Objective To revise the individual adaptability measure (I-ADAPT-M) developed by Ployhart & Bliese,and analyze the reliability and validity of its application in college freshmen.Methods Revise the I-ADAPT-M,One thousand and seven hundred freshmen were asked to complete the test,one month later,two hundred and seventy-seven freshmen were simple randomly chosen to report their General Life Satisfaction.Then,the data were analysis by SPSS 18.0 and Amos 4.0.Results The exploratory factor analysis showed that,the Chineseversion of the I-ADAPT-M consisted of 23 projects and 4 dimensions (crisis and creativity adaptability,interpersonal adaptability,stress tolerance adaptability,and resistant learning adaptability),which could account for over 45.344％ of total variance.The Cronbacha coefficient of the Chinese-version of the I-ADAPT-M was 0.82.The confirmatory factor analyzed further revealed the structure of four-dimensional scale(x2=708.80,x2/df =3.16,CFI =0.95,NNFI =0.94,RMSEA =0.051,SRMR =0.053).Male had significant high core in crisis and creativity adaptability and resistant learning adaptability than female.Female had significant high core in interpersonal adaptability than male.Colleges-leader had significant high core in 4 dimensions than general students,it suggested that the Chinese-version of the I-ADAPT-M had good discriminant validity.General Life Satisfaction of the subjects had significant positive correlation with crisis and creativity adaptability,stress tolerance adaptability and interpersonal adaptability,had little correlation with resistant learning adaptability.Conclusion The Chinese-version of the I-A-DAPT-M has good reliability and validity to measure the individual adaptability of the freshman.

Objective:To explore the effect of high glucose on formation of endogenetic toxins and expression of intercellular cell adhesion molecule-1(ICAM-1) and vascular cell adhesion molecule-1(VCAM-1) of human brain microvascular endothelial cells.Methods:Cultured HBMEC was used as target cells,anhydrous glucose was added to the cell medium to prepare the injury model of human endothelial cell.Methyl thiazolyl tetrazolium method was used to examine the cell activity in a high glucose environment.Immunocytochemistry method was used to detect the expression of ICAM-1 and VCAM-1 of HBMEC.Results:The expressions of ICAM-1 and VCAM-1of HBMEC were enhanced by high glucose after pretreating HBMEC for 24,48 and 72h(P

Objective We conducted a survey on the awareness rate of stroke in Yangquan residents and analyzed factors affecting awareness to provide basic information for Yangquan residents to prevent and treat stroke in Shanxi.MethodsA questionnaire regarding awareness and basic knowledge of stroke was used in this study and applied to Yangquan residents.A cluster stratified sample of 7983 residents were questionnaired by cross-sectional method.Results7921 returned copies were valid.The awareness rate of stroke in 7921 selected Yangquan residents was 30.14％ (2387/7921). Upon the occurrence of stroke,the awareness rates of the way to see a doctor,the right department to look for medical care and test manners to diagnose the illness as stroke were relatively high in these investigated people,which were 74.03％ (5864/7921),78.17％ (6192/7921) and 84.04％ (6657/7921),respectively.However,the number of people who knew characteristic symptoms and complications of stoke,risk factors that cause stroke and how to treat stroke was 2021 (25.51％),841 ( 10.62％ ),and 902 ( 11.39％ ),respectively,which was relatively low. After multivariate analysis,the awareness rate of stroke in Yangquan residents was positively correlated with an education degree.ConclusionsYangquan residents know little about stroke.Therefore,it is necessary to increase the level of their knowledge regarding stroke by extended propaganda and encourage them to live a healthy life to be able to treat stoke in time and to reduce the possibility of stroke occurring.

OBJECTIVE: To investigate the effect of miR-204 on the invasion and metastasis of breast cancer by targeted regulation of HNRNPA2B1. METHODS: The bioinformatics database was used to obtain data of the expressions of miR-204 in breast cancer patients and the survival rate of the patients. RT-qPCR was used to detect the expression of miR-204 in breast cancer cell lines. The expression vector GV369-miR-204 was used to overexpress miR-204 in MDA-MB-231 cells. Transwell assay was performed to detect the effect of miR-204 on the migration and invasion ability of the breast cancer cells. The key genes (hub genes) of miR-204 were determined by bioinformatics method. A dual luciferase assay was used to analyze the targeting relationship between miR-204 and HNRNPA2B1. The expression of HNRNPA2B1 in MDA-MB-231 cells after miR-204 overexpression was detected by Western blotting, and Transwell assay was used to examine the changes in the cell invasion ability. RESULTS: The expression of miR-204 was decreased in both breast cancer tissues, and was significantly lower in breast cancer MDA-MB-231 cells than in MCF-10A cells ( < 0.05). The decreased expression of miR-204 was associated with poorer prognosis of breast cancer patients ( < 0.05). Upregulation of miR-204 in MDA-MB-231 cells significantly inhibited the invasion and migration of the cells ( < 0.05). Analysis of the data from the Starbase revealed that the expression of miR-204-5p was negatively correlated with the expression of HNRNPA2B1, and the expression of HNRNPA2B1 was increased in breast cancer patients ( < 0.05) in association with a poorer prognosis of the patients ( < 0.05). Dual luciferase assay demonstrated that miR-204 could bind to HNRNPA2B1 in a target-specific manner. Western blotting and Transwell assay showed that miR-204 significant inhibited the migration and invasion ability of breast cancer cells by targeting HNRNPA2B1 ( < 0.05). CONCLUSIONS miR-204 expression is decreased in breast cancer tissues and cells, and its overexpression can inhibit the invasion and metastasis of breast cancer cells by targeted regulation of HNRNPA2B1.
Breast Neoplasms ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Gene Expression Regulation, Neoplastic ; Humans ; MicroRNAs ; genetics ; Neoplasm Invasiveness ; Neoplasm Metastasis

