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@#Objective To evaluate the effectiveness and safety of proximal aortic repair (PAR) versus total arch replacement (TAR) for treatment of acute type A aortic dissection (ATAAD). Methods An electronic search was conducted for clinical controlled studies on PAR versus TAR for patients with ATAAD published in Medline via PubMed, EMbase, The Cochrane Library, Web of Science, Wanfang Database and CNKI since their inception up to April 30, 2022. The quality of each study included was assessed by 2 evaluators and the necessary data were extracted. STATA 16 software was used to perform statistical analysis of the available data. Results A total of 28 cohort studies involving 7 923 patients with ATAAD were included in this meta-analysis, of whom 5 710 patients received PAR and 2 213 patients underwent TAR, and 96.43% of the studies (27/28) were rated as high quality. The meta-analysis results showed that: (1) patients who underwent PAR had lower incidences of 30 d mortality [RR=0.62, 95%CI (0.50, 0.77), P<0.001], in-hospital mortality [RR=0.64, 95%CI (0.54, 0.77), P<0.001], and neurologic deficiency after surgery [RR=0.84, 95%CI (0.72, 0.98), P=0.032] than those who received TAR; (2) the cardiopulmonary bypass time [WMD=–52.07, 95%CI (–74.19, –29.94), P<0.001], circulatory arrest time [WMD=–10.14, 95%CI (–15.02, –5.26), P<0.001], and operation time [WMD=–101.68, 95%CI (–178.63, –24.73), P<0.001] were significantly shorter in PAR than those in TAR; (3) there was no statistical difference in mortality after discharge, rate of over 5-year survival, renal failure after surgery and re-intervention, volume of red blood cells transfusion and fresh-frozen plasma transfusion, or hospital stay between two surgical procedures. Conclusion Compared with TAR, PAR has a shorter operation time and lower early and in-hospital mortality, but there is no difference in long-term outcomes or complications between the two procedures for patients with ATAAD.
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Objective Drug resistance is the main cause of chemotherapy failure in hepatocellular carcinoma (HCC), and thioredoxin reductase 1 (TXNRD1), as a major influencing factor for reactive oxygen species (ROS) metabolism, has been proven to be associated with the poor prognosis of patients with HCC. This study aims to explore the role of TXNRD1 in the mechanism of multidrug resistance in HCC. Methods BEL/FU cells in BEL-7402 cell line were selected as the multidrug-resistant cell line. The siRNA was used for the intervention of TXNRD1 expression; quantitative real-time PCR and Western blotting were used to measure the expression of TXNRD1; CCK-8 assay and flow cytometry were used to evaluate the effect of TXNRD1 on hepatocyte ROS accumulation, resistance to 5-fluorouracil (5-Fu) and doxorubicin (DOX), and apoptosis in vitro; a xenograft tumor model was established to investigate the effect of auranofin (AUR) on drug resistance in vivo. The two-independent-samples t test was used for comparison of continuous data between two groups. Results As a multidrug-resistant HCC cell line, BEL/Fu showed high mRNA and protein expression levels of TXNRD1 (both P < 0.05). Compared with 5-Fu or DOX treatment alone, the TXNRD1 inhibitor AUR combined with 5-Fu or DOX had had a significant reduction in the number of colony formation ( P < 0.01) and a significant increase in apoptosis ratio ( P < 0.001). The ROS scavenger N-acetylcysteine (NAC) significantly weakened the effect of TXNRD1 knockdown by siRNA on the drug resistance of BEL/Fu cells, and the application of NAC effectively reduced the apoptosis ratio of cells after siRNA interference ( P < 0.001). Animal experiments also confirmed that compared with the nude mice treated with 5-Fu alone, the nude mice treated with 5-Fu and AUR had a significantly lower tumor mass ( P < 0.001) and a significantly smaller tumor volume ( P < 0.001). Conclusion TXNRD1 plays an important role in the drug resistance of HCC, and inhibition of its level in cells can effectively improve drug resistance. As a TXNRD1 inhibitor, AUR has great application prospects in the multimodality therapy for HCC.
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Objective To investigate the expression of cyclin G1、cyclin G2 in gastric carcinoma and its significance. Methods The mRNA expression of cyclin G1、cyclin G2 in 55 cases of gastric carcinoma was measured with RT-PCR. The protein expression of cyclin G1 and cell cycle were detected by flow cytometry.Results Expression rate of cyclin G1 in gastric carcinoma was 58%,which was higher than that in normal tissue(P