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Y Kitaura

Publications and source records attributed to Y Kitaura.

At least 73 records · Page 4Linked to original sources
PubMed1985

Cell-mediated immunity in Coxsackie B3 virus myocarditis in mice--in situ characterization by monoclonal antibody of mononuclear cell infiltrates.

This light- and electron-microscopic study using monoclonal antibody and anti-immunoglobulin antibodies in murine Coxsackie B3 virus myocarditis provides an immunohistochemical demonstration of surface antigens of lymphocytes. On the 7th and 9th days after inoculation, many necrotic cardiocytes were surrounded by numerous cellular infiltrates, in which macrophages and T lymphocytes predominated, whereas immunoglobulin-bearing B lymphocytes represented a minority. Immuno-electron microscopy showed some T lymphocytes in close contact with other lymphocytes, macrophages, and the sarcolemma of cardiocytes. After the 30th day, significant numbers of T lymphocytes and macrophages were still identifiable in and around the fibrotic foci. Our study suggests that cell-mediated immunity plays a protective role by lysing and scavenging virus-infected cardiocytes and cell debris at least in the early stage of myocarditis. The residual T lymphocytes in the chronic stage suggest their involvement in sustained cardiocyte injury.

Animals↗
PubMed1985

Electron-microscopic and immunohistochemical studies on endomyocardial biopsies from a patient with eosinophilic endomyocardial disease.

Light- and electron-microscopic studies and immunohistochemical procedures were carried out on blood eosinophils and left ventricular endomyocardial biopsies from a 68-year-old man with an eosinophilia of 8.2 X 10(9)/l and congestive cardiac failure due to eosinophilic endomyocardial disease. Some blood eosinophils were vacuolated and degranulated, and reversal of the normal staining pattern of eosinophil granules was seen by means of electron microscopy. The biopsies showed degenerative changes in the cardiac myocytes, with interstitial fibrosis and infiltration by numerous eosinophils, mast cells, and macrophages. Eosinophils infiltrating the myocardium showed a decrease in the number of granules, many of which were indistinct or contained dissolving crystalloids, which occasionally were seen to be discharged onto the surface of adjacent cardiac myocytes. Immunohistochemical studies of the endomyocardial biopsies with a monoclonal antibody, which is specific for activated eosinophils and binds to the secreted forms of eosinophil cationic protein (ECP) and eosinophil protein-X (EP-X), demonstrated that the lesions contained numerous activated eosinophils and secreted ECP and EP-X. These findings support the concept that in eosinophilic endomyocardial disease, activated eosinophils infiltrate and degranulate in the myocardium, releasing eosinophil cationic proteins which then damage adjacent myocardial cells.

Aged↗
PubMed1985

Factors discriminating survivors and nonsurvivors in alcoholic heart disease.

Eighteen patients with dilated cardiomyopathy and a history of excessive ethanol intake were monitored for 3-98 months (mean 23 months). Six patients died (mean age 43.7 +/- 9.2 years) and 12 patients survived (mean age 48.8 +/- 9.5 years). Of the echocardiographic findings taken during heart failure, only the relative wall thickness to the internal dimension of the left ventricle (t/r ratio) differed significantly (survivors 0.33 +/- 0.77 vs. nonsurvivors 0.25 +/- 0.04, P less than 0.05). Of the hemodynamic data obtained after treatment of heart failure, left ventricular end-diastolic pressure differed significantly (survivors 6 +/- 2 vs. nonsurvivors 12 +/- 4 mmHg, P less than 0.001). The two groups could not be differentiated by ejection fraction, cardiac output, end-diastolic or end-systolic volumes, or semi-quantitative analysis of histologic findings obtained by right ventricular endomyocardial biopsy (light microscopy). Only two of six nonsurvivors (33%) succeeded in abstaining from alcohol, while eight of twelve survivors (67%) became teetotalers (P less than 0.05). Total abstinence from alcohol seems to be essential but was not necessarily followed by recovery in the most severe cases. Thus, the absence of adequate hypertrophy and high left ventricular filling pressure may predict the prognosis in alcoholic heart disease.

