Abstract. Free radicals play an important role in the

Abstract. Historically, clinical outcomes following spinal cord injury (SCI) have been dismal. Severe SCI leads to devastating neurological deficits, and there is no treatment available that restores the injury-induced loss of function to a degree that an independent life can be guaranteed. To address all the issues associated with SCI, a multidisciplinary approach is required, as it is unlikely that a single approach, such as surgical intervention, pharmacotherapy or cellular transplantation, will suffice. High mobility group box 1 (HMGB1) is an inflammatory cytokine. Various studies have shown that HMGB1 plays a critical role in SCI and that inhibition of HMGB1 release may be a novel therapeutic target for SCI and may support spinal cord repair. In addition, HMGB1 has been associated with graft rejection in the early phase. Therefore, HMGB1 may be a promising therapeutic target for SCI transplant patients. We hypothesize that inhibition of HMGB1 release rescues patients with SCI. Taken together, our findings suggest that anti-HMGB1 monoclonal antibodies or short hairpin RNA-mediated HMGB1 could be administered for spinal cord repair in SCI patients. Contents1. Introduction 2. HMGB1 as a therapeutic target in various diseases 3. HMGB1 in spinal cord injury 4. HMGB1 in transplantation 5. Hypothesis IntroductionOne of the most serious clinical conditions is spinal cord injury (SCI), the incidence of which has been increasing yearly (1). Spinal cord repair is a problem that has long puzzled neuroscientists (2,3). The repair of the injured human spinal cord with resultant functional recovery is one of the major challenges of contemporary neuroscience (4). Although the mortality rate of SCI has declined to less than 5%, the disability rate associated with SCI remains high (1). One of the most destructive complications after SCI is paraplegia, which has been a constant challenge in clinical medicine (1). Facilitating recovery of spinal cord structure and function after SCI is of great interest to neuroscientists (1

Abstract. Free radicals play major roles in the pathogenesis of tissue damage in many diseases and clinical conditions, and the removal of free radicals may offer a treatment option.

Abstract. Stroke is a major cause of mortality and disability worldwide. During the past three decades, major advances have occurred in secondary prevention, which have demonstrated the broader potential for the prevention of stroke. Risk factors for stroke include previous stroke or transient ischemic attack, hypertension, high blood cholesterol and diabetes. Proven secondary prevention strategies are antiplatelet agents, antihypertensive drugs, statins and glycemic control. In the present review, we evaluated the secondary prevention of stroke in light of clinical studies and discuss new pleiotropic effects beyond the original effects and emerging clinical evidence, with a focus on the effect of optimal oral pharmacotherapy. Contents1. Introduction 2. Antiplatelet agents 3. Antihypertensive drugs 4. Statins 5. Glycemic control 6. Conclusion IntroductionStroke is one of the leading causes of disability worldwide (1). In 2002, stroke-related disability was estimated to be the sixth most common cause of reduced disability-adjusted life-years (DALYs; the sum of life-years lost as a result of premature mortality and years lived with disability adjusted for severity) (2). However, due to the burgeoning elderly population in Western societies, it has been estimated that by 2030, stroke-related disability in such societies will be the fourth most significant cause of DALYs (3). Stroke also has substantial costs related to complications, including poststroke dementia, depression, falls, fractures and epilepsy (4). Risk factors and sources of stroke must be identified in order to take steps towards preventing stroke (5). Although primary prevention is most significant in the reduction of stroke burden, effective secondary prevention is also essential (4). Secondary prevention addresses all measures for avoiding recurrences following a first transient ischemic attack (TIA) or

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