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H Ishimoto

Publications and source records attributed to H Ishimoto.

At least 37 records · Page 2Linked to original sources
PubMed1996

Mastoparan elicits prostaglandin E2 generation and inhibits inositol phosphate accumulation via different mechanisms in rabbit astrocytes.

The effects of mastoparan on phosphoinositide hydrolysis and prostaglandin E2 (PGE2) generation were investigated in astrocytes cultured from rabbit brain. Mastoparan inhibited the accumulations of [3H]inositol phosphates induced by bradykinin (1 microM) in a time- and concentration-dependent manner. Mastoparan (3-30 microM) also released PGE2 in a time- and concentration-dependent manner. Mastoparan-induced release of PGE2 was inhibited by indomethacin, a cyclooxygenase inhibitor, by dexamethasone, a steroidal anti-inflammatory drug, and by pertussis toxin, an inactivator of some G proteins, such as Gi and Go. Mastoparan also caused [3H]arachidonic acid liberation, which was inhibited by dexamethasone or pertussis toxin. In contrast, indomethacin, dexamethasone and pertussis toxin failed to attenuate mastoparan-induced inhibition of [3H]inositol phosphate accumulation induced by bradykinin. Thus, mastoparan-induced inhibition of phosphoinositide hydrolysis does not involve pertussis toxin-sensitive G protein nor arachidonic acid metabolites. In addition to the inhibition of phospholipase C, mastoparan activates phospholipase A2 through pertussis toxin-sensitive G protein.

Animals↗
PubMed1996

A comparative study of arachidonic acid metabolism in rabbit cultured astrocytes and human astrocytoma cells (1321N1).

1. ATP, bradykinin (BK), and A-23187 activated the generation of prostaglandin (PG) E2 and thromboxane (TX) B2 in rabbit astrocytes, but not in human astrocytoma cells (1321N1). 2. In human astrocytoma cells, ATP, BK, and A-23187 could not release [3H]arachidonic acid (AA) from [3H]AA-labeled cells and exogenous AA was not converted to TXB2 and PGE2, suggesting the lack of phospholipase (PL) A2 and cyclooxygenase activities in 1321N1 human astrocytoma cells, although they express TXA2 receptors. 3. In rabbit astrocytes, ATP and BK, but not A-23187, showed increased accumulation of inositol phosphates, indicating that an increase in intracellular Ca2+ concentration alone would not be enough to activate PLC. Furthermore, indomethacin, a cyclooxygenase inhibitor, partially attenuated ATP-induced phosphoinositide hydrolysis, indicating that cyclooxygenase product(s) would secondarily activate PLC in response to ATP.

Adenosine Triphosphate↗
PubMed1995

Gq/11 communicates with thromboxane A2 receptors in human astrocytoma cells, rabbit astrocytes and human platelets.

Western blot analysis was performed to clarify the presence of trimeric G protein subfamily in membranes derived from human astrocytoma cells (1321N1), cultured rabbit astrocytes and human platelets, using G protein antisera GS alpha, Gi alpha, Gq/11 alpha, and G beta were found to exist in membranes derived from human astrocytoma cells and rabbit astrocytes as well as human platelets. However, only small amount of G(o) alpha was detected in any membranes. Gq/11 alpha was expressed much more in human platelets than in human astrocytoma cells or rabbit astrocytes. 9,11-Epithio-11,12-methanothromboxane A2 (STA2), a stable analogue of thromboxane A2 (TXA2), activated GTPase in membranes derived from human astrocytoma cells, rabbit astrocytes and human platelets with different potencies. STA2-induced GTPase activation in human platelet membranes was partly inhibited by treatment with QL antibody at 0 degrees C for 90 min. Furthermore, STA2-induced GTPase activation in membranes derived from human astrocytoma cells and rabbit astrocytes were potently inhibited by treatment with QL antibody. The results obtained indicate that TXA2 receptors in human astrocytoma cells and rabbit astrocytes communicate with Gq/11 as well as in human platelets.

Animals↗
PubMed1995

Extracellular ATP stimulates adenylyl cyclase and phospholipase C through distinct purinoceptors in NG108-15 cells.

