Understanding sciences behind fall-related hip fractures in older adults is important to develop effective interventions for prevention. The aim of this review is to provide biomechanical understanding and prevention strategies of falls and related hip fractures in older adults, in order to guide future research directions from biomechanical perspectives. While most hip fractures are due to a fall, a few of falls are injurious causing hip fractures, and most falls are non-injurious. Fall mechanics are important in determining injurious versus non-injurious falls. Many different biomechanical factors contribute to the risk of hip fracture, and effects of each individual factors are known well. However, combining effects, and correlation and causation among the factors are poorly understood. While fall prevention interventions include exercise, vision correction, vitamin D intake and environment modification, injury prevention strategies include use of hip protectors, compliant flooring and safe landing strategies, vitamin D intake and exercise. While fall risk assessments have well been established, limited efforts have been made for injury risk assessments. Better understanding is necessary on the correlation and causation among factors affecting the risk of falls and related hip fractures in older adults. Development of the hip fracture risk assessment technique is required to establish more efficient intervention models for fall-related hip fractures in older adults.

The majority of strokes are caused by ischemia and result in brain tissue damage, leading to problems of the central nervous system including hemiparesis, dysfunction of language and consciousness, and dysfunction of perception. The purpose of this study was to investigate the effects of Poly(ADP-ribose) polymerase(PARP) on necrosis in neuronal cells that have undergone needle electrode electrical stimulation(NEES) prior to induction of ischemia. Ischemia was induced in male SD rats(body weight 300g) by occlusion of the common carotid artery for 5 min, after which the blood was reperfused. After induction of brain ischemia, NEES was applied to Zusanli(ST 36), at 12, 24 and 48 hours. Protein expression was investigated using immuno-reactive cells, which react to PARP antibodies in cerebral nerve cells, and Western blotting. The results were as follows: In the cerebral cortex, the number of PARP reactive cells after 24 hours significantly decreased(p<.05) in the NEES group compared to the GI group. PARP expression after 24 hours significantly decreased(p<.05) in the NEES group compared to the GI group. As a result, NEES showed the greatest effect on necrosis- related PARP immuno-reactive cells 24 hours after ischemia, indicating necrosis inhibition, blocking of neural cell death, and protection of neural cells. Based on the results of this study, NEES can be an effective method of treating dysfunction and improving function of neuronal cells in brain damage caused by ischemia.