Objective To compare the efficacy between slanted bilateral lateral rectus recession(S-BLR)and conventional bilateral lateral recession(C-BLR)procedure in the treatment of convergence insuffi-ciency-type intermittent exotropia.Methods Relevant studies published before November 2023 were systematically searched in PubMed,Cochrane Library,EmBase,Web of Science,CNKI,Wanfang and VIP databases to compare the surgical effects of S-BLR and C-BLR,expressed by OR value and 95%CI.The success rate,recurrence rate,overcor-rection rate and stereoscopic improvement rate were analyzed by random effects model.Results A total of 5 studies involving 296 patients were included in the analysis.The success rate of the S-BLR procedure was significantly higher than that of C-BLR(OR=4.06,95%CI:2.47-6.67,P＜0.001),patients subjected to the C-BLR pro-cedure were more likely to be recurrent(OR=0.21,95%CI:0.08-0.52,P＜0.001).No statistically signifi-cant differences in the combined results for overcorrection rates(OR=0.43,95%CI:0.07-2.52,P=0.35)and stereoscopic improvement rates(OR=0.82,95%CI:0.36-1.83,P=0.62)were present between the S-BLR and C-BLR procedures(P＞0.05).Conclusion S-BLR procedure has a higher success rate and a lower recurrence rate in patients with aggregation-deficient intermittent exotropia.

Objective To explore the effects of nail-tail transverse connection in the treatment of atlantoaxial dislocation(AAD)and its impacts on bone metabolism,serum vascular endothelial growth factor(VEGF),and fibroblast growth factor-2(FGF-2)levels.Methods A total of 150 pa-tients with AAD were selected as the research subjects and divided into two groups using the random number table method,with 75 cases in each group.The observation group was treated with nail-tail transverse connection combined with posterior atlantoaxial pedicle screw internal fixation(C1-C2 PSR),while the control group was treated with C1-C2 PSR alone.Serum bone metabolism indicators[osteocalcin(BGP),type Ⅰ collagen N-terminal peptide(NTX),bone alkaline phosphatase(BALP),tartrate-resistant acid phosphatase(TRAP),type Ⅰ collagen carboxy-terminal peptide(CTX)],VEGF and FGF-2 levels were compared between the two groups at different time points.The Japanese Orthopaedic Association(JOA)score was used to evaluate the patients' neurological function before surgery and 3 years after surgery.Bone graft fusion was evaluated at 6 months,1 year,2 years,and 3 years after surgery.Results At 1,3 and 6 months after surgery,the serum VEGF and FGF-2 levels in the observation group were higher than those in the control group,and the differences were statistically significant(P＜0.05).After treatment,the BALP,BGP,NTX,TRAP and CTX levels in both groups were lower than those before treatment,and their levels in the observation group were lower than those in the control group,with statistically significant differences(P＜0.05).Before surgery,there was no statistically significant difference in the JOA scores be-tween the two groups(P＞0.05).At 3 years after surgery,the JOA scores in both groups were higher than those before surgery,and the JOA score and the score improvement rate in the observa-tion group were higher than those in the control group,with statistically significant differences(P＜0.05).At 6 months,1 year,2 years and 3 years after surgery,the success rate of bone graft fusion in the observation group was higher than that in the control group,with statistically significant differ-ences(P＜0.05).Conclusion Nail-tail transverse connection has significant effects in the treat-ment of AAD,which can effectively improve patients' bone metabolism and increase the serum VEGF and FGF-2 levels.

