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Biomedical subjects

S Mizuno

Publications and source records attributed to S Mizuno.

At least 541 records · Page 30Linked to original sources
PubMed1984

Salivary excretion of urea in dogs.

The salivary excretion of urea was investigated by collecting parotid saliva (Pr) and mandibular-sublingual saliva (MS) separately in beagle dogs. (1) After intravenous administration of urea (1.5 g/kg), urea concentrations in both Pr and MS were well correlated to but were lower than those in plasma. Urea concentrations in MS were significantly lower than those in Pr (p less than 0.05), indicating that there was glandular difference in salivary excretion of urea. (2) This glandular difference was not explained by Matin's equation, even if all variation factors in this equation were considered. (3) At relatively low salivary flow rates, the increase in saliva/plasma urea concentration ratio (S/P ratio) for both Pr and MS was found in the experiments for endogenous urea. (4) At relatively low salivary flow rates, glandular difference was observed in the S/P ratios of sodium ion. (5) Salivary clearance of urea was highly dependent on salivary flow rate under stimulated condition for salivation, and mean value of the salivary clearance of urea was about 20% of its total body clearance.

Absorption↗
PubMed1984

Relationships of structure to binding of gamma-aminobutyric acid (GABA) and related compounds with the GABA and benzodiazepine receptors.

The relationship of the structure of gamma-aminobutyric acid (GABA) and 45 related compounds to their binding with the GABA and benzodiazepine (BDZ) receptors was investigated. In the course of evaluating the cross-reactivity of the 45 GABA-related compounds in a GABA radioreceptor assay (GABA-RRA) using [3H]GABA and rat brain synaptic membranes, it became clear that for the molecule to react with GABA-receptors the amino group must be free, but that the carboxy group is not essential. It was also demonstrated that the molecule lost its cross-reactivity if the distance between the alpha-carbon and the amino group exceeded a certain limit, and, additionally, that the cross-reacting potency depended on the stereospecificity of the compound. When the cross-reactivity of GABA related compounds with the GABA receptor was compared with their enhancement of BDZ receptor affinity, a parallelism was found between the two actions. Between d-gamma-amino-beta-hydroxybutyric acid (d-GABOB) and 1-GABOB, however, no difference was found in the BDZ receptor affinity-enhancing effect, although there was a large difference in the cross-reactivity in the GABA-RRA. This indicates that the stereospecificity of the beta-carbon is crucial for the binding of the molecule to the GABA receptor but not essential for its binding to the BDZ receptor, suggesting that the GABA receptor and the BDZ receptor each recognize a different site of the molecule.

Animals↗
PubMed1984

[Etoposide effect on cell cycle kinetics of a human lung cancer cell line].

The lethal and kinetic effects of Etoposide on a cell line of human small cell carcinoma of the lung (PC-6) were analyzed in vitro using flow cytometric measurement of DNA content. The drug effect is dependent on concentration and exposure time. When PC-6 cells were exposed to Etoposide for 1 hour then washed, a increase of cells in G2 phase was observed followed by prompt recovery. Continuous treatment with Etoposide for 24 hours caused a retardation of S phase transit, and high concentrations (greater than 10 micrograms/ml) resulted in stoppage of the whole cell cycle. This drug may be useful in combination chemotherapy regimens.

Cell Count↗
PubMed1983

[Pituitary-thyroid function in patients with Cushing's syndrome--comparative study before and after extirpation of adrenal cortex tumor].

The pituitary-thyroid function and the metabolism of the thyroid hormones in the blood were investigated in 19 patients with Cushing's syndrome before and after an adrenalectomy, 16 patients had adrenal adenomas and 3 patients had modular adrenal hyperplasias. Serum T4, free T4 (FT4), T3, reverse T3 (rT3), TBG and TSH were measured in all patients by radioimmunoassay, and changes in serum TSH, PRL and HGH following the injection of TRH 500 micrograms in 10 out of 19 patients were observed to evaluate the pituitary functions. Serum T4, FT4 and rT3 were within normal limits and not significantly changed after the surgical treatment. Serum TBG levels in patients before the surgical treatment were also within the normal range. After the treatment, a small but significant increase in TBG levels was observed. Serum TSH levels were suppressed before the surgery and increased after the surgery, but a coefficient of correlation between serum cortisol and TSH levels was not statistically significant. The serum T3 levels were abnormally low in Cushing's syndrome and increased significantly (p less than 0.001), accompanying the normalization of serum cortisol levels, after the surgical treatment. Moreover, there was a negative correlation between serum T3 and cortisol levels before the treatment (r = -0.586), but it was not statistically significant (before the treatment: T3 0.71 +/- 0.04 ng/ml, cortisol 30.2 +/- 2.1 micrograms/dl, after the treatment: T3 1.58 +/- 0.15 ng/ml, cortisol 7.5 +/- 2.0 micrograms/dl). To evaluate further the metabolic changes in circulating thyroid hormones, T3/T4, T3/rT3, TBG/T4 and TBG/T3 were compared before and after the adrenalectomy. Significant decreases in T3/T4 (p less than 0.001) and T3/rT3 (p less than 0.05) and a significant increase in TBG/T3 (p less than 0.05) were observed before the surgery. On the other hand, TBG/T4 was not significantly different before or after the surgery. The TSH response to TRH was significantly higher in postoperative patients than in preoperative patients (p less than 0.05). Before the surgical treatment no responses of serum HGH to TRH were observed in any patients, while after the treatment, abnormal increases from 4.5 +/- 1.4 ng/ml to 10 +/- 1.1 ng/ml at 15 min. after TRH administration were observed. There was no difference between PRL response to TRH before or after the surgery.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1983

