Health communication aims to improve public health attitudes and behaviors by propagating health information. It plays an important role in promoting public health literacy and "Healthy China Initiative". The basic theories of health communication include "7 W" and Theory of Planned Behavior. Clinicians with profound medical expertise and a wealth of clinical practice play key roles in the communication, and they hold an unparalleled advantage in health communication by delivering authoritative and trustworthy information to the public. The capacity of health communication among clinicians in the nation is determined by various factors including professional characteristics, policy support, dissemination platforms and pathways, time and effort. Meanwhile, some problems in the research on the health communication capacity of clinicians remain, such as lack of well-established motivation systems, limited dissemination pathways, and imperfect evaluation frameworks. In some regions of China, health communication performance has been considered as part of the professional title evaluation for clinical physicians. Medical institutions and universities have also initiated relevant training and practice programs. It is crucial to improve evaluation frameworks, strengthen training pathways and effectiveness assessment, promote interdisciplinary integration, and enhance the role of clinicians in health communication in the future.

Objective To explore whether the environmental pollutant triclosan(TCS)has negative effects on the various biological characteristics of dental pulp stem cells(DPSCs),as well as the distribution and hazards of TCS in rat dental pulp tissue in vivo,which will provide a basis for the clinical application of DPSCs and the safety of TCS.Methods Tooth collection was approved by the Ethics Committee of Tianyou Hospital Affiliated to Wuhan University of Science and Technology.Human DPSCs were extracted,cultured,and identified.Up to 0.08 mmol/L of TCS was added to the in vitro culture medium of DPSCs.The proliferation ability of DPSCs was detected by CCK-8.The migration ability of DPSCs was detected via scratch assay.The differentiation ability of DPSCs was detected by inducing trilineage differenti-ation.The gene or protein expression levels of tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β),interleukin-6(IL-6),interleukin-10(IL-10),inducible nitric oxide synthase(iNOS),and transforming growth factor-β(TGF-β)in DPSCs were detected.The level of reactive oxygen species(ROS)generated by DPSCs was analyzed using fluorescence staining.Changes in mitochondrial membrane potential of DPSCs were detected using a fluorescent probe.The activity of PI3K/Akt/mTOR,p38,and JNK pathways of DPSCs were detected.Animal experiments were approved by the Animal Ethics Committee of Wuhan University of Science and Technology.A rat model of short-term oral exposure to 50 mg/kg/d of TCS for 2 months was established,and the TCS concentration in the liver,brain,and dental pulp tissues of rats was detected through liquid chromatography-mass spectrometry.Results TCS at 0.02 mmol/L,0.04 mmol/L,and 0.08 mmol/L significantly inhibited the proliferation ability of human-derived DPSCs on the 5th and 7th days of contact.TCS at 0.04 mmol/L and 0.08 mmol/L significantly inhibited the migration ability and tri-lineage differentiation ability of DPSCs on the 3rd day of contact.TCS induced the gene or protein expression of proinflammatory factors including TNF-α,IL-1β,IL-6,and iNOS,induced the gene or protein expression of TGF-β,and inhibited the protein expression of anti-inflammatory factor IL-10.On day 1,TCS at 0.04 mmol/L and 0.08 mmol/L induced the production of ROS in DPSCs and reduced the mitochondrial membrane potential of DPSCs.On day 3,TCS at these levels inhibited PI3K/Akt/mTOR pathway activity and enhanced p38 pathway activity of DPSCs,without affecting the pathway activity of JNK.After short-term intragastric exposure of rats to TCS,TCS was detected in liver(430 ng/mL)and brain(41.4 ng/mL)tissues but not in the dental pulp.The TCS concentration was highest in the liver,but no obvious histopathological changes were observed.Conclusion TCS inhibits a variety of biological characteristics of DPSCs and poses a potential risk to the organism.No TCS exists in the dental pulp tissue of rats exposed to TCS for a brief period of time,and the health of the rats is not damaged.

Acute-on-chronic liver failure(ACLF)is a group of clinical syndromes related to severe acute liver function damage and multiple organ failure caused by various acute inducing factors on the basis of chronic liver disease.Due to its serious condition,rapid progression and high mortality,it has attracted more and more attention.Recent studies have shown that the pathogenesis of ACLF mainly includes direct injury and immune injury.As the main immune cells in the liver,the immunoregulatory role of liver macrophages in ACLF has been increasingly recognized.Liver macrophages have excellent phenotype conversion function and plasticity characteristics under the influence of epigenetic reprogramming or local microenvironment.This adaptive expression ability can use key mediators to promote the early conversion of anti-inflammatory phenotype to alleviate liver injury.A large number of studies have shown that liver macrophages have a certain potential in reversing the process of ACLF.Therefore,from the perspective of the plasticity characteristics of liver macrophages,this paper expounds the role of liver macrophages in ACLF and the research on the intervention of ACLF disease process,and summarizes its potential significance in the treatment of ACLF.