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 explore the effect and mechanism of microRNA(miR)-155-5p on myocardial pyroptosis in rats with myocardial ischemia-reperfusion injury(IRI).Methods Sixty SD rats were randomly divided into sham group,IRI group,agomir-NC group,miR-155-5p agomir group,antagomir-NC group,and miR-155-5p antagomir group,with 10 rats in each group.Echocardiography was used to measure the left ventricular end-diastolic diameter(LVEDD),left ventricular end-systolic diameter(LVESD),left ventricular ejection fraction(LVEF),and left ventricular fractional shortening(LVFS)of rats.Enzyme-linked immune absorbent assay(ELISA)was used to detect the levels of creatine kinase isoenzyme(CK-MB),lactate dehydrogenase(LDH),and cardiac troponin T(cTnT)in serum,as well as the levels of interleukin(IL)-1β,IL-6,IL-18,and tumor necrosis factor(TNF)-α in myocardial tissue of rats.Hematoxylin-eosin staining was used to observe pathological changes in rat myocardial tissue.Real-time fluorescent quantitative polymerase chain reaction was used to detect the expression levels of miR-155-5p and silent information regulator 1(SIRT1)messenger RNA(mRNA)in myocardial tissue of rats.Dual-luciferase reporter gene assay was used to verify the targeting relationship between miR-155-5p and SIRT1.Western blot was used to detect the expression levels of SIRT1,NOD-like receptor protein 3(NLRP3),cleaved cysteine aspartate specific proteinase-1(Cleaved Caspase-1),and gasdermin D(GSDMD)proteins in myocardial tissue of rats.Results Compared with the sham group,the LVEDD and LVESD of rats in the IRI group were increased,LVEF and LVFS were decreased,serum levels of CK-MB,LDH,and cTnT were increased,IL-1β,IL-6,IL-18 and TNF-α levels in myocardial tissue were increased,myocardial tissue structure was severely damaged,myocardial fibers were disordered,relative expression of NLRP3,Cleaved Caspase-1,and GSDMD proteins were increased,and the relative expression of SIRT1 protein was decreased(all P<0.05/5).Compared with the IRI group,the rats in the miR-155-5p agomir group had increased LVEDD and LVESD,decreased LVEF and LVFS,increased serum levels of CK-MB,LDH,and cTnT,increased myocardial tissue levels of IL-1β,IL-6,IL-18,TNF-α,aggravated myocardial tissue lesions,increased relative expression of NLRP3,Cleaved Caspase-1,and GSDMD proteins,and decreased relative expression of SIRT1 protein,and the rats in the miR-155-5p antagomir group had decreased LVEDD and LVESD,increased LVEF and LVFS,decreased serum levels of CK-MB,LDH,and cTnT,decreased myocardial tissue levels of IL-1β,IL-6,IL-18,TNF-α,reduced myocardial tissue lesions,decreased relative expression of NLRP3,Cleaved Caspase-1,and GSDMD proteins,and increased relative expression of SIRT1 protein(all P<0.05/5).miR-155-5p was negatively correlated with the expression levels of SIRT1 in rat myocardial tissue,and SIRT1 was a target gene of miR-155-5p.Conclusions miR-155-5p may participate in the regulation of myocardial IRI in rats by targeting the downregulation of SIRT1 and promoting NLRP3-mediated myocardial pyroptosis.

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.

The aims of developing rapid and living guidelines is to keep the recommendations in the guideline up-to-date. Compared with the conventional guideline, the rapid and living guideline can make better use of the existing evidence and apply and transform the evidence in a timely manner. This paper introduces the advantages and usage of rapid and living guidelines, the development process and existing challenges, and offers some insights, in order to provide reference for domestic organizations and scholars engaged in guideline development.

Objective To study the changes of blood glutathione peroxidase (GSH-px),superoxide dis-mutase (SOD),malondialdehyde (MDA) and pathological tissues in the rat contrast-induced nephropathy (CIN) model,and to determine the role of oxidation mechanism in CIN.Methods A total of 40 adult male SD rats were selected and divided into three big groups and five small groups.After constructing the model,six rats with good status were taken from each group for conducting the experiment.The serum GSH-px,SOD and MDA levels were measured,the renal tissue biopsy was performed and the morphological changes of kid-ney cells were compared.Results There was no statistically significant difference in the baseline data among the blank control group,the control group and the experimental group (P>0.05).There was no statistically significant difference in serum GSH-px,SOD and MDA levels before model construction,at 24,48 h after model construction between the blank control group and the control group (P>0.05).There were statistical-ly significant differences in serum GSH-px,SOD and MDA levels of the experimental group between before model construction and after model construction (P<0.05).There was no statistically significant difference in serum GSH-px,SOD and MDA level in the experimental group between at 24 h after modelling and 48 h af-ter modeling (P>0.05).There was no statistically significant difference in serum GSH-px,SOD and MDA levels at 24 h after modeling among the three groups (P>0.05).There were statistically significant differ-ences in serum GSH-px,SOD and MDA levels at 48 h after modeling among the three groups and their pairs (P<0.05).The pathological sections of the blank control group and control group showed no obvious abnor-mal changes in glomeruli,renal tubule and renal interstitium.Renal interstitial fibrosis and inflammatory cell infiltration were seen after 24 h in the experimental group,but there was no obvious change in the renal tu-bules.After 48 h,moderate focal-like atrophy of renal tubules,epithelial cell granule degeneration and vacuolar changes were obviously seen.Conclusion The oxidative stress mechanism plays a role in CIN.The contrast a-gent acute renal injury mainly acts on the renal tubules and renal interstitium,and there is no obvious damage to the glomeruli.

