AIM:To investigate the effect of apoptosis stimulation protein 2(ASPP2)on the development of traumatic proliferative vitreoretinopathy(PVR)in a rabbit model.METHODS:A total of 30 New Zealand white rabbits were selected, and the right eyes of all rabbits were inflicted with a scleral penetrating wound of approximately 6 mm. Then rabbits were randomly and evenly divided into experimental and control group. The experimental group received an intravitreal injection of 0.1 mL of ARPE-19 cell suspension transfected with lentivirus-ASPP2, while the control group received an intravitreal injection of 0.1 mL of ARPE-19 cell suspension transfected with negative control lentivirus. At 1, 2, 3, and 4 wk after PVR modeling, a handheld tonometer was used to measure the intraocular pressure. Moreover, fundus photography and ocular ultrasound examination were performed to detect the retinal proliferation. At 4 wk after modeling, hematoxylin-eosin staining was used to observe the morphological retinal changes, and Western blot was used to determine the protein expressions of ASPP2 and the epithelial-mesenchymal transition(EMT)marker Vimentin in the rabbit retinas.RESULTS:At 1, 2, 3, and 4 wk after modeling, there were no significant changes in intraocular pressure within the experimental and control group of rabbit eyes, either before or after PVR modeling, the success rate of PVR modeling in the experimental group was lower than that in the control group(P<0.05), and the retinal proliferation and structural disorder was less severe in the experimental group. At 4 wk after modeling, the retinal protein expression level of ASPP2 in the experimental group was significantly higher than that in the control group(t=3.193, P=0.033), while the Vimentin protein expression level was significantly lower in the experimental group(t=-3.599, P=0.023).CONCLUSION:ASPP2 may be involved in regulating the process of EMT in retinal pigment epithelial cells, thereby delaying the development and progression of traumatic PVR in rabbit eyes.

Breast cancer， as one of the major cancers threatening women's health globally， is characterized by high aggressiveness， high malignancy， and poor prognosis. In 2022， according to the World Health Organization， breast cancer ranked second in the incidence of female cancers globally， accounting for 11.6% of all new cancer cases. Western medical doctors mainly use surgery， chemotherapy， radiotherapy， endocrine therapy， and molecular targeted therapy to treat breast cancer， which can effectively improve the recurrence rate and death rate of breast cancer patients and prolong the survival period of patients. However， its treatment process is often accompanied by a series of side effects， which bring challenges to patients' quality of life. However， traditional Chinese medicine （TCM） has demonstrated significant therapeutic effects in inhibiting the proliferation and metastasis of breast cancer cells， reducing toxic side effects produced by chemotherapy， and improving patients' survival rate and quality of life. It is therefore particularly necessary to investigate the pharmacological effects and mechanisms of TCM in breast cancer treatment. The authors combed the pharmacological effects and mechanisms of the etiology and pathogenesis of breast cancer， identification and treatment of breast cancer， TCM compound， TCM single medicine， TCM monomer， and external treatment of TCM to prevent and control breast cancer and found that TCM has a therapeutic effect on breast cancer. It can play a role in increasing the effectiveness， reducing the toxicity， and alleviating the adverse reactions. It can inhibit breast cancer cell proliferation， cell cycle， migration， invasion， immune escape， epithelial-mesenchymal transition （EMT）， aerobic glycolysis， mitochondrial biosynthesis， aminoacyl-tRNA biosynthesis， reduce drug resistance， promote apoptosis， ferroptosis， cell autophagy， and regulate the tumor immune microenvironment by regulating signaling pathways. This paper aims to provide new ideas and methods for experimental research and clinical treatment of breast cancer.

