Objective:To investigate the molecular markers involved in death related to acute myocardial infarction (AMI) and provide new targets for early intervention.Methods:Consecutive patients who hospitalized in department of cardiology, Xuanwu Hospital, Capital Medical University from January 2017 to December 2021 and diagnosed with AMI were enrolled. The clinical factors and markers associated with in-hospital death after AMI were analyzed. In addition, patients diagnosed with AMI hospitalized in department of cardiology, Xuanwu Hospital, Capital Medical University from September 2022 to April 2023 were enrolled. We prospectively analyzed the plasma protein of death related to AMI via Olink Precision Proteomics based on proximity extension assay (PEA) technology.Results:In the retrospective study, 2 325 patients with AMI were analyzed, including 75 patients in the in-hospital death group and 2 250 subjects in the survival group. The overall mortality rate during hospitalization was 3.23% (75/2325). The patients in the death group were older: 72 (64, 80) years vs. 63 (55, 71) years. And Interleukin-6 (IL-6), hypersensitive C-reactive protein (Hs-CRP), leukocyte counts and neutrophil counts were markedly higher in the death group than those in the survival group: 69.0 (26.7, 136.6) ng/L vs. 18.2 (9.4, 36.5) ng/L, 45.7 (28.7, 50.5) mg/L vs. 5.5 (2.0, 17.2) mg/L, 12.0 (9.8, 14.1) ×10 9/L vs. 8.9 (7.2, 11.2) × 10 9/L, 9.8 (7.8, 12.1) ×10 9/L vs. 6.5(4.7, 8.8) ×10 9/L ( P<0.01). In this prospective study, 86 patients with AMI were analyzed. 61 proteins including Insulin-like growth factor-binding protein 1, 2 (IGFBP-1, IGFBP-2), Chitotriosidase-1 (CHIT1), Complement component C1q receptor (CD93) were independently associated with in-hospital death related to AMI ( P<0.05). The differential proteins were mainly enriched in inflammatory response, cell adhesion, cytokine signaling pathway and apoptosis. Moreover, 22 proteins including Urokinase plasminogen activator surface receptor (U-PAR), Trefoil factor 3 (TFF3), Perlecan (PLC), Growth differentiation factor 15 (GDF-15), Junctional adhesion molecule A (JAM-A) were plotted according to a logistic regression model, and the area under the curve (AUC) was more than 0.9, showing the high accuracy in predicting in-hospital death after AMI. Conclusions:Molecular markers of the inflammatory response, cell adhesion, cell growth and apoptosis might be involved in death related to AMI, which provides new targets for early intervention.

Liver fibrosis is a chronic liver injury resulting from factors like viral hepatitis, autoimmune hepatitis, non-alcoholic steatohepatitis, fatty liver disease, and cholestatic liver disease. Liver transplantation is currently the gold standard for treating severe liver diseases. However, it is limited by a shortage of donor organs and the necessity for lifelong immunosuppressive therapy. Mesenchymal stem cells (MSCs) can differentiate into various liver cells and enhance liver function when transplanted into patients due to their differentiation and proliferation capabilities. Therefore, it can be used as an alternative therapy for treating liver diseases, especially for liver cirrhosis, liver failure, and liver transplant complications. However, due to the potential tumorigenic effects of MSCs, researchers are exploring a new approach to treating liver fibrosis using extracellular vesicles (exosomes) secreted by stem cells. Many studies show that exosomes released by stem cells can promote liver injury repair through various pathways, contributing to the treatment of liver fibrosis. In this review, we focus on the molecular mechanisms by which stem cell exosomes affect liver fibrosis through different pathways and their potential therapeutic targets. Additionally, we discuss the advantages of exosome therapy over stem cell therapy and the possible future directions of exosome research, including the prospects for clinical applications and the challenges to be overcome.

