Osteoporosis （OP） is a metabolic disorder characterized by microstructural deterioration of bone and increased bone fragility due to reduced bone mass， which can cause the development of bone-related diseases. This condition imposes significant economic and psychological burdens on patients. While modern medicine has extensively researched the pathogenesis of OP， it remains incompletely understood. Current clinical management primarily relies on anti-resorptive drugs and synthetic metabolic agents. However， long-term use of some medications may yield suboptimal therapeutic outcomes and lead to severe adverse reactions. Given the necessity for prolonged or lifelong treatment for OP， there is a critical need to identify highly effective， safe， and cost-effective pharmaceutical interventions. In light of evolving disease management paradigms and recent advancements in OP research， traditional Chinese medicine has demonstrated emerging advantages in addressing this condition. Through literature review， this study delves into the pathogenesis of OP from five perspectives： hormonal dysregulation， autophagy， ferroptosis， oxidative stress， and intestinal flora alteration. Furthermore， it summarizes the therapeutic efficacy and specific mechanisms of traditional Chinese medicine monomers and compound formulas against OP through regulating hormone levels， interfering with autophagy， inhibiting ferroptosis， counteract oxidative stress，and maintain intestinal flora balance. These multifaceted insights are expected to provide theoretical reference and guide future clinical traditional Chinese medicine approaches for preventing and managing OP.

Trophoblast cell surface antigen 2 (Trop2) is a glycoprotein that is barely expressed in normal tissues but highly expressed in malignant tumors; it is remarkably associated with poor prognosis. Various targeted therapeutics against Trop2, such as anti-Trop2 antibodies and antibody-drug conjugate drugs targeting Trop2, have been developed, and some therapeutics have been approved or are in clinical trials for cancer treatment. In this review, we comprehensively discuss the gene structure, mechanism of action, clinical research, drug development, and other aspects of Trop2 to provide references for the clinical development of effective and safe Trop2-targeting drugs.

Reactive astrocytes, which exhibit a correlation with the degeneration of dopaminergic neurons, are present in a considerable number during the progression of Parkinson's disease (PD). However, the underlying factors shaping astrocyte reactivity and neuroinflammation in PD remain inadequately elucidated. Here, we demonstrate that fibroblast growth factor 7 (FGF7)/FGF receptor 2 (FGFR2) autocrine signaling intensifies astrocyte reactivity and inflammation. Genetic deletion of Arrb2, β-Arrestin2 encoding gene, led to escalated astrocyte reactivity in MPTP-treated mice, which was further substantiated in astrocyte-specific Arrb2 knockdown mice. RNA sequencing profiling of Arrb2 knockout astrocytes identified Fgf7 as a critical effector of astrocyte reactivity. Subsequently, conditional knockdown of Fgf7 and its receptor Fgfr2 in astrocytes elicited advantageous effects for MPTP-treated mice by restraining the inflammatory phenotypic transition of reactive astrocytes. Furthermore, deletion of astrocytic Fgf7 mitigated MPTP-induced pathology in Arrb2 knockout mice. Mechanistically, STAT1 was distinguished as the transcription factor suppressing Fgf7 expression, while β-Arrestin2 counteracted the proteasomal degradation of STAT1 by binding to RNF220, an E3 ubiquitin ligase for STAT1. More importantly, selectively engaging dopamine D2 receptor (Drd2)/β-Arrestin2-biased signaling using the agonist UNC9995 exhibited therapeutic potential in MPTP-treated mice via moderation of astrocytic FGF7 production, thereby restoring balance in astrocyte reactivity. Collectively, our study bridges a crucial knowledge gap by elucidating the novel functions of FGF family members within the central nervous system, particularly within the context of PD. The autocrine signaling of FGF7/FGFR2 represents a novel mechanism and a potential druggable target for modulating astrocyte-derived inflammation.

Ovulatory dysfunction (OD) is one of the main causes of infertility in women of childbearing age, which not only affects their reproductive ability, but also physical and mental health. Traditional treatment strategies have limited efficacies, and the emergence of biomedicines provides a promising alternative solution via the strategies of combining engineered design with modern advanced technology. This review explores the pathophysiological characteristics and related induction mechanisms of OD, and evaluates the current cutting-edge advances in its treatments. It emphasizes the potentials of biomedicines strategies such as hydrogels, nanoparticles and extracellular vesicles in improving therapeutic precision and efficacy. By mimicking natural physiological processes, and achieving controlled drug release, these advanced drug carriers are expected to address the challenges in ovarian microenvironment reprogramming, tissue repair, and metabolic and immune regulation. Despite the promising progress, there are still challenges in terms of biomedical complexity, differences between animal models and human physiology, and the demand for intelligent drug carriers in the therapy of OD. Future researches are mainly dedicated to developing precise personalized biomedicines in OD therapy through interdisciplinary collaboration, promoting the development of reproductive regenerative medicine.