Adult↗
PubMed1984

Experimental coxsackie B3 virus myocarditis in golden hamsters. II. Evaluation of left ventricular function in intact in situ heart 14 months after inoculation.

The hemodynamic changes of the left ventricle (LV) of golden hamsters surviving for 14 months after acute coxsackie B3 virus myocarditis were assessed with the use of a high fidelity micromanometer pressure system. Of 25 infected hamsters, 10 survived to the 14th month, and 4 of these had cardiomegaly. Body weight (BW) was 150.0 +/- 20.7 g (mean +/- SD) (controls, 164.5 +/- 20.1 g, NS); heart weight (HW), 0.499 +/- 0.084 g (controls, 0.448 +/- 0.035 g, NS); and HW/BW, 3.39 +/- 0.79 X 10(-3) (controls, 2.74 +/- 0.23 X 10(-3), p less than 0.05). The hemodynamic data under anesthesia were: HR, 378 +/- 42 (controls, 414 +/- 43, NS); LVSP, 108 +/- 16 mmHg (controls, 126 +/- 16, NS); LVDP, 4.0 +/- 4.8 mmHg (controls, 0.6 +/- 0.7, NS); LVEDP, 9.7 +/- 7.5 mmHg (controls, 3.4 +/- 1.4, NS); peak positive dp/dt, 4960 +/- 1431 mmHg/sec (controls, 6714 +/- 1326, p less than 0.05); (dp/dt)/DP40, 56.8 +/- 9.8 sec-1 (controls, 73.1 +/- 7.0, p less than 0.01); peak negative dp/dt, 3876 +/- 1072 mmHg/sec (controls, 4971 +/- 599, p less than 0.05); and time constant T of LV pressure fall, 7.7 +/- 1.3 msec (controls, 5.9 +/- 0.7, p less than 0.01). Five hamsters had congestion of the lungs and liver with or without an elevation of LVEDP. One of them had an organizing thrombus in the left atrium, and one had an aneurysm in the LV free wall. Though markedly varied in extent, residual myocardial fibrosis was always evident in the hearts in which isovolumic contractility and early diastolic relaxation of the LV were significantly impaired. In a clinical extension of these findings, it may be that some cases of dilated cardiomyopathy in man develop in a way similar to the pathological processes noted in this experiment.

Animals↗
PubMed1983

Coxsackie B5 myopericarditis in a young adult--clinical course and endomyocardial biopsy findings.

An 18-year-old student with recent gastrointestinal symptoms was found to have Stokes-Adams syndrome. A transvenous pacemaker was successfully inserted with clinical improvement. Subsequent viral titer studies and serum enzyme changes supported the diagnosis of coxsackie B5 myopericarditis. The first cardiac catheterization and endomyocardial biopsy of the right ventricle were performed on the 14th hospital day; the former revealed no hemodynamic abnormalities, but the latter showed marked necrosis of the myofibers, disarray of the remaining ones, mononuclear cell infiltration and the appearance of fibroblasts with fine collagen fiber proliferation in the interstitium. A second biopsy of both ventricles, carried out on the 46th hospital day, showed no necrosis of the myofibers or inflammatory cell infiltration but increasing collagen fiber proliferation in the interstitium and disarray of the surviving myofibers. These pathological findings suggest the healing process of the myopericarditis. To the best of our knowledge, reports of viral myopericarditis with serial endomyocardial biopsies have been few.

Adolescent↗
PubMed1982

Studies on a new immunoactive peptide, FK-156. IV. Synthesis of FK-156 and its geometric isomer.

For the structural confirmation of FK-156, two possible structures, 1 and its geometric isomer 2, were synthesized. Di-Z-meso-diaminopimelic acid (4) was converted into 14 via a sequence of reactions involving, as key steps, an enzyme-mediated asymmetric hydrolysis (6 leads to 7), followed by carbobenzyloxylation using a copper chelate procedure (7 leads to 8). Condensation of 14 and the appropriately protected lactoyl dipeptide 17 and removal of the protecting groups of the resulting 18 afforded 1. Protection of 7 to 22, followed by coupling to glycine via an azide method, gave 25. Derivatization of 25 to 29 and condensation with 17 gave 30, which was deprotected to yield 2. Compound 1 proved to be identical in all respects with the natural product.

