Clinical analysis of minimally invasive McKeown esophagectomy in a single center by a single medical group / 浙江大学学报（英文版）（B辑：生物医学和生物技术）

OBJECTIVE@#McKeown esophagectomy followed by cervical and abdominal procedures has been commonly used for invasive esophageal carcinoma. This minimally-invasive operative procedure in the lateral prone position has been considered to be the most appropriate method. We describe our experiences in minimally invasive McKeown esophagectomy (MIME) for esophageal cancer.@*METHODS@#Between March 2016 and February 2018, a total of 82 patients underwent MIME by a single group in our department (a single center). All procedure, operation, oncology, and complication data were reviewed.@*RESULTS@#All MIME procedures were completed successfully, with no conversions to open surgery. The median operative time was 260 min, and median blood loss was 100 ml. The average number of total harvested lymph nodes was 20.1 in the chest and 13.5 in the abdomen. There were no deaths within 30 postoperative days. Twenty cases (24.4%) developed postoperative complications, including anastomotic leak in 4 (4.9%), single lateral recurrent nerve palsy in 4 (4.9%), bilateral recurrent nerve palsy in 1 (1.2%), pulmonary problems in 3 (3.7%), chyle leak in 1 (1.2%), and other complications in 7 (including pleural effusions in 4, incomplete ileus in 2, and neck incision infection in 1; 8.54%). Average postoperative hospitalization time was 12 d. Blood loss, operation time, morbidity rate, and the number of harvested lymph nodes were analyzed by evaluating learning curves in different periods. Significant differences were found in operative time (P=0.006), postoperative hospitalization days (P=0.015), total harvested lymph nodes (P=0.003), harvested thoracic lymph nodes (P=0.006), and harvested abdominal lymph nodes (P=0.022) among different periods.@*CONCLUSIONS@#Surgical outcomes following MIME for esophageal cancer are safe and acceptable. The MIME procedure for stages I and II could be performed proficiently and reached an experience plateau after approximately 25 cases.

Propofol ameliorates calpain-induced collapsin response mediator protein-2 proteolysis in traumatic brain injury in rats / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Collapsin response mediator protein-2 (CRMP2), a multifunctional cytosolic protein highly expressed in the brain, is degraded by calpain following traumatic brain injury (TBI), possibly inhibiting posttraumatic neurite regeneration. Lipid peroxidation (LP) is involved in triggering postinjury CRMP2 proteolysis. We examined the hypothesis that propofol could attenuate LP, calpain-induced CRMP2 degradation, and brain injury after TBI.</p><p><b>METHODS</b>A unilateral moderate controlled cortical impact injury was induced in adult male Sprague-Dawley rats. The animals were randomly divided into seven groups: Sham control group, TBI group, TBI + propofol groups (including propofol 1 h, 2 h, and 4 h groups), TBI + U83836E group and TBI + fat emulsion group. The LP inhibitor U83836E was used as a control to identify that antioxidation partially accounts for the potential neuroprotective effects of propofol. The solvent of propofol, fat emulsion, was used as the vehicle control. Ipsilateral cortex tissues were harvested at 24 h post-TBI. Immunofluorescent staining, Western blot analysis, and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling were used to evaluate LP, calpain activity, CRMP2 proteolysis and programmed cell death. The data were statistically analyzed using one-way analysis of variance and a paired t-test.</p><p><b>RESULTS</b>Propofol and U83836E significantly ameliorated the CRMP2 proteolysis. In addition, both propofol and U83836E significantly decreased the ratio of 145-kDa αII-spectrin breakdown products to intact 270-kDa spectrin, the 4-hydroxynonenal expression and programmed cell death in the pericontusional cortex at 24 h after TBI. There was no difference between the TBI group and the fat emulsion group.</p><p><b>CONCLUSIONS</b>These results demonstrate that propofol postconditioning alleviates calpain-mediated CRMP2 proteolysis and provides neuroprotective effects following moderate TBI potentially by counteracting LP and reducing calpain activation.</p>