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Biomedical subjects

T Nishimura

Publications and source records attributed to T Nishimura.

At least 1,567 records · Page 87Linked to original sources
PubMed1980

DNA repair synthesis in HeLa cell lysate.

In order to study the mechanism of DNA repair, we established an in vitro system for repair (unscheduled) DNA synthesis. HeLa cells synchronized at G2-G1 phase were irradiated with ultraviolet light in the presence of two DNA replication inhibitors, hydroxyurea and 1-beta-D-arabinofuranosyl cytosine (araCyt), to reduce the replicative DNA synthesis as much as possible. Hypotonic treatment of the cells was followed by gentle homogenization, and the resulting cell lysate was incubated with [3H]dTTP. The lysate system required all four dXTPs and Mg2+, but required no ATP. The incorporation of [3H]dTTP was dependent on the dose of ultraviolet light, was linear for 2 min, and reached the maximum at 5 min. The presence of hydroxyurea and araCyt during in vivo incubation was necessary for in vitro DNA synthesis. Accumulation of single-strand breaks was observed under these conditions, and this could explain the very high incorporation of [3H]dTTP in this system.

Adenosine Triphosphate↗
PubMed1980

Leiomyomatosis peritonealis disseminata.

The ninth documented case of leiomyomatosis peritonealis disseminata (LPD) combined with pregnancy is presented. Light and electron microscopic studies revealed that the smaller tumors were composed partly of decidual cells and partly of fibroblasts, and the larger tumors contained cells resembling smooth muscle cells. Plasma steroid levels were determined during pregnancy. Estrogen levels were within normal range, but progesterone levels were lower than normal, resulting in relative hyperestrogenism. In the case presented, pregnancy, especially with relative hyperestrogenism, may have been a major cause of LPD.

Adult↗
PubMed1980

Macrophages in prostatic fluid.

Non-specific esterase staining has been found useful in the detection of macrophages in prostatic fluid (PF). In the early stage of acute prostatitis most of the leucocytes in a smear of PF took up the stain, suggesting the dominant participation of macrophages in the inflammatory area in this stage of the disease. In chronic prostatitis, only a few leucocytes took up the stain. In female acute cystitis, none of the large numbers of leucocytes exhibited staining at any stage of the disease. The reason for this is still to be determined. Frozen sections of prostatic tissue from patients with chronic prostatitis revealed similar cells around the acini and these appeared to be the source of the macrophages which appeared in the PF.

Body Fluids↗
PubMed1980

Echocardiographic evaluation of long-term effects of exercise on left ventricular hypertrophy and function in professional bicyclists.

Echocardiographic examinations were performed in 60 professional bicyclists and control subjects to determine the effects of exercise on left ventricular hypertrophy and function. The athletes were separated by age into three groups: group 1 (n = 14), 20-29 years; group 2 (n = 17), 30-39 years; and group 3 (n = 29), 40-49 years. Echocardiograms showed enlargment of the left ventricular end-diastolic dimensions in all three groups compared with age-matched control groups (p less than 0.001). Thickness of the interventricular septum and the left ventricular posterior wall was more prominent in group 3 of the athletes than groups 1 and 2 of the athletes and control group (p less than 0.001). Resting left ventricular function evaluated with fractional shortening, ejection fraction and mean velocity of circumferential fiber shortening was significantly depressed in group 3 compared with the other groups. Moreover, 14% of group 3 subjects showed enlargement of left atrial dimension and T-wave inversion in the left precordial leads of the ECG. We conclude that left ventricular hypertrophy is an important ventricular adaptation in relatively young athletes. However, middle-aged athletes may be more susceptible to electrocardiographic abnormalities and prominent hypertrophy, and some may have slightly depressed left ventricular function.

Adult↗
PubMed1980

Radioimmunoassay method for baboon plasma gonadotropins.

Double antibody radioimmunoassay methods were developed for the determination of baboon luteinizing hormone (bLH) and follicle stimulating hormone (bFSH). The bLH radioimmunoassay employs a unique anti-ovine LH serum (GDN-15) and ovine LH (LER-1056-C2) for radioiodination, while the bFSH radioimmunoassay employs an heterologous system, i.e., an anti-ovine FSH serum (H-31) and purified human FSH for radioiodination. The reference standard used in both assays is a crude rhesus pituitary extract (LER-1909-2). Elevated endogeneous baboon plasma TSH and prolactin induced by the intravenous administration of 500 microgram of TRH had no influence on the levels of LH and FSH, whereas simultaneous intravenous administration of 100 microgram LHRH and 500 microgram TRH raised the levels of LH and FSH in plasma. hPRL, hCG, hTSH and hGH did not cross react with either the bLH or the bFSH assay system. The determination of plasma LH and FSH concentrations in daily samples from 6 mature female baboons throughout ovulatory menstrual cycles revealed patterns qualitatively similar to those of the rhesus monkey and human females.

