Objective:To analyze the developmental trajectories of depressive symptoms in middle school students and their relationship with school connection and self-efficacy,and to provide evidence for the prevention of early adolescent depressive symptoms.Methods:In March(T1),June(T2),December(T3),809 middle school students were followed up in 2023 using the Patient Health Questionnaire-9(PHQ-9),School Connection Scale(SCS)and General Self-Efficacy Scale(GSES).The heterogeneity of the developmental trajectory of depressive symptoms in early adolescents was analyzed by the latent variable growth mixed model(LGMM),and the relation-ship between the developmental trajectory of depressive symptoms and school connection and self-efficacy was ana-lyzed by multiple logistic regression.Results:LGMM results showed that the development trajectory of early de-pressive symptoms in adolescents could be divided into:"low level-remission group"(65.3％),"low level-stable group"(28.6％)and"medium level-worsening group"(6.1％).Logistic regression analysis showed that male students(OR=0.62,95％CI=0.44-0.86)and school connection(OR=0.91,95％CI=0.88-0.94)were the protective factors in the"low level-stable group".Boys(OR=0.26,95％CI=0.13-0.53),school connection(OR=0.93,95％CI=0.88-0.98),and self-efficacy(OR=0.90,95％CI=0.85-0.96)were the protective fac-tors in the"medium level-worsening".Conclusion:There is heterogeneity in the developmental trajectory of early adolescent depressive symptoms,and school connection and self-efficacy are protective factors for the development of early adolescent depressive symptoms.

Objective:To analyze the developmental trajectories of depressive symptoms in middle school students and their relationship with school connection and self-efficacy,and to provide evidence for the prevention of early adolescent depressive symptoms.Methods:In March(T1),June(T2),December(T3),809 middle school students were followed up in 2023 using the Patient Health Questionnaire-9(PHQ-9),School Connection Scale(SCS)and General Self-Efficacy Scale(GSES).The heterogeneity of the developmental trajectory of depressive symptoms in early adolescents was analyzed by the latent variable growth mixed model(LGMM),and the relation-ship between the developmental trajectory of depressive symptoms and school connection and self-efficacy was ana-lyzed by multiple logistic regression.Results:LGMM results showed that the development trajectory of early de-pressive symptoms in adolescents could be divided into:"low level-remission group"(65.3％),"low level-stable group"(28.6％)and"medium level-worsening group"(6.1％).Logistic regression analysis showed that male students(OR=0.62,95％CI=0.44-0.86)and school connection(OR=0.91,95％CI=0.88-0.94)were the protective factors in the"low level-stable group".Boys(OR=0.26,95％CI=0.13-0.53),school connection(OR=0.93,95％CI=0.88-0.98),and self-efficacy(OR=0.90,95％CI=0.85-0.96)were the protective fac-tors in the"medium level-worsening".Conclusion:There is heterogeneity in the developmental trajectory of early adolescent depressive symptoms,and school connection and self-efficacy are protective factors for the development of early adolescent depressive symptoms.

Objective: To explore the latent class characteristics and related factors of health risk behaviors among higher vocational college students (referred to as vocational students) in the Wuling Mountain Area, so as to provide references for promoting their healthy development and formulating effective intervention measures. Methods: From April to June 2024, a stratified random cluster sampling method was used to survey 1 737 students from three higher vocational colleges in the Wuling Mountain Area (Xiangxi in Hunan, Enshi in Hubei, and Tongren in Guizhou). The study employed the Health risk Behavior Questionnaire for College Students, the Parent-Child Relationship Scale, the Social Support Scale, and the School Connection Scale for data collection. Latent class analysis (LCA) was used to examine the heterogeneous distribution characteristics of health risk behaviors among vocational students, and multivariate Logistic regression was applied to analyze the related factors of latent classes. Results: The LCA results identified three latent classes based on 12 health risk behaviors: the comprehensive high risk group (151 students, 8.7% ), the psychological distress group (883 students, 50.8%), and the low risk group (703 students, 40.5%). The distribution of latent classes showed statistically significant differences in gender and only child status ( χ 2=121.25, 9.85, both P <0.05). The low risk group scored higher in parent-child relationship (29.26±6.19), social support (63.98±18.16), and school connection (35.97± 7.71 ) compared to the comprehensive high risk group (27.28±6.03, 57.67±15.60, 32.97±7.55) and the psychological distress group (27.52±5.19, 62.06±14.54, 33.80±6.14) ( F =20.37, 23.51, 9.89, all P <0.05). Multivariate Logistic regression revealed that boys( OR =3.29) were more likely to belong to the comprehensive high risk group, social support ( OR =0.03, 0.21) and school connection ( OR =0.92, 0.96) were less likely to belong to both the comprehensive high risk and psychological distress groups (all P < 0.05). Conclusions There are three potential categories of healthharmful behaviors among vocational college students in Wuling Mountain Area. Schools, families and society should enhance the levels of parent-child relationship, school connections and social support for vocational college students of different categories to promote their physical and mental health development.