Lung cancer has the highest morbidity and mortality rate among all cancers. Because of the complex pathogenesis， there are limitations in the common Western medicine treatment methods. Clinical and experimental studies have proved that traditional Chinese medicine （TCM） can not only effectively treat lung cancer and alleviate the clinical symptoms of cancer patients but also reduce the adverse reactions and complications caused by surgery， chemotherapy， and radiotherapy to improve the quality of life of the patients. The biological behaviors of lung cancer cells， such as proliferation， invasion， and metastasis， are closely related to their metabolic reprogramming. Metabolic reprogramming in lung cancer involves a series of metabolic changes such as increased glucose uptake and consumption， enhanced glycolysis， increased amino acid uptake and catabolism， and enhanced lipid and protein synthesis. Studies have reported that TCM active components， extracts， and compound prescriptions can effectively inhibit the biological behaviors of lung cancer by regulating metabolic reprogramming. Therefore， this paper reviews the pharmacological mechanisms of TCM active components， extracts， and compound prescriptions in regulating metabolic reprogramming of lung cancer， with the aim of providing a new way of thinking for the treatment of lung cancer by TCM regulation of metabolic reprogramming of lung cancer cells. The available studies suggest that TCM mainly inhibits the extracellular signal-regulated protein kinase （ERK）/c-Myc， phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt）/mammalian target of rapamycin （mTOR）， and hypoxia-inducible factor-α （HIF-1α） pathways. Furthermore， the expression of monocarboxylate transporter 4 （MCT4）， glucose transporter 1 （GLUT1）， pyruvate dehydrogenase （PDH）， phosphofructokinase 1 （PFK1）， pyruvate dehydrogenase kinase 1 （PDK1）， pyruvate kinase M2 （PKM2）， hexokinase （HK）， lactate dehydrogenase （LDH）， and lactate dehydrogenase A （LDHA） are inhibited. In this way， TCM inhibits the glucose uptake by lung cancer cells and glycolysis in lung cancer cells to reduce the energy metabolism of tumor cells， ultimately achieving the therapeutic effect on lung cancer.

ObjectiveTo explore the establishment of performance assessment indicators for the classification and grading of public health staff in district-level Centers for Disease Control and Prevention (CDCs), and to provide a basis for such evaluations. MethodsThrough literature review and group interviews, performance evaluation indicators were developed based on competency evaluation. Experts were invited to evaluate the weight of performance evaluation indicators for public health staff from different categories, with the average value used to represent the weight of each indicator. ResultsTwenty-nine experts from universities in Shanghai, municipal CDCs, and district CDCs participated, yielding an expert authority coefficient of 0.86. The performance evaluation indicators for department managers were categorized into three levels, with 4 indicators at the primary level, 16 indicators at the secondary level, and 42 indicators at the tertiary level, while those for general staff included 4 primary indicators, 15 secondary indicators, and 36 tertiary indicators. Significant differences were observed in the weight coefficients of the primary indicators (internal operations, professional work, and learning and growth) between department managers and general staff. The top three secondary indicators for department managers were department management, monitoring and prevention, and level of expertise. For mid-level and senior staff, the top three secondary indicators were monitoring and prevention, level of expertise, and research work. The top three secondary indicators for junior staff were monitoring and prevention, professional expertise, and professional attitude. No significant statistical differences were found among tertiary indicators. ConclusionThe developed performance evaluation indicators are reliable. Staff at different levels and classifications should be evaluated using different performance evaluation standards to accurately reflect individual performance and contributions.

Against the dual backdrop of increasingly mature big data applications and structural constraints in traditional human resource management models,comprehensive digital governance and reform of human resource management systems have become major challenges for public hospitals.By examining the core challenges faced by public hospitals in the big data era,it analyzes the implementation pathway of digital governance for human resource in public hospital,taking Guangdong Second People's Hospital as a practical case.lt summarizes the application effectiveness and the value of big data technology applucations in human resource management,providing support for talent system development.

