摘要：Chronic obstructive pulmonary disease(COPD)is incurable chronic disease which kills 3.3 million each year worldwide.Number of global cases of COPD is steadily rising alongside with life expectancy,disproportionally hitting middle-income countries like Russia and China,in such conditions,new approaches to the COPD management are desperately needed.DNA microarray technology is a powerful genomic tool that has the potential to uncover underlying COPD biological alteration and brings up revolutionized treatment option to clinicians.We executed systematic review studies of studies published in last 10 years regarding DNA microarray application in COPD management,with complacence to PRISMA criteria and using PubMed and Medline data bases as data source.Out of 920 identified papers,39 were included in the final analysis.We concluded that Genome-wide expression profiling using DNA microarray technology has great potential in enhancing COPD management.Current studied proofed this method is reliable and possesses many potential applications such as individual at risk of COPD development recognition,early diagnosis of disease,COPD phenotype identification,exacerbation prediction,personalized treatment optioning and prospect of oncogenesis evaluation in patients with COPD.Despite all the proofed benefits of this technology,researchers are still in the early stage of exploring it's potential.Therefore,large clinical trials are still needed to set up standard for DNA microarray techniques usage implementation in COPD management guidelines,subsequently giving opportunity to clinicians for controlling or even eliminating COPD entirely.

摘要：Kashin-Beck disease(KBD)is an endemic osteoarthropathy.Its distribution region covers a long and narrow belt on the Pacific side and belongs to continental climate with short summer,long frost period,and large temperature differences between day and night.In particular,KBD patients are typically scattered in the rural areas with seasonal features such as cold winters and rainy autumns.Etiological studies have demonstrated that the carrier of pathogenic factors is the grains produced in endemic areas.Risk factors for KBD include fungal contamination of grains due to poor storage conditions associated with cold weather.The epidemiological characteristics of KBD include agricultural area,early age of onset,gender equality,family aggregation,regional differences,and annual fluctuations.A series of preventive measures have been successfully taken in the past decades.National surveillance data indicate that the annual incidence of KBD is gradually declining.

摘要：Objective:Clinical manifestation of the inflammatory process in its relation to biochemical markers(total cysteine[Cys],cysteine-glycine[CysGly],glutathione[GSH],glutamate-cysteine[Glu-Cys],homocysteine[Hcy],the ratio of reduced to oxidized glutathione[GSH/GSSG],the ratio of reduced to oxidized cysteine[CySH/CySS],malondialdehyde-oxidized low-density lipoproteins[MDA-oxLDL])has been studied in patients with coronavirus disease 2019(COVID-19).Material and methods:48 patients with mild to severe COVID-19 and 20 healthy volunteers were included in our research.The participants were divided into 4 experimental groups according to inflammation intensity estimated based on the serum levels of interleukin 6(IL-6).Results:All 4 groups showed the prevalence of male patients and elevated serum levels of IL-6(by 54.6%).There was no comorbidity in patients with mild COVID-19(nasopharyngitis symptoms)and in healthy control subjects.50%of patients with lung damage had accompanying diseases.Alterations of aminoethyl metabolism were detected in COVID-19 patients:as reflected by the decreased levels of Cys,CysGly,and Glu-Cys and the increased levels of GSH as compared to the control group.Conclusion:Elevation of IL-6 over 7.5 pg/mL was associated with decreased GSH/GSSG and CySH/CySS ratios indicating enhanced oxidative stress and was followed by protein oxidation,specifically MDA-oxLDL.

