Objective To study the effects of human bronchial epithelial cells (BEAS-2B cells ) coculture together with human eosinophils on intercellular adhesion molecule (ICAM-1) expression on BEAS-2B cell surface.Methods BEAS-2B cells cocultured contact with eosinophils for 4 h and 12 h,total RNA was extracted and ICAM-1 gene in BEAS-2B cells were analyzed by reverse transcription polymerase chain reaction (RT-PCR); ICAM-1 protein on BEAS-2B cell surface was assayed by fluorescent antibody in flow cytometry.Results ICAM-1 gene expression in BEAS-2B cells was upregulated and ICAM-1 protein on BEAS-2B cell surface increased by coculture with eosinophils.Conclusion Coculture of BEAS-2B cells and eosinophils might induce BEAS-2B cells to express ICAM-1.

Objective To discuss the change of elasticity of common carotid artery(CCA) with velocity vector imaging(VVI) technique in perimenopausal women.Methods 68 women in perimenopausal period were divided into two groups:estrogen drop group(42 women) and normal control group(26 women) according to the level of estrogen in serum.All women were examined with color Doppler ultrasound,and the maximum time to peak of the velocity(VTTP),maximum velocity(Vmax),maximum radial strain (Smax),maximum strain rate(SRmax) and the change rate of area(ΔS) were measured and assessed in common carotid artery(CCA) including 6 segments:anterior wall,posterior wall,anterolateral wall,anterior internal wall,posterolateral wall and posterointernal wall.Results There were signicantly differences of the elastic parameters between two groups inculding VTTP,Smax and ΔS (P ＜0.01),and there were no statistical difference on the Vmax and SRmax in both two groups(P ＞0.05).Conclusions The change of elasticity in CCA can be observed susceptibly with VVI in perimenopausal women,and VVI is an effective and sensitive technique for detecting CCA elastic characteristics.

MicroRNAs (miRNAs) are small noncoding RNAs that have a pivotal role in the post-transcriptional regulation of gene expression by sequence-specifically targeting multiple mRNAs. Although miR-33a was recently reported to play an important role in lipid homeostasis, atherosclerosis, and hepatic fibrosis, the functions of miR-33a in tumor progression and metastasis are largely unknown. Here, we found that downregulated miR-33a in breast cancer tissues correlates with lymph node metastasis. MiR-33a expression is significantly lower in the highly metastatic breast cancer cell lines than the noncancerous breast epithelial cells and non-metastatic breast cancer cells. Moreover, the overexpression of miR-33a in metastatic breast cancer cells remarkably decreases cell proliferation and invasion in vitro and significantly inhibits tumor growth and lung metastasis in vivo, whereas its knockdown in non-metastatic breast cancer cells significantly enhances cell proliferation and invasion in vitro and promotes tumor growth and lung metastasis in vivo. Combining bioinformatics prediction and biochemical analyses, we showed that ADAM9 and ROS1 are direct downstream targets of miR-33a. These findings identified miR-33a as a negative regulator of breast cancer cell proliferation and metastasis.
ADAM Proteins ; deficiency ; genetics ; Animals ; Breast Neoplasms ; genetics ; pathology ; Cell Line, Tumor ; Cell Movement ; genetics ; Cell Proliferation ; genetics ; Female ; Humans ; Lung Neoplasms ; secondary ; Membrane Proteins ; deficiency ; genetics ; Mice ; MicroRNAs ; genetics ; Middle Aged ; Neoplasm Invasiveness ; Neoplasm Metastasis ; Protein-Tyrosine Kinases ; deficiency ; genetics ; Proto-Oncogene Proteins ; deficiency ; genetics