Pilot comparison of adhesion formation following colonic perforation and repair in a pig model using a transgastric, laparoscopic, or open surgical technique.

BACKGROUND AND STUDY AIM: Postoperative adhesions create significant morbidity and mortality. Natural orifice transluminal endoscopic surgery (NOTES) procedures may reduce or eliminate adhesions by avoiding disruption of the parietal peritoneum. The primary aim of this pilot study was to compare adhesion formation after performance and subsequent repair of colonic perforation via transgastric, laparoscopic, or open surgical techniques. The secondary aim was to test the feasibility and outcome of transgastric management of bowel perforation in a prepared model. MATERIAL AND METHODS: 15 Yorkshire pigs were divided into three groups of five: transgastric (needle-knife entry with balloon dilation over a wire), laparoscopic, and open surgical. Aspects of adhesion formation (density/vascularity, width of bands, and number of organ pairs involved) were compared after perforation and repair during the same procedure. Intra- and postoperative complications were documented during the 21-day survival period. RESULTS: All 15 pigs recovered fully with no immediate procedural complications. After 21 days, there was a trend towards a lower adhesion burden regarding density/vascularity and number of organ pairs involved, and a significant reduction in the width of the adhesive bands, when the transgastric group was compared with the surgical groups. Additionally, there was a trend towards decreased adhesions to the peritoneum in the transgastric group. CONCLUSIONS: Repair of colonic perforation during transgastric (NOTES) procedures appear feasible and safe in a porcine model. There appears to be a trend towards a lower rate of adhesion formation with the transgastric approach compared with laparoscopic or open surgery.

Pilot series of radiofrequency ablation of Barrett's esophagus with or without neoplasia.

BACKGROUND AND STUDY AIMS: Radiofrequency ablation is a rapidly evolving therapeutic modality for Barrett's esophagus. The aim of this ongoing 12-month trial is to assess Barrett's esophagus eradication after radiofrequency ablation using a balloon-based (HALO-360) and a plate-based (HALO-90) device. We report here our experience with the first 10 patients (out of 40) who have completed 12 months of follow-up. PATIENTS AND METHODS: Following radiofrequency ablation using the HALO-360 device all patients were maintained on double-dose proton pump inhibitor therapy. Endoscopic evaluation was performed at 3 and 12 months postablation. Patients with residual Barrett's esophagus at 3 months underwent repeat ablation. Ten patients, seven with nondysplastic Barrett's esophagus, two with low-grade and one with high-grade dysplasia have completed the study to date. RESULTS: Complete Barrett's esophagus eradication was achieved in seven patients, and partial eradication was achieved in three. There were no major complications. One case of buried Barrett's metaplasia was encountered and successfully re-ablated, with complete Barrett's esophagus eradication achieved at 12 months. CONCLUSIONS: In this study, Barrett's eradication rates were comparable to previously published reports. One case of buried Barrett's metaplasia was identified out of 247 biopsies and was eradicated with repeat ablation.

The Caenorhabditis elegans gene ham-2 links Hox patterning to migration of the HSN motor neuron.

The Caenorhabditis elegans HSN motor neurons permit genetic analysis of neuronal development at single-cell resolution. The egl-5 Hox gene, which patterns the posterior of the embryo, is required for both early (embryonic) and late (larval) development of the HSN. Here we show that ham-2 encodes a zinc finger protein that acts downstream of egl-5 to direct HSN cell migration, an early differentiation event. We also demonstrate that the EGL-43 zinc finger protein, also required for HSN migration, is expressed in the HSN specifically during its migration. In an egl-5 mutant background, the HSN still expresses EGL-43, but expression is no longer down-regulated at the end of the cell's migration. Finally, we find a new role in early HSN differentiation for UNC-86, a POU homeodomain transcription factor shown previously to act downstream of egl-5 in the regulation of late HSN differentiation. In an unc-86; ham-2 double mutant the HSNs are defective in EGL-43 down-regulation, an egl-5-like phenotype that is absent in either single mutant. Thus, in the HSN, a Hox gene, egl-5, regulates cell fate by activating the transcription of genes encoding the transcription factors HAM-2 and UNC-86 that in turn individually control some differentiation events and combinatorially affect others.

An antineutrophil cytoplasmic autoantibody associated with a propylthiouracil-induced adult respiratory distress-like syndrome: report of a case and review of the literature.

OBJECTIVE: To report the first case of propylthiouracil-induced adult respiratory distress-like syndrome associated with the presence of an antineutrophil cytoplasmic autoantibody. METHODS: We describe the initial manifestations, laboratory findings, and clinical course in a patient and discuss underlying factors potentially contributing to her condition. RESULTS: A 57-year-old woman with hyperthyroidism had an influenza-like illness and vasculitis during propylthiouracil therapy. Three days after she was admitted to the hospital, an adult respiratory distress-like syndrome developed. Results of perinuclear antineutrophil cytoplasmic antibody (pANCA) and antimyeloperoxidase antibody studies were positive. Her condition improved after the introduction of glucocorticoid therapy and the withdrawal of propylthiouracil treatment. The pANCA level, however, remained unchanged 3 months after her dismissal from the hospital. CONCLUSION: The propylthiouracil-induced adult respiratory distress-like syndrome may be a hypersensitivity phenomenon, and the presence of the pANCA could be a marker of a common mechanism of injury that stimulates its production rather than a pathogenic factor responsible for vascular injury in our patient.