Objective:To investigate the alterations in the brain structural network properties related to cognitive emotion regulation strategies in young, first-episode and drug-naive (FEDN) patients with major depressive disorder (MDD).Methods:One hundred and twelve young patients who were diagnosed with FEDN MDD were enrolled in the Second Xiangya Hospital of Central South University between October 2019 and October 2023, and 143 healthy controls (HC) were recruited for reference during the same period. Clinical data and T 1 structural images of high-resolution magnetic resonance imaging were collected from all participants, and the cognitive emotion regulation was assessed using the Chinese version of the Cognitive Emotion Regulation Questionnaire (CERQ-C). The brain structural alterations related to cognitive emotion regulation strategies were explored using whole-brain voxel-based morphometry (VBM) group analysis and individual differential structural covariance network (IDSCN) analysis. Partial correlation analysis was performed between the IDSCN anomalous structural concatenated edge and subdimensions of the CERQ-C. Results:The scores on the sub-dimension of negative cognitive emotion regulation (self-condemnation, rumination, catastrophization, blaming others) in the young FEDN MDD patients in CERQ-C were significantly higher than those in HC (14.28±2.30 vs 12.45±2.00, t=6.501, P<0.001;14.40±2.97 vs 11.31±2.93, t=7.934, P<0.001;12.19±3.75 vs 7.59±2.58, t=10.553, P<0.001;10.26±3.00 vs 8.74±2.89, t=3.916, P<0.001; respectively). There was no statistically significant difference in the VBM group analysis (all P>0.05). However, IDSCN single sample t test results showed significant group differences between the left orbitofrontal inferior gyrus and the left supplementary motor area, the left orbitofrontal middle gyrus and the bilateral precuneus, and the left superior temporal gyrus and the bilateral hippocampus (all P<0.05). With controlling for age, sex, and other factors, partial correlation analysis results showed that the left orbital inferior frontal gyrus-left supplementary motor area connection in patients with MDD was positively correlated with the self-condemnation and acceptance scores of the CERQ-C ( r=0.226, P=0.027; r=0.216, P=0.035), while negatively correlated with the score of blaming others ( r=-0.252, P=0.013). Additionally, connections between the right hippocampus and left superior temporal gyrus were significantly associated with the scores on catastrophization subdimension of the CERQ-C ( r=0.229, P=0.025). Conclusion:Due to its sensitivity to individualized analyses, the IDSCN analysis found that abnormal topological property changes were mainly manifested in the limbic system, the sensorimotor system, and the default network in young FEDN MDD patients, and were linked to their negative cognitive emotion regulation strategies, even though the VBM group analysis did not yield any significant results.

AIM:To investigate the modulatory role of E3 ubiquitin-protein ligase ITCH in Alzheimer disease(AD)-like pathology through the thioredoxin-interacting protein(TXNIP)-nucleotide-binding oligomerization domain-like receptor protein 3(NLRP3)signaling pathway using both in vivo and in vitro experimental models.METHODS:(1)Ten 5×FAD(AD model)mice and 10 wild-type(WT)mice at 2-,4-and 6-month-old were randomly allocated into AD and WT groups.Amyloid β-protein(Aβ)plaque burden in the brain was detected by thioflavin-S and immunofluorescence staining,with the latter method additionally applied to assess TXNIP protein expression.The protein levels of ITCH and TXNIP were determined by Western blot,while their interaction was verified by co-immunoprecipitation.(2)Mouse mi-croglia BV2 cells stimulated by lipopolysaccharide(LPS)were used to construct neuroinflammation model,and were di-vided into control(CON)group and LPS+ATP treatment group.The BV2 cells stimulated by Aβ were used to construct AD inflammation model.According to the different treatment time,they were divided into CON,and 12,24 and 48 h treatment groups.Western blot was used to evaluate the expression of ITCH,TXNIP,and NLRP3 inflammasome compo-nents(NLRP3 and caspase-1)as well as the downstream IL-1β.Adenovirus-mediated ITCH overexpression(OE-ITCH)in Aβ-stimulated BV2 cells comprised three experimental groups:negative control group,Aβ oligomer stimulation group,and OE-ITCH group,with subsequent immunoblotting of inflammatory mediators.RESULTS:The deposition of Aβ plaques in the cortex and hippocampus of 5×FAD transgenic mice exhibited an age-dependent progression(P<0.01).Compared with WT mice,the levels of TXNIP protein increased synchronously,and the levels of ubiquitin ligase ITCH was significantly down-regulated(P<0.05).Co-immunoprecipitation confirmed the interaction between ITCH and TXNIP proteins in the brain of 2-and 4-month-old 5×FAD mice,which exhibited marked attenuation by 4 months of age.In BV2 microglial models,Aβ/LPS stimulation provoked significant ITCH suppression,concurrently up-regulating TXNIP,core NLRP3 inflammasome components(NLRP3 and caspase-1),and downstream IL-1β(P<0.05).Overexpression of ITCH significantly inhibited Aβ-induced activation of TXNIP and NLRP3 and therelated inflammatory factors in BV2 cells.CONCLUSION:The results of in vitro and in vivo experiments showed that ITCH protein exerts effects against AD-like pathology by inhibiting the expression of TXNIP-NLRP3 signaling pathway.

