Objective To elucidate the molecular mechanism of sirtuin-3 (SIRT3) in regulating mitochondrial biogenesis in human renal tubular epithelial cells. Methods Cells were stimulated with different concentrations of H₂O₂ and divided into four groups: control (NC), 50 μmol/L H₂O₂, 110 μmol/L H₂O₂ and 150 μmol/L H₂O₂. SIRT3 protein expression was then measured. SIRT3 was knocked down with siRNA, and cells were further assigned to five groups: control (NC), negative-control siRNA (NCsi), SIRT3-siRNA (siSIRT3), NCsi+H₂O₂, and siSIRT3+H₂O₂. After 24 h, cellular adenosine triphosphate (ATP) and mitochondrial superoxide anion (O₂•⁻) levels were determined, together with mitochondrial expression of SIRT3, peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), nuclear respiratory factor 1 (NRF1), mitochondrial transcription factor A (TFAM), superoxide dismutase 2 (SOD2), acetylated-SOD2 and adenosine monophosphate activated protein kinase α1 (AMPKα1). Results The 110 and 150 μmol/L H₂O₂ decreased SIRT3 protein (both P<0.05). ATP and mitochondrial O₂•⁻ did not differ between NC and NCsi groups (both P>0.05). Compared to the NCsi group, the siSIRT3 group exhibited elevated O₂•⁻ level, decreased SIRT3 protein and increased expression levels of SOD2 and acetylated SOD2 protein (all P<0.05). Compared to the NCsi group, the NCsi+H₂O₂ group exhibited decreased cellular ATP levels, elevated mitochondrial O₂•⁻ levels, and reduced protein expression levels of SIRT3, SOD2, TFAM, AMPKα1, PGC-1α and NRF1 (all P<0.05). Compared with the siSIRT3 group, the siSIRT3+H₂O₂ group showed a decrease in cellular ATP levels, an increase in mitochondrial O₂•⁻ levels, a decrease in SIRT3, SOD2, TFAM, AMPKα1, PGC-1α and NRF1 protein expression levels and a decrease in acetylated SOD2 protein expression levels (all P<0.05). Compared with the NCsi+H₂O₂ group, the siSIRT3+H₂O₂ group showed a decrease in cellular ATP levels, an increase in mitochondrial O₂•⁻ levels, a decrease in SIRT3, AMPKα1, PGC-1α and NRF1, TFAM protein expression levels, and an increase in SOD2 and acetylated SOD2 protein expression levels (all P<0.05). Conclusions SIRT3 promotes mitochondrial biogenesis in tubular epithelial cells via the AMPK/PGC-1α/NRF1/TFAM axis, representing a key mechanism through which SIRT3 ameliorates oxidative stress-induced mitochondrial dysfunction.

Objective To investigate the effect of unilateral or bilateral transcranial direct current stimulation(tDCS)on post-stroke dysphagia.Methods From February,2023 to March,2025,27 stroke patients with dysphagia and nasal feeding in Beijing Bo'ai Hos-pital were randomly divided into healthy side stimulation group,bilateral stimulation group and sham stimulation group,with nine cases in each group.All the groups received conventional swallowing training and tDCS,while the healthy side stimulation group stimulated on the healthy side of oropharyngeal cortex;and the bilateral stimu-lation group alternatively stimulated bilateral oropharyngeal cortex,with one hour interval between bilateral stim-ulation;the sham stimulation group stimulated the healthy side of oropharyngeal cortex for 30 seconds and then stop.The course lasted two weeks.The scores of Standard Swallowing Function Assessment Scale(SSA),Modi-fied Mann Assessment of Swallowing Ability(MMASA)and Rosenbek Penetration-Aspiration Scale(PAS)were compared before and after treatment.Results The intra-group effect(F=16.185,P<0.01)was significant in the scores of SSA,the intra-group effect(F=28.650,P<0.01)and interaction effect(F=3.453,P<0.01)were significant in the scores of MMASA,and there was no significant difference in the inter-group effect,intra-group effect and interaction effect in the scores of PAS(P>0.05).Post hoc test showed that there was no significant difference in the scores of SSA,MMASA and PAS among three groups(P>0.05).There was significant difference in the score difference of MMASA be-fore and after treatment among three groups(F=4.698,P<0.05).Post hoc test showed that the score difference of MMAS was more in the healthy side stimulation group than in the bilateral stimulation group and the sham stimulation group(P<0.05),with no significant difference between the bilateral stimulation group and the sham stimulation group(P>0.05).Conclusion tDCS can partly improve post-stroke dysphagia.The healthy side anode stimulation is superior to the alter-nating bilateral hemisphere anode stimulation.

