Osteoarthritis (OA), a highly prevalent degenerative joint disease worldwide, is defined by articular cartilage degradation, abnormal bone remodeling, and persistent chronic inflammation. It severely compromises patients’ quality of life, and currently, there is no radical cure. Abnormal mechanical stress is widely regarded as a core driver of OA pathogenesis, and the exploration of mechanical signal perception and transduction mechanisms has become crucial for deciphering OA’s pathophysiological processes. Piezo1, a key mechanosensitive cation channel belonging to the Piezo protein family, has recently gained significant attention due to its pivotal role in mediating cellular responses to mechanical stimuli in joint tissues. This review systematically examines Piezo1’s expression patterns, regulatory mechanisms, and pathological functions in OA, with a particular focus on its dual roles in modulating chondrocyte homeostasis and bone metabolism disorders, while also delving into the underlying molecular signaling pathways and potential therapeutic implications. Piezo1, consisting of approximately 2 500 amino acids and forming a unique trimeric propeller-like structure, is widely expressed in chondrocytes, osteocytes, mesenchymal stem cells, and synovial cells. It exhibits permeability to cations such as Ca²⁺, K⁺, and Na⁺, and directly responds to membrane tension changes induced by mechanical stimuli like fluid shear stress and mechanical overload. In OA patients and animal models, Piezo1 expression is significantly upregulated, especially in cartilage regions subjected to abnormal mechanical stress (e.g., human temporomandibular joint cartilage). This overexpression is closely associated with aggravated cartilage degeneration, increased chondrocyte apoptosis, accelerated cellular senescence, and intensified inflammatory responses. Mechanical overload and pro-inflammatory cytokines (e.g., IL-1β) are key inducers of Piezo1 upregulation: IL-1β activates the PI3K/AKT/mTOR signaling pathway to enhance Piezo1 expression, forming a pathogenic positive feedback loop that inhibits chondrocyte autophagy, promotes apoptosis, and further accelerates joint degeneration. Mechanistically, Piezo1 mediates OA progression through multiple interconnected pathways. When activated by mechanical stress, Piezo1 triggers excessive Ca²⁺ influx, leading to endoplasmic reticulum stress (ERS) and mitochondrial dysfunction, which directly induce chondrocyte apoptosis. This process involves the activation of downstream signaling cascades such as cGAS-STING and YAP-MMP13/ADAMTS5. YAP, a transcriptional regulator, upregulates the expression of matrix metalloproteinase 13 (MMP13) and aggrecanase (ADAMTS5), thereby accelerating cartilage matrix degradation. Additionally, Piezo1-driven Ca²⁺ overload promotes the accumulation of reactive oxygen species (ROS) and upregulates senescence markers (p16 and p21), accelerating chondrocyte senescence via the p38MAPK and NF-κB pathways. Senescent chondrocytes secrete senescence-associated secretory phenotype (SASP) factors (e.g., IL-6, IL-1β), further amplifying joint inflammation. In terms of bone metabolism, Piezo1 maintains joint homeostasis by promoting the differentiation of fibrocartilage stem cells into chondrocytes and balancing bone formation and resorption through regulating the FoxC1/YAP axis and RANKL/OPG ratio. Therapeutically, targeting Piezo1 shows promising potential. Preclinical studies have demonstrated that Piezo1 inhibitors (e.g., GsMTx4) can reduce joint damage and alleviate pain in OA mice. Simultaneously, siRNA-mediated co-silencing of Piezo1 and TRPV4 (another mechanosensitive channel) decreases intracellular Ca²⁺ concentration, inhibits chondrocyte apoptosis, and promotes cartilage repair. Conditional knockout of Piezo1 using Gdf5-Cre transgenic mice alleviates cartilage degeneration in post-traumatic OA models by downregulating MMP13 and ADAMTS5 expression. Despite existing challenges, such as off-target effects of inhibitors, inefficient local drug delivery, and interindividual genetic variability, strategies like developing selective Piezo1 antagonists, optimizing targeted nanocarriers, and combining Piezo1-targeted therapy with physical therapy provide viable avenues for clinical translation. The authors propose that Piezo1 serves as a critical therapeutic target for OA, and future research should focus on deciphering its context-dependent regulatory networks, developing tissue-specific intervention strategies, and validating their efficacy and safety in clinical trials to address the unmet medical needs of OA patients.

