ObjectiveTo summarize the clinical effect of Da Vinci robot radical gastrectomy for gastric cancer.MethodsA retrospective analysis was performed on 200 patients undergoing radical surgery for Da Vinci robotic gastric cancer from the General Surgery of the 940th Hospital of the Chinese People's Liberation Army from December 2016 to January 2018.ResultsThere were 200 cases of robotic radical gastric cancer, 99 cases of radical distal gastrectomy, and 101 cases of radical total gastrectomy. The operative time was (241.0±33.3) min, intraoperative blood loss was (146.2±110.4) mL, and the number of lymph nodes cleaned was (42±14). The time of first anal exhaustion was (3.1±0.7) d, the time of first meal was (4.3±0.7) d, the postoperative extubation time was (5.3±0.5) d, and the postoperative hospitalization cost was (96 366.50±16 992.87) yuan. Tumor diameter was (4.5±2.0) cm. The degree of tumor differentiation was high differentiation in 7 cases, moderate differentiation in 61 cases and poor differentiation in 132 cases. TNM stage was 1 case in stage Ⅰ, 62 cases in stage Ⅱ and 137 cases in stage Ⅲ. Iauren was divided into intestinal type (78 cases), diffuse type (65 cases) and mixed type (57 cases). The tumor infiltrated into submucosa in 1 case, intrinsic muscularis in 3 cases, subserosal layer in 31 cases and serosal layer in 165 cases. The tumors were located in the upper part of the stomach in 45 cases, the lower part of the stomach in 106 cases, the body of the stomach in 46 cases, the whole stomach in 1 case, and the gastroesophageal junction in 2 cases. Postoperative complications occurred in 8 cases (4%), including anastomotic leakage in 4 cases, duodenal stump fistula in 1 case, tracheoesophageal fistula in 1 case, pulmonary infection in 1 case, and gastroparesis in 1 case.ConclusionThe DaVinci robotic surgical system has less surgical injuries, quicker postoperative recovery, and better clinical efficacy.
Objective To investigate the ameliorative effects of the traditional Chinese medicine formula Fuling Yin on heart failure and its potential mechanisms at the mitochondrial level. Methods Ninety SD rats were randomly divided into a blank control group (n=15) and a modeling group (n=75) using a random number table method. A chronic heart failure model was established in the modeling group by intraperitoneal injection of doxorubicin hydrochloride. One rat from the blank control group and five rats from the modeling group were randomly selected to verify the success of modeling. After confirming that the model was successfully established, the rest successfully modeled rats were randomly divided into the model group, positive drug (trimetazidine) group, and Fuling Yin low-, medium-, and high-dose groups (n=14 per group). Treatment groups were administered the respective drugs via gavage daily, while the blank control group and model group received an equal volume of pure water for 4 consecutive weeks. Cardiac function was assessed by echocardiography. Heart weight index (HWI) was calculated. Serum brain natriuretic peptide (BNP) levels and myocardial adenosine triphosphate (ATP) content were detected by enzyme-linked immunosorbent assay. Histopathological changes were observed via hematoxylin-eosin staining. Mitochondrial ultrastructure was examined using transmission electron microscopy. Mitochondrial membrane potential (MMP) and mitochondrial permeability transition pore (mPTP) opening were detected by JC-1 fluorescence probe and colorimetric assay, respectively. The expression of apoptosis-related proteins, peroxisome proliferator-activated receptor-gamma coactivator-1α (PGC-1α), and key proteins of the mitogen-activated protein kinase (MAPK) signaling pathway were determined by Western Blot. Results Compared with the blank control group, the HWI and serum BNP levels in the model group were increased (P<0.01). Compared with the model group, the HWI and serum BNP levels in Fuling Yin groups were decreased (P<0.01). Pathological and ultrastructural observations showed disordered myocardial fiber arrangement, mitochondrial swelling, and cristae rupture in the model group; whereas in the Fuling Yin groups, myocardial pathological injury was alleviated, mitochondrial swelling was reduced, and membrane structure tended to be intact. Regarding mechanism indicators, compared with the model group, the myocardial ATP content increased, the red fluorescence intensity of MMP enhanced, and the mPTP opening degree decreased in the Fuling Yin groups (P<0.01). Additionally, the Bax/Bcl-2 ratio decreased, and caspase-3 protein expression was downregulated (P<0.01). Furthermore, PGC-1α protein expression was upregulated, while the expression of MAPK proteins was downregulated (P<0.01). Conclusions Fuling Yin can alleviate myocardial injury and delay ventricular remodeling in doxorubicin-induced heart failure rats. Its mechanism may be related to regulating the PGC-1α/MAPK signaling pathway to maintain mitochondrial homeostasis, thereby inhibiting mitochondria-mediated cardiomyocyte apoptosis.