Liver fibrosis is a chronic liver injury resulting from factors like viral hepatitis, autoimmune hepatitis, non-alcoholic steatohepatitis, fatty liver disease, and cholestatic liver disease. Liver transplantation is currently the gold standard for treating severe liver diseases. However, it is limited by a shortage of donor organs and the necessity for lifelong immunosuppressive therapy. Mesenchymal stem cells (MSCs) can differentiate into various liver cells and enhance liver function when transplanted into patients due to their differentiation and proliferation capabilities. Therefore, it can be used as an alternative therapy for treating liver diseases, especially for liver cirrhosis, liver failure, and liver transplant complications. However, due to the potential tumorigenic effects of MSCs, researchers are exploring a new approach to treating liver fibrosis using extracellular vesicles (exosomes) secreted by stem cells. Many studies show that exosomes released by stem cells can promote liver injury repair through various pathways, contributing to the treatment of liver fibrosis. In this review, we focus on the molecular mechanisms by which stem cell exosomes affect liver fibrosis through different pathways and their potential therapeutic targets. Additionally, we discuss the advantages of exosome therapy over stem cell therapy and the possible future directions of exosome research, including the prospects for clinical applications and the challenges to be overcome.

Liver fibrosis is a chronic liver injury resulting from factors like viral hepatitis, autoimmune hepatitis, non-alcoholic steatohepatitis, fatty liver disease, and cholestatic liver disease. Liver transplantation is currently the gold standard for treating severe liver diseases. However, it is limited by a shortage of donor organs and the necessity for lifelong immunosuppressive therapy. Mesenchymal stem cells (MSCs) can differentiate into various liver cells and enhance liver function when transplanted into patients due to their differentiation and proliferation capabilities. Therefore, it can be used as an alternative therapy for treating liver diseases, especially for liver cirrhosis, liver failure, and liver transplant complications. However, due to the potential tumorigenic effects of MSCs, researchers are exploring a new approach to treating liver fibrosis using extracellular vesicles (exosomes) secreted by stem cells. Many studies show that exosomes released by stem cells can promote liver injury repair through various pathways, contributing to the treatment of liver fibrosis. In this review, we focus on the molecular mechanisms by which stem cell exosomes affect liver fibrosis through different pathways and their potential therapeutic targets. Additionally, we discuss the advantages of exosome therapy over stem cell therapy and the possible future directions of exosome research, including the prospects for clinical applications and the challenges to be overcome.

Objective:To explore the relationship between the changes of quadriceps femoris and ICU acquired weakness(ICU-AW)in children.Method:A prospective collection of pediatric patients treated in the intensive care unit of Shenzhen children's hospital from October 2022 to March 2023.The thickness and cross-sectional area of rectus femoris and the thickness of vastus intermedius were measured by ultrasound on the 1st,4th and 7th day after ICU.The first day served as the baseline to calculate the atrophy rate for each muscle.On the 7th day,the Medical Re-search committee muscle strength score(MRC score)and critical physical function test score(PFIT-s score)were performed.According to the MRC score＜48,patients were divided into ICU-AW group and non-ICU-AW group to analyze the relationship between ICU-AW and the changes of quadriceps femoris.Result:A total of 21 critically ill children were included,including 11 males and 10 females.The incidence of ICU-AW in children was 41.2％(4 cases were not evaluated because of delirium).Within 7 days after en-tering ICU,the atrophy rate of cross-sectional area of rectus femoris was the highest,reaching-8.00％±15.10％.Both groups showed the greatest rate of change in the vastus intermedius thickness over 7 days,with the ICU-AW group mainly showing an increase in thickness(19.51％±16.51％over 4 days,14.14％±28.13％over 7 days),while the non-ICU-AW group primarily showed atrophy(-16.07％±17.46％over 4 days,-15.55％±30.04％over 7 days).The ICU-AW group had an average increase in rectus femoris thickness of 4.51％±8.38％within 7 days of ICU admission,while the non-ICU-AW group had an average atrophy rate of-8.19％±11.79％.There was no correlation between muscular atrophy rate and PFIT-s score(all P＞0.05),but there was a moderate negative correlation between rectus femoris thickness atrophy rate and femoral intermediate muscle thickness atrophy rate and MRC score within 4 days,respectively(ritual color 0.541 million 0.657 million 0.004),and moderate negative correlation between MRC score and thickness atrophy rate of rectus femoris and vastus medius within 7 days.There was no significant correlation between the atrophy rate of cross-section-al area of rectus femoris and MRC score.Conclusion:Compared with the non-ICU-AW group,the muscle thickness in the ICU-AW group is mainly thickened rather than atrophied,which can be identified by ultrasound on the 4th day after ICU.The specific diagnostic threshold is worthy of further study.