Objective:To preliminarily evaluate the lumen gain of sonodynamic therapy (SDT) mediated by sinoporphyrin sodium at carotid and femoral atherosclerotic plaque sites, and to assess whether concomitant statin use, lesion location, plaque echogenicity/type, and baseline stenosis severity modify the therapeutic response.Methods:This single-center, prospective, exploratory pilot clinical study enrolled patients with peripheral artery disease who attended the outpatient cardiology clinic of the First Affiliated Hospital of Harbin Medical University between February and September 2016. All enrolled patients received optimized oral medical therapy in combination with a single session of SDT. Vascular evaluation was performed using color Doppler ultrasound before treatment and 1 and 4 weeks after treatment. The primary efficacy endpoint was the percent change from baseline in luminal diameter stenosis at the site of the atherosclerotic plaque (%Δ) at week 4, while the secondary efficacy endpoint was %Δ at week 1. Subgroup analyses were conducted according to prior statin use, plaque location, plaque characteristics, and baseline degree of luminal stenosis.Results:A total of 24 patients, aged (70.7±2.2) years were enrolled. There were 20 (83%) males. Compared to baseline, luminal diameter stenosis at the plaque site reduced by week 4 ((50.1±1.2)% vs. (57.2±1.1)%, P<0.001), %Δ was(12.32±1.05)%; and luminal diameter stenosis also reduced by week 1 ((51.7±1.2)% vs. (57.2±1.1)%, P<0.001)), %Δ was(9.61±0.85)%. In subgroup analyses, the treatment effect on diameter stenosis was independent of prior statin use; SDT reduced stenosis in both carotid and femoral plaques; with superior efficacy observed in hypoechoic and mixed-echo plaques; and efficacy was observed across mild, moderate, and severe baseline stenosis categories (all P<0.05). Conclusion:In this single-center pilot study, SDT demonstrates therapeutic efficacy across mild, moderate, and severe stenoses, as well as in hypoechoic and mixed-echo plaques, showing potential to rapidly promote luminal gain at carotid and femoral atherosclerotic plaque sites.

Objective:To investigate the effect and underlying mechanism of sonodynamic therapy (SDT) on inflammation-related atrial fibrillation (AF) susceptibility.Methods:Lipopolysaccharide (LPS)-stimulated mouse and HL-1 mouse atrial myocyte models were used. (1) In vivo study: experimental groups included control, LPS, LPS+SDT, and SDT groups, with 20 mice in each group. Atrial fibrillation inducibility and duration were assessed by electrical stimulation. Western blot was used to analyze atrial expression of NOD-like receptor family pyrin domain-containing protein 3 (NLRP3), interleukin (IL)-1β, and IL-18. Immunohistochemistry was used to detect calcium voltage-gated channel subunit alpha1 C (CACNA1C) expression. (2) In vitro study: cell counting kit-8 (CCK-8) and Western blot were used to determine the optimal and safe LPS concentration. The safe incubation condition for the sonosensitizer sinoporphyrin sodium was determined by CCK-8 and fluorometry. An LPS-induced inflammatory model in HL-1 atrial myocytes was used, with experimental groups including control, LPS, LPS+SDT, LPS+sinoporphyrin sodium, and LPS+ultrasound groups. NLRP3 was overexpressed using plasmid transfection, with experimental groups including control, NLRP3 plasmid, negative control plasmid, and NLRP3 plasmid+SDT groups. SDT was applied to LPS-stimulated or NLRP3-overexpressing HL-1 cells. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were used to measure mRNA and protein levels of NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC), Cleaved Caspase-1, IL-1β, IL-18, and CACNA1C. The NLRP3 inhibitor MCC950 was used to validate the relationship of NLRP3 and CACNA1C. The experimental groups included control, LPS, LPS+MCC950, and MCC950 groups. Intracellular reactive oxygen species (ROS) levels were detected using the probe DCFH-DA, and the ROS scavenger N-acetyl-L-cysteine (NAC) was used to test if the effects of SDT was ROS-dependent.Results:(1) In vivo: The LPS+SDT group exhibited a lower incidence of atrial fibrillation induction and a shorter duration of atrial fibrillation compared to the LPS group(both P<0.05). Protein expression levels of NLRP3 and IL-1β were lower than those in the LPS group (all P<0.05), while the expression of CACNA1C subunit tended to increase relative to the LPS group ( P>0.05). (2) In vitro: The safe concentration of LPS for administration was ≤20 μg/ml, with an optimal pro-inflammatory concentration of 4 μg/ml. The safe concentration of sinoporphyrin sodium for administration was 0.4 μmol/L, with an optimal incubation time of 4 hours. Compared to the LPS group or NLRP3 plasmid group, the LPS+SDT group or NLRP3 plasmid+SDT group exhibited lower expression levels of NLRP3, ASC, Cleaved Caspase-1, IL-1β, and IL-18, and higher mRNA and protein levels of CACNA1C (all P<0.05). The LPS+MCC950 group had higher CACNA1C protein expression than the LPS group ( P<0.05). SDT increased intracellular ROS levels, and NAC blocked the regulatory effects of SDT on NLRP3 and CACNA1C. Conclusion:SDT reduces atrial fibrillation susceptibility in mice by inhibiting NLRP3 inflammasome activation in atrial cardiomyocytes, thereby upregulating the L-type calcium channel subunit CACNA1C.

