PubMed Health⌕ Search

Biomedical subjects

K Hiwada

Publications and source records attributed to K Hiwada.

At least 37 records · Page 2Linked to original sources
PubMed2001

Myocardial ischemia induced by anomalous aortic origin of the right coronary artery in a patient with atrial septal defect.

A 27-year-old woman with atrial septal defect (ASD) and a sensation of squeezing in the anterior chest by effort was admitted to our hospital. In addition to the ASD, the coronary angiogram showed an abnormal anomalous position of the right coronary artery. Exercise thallium (Tl)-201 cardiac scintigram with an electrocardiogram clearly detected myocardial ischemia in the inferior area. In the operative findings, the orifice of the right coronary artery was positioned high above the commissure between the right and left sinuses of Valsalva, and it ran between the aorta and pulmonary trunk. Considering myocardial ischemia possibly caused by the anomalous origin of the right coronary artery, a coronary artery bypass graft (CABG) was simultaneously performed to the right coronary artery with direct closure of ASD. The myocardial ischemic finding in the inferior area disappeared after the operation, and she was also relieved from the chest pain. In view of these findings, we suggest that an active combination treatment such as CABG and ASD closure is highly successful in a patient with a threatening coronary anomaly and congenital heart disease.

Adult↗
PubMed2001

Congenitally corrected transposition of the great arteries in a 65-year-old woman.

A 65-year-old Japanese woman was admitted to hospital because of exertional dyspnea. Transthoracic echocardiography showed diffuse hypokinesis of the left-sided ventricular wall, but was not clear enough to provide useful information because of the rotation of the cardiac apex and the presence of lung tissue. Systemic ventriculography showed that the left-sided ventricle with heavy trabeculations was morphologically similar to a normal right ventricle. Magnetic resonance imaging (MRI) clearly revealed corrected transposition of the great arteries. Because this patient had no severe associated cardiac anomalies, systemic ventricular dysfunction is thought to be the major cause of exertional dyspnea. MRI is a useful non-invasive method for the rapid evaluation of cardiac morphology.

Aged↗
PubMed2001

Severe inclusion body myositis with interstitial pneumonia.

We report a patient with a severe inclusion body myositis (IBM). His illness was unusual in terms of a rapid progression, high creatine kinase levels, and complication with interstitial pneumonia. He responded well to immunosuppressive agents such as corticosteroids, cyclosporin A, cyclophosphamide, and immunoglobulin. The present patient indicates the wide range of the disease, and that immunosuppressive agents may be useful for treatment of IBM.

Aged↗
PubMed2001

[A case of sarcoidosis with muscle nodules].

A 65-year-old man with sarcoidosis, accompanied by muscle nodules, noticed a painless and enlarged nodule in his forearm. MRI of the nodule showed that a star-shaped area of lower signal intensity was surrounded by an area of higher signal intensity. Histological examination showed granulomas composed of multinuclear giant cells and epithelioid cells. Sarcoidosis was diagnosed. Eight months later, he was admitted to our hospital because of enlargement of the nodular region with pain and stiffness. Marked uptake of 67Ga was observed in the right arm and leg. MRI revealed sarcoid nodules in these regions. An enlargement of the higher signal intensity area was observed in the right forearm nodule. We started administration of prednisolone. Forty days later, his symptoms had disappeared and the size of higher signal intensity area of the nodule had reduced dramatically. 67Ga scintigram and MRI were useful for diagnosis and monitoring during therapy in this patient.

Aged↗
PubMed2001

Decreased E-cadherin augments beta-catenin nuclear localization: studies in breast cancer cell lines.