With the increasing proportion of human papilloma virus(HPV)infection in the pathogenic factors of oro-pharyngeal cancer,a series of changes have occurred in the surgical treatment.While the treatment mode has been im-proved,there are still many problems,including the inconsistency between diagnosis and treatment modes,the lack of popularization of reconstruction technology,the imperfect post-treatment rehabilitation system,and the lack of effective preventive measures.Especially in terms of treatment mode for early oropharyngeal cancer,there is no unified conclu-sion whether it is surgery alone or radiotherapy alone,and whether robotic minimally invasive surgery has better func-tional protection than radiotherapy.For advanced oropharyngeal cancer,there is greater controversy over the treatment mode.It is still unclear whether to adopt a non-surgical treatment mode of synchronous chemoradiotherapy or induction chemotherapy combined with synchronous chemoradiotherapy,or a treatment mode of surgery combined with postopera-tive chemoradiotherapy.In order to standardize the surgical treatment of oropharyngeal cancer in China and clarify the indications for surgical treatment of oropharyngeal cancer,this expert consensus,based on the characteristics and treat-ment status of oropharyngeal cancer in China and combined with the international latest theories and practices,forms consensus opinions in multiple aspects of preoperative evaluation,surgical indication determination,primary tumor re-section,neck lymph node dissection,postoperative defect repair,postoperative complication management prognosis and follow-up of oropharyngeal cancer patients.The key points include:① Before the treatment of oropharyngeal cancer,the expression of P16 protein should be detected to clarify HPV status;② Perform enhanced magnetic resonance imaging of the maxillofacial region before surgery to evaluate the invasion of oropharyngeal cancer and guide precise surgical resec-tion of oropharyngeal cancer.Evaluating mouth opening and airway status is crucial for surgical approach decisions and postoperative risk prediction;③ For oropharyngeal cancer patients who have to undergo major surgery and cannot eat for one to two months,it is recommended to undergo percutaneous endoscopic gastrostomy before surgery to effectively improve their nutritional intake during treatment;④ Early-stage oropharyngeal cancer patients may opt for either sur-gery alone or radiation therapy alone.For intermediate and advanced stages,HPV-related oropharyngeal cancer general-ly prioritizes radiation therapy,with concurrent chemotherapy considered based on tumor staging.Surgical treatment is recommended as the first choice for HPV unrelated oropharyngeal squamous cell carcinoma(including primary and re-current)and recurrent HPV related oropharyngeal squamous cell carcinoma after radiotherapy and chemotherapy;⑤ For primary exogenous T1-2 oropharyngeal cancer,direct surgery through the oral approach or da Vinci robotic sur-gery is preferred.For T3-4 patients with advanced oropharyngeal cancer,it is recommended to use temporary mandibu-lectomy approach and lateral pharyngotomy approach for surgery as appropriate;⑥ For cT1-2N0 oropharyngeal cancer patients with tumor invasion depth＞3 mm and cT3-4N0 HPV unrelated oropharyngeal cancer patients,selective neck dissection of levels ⅠB to Ⅳ is recommended.For cN+HPV unrelated oropharyngeal cancer patients,therapeutic neck dissection in regions Ⅰ-Ⅴ is advised;⑦ If PET-CT scan at 12 or more weeks after completion of radiation shows intense FDG uptake in any node,or imaging suggests continuous enlargement of lymph nodes,the patient should undergo neck dissection;⑧ For patients with suspected extracapsular invasion preoperatively,lymph node dissection should include removal of surrounding muscle and adipose connective tissue;⑨ The reconstruction of oropharyngeal cancer defects should follow the principle of reconstruction steps,with priority given to adjacent flaps,followed by distal pedicled flaps,and finally free flaps.The anterolateral thigh flap with abundant tissue can be used as the preferred flap for large-scale postoperative defects.

