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M Yoshimura

Publications and source records attributed to M Yoshimura.

At least 163 records · Page 9Linked to original sources
PubMed1999

Effect of 13-hydroperoxyoctadecadienoic acid on the supply of arachidonic acid for prostaglandin synthesis from arachidonoyl-CoA mediated by the cytosolic or microsomal acyl-CoA hydrolase in rabbit kidney medulla.

The effects of 13-hydroperoxyoctadecadienoic acid (13-HPODE) on the cytosolic or microsomal acyl-CoA hydrolase (ACH) activity in rabbit kidney medulla and on the ACH-mediated prostaglandin (PG) formation from arachidonoyl-CoA (AA-CoA) were examined. 13-HPODE (10, 20, and 50 microM) had no effect on the cytosolic ACH activity but significantly inhibited the activity of the microsomal enzyme (43-57% inhibition). PG formation was measured as follows: AA-CoA (20 nmol) was preincubated with the cytosolic or microsomal fraction (as the source of ACH) in the presence or absence of 13-HPODE for 5 min at 37 degrees C, followed by incubation with the microsomal fraction (as the source of PG-synthesizing enzymes), hydroquinone and reduced glutathione for 5 min at 37 degrees C, and the PGs formed were measured by HPLC, with use of 9-anthryldiazomethane for derivatization. 13-HPODE reduced the PG formation when the microsomal fraction, but not the cytosolic fraction, was used as the source of ACH (10, 20, and 50 microM; 28-55% inhibition). These results suggest that 13-HPODE may modulate PG levels in rabbit kidney medulla by inhibiting the microsomal ACH activity.

Acyl Coenzyme A↗
PubMed1999

Bovine milk antibodies against cell surface protein antigen PAc-glucosyltransferase fusion protein suppress cell adhesion and alter glucan synthesis of Streptococcus mutans.

Cell surface protein antigen (PAc) and glucosyltransferases (GTF) produced by Streptococcus mutans are considered major colonization factors of the organism, and the inhibition of these factors is thought to prevent dental caries. In this study, 8-mo-old pregnant Holstein cows were immunized with fusion protein PAcA-GB, a fusion of the saliva-binding alanine-rich region (PAcA) of PAc with the glucan binding (GB) domain of GTF-I, an enzyme catalyzing the synthesis of water-insoluble glucan from sucrose. High titers of immunoglobulin antibodies specific for the fusion protein were found in normal milk after reimmunization, and they persisted for approximately 3 mo. The immunoglobulin G (IgG) antibodies against PAcA-GB were purified from immunized milk. The antibodies significantly inhibited the adhesion of S. mutans cells to saliva-coated hydroxyapatite beads. IgG antibodies purified from immunized milk also inhibited total glucan synthesis by cell-associated GTF preparation and GTF-I from S. mutans. The immunized milk may be useful as a means of passive immunization for the prevention of dental caries in humans.

Animals↗
PubMed1999

Role of pleural lavage cytology before resection for primary lung carcinoma.

OBJECTIVE: To investigate the role of pleural lavage cytology (PLC) in resection for primary lung carcinoma. SUMMARY BACKGROUND DATA: The prognostic significance of PLC before manipulation is still controversial. METHODS: Cytology of pleural lavage immediately after thoracotomy but before any manipulation of the lung was examined in 500 consecutive patients with lung cancer with no pleural effusion who underwent pulmonary resections. Eighteen patients who already had pleural dissemination were excluded from this study. RESULTS: Eighteen of 482 patients (3.7%) had positive cytologic findings. The positivity of PLC was significantly correlated with histology, extension of tumor to pleura, and presence of lymphatic permeation or vascular involvement by tumor. Positive lavage findings were seen only in adenocarcinoma. Because 6.3% of the patients with adenocarcinoma had positive cytologic findings, it is vital to perform PLC before curative resections for lung cancer, especially adenocarcinoma. The 5-year survival rates of the patients having negative and positive lavage findings were 52.9% and 14.6%, respectively. The prognosis of the patients with positive lavage findings was as poor as that of the patients with stage IIIB disease and that of the patients with malignant effusion. CONCLUSIONS: Positive findings on PLC indicate exfoliation of cancer cells into the pleural cavity, which is an essential prognostic factor. In addition, we should regard positive cytologic findings as a subclinical malignant pleural effusion that is pathologic stage T4.