Objective:To preliminarily evaluate the lumen gain of sonodynamic therapy (SDT) mediated by sinoporphyrin sodium at carotid and femoral atherosclerotic plaque sites, and to assess whether concomitant statin use, lesion location, plaque echogenicity/type, and baseline stenosis severity modify the therapeutic response.Methods:This single-center, prospective, exploratory pilot clinical study enrolled patients with peripheral artery disease who attended the outpatient cardiology clinic of the First Affiliated Hospital of Harbin Medical University between February and September 2016. All enrolled patients received optimized oral medical therapy in combination with a single session of SDT. Vascular evaluation was performed using color Doppler ultrasound before treatment and 1 and 4 weeks after treatment. The primary efficacy endpoint was the percent change from baseline in luminal diameter stenosis at the site of the atherosclerotic plaque (%Δ) at week 4, while the secondary efficacy endpoint was %Δ at week 1. Subgroup analyses were conducted according to prior statin use, plaque location, plaque characteristics, and baseline degree of luminal stenosis.Results:A total of 24 patients, aged (70.7±2.2) years were enrolled. There were 20 (83%) males. Compared to baseline, luminal diameter stenosis at the plaque site reduced by week 4 ((50.1±1.2)% vs. (57.2±1.1)%, P<0.001), %Δ was(12.32±1.05)%; and luminal diameter stenosis also reduced by week 1 ((51.7±1.2)% vs. (57.2±1.1)%, P<0.001)), %Δ was(9.61±0.85)%. In subgroup analyses, the treatment effect on diameter stenosis was independent of prior statin use; SDT reduced stenosis in both carotid and femoral plaques; with superior efficacy observed in hypoechoic and mixed-echo plaques; and efficacy was observed across mild, moderate, and severe baseline stenosis categories (all P<0.05). Conclusion:In this single-center pilot study, SDT demonstrates therapeutic efficacy across mild, moderate, and severe stenoses, as well as in hypoechoic and mixed-echo plaques, showing potential to rapidly promote luminal gain at carotid and femoral atherosclerotic plaque sites.

Objective:To investigate the effect and underlying mechanism of sonodynamic therapy (SDT) on inflammation-related atrial fibrillation (AF) susceptibility.Methods:Lipopolysaccharide (LPS)-stimulated mouse and HL-1 mouse atrial myocyte models were used. (1) In vivo study: experimental groups included control, LPS, LPS+SDT, and SDT groups, with 20 mice in each group. Atrial fibrillation inducibility and duration were assessed by electrical stimulation. Western blot was used to analyze atrial expression of NOD-like receptor family pyrin domain-containing protein 3 (NLRP3), interleukin (IL)-1β, and IL-18. Immunohistochemistry was used to detect calcium voltage-gated channel subunit alpha1 C (CACNA1C) expression. (2) In vitro study: cell counting kit-8 (CCK-8) and Western blot were used to determine the optimal and safe LPS concentration. The safe incubation condition for the sonosensitizer sinoporphyrin sodium was determined by CCK-8 and fluorometry. An LPS-induced inflammatory model in HL-1 atrial myocytes was used, with experimental groups including control, LPS, LPS+SDT, LPS+sinoporphyrin sodium, and LPS+ultrasound groups. NLRP3 was overexpressed using plasmid transfection, with experimental groups including control, NLRP3 plasmid, negative control plasmid, and NLRP3 plasmid+SDT groups. SDT was applied to LPS-stimulated or NLRP3-overexpressing HL-1 cells. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were used to measure mRNA and protein levels of NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC), Cleaved Caspase-1, IL-1β, IL-18, and CACNA1C. The NLRP3 inhibitor MCC950 was used to validate the relationship of NLRP3 and CACNA1C. The experimental groups included control, LPS, LPS+MCC950, and MCC950 groups. Intracellular reactive oxygen species (ROS) levels were detected using the probe DCFH-DA, and the ROS scavenger N-acetyl-L-cysteine (NAC) was used to test if the effects of SDT was ROS-dependent.Results:(1) In vivo: The LPS+SDT group exhibited a lower incidence of atrial fibrillation induction and a shorter duration of atrial fibrillation compared to the LPS group(both P<0.05). Protein expression levels of NLRP3 and IL-1β were lower than those in the LPS group (all P<0.05), while the expression of CACNA1C subunit tended to increase relative to the LPS group ( P>0.05). (2) In vitro: The safe concentration of LPS for administration was ≤20 μg/ml, with an optimal pro-inflammatory concentration of 4 μg/ml. The safe concentration of sinoporphyrin sodium for administration was 0.4 μmol/L, with an optimal incubation time of 4 hours. Compared to the LPS group or NLRP3 plasmid group, the LPS+SDT group or NLRP3 plasmid+SDT group exhibited lower expression levels of NLRP3, ASC, Cleaved Caspase-1, IL-1β, and IL-18, and higher mRNA and protein levels of CACNA1C (all P<0.05). The LPS+MCC950 group had higher CACNA1C protein expression than the LPS group ( P<0.05). SDT increased intracellular ROS levels, and NAC blocked the regulatory effects of SDT on NLRP3 and CACNA1C. Conclusion:SDT reduces atrial fibrillation susceptibility in mice by inhibiting NLRP3 inflammasome activation in atrial cardiomyocytes, thereby upregulating the L-type calcium channel subunit CACNA1C.

