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Biomedical subjects

Y Moriyama

Publications and source records attributed to Y Moriyama.

At least 109 records · Page 6Linked to original sources
PubMed1999

Plasma level of homocysteine is correlated to extracranial carotid-artery atherosclerosis in non-hypertensive Japanese.

BACKGROUND: Results of some epidemiologic studies in Western countries have clarified that hyperhomocysteinemia is a plausible risk factor for atherosclerotic vascular disease, but its role in Japanese communities is not known. DESIGN: A community-based cross-sectional design. METHODS: We performed a cross-sectional study of 474 elderly men aged 60-74 years in two Japanese rural communities (Noichi in southwestern Japan and Ikawa in northeastern Japan). We examined the association between plasma concentrations of homocysteine and the maximum intima-media thickness (assessed by ultrasonography). RESULTS: The prevalence of thickening was 10.7% for the lowest tertile of homocysteine level and 21.1% for the highest tertile. For the subjects without hypertension, the odds ratio for having carotid intima-media thickening was 5.8; it was significantly higher for the highest tertile of homocysteine level than it was for the lowest after adjusting for age, hypercholesterolemia, hypoalphalipoproteinemia, diabetes, and smoking by using a multiple logistic regression model. However, its correlation was not evident for those with hypertension. CONCLUSIONS: High levels of plasma homocysteine are correlated to extracranial carotid artery atherosclerosis in elderly men without hypertension in Japanese rural communities.

Aged↗
PubMed1999

Inhibitory effects of H2-receptor antagonists on platelet function in vitro.

To evaluate in vitro inhibitory effects of four types of histamine H2-receptor antagonist (H2-receptor antagonists), famotidine, roxatidine, cimetidine and ranitidine, on platelet function, we examined aggregating potency and P-selectin levels with agonist-induced aggregation. Ranitidine and cimetidine inhibited, in concentration of 0.35 mM, the secondary aggregation induced by 5 microM adenosine diphosphate (ADP), the aggregation induced by 1 microg/mL collagen and 3 microM arachidonic acid. All of H2-receptor antagonists inhibited, in concentration of 1.4 mM, the aggregation induced by ADP, collagen and arachidonic acid. Ranitidine and cimetidine reduced markedly, in same concentration, P-selectin levels after induction of aggregation by 5 microm ADP, 1 microg/mL collagen and 3 microM arachidonic acid. When classified by the strength of inhibitory action, ranitidine and cimetidine were strong, followed by famotidine and roxatidine. It is considered that inhibitory effects of H2-receptor antagonists on platelet function are weaker than those of acetylsalicylic acid (ASA), since ASA inhibited platelet aggregation in concentration of 100 microM. No relationship was observed between inhibitory effects of H2-receptor antagonists on platelet aggregation induced by above agonists and the presence or absence of imidazole ring in the chemical structure.

Adenosine Diphosphate↗
PubMed1999

Cycloprodigiosin hydrochloride obtained from Pseudoalteromonas denitrificans is a potent antimalarial agent.

Cycloprodigiosin hydrochloride (cPrG*HCl) is a stable fluorescent red pigment obtained from the marine bacterium Pseudoalteromonas denitrificans. It was found that the compound was incorporated into Plasmodium falciparum cells upon incubation and exhibited a potent antimalarial activity with the concentration required for 50% of the activity being 11 nM, which is stronger than that of chloroquine, a well-known antimalarial agent. The compound did not affect growth rate of mammalian cells. Antimalarial activity of cPrG*HCl was also observed in vivo. These results indicate that cPrG*HCl is a potent antimalarial drug.

Animals↗
PubMed1999

[Effects of aging and hyperlipidemia on plasma osteopontin level].

In order to elucidate a possible mechanism for accelerated atherogenesis as well as enhanced vascular calcification observed during the normal aging process, we measured plasma osteopontin (OPN) levels and examined their relation to aging and certain disease parameters. In all cases examined, no significant relation was found between the plasma OPN level and age, body mass index, blood pressure, plasma levels of glucose and insulin, serum levels of creatinine, triglyceride, and high density lipoprotein cholesterol. On the other hand, a significant negative correlation was found between the plasma OPN level and serum total cholesterol concentration (n = 78, r = -0.355, p = 0.0014). The serum level of low density lipoprotein (LDL) cholesterol, calculated by the formula of Friedewald, also showed a significant negative correlation to the plasma OPN level (n = 78, r = -0.301, p = 0.0075). In cases without diabetes mellitus and hypertension, a significant positive correlation was found between the plasma OPN level and age (n = 22, r = 0.445, p = 0.0378). It is postulated that OPN plays a negative regulatory role in the development of vascular calcification. Therefore, the observed negative relationship between the plasma OPN level and the serum levels of total cholesterol and LDL cholesterol, suggests a possibility that hypercholesterolemia facilitates vascular calcification by suppressing OPN synthesis. On the other hand, in non-diabetic and normotensive cases, the positive relationship between the plasma OPN level and age may reflect a defense mechanism against age-related increase of vascular calcification.