Bronchoalveolar Lavage↗
PubMed1999

Enhancement of constrictor response of spastic coronary arteries to acetylcholine but not to phenylephrine in patients with coronary spastic angina.

This study examined the direct response of smooth muscle of coronary spasm sites to alpha1-adrenergic stimulation in patients with coronary spastic angina. Phenylephrine (1 microM in the coronary circulation, for 5 min), a stimulator of alpha1-adrenoreceptors, was directly infused into coronary arteries with spasm in 10 patients with coronary spastic angina and into normal coronary arteries in 10 control patients. The luminal diameter of epicardial coronary arteries was determined by computer-assisted quantitative angiography. The constrictor response to intracoronary injection of acetylcholine (ACh; 50 microg) was greater in spastic arteries than in control arteries (decrease from baseline, 48+/-2% vs. 12+/-2%, respectively; p<0.001). ACh (50 or 100 microg) induced coronary spasm associated with myocardial ischemia in all of patients with coronary spastic angina but not in any control patients. On the other hand, phenylephrine infusion did not induce coronary spasm in any of patients with coronary spastic angina or in control subjects. The constrictor response to phenylephrine infusion was comparable between spasm and control coronary arteries (decrease from baseline, 11+/-2% vs. 9+/-2%, respectively; p = NS). The results indicate that smooth muscle of spastic coronary arteries does not exhibit enhancement of constrictor response to direct stimulation of alpha1-adrenoreceptor on coronary smooth muscle. There may be receptor-specific enhancement of constrictor response to agonists in smooth muscle of spastic coronary arteries in patients with coronary spastic angina.

Acetylcholine↗
PubMed1999

EP receptor-mediated inhibition by prostaglandin E(1) of cardiac L-type Ca(2+) current of rabbits.

Prostaglandin E(1) (PGE(1)) has cardioprotective effects on the ischemic-reperfused heart. To clarify the mechanisms underlying the protective action of PGE(1) on myocardium, we examined the effect of PGE(1) on the L-type Ca(2+) current (I(Ca)) using single atrial cells from rabbits. PGE(1) did not show a significant effect on basal I(Ca) but inhibited the I(Ca) prestimulated by isoproterenol (Iso, 30 nM). This inhibition was concentration dependent (EC(50) = 0.027 microM). Both sulprostone, a specific PGE receptor subtype (EP(1) and EP(3)) agonist, and 11-deoxy-PGE(1), an EP(3) agonist, inhibited the Iso-stimulated I(Ca), similar to PGE(1). Pretreatment with pertussis toxin (PTX) abolished the PGE(1) inhibition of I(Ca). Both the application of forskolin plus IBMX and intracellular dialysis with 8-bromoadenosine 3',5'-cyclic monophosphate eliminated the effect of PGE(1). PGE(1) did not show any further inhibition of I(Ca) when the effect of Iso was almost fully antagonized by acetylcholine. Methylene blue (guanylate cyclase inhibitor), KT-5823 (cGMP-dependent protein kinase inhibitor), and erythro-9-(2-hydroxy-3-nonyl)adenine (type II phosphodiesterase inhibitor) did not significantly change the inhibitory effect of PGE(1). These findings suggest that 1) PGE(1) inhibits Iso-stimulated I(Ca) by binding to the EP(3) receptor and 2) the PTX-sensitive and cAMP-dependent pathway is involved in the PGE(1) inhibition of I(Ca), but the nitric oxide-cGMP-dependent pathway is not. The PGE(1)-induced antiadrenergic effect shown in this study may contribute to the PGE(1) protection of myocardium against ischemia.

Adrenergic beta-Agonists↗
PubMed1999

Regulation of brain renin-angiotensin system by benzamil-blockable sodium channels.