摘要：Background:Myocardial infarctions(MI)is a major threat to human health especially in people exposed to cold environment.The polarization of macrophages towards different functional phenotypes(M1 macrophages and M2 macrophages)is closely related to MI repairment.The growth differentiation factor 11(GDF11)has been reported to play a momentous role in inflammatory associated diseases.In this study,we examined the regulatory role of GDF11 in macrophage polarization and elucidated the underlying mechanisms in MI.Methods:In vivo,the mice model of MI was induced by permanent ligation of the left anterior descending coronary artery(LAD),and mice were randomly divided into the sham group,MI group,and MI+GDF11 group.The protective effect of GDF11 on myocardial infarction and its effect on macrophage polarization were verified by echocardiography,triphenyl tetrazolium chloride staining and immunofluorescence staining of heart tissue.In vitro,based on the RAW264.7 cell line,the effect of GDF11 in promoting macrophage polarization toward the M2 type by inhibiting the Notch1 Signaling pathway was validated by qRT-PCR,Western blot,and flow cytometry.Results:We found that GDF11 was significantly downregulated in the cardiac tissue of MI mice.And GDF11 supplementation can improve the cardiac function.Moreover,GDF11 could reduce the proportion of M1 macrophages and increase the accumulation of M2 macrophages in the heart tissue of MI mice.Furthermore,the cardioprotective effect of GDF11 on MI mice was weakened after macrophage clearance.At the cellular level,application of GDF11 could inhibit the expression of M1 macrophage(classically activated macrophage)markers iNOS,interleukin(IL)-1β,and IL-6 in a dose-dependent manner.In contrast,GDF11 significantly increased the level of M2 macrophage markers including IL-10,CD206,arginase 1(Arg1),and vascular endothelial growth factor(VEGF).Interestingly,GDF11 could promote M1 macrophages polarizing to M2 macrophages.At the molecular level,GDF11 significantly down-regulated the Notch1 signaling pathway,the activation of which has been demonstrated to promote M1 polarization in macrophages.Conclusions:GDF11 promoted macrophage polarization towards M2 to attenuate myocardial infarction via inhibiting Notch1 signaling pathway.

摘要：Brown adipose tissue(BAT),crucial for mammalian thermoregulation and energy metabolism,boasts a dense concentration of mitochondria.As a vital cellular organelle,mitochondria undergo substantial remodeling in cold environments,playing a pivotal role in maintaining body temperature and energy balance[1].

摘要：1 Introduction Infants are born with a substantial amount of brown adipose tissue(BAT),primarily clustered around their upper back,shoulders,and upper chest[1].As age progresses,the primary BAT gradually diminishes,and concomitantly,de novo lipogenesis(DNL)continues to occur in subcutaneous adipose tissue throughout the body.

摘要：Objective:Cold exposure has been suggested to be advantageous for the spread and infection of the coronavirus,and the gut microbiota influences the severity of the infection by modulating host inflammatory and immune responses.However,it remains unclear whether the promotion of viral infection through cold exposure is linked to the gut microbiota.Methods:In this study,we performed an unbiased analysis of gut microbiota,serum,and lung tissue metabolome changes in cold-exposed and virus-infected mice,alongside the assessment of immune-inflammatory indicators in serum and lung tissue.Results:The results revealed that both cold exposure and viral infection significantly decreased the percentage of peripheral blood lymphocytes(CD4+T cells,CD8+T cells,and B cell)and increased the expression of inflammatory factors(IL-6,IL-1 β,TNF-α,and IFN-γ).Meanwhile,cold exposure disrupted the homeostasis of gut microbiota,elevating the abundance of pathogenic bacteria(Staphylococcus)and diminishing the abundance of beneficial bacteria(Alistipes).Notably,in virus-infected mice exposed to a cold environment,the reduction in the abundance of beneficial bacteria Alistipes was more pronounced than in cases of single virus infection and cold exposure.Analysis of altered serum and lung tissue metabolites highlighted glycerophospholipids,fatty acids,and eicosanoids as the most affected metabolites by cold exposure.These metabolites,closely associated with virus infection,exhibited a significant correlation with immune-inflammatory indicators.Conclusion:These findings establish a mechanistic connection between cold exposure and virus infection,suggesting that cold exposure-induced dysregulation of gut microbiota and lipid metabolism diminishes host immunity,promoting virus infection.

