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Involvement of Orai1 in tunicamycin-induced endothelial dysfunction
Hui Yang,Yumei Xue,Sujuan Kuang,Mengzhen Zhang,Jinghui Chen,Lin Liu,Zhixin Shan,Qiuxiong Lin,Xiaohong Li,Min Yang,Hui Zhou,Fang Rao,Chunyu Deng 대한약리학회 2019 The Korean Journal of Physiology & Pharmacology Vol.23 No.2
Endoplasmic reticulum (ER) stress is mediated by disturbance of Ca2+ homeostasis. The store-operated calcium (SOC) channel is the primary Ca2+ channel in non-excitable cells, but its participation in agent-induced ER stress is not clear. In this study, the effects of tunicamycin on Ca2+ influx in human umbilical vein endothelial cells (HUVECs) were observed with the fluorescent probe Fluo-4 AM. The effect of tunicamycin on the expression of the unfolded protein response (UPR)-related proteins BiP and CHOP was assayed by western blotting with or without inhibition of Orai1. Tunicamycin induced endothelial dysfunction by activating ER stress. Orai1 expression and the influx of extracellular Ca2+ in HUVECs were both upregulated during ER stress. The SOC channel inhibitor SKF96365 reversed tunicamycin-induced endothelial cell dysfunction by inhibiting ER stress. Regulation of tunicamycin-induced ER stress by Orai1 indicates that modification of Orai1 activity may have therapeutic value for conditions with ER stress-induced endothelial dysfunction.
Shan Shan Gao,Jia-Lin Li,Hui Min Qiao 대한전기학회 2019 Journal of Electrical Engineering & Technology Vol.14 No.5
A planar slot antenna operating at 2.75–9.75 GHz is studied for ultra-wideband (UWB) applications, where three controllable notched bands centered at 4, 5.9 and 8.45 GHz are further introduced to avoid some potential interferences. The elliptical slots and coplanar waveguide feeding lines are incorporated to achieve desired UWB operation. By introducing a V-shaped and two U-shaped slots on the CPW signal line, three notched bands are implemented, and each notch band can be adjusted independently. Measurements on the developed demonstrator match with the numerical simulations.
Involvement of Orai1 in tunicamycin-induced endothelial dysfunction
Yang, Hui,Xue, Yumei,Kuang, Sujuan,Zhang, Mengzhen,Chen, Jinghui,Liu, Lin,Shan, Zhixin,Lin, Qiuxiong,Li, Xiaohong,Yang, Min,Zhou, Hui,Rao, Fang,Deng, Chunyu The Korean Society of Pharmacology 2019 The Korean Journal of Physiology & Pharmacology Vol.23 No.2
Endoplasmic reticulum (ER) stress is mediated by disturbance of $Ca^{2+}$ homeostasis. The store-operated calcium (SOC) channel is the primary $Ca^{2+}$ channel in non-excitable cells, but its participation in agent-induced ER stress is not clear. In this study, the effects of tunicamycin on $Ca^{2+}$ influx in human umbilical vein endothelial cells (HUVECs) were observed with the fluorescent probe Fluo-4 AM. The effect of tunicamycin on the expression of the unfolded protein response (UPR)-related proteins BiP and CHOP was assayed by western blotting with or without inhibition of Orai1. Tunicamycin induced endothelial dysfunction by activating ER stress. Orai1 expression and the influx of extracellular $Ca^{2+}$ in HUVECs were both upregulated during ER stress. The SOC channel inhibitor SKF96365 reversed tunicamycin-induced endothelial cell dysfunction by inhibiting ER stress. Regulation of tunicamycin-induced ER stress by Orai1 indicates that modification of Orai1 activity may have therapeutic value for conditions with ER stress-induced endothelial dysfunction.
IGF-1 from Adipose-Derived Mesenchymal Stem Cells Promotes Radioresistance of Breast Cancer Cells
Yang, Hui-Ying,Qu, Rong-Mei,Lin, Xiao-Shan,Liu, Tong-Xin,Sun, Quan-Quan,Yang, Chun,Li, Xiao-Hong,Lu, Wei,Hu, Xiao-Fang,Dai, Jing-Xing,Yuan, Lin Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.23
Purpose: The aim of this study was to investigate effects of adipose-derived mesenchymal stem cells (AMSCs) on radioresistance of breast cancer cells. Materials and Methods: MTT assays were used to detect any influence of AMSC supernatants on proliferation of breast cancer cells; cell migration assays were used to determine the effect of breast cancer cells on the recruitment of AMSCs; the cell survival fraction post-irradiation was assessed by clonogenic survival assay; ${\gamma}$-H2AX foci number post-irradiation was determined via fluorescence microscopy; and expression of IGF-1R was detected by Western blotting. Results: AMSC supernatants promoted proliferation and radioresistance of breast cancer cells. Breast cancer cells could recruit AMSCs, especially after irradiation. IGF-1 derived from AMSCs might be responsible for the radioresistance of breast cancer cells. Conclusions: Our results suggest that AMSCs in the tumor microenvironment may affect the outcome of radiotherapy for breast cancer in vitro.
