Objective: To analyse the influence path of family economic status on adolescent depressive symptoms, and to explore the chained mediation role of peer relationship and self satisfaction, as well as the moderating effect of the parent-child relationship, so as to provide a theoretical basis for the prevention and control of adolescent depressive symptoms. Methods: Data were obtained from the Database of Youth Health （DYH） in the National Population Health Science Data Center, and a total of 11 277 samples were included. Questionnaires were used to obtain information on family economic status, peer relationship, self satisfaction, parent-child relationship and depressive symptoms. Spearman correlation analysis was used to examine correlations among variables. Hierarchical linear regression analysis was used to analyze effects of family economic status and parent-child relationship on depressive symptom scores. The Process macro program was adopted to test the chained mediating effects of peer relationship and self satisfaction and the moderating effect of parent-child relationship. Results: The prevalence rate of depressive symptoms among adolescents was 24.2%. The prevalence rates of depressive symptoms significantly differed among adolescents with different family economic status and places of residence( χ 2=210.12, 4.18, both P ＜0.05). Adolescents with depressive symptoms had significantly lower scores on peer relationship, self satisfaction, and parent-child relationship compared to those without depressive symptoms ( t = 27.76 , 42.43, 31.12, all P ＜0.05). Family economic status were negatively correlated with adolescent depressive symptom scores ( B =-0.12, P <0.05).Parent-child relationship was negatively correlated with depressive symptom scores ( B = -0.02 , P < 0.05 ). After introducing the parent-child relationship, the negative effect of family economic conditions was reduced ( B = -0.08, P ＜ 0.01). Family economic conditions affected depressive symptoms through the chained mediating pathway involving peer relationship ( B = 2.07 ) and self satisfaction ( B =3.88)(both P <0.05). The parent-child relationship moderated this pathway: under conditions of high quality parent child relationship, the effect of family economic status on peer relationships was weaker ( B = 0.15); under low quality parent-child relationship, the positive effect of family economic status on peer relationships was enhanced ( B = 1.15 ) (both P ＜0.01). Conclusions Family economic status exert both direct and chain mediating effects on adolescent depression, and high quality parent-child relationship can play a protective moderation role. For economically disadvantaged families, it is critical to synergistically enhance parent-child relationship and social support in order to reduce depression risk among adolescents.

Objective To reveal the molecular mechanism by which nuclear epidermal growth factor receptor(nEGFR)synergistically regulates the expression of cell migration-inducing protein(CEMIP)by forming a complex with the transcription factor Yin Yang 1(YY1),and to investigate the biological functions of the nEGFR-YY1-CEMIP signaling axis in invasion of hepatocellular carcinoma(HCC).Methods After HCC cells were serum-starved for 24 h,the cells were treated with 100 ng/mL EGF.Thus,the cells were divided into a control group and EGF-treated groups at different time points.Nuclear expression and localization changes of EGFR were detected by Western blotting and immunofluorescence(IF).To investigate the interaction between nEGFR and YY1,their nuclear colocalization and interaction were examined by IF and co-immunoprecipitation(Co-IP),respectively.Transcriptional profiling was performed using RNA sequencing(RNA-seq)to identify differentially expressed genes at the genome-wide level.Combined with Gene Ontology(GO)functional enrichment analysis and transcription factor binding profiles via using the JASPAR database,CEMIP was identified as a candidate target gene.To validate the regulatory mechanism,the following experimental groups were established,Control,EGF,siYY1,and siYY1+EGF.The expression of CEMIP at protein and mRNA levels was detected by Western blotting and RT-qPCR.To elucidate the molecular mechanism of nEGFR/YY1 binding to the CEMIP promoter,the control and EGF-treated groups were established.Chromatin immunoprecipitation followed by quantitative PCR(ChIP-qPCR)was performed to assess the enrichment of nEGFR/YY1 at the CEMIP promoter region.Luciferase reporter assay was conducted following transfection with either wild-type EGFR(EGFR-WT),nuclear localization-deficient mutant(EGFR-dNLS),YY1 overexpression plasmid(YY1-OE),or dominant-negative YY1 mutant(YY1-DN)to