ObjectiveTo delineate imaging findings using an imaging platform and investigate the correlation between MRI characteristics of spinal cord atrophy and clinical diagnosis in children with spinal cord injury (SCI). MethodsImaging data of 150 children with SCI admitted to Beijing Bo'ai Hospital, China Rehabilitation Research Center, from January, 2002 to March, 2024 were collected and imported into the imaging platform. The anteroposterior and transverse diameters of the middle part of the spinal cord at the cross-section with the most severe atrophy were measured, and the relevant indicators of the previous normal spinal cord segment were measured as controls; the radiomic features were extracted. Clinical data of the children including gender, age, cause of injury, sensory level, motor level, spinal cord injury level, injury severity and disease course were collected. ResultsSpinal cord atrophy was identified in 81 cases (54%), among which 78 cases (96%) were American Spinal Injury Association Impairment Scale (AIS) grade A and 3 cases (4%) were AIS grade C. The upper boundary of the spinal cord atrophy site strongly correlated with the injury level, motor level and sensory level (r > 0.8, P < 0.001). ConclusionMore than half of children with SCI may develop secondary spinal cord atrophy, the vast majority of whom suffer from complete spinal cord injury; the upper boundary of spinal cord atrophy is correlated with the injury level.

Background: s/Aims: Non-invasive models stratifying clinically significant portal hypertension (CSPH) are limited. Herein, we developed a new non-invasive model for predicting CSPH in patients with compensated cirrhosis and investigated whether carvedilol can prevent hepatic decompensation in patients with high-risk CSPH stratified using the new model. Methods: Non-invasive risk factors of CSPH were identified via systematic review and meta-analysis of studies involving patients with hepatic venous pressure gradient (HVPG). A new non-invasive model was validated for various performance aspects in three cohorts, i.e., a multicenter HVPG cohort, a follow-up cohort, and a carvediloltreating cohort. Results: In the meta-analysis with six studies (n=819), liver stiffness measurement and platelet count were identified as independent risk factors for CSPH and were used to develop the new “CSPH risk” model. In the HVPG cohort (n=151), the new model accurately predicted CSPH with cutoff values of 0 and –0.68 for ruling in and out CSPH, respectively. In the follow-up cohort (n=1,102), the cumulative incidences of decompensation events significantly differed using the cutoff values of <–0.68 (low-risk), –0.68 to 0 (medium-risk), and >0 (high-risk). In the carvediloltreated cohort, patients with high-risk CSPH treated with carvedilol (n=81) had lower rates of decompensation events than non-selective beta-blockers untreated patients with high-risk CSPH (n=613 before propensity score matching [PSM], n=162 after PSM). Conclusions Treatment with carvedilol significantly reduces the risk of hepatic decompensation in patients with high-risk CSPH stratified by the new model.

Radiation-induced heart disease(RIHD)is a severe complication in patients with thoracic cancer undergoing radiotherapy,with important impacts on long-term survival among cancer survivors.There is an urgent need to investigate the pathogenesis of RIHD and to develop effective therapeutic agents,and the establishment of high-quality RIHD animal models is pivotal to addressing these issues.This review summarizes the critical factors to consider in establishing RIHD animal models,including species selection,radiation type,dosage,fractionation,and target fields,and modeling timeline,along with the evaluation method and success criteria.We also consider the potential pathogenic mechanisms underlying RIHD,including DNA damage,oxidative stress,inflammatory responses,mitochondrial dysfunction,renin-angiotensin-aldosterone system activation,and myocardial fibrosis,as well as their interrelationships.These insights provide a comprehensive reference framework for constructing RIHD animal models and advancing mechanistic investigations into this condition.