AIM:To investigate the modulatory role of E3 ubiquitin-protein ligase ITCH in Alzheimer disease(AD)-like pathology through the thioredoxin-interacting protein(TXNIP)-nucleotide-binding oligomerization domain-like receptor protein 3(NLRP3)signaling pathway using both in vivo and in vitro experimental models.METHODS:(1)Ten 5×FAD(AD model)mice and 10 wild-type(WT)mice at 2-,4-and 6-month-old were randomly allocated into AD and WT groups.Amyloid β-protein(Aβ)plaque burden in the brain was detected by thioflavin-S and immunofluorescence staining,with the latter method additionally applied to assess TXNIP protein expression.The protein levels of ITCH and TXNIP were determined by Western blot,while their interaction was verified by co-immunoprecipitation.(2)Mouse mi-croglia BV2 cells stimulated by lipopolysaccharide(LPS)were used to construct neuroinflammation model,and were di-vided into control(CON)group and LPS+ATP treatment group.The BV2 cells stimulated by Aβ were used to construct AD inflammation model.According to the different treatment time,they were divided into CON,and 12,24 and 48 h treatment groups.Western blot was used to evaluate the expression of ITCH,TXNIP,and NLRP3 inflammasome compo-nents(NLRP3 and caspase-1)as well as the downstream IL-1β.Adenovirus-mediated ITCH overexpression(OE-ITCH)in Aβ-stimulated BV2 cells comprised three experimental groups:negative control group,Aβ oligomer stimulation group,and OE-ITCH group,with subsequent immunoblotting of inflammatory mediators.RESULTS:The deposition of Aβ plaques in the cortex and hippocampus of 5×FAD transgenic mice exhibited an age-dependent progression(P<0.01).Compared with WT mice,the levels of TXNIP protein increased synchronously,and the levels of ubiquitin ligase ITCH was significantly down-regulated(P<0.05).Co-immunoprecipitation confirmed the interaction between ITCH and TXNIP proteins in the brain of 2-and 4-month-old 5×FAD mice,which exhibited marked attenuation by 4 months of age.In BV2 microglial models,Aβ/LPS stimulation provoked significant ITCH suppression,concurrently up-regulating TXNIP,core NLRP3 inflammasome components(NLRP3 and caspase-1),and downstream IL-1β(P<0.05).Overexpression of ITCH significantly inhibited Aβ-induced activation of TXNIP and NLRP3 and therelated inflammatory factors in BV2 cells.CONCLUSION:The results of in vitro and in vivo experiments showed that ITCH protein exerts effects against AD-like pathology by inhibiting the expression of TXNIP-NLRP3 signaling pathway.

