Objective:To analyze the anatomical characteristics and surgical management measures of acute Stanford type A aortic dissection (AAD) involving coronary arteries, and to preliminarily explore the clinical efficacy of different coronary artery treatment techniques.Methods:A retrospective analysis was conducted on the clinical data of 42 patients who underwent surgery for AAD involving coronary arteries in Hunan Provincial People′s Hospital from January 2022 to May 2025. They were divided into the MI group (14 cases) and the nMI group (28 cases) according to whether they had acute myocardial infarction before surgery. The clinical data such as the actual surgical methods and mortality in the two groups were summarized.Results:Among 294 surgeries, 42 cases (14.3%) had definite coronary artery involvement, including 14 cases in the MI group and 28 cases in the nMI group; 1 case had bilateral coronary artery involvement and 41 cases had right coronary artery involvement. Regarding injury types: 16 cases were of the coronary trunk compression type, 12 cases were of the sinus intimal tear neal to ostium type, and 14 cases were of the coronary trunk intimal type. There was no statistically significant difference in the types of coronary artery involvement between the two groups ( P>0.05). There were 18 cases of Sun′s procedure with preserved aortic sinus and aortic valve, 7 cases of Bentall procedure without bypass, and 17 cases of Bentall procedure plus bypass. There was no statistically significant difference in the surgical plans between the two groups ( P>0.05). There were 4 deaths within 30 days (2 cases in each group). Conclusions:AAD involving coronary arteries is a critical condition, and accurate diagnosis is somewhat difficult. Myocardial ischemia is not significantly associated with the type of coronary artery involvement. The surgical plan depends on the type of coronary artery involvement. The classification method in this study is conducive to selecting appropriate surgical methods and improving surgical prognosis.

Objective:To investigate the miRNA-mRNA regulatory network in a rat model of Tourette syndrome(TS)using transcriptomic technology and to screen key signaling pathways and potential traditional Chinese medicine(TCM)candidates for intervention.Methods:A TS rat model was established using iminodipropionitrile(IDPN).RNA sequencing was performed to identify differentially expressed miRNAs and mRNAs in the brain tissues of TS rats.Bioinformatics analysis was applied to construct interaction networks,and network pharmacology was further employed to screen potential TCM compounds.Results:After 7 days of IDPN modeling,the model group exhibited motor and stereotypical behavioral changes,with behavioral scores greater than 3 points.Hema toxylin-eosin(HE)staining revealed irregular neuronal nuclear morphology,uneven chromatin distribution,nuclear pyknosis,and increased glial cell density.KEGG enrichment analysis identified key pathways:calcium signaling pathway,neuroactive ligand-receptor interaction,p53 signaling pathway,ECM-receptor interaction,and TGF-β signaling pathway.miR-125a-3p,miR-106-3p,and miR-760-3p were identified as pivotal miRNAs.Potential TCM candidates included Ajuga decumbens,Acanthopanax bark,Codonopsis pilosula,Stephania japonica,Os Draconis,Notopterygium root,Siraitia grosvenorii,Zanthoxylum nitidum root,Morinda officinalis,and Corydalis yanhusuo.Conclusion:The miRNAs miR-106-3p,miR-125a-3p,and miR-760-3p may mediate TS pathogenesis by altering critical signaling networks,including the calcium signaling pathway,neuroactive ligand-receptor interaction,and ECM-receptor interaction pathways,leading to neuroimmune inflammation and dopaminergic system dysregulation.TCM compounds such as Corydalis yanhusuo and Ajuga decumbens may exert therapeutic effects through multi-component synergistic regulation of these miRNAs and downstream pathways.

