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This article discusses a first-in-human trial comparing laser speckle contrast imaging (LSCI) and indocyanine green fluorescence angiography (ICG-FA) for assessing tissue perfusion in minimally invasive colorectal and bariatric surgery. The study used the ActivSight™ device, which displayed LSCI and ICG-FA signals in various modes. The results showed that LSCI was concordant with ICG-FA and demonstrated more accuracy on repeat assessments. Surgeons found the device to be safe, usable, and effective in assessing tissue perfusion. However, the study had limitations, such as the lack of a control group and case heterogeneity. Overall, the dual-mode LSCI and ICG-FA imaging device shows promise for real-time, continuous assessment of tissue perfusion in minimally invasive surgery. [Extracted from the article]

The role of routine preoperative endoscopy before primary weight loss surgery remains controversial. We reviewed our experience to determine the frequency of abnormal findings in patients undergoing routine preoperative endoscopy before bariatric surgery. A tertiary level, academic-affiliated bariatric surgery practice. A retrospective chart review was performed between July 2014 and June 2016 of patients undergoing routine preoperative endoscopy before primary bariatric surgery. Variables evaluated included preendoscopy symptoms, planned bariatric surgical procedure, abnormal findings on endoscopy, and changes in planned bariatric surgical procedure after endoscopy. A total of 631 patients met inclusion criteria. Of patients, 72% (457) were female. The median age was 44 (interquartile range 36–55). The median body mass index was 46 (interquartile range 42–51). Most patients had no preendoscopy clinical symptoms (61.3%). The most frequent abnormal findings included esophagitis (26.5%), hiatal hernia (27.1%), gastric ulcer (4.9%), and biopsy-proven Barrett's esophagus (4.6%). Although patients with preoperative symptoms were more likely to have abnormal findings on endoscopy, there were no significant differences in rates of Barrett's esophagus in patients with (5.3%) or without (4.1%) symptoms. Of the total cohort, 18.4% had a change in their planned operation after endoscopy results. The findings in our large series suggest selective screening in symptomatic patients only may lead to failure of discovery of foregut pathology that should prompt consideration for changes in the planned bariatric surgical procedure. Further study is necessary to see if our findings have broad applicability. [ABSTRACT FROM AUTHOR]

Bone marrow–derived mesenchymal stromal cells (MSCs) used as “MSC therapy” after traumatic brain injury act as remote “bioreactors” via stimulation of lung macrophages and augmention of T regulatory cell production by the spleen, leading to systemic increases in circulating anti-inflammatory cytokines and alteration of the locoregional milieu of the central nervous system. The altered intracerebral microenvironment leads to modulation of the resident microglia population, thereby stimulating an increase in the ratio of M2 (anti-inflammatory) macrophage to M1 (proinflammatory) macrophage, and it is this effect that accounts for the observed neuroprotection. [ABSTRACT FROM AUTHOR]

Abstract: Background: Recent studies suggest that peritoneal fluid (PF) may be an important mediator of inflammation. The aim of this study was to test the hypothesis that PF may drive systemic inflammation in intra-abdominal sepsis by representing a priming agent for neutrophils. Methods: PF was collected 12 hours after the initiation of intra-abdominal sepsis in swine. Naive human neutrophils were primed with PF before treatment with N-formyl-Met-Leu-Phe or phorbol 12-myristate 13-acetate to elucidate receptor-dependent and receptor-independent mechanisms of neutrophil activation. Flow cytometry was used to quantify neutrophil surface adhesion marker expression of integrins and selectins and superoxide anion production. Additionally, proinflammatory cytokines were quantified in PF. Results: PF primed neutrophils via receptor-dependent and receptor-independent mechanisms. There were significant increases in the proinflammatory cytokines interleukin-6 and tumor necrosis factor–α in PF correlating with the development of intra-abdominal sepsis. Conclusions: PF represents a priming agent for naive polymorphonuclear cells in intra-abdominal sepsis. This may be secondary to increased levels of proinflammatory cytokines. Strategies to reduce the amount of PF may decrease the systemic inflammatory response by reducing a priming agent for neutrophils. [Copyright &y& Elsevier]

Background: Resuscitation-induced intestinal edema is associated with early and profound mechanical changes in intestinal tissue. We hypothesize that the sodium hydrogen exchanger (NHE), a mechanoresponsive ion channel, is a mediator of edema-induced intestinal contractile dysfunction. Methods: An animal model of hydrostatic intestinal edema was used for all experiments. NHE isoforms 1-3 mRNA and protein were evaluated. Subsequently, the effects of NHE inhibition (with 5-(N-ethyl-N-isopropyl) amiloride [EIPA]) on wet-to-dry ratios, signal transduction and activator of transcription (STAT)-3, intestinal smooth muscle myosin light chain (MLC) phosphorylation, intestinal contractile activity, and intestinal transit were measured. Results: NHE1-3 mRNA and protein levels were increased significantly in the small intestinal mucosa with the induction of intestinal edema. The administration of EIPA, an NHE inhibitor, attenuated validated markers of intestinal contractile dysfunction induced by edema as measured by decreased STAT-3 activation, increased MLC phosphorylation, improved intestinal contractile activity, and enhanced intestinal transit. Conclusion: The mechanoresponsive ion channel NHE may mediate edema-induced intestinal contractile dysfunction, possibly via a STAT-3 related mechanism. [ABSTRACT FROM AUTHOR]

