Surgery
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Ventral abdominal wall hernias are common lesions and may be associated with life-threatening complications. The application of laparoscopic principles to the treatment of ventral hernias has reduced recurrence rates from a range of 25% to 52% to a range of 3.4% to 9%. In this study, we review our experience and assess the clinical outcome of patients who have undergone laparoscopic repair of ventral hernias. ⋯ The laparoscopic repair of ventral hernias is safe, effective, and durable with minimal morbidity. It is particularly successful in patients with recurrent lesions. The laparoscopic approach to ventral hernia repair should be considered the standard of care.
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Secretory immunoglobulin A (SIgA) is the principal immune defense against luminal pathogens at gut mucosal surfaces. It also has anti-inflammatory activities that may be important for the maintenance of mucosal surface integrity. Enterocyte apoptosis (Apo) is increased after challenge with invasive bacteria and ischemia-reperfusion insults. Increased Apo also has been associated with impaired intestinal barrier function. However, the impact of SIgA on enterocyte apoptosis and mucosal barrier integrity after challenge with commensal bacteria and ischemia-reperfusion is unknown. ⋯ Modulation of enterocyte Apo by SIgA may serve to maintain intestinal barrier function and thereby decrease the systemic inflammatory response after clinical conditions associated with gut ischemia-reperfusion insults.
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Linking the process of evidence-based guidelines to outcomes is difficult. We hypothesized that the process of implementing an evidence-based clinical guideline for blunt splenic trauma would reduce resource consumption and improve outcome. ⋯ Compliance with evidence-based data in the management of blunt splenic injury improved rates of nonoperative management, decreased hospital days, and did not change mortality rates. An evidence-based clinical guideline evaluated with process measures can reduce resource use and improve outcome in a trauma program.
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Resuscitated hemorrhagic shock predisposes patients to the development of organ dysfunction, particularly to lung injury. Ischemia/reperfusion during shock is believed to prime the immune system for an exaggerated inflammatory response to a second delayed stimulus. We previously reported an in vitro model of oxidant-induced priming of the macrophage to lipopolysaccharide (LPS) involves the Src family of tyrosine kinases. Because the Src family has been shown to activate the p38 mitogen-activated protein kinase (MAPK) pathway, we hypothesize that LPS signaling after oxidant stress involves the p38 pathway and is activated by Src kinases. ⋯ Oxidant stress generated during global ischemia/reperfusion activates p38 MAPK in an Src-dependent manner. Oxidants seem to alter the LPS-induced activation of p38. P38 does not seem to have a direct role in leading to oxidant-induced NF-kappaB translocation but may affect other oxidant-induced transcription factors. This altered pathway provides an alternative avenue to target therapy during the oxidant-induced priming of the macrophage induced by trauma resuscitation.
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Heme oxygenase (HO)-1 system has been shown to provide protection against oxidative stress through the degradation of heme to biliverdin, free iron, and carbon monoxide (CO). This study investigated cytoprotective efficacy of CO at a low concentration on cold ischemia/reperfusion (I/R) injury of transplanted intestine. ⋯ These results indicate a significant role for CO in protecting the intestine from cold I/R injury associating with small intestinal transplantation.