Objective:To study the differential gene expression and immune cell infiltration of gout patients,to find the key genes and immune cells of gout pathogenesis,and to explore the relationship between immune cells and gout.Methods:The gout chip GSE160170 was downloaded from the GEO database,and the differential gene expression analysis was carried out with the help of R language.Then,the STRING database was used to analyze the differential gene,and the Cytoscape software was used to screen the key genes,and then carry out enrichment analysis.At the same time,the infiltration of immune cells were analyzed.Results:The study found that IL-6,IL-1β,TNF,CCL3,CXCL8 and CXCL1 were key genes in the pathogenesis of gout,which were mainly exerted by IL-17,Toll-like receptor,NOD-like receptor,NF-κB and other signaling pathways.Processes such as cellular responses to lipo-polysaccharides,bacteria-derived molecules,and biological stimuli lead to disease;immune infiltration results indicate that memory B cells,activated NK cells,activated dendritic cells,activated mast cells and eosinophils were involved in the disease.It was signifi-cantly expressed in gout patients;the correlation analysis between immune cells showed that the expression of follicular helper T cells were positively correlated with the expression of activated mast cells,and the expression of unactivated NK cells and monocyte were negatively correlated.Conclusion:Key genes and differentially expressed immune cells are closely related to the pathogenesis of gout,providing new ideas for the study of the molecular mechanism of gout.

Objective:To explore the clinical characteristics and prognosis of children with chronic myeloid leukemia in the blast phase (CML-BP) .Methods:The clinical characteristics, treatment measures, and survival outcomes of 28 children with CML-BP were analyzed in our hospital from January 2008 to November 2022.Results:The male to female ratio of the 28 children with CML-BP was 1.15∶1. The median age of diagnosis of CML-BP was 10 years, and the median follow-up time was 79 months. During the diagnosis of CML, four children were in the BP, one was in the accelerated phase (AP) and 23 children were in the chronic phase (CP). Among the 23 children with CML-CP, 75% had progressed directly from CP to BP without experiencing the AP. Among the children diagnosed with CML-BP, 71.4% were classified as chronic myeloid leukemia lymphoid blast phase (CML-LBP), 25.0% belonged to the chronic myeloid leukemia myeloid blast phase (CML-MBP), and 3.6% belonged to the chronic myeloid leukemia mixed phenotype acute leukemia (CML-MPAL). Treatment with hemaopoietic stem cell transplantation (HSCT) after tyosine kinase inhibitor (TKI) combined with chemotherapy was administered to 19 children, two children received HSCT after TKI alone, and seven children received TKI combined with chemotherapy but without HSCT. The 5-year overall survival of the 28 children with CML-BP was 59.3%.Conclusion:The direct progression of BP from CP is greater in children with CML-BP compared with adults, and the overall prognosis of children with CML-BP is poor.

Objective To observe the expression of GLIS3 in triple negative breast cancer(TNBC)and analyze its relationship with the prognosis of TNBC patients.Methods Bioinformatic analysis was applied to analyze the expression level of GLIS3 in Gene Expression Omnibus(GEO).Kaplan-Meier survival curve was plotted to evaluate the impact of GLIS3 expression on the survival rate of patients based on DNA chip data.A total of 125 patients pathologically diagnosed as TNBC in the Fourth Hospital of Hebei Medical University from January to December 2014 were enrolled by cluster random sampling.Among them,53 patients had complete tissue specimens,medical records and follow-up data.Immunohistochemical assay was used to detect the expression of GLIS3 in TNBC and adjacent tissues to tumors,while the relationships between GLIS3 protein expression in breast cancer tissues and clinicopathological parameters such as age,menstrual status,tumor size,clinical stage,histological grade,pathological type,axillary lymph node metastasis,vascular tumor thrombus,and expression of TP53 and Ki-67 were analyzed.Kaplan-Meier survival curve was plotted to analyze the effect of GLIS3 on the overall and disease-free survival of TNBC patients.Cox regression model was established to identify the risk factors impacting the prognosis of the patients.Results Analysis of GEO data showed that the expression of GLIS3 in TNBC was significantly higher than that in paracancer tissues(P＜0.05).The expression of GLIS3 was notably higher in the TNBC tissue than the adjacent tissue to tumor(P＜0.05).A marked augmentation of GLIS3 expression was observed in both the advanced and larger-sized tumors(P＜0.05).Univariate analysis of Cox regression model revealed that lymph node metastasis,TNM stage and GLIS3 expression were all related to disease-free survival of TNBC patients(P＜0.05).Univariate and multivariate analyses displayed that TNM stage was related to the overall survival of TNBC patients(P＜0.05).The patients with high expression of GLIS3 had significant shorter disease-free survival time than those with low expression(P＜0.05),but had no statistical difference in overall survival(P＞0.05).Conclusion GLIS3 protein is highly expressed in TNBC tissues,and tumor size and TNM stage are correlated with its high expression.The high expression of GLIS3 suggests that the patients have poor prognosis and low disease-free survival rate.