Objective:To investigate the alterations in the brain structural network properties related to cognitive emotion regulation strategies in young, first-episode and drug-naive (FEDN) patients with major depressive disorder (MDD).Methods:One hundred and twelve young patients who were diagnosed with FEDN MDD were enrolled in the Second Xiangya Hospital of Central South University between October 2019 and October 2023, and 143 healthy controls (HC) were recruited for reference during the same period. Clinical data and T 1 structural images of high-resolution magnetic resonance imaging were collected from all participants, and the cognitive emotion regulation was assessed using the Chinese version of the Cognitive Emotion Regulation Questionnaire (CERQ-C). The brain structural alterations related to cognitive emotion regulation strategies were explored using whole-brain voxel-based morphometry (VBM) group analysis and individual differential structural covariance network (IDSCN) analysis. Partial correlation analysis was performed between the IDSCN anomalous structural concatenated edge and subdimensions of the CERQ-C. Results:The scores on the sub-dimension of negative cognitive emotion regulation (self-condemnation, rumination, catastrophization, blaming others) in the young FEDN MDD patients in CERQ-C were significantly higher than those in HC (14.28±2.30 vs 12.45±2.00, t=6.501, P<0.001;14.40±2.97 vs 11.31±2.93, t=7.934, P<0.001;12.19±3.75 vs 7.59±2.58, t=10.553, P<0.001;10.26±3.00 vs 8.74±2.89, t=3.916, P<0.001; respectively). There was no statistically significant difference in the VBM group analysis (all P>0.05). However, IDSCN single sample t test results showed significant group differences between the left orbitofrontal inferior gyrus and the left supplementary motor area, the left orbitofrontal middle gyrus and the bilateral precuneus, and the left superior temporal gyrus and the bilateral hippocampus (all P<0.05). With controlling for age, sex, and other factors, partial correlation analysis results showed that the left orbital inferior frontal gyrus-left supplementary motor area connection in patients with MDD was positively correlated with the self-condemnation and acceptance scores of the CERQ-C ( r=0.226, P=0.027; r=0.216, P=0.035), while negatively correlated with the score of blaming others ( r=-0.252, P=0.013). Additionally, connections between the right hippocampus and left superior temporal gyrus were significantly associated with the scores on catastrophization subdimension of the CERQ-C ( r=0.229, P=0.025). Conclusion:Due to its sensitivity to individualized analyses, the IDSCN analysis found that abnormal topological property changes were mainly manifested in the limbic system, the sensorimotor system, and the default network in young FEDN MDD patients, and were linked to their negative cognitive emotion regulation strategies, even though the VBM group analysis did not yield any significant results.

Objective To establish a genetic monitoring method for laboratory quails.Methods Quail microsatellite loci were searched in the literature,and microsatellite DNA loci suitable for quails were screened by an interspecific transfer method in closely related species,namely chickens and ducks.Quail liver DNA was extracted as a template,and the corresponding loci were screened by PCR amplification and agarose gel electrophoresis.On the basis of amplification of the selected microsatellite loci,the number of alleles,polymorphisms,and microsatellite loci combinations for quail genetic quality detection were selected and detection method were developed.Results We preliminary determined 23 microsatellite loci for genetic monitoring of closed-colony laboratory quails.Conclusions A genetic monitoring method for laboratory quails was preliminary developed.

Objective To systematically evaluate the risk factors for new-onset atrial fibrillation after off-pump coronary artery bypass grafting (OPCABG). Methods PubMed, EMbase, The Cochrane Library, CNKI, Wanfang, VIP, SinoMed were searched to collect published literature on risk factors for new-onset atrial fibrillation after OPCABG from inception to September 2022. Two authors independently screened, extracted data and evaluated the quality. The Newcastle-Ottawa Scale (NOS) was used to evaluate the quality of the included studies, and Stata 12.0 and RevMan 5.4 softwares were used for meta-analysis. Results A total of 18 researches were included, including 6 354 patients of OPCABG. The NOS scores of the included studies were 6-8 points. Meta-analysis showed that age [MD=2.56, 95%CI (1.61, 3.52), P<0.001], hypertension [OR=1.77, 95%CI (1.18, 2.66), P<0.001], EuroSCORE Ⅱ score [MD=0.70, 95%CI (0.34, 1.06), P<0.001], frequent atrial premature beats or atrial tachycardia [OR=3.77, 95%CI (2.13, 6.68), P<0.001], left atrium diameter (LAD) [MD=1.64, 95%CI (0.26, 3.03), P=0.010], left ventricular ejection fraction (LVEF) [MD=−1.84, 95%CI (−2.85, −0.83), P<0.001], right coronary stenosis [OR=2.49, 95%CI (1.29, 4.81), P=0.006], three-vessel coronary artery lesions [OR=0.73, 95%CI (0.54, 0.97), P=0.030], not using β blockers [OR=0.81, 95%CI (0.69, 0.96), P=0.010], operation time [MD=10.13, 95%CI (8.15, 12.10), P<0.001], duration of mechanical ventilation [OR=2.85, 95%CI (1.79, 3.91), P<0.001] were risk factors for new-onset atrial fibrillation after OPCABG. Conclusion Advanced age, hypertension, high EuroSCOREⅡ score, frequent atrial premature beats or atrial tachycardia, increased LAD, decreased LVEF, right coronary stenosis, three-vessel coronary artery lesions, not using β blockers, prolonged operation time and mechanical ventilation are risk factors for new-onset atrial fibrillation after OPCABG. Due to factors such as the methodology, content and quality of the included literature, the conclusion of this study need to be supported by more high-quality studies.