Changes in the renin-angiotensin system (RAS) mRNAs in the brain and the kidney of rats after administration of DOCA and/or sodium chloride were assessed by use of a competitive PCR method. Benzamil, a blocker of amiloride-sensitive sodium channels, was infused intracerebroventricularly or intravenously for 7 days in DOCA-salt or renal hypertensive rats, and the effects of benzamil on the brain RAS mRNAs were determined. Renin and ANG I-converting enzyme (ACE) mRNAs were not downregulated in the brain of rats administered DOCA and/or salt; however, these mRNAs were decreased in the kidney. Intracerebroventricular infusion of benzamil decreased renin, ACE, and ANG II type 1 receptor mRNAs in the brain of DOCA-salt hypertensive rats but not in the brain of renal hypertensive rats. The gene expression of the brain RAS, particularly renin and ACE, is regulated differently between the brain and the kidney in DOCA-salt hypertensive rats, and benzamil-blockable brain sodium channels may participate in the regulation of the brain RAS mRNAs.

Amiloride↗
PubMed1999

Serum hepatocyte growth factor levels in patients with renal diseases.

The serum levels of hepatocyte growth factor (HGF) were determined in patients with various renal diseases. In patients with acute-phase acute renal failure (ARF) and chronic tubulointerstitial nephritis (chronic TIN), the serum HGF levels were 0.55 +/- 0.24 and 0.44 +/- 0.37 ng/ml (mean +/- SD), respectively, and were significantly higher than that in the control group (0.12 +/- 0.12 ng/ml). The serum HGF level tended to be high also in patients with active-phase steroid-sensitive nephrotic syndrome (SSNS). The serum levels of HGF were not elevated in patients with IgA nephropathy (IgAN), Henoch-Schönlein purpura nephritis (HSPN), membranoproliferative glomerulonephritis (MPGN), poststreptococcal acute glomerulonephritis (PSAGN), unilateral renal atrophy, unilateral nephrectomy, or proximal tubular dysfunction. These observations suggest that glomerular disorders cause no apparent elevation of the serum HGF level, and that elevation of the serum HGF level may be associated with tubulointerstitial damage in renal diseases.

Adolescent↗
PubMed1999

Increased vitreous concentrations of human hepatocyte growth factor in proliferative diabetic retinopathy.

Human hepatocyte GF (hHGF) has strong neoangiogenesis activity. The present study was designed to investigate the possible involvement of hHGF in neovascularization in proliferative diabetic retinopathy (PDR) by measuring vitreous hHGF concentrations. The mean vitreous hHGF concentration was higher in subjects with PDR (5.70 +/- 0.68 ng/mL, n = 33) than in nondiabetic control subjects (1.50 +/- 0.20 ng/mL, n = 18, P < 0.01), nondiabetic subjects with proliferative vitreoretinopathy (3.31 +/- 0.57 ng//mL, n = 10, P < 0.05), or diabetic subjects without PDR (1.29 +/- 0.28 ng/mL, n = 8, P < 0.01). PDR subjects with neovascularization of iris, which suggests advanced retinal ischemia, showed a higher mean vitreous hHGF concentration than those without iridal neovascularization [7.33 +/- 1.16 ng/mL (n = 14) vs. 4.49 +/- 0.72 ng/mL (n = 19), P < 0.05]. The mean vitreous hHGF concentration was higher in PDR subjects with retinal neovascularization at the optic disc than in those with neovascularization elsewhere [7.3 +/- 1.1 ng/mL (n = 15) vs. 4.4 +/- 0.7 ng/mL (n = 18), P < 0.05]. Our results indicate that vitreous hHGF may play a role in retinal neovascularization in PDR.

Aged↗
PubMed1999

Serum hepatocyte growth factor as a possible indicator of vascular lesions.

