Induction of Apoptosis of Rat Neonatal Cardiomyocytes by Chemical Ischemia and Reoxygenation: The Role of Phosphatidylserine

Ischemia/reperfusion injury plays a crucial role in the induction of the cell death of myocytes. The precise mechanism of the cell death, however, has not been elucidated enough. This study examined the cell death of rat neonatal myocytes induced by chemical ischemia and reoxygenation with an in vitro model, in terms of apoptosis, and the role of phosphatidylserine, which is recognized with annexin V. Chemical ischemia and reoxygenation were conducted on the cultured myocytes obtained from 1- or 2-day-old Wistar rats. The cells were divided into 4 groups exposed to chemical ischemia for 9 h (Group A), 18 h (Group B) and 24 h (Group C) and one group not exposed to chemical ischemia (Control Group). DNA ladder formation on agarose gel electrophoresis was noted in Groups B and C followed by reoxygenation, but not in Group A, as well as all 4 groups without reoxygenation. There were cells positive to terminal deoxynucleotidyl transferase-mediated dUDP-biotin nick end labeling in all 3 groups except for the Control Group; after reoxygenation, the number of cells became larger in Groups B and C than in Group A. Flow cytometry revealed that annexin V-positive cells were 1.15 ± 0.82% in the Control Group, 4.07 ± 3.8% in Group A without reoxygenation and 15.5 ± 6.3% in Group A after 30-min reoxygenation, respectively; the value was significantly higher in the latter than the former two (P < 0.01). Although 18-h and 24-h ischemia increased the annexin V-positive cells, reoxygenation did not alter the number of cells in Groups B and C. These results indicate that i) chemical ischemia followed by reoxygenation variably induces apoptosis of rat myocytes, ii) long-term ischemia causes phosphatidylserine translocation on the cell surface membrane, regardless of reoxygenation and iii) mild ischemia necessitates reoxygenation to translocate phosphatidylserine, which might play a crucial role in the initiation of apoptosis of the myocytes

Simulation Data Analysis by Virtual Reality System

We introduce new software for analysis of time-varying simulation data and new approach for contribution of simulation to experiment by virtual reality (VR) technology. In the new software, the objects of time-varying field are visualized in VR space and the particle trajectories in the time-varying electromagnetic field are also traced. In the new approach, both simulation results and experimental device data are simultaneously visualized in VR space. These developments enhance the study of the phenomena in plasma physics and fusion plasmas

Sorafenib-induced Prostate Volume Reduction, a New Adverse Effect Detected by Imaging: A Pilot Study

Background: Sorafenib has been used in the treatment of advanced hepatocellular carcinoma (HCC) and renal cell carcinoma (RCC). Sorafenib-associated organ reduction have been reported on imaging, such as thyroid, pancreas and muscle, but there has been no research on prostate volume reduction (PVR).Methods: We retrospectively analyzed 26 patients (twenty with HCC and six patients with RCC) who underwent sorafenib therapy for 31 to 1225 days (median, 100 days). PVR was estimated by two independent readers using CT volumetry.Results: The sum of all prostate volumes measured by reader 1 was 24.2 ± 13.8 cm3 on the baseline CT and 20.4 ± 10.6 cm3 on the follow-up CT (p < 0.001), and that measured by reader 2 was 22.3 ± 13.9 cm3 on the baseline CT and 19.2 ± 10.6 cm3 on the follow-up CT (p < 0.001). The concordance correlation coefficient for the prostate volume measured by the two readers was 0.95 on the baseline CT scans and 0.94 on the follow-up CT scans. Sorafenib-associated PVR demonstrated slight dependence to the exposure time (r = –0.23). One patient with benign prostatic hyperplasia (BPH) showed PVR (from 80.4 to 61.5 cm3 [reader 1]; 83.4 to 61.6 cm3 [reader 2]) after sorafenib administration. Sorafenib-associated PVR occurred in patients both with and without underlying liver dysfunction with relative prostate volume changes of 86.7 ± 12.0% and 85.0 ± 9.0%, respectively.Conclusion: Our study demonstrated significant PVR with sorafenib treatment in patients regardless of the presence of BPH and underlying liver dysfunction