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Postconditioning (POC), a novel strategy of cardioprotection against ischemia-reperfusion injury, is clinically attractive because of its therapeutic application at the predictable onset of reperfusion. POC activates several intracellular kinase signaling pathways, including phosphatidylinositol 3-kinase (PI3K)-Akt (RISK). The regulation of POC-induced survival kinase signaling, however, has not been fully characterized. JAK-STAT activation is integral to cardiac ischemic tolerance and may provide upstream regulation of RISK. We hypothesized that POC requires the activation of both JAK-STAT and RISK signaling. Langendorff-perfused mouse hearts were subjected to 30 min of global ischemia and 40 min of reperfusion, with or without POC immediately after ischemia. A separate group of POC hearts was treated with AG 490, a JAK2 inhibitor, Stattic, a specific STAT3 inhibitor, or LY-294002, a PI3K inhibitor, at the onset of reperfusion. Cardiomyocyte-specific STAT3 knockout (KO) hearts were also subjected to non-POC or POC protocols. Myocardial performance (+dP/dt(max), mmHg/s) was assessed throughout each perfusion protocol. Phosphorylated (p-) STAT3 and Akt expression was analyzed by Western immunoblotting. POC enhanced myocardial functional recovery and increased expression of p-STAT3 and p-Akt. JAK-STAT inhibition abrogated POC-induced functional protection. STAT3 inhibition decreased expression of both p-STAT3 and p-Akt. PI3K inhibition also attenuated POC-induced cardioprotection and reduced p-Akt expression but had no effect on STAT3 phosphorylation. Interestingly, STAT3 KO hearts undergoing POC exhibited improved ischemic tolerance compared with KO non-POC hearts. POC induces myocardial functional protection by activating the RISK pathway. JAK-STAT signaling, however, is insufficient for effective POC without PI3K-Akt activation.

BACKGROUND: Multidisciplinary tracheostomy teams have been successful in improving operative outcomes; however, limited data exist on their effect on postoperative care. We aimed to determine the effectiveness of a multidisciplinary tracheostomy service alone and following implementation of a post-tracheostomy care bundle on rates of decannulation and tolerance of oral diet before discharge. METHODS: Prospective data on all subjects requiring tracheostomy by any trauma/ critical care surgeon were collected from January 2011 to December 2013 following development of a tracheostomy service and continued following implementation of the post-tracheostomy care bundle. Rates of decannulation and tolerance of oral diet were compared between all groups: pre-tracheostomy service (baseline, historical control), tracheostomy service alone, and tracheostomy service with post-tracheostomy care bundle. RESULTS: Three hundred ninety-three subjects met the criteria for analysis with 61 in the baseline group, 124 following initiation of a tracheostomy service, and 208 after the addition of the post-tracheostomy care bundle. There were significant overall differences between all groups in the proportion of subjects decannulated, proportion of subjects tolerating oral diet, and number of subjects receiving speech evaluations. Pairwise comparisons showed no differences in decannulation or tolerance of oral diet following implementation of the tracheostomy service alone but significant improvement with the addition of the posttracheostomy care bundle compared with baseline. (P ‫؍‬ .002 and P ‫؍‬ .005, respectively). Likewise, the number of speech language pathologist consults significantly increased compared with baseline only after the post-tracheostomy care bundle (P ‫؍‬ .004). Time to speech evaluation significantly decreased with the post-tracheostomy care bundle compared with baseline and tracheostomy service (P < .013). CONCLUSIONS: The addition of a post-tracheostomy care bundle to a multidisciplinary tracheostomy service significantly improved rates of decannulation and tolerance of oral diet.

Novel technique of aortic banding followed by gene transfer during hypertrophy and heart failure. Physiol Genomics 9: 49-56, 2002; 10.1152/physiolgenomics.00035.2001.-Aortic banding in the rat has become a popular method to induce left ventricular (LV) hypertrophy and heart failure. However, because of often extensive intrathoracic adhesions and inflammatory cell infiltrates resulting from the traditional surgical approach, an uncomplicated second thoracic incision for genetic manipulation is impeded. In this study, we describe a novel surgical technique of aortic banding which avoids opening the sternum and thereby avoids adhesions and surgery-related inflammation. Placing a clip on the ascending aorta using a suprasternal approach in SpragueDawley rats created proximal aortic constriction. The present study was initiated to determine whether a replication-deficient adenovirus would enable efficient gene transfer to adult cardiac myocytes undergoing hypertrophy and transitioning to heart failure. Echocardiography performed at week 24 revealed significant concentric hypertrophy and increased fractional shortening followed by LV dilatation with decreased fractional shortening after 27 wk of banding. An adenoviral solution encoding for the reporter green fluorescent protein gene (GFP) was delivered to the heart. Fluorescent microscopy revealed global gene expression throughout hypertrophied and failing hearts. Our studies demonstrate that a novel suprasternal approach can be applied to create an LV hypertrophy model followed by heart failure which also allows investigators to perform genetic manipulations in vivo through gene transfer without the complication of adhesions and surgical trauma-induced inflammation. Furthermore, our approach to delivery of transgenes results in homogenous gene expression in both hypertrophied and failing hearts.

Surgical resident experience on most trauma services is heavily weighted to nonoperative management, with a relatively low number of procedures, little experience with DPL, and highly variable experience with ultrasound. These data have serious implications for resident training and recruitment into the specialty.

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A significant portion of patients sustaining traumatic brain injury (TBI) take antiplatelet medications (aspirin or clopidogrel), which have been associated with increased morbidity and mortality. In an attempt to alleviate the risk of increased bleeding, platelet transfusion has become standard practice in some institutions. This study was designed to determine if platelet transfusion reduces mortality in patients with TBI on antiplatelet medications. Databases from two Level I trauma centers were reviewed. Patients with TBI 50 years of age or older with documented preinjury use of clopidogrel or aspirin were included in our cohort. Patients who received platelet transfusions were compared with those who did not to assess outcome differences between them. Demographics and other patient characteristics abstracted included Injury Severity Score, Glasgow Coma Scale, hospital length of stay, and warfarin use. Three hundred twenty-eight patients comprised the study group. Of these patients, 166 received platelet transfusion and 162 patients did not. Patients who received platelets had a mortality rate of 17.5 per cent (29 of 166), whereas those who did not receive platelets had a mortality rate of 16.7 per cent (27 of 162) ( P = 0.85). Transfusion of platelets in patients with TBI using antiplatelet therapy did not reduce mortality.