ObjectiveTo analyze the development trajectory， research hotspots， and trends in medical humanities research in China since the new era. MethodsA search was conducted on the CNKI （China National Knowledge Infrastructure） advanced search page using the themes“medical humanities”or “humanistic medicine，”retrieving a total of 5，758 articles. After applying specific screening criteria， 5，095 articles were included in the analysis. Citespace6.1.R6 was used to visualize and analyze the authors， institutions， and keywords of the 5，095 articles. ResultsSince the new era， the volume of publications on medical humanities in China has shown an overall upward trend， with limited collaboration between core institutions and core authors. The research content of medical humanities has evolved from broad to specific， from abstract to concrete， and from theoretical to practical. ConclusionThe development of medical humanities research in China has generally gone through three stages： defining related concepts， integrating medical humanistic spirit into clinical practice， and applying empirical methods. Narrative medicine， ideological and political education in curricula， and medical humanities education are potential future research directions.

BACKGROUND:Estrogen receptor α can act as an upstream protein to regulate the expression and phosphorylation level of adenosine monophosphate-activated protein kinase(AMPK).Activation of the estrogen receptor α-AMPK signaling pathway promotes osteogenic proliferation and differentiation.OBJECTIVE:To explore the molecular mechanism of estrogen receptor α regulating AMPK and its effect on osteoblast proliferation and differentiation at osteoblast cell line and molecular biology levels.METHODS:(1)The passaged MC3T3-E1 mouse embryonic osteoblasts were divided into three groups:blank control group,mock group(transfected with pCDNA3.1 control plasmid),and estrogen receptor α group(transfected with pCDNA3.1-estrogen receptor α overexpression plasmid),and RT-qPCR and western blot methods were used to detect the hepatic kinase B1,CaMKKβ,and AMPKα1 mRNA,protein and phosphorylation levels.(2)ChIP-qPCR was used to demonstrate that estrogen receptor α interacts with the hepatic kinase B1 promoter.Dual luciferase assay was used to demonstrate that estrogen receptorα interacts with the hepatic kinase B1 promoter region to activate its transcriptional expression.(3)The cells were divided into three groups:mock+shNC group,estrogen receptor α+shNC group,and estrogen receptor α+shLKB1 group.Changes in the expression levels of hepatic kinase B1,phosphorylated hepatic kinase B1,and phosphorylated AMPKα1 proteins in the cells were detected by western blot.(4)The cells were divided into four groups:mock group,estrogen receptor α group,estrogen receptor α+5 μmol/L Compound C(AMPK inhibitor)group,and estrogen receptor α+10 μmol/L Compound C group.The expression of proteins related to the AMPK signaling pathway and related to osteogenesis and osteoinductivity were detected by western blot method.Cells were transfected for 24 hours and then subjected to osteogenic induction for 14 days.Alkaline phosphatase staining was performed and cell viability in each group was detected.Mineralized nodule formation was detected by alizarin red staining at 21 days of osteogenic induction.(5)The cells were transfected and pretreated with different concentrations of AMPK inhibitor in corresponding groups,and cell viability was detected by cell counting kit 8.RESULTS AND CONCLUSION:(1)Estrogen receptor α activates the AMPK signaling pathway in MC3T3-E1 cells.(2)Estrogen receptor α promotes liver kinase B1 transcription and mediates AMPK signaling pathway activation.(3)Estrogen receptor α promotes the proliferation and differentiation of MC3T3-E1 cells by activating the AMPK signaling pathway,and the expression of AMPKα1,p-AMPKα,osteoprotegerin,osteopontin,and Runx2 proteins was down-regulated under the intervention of AMPK inhibitor,and the viability of osteoblasts was decreased.(4)To conclude,estrogen receptor α activates the AMPK signaling pathway by acting on liver kinase B1 promoter,promotes osteoblast proliferation and osteogenic differentiation,and prevents osteoporosis.

Pancreatic cancer is a highly malignant tumor of the digestive system and has an extremely poor prognosis.Due to its insidious onset and rapid progression,major surrounding vessels are frequently invaded at the time of diagnosis.Consequently,resection and reconstruction of the portal vein and/or superior mesenteric vein are often required during pancreatectomy.Various methods of venous resection and reconstruction have been developed,each with its own advantages,limitations,and specific applicability.Compared with open surgery,laparoscopic pancreatectomy requires higher technical proficiency and more precise intraoperative decision-making.To promote the advancement of venous reconstruction techniques in laparoscopic pancreatectomy,in this article,we summarize and evaluate our team's practical experience and relevant literature,focusing on graft selection,technical difficulty,operative risk,and short-and long-term patency.Special emphasis was placed on the applicability of different approaches and materials.In addition,regarding postoperative reconstruction of venous patency,we introduced the"Cross-sectional Area Algorithm",a method simulating the evaluation mode of coronary artery patency,to accurately quantify postoperative venous patency.The evaluation method was first proposed by the team but has not yet been externally validated.By reviewing the current status of venous reconstruction strategies and the prognosis of laparoscopic pancreatic surgery,we aim to inform the development of standardized technical guidelines,enable individualized assessment of venous patency after surgery,and ultimately improve minimally invasive pancreatic surgery and the long-term prognosis of patients.

