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Biomedical subjects

S Kuwao

Publications and source records attributed to S Kuwao.

88 records · Page 5Linked to original sources
PubMed1991

[Histopathological study of aortic wall dissection].

To determine the etiology of aortic wall dissection, a histopathological study of the aorta in 20 cases with dissecting aortic aneurysm (DA), 3 cases with Marfan syndrome and 3 cases with annulo-aortic ectasia (AAE) was performed. Controls consisted of 348 cases of normally-aging aorta. In cases with aortic wall dissection, the histopathological changes in the undissected media were also carefully examined. In Marfan syndrome and AAE, there was a marked accumulation of acid mucopolysaccharide (AMPS) and its distribution in the wall was diffuse in patients under 50 years old, resulting in changes in elastic fibers including fragmentation, elastolysis and reticulation. In contrast, DA was histopathologically characterized by zonal fibrosis and abnormally-dilated vessels in the aortic media. These lesions were found in 8 (40%) of the 20 DA cases. The remaining 12 cases also had increased vascularization and fragmentation of elastic fibers. This medial fibrosis and increased vascularization were particularly marked in older patients. Among the 3 diseased entities responsible for aortic wall dissection, DA differed distinctly from Marfan syndrome or AAE as to the amount and site of AMPS accumulation in the media as well as fibrosis and hypervascularity in the outer half of the aortic media. In conclusion, aortic wall dissection in younger patients may be etiologically associated with the increased AMPS accumulation in the aortic media which may always be accompanied by degeneration of elastic fibers in this study, however, in older patients zonal fibrosis and abnormal vessels developing in the media are responsible for the dissection.

Adolescent↗
PubMed1990

Relationships among expression, transcription and rearrangement of T-cell receptor beta gene in T-cell lymphomas.

The expression of T-cell receptors (TCR) in malignant lymphomas was examined immunohistochemically by monoclonal antibodies which react with the TCR beta or TCR delta chain. TCR beta was expressed in 16 out of 47 non-Hodgkin's lymphomas. These included 15 T-cell lymphomas and 1 Ki-1 lymphoma. The anti-TCR beta chain antibody, beta F1, did not react with 26 B-cell lymphomas, 1 Ki-1 lymphoma or 6 Hodgkin's disease. This anti-TCR delta chain antibody, TCR delta 1, did not react with any type of malignant lymphoma. Although TCR beta and CD3 were co-expressed in normal lymphoid tissues and most T-cell lymphomas, 3 cases of CD3+ CD4+ CD8- T-cell lymphoma failed to express TCR beta. TCR beta and Ig JH gene configurations in malignant lymphomas were examined by Southern hybridization. Although each of 9 T-cell lymphomas had a rearranged TCR beta locus, TCR beta gene rearrangement in the 3 cases of beta F1- CD3+ T-cell lymphomas was demonstrated by Southern blot. No transcripts of the TCR beta gene could be found in 2 out of the 3 beta F1- CD3+ T-cell lymphomas by Northern blot, indicating the lack of TCR beta protein expression to be due to non-transcription of the TCR gene. Loss of TCR beta proteins in these T-cell lymphomas is thus quite likely to be associated with T-cell tumour activation and progression, since 3 beta F1- CD3+ T-cell lymphomas expressed CD25 (interleukin-2 receptor) to a high degree.

Adolescent↗
PubMed1990

An angiographic study of intracardiac coronary arteries from human autopsy hearts: their clinicopathologic significance and characterization during transmural myocardial infarction.

In this study of human autopsy hearts, coronary arteries were divided by morphologic criteria into classes A (branching-type) and B (straight-type) arteries. Infarcted hearts and normal hearts were investigated mainly by means of coronary angiography, as well as by gross and histologic examinations. Transmural myocardial infarction originated in the inner half of the myocardial layer, which was predominantly supplied by class A arteries, followed by gradual extension to the outer layer. The early infarcted focus revealed an angiographically avascular state. This may have been the result of shrinkage of the peripheral branches of class A arteries due to increased extravascular resistance rather than to arteriolar obstruction by small thrombi and/or leukocyte plugs. By contrast, class B arteries remained patent and were almost entirely free from such phenomena. They usually penetrated the infarcted focus to drain into the papillary muscles and trabeculae carnae. As the process of myocardial infarction progressed, various patterns of vascular reactions corresponding to the healing phase were demonstrated by these branches within the infarcted foci. The passive response of class A arteries during acute ischemia characterized the early myocardial lesion. Subsequently, neovascularization from the surviving class B arteries in the infarcted focus occurred as a part of the formation of granulation tissue. Newly formed small arteries from class A arteries also participated in this reaction at the marginal area of the lesion. These well-coordinated vascular reactions revealed in greater detail the initiation and progression of the healing process and were reflective of the clinical prognosis.

Angiography↗
PubMed1989

[A case report of tricuspid valve endocarditis due to Staphylococcus aureus with successful surgical treatment].

