Objective:To extract and evaluate the relevant evidence to improve the family discharge preparation of premature infants with bronchopulmonary dysplasia, so as to provide evidence-based basis for clinical formulation of scientific and effective discharge plans.Methods:All the evidence on the family discharge readiness of premature infants with bronchopulmonary dysplasia was collected from Chinese and English databases or websites, and the quality of various studies was evaluated. JBI′s evidence grading and recommendation level system (2014 edition) was used to extract and summarize the evidence.Results:A total of 21 articles were included, and 24 pieces of evidence were summarized, which were divided into seven themes: pre-discharge planning, environmental preparedness, parent education and training, support systems, feeding and nutrition, respiratory management, and discharge follow-up.Conclusions:For preterm infants with bronchopulmonary dysplasia, discharge readiness should be improved in terms of standardizing discharge criteria and implementing a discharge plan; improving family care preparation to ensure discharge support; strengthening health management and implementing a personalized plan; and continuing high-quality follow-up to ensure long-term health.

Aim To explore the mechanism of the syn-ergistic effect of the ferroptosis inducer erastin com-bined with shikonin in promoting ferroptosis in human hypertrophic scar fibroblasts(HSFBs).Methods Hypertrophic scar tissues provided by the General Hos-pital of Ningxia Medical University were collected,and HSFBs were extracted.HSFBs were identified by HE staining and immunofluorescence.The inhibitory rates of Era and SHK on HSFBs at different concentrations were detected by CCK-8 assay,and the IC50 value was calculated.CompuSyn software was used to calculate the co-use index(CI).Control group,Erastin(Era)group,shikonin(SHK)group and Era+SHK group were set up,and the number and morphological chan-ges of cells were observed after 24 hours of interven-tion.The ability of cell migration and invasion was de-tected by scratch test and Transwell test.The changes of malondialdehyde(MDA),total iron ion and reactive oxygen species(ROS)were detected by corresponding biochemical kits.The expressions of collagen I,α-SMA and GOT1,SLC7A11,GPX4 and FTH1 were detected by Western blot.Results The IC50 value of Era and SHK of primary HSFBs was 2.22 μmol·L-1 and 3.94μmol·L-1 respectively,which was used as the single drug concentration for subsequent experiments.The CompuSyn software was employed to calculate the CI value when the two drugs were used in combination,and the concentrations corresponding to CI=0.39597(Era:1.2 μmol·L-1+SHK:1.5 μmol·L-1)were selected as subsequent combination concentrations(Because when CI was equal to 0.395 97,the concen-tration of each drug was lower than the concentration of single drug,and the inhibition rate of combined drug was greater than 50％).Compared with the monother-apy group,the number of HSFBs in the SHK+Era group was significantly reduced,cell membrane showed breakage and vesiculation,cell wrinkling became smal-ler,and cytoplasm was concentrated.The migration and invasion ability of HSFBs in the SHK+Era group were obviously weakened(P＜0.05),and the expres-sion of fibrosis-related proteins collagen Ⅰ and α-SMA was reduced(P＜0.05);the contents of MDA,total i-ron ions,and ROS in HSFBs of the SHK+Era group increased(P＜0.05),and the protein expression lev-els of SLC7A11,GOT1,GPX4,and FTH1 further de-creased(P＜0.05).Conclusions Erastin in combi-nation with shikonin can synergistically inhibit the pro-liferation,migration and fibrosis levels of HSFBs.The mechanism may be that erastin enhances the inhibition of shikotin on GOT1,increases the levels of cellular i-ron ions,ROS,and lipid peroxides,thereby promoting ferroptosis in HSFBs.

Aim To study the role and mechanism of ML210 in glioma.Methods The cell viability was detected by CCK8 assay.The percentage of dead cells was detected by SYTOXstaining.The role of ferroptosis-signaling pathway in gliomas was detected bygenomics.Cell proliferation was observed by EdU staining and clone formation assay.Cell migration ability was detec-ted by scratch healing assay.The apoptosis was detec-ted by flow cytometry.Cell mitochondrial function was assesses by JC-1 staining.The mechanism of action of ML210 was detected by molecular docking coupled with immunoblotting assay(Western blot).The levels of ROS,MDA were observed by ELISA.Results Compared with the control group,ML210 treatment dose-dependently decreased glioma cell viability,in-hibited cell proliferation,migration,and increased cell apoptosis and mitochondrial dysfunction,which were reversed by ferroptosis antagonists.Gene microarray screening showed that 688 genes of the ferroptosissig-naling pathway were aberrant and 10 signaling path-ways were altered in gliomas.Molecular docking re-sults showed that ML210 binding to GPX4 significantly inhibited the protein expression level of GPX4 and pro-moted the elevation of ROS and MDA levels.Conclu-sions ML210 produces anti-glioma cells via GPX4-mediated ferroptosis pathway.