In neuroblastoma x glioma hybrid NG108-15 cells, ATP induced a concentration-dependent increase in the intracellular Ca2+ concentration ([Ca2+]i), accompanied by inositol phosphate formation. Under the same conditions, we found a marked increase in cAMP levels produced by ATP at concentrations similar to those required to increase [Ca2+]i. The Ca2+ ionophore A23187 or bradykinin, which evoked inositol phosphate formation and increases in [Ca2+]i, did not increase, and instead slightly decreased, cAMP content, indicating that ATP-induced cAMP accumulation was not due to activation of Ca(2+)-sensitive adenylyl cyclase. The effect of ATP on cAMP production was not dependent on generation of adenosine caused by ATP hydrolysis. Among several P2 purinoceptor agonists, adenosine-5'-O-(3-thio)triphosphate, 5'-adenylylimidodiphosphate, and adenosine-5'-O-(2-thio)diphosphate evoked both cAMP accumulation and Ca2+ mobilization. In contrast, beta,gamma-methylene-ATP selectively elicited cAMP accumulation, whereas 2-methylthio-ATP and UTP induced only Ca2+ mobilization, without affecting cAMP levels. The potent P2x purinoceptor agonist alpha,beta-methylene-ATP did not induce cAMP accumulation or Ca2+ mobilization. The cAMP accumulation induced by ATP was not affected by the P2 receptor antagonist suramin but was inhibited by P1 receptor antagonists such as 8-(p-sulfophenyl)theophylline, 3-isobutyl-1-methylxanthine, and xanthine amine congener. However, the ATP-induced increase in [Ca2+]i was not affected by suramin or xanthine amine congener. Taken together, these results indicate that ATP activates two distinct purinoceptors that are coupled to different signal transduction systems, one being adenylyl cyclase and the other phospholipase C, in NG108-15 cells. Furthermore, pharmacological profiles of the adenylyl cyclase-coupled receptor were quite different from those of any known purinoceptor subtypes, especially in the unusual sensitivity of the receptor to P1 and P2 receptor agonists and antagonists. It is therefore suggested that ATP-induced cAMP accumulation may be mediated by a novel subtype of purinoceptor in NG108-15 cells.

Adenosine↗
PubMed1994

Experimental growth retardation produced by transient period of uteroplacental ischemia in pregnant Sprague-Dawley rats.

OBJECTIVE: Introduction of experimental growth retardation, which was based on the hypothesis of uteroplacental postischemic hypoperfusion, was attempted by a transient period of uteroplacental ischemia in dated-pregnant Sprague-Dawley rats. STUDY DESIGN: On day 17 of gestation right uterine horn circulation was occluded for 5 to 60 minutes in 35 dams. The fetuses were delivered by cesarean section and studied on day 21 of gestation. For each experiment the fetuses in the right horn served as the ischemia group and those in the left horn were used as the control group. RESULTS: Statistical analysis by Wilcoxon signed-rank test demonstrated a significant decrease in the fetal weights and in the liver-to-body weight ratios, in contrast to an increase in the brain-to-body weight ratios in the 60-minute ischemia group, compared with those in the control group. This ischemia resulted in a 14% incidence of fetal deaths. CONCLUSION: Ischemia of a single uterine horn circulation in pregnant rat for 60 minutes should readily serve as a suitable model for asymmetric intrauterine growth retardation.

Animals↗
PubMed1994

Dual effects of mastoparan on intracellular free Ca2+ concentrations in human astrocytoma cells.

1. The effect of mastoparan, a wasp venom toxin, on intracellular free Ca2+ concentration ([Ca2+]i) was examined in human astrocytoma cells. Mastoparan inhibited [Ca2+]i induced by carbachol (100 microM) in a concentration-dependent manner in the absence of extracellular Ca2+, consistent with our previous results showing that mastoparan inhibits phosphoinositide hydrolysis in human astrocytoma cells. 2. In contrast, mastoparan itself increased [Ca2+]i and augmented carbachol-induced increase in the [Ca2+]i in the presence of extracellular Ca2+, suggesting that mastoparan elicited Ca2+ influx from the extracellular medium. The increase appeared to be maximum at extracellular Ca2+ concentrations of 0.1-0.2 mM. The higher concentrations of extracellular Ca2+ depressed the influx. 3. Pertussis toxin did not affect mastoparan-induced inhibition of [Ca2+]i in the absence of extracellular Ca2+, consistent with the previous results that pertussis toxin did not affect mastoparan-induced inhibition of phosphoinositide hydrolysis. 4. Pertussis toxin augmented mastoparan-induced increase in [Ca2+]i in the presence of extracellular Ca2+, suggesting that pertussis toxin substrate(s) seems to be inhibitory for Ca2+ influx induced by mastoparan. 5. Verapamil, nifedipine and diltiazem (each 10 microM), L-type Ca2+ antagonists, did not affect mastoparan-induced Ca2+ influx. However, verapamil (10 microM) slightly inhibited the increase in [Ca2+]i induced by carbachol in the presence of mastoparan. 6. The results obtained in the present study indicate that mastoparan has two opposite effects on [Ca2+]i in human astrocytoma cells and possibly has at least two sites of action.