To investigate the role of human hepatocyte growth factor (hHGF) in vascular lesions associated with endothelial injury, we measured serum hHGF concentrations in subjects with retinal arteriosclerosis, coronary atherosclerosis, or arteriolitis due to Henoch-Schönlein purpura. Individuals with more advanced grades of retinal arteriosclerosis showed higher serum hHGF concentrations [grade 0, 0.053+/-0.005 ng/mL (n = 68); grade 1, 0.144+/-0.022 ng/mL (n = 21; P<0.01 vs. grade 0); grade 2, 0.338+/-0.036 ng/mL (n = 20; P<0.01 vs. grade 0 or 1); grade 3, 0.526+/-0.051 ng/mL (n = 9; P<0.01 vs. grade 0, 1, or 2)]. Patients with active arteriolitis due to Henoch-Schönlein purpura showed higher (P<0.01) serum hHGF concentrations (0.347+/-0.038 ng/mL; n = 14) than those in the remission phase (0.097+/-0.017 ng/mL; n = 19). Mean serum hHGF concentrations were higher in subjects with coronary atherosclerosis than in those without, but a significant overlap in serum hHGF concentrations was found between subjects with and those without coronary atherosclerosis. Serum hHGF may be an indicator of the presence or development of arteriolar lesions.

Aged↗
PubMed1999

Effects of the central pair apparatus on microtubule sliding velocity in sea urchin sperm flagella.

To produce oscillatory bending movement in cilia and flagella, the activity of dynein arms must be regulated. The central-pair microtubules, located at the centre of the axoneme, are often thought to be involved in the regulation, but this has not been demonstrated definitively. In order to determine whether the central-pair apparatus are directly involved in the regulation of the dynein arm activity, we analyzed the movement of singlet microtubules that were brought into contact with dynein arms on bundles of doublets obtained by sliding disintegration of elastase-treated flagellar axonemes. An advantage of this new assay system was that we could distinguish the bundles that contained the central pair apparatus from those that did not, the former being clearly thicker than the latter. We found that microtubule sliding occurred along both the thinner and the thicker bundles, but its velocity differed between the two kinds of bundles in an ATP concentration dependent manner. At high ATP concentrations, such as 0.1 and 1 mM, the sliding velocity on the thinner bundles was significantly higher than that on the thicker bundles, while at lower ATP concentrations the sliding velocity did not change between the thinner and the thicker bundles. We observed similar bundle width-related differences in sliding velocity after removal of the outer arms. These results provide first evidence suggesting that the central pair and its associated structures may directly regulate the activity of the inner (and probably also the outer) arm dynein.

Adenosine Triphosphate↗
PubMed1999

Significance of exercise QT dispersion in patients with coronary artery disease who do not have exercise-induced ischemic ST-segment changes.

The poor sensitivity and the poor predictive value of ST-segment depression have limited the usefulness of the exercise electrocardiogram (ECG) in the diagnosis and evaluation of coronary artery disease (CAD). The QT dispersion (QTD), recorded as the difference between maximal and minimal QT intervals on a 12-lead exercise ECG, is sensitive to myocardial ischemia and may improve the accuracy of exercise testing in patients with CAD who do not show an ST-segment depression. Exercise ECGs were analyzed in 50 subjects who had undergone coronary angiography for clinical indications. None of them showed an ST-segment depression during or after exercise: There were 25 patients with significant coronary artery stenosis and 25 without significant stenosis. The QTD measured before, immediately after, and 1 min after exercise was similar in the 2 groups. The QTD at 3 and 5 min after exercise was significantly greater in patients with CAD than in the controls, and the most marked difference in QTD was observed at 3 min after exercise. A QTD at 3 min after exercise of >60 ms had a sensitivity of 80% and specificity of 88% regarding the diagnosis of CAD. When a deltaQTD (post-exercise QTD minus QTD at rest) at 3 min after exercise of >0 ms was added to a QTD of >60 ms as a condition for positivity, the specificity increased to 96%. QTD measured at 3 min after exercise increases the accuracy of exercise testing in patients with CAD who do not show an ST-segment depression.

Adult↗
PubMed1999

Influence of exercise on QT dispersion in hypertensive patients with left ventricular hypertrophy without coronary artery disease.