Objective To study the role of microRNA(miR)-483-3p in reducing myocardial fibrosis in rats,and explore the relationship between its mechanism and autophagy.Methods A total of 24 male SD rats were randomly divided into sham operation group,model group,blank transfec-tion group and high expression group,with 6 rats in each group.The blank transfection group and the high-expression group were pretreated with a single injection of adeno-associated virus(AAV)-blank transfection and AAV-miR-483-3p(5×1011 vg)in the tail vein,respectively.In 14 d later,the sham group was injected with 2.5 ml/(kg·d)normal saline for 14 d,and rat model of myocardial fibrosis was established by 2 mg/ml isoproterenol[2.5 ml/(kg·d)]injection through tail vein for 14 consecutive days.Myocardial pathological damage,severity of myocardial fibrosis,and expression levels of collagen-Ⅰ,microtubule-associated protein light chain 3(LC3),autoph-agy-related protein 5(Atg5)and autophagy degradation substrate(P62)in cardiomyocytes were evaluated and measured.Results Compared with the sham operation group,the model group had obviously larger myocardial fibrosis area,higher positive expression of Collagen-Ⅰ,and increased protein levels of Atg5 and LC3-Ⅱ/LC3-Ⅰ,and decreased expression level of P62 protein(P＜0.05).The myocardial fibrosis area,positive expression of Collagen-Ⅰ,the expression levels of Atg5 and LC3-Ⅱ/LC3-Ⅰ protein[(13.64±1.51)％vs(27.47±1.55)％,(13.48±3.07)％vs(30.91±2.45)％,0.98±0.17 vs 1.24±0.28,0.66±0.05 vs 1.26±0.09,P＜0.05]were significant-ly decreased,and the expression level of P62 was notably increased(0.91±0.11 vs 0.74±0.06,P＜0.05)in the high expression group than the model group.Conclusion MiR-483-3p attenuates myocardial fibrosis in rats,and the mechanism may be related to the inhibition of cardiomyocyte autophagy.

Objective To analyze the clinical characteristics and prognosis of patients with coronary slow flow(CSF)or no reflow(CNR)after emergency PCI.Methods A total of 443 elderly STEMI patients who underwent emergency PCI in Department of Cardiology of the First Affilia-ted Hospital of Tsinghua University from January 2017 to August 2023 were recruited,and ac-cording to thrombolysis in myocardial infarction(TIMI)flow grading after operation,they were divided into CSF/CNR group(TIMI grade≤2 flow,n=40)and normal flow(NCF)group(TIMI grade 3 flow,n=403).Logistic regression analysis was used to analyze the risk factors for CSF/CNR in STEMI patients after PCI.The prognosis was analyzed in the two groups.Results The CSF/CNR group had advanced age,longer durations from onset to admission and from onset to balloon opening,higher mortality rate,and larger proportions of chronic heart failure(CHF),type 2 diabetes mellitus(T2DM),pulse rate＞100 times/min,SBP＜100 mm Hg(1 mm Hg=0.133 kPa),Killip grade＞1,left anterior descending artery disease,LVEF＜50％,and using glycopro-tein Ⅱb/Ⅲa inhibitors and intraaortic balloon counterpulsation,but lower male ratio and DBP when compared with the control group(P＜0.05,P＜0.01).Multiple logistic regression analysis revealed that T2DM(OR=1.320,95％CI:0.618-2.123,P=0.046),mean SBP(OR=1.239,95％CI:0.752-1.525,P=0.04)and SBP＜100 mm Hg(OR=1.330,95％CI:0.836-1.675,P=0.013)were independent risk factors,while male was a protective factor(OR=-1.755,95％CI:-2.338--1.171,P=0.002)for CSF/CNR in STEMI patients after PCI.Conclusion T2DM and lower SBP are independent risk factors,while male is a protective factor for CSF/CNR in STEMI patients after emergency PCI.

