The p53-deficient hemopoietic stem cells: their resistance to radiation-apoptosis, but lasted transiently.

Hemopoietic stem cells lacking with p53 are known to be resistant to radiation apoptosis: p53-product induces, on one hand, the cells that have been injured by radiation to stop cell-cycle at G, phase, and on the other hand the cells that have not been repaired to go into apoptosis. Thus, in the p53-deficient mice, the hemopoietic stem cells after graded dose of radiation show a flatter survival curve for radiation, i.e., like a curve for radio-resistant phenotype. However, we found the radio-resistance in the stem cell was only transient, and an apoptosis in p53-deficient hemopoietic stem cells, we made concentrated analysis including the end-labeling technique to detect double strand breaks of DNA. Results clearly showed that, according to the end-labeling for spleen colonies, the p53-deficiency showed rather higher incidence of apoptosis (30-50%) as compared with the wild-control (17%). Irradiation with 200cGy for the recipient mice two months after transplantation, showed an induction of higher incidence of hemopoietic malignancies, when the heterozygous marrow was repopulated, however, none of increase was observed in the recipient mice repopulated with the homozygous bone marrow. Clear difference between the hetero- and the homozygous in inducing hemopoietic malignancies with the 200cGy-radiation may be reflected by the different degree of delayed appearance of apoptosis during the development of the spleen colonies.

Transient increase in wall thickness of the left ventricular apex after stunned myocardium: a case report.

A case of transiently increased wall thickness in the left ventricular apex after stunned myocardium due to severe attack of vasospastic angina is described. "Ace of spades" configuration, documented by left ventriculogram and increased apical wall thickness of the left ventricle, as revealed by two-dimensional echocardiograms returned to normal in 2 months. This transiently increased left ventricular mass may have been due to myocardial edema, which is occasionally seen in the recovery course of active myocarditis.

[Two cases of atrial septal defect diagnosed by two-dimensional Doppler echocardiography: comparison with other methods for detecting atrial septal defect].

We describe two cases of atrial septal defect(ASD) diagnosed by chance with two-dimensional Doppler echocardiography(2DD) which was carried out for another purpose. There were no findings characteristic of ASD such as systolic murmurs in the pulmonary area, incomplete right bundle branch block pattern on electrocardiograms, increased hilar shadow on chest films or increased right ventricular chamber diameter in two-dimensional echocardiography. However, the 2DD showed blood flow crossing through the atrial septum. Cardiac catheterization confirmed the presence of a small ASD. ASD diagnosed by 2DD alone without other classical characteristic signs of ASD indicates that the ASD is small and clinically insignificant as it is with Doppler valvular heart disease.

[Congestive heart failure in the elderly: severe tricuspid regurgitation by two-dimensional Doppler echocardiography].

We studied five cases of atrial fibrillation in the elderly showing severely decreased exercise tolerance (NYHA III) and normal left ventricular function. There were no signs of classical tricuspid regurgitation. Both atria were enlarged and right ventricular sizes were shown by two-dimensional echocardiography to have mildly increased. Two-dimensional Doppler echocardiography revealed severe tricupid regurgitation but at a maximal velocity less than 2.3 m/sec, meaning that right ventricular pressure was not increased. Cardiac output (CO) and circulating blood volume (BV), measured by radiocardiography showed CO to have decreased and BV to have increased. No intracardiac shunt was detected. The cause of this decreased exercise tolerance in the group in our study is thought to be right ventricular dysfunction due to the aging process. This also occurs in a similar pattern in younger people who have arrhythmogenic right ventricular dysplasia (ARVD), Uhl's disease, or right ventricular dilated cardiomyopathy.

Experimental study of the maternal effects on tumor immunity of infant mice with C1300 mouse neuroblastoma.

The spontaneous regression of neuroblastoma (NB), one of the most common malignant tumors in childhood, is found to occur in 1% to 2% of patients with NB, especially in young infants. An unexpectedly favorable response to therapy is also noticed in infants suggesting the potential presence of an immune mechanism. Monoclonal C1300-S and C1300A-4 cell lines were established from polyclonal C1300 cells in our laboratory. Adult female A/J mice that had rejected 1 x 10(3) NB cells (C1300S-3) or 1 x 10(5)-10(6) NB cells (C1300A-4) were used as immunized mothers. The immunized mothers with C1300A-4 or C1300S-3 were found to have specific antibodies to C1300S-3 cells by 51Cr release assay of complement dependent cytotoxicity. Newborn mice, 24 hours after birth from immunized or nonimmunized mothers, were inoculated with 1 x 10(3) C1300S-3 NB cells. The same antibody that was assayed in the immunized mothers was detected in this offspring by the antibody-dependent cell cytotoxicity (ADCC). The tumor incidence in the offspring of the immunized mothers was found to be less than that of the offspring of the nonimmunized mothers. This study suggests that the lower tumor incidence in the offspring of immunized mothers compared with offspring of nonimmunized mothers may be attributed to their ADCC activity. Furthermore, the antibody that has the ADCC activity was proven to be immunoglobulin G by a serum absorption test using IgG absorbant. This study offers insight into the relationship between transported mother-infant immunoglobulins and on its potential control of NB.