Objective To understand the impact of bed-making manipulation on the air surrounding bed units in hemodialysis room,evaluate the effectiveness of routine terminal disinfection,and provide scientific basis for optimi-zing infection control measures.Methods Air specimens(pre-bed-making group)and environmental object surface specimens(pre-terminal disinfection group)around bed units were collected when hemodialysis was about to be fi-nished.Air specimens after bed-making(bed-making group)and environmental object surface specimens after ter-minal disinfection(terminal disinfection group)were also collected.Bacterial colonies were counted and identified.Results A total of 714 air specimens were collected from 238 bed units of 45 hemodialysis units before and during bed-making.The average bacterial colony count during bed-making was higher than that before bed-making([2.72±3.43]CFU/plate vs[0.69±1.50]CFU/plate,P＜0.05).The qualified rate of microbial colony count before bed-making was higher than that during bed-making(96.64％vs 64.71％,P＜0.05).A total of 450 environmental ob-ject surface specimens from 90 bed units of 45 hemodialysis units were collected before and after terminal disinfec-tion.The average bacterial colony count before terminal disinfection was higher than that after terminal disinfection([8.18±20.6]CFU/cm2 vs[1.49±3.44]CFU/cm2.P＜0.05).The qualified rate of microbial colony count after terminal disinfection was higher than that before terminal disinfection(98.22％vs 92.44％,P＜0.05).The micro-organisms in the air and environment were mainly coagulase negative Staphylococcus.Conclusion Bed-making has a certain impact on the air microorganisms around the bed units,and terminal disinfection can reduce the bacterial co-lony count of the environment.It is necessary to pay attention to the cleaning and disinfection of the environment for medical treatment,and carry out bed-making manipulation under clear condition to minimize the risk of infection.

Objective:To investigate the mechanisms by which calpain small subunit 1(CAPN4)regulates cisplatin resistance and cancer stem cell(CSC)stemness in lung adenocarcinoma,and to provide experimental evidence for reversing drug resistance through targeting CSC stemness.Methods:Tissue samples were collected from 10 lung adenocarcinoma patients who underwent surgical resection at Fujian Cancer Hospital from January 2023 to January 2024.Immunohistochemistry(IHC)stining was used to detect the differential expression of CAPN4 in five cisplatin-resistant and five cisplatin-sensitive lung adenocarcinoma tissues,followed with a histological scoring(H-score).CAPN4 gene expression-related survival analysis in lung cancer patients was conducted using The Cancer Genome Atlas(TCGA)database and Gene Expression Profiling Interactive Analysis(GEPIA)platform.Additionally,tissue samples from two cisplatin-resistant and two cisplatin-sensitive lung adenocarcinoma cases were collected to establish lung adenocarcinoma organoid(PDO)models.H-E and IHC staining were used to assess the morphological consistency between PDOs and the primary tumors.CAPN4 gene expression was silenced using lentivirus-mediated shRNA transduction.The expression levels of stem cell markers ALDH1A1,CD133,Nanog,and SOX9 were detected at both the gene and protein levels using quantitative polymerase chain reaction(qPCR)and Western blotting(WB),respectively.The sensitivity of CAPN4-knockdown PDOs to cisplatin was evaluated using the adenosine triphosphate(ATP)assay,and the apoptosis was assessed using the caspase-3 assay.Results:IHC results showed that CAPN4 protein expression was significantly upregulated in cisplatin-resistant lung adenocarcinoma tissues(P<0.05).TCGA cohort analysis revealed that high CAPN4 expression was significantly associated with poor prognosis(reduced OS)in lung adenocarcinoma patients(HR=1.4,P<0.05).PDOs derived from cisplatin-resistant patients exhibited significant upregulation in CAPN4 protein and stemness markers at both gene and protein levels(all P<0.05).Cisplatin sensitivity assays demonstrated that PDOs derived from cisplatin-resistant patients had significantly higher IC50 values than those from cisplatin-sensitive patients(P<0.05).After CAPN4 knockdown,the expression of stem cell makers in PDOs derived from cisplatin-resistant patients were significantly reduced,and their sensitivity to cisplatin was enhanced(P<0.05).Conclusion:Knockdown of CAPN4 reduces stem cell marker expression and enhances cisplatin sensitivity in lung adenocarcinoma PDOs,providing a potential therapeutic target for reversing cisplatin resistance in lung cancer.

