Objective To investigate the changes of C1q tumor necrosis factor-related protein-12(CTRP12)levels in serum of the pa-tients with acute myocardial infarction(AMI)before and after percutaneous coronary intervention(PCI),and explore its clinical sig-nificance.Methods A total of 50 patients with AMI who underwent emergency PCI and 35 patients with normal coronary angiography results in Danyang People's Hospital from November 2021 to October 2022 were enrolled.The CTRP12 levels in peripheral venous ser-um were compared between the two groups.The levels of serum CTRP12 levels were measured before,during and on the 3rd,5th and 7th day after PCI.The serum CTRP12 levels in culprit coronary ostium and peripheral vein were compared.CTRP12 levels in peripher-al venous serum were compared at different time points after PCI.The severity of coronary artery disease was evaluated by SYNTAX score system,and the AMI patients were divided into two groups:SYNTAX score ≤22 and SYNTAX score＞22.The serum CTRP12 levels were compared between the two groups and before and after PCI.The correlation between CTRP12 and age,body mass index(BMI),fasting blood glucose,blood lipid and other factors was analyzed.The influencing factors of the severity of coronary artery le-sions were analyzed by logistic regression.Results The serum CTRP12 level in the patients with AMI was significantly lower than that in healthy controls(P＜0.05).There was no significant difference between the serum CTRP12 levels between preoperative peripheral vein and intraoperative culprit coronary orifice(P＞0.05).Compared with that before PCI,the serum CTRP12 level was lower on the 3rd day after PCI(P＜0.05),and increased on the 5th and 7th days after PCI,but no statistically significant difference was found(P＞0.05).Compared with those on the 3rd day after PCI,the serum CTRP12 levels were increased on the 5th and 7th day after PCI,but no statistically significant differences were found(all P＞0.05).Compared with that in the SYNTAX≤22 group,the CTRP12 levels were significantly lower than those before PCI and on the 3rd day after PCI(all P＜0.05),while there was no significant difference on the 5th and 7th day after PCI in SYNTAX＞22 group(all P＞0.05).CTRP12 was negatively correlated with the level of total cholesterol(TC)and positively correlated with high-density lipoprotein cholesterol(HDL-C).Univariate logistic regression analysis showed that CTRP12 was an independent influencing factor for the severity of coronary artery disease in the patients with AMI(β=-1.671,OR=0.188,P＜0.05).After adjusting for the effects of age,gender,BMI,smoking,hypertension,diabetes,fasting blood glucose,total cholesterol(TC),triglyceride(TG),HDL-C and low-density lipoprotein cholesterol(LDL-C),CTRP12 was still an independent in-fluencing factor for the severity of coronary artery disease in the patients with AMI(β=-3.441,OR=0.032,P＜0.05).Conclusion The serum CTRP12 level was significantly decreased in the patients with AMI before PCI,and showed continuous decline on the 3rd day after PCI,but increased on the 5th and 7th day after PCI.CTRP12 should be an independent influencing factor for the severity of coronary artery disease in the patients with AMI.

Objective This study examined the influence of c-Myc regulated long noncoding RNA TBL1XR1-5(lnc-TBL1XR1-5)on the progression of oral squamous cell carcinoma(OSCC).Methods Based on the expres-sion of c-Myc,bioinformatics analysis was performed on head and neck squamous cell carcinoma samples in the TCGA database,and lnc-TBL1XR1-5 with closely related c-Myc expression was screened.The effects of c-Myc overexpression and knockdown on lnc-TBL1XR1-5 were detected.Expression relationship of c-Myc and lnc-TBL1XR1-5 in OSCC and para-cancer tissues.Dual-luciferase reporter assays were used to verify the binding of c-Myc to the lnc-TBL1XR1-5 promoter region.RNA FISH were used to determine the localization of lnc-TBL1XR1-5 in OSCC cell lines.The effects of overexpression,knockdown of lnc-TBL1XR1-5 on migration,metabolism,and proliferation of OSCC cells were observed by quantitative real-time polymerase chain reaction(qRT-PCR),scratch tests,transwell assays,medium color and pH changes,cell counts,CCK-8 assay,and colony formation assays.Results It was found that c-Myc positively regulated the expression of lnc-TBL1XR1-5 in OSCC cell lines and tis-sues.The binding of c-Myc to the lnc-TBL1XR1-5 promoter region was verified by dual-luciferase reporter assays.RNA FISH showed that lnc-TBL1XR1-5 was localized in the nuclei in OSCC cells.Overexpression of lnc-TBL1XR1-5 promoted migration,metabolism and proliferation in OSCC cell lines,while knockdown of it had the opposite effect.Conclusion c-Myc positively regulates lnc-TBL1XR1-5 in OSCC.Lnc-TBL1XR1-5 affect the mi-gration,proliferation,and metabolism of OSCC by influencing the tumor microenvironment.