Non-alcoholic fatty liver disease (NAFLD) is a metabolic disease characterized by abnormal deposition of lipid in hepatocytes. If not intervened in time, NAFLD may develop into liver fibrosis or liver cancer, and ultimately threatening life. NAFLD has complicated etiology and pathogenesis, and there are no effective therapeutic means and specific drugs. Currently, insulin sensitizers, lipid-lowering agents and hepatoprotective agents are often used for clinical intervention, but these drugs have obvious side effects, and their effectiveness and safety need to be further confirmed. Adenosine monophosphate (AMP)-activated protein kinase (AMPK) plays a central role in maintaining energy homeostasis. Activated AMPK can enhance lipid degradation, alleviate insulin resistance (IR), suppress oxidative stress and inflammatory response, and regulate autophagy, thereby alleviating NAFLD. Natural herbal medicines have received extensive attention recently because of their regulatory effects on AMPK and low side effects. In this article, we reviewed the biologically active natural herbal medicines (such as natural herbal medicine formulas, extracts, polysaccharides, and monomers) that reported in recent years to treat NAFLD via regulating AMPK, which can serve as a foundation for subsequent development of candidate drugs for NAFLD.

Objective To investigate the therapeutic efficacy of artesunate(AS)on polycystic ovary syndrome(PCOS)in mice and explore the potential mechanism primarily.Methods Twenty-five female C57BL/6J mice were randomly divided into Control group,model group(PCOS group),low-and high-dose AS groups(AS15 and AS30 groups)and metformin group(Met group).In addition to the Control group,the mouse model of PCOS was established by subcutaneous injection of dehydroepiandrosterone(DHEA,60 mg/kg)following by a high-fat diet for 21 d.After modeling,AS of 15 and 30 mg/kg was intraperitoneally injected into the mice of the AS 15 and AS30 groups,respectively,and 200 mg/kg Met was given to those of the Met group by gavage,once per day,for 6 weeks.ELISA was used to detect serum testosterone(T),fasting insulin(FINS),luteinizing hormone(LH)and follicle-stimulating hormone(FSH),and the LH/FSH ratio was calculated.The levels of fasting blood glucose(FBG),triglyceride(TG)and total cholesterol(TC)were detected by automatic biochemical analyzer,and the homeostasis model assessment of insulin resistance(HOMA-IR)was calculated.The estrous cycle was observed,and HE staining was performed for pathological changes in the ovary and uterus.Immunofluorescence assay was employed to measure the expression of p-eIF2α,ATF4 and CHOP in the ovarian tissue.After steroidogenic human granulosa-like tumor cell line KGN were exposed to 100 μmol/L DHEA to simulate the hyperandrogen environment of PCOS,and then treated with 5 and 10 μg/mL AS for 24 h,the protein levels of endoplasmic reticulum stress signaling pathway was detected by Western blotting.Results Compared with the Control group,the PCOS mice had disturbed estrous cycle,polycystic changes in the ovaries,and significantly increased serum T level and LH/FSH ratio(P＜0.05),and obviously elevated HOMA-IR,TC and TG levels in terms of metabolism(P＜0.01).The expression levels of p-eIF2α,ATF4 and CHOP were notably up-regulated in the ovarian granulosa cells of PCOS mice and KGN cells after DHEA exposure(P＜0.05).Additionally,AS treatment attenuated the pathological changes of ovary and uterine expression,decreased the serum T level and the LH/FSH ratio(P＜0.05),and reduced HOMA-IR,TC and TG levels(P＜0.05)when compared with the PCOS mice.Moreover,the expression levels of p-eIF2α,ATF4 and CHOP were significantly down-regulated after AS treatment in both ovarian granulosa cells of PCOS mice and KGN cells(P＜0.05).Conclusion AS significantly improves glycolipid metabolic disorder and reproductive dysfunction in PCOS mice,which may be associated with its suppressing endoplasmic reticulum stress by inhibiting the PERK/eIF2α/ATF4/CHOP pathway.