Objective:To extract and evaluate the relevant evidence to improve the family discharge preparation of premature infants with bronchopulmonary dysplasia, so as to provide evidence-based basis for clinical formulation of scientific and effective discharge plans.Methods:All the evidence on the family discharge readiness of premature infants with bronchopulmonary dysplasia was collected from Chinese and English databases or websites, and the quality of various studies was evaluated. JBI′s evidence grading and recommendation level system (2014 edition) was used to extract and summarize the evidence.Results:A total of 21 articles were included, and 24 pieces of evidence were summarized, which were divided into seven themes: pre-discharge planning, environmental preparedness, parent education and training, support systems, feeding and nutrition, respiratory management, and discharge follow-up.Conclusions:For preterm infants with bronchopulmonary dysplasia, discharge readiness should be improved in terms of standardizing discharge criteria and implementing a discharge plan; improving family care preparation to ensure discharge support; strengthening health management and implementing a personalized plan; and continuing high-quality follow-up to ensure long-term health.

Objective To evaluate the association of different obesity phenotypes and their components with the risk of cognitive impairment in older Chinese adults,and to assess the association between obesity and cognitive impairment in different cognition-related genetic backgrounds.Methods A cross-sectional study based on the West China Health and Aging Cohort was conducted.Logistic regression was applied to estimate the association of obesity phenotypes and components with cognitive impairment in older Chinese adults stratified by APOE gene and polygenic risk scores.Results A total of 7 316 participants were enrolled,of whom 1 820 had cognitive impairment.Weight gains were associated with a reduced risk of cognitive impairment(odds ratio[OR]=0.96,95%CI,0.95-0.97).Being overweight with a normal waist-to-hip ratio was a protective factor for cognition(OR=0.74,95%CI,0.61-0.90),whereas the coexistence of elevated waist-to-hip ratio and overweight did not increase the risk of cognitive impairment.Sarcopenia was associated with an elevated risk of cognitive impairment.This association was found in both overweight(OR=2.03,95%CI,1.71-2.41)and non-overweight older adults(OR=1.86,95%CI,1.58-2.20),and was significant across all polygenic risk score strata.Conclusion Increasing body mass may serve as a key protective factor against cognitive decline in older adults.Having sarcopenia and obesity is associated with an elevated risk of cognitive impairment,independent of genetic susceptibility.

Objective To investigate the correlations of expression levels of serum transforming growth factor-β1(TGF-β1)and insulin-like growth factor-1(IGF-1)with clinicopathological features of patients with adenomyosis,and the clinical value of their prediction of postoperative recurrence.Methods Eighty-two patients with adenomyosis were selected as study subjects(study group).Patients were followed up for two years after surgery and divided into recurrence group(n=15)and non-recur-rence group(n=67)based on their postoperative status.An additional 85 healthy individuals who un-derwent physical examinations during the same period were selected as control group.Serum TGF-β1 and IGF-1 levels were compared between the study group and the control group.The correlations of se-rum TGF-β1 and IGF-1 levels with the clinicopathological characteristics of adenomyosis patients was analyzed.Serum TGF-β1 and IGF-1 levels were compared between the recurrence and non-recurrence groups.Receiver operating characteristic(ROC)curve analysis was used to evaluate the diagnostic efficacy of serum TGF-β1 and IGF-1 levels in predicting postoperative recurrence in adenomyosis pa-tients.Results Serum TGF-β1 and IGF-1 levels in the study group were significantly higher than those in the control group(P＜0.05).Serum TGF-β1 levels were correlated with menstrual vol-ume,history of curettage,uterine volume,pathological type,lesion volume,endometrial status and ectopic gland cycle(P＜0.05).Serum IGF-1 levels were correlated with menstrual volume,history of curettage,uterine volume,pathological type,endometrial status and ectopic gland cycle(P＜0.05).Postoperative serum TGF-β1 and IGF-1 levels in the recurrence group were significantly higher than those in the non-recurrence group(P＜0.05).ROC curve analysis showed that the area under the curve(AUC)for predicting postoperative recurrence using serum TGF-β1,IGF-1 and their combination were 0.823,0.803 and 0.940,respectively.The clinical efficacy of TGF-β1 and IGF-1 in combination in predicting postoperative recurrence was superior to that of TGF-β1 alone(ZcombinedwithTGF-β1=2.001,ZcombinedwithIGF-1=2.318,P=0.045,0.021).Conclusion The serum levels of TGF-β1 and IGF-1 in patients with adenomyosis are significantly increased,which are closely related to the clinicopathological features of the patients.The combination of serum TGF-β1 and IGF-1 levels has high clinical efficacy in predicting postoperative recurrence.