Chronic thyrotropin releasing hormone (TRH) administration on TRH receptors and muscarinic cholinergic receptors in CNS.

Intraperitoneal injections of thyrotropin releasing hormone (TRH, 6 mg/kg/day) to rats for 14 days resulted in a significant loss (20 25%) of TRH binding sites in the hippocampus, hypothalamus and cerebral cerebral cortex. The TRH-mediated loss was reversible and reflected a decrease in binding sites but no change in affinity. On the other hand, this TRH treatment did not affect the specific brain binding of [3H]QNB. The results suggest that TRH participates in regulating CNS-TRH receptors.

Animals↗
PubMed1983

Differential effects of some transition metal cations on the binding of beta-carboline-3-carboxylate and diazepam.

The interaction of benzodiazepines and beta-carbolines with metal cations was investigated. Among numerous transition metal cations, only three, CO2+, Ni2+ and Zn2+, specifically inhibited the binding of [3H]beta-carboline-3-carboxylate ethyl ester (beta-CCE). The effects of these cations on [3H]beta-CCE binding were exactly opposite to those on [3H]diazepam binding. The effects of these cations was not dependent on lipid peroxidation. The differential effect of these cations may reflect a general difference in the way agonists and antagonists bind to the benzodiazepine receptor.

Animals↗
PubMed1983

Clinical evaluation of three-day treatment of vaginal mycosis with clotrimazole vaginal tablets.

A double-blind study was conducted comparing a 3-day (200 mg once a day for 3 consecutive days) treatment with a 6-day (100 mg once a day for 6 consecutive days) treatment of clotrimazole in patients with vaginal mycoses. Two days after therapy, fungal eradication was achieved in 87.7% of the patients who received 3-day therapy and 89.1% of patients who received 6-day therapy. With regard to the clinical assessment, 2 days after therapy the symptoms had disappeared in 54.4%, improvement in 42.1%, were unchanged in 1.8%, and aggravated in 1.8% of the 3-day therapy group. The corresponding values in the 6-day group were 63.6%, 34.5%, 1.8% and 0%. Reappearance of fungi was found 2 weeks after therapy in 15.6% of the 3-day treatment group and 8.7% of the 6-day treatment group. No adverse reactions were seen in either group which necessitated the discontinuation of therapy. There were no statistical differences between any of the above results and it is therefore concluded that 3-day clotrimazole therapy is an effective treatment for primary vaginal mycosis.

Candidiasis, Vulvovaginal↗
PubMed1983

Differential cytotoxicity to human lung normal diploid, virus-transformed and carcinoma cells by the antitumor antibiotics, auromomycin and macromomycin, and their non-protein chromophores.

With the use of three human lung cultured cell lines: normal diploid fibroblasts (WI38), their SV40-transformants (VA13) and carcinoma cells (A549), whose doubling times were similar, the cytotoxicity of the protein antitumor antibiotics, auromomycin (AUR) and macromomycin (MCR), was studied by colony formation method. The susceptibilities of the three cell lines to these antibiotics were in the order: WI38 less than VA13 less than A549. This differentiality in the cytotoxic effect was similar between AUR and MCR. The differential cytotoxic effect did not depend on cell densities of each cell line at the time of the antibiotic-treatment. Alcohol-extracted chromophores of the antibiotics also showed a similar differential cytotoxic effect, while the apo-proteins of the antibiotics showed no cytotoxicity. It is concluded that the differential cytotoxic effect of AUR and MCR to normal, transformed and carcinoma cells is attributed to the chromophore moiety and the protein moiety is not involved in this effect.

Anti-Bacterial Agents↗
PubMed1983

Role of pronase-resistant peptide segments of the antitumor protein antibiotics, auromomycin and macromomycin, in stabilizing cytocidal activity of the chromophore moieties to carcinoma cells.

