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Biomedical subjects

C Yutani

Publications and source records attributed to C Yutani.

At least 19 recordsLinked to original sources
PubMed1998

Serum amyloid P component associates with high density lipoprotein as well as very low density lipoprotein but not with low density lipoprotein.

Serum amyloid P component (SAP) is a glycoprotein in human plasma. We previously showed that SAP is specifically localized in human atherosclerotic lesions, suggesting that SAP may play a role in atherogenesis. In this study, the interactions between human SAP and high density lipoprotein (HDL), low density lipoprotein (LDL) and very low density lipoprotein (VLDL) were investigated by using a solid phase plate assay. Biotinylated SAP bound to immobilized HDL and VLDL in a calcium-dependent, saturable manner. The SAP-HDL and SAP-VLDL bindings reached saturation at 4 nM and 16 nM of SAP, respectively. The bindings were inhibited by native SAP in a dose-dependent manner. No binding between SAP and LDL was found in the presence of calcium or EDTA, which indicates the specificity of SAP-lipoproteins interactions. These results suggest that the function of SAP is related to its capability to interact with lipoproteins and this may have important implications in atherosclerosis and in amyloidosis.

Binding, Competitive↗
PubMed1998

Two cases of mesothelial/monocytic incidental cardiac excrescences of the heart.

Two cases of mesothelial/monocytic incidental cardiac excrescences in a 66-year-old female and an 80-year-old male are presented. Lesions had solid and tubular pattern formations which were composed of two predominant cell types of histiocytoid cells and cuboidal cells arranged in strips. The histiocytoid cells were round and had well-defined nuclei with prominent nuclear grooves. They had a low nuclear to cytoplasmic ratio. There were no atypical mitoses. Immunohistochemically, these cells were positive for leukocyte common antigen (LCA) and CD68 (KP-1) but negative for keratin. The cuboidal cells were present in strips, had haphazardly arranged surface microvilli and had small round non-cleaved nuclei. These cells were positive for keratin but negative for LCA, CD68, p53, proliferative cell nuclear antigen, alpha-smooth muscle actin, Factor VIII, epithelial membranous antigen and vimentin. These lesions are probably reactive because of their heterogeneous components; an expected feature for an essentially artifactual lesion that is related to cardiac surgery and invasive catheterization. Immunohistochemical studies are useful for avoiding misdiagnosis of neoplasms.

Aged↗
PubMed1998

A huge coronary aneurysm resulting from a coronary artery-to-left ventricle fistula.

A huge coronary aneurysm resulting from a coronary artery-to-left ventricle fistula is a rare condition. A 57-year-old male had severe recurrent angina attacks. The cause of angina pectoris was a right coronary artery-to-left ventricle fistula with a huge coronary aneurysm. The histological examination of surgically excised specimens revealed that two vertical smooth muscle layers of media of the aneurysm might be associated with dysplasia. Mucoid degeneration was also shown in the intima and around the vasa-vasorum. Abnormal hemodynamics related to the fistula might have induced these vessel wall changes resulting in the huge coronary aneurysm.

Angina Pectoris↗
PubMed1998

Hereditary angioneurotic edema and thromboembolic diseases: I: How symptoms of acute attacks change with aging.

Localized edema of the larynx and pharynx leading to death from asphyxia has long been recognized as a characteristic symptom of hereditary angioneurotic edema (HANE). Long-term follow-up of younger HANE patients has revealed that transient localized acute attacks of edema affect tissues where the microcirculation maintains the blood supply. However, with aging, HANE attacks precipitate disseminated intravascular coagulation (DIC) or multiple organ failure (MOF). Substitution with a C1-inhibitor (C1-INH) has resulted in a fulminant lethal end with a rapid and profound decrease in antithrombin-III (AT-III) activity. A possible mechanism is as follows: Exogenous stimuli activate plasma proteinase systems with the generation of plasma kallikrein that activates the tissue factor pathway (TF) and liberates bradykinin (BK). In younger patients, BK enhances vascular permeability. In the elderly, activated TF is controlled by tissue factor pathway inhibitor (TFPI) and generates thrombin, which is the target enzyme of AT-III and precipitates DIC or MOF. In elderly patients, the characteristic symptom of HANE is hypercoagulation by age-related changes in the biosynthesis of AT-III or TFPI.

