The durability of revisional sleeve gastrectomy and Roux-en-Y gastric bypass after previous adjustable gastric band.

Background: Patients with adjustable gastric banding (AGB) often require revision to one-stage or two-stage sleeve gastrectomy (SG) or Roux-en-Y gastric bypass (RYGB).

Objective: To compare the long-term durability of revisional SG and RYGB, in terms of subsequent revision or conversion (RC).

Methods: The New York Statewide Planning and Research Cooperative Systems dataset was queried from 2006 to 2013 for patients who underwent primary SG and RYGB, one-stage, and two-stage conversion from AGB to SG and RYGB.

Contact Isolation Precautions in Trauma Patients: An Analysis of Infectious Complications.

Background: Victims of traumatic injuries represent a population at risk for a wide variety of complications. Contact isolation (CI) is a set of restrictions designed to help prevent the transmission of medically significant organisms in the healthcare setting. A growing body of literature demonstrates that CI can have significant implications for the individual isolated patient.

Putting the MeaT into TeaM Training: Development, Delivery, and Evaluation of a Surgical Team-Training Workshop.

Background: Despite importance to patient care, team training is infrequently used in surgical education. To address this, a workshop was developed by the Association for Surgical Education Simulation Committee to teach team training using high-fidelity patient simulators and the American College of Surgeons-Association of Program Directors in Surgery team-training curriculum.

Methods: Workshops were conducted at 3 national meetings.

Oxidative Stress Increases Surface Toll-Like Receptor 4 Expression in Murine Macrophages Via Ceramide Generation.

Multiorgan failure is a major cause of late mortality following trauma. Oxidative stress generated during shock/resuscitation contributes to tissue injury by priming the immune system for an exaggerated response to subsequent inflammatory stimuli, such as lipopolysaccharide (LPS). We recently reported that oxidative stress causes rapid recruitment of the LPS receptor Toll-like receptor 4 (TLR4) to membrane lipid rafts, thus increasing LPS responsiveness and cellular priming.

Simulated laparoscopic operating room crisis: An approach to enhance the surgical team performance.

Objective: Diminishing human error and improving patient outcomes is the goal of task training and simulation experience. The fundamentals of laparoscopic surgery (FLS) is a validated tool to assess technical laparoscopic skills. We hypothesize that performance in a crisis depends on technical skills and team performance.

Financial impact of obesity and bariatric surgery.

Obesity constitutes a major health problem with serious social and economic consequences worldwide. In North America, nearly one third of the population is obese, and this figure includes children and adolescents who are likely to become obese adults. Obesity carries a great financial impact on society; consequently, treating morbidly obese patients with surgery may offer substantial economic savings.

Oxidative stress generated by hemorrhagic shock recruits Toll-like receptor 4 to the plasma membrane in macrophages.

Oxidative stress generated by ischemia/reperfusion is known to prime inflammatory cells for increased responsiveness to subsequent stimuli, such as lipopolysaccharide (LPS). The mechanism(s) underlying this effect remains poorly elucidated. These studies show that alveolar macrophages recovered from rodents subjected to hemorrhagic shock/resuscitation expressed increased surface levels of Toll-like receptor 4 (TLR4), an effect inhibited by adding the antioxidant N-acetylcysteine to the resuscitation fluid.

Impaired induction of IL-10 expression in the lung following hemorrhagic shock.

The balance between pro- and anti-inflammatory cytokines is considered to be an important determinant of the magnitude of inflammation in a number of disease states. We previously showed that resuscitated hemorrhagic shock augmented LPS-induced release of proinflammatory molecules by alveolar macrophages (AM). In the present studies, we evaluated the expression and regulation of the counter inflammatory cytokine IL-10 in the lung using this model.

The role of the Src family of tyrosine kinases after oxidant-induced lung injury in vivo.

Background: Patients sustaining major trauma are predisposed to the development of organ dysfunction. We have shown that oxidant stress generated by hemorrhagic shock/resuscitation (S/R) in rodents increases lipopolysaccharide (LPS)-induced lung injury and translocation of nuclear factor kappa B (NF-kappaB) in alveolar macrophages (AMs). In addition, using a cellular model, we have shown that priming with oxidants reprograms LPS signaling through an Src-dependent pathway.

Twenty-five percent albumin prevents lung injury following shock/resuscitation.

Objective: To evaluate novel indications for the use of human albumin solutions in the prevention and treatment of acute lung injury following shock/resuscitation and to test the hypothesis that 25% human albumin is an effective resuscitation fluid as well as an immunomodulatory agent protective against lung injury in our model.

Design: A previously developed rodent model of acute lung injury in which resuscitated shock primes for increased lung injury in response to a small dose of intratracheal lipopolysaccharide.

Setting: University-affiliated hospital.

Hypertonic resuscitation of hemorrhagic shock upregulates the anti-inflammatory response by alveolar macrophages.

Background: Resuscitated hemorrhagic shock predisposes patients to the development of acute respiratory distress syndrome (ARDS). Hypertonic saline (HTS) has been shown to inhibit immune cell activation in response to lipopolysaccharide (LPS) in vitro and to reduce lung damage when used for resuscitation of hemorrhagic shock in vivo. We hypothesize that HTS resuscitation of hemorrhagic shock may exert this anti-inflammatory effect by modulating alveolar macrophage function leading to an altered balance between the proinflammatory and the counter-inflammatory response.

Oxidant-induced priming of the macrophage involves activation of p38 mitogen-activated protein kinase through an Src-dependent pathway.

Background: 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.

Oxidative stress reprograms lipopolysaccharide signaling via Src kinase-dependent pathway in RAW 264.7 macrophage cell line.

Oxidative stress generated during ischemia/reperfusion injury has been shown to augment cellular responsiveness. Whereas oxidants are themselves known to induce several intracellular signaling cascades, their effect on signaling pathways initiated by other inflammatory stimuli remains poorly elucidated. Previous work has suggested that oxidants are able to prime alveolar macrophages for increased NF-kappa B translocation in response to treatment with lipopolysaccharide (LPS).

25% Albumin modulates adhesive interactions between neutrophils and the endothelium following shock/resuscitation.

Background: Polymorphonuclear neutrophil (PMN) sequestration in the lung is a hallmark of acute respiratory distress syndrome (ARDS). We have shown that 25% Albumin (A25) resuscitation attenuates lung injury after hemorrhagic shock and lipopolysaccharide (LPS) exposure by reducing lung leukosequestration. We hypothesize that this protective property is mediated by alteration of neutrophil-endothelial cell adhesive interactions.

Impaired activation of mitogen-activated protein kinases after hemorrhagic shock.

Background: Patients sustaining major trauma are at risk of developing organ dysfunction. We have previously shown that resuscitated hemorrhagic shock primes for increased lung injury in response to lippolysaccharide (LPS), in part by preventing upregulation of the counterinflammatory cytokine IL-10. Because the mitogen-activated protein kinase (MAPK) family is known to participate in LPS signaling, we hypothesized that altered upstream signaling through these kinases might contribute to impaired LPS-simulated IL-10 release after shock and resuscitation.