The free chromophores isolated from the antitumor protein antibiotics, auromomycin (AUR) and macromomycin (MCR), were rapidly inactivated by incubation in serum-containing medium at 37 degrees C in the dark with respect to cytocidal activity to human lung carcinoma A549 cells. Under the same conditions, the intact antibiotics, their pronase-hydrolysates and reconstituents from the chromophores and apo-proteins were stable. Intact and reconstituted AUR and MCR were more resistant to pronase digestion than the apo-proteins. The analyses of the pronase-hydrolysates of AUR and MCR by SDS-polyacrylamide gel electrophoresis and ultrafiltration showed that the antibiotics (13 kilodaltons (kDa] were degraded to produce peptide fragments (1-3 kDa) in which most cytotoxicity of the pronase-hydrolysates resided. The pronase-hydrolysates exhibited a differential cytocidal activity to normal diploid fibroblasts (WI38), their SV40-transformants (VA13) and carcinoma cells (A549) of human lung origin as was observed for the intact antibiotics. These results indicate that specific interaction between the chromophores and the pronase-resistant peptide segments (1-3 kDa) of the protein moiety stabilizes the cytocidal activity of the chromophores and also protects the peptide segments from pronase digestion.

Anti-Bacterial Agents↗
PubMed1983

Modulation of the cytotoxicity of the antitumor antibiotic peplomycin by membrane-interacting drugs and by increased levels of calcium ions.

The cytotoxic effect of peplomycin (PEP), a new derivative of bleomycin glycopeptide antibiotics, toward HeLa cells and mouse FM3A cells was markedly enhanced by combination of PEP with non-toxic doses of the membrane-interacting drugs verapamil (0.1-0.2mM) and dibucaine (0.15-0.25mM), or with CaCl2 (10-16 mM). Treatment with verapamil or CaCl2 following PEP treatment also effectively enhanced the cytotoxic effect of PEP, suggesting an interaction with PEP-induced damage. Cellular uptake of PEP did not increase in dibucaine-treated cells, suggesting no correlation between membrane permeability to PEP and enhanced cytotoxicity. Increased Ca2+ did not enhance the cytotoxic effects of adriamycin, mitomycin C, cis-diamminedichloroplatinum (II), vinblastine or macromomycin, thus suggesting a unique interaction with PEP. The enhancing action of verapamil and Ca2+ was greatly promoted by 41 degrees hyperthermia, although 41 degrees alone scarcely enhanced PEP cytotoxicity. Cytochalasin B and alpha-tocopherol, but not cytochalasin D, reversed the enhanced cytotoxicity produced by PEP and verapamil or dibucaine, but did not reverse the enhanced cytotoxicity by PEP combined with increased Ca2+. The enhancing action of Ca2+ was, however, antagonized by ruthenium red and lanthanum chloride, which are potent inhibitors of Ca2+ uptake by cells, or by magnesium chloride. Verapamil and increased Ca2+ promoted the decomposition of the DNA-membrane complex induced by PEP in HeLa cells, and also impaired the regeneration of the decomposed DNA complex.

Animals↗
PubMed1983

Differential enhancement of cytotoxicity by combination of the carcinostatic agent benzaldehyde and hyperthermia in simian virus 40-transformed and normal cell lines.

The effect of the carcinostatic drug benzaldehyde (BA) on hyperthermia-induced cytotoxicity was studied in various types of cultured mammalian cell lines by colony formation assay. The treatment of HeLa cells with nontoxic doses of BA (1 to 4 mM) at 42 and 43 degrees for up to 3 hr induced enhancement of cell killing. BA-induced enhancement of hyperthermic cell killing was much greater in SV40-transformed rat fibroblast cells than in the untransformed cell line. This BA-induced differential enhancement of hyperthermic cell killing increased as the time and dose of BA treatment were increased at elevated temperatures. For example, BA (2 mM) treatment for 4 hr at 42 degrees decreased the survival of transformed cells to 2 X 10(-4), but decreased the survival of untransformed cells to only 0.1. Furthermore, BA (4 mM) treatment for 2 hr at 42 degrees reduced the survival of transformed cells to less than 10(-5), but reduced the survival of untransformed cells to 5 X 10(-2). Differential enhancement of hyperthermic cytotoxicity by BA was also evident between normal human diploid fibroblast W138 cells and its SV40-transformed cell line, although the magnitude of the enhancement was less than that observed with rat cell lines. The determination of BA remaining in the medium after incubation with transformed and untransformed rat cells at 37, 42, and 43 degrees suggested that greater amounts of BA reacted with or were consumed by transformed cells irrespective of temperature.

Animals↗