The Journal of surgical research
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Hemorrhagic shock (HS) followed by a subsequent insult ("second hit") often initiates an exaggerated systemic inflammatory response and multiple organ failure. We have previously demonstrated that valproic acid, a pan histone deacetylase inhibitor, could improve survival in a rodent "two-hit" model. In the present study, our goal was to determine whether selective inhibition of histone deacetylase 6 with Tubastatin A (Tub-A) could prolong survival in a two-hit model where HS was followed by sepsis from cecal ligation and puncture (CLP). ⋯ Tub-A treatment significantly improves survival, attenuates inflammation, and downregulates TNF-α and IL-6 gene expression in a rodent two-hit model.
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Randomized Controlled Trial
Parecoxib for the prevention of shivering after general anesthesia.
Shivering is the most common complication during the recovery period after general anesthesia, and there is no clear consensus about the best strategy for its prophylactic. The aim of the study was to evaluate the efficacy of parecoxib in prevention of postoperative shivering. ⋯ Prophylactic administration of parecoxib produces dual effects on antishivering and postoperative analgesia. This implies that cyclooxygenase 2-prostaglandin E2 pathways may be involved in the regulation of shivering.
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Epithelial to mesenchymal transition (EMT) of alveolar epithelial cells occurs in lung fibrotic diseases. Tanshinone IIA (Tan IIA) has been reported to exert anti-inflammatory effects in pulmonary fibrosis. Nonetheless, whether Tan IIA affects lung fibrosis-related EMT remains unknown and requires for further investigations. ⋯ Our research suggests that Tan IIA mitigates BLM-induced pulmonary fibrosis and suppresses TGF-β-dependent EMT of lung alveolar epithelial cells.
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The pathophysiology that drives the subacute hypercoagulable state commonly seen after traumatic brain injury (TBI) is not well understood. Alterations caused by TBI in platelet and microparticle (MP) numbers and function have been suggested as possible causes; however, the contributions of platelets and MPs are currently unknown. ⋯ MPs generated after TBI likely contribute to altered coagulation after head injury and may play a key role in the development of a posttraumatic hypercoagulable state in TBI patients.