1.High-altitude exposure induces lung injury in mice by altering expres-sion of genes associated with vascular function,extracellular matrix,apoptosis,and proliferation
Xingyu ZHANG ; Shiguan LE ; Yi LI ; Xiangguang SHI ; Jiucun WANG
Chinese Journal of Pathophysiology 2025;41(9):1703-1712
AIM:To investigate the types and mechanisms of lung injury induced by high-altitude exposure in mice.METHODS:Eight-week-old male C57BL/6 mice were randomly assigned to a normoxia group and a hypobaric hy-poxia exposure group,with 10 mice in each group.The hypobaric hypoxia group was continuously exposed to a hypobaric hypoxia environment simulating an altitude of 6 000 m for 3 d to establish an acute lung injury model.Lung tissues were collected.Lung pathological changes were evaluated using HE and Masson staining.Transcriptome analysis was conducted using DESeq2 and ClusterProfiler to identify differentially expressed genes and pathways,and hub genes were screened us-ing the STRING database.RESULTS:Compared with the normoxia group,the hypobaric hypoxia group exhibited signifi-cant increases in alveolar septal thickness,hyaline membrane formation,and neutrophil infiltration both in the alveolar space and the interstitial space,along with elevated lung injury scores(P<0.01),with no significant fibrosis observed.The mRNA levels of Alas2,Slc4a1,Rhag,Car1,Car2,Hbb,Agtr1b,Bmp2,Bmper,Vegfc,Foxm1,Fgf18,Igf1,Cx-cl12 and Mmp14 genes were significantly elevated(P<0.01),while Notch1,Notch4 and Cxcr4 mRNA levels were signifi-cantly decreased(P<0.01).Protein levels of inducible nitric oxide synthase(iNOS),cleaved caspase-3,cleaved PARP,fibronectin,elastin,tenascin C,tissue inhibitor of metalloproteinase-1(TIMP1),WNT3a,and β-catenin were signifi-cantly increased(P<0.05).CONCLUSION:Short-term high-altitude hypobaric hypoxia exposure induced acute lung in-jury in mice by significantly altering the expression of genes involved in apoptosis,vascular permeability regulation,extra-cellular matrix remodeling,and type Ⅱ alveolar epithelial cell proliferation.
2.High-altitude exposure induces lung injury in mice by altering expres-sion of genes associated with vascular function,extracellular matrix,apoptosis,and proliferation
Xingyu ZHANG ; Shiguan LE ; Yi LI ; Xiangguang SHI ; Jiucun WANG
Chinese Journal of Pathophysiology 2025;41(9):1703-1712
AIM:To investigate the types and mechanisms of lung injury induced by high-altitude exposure in mice.METHODS:Eight-week-old male C57BL/6 mice were randomly assigned to a normoxia group and a hypobaric hy-poxia exposure group,with 10 mice in each group.The hypobaric hypoxia group was continuously exposed to a hypobaric hypoxia environment simulating an altitude of 6 000 m for 3 d to establish an acute lung injury model.Lung tissues were collected.Lung pathological changes were evaluated using HE and Masson staining.Transcriptome analysis was conducted using DESeq2 and ClusterProfiler to identify differentially expressed genes and pathways,and hub genes were screened us-ing the STRING database.RESULTS:Compared with the normoxia group,the hypobaric hypoxia group exhibited signifi-cant increases in alveolar septal thickness,hyaline membrane formation,and neutrophil infiltration both in the alveolar space and the interstitial space,along with elevated lung injury scores(P<0.01),with no significant fibrosis observed.The mRNA levels of Alas2,Slc4a1,Rhag,Car1,Car2,Hbb,Agtr1b,Bmp2,Bmper,Vegfc,Foxm1,Fgf18,Igf1,Cx-cl12 and Mmp14 genes were significantly elevated(P<0.01),while Notch1,Notch4 and Cxcr4 mRNA levels were signifi-cantly decreased(P<0.01).Protein levels of inducible nitric oxide synthase(iNOS),cleaved caspase-3,cleaved PARP,fibronectin,elastin,tenascin C,tissue inhibitor of metalloproteinase-1(TIMP1),WNT3a,and β-catenin were signifi-cantly increased(P<0.05).CONCLUSION:Short-term high-altitude hypobaric hypoxia exposure induced acute lung in-jury in mice by significantly altering the expression of genes involved in apoptosis,vascular permeability regulation,extra-cellular matrix remodeling,and type Ⅱ alveolar epithelial cell proliferation.
3.Relationship between workplace procrastination and illegitimate tasks in kindergarten teachers
Xingyu LE ; Lingfeng WANG ; Jiameng YE ; Luyi SUN ; Siyue DONG
Chinese Mental Health Journal 2023;37(12):1071-1077
Objective:To explore the relationship between workplace procrastination and illegitimate tasks in-kindergarten teachersand the role of work disengagement and coworker support in their relationship.Methods:A to-tal of 245 kindergarten teachers were selected from 3 cities in Zhejiang Province.They were assessed with the Workplace Procrastination Scale(WPS),Bern Illegitimate Tasks Scale(BITS),Work Disengagement Scale(WDS),Colleague Support Scale(CSS).The models were tested by using Process macro for SPSS,and non-para-metric percentile bootstrap method was used to analyze the mediating effect and moderating effect.Results:There were significant differences in the total scores of workplace procrastination among kindergarten teachers in different marital status,age,teaching age,education level,teaching gradeand kindergarten level(Ps<0.05).Work disengage-ment played a significant mediating role between workplace procrastination and illegitimate tasks(indirect effect=0.26,95%CI:0.16-0.37).Coworker support played a significant moderating role in the impact of illegitimate tasks on work disengagement(simple slope=0.72,0.39;P<0.001).Conclusion:It suggests that workplace pro-crastination is related to illegitimate tasksin kindergarten teachers.Work disengagement plays a mediating role in their relationship,and coworker support plays a moderating role in the first half of this mediating role.

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