Objective To explore the influence of hsa_circ_0004535 on type 2 diabetes(T2DM)combined with metabolic-associated fatty liver disease(MAFLD)model mice.Methods Forty-eight healthy SPF grade Balb/c mice were selected for modeling and divided into the following groups(n=6 per group):Control group:normal feed;T2DM group:diabetes model induced by high-glucose and high-fat diet;T2DM combined MAFLD group:non-alcoholic fatty liver high-glucose and high-fat diet-induced diabetes combined with fatty liver model;T2DM combined MAFLD+hsa_circ_NC group:after 4 weeks of modeling,10 nmol hsa_circ_NC injected into the tail vein;T2DM combined MAFLD+hsa_circ_0004535 group:after 4 weeks of modeling,10 nmol circ_0004535 injected into the tail vein;T2DM combined MAFLD+miRNA_NC group:after 4 weeks of modeling,10 nmol miRNA blank control injected into the tail vein;T2DM combined MAFLD+miR-1827 agomir group:after 4 weeks of modeling,10 nmol miR-1827 agomir injected into the tail vein;and T2DM combined MAFLD+miR-1827 antagomir group:after 4 weeks of modeling,10 nmol miR-1827 antagomir injected into the tail vein.Mouse body weight was measured after the interventions and recorded weekly.Glucose and insulin tolerance tests were performed,blood lipids and liver function were measured,the liver and insulin resistance indexes were calculated,and pathological tests(hematoxylin/eosin(HE),oil red O,and Masson staining,immunohistochemistry,terminal deoxynucleotidyl transferase dUTP nick end labeling(TUNEL))were performed to measure the degree of hepatic inflammation,fat deposition,and fibrosis.Results(1)Body weight,liver weight,liver index,insulin resistance index,and biochemical indexes were all significantly lower in the hsa_circ_0004535 injection group compared with the hsa_circ_NC injection group and the T2DM combined MAFLD group(both P＜0.05).(2)Steatosis vacuoles were reduced and smaller and inflammatory cell infiltration was reduced in the T2DM combined MAFLD+circ_0004535 group,as shown by HE and oil red staining.(3)TUNEL-positive cells were significantly reduced in the T2DM combined MAFLD+hsa_circ_0004535 group(P＜0.05).(4)Collagen fiber deposition was significantly reduced in the T2DM combined MAFLD+hsa_circ_0004535 group,as shown by Masson staining(P＜0.05).Conclusions The expression of hsa_circ_0004535 and miRNA-1827 play important roles in regulating lipid metabolism,insulin sensitivity,inflammatory pathways,hepatocyte apoptosis,and hepatic fibrosis-related pathways in an animal model of T2DM combined with MAFLD.

Objective To compare the effect of different intensity of neuromuscular training(NMT)on muscle strength and knee joint function of patients after anterior cruciate ligament reconstruction(ACLR).Methods From January,2023 to January,2024,60 ACLR patients in Changhai Hospital were selected,and they received the same intensity of NMT from one to eight weeks after surgery.Eight weeks after surgery,they were randomly divided into low intensity group(n=30)and high intensity group(n=30),and then they received different inten-sities of NMT from nine to 16 weeks after surgery,each training session lasted one hour,with three sessions per week,totaly 48 sessions.The Lysholm score,knee flexor and extensor muscle strength and muscle endurance-were compared at eight weeks and 16 weeks after surgery.Results After group training,the Lysholm score significantly increased in both groups(|t|>13.739,P<0.001),and was higher in the high intensity group than in the low intensity group(t=-2.574,P<0.05);in the high intensity group,the relative peak torque and endurance of the extensor and flexor muscles improved at angular velocities of 60°/s,120°/s and 180 °/s(|t|>2.320,P<0.05);in the low intensity group,the flexor peak torque improved at all the three angular velocities(t>2.177,P<0.05),the extensor peak torque improved at angular velocities of 60°/s and 180°/s(|t|>1.715,P<0.05),and the extensor endurance improved at angular velocity of 60°/s(t=-2.293,P<0.05).However,there was no significant difference in the relative peak torque and endurance of the extensor and flexor muscles at all the three angular velocities(P>0.05).Conclusion Both high and low intensity NMT could improve the muscle strength,muscle endurance and knee joint func-tion.Maybe,high intensity is superior to low intensity.Further verification is still needed.

