Background: Disorders of the blood-brain barrier (BBB) arising from diabetes mellitus are closely related to diabetic encephalopathy. Previous research has suggested that neuron-glia antigen 2 (NG2)-glia plays a key role in maintaining the integrity of the BBB. However, the mechanism by which NG2-glia regulates the diabetic BBB remains unclear. Methods: Type 2 diabetes mellitus (T2DM) db/db mice and db/m mice were used. Evans-Blue BBB permeability tests and transmission electron microscopy techniques were applied. Tight junction proteins were assessed by immunofluorescence and transmission electron microscopy. NG2-glia number and signaling pathways were evaluated by immunofluorescence. Detection of matrix metalloproteinase-9 (MMP-9) in serum was performed using enzyme-linked immunosorbent assay (ELISA). Results: In T2DM db/db mice, BBB permeability in the hippocampus significantly increased from 16 weeks of age, and the structure of tight junction proteins changed. The number of NG2-glia in the hippocampus of db/db mice increased around microvessels from 12 weeks of age. Concurrently, the expression of MMP-9 increased in the hippocampus with no change in serum. Sixteen- week-old db/db mice showed activation of the Wnt/β-catenin signaling in hippocampal NG2-glia. Treatment with XAV-939 improved structural and functional changes in the hippocampal BBB and reduced MMP-9 secretion by hippocampal NG2-glia in db/db mice. It was also found that the upregulation of β-catenin protein in NG2-glia in the hippocampus of 16-week-old db/db mice was significantly alleviated by treatment with XAV-939. Conclusion The results indicate that NG2-glia can lead to structural and functional disruption of the diabetic BBB by activating Wnt/β-catenin signaling, upregulating MMP-9, and degrading tight junction proteins.

This study reports a new species of Culicoides(Avaritia)isolated from Xunke County, Heilongjiang Province, China. The new species, Culicoides(Avaritia)dongshanensis Liu et Wang, sp. nov., was identified and illustrated based on female adults. Its diagnostic characteristics are as follows: eyes contiguous over a short distance, with short interfacetal hair, antennal ratio(AR)of 1.20, palpal ratio(PR)of 2.16, wing length of 0.83 mm, mandible with 15 teeth, one pale spot in base cell M1, one pale spot in cell M4, two pale spots in cell A, and two unequal spermathecae. Type specimens were deposited at the Center for Disease Control and Prevention of the Northern Theater Command.

Precise management of the activity dose is a core component of the(early mobilization,EM)plan for ICU patients.However,the lack of clinical practice guidelines related to EM dose of existing programs hinders the implementation and development of EM in ICU patients to some extent.Therefore,this review focuses on 4 aspects,covering the definition of activity dose,assessment tools,the current clinical implementation status,and implications for future nursing.The aim is to systematically review the assessment tools and intervention strategies for the activity dose of EM in ICU patients,providing a reference for optimization of EM programs.

In June 2018,sows at a pig farm in Jiamusi,Heilongjiang Province,suffered a large num-ber of miscarriages,and subsequently weaned piglets at the farm began to show persistent high fe-ver symptoms at around 35 days of age,with some pigs having a fever of more than 41.5 ℃.In or-der to determine the cause of this outbreak,63 clinical samples from this farm were tested.The re-sults showed that 60 out of 63 samples were positive for the porcine reproductive and respiratory syndrome virus(PRRSV)antigen.Subsequently,PRRSV antigen-positive plasmid was transfected into African green monkey embryonic kidney cells(Marc-145),and after three generations of blind transmission,indirect immunofluorescence assay(IFA)was performed.The results showed that one PRRSV strain,named HLJ38,was successfully isolated.Then the whole genome of HLJ38 strain was sequenced and then analyzed in detail by bioinformatics software.Sequence analysis showed that there were three deletions of 131 amino acids(323-433 aa,483 aa and 504-522 aa)in the derived sequence of Nsp2 gene of HLJ38 strain,which was consistent with the molecular ge-netic marker of NADC30 PRRSV.The phylogenetic tree analysis showed that HLJ38 and NADC30 PRRSV in GenBank belong to lineage 1 subgroup,and the nucleotide homology of HLJ38 and NADC30 PRRSV in GenBank was only 85.2％and 84.6％.Recombinant analysis showed that HLJ38 was a recombinant NADC30-like PRRSV,and the recombinant gene fragments were de-rived from multiple strains,among which the fragment of 1-201 nt was provided by VR2332 strain and fragment of 6 641-8 061 nt derived from the HP-PRRSV strain.In summary,the re-sults showed that the outbreak in this pig farm may be caused by the recombination of PRRSV strains among different lineages,and the recombinant circulating strains not only have certain pathogenicity but also suggest that the existing commercial vaccines provide limited cross-protec-tion against them.Recombination between different lineages increases the genetic diversity of PRRSV and aggravates the difficulty of prevention and control of PRRS in pig farms.Therefore,it is necessary to continuously monitor the epidemic dynamics of PRRSV in pig farms and take effec-tive measures in time to curb the spread of PRRS.

Objective To identify key proteins associated with sudden cardiac death(SCD)caused by lethal arrhythmia and to explore their potential molecular mechanisms through integrated proteomic analysis,data mining,and bioinformatics.Methods A lethal arrhythmia model was established in 8-week-old male Sprague-Dawley rats,which were divided into an arrhythmia group and a control group.Proteomic techniques were applied to identify and quantify proteins in left ventricular myocardial tissue,and differentially expressed proteins related to arrhythmia were screened.Key proteins were further identified through comparison with target proteins in databases combined with joint analyses.Bioinformatics methods were then used to investigate potential molecular mechanisms.Results A total of 356 differentially expressed proteins were identified,including 189 upregulated and 167 downregulated.Association analysis with target gene proteins identified 71 key proteins,and a protein-protein interaction network was constructed.GO enrichment and KEGG pathway analyses indicated that these key proteins were primarily involved in ion channel dysfunction,enhanced oxidative stress,and autonomic nervous system imbalance.Conclusion This study,through the integration of proteomics,data mining,and bioinformatics,revealed critical molecular mechanisms underlying SCD associated with lethal arrhythmia.These findings provide new perspectives and potential biomarkers for forensic identification and research on the mechanisms of death.