Objective To systematically evaluate the risk prediction models for acute kidney injury in patients with acute coronary syndrome (ACS) based on machine learning, providing a reference for clinical selection of appropriate risk assessment tools. Methods Clinical studies using machine learning methods for predicting the risk of acute kidney injury in ACS patients were retrieved from PubMed, Cochrane Library, Embase, Web of Science core database, CNKI, Wanfang Database, CBM, and VIP. The retrieval time was from the establishment of the database to May 24, 2025. The quality of the models were evaluated using the prediction model risk of bias assessment tool. Results Nine articles were included, and a total of 58 prediction models were constructed using 20 machine learning methods. The area under the receiver operating characteristic curve ranged from 0.733 to 0.894. The most commonly used predictors were age and creatinine. The overall bias risk of the included studies was relatively high, but the applicability was good.Conclusion Machine learning models can identify the risk of acute kidney injury in ACS patients. All models have good predictive potential, but they are still in the development stage. It is recommended that future studies adopt prospective design with external validation to improve the stability and predictive accuracy of the models.

The essential public health services is an important component of China's health risk governance system.It possesses both institutional and emotional attributes and addresses potential risk factors in health risk governance by forming a rational pathway and an emotional pathway:essential public health services guide-trust in government enhancement-improve health risk governance capacity.The rational pathway strengthens calculative trust through institutional reinforcement mechanisms,fostering the public's cognitive trust in government departments.The emotional pathway follows the principle of satisfaction,strengthening non-calculative trust through emotional communication and cultivating the public's emotional trust in government departments.By reinforcing both cognitive and emotional trust among the public,essential public health services improved the level of health information reserves and the guidance of medical service order,thereby improving health risk governance capacity.

OBJECTIVE To explore the risk factors for hospital-associated infections(HAI)in dead patients so as to provide bases for development of prevention strategies for the hospital-associated infections.METHODS Totally 560 patients who died due to non-SARS-CoV-2 infections and hospitalized in Gansu Provincial People's Hospital for more than 48 hours in 2019 and 2023 were retrospectively analyzed,70 of whom had HAI and were assigned as the HAI group,and the rest of 490 patients were assigned as the non-HAI group.The incidence of HAI,major causes of death,risk factors and economic burden were observed.RESULTS The incidence of HAI was 12.50％a-mong the dead patients,the lower respiratory tract infection was the predominant type of infection,and the re-spiratory failure was the primary and direct cause of death in the HAI group;the total treatment cost of the HAI group was higher than that of the non-HAI group(P＜0.05).Univariate analysis showed that there were signifi-cant differences in the length of hospital stay,multidrug-resistant organisms infections,combined use of antibiot-ics,surgery,hemodialysis/peritoneal dialysis,invasive procedures(drainage,puncture,intubation,tracheoto-my),use of equipment like ventilator or urinary catheter,central venous catheter indwelling,blood transfusion,and use of immunosuppressors/glucocorticoids between the HAI group and the non-HAI group(P＜0.05),while there were no significant differences in the sex,age,underlying diseases,modified early warning score(MEWS)and major diagnosis and chemoradiotherapy between the two groups.Multivariate analysis indicated that the length of hospital stay more than 14 days,history of surgery and combined use of antibiotics were the risk factors for HAI in the dead patients(P＜0.05).CONCLUSION It is necessary for the hospital to identify the high-risk pa-tients as early as possible,pay close attention to the lower respiratory tract infection,reduce the risk of HAI by shortening the length of hospital stay,standardizing the invasive procedures and reasonably using antibiotics so as to improve the prognosis of the patients.

