Aerobic exercise function of patients with persistent coronary artery aneurysms secondary to Kawasaki disease

Nine patients with persistent coronary artery aneurysms 1.7–14.0 years after an episode of Kawasaki disease underwent progressive bicycle ergometry with expiratory gas analysis. Two of the patients had aneurysms complicated by angiographically documented coronary artery stenosis. Results of the exercise tests were compared to those obtained from a group of age- and gender-matched normal control subjects. The Kawasaki disease patients did not differ significantly from the control subjects with regard to peak oxygen consumption (81 ± 7% versus 79 ± 12% predicted), peak workload (75 ± 13% versus 77 ± 9% predicted), anaerobic threshold (21.9 ± 6.5 versus 18.9 ± 4.0 ml/kg per minute) or oxygen pulse (96 ± 7% versus 90 ± 14% predicted). None of the patients developed significant ST segment changes or rhythm disturbances during exercise. The exercise function of the patients with coronary artery stenosis did not differ from that of patients without stenosis. It was concluded that the aerobic exercise function of patients with persistent coronary artery aneurysms after an episode of Kawasaki disease appears to be well preserved. Kawasaki disease patients with significant coronary artery pathology are not accurately identified by a single assessment of aerobic exercise function.     

Hyperglycemia and reactive oxygen species mediate apoptosis in aortic endothelial cells through Janus kinase 2

The generation of reactive oxygen species (ROS) has been implicated in the perturbation of endothelial function and cell death. However, the specific signaling pathways which mediate and modifying this response have not been fully elucidated. Therefore, in this study we tested the hypothesis that activation of JAK2 is involved in the aortic endothelial cell (EC) response to ROS. When ECs were exposed to HG (25 mM) for 6 h or ROS (i.e., H(2)O(2) (100 microM)) for 1 h and returned to normal medium we found a decrease in cell density and morphologic signs of apoptosis. Furthermore, incubation of ECs with HG and H(2)O(2) also resulted in the tyrosine phosphorylation of JAK2. In addition, pretreatment of ECs with AG-490, an inhibitor of JAK2, prevented nuclear fragmentation, whereas inhibitors of Jun kinase (SP 600125), MAP kinase (PD 98059), Src kinase (PP2) or PI-3 kinase (wortmannin) were without effect. Finally, immunoblot analysis of caspase-3 and PARP cleavage confirmed a role for activation of JAK2 in both HG- or ROS-induced apoptosis, based on inhibition by either AG-490 or adenoviral transfection with a dominant-negative JAK2 mutant. In conclusion the activation of JAK2 plays a pivotal role in oxidant stress-induced commitment of ECs to apoptosis, based on studies with HG and H(2)O(2).     

Interferon production by bovine tracheal organ cultures infected with bovid herpesvirus 1 strains

Studies have been made of antiviral inhibitors produced by bovine tracheal organ cultures inoculated with strains of bovid herpesvirus 1. The inhibitors, which had properties of interferon, were assayed by a plaque-reduction method in bovine turbinate cell cultures with vesicular stomatitis virus as challenge virus. Each of the four strains of bovid herpesvirus 1 studied induced interferon in bovine tracheal organ cultures.