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.

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 identify key proteins associated with sudden cardiac death(SCD)caused by lethal arrhythmia and to explore their potential molecular mechanisms through integrated proteomic analysis,data mining,and bioinformatics.Methods A lethal arrhythmia model was established in 8-week-old male Sprague-Dawley rats,which were divided into an arrhythmia group and a control group.Proteomic techniques were applied to identify and quantify proteins in left ventricular myocardial tissue,and differentially expressed proteins related to arrhythmia were screened.Key proteins were further identified through comparison with target proteins in databases combined with joint analyses.Bioinformatics methods were then used to investigate potential molecular mechanisms.Results A total of 356 differentially expressed proteins were identified,including 189 upregulated and 167 downregulated.Association analysis with target gene proteins identified 71 key proteins,and a protein-protein interaction network was constructed.GO enrichment and KEGG pathway analyses indicated that these key proteins were primarily involved in ion channel dysfunction,enhanced oxidative stress,and autonomic nervous system imbalance.Conclusion This study,through the integration of proteomics,data mining,and bioinformatics,revealed critical molecular mechanisms underlying SCD associated with lethal arrhythmia.These findings provide new perspectives and potential biomarkers for forensic identification and research on the mechanisms of death.

In recent years,more and more researches has focused on the correlation between cognitive activity and physiological variables.The change of pupil is regarded as an important target in the cognitive process,and has become a hot research field.This review focuses on the three key brain regions that regulate pupil change,and reflects the neurophysiological mechanism behind pupil change by elaborating the neural pathways related to pupil change and cognitive performance.Based on recent studies on pupil change in cognitive diseases,it aims to promote the application of pupil change in the field of cognitive science in the future.

Objective:To investigate the expression of heat shock factor binding protein 1 (HSPB1) in endometrial carcinoma and its clinical significance.Methods:The pan-cancer dataset after standardization and unification was downloaded from the University of California Santa Cruz (UCSC) Genome database (updated to December 6, 2019), and the expression of HSPB1 in pan-cancer was analyzed. The transcriptome data of endometrial carcinoma of the uterus from the Cancer Genome Atlas (TCGA) database were downloaded (updated to July 21, 2016), including 552 cases of endometrial carcinoma and 35 cases of corresponding adjacent tissue samples. The clinical data of 543 patients with endometrial cancer were obtained. The differences in the expression levels of HSPB1 in patients with different clinicopathological features were compared. R 4.3.1 software maxstat was used to calculate the optimal critical value (>46.30) of HSPB1 expression, and the patients were divided into HSPB1 low expression group (<46.30) and HSPB1 high expression group (≥46.30). Kaplan-Meier method was used to analyze the difference in prognosis between the 2 groups, and log-rank test was performed. The top 50 genes with positive and negative correlation with HSPB1 were screened by LinkedOmics database. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis were performed on HSPB1. The interaction network of HSPB1 protein was analyzed by STRING database and Cytoscape 3.9.1 software. The correlation between HSPB1 expression and various immune cell infiltration levels was analyzed by using the TIMER2.0 database.Results:The expression of HSPB1 in 27 kinds of tumor tissues was higher than that in paracancerous tissues, and the expression of HSPB1 in 2 kinds of tumor tissues was lower than that in paracancerous tissues (all P < 0.05). In the transcriptome data of 552 cases of endometrial cancer and 35 cases of corresponding paracancerous tissues in the TCGA database, the relative expression level of HSPB1 in endometrial cancer tissues was higher than that in corresponding paracancerous tissues ( t = -2.90, P = 0.005). The result of the comparison of relative expression level of HSPB1 in endometrial cancer patients with different clinicopathological features showed that patients aged < 65 years had higher expression level compared to those aged ≥ 65 years, patients at clinical stage Ⅰ-Ⅱ had higher expression level compared to those at stage Ⅲ-Ⅳ, patients with Grade grading G 1-G 2 had higher expression level compared to those with G 3, and patients with pathological type I had higher expression level compared to those with type Ⅱ (all P < 0.05). Of the 543 patients, 2 were lost to follow-up, and the overall survival of the remaining 541 patients with high HSPB1 expression was better than that of those with the low expression ( HR = 0.532, 95% CI: 0.333-0.849, P = 0.008). HSPB1 and its related genes were mainly involved in estrogen signaling, p53 signaling and other pathways; HSPB1 was involved in cysteine-type endopeptidase inhibitor activity and calcium-dependent protein binding. The top 10 genes with the strongest correlation with HSPB1 in protein-protein interaction analysis were DSG3, EVPL, PKP1, DSC3, PKP3, PPL, KRT5, IVL, TGM1 and CSTA. The expression of HSPB1 was negatively correlated with tumor purity ( r = -0.025, P < 0.01), and positively correlated with CD4 + T cells ( r = 0.204, P < 0.01), CD8 + T cells ( r = 0.225, P < 0.01), B cells ( r = 0.285, P < 0.01), NK cells ( r = 0.269, P < 0.01), macrophages ( r = 0.234, P < 0.01) and dendritic cells ( r = 0.354, P < 0.01). Conclusions:The high expression of HSPB1 is associated with clinicopathological features, prognosis and immune infiltration in patients with endometrial carcinoma. It may be one of the reference indexes for predicting the prognosis of patients with endometrial cancer.