In recent decades,the incidence of human papillomavirus(HPV)-associated oropharyngeal squamous cell carcinoma(OPSCC)has shown a marked increase.Significant changes have also occurred in the OPSCC diagnosis and treatment paradigm.Deter-mining HPV status prior to treatment is now essential,and radiotherapy/chemotherapy,immunotherapy,and minimally invasive surgical techniques have progressively emerged as key modalities for managing OPSCC.However,alongside these paradigm shifts,a comprehen-sive technical consensus guiding the entire diagnostic and therapeutic process for OPSCC patients is currently lacking.Given China's large population base and the rising incidence of OPSCC,an expert panel convened to develop a clinical technical consensus on OPSCC diagno-sis and management tailored to China's specific context.This consensus aims to further enhance and standardize understanding of OPSCC management techniques among relevant healthcare professionals.

A recombinant adenovirus(rAd)for expression of Mycobacterium tuberculosis(M.tb)c-di-AMP phosphodiesterase CnpB was constructed,and its induced humoral immune response was detected.The codon-optimized gene of M.tb CnpB was cloned into the adenoviral plasmid pcADV.The recombinant plasmid pcADV-CnpB was transfected into HEK293T cells,and expression was detected with Western blot.The recombinant plasmid pcADV-CnpB and the backbone plasmid were co-transfected into HEK293T cells to obtain the recombinant adenovirus rAd-CnpB.rAd-CnpB was amplified in HEK293T cells,and the target protein expression of rAd-CnpB was detected with Western blot and immunofluorescence.Mice were immunized with rAd-CnpB intranasally,and their sera and bronchoalveolar lavage fluid(BALF)were collected.ELISA was used to detect levels of antigen-specific antibodies.Restriction enzyme digestion and sequencing indicated that the recombinant plasmid pcADV-CnpB was successfully constructed and led to protein expression in eukaryotic cells.rAd-CnpB was packaged and produced in HEK293T cells.After amplification and purification,rAd-CnpB with a titer of 5.53×1010 PFU/mL was obtained.rAd-CnpB led to CnpB expression in HEK293T cells.Intranasal immunization with rAd-CnpB increased levels of IgG and secretory IgA in BALF and led to high levels of IgG in sera.rAd-CnpB,the recombinant adenovirus for expression of c-di-AMP phosphodiesterase CnpB was successfully constructed,and was found to induce antigen-specific humoral and mucosal immune responses through mucosal immunization.Thus,rAd-CnpB may be used in further research on new TB vaccine strategies.

This study was aimed at investigating the presence of Helicobacter hepaticus(Hh)infection in patients with digestive tract diseases and evaluating Helicobacter pylori(Hp)infection status in patients with digestive tract cancers other than gastric cancer.Fecal samples were collected from 197 patients with digestive tract diseases at the Affiliated Cancer Hospital of Guizhou Medical Uni-versity and from 149 healthy volunteers residing in Guiyang.Hp stool antigen(HpSA)was detected with the colloidal gold method.Af-ter the extraction of fecal DNA,the Hp specific ureA gene and the Hh specific 16S rRNA gene were amplified via nested PCR,and the amplified products were subsequently confirmed through sequencing analysis.The study included 197 patients with digestive system diseases,comprising 135 cases of colorectal cancer,32 cases of chronic gastritis,22 cases of gastric cancer,5 cases of liver cancer,and 3 cases of cholangiocarcinoma.The detection rate of HpSA was 31.5%(62/197).HpSA was detected across all five disease catego-ries,and the highest detection rate was observed in patients with gastric cancer,at 50.0%(11/22),or colorectal cancer,at 24.4%(33/135).The positivity rate of Hp ureA gene PCR was 7.6%(15/197),and sequencing confirmed that the amplified products were in-deed Hp ureA gene fragments.Notably,the highest detection rate was observed in patients with colorectal cancer,at 8.9%(12/135).The positivity rate of Hh 16S rRNA gene PCR was 11.2%(22/197),and sequencing confirmed that the amplified products were in-deed Hh 16S rRNA gene fragments.Hh 16S rRNAgene presence was detected in patients with all five diseases,and the highest detec-tion rate was observed in patients with colorectal cancer,at 11.1%(15/135).Among 149 healthy volunteers,the detection rate of HpSA was 11.4%(17/149),only one case tested positive for the Hp ureA gene,and the Hh 16S rRNA gene was undetectable in all samples.In conclusion,Hh infection was detected in patients with digestive tract diseases.Beyond patients with gastric cancer,the prevalence of Hp infection was also notably high among patients with colorectal cancer,liver cancer,and cholangiocarcinoma.Further investigation is warranted to elucidate the roles of the two species of Helicobacter in the occurrence and progression of digestive tract cancers.