摘要：Background and Objective:Self-monitoring of blood glucose(SMBG)is crucial for achieving a glycemic target and upholding blood glucose stability,both of which are the primary purpose of anti-diabetic treatments.However,the association between time in range(TIR),as assessed by SMBG,and β-cell insulin secretion as well as insulin sensitivity remains unexplored.Therefore,this study aims to investigate the connections between TIR,derived from SMBG,and indices representing β-cell functionality and insulin sensitivity.The primary objective of this study was to elucidate the relationship between short-term glycemic control(measured as points in range[PIR])and both β-cell function and insulin sensitivity.Methods:This cross-sectional study enrolled 472 hospitalized patients with type 2 diabetes mellitus(T2DM).To assess β-cell secretion capacity,we employed the insulin secretion-sensitivity index-2(ISSI-2)and(ΔC-peptide0-120/Δglucose0-120)× Matsuda index,while insulin sensitivity was evaluated using the Matsuda index and HOMA-IR.Since SMBG offers glucose data at specific point-in-time,we substituted TIR with PIR.According to clinical guidelines,values falling within the range of 3.9-10 mmol were considered"in range,"and the corresponding percentage was calculated as PIR.Results:We observed significant associations between higher PIR quartiles and increased ISSI-2,(ΔC-peptide0-120/Δglucose0-120)× Matsuda index,Matsuda index(increased)and HOMA-IR(decreased)(all P＜0.001).PIR exhibited positive correlations with log ISSI-2(r=0.361,P＜0.001),log(ΔC-peptide0-120/Δglucose0-120)× Matsuda index(r=0.482,P＜0.001),and log Matsuda index(r=0.178,P＜0.001)and negative correlations with log HOMA-IR(r=-0.288,P＜0.001).Furthermore,PIR emerged as an independent risk factor for log ISSI-2,log(ΔC-peptide0-120/Δglucose0-120)× Matsuda index,log Matsuda index,and log HOMA-IR.Conclusion:PIR can serve as a valuable tool for assessing β-cell function and insulin sensitivity.

摘要：Background:Nonalcoholic fatty liver disease(NAFLD)is a chronic condition characterized by a progressive decline in liver function,leading to disruptions in liver integrity and metabolic function,resulting in lipid deposition and excessive accumulation of extracellular matrix(ECM).The pathogenesis of NAFLD is complex and not yet fully understood,contributing to the absence of specific therapeutic strategies.Peroxisome proliferator-activated receptor gamma(PPARγ)is a ligand-activated transcription factor pivotal in regulating lipid and glucose metabolism.However,the impacts of PPARγ on NAFLD remains insufficiently explored.Thus,this study aimed to investigate the role of PPARγ in NAFLD and its underlying molecular mechanisms.Methods:Chemical detection kits were utilized to quantify collagen content,alanine aminotransferase(ALT),and aspartate aminotransferase(AST)level variations.Quantitative real-time polymerase chain reaction(qRT-PCR)was employed to assess alterations in extracellular matrix-related genes and inflammatory response genes in liver tissue and HepG2 cells,while western blotting was conducted to analyze the levels of both PPARγ and the TGF-β/Smad signaling pathway.Results:Our findings unveiled significantly reduced PPARγ expression in a rat model of NAFLD,leading to subsequent activation of the TGF-β/Smad signaling pathway.Furthermore,PPARγ activation effectively mitigated NAFLD progression by inhibiting inflammation and fibrosis-related gene expression and collagen production.On a cellular level,PPARγ activation was found to inhibit the expression of extracellular matrix-related genes such as matrix metalloproteinase 2(MMP2)and matrix metalloproteinase 9(MMP9),along with inflammatory response genes interleukin(IL)-1β and IL-6.Additionally,PPARγ activation led to a significant decrease in the levels of ALT and AST.At the molecular level,PPARγ notably down-regulated the TGF-β/Smad signaling pathway,which is known to promote liver fibrosis.Conclusion:These groundbreaking findings underscore PPARγ activation as a promising therapeutic approach to delay NAFLD progression by targeting the TGF-β/Smad signaling pathway in hepatic cells.This highlights the potential of PPARγ as a promising therapeutic target for NAFLD management in clinical settings.

