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Biomedical subjects

C Yutani

Publications and source records attributed to C Yutani.

At least 181 records · Page 10Linked to original sources
PubMed1986

Autolysis of the granular layer of the cerebellar cortex in brain death.

In a study of duration of brain death, granular layer autolysis (GLA) of the cerebellar cortex was analyzed in 45 patients who died of acute cerebrovascular diseases (CVDs). Twelve patients who died of causes other than intracranial disease served as controls. Tonsillar herniation occurred in all who died of acute CVDs. More advanced GLA was seen in the central folia adjacent to the central white medullary body of the cerebellum as compared with the peripheral folia. Widespread GLA involving the most of the peripheral folia was found solely in patients in whom brain death had been present over 18 h. Of the 12 control patients, 4 showed GLA only in the central folia. Although GLA of the central folia might develop during immersion fixation of the brain, the alteration of the peripheral folia is assumed to develop in the period of brain death. Widespread GLA extending to the peripheral folia could be a pathological finding characteristic of brain death, where intracranial blood flow could be absent or significantly reduced. Brain death for little less than 1 day would be necessary for GLA to develop.

Adult↗
PubMed1986

Rearrangement of immunoglobulin heavy chain genes and T3 expression in the absence of rearrangement of T-cell receptor beta-chain gene in a patient with T-cell malignant lymphoma.

We describe the rearrangement of immunoglobulin genes and T3 expression in the absence of rearrangement of T-cell receptor beta-chain genes in a patient with T-cell malignant lymphoma. He had a mediastinal mass and his lymphoma cells expressed T-cell antigens (OKT3+, OKT9+, and OKT10+). When we examined genomic DNA from the lymphoma cells, we detected the rearrangement of immunoglobulin heavy chain genes with a germ-line configuration of light chain genes and no rearrangement of T-cell receptor beta-chain gene. These results indicated that the rearrangement of immunoglobulin genes could occur in T-cell malignant lymphoma, and that T3 antigen could be expressed prior to the rearrangement of T-cell receptor beta-chain genes under certain circumstances.

Adult↗
PubMed1986

Purification and characterization of human kidney renin.

By means of a new rapid and small scale purification method, human kidney renin has been purified from a single kidney in a homogeneous state, as judged on SDS-PAGE. The kidney which showed unusually high renin activity was from a patient with cardiomyopathy. 8,000-fold purification was attained by means of only pepstatin-aminohexyl-Sepharose chromatography and FPLC on a Mono Q column, and the yield was 34%. The specific activity was 5.63 mg angiotensin I per mg protein per h at 37 degrees C and pH 6.5 with porcine angiotensinogen as the substrate. The molecular weight was estimated to be 37,000 by SDS-PAGE and 38,000 by HPLC on a TSK G-3000 SW column. The preparation showed three bands on isoelectric focusing. The molecular weight and the profile on isoelectric focusing of the purified renin agreed with those found for the extracts of both the patient's kidney and a kidney with the usual low renin activity.

Adolescent↗
PubMed1986

Polymyositis associated with dissecting aneurysm of arteries and intracerebral hemorrhage.

Dissecting aneurysm and stroke are a rare complication of polymyositis. The present report describes an autopsy case of a 53-year-old woman, who suffered from polymyositis accompanied by dissecting aneurysms of right external iliac and right renal arteries, and furthermore, intracerebral hemorrhage. The latter was caused by necrotizing angiitis. The patient had no abnormal anatomical changes such as coarctation of aorta, aortic stenosis, bicuspid aortic valve or Marfan's syndrome. Atherosclerosis in the patient was mild, and cystic medial necrosis of aorta and arteries was not found. Since the patient was attacked by dissections of arteries following long-term steroid therapy, a possibility can be raised that arterial dissection was attributable to steroid treatment besides necrotizing angiitis complicating in polymyositis.

Aortic Dissection↗
PubMed1986

[Hereditary angioneurotic edema: pathophysiology and therapy].

The hereditary angioneurotic edema (HANE), owing to its characteristic clinical symptom, episodic formation of localized edema, has been the subject to be discussed in relation to the problems of the mechanism for the edema formation. On the other hand, when HANE is considered from the point of view on the abnormality in the plasma proteinase systems, it has been thought to be a suitable hereditary defect which enables to investigate into the interactions of the plasma proteinase systems. However, when the clinical course of the disease is correlated with the changes in the plasma proteinase systems, it appears very likely to state that HANE is a very unique model disease, in which edema attacks are elicited by the interactions between plasma proteinase systems and vascular system of the microcirculation, that are triggered by the exogenous stimuli under the influence of the control functions of the endocrine systems.

Angioedema↗
PubMed1986

[Progressive left ventricular dilatation in a child with hypertrophic cardiomyopathy: a case report].

Clinical pictures of a patient with progression from hypertrophic cardiomyopathy to dilated cardiomyopathy features in the end stage was described. Echocardiography performed at the age of five years revealed septal hypertrophy without systolic anterior motion (SAM). At 7 years of age, it revealed ventricular septal thickness of 18 mm, left ventricular posterior wall thickness of 24 mm, and marked SAM. Echocardiography at 14 years of age revealed left ventricular dilatation (52 mm in diastole) with poor contraction. Ventricular septal thickness was 18 mm and left ventricular posterior wall thickness was 16 mm. The SAM was no longer present. At autopsy, the heart weighed 590 g, and there was moderate dilatation of the right and left ventricular cavities. Histologically, there were massive fibrosis and myocardial disarray in the right and left ventricular walls.

Cardiomyopathy, Dilated↗
PubMed1986

[Asymmetric septal hypertrophy of sporadic form with abnormal thallium perfusion and myocardial enzymes].