Aim To explore the neuroprotective effects of salidroside on Parkinson's disease(PD)through modulation of inflammatory responses and the underly-ing mechanisms.Methods Mice were divided into five groups:healthy control group,1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP)disease group,low-dose Rhodioloside intervention group,medium-dose salidroside intervention group,and high-dose salidro-side intervention group.MPTP-induced PD mouse model was established,and salidroside intervention was administered.Behavioral changes,inflammatory cyto-kine levels,autophagy-related protein expression,and neurons were observed through histological analysis and immunohistochemical staining.Results After MPTP treatment,mice exhibited significant behavioral chan-ges,increased pro-inflammatory cytokines,decreased anti-inflammatory cytokines,reduced autophagy-related proteins,and evident pyroptosis.Salidroside interven-tion alleviated these changes in a dose-dependent man-ner.Conclusions Salidroside exerts neuroprotective effects on PD by alleviating inflammatory responses and promoting autophagy,thereby protecting neurons.

Objective To observe the association between afterschool physical exercise and sleep quality among preschool children,and to explore the proper afterschool physical exercise model for better sleep quality.Methods A cross-sectional study was conducted.From Apr to Jun 2024,a total of 1 430 children from three public kindergartens in Minhang district were enrolled to participate in the survey.Parents were invited to complete the basic sociodemographic information,afterschool physical exercise information and the Children's Sleep Habits Questionnaire.One-way ANOVA and linear mixed effects models were used to explore the relationship between afterschool exercise and sleep quality.Results A total of 1 430 questionnaires were sent out and 1 384 were recovered with a recovery rate of 96.78%.Among them 1 366 were valid,with an effective rate of 95.52%.The average age of the children was(5.19±0.87)years old with gender ration of 1.07∶1(male:female).The prevalence of poor sleep quality was 80.60%(regarding a CSHQ total score>41 as cutoff).A one-way ANOVA indicated that time on afterschool physical exercise was significantly associated with sleep duration,Night waking,and sleep onset delay(P<0.05).After adjusting for age,gender,the only child or not,main caregiver,and parental education and occupation,linear mixed effects models showed that engaging in afterschool physical activity for at least 180 mins per week has a statistically significant predictive effect on sleep duration scores(β=-0.50,z=-4.52,95%CI:-0.72,-0.28,P<0.001),night waking scores(β=-0.16,z=-2.34,95%CI:-0.29,-0.02,P=0.020),and sleep onset delay scores(β=-0.14,z=-2.35,95%CI:-0.26,-0.02,P=0.019).Conclusion Afterschool exercise was significantly associated with sleep quality among preschool children in Minhang district of Shanghai.The time≥180 min on afterschool exercise per week in preschool children was significantly positively associated with maintaining sleep duration,reducing night wakings and shortening the latency to fall asleep.The habit of afterschool exercise and the time on afterschool exercise should be emphasized by parents and the society to improve sleep quality among preschool children.

Fibroblast growth factor,as a critical protein regulating cell growth and differentiation,exhibits aberrant signaling closely associated with various pathological pathologies,including cancer.Among the members of the fibroblast growth factor family,fibroblast growth factor 9(FGF9)has been identified as a critical player in cancer initiation and progression.While numerous studies have investigated the molecular mechanisms of FGF9 individually,comprehensive reviews addressing its impact in cancer remain scarce.This article systematically reviews the functional mechanisms and regulatory networks of FGF9 in cancer,with a focus on its roles in common malignancies such as lung cancer,liver cancer,gastric cancer,colorectal cancer,breast cancer,and ovarian cancer.The aim is to facilitate translational research on FGF9 for targeted cancer diagnosis and therapy.