OBJECTIVE To provide reference for improving the work efficiency of staff and promoting the discipline construction of pharmacy department. METHODS By analyzing the current situation of performance management in the pharmacy department of our hospital， the key successful factors were sorted out， strategic decoding was carried out and key performance indicators were extracted. The quarterly and annual performance appraisal forms were formulated for the departments of pharmacy warehouse， outpatient pharmacy， ward pharmacy， clinical pharmacy department， prescription examination center， laboratory and other departments； the performance management information platform was built. The work efficiency and output of each department were compared half a year before and after the implementation of the performance management plan. RESULTS After the implementation of the program， the average queuing time for drug collection in the outpatient department was shortened from 5 minutes to 3 minutes， the average number of dispensing infusion bags per hour in the pharmacy intravenous admixture services increased from 50 bags to 60 bags， and antibacterial use density of the hospital decreased from 42.7 DDD（defined daily doses） to 40.2 DDD. The number of academic papers published had increased from 8 to 10， and the satisfaction of clinical departments with ward pharmacies increased from 85% to 95%. CONCLUSIONS The performance management system has been successfully established in pharmacy department of our hospital， which can improve the enthusiasm of pharmacists， reflect the value of pharmaceutical care， and promote the discipline construction of pharmacy.

Objective:To explore the research hotspots and effective promotion paths of post market surveillance and supervise of medical consumables with non-active medical devices.Methods:Data mining methods were used to collect related journal literatures and documents from the websites of China regulatory institutions and the China National Knowledge Infrastructure(CNKI),order sub item data of medical device adverse event reports,extract the MeSH element words of literatures and documents,perform bibliometric analysis and visual display.Results:The number of medical devices adverse event reports in China has been increasing year by year,reaching 694 866 in 2022,in the four statistical years from 2019 to 2022,the number of reports on non-active medical devices and IVD reagents also showed a parallel increasing trend,accounting for about 65.00% of the total number of adverse event reports on medical devices in the year.The bibliometric analysis of journal literature shows that research in this field has received varying degrees of participation from regulatory institutions,universities,medical institutions,and enterprises.Regulatory institutions have contributed 46 articles,accounting for 56.79% of the total number of articles,followed by 28 articles from universities.The co-occurrence analysis shows that hot topic is focused in 5 clusters:quality management,risk management,international experiences discussion and adverse event surveillance and re-evaluation and real-world research.China regulatory institutions attach great importance to post market surveillance and supervise,and have issued more than 20 relevant documents since 2006,focusing on specific topics and gradually deepening around safety and effectiveness.Conclusion:The post market surveillance and supervise of medical devices,especially medical consumables based on non-active medical devices,need to be promoted synchronously in three dimensions:regulatory institutions,medical institutions,and enterprises.Universities,research institutes,and industry organizations should work in coordinating to strengthen the collection,identification,and active surveillance of risk signals based on adverse event surveillance,safety evaluation based on risk management,and conducting real-world research,research and develop risk control and corrective and preventive measures.