evaluate changes in promoter activity.Subsequently,cell migration and invasion capabilities were evaluated using scratch wound healing assay and Transwell assay,while hyaluronic acid(HA)level was quantified by ELISA.The expression of matrix metalloproteinases(MMP2/9)was analyzed via Western blotting to assess the regulatory role of the nEGFR/YY1-CEMIP axis in the migration and invasion of HCC cells.By analyzing the CEMIP expression profiles in HCC patients from National Center for Biotechnology Information(NCBI)public databases,its potential association with tumor metastasis risk was validated.Results Western blotting and IF demonstrated that EGF treatment significantly induced nuclear translocation of EGFR,peaking at 30 min(P<0.001).Co-IP and IF assays indicated both physical interaction and nuclear co-localization between nEGFR and YY1.RNA-seq analysis identified CEMIP as a significantly differentially expressed gene.GO enrichment analysis revealed that CEMIP was significantly enriched in biological processes related to cell invasion promotion.JASPAR prediction identified conserved YY1 potential binding region within the CEMIP promoter region.Western blot and RT-qPCR analyses confirmed that EGF treatment up-regulated CEMIP at both protein and mRNA levels(P<0.05).Notably,YY1 knockdown significantly suppressed CEMIP expression,while exogenous EGF supplementation restored CEMIP level in YY1-deficient cells(P<0.05).ChIP-qPCR analysis demonstrated specific enrichment of the nEGFR/YY1 complex at the CEMIP promoter region,with EGF stimulation significantly enhancing its binding affinity(P<0.001).Luciferase reporter assay confirmed that nEGFR/YY1 robustly enhanced CEMIP promoter activity(P<0.01),while either the EGFR-dNLS or the YY1-DN substantially attenuated this transcriptional activation.Functional phenotyping showed that the nEGFR/YY1-CEMIP axis significantly enhanced the migration and invasion of HCC cells by promoting HA catabolism and up-regulating MMP2/9 expression(P<0.05).Analysis of NCBI datasets revealed that CEMIP expression was significantly up-regulated in HCC tumor tissues than adjacent normal tissues(P<0.001).Moreover,HCC patients with elevated CEMIP expression exhibited higher risk of metastasis(P<0.001).Conclusion nEGFR promotes HCC invasion by forming a transcriptional complex with YY1 to cooperatively activate CEMIP expression.

Objective To reveal the mechanism by which the programmed death-ligand 1(PD-L1)-protein tyrosine phosphatase 1B(PTP1B)-focal adhesion kinase(FAK)signaling axis promotes the progression of hepatocellular carcinoma(HCC)and elucidate its effector functions in HCC.Methods GEPIA database was used to plot a 10-year survival curve for PD-L1 and FAK expression levels in HCC patients.Immunohistochemical(IHC)staining was utilized to analyze the relative expression levels of PD-L1 and FAK phosphorylated at the Y397 site[p-FAK(Y397)]in HCC tissues,and the results were compared to those in the adjacent non-tumor tissues.Subsequently,endogenous PD-L1 expression was detected with Western blotting in HCC cell lines with low(SNU-387)and high(Hep3B)PD-L1 expression levels.After lentivirus-transduced SNU-387PDL1+and Hep3BPDL1-cells were constructed,the effect of high and low expression of PD-L1 on the expression of p-FAK(Y397)with Western blotting.To elucidate the functional mechanism of FAK in HCC,functional rescue experiments were performed by administering a FAK inhibitor to SNU-387PDL1+cells and a FAK activator to Hep3BPDL1-cells,combined with wound healing scratch assay,Transwell invasion assay,EdU proliferation assay,and colony formation assay to evaluate tumor malignant effects.The GENEMANIA database predicted functional interactions between protein tyrosine phosphatase 1B(PTP1B),PD-L1,and FAK.IHC staining was performed to analyze the correlation among PD-L1,PTP1B,and p-FAK(Y397)expression.Co-immunoprecipitation(Co-IP)and indirect immunofluorescence(IF)were applied to validate the interaction between PD-L1 and PTP1B.Western blotting was utilized to confirm the regulatory relationship between PD-L1 and PTP1B.In vitro PTP1B phosphatase activity assay measured the changes in PTP1B activity.Subsequently,Western blotting was used to screen cell lines with high endogenous PTP1B expression(SNU-387)and low endogenous PTP1B expression(Hep3B).Furthermore,Hep3BPTP1B+and SNU-387PTP1B-cell lines were generated,and then p-FAK(Y397)levels were then detected in these modified cell lines,and the aforementioned functional effect assays(migration,invasion,proliferation and colony formation)and rescue experiments were repeated.Furthermore,Western blotting was employed to detect changes in downstream signaling pathways following enhancement