Acute Disease↗
PubMed1998

[Evaluation of cardiac function by various cardiac imaging techniques in mitochondrial cardiomyopathy: a case report].

A 39-year-old man with cardiomyopathy due to point mutation of mitochondrial DNA(3243) was admitted to our hospital because of exertional dyspnea accompanied by hearing disturbance and diabetes mellitus. Echocardiography revealed asymmetric hypertrophy of the anterolateral and posterior walls and systolic dysfunction of the left ventricle (fractional shortening = 18%). Pulsed Doppler mitral inflow velocity wave showed a pseudonormalized pattern. Iodine-123 betamethyl-p-iodophenyl-pentadecanoic acid (123I-BMIPP) myocardial scintigraphy showed decreased accumulation in the anterolateral, posterior, and apical walls. Left ventriculography showed moderately decreased ejection fraction (43%), and left ventricular end-diastolic pressure was mildly elevated (18 mmHg). Angiography showed normal coronary arteries, but coronary flow reserve measured by administering intravenous adenosine triphosphate was impaired in the left anterior descending and left circumflex arteries compared to the right coronary artery. Intracellular accumulations of abnormal mitochondria were detected by histologic examination of the cardiac and skeletal muscles. Evaluation of cardiac function showed that the area of myocardial hypertrophy was nearly consistent with the region of decrease in 123I-BMIPP accumulation and coronary flow reserve.

Adult↗
PubMed1998

[Surgical treatment for prosthetic valve endocarditis].

From April 1993 to May 1997, 21 patients underwent surgical treatment for prosthetic valve endocarditis (PVE). There were 13 males and eight females aged from 46 to 79 years old (mean 62 years). There were four cases of early PVE (onset of PVE within 60 days from previous valve replacement), and 17 cases of late PVE (after 60 days). The predominant organisms were Staphylococcus epidermidis (eight cases), Staphylococcus aureus (two cases), MRSA (one case), streptococcal species (three cases), Candida (two cases), Pseudomonas cepacia (one case) and Enterococcus (one case). The predominant organisms were identified in 16 of 20 cases by preoperative blood culture, and in 11 of 20 cases by intraoperative tissue culture, and in 19 cases in all. There were four cases of preoperative cerebral complications, and three cases resurged. The hospital mortality rate was 24% (five patients). Reoperation was required in four patients for recurrence of PVE. Autopsy was performed in four of five patients. Intramyocardial abscess was detected in three patients. Earlier diagnosis and earlier surgical treatment could prevent emboli due to vegetations, which might cause catastrophic results, and could achieve better outcomes. Identification of the predominant organisms, especially from operative tissue cultures, is required.

Aged↗
PubMed1997

Prevalence and predictors of renal artery stenosis in patients with myocardial infarction.

In recent years, the importance of renovascular disease as a cause of end-stage renal disease has been emphasized. Among 1,788 cases autopsied during the 12-year period between 1981 and 1992 at the National Cardiovascular Center Hospital, we examined cases over 40 years of age with autopsy evidence of myocardial infarction to determine the prevalence and predictors of atherosclerotic renal artery stenosis in the atherosclerotic population. Two hundred ninety-seven patients remained for analysis. In this population, atherosclerotic renal artery stenosis was found in 35 patients (12%), and 10 of them had bilateral renal artery stenosis. In patients with hypertension, proteinuria, and renal insufficiency, renal artery stenosis was found in 19%, 39%, and 39%, respectively. As the number of coronary vessels with significant stenosis increased, the prevalence of renal artery stenosis increased. The severity of stenotic lesions of coronary artery was also correlated with the presence of renal artery stenosis. Multiple logistic regression analysis identified age, hypertension, proteinuria, and renal insufficiency as independent predictors of renal artery stenosis. Patients with hypertension, proteinuria, and renal insufficiency had 3.4-, 13.5-, and 4.8-fold increased risk of renal artery stenosis in the population with myocardial infarction. The number of coronary arteries with severe stenosis was also an independent predictor of renal artery stenosis, and had a relative risk of 2.1. These results indicated that atherosclerotic renal artery stenosis is common in patients with myocardial infarction, particularly when hypertension, proteinuria, or renal insufficiency is present. The presence of severe multivessel coronary artery disease suggests a higher incidence of renal artery stenosis.