Objective To investigate the role of p300 in lipid metabolism disorders.Methods Bioinformatics analysis was performed to analyze the expression patterns of p300 in lipid metabolism disorder-related diseases and its correlation with SREBP-1c and downstream lipid metabolic enzymes.Immunofluorescence assay was used to detect the expression of p300 in the liver tissues of the patients with varying disease severity of non-alcoholic fatty liver disease(NAFLD).A mouse model of lipid metabolism disorder was established in male C57BL/6J mice by feeding high-fat diet(HFD)for 12 weeks.Western blotting was employed to assess p300 expression level in the liver tissues of HFD-fed mice.A cell model of lipid metabolism disorder was established in HepG2/AML-12 cells induced with free fatty acid(FFA).The effects of siRNA-mediated knockdown of p300 was observed to measure the levels of intracellular total cholesterol(TC)and triglyceride(TG),lipid deposition,and production of reactive oxygen species(ROS).Results Clinically,p300 was highly expressed in lipid metabolism disorders,and its level was positively correlated with NAFLD severity(P<0.05).Gene Set Enrichment Analysis(GSEA)revealed that p300 expression was significantly associated with fatty acid metabolism,cholesterol homeostasis,lipogenesis,PPAR signaling pathway,and peroxisome pathway.In vivo,p300 was significantly up-regulated in the livers of HFD-fed mice(P<0.01).In vitro,FFA stimulation markedly increased p300 expression in both HepG2 and AML-12 cells(P<0.01),whereas p300 knockdown significantly reduced intracellular TG and TC levels(P<0.01),attenuated lipid droplet accumulation,and reversed FFA-induced ROS elevation(P<0.01).Furthermore,p300 expression was positively correlated with the expression of SREBP-1c and its downstream key lipid synthesis enzymes.Conclusion p300 may promote hepatic lipid accumulation by acetylating and activating SREBP-1c and regulating downstream lipid metabolic enzymes,thereby affecting lipid synthesis and oxidative stress.These findings suggest that p300 may be a potential therapeutic target for lipid metabolism disorder-related diseases.

Objective To investigate the role of autophagy involving the protein kinase B/sterol regulatory element binding protein 1(Akt/SREBP-1)signaling pathway in diabetic retinopathy(DR).Methods DR rat models were estab-lished via the intraperitoneal injection of streptozotocin.Rats were randomized into control(normal rats)and DM-DR groups(DR rats).The expression of autophagy-related proteins(autophagy markers LC3-Ⅱ and LC3-Ⅰ,autophagy specific substrate p62,and autophagy-related protein Beclin1)in rat retinas was compared between the two groups.Rats were di-vided into control B(normal rats injected with 1 μL saline),DR(DR rats injected with 1 μL saline),DR+si-NC(DR rats injected with 1 μL of the negative control siRNA),and DR+si-SREBP-1 groups(DR rats injected with 1 μL of the SREBP-1 siRNA).All interventions were given 1 day before modeling and 8 weeks after modeling.Akt/SREBP-1 expression and retinal ganglion cell(RGC)survival were compared among groups.R28 rat retinal precursor cells were classified into con-trol C(normal glucose,24 h),HG(high glucose,24 h),HG+si-NC(si-NC transfection+high glucose,24 h),and HG+si-SREBP-1 groups(si-SREBP-1 transfection+high glucose,24 h).The expression of autophagy-related proteins and au-tophagosome-lysosome fusion were compared among groups.Western blot and immunofluorescence were used to examine the expression of Akt,SREBP-1 and autophagy-related proteins.Results The relative expression of Beclin1 and p62 pro-teins and the LC3-Ⅱ/Ⅰ ratio in the DM-DR group were significantly higher than those in the control group 1 and 8 weeks after modeling(all P＜0.001).Compared with the control B group,the DR group exhibited elevated SREBP-1 and reduced Akt protein levels 1 and 8 weeks after modeling(all P＜0.01).RGC counts in the DR and DR+si-NC groups were significantly lower than those in the control B group(P＜0.001).The RGC count in the DR+si-SREBP-1 group was significantly higher than that in the DR+si-NC group(P＜0.001).Compared with those in the control C group,the Beclin1 and p62 protein levels and the LC3-Ⅱ/Ⅰ ratio were increased in the HG and HG+si-NC groups(all P＜0.01).Compared with those in the HG+si-NC group,the Beclin1 and p62 protein levels and the LC3-Ⅱ/Ⅰ ratio were reduced in the HG+si-SREBP-1 group(all P＜0.05).The HG and HG+si-NC groups showed significantly more LC3B/LAMP1 dual-positive puncta than the control C group(P＜0.001).The HG+si-SREBP-1 group showed significantly less LC3B/LAMP1 dual-positive puncta than the HG+si-NC group(P＜0.001).Conclusion SREBP-1 knockdown enhances autophagic flux in early DR to attenuate RGC loss.Thus,the Akt/SREBP-1 axis represents a promising therapeutic target for DR.