or attenuation of p-FAK(Y397)in SNU-387 and Hep3B cells.Results IHC staining revealed a positive correlation between PD-L1 and p-FAK(Y397)expression in HCC tissues(95%CI:1.065～3.801,P<0.01).In SNU-387PDL1+cells,PD-L1 overexpression significantly enhanced phosphorylation at the FAK Y397 site(P<0.01)and increased cell migration,invasion,proliferation,and colony formation capabilities(P<0.01),and these effects could be reversed by FAK inhibitor treatment(P<0.05).Conversely,in Hep3BPDL1-cells,PD-L1 knockdown significantly reduced FAK Y397 phosphorylation(P<0.01)and decreased cell migration,invasion,proliferation,and colony formation abilities(P<0.01),and these effects were restored by FAK activator treatment(P<0.05).IHC staining further showed a negative correlation between PTP1B expression and both PD-L1 and p-FAK(Y397)in HCC tissues(95%CI:1.886～3.514,P<0.05).Co-IP and IF assays confirmed a direct interaction between PD-L1 and PTP1B,with PD-L1 suppressing PTP1B expression level and reducing its activity(P<0.01).In SNU-387PTP1B-cells,PTP1B knockdown significantly increased FAK Y397 phosphorylation(P<0.01)and enhanced cell migration,invasion,proliferation,and colony formation(P<0.01),and these effects were reversed by FAK inhibitor(P<0.05).While in Hep3BPTP1B+cells,PTP1B overexpression significantly decreased FAK Y397 phosphorylation(P<0.01)and reduced cell migration,invasion,proliferation,and colony formation(P<0.01),and those effects were restored by FAK activator treatment(P<0.05).Furthermore,enhanced phosphorylation at the FAK Y397 site in SNU-387 cells activated downstream PI3K/AKT and MEK/ERK signaling pathways(P<0.01),whereas inhibition of FAK(Y397)phosphorylation in Hep3B cells attenuated the activation of these signaling pathways(P<0.01).Conclusion PD-L1 activates FAK by suppressing PTP1B,thereby promoting migration,invasion,and proliferation in HCC.

Objective:To evaluate the role of neuronal nitric oxide synthase (nNOS)-nitric oxide synthase 1 adaptor protein (NOS1AP) coupling in remifentanil-induced hyperalgesia in rats.Methods:Forty clean-grade healthy adult male Sprague-Dawley rats, weighing 240-260 g, aged 2-3 months, were divided into 4 groups ( n=10 each) using a random number table method: control group (group C), remifentanil group (group R), nNOS-NOS1AP inhibitor ZLc002 group (group C+ Z) and remifentanil + ZLc002 group (group R+ Z). Normal saline was intravenously infused at a rate of 0.1 ml·kg -1·min -1 for 60 min in C group. Remifentanil was intravenously infused at a rate of 1.0 μg·kg -1·min -1 for 60 min in R group. ZLc002 10 mg/kg was intraperitoneally injected for 3 consecutive days, and then normal saline 0.1 ml·kg -1·min -1 and remifentanil 1.0 μg·kg -1·min -1 were intravenously infused for 60 min in C+ Z group and R+ Z group. The mechanical paw withdrawal threshold (MWT) and thermal paw withdrawal latency (TWL) were measured at 24 h before intravenous infusion and 6, 24 and 48 h after intravenous infusion (T 0-3). All the rats were sacrificed after the last measurement of pain thresholds, and the L 4-6 segments of the spinal cord were removed for determination of the expression of nNOS, NOS1AP and Dexamethasone-induced Ras-related protein 1 (Dexras1) protein and mRNA using the real-time polymerase chain reaction. Nitrosylated proteins were extracted by biotin conversion for determination of the expression of nNOS, NOS1AP and total and nitrosylated Dexras1 (by Western blot) and co-expression of nNOS-NOS1AP (by co-immunoprecipitation). The content of NO in the spinal cord was measured. Results:Compared with group C, the MWT was significantly decreased, and the TWL was shortened at T 1-3, the expression of nNOS and NOS1AP protein and mRNA was up-regulated, the co-expression of nNOS-NOS1AP and NO production were increased, and the expression of nitrosylated Dexras1 was up-regulated in group R ( P<0.05), and no significant change was found in each aforementioned parameter in group C+ Z ( P>0.05). Compared with group R, the MWT was significantly increased, and the TWL was prolonged at T 1-3, the co-expression of nNOS-NOS1AP and NO production were decreased, the expression of nitrosylated Dexras1 was down-regulated ( P<0.05), and no significant change was found in the expression of nNOS and NOS1AP protein and mRNA in group R+ Z ( P>0.05). There were no significant differences in total Dexras1 protein and mRNA expression among the four groups ( P>0.05). Conclusions:The mechanism by which remifentanil induces hyperalgesia may be related to up-regulating the expression of nNOS and NOS1AP in the spinal cord, promoting interaction between nNOS and NOS1AP and mediating NO generation and Dexras1 nitrosylation modification in rats.