Objective:To explore the relationship between the changes of quadriceps femoris and ICU acquired weakness(ICU-AW)in children.Method:A prospective collection of pediatric patients treated in the intensive care unit of Shenzhen children's hospital from October 2022 to March 2023.The thickness and cross-sectional area of rectus femoris and the thickness of vastus intermedius were measured by ultrasound on the 1st,4th and 7th day after ICU.The first day served as the baseline to calculate the atrophy rate for each muscle.On the 7th day,the Medical Re-search committee muscle strength score(MRC score)and critical physical function test score(PFIT-s score)were performed.According to the MRC score＜48,patients were divided into ICU-AW group and non-ICU-AW group to analyze the relationship between ICU-AW and the changes of quadriceps femoris.Result:A total of 21 critically ill children were included,including 11 males and 10 females.The incidence of ICU-AW in children was 41.2％(4 cases were not evaluated because of delirium).Within 7 days after en-tering ICU,the atrophy rate of cross-sectional area of rectus femoris was the highest,reaching-8.00％±15.10％.Both groups showed the greatest rate of change in the vastus intermedius thickness over 7 days,with the ICU-AW group mainly showing an increase in thickness(19.51％±16.51％over 4 days,14.14％±28.13％over 7 days),while the non-ICU-AW group primarily showed atrophy(-16.07％±17.46％over 4 days,-15.55％±30.04％over 7 days).The ICU-AW group had an average increase in rectus femoris thickness of 4.51％±8.38％within 7 days of ICU admission,while the non-ICU-AW group had an average atrophy rate of-8.19％±11.79％.There was no correlation between muscular atrophy rate and PFIT-s score(all P＞0.05),but there was a moderate negative correlation between rectus femoris thickness atrophy rate and femoral intermediate muscle thickness atrophy rate and MRC score within 4 days,respectively(ritual color 0.541 million 0.657 million 0.004),and moderate negative correlation between MRC score and thickness atrophy rate of rectus femoris and vastus medius within 7 days.There was no significant correlation between the atrophy rate of cross-section-al area of rectus femoris and MRC score.Conclusion:Compared with the non-ICU-AW group,the muscle thickness in the ICU-AW group is mainly thickened rather than atrophied,which can be identified by ultrasound on the 4th day after ICU.The specific diagnostic threshold is worthy of further study.

Objective:To investigate the molecular markers involved in death related to acute myocardial infarction (AMI) and provide new targets for early intervention.Methods:Consecutive patients who hospitalized in department of cardiology, Xuanwu Hospital, Capital Medical University from January 2017 to December 2021 and diagnosed with AMI were enrolled. The clinical factors and markers associated with in-hospital death after AMI were analyzed. In addition, patients diagnosed with AMI hospitalized in department of cardiology, Xuanwu Hospital, Capital Medical University from September 2022 to April 2023 were enrolled. We prospectively analyzed the plasma protein of death related to AMI via Olink Precision Proteomics based on proximity extension assay (PEA) technology.Results:In the retrospective study, 2 325 patients with AMI were analyzed, including 75 patients in the in-hospital death group and 2 250 subjects in the survival group. The overall mortality rate during hospitalization was 3.23% (75/2325). The patients in the death group were older: 72 (64, 80) years vs. 63 (55, 71) years. And Interleukin-6 (IL-6), hypersensitive C-reactive protein (Hs-CRP), leukocyte counts and neutrophil counts were markedly higher in the death group than those in the survival group: 69.0 (26.7, 136.6) ng/L vs. 18.2 (9.4, 36.5) ng/L, 45.7 (28.7, 50.5) mg/L vs. 5.5 (2.0, 17.2) mg/L, 12.0 (9.8, 14.1) ×10 9/L vs. 8.9 (7.2, 11.2) × 10 9/L, 9.8 (7.8, 12.1) ×10 9/L vs. 6.5(4.7, 8.8) ×10 9/L ( P<0.01). In this prospective study, 86 patients with AMI were analyzed. 61 proteins including Insulin-like growth factor-binding protein 1, 2 (IGFBP-1, IGFBP-2), Chitotriosidase-1 (CHIT1), Complement component C1q receptor (CD93) were independently associated with in-hospital death related to AMI ( P<0.05). The differential proteins were mainly enriched in inflammatory response, cell adhesion, cytokine signaling pathway and apoptosis. Moreover, 22 proteins including Urokinase plasminogen activator surface receptor (U-PAR), Trefoil factor 3 (TFF3), Perlecan (PLC), Growth differentiation factor 15 (GDF-15), Junctional adhesion molecule A (JAM-A) were plotted according to a logistic regression model, and the area under the curve (AUC) was more than 0.9, showing the high accuracy in predicting in-hospital death after AMI. Conclusions:Molecular markers of the inflammatory response, cell adhesion, cell growth and apoptosis might be involved in death related to AMI, which provides new targets for early intervention.

