Pyloroplasty for Refractory Gastroparesis.

Gastroparesis is a chronic gastric motility disorder in which the pathophysiology mimics a postvagotomy state. Pyloroplasty is beginning to emerge as a successful drainage procedure for refractory gastroparesis. Here we report our experience using pyloroplasty in the surgical management of diabetic and nondiabetic gastroparesis. A retrospective study was performed of 46 patients undergoing pyloroplasty for refractory gastroparesis from January 2010 through December 2013. Gastric emptying scintigraphy and the Gastroparesis Cardinal Symptom Index were assessed pre- and postoperatively. Laparoscopic pyloroplasty was performed in 42 patients, open pyloroplasty in three, and one patient was converted from laparoscopic to open pyloroplasty. Studies were repeated during the six to 12 month postoperative interval. The postoperative gastric emptying scintigraphy improved in 90 per cent of patients and normalized in 60 per cent. Postoperative T½ was significantly reduced (P = 0.001) as was four-hour retention (P < 0.001). The Gastroparesis Cardinal Symptom Index showed statistically significant reduction in symptom severity for all nine categories (P < 0.0005) as well as total symptom score (P < 0.005). No patients developed dumping syndrome. Pyloroplasty is a highly effective therapy for refractory gastroparesis, offering significant reduction in symptom severity, improvement in quality of life, and acceleration of gastric emptying.

The PLEXIN PLX-2 and the ephrin EFN-4 have distinct roles in MAB-20/Semaphorin 2A signaling in Caenorhabditis elegans morphogenesis.

Semaphorins are extracellular proteins that regulate axon guidance and morphogenesis by interacting with a variety of cell surface receptors. Most semaphorins interact with plexin-containing receptor complexes, although some interact with non-plexin receptors. Class 2 semaphorins are secreted molecules that control axon guidance and epidermal morphogenesis in Drosophila and Caenorhabditis elegans. We show that the C. elegans class 2 semaphorin MAB-20 binds the plexin PLX-2. plx-2 mutations enhance the phenotypes of hypomorphic mab-20 alleles but not those of mab-20 null alleles, indicating that plx-2 and mab-20 act in a common pathway. Both mab-20 and plx-2 mutations affect epidermal morphogenesis during embryonic and in postembryonic development. In both contexts, plx-2 null mutant phenotypes are much less severe than mab-20 null phenotypes, indicating that PLX-2 is not essential for MAB-20 signaling. Mutations in the ephrin efn-4 do not synergize with mab-20, indicating that EFN-4 may act in MAB-20 signaling. EFN-4 and PLX-2 are coexpressed in the late embryonic epidermis where they play redundant roles in MAB-20-dependent cell sorting.