Human milk is a product of human evolution and is crucial for the early growth and development of infants as well as maternal health. This paper discusses the research and application of human milk science in China, aiming to clarify the research pathways in this field and contribute to the promotion of breastfeeding initiatives and the realization of the Healthy China 2030 goals.

A comprehensive understanding of the nutritional composition and active components of human milk are important for promoting infant health. However, in the design and implementation of scientific research on human milk, the lack of standardized research and implementation methods have led to the collection, storage, and testing processes of human milk samples being largely based on reference literature and practical experience. This has resulted in variability in the representativeness of human milk samples and differences in the comparability of research results between different studies. This article summarizes the principles and guidelines for the " Specification for collection and storage of human milk samples for research", published by the Chinese Nutrition Society on December 30, 2022, and discusses the feasibility and importance of standardized management in the process of scientific research on human milk.

Objective To investigate the relationship between exposure to famine in early life stage and hypertension phenotype and grade in middle and old age. Methods People born between 1951 and 1965 in the 2015 China Health and Elderly Care Follow-up Survey were included in the study, and were divided into unexposed group, fetal exposed group, childhood exposed group and adolescent exposed group according to the time of famine occurrence and birth year of the participants. Logistic regression model was used to explore the effects of different famine exposure periods in early life stage on hypertension classification （including normal high value, grade I, grade II and grade III） and phenotype （including isolated systolic hypertension[ISH], isolated diastolic hypertension [IDH] and combined systolic and diastolic hypertension [SDH]）. Results Compared with unexposed group, fetal famine exposure （OR=1.59, 95% CI :1.10-2.30）, childhood famine exposure （OR=1.67, 95% CI :1.04-2.70） and adolescent famine exposure （OR=3.42, 95% CI : 2.51-4.66） were the risk factors for ISH. Only famine exposure during adolescence （OR=1.54, 95% CI: 1.07-2.21） was a risk factor for SDH. In addition, fetal famine exposure （OR=1.41, 95% CI: 1.05-1.89） and adolescent famine exposure （OR=2.22 , 95% CI: 1.71-2.88） were risk factors for developing grade I hypertension. Famine exposure in childhood （OR=2.45, 95% CI: 1.21-4.94） and famine exposure in adolescence （OR=2.45, 95% CI: 1.44-4.19） were risk factors for grade 2 hypertension. Conclusion Famine exposure in early life stage was associated with the phenotype and grade of hypertension. Therefore, balanced nutrition in early life is important to prevent hypertension in adulthood.

Objective: To analyze the expression and clinical prognostic significance of nuclear Dbf2-related kinase 1 ( NDR1 ) in hepatocellular carcinoma ，and to investigate the biological function and regulatory mechanism of NDR1 in hepatocellular carcinoma cells． Methods: ENCORI database was used to analyze the correlation of NDR1 and c-Myc．Cycloheximide ( CHX) experiment analyzed the relationship between NDR1 and c-Myc protein stability．The expression levels of NDR1 in liver cancer tissues and normal tissues and its relationship with the survival rate of liver cancer patients were analyzed using the ENCORI database．MYC-NDR1 eukaryotic expression vector was constructed，transfected with hepatocellular carcinoma HepG2 cells，and its expression was verified by protein immuno blotting (Western blot) ; cell proliferation and migration ability were detected by CCK-8 assay，cell clone formation assay and scratch assay，respectively．The correlation between NDR1 and c-Myc expression was analyzed using the ENCORI database，and the relationship between NDR1 and c-Myc protein was investigated using a protein synthesis inhibitor CHX dosing assay. Results: The results of the ENCORI database showed that the expression of NDR1 in liver cancer tissues was higher than that in normal tissues and the overall survival rate of patients with high NDR1 expression was lower than that of patients with low NDR1 expression，and the difference was statistically significant (P＜0. 001) ．The results of the CCK-8 assay showed that the MYC-NDR1 group grew faster than the empty vector group (P＜0. 001) ．The clone formation assay showed that the number of clones in the MYC-NDR1 group was higher than that in the empty vector group (P＜0. 001) ．The cell scratch assay showed that the mean migration distance in the MYC-NDR1 group was greater than that in the empty vector group (P＜0. 001) ．ENCORI database analysis showed that NDR1 correlated with c-Myc expression (R = 0. 184，P＜0. 001) ; CHX dosing assay showed that the reduction of c-Myc protein in the MYC-NDR1 group was lower than that in the empty vector group during the same time． Conclusion NDR1 is highly expressed in hepatocellular carcinoma tissues，closely correlated with poor prognosis of hepatocellular carcinoma patients ，and positively correlated with the expression of c-Myc gene. The study successfully constructes MYC-NDR1 eukaryotic expression vector ，and the expression product MYC- NDR1 can increase the stability of c-Myc protein and promote the proliferation and migration of human hepatocellu- lar carcinoma cells.

