Abstract Among women of reproductive age, pelvic inflammatory disease is a prevalent gynecological condition. In its early stages, it may be mild or asymptomatic. If treatment is delayed, there is a high likelihood of recurrence, which can have a major impact on women′s reproductive health and raise the financial, emotional, and physical load on the family. Significant advancements in the treatment of chronic pelvic inflammatory disease have been made possible by the thorough investigation of this condition. In an effort to advance the health management of this illness and offer fresh concepts for clinical treatment, this review discusses a number of facets of both Chinese and Western medicine.

Juvenile idiopathic arthritis（JIA）is a pediatric rheumatic disease characterized by chronic arthritis as its core manifestation，with pathogenesis closely linked to inflammatory responses mediated by pro-inflammatory factors such as tumor necrosis factor alpha（TNF-α）. Tumor necrosis factor inhibitors（TNFi）have significantly improved disease activity and prognosis in JIA patients by targeting and blocking inflammatory pathways. Commonly used TNFi agents，including etanercept，infliximab，adalimumab，and golimumab，have demonstrated favorable efficacy in multiple studies. However，infection risks-particularly the increased risk of tuberculosis associated with TNFi require heightened attention，necessitating pre-treatment screening and ongoing monitoring. The immunogenicity of these agents may also impact long-term therapeutic outcomes. Monoclonal antibody-based TNFi agents demonstrate superior efficacy in JIA patients with concomitant uveitis，whereas fusion protein TNFi show limited therapeutic benefits. Vaccination with live vaccines should be avoided，whereas inactivated vaccines generally demonstrate satisfactory immunogenicity. This review summarizes the efficacy，safety，and current research status of TNFi in JIA treatment，explores limitations of existing studies，and aims to advance precision medicine for JIA，optimize clinical practice，and provide direction for future research.

Objective: To evaluate the clinical effectiveness of transcutaneous electrical acupoint stimulation (TEAS) in the treatment of sequelae of inflammatory pelvic diseases in women. Methods: A total of 100 patients diagnosed with sequelae of inflammatory pelvic diseases were selected . They were randomly divided into three groups : transcutaneous electrical acupoint stimulation (TEAS) treatment group (40 cases) , drug treatment group (30 cases) and combined treatment group (30 cases) . The three groups received treatment for four weeks : the medication group received Kangfu xiaoyan shuan ; the combination treatment group received TEAS combined with Kangfu xiaoyan shuan ; and the TEAS treatment group received the highest level of electrical stimulation that the human body could withstand via medium_low frequency pulsed electrotherapy instrument on the Guanyuan acupoints or the uterine acupoints . Prior to and following treatment , the three patient groups ’local sign score , symptom and sign score (McCormack score) , visual analogue scale ( VAS) score for lower abdomen pain , and SF_36 scale score were observed . Additionally , the three groups ’incidence of adverse events was noted . Results: Following the intervention , all three groups ’local sign score , McCormack score , and VAS score for lower abdomen pain were considerably lower than they were before the intervention (P < 0. 05) . These three scores showed significant differences (P < 0. 05) between the combination treatment group and the TEAS treatment and drug treatment groups . The combined treatment group ’s scores were lower. The three groups ’total somatic health score and total mental health score before and after the intervention differed significantly (P < 0. 05) after the period of therapy. Additionally , the combined treatment group ’s total somatic health score and total mental health score were higher than those of the medication group . In all three groups , there were no notable negative reactions . Conclusion TEAS treatment is effective in relieving the symptoms of chronic pelvic pain due to the sequelae of inflammatory pelvic disease , and the combination of medication is better than monotherapy in improving pain symptoms and quality of life . Key words sequelae of inflammatory pelvic diseases ; chronic pelvic pain ; transcutaneous electrical acupoint stimulation ; randomized controlled trial;clinical efficacy

