The utility of intraoperative endoscopy to assist novice surgeons in the detection of gastric stenosis during laparoscopic sleeve gastrectomy.

BACKGROUND: Laparoscopic sleeve gastrectomy (LSG) is a commonly performed bariatric surgery. Gastric stenosis and leaks are 2 major complications associated with LSG and revision surgery might be needed. Herein, we report our experience of intraoperative endoscopy (IOE) to evaluate stenosis and leaks during LSG. METHODS: LSG was performed by three surgeons. Patients who underwent LSG and IOE between January 2016 and March 2020 were enrolled and assigned to two groups: group 1 (1st-30th LSG case for each surgeon) and group 2 (> 30th LSG for each surgeon). Patients' anthropometric and biochemical data pre- and post-LSG, as well as IOE findings and follow-up esophagogastroduodenoscopy records were reviewed. RESULTS: In total, 352 patients were enrolled including 90 patients in group 1 and 262 patients in group 2. Three out of 352 patients (0.9%) were found to have stenosis by IOE, which was related to tightly gastropexy stitch or reinforcement stitch, all of which were in group 1. Stenosis was resolved after removal of the stitch during LSG. The incidence of gastric stenosis detected by IOE was 3.3% (3/90) and 0% (0/262) in group 1 and group 2, respectively (P = 0.003). No leakage was found in this study and no patient developed clinical or endoscopic stenosis after LSG. CONCLUSIONS: The existing evidence showed that IOE can help detect gastric stenosis during LSG, especially for novice surgeons, and the stenosis could be resolved during operation.

A prospective, randomized trial of thrombin versus cyanoacrylate injection in the control of acute gastric variceal hemorrhage.

BACKGROUND: Acute gastric variceal hemorrhage (AGVH) is a serious complication of portal hypertension. Endoscopic cyanoacrylate glue injection is standard therapy for acute hemostasis; however, it may be associated with serious complications. The role of thrombin injection has not been confirmed. This study compared endoscopic thrombin and glue injections in the hemostasis of AGVH. METHODS: 68 eligible patients with AGVH were randomized to receive thrombin injection (33 patients) or glue injection (35 patients). The primary end point was injection-induced gastric ulcers. Secondary end points were acute hemostasis, rebleeding, and mortality within 42 days. RESULTS: Both groups had comparable baseline data. Hemostasis of active bleeding at endoscopy was 90.0 % (9/10) in the thrombin group and 90.9 % (10/11) in the glue group (P = 0.58), and 48-hour hemostasis was achieved in 93.9 % (31/33) and 97.1 % (34/35), respectively (P = 0.60). Treatment failure at 5 days occurred in two patients (6.1 %) in the thrombin group and two patients (5.7 %) in the glue group (P > 0.99). Gastric ulcers occurred in none of the thrombin group and 11/30 (36.7 %) of the glue group (P < 0.001, 95 % confidence interval [CI] 8 % - 27 %). Complications occurred in 4 (12.1 %) and 18 (51.4 %) patients in the thrombin and glue groups, respectively (P < 0.001, 95 %CI 22 % - 45 %). Two patients who received glue had post-treatment gastric ulcer bleeding. One patient in each group died. CONCLUSIONS: Endoscopic thrombin injection was similar to glue injection in achieving successful hemostasis of AGVH. However, a higher incidence of complications may be associated with glue injection.

Lymphatic absorption of quercetin and rutin in rat and their pharmacokinetics in systemic plasma.

Substances and macromolecules absorbed by the lymphatic system avoid hepatic first-pass effect and directly enter the blood circulation system. In this study, an anesthetized, mesenteric lymphatic/duodenum-cannulated rat model was used to investigate the role of lymphatic absorption with intraduodenally administered drugs. Quercetin and rutin were administered, respectively, at dosages of 30 and 300 mg/kg intraduodenally. Lymph and plasma samples were collected every 30 min. These samples were prepared by protein precipitation and then analyzed by high-performance liquid chromatography with a photodiode array detector (HPLC-PDA) and verified by LC tandem mass spectrometry (LC-MS/MS). Quercetin was separated by a C18 reversed-phase column, and rutin was separated by a phenyl reverse-phase column. Pharmacokinetic parameters were calculated using the software WinNonlin Standard Edition Version. The maximum concentration (Cmax) of quercetin recovered in lymph, 1.97+/-0.96 microg/mL, was about 5-fold higher than that in plasma, 0.41+/-0.08 microg/mL. The time to reach the highest concentration (Tmax) of quercetin in lymph was 30 min longer than that in plasma. The maximum concentration (Cmax) of rutin recovered in lymph, 0.86+/-0.13 microg/mL, was slightly lower than that in plasma, 1.35+/-0.37 microg/mL. The area under curve (AUC) of rutin recovered in lymph, 359+/-41 min microg/mL, was about 2-fold higher than the AUC of rutin in plasma, 150+/-22 min microg/mL. This phenomenon was due to the milder concentration decline of rutin in the lymphatic system. These results demonstrate the pharmacokinetic data of lymphatic and systemic absorption after intraduodenally administered quercetin and rutin. It is also the first report revealing the lymphatic absorption of rutin. Although both quercetin and rutin are absorbed and transported mainly via the blood circulation system, the AUC of these two drugs in lymph fluid appeared higher than their respective AUC in plasma.

Antidepressant administration modulates neural stem cell survival and serotoninergic differentiation through bcl-2.

The hippocampus has long been associated with learning, memory, and modulation of emotional responses. Previous studies demonstrated that stress-induced loss of hippocampal neurons may contribute to the pathogenesis of depression. The recent observations supported that antidepressant drugs increase the production of serotoninergic neurotransmitter and they play a critical role in the initiation of neurogenesis in the hippocampus. In order to explore the possible new mechanism of the treatment of depression, we cultured neural stem cells (NSCs) derived from the hippocampus of adult rats as an in vitro model to evaluate the capabilities of neuroprotection and neural differentiation in NSCs by fluoxetine (FL) treatment. Our results showed that 20 microM FL treatment can significantly increase the proliferation rate of NSCs (p<0.05), and up-regulate the mRNA and protein expressions of Bcl-2 in Day-7 FL-treated NSCs (p<0.01). Using Bcl-2 gene silencing with small interfering RNA, our data verified that FL can prevent Fas ligand-induced caspase-dependent apoptosis in NSCs through the activation of Bcl-2. The in vitro observation and immunofluorescent study further demonstrated that FL treatment can stimulate the neurite development and serotoninergic differentiation of NSCs through the activation of Bcl-2. Using microdialysis with high performance liquid chromatography- electrochemical detection, the functional release of serotonin in the differentiating NSCs with FL treatment was increased and simultaneously regulated by the Bcl-2 expressions. In sum, the study results indicate that antidepressant administration can increase NSCs survival, promote the neurite development, and facilitate NSCs differentiating into the functional serotoninergic neurons via the modulation of Bcl-2 expression.