Astrocytoma↗
PubMed1994

[Relation of gestational age, maternal body weight and age or serum alpha-fetoprotein and human chorionic gonadotropin at second-trimester].

Serum levels of alpha-fetoprotein (AFP) and human chorionic gonadotropin (hCG) were measured in serum samples of 1,964 pregnant Japanese women whose gestational age and singleton pregnancy were confirmed by ultrasound examination during the first trimester of pregnancy. Statistical analysis of log-linear regression to calculate multiples of the median (MoM) was accomplished by the SAS statistical method. The levels of the two analytes noticeably decreased as maternal body weight increased. However, maternal age did not have a significant effect on either of them. The MoM formulae were as follows: MSAFPMoM = AFP/exp(0.861 + 0.0685 x gestational age(weeks) - 0.00572 x body weight(kg)). MShCGMoM = hCG/exp(6.12 - 0.787 x gestational age(weeks) - 0.00613 x body weight(kg)). Gestational age and maternal body weight should be considered as regression functions for the adjustment of serum levels in risk estimation of fetal anomalies and fetal demise in Japan.

Adult↗
PubMed1994

[Screening for adverse perinatal outcome by biomarkers in maternal serum; a comparison of elevated maternal serum alpha-fetoprotein versus human chorionic gonadotropin].

We conducted a cohort analytic study to determine whether an unexplained increase in maternal serum alpha-fetoprotein (MSAFP) or human chorionic gonadotropin (MShCG) is effective in screening for adverse perinatal outcomes. MSAFP and MShCG levels were measured in 1,097 consecutive pregnant women in whom gestation was dated by ultrasonography and who later delivered a single infant. Patients with high MSAFP or MShCG had a much higher risk of low birth weight, intrauterine growth retardation and fetal death. But a screening test with MShCG for predicting preterm birth, low birth weight and intrauterine growth retardation had an approximately twice higher sensitivity than that with MSAFP. A combination of MSAFP and MShCG had little effect on the sensitivity. We concluded that a screening test with MShCG alone might be useful in predicting adverse perinatal outcomes.

Biomarkers↗
PubMed1994

Epidemiological study on relationship between breast cancer mortality and dietary factors.

To elucidate the effects of nutritional factors on regional differences in breast cancer mortality in Japan, the statistical analysis was made using the results of the national nutrition surveys in 12 districts from 1966 to 1980 and age-adjusted mortality from breast cancer from 1966 to 1990. The correlation analysis between food or nutrient intake and breast cancer mortality was performed with a fixed time lag of 10 years. Dietary factors such as wheat, milk, meats, animal fat, animal protein, total fat, saturated fatty acid (SF) and monounsaturated fatty acid (MUF) were correlated highly positively with breast cancer mortality. The correlation analysis between increase rates in age-adjusted mortality from breast cancer and increase rates in food or nutrient intake was also examined. Highly positive correlations were obtained between breast cancer mortality and following dietary factors; oils and fats, fruits, milk, total fat, vegetable fat, SF, MUF and n-6 polyunsaturated fatty acid. Factor analysis using fat intake by 12 districts revealed the factor representing the intake of fat component resulting from ingestion of animal fat. This factor showed a positive correlation with age-adjusted mortality from breast cancer. The findings suggested that the dietary factors due to intake of Westernized meals, especially SF had the effect on breast cancer mortality in Japan.

Adult↗
PubMed1993

Incidence of anemia in women in fishing villages.