We showed that the YMB-1-derived breast cancer cell line YMB-S, which proliferates in suspension without aggregation, exhibits complete loss of cell-cell adhesion despite the presence of E-cadherin-catenin complex and expression of free beta-catenin in the cytoplasm. Here, we describe beta-catenin gene regulation, interaction with E-cadherin, immunocytochemical localization, and their relation to growth rate in the YMB-1-derived cell line YMB-A, which forms tight junctions and displays anchorage-dependent growth. YMB-A cells proliferated more slowly than YMB-S cells. E-cadherin and APC gene product expression in YMB-A cells was significantly higher than that in YMB-S cells, whereas expression of beta-catenin, MUC1, and c-myc was lower in YMB-A cells than in YMB-S cells. According to immunocytochemical analysis, beta-catenin in YMB-A cells displayed membranous or submembranous localization, indicating that beta-catenin is mostly tethered to E-cadherin. Inhibition of E-cadherin expression in YMB-A cells by an antisense oligonucleotide did not change expression of whole cell beta-catenin protein, but increased nuclear beta-catenin protein level, c-myc expression, and cell growth rate. These results suggest that decreased expression of E-cadherin and APC and increased amount of beta-catenin in YMB-S cells lead to accumulation of beta-catenin in the nucleus, activate beta-catenin-LEF/TCF signaling pathway, and trigger c-myc proto-oncogene expression. c-Myc overexpression in breast cancer may be related to activated Wnt independent beta-catenin-LEF/TCF signaling.

Blotting, Southern↗
PubMed2001

Role of GADD153 (growth arrest- and DNA damage-inducible gene 153) in vascular smooth muscle cell apoptosis.

GADD153 (growth arrest- and DNA damage-inducible gene 153) is expressed at very low levels in growing cells, but is markedly induced in response to a variety of cellular stresses, including glucose deprivation, exposure to genotoxic agents and other growth-arresting situations. Forced expression of GADD153 induces cell cycle arrest in many types of cells. It is also reported that GADD153 is directly associated with apoptosis. Recently we have reported that platelet-derived growth factor (PDGF)-BB induces apoptosis in cultured vascular smooth muscle cells (VSMC), but only when 100% confluency is reached. These results suggested that cell-cell contact inhibition (cell growth arrest) may be a critical factor for induction of VSMC apoptosis by PDGF-BB. In the present study, we explored the role of GADD153, one of a number of growth-arrest-related gene products, in the molecular mechanisms of VSMC apoptosis in vitro and in vivo. GADD153 was markedly induced at both the mRNA and protein levels, in parallel with the induction of VSMC apoptosis, after treatment with PDGF-BB. Moreover, overexpression of GADD153 in VSMC significantly reduced cell viability and induced apoptosis. In the carotid artery balloon injury model in rats, GADD153 protein was expressed in apoptotic VSMC which were positively stained by in situ DNA labelling. These results demonstrate an important role for GADD153 in the molecular mechanisms of VSMC apoptosis.

Analysis of Variance↗
PubMed2001

[Diagnosis of hypertension and outline of hypertension treatment].

In this review first I described the procedures of diagnosis in patients with essential hypertension. Blood pressure level, risk factor for cardiovascular disease and organ damage due to hypertension are essential in evaluating a patient with hypertension at outpatient clinic. Those criteria are based on Hypertension Treatment Guidelines 2000 published by Japanese Society of Hypertension last year. Next I described the outline of treatment of hypertensive patients according to the above guidelines. The guidelines is our interpretation of the world literature and of current opinions together with our largely documented experience based on the management of many hypertensive patients in Japan. The first-line antihypertensive drugs are long-acting Ca antagonists, ACE inhibitors, angiotensin II receptor antagonists, diuretics, beta-blockers and alpha-blockers.

Antihypertensive Agents↗
PubMed2001

Beneficial effect of beta-adrenergic blockade on left ventricular function in haemodialysis patients.

