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Y Masaki

Publications and source records attributed to Y Masaki.

At least 145 records · Page 8Linked to original sources
PubMed1990

Chloranil-photosensitized monomerization of dimethylthymine cyclobutane dimers and effect of magnesium perchlorate.

The photosensitized monomerization of the cyclobutane dimers of 1,3-dimethylthymine by p-chloranil was investigated by means of steady-state irradiation and laser-flash photolysis. Quantum yields for the monomerization are 0.34 for the cis,syn dimer, 0.39 for the trans,syn dimer, and much less than 10(-2) for the cis,anti isomer. Formation of the chloranil anion radical associated with quenching of triplet chloranil by the dimers demonstrates that electron transfer from dimers to triplet chloranil occurs to initiate the monomerization. Kinetic analysis suggested that the syn-dimer cation radicals undergo the ring cleavage at greater than or equal to 10(9) s-1 before escaping from the solvent cage, while the reactivity of the anti-dimer cation radical is very low. The different reactivities of the syn and anti dimer cation radicals are discussed in terms of through-bond coupling between the n orbitals of N(1) and N(1') involving the cyclobutane-ring sigma orbitals. In the cases of the syn-dimers, the sensitizer-dimer ion-radical pairs undergo the rapid geminate recombination that works as a major energy dissipating channel responsible for the lower-than-unity quantum yields. It has been found that the presence of Mg(ClO4)2 at 0.1 M enhances approximately 1.5 times either the monomerization of the syn dimers or the formation of the chloranil anion radical. A laser-flash photolysis study shows that Mg2+ forms a complex with either the triplet or the anion radical of chloranil. The net salt effects are attributed to the retardation of the rapid geminate recombination by the participation of Mg2+ in the sensitizer-dimer ion-radical pairs.

Chloranil↗
PubMed1990

Pharmacological differentiation of epithelium-derived relaxing factor from nitric oxide.

We examined the possibility that nitric oxide is one of the epithelium-derived relaxing factors in guinea pig airways. First we studied whether nitric oxide could relax isolated tracheal strips, and then we examined the effects of known inhibitors of endothelium-dependent relaxation (EDR) in the vascular system [hemoglobin, methylene blue, and NG-monomethyl-L-arginine (L-NMMA)] on epithelium-dependent relaxation (EpDR) induced by hyperosmotic stimuli in perfused whole tracheal preparations. Mannitol (160 mM in Krebs-Henseleit solution) applied to the epithelial surface was used as an osmotic stimulus to induce EpDR after carbachol-induced contraction (2 microM, serosal side). Nitric oxide produced concentration-dependent and complete relaxation of epithelium-denuded tracheal strips. Preincubation of the whole trachea with hemoglobin significantly inhibited osmotic-induced EpDR (P less than 0.05), but preincubation with methylene blue and L-NMMA did not. Hemoglobin introduced into the epithelial side after EpDR induced by hyperosmotic stimuli reversed relaxation, but methylene blue and L-NMMA did not. These results suggest that, although EpDR and vascular EDR have some pharmacological similarities and nitric oxide can relax airway smooth muscle, nitric oxide is not responsible for osmotic-induced EpDR.

Animals↗
PubMed1990

[The normal response process of the dynamic topography of pattern visual evoked potentials].

The dynamic topography of pattern visual evoked potentials (PVEPs) were studied in 20 normal subjects. PVEPs, recorded from 16 electrodes referenced to balanced non-cephalic electrode (BNE), were elicited by a binocular checkerboard pattern (15 min) that alternated at 1 Hz rate on a 14 x 8.5 degree TV monitor 1m distant from the eyes. N70, P100, N100, N150 and P200 components were recorded each time. In 65% of subjects the P100 components appeared in the lateral region in 120-150 msec. In flash VEP, the P100 component did not appear in the lateral region. Recorded on lateral electrodes, N100 components first appeared in the deep frontal region and gradually distributed throughout the frontal region while the P100 component was localized at the occipital pole. In the focused state, the peak latency of the N100 component was the same as that of the P100 component, but in the moderately defocused state, the peak latency of the N100 component was delayed compared with that of the P100 component. This study suggested that the appearance of the P100 component in the lateral region is related to form recognition, and that the N100 component is not the inverse dipole of the P100 component.

Adult↗
PubMed1989

Effect of starvation on nutrition and insulin secretion in pregnant rats and their fetuses.

Pregnancy is thought to create a metabolic condition of accelerated starvation. To clarify this idea, the effect of fasting on pregnant rats (day 21 of gestation) and their fetuses was examined. Although pregnancy significantly increased plasma insulin, plasma ketone body concentrations in fed pregnant rats were higher than those of age-matched fed virgin rats. After 48 hr fasting (i.e., fasting during days 19-21 of gestation), plasma insulin was markedly decreased in virgin rats compared with term pregnant rats, while ketone bodies were significantly higher in pregnant rats than in virgin rats. Body weight was lower in fetuses from fasted mothers than those from fed mothers. Starvation also markedly diminished the insulin response to glucose in isolated, perfused pancreases in both virgin and pregnant rats. The amount of insulin released during glucose stimulation was greater in pregnancy, and the inhibitory effect of 48 hr fasting on insulin release was greater in virgin rats than in pregnant rats. It is possible, therefore, that in term pregnant rats a decrease in insulin release caused by fasting may cause more profound catabolism than in nongravid rats.

Animals↗
PubMed1989

Subacute toxicity of (-)15-deoxyspergualin in BALB/c mice. I. Hematological study.