Objective:To investigate the relationship between S-nitrosylation of spinal divalent metal transporter 1 (DMT1) modification and mechanism of remifentanil-induced hyperalgesia in rats.Methods:Forty pathogen-free healthy male Sprague-Dawley rats, aged 2-3 months, weighing 240-260 g, were divided into 4 groups ( n=10 each) using a random number table method: control group (group C), remifentanil group (group R), L-NAME group (group C+ L) and remifentanil+ L-NAME group (group R+ L). Normal saline was infused at a rate of 0.1 ml·kg -1·min -1 for 60 min via the caudal vein in C group. Remifentanil was infused at a rate of 1.0 μg·kg -1·min -1 for 60 min via the caudal vein in R group. L-NAME 30 mg/kg was intraperitoneally injected, and 10 min later normal saline was infused at a rate of 0.1 ml·kg -1·min -1 for 60 min in C+ L group. L-NAME 30 mg/kg was intraperitoneally injected, and 10 min later remifentanil was infused at a rate of 1.0 μg·kg -1·min -1 for 60 min in R+ L group. The mechanical paw withdrawal threshold (MWT) and thermal paw withdrawal latency (TWL) were measured at 24 h before iv infusion and 6, 24 and 48 h after the end of infusion (T 0-3). All the rats were sacrificed under anesthesia after the last measurement of pain thresholds, and the L 4-6 segments of the spinal cord were removed for determination of the expression of neuronal nitric oxide sythases (nNOS) and DMT1 mRNA (using quantitative real-time polymerase chain reaction), extraction of nitrosylated proteins (by biotin switch assay), expression of nNOS, total DMT1 and S-nitrosylation of DMT1 (by Western blot), nitric oxide (NO) content (by spectrophotometry) and iron content (using atomic absorption spectrophotometer). Results:Compared with group C, the MWT was significantly decreased, and the TWL was shortened at T 1-3 in group R ( P<0.05), and the expression of nNOS protein and mRNA and S-nitrosylation of DMT1 was significantly up-regulated, and contents of NO and iron were increased in R and R+ L groups ( P<0.05), and no significant change was found in each index in group C+ L ( P>0.05). Compared with group R, the MWT was significantly increased, and the TWL was prolonged at T 1-3, and the expression of nNOS protein and mRNA and S-nitrosylation of DMT1 was down-regulated, and contents of NO and iron were decreased in group R+ L ( P<0.05). Compared with group C+ L, the MWT was significantly decreased, and the TWL was shortened at T 1-3, and the expression of nNOS protein and mRNA and S-nitrosylation of DMT1 was up-regulated, and the contents of NO and iron were increased in group R+ L ( P<0.05). There were no significant differences in the expression of DMT1 mRNA and total DMT1 in spinal cord among all the groups ( P>0.05). Conclusions:Activation of nNOS induces an increase in NO generation in the spinal cord and mediates the S-nitrosylation of DMT1, which may be related to the mechanism of remifentanil-induced hyperalgesia in rats.

