The present study examines the effects of ionizing radiation in combination with rituximab (RTX), a chimeric human anti-CD20 monoclonal antibody, on proliferation, cell cycle distribution and apoptosis in B-lymphoma RL and Raji cells. Exposure to ionizing radiation (9 Gy) induced cell growth delay and apoptosis in RL cells, whereas Raji cells showed moderate radio-resistance. The simultaneous exposure of lymphoma cells to ionizing radiation and RTX (10 microg/mL) markedly enhanced apoptosis and cell growth delay in RL and Raji cells. Cooperative antiproliferative and apoptotic effects of RTX and radiation were achieved through the inhibition of c-myc and bcl-XL expression. Furthermore, RTX-modulated expression of cell cycle regulating proteins, such as p53, p21/WAF1, p27/KIP1, contributed to the development of radiation-induced cell killing and growth arrest. Each NHL cell line that underwent apoptosis induced by combination treatment revealed enhanced caspase-3 and poly (ADP-ribose) polymerase (PARP) cleavage as compared to only irradiated cells. These findings show that rituximab synergistically enhances radiation-induced apoptosis and cell growth delay through the expression of proteins involved in the programmed cell death and cell cycle regulation pathways.

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Three cases with the triad of ventricular septal defect, atrioventricular heart block, and corrected transposition of the great vessels are presented. In each instance the patient successfully underwent open heart surgery on the pump-oxygenator for closure of the ventricular septal defect. A review of the literature suggests a frequent association of these 3 conoenital anomalies. In our experience atrioventricular heart block is rarely encountered with simple ventricular septal defect. The finding of atrioventricular heart block in a patient with an interventricular septal defect warrants consideration of an associated corrected transposition of the great vessels.CORRECTED transposition of the great vessels is a rare anomaly in which the root of the aorta arises anterior to the pulmonary artery, yet each major vessel receives blood from its "correct" ventricle, (the aorta from the left ventricle, the lpulmonary artery from the right). As illustrated in figure 1, the main pulmonary artery fails to arch in front of the aorta in the iiormnal manner, and the left pulmonary artery passes behind the ascending aorta. Figure 2 illustrates the medial displacement of the cardiac catheter as it passes through the main pulmonary artery in corrected transposition. In complete transposition of the great vessels the position of the major trunks is similarly altered but they originate from reversed ventricles, the aorta from the right, and the pulmonary artery from the left ventricle.We are reporting 3 cases that represent combinations of defects that have been reported previously but whose association has not been stressed, namely "corrected tramisposition" of the aorta and pulmonary ar-