Aging↗
PubMed1999

Effect of granulocyte-colony stimulating factor on empiric therapy with flomoxef sodium and tobramycin in febrile neutropenic patients with hematological malignancies. Kan-etsu Hematological Disease and Infection Study Group.

The clinical effects of concomitant use of granulocyte-colony stimulating factor (G-CSF) on empiric antibiotic therapy in febrile neutropenic patients were evaluated in a randomized fashion. Two hundred and fourteen neutropenic febrile episodes (neutrophil counts < 1.0 x 10(9)/l) were treated with flomoxef sodium and tobramycin with or without G-CSF. The resolution of fever at day 4 (excellent response) or at day 7 (good response) was deemed effective. Among 157 evaluable episodes, the observed excellent responses were 31 (38.8%) and the good responses were 20 (25.0%) in the G-CSF group; those in the control group were 26 (33.8%) and 25 (32.5%), respectively. The overall efficacy rate was 63.8% (51/80) in the G-CSF group and 66.2% (51/77) in the control group (not significant). The initial neutrophil count was 0.186 +/- 0.249 x 10(9)/l in the G-CSF group and 0.235 +/- 0.290 x 10(9)/l in the control group, and rose to 2.889 +/- 4.198 x 10(9)/l and 0.522 +/- 0.844 x 10(9)/l, respectively, at day 7. These results indicate that G-CSF does not affect the rate of response to empiric antibiotic therapy in febrile neutropenic patients, although a significant effect of G-CSF was observed on neutrophil recovery.

Adolescent↗
PubMed1999

[Ex vivo and in vivo purging for PBSCT].

Relapse due to either residual host disease or reinfused tumor cells remains the principal cause of treatment failure after autologous stem cell transplantation. It is very attractive to remove contaminated tumor cells from autologous grafts prior to transplant and many purging techniques including hyperthermia we developed, have been reported on this subject. However, there are only limited data suggesting that purging autografts have any favorable effect on relapses or disease-free survival. Drug-treated purging and CD34 positive cell selections that remove substantial numbers of T cells or destroy stem cells may have adverse effects such as delayed hematopoietic or T cell recovery. Therefore, there is a critical need for large, well-designed trials to re-evaluate ex vivo and in vivo purging effects on relapses and disease-free survival after autologous stem cell transplantation.

Animals↗
PubMed1999

Clinical experience of 473 patients with the omnicarbon prosthetic heart valve.

BACKGROUND AND AIM OF THE STUDY: The long-term clinical experience of patients receiving Omnicarbon heart valve prostheses between January 1985 and December 1996 was investigated. METHODS: In total, 473 patients (255 males, 218 females; mean age 57.5 +/- 10.1 years (range: 20n-73 years) received 523 prostheses. These included 253 mitral (MVR), 170 atrial (AVR) and 50 double (DVR) valve replacements. RESULTS: The 30-day mortality rate was 4.7% (n = 22); in addition eight patients died more than 30 days after surgery, but during the same hospital stay. Mean follow up was 3.9 years (maximum 11 years and 7 months). Cumulative follow up was 1,750.1 patient-years (pt-yr); follow up was 97.5% complete. Among 39 late deaths, 20 were valve-related (seven cerebral infarction, seven cerebral bleeding, six endocarditis) and four cardiac-related. The overall five-year cumulative survival rate (excluding early mortality) was 90.2 +/- 11.7% (MVR 88.0 +/- 2.5%, AVR 93.1 +/- 2.3%, DVR 93.7 +/- 4.8%). At 10 years, the overall survival rate was 76.4 +/- 7.7%. Valve-related complications included thromboembolism (n = 13, 0.7%/pt-yr), anticoagulation-related hemorrhage (n = 12, 0.7%/pt-yr) and endocarditis (n = 7, 0.4%/pt-yr). Neither mechanical failure nor clinical hemolysis was observed. The overall valve-related event-free rate after five years was 89.3 +/- 2.0% (MVR 89.8 +/- 2.4%, AVR 93.5 +/- 2.6%, DVR 89.4 +/- 5.7%) and after 10 years it was 87.6 +/- 2.6% (MVR 85.4 +/- 3.7%, AVR 93.5 +/- 2.6%, DVR 82.5 +/-10.1%). CONCLUSIONS: These long-term results with the Omnicarbon valve are excellent; especially satisfactory results were achieved in terms of the low rate of thromboembolic complication.

