A multidisciplinary approach to intestinal rehabilitation allows for fully integrated care of inpatients and outpatients with SBS by fostering coordination of surgical, medical, and nutritional management. Our experience with 2 comparable cohorts demonstrates that this multidisciplinary approach is associated with improved survival.

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Stroke is a devastating complication of thoracic endovascular aortic repair (TEVAR). Whether left subclavian artery (LSA) coverage and LSA revascularization affect stroke rate is debated. Whether patients with aneurysms or dissections undergoing TEVAR have higher stroke rates is also debated. We report a systematic review of 63 studies comprising more than 3,000 patients. We conclude that stroke risk after TEVAR is increased by LSA coverage, and that LSA revascularization reduces stroke risk. LSA revascularization may lower the rate of posterior stroke. TEVAR for aneurysm is associated with increased stroke risk compared to TEVAR for dissection.

Supramaximal concentrations of cholecystokinin or its analogue caerulein have been shown to stimulate the proteolytic activation of zymogens within the pancreatic acinar cell and initiate acute pancreatitis. Previous studies suggest that a low pH compartment might be required for activation. To test this hypothesis, the effects of agents that modulate intracellular pH on caerulein-induced trypsin and chymotrypsin activation were studied. Pretreatment of pancreatic acini with the proto-ionophore monensin (10 M) and the weak base chloroquine (40 M) inhibited activation. Pre-incubation with the vacuolar ATPase (V-ATPase) inhibitors bafilomycin A 1 and concanamycin A also decreased activation in a concentration-dependent manner with 50% inhibition at ϳ50 and 25 nM, respectively. Caerulein stimulation caused a time-and concentration-dependent translocation of soluble V-ATPase V 1 subunits to a membrane fraction, a marker of V-ATPase activation. Carbachol also stimulated translocation at supramaximal concentrations. Elevation of cytosolic Ca 2؉ by thapsigargin was sufficient to induce translocation. Thus, stimulation of VATPase activity appears to be required for agonist-induced zymogen activation in the pancreatic acinar cell.The premature activation of digestive zymogens in the pancreatic acinar cell plays a central role in the initiation of acute pancreatitis, but the mechanisms leading to activation remain unclear. Concentrations of cholecystokinin that are at least 10-fold greater than that generated by the physiologic response to a meal, a treatment known as hyperstimulation, cause zymogen activation and pancreatitis in vivo. Similarly, hyperstimulation of isolated pancreatic acini by cholecystokinin or its analogue caerulein causes zymogen activation in vitro (1, 2). Such activation appears to take place in unidentified membrane-bound organelles. Previous findings suggest that the generation of a low pH compartment in acinar cells is a feature of acute pancreatitis and may be required for zymogen activation. First, in both the caerulein hyperstimulation and the choline-deficient, ethionine-supplemented diet models of acute pancreatitis, acidic vacuoles are generated within acinar cells (3). Second, chloroquine, a weak base that non-selectively increases pH in acidic organelles, reduces the severity of pancreatitis in the caerulein hyperstimulation and choline-deficient, ethionine-supplemented diet models of pancreatitis (4, 5). Third, both proposed mechanisms of zymogen activation, trypsinogen autoactivation and trypsinogen activation by the lysosomal protease cathepsin B, proceed optimally at an acidic pH (6). Finally, chloroquine and monensin, agents that non-selectively increase intracellular pH, block the proteolytic conversion of procarboxypeptidase A 1 to its active form in isolated acini following caerulein hyperstimulation (1). Although these studies support a role for acidification in zymogen activation, they provide no information on the mechanism.Because vacuolar ATPase (V-ATPase) 1 acidifies many in...