摘要：Background:Myocardial infarction(MI)is associated with higher morbidity and mortality in the world,especially in cold weather.YBX1 is an RNA-binding protein that is required for pathological growth of cardiomyocyte by regulating cell growth and protein synthesis.But YBX1,as an individual RNA-binding protein,regulates cardiomyocytes through signaling cascades during myocardial infarction remain largely unexplored.Methods:In vivo,the mouse MI model was induced by ligating the left anterior descending coronary artery(LAD),and randomly divided into sham operation group,MI group,MI+ YBX1 knockdown/overexpression group and MI+ negative control(NC)group.The protective effect of YBX1 was verified by echocardiography and triphenyltetrazolium chloride staining.In vitro,mitochondrial-dependent apoptosis was investigated by using CCK8,TUNEL staining,reactive oxygen species(ROS)staining and JC-1 staining in hypoxic neonatal mouse cardiomyocytes(NMCMs).Results:YBX1 expression of cardiomyocytes was downregulated in a mouse model and a cellular model on the ischemic condition.Compared to mice induced by MI,YBX1 overexpression mediated by adeno-associated virus serotype 9(AAV9)vector reduced the infarcted size and improved cardiac function.Knockdown of endogenous YBX1 by shRNA partially aggravated ischemia-induced cardiac dysfunction.In hypoxic cardiomyocytes,YBX1 overexpression decreased lactic dehydrogenase(LDH)release,increased cell viability,and inhibited apoptosis by affecting the expression of apoptosis related proteins,while knockdown of endogenous YBX1 by siRNA had the opposite effect.Overexpression of YBX1 restored mitochondrial dysfunction in hypoxic NMCMs by increasing mitochondrial membrane potential and ATP content and decreasing ROS.In hypoxic NMCMs,YBX1 overexpression increased the expression of phosphorylated phosphatidylinositol 3 kinase(PI3K)/AKT,and the anti-apoptosis effect of YBX1 was eliminated t by LY294002,PI3K/AKT inhibitor.Conclusion:YBX1 protected the heart from ischemic damage by inhibiting the mitochondrial-dependent apoptosis through PI3K/AKT pathway.It is anticipated that YBX1 may serve as a novel therapeutic target for MI.

摘要：Background and Objective:Some patients continue to experience major adverse cardiovascular and cerebrovascular events(MACCE)after percutaneous coronary intervention(PCI)in frigid places.Indexes of inflammation and nutrition alone were shown to predict outcomes in patients with PCI.However,the clinical predictive value of mixed indicators is unclear.This study aimed to assess the predictive value of the albumin/neutrophil/lymphocyte ratio(NLR)on the long-term prognosis of patients with coronary heart disease(CHD)following percutaneous coronary intervention(PCI).Methods:A total of 608 post-PCI CHD patients were categorized into low-and high-index groups based on the optimal cut-off values for albumin and NLR.The primary outcome was a composite endpoint comprising all-cause mortality and major adverse cerebrovascular events.The secondary outcome was the comparison of the predictive efficiency of the new nutritional index,albumin/NLR,with that of albumin or NLR alone.Results:Over the five-year follow-up period,45 patients experienced the composite endpoint.The incidence of endpoint events was significantly higher in the low-index group(12%)compared to the high-index group(4.9%).Receiver operating characteristic(ROC)curve analysis revealed that the albumin/NLR index had a larger area under the curve(AUC:0.655)than albumin(AUC:0.621)or NLR(AUC:0.646),indicating superior predictive efficiency.The prognostic nutritional index had an AUC of 0.644,further supporting the enhanced predictive value of the albumin/NLR index over individual nutritional and inflammatory markers.Conclusion:The albumin/neutrophil/lymphocyte ratio is independently associated with the long-term prognosis of CHD patients post-PCI and demonstrates superior predictive efficiency compared to individual nutritional and inflammatory markers.