Objective To elucidate the clinical significance in facilitating timely diagnosis and treatment of RMPP in children by investigating the association between infection caused by macrolide-resistant Mycoplasma pneu-moniae(MRMP)and refractory Mycoplasma pneumoniae pneumonia(RMPP)in pediatric patients.Methods The clinical data of 714 hospitalized children with refractory Mycoplasma pneumoniae pneumonia(RMPP)were retro-spectively analyzed.Bronchoscopy and bronchoalveolar lavage fluid(BALF)were performed on each subject,and the BALFs were collected to detect mutation sites in the V region of 23S rRNA for Mycoplasma pneumoniae DNA.Based on the gene detection results,children with RMPP were categorized into a macrolide-resistant group and a control group(non-macrolide-resistant group).Results A total of 714 children diagnosed with refractory Mycoplasma pneumoniae pneumonia(RMPP)were enrolled in this study,including 509 cases in the macrolide-resistant group and 205 cases in the control group.Among them,there were 369 males(54.7%)and 345 females(45.3%).The macrolide-resistant group exhibited higher average age,fever duration,and hospitalization days compared to the control group.Furthermore,elevated levels of white blood cell count(WBC),neutrophil percentage(NE%),high-sensitivity C-reactive protein(hs-CRP),lactate dehydrogenase(LDH),and interleukin-6(IL-6)were observed in the macrolide-resistant group when compared to the control group(P<0.05 or P<0.000 1).Compared to the control group,children with macrolide-resistant Mycoplasma pneumoniae pneumonia(RMPP)exhibited higher incidences of lung consolidation,pleural effusion,necrotic pneumonic lesions,severe MPP(SMPP)/fulminant MPP(FMPP),flocculent and viscous tracheal secretions,severe mucosal lesions(erosion,ulceration or necrosis),bronchial inflammatory stenosis,endo-bronchial plastic phlegm plugs and extra-pulmonary complications(P<0.05 or P<0.0001).Conclusions MRMP infection can contribute to the development of RMPP,potentially exacerbating respi-ratory conditions in affected children.Timely bronchoscopy and collection of BALF samples for accurate evaluation of respiratory tract lesions and detection of MRMP infection have significant implications for guiding precise clinical diagnosis and treatment.

AIM:To investigate the impact of Bruton tyrosine kinase(BTK)on Alzheimer disease(AD)-like pathology through the NIMA(never in mitosis gene A)-related kinase 7(NEK7)-nucleotide-binding oligomerization do-main-like receptor protein 3(NLRP3)pathway.METHODS:5xFAD and wild-type(WT)mice aged 2,4 and 6 months were utilized to assess the expression of BTK,NEK7 and NLRP3 proteins in the hippocampus and cortex via Western blot and immunofluorescence.Co-immunofluorescence was conducted to identify the interaction between NEK7 and NLRP3 in the brains of 4-month-old mice.Three-month-old mice were divided into a control group and an ibrutinib treatment group,receiving intraperitoneal injections of ibrutinib(10 mg/kg)or solvent for 14 d,and were then subjected to behavioral as-sessments including learning and memory tests using the Morris water maze and Y-maze.Wild-type mice were induced with an AD model by intracerebroventricular injection of Aβ42.Morris water maze tests were performed after 14 d to eva-luate learning and memory,followed by measurement of BTK protein levels in the brain via Western blot.BV2 microglial cells were treated with ibrutinib,followed by LPS or Aβ42 stimulation.Western blot analysis was conducted to measure the protein levels of NEK7,NLRP3,BTK and p-BTK(Y223),while immunofluorescence was used to assess the protein expression of ASC,caspase-1,NEK7 and NLRP3.RESULTS:The levels of BTK,NEK7 and NLRP3 in the brains of 5×FAD mice were significantly elevated compared to WT mice,with observed interaction between NEK7 and NLRP3 in the 5xFAD mouse brains.Ibrutinib treatment significantly improved learning and memory functions in mice compared to the AD group.In BV2 cells,pre-treatment with ibrutinib effectively suppressed the NLRP3 inflammasome pathway and NEK7 proteins in response to Aβ42 stimulation.CONCLUSION:BTK plays a regulatory role in AD-like pathology through the NEK7-NLRP3 pathway both in vivo and in vitro.

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.