By B. M. Tang, S. J. Huang, A. S. McLean (auth.), Prof. Jean-Louis Vincent (eds.)
The Yearbook compiles the latest advancements in experimental and medical study and perform in a single complete reference e-book. The chapters are written via good famous specialists within the box of in depth care and emergency medication. it truly is addressed to every body thinking about inner drugs, anesthesia, surgical procedure, pediatrics, extensive care and emergency medicine.
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Yang Y, Shou Z, Zhang P, et al (2008) Mitochondrial DNA haplogroup R predicts survival advantage in severe sepsis in the Han population. Genet Med 10: 187 – 192 32. Torroni A, Petrozzi M, D’Urbano L, et al (1997) Haplotype and phylogenetic analyses suggest that one European-specific mtDNA background plays a role in the expression of Leber hereditary optic neuropathy by increasing the penetrance of the primary mutations 11778 and 14484. Am J Hum Genet 60: 1107 – 1121 33. Ruiz-Pesini E, Lapena AC, Diez-Sanchez C, et al (2000) Human mtDNA haplogroups associated with high or reduced spermatozoa motility.
References 1. Laterre PF (2007) Clinical trials in severe sepsis with drotrecogin alfa (activated). Crit Care 11 (Suppl 5):S5 2. Ely EW, Laterre P-F, Angus D, et al (2003) Drotrecogin alfa (activated) administration across clinically important subgroups of patients with severe sepsis. Crit Care Med 31: 12 – 19 3. Carlet J, Cohen J, Calandra T, Opal S, Masur H (2008) Sepsis: Time to reconsider the concept. Crit Care Med 36: 1 – 3 4. Levy M, Fink M, Marshall J, et al (2003) 2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference.
Apoptosis is triggered by both intrinsic and extrinsic pathways. Oxidative stress can induce the intrinsic pathway of apoptosis. The mitochondrial regulation of apoptosis occurs during the initiation and regulation of the intrinsic pathway. Lethal agents cause the mitochondria to release cyto- 15 I 16 I A. Pyle, P. Chinnery, and S. Baudouin chrome c and other pro-apoptotic proteins into the cytosol. Here they induce or amplify the activation of apoptotic caspases [6]. Mitochondrial oxidative stress has been implicated in cell death.