摘要：Objective:The benefits of phytosterols have attracted growing interest,but their association with Metabolic Dysfunction-Associated Fatty Liver Disease(MAFLD)has rarely been reported in population-based studies.This research aimed to investigate the correlation between dietary phytosterols and MAFLD.Methods:Phytosterols intake was evaluated using an internet-based dietary questionnaire targeted at the Chinese population.Conditional logistic regression models were employed to investigate dose-response relationships between phytosterol intake and MAFLD,as well as the potential preventive role of phytosterols.Restricted Cubic Spline(RCS)analyses were conducted to examine associations between phytosterols intake and MAFLD.Additionally,a quantile-based g-computation(qgcomp)method was applied to explore the combined effect of campesterol,stigmasterol,β-sitostelane,campestane,and β-sitosterol on MAFLD.Results:Significant inverse relationships were found between total phytosterols and MAFLD(OR,0.19;95%CI,0.11-0.32;P<0.001),campesterol(OR,0.22;95%CI,0.13-0.37;P<0.001),stigmasterol(OR,0.17;95%CI,0.10-0.30;P<0.001),β-sitostelane(OR,0.26;95%CI,0.16-0.45;P<0.001),campestane(OR,0.23;95%CI,0.14-0.39;P<0.001),and β-sitosterol(OR,0.17;95%CI,0.10-0.29;P<0.001).The qgcomp analysis showed a significant negative association between the five phytosterols and MAFLD(OR,0.58;95%CI,0.50-0.67;P<0.001).Additionally,the qgcomp analysis revealed that the combination of these five phytosterols was inversely associated with MAFLD,with stigmasterol contributing the most(weight=0.70).Conclusion:Higher intake of phytosterols was associated with a reduced prevalence of MAFLD,with stigmasterol showing the most significant inverse relationship.Further research is needed to clarify the relationship between phytosterols and MAFLD.

摘要：Background and Objectives:Non-Communicable Diseases(NCDs)represent a significant public health burden in China,particularly in cold regions where environmental factors further limit access to healthcare.To address this challenge,China has implemented the National Essential Public Health Service Package(NEPHSP)to improve NCD management through primary healthcare services.However,research on the effectiveness of NEPHSP in cold regions is limited.This study aims to identify the key factors influencing the implementation of NCD management services in cold regions,focusing on both barriers and facilitators.Methods:This qualitative study was conducted in three purposively selected cold regions in Northeast China(Harbin,Qiqihar,and Jiamusi).Data were collected through semi-structured interviews and focus group discussions,guided by the RE-AIM framework.Participants included local health administrators,primary healthcare workers,and community-dwelling individuals with NCDs.Thematic analysis was employed to code and extract key themes from the data.Results:A total of 72 participants(59.7%female,mean age 49.1±6.24 years)took part in the study.Major barriers to NCD management included low health literacy,limited awareness of NCDs,insufficient medical resources,poor public awareness,inadequate multisectoral collaboration,and the absence of effective audit and feedback systems.Key facilitators included the affordability and accessibility of primary healthcare services,strong patient-physician relationships,and the high priority given to NCD management by local governments.Furthermore,harsh environmental conditions and limited healthcare accessibility in cold regions complicated the management of NCDs,highlighting the need for tailored interventions that address the specific challenges of these regions.Conclusion:This study identifies significant facilitators and barriers to the implementation of NCD management services under the NEPHSP in cold regions of China.The unique challenges posed by cold climates necessitate the adaptation of healthcare services to local needs,with a focus on improving health literacy,enhancing healthcare infrastructure,and fostering multisectoral collaboration.These findings provide valuable insights for optimizing NCD prevention and management strategies within China's primary healthcare system.

摘要：Objective:This study aims to evaluate the relationship between PM2.5 concentration and daily mortality rate from cardiovascular and cerebrovascular diseases(CCVD)in cold regions of northern China,as well as to identify the primary sources of PM2.5.Methods:A time series analysis model was used to calculate the exposure-response relationship between PM2.5 and CCVD mortality in Harbin.Positive matrix factorization(PMF)was employed to analyze the sources of PM2.5.Results:After adjusting for multiple pollutant combinations,the maximum excess risk of cardio-cerebrovascular death on the day of PM2.5 exposure was 0.42%(95%CI:0.15%-0.70%).Stratification by gender and age revealed that the elderly individuals and men were particularly susceptible to PM2.5 exposure.The source analysis identified seven major pollution sources contributing to PM2.5 in Harbin.Conclusion:Our findings strengthen the evidence that PM2.5 is an independent risk factor for daily CCVD mortality,identify vulnerable populations that require special attention,and pinpoint the primary sources of PM2.5 in Harbin.These findings provide reference points for effectively reducing the health risks associated with PM2.5 exposure.