Objective To evaluate the pharmacokinetics(PK)and pharmacodynamics(PD)of propofol injectable emulsion,and to assess the bioequivalence of test and reference formulations in healthy Chinese adult volunteers.Methods Thirty-two healthy Chinese adult volunteers were recruited and randomly assigned to a fasting.single-dose,two-period and double-crossover study.Propofol was given to eligible subjects at a speed of 30 μg·kg-1·min-1 for 30 min.The concentration of propofol in plasma was determined by avalidated high performance liquid chromatography-tandem mass spectrometery(HPLC-MS/MS)method.The PK parameters of the two preparations were calculated.Bispectral index(BIS)was measured to calculate the PD parameters of two formulations.Adverse events during the trial were recorded.Results Thirty-one volunteers were included in the pharmacokinetic parameter set.The mean values of PK parameters of test andreference formulations were as follows:Cmax were(660.87±110.25)and(683.13±125.75)ng·mL-1;AUC0-t were(473.50±86.03)and(478.40±80.25)h·ng·mL-1;AUC0-∞ were(500.45±96.49)and(507.84±88.00)h·ng·mL-1;tmax were 0.47(0.25,0.53)and 0.50(0.40,0.54)h;t1/2 were(2.97±1.74)and(3.08±1.82)h.Thirty-one volunteers were included in the bioequivalence set.The 90％confidence intervals(CI)for the geometric mean ratios of Cmax,AUC0-t,AUC0-∞ were 92.64％-101.39％,96.43％-101.00％,95.67％-100.70％,respectively.The mean values of PD parameters of test and reference formulations were as follows:BISmin were(75.94±13.66)and(74.39±12.32);BISAUC0-60minwere 5 569.85±182.78 and 5 575.68±166.19;T-BISmin were 23.00 and 29.00 min,respectively.There were no serious adverse events.Conclusion Two formulations of propofol injectable emulsion were bioequivalent and both of them exhibited good safety.

To meet the domestic clinical demand timely,the national health commission has released three batches of encourage generic drug catalogues,which plays a good guiding role in improving the supply level and accessibility of generic drugs.Based on literature investigation,the typical cases of novel pharmaceutical preparations were analyzed,and the pharmaceutical considerations were put forward in terms formulation,manufacturing process and quality control,aimed to provide scientific reference for research and development of such drugs.

Aim To study the role and mechanism of ML210 in glioma.Methods The cell viability was detected by CCK8 assay.The percentage of dead cells was detected by SYTOXstaining.The role of ferroptosis-signaling pathway in gliomas was detected bygenomics.Cell proliferation was observed by EdU staining and clone formation assay.Cell migration ability was detec-ted by scratch healing assay.The apoptosis was detec-ted by flow cytometry.Cell mitochondrial function was assesses by JC-1 staining.The mechanism of action of ML210 was detected by molecular docking coupled with immunoblotting assay(Western blot).The levels of ROS,MDA were observed by ELISA.Results Compared with the control group,ML210 treatment dose-dependently decreased glioma cell viability,in-hibited cell proliferation,migration,and increased cell apoptosis and mitochondrial dysfunction,which were reversed by ferroptosis antagonists.Gene microarray screening showed that 688 genes of the ferroptosissig-naling pathway were aberrant and 10 signaling path-ways were altered in gliomas.Molecular docking re-sults showed that ML210 binding to GPX4 significantly inhibited the protein expression level of GPX4 and pro-moted the elevation of ROS and MDA levels.Conclu-sions ML210 produces anti-glioma cells via GPX4-mediated ferroptosis pathway.

Objective To investigate the regulatory effect of lipocalin 2(LCN2)on epidermal growth factor receptor(EGFR)phosphorylation and its impact on inflammatory damage in human fallopian tube epithelial cells.Methods Human fallopian tube epithelial cells were isolated and a lipopolysaccharide(LPS)intervention was applied to establish an in vitro cell model.The cells were randomly assigned into the following groups:a blank control group(Control),a model group(Model),experimental groups(Model+si-LCN2 or Model+oe-LCN2),and negative control groups(Model+si-NC or Model+oe-NC).Changes in cell viability,apoptosis rates,inflam-matory levels,as well as the expression of EGFR mRNA,LCN2,EGFR,p-EGFR,and the ratio of p-EGFR/EGFR proteins were evaluated.Results Compared to the Model group,the Model+si-LCN2 group exhibited enhanced cell viability,a reduced apoptosis rate,and decreased expression of inflammatory factors(P＜0.05).Immunopre-cipitation analysis confirmed a direct interaction between LCN2 and EGFR.In comparison with the Model group,the Model+oe-LCN2 group demonstrated elevated levels of p-EGFR and the p-EGFR/EGFR ratio(P＜0.05),while no significant change was observed in total EGFR expression(P＞0.05).Conclusion Inhibition of LCN2-mediated EGFR phosphorylation enhances cell viability,reduces apoptosis,and mitigates inflammatory responses,thereby ameliorating LPS-induced inflammatory injury in human fallopian tube epithelial cells.