ObjectiveTo develop a community-family management model for older adults with mild cognitive impairment (MCI) and to formulate detailed application specifications, and to fully leverage the initiative of communities and families under limited resource conditions, for achieving community-based early detection and early intervention for older adults with MCI. MethodsA systematic literature review was conducted to identify pertinent publications. Corpus-based research methodologies were employed to extract, refine, integrate and synthesize management elements, thereby establishing the specific content and service processes for each stage of the management model. Utilizing the 5W2H analytical framework, essential elements such as management stakeholders, target populations, content and methods for each stage were delineated. The model and its application guidelines were finalized through expert consultation and demonstration. ResultsAn expert evaluation of the management model yielded mean scores of 4.84, 4.32 and 4.84 for acceptability, feasibility and systematicity, respectively. By integrating the identified core elements with expert ratings and feedback, the final iteration of the community-family management model for older adults with MCI was formulated. This model comprised of five stages: screening and identification, comprehensive assessment, intervention planning, monitoring and referral pathways to ensure implementation, and enhanced support for communities, family members and caregivers. Additionally, it included 18 specific application guidelines. ConclusionThe proposed management model may theoretically help delay cognitive decline, improve cognitive function and potentially promote reversal from MCI to normal cognition. It may also enhance the awareness and coping capacity of older adults and their families, strengthen community healthcare professionals' ability to early identify and manage MCI.

ObjectiveTo investigate the clinical characteristics and risk factors of Mycoplasma pneumoniae pneumonia （MPP） in children based on a dual classification integrating imaging features and clinical severity. MethodsMedical records of 2 054 pediatric patients with MPP were retrospectively analyzed. The cohort was stratified into severe consolidation （n=253）， severe non-consolidation （n=118）， non-severe consolidation （n=393）， and non-severe non-consolidation groups （n=1 290） based on clinical and radiological findings. Inter group data and characteristics were compared and multiple regression analysis was conducted to construct a prediction model for severe consolidation group. ResultsSignificant differences were observed among the groups in terms of age， duration of fever， length of hospital stay， presence of pulmonary rales， inflammatory markers ［C-reactive protein （CRP） and lactate dehydrogenase （LDH）］， the use of hormones， and bronchoscopic treatment （all P < 0.05）. Compared with the severe non-consolidation group， non-severe consolidation group， and non-severe non-consolidation group， children in severe consolidation group exhibited the longest duration of fever ［8 （6， 11） days vs 6 （2， 9）， 7 （6， 9） and 6 （3， 8） days， respectively］ and the longest length of hospital stay ［7 （5， 8） days vs 6 （5， 8）， 6 （5， 8） and 6 （4， 7） days， respectively］. They also had the highest incidence of reduced breath sounds ［34 cases （13.4%） vs 2 cases （1.7%）， 29 cases （7.4%） and 13 cases （1.0%）， respectively］ and a substantially higher rate of coinfections， particularly viral infections ［63 cases （24.9%） vs 23 cases （19.5%）， 60 cases （15.3%） and 190 cases （14.7%）， respectively］. Multivariate analysis indicated that the independent risk factors for severe MPP （SMPP） were age > 4.5 years， length of hospital stay > 6.5 days， reduced breath sounds， neutrophil-to-lymphocyte ratio （NLR） > 1.66， LDH > 370.5 U/L， CRP > 9.5 mg/L， and coinfection with viruses. Reduced breath sounds （OR = 5.58， 95% CI： 2.45 - 12.69） and coinfection with bacteria （OR = 3.11， 95% CI： 1.43 - 6.75） were identified as the most significant risk factors for pulmonary consolidation in non-severe MPP children. Additionally， reduced breath sounds， coinfection with viruses， LDH > 365.5 U/L， and CRP > 32.1 mg/L were risk factors for severe pneumonia in children with pulmonary consolidation. For non-consolidation MPP children， the presence of pulmonary dry rales （OR = 2.28， 95% CI： 1.46 - 3.56） was the primary independent risk factor for the development of severe pneumonia. ConclusionThe chest imaging findings of MPP are associated with clinical severity， and the risk factor model constructed based on this imaging-clinical classification can assist in achieving precise hierarchical diagnosis and treatment in clinical practice.

