Objective: To explore the effects of personality and sleep quality with psychological distress of junior and senior high school stduents, so as to provide a reference basis for precise interventions of junior and senior high school students mental health. Methods: In October 2023, a convenience sampling method was used to select 9 034 students aged 12-17 from Shiyan City as the study subjects. The Pittsburgh Sleep Quality Index (PSQI) and Kessler Psychological Distress Scale (K10) were used to collect information on sleep quality and psychological distress of junior and senior high school stduents. Between group comparison was conducted by using t-test and Chi-square test. Generalized linear models were employed to analyze the interaction and joint effects of personality and sleep quality on psychological distress. Results: The generalized linear model analysis showed that the interaction between personality and sleep quality on psychological distress was statistically significant of junior and senior high school students(effect size=0.80, P <0.01). The general linear model analysis indicated that, after adjusting for variables such as age, gender, screen time, and daily sitting time with the extroverted and good sleep quality group as the reference, the introverted and poor sleep quality group had the largest mean difference in psychological distress scores (difference=0.51, P <0.05). When stratified by sleep quality, psychological distress scores were higher in the introverted and neutral personality groups with both poor and good sleep quality compared to the extroverted group (poor sleep quality: introverted difference=3.71, neutral difference=1.14; good sleep quality: introverted difference=2.23, neutral difference=0.57, all P < 0.05). When stratified by personality, psychological distress scores were higher in the poor sleep quality groups for introverted, neutral, and extroverted individuals compared to their good sleep quality counterparts (differences=8.66, 7.83, 7.34, all P < 0.05 ). Conclusions Personality and sleep quality have interactive and joint effects on psychological distress of junior and senior high school stduents. Personalized psychological interventions should be developed based on personality and sleep quality.

Background: Influenza A virus (IAV) is a negative-sense RNA virus of the Orthomyxoviridae family and is the etiological agent of a highly contagious acute respiratory disease that can lead to acute lung injury. Objective: To elucidate the molecular mechanisms of IAV infection, an integrative research approach combining gene expression profiling, multinetwork analysis, and in vivo experimental validations was employed. Methods: First, a series of network-based analyses were performed, including protein-protein interaction network construction, weighted gene co-expression network analysis, and subsequent gene set enrichment analysis, to identify the major underlying mechanisms of IAV infection. Following gene expression analysis, core targets, both direct and indirect regulators, were screened. An IAV (H1N1) strain A/PR/8/34-induced acute lung injury mouse model was constructed for in vivo validations. Batch one included two groups to evaluate findings from the multi-network analysis: Mock (n = 10; 5 males and 5 females) and IAV (n = 10; 5 males and 5 females). Batch two included three groups to assess the role of toll-like receptor 3 (TLR3) in IAV infection: Mock (n = 6; 3 males and 3 females), IAV (n = 6; 3 males and 3 females), and TLR3 inhibitor (n = 6; 3 males and 3 females). Body weight was measured on days 0, 3, and 5 after infection. On day 5, lung tissues were collected to assess viral load and histopathological changes. Key targets were examined using enzyme-linked immunosorbent assay, Western blotting, and immunofluorescence staining, both in sera and lung tissues. Results: IAV infection was significantly associated with dysregulation of the immune-inflammation system, such as the LTR, nucle-otide-binding oligomerization domain-(NOD) like receptor, retinoic acid-inducible gene I-like receptor, and nuclear factor kappa-B signaling pathways. Gene set enrichment analysis further indicated that the TLR and necroptosis signaling pathways played crucial roles in the progression of IAV infection (TLR signaling pathway normalized enrichment score = 2.3941, P = 1.00 × 10 ⁻¹⁰; necroptosis normalized enrichment score = 1.9421, P = 6.21 × 10 ⁻⁷). Among the core targets, TLR3 and mixed lineage kinase domain-like protein (MLKL) may regulate gene expression at the transcriptional level (all P < 0.05). In vivo validation using an IAV (PR8) infected acute lung injury mouse model demonstrated increased viral load and lung index, alveolar structural damage, and inflammatory cell infiltration. Immunofluorescence staining exhibited large gaps in Lamin B1 staining and breaches in Emerin signals following IAV-PR8 infection. Expression levels of TLR3, p-receptor-interacting serine/threonine-protein kinase 3 (RIPK3)/RIPK3, and p-mixed lineage kinase domain-like protein (MLKL)/MLKL proteins in lung tissues, as well as proinflammatory factors and mediators in sera, were significantly elevated after IAV infection. Moreover, enhanced neutrophil infiltration (myeloperoxidase) and citrullinated histone H3 (a neutrophil extracellular trap-specific marker), both established indicators of neutrophil extracellular trap formation, were observed. Notably, treatment with a TLR3 inhibitor significantly ameliorated IAV-induced acute lung injury by regulating necroptosis-related targets. Conclusion: Our study provides network-based in vivo evidence that TLR3-receptor-interacting serine/threonine-protein kinase 3-MLKL-mediated necroptosis may underlie IAV-induced acute lung injury and could serve as a potential therapeutic target in severe influenza cases.