Adjuvants, Immunologic↗
PubMed1981

Virological study of idiopathic cardiomyopathy: serological study of virus antibodies and immunofluorescent study of myocardial biopsies.

In 113 patients with idiopathic cardiomyopathy paired sera obtained 2--4 weeks apart were examined for neutralizing antibody to coxsackie B 1--6, and echo 4, 6, 7, 9 and 11 viruses. Only eight cases (6.9 per cent) showed a significant change in titer, indicating a virus infection during or shortly before the study. Complement-fixing antibody titers were measured in 126 patients and neutralizing antibodies in 116 patients with idiopathic cardiomyopathy. More patients had complement-fixing antibody titers greater than or equal to 1 : 4 to coxsackie B and herpes simplex virus than did controls (p less than 0.05). Neutralizing antibody titers to coxsackie B 1 and B 3 virus were also higher in patients (p less than 0.01 for titers greater than or equal to 1 : 4 and p less than 0.05 for titers greater than or equal to 1 : 16). Complement-fixing antibody titers greater than or equal to 1 : 4 to herpes simplex virus were more frequent (p less than 0.05) in hypertrophic cardiomyopathy and those to coxsackie B, herpes simplex and influenza A virus were more frequent in congestive cardiomyopathy. Neutralizing antibody titers were more common to coxsackie B 3 (p less than 0.05 for titers of greater than or equal to 1:4) in hypertrophic cardiomyopathy, while in congestive cardiomyopathy they were more common to B 1 (p less than 0.01 for titers greater than or equal to 1 : 4 and p less than 0.05 for titers greater than or equal to 1 : 16), to coxsackie B 3 virus (p less than 0.001 for titers greater than or equal to 1 : 4 and p less than 0.04 for titers greater than or equal to 1 : 16) and to coxsackie B 5 (p less than 0.05 for titers greater than or equal to 1 : 4 or more) and to echo 6 virus (p less than 0.05 for titers greater than or equal to 1 : 4 and greater than or equal to 1 : 128). Immunofluorescent study of 61 cases showed no virus antigens in the biopsied myocardium even in patients who had significant changes in neutralizing antibody titers in paired sera. These results suggest a relationship between virus infection and idiopathic cardiomyopathy not only of the congestive type but also of the hypertrophic type. However, they do not provide definite proof of the virus infection theory of the disease.

Adult↗
PubMed1981

[A result of mass-screening for uterine cervical cancer in Hyogo prefecture (author's transl)].

A result of mass-screening for uterine cervical cancer conducted by Hyogo Cancer Hospital performed using mobilunit from 1965 to 1978 was analyzed and presented in this paper. The total number of women taking our initial screening examination was 188, 183.5% women screened or 9,447 were transferred for the further accurate examination. The rate of participants for this 2nd examination was 93.8% on the average. In this initial screening examination, a result of cytological examination on Papanicolaou's classification was as follows; 94.87% for class I and II, 4.81% for class III, and 0.21% for class IV and V. In the 2nd examination, the rate of the negative, suspected positive were 70.6%, 22.5% and 6.9% respectively. 759 cervical cancers were detected in our screening. The detecting rate of cervical cancer was 0.4% among initially screened women and 8.6% among women who appeared for the accurate examination. As the detecting rate among women for the 2nd examination became higher year by year (20% increase during recent 3 years), the accuracy of our screening methodology appeared to be improving. The incidence rate of cervical cancer in our screening was classified as stage 0; 49.0%, Ia; 36.4%, Ib; 9.1%, II; 3.9% an III; 1.6%. The most of detected cancer was occupied by cancer in situ and early invasive cancer. Annual review showed there is a gradual and steady increase in incidence rate to stage 0 in our screening.

Female↗