Objective:To investigate the impact of cleavage factor Im25(CFIm25)on VSMCs-specific knockdown in the context of hyperlipidemia.Methods:Mice models were constructed with specific knockout of CFIm25 in VSMCs(CFIm25f/+ TaglnCre)and control mice(TaglnCre).The mice were fed a normal diet or high-fat diet(HFD)for 18 weeks and their body weight changes were monitored.ELISA was used to measure serum total cholesterol(TC), triacylglycerol(TG), high-density lipoprotein(HDL-C)and low-density lipoprotein(LDL-C)levels.The extent of aortic lipid deposition in mice was assessed by oil red O staining.Results:During the feeding of a high-fat diet, CFIm25f/+ TaglnCre mice showed a significant increase in body weight compared to the control group[Male(1.01±0.06)g and(0.87±0.31)g, t=7.53, P<0.05; Female: (0.64±0.02)g and(0.35±0.04)g, t=9.68, P<0.05].After 18 weeks of high-fat diet feeding, CFIm25f/+ TaglnCre mice had significantly higher levels of TC[(6.80±0.35)mmol/L and(3.76±0.87)mmol/L, t=5.63, P=0.004], TG[(0.97±0.21)mmol/L and(0.42±0.10)mmol/L, t=4.08, P=0.015], and LDL-C[(5.20±0.30)mmol/L and(2.00±0.98)mmol/L, t=5.40, P=0.006]compared to the TaglnCre group.Specifically, TC levels increased by 80.72%, TG increased by 132.79%, and LDL-C increased by 160.32%.There was a significant increase in aorta lipid deposition and atherosclerotic plaque area in CFIm25f/+ TaglnCre mice( P<0.05). Conclusions:The research indicated that VSMCs-specific CFIm25 knockdown in mice further worsened hyperlipidemia and atherosclerotic lesions.

Traumatic brain injury (TBI) contributes to the key causative elements of neurological deficits. However, no effective therapeutics have been developed yet. In our previous work, extracellular vesicles (EVs) secreted by stem cells from human exfoliated deciduous teeth (SHED) offered new insights as potential strategies for functional recovery of TBI. The current study aims to elucidate the mechanism of action, providing novel therapeutic targets for future clinical interventions. With the miRNA array performed and Real-time PCR validated, we revealed the crucial function of miR-330-5p transferred by SHED-derived EVs (SHED-EVs) in regulating microglia, the critical immune modulator in central nervous system. MiR-330-5p targeted Ehmt2 and mediated the transcription of CXCL14 to promote M2 microglia polarization and inhibit M1 polarization. Identified in our in vivo data, SHED-EVs and their effector miR-330-5p alleviated the secretion of inflammatory cytokines and resumed the motor functional recovery of TBI rats. In summary, by transferring miR-330-5p, SHED-EVs favored anti-inflammatory microglia polarization through Ehmt2 mediated CXCL14 transcription in treating traumatic brain injury.
Animals ; Brain Injuries, Traumatic/therapy* ; Chemokines, CXC/metabolism* ; Extracellular Vesicles/metabolism* ; Histocompatibility Antigens/metabolism* ; Histone-Lysine N-Methyltransferase/metabolism* ; Humans ; MicroRNAs/metabolism* ; Microglia/metabolism* ; Rats ; Stem Cells/metabolism*

Purpose: This study aims to comprehensively evaluate the clinical efficacy of chemotherapy or endocrine therapy maintenance in metastatic breast cancer (MBC) patients. Materials and Methods: The meta-analysis of randomized clinical trials (RCTs) and propensity score matching of multicenter cohort study evaluated MBC patients who underwent first-line chemotherapy or endocrine therapy maintenance. This study is registered with PROSPERO: CRD42017071858 and ClinicalTrials.gov: NCT04258163. Results: A total of 2,867 patients from 15 RCTs and 760 patients from multicenter cohort were included. The results from meta-analysis showed that chemotherapy maintenance improved progression-free survival (PFS) (hazard ratio [HR], 0.63; 95% confidence interval [CI], 0.54 to 0.73; p < 0.001; moderate-quality evidence) and overall survival (OS) (HR, 0.87; 95% CI 0.78 to 0.97; p=0.016; high-quality evidence) than observation. In the cohort study, for hormone receptor–positive MBC patients, chemotherapy maintenance improved PFS (HR, 0.67; 95% CI, 0.52 to 0.85; p < 0.001) and OS (HR, 0.55; 95% CI 0.42 to 0.73; p < 0.001) compared with observation, and endocrine therapy maintenance also improved PFS (HR, 0.65; 95% CI, 0.53 to 0.80; p < 0.001) and OS (HR, 0.55; 95% CI, 0.44 to 0.69; p < 0.001). There were no differences between chemotherapy and endocrine therapy maintenance in PFS and OS (all p > 0.05). Regardless of the continuum or switch maintenance therapy, showed prolonged survival in MBC patients who were response to first-line treatment. Conclusion This study provided evidences for survival benefits of chemotherapy and endocrine therapy maintenance in MBC patients, and there was no difference efficacy between chemotherapy and endocrine therapy maintenance for hormone receptor–positive patients.