Objective To explore the effect of a phased rehabilitation training programme to relieve shoulder dys-function in patients after neck dissection and to provide effective solutions for postoperative shoulder joint function recov-ery of patients.Methods This study has been reviewed and approved by the Ethics Committee,and informed consent has been obtained from patients.A phased rehabilitaiton training programme for the shoulder after neck dessection was developed through literature review and discussion,and 70 eligible patients from Hospital of Stomatology,Sun Yat-sen University from December 2020 to April 2021 were selected and randomly divided into the test group and control group(35 patients in each group).The control group underwent motor rehabilitation training from 6 weeks postoperative to 1 year after surgery,such as shoulder mobility and coordination training and small range of motion training of the neck,while the test group took part in a rehabilitation training program that included familiarization maneuver training,protective rehabilitation,exercise rehabilitation,and resistance training in the following four stages:preoperative,postop-erative general anesthesia and awake until the removal of stitches,the removal of stitches until 6 weeks after surgery,and 6 weeks after surgery until 1 year after surgery.The frequency of training in both groups was at least 3 days per week,and the length of each training session was 10-15 min.The intensity of exercise was 2-3 points on the Borg Conscious Ex-ercise Intensity Scale(i.e.,mild-to-moderate tachypnea or fatigue).The neck dissection injury index(NDII)was used to evaluate the quality of life related to shoulder joint function at four time points:preoperative,postoperative 3 months,postoperative 6 months,and postoperative 12 months.The higher the score,the better the quality of life.Results 28 cases in the test group and 32 cases in the control group completed a one-year follow-up.At 3 and 6 months postopera-tive,the NDII of the test group was significantly higher than that of the control group[3 months postoperative:test group(93.48±9.36)vs.control group(80.00±11.34)(P＜0.001),6 months postoperative:test group(98.21±4.76)vs.control group(90.70±9.12)(P＜0.001)];12 months after surgery,the NDII of the test group(97.23±4.88)was still higher than that of the control group(96.33±4.49),but the difference was not statistically significant(P=0.458).The difference in NDII scores among subjects at 3,6,and 12 months after surgery was statistically significant in each group(P＜0.001).Conclusion The application of the phased rehabilitation training method in neck dissection patients has a feasibility and could improve the quality of life of patients'shoulder joint function within 6 months after surgery.

Objective:To study the inhibitory effect of endothelial progenitor cells (EPCs) on aortic injury in mice with systemic lupus erythematosus (SLE) arteriosclerosis.Methods:APOE -/- mice were injected with norphytane and high fat diet to establish lupus vascular injury model. Then the mice were divided into normal control group (ND group), high fat diet group (HFD group), high fat diet+ SLE vascular injury group (HFD+ SLE group), high fat diet+ SLE vascular injury+ hydroxychloroquine treatment group (HFD+ SLE+ Hydro group), high fat diet+ SLE vascular injury+ EPCs treatment group (HFD+ SLE+ EPCs group). At the end of the experiment, urine, blood and aortic tissues of mice in each group were collected, and the content of urinary protein and the depth of serum type I interferon (IFN-Ⅰ) were detected by enzyme linked immunosorbent assay (ELISA). The activation of cyclic guanosine monophosphate synthase/interferon gene stimulating factor/type I interferon (cGAS/STING/IFN-Ⅰ) pathway, the levels of inflammatory factors, adhesion fractions and chemokines in the aorta of mice in each group were detected by immunohistochemistry and Western blotting (WB). The lipid deposition in the aorta was detected by oil red staining. Results:The results of ELISA showed that the levels of urinary protein and serum IFN-Ⅰ in HFD+ SLE group were higher than those in normal control group. EPCs treatment could reduce the levels of urinary protein and serum IFN-Ⅰ in SLE atherosclerotic mice. WB results showed that the expression of CD19, CD68, CD34, chemokine, cGAS, p-STING, phosphorylated TANK binding kinase 1 (p-TBK1), phosphorylated interferon regulatory factor 3 (p-IRF3) and IFN-Ⅰ increased in HFD+ SLE group, and hydroxychloroquine and EPCs decreased the levels of these factors. CGAS/STING/IFN-Ⅰ signal pathway is involved in the occurrence and development of atherosclerosis in SLE patients; both EPCs and hydroxychloroquine can inhibit the activation of cGAS/STING/IFN-Ⅰ signal, thus reducing atherosclerosis in SLE mice.Conclusions:cGAS/STING/IFN-Ⅰ pathway is involved in the development of SLE atherosclerosis. EPCs can inhibit the activation of cGAS/STING signal, reduce the expression and secretion of IFN-Ⅰ, and then reduce vascular inflammation and inhibit the development of SLE-related atherosclerosis.