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IntroductionGastrointestinal anastomoses with classical sutures and/or metal staples have resulted in significant bleeding and leak rates. This multi-site study evaluated the feasibility, safety, and preliminary effectiveness of a novel linear magnetic compression anastomosis device, the Magnet System (MS), to form a side-to-side duodeno-ileostomy (DI) diversion for weight loss and type 2 diabetes (T2D) resolution. MethodsIn patients with class II and III obesity (body mass index [BMI, kg/m2] ≥ 35.0– ≤ 50.0 with/without T2D [HbA1C > 6.5%]), two linear MS magnets were delivered endoscopically to the duodenum and ileum with laparoscopic assistance and aligned, initiating DI; sleeve gastrectomy (SG) was added. There were no bowel incisions or retained sutures/staples. Fused magnets were expelled naturally. Adverse events (AEs) were graded by Clavien-Dindo Classification (CDC).ResultsBetween November 22, 2021 and July 18, 2022, 24 patients (83.3% female, mean ± SEM weight 121.9 ± 3.3 kg, BMI 44.4 ± 0.8) in three centers underwent magnetic DI. Magnets were expelled at a median 48.5 days. Respective mean BMI, total weight loss, and excess weight loss at 6 months (n = 24): 32.0 ± 0.8, 28.1 ± 1.0%, and 66.2 ± 3.4%; at 12 months (n = 5), 29.3 ± 1.5, 34.0 ± 1.4%, and 80.2 ± 6.6%. Group mean respective mean HbA1C and glucose levels dropped to 1.1 ± 0.4% and 24.8 ± 6.6 mg/dL (6 months); 2.0 ± 1.1% and 53.8 ± 6.3 mg/dL (12 months). There were 0 device-related AEs, 3 procedure-related serious AEs. No anastomotic bleeding, leakage, stricture, or mortality.ConclusionIn a multi-center study, side-to-side Magnet System duodeno-ileostomy with SG in adults with class III obesity appeared feasible, safe, and effective for weight loss and T2D resolution in the short term.

Background Hyperdynamic circulation in portal hypertension (PHT) depends on central neural activation. However, the initiating mechanism that signals PHT to the central neural cardiovascular-regulatory centers remains unclear. We aimed to test the hypothesis that oxidative stress in the gut initiates the signal that activates central cardiovascular nuclei in portal hypertensive rats. Methods Two groups of rats were used. One had portal hypertension produced by partial portal vein ligation, while controls underwent sham operation. Hemodynamics including portal pressure, cardiac output, mean arterial pressure (MAP) and peripheral vascular resistance were measured. Activation of central cardiovascular nuclei was determined by immunohistochemical Fos expression in the paraventricular nucleus (PVN) of the hypothalamus. Myeloperoxidase activity, an oxidative stress marker, was measured in the jejunum. Hydrogen peroxide, the antioxidant N -acetyl-cysteine (NAC) or saline controls were administered for 12–14 days by gavage or osmotic minipumps placed in the peritoneal cavity. Results Compared with controls, PHT rats showed increased cardiac output (54.2 ± 9.5 vs 33.6 ± 2.4 ml/min/100 g BW, p  < 0.01), decreased MAP (96.2 ± 6.4 mmHg vs 103.2 ± 7.8, p  < 0.01) and systemic vascular resistance (1.84 ± 0.28 vs 3.14 ± 0.19 mmHg/min/ml/100 g BW, p  < 0.01). PHT rats had increased jejunal myeloperoxidase and PVN Fos expression. NAC treatment eliminated the hyperdynamic circulation, decreased jejunal myeloperoxidase and PVN Fos expression in PHT rats, but had no effect on sham controls. H 2 O 2 significantly increased PVN Fos expression and decreased MAP. Conclusion These results indicate that in PHT, mesenteric oxidative stress is the initial signal that activates chemoreceptors and triggers hyperdynamic circulation by central neural cardiovascular-regulatory centers.