Objective To explore the action mechanism of long non-coding RNA(lncRNAs)lncRNA KCTD13-DT in oral squamous cell carcinoma(OSCC)and its potential interaction with transcription factor c-Myc,providing a potential diagnostic and therapeutic target for patients with OSCC.Methods The expression of lncRNA KCTD13-DT in OSCC and paracancerous tissues was detected by qRT-PCR.The effects of c-Myc overexpression and knock-down on human tongue squamous carcinoma cells HN6 and CAL27 were detected by qRT-PCR.Fluorescence in si-tu hybridization(FISH)assessed the localization of lncRNA KCTD13-DT in cells.A dual luciferase reporter gene was used to analyze the role of c-Myc in target binding to the promoter region of lncRNA KCTD13-DT.Stable cell lines with knockdown or overexpression of lncRNA KCTD13-DT were constructed in human OSCC cell lines HN6 and CAL27 by lentiviral infection,and the knockdown and overexpression efficiencies of lncRNA KCTD13-DT were detected by qRT-PCR.Cell proliferation changes were detected by growth curve assay,CCK-8 assay,colony forma-tion assay,and cell migration was detected by scratch assay and Transwell.Results lncRNA KCTD13-DT expres-sion level was reduced in OSCC tissues and OSCC cells(HN6,CAL27),and Western blot verified that after knoc-king down and overexpression of c-Myc in HN6 and CAL27,the qRT-PCR experiments showed that c-Myc nega-tively regulated lncRNA KCTD13-DT,and overexpression of c-Myc significantly down-regulated lncRNA KCTD13-DT;knockdown of c-Myc significantly up-regulated lncRNA KCTD13-DT levels.Dual luciferase reporter gene showed that c-Myc could target lncRNA KCTD13-DT,and c-Myc could be involved in regulating and repressing the transcriptional activity of lncRNA KCTD13-DT.FISH showed that lncRNA KCTD13-DT mainly existed in the nu-cleus.Growth curve assay,CCK-8 assay,cell scratch assay,Transwell,and colony formation assay showed that knockdown of lncRNA KCTD13-DT promoted the growth and proliferation of OSCC cells,and overexpression of ln-cRNA KCTD13-DT significantly inhibited the proliferation and migration of OSCC cells.Conclusion lncRNA KCTD13-DT is negatively regulated by c-Myc.Knockdown of lncRNA KCTD13-DT promotes cell proliferation,while overexpression of it inhibits cell growth.

Cuproptosis is a new type of cell death that depends on intracellular copper accumulation to trigger the aggregation of mitochondrial lipoacylated protein and the degradation of iron-sulfur cluster protein,with a different mechanism of action from autophagy,ferroptosis,pyroptosis,and necroptosis.Cuproptosis is closely association with the development of liver cancer and resistance to antitumor drugs,as well as the progression of various liver diseases such as hereditary liver diseases,nonalcoholic fatty liver disease,viral hepatitis,and liver cirrhosis.This article summarizes the mechanism of cuproptosis and its role in liver diseases,in order to provide a reference for further research and treatment of liver diseases.

Objective To investigate changes in serum complement C1 tumor necrosis factor-related pro-tein family 12(CTRP12)level before and after percutaneous coronary intervention(PCI)in patients with acute myocardial infarction(AMI)and the relationship of CTRP12 level with in-stent restenosis(ISR).Methods A total of 104 patients who had been diagnosed with AMI and had undergone PCI at Danyang People's Hospital in Jiangsu Province from January 2021 to June 2023 were selected.The incidence of ISR within 12 months after PCI was counted,and they were divided into an ISR group and a non-ISR group according to the results of reviewed coronary angiography.Serum CTRP12 levels were compared between the two groups before PCI and on one day before discharge.Logistic regression was used to analyze the influencing factors of ISR in AMI patients after PCI.Receiver operating characteristic(ROC)curve was used to analyze the predictive value of CTRP12 for ISR in AMI patients after PCI.Results The incidence of ISR in 104 AMI patients at 12 months after PCI was 14.4%(15/104).As compared with the non-ISR group,the ISR group had significant increases in preoperative TIMI flow of≤1,white blood cell count,neutrophil count,TC,and LDL-C,and a significant decline in serum CTRP12 level on one day before discharge(P<0.05).In the non-ISR group,serum CTRP12 level was significantly higher on one day before discharge than its baseline(P<0.05).In the ISR group,serum CTRP12 level on one day before discharge was lower than its baseline,but the difference was not statistically significant(P>0.05).Logistic regression analysis showed that a lower CTRP12 level on one day before discharge was an independent risk factor for ISR in AMI patients after PCI(P<0.05).ROC curve analysis showed that the optimal cut-off point of serum CTRP12 on one day before discharge for predicting ISR in AMI patients after PCI was 3.89 ng/mL(sensitivity 93.3%and speci-ficity 73.0%),and the area under the ROC curve(AUC)was 0.849.Conclusions Serum CTRP12 level inone day before discharge has certain predictive value for ISR in AMI patients after PCI.CTRP12 may be a therapeutic target for ISR in AMI patients after PCI.