Asymmetric septal hypertrophy with abnormal thallium scintigram and elevated cardiac enzymes were observed in five patients and were studied with special reference to the clinical significance of their clinicopathological features. They were not familial cardiomyopathy patients. Two of the five patients (Cases 1 and 2) exhibited the clinical features characteristic of hypertrophic cardiomyopathy without abnormal thallium perfusion and serum cardiac enzyme levels. A right endomyocardial biopsy for Case 1 disclosed myocardial fibrosis in addition to hypertrophy and disarray of myocardial fibers. The left ventricular cavities of two other patients (Cases 4 and 5) tended to be dilated with signs of impaired systolic function and asymmetric septal hypertrophy. A regional area of reduced thickness was observed in the medial portion of the left ventricular posterior wall of Case 4. The remaining case (Case 3) exhibited left ventricular dilatation and reduced left ventricular systolic function, disproportionate hypertrophy, and had clinical signs of congestive heart failure. Necropsy disclosed massive fibrosis and diffuse disarray of myocardial fibers. Some patients with familial hypertrophic cardiomyopathy progress to exhibit clinical features of dilated cardiomyopathy in the terminal stages, and have massive fibrosis of the myocardium histologically. Thallium scintigraphic abnormalities and elevated serum levels of cardiac enzymes, especially the LDH1 isoenzyme, in patients with hypertrophic cardiomyopathy may be a meaningful indicator of such progression in its early stages. The five patients in the present study exhibited a variety of clinical and histological features which may comprise a spectrum of clinical conditions during the progression from hypertrophic cardiomyopathy to a condition like dilated cardiomyopathy, similar to that in familial patients. This progression and the factors promoting it should be studied further in the near future.

Adult↗
PubMed1985

Thallium perfusion and cardiac enzyme abnormalities in patients with familial hypertrophic cardiomyopathy.

Twelve patients of five families with familial hypertrophic cardiomyopathy were examined. Within each family, the older patients showed dilation or diminished contraction of the left ventricle by echocardiography or angiocardiography more frequently than did younger patients. LDH1 fraction (lactic dehydrogenase isoenzyme) and MB-CPK (creatinine phosphokinase isoenzyme) were increased in 7 of 10 patients. Thallium-201 myocardial scintigraphy showed perfusion defect or hypoperfusion in 9 of 10 patient. Eleven cases demonstrated remarkable hypertrophy at the macroscopic level. Marked fibrosis was observed in all 5 of the 11 patients whose histologic findings were obtained. In two necropsy cases, disarray was found throughout the right and left ventricles and the pattern of fibrosis was massive. These findings were different from those of ordinary hypertrophic cardiomyopathy. It is possible that each patient with familial hypertrophic cardiomyopathy may develop more prominent thallium and enzyme abnormalities as he becomes older, regardless of whether he develops a dilated cardiomyopathy picture.

Adolescent↗
PubMed1985

Three autopsy cases of progression to left ventricular dilatation in patients with hypertrophic cardiomyopathy.

The hearts of three cases of congestive heart failure with dilated left ventricles developing in patients with symptomatic hypertrophic cardiomyopathy (HCM) were morphologically investigated. The results showed that disproportionate hypertrophy and dilatation of the left ventricles, accompanied by massive fibrosis and myocardial disarray, were present in the three patients. The mean percent area of fibrosis of the left ventricle was 34.7% and 47.4% at the upper third and lower third levels, respectively, and was much more frequently associated with disarray (84.4 +/- 12.3%). Moreover, the fibrosis was most extensive in the lateral wall of the left ventricle, followed by the posterior, anterior, and interventricular walls. The fibrosis was also diffuse regardless of the subendocardial or subepicardial region of the heart. The findings in the present study suggest that the disarray in this particular series of HCM might be responsible for the mechanism of the fibrosis leading to dilatation of the left ventricle.

Adolescent↗
PubMed1985

Cerebro-spinal infarction caused by atheromatous emboli.

Cholesterol embolization to the abdominal viscera is common, but rare in the central nervous system. Fourteen cases of atheromatous embolization to the central nervous system were morphologically investigated. Among the 800 consecutive autopsy cases, 38 cases had atheromatous emboli in various organs. Cerebro-spinal infarction caused by atheromatous emboli was found in 11 cases. Infarction rate (11/14) was relatively higher than in other organs and 5 of these cases were thought to be due to direct injury to the erosive surface of the aorta; cardiac catheterization (2 cases), intra-aortic balloon pumping (2 cases), and extra-anatomical bypass graft operation (1 case). These 14 patients consisted of elderly patients (70.1 +/- 6.3 years old) usually associated with hypertension (78.6%) and diabetes mellitus (42.8%). Anatomically, aortic aneurysms were seen in 10 cases (71.4%), in which aortic arch aneurysm was seen in 6 cases. Hence, aortic mechanical procedure is of great importance for denuding atheromatous materials from erosive atherosclerosis to the central nervous system.

Aged↗
PubMed1985

A case of foamy myocardial transformation of infancy.

A case of infantile cardiomyopathy in a year and four months old girl, which was clinically characterized by tachycardia resistant to any drugs and marked hyperplasia of mitochondria in their cytoplasms on electron microscopic observation, was presented. In the present case light and electron microscopical proof of the diagnosis was obtained by right endomyocardial biopsy, while most of this condition has not been recognized prior to autopsy. In Japan this newly recognized infantile cardiomyopathy has not been reported, and we proposed that this condition could be designated as mitochondrial cardiomyopathy caused by unknown etiology. The literatures described previously in the world have been reviewed.

Cardiomyopathies↗