulted in solubilization of membrane proteins with recoveries of 25-30%, whereas increasing the concentration of Triton X-100 in the assay medium caused a decrease of [125I]bTSH binding to the solubilized membranes. Thus, the solubilized membranes were found to retain the capacity to bind [125I]bTSH below the Triton X-100 concentration of 0.4% in the assay medium. Incubation of the solubilized membranes with [125I]bTSH for 24 h at 4 C led to a steady state of specific binding, while incubation at 37 C resulted in more rapid but less specific binding, with a shorter duration of the steady state. Maximum binding occurred within the physiological pH range. Both TSH and Graves' immunoglobulins (Igs) specifically inhibited [125I]bTSH binding to the solubilized membranes, as demonstrated by polyethylene glycol separation of the [125I]bTSH-solubilized membrane complex from unbound [125I]-bTSH. Scatchard analysis of [125I]bTSh displacement curves for both TSH and Graves' Igs indicated a single class of binding site for each, with an affinity constant of 1.8 x 10(9) M-1. In addition, Igs capable of inhibiting [125I]bTSH binding to the solubilized membranes were detected predominantly in the serum of patients with Graves' disease. These results strongly suggest that TBII are antibodies directed to the TSh receptor itself without strict organ and species specificity.
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Decreased erythrocyte membrane fluidity was revealed by analyses with fluorescence depolarization using 1,6-diphenyl-1,3,5-hexatriene (DPH) and with electron paramagnetic resonance using spin-labelled stearates (EPR). The decreased membrane fluidity measured by DPH appeared to be related to the increase in membrane or plasam free cholesterol to phospholipid (C/PL) mol ratios. The decreased membrane fluidity observed by EPR appeared to be located, at least in part, in a deeper portion of membrane lipid core and the change may not be derived principally from the effect of cholesterol. Increases of membrane sphingomyelin (+ lysophosphatidylcholine) and decreases of phosphatidylethanolamine were found in erythrocytes of diabetic patients. The contributing factors to the decreased erythrocyte membrane fluidity in diabetic patients were suggested to be not only an increase in membrane C/PL mol ratios but also multifactorial changes involving membrane phospholipid fractions and other complex factors. It is considered that the determinant factors of membrane fluidity are so complex that the decreased membrane fluidity observed with diabetic erythrocytes cannot be closely correlated with any single constituent measured. The decreased membrane fluidity observed in this study appears to be related to poor metabolic control and is often associated with diabetic microangiopathy.
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