Creutzfeldt-Jakob disease(CJD)is a rapidly progressive and fatal neurodegenerative disorder caused by prions,with certain infectivity and iatrogenic transmission risks.With the rapid progress and application of new dia-gnostic biomarkers and detection methods,as well as the construction and improvement of surveillance and reporting systems,the detection of CJD in patients domestically and internationally has shown an increasing trend year by year.Due to its long incubation period and heterogeneity of early symptoms,early identification and diagnosis of the disease is difficult,increasing the risk of transmission within medical institutions.Currently,there is a lack of con-sensus on the infection prevention and control of CJD.In order to timely identify and diagnose CJD as well as effec-tively block its transmission in medical institutions,this consensus summarizes 15 clinical concerns and formulates 24 specific recommendations based on the latest domestic and international research findings and clinical evidence,as well as combines with clinical practice,aiming to standardize healthcare-associated infection prevention and control measures for CJD and reduce its transmission risk in medical institutions.

Objective To investigate the correlation between the expression of lectin galactoside binding soluble-3 binding protein(LGALS3BP),GTP enzyme activating protein SH3 functional region binding protein 1(G3BP1)and Wnt/β-catenin pathway genes in endometrial cancer(EC)tissues and its clinical prognostic significance.Methods 138 patients with EC treated in Cangzhou Central Hospital from February 2016 to February 2019 were selected.qRT-PCR was used to detect the expression of LGALS3BP mRNA,G3BP1 mRNA and Wnt/β-catenin pathway genes Wnt5a mRNA,β-catenin mRNA and matrix metalloproteinase-9(MMP-9)mRNA in cancer and adjacent tissues.The expression of LGALS3BP protein and G3BP1 protein in cancer and adjacent tissues was detected by immunohistochemistry.Pearson correlation analysis was used to analyze the correlation between LGALS3BP mRNA,G3BP1 mRNA and Wnt/β-catenin pathway genes.Kaplan-Meier curve was used to analyze the effect of LGALS3BP mRNA and G3BP1 mRNA on the survival and prognosis of EC patients.COX regression model was used to analyze the factors affecting the prognosis of EC patients.Results The expression of LGALS3BP mRNA(3.01±0.34),G3BP1 mRNA(2.87±0.33),Wnt5a mRNA(2.29±0.26),β-catenin mRNA(3.25±0.41)and MMP-9 mRNA(2.68±0.36)in EC cancer tissues were higher than those in adjacent tissues(1.10±0.23,1.06±0.24,0.84±0.17,0.88±0.26,0.69±0.17),and the differences were statistically significant(t=52.109～58.719,all P<0.001).The expression of LGALS3BP mRNA and G3BP1 mRNA in EC was positively correlated with the expression of Wnt5a mRNA,β-catenin mRNA and MMP-9 mRNA(r=0.675～0.781,all P<0.001).The expression of LGALS3BP protein(3.54±0.47 vs 0.51±0.16)and G3BP1 protein(2.84±0.44 vs 0.42±0.13)in EC cancer tissues were higher than that in adjacent tissues,and the differences were statistically significant(t=71.692,61.962,all P<0.001).The expression of LGALS3BP mRNA and G3BP1 mRNA in cancer tissues of EC patients with FIGO stage Ⅲ and lymph node metastasis were higher than that of FIGO stage Ⅰ～Ⅱ and no lymph node metastasis,and the differences were statistically significant(t=40.279～557.671,all P<0.001).The 5-year survival rate of LGALS3BP mRNA high expression group was 58.82%(40/68),which was lower than that of low expression group 94.29%(66/70),and the difference was statistically significant(Log-rank χ2=24.970,P<0.001).The 5-year survival rate of G3BP1 mRNA high expression group was 62.12%(41/66),which was lower than that of low expression group 90.28%(65/72),and the difference was statistically significant(Log-rank χ2=15.960,P<0.001).FIGO stage Ⅲ,lymph node metastasis,high expression of LGALS3BP mRNA and high expression of G3BP1 mRNA were risk factors for poor prognosis of EC patients(Wald χ2=7.847～12.054,all P<0.001).Conclusion The expression of LGALS3BP and G3BP1 mRNA is elevated in EC,both of which are associated with Wnt/β-catenin pathway genes,promoting the malignant progression of EC tumors,and are new tumor markers for evaluating the prognosis of EC patients.