ObjectiveTo investigate the effect of transplantation of bone marrow mesenchymal stem cells （BMSCs） co-cultured with bone marrow-derived M2 macrophages （M2-BMDMs）， named as BMSC^M2， on a rat model of liver cirrhosis induced by carbon tetrachloride （CCl₄）/2-acetaminofluorene （2-AAF）. MethodsRat BMDMs were isolated and polarized into M2 phenotype， and rat BMSCs were isolated and co-cultured with M2-BMDMs at the third generation to obtain BMSC^M2. The rats were given subcutaneous injection of CCl₄ for 6 weeks to establish a model of liver cirrhosis， and then they were randomly divided into model group （M group）， BMSC group， and BMSC^M2 group， with 6 rats in each group. A normal group （N group） with 6 rats was also established. Since week 7， the model rats were given 2-AAF by gavage in addition to the subcutaneous injection of CCl₄. Samples were collected at the end of week 10 to observe liver function， liver histopathology， and hydroxyproline （Hyp） content in liver tissue， as well as changes in the markers for hepatic stellate cells， hepatic progenitor cells， cholangiocytes， and hepatocytes. A one-way analysis of variance was used for comparison of continuous data between multiple groups， and the least significant difference t-test was used for further comparison between two groups. ResultsCompared with the N group， the M group had significant increases in the activities of serum alanine aminotransferase （ALT） and aspartate aminotransferase （AST） （P<0.01）； compared with the M group， the BMSC and BMSC^M2 groups had significant reductions in ALT and AST （P<0.01）， and the BMSC^M2 group had significantly better activities than the BMSC group （P<0.05）. Compared with the N group， the M group had significant increases in Hyp content and the mRNA and protein expression levels of alpha-smooth muscle actin （α-SMA） in the liver （P<0.01）； compared with the M group， the BMSC and BMSC^M2 groups had significant reductions in Hyp content and the expression of α-SMA （P<0.05）， and the BMSC^M2 group had a significantly lower level of α-SMA than the BMSC group （P<0.01）. Compared with the N group， the M group had significant increases in the mRNA expression levels of the hepatic progenitor cell markers EpCam and Sox9 and the cholangiocyte markers CK7 and CK19 （P<0.01） and significant reductions in the expression levels of the hepatocyte markers HNF-4α and Alb （P<0.01）； compared with the M group， the BMSC and BMSC^M2 groups had significant reductions in the mRNA expression levels of EpCam， Sox9， CK7， and CK19 （P<0.05） and significant increases in the mRNA expression levels of HNF-4α and Alb （P<0.05）， and compared with the BMSC group， the BMSC^M2 group had significant reductions in the mRNA expression levels of EpCam and CK19 （P<0.05） and significant increase in the expression level of HNF-4α （P<0.05）. ConclusionM2-BMDMs can enhance the therapeutic effect of BMSCs on CCl₄/2-AAF-induced liver cirrhosis in rats， which provides new ideas for further improving the therapeutic effect of BMSCs on liver cirrhosis.

Objective To investigate the regulatory effect of KHSRP on progression of gastric adenocarcinoma and the role of the JAK1/STAT3 signaling axis in mediating its effect.Methods KHSRP mRNA expression level was detected using qRT-PCR in 120 pairs of gastric adenocarcinoma and adjacent tissues,4 gastric adenocarcinoma cell lines(MKN-28,HGC-27,CRL-5822,and SNU-1)and normal human gastric mucosal GES-1 cells.In HGC-27 cells with KHSRP knockdown and SNU-1 cells with KHSRP overexpression,cell proliferation,migration,invasion and expression levels of JAK/STAT were evaluated using CCK-8 assay,Transwell migration and invasion assays,and Western blotting.In BALB/c-nude mice,HGC-27 cells with KHSRP knockdown and SNU-1 cells overexpressing KHSRP were injected either subcutaneous or via the tail vein to observe subcutaneous xenograft growth and lung metastasis of the tumor cells.Results Gastric adenocarcinoma tissues and cell lines all showed significantly increased KHSRP expression as compared with the adjacent tissues and GES-1 cells.In HGC-27 cells,KHSRP knockdown significantly inhibited cell proliferation,migration and invasion,while KHSRP overexpression enhanced the malignant behaviors of SNU-1 cells.In nude mice,inoculation of HGC-27 cells with KHSRP knockdown resulted in smaller tumor volume and weight,slower cell proliferation rate and fewer lung metastatic foci,and KHSRP-overexpressing SNU-1 cells produced the opposite results.KHSRP knockdown in HGC-27 cells significantly down-regulated the expression levels of JAK1 and STAT3,which were obviously increased in KHSRP-overexpressing SNU-1 cells.Conclusion High expressions of KHSRP promote progression and metastasis of gastric adenocarcinoma possibly by regulating the JAK1/STAT3 signaling axis.