Animals↗
PubMed1980

Ovulatory changes in the wall at the apex of the human Graafian follicle.

The apical wall was studied ultrastructurally in 16 human follicles at various stages of development. In the theca externa and tunica albuginea at the apex of growing follicles, fibroblasts with little cytoplasm and abundant collagen fibres were observed. In the mature follicles, the fibroblastic cytoplasm was well developed, rich in lysosome-like granules and contained peripheral multivesicular structures. Intercellular collagen fibres were sparse. It is suggested that the collagen fibres are digested by the content of lysosomal granules and multivesicular structures, thus aiding follicular rupture.

Adult↗
PubMed1980

Inhibition by indomethacin of ovulation induced by human chorionic gonadotrophin in immature rats primed with pregnant mare serum gonadotrophin.

Treatment of immature rats with pregnant mare serum gonadotrophin followed by human chorionic gonadotrophin (HCG) caused an acute and temporary increase in concentrations of progesterone, testosterone and oestradiol in plasma with maximum levels 3 h after the administration of HCG. Concurrent injection of indomethacin and HCG reduced, in a dose-dependent manner, the mean number of ova shed and this was accompanied by a dose-dependent decrease in concentrations of plasma progesterone and testosterone but not of oestradiol when they were measured 3 h after the injection of HCG. The minimum effective dose that blocked ovulation completely at 0 h abolished the acute increase of progesterone and testosterone, suggesting that prostaglandins act on ovulation by stimulating steroidogenesis at an early stage in the preovulatory process. The anti-ovulatory action of the minimum effective dose at 0 h became progressively less potent as the time between injection of HCG and administration of indomethacin was increased, although plasma concentrations of progesterone and testosterone measured at autopsy 18 h after treatment with HCG had not changed appreciably. When indomethacin was administered 10 h after HCG, the relationship between the dose of indomethacin and the mean number of ova differed from that observed when simultaneous injections of indomethacin and HCG were given, and the minimum effective dose that prevented ovulation was much higher than that at 0 h, suggesting that prostaglandins act differently on ovulation in the later stage of the preovulatory process. It was concluded that prostaglandins may mediate the action of HCG on ovulation through two mechanisms which operate at different stages of the preovulatory process.

Animals↗
PubMed1980

A progesterone-dependent step in ovulation induced by human chorionic gonadotrophin in immature rats primed with pregnant mare serum gonadotrophin.

In immature rats primed with pregnant mare serum gonadotrophin, antiserum to progesterone could prevent or reduce ovulation in response to injected human chorionic gonadotrophin (HCG). To be effective, antiserum treatment had to be within 6 h of gonadotrophin treatment; antiserum given 9 h after HCG was ineffective. Progesterone restored the antiserum blocked ovulation completely or incompletely when administered intravenously within 6 h of treatment with HCG. The first 6 h was shown to be a progesterone-dependent step in the ovulatory process in this experimental system.

Animals↗
PubMed1980

In vivo and in vitro cross-resistance of kanamycin-resistant mutants of E. coli to other aminoglycoside antibiotics.

Cross resistance of kanamycin-resistant mutants of E. coli Q13 to other aminoglycosides (streptomycin, neomycin, gentamicin and dibekacin) was demonstrated in vivo (growth) and in vitro (polyphenylalanine synthesis, codon misreading and translocation on the ribosomes). Kanamycin-resistant mutants, R1-4, R2-1, R2-2, R3-3 and R3-5 showed various degrees of cross-resistance to streptomycin, gentamicin, neomycin and dibekacin in vivo. In vitro, polyphenylalanine synthesis was more resistant to kanamycin, streptomycin, neomycin and gentamicin on the ribosomes of the kanamycin-resistant mutants than on those of the parental strain. In the presence of kanamycin, neomycin or gentamicin, less degrees of [14C]isoleucine uptake with poly[U] (codon misreading) were observed on the ribosomes obtained from the resistant mutants than on the sensitive cell ribosomes. The N-acetyl-[14C]phenylalanyl-puromycin synthesis enhanced by an elongation factor, EF-G and GTP (translocation) was more resistant to kanamycin and dibekacin on the mutant ribosomes than on the parental ribosomes. The results indicate that the cross-resistance to other aminoglycoside antibiotics, as well as the kanamycin resistance, are attributed to mutational alterations of the ribosomes in these mutants.