Objective To investigate the correlation between the expression of lectin galactoside binding soluble-3 binding protein(LGALS3BP),GTP enzyme activating protein SH3 functional region binding protein 1(G3BP1)and Wnt/β-catenin pathway genes in endometrial cancer(EC)tissues and its clinical prognostic significance.Methods 138 patients with EC treated in Cangzhou Central Hospital from February 2016 to February 2019 were selected.qRT-PCR was used to detect the expression of LGALS3BP mRNA,G3BP1 mRNA and Wnt/β-catenin pathway genes Wnt5a mRNA,β-catenin mRNA and matrix metalloproteinase-9(MMP-9)mRNA in cancer and adjacent tissues.The expression of LGALS3BP protein and G3BP1 protein in cancer and adjacent tissues was detected by immunohistochemistry.Pearson correlation analysis was used to analyze the correlation between LGALS3BP mRNA,G3BP1 mRNA and Wnt/β-catenin pathway genes.Kaplan-Meier curve was used to analyze the effect of LGALS3BP mRNA and G3BP1 mRNA on the survival and prognosis of EC patients.COX regression model was used to analyze the factors affecting the prognosis of EC patients.Results The expression of LGALS3BP mRNA(3.01±0.34),G3BP1 mRNA(2.87±0.33),Wnt5a mRNA(2.29±0.26),β-catenin mRNA(3.25±0.41)and MMP-9 mRNA(2.68±0.36)in EC cancer tissues were higher than those in adjacent tissues(1.10±0.23,1.06±0.24,0.84±0.17,0.88±0.26,0.69±0.17),and the differences were statistically significant(t=52.109～58.719,all P<0.001).The expression of LGALS3BP mRNA and G3BP1 mRNA in EC was positively correlated with the expression of Wnt5a mRNA,β-catenin mRNA and MMP-9 mRNA(r=0.675～0.781,all P<0.001).The expression of LGALS3BP protein(3.54±0.47 vs 0.51±0.16)and G3BP1 protein(2.84±0.44 vs 0.42±0.13)in EC cancer tissues were higher than that in adjacent tissues,and the differences were statistically significant(t=71.692,61.962,all P<0.001).The expression of LGALS3BP mRNA and G3BP1 mRNA in cancer tissues of EC patients with FIGO stage Ⅲ and lymph node metastasis were higher than that of FIGO stage Ⅰ～Ⅱ and no lymph node metastasis,and the differences were statistically significant(t=40.279～557.671,all P<0.001).The 5-year survival rate of LGALS3BP mRNA high expression group was 58.82%(40/68),which was lower than that of low expression group 94.29%(66/70),and the difference was statistically significant(Log-rank χ2=24.970,P<0.001).The 5-year survival rate of G3BP1 mRNA high expression group was 62.12%(41/66),which was lower than that of low expression group 90.28%(65/72),and the difference was statistically significant(Log-rank χ2=15.960,P<0.001).FIGO stage Ⅲ,lymph node metastasis,high expression of LGALS3BP mRNA and high expression of G3BP1 mRNA were risk factors for poor prognosis of EC patients(Wald χ2=7.847～12.054,all P<0.001).Conclusion The expression of LGALS3BP and G3BP1 mRNA is elevated in EC,both of which are associated with Wnt/β-catenin pathway genes,promoting the malignant progression of EC tumors,and are new tumor markers for evaluating the prognosis of EC patients.

Creutzfeldt-Jakob disease(CJD)is a rapidly progressive and fatal neurodegenerative disorder caused by prions,with certain infectivity and iatrogenic transmission risks.With the rapid progress and application of new dia-gnostic biomarkers and detection methods,as well as the construction and improvement of surveillance and reporting systems,the detection of CJD in patients domestically and internationally has shown an increasing trend year by year.Due to its long incubation period and heterogeneity of early symptoms,early identification and diagnosis of the disease is difficult,increasing the risk of transmission within medical institutions.Currently,there is a lack of con-sensus on the infection prevention and control of CJD.In order to timely identify and diagnose CJD as well as effec-tively block its transmission in medical institutions,this consensus summarizes 15 clinical concerns and formulates 24 specific recommendations based on the latest domestic and international research findings and clinical evidence,as well as combines with clinical practice,aiming to standardize healthcare-associated infection prevention and control measures for CJD and reduce its transmission risk in medical institutions.

