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Objective:To develop and validate a nomogram model for predicting microvascular invasion (MVI) in hepatocellular carcinoma (HCC) based on preoperative enhanced computed tomography imaging features and clinical data.Methods:The clinical data of 210 patients with HCC undergoing surgery in the Second Affiliated Hospital of Anhui Medical University from May 2018 to May 2022 were retrospectively analyzed, including 172 males and 38 females, aged (59±10) years old. Patients were randomly divided into the training group ( n=147) and validation group ( n=63) by systematic sampling at a ratio of 7∶3. Preoperative enhanced computed tomography imaging features and clinical data of the patients were collected. Logistic regression was conducted to analyze the risk factors for HCC with MVI, and a nomogram model containing the risk factors was established and validated. The diagnostic efficacy of predicting MVI status in patients with HCC was assessed by receiver operating characteristic (ROC) curve, calibration curves, decision curve analysis (DCA), and clinical impact curve (CIC) of the subjects in the training and validation groups. Results:The results of multifactorial analysis showed that alpha fetoprotein ≥400 μg/ml, intra-tumor necrosis, tumor length diameter ≥3 cm, unclear tumor border, and subfoci around the tumor were independent risk factors predicting MVI in HCC. A nomogram model was established based on the above factors, in which the area under the curve (AUC) of ROC were 0.866 (95% CI: 0.807-0.924) and 0.834 (95% CI: 0.729-0.939) in the training and validation groups, respectively. The DCA results showed that the predictive model thresholds when the net return is >0 ranging from 7% to 93% and 12% to 87% in the training and validation groups, respectively. The CIC results showed that the group of patients with predictive MVI by the nomogram model are highly matched with the group of patients with confirmed MVI. Conclusion:The nomogram model based on the imaging features and clinical data could predict the MVI in HCC patients prior to surgery.
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Objective:To investigate the expression of RASAL3 in intrahepatic cholangiocarcinoma (iCCA) and the mechanism of promoting iCCA development.Methods:Tumor and paracancerous tissues were collected from 185 iCCA patients, the expression of RASAL3 was detected by immunohistochemistry, RT-qPCR and Western blot. The expression of RASAL3 and FXYD6 mRNA and protein in human cholangiocarcinoma cell line and human bile duct epithelial cells were detected with RT-qPCR and Western blot, the cell proliferation was detected with CCK-8 assay, and the activity of Na +-K +-ATPase was also detected. Results:RASAL3 was highly expressed in cholangiocarcinoma tissues and cell lines; Survival analysis showed that RASAL3 overexpression was associated with poor prognosis of cholangiocarcinoma( P<0.05) and knockdown of RASAL3 inhibits the proliferation of cholangiocarcinoma cells; Silencing RASAL3 decreases the expression of FXYD6 inhibiting the activity of Na +-K +-ATPase. Conclusion:RASAL3 is up-regulated in human cholangiocarcinoma, which can promote the occurrence and development of cholangiocarcinoma by activating FXYD6 and affecting Na +-K +-ATPase activity.
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Objective To establish the canine model of esophageal variees caused by portal hyper-tension. Methods The model was established in 12 dogs with a side-to-side portacaval shunt, an ameroid constrictor around the portal vein and double ligation and cross suture of the cephalic part of the inferior vena cava (IVC), and the development of esophageal varices was confirmed 6 weeks later by endoscopy and portal vein angiography. Results The mean pre- and postoperative portal pressure were (11.0 ± 1.1) mm Hg and (22. 9 ± 1.2) nun Hg, respectively (P =0. 010). Endoscopy detected mild to moderate esophageal varices in all dogs, which was confirmed by portal vein angiography, and varices was also seen in abdominal wall. Conclusion Canine model of esophageal varices induced by portal hypertension can be established with the procedure.