Objective:To investigate the relationship between the polymorphisms of two SNP loci (rs901823 and rs3736228) in the low density lipoprotein receptor-associated protein 5 (LRP5) gene and glucocorticoids-induced osteoporosis (GIOP) in children.Methods:87 children with GIOP who were treated in Beijing Aiyuhua Women’s and Children’s Hospital and Beijing Children’s Hospital affiliated to Capital Medical University from Jan. 2015 to Dec. 2020 were selected as the research objects, and 100 children with normal bone mass who were treated with corticosteroids in this hospital during the same period were enrolled as the control group. Capillary electrophoresis and fragment analysis (SNaPshot) technology were used to genotype SNP sites rs901823 (T>C) and rs3736228 (C>T) ; Quantitative real-time fluorescence quantitative polymerase chain reaction detection method was employed to determine the relative mRNA of LPR5 gene The amount of expression.Results:For the rs901823 locus of the LRP5 gene, the TT, TC, and CC genotype distribution differences between the GIOP group and the control group were statistically significant ( χ2=14.176, P=0.001) . Compared with the TT genotype, carriers of the TC and CC genotypes had a higher risk of GIOP, with OR values of 3.022 (1.189-6.387) and 5.483 (1.452-20.883) ; For academic significance, OR values were 3.412 (1.795-6.587) and 4.352 (1.215-15.982) . For the rs3736228 locus, the distribution of CC, CT, TT genotypes between the GIOP group and the control group was significantly different ( χ2=9.597, P=0.008) . Compared with CC carriers, CT genotype carriers had a significantly increased risk of GIOP, with an OR value of 5.125 (1.721-16.241) . The result of a dominant model was statistically significant, with an OR value of 4.165 (1.335-14.652) , while for TT there was no statistically significant difference between the carrier and the CC genotype ( P=0.512) , and the results of the recessive model also showed no significant statistical significance ( P=0.887) . There was a statistically significant difference in the frequency distribution of T and C alleles at rs901823 between the GIOP group and the control group ( χ2=17.298, P<0.001) , and the difference in the frequency distribution of C and T alleles at rs3736228 was also statistically significant ( χ2=9.356, P=0.002) . The relative expression level of LRP5 gene mRNA in children with GIOP was 1.34±0.26, which was significantly lower than the expression level of LRP5 gene mRNA in children in the control group of 3.06±0.42 ( t=8.248, P<0.001) . Among children with GIOP, the relative expression of LRP5 gene mRNA in patients with rs901823 locus TT, TC, and CC genotypes was statistically significant ( P<0.001) ; the differences in rs901823 locus CC, CT, TT genotype patients were significant. Pairwise comparison of the relative expression of LRP5 gene mRNA showed that there was no significant difference between the TT group and the CT group ( P>0.05) , but the expression of the CC group was significantly higher than that of the CT group and the TT group ( P<0.05) . Conclusion:The rs901823 and rs3736228 polymorphisms of LRP5 gene are correlated with the occurrence of GIOP and can be used as genetic markers for predicting GIOP in children.

OBJECTIVES: Human papillomavirus (HPV) is a kind of spherical DNA virus, which is related to many factors such as immune status and pregnancy. Due to the decrease of immunity, pregnant women are more likely to have HPV infection, which causes serious imbalance of vaginal microecology and is not beneficial to pregnancy outcome. Therefore, this study focuses on the impact of HPV infection on vaginal microecology and maternal and neonatal outcomes. METHODS: A total of 140 pregnant women with HPV infection during pregnancy, who received obstetric examination in the First Affiliated Hospital of Hainan Medical College from November 2017 to July 2019, were selected as a HPV infection group, and 150 normal pregnant women with HPV negative in the same period were selected as a control group. Vaginal secretions were collected from all the pregnant women at 28-34 weeks of gestation to evaluate vaginal pH, cleanliness and microecological status, and to record pregnancy outcomes for all pregnant women. RESULTS: The proportions of vaginal pH>4.5, constituent ratio of flora density and diversity of I-II, positive detection rate of vulvovaginal candidiasis (VVC) and bacterial vaginosis (BV) in HPV infected pregnant women were significantly higher than those in the control group (all CONCLUSIONS Pregnant women with HPV infection during pregnancy are more likely to have vaginal microecological disorders, and can increase the risk of adverse pregnancy outcomes such as premature delivery and chorioamnionitis.
Candidiasis, Vulvovaginal ; Cesarean Section ; Female ; Humans ; Infant, Newborn ; Papillomavirus Infections/epidemiology* ; Pregnancy ; Vaginosis, Bacterial

Purpose: Most lung adenocarcinoma (LUAD) patients are diagnosed at the advanced stage and have poor prognosis. DNA methylation plays an important role in the prognosis prediction of cancers. The objective of this study was to identify new DNA methylation sites as biomarkers for LUAD prognosis. Materials and Methods: We downloaded DNA methylation data from The Cancer Genome Atlas data portal. Cox proportional hazard regression model and random survival forest algorithm were applied to identify the DNA-methylation sites. Methylation of sites were validated in the Gene Expression Omnibus cohorts. Function annotation were done to explore the biological function of DNA methylated sites signature. Results: Six DNA methylation sites were identified as prognosis signature. The signature yielded acceptable discrimination between the high-risk group and low-risk group. The discrimination effect of this DNA methylation signature for the OS was obvious, with a median OS of 21.89 months vs. 17.74 months for high-risk vs. low-risk groups. This prognostic prediction model was validated by the test group and GEO dataset. The predictive survival value was higher for the prognostic prediction model than that for the tumor node metastasis stage. Adjuvant hemotherapy could not affect the prediction of the signature. Functional analysis indicated that these signature genes were involved in protein binding and cytoplasm. Conclusion We identified the prognostic signature for LUAD by combining six DNA methylation sites. This could service as potential robust and specificity signature in the prognosis prediction of LUAD.