Objective:Bidirectional causal associations of 41 cytokines with atopic dermatitis(AD)were explored based on a Mendelian randomization(MR)approach.Methods:Pooled data from genome wide association study(GWAS)of 41 cytokines and AD were utilized for instrumental variable(IV)screening,and single nucleotide polymorphism(SNP)affecting the results of MR analyses was excluded by the MR-PRESSO outlier test as well as by the MR Steiger filtering method.Two-sample bidirectional MR analyses were performed using inverse variance weighting(IVW),MR-Egger regression,and weighted median methods(WM).MR-Egger intercept term test and Cochran's Q test were performed to test the pleiotropy and heterogeneity of IV,and MR results were visu-alized by scatterplots,funnel plots,and leave-one-out plots.Results:Forward MR analysis showed that MIG(IVW:OR=0.89;95%CI:0.81～0.97;P=0.006)reduced the risk of AD development.In contrast,IL-5(IVW:OR=1.17;95%CI:1.01～1.36;P=0.042)and IL-18(MR Egger:OR=1.17;95%CI:1.03～1.33;P=0.030)increased the risk of AD development.Inverse MR analysis showed a potential causal association between AD and increased MIG(IVW:Beta=0.10;95%CI:0.02～0.17;P=0.014).None of the sensitivity analyses indicated pleiotropy and heterogeneity of the included IV.Conclusion:MIG may be an important marker in the progression of AD with a potential bidirectional causal association with risk of morbidity.IL-5 and IL-18 have a potential positive causal association for AD.

Objective To understand the impact of bed-making manipulation on the air surrounding bed units in hemodialysis room,evaluate the effectiveness of routine terminal disinfection,and provide scientific basis for optimi-zing infection control measures.Methods Air specimens(pre-bed-making group)and environmental object surface specimens(pre-terminal disinfection group)around bed units were collected when hemodialysis was about to be fi-nished.Air specimens after bed-making(bed-making group)and environmental object surface specimens after ter-minal disinfection(terminal disinfection group)were also collected.Bacterial colonies were counted and identified.Results A total of 714 air specimens were collected from 238 bed units of 45 hemodialysis units before and during bed-making.The average bacterial colony count during bed-making was higher than that before bed-making([2.72±3.43]CFU/plate vs[0.69±1.50]CFU/plate,P＜0.05).The qualified rate of microbial colony count before bed-making was higher than that during bed-making(96.64％vs 64.71％,P＜0.05).A total of 450 environmental ob-ject surface specimens from 90 bed units of 45 hemodialysis units were collected before and after terminal disinfec-tion.The average bacterial colony count before terminal disinfection was higher than that after terminal disinfection([8.18±20.6]CFU/cm2 vs[1.49±3.44]CFU/cm2.P＜0.05).The qualified rate of microbial colony count after terminal disinfection was higher than that before terminal disinfection(98.22％vs 92.44％,P＜0.05).The micro-organisms in the air and environment were mainly coagulase negative Staphylococcus.Conclusion Bed-making has a certain impact on the air microorganisms around the bed units,and terminal disinfection can reduce the bacterial co-lony count of the environment.It is necessary to pay attention to the cleaning and disinfection of the environment for medical treatment,and carry out bed-making manipulation under clear condition to minimize the risk of infection.

Objective To analyze the potential biological relationship between Alzheimer disease(AD)and chronic periodontitis(CP)by bioinformatics.Methods We analyzed two datasets of AD and CP from the Gene Expression Omnibus database,and differentially expressed genes(DEGs)were identified from these datasets.Weighted gene co-expression network analysis(WGCNA)was used to identify the most relevant modules.Functional enrichment analysis of shared genes was performed,and a protein-protein interaction(PPI)network was constructed.MCODE was used to identify key modules,and machine learning was used to discover key genes.In addition,Gene Set Enrichment Analysis(GSEA)and CIBERSORT were used to investigate KLRB1-related molecular pathways and immune cell distribu-tion.Results The study identified 18 genes common to both AD and CP.MCODE analysis revealed five pivotal genes,machine learning identified 13 genes for AD,eight for CP,and KLRB1 was determined as a common gene for AD and CP.GSEA demonstrated the intricate involvement of these genes in disease-related pathways.Immunocellular analysis underscored a significant association between KLRB1 and γδT cells.Conclusion This research highlighted KLRB1 as a key gene for AD and CP,providing new insights into their molecular linkages.