Objective N-methyl-D-aspartate(NMDA)receptor subunit 2B(NR2B)and its phosphorylation are involved in cerebral ischemia/hypoxic neural injury.Hypoxic preconditioning(HPC)can serve as an endogenous protective intervention to protect the brain from ischemic/hypoxic injury.This study intended to explore the effect of HPC on NR2B and the phosphorylation of its two tyrosine sites(1252 and 1336)in hippocampal cells through in vivo and in vitro experiments and thus determine the role of NR2B in HPC neuroprotection.Methods 6～8 weeks-old male SPF-grade ICR mice and the mouse hippocampal neuron cell line HT22 were repeatedly exposed to hypoxia to replicate HPC animal and cell models.Western blot and immunofluorescence were applied to detect the levels of NR2B and the phosphorylation levels of its tyrosine 1336(pY1336NR2B)and 1252(pY1252NR2B)residues in the hippocampus of mice and HT22 cells.The distributions of NR2B,pY1336NR2B,and pY1252NR2B in the synaptic site(TxP)and extrasynaptic site(TxS)were analyzed by Western blot.The levels of cleaved caspase-3 and α-spectrin,which indicate cell apoptosis,were also detected.Results HPC downregulated the levels of NR2B and pY1336NR2B in the mouse hippocampus and HT22 cells.Changes in NR2B and pY1336NR2B levels in the TxS of the mouse hippocampus were similar to those in hippocampus and HT22 cells,whereas changes in the TxP showed the opposite trend.Conclusions Downregulation of NR2B and pY1336NR2B may be involved in HPC-induced neuroprotection,and their localization at synapses and extrasynapses may play different roles in neuroprotection.

The ezrin,radixin,moesin(ERM)protein family plays a pivotal role in cell morphology,migration,and signal transduction.Ezrin,as a prominent member of this family,is highly involved in these processes.Ezrin phosphorylation is particularly crucial,by regulating the interaction between ezrin and the actin cytoskeleton.This interaction is a key mediator of cytotoxicity in host cells infected with Helicobacter pylori,significantly impacting cell morphology.In this review,we comprehensively summarize the multifaceted role of ezrin protein in H.pylori-induced nodular gastritis.We consider the relationships between ezrin's structure,function,signaling pathways,and phosphorylation in the context of nodular gastritis.Moreover,this review highlights the role of ezrin protein as a potential therapeutic target,offering novel insights for the prevention and treatment of nodular gastritis.

Mild cognitive impairment (MCI) is the transitional stage between healthy aging and dementia, enjoying high risk of progression to Alzheimer's disease (AD). Therefore, MCI stage becomes the most important node for early identification, diagnosis and prevention of AD. At present, MCI clinical diagnosis lacks neuroimaging markers with non-invasive, timely and economic advantages. Recent studies suggest that microstructural and/or functional changes may occur in brain regions such as the hippocampus, amygdala, cingulate gyrus, thalamus, putamen, caudate nucleus and corpus callosum during MCI stage, and imaging features of these abnormal changes may serve as neuroimaging markers for early diagnosis of MCI. This article reviews the research progress on the abnormal changes of MCI related brain regions in neuroimaging.