Adult↗
PubMed1997

Extension of hemorrhage after reperfusion of occluded coronary artery: contrast echocardiographic assessment in dogs.

OBJECTIVES: The aim of this study was to elucidate the progression of intramural hemorrhage complicated by reperfusion with the use of myocardial contrast echocardiography. BACKGROUND: Although hemorrhagic infarction is known to occur in ischemia followed by reperfusion, its onset and sequence have not been well characterized. METHODS: In 20 anesthetized dogs, 3-h occlusion of the left circumflex-coronary artery was followed by reperfusion. The area at risk during coronary occlusion was approximately 25%. Myocardial contrast echocardiogram was examined, and the time-intensity curves for both ischemic and nonischemic areas were obtained at baseline, at 3 min after reperfusion and then at 15-min intervals until 90 min after reperfusion. The wall thickness of both areas was also measured. RESULTS: Gross hemorrhage in the reperfused areas was observed in five dogs (Group H) but not in seven dogs (Group NH). All wall segments were opacified at 3 min after reperfusion in both groups. However, the contrast defect spread significantly with time after reperfusion in Group H but not in Group NH (18.7 +/- 3.4% and 3.3 +/- 1.8%, respectively, at 90 min after reperfusion p < 0.005). The wall of the risk area at 90 min after reperfusion had thickened to 1.3 times baseline thickness in Group H but was unchanged in Group NH. The other eight dogs were excluded from study because of fatal arrhythmias or the existence of collateral circulation during coronary occlusion. CONCLUSIONS: Both progression of the contrast defect area on myocardial contrast echocardiography and a gradual thickening of the wall with reperfusion are characteristic of hemorrhagic infarction.

Animals↗
PubMed1997

A Japanese family with a variant of Gerstmann-Sträussler-Scheinker disease.

OBJECTIVE: A new variant of Gerstmann-Sträussler-Scheinker disease (GSS) was reported, which had a substitution of glutamate to lysine at codon 219 (E219K) in addition to a P102L mutation on the same allele of the PrP gene. However, clinical features were not detailed and pathological studies were not done. Unusual clinical, neuroradiological, and pathological findings are reported for these patients. METHODS AND RESULTS: Clinical presentations of the patients in the same family were variable; progressive dementia with minimal ataxia in some patients but ataxia without dementia in others. PET studies with 18F-2-fluoro-2-deoxyglucose (FDG) disclosed a relative decrease of FDG uptake in bilateral temporoparietal cortices of a patient with dementia, but in the cerebellar cortices in a patient with ataxia. At necropsy, a patient with dementia had multicentric and diffuse plaques stained with PrP antiserum, but not with haematoxylin and eosin or Congo red, in the cerebral and cerebellar cortices. CONCLUSION: Neurological and neuropathological features in the patients were atypical of the classic form of GSS with P102L mutation. The absence of Congo red staining prion protein plaques is probably attributable to E219K polymorphism on the same allele of the PrP gene.

Adult↗
PubMed1997

Crescentic glomerulonephritis and elevated antimyeloperoxidase antibody in a patient with Churg-Strauss syndrome.

A 45-year-old man with a long history of bronchial asthma was admitted to the National Cardiovascular Center with complaints of severe pain, swelling, and ecchymoses of the lower extremities. A diagnosis of Churg-Strauss syndrome was made because of marked eosinophilia, vasculitis, and a history of asthma. Urinalysis revealed severe proteinuria and microscopic hematuria. A renal biopsy demonstrated extensively crescentic glomerulonephritis. The antineutrophil cytoplasmic antibody against myeloperoxidase (MPO-ANCA) level, determined by enzyme-linked immunosorbent assay (ELISA), was 494 ELISA units. Under treatment with prednisolone, the symptoms and eosinophilia improved within 3 days. The MPO-ANCA level decreased to its lowest value, and renal function was ameliorated within 3 months. The patient has been followed regularly on an ambulatory basis with a regimen of prednisolone.

Anti-Inflammatory Agents↗
PubMed1997

A case of dilated cardiomyopathy with abnormal atrioventricular conduction 5 years before the appearance of left ventricular systolic dysfunction.

