Hot Topics in Burn Injuries

The aim of this book is to give readers a broad review of burn injuries, which may affect people from birth to death and can lead to high morbidity and mortality. The book consists of four sections and seven chapters. The first section consists of the introductory review chapter, which overviews the burn injuries. The second section includes chapter ""Burn Etiology and Pathogenesis,"" which focuses on burn injuries and clinical findings. The third section consists of chapter ""Controlling Inflammation in Burn Injury"" and is devoted to the role of inflammatory response, which is fundamental to the healing process, while a prolonged inflammation may lead to scarring and fibrosis. The fourth section consists of four chapters as follows: ""Therapeutic Effects of Conservative Treatments on Burn Scars,"" ""Herbal Therapy for Burns and Burn Scars,"" ""Platelet-Rich Plasma in Burn Treatment,"" and ""Surgical Treatment of Burn Scars."" The book is easy to read and includes hot topics on burn injury to enhance the reader's understanding and knowledge

The Link Between Unpredictable Chronic Mild Stress Model for Depression and Vascular Inflammation?

Abstract-Inflammation has been suggested to be associated with stress-induced depression and cardiovascular dysfunction. Tumor necrosis factor alpha (TNF-α) is a major cytokine in the activation of neuroendocrine, immune, and behavioral responses. In this study, we investigated the effects of infliximab (a TNF-α inhibitor) on endothelium-dependent vascular reactivity, systemic blood pressure, and endothelial nitric oxide synthase (eNOS) immunoreactivity in the unpredictable chronic mild stress (UCMS) model of depression in rats. There was no significant change between all groups in the systemic blood pressure. In UCMS, endothelium-dependent relaxation of the smooth muscle in response to carbachol was significantly decreased with 50 % maximal response (E max ) and pD2 values compared with the controls. Infliximab was able to reverse this UCMS effect. Relaxation in response to the nitric oxide (NO) donor sodium nitroprusside and papaverine and KCl-induced contractile responses was similar between groups. In UCMS, decreased expression of eNOS was detected. Moreover, there was no significant change in UCMS+infliximab group with respect to control rats. Our results suggest that tumor necrosis factor-alpha (TNF-α) could be a major mediator of vascular dysfunction associated with UC-MS, leading to decreased expression of eNOS