The trillions of commensal microorganisms living in the gut lumen profoundly influence the physiology and pathophysiology of the liver through a unique gut-liver axis. Disruptions in the gut microbial communities, arising from environmental and genetic factors, can lead to altered microbial metabolism, impaired intestinal barrier and translocation of microbial components to the liver. These alterations collaboratively contribute to the pathogenesis of liver disease, and their continuous impact throughout the disease course plays a critical role in hepatocarcinogenesis. Persistent inflammatory responses, metabolic rearrangements and suppressed immunosurveillance induced by microbial products underlie the pro-carcinogenic mechanisms of gut microbiota. Meanwhile, intrahepatic microbiota derived from the gut also emerges as a novel player in the development and progression of liver cancer. In this review, we first discuss the causes of gut dysbiosis in liver disease, and then specify the pivotal role of gut microbiota in the malignant progression from chronic liver diseases to hepatobiliary cancers. We also delve into the cellular and molecular interactions between microbes and liver cancer microenvironment, aiming to decipher the underlying mechanism for the malignant transition processes. At last, we summarize the current progress in the clinical implications of gut microbiota for liver cancer, shedding light on microbiota-based strategies for liver cancer prevention, diagnosis and therapy.

The trillions of commensal microorganisms living in the gut lumen profoundly influence the physiology and pathophysiology of the liver through a unique gut-liver axis. Disruptions in the gut microbial communities, arising from environmental and genetic factors, can lead to altered microbial metabolism, impaired intestinal barrier and translocation of microbial components to the liver. These alterations collaboratively contribute to the pathogenesis of liver disease, and their continuous impact throughout the disease course plays a critical role in hepatocarcinogenesis. Persistent inflammatory responses, metabolic rearrangements and suppressed immunosurveillance induced by microbial products underlie the pro-carcinogenic mechanisms of gut microbiota. Meanwhile, intrahepatic microbiota derived from the gut also emerges as a novel player in the development and progression of liver cancer. In this review, we first discuss the causes of gut dysbiosis in liver disease, and then specify the pivotal role of gut microbiota in the malignant progression from chronic liver diseases to hepatobiliary cancers. We also delve into the cellular and molecular interactions between microbes and liver cancer microenvironment, aiming to decipher the underlying mechanism for the malignant transition processes. At last, we summarize the current progress in the clinical implications of gut microbiota for liver cancer, shedding light on microbiota-based strategies for liver cancer prevention, diagnosis and therapy.

Objective To describe the significance of the pretreatment inflammatory indicators in predicting the prognosis of patients with esophageal squamous cell carcinoma (ESCC) after undergoing radical radiotherapy. Methods The data of 246 ESCC patients who underwent radical radiotherapy were retrospectively collected. Receiver operating characteristic (ROC) curves were drawn to determine the optimal cutoff values for platelet-lymphocyte ratio (PLR), neutrophil-lymphocyte ratio (NLR), and systemic immune-inflammation index (SII). The Kaplan-Meier method was used for survival analysis. We conducted univariate and multivariate analyses by using the Cox proportional risk regression model. Software R (version 4.2.0) was used to create the nomogram of prognostic factors. Results The results of the ROC curve analysis showed that the optimal cutoff values of PLR, NLR, and SII were 146.06, 2.67, and 493.97, respectively. The overall response rates were 77.6% and 64.5% in the low and high NLR groups, respectively (P<0.05). The results of the Kaplan-Meier survival analysis revealed that the prognosis of patients in the low PLR, NLR, and SII group was better than that of patients in the high PLR, NLR, and SII group (all P<0.05). The results of the multivariate Cox regression analysis showed that gender, treatment modalities, T stage, and NLR were independent factors affecting the overall survival (OS). In addition, T stage and NLR were independent factors affecting the progression-free survival (PFS) (all P<0.05). The nomogram models of OS and PFS prediction were established based on multivariate analysis. The C-index values were 0.703 and 0.668. The calibration curves showed excellent consistency between the predicted and observed OS and PFS. Conclusion The pretreatment values of PLR, NLR, and SII are correlated with the prognosis of patients with ESCC who underwent radical radiotherapy. Moreover, NLR is an independent factor affecting the OS and PFS of ESCC patients. The NLR-based nomogram model has a good predictive ability.

The trillions of commensal microorganisms living in the gut lumen profoundly influence the physiology and pathophysiology of the liver through a unique gut-liver axis. Disruptions in the gut microbial communities, arising from environmental and genetic factors, can lead to altered microbial metabolism, impaired intestinal barrier and translocation of microbial components to the liver. These alterations collaboratively contribute to the pathogenesis of liver disease, and their continuous impact throughout the disease course plays a critical role in hepatocarcinogenesis. Persistent inflammatory responses, metabolic rearrangements and suppressed immunosurveillance induced by microbial products underlie the pro-carcinogenic mechanisms of gut microbiota. Meanwhile, intrahepatic microbiota derived from the gut also emerges as a novel player in the development and progression of liver cancer. In this review, we first discuss the causes of gut dysbiosis in liver disease, and then specify the pivotal role of gut microbiota in the malignant progression from chronic liver diseases to hepatobiliary cancers. We also delve into the cellular and molecular interactions between microbes and liver cancer microenvironment, aiming to decipher the underlying mechanism for the malignant transition processes. At last, we summarize the current progress in the clinical implications of gut microbiota for liver cancer, shedding light on microbiota-based strategies for liver cancer prevention, diagnosis and therapy.

