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Biomedical subjects

H Nagoshi

Publications and source records attributed to H Nagoshi.

At least 55 records · Page 3Linked to original sources
PubMed1987

Chromosome aberrations and clinical features of adult T cell leukemia-lymphoma not associated with human T cell leukemia virus type I.

Chromosome aberrations and clinical features of three patients with adult T cell leukemia-lymphoma (ATL) not associated with human T cell leukemia virus type I (HTLV-I) are described. From their clinical features, two patients were diagnosed as acute type and one patient was diagnosed as chronic type, which later converted to acute crisis. Clonal and many chromosomal abnormalities were observed before therapy in the two acute type cases and at relapse in the chronic type case. Karyotype aberrations, including trisomy 3, trisomy 7, trisomy 21, del(6)(q21), del(10)(p13), 14q11 translocation, and loss of X chromosome, all of which are frequently found in HTLV-I associated ATL, were also seen in these cases of HTLV-I-negative ATL.

Acute Disease↗
PubMed1984

Clinical implications of anti-HTLV antibody titer, abnormal lymphocytes in HTLV carriers and HTLV genome negative adult T-cell leukemia-lymphoma.

Abnormally large lymphocytes with Pelger-like nuclear lobulation have been found in peripheral blood of smoldering adult T-cell leukemia-lymphoma (ATL) patients. They are also found in quite low percentage in peripheral blood of healthy HTLV carriers. Therefore, it has become difficult to discriminate smoldering ATL having only abnormal lymphocytes from a healthy human T-cell leukemia virus (HTLV) carrier only by morphology and serology. We found that patients with smoldering ATL with visceral organ involvement such as skin or lung lesions had much higher titer (about 1 : 1,000) of anti-HTLV antibodies than those with other subtypes of ATL (about 1 : 250); the difference was highly significant (p less than 0.001). In addition, the period of survival of patients with smoldering ATL having antibody with high titer was much longer than that of patients with other subtypes of ATL, suggesting the role of a host immune response. Four cases of HTLV-negative ATL were found to have the same chromosomal abnormality as that has been seen in HTLV-positive typical ATL; the situation was quite similar to Burkitt's lymphoma. Since it has been considered that HTLV does not include oncogenes, a common oncogenic mechanism, ATL specific cellular oncogenes, might exist: they might be activated by HTLV or a mechanism other than a virus.

Antibodies, Viral↗
PubMed1983

Anti-ATLA (antibody to adult T-cell leukemia-lymphoma virus-associated antigen)-negative adult T-cell leukemia-lymphoma.

Five cases of adult T-cell leukemia-lymphoma (ATL) having typical clinicohematologic and morphologic features but negative for anti-ATLA [antibody to ATL virus (ATLV)-associated antigen (ATLA)] are presented. Some differences in immunologic, epidemiologic, and serologic data between anti-ATLA-positive and -negative ATLs are also described. Expression of ATLA in early primary cultured leukemic cells was found to be negative in three patients tested (Cases 1, 2 and 4), however, a long-term cultured cell line, ATL-6A, derived from peripheral blood leukemia cells from Case 1, was found to express ATLA. Mother of Case 1 and a daughter of Case 2 were anti-ATLA negative. These results indicate that ATLV was involved in certain anti-ATLA-negative ATL patients, at least in Case 1, and that the patient had no detectable immune response against ATLV and ATLA. However, in other cases in which no ATLA reactivity of serum and no ATLA expression in cultured leukemic cells were observed, another possibility such as activation of an unknown cellular oncogene specific for ATL without ATLV involvement may be considered. In order to prove these possibilities definitely, it is necessary to elucidate whether or not proviral DNA of ATLV is integrated into chromosomal DNA of ATL cells and to find a cellular oncogene specific for ATL in the future.

Adult↗
PubMed1983

[Backward flow signal in the left atrium studied by Doppler echocardiography. Differentiation from mitral regurgitation].

A backward flow signal in the left atrium masquerading as mitral regurgitation was studied by a pulsed Doppler method. The subjects consisted of 20 normal volunteers, 12 cases with mitral valve prolapse syndrome, five cases with rheumatic mitral regurgitation, five cases with lone atrial fibrillation, four cases with asymmetric septal hypertrophy and three cases with the Björk-Shiley tilting disc valve in the mitral position. In two-dimensional echocardiography combined with pulsed Doppler method, a Doppler signal was recorded by locating a sample volume in the left atrium. In all of the cases with mitral valve prolapse syndrome and the cases with the prosthetic valve as well as in all of the normal subjects, the backward flow signal was observed in the left atrium. In three cases with mitral valve prolapse syndrome, it was differentiated from a transvalvular regurgitant flow signal. In all cases with rheumatic mitral regurgitation, the backward flow signal was masked by a turbulent flow signal representing regurgitation. In cases with mitral stenosis, the backward flow signal was scarcely recognized. The duration of the backward flow signal had no relationship with heart rate. The histogram of incidence on the scale of R-R interval revealed normal distribution with a mean value of 0.24 sec (+/- 0.09 sec). Therefore, in cases with tachycardia, the backward flow signal was seen throughout systole. The peak backward flow velocity of Doppler signals was correlated (r = 0.71, p less than 0.01) with the peak forward flow velocity in diastole. The faint backward flow signal seen in cases with mitral stenosis and post-extrasystolic potentiation of the backward flow signal were suggestive of the foregoing relationship. The mechanism producing the backward flow was postulated as a water hammer phenomenon caused by closure of the mitral valve.

Adult↗
PubMed1977

Studies on the coronary circulation by a simulation method.

Some aspects of the control mechanism in the coronary circulation were investigated by using analog simulation. The simulation is designed to separate passive or mechanical factor from entire influence on the change in coronary flow consisting of passive and active factors, under different hemodynamic conditions. Simulated waveform was very similar to the blood flow pattern of the left circumflex artery actually obtained by an electromagnetic flowmeter. Pressure flow relationship was almost linear. Coronary flow increased with rise of aortic pressure, with the influence of active factors exceeding greatly that of the passive factors. When the heart rate was increased, the decrease in coronary flow due to the passive factors themselves was found. After the occlusion of the coronary artery the slight reactive hyperemia due to only passive factors was observed in the simulated flow.

Animals↗