Dang-Hui Wang,Sheng-Rui Xu,Jin-Cheng Zhang,Ke Chen,Zhi-Wei Bi,Lin-Xia Zhang,Fan-Na Meng,Shan Ai,Yue Hao 한국물리학회 2012 THE JOURNAL OF THE KOREAN PHYSICAL SOCIETY Vol.61 No.4
In this study, we report on the crystal quality of InGaN epifilms with different indium fractions grown at different growth temperatures on c-plane sapphire substrates with an AlN nucleation layer by using low-pressure metal-organic chemical-vapor deposition (MOCVD). High-resolution X-ray diffraction (HRXRD), atom force microscopy (AFM), photoluminescence (PL) and Raman scattering measurements were employed to study the crystal quality, optical properties and strain condition of InGaN epifilms with increasing indium fraction (from 4.36% to 15.36%). Results show that InGaN epitaxial layers can be realized with a higher indium fraction at a lower temperature by inserting an AlN nucleation layer between the sapphire substrate and the GaN buffer layer and that the obtained InGaN epifilms have an improved crystal quality and a lower threading dislocation density.
Rhodococcus soli sp. nov., an actinobacterium isolated from soil using a resuscitative technique.
Li, Shan-Hui,Yu, Xiao-Yun,Park, Dong-Jin,Hozzein, Wael N,Kim, Chang-Jin,Shu, Wen-Sheng,Wadaan, Mohammed A M,Ding, Lin-Xian,Li, Wen-Jun N.V. Swets en Zeitlinger 2015 Antonie van Leeuwenhoek Vol.107 No.2
<P>A Gram-positive, aerobic, non-motile, non-spore forming strain, designated DSD51W(T), was isolated using a resuscitative technique from a soil sample collected from Kyoto park, Japan, and characterized by using a polyphasic approach. The morphological and chemotaxonomic properties of the isolate were typical of those of members of the genus Rhodococcus. Strain DSD51W(T) was found to form a coherent cluster with Rhodococcus hoagii ATCC 7005(T), Rhodococcus equi NBRC 101255(T), Rhodococcus defluvii Call(T) and Rhodococcus kunmingensis YIM 45607(T) as its closest phylogenetic neighbours in 16S rRNA gene sequence analysis. However, the DNA-DNA hybridization values with the above strains were 58.2 ± 2.2, 58.4 ± 1.9, 45.1 ± 1.4 and 40.3 ± 4.7 %, respectively. In combination with differences in physiological and biochemical properties, strain DSD51W(T) can be concluded to represent a novel species of the genus Rhodococcus, for which the name Rhodococcus soli sp. nov. is proposed, with the type strain DSD51W(T) (=KCTC 29259(T) = JCM 19627(T) = DSM 46662(T) = KACC 17838(T)).</P>
Suppression of GHS-R in AgRP Neurons Mitigates Diet-Induced Obesity by Activating Thermogenesis
Wu, Chia-Shan,Bongmba, Odelia Y. N.,Yue, Jing,Lee, Jong Han,Lin, Ligen,Saito, Kenji,Pradhan, Geetali,Li, De-Pei,Pan, Hui-Lin,Xu, Allison,Guo, Shaodong,Xu, Yong,Sun, Yuxiang MDPI AG 2017 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.18 No.4
<P>Ghrelin, an orexigenic hormone released primarily from the gut, signals the hypothalamus to stimulate growth hormone release, enhance appetite and promote weight gain. The ghrelin receptor, aka Growth Hormone Secretagogue Receptor (GHS-R), is highly expressed in the brain, with highest expression in Agouti-Related Peptide (AgRP) neurons of the hypothalamus. We recently reported that neuron-specific deletion of GHS-R completely prevents diet-induced obesity (DIO) in mice by activating non-shivering thermogenesis. To further decipher the specific neuronal circuits mediating the metabolic effects of GHS-R, we generated AgRP neuron-specific GHS-R knockout mice (<I>AgRP-Cre</I>;<I>Ghsr<SUP>f/f</SUP></I>). Our data showed that GHS-R in AgRP neurons is required for ghrelin’s stimulatory effects on growth hormone secretion, acute food intake and adiposity, but not for long-term total food intake. Importantly, deletion of GHS-R in AgRP neurons attenuated diet-induced obesity (DIO) and enhanced cold-resistance in mice fed high fat diet (HFD). The HFD-fed knockout mice showed increased energy expenditure, and exhibited enhanced thermogenic activation in both brown and subcutaneous fat; this implies that GHS-R suppression in AgRP neurons enhances sympathetic outflow. In summary, our results suggest that AgRP neurons are key site for GHS-R mediated thermogenesis, and demonstrate that GHS-R in AgRP neurons plays crucial roles in governing energy utilization and pathogenesis of DIO.</P>