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.

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 explore the application effect of advanced lung rehabilitation programs in patients un-dergoing high flow nasal cannula oxygen therapy(HFNC).Methods Convenience sampling method was used to se-lect 40 HFNC patients admitted to the respiratory department,ICU,coronary heart disease monitoring unit,and other departments of a tertiary A comprehensive hospital in Tianjin from January to June 2023 as the experimental group,and 40 HFNC patients admitted from June to December 2022 as the control group.Both groups of patients received HFNC treatment during hospitalization and continued at home,while the experimental group adopts the information-motivation-behavioral skills(IMB)model as the theoretical basis,implements advanced pulmonary rehabili-tation during the stable condition period,discharge preparation period,and home rehabilitation period,and imple-ments compliance management of home pulmonary rehabilitation through cloud follow-up,and the control group re-ceived routine lung rehabilitation and home follow-up.The degree of respiratory distress,6-minute walking distance,exercise self-efficacy,quality of life were compared between the 2 groups before intervention,2 months and 6 months after intervention,and compliance with home pulmonary rehabilitation was compared between the 2 groups 6 months after intervention.Results The repeated measures analysis of variance showed that there was an interaction effect between time and the 2 groups in terms of difficulty in breathing,6-minute walking distance,exercise self-ef-ficacy,and quality of life(P＜0.05).Simple effect analysis showed that after 2 and 6 months of intervention,the ex-perimental group performed better than the control group in the respiratory distress,6-minute walking distance,exer-cise self-efficacy,and quality of life(P＜0.05).Within 6 months of intervention,the compliance of home pulmonary rehabilitation in the experimental group was better than that in the control group,and the difference was statistically significant(P＜0.05).Conclusion The application of advanced pulmonary rehabilitation programme based on IMB can improve respiratory symptoms and improve exercise self-efficacy and adherence to pulmonary rehabilitation,en-hance activity endurance and improve quality of life.

Objective To investigate the changes in the expression of complement C3,high mobility group protein B1(HMGB1),and glutathione peroxidase 4(GPX4)in brain tissue at different time points after cerebral ischemia-reperfusion injury in rats.Methods A total 72 SPF male SD rats were randomly divided into a sham operation group(36 rats)and a model group(36 rats).A rat model of middle cerebral artery occlusion was established using thread occlusion,and then the rats from the model group were further assigned into 4 subgroups with reperfusion time for 3,6 and 24 h and 3 d,respectively,with 9 rats in each subgroup.Zea Longa scoring was used to assess neu-rological function.R2StarMap imaging,diffusion-weighted imaging(DWI),T1 weighted imaging,and T2 weighted imaging were performed on all the rats.The volume of abnormal DWI signals were detected and the volume of cerebral infarction was measured.The original R2StarMap images were post-processed to generate R2*pseudo color images,and then the R2*values of the areas with blood supply from bilateral middle cerebral artery were measured to detect iron deposition in the brain.The protein expression of C3,HMGB1,and GPX4 was detected by Western blotting.Results The sham operation group showed no neurological damage,while the model group had a significant increase in neurological function scores at 3,6 and 24 h and 3 d after modeling when compared to the sham surgery group(P＜0.05).While the size of right cerebral infarct was in-creased significantly at 3,6 and 24 h and 3 d in the rats of the model group(P＜0.05).The R2*value of the area with blood supply from the right middle cerebral artery in the model group was significantly higher than that in the left side at 3,6 and 24 h and 3 d(P＜0.05,P＜0.01),and it was also obviously higher than that in the right side of the sham operation group at these time points(P＜0.05,P＜0.01).The R2*ratio of the right and left blood supply areas in the model group at 3,6 and 24 h and 3 d was also statistically higher than that in the sham operation group at corresponding time points(1.82±0.82 vs 1.12±0.31,P＜0.05;1.31±0.26 vs 1.04±0.14,P＜0.05;1.94±0.74 vs 1.06±0.10,P＜0.01;1.99±0.39 vs 1.02±0.11,P＜0.01).Compared with the sham operation group,the expression levels of C3 and HMGB1 was significantly increased in the model group at 3,6 and 24 h and 3 d,while that of GPX4 was notably reduced(P＜0.01).Conclu-sion Cerebral ischemia-reperfusion injury impairs the neurological function of rats and signifi-cantly affects the cerebral expression of complement C3,HMGB1,and GPX4.

