Novel endoscopic management of buried bumper syndrome in percutaneous endoscopic gastrostomy: The Olympus HookKnife.

Buried bumper syndrome (BBS) is an uncommon but serious complication of percutaneous endoscopic ga-strostomy. It involves the internal fixation device, or "bumper", migrating into the gastric wall and subsequent mucosal overgrowth. We described a case series of four patients with BBS treated with a novel endoscopic technique using a HookKnife between June 2016 and February 2017. The HookKnife is a rotating L-shaped cutting wire designed for hooking tissue and pulling it away from the gastric wall towards the lumen. The technique was successful in all four cases with no complications. Each patient was discharged on the day of treatment. The HookKnife is a manoeuvrable, safe and effective device for endoscopic removal of buried bumpers and could avoid surgery in a high risk group of patients. To our knowledge this technique has not been described previously. We suggest that this technique should be added to the treatment algorithms for managing BBS.

Innovative use of Octopus IV stabilizer in cardiac trauma.

We report an innovative use of the Octopus IV cardiac stabilizer in a case of penetrating thoracic injury. In this case, we used the Octopus IV cardiac stabilizer to immobilize the right ventricular outflow tract during the repair of a stab wound. To date, there have been no reports of such an application of the Octopus IV cardiac stabilizer.

Preconditioning the diabetic heart: the importance of Akt phosphorylation.

Conflicting evidence exists whether diabetic myocardium can be protected by ischemic preconditioning (IPC). The phosphatidylinositol 3-kinase (PI3K)-Akt pathway is important in IPC. However, components of this cascade have been found to be defective in diabetes. We hypothesize that IPC in diabetic hearts depends on intact signaling through the PI3K-Akt pathway to reduce myocardial injury. Isolated perfused Wistar (normal) and Goto-Kakizaki (diabetic) rat hearts were subjected to 1) 35 min of regional ischemia and 120 min of reperfusion with infarct size determined; 2) preconditioning (IPC) using 5 min of global ischemia followed by 10 min of reperfusion performed one, two, or three times before prolonged ischemia; or 3) determination of Akt phosphorylation after stabilization or after one and three cycles of IPC. In Wistar rats, one, two, and three cycles of IPC reduced infarct size 44.7 +/- 3.8% (P < 0.05), 31.4 +/- 4.9% (P < 0.01), and 34.3 +/- 6.1% (P < 0.01), respectively, compared with controls (60.7 +/- 4.5%). However, in diabetic rats only three cycles of IPC significantly reduced infarction to 20.8 +/- 2.6% from 46.6 +/- 5.2% in controls (P < 0.01), commensurate with significant Akt phosphorylation after three cycles of IPC. To protect the diabetic myocardium, it appears necessary to increase the IPC stimulus to achieve the threshold for cardioprotection and a critical level of Akt phosphorylation to mediate myocardial protection.

The reperfusion injury salvage kinase pathway: a common target for both ischemic preconditioning and postconditioning.

Novel treatment approaches, as potential adjunctive therapy to current reperfusion strategies (such as thrombolysis, primary coronary angioplasty, and cardiac surgery), are required to provide further cardioprotection in the setting of an acute myocardial infarction to effect further reductions in morbidity and mortality. In this regard, the activation of prosurvival kinases, such as Akt and Erk1/2 (which we have termed the reperfusion injury salvage kinase [RISK] pathway), at the time of reperfusion, has been demonstrated to confer powerful cardioprotection against myocardial ischemia-reperfusion injury. In this review, we present evidence suggesting that the cardioprotective phenomena of ischemic preconditioning and the recently described ischemic postconditioning exert their cardioprotective effects through the recruitment of the RISK pathway, at the time of reperfusion, and that the protection in these settings is mediated through the inhibition of mitochondrial permeability transition pore (mPTP) opening at this time. Therefore, the pharmacologic manipulation of the RISK pathway at the time of reperfusion may enable one to harness the powerful cardioprotective benefits of both ischemic preconditioning and postconditioning, and provide a novel approach to cardioprotection.

Postconditioning: a form of "modified reperfusion" protects the myocardium by activating the phosphatidylinositol 3-kinase-Akt pathway.

Brief intermittent episodes of ischemia and reperfusion, at the onset of reperfusion after a prolonged period of ischemia, confer cardioprotection, a phenomenon termed "ischemic postconditioning" (Postcond). We hypothesized that this phenomenon may just represent a modified form of reperfusion that activates the reperfusion injury salvage kinase (RISK) pathway. Isolated perfused rat hearts were subjected to: (a) 35 minutes of ischemia and 120 minutes of reperfusion, and infarct size was determined by tetrazolium staining; or (b) 35 minutes of ischemia and 7 minutes of reperfusion, and the phosphorylation states of Akt, endothelial NO synthase (eNOS), and p70S6K were determined. Postcond reduced infarct size from 51.2+/-3.4% to 31.5+/-4.1% (P<0.01), an effect comparable with ischemic preconditioning (IPC; 27.5+/-2.3%; P<0.01). Of interest, the combined protective effects of IPC and Postcond were not additive (30.1+/-4.8% with IPC+Postcond; P=NS). Inhibiting phosphatidylinositol 3-kinase (PI3K) at reperfusion using LY or Wortmannin (Wort) during the first 15 minutes of reperfusion completely abolished Postcond-induced protection (31.5+/-4.1% with Postcond versus 51.7+/-4.5% with Postcond+LY, P<0.01; 56.2+/-10.1% with Postcond+ Wort; P<0.01), suggesting that Postcond protects the heart by activating PI3K-Akt. Western blot analysis demonstrated that Postcond induced a significant increase in phosphorylation of Akt, eNOS, and p70S6K in an LY- and Wort-sensitive manner. In conclusion, we show for the first time that ischemic Postcond protects the myocardium by activating the prosurvival kinases PI3K-Akt, eNOS, and p70S6K in accordance with the RISK pathway.

The role of salivary function in modulating chemotherapy-induced oropharyngeal mucositis: a review of the literature.

Oropharyngeal mucositis is a common and significant complication of cancer chemotherapy and limits the delivery of chemotherapy, affects the quality of life, and increases the cost of care. Oral mucositis caused by cancer chemotherapy is associated with specific agents, but the origin of oral mucositis is poorly understood. These drugs may have direct toxic effects on the rapidly dividing cells of the oral mucosa and on cellular elements of the connective tissue. Microbial flora may play a role in the development of ulcerative mucositis. Chemotherapy may be directly toxic and affect the mucosa by systemic circulation and may be related to secretion of some chemotherapeutic drugs in the saliva, resulting in topical exposure to the oral environment. Other potential mechanisms include reduced saliva volume and change in saliva constituents that may affect epithelial maintenance and repair, the physiology of the oral microflora, and the interaction between the oral flora and the epithelium. Improved understanding of the mechanisms whereby specific chemotherapeutic agents cause mucositis may lead to management approaches that will reduce the incidence and severity of mucositis, improving quality of life and ensuring delivery of the necessary chemotherapy to improve cancer cure rates.