Congestive heart failure is a common and serious complication in patients undergoing chronic dialysis. However, there have been no studies on preferential medical therapies to improve left ventricular function in haemodialysis patients. Beta-blocker treatment is known to improve left ventricular function in patients with dilated cardiomyopathy; moreover, plasma levels of noradrenaline and natriuretic peptides are sensitive markers of left ventricular dysfunction. The present study investigated whether beta-blocker treatment could improve left ventricular function in haemodialysis patients with a dilated left ventricle. Our study group comprised 14 haemodialysis patients with a dilated left ventricle, who had undergone maintenance haemodialysis for a mean of 11 years. The following haemodynamic parameters were evaluated before and after 4 months of treatment with the beta-blocker metoprolol: left ventricular dimension at end-systole and end-diastole, and fractional shortening. Plasma levels of noradrenaline, atrial natriuretic peptide and brain natriuretic peptide were also determined. Dry body weight and haemoglobin concentration showed no significant change after compared with before treatment with metoprolol. Heart rate decreased significantly, from 79+/-9 beats/min to 69+/-9 beats/min, but systolic blood pressure remained unchanged. The left ventricular dimension both at end-systole and at end-diastole was decreased, and fractional shortening increased significantly. Plasma levels of noradrenaline did not change significantly, but those of atrial natriuretic peptide and brain natriuretic peptide decreased markedly [from 100+/-89 pg/ml to 46+/-29 pg/ml (P=0.0051) and from 549+/-516 pg/ml to 140+/-128 pg/ml (P=0.0035) respectively]. In conclusion, beta-blocker therapy with metoprolol can markedly attenuate left ventricular remodelling and decrease the plasma levels of natriuretic peptides in haemodialysis patients with a dilated left ventricle.

Adrenergic beta-Antagonists↗
PubMed2000

Troglitazone induces apoptosis via the p53 and Gadd45 pathway in vascular smooth muscle cells.

Thiazolidinediones, activators of peroxisome proliferator-activated receptor (PPAR)gamma, have been reported to induce apoptosis in many types of cells. In the present study, we investigated the effects of thiazolidinediones, troglitazone, and pioglitazone on the cell growth of vascular smooth muscle cells, and identified a specific effect of troglitazone in addition to PPARgamma activation. Subconfluent rat culture vascular smooth muscle cells were treated with or without PPARgamma activators, troglitazone (1-30 microM), or pioglitazone (1-30 microM) for 72 h. After treatment, cell viability was significantly reduced by troglitazone in concentrations of 5-30 microM but not by pioglitazone. Vascular smooth muscle cells appeared to float and shrink 48 h after treatment with 20 microM of troglitazone. In situ DNA labeling showed that the nuclei of these cells were positively stained, and genomic DNA extracted from the cells showed nucleosomal laddering. Messenger RNA expression levels of c-myc, p21, bax, bcl-2, and bcl-x were not changed by the treatment with troglitazone. In contrast, along with the induction of vascular smooth muscle cell apoptosis, both the mRNA and protein expression levels of p53 and Gadd45 markedly increased in response to troglitazone. These results strongly suggest that troglitazone can induce vascular smooth muscle cell apoptosis and that this effect is caused primarily by activation of the p53 and Gadd45 pathway but not by PPARgamma activation.

Animals↗
PubMed2000

Association between elevated brain natriuretic peptide levels and the development of left ventricular hypertrophy in patients with hypertension.

PURPOSE: To examine whether plasma levels of brain natriuretic peptide identify hypertensive patients at risk for progressive cardiac hypertrophy. SUBJECTS AND METHODS: We examined the association between plasma brain natriuretic peptide levels and left ventricular structural changes in 54 hypertensive patients and 28 normotensive control subjects. Patients were divided into those with elevated (n = 14) or normal (n = 40) levels of brain natriuretic peptide, based on a cutoff level of 41 pg/mL (2 SD above the mean in the control subjects). Left ventricular function and geometry were assessed echocardiographically at baseline and follow-up. RESULTS: At baseline, initial left ventricular chamber size, wall thickness, and systolic function did not differ between the hypertensive patients and normotensive subjects. After a mean (+/- SD) follow-up of 9 +/- 3 months, blood pressure was relatively unchanged in the hypertensive patients with normal brain natriuretic peptide levels, whereas there were significant increases in systolic blood pressure and pulse pressure (both P <0.05 versus baseline) in patients with elevated brain natriuretic peptide levels. Moreover, left ventricular midwall systolic function had decreased significantly at follow-up in those with elevated levels (P <0.05 versus baseline). At follow-up, the hypertensive patients with elevated brain natriuretic peptide levels had a significantly greater left ventricular mass index and relative wall thickness than those with normal levels. Multiple regression analyses determined that only initial plasma brain natriuretic peptide was significantly (P <0.01) associated with subsequent left ventricular hypertrophy. CONCLUSION: Plasma brain natriuretic peptide levels may identify hypertensive patients who are likely to have progressive cardiac hypertrophy.