Alzheimer's disease(AD)is the most common neurodegenerative disorder worldwide,characterized primarily by cognitive impairment and memory dysfunction.Its pathological mechanisms involve the toxic accumulation of amyloid β-protein(Aβ),hyperphosphorylation of Tau protein leading to neurofibrillary tangles,mitochondrial dysfunction,synaptic impairment,cholinergic system dysfunction,neuroinflammation,and oxidative stress.Current clinical treatments for AD include acetylcholinesterase inhibitors and N-methyl-D-aspartate antagonists,which can improve cognitive function but fail to slow disease progression and often have side effects.Research indicates that traditional Chinese medicine(TCM)may regulate the phosphatidylinositol 3-kinase/protein kinase B(PI3K/AKT)signaling pathway,promoting neuronal survival,inhibiting neuroinflammation,reducing oxidative stress,preventing apoptosis,and decreasing Aβ deposition,thus improving the symptoms of AD.This review summarizes the mechanisms by which individual TCM components,extracts,and formulas may regulate the PI3K/AKT pathway in the treatment of AD,with the aim of providing a theoretical foundation for the application of TCM in AD therapy.

Objective:Bidirectional causal associations of 41 cytokines with atopic dermatitis(AD)were explored based on a Mendelian randomization(MR)approach.Methods:Pooled data from genome wide association study(GWAS)of 41 cytokines and AD were utilized for instrumental variable(IV)screening,and single nucleotide polymorphism(SNP)affecting the results of MR analyses was excluded by the MR-PRESSO outlier test as well as by the MR Steiger filtering method.Two-sample bidirectional MR analyses were performed using inverse variance weighting(IVW),MR-Egger regression,and weighted median methods(WM).MR-Egger intercept term test and Cochran's Q test were performed to test the pleiotropy and heterogeneity of IV,and MR results were visu-alized by scatterplots,funnel plots,and leave-one-out plots.Results:Forward MR analysis showed that MIG(IVW:OR=0.89;95%CI:0.81～0.97;P=0.006)reduced the risk of AD development.In contrast,IL-5(IVW:OR=1.17;95%CI:1.01～1.36;P=0.042)and IL-18(MR Egger:OR=1.17;95%CI:1.03～1.33;P=0.030)increased the risk of AD development.Inverse MR analysis showed a potential causal association between AD and increased MIG(IVW:Beta=0.10;95%CI:0.02～0.17;P=0.014).None of the sensitivity analyses indicated pleiotropy and heterogeneity of the included IV.Conclusion:MIG may be an important marker in the progression of AD with a potential bidirectional causal association with risk of morbidity.IL-5 and IL-18 have a potential positive causal association for AD.

Charcoal-processed traditional Chinese herbal medicine has various therapeutic effects， including astringing， hemostasis， anti-diarrhea， clearing heat， tonifying， and warming the interior. This paper summarizes the clinical application features， compatible experiences， dosages， and precautions for over 20 types of charcoal-processed herbal medicine in the treatment of gynecological bleeding disorders caused by dysfunctions such as dysfunctional uterine bleeding， endometriosis， uterine incision pseudocavity， and vaginal bleeding resulting from threatened miscarriage. The charcoal-processed herbal medicine include Huangqin （Scutellaria Baicalensis） Charcoal， Dahuang （Rheum Palmatum） Charcoal， Cebai （Platycladus Orientalis） Charcoal， Diyu （Sanguisorba Officinalis） Charcoal， Daji （Cirsium Setosum） Charcoal， Xiaoji （Cirsium Japonicum） Charcoal， Shengdi （Rehmannia Glutinosa） Charcoal， Aiye （Artemisia Argyi） Charcoal， Paojiang （Zingiber Officinale） Charcoal， Xuduan （Dipsacus Asper） Charcoal， Duzhong （Eucommia Ulmoides） Charcoal， Qiancao （Rubia Cordifolia） Charcoal， Puhuang （Typha Angustifolia） Charcoal， Shanzha （Crataegus Pinnatifida） Charcoal， Jingjie （Schizonepeta Tenuifolia） Charcoal， Xueyu （Carthamus Tinctorius） Charcoal， Zonglyu （Areca Catechu） Charcoal， Wumei （Prunus Mume） Charcoal， Shudahuang （Rheum Officinale） Charcoal， Lianfang （Nymphaea Alba） Charcoal， Mianmaguanzhong （Clematis Armandii） Charcoal， and Oujie （Nelumbo Nucifera） Charcoal.