Objective To analyze Clopidogrel Resistance (CR) and influencing factors of coronary heart disease (CHD) with diabetes (DM) patients and evaluatc the relationship of CR and major adverse cardiovascular events (MACE) and readmission of CHD with DM patients.Methods 270 CHD patients were enrolled.Clinical conditions of CR were measured by adenosine diphosphate (ADP) induced maximum platelet aggregation rate (MPAR).After 1-year follow-up,MACE events and rehospitalization were recorded.Results CR of NDM and DM patients were 45 (33.1％) and 78 cases (58.2％) respectively,and the difference was significant (P ＜ 0.001).Factors of CR of CHD DM patients included heart rate,TG level,the number of severe coronary artery disease.MACE events of CS and CR patients were 35 (23.8％) and 47 patients (38.2％) respectively,and the difference was significant (P =0.010).The readmitted patients of CS and CR groups were 15 cases (10.2％) and 27 patients (22.0％) respectively,and the differcnce was significant (P =0.008).The MACE of CR and CS patients in DM group were 32 (41.0％) and 12 cases (21.4％) respectively,and thc difference was significant (P ＜ 0.05).The Readmitted cases of CR and CS patients in DM group were 19 (24.4％) and 5 (8.9％) respectively,and the diffcrcnce was significant (P ＜ 0.05).Conclusions CR of CHD DM patients increased significantly.The influencing factors of CR of CHDDM are including heart rate,TG level,the number of severe coronary artery disease.MACE events and rehospitalization rate were significantly increased in CHD patients with DM AR.Therefore,it should be further strengthened the anti-platelet therapy for CHD patients with DM.

Objective To analyze the dTP value in the patients with coronary heart disease (CHD) complicating diabetes mellitus (DM) and its relationship with major adverse cardiovascular events (MACE) and rehospitalization.Methods Two hundreds and seventy CHD patients were selected as the research subjects,including 136 cases of non-MD and 134 cases of DM.Their clinical condition was recorded.The indicators such as height,body mass,blood pressure and heart rate were measured.ECG,echocardiography,coronary angiography and other examiantions were carried out.The various indicators were detected.11-dh-TXB2 and 6-k-PGF1a levels were detected in the two groups and then dTP value was calculated.The 1-year follow-up was performed,MACE and rehospitalization were recorded.Epdate software was used for building a database and SPSS 17.0 software was applied for conducting the statistical analysis.Results The dTP level in the f non-DM and DM patients were 1.8 ± 0.6 and 2.0 ± 0.7 respectively,the difference was statistically significant (P＜ 0.05).For the non-DM CHD group,hs-CRP,systolic blood pressure,diastolic pressure,lesions number and severe lesions number were correlated with dTP level(P＜0.05).For the complicating DM CHD group,hs CRP,blood glucose,CHO level,lesions number and severe lesions number were correlated with dTP level(P＜0.05).After 1-year follow-up,MACE had 33 cases (24.3％) in the non-DM group and 44 cases (32.8％) in the DM group respectively,the difference was not statistically significant (P＞0.05).The rehospitalized cases had 12 cases (8.8％) in the non-DM group and 24 cases (17.9 ％).in the DM group respectively,the difference was statistically significant (P＜ 0.05).The dTP levels of MACE occurrence and non-MACE occurrence were 2.3 ± 0.8 and 1.8 ± 0.6 respectively,the difference was statistically significant (P＜0.05).The dTP levels of rehospitalized patients and non-rehospitalized patients were 2.4 ± 1.0 and 1.9 ±-0.6 respectively,the difference was statistically significant(P＜0.05).Conclusion The dTP level in the patients with CHD complicating DM is significantly increased,suggesting that platelet is obviously activated,moreover higher dTP level increases the risk of MACE and rehospitalization.So the anti-platelet therapy should be strengthened.