Aged↗
PubMed2000

Low wall shear stress in carotid arteries in subjects with left ventricular hypertrophy.

Left ventricular hypertrophy (LVH) is an independent risk factor for cardiovascular complications including atherosclerosis. The close linkage between LVH and carotid atherosclerosis has been the focus of much research. However, the underlying mechanism linking the two conditions is not fully understood. Low wall shear stress contributes to intimal thickening and atherosclerosis development as a local mechanism. In the present study, we investigated the relationship between wall shear stress and LVH in subjects with risk factors for atherosclerosis. Eighty subjects with at least one risk factor for atherosclerosis; ie, hypertension, diabetes mellitus, hyperlipidemia, or smoking, were enrolled. Intimal-medial thickness (IMT), number of plaques, internal dimensions, and blood flow velocity in the common carotid artery were evaluated. Wall shear stress was calculated using a Poiseuillean parabolic model of velocity distribution: shear stress = 4 x blood viscosity x central flow velocity/internal dimension. Subjects were divided into two groups; LVH(-) (n = 36) and LVH(+) (n = 44), according to their left ventricular mass index (LVMI). Mean shear stress and systolic peak shear stress were significantly lower in subjects with LVH compared with subjects without LVH. Furthermore, mean shear stress (r = -0.42, P < .0001) and peak shear stress (r = -0.31, P < 0.01) were significantly inversely related to LVMI. Stepwise regression analysis revealed that wall shear stress independently correlated with LVMI as well as IMT. These results indicate that low shear stress could function as a local factor in the development of atherosclerosis in subjects with LVH.

Arteriosclerosis↗
PubMed2000

Left ventricular mass and atrial volume determined by cine magnetic resonance imaging in essential hypertension.

To evaluate the relationship between left atrial volume determined by cine magnetic resonance imaging and progression of left ventricular hypertrophy (LVH), left atrial volume and echocardiographic left ventricular mass (LVM) were measured in 30 hypertensive patients (15 without LVH and 15 with LVH) and 10 normotensive control subjects. We also evaluated the effects of antihypertensive therapy on the cardiac chamber volumes and LVM in hypertensive patients. The cardiac chamber volumes and LVM were indexed by body surface area. Although there were no significant differences in left ventricular chamber volumes among the three groups, both maximum and minimum left atrial volume indexes, and the LVM index were greater in hypertensive patients with LVH than in the other two groups. The LVM index was correlated with maximum left atrial volume index (r = 0.74, P < .0001), and minimum left atrial volume index (r = 0.76, P < .0001), respectively. Furthermore, in multivariate models, the LVM index was significantly correlated with maximum left atrial volume index. In hypertensive patients with LVH, both maximum and minimum left atrial volume indexes, and the LVM index significantly reduced after treatment. The percent of changes in maximum left atrial volume index after treatment was significantly correlated with the percent of changes in LVM index after treatment. In conclusion, our data indicate that LVH is an independent determinant of left atrial enlargement, and both LVH and left atrial enlargement may be reversed by some effective therapeutic interventions.

Antihypertensive Agents↗
PubMed2000

Effect of suplatast tosilate (IPD-1151T) on a mouse model of asthma: inhibition of eosinophilic inflammation and bronchial hyperresponsiveness.

