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Biomedical subjects

R Sone

Publications and source records attributed to R Sone.

26 records · Page 2Linked to original sources
PubMed1992

An improved method for measurement of sweat expulsions during profuse sweating.

We present an improved ventilated-capsule method of recording for clear sweat expulsion patterns using nitrogen gas as a carrier gas heated to promote sweat evaporation. With this method, sweat expulsion patterns were more clearly recorded than with the conventional ventilated-capsule method. Taking the derivatives of these recordings of sweating expulsions could eliminate slow fluctuation components in the patterns of sweating. The results indicate that this method is useful in providing more-accurate measurements of sweat expulsion frequencies during profuse sweating.

Adult↗
PubMed1992

[Pathological and immunohistochemical evaluation of keratoepithelioplasty in rats].

Keratoepithelioplasty was performed in the rat and epithelial rejection and epithelial regeneration were evaluated pathologically and immunohistochemically. A mechanical corneal epithelial defect was prepared in Lewis rats. Two lenticules, obtained from DA rats were grafted and postoperative observations were performed using a slit lamp microscope up to the 21st day. The same procedure was performed between Lewis rats only, as the control group (syngeneic model). Eyeballs were enucleated, and Hematoxylin-eosin (H-E) and Periodic Acid Shiff (PAS) staining were performed to allow observation by light microscopy. In addition, eyeballs were examined after staining by the Peroxidase-antiperoxidase (PAP) method using three kinds of monoclonal antibodies (W3/25, OX8 and OX6). Reepithelialization was completed by approximately postoperative day 6. Superficial keratitis occurred at postoperative day 10. Intense infiltration of helper T cells, cytotoxic T cells, Ia antigen positive cells, and neutrophils in the lenticules, regenerated epithelium, and beneath the regenerated epithelium was accompanied by rejection. On postoperative day 21, goblet cells were observed in the lenticules and its regenerated epithelial layer. There were no goblet cells in the lenticule and its regenerated epithelial layer of the control groups. Epithelial rejection began on the lenticular side, and rejected both the lenticules and the regenerated epithelium. The recovered corneal epithelium, migrated from the lenticules seemed to be replaced by regenerating conjunctival epithelium of the recipient.

Animals↗
PubMed1991

Inhibitory effects of prostanoids on the proliferation of transformed human epidermal cells in culture.

The cytotoxic action of various prostanoids was examined on a transformed human epidermal cell line (HSC-1), and methyl(5S,6S,7Z)-5,6-diacetoxy-7-((2S)-4-chloro-2-hydroxy-2-((2 Z+ ++)-2-octenyl)-5-oxo-3-cyclopentenylidene)heptanoate (YM-11), which is a punaglandin compound, was found to be most active. YM-11 exerted a dose-dependent inhibition of HSC-1 cell growth over 0.03 microM (0.01 micrograms/ml), and at 0.3 microM (0.1 micrograms/ml) its growth was completely inhibited. The IC50 value of YM-11 on HSC-1 cell growth was calculated as 0.15 microM (0.05 micrograms/ml). Methyl(E)-7-(5-chloro-2-hydroxy-2-octyl-5-oxo-3-cyclopentenylidene )heptanoate (YM-3), which is also a punaglandin derivative, showed remarkable cytotoxicity on HSC-1 cells with an IC50 of 0.24 microM (0.08 micrograms/ml). Concerning other cytotoxic prostaglandins (PGs), the IC50 values of delta 7-PGA1, delta 12-PGJ2 and PGD2 were 1.5 microM (0.5 micrograms/ml), 2.1 microM (0.75 micrograms/ml) and 5.7 microM (2 micrograms/ml), respectively. On the basis of the present data and previous in vitro and in vivo evidence, punaglandin derivatives may be useful antineoplastic agents for skin cancer.

Cell Division↗
PubMed1991

[Response of respiratory exchange ratio (R) to sinusoidal work load in humans].