Objective To elucidate the changes in the gut microbiota and molecular mechanism of huaier in enhancing the efficacy of oxaliplatin (OXA) chemotherapy in gastric cancer (GC). Methods The effects of huaier on the gut microbiota structure and intestinal barrier function in MKN45-bearing mice were analyzed by using 16S rRNA sequencing, RT-qPCR, and IHC. UPLC-MS and network pharmacology, as well as in vivo experimental approaches, were employed to investigate the key bioactive constituents of huaier systematically and elucidate the underlying mechanisms by which huaier exerts therapeutic effects against GC. The expression of the PI3K/AKT/SREBP pathway was detected in cancer cells and tissues via Western blot analysis. The safety profile of huaier combined with OXA was verified through serum biochemistry and HE-stained tissue section analyses. Results Huaier inhibited the PI3K/AKT/SREBP pathway by increasing the abundance of Akkermansia muciniphila, reduced lipid droplet deposition, and ultimately enhanced the sensitivity to OXA in the treatment of GC. Conclusion This study demonstrates the value of huaier in gastric cancer treatment by enhancing chemosensitivity and provides novel insights into its systemic therapeutic effects through molecular mechanisms and gut microbiota modulation.

Yi and Gui,its physiological characteristics and pathological manifestations are closely related to the lumbar spine.The intervertebral disc,chamber of arthrosis,requires nourishment from qi and blood circulation,as well as support from liver and kidney functions to maintain its health.Chinese medicine master Shi Qi has based on the pathological manifestations of discogenic low back pain patients at different stages and followed the guidelines of the Visceral manifestation theory.Combining more than 60 years of experience in traditional Chinese medicine diagnosis and treatment,he has used external observations to infer internal conditions and examined causes to find solutions.By entering the body from the outside and focusing on the"Homology of Yi and Gui"as a benchmark,he emphasizes the distinctive characteristic of traditional Chinese medicine in medical treatment.He states that"visceral pattern is fundamental"and"qi-blood is first,"emphasizing the importance of treating liver and kidney together.This article aims to draw on the wisdom of Taishan to provide a bridge for colleagues.

Objective To investigate the association between gout-related gene polymorphisms and clinical phenotypic heterogeneity among gout patients in the Foshan region,thereby providing a scientific basis for stratified clinical management.Methods A total of 125 gout patients diagnosed at the Foshan Hospital of Traditional Chinese Medicine between June 2022 and May 2025 were enrolled in this study.The collected data included demo-graphic characteristics,frequency of gout attacks,presence of tophi,levels of uric acid,creatinine,C-reactive protein(CRP),erythrocyte sedimentation rate(ESR),gout-related genes(ABCG2,SLC2A9,SLC22A12,MTHFR),and joint ultrasound findings.Group comparisons and rank correlation analyses were conducted to explore potential associations between gene polymorphisms and clinical heterogeneity.Results The male-to-female ratio was 11∶1;the mean age was(35.28±2.67)years;the mean disease duration was(6.03±0.68)years;and the mean frequency of acute attacks in the past 12 months was 4(2.0,7.25).Genotype distributions were as follows:ABCG2:wild-type(C/C),23.8%;heterozygous(C/A),53.2%;homozygous(A/A),23%.SLC2A9:wild-type(A/A),24.6%;heterozygous(A/G),50%;homozygous(G/G),25.4%.SLC22A12:wild-type(A/A),4.8%;heterozygous(A/C),31.7%;homozygous(C/C),63.5%.MTHFR:wild-type(C/C),68.3%;heterozygous(C/T),28.6%;homozygous(T/T),3.2%.Rank correlation analysis revealed that SLC2A9 polymorphisms were significantly correlated with tophi formation(ρ=0.193,P=0.031)and crystal deposition on ultrasound(ρ=0.202,P=0.025).SLC22A12 polymorphisms were associated with hypertension(ρ=0.269,P=0.003)and diabetes(ρ=0.200,P=0.026).MTHFR polymorphisms showed a correlation with diabetes(ρ=0.224,P=0.012).Conclusions Polymorphisms in SLC2A9,SLC22A12,and MTHFR are significantly linked to clinical phenotypic heterogeneity among gout patients.Genetic testing could facilitate the early identification of individuals at high risk for complications and support the development of stratified and individualized treatment approaches.