A 14-year-old boy had previously received right temporal lobectomy under the diagnosis of a malignant brain tumor. About one month after lobectomy, ventriculo-peritoneum shunt and ventriculo-atrium shunt were placed because hydrocephalus was progressed. The patient subsequently had a high fever probably due to wound infection of the shunt operation. Several blood cultures demonstrated Methicillin Resistant Staphylococcus Aureus (MRSA). Several sensitive antibiotics were administered for about 30 days, however these drugs were not effective. According to echocardiography, moderate tricuspid regurgitation and a large vegetation at the tricuspid valve were detected and isolated tricuspid valve endocarditis was diagnosed. Surgical intervention was necessary because of recurrent pulmonary emboli. After tricuspid valve replacement with a Björk-Shiley mechanical valve (31 mm), fever subsided and the patient was discharged on the 38th postoperative day. It is concluded that the surgical indications of the tricuspid valve endocarditis are as follows: 1. recurrent pulmonary emboli, 2. refractory right heart failure, 3. resistance against antibiotics.

Adolescent↗
PubMed1989

[Effect of oral-adsorbent (AST-120) in chronic renal failure (CRF) in rats].

The progression of renal failure has been suggested to be altered by dietary manipulation of protein based on the presumption that the progressive nature of CRF may be caused by the vicious cycle driven by some toxic metabolite uncleared by failing kidney. We studied 29 female Sprague-Dawley rats aged 12 weeks weighing 226 to 290 gm subjected to a 5/6 nephrectomy. 2 days after, group C (16 rats) were given a commercially prepared diet (CE-2, Japan Kurea). While group A (13 rats) were given the same diet and 5% AST-120. Initial serum creatinine of both group was 2.2 mg/dl. After 9 weeks, all surviving rats were sacrificed for evaluation of renal histology. During the observation period, survival rate, Ccr, urinary creatinine and urea excretion were significantly better in group A rats. Result also showed a better weight increase with concomitant increase in protein catabolic rate in group A rats. These result showed the beneficial effect of AST-120 in uremic rats in terms of survival rate and delaying the progression of CRF despite the presence of increased protein catabolic rate. Based on this study, one way of preventing the progression of renal failure is through removal of some toxic metabolite in the gastrointestinal tract by the use of oral adsorbent as exemplified by AST-120.

Age Factors↗
PubMed1985

An ultrastructural study on ischemic lesions in rabbits' hearts with pressure overload and hyperlipidemia.

The effect of hypertension, hyperlipidemia, and the combination of both on acute and chronic myocardial ischemia were evaluated in a total of 30 male rabbits. After preliminary hypertension and/or hyperlipidemic load by loading of the abdominal aorta and/or cholesterol feeding, acute ischemia was produced by clipping of the left coronary artery. The banding produced elevation of carotid arterial pressure and left ventricular hypertrophy. Cholesterol feeding resulted in severe atheromatous changes in all sizes of coronary arteries. The intimal thickening was due to foam cell accumulation in all arteries examined. Animals pretreated with the combination of hypertension and hyperlipidemia displayed the most severe cardiolmegaly with advanced coronary atherosclerosis and chronic ischemic lesions of the myocardium, i.e., perivascular patchy fibrosis in the subendocardial area. Furthermore, electron microscopic detection of ultrastructural myocardial damage, involving glycogen depletion, sarcoplasmic edema, mitochondrial swelling, and contractile abnormalities, was also most frequent in this group. These changes were quantitated using the ischemic score. These results confirm the hypothesis that fatal ischemic injuries may occur clinically in human hearts with coronary insufficiency due to coexistence of hypertensive cardiomegaly and severe coronary atherosclerosis. They offer a model for further study of these combined effects.

Animals↗
PubMed1983

Glomerular tissue injury in IgA nephritis.

The glomerular lesions in 129 cases of IgA nephritis were analyzed. The development of glomerular injury occurred in two ways, one being a chronic mesangial depositive and sclerosing lesion commonly found in most glomeruli, and the other an acute but local injury initiating from the local peripheral glomerular basement membrane abnormality, i.e., thinning and/or splitting, which was seen at least in one third of all cases. The activation of the local coagulatory process could add segmental glomerular changes including small crescents, adhesion, and local tuft necrosis to the mesangial lesion.

Adolescent↗
PubMedDate not supplied

Three-dimensional reconstruction of colorectal tumors from serial tissue sections by computer graphics: a preliminary study.

BACKGROUND/AIMS: We present herein the three-dimensional reconstruction of colorectal tumors, with particular reference to growth pattern into each layer of the colorectal wall, and measurement of tumor volume and surface area. METHODOLOGY: Conventional tissue section images of colorectal tumors were analyzed using a computer graphics analysis program. The two-dimensional extent of invasion by each tumor into each layer of intestinal wall were determined from the images of each section. Based on data from multiple sections, tumor and surrounding normal tissue layers were reconstructed three-dimensionally, and volume and surface area of the tumors were determined. RESULTS: Using this technique, three-dimensional morphology of tumor and tumor progression into colorectal wall could be determined. Volume and surface area of the colon tumor were 4871 mm3 and 1741 mm2, respectively. Volume and surface area of the rectal tumor were 1090 mm3 and 877 mm2, respectively. CONCLUSIONS: This technique may provide a new approach for pathological analysis of colorectal carcinoma.

Colonic Neoplasms↗