Objective:To investigate the features of the brain structural network in patients with postpartum depression (PPD).Methods:This cross-sectional study included PPD patients who visited the mental health counseling clinic after delivery at the Jiangsu University Affiliated Yixing Hospital from June 2013 to September 2022 (PPD group). Matched non-PPD postpartum women based on age, years of education, and body mass index who came for postpartum follow-up (non-PPD postpartum group), and non-pregnant women who visited the hospital or underwent physical examinations during the same period (non-pregnant group) were also included. Demographic data and diffusion tensor imaging (DTI) data were collected for all three groups. The brain was partitioned into 90 regions using an anatomical template to construct the brain structural network. Network-based statistics (NBS) were applied to further screen and construct subnetworks. The efficacy of the subnetworks in identifying PPD was evaluated through multivariable logistics regression models and receiver operating characteristic curves. A comparison of the connectivity strength of white matter tracts and topological attributes of brain structural network parameters was conducted using independent samples t-tests, and the results were corrected using the false discovery rate (FDR) method. Results:(1) A total of 116 subjects were included, with 40 in the non-pregnant group, 40 in the non-PPD postpartum group, and 36 in the PPD group. PPD group had higher Edinburgh Postnatal Depression Scale (EPDS) scores than the non-pregnant and non-PPD postpartum groups [(18.0±4.1) scores vs. (2.5±1.2) and (6.1±2.1) scores, F=340.40; t=24.65,10.60 and 16.16 in pairwise comparison; all P<0.001]. (2) Compared to the non-pregnant group, there was a decrease in the connectivity strength of nine white matter tracts within the brain structural network of the postpartum group (including left dorsolateral superior frontal gyrus-left anterior cingulate and paracingulate gyrus, left dorsolateral superior frontal gyrus-right amygdala, left dorsolateral superior frontal gyrus-left insula, left insula-left lentiform nucleus, left insula-left hippocampus, left hippocampus-right amygdala, left hippocampus-left precuneus, left anterior cingulate and paracingulate gyrus-right amygdala, and right amygdala-right hippocampus) (all P<0.05, FDR corrected). No increased connection strengths were observed. There were no significant differences in the connection strengths of these nine tracts between the non-PPD and PPD groups. (3) A characteristic subnetwork for the maternal group was successfully constructed based on the nine tracts, which exhibited typical small-world properties (σ>1). Compared to the non-PPD maternal group, the characteristic path length in the PPD group was increased [(3.904±0.328) vs. (4.130±0.433), t=－2.58], and global efficiency was decreased [(0.361±0.036) vs. (0.331±0.053), t=2.91] (both P<0.05). Local property comparisons showed that the node efficiency values for the left dorsolateral superior frontal gyrus, left insula, left anterior cingulate and paracingulate gyrus, left hippocampus, right hippocampus, right amygdala, left precuneus and left putamen in the PPD group were significantly reduced [(0.273±0.023) vs. (0.267±0.030), t=0.98; (0.299±0.035) vs. (0.276±0.041), t=2.64; (0.265±0.019) vs. (0.258±0.025), t=1.38; (0.318±0.028) vs. (0.305±0.031), t=1.92; (0.312±0.027) vs. (0.302±0.031), t=1.50; (0.322±0.030) vs. (0.298±0.026), t=3.71; (0.356±0.040) vs. (0.338±0.056), t=1.62; (0.346±0.028) vs. (0.331±0.036), t=1.74; all P<0.05]. However, only the differences in node efficiency values for the left insula and right amygdala remained significant after FDR correction (corrected P=0.041 and 0.003). (4) Global efficiency, as well as node efficiency for the left insula and right amygdala, demonstrated good value for identifying PPD [areas under the curve (AUC) and their 95% CI were 0.827 (0.732-0.922), 0.741 (0.628-0.854), and 0.761 (0.653-0.867), respectively], with even better performance when combined [0.897 (0.828-0.969)]. (5) In the PPD group, global efficiency ( r=－0.43, P=0.008), node efficiency for the left insula ( r=－0.39, P=0.019), and node efficiency for the right amygdala ( r=－0.42, P=0.011) were all negatively correlated with EPDS scores. Conclusion:Aberrations in global efficiency, node efficiency for the left insula, and node efficiency for the right amygdala may serve as characteristic neuroimaging biomarkers for PPD.

Objective To construct and apply an intelligent follow-up information system for patients with cancer pain,providing references for improving the efficiency of hospital follow-up and promoting pain management of patients at home.Methods The intelligent discharge follow-up system for patients with cancer pain includes 2 platforms,namely a patient self-report platform and an administrator operation platform.The administrator operation platform consists of 5 modules,namely the workbench module,the follow-up plan module,the follow-up results module,the health education module and the data statistics module.In January 2022,the system was officially put into clinical application.The use of the system was analyzed,and patients'completion rate,medication compliance,incidence of moderate and severe pain and satisfaction with pain control were compared before(from January 2020 to December 2021)and after(from January 2022 to November 2023)the application of the system.Results At present,this system has been applied in 95 cancer-related wards of our hospital.From January 2022 to November 2023,the number of people who should be followed up was 4 248,and the number of people who actually completed the follow-up was 4 127;the rate of follow-up completion was 97.2%;the rate of timely completion of the follow-up was 94.9%;the rate of automatic follow-up by the system was 40.1%;the rate of patient abnormality report was 31.9%;the rate of timely treatment of patient abnormality report was 89.1%.After the application of the system,the completion rate of pain follow-up was increased,and the difference was statistically significant(P<0.001).After the application of the system,the medication compliance rate of patients with cancer pain increased from 86.9%to 91.0%;the incidence of moderate and severe pain decreased from 6.8%to 5.2%;the satisfaction with pain control increased from 81.0%to 83.5%(P<0.05).Conclusion The intelligent discharge follow-up system for patients with cancer pain can effectively improve the discharge follow-up efficiency and promote the management of patients with cancer pain at home.