Objective To discuss the potential mechanisms by which programmed cell death(PCD)might contribute to the pathogenesis of diabetic kidney disease(DKD).Methods Retrieve the datasets GSE30529 and GSE30122 from the Gene Expression Omnibus database and analyze them to obtain differentially expressed genes(DEGs)associated with DKD.Utilize the Gene Set Enrichment Analysis website,the ferroptosis database,and the autophagy database,along with relevant literature,to identify genes associated with apoptosis,necroptosis,pyroptosis,autophagy,and ferroptosis.Cross-reference these genes with the DKD DEGs to identify PCD-related genes that are differentially expressed in DKD.Perform Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway enrichment analyses to explore the biological functions and potential pathways of the core genes.Conduct a protein-protein interaction network analysis to examine the interaction relationships of the target genes,and use the CytoHubba plugin in Cytoscape to screen for Hub genes.Results In the GSE30529 dataset,a total of 460 DEGs were identified,while the GSE30122 dataset yielded 992 DEGs.After merging and removing duplicates,932 DEGs were obtained.By intersecting these DEGs with PCD-related genes,61 apoptosis-related genes,7 necroptosis-related genes,39 pyroptosis-related genes,18 autophagy-related genes,and 16 ferroptosis-related genes associated with DKD were identified.The KEGG analysis results indicated that the DEGs related to apoptosis,necroptosis,pyroptosis,and autophagy in PCD were primarily enriched in pathways associated with diabetic complications,including the AGE-RAGE,IL-17,NF-κB,and TNF signaling pathways.In contrast,DEGs related to ferroptosis were mainly enriched in the fatty acid degradation pathway.GO enrichment analysis revealed that the biological processes of the differentially expressed PCD related genes in DKD were primarily involved in the regulation of signals such as NF-κB-inducing kinase/NF-κB,IL-1,and IL-17.Conclusions Differentially expressed PCD-related genes in DKD are mainly enriched in related signal pathways such as AGE-RAGE,IL-17,NF-κB and TNF,suggesting a critical role of PCD in the pathogenesis of DKD.

Aim To investigate the effects of Mdivi-1 on A1 astrocyte activation and its associated signaling molecules.Methods CTX-TNA2 astrocytes were di-vided into the control,ACM,and low-,medium-,and high-dose Mdivi-1 groups based on concentration screening via CCK-8 assay.ACM,a DMEM high-glu-cose medium containing preset concentrations of IL-1α,TNF-α,and C1q,was used to induce A1 activa-tion.The ACM group was stimulated with ACM for 24 hours.Mdivi-1 groups were pretreated with correspond-ing concentrations of Mdivi-1 for 2 hours,followed by ACM stimulation for 24 hours.Real-time quantitative PCR and Western blot were employed to assess mRNA levels and protein expression of IL-1β,C3,and iNOS in all groups.Immunofluorescence and Western blot were used to detect the expression of signaling molecules NLRP3,caspase-1,and ASC.DHE labeling was used to assess and flow cytometry was used to examine reac-tive oxygen species(ROS)levels.Results The CCK-8 assay identified 5,10,and 25 μmol·L-1as ap-propriate concentrations for Mdivi-1 intervention in CTX-TNA2 cells.Real-time quantitative PCR and Western blot results indicated that,compared to the control group,IL-1 β,C3,and iNOS mRNA levels and protein expression were significantly elevated in the ACM group(P＜0.05).In contrast,these levels were significantly reduced in the 10 and 25 μmnol·L-1 Mdi-vi-1 groups compared to the ACM group(P＜0.05).Immunofluorescence and Western blot results confirmed that ACM stimulation significantly activated the NLRP3 inflammasome in astrocytes,while Mdivi-1 intervention effectively reversed the ACM-induced upregulation of NLRP3,caspase-1,and ASC.DHE staining results demonstrated that 5,10,and 25 μmol·L-1Mdivi-1 in-terventions partially reversed the ACM-induced in-crease in ROS levels in a dose-dependent manner.Conclusion Mdivi-1 effectively inhibits A1 astrocyte activation,potentially through modulation of ROS and the NLRP3 inflammasomes.

Transfer-RNA derived small RNA(tsRNA),a re-cently discovered class of non-coding RNA,is produced by ma-ture tRNA or tRNA precursor through the mediation of specific endonucleases.By regulating gene expression at the transcrip-tional and post transcriptional levels and acting as an epigenetic regulator,tsRNA plays an important role in the physiological and pathological processes of many organisms.Therefore,it has gradually become a research hotspot in biomedicine and attracted widespread attention.Moreover,there is increasing evidence that tsRNA is involved in the occurrence and development of many neuropsychiatric diseases through participating in stress re-sponse,cell proliferation and apoptosis,neural development,synaptic plasticity,neuroinflammation and immune regulation,epigenetic regulation,RNA processing,and protein translation regulation.This article mainly discusses the generation,classifi-cation and biological functions of tsRNA,and elaborates on the role and possible mechanisms of tsRNA in neurodevelopment and neuropsychiatric disorders,thereby further revealing the poten-tial of tsRNA as a reliable biomarker and therapeutic target for neuropsychiatric disorders.

