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Biomedical subjects

R Okada

Publications and source records attributed to R Okada.

447 records · Page 25Linked to original sources
PubMedDate not supplied

Multicore myopathy associated with multiple pterygium syndrome and hypertrophic cardiomyopathy.

A boy with multicore myopathy associated with multiple pterygium syndrome and hypertrophic cardiomyopathy is described. Light microscopy of biopsy samples from the skeletal muscle and myocardium revealed multiple cores in the muscle fibers in the former but their absence in the latter. These results suggest that the pathogenesis of the histologic changes might differ between skeletal muscle and myocardium, and that further electron microscopic examination be done on both types of specimen. The prognosis of multicore myopathy is not usually good when cardiac involvement is present.

Abnormalities, Multiple↗
PubMedDate not supplied

Clinicopathologic characteristics of hypertrophic cardiomyopathy detected during mass screening for heart disease.

Between 1981 and 1992 a total of 10 patients with hypertrophic cardiomyopathy (HCM) were detected by mass screening for heart disease in Tokyo's Adachi Ward. Four were first grade elementary school children and six were first grade junior high school adolescents. Two-dimensional echocardiography at the initial evaluation revealed asymmetric septal hypertrophy in four patients, diffuse hypertrophy of the left ventricle in five, and poor left ventricular contractility with wall thinning in one (dilated phase). Three of the five patients with diffuse hypertrophy progressed to asymmetric septal hypertrophy during the average 4-year follow-up period. The degree of septal thickness and the left ventricular wall thickness index were significantly less than in those of young adult controls (12 +/- 3 versus 21 +/- 9 mm, p < 0.05; and 22 +/- 4 versus 28 +/- 16 mm, p < 0.05, respectively). Right ventricular endomyocardial biopsy specimens obtained from 9 of the 10 patients showed features typical of HCM (e.g., myocyte hypertrophy with myofibril disarray) in five patients and atypical features (mainly interstitial fibrosis with perivascular cell infiltration) in another four. One patient with dilated phase disease died of congestive heart failure 6 months after the initial evaluation. These results indicate that HCM detected during mass screening is a mild form of the disease and may have atypical pathologic features, such as interstitial fibrosis and perivascular cell infiltration, mimicking the sequela of chronic myocarditis.

Adolescent↗
PubMedDate not supplied

Circulating leptin: a marker of health in female students.

We studied the relationship between serum leptin concentration and lifestyle factors in female nursing students. Serum leptin was estimated by radioimmunoassay and the correlation between these concentrations with serum lipids, physical fitness and Health-promoting Lifestyle Profile score was investigated. A total of 247 students took part in the study: mean age, 19.0 +/- 2.0 years; mean body mass index (BMI), 21.7 +/- 2.9 kg/m2; and mean serum leptin concentration, 10.8 +/- 11.5 ng/ml. Serum leptin was positively correlated with BMI, systolic and diastolic blood pressure, total cholesterol and serum triglyceride. Serum leptin level concentration inversely correlated with physical fitness score and lifestyle score. When the subjects were grouped according to BMI, the high-BMI group (BMI: > or = 24 kg/m2; n = 40) showed significantly lower fitness and lifestyle scores than the low-BMI group (BMI < or = 20 kg/m2; n = 70). Higher leptin, blood pressure, total cholesterol and triglyceride were seen in high-BMI compared with low-BMI subjects. We suggest that leptin is a useful marker for monitoring good health and may be useful as a motivational aid towards achieving and maintaining a healthy lifestyle.

Adolescent↗
PubMedDate not supplied

Histopathological study of hypertrophied myocardium of known etiologies with special reference to correlation of ECG changes.

Sixty-two autopsied hearts, with left ventricular hypertrophy (LVH) caused by mitral regurgitation (MR), aortic failure (AR), combined valvular disease (CVD), hypertension (HHD), or ischemia (IHD), and 23 control hearts with normal left ventricles were studied morphologically for analysis of modes of hypertrophy and for ECG-pathology correlation. Basic disorders modify the mode of hypertrophy; that is, elongated AR-type LV makes muscle fiber orientation in the outer layer more vertical, and globular MR-type LV makes it more horizontal than normal. High-voltage QRS correlates with hypertrophy of the outer layer which is often associated with that of the inner layer. ST depression and T changes correspond to relative deterioration of the inner and median layers, respectively.

Cardiomegaly↗
PubMedDate not supplied

Histopathological study of cardiac rupture following myocardial infarction with and without thrombolytic therapy.

The characteristics of cardiac rupture associated with thrombolytic therapy for acute myocardial infarction (MI) were studied in the hearts of 10 autopsy patients, 7 men and 3 women aged 41-80 years (mean 59.9 +/- 13.2 years), who died of rupture of the free wall of the left ventricle following acute MI. The site of rupture was examined histologically and the percentage areas of living myocytes, the processes of organization, necrosis and degeneration, and hemorrhage were compared in four patients who received thrombolytic therapy (group R) and six patients without thrombolytic therapy (group N). There were four pathological findings at the site of rupture: necrosis, neutrophil infiltration, hemorrhage, and evidence of the process of absorption. Group R consisted of two patients with hemorrhage, one with absorption, and one with unsuccessful reperfusion and neutrophilic infiltration. Group N included three patients with necrosis, two with neutrophilic infiltration, and one with hemorrhage. The percentage area involved by necrosis and degeneration was significantly lower in group R than in group N. Therefore, local stress produced by more surviving myocardium around the smaller necrosis area and the weakness of myocardium due to hemorrhage and absorption may provoke cardiac rupture in acute MI patients receiving thrombolytic agent.

Adult↗