In hypertensive patients with left ventricular hypertrophy (LVH), the influence of exercise on the regional variations in ventricular repolarization is not well understood. The present study compared dispersions of QT and QT apex (QTD and QTaD), which are indices of regional variations in ventricular repolarization, between hypertensive patients with echocardiographic evidence of LVH and those without LVH. Seventy essential hypertensive patients underwent a modified Bruce protocol exercise test, and QTD and QTaD were measured at rest and at peak exercise level. All subjects had undergone coronary angiography and did not have coronary artery disease. None of them showed ST-segment depression during or after exercise. There were 20 patients with LVH and 50 patients without LVH. The QTD and QTaD at rest were not different between the patients with LVH and those without LVH (56+/-32 vs 57+/-28 ms, 52+/-20 vs 49+/-23 ms). At peak exercise level, QTaD was significantly decreased compared with the baseline in hypertensive patients without LVH (49+/-23 to 42+/-16ms, p<0.05), whereas in patients with LVH QTaD increased (52+/-20 to 67+/-17ms, p<0.05). QTaD at peak exercise level was positively correlated with the left ventricular mass index (r=0.357, p=0.0024). These data were unchanged after correction for heart rate using Bazett's equation. In conclusion, QTaD increased after exercise in hypertensive patients with LVH. Inhomogeneity of repolarization is induced by exercise stress in hypertensives with LVH.

Adult↗
PubMed1999

[A case of atypical polypoid adenomyoma with intramural myoma-like growth].

We encountered a case of a large atypical polypoid adenomyoma (APA) which showed characteristic intramural appearance. As many cases of APA of the uterus have been reported in recent years, macro- and microscopic findings of the lesion and its clinical characteristics have been investigated. However the pathogenesis and the natural history of the lesion remained to be solved owing to still limited number of the cases. We report this case to discuss the macroscopic findings and clinicopathologic characteristics of the lesion.

Adenomyoma↗
PubMed1999

[Creatinine].

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Adult↗
PubMed1999

Ethanol's actions on cAMP-mediated signaling in cells transfected with type VII adenylyl cyclase.

BACKGROUND: Adenylyl cyclase (AC) activity is increased in the presence of ethanol. The magnitude of ethanol's action on AC depends on the isoform of AC expressed in a particular cell type. Type VII AC demonstrates the greatest potentiation of activity in the presence of ethanol, but questions have arisen regarding the effects of pharmacologically relevant (approximately 50 mM) concentrations of ethanol on type VII AC activity. Questions also remain as to whether the potentiation of AC activity by ethanol initiates downstream effects on protein kinase A activity. METHODS: HEK293 (human embryonic kidney 293) cells overexpressing type VII AC were used to study the dose-dependent actions of ethanol on cyclic adenosine monophosphate (cAMP) production. Studies were performed in the presence and absence of phosphodiesterase inhibitors. Protein kinase A activity was assessed under conditions similar to those used to measure ethanol's actions on AC. RESULTS: A significantly greater percent stimulation of prostaglandin E1-mediated cAMP accumulation was evident in the absence of the phosphodiesterase inhibitors 3-isobutyl-1-methylxanthine and Ro 20-1724 than in the presence of the phosphodiesterase inhibitors. We also showed that ethanol was not, itself, acting as a phosphodiesterase inhibitor. The calculated percent stimulation of AC activity by ethanol depended on the baseline levels of cAMP production in the absence of ethanol. In the absence of 3-isobutyl-1-methylxanthine (or other phosphodiesterase inhibitors), a 50 mM concentration of ethanol produced a 56% increase in prostaglandin E1-stimulated cAMP production in the type VII AC transfected HEK293 cells. This concentration of ethanol also produced a significant activation of protein kinase A beyond that produced by prostaglandin E1 alone. CONCLUSIONS: The present study indicates that, in the presence of a particular isoform of AC, moderately intoxicating concentrations of ethanol will significantly potentiate the transmitter-mediated activation of the cAMP signaling cascade. Activation of this signaling cascade may have important implications for the mechanisms by which ethanol produces intoxication and/or in the mechanisms of neuroadaptation leading to tolerance to, and physical dependence on, ethanol.

Adenylyl Cyclases↗
PubMed1999

[Dopamine].

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Dopamine↗
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↗