BACKGROUND:Estrogen receptor α can act as an upstream protein to regulate the expression and phosphorylation level of adenosine monophosphate-activated protein kinase(AMPK).Activation of the estrogen receptor α-AMPK signaling pathway promotes osteogenic proliferation and differentiation.OBJECTIVE:To explore the molecular mechanism of estrogen receptor α regulating AMPK and its effect on osteoblast proliferation and differentiation at osteoblast cell line and molecular biology levels.METHODS:(1)The passaged MC3T3-E1 mouse embryonic osteoblasts were divided into three groups:blank control group,mock group(transfected with pCDNA3.1 control plasmid),and estrogen receptor α group(transfected with pCDNA3.1-estrogen receptor α overexpression plasmid),and RT-qPCR and western blot methods were used to detect the hepatic kinase B1,CaMKKβ,and AMPKα1 mRNA,protein and phosphorylation levels.(2)ChIP-qPCR was used to demonstrate that estrogen receptor α interacts with the hepatic kinase B1 promoter.Dual luciferase assay was used to demonstrate that estrogen receptorα interacts with the hepatic kinase B1 promoter region to activate its transcriptional expression.(3)The cells were divided into three groups:mock+shNC group,estrogen receptor α+shNC group,and estrogen receptor α+shLKB1 group.Changes in the expression levels of hepatic kinase B1,phosphorylated hepatic kinase B1,and phosphorylated AMPKα1 proteins in the cells were detected by western blot.(4)The cells were divided into four groups:mock group,estrogen receptor α group,estrogen receptor α+5 μmol/L Compound C(AMPK inhibitor)group,and estrogen receptor α+10 μmol/L Compound C group.The expression of proteins related to the AMPK signaling pathway and related to osteogenesis and osteoinductivity were detected by western blot method.Cells were transfected for 24 hours and then subjected to osteogenic induction for 14 days.Alkaline phosphatase staining was performed and cell viability in each group was detected.Mineralized nodule formation was detected by alizarin red staining at 21 days of osteogenic induction.(5)The cells were transfected and pretreated with different concentrations of AMPK inhibitor in corresponding groups,and cell viability was detected by cell counting kit 8.RESULTS AND CONCLUSION:(1)Estrogen receptor α activates the AMPK signaling pathway in MC3T3-E1 cells.(2)Estrogen receptor α promotes liver kinase B1 transcription and mediates AMPK signaling pathway activation.(3)Estrogen receptor α promotes the proliferation and differentiation of MC3T3-E1 cells by activating the AMPK signaling pathway,and the expression of AMPKα1,p-AMPKα,osteoprotegerin,osteopontin,and Runx2 proteins was down-regulated under the intervention of AMPK inhibitor,and the viability of osteoblasts was decreased.(4)To conclude,estrogen receptor α activates the AMPK signaling pathway by acting on liver kinase B1 promoter,promotes osteoblast proliferation and osteogenic differentiation,and prevents osteoporosis.

Pancreatic cancer is a highly malignant digestive system tumor with poor prognosis.Its incidence is closely related to the level of regional development.Epidemiology shows that with the progress of urbanization,the proportion of obese people in the world is increasing over the years.Meanwhile,obesity has also been found to be one of the risk factors for pancreatic cancer.However,the mechanism of obesity regulating pancreatic cancer is still unclear at present.Researches show that obese people with pancreatic cancers have different tumor pathological mechanisms and higher risk of surgical complications.Therefore,this article will review the potential transformation mechanism between microscopic pathological changes and clinical manifestations of obesity related pancreatic cancer.