(-)15-Deoxyspergualin (DSP), a bacterial metabolite obtained from Bacillus laterosporus, was shown to effectively suppress autoantibody production in mice and alloimmune reaction in mice and rats. Its potential toxicity and safety margin in BALB/c mice were studied by administering the drug, 0.5-5.0 mg/kg body weight, s.c., 6 days/week for 3 months. The animals were weighted every two weeks, and their blood was drawn for hematological and liver function studies. Control animals showed a gradual increase in body weight from 17.8 +/- 1.1 g (SD) to 20.2 +/- 3.2 g during the 3 months of treatment. The body weight of 0.5 mg- and 2.5 mg-DSP group was not significantly different from that of the control group. In contrast, 5.0 mg-DSP group of animals showed significant decrease in their weight compared with the control after 5 weeks of treatment (P less than 0.01). They were then sacrificed. WBC in 0.5 mg-, 2.5 mg- and 5.0 mg-DSP groups were significantly lower compared with the control after 3 months of treatment. On the other hand, only 5.0 mg-DSP group showed significantly lower level in their RBC, Hb and Hct values (P less than 0.05). In contrast, platelet counts in 2.5 mg- and 5.0 mg-DSP group significantly increased. No manifest effect due to DSP on differential count of leukocytes was observed, although on day 92, a significant difference was shown in the stab cells of the 0.5 mg-DSP group and in the eosinophils in the 2.5 mg-DSP.(ABSTRACT TRUNCATED AT 250 WORDS)

Alanine Transaminase↗
PubMed1989

Subacute toxicity of (-)15-deoxyspergualin in BALB/c mice. II. Histopathological study.

Following the preceding report on hematological aspects in subacute toxicity of (-)15-deoxyspergualin (DSP), the present report dealt with the histopathological changes produced by DSP, 0.5-5.0 mg/kg, given to BALB/c mice for three months. At sacrifice, various internal organs such as heart, lungs, liver, spleen and kidneys, were taken, and their wet weights immediately measured. HE- or PAS-stained sections were histopathologically studied under light microscope. Additionally, frozen sections of the spleen were prepared to evaluate the effect of DSP on the lymphocyte surface markers like thy 1 and B220 by avidin-biotin complex (ABC) technique. Although the mean weights of lungs, liver, spleen and kidneys in the 0.5 mg- and 2.5 mg-DSP groups were not significantly different from those in the control animals, the weights of the heart, lungs, liver and spleen in the 5 mg-DSP group were significantly lower. Histopathological studies by light microscopy revealed no abnormalities in the heart, lungs, liver or kidneys taken from the mice given 0.5-5.0 mg/kg DSP. In contrast, significant changes were observed in the spleen and bone marrow of the 5.0 mg group of mice. Likewise, in the intestine of the 0.5-5.0 mg groups dose-dependent lesions, such as degeneration or disappearance of the mucosal epithelium, infiltration by inflammatory cells, and pseudo-membrane formation, was observed. By ABC technique, preferential decrease of B cells was seen in the splenic corpuscles of the DSP-treated mice. Histopathological changes due to DSP predominantly seen in the lymphoid and/or hematopoietic organs may be directly related to the immunosuppressive potency inherent to this drug.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Lupus nephropathy in New Zealand F1 hybrid mice treated by (-)15-deoxyspergualin.

The effect of (-)15-deoxyspergualin (15-dsp), a new immunosuppressant which was originally separated from the culture filtrate of a strain of Bacillus laterosporus, was evaluated in this study. Various doses of 15-dsp were subcutaneously administered to New Zealand black/white F1 hybrid mice (B/WF1) four times a week starting at 14 weeks of age, just prior to the onset of nephropathy. The life span of the treated animals, studied at 0.6 to 6.0 mg/kg body weights, compared with the control mice was significantly prolonged by 15-dsp treatment (percent survival of the treated mice at 50 to 70 weeks of age was significantly higher than that of the control mice, except that of the 0.6 mg group at 60 wks of age, P less than 0.05 by Fisher's exact test). In the 6.0 mg group of mice, complete suppression of spontaneously progressive splenomegaly with decreased total spleen cells was observed at 24 through 36 weeks of age compared with the same-aged control group of mice (P less than 0.01). Absolute numbers of L3T4+ splenocytes determined by flow cytometry, as well as L3T4+/Lyt2+ ratio, were decreased, while in vitro interleukin 2 production by splenocytes induced with staphylococcal enterotoxin A was significantly enhanced. Serum IgG anti-ds DNA antibody levels, measured by radioimmunoassay in the treated mice, were significantly lower at 24 through 36 weeks of age than those in the control mice (P less than 0.01), and the incidence of significant proteinuria (greater than or equal to 100 mg/dl) in the 15-dsp group was lower at both 32 and 36 weeks of age (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed1988

The presence of atrial natriuretic peptide in canine cerebrospinal fluid and its possible origin in the brain.

The presence of atrial natriuretic peptide (ANP) in canine cerebrospinal fluid (CSF) was clearly demonstrated and an attempt was made to determine its origin as either the brain or the atrium. The concentration of ANP in canine CSF was 0.78 +/- 0.37 pmol/l (n = 31) and showed no evident correlation with that in plasma (r = 0.12). Physiological doses of human alpha-ANP (alpha-hANP) were continuously infused intravenously into nine dogs, and ANP concentrations in CSF and plasma were examined six to eight times within a 120-min period following this. The ANP level in CSF was not influenced by the systemic administration of alpha-hANP up to 180 min. Only one low molecular weight peak corresponding to alpha-hANP could be obtained from the CSF samples, while both low and high molecular weight peaks were observed for plasma ANP by gel permeation chromatography. In the atrial and hypothalamic tissue extracts the same kinds of peaks were also evident. These results prove the presence of ANP in canine CSF and that it does not come from blood that has seeped across the blood-CSF barriers, but suggest that it may originate from the brain.

Animals↗