Background and purpose:Heterogeneous nuclear ribonucleoprotein K(hnRNPK)is an RNA special binding protein that participates in regulating the expression of related genes and protein translation.It has been linked to the malignant occurrence and development of various tumors,but its role in breast cancer remains unclear.The aim of this study was to investigate the effects of hnRNPK on ferroptosis in breast cancer cells and the underlying mechanisms.Methods:Based on The Cancer Genome Atlas(TCGA)and Gene Expression Omnibus(GEO)databases,hnRNPK expression in breast cancer tissues and normal tissues and its relationship with clinical prognosis were analyzed by bioinformatics.We detected hnRNPK expression in breast cancer cells and tissues using real-time quantitative reverse transcription polymerase chain reaction(qRT-PCR),Western blot,and immunohistochemistry staining diagnosis methods.MCF-7 and MDA-MB-231 breast cancer cells were transfected with siRNA,and divided into control group(control),empty body group(NC),and interference vector group(si-hnRNPK).Cell proliferation was detected by cell counting kit-8(CCK-8)and plate clone formation assays.RNA-seq analysis was applied to explore potential targeted biological functions and signaling pathways affected by hnRNPK.Additionally,we investigated the impact of hnRNPK on ferroptosis phenotype using Western blot and commercial kits for reactive oxygen species(ROS),malondialdehyde(MDA),glutathione(GSH),and Fe2+,ferroptosis inhibitor(ferrostatin-1,Fer-1)was used to detect the rescue effect of hnRNPK knockdown on ferroptosis.The impact of hnRNPK on the expressions of Wnt/β-catenin pathway-related proteins were determined by Western blot.Results:The bioinformatics analyses indicated hnRNPK was upregulated in breast cancer tissues(P＜0.01),and the overall survival of patients in the high expression group was poorer compared with those in the low expression group(P＜0.05).hnRNPK was highly expressed in breast cancer tissues and cells,and knocking down hnRNPK weakened the proliferation ability of breast cancer cells(P＜0.05).The RNA-seq analysis showed that hnRNPK was significantly enriched in ferroptosis,apoptosis,and the Wnt/β-catenin signaling pathway.Knocking down hnRNPK promoted ferroptosis in breast cancer cells by inducing lipid ROS and MDA,as well as Fe2+accumulation(P＜0.05).Interestingly,the ferroptosis inhibitor ferrostatin-1(Fer-1)reversed the promotive effect of hnRNPK knockdown on ferroptosis(P＜0.05).Downregulation of hnRNPK led to a decrease in the expressions of β-catenin and c-Myc in the Wnt/β-catenin signaling pathway,while expressions of CK1α,APC and the GSK-3β complex were elevated(P＜0.05).Conclusion:hnRNPK is highly expressed in breast cancer,and knocking down hnRNPK promotes ferroptosis in breast cancer cells by inhibiting the Wnt/β-catenin signaling pathway,thereby suppressing the malignant progression of breast cancer.

Objective To investigate the mechanism by which fragile X mental retardation protein(FMRP)regulates ferroptosis evasion in colorectal cancer(CRC)cells.Methods We examined FMRP expression levels in CRC cell lines using RT-qPCR and Western blotting and analyzed the biological functions and signaling pathways involved in FMRP-mediated regulation of CRC progression using the TCGA database.A lentiviral FMRP overexpression vector(Lv-FMRP)and 3 knockdown vectors(siFMRP-1,siFMRP-2,and siFMRP-3)were constructed,and their effects on proliferation of HCT116 cells were examined using CCK8 assay and plate clone formation assay;the changes in cell ferroptosis level was determined using MDA/ROS/GSH/Fe2+kits,mitochondrial membrane potential changes were detected using JC-1 fluorescence staining,and the expressions of proteins associated with ferroptosis and the RAS/MAPK signaling pathway were detected using Western blotting.The subcutaneous tumorigenic potential of the transfected cells was evaluated in nude mice.Results Compared with normal colonic mucosal epithelial NCM460 cells,the CRC cell lines had significantly higher FMRP expression level.Bioinformatics analysis suggested the involvement of FMRP in regulation of reactive oxygen,oxidative stress-induced cell death,mitochondrial respiration,and glutathione metabolism pathways.In the cell experiments,FMRP knockdown significantly inhibited proliferation of HCT116 cells,lowered cellular GSH content,increased MDA and ROS levels,Fe2+fluorescence intensity,and mitochondrial membrane potential,and decreased SLC7A11/GPX4 protein expressions and the phosphorylation levels of ERK,MEK,MAPK,and RAS proteins;FMRP overexpression resulted in the opposite changes in the cells.In the tumor-bearing nude mice,HCT116 cells with FMRP knockdown showed attenuated tumorigenic potential with lowered xenograft growth rate and reduced SLC7A11 expression in the xenograft.Conclusion The high expression of FMRP inhibits ferroptosis in CRC cells and promotes progression of CRC by activating the RAS/MAPK signaling pathway.