Macrophage extracellular traps(METs)are extracellular fibrous web-like structures produced by macrophages.METs play a crucial role in the development and progression of various cardiovascular diseases(CVDs),including atherosclerosis and myocardial infarction.This article summarizes the mechanism of METs in CVDs,future research directions and the possibility of using METs as potential therapeutic targets for clinical diseases.

Objective By population survey,to explore the epidemiological characteristics of gastric precancerous lesions in Lishui District of Nanjing and provide objective basis for the prevention and treatment of early gastric cancer.Methods From July 2021 to December 2022,21 977 patients who received endoscopy and/or 13C-UBT in Lishui District People's Hospital and 6 medical community units in Nanjing City were retrospectively analyzed for demography characteristics,detection rate of gastric precancerous lesions,and H.Pylori infection rate.Results(1)590 cases of gastric precancerous lesions were detected(detection rate 2.68%);(2)The total detection rate of precancerous lesions and three pathological types in males were all higher than those in females(all P<0.001);(3)The minimum age for the total detection rate of precancerous lesions in males and the mini-mum age for each pathological type were lower than in females(P<0.001,0.009,0.005,0.002);(4)The popu-lation total H.pylori infection rate was 23.10%,the H.pylori infection rate in patients with precancerous lesions was higher than that in non-precancerous lesions(P<0.001),both H.pylori infection rate of male and female in precancerous lesions were all higher than those of non-precancerous lesions of the same sex(all P<0.001),in addition,the H.pylori infection rate of male whether in precancerous or non-precancerous lesions was higher than that of female(all P<0.001);(5)The precancerous lesions detection rate in male,female,and the overall age range of 20～29 to 70～79 years is positively correlated with age growth(P<0.001),and rapidly decreases after the age of 79,the of H.pylori infection rate was also positively correlated with age growth(P<0.001),and the trend of age change(P<0.001)was parallel to the precancerous lesions detection rate.Conclusions The detec-tion rate of gastric precancerous lesions in this region is above the average level in China;the total H.pylori infec-tion rate is at a relatively low level in China;the H.pylori infection rate is parallel to the age trend of the detection rate of gastric precancerous lesions,and increases with age.

Background:Knockdown of ribosomal RNA processing 15 homolog(RRP15)inhibited the proliferation and growth of hepatocellular carcinoma(HCC),but its relationship with the sensitivity of HCC to sorafenib has not been reported.Aims:To elucidate the role of RRP15 in modulating the sensitivity of HCC to sorafenib and to unravel the underlying mechanisms.Methods:The constitutive expression of RRP15 in human HCC cell lines was assessed using real-time PCR and Western blotting,and then manipulated via infection with either RRP15 knockdown or overexpression lentivirus.The impact of RRP15 expression on sorafenib sensitivity of HCC cells was investigated by CCK-8 and colony formation assays.Changes in ferroptosis markers,including reactive oxygen species(ROS),Fe2+,lipid peroxide,reduced glutathione,etc in HCC cells were measured to determine the effect of RRP15 on ferroptosis.The combination of the ferroptosis inhibitor Ferrostatin-1 and RRP15 knockdown was used to verify the modulatory effect of RRP15 on sorafenib sensitivity and ferroptosis.Furthermore,xenograft tumor in nude mice was used to confirm the relationship between RRP15 and sorafenib sensitivity.Results:Sorafenib treatment induced RRP15 expression in HCC cells.The expression levels of RRP15 in HCC cells were negatively associated with the sensitivity to sorafenib.RRP15 knockdown enhanced the sorafenib sensitivity and sorafenib-induced ferroptosis in HCC cells,presenting as reduced cell viability,decreased colony formation ability,and increased intracellular ROS,Fe2+,and lipid peroxidation.Treatment with Ferrostatin-1 effectively compromised the increased ferroptosis and sorafenib sensitivity caused by RRP15 downregulation.Mechanistically,inactivation of p62-KEAP1-NRF2 pathway was involved in the RRP15 depletion-mediated ferroptosis and sorafenib sensitization in HCC cells.In in vivo study,RRP15 knockdown combined with sorafenib treatment notably inhibited the subcutaneous xenograft tumor growth in nude mice.Conclusions:This study demonstrates that inhibition of RRP15 significantly enhances the sensitivity of HCC to sorafenib,potentially through the promotion of ferroptosis.These findings may provide new strategies for improving the therapeutic response of HCC to sorafenib treatment.