The first manifestation of dilated cardiomyopathy is usually dyspnea as a result of left heart failure. In this report we describe an unusual patient with third-degree atrioventricular (AV) block unaccompanied by left ventricular dysfunction. Severe left ventricular dysfunction occurred 5 years after the implantation of a permanent pacemaker. We conclude that AV block should not be overlooked as an initial clinical manifestation of dilated cardiomyopathy.

Adult↗
PubMed1996

Wall composition in intravascular ultrasound layered appearance of human coronary artery.

To evaluate the impact of histological factors on the appearance of the wall of the coronary artery by intravascular ultrasound (IVUS), we performed an in vitro study of 34 coronary artery segments from eight autopsied patients. We assumed the coronary cross section to be divided into four equal parts, and assessed the quadrants with maximal and minimal wall thickness by IVUS (30 MHz; 4.3 Fr; 1800 rpm) and by a histological study. The histological layer thickness and composition were also evaluated in terms of their contribution to the appearance of the ultrasound layer. Fifty-eight quadrants were clearly visible on ultrasound. A three-layered appearance, with inner echogenic, subjacent sonolucent, and outer echogenic layers, was observed in 32 quadrants, while 26 quadrants showed a two-layered appearance with inner and outer echogenic layers. The thickness of the inner echogenic layer (0.77 +/- 0.38 mm) was moderately correlated with the intimal thickness (0.51 +/- 0.45 mm; r = 0.85, standard error of estimate [SEE] = 0.24 mm); however, the correlation was significantly improved when the thickness of the inner echogenic plus sonolucent layers (0.89 +/- 0.47 mm) was compared with that of the intima plus media (0.69 +/- 0.47 mm; r = 0.94, SEE = 0.15 mm; P = 0.012 between the coefficients). Discriminant analysis showed that intimal hyalinization, associated with intimal thickening, was strongly related to the presence of the three-layered appearance on IVUS (F to enter 40.0, P < 0.0001). These results indicate that the ultrasound layered appearance of human coronary arteries varies with histological alterations. We suggest that the thickness of the inner echogenic plus sonolucent layers on IVUS represents the intimal plus medial thickness observed by histology, and that the use of this value may be appropriate in the assessment of coronary wall thickening associated with atherosclerosis.

Aged↗
PubMed1996

A case of splenic artery aneurysm with Cushing's syndrome.

We report here a case of splenic artery aneurysm with Cushing's syndrome. Pregnancy and the increased secretion of cortisol from an adrenal adenoma in Cushing's syndrome may affect the intimal and medial degeneration. Factors other than glucocorticoids may influence the pathological changes.

Adrenal Glands↗
PubMed1996

Genomic imprinting of human p57KIP2 and its reduced expression in Wilms' tumors.

p57KIP2 is a potent tight-binding inhibitor of several G1 cyclin complexes, and is a negative regulator of cell proliferation. The gene encoding human p57KIP2 is located on chromosome 11p15.5, a region implicated in both sporadic cancers and Beckwith-Wiedemann syndrome (BWS), a cancer syndrome, making it a tumor suppressor candidate. Several types of childhood tumors including Wilms' tumor, adrenocortical carcinoma and rhabdomyosarcoma display a specific loss of maternal 11p15 alleles, suggesting that genomic imprinting plays an important part. Genetic analysis of the familial BWS has indicated maternal carriers and suggested a role in genomic imprinting. Previously, we demonstrated that p57KIP2 is imprinted in the mouse. Here we describe the genomic imprinting of human p57KIP2 and the reduction of its expression in Wilms' tumors. High resolution mapping locates p57KIP2 in the region responsible for both tumor suppressivity and BWS.

Alleles↗
PubMed1996

Sudden death in a patient with apparent idiopathic ventricular tachycardia.

Idiopathic ventricular tachycardia is widely believed to carry a favorable prognosis, although there have also been reports of sudden cardiac deaths. We present a case of sudden death in a patient with apparent idiopathic right ventricular tachycardia. This patient had long-standing and exercise-related symptoms, an essentially negative non-invasive cardiac evaluation, and spontaneous and inducible ventricular tachycardia of left bundle branch block and inferior axis morphology, that was treated with propranolol. After an uneventful 5-year course, the patient died suddenly. Postmortem examination revealed a severely dilated right ventricle and significant replacement of the right ventricular wall with adipose tissue. Interstitial fibrosis was also seen, but only to a very slight degree.

Bundle-Branch Block↗