Adult↗
PubMed1998

Vitamin E administration improves impairment of endothelium-dependent vasodilation in patients with coronary spastic angina.

OBJECTIVES: We examined the effects of oral administration of vitamin E, an antioxidant, on endothelium-dependent vasodilation in patients with coronary spastic angina. BACKGROUND: We have recently reported that endothelium-dependent vasodilation is impaired in patients with coronary spastic angina (CSA). Furthermore, it is known that oxidative stress may play an important role in the impairment of endothelium-dependent vasodilation in cardiovascular diseases. METHODS: With the ultrasound technique, flow-dependent vasodilation of the brachial arteries during reactive hyperemia was examined before and after treatment for a month with either oral administration of vitamin E (alpha-tocopherol acetate, 300 mg/day) or placebo, which is randomly assigned, in patients with CSA (n=60). RESULTS: Before treatment, patients with CSA had impaired flow-dependent vasodilation, lower plasma levels of alpha-tocopherol and higher plasma levels of thiobarbituric acid reactive substances (TBARS), as compared with age- and sex-matched control subjects (n=60) (flow-dependent vasodilation: 3.1+/-1.8 vs. 7.1+/-2.5%, p < 0.001; alpha-tocopherol levels: 8.9+/-1.8 vs. 10.8+/-1.8 microg/ml, p < 0.001). In patients with CSA, treatment with vitamin E restored flow-dependent vasodilation (3.1+/-1.7 vs. 8.3+/-2.0%, p < 0.001), and this improvement was associated with the decreases in plasma TBARS levels and anginal attacks. CONCLUSIONS: The results indicate that vitamin E treatment improved endothelium-dependent vasodilation and decreased plasma TBARS levels in patients with CSA. Thus, increased oxidative stress may contribute to endothelial dysfunction and anginal attacks in patients with CSA.

Adult↗
PubMed1998

Acetylcholine triggers L-glutamate exocytosis via nicotinic receptors and inhibits melatonin synthesis in rat pinealocytes.

Rat pinealocytes, melatonin-secreting endocrine cells, contain peripheral glutaminergic systems. L-Glutamate is a negative regulator of melatonin synthesis through a metabotropic receptor-mediated inhibitory cAMP cascade. Previously, we reported that depolarization of pinealocytes by externally added KCl and activation of L-type Ca2+ channels resulted in secretion of L-glutamate by microvesicle exocytosis. What is unknown is how and what kinds of stimuli trigger glutamate exocytosis under physiological conditions. Here, we report that the nicotinic acetylcholine receptor can trigger glutamate exocytosis from cultured rat pinealocytes. Moreover, acetylcholine or nicotine inhibited norepinephrine-dependent serotonin N-acetyltransferase activity, which results in decreased melatonin synthesis. These activities were blocked by (2S,3S, 4S)-2-methyl-2-(carboxycyclopropyl)glycine, an antagonist of the metabotropic glutamate receptor. These results suggest that cholinergic stimulation initiates the glutaminergic signaling cascade in pineal glands and that parasympathetic neurons innervating the gland exert negative control over melatonin synthesis by way of the glutaminergic systems.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1998

D-aspartate modulates melatonin synthesis in rat pinealocytes.

It has been known that pinealocytes contain the highest level of D-aspartate among various neuroendocrine cells in the rat. Here, we report that exogenous D-aspartate strongly inhibited norepinephrine-dependent melatonin synthesis in the rat pineal gland, the concentration required for 50% inhibition being 75 microM. This inhibition was due at least partly to decreased norepinephrine-dependent serotonin N-acetyltransferase activity. Upon incubation, D-aspartate was gradually released from pinealocytes and accumulated in the incubation medium as determined by high-performance liquid chromatography on a Pirkle-type chiral column. These results suggest that D-aspartate acts as a negative regulator for melatonin synthesis in the pineal gland.

Animals↗
PubMed1998

Identification of D-aspartate in rat pheochromocytoma PC12 cells.

D-Aspartate is now known to be present in mammalian neuronal and endocrine cells in vivo, and may play some role(s) in neurocrine and endocrine functions. However, origin of D-aspartate is unknown. Here, we report that free D-aspartate (108 pmoles/3 x 10(7) cells) is present in the cultured PC12 cells, a rat pheochromocytoma cell line, as determined with immunohistochemical techniques as well as high performance liquid chromatography (HPLC) on a Pirkle-type chiral column. The amount of D-aspartate does not change with the passage. The culture medium does not contain D-aspartate. These results strongly suggest the presence of a de novo biosynthetic pathway for D-aspartate in the endocrine cells.