Objective:To analyze the effect of emodin on apoptosis and oxidative damage of PC12 cells induced by hypoxia/re-oxygenation and its corresponding mechanism.Methods:PC12 cells were cultured in vitro and their neural differentiation was induced.Cells were divided into control group,model group,low concentration emodin group(30 mmol/L),high concentration emodin group(90 mmol/L)and high concentration emodin+GW441756(90 mmol/L+6.3 μmol/L)group,excepted for control group,other groups were treated with hypoxia and reoxygenation,and viability of PC12 cells was determined by CCK-8 method;levels of LDH release,SOD,MDA,IL-1β and TNF-α were measured by kits;PC12 cell apoptosis was detected by flow cytometry,expressions of nerve growth factor(NGF)/tropomyosin receptor kinase A(TrkA)pathway proteins in PC12 cells were determined by Western blot.Results:Compared with control group,PC12 cell activity,SOD level,NGF,and p-TrkA/TrkA in model group were decreased(P<0.05),while LDH release,apoptosis rate,MDA,IL-1β and TNF-α levels were increased(P<0.05);compared with model group,PC12 cell activity,SOD level,NGF,and p-TrkA/TrkA in low concentration emodin group and high concentration emodin group were increased(P<0.05),while LDH release,apoptosis rate,MDA,IL-1β and TNF-α levels were decreased(P<0.05);compared with high concen-tration emodin group,PC12 cell activity,SOD level,NGF,and p-TrkA/TrkA in high concentration emodin+GW441756 group were decreased(P<0.05),while LDH release,apoptosis rate,MDA,IL-1β and TNF-α levels were increased(P<0.05).Conclusion:Emodin can inhibit oxidative stress and inflammatory damage of PC12 cells induced by hypoxia/reoxygenation,and inhibit apoptosis by activating NGF/TrkA pathway.

Objective:To investigate the determinants of hospitalization costs for joint replacement surgeries in a tertiary public hospital in Beijing from 2011 to 2023.Methods:Structural variation degree,grey relational analysis,and multiple linear regression were applied to assess the impact of policy reforms and clinical factors.Results:Average hospitalization cost per visit decreased markedly in 2013,rose steadily to a peak in 2019,and then declined.Medical pricing policies significantly influenced both cost levels and structure.Material cost consistently showed the strongest association with total cost,while treatment cost became the second most influential factor after four rounds of price adjustments.Length of stay,number of secondary diagnoses,number of additional surgeries,number of procedures,and ICU admission had impact on the average hospitalization cost per visit,with statistical significance.Conclusion:Price adjustments for consumables and treatment services are the main drivers of average hospitalization costs for joint replacement surgeries.Further optimization of cost structures and medical service pricing is required to better reflect labor value,while the labor value is required to be promoted.The length of stay and operation amount have impact on the average hospitalization cost per visit.It is needed to focus on improving efficiency and care quality.