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Objective To investigate the effects of lipoxygenase inhibitor NDGA on expression of 5-LOX and its apoptosis related genes in HepG2 cell line.Methods The expression of 5-LOX and apoptosis related genes hTERT,bcl-2 and bax mRNA was determined by reverse transcriptasepolymerase chain reaction (RT-PCR).Results After 25,50,100,200 μmol/L NDGA treatment for24,48 h,the expression of 5-LOX of HepG2 cell decreased,but the expression of bax was up-regulated and the expressions of bcl-2 and hTERT mRNA were down-regulated,(P＜0.05 compared with the control group).The decrease in the expression of 5-LOX,hTERT and bcl-2 in HepG2 cell was negtively correlated with the dose duration of action of NDGA.Conclusion In vitro,5-LOX is expressed highly in HepG2 cell.Overexpression of 5-LOX may be related to the progression of hepatocellular carcinoma,NDGA can significantly decrease the expression of 5-LOX,up-regulate of bax and downregulation of bcl-2 and telomerse.Lipoxygenase might be a novel therapeutic target for the hepatocellular carinoma.
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Death-associated protein kinase (DAPK) is a muhidomain calcium/calmodulin (CaM)-de- pendent Ser/Thr protein kinase with an important role in apoptosis regulation and tumor suppression. DAPK may serve as a diagnostic and prognostic tool to evaluate disease severity, progression, metastatic rate, and re- currence, and may serve as a target for therapeutic intervention.
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ObjectiveTo investigate the clinical results of hepatectomy for bleeding of spontaneous rupture of hepatocellular carcinoma (HCC). MethodsThe clinical data of 24 cases admitted to our hospital from Jan 1990 to Mar 2004 was analyzed retrospectively.ResultsSurgical hemostasis was achieved successfully in 100.0% (24/24) of patients. The postoperative mortality rate was 4.1% (1/24), and the (complication) rate 12.5%(4/24). Liver function recovered within two weeks after operation. The length of hospital stay was 14.756.25 days.Twenty-one patients were followed-up from 6 month to 36 months. 8 patients died from recurrence within 10 months postoperatively; 10 patients survived over 1 year, 1 patient over 2 years and 1 over 3 years. The overall 1-year survival rate was 58.3%(13/24).ConclusionsIn the management of bleeding of spontaneous rupture of HCC, hepatectomy can effectively stop the bleeding and excise the tumor at the same operation. In some patients, a radical excision can be achieved, and, if the (patient)s condition permits it, hepatectomy should be the treatment of choice.
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AIMTo study whether Mel has protective role in liver c old preservation and its mechanism. METHODSTo study the role of Mel at the different concentration and time in liver cold preservation, we colle cted liver washing liquid and liver tissue from male SD rats. We analysed ALT, AST, LDH, HA, ET 1, MDA and SOD to see the function of liver cell and sinusoida l lining cell and mechanism of cell injury. At the same time, we studied the eff ects of Mel at different concentration and different time on liver cold preserva tion. RESULTS① The damage to liver function and change of its histology was aggravated with the prolongation of UW co ld preservation time, and injury of the sinusoidal lining cell was also aggravated gr adually. ② Indexes of the liver function and the sinusoidal lining cell functio n in the Mel solution cold preservation group were lower than that in the UW sol ution cold preservation group. These suggest protective role of Mel against live r injury caused by cold preservation. Its mechanism may be related to powerful a nti-oxidative effect of Mel. ③ The protective effect of Mel at 1?10 -5 m ol?L -1 ,1?10 -7 mol?L -1 was better than that of Mel at 1?10 -9 mol?L -1 . We found no obvious difference between the protection of Mel 1?10 -5 mol?L -1 and 1?10 -7 mol?L -1 indicati ng a concentration-effect relationship. CONCLUSIONProtective ef fect of UW solution used in clinic weakens gradually as cold preservation time increases. Mel solution has protective effect on liver cold preservation injury and is better than the simple UW solution. Its mechanism is related to anti-oxi dative effect of Mel.