ABSTRACT
@#Objective To explore the efficacy of artificial intelligence (AI) detection on pulmonary nodule compared with multidisciplinary team (MDT) in regional medical center. Methods We retrospectively analyzed the clinical data of 102 patients with lung nodules in the Xiamen Fifth Hospital from April to December 2020. There were 57 males and 45 females at age of 36-90 (48.8±11.6) years. The preoperative chest CT was imported into AI system to record the detected lung nodules. The detection rate of pulmonary nodules by AI system was calculated, and the sensitivity, specificity of AI in the different diagnosis of benign and malignant pulmonary was calculated and compared with manual film reading by MDT. Results A total of 322 nodules were detected by AI software system, and 305 nodules were manually detected by physicians (P<0.05). Among them, 113 pulmonary nodules were diagnosed by pathologist. Thirty-eight of 40 lung cancer nodules were AI high-risk nodules, the sensitivity was 95.0%, and 25 of 73 benign nodules were AI high-risk nodules, the specificity was 65.8%. Lung cancer nodules were correctly diagnosed by MDT, but benign nodules were still considered as lung cancer at the first diagnosis in 10 patients. Conclusion AI assisted diagnosis system has strong performance in the detection of pulmonary nodules, but it can not content itself with clinical needs in the differentiation of benign and malignant pulmonary nodules. The artificial intelligence system can be used as an auxiliary tool for MDT to detect pulmonary nodules in regional medical center.
ABSTRACT
To explore the effect of growth hormone releasing peptide (GHRP) on myocardial cell apoptosis in heart failure (HF) rats. Methods: Rat's HF model was established by the ligation of left anterior descending coronary artery induced ischemia. 40 male SD rats were randomly assigned into 4 groups: Normal control group, Sham operation group, HF group and GHRP treated HF group. n=10 in each group and the rats were fed for 4 weeks after the operation. Cardiac function was examined and myocardial cell morphology was observed; protein expressions of Smac/DIABL0 and Bcl-2 were measured by Western blot analysis; cell apoptosis was evaluated by FCM technique. The differences for above parameters were compared among groups to explore the effect of GHRP on myocardial cell apoptosis in HF rats. Results: Compared with HF group, GHRP treated HF group showed the less heart dilation, higher LVEF, lighter pathological changes in myocardial cells and decreased protein expression of Smac/DIABL0, all P<0.05. Bcl-2 level was lower in HF group than the other 3 groups, P<0.05. Compare with Normal control group, GHRP treated HF group had elevated Bcl-2 level, all P<0.05. Myocardial cell apoptosis index was different between HF group and GHRP treated HF group, P<0.05. Conclusion: The effect of GHRP on anti-HF should be via inhibiting myocardial cell apoptosis; the mechanism may partly be through promoting Bcl-2 protein expression and depressing Smac/DIABLO mediated mitochondrial pathway of apoptosis.
ABSTRACT
Objective In order to improve the surgical treatment for midpiece esophageal carcinoma, different surgical ways were com-pared. Methods From January 2010 to June 2012, 110 patients with midpiece esophageal cancer in our hospital were divided into the Ivor-Lewis group (55 cases) and the Sweet group (55 cases) according to different surgical ways, that is to say Ivor-Lewis surgery via right chest and Sweet surgery through left chest. Length of specimens, rang of tumor invasion, distance of removal, incidence of residual carcinoma in the esophageal edges, number of lymph nodes removed in chest and abdomen, and positive rate of carcinoma infiltrated lymph nodes were compared between the two groups. Questions of surgical anatomy were investigated through questionnaire among surgeons of the two groups, and the scores of both groups were analysed. Results The length of resected specimens and number of lymph nodes removed in Ivor-Lewis group was significantly lager than that of the Sweet group (P<0. 01). The positive rate of carcinoma infiltrated lymph nodes in Ivor-Lewis group was 1. 82%, which was significantly lower than 21. 82% in the Sweet group (P<0. 01). Results of questionnaire showed surgeons have gieven higher scores to Ivor-Lewis group. Conclusion Ivor-Lewis surgery is recommend for upper and midpiece esophageal carcinoma while Sweet surgery is more suitable for cardial and lower esophageal cancer.
ABSTRACT
The opening of mitochondrial permeability transition pore (PTP) during reperfusion injury of heart has been well demonstrated and thus controlling PTP would attenuate the myocardial damage and cell death. Ursodeoxycholic acid (UDCA) is a hydrophilic bile salt and has been shown to prevent apoptosis in hepatocytes by inhibiting the opening of PTP. Here we demonstrate the role of UDCA in preventing the reperfusion injury of heart through its ability to inhibit PTP. Wistar rats underwent 30 min left coronary artery occlusion (LCA) followed by 180 min reperfusion after treatment with 40 mg/kg per iv infusion of UDCA over 30 min before LCA occlusion. Other groups of rats were treated with PTP agonist atractyloside(5 mg/kg) or PI3 kinase inhibitor wortmannin (16 ug/kg) before UDCA treatment. UDCA treatment prior to LCA occlusion, activated phosphorylation of Akt and Bad. Phosphorylating Bad prevented its translocation in to mitochondria, there by preventing the down regulation of Bcl-2 expression and PTP opening. This was confirmed by reduced cytochrome C release from intramitochondrial space in to the cytosol and hence reduced cell death either by apoptosis (4.8 vs 11.8%, P<0.001, UDCA treated against control group) or necrosis (reduced MI area in UDCA treated group (22.1%) compared to control group(46.4%), P<0.001). In contrast, inhibition of Akt activation with PI3K inhibitor wortmannin or opening the PTP with atractyloside abolished, UDCA mediated cytoprotective effects. Studies on primary culture cardiomyocytes also confirmed our in vivo results of UDCA on cell survival. These results altogether demonstrate that UDCA protect the heart against reperfusion injury by inhibiting the PTP in a PI3K/Akt dependent pathway.