Objective To examine the level of sperm flagellar tubulin glycosylation(Gly-Tubulin)in asthenospermia patients(AP)and discuss its significance.Methods According to the principle of inclusion and exclusion criteria,108 patients treated in the Department of Andrology in Xinjiang Uygur Autonomous Region Maternal and Child Health Hospital from June 2021 to May 2022 were rolled in this study.According to the results of semen examine,they were divided into group AP(n=74),and normal control(NC)group(n=34).Colleced the clinical date of both group,such as the age,the sterility period.The levels of sex hormones were detected by chemiluminescence method.The glycosylated Tubulin levels of the sperm were detected by Western blot and immunofluorescence was used for localization analysis,and the relationship between the Gly-Tubulin of sperm flagellar and asthenospermia was analyzed by Multivariate Logistic regression analysis.Results Compared to NC group,the sterility period of group AP was prolong(3.98±0.30 vs 0.78±0.08),the percent of forward sperm motility was decreased(18.55±0.97 vs 46.24±1.89)and the expression level of Gly-Tubulin in the sperm flagellar was decreased(0.64±0.11 vs 1.00±0.00),the differences with statistical significance(t=62.038,χ2=14.394,3.148,all P＜0.05).There were no significant differences in follicle-stimulating hormone(FSH),luteinizing hormone(LH),prolactin(PRL),estradiol(E2),testosterone,semen volume,sperm concentration and total sperm between the two groups(t/χ2=0.043～1.503,all P>0.05).Multivariate Logistic regression analysis showed that the percent of forward sperm motility and the sperm flagellar Gly-Tubulin expression level were independent risk factors for male asthenospermia(Wald χ2=4.406,7.492,P<0.05).Conclusion Abnormal level of Gly Tubulin in sperm flagella may be closely related to the occurrence and development of asthenospermia.

Epilepsy is a chronic neurological disorder caused by an imbalance between excitation and inhibition in the central nervous system.Recently,the role of the orexin system in the pathogenesis of epilepsy has garnered significant attention.Orex-in primarily regulates arousal states and enhances neuronal excit-ability through activation of OX1-R/OX2-R receptors.Studies have shown that elevated orexin levels lower the seizure thresh-old,while orexin receptor antagonists(ORAs)exhibit potential antiepileptic effects.ORAs suppress epileptiform discharges by reducing glutamate release,enhancing GABAergic inhibitory effects,and modulating the thalamocortical circuit.Animal ex-periments and preliminary clinical studies demonstrate that OX1R antagonists decrease excitatory synaptic transmission,whereas OX2 R antagonists primarily strengthen GABA-mediated inhibition.With the widespread application of ORAs in sleep disorders,exploring their clinical value as antiepileptic drugs will become a key focus for future research.This review summa-rizes the role of the orexin system in epileptogenesis and discus-ses the research progress and future directions of ORAs as poten-tial antiepileptic agents.

Angiopoietin-like proteins(ANGPTLs)are a family of proteins that are structurally similar to angio-poietin.So far,eight ANGPTLs have been discovered,namely ANGPTL1 to ANGPTL8.They are not only angiogenic fac-tors,but also play a pivotal role in various pathophysiological processes such as glucose and lipid metabolism,redox regu-lation,chronic inflammation and cancer,and having a close connection with the occurrence and development of metabolic diseases.This review focuses on the mechanism of action of ANGPTLs in metabolic associated fatty liver disease,in order to make a contribution to the prevention and treatment of MAFLD and concurrent diseases.

Angiopoietin-like proteins(ANGPTLs)are a family of proteins that are structurally similar to angio-poietin.So far,eight ANGPTLs have been discovered,namely ANGPTL1 to ANGPTL8.They are not only angiogenic fac-tors,but also play a pivotal role in various pathophysiological processes such as glucose and lipid metabolism,redox regu-lation,chronic inflammation and cancer,and having a close connection with the occurrence and development of metabolic diseases.This review focuses on the mechanism of action of ANGPTLs in metabolic associated fatty liver disease,in order to make a contribution to the prevention and treatment of MAFLD and concurrent diseases.