An examination was made of the response of respiratory exchange ratio (R), carbon dioxide output (VCO2) and oxygen uptake (VO2) to sinusoidal work load with periods (T) of 1-16 min in six healthy men to determine whether R response is sinusoidal. The influence of the ratio of the amplitude of VCO2 to that of VO2 and the phase lag between them on R response was also studied by computer simulation. The results and conclusions obtained are as follows: 1) With decrease in the period, the amplitudes of VO2 and VCO2 dropped exponentially, becoming least at T of 1 min (T = 1 min). In contrast, the amplitude of R was largest at T = 4 min and subsequently decreased progressively. 2) The peak amplitude of R at T = 4 min can be explained by the larger phase lag and relatively low of amplitude of VCO2 to VO2. 3) The smallest amplitude of R at T = 1 min was due not to the ratio of amplitude or phase lag, but to remarkably smaller amplitudes of VO2 and VCO2. 4) The phase lag of VO2 to sinusoidal work load was smaller than that of VCO2. Phase lag of R was considerably larger than that of VO2 or VCO2. 5) The response curve of VO2 and VCO2 is a sinusoidal curve with the same period as exercise. However, the response of R is not a real sinusoidal but a deformed biphasic curve with a high crest and low trough. The deformity is determined by the phase lag between VO2 and VCO2 response and also the ratio of amplitude of VCO2 to that of VO2.

Adult↗
PubMed1989

Combination therapy with low-dose aspirin and ticlopidine in cerebral ischemia.

We compared combination therapy with low-dose aspirin plus ticlopidine to therapy with aspirin alone or ticlopidine alone in patients suffering transient ischemic attack or cerebral infarction. In 17, 24, and 23 patients, respectively, 300 mg/day aspirin, 200 mg/day ticlopidine, and 81 mg/day aspirin plus 100 mg/day ticlopidine were administered orally. Aspirin alone markedly inhibited platelet aggregation induced by arachidonic acid, partially inhibited platelet aggregation induced by adenosine diphosphate, and did not inhibit platelet aggregation induced by platelet activating factor. Ticlopidine alone inhibited platelet aggregation induced by adenosine diphosphate and platelet activating factor, but did not inhibit platelet aggregation induced by arachidonic acid. Combination therapy with aspirin plus ticlopidine markedly inhibited platelet aggregation induced by all three agonists. Plasma concentrations of beta-thromboglobulin and platelet factor 4 remained unchanged by aspirin alone, were slightly reduced by ticlopidine alone, and were markedly reduced by aspirin plus ticlopidine. Plasma concentration of thromboxane B2 was reduced by aspirin alone or with ticlopidine, but not by ticlopidine alone. The level of 6-ketoprostaglandin F1 alpha was reduced only by aspirin alone. Bleeding time was significantly prolonged by aspirin alone and by ticlopidine alone, although the greatest prolongation was produced by aspirin plus ticlopidine. Our results indicate that the combination of aspirin plus ticlopidine is a potent antiplatelet strategy, although the clinical importance of the changes observed need to be determined by a properly designed and controlled prospective study.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Glycogen storage disease confined to the heart with deficient activity of cardiac phosphorylase kinase: a new type of glycogen storage disease.

The case of a male infant with marked deposition of glycogen, confined to the heart, is presented. Clinically, prominent cardiomegaly had been evident from immediately after birth until the infant's death due to heart failure. There were no significant clinical manifestations in other organs, including liver and skeletal muscle, during the clinical course. Autopsy revealed abnormal deposition of normally structured glycogen in the heart, but no deposition in the liver, skeletal muscle, or other systemic organs. This unusual pattern of glycogen deposition was also confirmed by measurement of the glycogen content of each organ. This is the first report of glycogen storage disease confined to the heart. Enzymatic analysis revealed no decrease in the activities of acid maltase, amylo-1,6-glucosidase, and phosphorylase in the heart or in the liver or skeletal muscle. However, phosphorylase kinase activity was not detectable in the heart, although high activity levels were observed in the liver and skeletal muscle. In this case the inborn error of metabolism responsible for the isolated deposition of glycogen in heart muscle may have been due to a deficiency of cardiac phosphorylase kinase.

Cardiomyopathies↗