Acute respiratory distress syndrome(ARDS)is a common respiratory emergency,but current clinical treatment remains at the level of symptomatic support and there is a lack of effective targeted treatment measures.Our previous study confirmed that inhalation of hydrogen gas can reduce the acute lung injury of ARDS,but the application of hydrogen has flammable and explosive safety concerns.Drinking hydrogen-rich liquid or inhaling hydrogen gas has been shown to play an important role in scavenging reactive oxygen species and maintaining mitochondrial quality control balance,thus improving ARDS in patients and animal models.Coral calcium hydrogenation(CCH)is a new solid molecular hydrogen carrier prepared from coral calcium(CC).Whether and how CCH affects acute lung injury in ARDS re-mains unstudied.In this study,we observed the therapeutic effect of CCH on lipopolysaccharide(LPS)induced acute lung injury in ARDS mice.The survival rate of mice treated with CCH and hydrogen inhalation was found to be comparable,demonstrating a significant improvement compared to the untreated ARDS model group.CCH treatment significantly reduced pulmonary hemorrhage and edema,and improved pulmonary function and local microcirculation in ARDS mice.CCH promoted mitochon-drial peripheral division in the early course of ARDS by activating mitochondrial thioredoxin 2(Trx2),improved lung mitochondrial dysfunction induced by LPS,and reduced oxidative stress damage.The results indicate that CCH is a highly efficient hydrogen-rich agent that can attenuate acute lung injury of ARDS by improving the mitochondrial function through Trx2 activation.

The incomplete degradation of tumour cells by macrophages(Mφ)is a contributing factor to tumour progression and metastasis,and the degradation function of Mφ is mediated through phagosomes and lysosomes.In our preliminary experiments,we found that overactivation of NADPH oxidase 2(NOX2)reduced the ability of Mφ to degrade engulfed tumour cells.Above this,we screened out liquiritin from Glycyrrhiza uralensis Fisch,which can significantly inhibit NOX2 activity and inhibit tumours,to elucidate that suppressing NOX2 can enhance the ability of Mφ to degrade tumour cells.We found that the tumour environment could activate the NOX2 activity in Mφ phagosomes,causing Mφ to produce excessive reactive oxygen species(ROS),thus prohibiting the formation of phagolysosomes before degradation.Conversely,inhibiting NOX2 in Mφ by liquiritin can reduce ROS and promote phagosome-lysosome fusion,therefore improving the enzymatic degradation of tumour cells after phagocytosis,and subse-quently promote T cell activity by presenting antigens.We further confirmed that liquiritin down-regulated the expression of the NOX2 specific membrane component protein gp91 phox,blocking its binding to the NOX2 cytoplasmic component proteins p67 phox and p47 phox,thereby inhibiting the activity of NOX2.This study elucidates the specific mechanism by which Mφ cannot degrade tumour cells after phagocytosis,and indicates that liquiritin can promote the ability of Mφ to degrade tumour cells by suppressing NOX2.

AIM To investigate the effects of Wenfei Jiangzhuo Formula on mitochondrial function of Aβ25-35-induced BV-2 cells.METHODS In the establishment of cell model of Alzheimer's disease(AD)using Aβ25-35 on the BV-2 cells,the optimal concentration and time point of Aβ25-35 intervention were determined;and the groups for the intervention of LFHP-1c group(inhibitor)or the serum containing Wenfei Jiangzhuo Formula were set up.The detection of the optimal intervention concentration and time point by CCK-8 assay;the observation of cell migration and apoptosis by Transwell assay and Hoechst 33342 staining;the detection of the positive expressions of PGAM5 and Drp1 by immunofluorescence;and the detection of cellular PGAM5,Drp1,OPA1,and Mfn1/2 mRNA and protein expressions by RT-qPCR and Western blot were conducted.RESULTS The best AD cell model was established by 48 h exposure to 5 μmol/L of Aβ25-35,and most active cell viability was achieved with the 48 h use of serum containing 20％Wenfei Jiangzhuo Formula.Compared with the control group,the model group displayed decreased number of cell migration,more bright blue positive apoptotic cells,increased number of PGAM5 and Drp1 positive cells and their mRNA and protein expressions(P＜0.05);and decreased mRNA and protein expressions of OPA1 and Mfn1/2(P＜0.05).Compared with the model group,the groups intervened with the medicines shared increased number of cell migration,less bright blue positive apoptotic cells,decreased number of PGAM5 and Drp1 positive cells and their mRNA and protein expressions(P＜0.05);and elevated OPA1 and Mfn1/2 mRNA and protein expressions(P＜0.05).CONCLUSION Wenfei Jiangzhuo Formula exerts cerebroprotective effects to improve cognition by reducing cell damage and improving the balance of mitochondrial homeostasis through PGAM5-Drp1 axis in AD model.