Traditional Chinese medicine is a treasure of Chinese civilization,which has undergone thousands of years of precipitati-on and clinical verification.According to the theory of traditional Chinese medicine,ancient doctors used natural medicines and natural means to promote self-regulation and damage repair of the body.In recent years,as an important tool to repair body damage,stem cells have set off a research upsurge.With the continuous deepening of stem cell research and the continuous expansion of the fields in-volved,the potential correlation between traditional Chinese medicine and stem cells has attracted more and more domestic and foreign researchers to invest in research.This paper expounds regenerative medicine and stem cells,the advantages of Chinese medicine in regulating stem cells,and the opportunities and challenges faced by Chinese medicine and regenerative medicine,and reviews the cur-rent research trends and frontier trends in this field,in order to provide useful references for subsequent studies.

Objective·To further clarify the mechanism of podocyte damage by studying the expression of cartilage oligomeric matrix protein(COMP)in glomerular podocytes and its relationship with podocyte autophagy under high glucose environment.Methods·The gene expression dataset GSE104948 was downloaded from the GENE EXPRESSION OMNIBUS(GEO)database,and differentially expressed genes(DEGs)were obtained via GEO2R.The molecular functions and signaling pathways related to differential genes were summarized.The most correlated key genes(hub genes)were acquired by Weighted Gene Co-Expression Network Analysis(WGCNA)and the protein-protein interaction network(PPI)of DEGs was constructed with STRING database.The enrichment analysis was performed again.Conditionally immortalized mouse podocyte cells were cultured in vitro.After being fully differentiated,they were stimulated with high glucose,and the expressions of COMP,mammalian target of rapamycin(mTOR),microtubule-associated protein 1 light chain3(LC3)and other proteins in podocytes were detected by Western blotting.The shRNA constructed by lentiviral vector was further used to infect podocytes to inhibit the expression of COMP,and the stable cell strains were screened by puromycin.The expression of COMP,mTOR,and LC3 of stable strains were detected by Western blotting,in order to observe the effect of COMP on autophagy.Results·A total of 362 DEGs were filtered for subsequent analysis.Among these DEGs,284 genes were up-regulated and 78 genes were down-regulated.The results of Gene Onotology(GO)term analysis showed that DEGs in diabetic nephropathy(DN)were mainly enriched in cell surface receptor signaling pathway,receptor binding,etc.The main enriched Kyoto Encyclopedia of Genes and Genomes(KEGG)pathways included phosphatidylinositol 3-kinase(PI3K)/protein kinase B(PKB/AKT)signaling pathway,extracellular matrix(ECM)-receptor interaction,etc.Sixty-four hub genes were refined through the intersection of WGCNA and PPI hub genes,and the hub genes with significantly increased or decreased expression were sifted.The hub genes were annotated with KEGG again,and it was found that most of the hub genes were enriched in"ECM-receptor interaction"and"PI3K/AKT signaling pathway".The PI3K/AKT/mTOR signaling pathway is a classic autophagy pathway,and COMP was absolutely overexpressed(logFC>2)in the 64 hub genes,suggesting that it may affect autophagy through this pathway.Western blotting showed that compared with the mannitol control group and the low glucose group,the expression of COMP in podocytes was significantly increased under high glucose stimulation.Compared with the control group,the expression of LC3-Ⅱ in the high glucose group was significantly decreased,indicating that the autophagy initiation of podocytes was inhibited under the high glucose environment.Compared with the negative control,the expression of LC3-Ⅱ in renal podocytes of mice with knockdown of COMP was significantly increased,and the mTOR decreased with the decrease of the expression of COMP,indicating that inhibiting COMP contributed to the recovery of autophagy in podocytes.Conclusion·COMP is highly expressed in DN patients and highly enriched in ECM receptor and PI3K/AKT signaling pathway.Autophagy in mouse renal podocytes is inhibited under high glucose conditions,and the high expression of COMP induced by high glucose may be a key factor in autophagy inhibition.Inhibiting COMP helps to restore autophagy in mouse renal podocytes.