摘要：Objective:Psoriasis is a common chronic,recurrent,immune-mediated inflammatory skin disease,which tends to occur in cold areas.Its pathogenesis is currently unclear.This study aims to screen differentially expressed genes in the psoriasis dataset,identify the central genes,detect the expression of central genes in psoriasis lesions of patients in the cold regions and then conduct further research.Methods:Differential genes associated with psoriasis in the GEO database were analyzed,and functional enrichment analysis and protein-protein interaction network analysis.The expression results of the identified genes were validated in psoriasis cell models.The ISG15 gene,which showed the most significant difference in expression,was further studied.The expression level of ISG15 protein in psoriasis was examined.Then,we knocked out ISG15 in psoriasis cell models and detected keratinocyte proliferation by MTT,Real-Time PCR and Western Blot.Western Blot showed the expression of β-catenin after ISG15 gene knockout.Results:We detected the protein expression of ISG15 in the cold area of Northeast China,and found that the expression of ISG15 increased in patients with psoriasis,and the proliferation of keratinocytes and the expression of β-catenin decreased in psoriasis cell model after ISG15 was knocked down.ISG15 regulates keratinocyte proliferation through Wnt signaling pathway in psoriasis.Conclusions:ISG15 expression is increased in psoriatic cells and skin lesions of patients with psoriasis.In psoriasis,ISG15 promotes keratinocyte proliferation through the Wnt signaling pathway.

摘要：Background:Cold exposure is linked to numerous diseases,yet the changes in key genes and pathways in mice under cold exposure remain unexplored.Understanding these alterations could offer insights into the mechanisms of cold resistance and contribute valuable ideas for treating cold-related diseases.Methods:The dataset GSE148361 was obtained from the Gene Expression Omnibus(GEO)database.Differentially expressed genes(DEGs)were identified using the"limma"package in R software.Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway analyses were performed on DEGs.The STRING(Search Tool for the Retrieval of Interacting Genes)database was used to construct a protein-protein interaction(PPI)network.Additionally,gene set enrichment analysis(GSEA)was conducted to identify pathways associated with key genes.miRNAs and upstream transcription factors(TFs)were predicted using the miRNet database.Results:A total of 208 DEGs were identified,with 137 upregulated and 71 downregulated.In biological processes,DEGs were enriched in nucleotide and purine-containing compound metabolism.For cellular components,DEGs were involved in condensed chromosomes and mitochondrial protein complexes.In molecular functions,proton transmembrane transporter activity was enriched.KEGG pathway analysis showed significant enrichment in biosynthesis of unsaturated fatty acids,fatty acids,and pyruvate metabolism.From the PPI network,12 hub genes were identified using MCODE.Four hub genes(Col3a1,Ifi203,Rtp4,Vcan)demonstrated similar trends in a validation set(GSE110420)and were significantly differentially expressed.GSEA analysis indicated that these four genes were enriched in pathways such as ECM-receptor interaction and cytokine-cytokine receptor interaction.The hub gene network included 93 miRNAs and one TF.Conclusion:This study identified four hub genes as potential diagnostic biomarkers for cold exposure,providing insights for further research on the effects of cold on gene expression and disease.

摘要：Objective:Heilongjiang Province is part of the northern cold areas of China,where gastric cancer is one of the most common gastrointestinal malignancies.Peritoneal metastases(PM)are the leading cause of mortality among patients.This study conducted bioinformatics and basic research on the gene ANXA2(Annexin A2),which may influence the prognosis of patients.Methods:Genome sequencing was performed on patients from Heilongjiang to identify potential genes impacting survival time.The function of ANXA2 in gastric cancer was analyzed using multiple bioinformatics databases,focusing on its pathways and mechanisms.ANXA2-knockout gastric cancer cell lines were constructed,and in vitro assays,including CCK-8,flow cytometry,scratch,and Transwell experiments,were conducted.A nude mouse tumorigenesis model was also developed to analyze in vivo effects.Results:ANXA2 was found to be expressed at higher levels in gastric cancer tissue than in normal gastric tissue,and its mRNA levels were associated with short overall survival(OS).Enrichment analysis indicated that ANXA2 is primarily localized on the cell membrane and primarily influences the PI3K-AKT signaling pathway.Cytological experiments demonstrated that knockdown of ANXA2 suppresses the growth and migration of gastric carcinoma cells,an effect that was also observed in vivo.Conclusions:ANXA2 is essential for gastric cancer growth and may represent a potential risk factor affecting the survival probability of patients in cold regions.