BACKGROUND: Derlin 3 (DERL3) is downregulated in colorectal cancer (CRC) samples. Its level is closely linked to lymphatic metastasis or distant metastasis rate in CRC patients. However, its biological behavior in lung adenocarcinoma were rarely reported. The aim of this study is to investigate the ectopic expression of DERL3 in lung adenocarcinoma tissues and its effect on the invasion and metastasis of lung adenocarcinoma A549 cell line to reveal the possible mechanism of invasion and metastasis of lung adenocarcinoma. METHODS: Lung adenocarcinoma microarray gene chip data included 3 cases of lymph node metastasis and 3 cases of lung adenocarcinoma tissue without lymph node metastasis. The GEDS and Kaplan-Meier plot queries the survival curve and expression level of DERL3. Western blot was used to detect the expression of DERL3 in lung adenocarcinoma cells. The efficiency of knockdown DERL3 gene was detected by Western blot assay. Transwell detected the number of cells passing through the basement membrane of the transwell. EDU assay detected cell proliferation ability. Western blot detected the expression of epithelial-mesenchymal transition related proteins E-cadherin and Vimentin. RESULTS: The microarray gene chip results showed that compared with lung adenocarcinoma tissues without lymph node metastasis, 1,314 mRNAs in lung adenocarcinoma tissues with lymph node metastasis were up-regulated, 400 mRNAs were down (P<0.05). The expression of DERL3 increased in lung adenocarcinoma (P<0.05). The results of survival curve showed that the lung cancer patients with high expression of DERL3 with poor prognosis (P<0.05). Western blot results indicated that plasmid transfection was successful. Knockdown of DERL3 suppressed the ability of proliferation, invasion and migration in A549 cells (P<0.05). After knockdown of DERL3, the expression level of Vimentin was decreased, while E-cadherin expression increased (P<0.05). CONCLUSIONS Knockdown of DERL3 inhibited the proliferation, invasion and metastasis of A549 cells.

Objective : To investigate the effect of long non⁃coding RNA (LncRNA) anoctamin 1 antisense RNA⁃1 (ANO1⁃AS1) on the proliferation and apoptosis of esophageal squamous cell carcinoma (ESCC) cells and its possible mechanisms. Methods : Silenced ANO1⁃AS1 lentivirus was transfected in ESCC cells TE⁃1 and EC109. Subsequently, the expression levels of ANO1⁃AS1 and calcium⁃activated chloride channel protein 1 (ANO1) in the cells were detected by qRT⁃PCR. CCK⁃8 and colony formation assays were used to detect the proliferation of TE⁃1 and EC109 cells. ANO1 positively related expressed genes were obtained from the LinkedOmics database and then the gene set was enriched for pathways and possible pathways were validated. The expression levels of proliferating cell nuclear antigen(PCNA), P53 protein, apoptosis⁃related protein ( Bax and Bcl⁃2), ANO1 protein and phosphatidylinositol⁃3⁃kinase/protein kinase B (PI3K/Akt) pathway⁃related protein were assessed by Western blot. Results: After transfection of lentivirus with silent expression function, the expression level of ANO1⁃AS1 was significantly reduced in TE⁃1 and EC109 cells (P < 0. 05); After down⁃regulation of ANO1⁃AS1, compared with the negative control group, the proliferation ability of ESCC cells was reduced (P < 0. 05) and the rate of clone formation decreased (P < 0. 05); Western blot results showed that, compared with negative controls, the expression of PCNA decreased, the expression of oncogene P53 protein increased ( P < 0. 05 ), the expression of proteins ( Bax) increased, Bcl⁃2 decreased and the levels of phosphorylation of the pathway proteins PI3K and Akt decreased (P < 0. 05) . Conclusion Knockdown of ANO1⁃AS1 can decrease proliferation and promote apoptosis in ESCC, which may be achieved by affecting PI3K/Akt pathway activation.