Objective:To evaluate the role of spinal Leucine-rich Repeat Kinase 2 (LRRK2) in neuropathic pain in rats.Methods:Fifty SPF healthy male Sprague-Dawley rats, aged 6-7 weeks, weighing 210-245 g, were divided into 5 groups ( n=10 each) using a random number table method: control group (C group), neuropathic pain group (NP group), low dose GNE-7915 group (low-dose GNE-7915 group), medium-dose GNE-7915 group (medium-dose GNE-7915 group), and high-dose GNE-7915 group (high-dose GNE-7915 group). Neuropathic pain was induced by the spared nerve injury in anesthetized rats. At 7 days after developing the model, LRRK2 inhibitor GNE-7915 12.5, 25.0 and 50.0 mg/kg were intraperitoneally injected in low-, medium- and high-dose GNE-7915 groups, respectively. The mechanical paw withdrawal threshold (MWT) and thermal paw withdrawal latency (TWL) were measured before developing the model, at 7 days after developing the model, and at 4 h after injecting the inhibitor. After measurement of the pain threshold, the rats were sacrificed and the spinal cord tissues were taken for determination of the positive expression of ionized calcium-binding adapter molecule 1(Iba-1) (by immunofluorescence staining), contents of interleukin-1β (IL-1β), monocyte chemotactic protein-1 (MCP-1) and IL-18 (by enzyme-linked immunosorbent assay), positive expression of phosphorylated LRRK2 (p-LRRK2) (by immunofluorescence staining), and expression of LRRK2, IL-1β, MCP-1 and IL-18 (by immunoblotting). The ratio of p-LRRK2/LRRK2 was calculated. Results:Compared with C group, the MWT was significantly decreased, the TWL was shortened, the proportion of Iba-1 and p-LRRK2 positive cells in spinal cord tissues, contents of IL-1β, MCP-1 and IL-18, and p-LRRK2/LRRK2 ratio were increased, and the expression of IL-1β, MCP-1 and IL-18 proteins was up-regulated in NP group ( P<0.05). Compared with NP group, the MWT was significantly increased, the TWL was prolonged, the proportion of Iba-1 and p-LRRK2 positive cells in spinal cord tissues, contents of IL-1β, MCP-1 and IL-18, and p-LRRK2/LRRK2 ratio were decreased, and the expression of IL-1β, MCP-1 and IL-18 proteins was down-regulated in low-, medium- and high-dose GNE-7915 groups ( P<0.05). Conclusions:LRRK2 in the spinal cord may be involved in the pathophysiological mechanism of neuropathic pain by activating microglia and inducing inflammatory responses in rats.

Demyelinating disorders of the nervous system constitute a broad spectrum of neurological conditions characterized by the depletion of myelin sheaths accompanied by inflammatory cell infiltration, manifesting in either the central or peripheral nervous system. The former primarily encompasses conditions such as multiple sclerosis (MS) and neuromyelitis optica spectrum disorders (NMOSD), while the latter is exemplified predominantly by Guillain-Barre syndrome (GBS). Recent investigations have revealed that dyslipidemia may be related to the occurrence and development of neurological demyelination, but there are fewer analyses and summaries of related advances in China. Consequently, this review aims to comprehensively outline advancements in research concerning the correlation between dyslipidemia and neurological demyelinating disordersand discusses in depth the interrelationship between dyslipidemia and neurological demyelinating diseases, so as to provide reference for the prevention and treatment of neurological demyelinating diseases.

Demyelinating disorders of the nervous system constitute a broad spectrum of neurological conditions characterized by the depletion of myelin sheaths accompanied by inflammatory cell infiltration, manifesting in either the central or peripheral nervous system. The former primarily encompasses conditions such as multiple sclerosis (MS) and neuromyelitis optica spectrum disorders (NMOSD), while the latter is exemplified predominantly by Guillain-Barre syndrome (GBS). Recent investigations have revealed that dyslipidemia may be related to the occurrence and development of neurological demyelination, but there are fewer analyses and summaries of related advances in China. Consequently, this review aims to comprehensively outline advancements in research concerning the correlation between dyslipidemia and neurological demyelinating disordersand discusses in depth the interrelationship between dyslipidemia and neurological demyelinating diseases, so as to provide reference for the prevention and treatment of neurological demyelinating diseases.