Objective To construct a prokaryotic expression vector of of the long QT syndrome(LQTS)associated C-terminal lobe of calmodulin(CaM)mutant E141G(C-lobeE141G)and to identify the expression,purification,and activity of C-lobeE141G.Methods A cDNA fragment was inserted into a PGEX-6p-3 plasmid vector and transferred into Escherichia coli BL21 receptor cells,and glutathione-S-trans-ferase(GST)fusion protein was induced by isopropyl thio-β-D galactoside(IPTG).Glutathione-Sepharose 4B beads were used to separate and purify GST-C-lobeE141G.After removing the GST label with protease,the purity and concentration of purified C-lobeE141G were detected using SDS-PAGE and BCA,respectively.The activity of purified C-lobeE141G was detected using the GST pull-down method and patch clamp technique.Results GST-C-lobeE141G fusion protein was highly expressed,and C-lobeE141G with high purity and concentration was obtained.The purified C-lobeE141G protein not only bound to CaV1.2 calcium channels,but also rescued the channel activity from run-down in the ventricular myocytes of rat hearts.Conclusion This study successfully constructed a prokaryotic expression vector of C-lobeE141G,which provides a material basis for the study of the mechanism of LQTS mediated by C-lobe mutations in CaM.

Objectives:This study aims to investigate the association between cumulative fasting blood glucose(FBG)and presence of coronary artery calcification(CAC). Methods:A total of 1 113 participants were recruited from the Beijing Community-based Cohort of Atherosclerosis.Anthropometric measurements and laboratory examinations including FBG were performed in 1998,2008-2009 and 2013-2014 respectively,and coronary CT scan was performed in 2013-2014.Participants were classified into 4 groups according to the level of cumulative FBG(10-year weighted cumulative value of at least 2 FBGs):<50.0 mmol/L group(n=495),50.0-55.9 mmol/L group(n=345),56.0-69.9 mmol/L group(n=176),and≥70.0 mmol/L group(n=97).CAC score>0 was defined as presence of CAC.Multivariable logistic regression model was applied to analyze the impact of cumulative FBG exposure on the risk of CAC,and subgroup analyses were conducted according to factors such as sex and age. Results:The mean age of enrolled participants was(59.7±6.4)years,523(47.0%)were male and 478(42.9%)had CAC.The proportion of subjects with CAC increased with the increment of cumulative FBG.Compared with the<50.0 mmol/L group,the multivariable-adjusted OR(95%CI)for CAC in the 50.0-55.9 mmol/L group,56.0-69.9 mmol/L group,and≥70.0 mmol/L group were 1.43(1.04-1.98),1.92(1.24-2.99)and 2.79(1.35-5.77),respectively(Ptrend<0.05).The risk for CAC increased by 34%per 10 mmol/L increase in cumulative FBG,with OR(95%CI)of 1.34(1.12-1.59).There was no statistically significant difference in the risk of CAC presence for each 10 mmol/L increase in cumulative FBG level between the subgroups(all P≥0.05). Conclusions:Elevated cumulative FBG is a risk factor for the prevalence of CAC,indicating the importance of maintaining healthy FBG in preventing the occurrence of CAC.

Objective The existing evidence of exercise rehabilitation in patients undergoing surgery for valvular heart disease was analyzed,described and evaluated by using evidence mapping methods.Methods Systematic reviews and randomized controlled trials on exercise rehabilitation of patients undergoing valvular heart disease surgery were searched from CNKI,Wanfang Data,VIP,CBM,Embase,PubMed,Cochrane Library,Web of Science,Ovid,CINAHL and other databases,and the search period was established until April 23,2024.The quality of the included literature was evaluated,and the feature information of the included literature was visualized in the form of bubble map and table.Results Fifty-one literatures(including 44 randomized controlled trials and 7 systematic evaluations)were finally included.Among the 44 randomized controlled trials,the types of exercise were mainly related to anaerobic exercise(3 literatures),aerobic exercise(11 literatures),flexibility training(8 literatures),and multisport exercise(22 literatures);postoperative inpatient rehabilitation accounted for a relatively high proportion(16 literatures),followed by overall postoperative rehabilitation(13 literatures)and pre-operative prehabilitation(7 literatures).Twenty-seven conclusions were categorized as"beneficial",15 as"possibly beneficial,"and one ach as"unclear"and"no effect".Seven systematic evaluations were subjected to Meta-analysis,and in terms of the design of the included studies,there were only 3 systematic reviews that included randomized controlled trials.Of the study conclusions,three were"beneficial",three were"possibly beneficial"and one was"unclear".Conclusion The evidence mapping shows that exercise rehabilitation is generally beneficial or potentially beneficial in the rehabilitation of valvular heart disease surgery,mainly in the postoperative inpatient rehabilitation phase.High-quality studies are needed to further investigate the effectiveness of exercise programs with different intensities,frequencies,and durations,as well as different valve types,adverse effects of exercise,and other outcome indicators.