Objective To investigate the mechanism by which fragile X mental retardation protein(FMRP)regulates ferroptosis evasion in colorectal cancer(CRC)cells.Methods We examined FMRP expression levels in CRC cell lines using RT-qPCR and Western blotting and analyzed the biological functions and signaling pathways involved in FMRP-mediated regulation of CRC progression using the TCGA database.A lentiviral FMRP overexpression vector(Lv-FMRP)and 3 knockdown vectors(siFMRP-1,siFMRP-2,and siFMRP-3)were constructed,and their effects on proliferation of HCT116 cells were examined using CCK8 assay and plate clone formation assay;the changes in cell ferroptosis level was determined using MDA/ROS/GSH/Fe2+kits,mitochondrial membrane potential changes were detected using JC-1 fluorescence staining,and the expressions of proteins associated with ferroptosis and the RAS/MAPK signaling pathway were detected using Western blotting.The subcutaneous tumorigenic potential of the transfected cells was evaluated in nude mice.Results Compared with normal colonic mucosal epithelial NCM460 cells,the CRC cell lines had significantly higher FMRP expression level.Bioinformatics analysis suggested the involvement of FMRP in regulation of reactive oxygen,oxidative stress-induced cell death,mitochondrial respiration,and glutathione metabolism pathways.In the cell experiments,FMRP knockdown significantly inhibited proliferation of HCT116 cells,lowered cellular GSH content,increased MDA and ROS levels,Fe2+fluorescence intensity,and mitochondrial membrane potential,and decreased SLC7A11/GPX4 protein expressions and the phosphorylation levels of ERK,MEK,MAPK,and RAS proteins;FMRP overexpression resulted in the opposite changes in the cells.In the tumor-bearing nude mice,HCT116 cells with FMRP knockdown showed attenuated tumorigenic potential with lowered xenograft growth rate and reduced SLC7A11 expression in the xenograft.Conclusion The high expression of FMRP inhibits ferroptosis in CRC cells and promotes progression of CRC by activating the RAS/MAPK signaling pathway.

Objective To observe the correlations of subchondral insufficiency fracture(SIF)of medial femoral condyle with medial meniscus injury pattern and medial meniscus extrusion(MME).Methods Data of 36 patients with clinically confirmed unilateral medial femoral condyle SIF were retrospectively analyzed.The patients were divided into low-grade and high-grade groups according to SIF grade.Cartilage injury,medial meniscus injury and MME were compared between groups,and the correlations of SIF grade with cartilage injury,osteonecrosis volume(OV)and MME were analyzed.Cartilage injury grade,OV and MME were compared between groups,and the correlations were explored.Results There were 18 cases in each group.The percentage of cartilage injury grade Ⅲ-Ⅳ,OV and MME value(the distance between the vertical line of medial meniscus and the vertical line of tibial plateau cartilage)in high-grade group were greater than those in low-grade group(all P＜0.05).Significant difference of injury grades of meniscus posterior horn was found between groups(P=0.007).SIF grade was positively correlated with cartilage injury grade,OV and MME value(rs=0.710,0.765,0.540,all P≤0.01).MME value was positively correlated with meniscal injury degree and tear range(rs=0.502,0.520,both P＜0.01).There were 4,19 and 13 cases with 0,1 and 2 grade MME,respectively,and significant differences of cartilage injury grades,OV and MME values were found among different MME grades(all P＜0.05).MME value was positively correlated with cartilage injury grade and OV(rs=0.451,0.579,both P＜0.01).Conclusion In SIF patients,OV and cartilage injury were both correlated with medial meniscus injury pattern and MME.

