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Urocortin 1 (Ucn1) is a neuropeptide that regulates vascular tone and is implicated in both the vascular and immune cell-mediated responses to inflammation. The role of Ucn1 in regulating microvascular permeability has not been determined. We hypothesized that local Ucn1 release promotes microvascular permeability and that this effect augments the local gastrointestinal vascular response to lipopolysaccharide (LPS)-induced systemic inflammation. We measured hydraulic (L(p)) and macromolecule permeability in mesenteric venules. We show that a continuous infusion of 10(-7) m Ucn1 in a postcapillary venule increased L(p) 2-fold over baseline, as did LPS-induced inflammation. However, simultaneous infusion of Ucn1 and LPS markedly increased L(p) by 7-fold. After local knockdown of Ucn1 using RNA interference, infusion of Ucn1 with LPS resulted in return to 2-fold increase, confirming that Ucn1 synergistically augments hydraulic permeability during inflammation. LPS and Ucn1 treatment also resulted in increased numbers of interstitial microspheres, which colocalized with CD31(+) immune cells. Ucn1 activity is mediated through two receptor subtypes, CRH-R(1) and CRH-R(2). CRH-R(1) receptor blockade exacerbated, whereas CRH-R(2) receptor blockade decreased the LPS-induced increase in L(p). Finally, treatment with the c-JUN N-terminal kinase (JNK) antagonist SP600125 during infusion of LPS, but not Ucn1, decreased L(p). These findings suggest that Ucn1 increases microvascular permeability and acts synergistically with LPS to increase fluid and macromolecule losses during inflammation. Knockdown of endogenous Ucn1 during inflammation attenuates synergistic increases in L(p). Ucn1's effect on L(p) is partially mediated by the CRH-R(2) receptor and acts independently of the c-JUN N-terminal kinase signal transduction pathway.

SCCT is safe and effective for triaging hemodynamically stable patients with penetrating torso trauma. It successfully determined the need for operative intervention with appropriate clinical accuracy without the additional costs, morbidity, and delay of oral and rectal contrast. Trauma surgeons can reproducibly interpret SCCT with high-predictive accuracy as to whether patients with penetrating torso trauma require operative exploration.

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Background The release of proinflammatory cytokines during inflammation disturbs the endothelial barrier and can initiate significant intravascular volume loss. Proinflammatory cytokines also induce the expression of anti-inflammatory mediators, such as lipoxin, which promote the resolution of inflammation. Our hypothesis is that lipoxin A4 (LXA4) reverses the increased microvascular fluid leak observed during inflammatory conditions. Materials And Methods Microvascular fluid leak (Lp) was measured in rat mesenteric venules using a micro-cannulation technique. Lp was measured under the following conditions: 1) LXA4 (100nM) alone (n=5), 2) LXA4 (100nM) administered after endothelial hyperpermeability induced by a continuous perfusion of 10nM platelet activating factor (PAF) (n=5), 3) LXA4 (100nM) perfused after inflammation induced by a systemic bolus of 10mg/kg lipopolysaccharide (LPS) (n=5), and 4) LXA4 (100nM) perfused after LPS-induced inflammation during inhibition of c-Jun N-terminal kinase (n=4). Results LXA4 alone slightly increased Lp from baseline (Lp-baseline=1.05±0.03, Lp-LXA4=1.55±0.04; p<0.0001). PAF increased Lp fourfold (Lp-baseline=1.20±0.10, Lp-PAF=4.49±0.95; p<0.0001). LXA4 administration after PAF decreased Lp 66% versus PAF alone (from 4.49±0.95 to 1.54±0.13; p=0.0004). LPS-induced inflammation increased Lp over 2-fold (Lp-baseline=1.05±0.03, Lp-LPS=2.27±0.13; p<0.0001). LXA4 administration after LPS decreased Lp 42% versus LPS alone (from 2.27±0.13 to 1.31±0.05; p<0.0001). The effect of c-Jun N-terminal kinase inhibition during LPS-induced inflammation attenuated the decrease in leak cause by LXA4 by 51% (p=0.0002). Conclusion After either LPS or PAF, LXA4 attenuated the intravascular volume loss caused by these inflammatory mediators. LXA4’s activity may be partly mediated by the c-Jun N-terminal kinase signaling pathway. These data support an anti-inflammatory role for LXA4 and suggests a potential pharmacologic role for LXA4 during inflammation.

Military field hospitals and rural medical centers may lack surgical subspecialists. Robotic technology can enable proctoring of remotely located general surgeons by subspecialists. Our objective compared three proctoring platforms: (1) 6-degree-of-freedom (DOF) computer input devices controlling a camera and laser pointer mounted on robotic arms, (2) a computer mouse controlling a pan-tilt-zoom (PTZ) camera and robotic laser scanner, and (3) a computer pen/tablet controlling a PTZ-camera and robotic laser scanner. Our hypothesis was that a pen/tablet or mouse platform would be superior to the 6-DOF-input device platform. Five surgeons used each platform by simulating the creation of operative incisions. Qualitative (instrument handling, time, motion, spatial awareness) and quantitative performance (accuracy, speed) was assessed on a five-point scale. Each surgeon completed a satisfaction survey. Both mouse and pen/tablet had higher mean performance scores than the 6-DOF-input device in all quantitative (6-DOF = 1.7 +/- 0.8, mouse = 4.3 +/- 0.2, pen = 4.1 +/- 0.6; p < 0.001) and qualitative measures (6-DOF = 1.7 +/- 0.2, mouse = 4.8 +/- 0.0, pen = 4.6 +/- 0.1; p < 0.001). Handling, motion, and instrument awareness were superior with the mouse and pen/tablet versus 6-DOF-input devices (p < 0.0001). Speed and accuracy were also superior using the mouse or pen/tablet versus 6-DOF-input devices (p < 0.0001). Surgeons completed tasks faster using the mouse versus pen/tablet (p = 0.02). Satisfaction surveys revealed a preference for the mouse. This study demonstrates the superiority of a mouse or pen/tablet controlling a PTZ-camera and robotic laser scanner for remote surgical teleproctoring versus 6-DOF-input devices controlling a camera and laser pointer. Either a mouse or pen/tablet platform allows subspecialists to proctor remotely located surgeons.

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