Ferroptosis is a form of programmed cell death characterized by iron metabolic imbalance and lipid peroxidation.Alzheimer disease(AD)is a neurodegenerative condition.Studies have shown that lipid peroxidation through ferroptosis plays a significant role in the progression of AD.Ferroptosis suppressor protein 1(FSP1)/coenzyme Q10(CoQ10)signaling axis serves as a crucial regulatory element in the process of lipid peroxidation associated with ferropto-sis.This review explores the mechanisms of the FSP1/CoQ10 signaling axis in AD,aiming to present a novel therapeutic ap-proach for AD treatment.

Objective:To investigate the applied effect of airway lavage of fiberoptic bronchoscope under computed tomography(CT)location combined with ultrasound monitoring diaphragmatic movement in mechanical ventilation of pediatric severe pneumonia.Methods:A total of 70 pediatric patients with severe pneumonia who received mechanical ventilation in The People's Hospital of Liupanshui City and Liupanshui Maternal and Child Health Care Hospital from October 2022 to October 2023 were selected,and they were divided into a control group and an observation group according to the random number table method,with 35 cases in each group.The control group did not undergo CT examination for lung before lavage with bronchoscopy,while the observation group received CT examination before airway lavage.Both two groups simultaneously adopted B ultrasound to monitor diaphragm movement.Heart rate,respiration,oxygen saturation,respiratory mechanics index,pediatric early warning score(PEWS)and modified pneumonia survivor index(mPIRO)score were detected before and after lavage,and the movement and thickness of diaphragm of children were measured by B ultrasound.Results:The heart rate and respiratory frequency of two groups after treatment were significantly lower than those before treatment,and the blood oxygen saturation was significantly higher than that before treatment.The heart rate and respiratory frequency of the observation group were respectively(80.23±10.07)times/min and(18.11±5.03)times/min,which were significantly lower than those of the control group,and the blood oxygen saturation was significantly higher than that of the control group,and the differences were statistical significance(t=3.397,3.939,7.719,P<0.05),respectively.The pulmonary pressure,peak pressure,plateau pressure,average airway pressure,chest pressure and abdominal pressure of two groups after treatment were significantly lower than those before treatment,and the levels of the above indicators in the observation group were significantly lower than those in the control group,with statistical significances(t=12.323,8.141,16.733,12.298,11.375,18.248,P<0.05),respectively.The PEWS scores and total scores of body temperature,pulse,respiration and blood pressure of two groups after treatment were significantly lower than those after treatment,and the above scores in the observation group were significantly lower than those in the control group,with statistical significance(t=67.309,58.148,35.997,30.218,5.271,P<0.05),respectively.The mPRIO scores and total scores of age,test indicators of laboratory,symptom duration,respiratory distress index and treatment plan in two groups after treatment were significantly higher than those before treatment,and the above scores in the observation group were significantly higher than those in the control group,with statistical significances(t=7.432,7.153,7.268,5.088,4.645,4.091,P<0.05),respectively.The diaphragm movement and thickness of two groups after treatment were significantly higher than those before treatment,and the above indicators in the observation group were significantly higher than those in the control group,with statistical significances(t=63.444,6.803,P<0.05),respectively.Conclusion:Compared with conventional airway lavage,the airway lavage of fiberoptic bronchoscope under CT location combined with B ultrasound of monitoring diaphragm has higher accuracy and reliability.