On August 2-4,2023,the"Third Summit Forum on'Building a Community of Shared Future for Doctors and Patients'"was jointly organized by institutions such as the Chinese Medical Ethics,the Hospital Humanities Management and Talent Training Special Committee of the China Population and Culture Promotion Association,Center for Ethical Studies of Renmin University of China,the Newspaper for China's Physicians,the China Health Law Society,the China Anti-Cancer Association,and the China Association For Ethical Studies in Harbin.The conference arranged a sub-forum for the"Seminar on the Construction of Chinese Medical Humanities",with domestic medical humanities scholars attending the conference.After heated discussions at the seminar,the Scholars'Consensus on the Construction and Development of Chinese Medical Humanities was formed.It was proposed that in the new era,it is urgent to build the medical humanities discipline,as well as lead the academic integration and development of medical humanities under the core socialist values.At the same time,for the construction of the medical humanities discipline,it is necessary to optimize the organizational mechanism,prosper and develop the overall framework of the medical humanities discipline,accelerate the construction of a professional teaching team for the medical humanities discipline,promote the establishment of a new carrier medical humanities education and teaching in cultivating morality and nurturing talents,as well as focus on solving problems related to the cultivation of medical humanities graduate students.

Pancreatic cancer is a highly malignant digestive system tumor with poor prognosis.Its incidence is closely related to the level of regional development.Epidemiology shows that with the progress of urbanization,the proportion of obese people in the world is increasing over the years.Meanwhile,obesity has also been found to be one of the risk factors for pancreatic cancer.However,the mechanism of obesity regulating pancreatic cancer is still unclear at present.Researches show that obese people with pancreatic cancers have different tumor pathological mechanisms and higher risk of surgical complications.Therefore,this article will review the potential transformation mechanism between microscopic pathological changes and clinical manifestations of obesity related pancreatic cancer.

Objective To propose specific suggestions for exemption management of X-ray devices applying for exemption management. Methods The weight analysis of influence of shielding thickness and tube voltage on the radiation dose leakage of low-energy X-ray devices was carried out through test analysis, and the radiation status of 50 X-ray devices applied for end-user exemption in Shenzhen, China was investigated. Results There was no significant correlation between the ambient dose equivalent rate and the tube voltage and tube current of the X-ray device. The ambient dose equivalent rate of 50 X-ray devices was 0.16-1.20 μSv/h. Among them, 8 X-ray devices had radiation dose leakage, that is, the ambient dose equivalent rate was greater than 0.36 μSv/h; the ambient dose equivalent rate of one X-ray device was 1.2 μSv/h, exceeding exemption management requirements. Conclusion Applications for exemption management and filing of X-ray devices should be treated differently, and their own shielding effect and inherent safety have a greater impact on radiation safety, which should be focused on.

To promote the ideological and political construction of the doctor-patient communication course, the research group discussed the subject characteristics and proposed the goals, principles, elements, and paths of the ideological and political construction of the doctor-patient communication course combined with practical teaching and relevant policy documents. Besides, this paper put forward the top-level framework design for the implementation, curriculum assessment, and evaluation indicators of the ideological and political construction, and developed the Guidelines for Ideological and Political Teaching of the Doctor-patient Communication Course and related teaching evaluation indicators, with a view to providing reference evaluation standards for the ideological and political construction of the doctor-patient communication course in China.

Objective:To explore the differences of risk stratification of very high-risk or extreme high-risk atherosclerotic cardiovascular diseases (ASCVD) and the attainment rates of low-density lipoprotein cholesterol (LDL-C) management targets evaluated by three different criteria, and the causal attributions of these differences.Methods:Patients with ASCVD were consecutively enrolled from January 1 to December 31 in 2019, and were evaluated for very high-risk or extreme high-risk and LDL-C goal attainment rates with 2018 American guideline on the management of blood cholesterol (2018AG), 2019 China Cholesterol Education Program (CCEP) Expert Advice for the management of dyslipidemias (2019EA) and 2020 Chinese expert consensus on lipid management of very high-risk ASCVD patients(2020EC), respectively. The causal attributions of the differences in attainment rates were analyzed as well.Results:A total of 1 864 ASCVD patients were included in this study. According to 2018AG, 2019EA and 2020EC, the proportions of the patients with very high-risk or extreme high-risk were 59.4%, 90.7%, and 65.6%, respectively. The absolute LDL-C target attainment rates were 37.2%, 15.7%, and 13.7%, respectively, the differences between each two rates were statistically significant (all P<0.001). As to the differences in attainment rates between 2020EC and 2018AG, 61.5% were due to the different LDL-C goal attainment values and 38.5% were caused by the different risk stratifications, while for the differences between 2020EC and 2019EA attainment rates, different LDL-C goal attainment values were responsible for 13.2%, and different risk stratifications were responsible for 86.8% of the differences. Conclusions:There are significant differences in the proportions and LDL-C attainment rates among the three different criteria for very high-risk or extreme high-risk ASCVD. 2020EC showed a moderate proportion of patients with extreme high-risk, and had the lowest LDL-C attainment rate. The differences between 2020EC and 2018AG are mainly due to the LDL-C target values, and the differences between 2020EC and 2019EA are mainly caused by the risk stratifications.