BACKGROUND: Suplatast tosilate (IPD) is a newly developed 'anti-allergic' drug. It seems to be a unique compound because of its ability to suppress IgE but not IgG or IgM production in vivo and cytokine production from type 2 helper T cells (Th2) in vitro. However, information on its in vivo effect on an animal model of asthma is limited. METHOD: BALB/c mice sensitized to ovalbumin (3 times, 2-week interval) were challenged with ovalbumin by inhalation (50 mg/ml for 20 min, once a day for 6 days). In this study, we explored the influence of IPD on eosinophil infiltration into the airways, bronchial hyperresponsiveness (BHR) to methacholine, specific IgE antibody production, and cytokines in bronchoalveolar lavage fluid (BALF) using this murine model. RESULTS: Treatment with IPD significantly reduced the number of total cells and eosinophils in BALF (around -40%) and almost completely inhibited the development of antigen-induced BHR. Histological findings confirmed the reduction of submucosal cell infiltration in the lung, and disclosed the marked inhibition of bronchial epithelial cell damage. Ovalbumin-specific IgE was slightly but significantly reduced. The levels of IL-4, IL-5 and IL-13 in BALF were significantly decreased in mice treated with the compound compared to those in untreated mice. CONCLUSION: These results suggest that IPD is capable of inhibiting the production of Th2 cytokines, which inhibit eosinophil infiltration into the murine airway, IgE synthesis, and development of BHR, in a murine model of asthma.

Animals↗
PubMed2000

Effect of aerosolized docosahexaenoic acid in a mouse model of atopic asthma.

BACKGROUND: Docosahexaenoic acid (DHA) found in fish oil is known to depress inflammation-related mediators. We investigated a novel delivery method of tridocosahexaenoyl-glycerol (DHA-TG). METHODS: BALB/c mice (6-8 weeks old) were primed intraperitoneally with ovalbumin (OVA) and Al(OH)(3) on days 0 and 7, and with aerosolized OVA on day 7. Primed mice were challenged by repeated exposure to aerosolized OVA on days 15-17. Just before each exposure to aerosolized OVA, the mice were also exposed to an aerosol of emulsified DHA-TG or soybean oil, or saline (days 7 and 15-17). Bronchial hyperresponsiveness (BHR) to methacholine was measured, and bronchoalveolar lavage fluid was obtained 24 h after the last challenge (day 18). Lungs were histologically examined. RESULTS: Bronchoalveolar lavage fluid of saline-treated mice showed an increased cellularity with predominant eosinophils. Exposure to DHA-TG significantly reduced the total cell number and the eosinophil percentage in lavage fluid, whereas soybean oil did not. CONCLUSION: DHA but not soybean oil exposure reduced BHR and cell infiltration to bronchovascular bundles. This type of DHA administration could be studied in clinical trials.

Aerosols↗
PubMed2000

Association between risk factors for atherosclerosis and mechanical forces in carotid artery.

BACKGROUND AND PURPOSE: Mechanical stresses on the arterial wall participate in the pathogenesis of atherosclerosis as local factors. The relationships between local mechanical forces and risk factors for atherosclerosis were investigated. METHODS: Mechanical forces on the arterial wall were evaluated in the carotid artery in 117 patients with risk factors for atherosclerosis including hypertension, dyslipidemia, diabetes mellitus, and smoking, as well as in 20 age- and sex-matched normal controls. Circumferential wall tension and shear stress were evaluated with Laplace's law and a poiseuillean parabolic model of velocity distribution. Circumferential wall strain was also evaluated as carotid mechanical force. RESULTS: Mechanical forces in subjects with risk factors were characterized by low wall shear stress, high circumferential wall tension, and reduced strain. Systolic blood pressure was significantly negatively associated with shear stress and circumferential wall strain. HDL cholesterol showed a significant positive correlation with shear stress and a negative correlation with wall tension. Fasting blood glucose was significantly associated with shear stress, while smoking showed a negative correlation with shear stress and a positive correlation with wall tension. Accumulation of risk factors was associated with further deterioration of mechanical forces. Furthermore, stepwise regression analysis showed that the number of risk factors was significantly associated with mechanical forces independently of carotid intima-media thickness. CONCLUSIONS: These findings suggest that risk factors for atherosclerosis were associated with alteration of mechanical forces. Consequent alteration in mechanical forces could be an underlying local mechanism for the progression of atherosclerosis.

Arteriosclerosis↗