The anti-tumor effect of anti-PD-1 antibody has long been shown to be strongly related to the tumor immune microenvironment (TIME). This study aimed to mechanistically assess whether Chang Wei Qing (CWQ) Decoction can enhance the anti-tumor effect of PD-1 inhibitor therapy. PD-1 inhibitor therapy showed the significant anti-tumor effect in patients with mismatch repair-deficient/microsatellite instability-high (dMMR/MSI-H) colorectal cancer (CRC), rather than those with mismatch repair-proficient/microsatellite stable (pMMR/MSS) CRC. Hence, immunofluorescence double-label staining was utilized to explore the difference in the TIME between dMMR/MSI-H and pMMR/MSS CRC patients. Flow cytometry was used to analyze T-lymphocytes in tumors from mice. Western blot was used to measure the expression of PD-L1 protein in mouse tumors. The intestinal mucosal barrier of mice was evaluated by hematoxylin-eosin staining and immunohistochemistry. 16S rRNA-gene sequencing was used to examine the structure of the gut microbiota in mice. Subsequently, Spearmanapos;s correlation analysis was used to analyze the relationship between the gut microbiota and tumor-infiltrating T-lymphocytes. The results showed that dMMR/MSI-H CRC patients had more CD8⁺T cells and higher expression of PD-1 and PD-L1 proteins. In vivo, CWQ enhanced the anti-tumor effect of anti-PD-1 antibody and increased the infiltration of CD8⁺ and PD-1⁺CD8⁺ T cells in tumors. Additionally, the combination of CWQ with anti-PD-1 antibody resulted in lower inflammation in the intestinal mucosa than that induced by anti-PD-1 antibody alone. CWQ and anti-PD-1 antibody co-treatment upregulated PD-L1 protein and reduced the abundance of Bacteroides in the gut microbiota but increased the abundance of Akkermansia,Firmicutes, andActinobacteria. Additionally, the proportion of infiltrated CD8⁺PD-1⁺, CD8⁺, and CD3⁺ T cells were found to be positively correlated with the abundance of Akkermansia. Accordingly, CWQ may modulate the TIME by modifying the gut microbiota and consequently enhance the anti-tumor effect of PD-1 inhibitor therapy.
Animals ; Mice ; Immune Checkpoint Inhibitors/therapeutic use* ; Gastrointestinal Microbiome ; CD8-Positive T-Lymphocytes ; B7-H1 Antigen ; RNA, Ribosomal, 16S ; Colorectal Neoplasms/metabolism* ; Colonic Neoplasms ; Tumor Microenvironment

Objective:To investigate the effects of endocrine drugs on tumor markers and endometrium after breast cancer surgery.Methods:Eighty-eight patients with endocrine therapy for breast cancer admitted to the Heping Hospital Affiliated to Changzhi Medical College from November 2018 to March 2022 were selected, 44 patients taken orally tamoxifen citrate tablets were enrolled in the study group, 44 patients taken orally anastrozole tablets were enrolled in the control group, the patients in the two groups were treated for 12 months. The tumor markers, endometrial thickness were compared between the two groups before treatment and 12 months after treatment. The drug safety was compared too.Results:After treatment, the serum levels of carcinoembryonic antigen (CEA), carbohydrate antigen 125 (CA125) and glycochain antigen 15-3 (CA15-3) in both groups were decreased, and the level of tumor markers in the study group were lower than those in the control group: (3.01 ± 0.23) μg/L vs.(3.89 ± 1.15) μg/L, (4.22 ± 1.21) kU/L vs. (7.38 ± 2.19) kU/L, (16.76 ± 2.19) kU/L vs. (19.87 ± 2.21) kU/L, there were statistical differences ( P<0.05). The endometrial thickness in the study group at 6 months and 12 months after treatment were higher than those in the control group: (7.23 ± 0.22) mm vs. (6.21 ± 0.19)mm, (7.98 ± 0.24) mm vs. (6.47 ± 0.22) mm, there were statistical differences ( P<0.05). At 12 months after treatment, the scores of functional dimension, emotional dimension, social/family dimension and physical dimension in functional assessment of cancer therapy (FACT-G) scale in the study group were significantly higher than those in the control group ( P<0.05). There was no statistically significant difference in adverse reactions between the two groups ( P>0.05). Conclusions:Tamoxifen citrate tablets can effectively inhibit the levels of serum tumor markers and improve the quality of life of patients, and anastrozole tablets can significantly reduce the endometrial thickness of breast cancer patients.