Aminoglycosides↗
PubMed1980

Studies on aclacinomycin A resistance in mouse lymphoblastoma.

An aclacinomycin A-resistant subline of mouse lymphoblastoma L5178Y cells was isolated by successive treatment of tumor-bearing mice with the antibiotic. IC50 (50% growth inhibition) in culture was observed at a drug concentration of 0.22 micrograms/ml, which was ca. 11 times higher than IC50 for the parental cells. The resistant cell line exhibited cross resistance to mitomycin C, actinomycin D, macromomycin, auromomycin, vinblastine, cytochalasin B, and other anthracyclines: daunorubicin, adriamycin, 4'-O-tetrahydropyranyladriamycin, baumycins A1 and A2, aclacinomycins B and Y, MA144-S1, 1-deoxypyrromycin, cinerubin A, musettamcyin, and pyrromycin. The 1-deoxy group of anthracyclines showed higher degree of cross resistance than the 1-hydroxy group. No significant cross resistance was found with bleomycin A2, neothramycin and blasticidin S. The resistance to aclacinomycin A and cross resistance to adriamycin were also demonstrated by the method of uridine incorporation. The accumulation or retention studies with [3H]adriamycin revealed that the resistance may be due to decreased uptake and increased efflux of the antibiotic in the resistant cells.

Aclarubicin↗
PubMed1980

[The effect of atenolol on the cardiovascular system (author's transl)].

Effects of atenolol on the cardiovascular system were studied in rats and dogs. Atenolol (10 microgram/kg - 3 mg/kg) did not increase heart rate significantly in rats pretreated with reserpine (5 mg/kg), while a significant increase occurred with practolol (30 microgram/kg - 3 mg/kg). Atenolol (100 microgram/kg) inhibited the response of canine heart (heart rate and myocardial contractile force) to isoproterenol to a similar degree as seen with propranolol (100 microgram/kg) did. The ability of atenolol to inhibit vasodilating action of isoproterenol, however, was about 1/12 of that of propranolol. Atenolol (0.5 mg/kg) did not inhibit hemodynamic responses to ouabain and CaCl2 in dogs, while this drug inhibited these responses to isoproterenol. Atenolol decreased heart rate, myocardial contractile force, left ventricular pressure, and rate of rise of the left ventricular pressure (dp/dt LV max) dose-dependently. Atenolol (1 mg/kg) decreased coronary venous outflow and myocardial oxygen consumption in dogs, but did not alter the myocardium to a more reduced state, as determined by coronary arterial and venous lactate and pyruvate levels. These results confirmed that atenolol is a potent cardioselective beta-blocker devoid of intrinsic sympathomimetic action. The results also suggest that atenolol inhibits cardiac function without disturbing the intracellular redox state of the myocardium.

Adrenergic beta-Antagonists↗
PubMed1980

[Atenolol, its cardioselective property for adrenergic beta-receptor blocking action and effect on the cardiac function (author's transl)].

Cardioselective property of the beta-adrenoceptor blocking action of atenolol and its effect on the AV conduction, the atrial muscle refractory period and the cardiac contractility were studied in comparison with these of propranolol. A ratio of pA2 values obtained in the isolated right-atrial preparations and the isolated tracheal preparations of guinea pigs demonstrated that atenolol was highly cardioselective, while propranolol was non-selective. This cardioselective property of atenolol was confirmed in in vivo experiments using guinea pigs. Atenolol increased the AV conduction time and decreased the cardiac contractility dose-dependently in anesthetized dogs of which the heart was electrically driven at fixed rates. At 140 beats/min, AV block was observed at 10 mg/kg, i.v. in 3 of 8 dogs, and further increase in a dose ti 30 mg/kg resulted in acute heart failure in one of remaining 5 dogs, while propranolol, though showing a tendency to be less potent in depressing AV conduction in a dose range less than 0.3 mg/kg, produced a state of heart failure in 2 of 5 dogs at 3 mg/kg, i.v. and AV block in all of the remainder at 10 mg/kg, i.v. Functional refractory period of AV node as well as functional and effective refractory period the the atrial muscle were increased dose-dependently by atenolol and propranolol. There were no significant differences between both drugs regarding these effects. Further increase in a pacing rate to 160 and 180 beats/min augmented the depressing effect of both drugs on the AV conduction.

Adrenergic beta-Antagonists↗