Critical care medicine
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Critical care medicine · Feb 2014
Case ReportsNeurologic Recovery From Profound Accidental Hypothermia After 5 Hours of Cardiopulmonary Resuscitation.
To describe the successful neurologic recovery from profound accidental hypothermia with cardiac arrest despite the longest reported duration of cardiopulmonary resuscitation. ⋯ With no evidence of trauma or asphyxia, profound accidental hypothermia with cardiac arrest represents a specific condition for which successful neurologic recovery is feasible despite prolonged cardiopulmonary resuscitation.
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Critical care medicine · Feb 2014
Prolonged Therapeutic Hypothermia Is More Effective in Attenuating Brain Apoptosis in a Swine Cardiac Arrest Model.
To investigate whether 48 hours of therapeutic hypothermia is more effective to attenuate brain apoptosis than 24 hours and to determine whether the antiapoptotic effects of therapeutic hypothermia are associated with the suppressions of the cleavage of protein kinase C-δ, the cytosolic release of cytochrome c, and the cleavage of caspase 3 in a swine cardiac arrest model. ⋯ We found that 48 hours of therapeutic hypothermia was more effective in attenuating brain apoptosis than 24 hours of therapeutic hypothermia. We also found that the antiapoptotic effects of therapeutic hypothermia were associated with the suppressions of the cleavage of protein kinase C-δ, the cytosolic release of cytochrome c, and the cleavage of caspase 3.
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Critical care medicine · Feb 2014
Inhibiting the Toll-Like Receptor 4 Toll/Interleukin-1 Receptor Domain Protects Against Hepatic Warm Ischemia and Reperfusion Injury in Mice.
During Toll-like receptor 4 signaling, the Toll/interleukin-1 receptor domain is essential for interactions with downstream Toll/interleukin-1 receptor domain-containing adaptor proteins. The aim of this study is to investigate the role of the Toll/interleukin-1 receptor domain in the Toll-like receptor 4 signaling pathway during hepatic ischemia and reperfusion injury. ⋯ Toll/interleukin-1 receptor domain inhibition disrupts the interaction of Toll-like receptor 4 with its adaptor proteins, which abrogates downstream signaling pathways and prevents the activation of nuclear factor-κB and Jun N-terminal kinase/p38. This reduction in signaling consequently reduces hepatic inflammation, cell apoptosis, and hepatic damage. Toll/interleukin-1 receptor domain-targeted therapy thus represents a new approach to inhibit the intracellular Toll-like receptor 4 signaling pathway and reveals novel therapeutic target sites, which will facilitate the development of specific therapeutic agents.