Objective To investigate the effect of transcutaneous auricular vagus nerve stimulation(taVNS)on quality of early postoperative recovery in patients undergoing thoracoscopic lung resection.Methods A total of 168 patients scheduled for elective thoracoscopic lung resection(wedge resection,segmentectomy,lobectomy)under general anesthesia were enrolled and randomly assigned to active-taVNS group(group T)or sham-taVNS group(group S)(n=84).Participants received four consecutive 30-minute sessions of active stimulation or sham stimulation at four time points:(1)the afternoon prior to the surgery,(2)the morning of the surgery,(3)following extubation,and(4)the first afternoon post-surgery.The Quality of Recovery-15(QoR-15)scores of the patients,the Numerical Rating Scale(NRS)scores at rest and during cough at 24,48,and 72 hours after surgery were recorded;and the usage of opioids within 48 hours after surgery was recorded;the duration of chest tube indwelling,incidence of severe pulmonary complications,postoperative hospital stay and adverse reactions to the stimulation(such as nausea and vomiting,fever,constipation,dizziness and itching)were observed.Results Compared with group S,group T exhibited significantly higher QoR-15 scores at 24,48,and 72 h postoperatively,lower NRS pain scores during resting and coughing,and reduced opioid consumption within 48 hours postoperatively(P<0.05).There were no significant differences between the two groups in the duration of chest tube indwelling,incidence of severe pulmonary complications,hospital stay,and the incidence of adverse reactions to the stimula-tion(P>0.05).Conclusion TaVNS can significantly improve quality of early postoperative recovery in patients undergoing thoracoscopic lung resection,and provide more effective postoperative analgesia without increasing the risk of postoperative complications.

FLASH radiotherapy is moving from animal experiments to clinical trials. However, the research on radiation shielding of FLASH radiotherapy rooms has been still in the initial stage. This paper analyses the structural characteristics of the beam pulse of FLASH radiotherapy devices of different technical routes, and discusses the radiation shielding challenges facing the radiotherapy room from FLASH radiotherapy technology based on the current protection standards for the radiotherapy room at home and abroad. The purpose is to provide input to the research on radiation protection of FLASH radiotherapy and to promote the clinical development of FLASH radiotherapy.

AIM:To investigate the role of NLR family CARD domain containing 3(NLRC3)in endothelial cells and evaluate its diagnostic value in coronary artery disease.METHODS:Twenty male ApoE-/-C57BL/6 mice,aged eight weeks,were randomly assigned into two groups:an experimental group and a control group,with each group com-prising ten mice.The experimental group was subjected to a high-fat diet for 8 weeks to induce atherosclerosis(AS),whereas the control group was maintained on a standard diet.The expression of NLRC3 in the aorta was evaluated using RT-qPCR and immunofluorescence techniques.Additionally,human umbilical vein endothelial cells(HUVECs)were ex-posed to interleukin-1β(IL-1β)to investigate the expression levels of NLRC3.Lentiviral vectors or plasmid vectors were employed to either overexpress or knock down NLRC3 in endothelial cells,and subsequently subjected to inflammation in-duced by IL-1β.The RT-qPCR and ELISA were employed to assess the impact of NLRC3 on inflammation in endothelial cells.Western blot and immunofluorescence techniques were utilized to investigate the modulation of the NF-κB signaling pathway in endothelial cells by NLRC3.Plasma NLRC3 levels in coronary artery disease patients and healthy controls were measured using ELISA,and its diagnostic potential was assessed through ROC curve analysis.RESULTS:In AS mice,distinct plaque lesions were observed in the aorta,accompanied by a significantly reduced expression of NLRC3 in the aortic arch relative to the control group.Expression of NLRC3 exhibited a significant down-regulation in IL-1β-stimu-lated HUVECs,demonstrating both time-dependent and dose-dependent effects(P<0.01).Overexpression of NLRC3 markedly suppressed the levels of IL-6,IL-8,monocyte chemoatbactant protein-1(MCP-1),p-p65,and p-IκBα in endo-thelial cells stimulated with IL-1β(P<0.01).Conversely,knockdown of NLRC3 resulted in elevated levels of IL-6,IL-8,MCP-1,p-p65 and p-IκBα in endothelial cells(P<0.01).Coronary artery disease patients had significantly lower plasma NLRC3 levels than controls,with an AUC of 0.851(95%CI:0.785～0.918,P<0.01).A diagnostic threshold of 1.605 μg/L yielded a sensitivity of 93.8%and a specificity of 71.3%.CONCLUSION:The NLRC3 may modulate endothelial inflammation and suppress AS progression through inhibition of the NF-κB signaling pathway,and it holds potential as a diagnostic biomarker for coronary artery disease.