Objective:To investigate the relationship between body mass index (BMI) and gestational hypertension using two-sample Mendelian randomization analysis.Methods:The summary level data for BMI and gestational hypertension were obtained from the genome-wide association study (the deadline for data inclusion was October 31, 2023). All data were analyzed by inverse variance weighting, MR-Egger regression, weighted median, simple model and weighted model methods. Cochrane Q test was used to evaluate heterogeneity, MR-Egger regression intercept test and funnel plot were used to assess horizontal pleiotropy. Results:Inverse variance weighting result under fixed effects and random effects models showed that the risk of gestational hypertension increased with the increase of BMI ( OR = 1.62 and 1.62, 95% CI 1.39 to 1.88 and 1.39 to 1.88, P<0.01). Sensitivity analysis results including MR-Egger regression, weighted median and weighted model methods showed that BMI increased the risk of gestational hypertension ( OR = 1.51, 1.56 and 1.71; 95% CI 1.01 to 2.26, 1.23 to 1.99 and 1.09 to 2.69; P<0.05 or <0.01). Although Cochrane Q test result showed evidence of heterogeneity ( P = 0.04), inverse variance weighting under a random model suggested that BMI increased the risk of gestational hypertension. Horizontal pleiotropy was not observed in the above analysis ( P = 0.73). Conclusions:Obesity may increase the risk of gestational hypertension. Pregnant women should pay attention to weight control to decrease the risk of gestational hypertension.

Objective To explore the correlation between serum levels of miR-193a-3p,activated transcription factor 5(ATF5),clinicopathological characteristics and chemotherapy efficacy in patients with triple negative breast cancer(TNBC).Methods A total of 120 patients with TNBC admitted to our hospital were collected as the research group.In the same period,120 cases with benign breast disease in our hospital were selected as the control group.Serum levels of miR-193a-3p and ATF5 were detected,and the relationship between them and clinicopathological characteristics were detected in two groups.According to the therapeutic effect,TNBC patients were divided into the treatment ineffective group(n=50)and the treatment effective group(n=70).The expression levels of miR-193a-3p and ATF5 were compared between the two groups,and factors affecting the chemotherapy efficacy of TNBC patients were analyzed.Results Compared with before chemotherapy,the serum miR-193a-3p level increased and ATF5 level decreased in TNBC patients after chemotherapy(P＜0.05).Compared with the control group,the serum miR-193a-3p level of TNBC patients decreased in the research group before chemotherapy,and ATF5 level increased(P＜0.05).The expression level of miR-193a-3p was lower and the expression level of ATF5 was higher in patients with tumor diameter≥3 cm,lymph node metastasis,low histological grade,clinical stage Ⅲ and Ki-67＞30%(P＜0.05).In TNBC patients,compared with the treatment effective group,patients in the treatment ineffective group showed a decreased serum miR-193a-3p level and an increased ATF5 level(P＜0.05).Lower level of miR-193a-3p,higher level of ATF5,lymph node metastasis,tumor diameter≥3 cm,low histological grade,and TNM stage Ⅲ were risk factors affecting the efficacy of chemotherapy in TNBC patients(P＜0.05).Conclusion Low level of miR-193a-3p and high level of ATF5 in the serum of TNBC patients are risk factors for chemotherapy efficacy.

This paper reports the inpatient care and nine-year follow-up management experience of a patient with Type 3 Long QT Syndrome.During hospitalization,efforts were focused on accurate symptom identification and emergency intervention.Key points in post-discharge follow-up care include medication education to prevent the use of drugs that prolong the QT interval on ECG,the application of anticipatory care to enhance the patient's self-management skills,and the joint development of a family emergency plan by relatives and healthcare providers.Additionally,the comprehensive family genetic health management was implemented.Through systematic screening,disease education,and continuous follow-up,the patient was maintained on long-term oral metoprolol post-discharge,with no further cardiac adverse events.The cardiac function of the patient improved,and during follow-up,the patient exhibited good recovery,being able to perform self-monitoring as required,and retumed to normal life.