Objective:To analyze the activity of lithium chloride (LiCl) against influenza virus A (H3N2) in human non-small cell lung cancer cells (A549).Methods:Different concentrations of LiCl were incubated with A549 cells, and the cytopathic effect (CPE) was observed after 24 hours, and the effect of LiCl on cell activity was determined by CCK-8 method. After H3N2 (MOI=1) infected A549 cells, different concentrations of LiCl were added and incubated for 24 hours, and the viral load was measured by real time/reverse transcription quantitative polymerase chain reaction (RT-qPCR), and the CPE was observed, and the viral titer was determined. Different concentrations of LiCl were incubated with A549 at 37 ℃ and 5% CO 2 for 2 hours, virus was added and incubated for 24 hours, and the viral load was determined by RT-qPCR. LiCl, H3N2 and A549 were incubated at 4 ℃ for 1 hour, 35 ℃, 5% CO 2 for 24 hours, and viral load was determined by RT-qPCR. H3N2 and A549 were incubated at 4 ℃for 1 hour, then different concentrations of LiCl were added, incubated at 35 ℃ with 5% CO 2 for 24 hours, and the viral load was determined by RT-qPCR. After H3N2 infected A549 cells, different concentrations of LiCl were added and incubated for 24 hours, and the viral RNA load and viral titer of the supernatant and cells were measured, respectively, and then the corresponding ratios of the supernatant and the cells were calculated. After H3N2 (MOI=10) and BV (MOI=1) infected A549 cells, different concentrations of LiCl were added for 24 h, and the viral load was determined by RT-qPCR. Results:When the concentration of LiCl was<50 mmol/L, the cell viability of A549>90%. Different concentrations of LiCl could significantly reduce the viral load of H3N2 ( P<0.000 1), and the CPE of the LiCl treatment group was more dose-dependent than that of the control group. LiCl did not inhibit viral replication by affecting the cell itself; Different concentrations of LiCl significantly inhibited the entry of H3N2 into A549 ( P<0.000 1), and also had a certain inhibitory effect on the adsorption of A549 cells ( P<0.1). LiCl did not affect the assembly and release of H3N2 ( P>0.05), and it was also found that LiCl had a broad spectrum of antiviral effects against multiple influenza virus strains ( P<0.000 1). Conclusions:LiCl may exert antiviral effect by inhibiting the adsorption and entry of H3N2 into A549 cells and the replication of H3N2 in A549 cells, which provides a data reference for the prevention and treatment of viral infection by LiCl.

Objective To clarify the changes in CXCL5 in serum and gastric tissues of patients with chronic atrophic gastritis(CAG)and precancerous lesions of gastric cancer(PLGC)and to investigate the predictive value of CXCL5 for the diagnosis of CAG and PLGC.Methods This study enrolled 72 participants of CAG admitted to the Department of Splenology and Gastroenterology of the Second Affiliated Hospital of Anhui University of Chinese Medicine from June 2022 to June 2023,with gastroscopy and pathologically confirmed diagnosis,as well as 68 healthy participants who underwent gastroscopy in the same period at our department.We collected clinical information and laboratory results from all participants.The logistic regression analysis methods were used to identify the diagnostic value of serum CXCL5.Furthermore,in order to clarify the role of CXCL5 in the developent of CAG,a total of 15 patients each with CAG,intestinal metaplasia,and dysplasia treated at our hospital from June 2023 to December 2023,and 15 healthy participants were selected.The relationship between the expression of CXCL5 and the degree of clinicopathology was analysed in each group using ELISA,PCR,and immunohistochemistry staining to validate and assess the diagnostic efficacy of CXCL5.Results The study found that several factors were associated with CAG,including family history of tumours,smoking and alcohol consumption history,dietary regularity,Helicobacter pylori infection,the number of lesions,gastric function scores and CXCL5(P<0.05).The ROC curve had an AUC of 1.00 and a Youden index of 0.986,indicating excellent predictive ability.The ELISA results indicated a significantly higher serum CXCL5 expression level in the CAG,intestinal metaplasia,and dysplasia groups compared to the normal group.There was a positive correlation between the serum CXCL5 expression level and the degree of pathology.The PCR and immunohistochemistry staining results indicate that the mRNA and pro-tein expression levels of CXCL5 in gastric tissues of patient groups were significantly higher compared to the nor-mal group.Furthermore,the mRNA and protein expression levels of CXCL5 in gastric tissues were positively correlated with the degree of pathology.Conclusions The results indicate that CXCL5 is highly expressed in the serum and gastric tissues of patients with CAG and PLGC,and its expression level is positively correlated with the degree of pathology.Therefore,CXCL5 could serve as a predictive indicator and a potential therapeutic target for the diagnosis of CAG and PLGC.