Objective To investigate the risk factors of infection after hepatectomy for liver cancer, and to establish and validate a risk prediction model. Methods The clinical data of 167 patients with primary liver cancer who underwent hepatectomy in People's Hospital of Wuhan University from January 2020 to March 2022 were retrospectively collected. All patients were divided into postoperative infection group ( n =28) and non-infection group ( n =139) according to whether postoperative infection complications occurred. The t -test or Mann-Whitney U test was used for comparison of continuous data between two groups and the chi-square test was used for comparison of categorical data between two groups. Univariate analysis and logistic regression analysis were used to screen the risk factors of infection after hepatectomy for hepatocellular carcinoma, and a nomogram risk prediction model for postoperative infection was established. All patients were randomly divided into training cohort ( n =119) and the validation cohort ( n =48) according to the ratio of 7∶ 3, the Bootstrap method was used for internal validation of the model, and the model calibration curve and ROC curve were used to evaluate the calibration and discrimination of the nomogram model. Results Postoperative infection occurred in 28 of 167 patients (16.8%). Logistic regression analysis showed that diabetes, CONUT score ≥4 points, preoperative NLR, operation time, intraoperative blood loss, and drainage tube placement time > 7 d were independent risk factors for infection after hepatectomy for liver cancer (all P < 0.05). Based on the nomogram constructed from the above six risk factors, the area under the ROC curve of the training cohort and the validation cohort was 0.848, and 0.853, respectively. The calibration curve of the nomogram model shows that the predicted value is basically consistent with the actual observed value, indicating that the accuracy of the nomogram model prediction is better. Conclusion The individualized nomogram risk prediction model based on diabetes, CONUT score ≥4 points, preoperative NLR, operation time, intraoperative blood loss, and drainage tube placement time > 7 d has good predictive performance and has high predictive value for high-risk patients.

Objective To analyze the serological markers and surgical indicators associated with biliary complications after orthotopic liver transplantation, explore their influencing factors and predictive indicators. Methods A retrospective analysis was performed for the clinical data of 101 patients who underwent orthotopic liver transplantation in Renmin Hospital of Wuhan University from January 2016 to June 2022, according to the presence or absence of biliary complication (BC) at 6 months after surgery, they were divided into BC group with 21 patients and non-BC group with 80 patients.The t -test or the Mann-Whitney U test was used for comparison of continuous data between groups, and the chi-square test was used for comparison of categorical data between groups.Univariate and multivariate Logistic regression analyses were performed, and the receiver operating characteristic (ROC) curve was used to evaluate the predictive performance of combined indicators. Results Among the 101 patients, 21(20.8%) experienced BC.The multivariate Logistic regression analysis showed that MELD score (odds ratio[ OR ]=0.134, 95% confidence interval[ CI ]: 0.031-0.590, P =0.008), SⅡ/Alb ( OR =1.415, 95% CI : 1.181-1.696, P =0.001), and plasma transfusion volume ( OR =1.001, 95% CI : 1.000-1.002, P =0.032) were independent risk factors for the development of BC in patients after liver transplantation.MELD score, SⅡ/Alb, plasma transfusion volume, MELD+SⅡ/Alb, and MELD+SⅡ/Alb+plasma transfusion volume had an area under the ROC curve of 0.712, 0.870, 0.712, 0.900, and 0.918, respectively, in predicting BC after liver transplantation. Conclusion SⅡ/Alb, plasma transfusion volume and MELD score are independent risk fators for BC after liver transplantation.The combination of three indicators has good predictive value and clinical guiding significance for BC after liver transplantation.