Background: We sought to determine the effect of peritoneal fluid from a novel animal model of abdominal compartment syndrome (ACS) on the proinflammatory status of polymorphonuclear leukocytes (PMNs) and monocytes. We hypothesize that peritoneal fluid is a potential priming and/or activating agent for PMNs/monocytes. Methods: ACS was induced in female Yorkshire swine, and peritoneal fluid was collected at the time of decompressive laparotomy. Naïve PMNs/monocytes were primed and/or activated with peritoneal fluid, phosphatidylcholine (PAF) plus peritoneal fluid, peritoneal fluid plus n-formyl-met-leu-phe (fMLP), and peritoneal fluid plus phorbol 12-myristate 13-acetate (PMA). Activation was determined by surface marker expression of integrins (CD11b an CD18) and selectins (CD62L). Additionally, proinflammatory cytokines in peritoneal fluid were analyzed. Results: Peritoneal fluid did not activate PMNs but increased CD11b expression on monocytes. When used as a primer for fMLP- or PMA-induced activation, peritoneal fluid significantly increased CD11b and CD18 expression on PMNs and monocytes. Peritoneal fluid collected at 6 and 12 h post decompressive laparotomy had similar effects. Interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) levels were increased in peritoneal fluid. Conclusion: Peritoneal fluid represents a primer for PMNs/monocytes and seems to act through receptor-dependent and receptor-independent pathways. Strategies to reduce the amount of peritoneal fluid may decrease the locoregional and systemic inflammatory response by reducing priming and activation of neutrophils/monocytes. [Copyright &y& Elsevier]

Background: Hydrostatic intestinal edema initiates a signal transduction cascade that results in smooth muscle contractile dysfunction. Given the rapid and concurrent alterations in the mechanical properties of edematous intestine observed with the development of edema, we hypothesize that mechanical forces may serve as a stimulus for the activation of certain signaling cascades. We sought to examine whether isolated similar magnitude mechanical forces induced the same signal transduction cascades associated with edema. Methods: The distal intestine from adult male Sprague Dawley rats was stretched longitudinally for 2 h to 123% its original length, which correlates with the interstitial stress found with edema. We compared wet-to-dry ratios, myeloperoxidase activity, nuclear signal transduction and activator of transcription (STAT)-3 and nuclear factor (NF)-kappa B DNA binding, STAT-3 phosphorylation, myosin light chain phosphorylation, baseline and maximally stimulated intestinal contractile strength, and inducible nitric oxide synthase (iNOS) and sodium hydrogen exchanger 1–3 messenger RNA (mRNA) in stretched and adjacent control segments of intestine. Results: Mechanical stretch did not induce intestinal edema or an increase in myeloperoxidase activity. Nuclear STAT-3 DNA binding, STAT-3 phosphorylation, and nuclear NF-kappa B DNA binding were significantly increased in stretched seromuscular samples. Increased expression of sodium hydrogen exchanger 1 was found but not an increase in iNOS expression. Myosin light chain phosphorylation was significantly decreased in stretched intestine as was baseline and maximally stimulated intestinal contractile strength. Conclusion: Intestinal stretch, in the absence of edema/inflammatory/ischemic changes, leads to the activation of signaling pathways known to be altered in intestinal edema. Edema may initiate a mechanotransductive cascade that is responsible for the subsequent activation of various signaling cascades known to induce contractile dysfunction. [Copyright &y& Elsevier]

Abstract: Background: Pediatric truncal vascular injuries occur infrequently and have a reported mortality rate of 30% to 50%. This report examines the demographics, mechanisms of injury, associated trauma, and outcome of patients presenting for the past 10 years at a single institution with truncal vascular injuries. Methods: A retrospective review (1997-2006) of a pediatric trauma registry at a single institution was undertaken. Results: Seventy-five truncal vascular injuries occurred in 57 patients (age, 12 ± 3 years); the injury mechanisms were penetrating in 37%. Concomitant injuries occurred with 76%, 62%, and 43% of abdominal, thoracic, and neck vascular injuries, respectively. Nonvascular complications occurred more frequently in patients with abdominal vascular injuries who were hemodynamically unstable on presentation. All patients with thoracic vascular injuries presenting with hemodynamic instability died. In patients with neck vascular injuries, 1 of 2 patients who were hemodynamically unstable died, compared to 1 of 12 patients who died in those who presented hemodynamically stable. Overall survival was 75%. Conclusions: Survival and complications of pediatric truncal vascular injury are related to hemodynamic status at the time of presentation. Associated injuries are higher with trauma involving the abdomen. [Copyright &y& Elsevier]

Objective: The objective of the study was to examine whether the size of silicon nanovectors (SNVs) inhibits their entrance into the fetal circulation. Study Design: Pregnant rats were intravenously administered with SNVs or saline. The SNVs were spherical particles with 3 escalating diameters: 519 nm, 834 nm, and 1000 nm. The maternal and fetal distribution of SNVs was assessed. Results: In animals that received 1000 or 834 nm SNV, silicon (Si) levels were significantly higher in the maternal organs vs the saline group, whereas the silicon levels in fetal tissues were similar to controls. However, in animals receiving 519 nm SNVs, fetal silicon levels were significantly higher in the SNV group compared with the saline group (5.93 ± 0.67 μg Si per organ vs 4.80 ± 0.33, P = .01). Conclusion: Larger SNVs do not cross the placenta to the fetus and, remaining within the maternal circulation, can serve as carriers for harmful medications in order to prevent fetal exposure. [Copyright &y& Elsevier]