Background: s/Aims: Non-invasive models stratifying clinically significant portal hypertension (CSPH) are limited. Herein, we developed a new non-invasive model for predicting CSPH in patients with compensated cirrhosis and investigated whether carvedilol can prevent hepatic decompensation in patients with high-risk CSPH stratified using the new model. Methods: Non-invasive risk factors of CSPH were identified via systematic review and meta-analysis of studies involving patients with hepatic venous pressure gradient (HVPG). A new non-invasive model was validated for various performance aspects in three cohorts, i.e., a multicenter HVPG cohort, a follow-up cohort, and a carvediloltreating cohort. Results: In the meta-analysis with six studies (n=819), liver stiffness measurement and platelet count were identified as independent risk factors for CSPH and were used to develop the new “CSPH risk” model. In the HVPG cohort (n=151), the new model accurately predicted CSPH with cutoff values of 0 and –0.68 for ruling in and out CSPH, respectively. In the follow-up cohort (n=1,102), the cumulative incidences of decompensation events significantly differed using the cutoff values of <–0.68 (low-risk), –0.68 to 0 (medium-risk), and >0 (high-risk). In the carvediloltreated cohort, patients with high-risk CSPH treated with carvedilol (n=81) had lower rates of decompensation events than non-selective beta-blockers untreated patients with high-risk CSPH (n=613 before propensity score matching [PSM], n=162 after PSM). Conclusions Treatment with carvedilol significantly reduces the risk of hepatic decompensation in patients with high-risk CSPH stratified by the new model.

Background: s/Aims: Non-invasive models stratifying clinically significant portal hypertension (CSPH) are limited. Herein, we developed a new non-invasive model for predicting CSPH in patients with compensated cirrhosis and investigated whether carvedilol can prevent hepatic decompensation in patients with high-risk CSPH stratified using the new model. Methods: Non-invasive risk factors of CSPH were identified via systematic review and meta-analysis of studies involving patients with hepatic venous pressure gradient (HVPG). A new non-invasive model was validated for various performance aspects in three cohorts, i.e., a multicenter HVPG cohort, a follow-up cohort, and a carvediloltreating cohort. Results: In the meta-analysis with six studies (n=819), liver stiffness measurement and platelet count were identified as independent risk factors for CSPH and were used to develop the new “CSPH risk” model. In the HVPG cohort (n=151), the new model accurately predicted CSPH with cutoff values of 0 and –0.68 for ruling in and out CSPH, respectively. In the follow-up cohort (n=1,102), the cumulative incidences of decompensation events significantly differed using the cutoff values of <–0.68 (low-risk), –0.68 to 0 (medium-risk), and >0 (high-risk). In the carvediloltreated cohort, patients with high-risk CSPH treated with carvedilol (n=81) had lower rates of decompensation events than non-selective beta-blockers untreated patients with high-risk CSPH (n=613 before propensity score matching [PSM], n=162 after PSM). Conclusions Treatment with carvedilol significantly reduces the risk of hepatic decompensation in patients with high-risk CSPH stratified by the new model.

Epilepsy is a chronic neurological disorder caused by an imbalance between excitation and inhibition in the central nervous system.Recently,the role of the orexin system in the pathogenesis of epilepsy has garnered significant attention.Orex-in primarily regulates arousal states and enhances neuronal excit-ability through activation of OX1-R/OX2-R receptors.Studies have shown that elevated orexin levels lower the seizure thresh-old,while orexin receptor antagonists(ORAs)exhibit potential antiepileptic effects.ORAs suppress epileptiform discharges by reducing glutamate release,enhancing GABAergic inhibitory effects,and modulating the thalamocortical circuit.Animal ex-periments and preliminary clinical studies demonstrate that OX1R antagonists decrease excitatory synaptic transmission,whereas OX2 R antagonists primarily strengthen GABA-mediated inhibition.With the widespread application of ORAs in sleep disorders,exploring their clinical value as antiepileptic drugs will become a key focus for future research.This review summa-rizes the role of the orexin system in epileptogenesis and discus-ses the research progress and future directions of ORAs as poten-tial antiepileptic agents.