Objective To systematically review the efficacy of enhanced recovery after surgery(ERAS)nursing on patients with dissection of aorta.Methods Nine databases,including PubMed,CNKI,etc were searched to identify randomized controlled trials involving dissection of aorta patients undergoing ERAS nursing.The retrieval time was from setting up of the databases until March 2024.Literature quality assessment followed by"Cochrane handbook for systematic reviews of interventions.Version 5.1.0",and Meta-analysis was conducted utilizing software of RevMan 5.4.Results Nine literatures with a total of 723 patients were included.The results of Meta-analysis showed that compared with the conventional nursing model,the application of ERAS nursing model could effectively promote the process of patients'postoperative recovery,and there were significant differences in indicators such as the time of postoperative mechanical ventilation,the time of the first postoperative out-of-bed activity,the time of tubing removal,the incidence of complications,the length of hospital stay,and the degree of perceived pain(P＜0.05).Conclusion Implementing nursing model based on ERAS on dissection of aorta patients can effectively enhance patients'postoperative recovery outcomes,thus worth clinical promotion and application.

Objective To evaluate the effect of mindfulness-based intervention in patients after percutaneous coronary intervention(PCI)through Meta-analysis.Methods Nine databases,including CNKI and PubMed,were searched for randomized controlled trials on the effect of mindfulness intervention in patients after PCI,and the search period was from the establishment of the database to May 31,2024.Two researchers independently screened the literature,extracted data and evaluated the quality,and used Revman 5.4 software for Meta-analysis.Results A total of 11 randomized controlled trials involving 998 patients were included.The results of Meta-analysis showed that compared with conventional care,the use of mindfulness-based intervention therapy could positively improve patients'postoperative anxiety,perceived stress level,mindfulness awareness and other indicators.In terms of safety measures,the incidence of cardiac adverse events was not statistically significant compared with usual care(P＞0.05).Conclusion Mindfulness intervention has a significant effect in patients after PCI.

AIM:To investigate the effect of vaccarin(VAC)on endothelial dysfunction in type 2 diabetes mellitus(T2DM),and to uncover the underlying mechanisms.METHODS:(1)C57BL/6 mice received intraperitoneal injection of streptozotocin and were fed with a high-fat diet(21.8 kJ/kg,60%of the energy source was fat)to construct a T2DM mouse model.Thirty mice were randomly divided into control,T2DM and T2DM+VAC groups,with 10 mice in each group.The mice in T2DM+VAC group were given 1 mg/kg VAC via oral gavage for 6 weeks,while those in control and T2DM groups were given the same volume of PBS.The mRNA and protein expression levels of BCL2-interacting pro-tein 3(BNIP3),PTEN-induced kinase 1(PINK1)and parkin in the thoracic aorta were detected by RT-qPCR and West-ern blot.(2)Human umbilical vein endothelial cells(HUVECs)were stimulated by high glucose(HG;35 mmol/L glu-cose).Mitochondrial membrane potential,autophagy and mitochondrial superoxide levels were detected using JC-1,acri-dine orange(AO)and MitoSOX staining,respectively.RESULTS:Compared with control group,the mRNA and protein levels of BNIP3,PINK1 and parkin were significantly increased in the thoracic aorta of T2DM mice(P<0.05).Compared with T2DM group,the mRNA and protein levels of BNIP3,PINK1 and parkin in the thoracic aorta were significantly re-duced in T2DM+VAC group(P<0.05).The results of JC-1,AO and MitoSOX staining showed that VAC attenuated the decrease in mitochondrial membrane potential and the increase in autophagy and mitochondrial superoxide levels in HG-in-duced HUVECs.Treatment with VAC also inhibited HG-mediated mitochondrial damage in HUVECs after BNIP3 overex-pression.The effect of miR-570-3p mimic on mitochondrial damage was similar to VAC.RT-qPCR and Western blot showed that both miR-570-3p mimic and VAC significantly reduced the mRNA and protein levels of BNIP3,PINK1 and parkin.In contrast,inhibition of miR-570-3p exhibited the opposite effects.CONCLUSION:Treatment with VAC alle-viated endothelial dysfunction in T2DM by inhibiting HG-induced mitochondrial dysfunction through miR-570-3p/BNIP3.