WS9326A is a peptide antibiotic containing a highly unusual N-methyl-E-2-3-dehydrotyrosine (NMet-Dht) residue that is incorporated during peptide assembly on a non-ribosomal peptide synthetase (NRPS). The cytochrome P450 encoded by sas16 (P450_Sas) has been shown to be essential for the formation of the alkene moiety in NMet-Dht, but the timing and mechanism of the P450_Sas-mediated α,β-dehydrogenation of Dht remained unclear. Here, we show that the substrate of P450_Sas is the NRPS-associated peptidyl carrier protein (PCP)-bound dipeptide intermediate (Z)-2-pent-1'-enyl-cinnamoyl-Thr-N-Me-Tyr. We demonstrate that P450_Sas-mediated incorporation of the double bond follows N-methylation of the Tyr by the N-methyl transferase domain found within the NRPS, and further that P450_Sas appears to be specific for substrates containing the (Z)-2-pent-1'-enyl-cinnamoyl group. A crystal structure of P450_Sas reveals differences between P450_Sas and other P450s involved in the modification of NRPS-associated substrates, including the substitution of the canonical active site alcohol residue with a phenylalanine (F250), which in turn is critical to P450_Sas activity and WS9326A biosynthesis. Together, our results suggest that P450_Sas catalyses the direct dehydrogenation of the NRPS-bound dipeptide substrate, thus expanding the repertoire of P450 enzymes that can be used to produce biologically active peptides.

Objective : To clarify the targeted regulatory relationship between long non-coding RNA ( lncRNAs) lnc-CCDC117-1 and oncogenic transcription factor c-Myc，and to explore the effect of lnc-CCDC117-1 knockdown and overexpression on the development of tongue squamous cell carcinoma cells． Methods : Lentiviral vectors car- rying flag-c-Myc，plko．1-shc-Myc and their controls were transfected into HN6，SCC9 and CAL27 cells respective- ly，and real-time quantitative PCR(qRT-PCR) was used to detect the expression of lnc-CCDC117-1．In addition， the intracellular localization of lnc-CCDC117-1 was detected by fluorescence in situ hybridization．On this basis，the lnc-CCDC117-1 expression vector and knockdown vector were constructed and transfected with HN6 ，SCC9， CAL27 cells，CCK-8 method，cloning and formation to verify the proliferation of tongue squamous cell. Results: LncRNAs positively regulated by c-Myc were initially screened by gene chip technology．After overexpression or c- Myc knockdown in tongue squamous cell HN6，these lncRNAs were verified to be consistent with the results of the chip，and the expression difference of lnc-CCDC117-1 was found to be the most significant．qRT-PCR test showed that c-Myc had a positive regulatory effect on lnc-CCDC117-1．When c-Myc was overexpressed，the expression of lnc-CCDC117-1 could be significantly up-regulated．lnc-CCDC117-1 expression was significantly down-regulated by c-Myc knockdown．Dual luciferase reporter genes showed that c-Myc could target the regulation of lnc-CCDC117-1， and c-Myc was involved in regulating and enhancing the transcriptional activity of lnc-CCDC117-1．lnc-CCDC117- 1 mainly existed in the nucleus of the cell．qRT-PCR results showed that the expression of lnc-CCDC117-1 and c- Myc significantly decreased by sh-lnc-CCDC117-1．The expression of lnc-CCDC117-1 was significantly up-regula- ted by + lnc-CCDC117-1．The results of growth curve assay，CCK-8 assay，cell scratch assay and cloning forma- tion showed that overexpression of lnc-CCDC117-1 significantly promoted the proliferation and migration of tongue squamous cell cells，while knockdown of lnc-CCDC117-1 could inhibit the growth and proliferation of tongue squa- mous cell carcinoma cells． Conclusion lnc-CCDC117-1 is positively regulated by c-Myc，and overexpression of lnc-CCDC117-1 can promote cell proliferation，on the contrary，inhibit cells growth.

Liver cancer has a high degree of malignancy and its prognosis is poor. The biological behavior of liver cancer with its high degree of malignancy and high tumor heterogeneity impact on its therapeutic effect. The rapid development of precision therapy in the field of cancer provides a platform for application of the precision therapy mode in liver cancer treatment. This article reviews the combined impact by using immune checkpoint inhibitors therapy under precision medicine with targeted therapy, radiotherapy, chemotherapy, oncolytic viruses, tumor vaccines, fecal bacteria transplantation and other therapies.