Studies were made on the incidence of anemia among women in fishing villages in Tokushima prefecture. In 839 women in the fishing villages, the mean values for hemoglobin (Hb) and the hematocrit (Ht) were 12.5 +/- 1.3 g/dl and 37.9 +/- 3.3%, respectively, and the incidence of anemia was 20.1%. The incidence of anemia was high in elderly women. In 158 women in the fishing villages, the mean serum level of iron was 80.0 +/- 41.6 micrograms/dl and the incidences of iron deficiency anemia in the women with serum iron levels of under 50 and 70 micrograms/dl were as high as 25.9 and 41.1%, respectively. Almost all women with Hb values of under 11.0 g/dl had iron-deficiency anemia. The mean values for the total iron binding capacity (TIBC), unsaturated iron binding capacity (UIBC) and percentage iron saturation, were 365.6 +/- 65.1, 286.3 +/- 92.8 micrograms/dl and 23.3 +/- 13.0%, respectively. The incidence of anemia was 40.0% in the women with percentage iron saturation value of under 20%.

Adult↗
PubMed1993

Influence of living conditions on the incidence of anemia and effects of health guidance and diet supplementation on recovery from anemia of women in fishing villages.

Studies were made on the relationship between the incidence of anemia and living conditions of women in fishing villages in Tokushima prefecture, and also on the effects of health guidance and supplementation of the diet with iron enriched food on recovery from anemia. With regard to economic conditions, Hb values were found to be higher in women who spent more money on food and who had much leisure time compared with working hours. With regard to diet, Hb values were higher in women with higher intakes of animal protein and vitamin C. Intake of vitamin C was significantly higher in a group with hemoglobin value of over 12.0 g/dl than in a group with hemoglobin value of under 12.0 g/dl. The cumulative recovery rate from anemia of women receiving health guidance was 61.5% and the cumulative recovery rate from anemia of women receiving Tsukudani (a preparation of small dried sardines) enriched with iron for 60 to 105 days (30 to 75 mg iron per day: average 59.3 mg per day) was 53.3%. But the recovery rate of serum iron was lower than those of Hb and Ht, being about 40% on the average.

Adult↗
PubMed1993

Fetal growth in patients with elevated maternal serum hCG levels.

OBJECTIVE: To determine the relationship between maternal serum hCG levels and small for gestational age (SGA) infants. METHODS: Maternal serum hCG levels were measured in 638 consecutive pregnant women in whom gestation was dated by crown-rump length and who later delivered a singleton infant. Fetal growth was compared between the women with elevated maternal hCG (above 2 multiples of the median) and those with normal levels. RESULTS: Elevated maternal hCG values were found in 6.6%, of whom 19% delivered SGA infants. In the normal maternal hCG group, 3.9% of the infants were SGA. These differences were statistically significant by chi 2 analysis. Mothers with elevated hCG also had a significantly higher risk for fetal death, preterm rupture of the membranes, and abruptio placentae by the Fisher exact probability test. CONCLUSION: Elevated maternal serum hCG levels correlate with SGA infants.

Adult↗
PubMed1992

The presence of thromboxane A2 receptors in cultured astrocytes from rabbit brain.

We have previously shown that human astrocytoma cells (1321N1) express thromboxane A2 (TXA2) receptors, of which stimulation activates phosphoinositide hydrolysis (Nakahata et al., Eur. J. Pharmacol. 162 (1989) 407). In order to examine whether TXA2 receptors exist in native astrocytes or not, rabbit cultured astrocytes were used. Glial fibrillary acidic protein (GFAP)-positive astrocytes were obtained three weeks after culture of brain. [3H]ONO NT-126, a TXA2 antagonist, bound to the membranes derived from cultured rabbit astrocytes with the dissociation constant (Kd) of 0.23 nM and the maximum binding site (Bmax) of 69.5 fmol/mg protein. STA2, a stable TXA2 receptor agonist, activates phosphoinositide hydrolysis in a concentration-dependent manner, and S-145, a TXA2 antagonist, inhibited STA2-induced phosphoinositide hydrolysis. The results indicate that TXA2 receptors exist in cultured rabbit astrocytes and the activation of TXA2 receptors results in phosphoinositide hydrolysis.

Animals↗
PubMed1992

Intravascular pancuronium bromide infusion for prenatal diagnosis of twin-twin transfusion syndrome.

The diagnosis of twin-twin transfusion syndrome remains a problem. Intravascular infusion of pancuronium bromide, a nondepolarizing neuromuscular blocking agent, for the smaller of a set of twins demonstrated paralysis of both twins in one case. However, in a second case, paralysis was shown only in the smaller twin who demonstrated no transplacental vascular communications postnatally. We suggest that infusion of pancuronium bromide, 'pancuronium test', is a simple and safe method for confirming transplacental communications and aids in the diagnosis of twin-twin transfusion syndrome.

Adult↗