Werner's syndrome: in vivo and in vitro characteristics as a model of aging.
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Biomedical subjects
Publications and source records attributed to N Sakamoto.
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Inhibitory factors were investigated, using 51Cr-labelled Chang cells as targets, based on the inhibition of lymphocyte-mediated cytotoxicity (LMC) in patients with chronic active hepatitis (CAH). A significant reduction of LMC was noted (P less than 0.001) when autologous sera of patients with CAH was added. The addition of HBsAg-positive and -negative homologous sera from CAH, which were as capable of inhibiting LMC as autologous sera, decreased LMC significantly (P less than 0.001). The LMC fell significantly (P less than 0.001) in the presence of sera of patients with rheumatoid arthritis. A significantly higher inhibition (P less than 0.001) by rheumatoid factor (RF) positive autologous sera of patients with CAH was observed when compared to that of RF-negative sera. Such autologous sera inhibiting LMC contained increased IgG levels (P less than 0.01) when compared to those that failed to inhibit LMC. A significant reduction of LMC was also induced with the addition of anti-HBs (P less than 0.05), HBsAg--anti-HBs (P less than 0.001) and IgG--anti-IgG (P less than 0.01) complexes, or aggregated IgG (P less than 0.001). The LMC was reduced significantly (P less than 0.001) after adding a purified liver-specific membrane lipoprotein (LSP) from human livers. There was some evidence for the inhibition of LMC being effected by these additives as a result of their acting on an effector cell level. These findings suggest that humoral factors including immune complexes, aggregated IgG and LSP play an important role for lymphocyte cytotoxicity in the pathogenesis of CAH.
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The present study was undertaken to discuss the echo source of systolic hump in hypertrophic obstructive cardiomyopathy (HOCM) from a viewpoint of B-mode echocardiography. Cross-sectional images were obtained from 4 patients with HOCM using a Sonolayergraph of Toshiba, SSL-51H. This equipment is characterized by its high speed mechanical sector scanning and wider angle. Recordings were made with ordinary 35 mm camera or Polaroid in conjunction with 8 mm cinecamera. Our data showed that systolic hump in this lesion was not caused by anterior systolic movement of anterior mitral leaflet, but was emanated from the chordae tendineae attached to the anterior or posterior mitral leaflet. In systole, the anterior mitral leaflet moved backward for closure, while the chordae tendineae approached the bulged interventricular septum resulting in the formation of systolic hump.
In order to study the intracardiac murmurs in coronary venous system, right heart catheterization was carried out on 35 patients with or without mitral regurgitation. The double-lumen phonocatheter of A. E. L. was used for 33 cases but for 2 the microtip phonocatheter of Millar was employed. As a rule, simultaneous recording of intracardiac and external phonocardiograms was made with the pressure tracing in the majority of cases. The examined subjects were divided into 3 groups; 9 cases with mitral regurgitation confirmed by left ventriculography (Group I), 20 without mitral regurgitation (Group II), and 6 with functional systolic murmur (Group III). In Group I, a loud systolic murmur was recorded in 7 cases (MR 5, MR + AR 1, ECD 1), but in none of IHSS in the coronary sinus or great coronary vein. In Group II, no systolic bruit was noted in VSD and other lesions except ASR in the coronary venous system. The same was true in patients with functional systolic murmur (Group III). Intracardiac phonocardiography is thought to be useful to record mitral regurgitant murmurs in the coronary venous system, since the latter is in the close proximity to the mitral posterior commissure or mitral annulus.
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