Objective:To explore the impact of female body mass index (BMI) on pregnancy outcomes in artificial insemination with donor sperm (AID).Methods:A retrospective cohort study was conducted on 4 484 couples with 9 852 AID treatment cycles treated at Reproductive Center of Guangdong Institute of Reproductive Science from January 2011 to September 2024. Participants were divided into four groups based on BMI: low BMI group (BMI<18.5 kg/m 2), normal BMI group (18.5 kg/m 2≤BMI<24.0 kg/m 2), overweight group (24.0 kg/m 2≤BMI<28.0 kg/m 2), and obese group (BMI≥28.0 kg/m 2). General characteristics and pregnancy outcomes were compared across groups. Kaplan-Meier survival analysis was used to calculate cumulative pregnancy rates from one to six cycles. Generalized estimating equations (GEE), univariate and multivariate logistic and Cox regression analysis were performed, adjusting for age, basal follicle-stimulating hormone, basal luteinizing hormone, endometrial thickness, clinical diagnosis, and treatment protocol, to explore correlations between female BMI and clinical pregnancy rate, spontaneous abortion rate, and cumulative pregnancy rate. Results:1) There were no statistically significant differences in clinical pregnancy rate and spontaneous abortion rate among the low BMI group, the normal BMI group, the overweight group, and the obesity group (all P>0.05). 2) Cumulative pregnancy rates for AID cycles 1-6 were 17.60%, 31.60%, 43.08%, 54.37%, 61.83% and 73.68%, respectively. 3) Multivariate GEE analysis revealed that female age ( OR=0.962, 95% CI: 0.950-0.974, P<0.001), endometrial thickness ( OR=1.040, 95% CI:1.011-1.069, P=0.006), and natural cycles ( OR=1.171, 95% CI: 1.060-1.294, P=0.002) influenced clinical pregnancy rates. Compared with the normal BMI group, there were no statistically significant differences in clinical pregnancy rates of low BMI group, overweight group, and obese group (all P>0.05). Multivariate logistic analysis showed that female age ( OR=1.051, 95% CI: 1.012-1.091, P=0.010), endometrial thickness ( OR=0.920 , 95% CI: 0.847-1.000, P=0.049) and polycystic ovary syndrome ( OR=1.927, 95% CI: 1.044-3.556, P=0.036) influenced spontaneous abortion rates. Compared with the normal BMI group, there were no statistically significant differences in spontaneous abortion rates of low BMI group, overweight group and obese group (all P>0.05). 4) Cox regression analysis indicated that female age ( HR=0.939, 95% CI: 0.928-0.950, P<0.001), endometrial thickness ( HR=1.039, 95% CI: 1.013-1.066, P=0.003) and natural cycles ( HR=1.957, 95% CI: 1.785-2.146, P<0.001) influenced cumulative pregnancy rates. Compared with the normal BMI group, there were no statistically significant differences in cumulative pregnancy rates of low BMI group, overweight group and obese group (all P>0.05). Conclusion:Female BMI does not significantly affect clinical pregnancy rates, spontaneous abortion rates and cumulative pregnancy rates in AID.