Animals↗
PubMed1998

Metabotropic glutamate receptors negatively regulate melatonin synthesis in rat pinealocytes.

Rat pinealocytes receive noradrenergic innervation that stimulates melatonin synthesis in a cAMP-mediated manner. In addition to melatonin, we showed previously that pinealocytes secrete L-glutamate through an exocytic mechanism. The released glutamate inhibits norepinephrine (NE)-dependent melatonin synthesis. Consistent with this observation, specific agonists of class II metabotropic glutamate receptors (mGluRs), including 1-(1S,3R)-aminocyclopentane-1,3-dicarboxylic acid (tACPD), inhibited NE-dependent melatonin synthesis, whereas agonists for other types of glutamate receptors did not. Furthermore, reverse transcription-PCR, Northern blotting, and immunohistochemistry analyses indicated expression of class II mGluR3 in pinealocytes. Inhibitory guanine nucleotide-binding protein (Gi) was also detected in pinealocytes. L-Glutamate or agonists of class II receptors decreased NE- or forskolin-dependent increase of cAMP and serotonin-N-acetyltransferase activities to similar extents. These effects were blocked by pertussis toxin or dibutyryl cAMP. These results indicate that the inhibitory cAMP cascade is involved in the glutamate-evoked inhibition of melatonin synthesis. We propose that the glutaminergic system negatively regulates NE-dependent melatonin synthesis in rat pinealocytes.

Animals↗
PubMed1998

Serial changes in plasma levels of soluble P-selectin in patients with acute myocardial infarction.

The present study examines whether an acute inflammatory response occurs during acute myocardial infarction (AMI) by measuring soluble P-selectin levels. We examined plasma soluble P-selectin levels in 16 consecutive patients with AMI, in 15 patients with angina, and in 13 control subjects with chest pain but normal coronary arteries and no coronary spasm. In patients with AMI, blood samples were obtained immediately after admission and at 1, 4, 24, and 48 hours, and 1 week after initiation of reperfusion therapy. The plasma soluble P-selectin levels were significantly higher in the AMI group on admission than in the other 2 groups (83 +/- 13 ng/ml, p < 0.01). The plasma soluble P-selectin levels at baseline were not significantly different between the angina and control groups (28 +/- 4 vs 24 +/- 5 ng/ml, p = NS). Plasma soluble P-selectin levels reached their peak significantly at 4 hours after initiation of the reperfusion therapy in patients with AMI. The peak level was significantly higher than the level on admission (115 +/- 17 vs 83 +/- 13 ng/ml, p < 0.05). The plasma soluble P-selectin levels were higher in the AMI group than in the angina and control groups over the time course (p < 0.01). Our data indicate that the plasma soluble P-selectin levels are increased in patients with AMI, and that the levels are increases after reperfusion therapy more than before reperfusion. We suggest that the increase in the plasma soluble P-selectin levels may be caused by the activation of endothelial cells and platelets after myocardial ischemia and reperfusion during AMI.

Aged↗
PubMed1998

Gain-of-function mutations of c-kit in human gastrointestinal stromal tumors.

Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumors in the human digestive tract, but their molecular etiology and cellular origin are unknown. Sequencing of c-kit complementary DNA, which encodes a proto-oncogenic receptor tyrosine kinase (KIT), from five GISTs revealed mutations in the region between the transmembrane and tyrosine kinase domains. All of the corresponding mutant KIT proteins were constitutively activated without the KIT ligand, stem cell factor (SCF). Stable transfection of the mutant c-kit complementary DNAs induced malignant transformation of Ba/F3 murine lymphoid cells, suggesting that the mutations contribute to tumor development. GISTs may originate from the interstitial cells of Cajal (ICCs) because the development of ICCs is dependent on the SCF-KIT interaction and because, like GISTs, these cells express both KIT and CD34.

Amino Acid Sequence↗
PubMed1998

Penetrating atherosclerotic ulcers in an abdominal aortic aneurysm: report of a case.

We report the case of a 74-year-old man found to have an extensive intramural hematoma (IMH) in the infrarenal abdominal aorta during a follow-up imaging study performed after repair of a DeBakey type II aortic dissection with an aortic arch true aneurysm. Enhanced computed tomographic scan and angiography revealed an extensive IMH and multiple penetrating atherosclerotic ulcers in the abdominal aorta. The patient underwent a successful replacement of the affected abdominal aorta using a collagen-impregnated woven Dacron graft. Atheromatous ulcers are known to occur frequently in patients with advanced atherosclerosis. Hence, the elderly hypertensive patient, being at high risk of developing a variety of aortic disorders, requires careful follow-up imaging studies to assess the aorta on a regular basis.

Aged↗