Objective To investigate the regulatory effect of KHSRP on progression of gastric adenocarcinoma and the role of the JAK1/STAT3 signaling axis in mediating its effect.Methods KHSRP mRNA expression level was detected using qRT-PCR in 120 pairs of gastric adenocarcinoma and adjacent tissues,4 gastric adenocarcinoma cell lines(MKN-28,HGC-27,CRL-5822,and SNU-1)and normal human gastric mucosal GES-1 cells.In HGC-27 cells with KHSRP knockdown and SNU-1 cells with KHSRP overexpression,cell proliferation,migration,invasion and expression levels of JAK/STAT were evaluated using CCK-8 assay,Transwell migration and invasion assays,and Western blotting.In BALB/c-nude mice,HGC-27 cells with KHSRP knockdown and SNU-1 cells overexpressing KHSRP were injected either subcutaneous or via the tail vein to observe subcutaneous xenograft growth and lung metastasis of the tumor cells.Results Gastric adenocarcinoma tissues and cell lines all showed significantly increased KHSRP expression as compared with the adjacent tissues and GES-1 cells.In HGC-27 cells,KHSRP knockdown significantly inhibited cell proliferation,migration and invasion,while KHSRP overexpression enhanced the malignant behaviors of SNU-1 cells.In nude mice,inoculation of HGC-27 cells with KHSRP knockdown resulted in smaller tumor volume and weight,slower cell proliferation rate and fewer lung metastatic foci,and KHSRP-overexpressing SNU-1 cells produced the opposite results.KHSRP knockdown in HGC-27 cells significantly down-regulated the expression levels of JAK1 and STAT3,which were obviously increased in KHSRP-overexpressing SNU-1 cells.Conclusion High expressions of KHSRP promote progression and metastasis of gastric adenocarcinoma possibly by regulating the JAK1/STAT3 signaling axis.

In the central nervous system,CX3CL1 is a transmembrane chemokine expressed on neurons,and its specific receptor CX3CR1 is located on microglia.The combination of CX3CL1 and CX3CR1 is regarded as the bond of interaction between neurons and microglia.Bidirectional communication between microglia and neurons is essential for maintaining brain homeostasis and overcoming neuroinflammation,which is thought to play an important role in neurode-generative and cerebrovascular diseases.This article reviews the mechanisms of CX3CL1/CX3CR1 signaling pathway in the proliferation,metabolism,activation,polarization and regulation of synaptic plasticity of microglia,and uses this sig-naling pathway as a target to regulate the role of microglia in the disease process,which may provide a new target for the treatment of inflammation-related diseases.

Objective:To investigate the status and influencing factors of different types of cognitive frailty in aged inpatients with hypertension.Methods:Totally 300 aged patients with hypertension admitted to the Cardiology, Geriatrics, and Endocrinology Departments of Xuanwu Hospital, Capital Medical University, from April to October 2022 were selected by convenience sampling. Data were collected using a general information questionnaire, the Fried Frailty Phenotype (FP), the Mini-Mental State Examination (MMSE), the 9-item Subjective Cognitive Decline Questionnaire-9 (SCD-Q9), the Morisky Medication Adherence Scale (MMAS), the Pittsburgh Sleep Quality Index (PSQI), the Hospital Anxiety and Depression Scale (HADS), the Social Support Rating Scale (SSRS), and the Mini Nutritional Assessment (MNA) .Results:A total of 300 questionnaires were distributed and returned, yielding a 100.00% response rate. Among the 300 aged hypertensive patients, 74 were diagnosed with reversible cognitive frailty (RCF) and 98 with potentially reversible cognitive frailty (PRCF). Logistic vegression analysis showed that, factors influencing RCF included daily exercise habits and the use of thiazide diuretics ( P<0.05) ; factors influencing PRCF included age, pre-retirement occupation, daily exercise habits, sleep quality, Barthel Index score, and serum albumin levels ( P<0.05) . Conclusions:The status of both RCF and PRCF is relatively high among aged inpatients with hypertension. The influencing factors for different types of cognitive frailty vary. Targeted interventions based on both common and specific influencing factors should be developed to reverse or slow the progression of cognitive frailty in aged hypertensive patients.