摘要：Objective:To evaluate the clinical efficacy of combining arthroscopic patellar denervation with microfracture in the treatment of patellofemoral arthritis under cold weather conditions.Methods:A total of 134 patients with patellofemoral arthritis who underwent treatment between June 2019 and June 2021 were included in this study.Patients were randomly divided into two groups:the control group,which received standard arthroscopic debridement and conventional therapy,and the study group,which underwent additional peripatellar denervation and microfracture procedures.Clinical outcomes,including Tegner scores,hospital for special surgery(HSS)scores,and treatment-related adverse events,were evaluated and compared between the two groups.Results:The study group achieved a significantly higher excellent treatment rate(95.52%,64/67)compared to the control group.Post-treatment Tegner scores(5.48±1.86)and HSS scores(86.37±11.25)were also significantly better in the study group than in the control group.Furthermore,the incidence of adverse reactions was lower in the study group(4.48%,3/67),with statistically significant differences observed(P<0.05).Conclusions:Arthroscopic patellar denervation combined with microfracture markedly improves clinical outcomes,including Tegner and HSS scores,in the treatment of patellofemoral arthritis,particularly under cold weather conditions.The procedure is effective and safe,supporting its broader clinical application.

摘要：Bladder cancer(BC)ranks as the tenth most common cancer globally.Histopathologically,BC is broadly categorized into urothelial and non-urothelial BC.Urothelial carcinoma represents over 90％of BC in most regions worldwide.The standard treatment procedure for diagnosing and treating non-muscle-invasive bladder cancer(NMIBC)is transurethral resection of bladder tumors(TURBT).Currently,the standard of care for muscle-invasive bladder cancer(MIBC)is neoadjuvant chemotherapy followed by radical cystectomy.Cryoablation therapy is a medical technique that uses extremely low temperatures to destroy diseased tissue.This treatment serves as a therapeutic tool for both benign and malignant diseases in organs such as the kidney,prostate gland,lung,liver,and breast,and is particularly effective for unresectable tumors,offering less trauma,quick recovery,good tolerability,and symptom control.However,cryoablation has its limitations.Over the past few years,cryoablation therapy has emerged as a new method for treating early BC.This treatment is minimally invasive,precise,and offers quick recovery,providing patients with a new treatment option.Although randomized studies are still limited,increasing evidence suggests its potential application in bladder cancer combined with transurethral resection(TURBT)or medication.Cryoablation is not standard therapy for bladder cancer.Treatment decisions should be discussed by a multidisciplinary team of urologists,oncologists,and interventional physicians and require more randomized controlled trials to define patient selection criteria and treatment approaches.

摘要：Background and objective:Commonly plaguing in the frigid zone of the world,vitamin D deficiency,as indicated by low levels of 25-hydroxyvitamin D,exacerbated inflammatory responses and impaired endothelial function.Leukoaraiosis(LA)is a prevalent cause of cognitive dysfunction in the elderly and is potentially associated with inflammatory responses.This study aimed to investigate the impact of vitamin D on the severity of LA.Methods:Patients with LA were categorized based on 3.0 T brain MRI findings into mild(N=43),moderate(N=40),or severe groups(N=29)using the Fazekas scale(scoring 1-6).A control group consisting of 41 healthy individuals was included.Serum fibrinogen C,homocysteine,plasma 25-hydroxyvitamin D,and intercellular cell adhesion molecule-1(ICAM-1)levels were measured using ELISA.Results:All LA severity groups exhibited lower plasma 25-hydroxyvitamin D levels compared to the control group,with a more pronounced decrease observed as LA severity increased.Low plasma 25-hydroxyvitamin D was identified as an independent risk factor for LA(P＜0.05)according to Multiple logistic regression analysis.Additionally,a negative association was observed between 25-hydroxyvitamin D and vascular inflammatory factor ICAM-1.Conclusions:Disease severity positively correlated with levels of the inflammatory marker ICAM-1,worsening as plasma 25-hydroxyvitamin D concentration decreased.Low 25-hydroxyvitamin D emerged as an independent risk factor for LA,potentially exacerbating the inflammatory response.These findings suggest 25-hydroxyvitamin D supplementation as a potential therapeutic approach for LA.