Objective: To investigate the effects of transient cerebral ischemia-reperfusion injury on the expression of CaMKK?, Bcl-2, Bax, and apoptosis in hippocampal region of young and aged rat. Materials and methods: A total of 48 young Sprague-Dawley?SD? rats and 48 aged SD rats were randomly divided into four groups: sham-operated (S) group and transient cerebral ischemia/reperfusion injury (IR) group. For S group, SD male rats were exposed bilateral common carotid arteries without blocked. For IR group, SD male rats were subjected to middle cerebral artery occlusion for 3 mins followed by reperfusion. After 1, 3, 5 and 7 days of reperfusion, all rats in each group was sacrificed, respectively. Western Blot were adopt for the expression of Calcium/calmodulin dependent protein kinase kinase ? (CAMKK?), Bcl-2 and Bax in hippocampus tissues after transient cerebral ischemia-reperfusion injury. Terminal deoxynucleotidyl transferase-mediated dNTP nick end labeling (TUNEL) staining was used to detect cell apoptosis. Results: Western blot showed that the expression of CaMKK?, Bcl-2 and Bax were increased in both young and aged groups after 1, 3, 5 and 7 day of sham-operated and reperfusion. The aged male rats had a higher levels of CaMKK? compared with young male rats after 1, 3, 5 and 7 day of reperfusion, and Bcl-2 only after 3 and 5 day of reperfusion, Bax only after 3 day of reperfusion (P <0.05). TUNEL staining showed that apoptotic cell in aged male rats increased significantly compared with young rats after 1, 3, 5 and 7 day of sham-operated and reperfusion. The aged male rats had more number of TUNEL-positive cells compared with young male rats after 1, 3, 5 and 7 day of reperfusion The expression of CaMKK?, Bcl-2, Bax and TUNEL-positive cells reached the peak level on 1st day in young male rats, however, on 3st day in aged male rats. Conclusion: our present findings demonstrate CaMKK? take part in transient cerebral ischemia-reperfusion injury, and different profiles of CaMKK? activation are exhibited in young and aged animals after transient cerebral ischemia-reperfusion injury.

Abstract \nBone thickness measured ultrasonically, requires knowledge of its velocity and its propagation-timealomg a path in the bone. This velocity is required to define intraoperatively the residual thickness of bone, which is in front of an inserted hardware (a drill, or an implant).There is a special importance in these measurements, during the ‘final stage’ of the insertion, when the residual thickness gets smaller. \nThe general problem being addressed by this study is to assess intraoperatively the intraosseous speed-of-sound. We present here and compare three novel methods for assessing intraoperatively the speed-of-sound in trabecular bone.\nThese methods are based on ultrasonic waves that propagate in both directions through a tiny stream of normal saline. Part of these echoes are detected by the same ultrasonic transducer. For assessing the ultrasonic speed-of-sound, these methods require additional drilled path, measured mechanically and its accuracy is smaller than the propagation time. In two of these methods, the assessed speed-of-sound depends on the accuracy of the additional drilled path and the propagation time, where in the third method, it depends only on the propagation time. Therefore, the second method is more accurate. \nOne of the methods provides the ultrasonic speed-of-sound (and therefore the residual thickness) in real-time. The signal processing and displaying the data are automatic in these methods; therefore, it is less human-dependent and more objective.\nThese methods have the potential in applications of skeletal surgeries (orthopedic, neurosurgery and also in dentistry), as they improve the time, objectivity and residual thickness accuracy during such surgical procedures.