Chemokine receptor 4 (CXCR4) belongs to G protein-coupled receptor superfamily.It can induce immune cells-directed chemotaxis,thus keeping their homeostasis.CXCR4 expresses on a variety of tissues and cells.In different tumors and at different stages of tumors,CXCR4 expression is significantly higher than that in normal tissues.CXCR4 plays an important role in tumor progression since it is involved in tumor cell proliferation,adhesion,invasion and metasta.

Objective To observe clinical therapeutic effect of treating insomnia by moxibustioning Balhui (DU20)and Sisbencong(EX-HN 1) . Methods 276 cases of insomnia were divided into treatment group and control group. The treatment group was treated by moxibustioning on Baihui (DU 20) and Sishencong(EX-HN 1); while the control group was treated by moxibutioning on Zusanli (ST 36). Evaluate the therapeutic effects and PSQI index of the two groups. Results Clinical symptoms got improvement in the both groups. The treatment group was better than the control group in terms of therapeutic effect of the (P＜0.05) and the improvement of PSQI (P＜0.01). Conclusion Moxibustioning on Baihui(DU 20)and Sishencong (EX-HN 1) has a good therapeutic effect for insomnia.

Objective To investigate the effect of miR-27a mimic and inhibitor on proliferation and apoptosis in melanoma cell line WM239. Methods The miR-27a mimic,inhibitor and its negative control were transfected into WM239 cells. The transfection efficiency was evaluated by fluorescence microscope. The expres-sion of miR-27a was detected by real-time fluorescent quantitative PCR. The proliferation of cells was detected by MTT. The cell apoptosis and cell cycle were analyzed by flow cytometry. Results The transfection efficiency in WM239 cells was 80% to 90%. The expression of miR-27a was markedly up-regulated in miR-27a mimic group (2-△△CT value is 26. 98 ± 0. 01),with statistically significant difference(t= -1 123. 67,P=0. 00);and the miR-27a inhibitor group showed lower expression of miR-27a(2-△△CT value is 0. 96 ± 0. 02),there was no statisti-cally significant difference compared with normal control group(t=0. 04,P=0. 06). The proliferation of cells was obviously inhibited in miR-27a mimic group,and there was statistically significant difference compared with normal control group[absorbance of 72 h(0. 45 ± 0. 02)∶(0. 72 ± 0. 01),F=129. 56,P﹤0. 05]. The percent-age of WM239 cells in G0-G1 phase was increased[(74. 83 ± 1. 46)∶(63. 73 ± 1. 25),F=30. 33,P﹤0. 05], and the percentage of WM239 cells in S phase and G2-M phase were decreased[(21. 33 ± 1. 75)∶(27. 50 ± 1. 25),F=14. 98,P﹤0. 05;(3. 90 ± 1. 31)∶(8. 80 ± 2. 10),F=3. 66,P﹤0. 05]. The apoptosis rate of cells was significantly increased in miR-27a mimic group compared with normal group[(29. 67 ± 0. 91)%∶(1. 44 ± 0. 85)%,F=530. 90,P﹤0. 01],but the inhibitor group had no obvious effect on cell cycle and cell apoptosis. Conclusion MiR-27a can suppress melanoma cell proliferation and act as a tumor suppressor gene,which is rel-evant to induce cell apoptosis and block cell cycle in G0-G1 phase.

Abstract Fear of missing out is an emerging type of anxiety disorder in the context of the Internet and has showed significant impacts on physical and mental health of college students. The review provides an overview on the connotation, extension, and adverse effects, as well as potential underlying mechanisms of fear of missing out in mobile social media among college students, which aims to highlight future attention, as well as prevention and intervention reference on fear of missing out in college students.

OBJECTIVE To investigate the effects of β-sitosterol on the function of rheumatoid arthritis （RA） fibroblastic synoviocytes MH7A cells and its mechanism. METHODS Network pharmacology was adopted to screen the targets of β-sitosterol and the targets for the treatment of RA. After the intersection of them， topological analysis was performed to find the most critical target in the treatment of RA. MH7A cells were treated with different concentrations （0， 5， 10， 20， 40 μmol/L） of β-sitosterol， and CCK-8 was used to assay cell viability for screening the optimal concentration of β-sitosterol. MH7A cells were induced by 10 ng/mL TNF-α in vitro and treated with β-sitosterol （the optimum concentration）. CCK-8 and EdU were used to detect the ability of cell proliferation. Scratch experiment and Transwell invasion assay were used to analyze cell migration and invasion. The levels of interleukin-1β （IL-1β） and IL-6 in cell supernatant were detected by enzyme-linked immunosorbent assay （ELISA）. The mRNA and protein expressions of peroxisome proliferator-activated receptor α （PPARα） were measured by qRT-PCR and Western blot， respectively. The siRNA targeting PPARα was transfected into MH7A cells， and the effects of β-sitosterol on cell proliferation， migration， invasion， the secretion of inflammatory factors and the expression of PPARα after PPARα knockdown were detected by the above experimental methods. RESULTS PPARα was the most critical target of β-sitosterol in the treatment of RA. The optimal concentration of β-sitosterol was 20 μmol/L. Compared with model group， β-sitosterol decreased the viability of MH7A cells， and the number of proliferating cells also decreased significantly （P＜0.05）； the cell migration rate and the number of cell invasion decreased significantly （P＜0.05）. The levels of IL-1β and IL-6 were also significantly decreased （P＜0.05）， and the mRNA 15 and protein expression levels of PPARα were significantly increased （P＜0.05）. Compared with negative control small interfering RNA group， after PPARα knockdown， the cell viability increased by about 35.6% （P＜0.05）， the number of cell proliferation， the cell migration rate and the number of cell invasion increased significantly （P＜0.05）， and the levels of IL-1β and IL-6 also increased significantly （P＜0.05）. CONCLUSIONS β-sitosterol could effectively inhibit the proliferation， migration， invasion and secretion of inflammatory factors in MH7A cells， the mechanism of which may be associated with activating PPARα pathway.