Search

Ren-Duan Cai,1 Chao-Cai Zhang,1 Li-Li Xie,2 Peng-Cheng Wang,3 Chui-Xue Huang,3 Jian-Long Chen,3 Hong-Tao Lv4,* 1Department of Neurosurgery, Hainan General Hospital/Hainan Affiliated Hospital of Hainan Medical University, Haikou, Hainan Province, People’s Republic of China; 2Department of Neurology, Dalian Central Hospital, Dalian, Liaoning Province, People’s Republic of China; 3Department of Neurosurgery, Hainan People’s Hospital, Haikou, Hainan Province, People’s Republic of China; 4Department of Neurosurgery, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning Province, People’s Republic of China*These authors contributed equally to this workCorrespondence: Hong-Tao LvDepartment of Neurosurgery, The First Affiliated Hospital of Dalian Medical University, No. 222 Zhongshan Road, Xigang District, Dalian 116011, Liaoning Province, People’s Republic of ChinaTel +86-18098876125Email lht_725@163.comPurpose: To explore the regulatory mechanism of long non-coding RNA small nucleolar RNA host gene 1 (SNHG1) in glioma.Materials and Methods: The expression of SNHG1 and miR-140-5p in glioma tissues and glioma cell lines (LN-18, KNS-81, and KALS-1) was determined, and the effect of the two on cell proliferation, invasion, and PI3K/AKT pathway was analyzed.Results: SNHG1 was overexpressed in glioma tissues, while miR-140-5p was underexpressed in them, and there was a significant negative correlation between SNHG1 and miR-140-5p. In addition, both down-regulation of SNHG1 and up-regulation of miR-140-5p significantly inhibited the malignant proliferation and invasion of glioma, intensified the apoptosis, and also significantly suppressed the activation of the PI3K/AKT pathway. The dual-luciferase reporter assay, RNA pull-down assay, and RIP determination all confirmed that there was a targeting relationship between SNHG1 and miR-140-5p, and there was no difference between KNS-81 and KALS-1 cells transfected with SNHG1+mimics and si-SNHG1+inhibitor and those in the si-NC group with unrelated sequences in terms of cell malignant progression.Conclusion: SNHG1/miR-140-5p axis and its regulation on PI3K/AKT pathway might be a novel therapeutic direction to curb the malignant progression of glioma.Keywords: SNHG1, glioma, miR-140-5p, PI3K/AKT pathway

A novel method that without aluminum substrate high-power LED encapsulation is proposed.The thermal properties of traditional structure and this new structure is simulated by using finite element analysis software.The simulation results show that the maximum temperatures appear in the LED chips.Comparing with the traditional structure,the maximum temperatures of the new structure respectively lower 6.436,9.468 and 19.309 ℃ when the input power is 1×1 W,3×1 W and 1×3 W.Even if the thermal conductivity of substrate reaches as high as 200 W/(m·K),the heat dissipation effect is still better than the structure with aluminum substrate.The heat dissipation effect of the new structure is obviously superior to that of aluminum substrate structure.With the increase of input power,the advantage of the new structure is more remarkable.It provides a new way to solve the heat dissipation problem of high power LED.

Perfluoroalkanesulfonyl bromides reacted with vinyl bromide, vinyl acetate and trimethyl vinyl silane to give the corresponding adducts with the evolution of SO2. Perfluoroalkanesulfonyl bromide reacted with trimethyl silyl enol ether followed by hydrolysis to give the corresponding α-bromoketones and perfluoroalkanesulfinic acid. However, perfluoroalkanesulfonyl chlorides reacted with trimethyl silyl enol ether of pinacolone on UV irradiation to give the corresponding α-perfluoroalkyl derivatives of pinacolone. Under mild condition, perfluoroalkanesulfonyl bromide also brominated phenol and anisole to give the corresponding p-bromo derivatives. Sodium α, α-dichlorotrifluoroethanesulfinate reacted with bromine in water at 25°C to form α, α-dichlorotrifluoroethanesulfonyl bromide which was thermally less stable than but similar in reactivity to perfluoroalkanesulfonyl bromide.