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Yin, Fugui,Yin, Yulong,Kong, Xiangfeng,Liu, Yulan,He, Qinghua,Li, Tiejun,Huang, Ruilin,Hou, Yongqing,Shu, Xugang,Tan, Liangxi,Chen, Lixiang,Gong, Jianhua,Kim, Sung Woo,Wu, Guoyao Asian Australasian Association of Animal Productio 2008 Animal Bioscience Vol.21 No.9
This study was conducted to investigate the effects of Acanthopanax senticosus extract (ASE) as a dietary additive on gut microflora in weaned piglets. A total of sixty pigs were weaned at 21 d of age (BW = $5.64{\pm}0.23kg$) and allocated on the basis of BW and litter to three dietary treatments in a randomized complete block design. The dietary treatments were: control group (basal diet), antibiotics group (basal diet+0.02% colistin), and ASE group (basal diet+0.1% ASE). On d 7, 14 and 28 after consuming the experimental diets, five piglets per group were sacrificed and then the contents from the jejunum, ileum and cecum were collected to determine changes in the microbial community by using a polymerase chain reaction-denaturing gradient gel electrophoresis (PCR-DGGE) technique and estimating the contents of Lactobacillus and E. coli by in vitro culturing methods. The results showed that the ASE promoted the microflora diversity in the cecum. Enumeration of bacteria in the gut contents showed that the number of Lactobacillus increased (p<0.05), while that of E. coli decreased (p<0.05) when compared with the other 2 groups as the days of age progressed post-weaning. These findings suggested that the ASE, as a substitute for dietary antimicrobial products, could improve the development of the normal gut microflora and suppress bacterial pathogens, and effectively promote a healthy intestinal environment.
Energy Efficiency of Distributed Massive MIMO Systems
He, Chunlong,Yin, Jiajia,He, Yejun,Huang, Min,Zhao, Bo The Korea Institute of Information and Commucation 2016 Journal of communications and networks Vol.18 No.4
In this paper, we investigate energy efficiency (EE) of the traditional co-located and the distributed massive multiple-input multiple-output (MIMO) systems. First, we derive an approximate EE expression for both the idealistic and the realistic power consumption models. Then an optimal energy-efficient remote access unit (RAU) selection algorithm based on the distance between the mobile stations (MSs) and the RAUs are developed to maximize the EE for the downlink distributed massive MIMO systems under the realistic power consumption model. Numerical results show that the EE of the distributed massive MIMO systems is larger than the co-located massive MIMO systems under both the idealistic and realistic power consumption models, and the optimal EE can be obtained by the developed energy-efficient RAU selection algorithm.
Energy Efficiency of Distributed Massive MIMO Systems
Chunlong He,Jiajia Yin,Yejun He,Min Huang,Bo Zhao 한국통신학회 2016 Journal of communications and networks Vol.18 No.4
In this paper, we investigate energy efficiency (EE) of thetraditional co-located and the distributed massive multiple-inputmultiple-output (MIMO) systems. First, we derive an approximateEE expression for both the idealistic and the realistic power consumptionmodels. Then an optimal energy-efficient remote accessunit (RAU) selection algorithm based on the distance between themobile stations (MSs) and the RAUs are developed to maximizethe EE for the downlink distributedmassive MIMO systems underthe realistic power consumption model. Numerical results showthat the EE of the distributedmassiveMIMOsystems is larger thanthe co-locatedmassiveMIMOsystems under both the idealistic andrealistic power consumptionmodels, and the optimal EE can be obtainedby the developed energy-efficient RAU selection algorithm.
He, Zongze,Chen, Longyi,Wang, Qi,Yin, Cheng,Hu, Junting,Hu, Xiao,Fei, Fan,Tang, Jian The Korean Society of Pharmacology 2019 The Korean Journal of Physiology & Pharmacology Vol.23 No.3
Pituitary tumors are usually benign but can occasionally exhibit hormonal and proliferative behaviors. Dysregulation of the G1/S restriction point largely contributes to the over-proliferation of pituitary tumor cells. F-box protein S-phase kinase-interacting protein-2 (SKP2) reportedly targets and inhibits the expression of $p27^{Kip1}$, a well-known negative regulator of G1 cell cycle progression. In this study, SKP2 expression was found to be upregulated while $p27^{Kip1}$ expression was determined to be downregulated in rat and human pituitary tumor cells. Furthermore, SKP2 knockdown induced upregulation of $p27^{Kip1}$ and cell growth inhibition in rat and human pituitary tumor cells, while SKP2overexpression elicited opposite effects on $p27^{Kip1}$ expression and cell growth. The expression of microRNA-186 (miR-186) was reported to be reduced in pituitary tumors. Online tools predicted SKP2 to be a direct downstream target of miR-186, which was further confirmed by luciferase reporter gene assays. Moreover, miR-186 could modulate the cell proliferation and $p27^{Kip1}$-mediated cell cycle alternation of rat and human pituitary tumor cells through SKP2. As further confirmation of these findings, miR-186 and $p27^{Kip1}$ expression were downregulated, while SKP2 expression was upregulated in human pituitary tumor tissue samples; thus, SKP2 expression negatively correlated with miR-186 and $p27^{Kip1}$ expression. In contrast, miR-186 expression positively associated with $p27^{Kip1}$ expression. Taken together, we discovered a novel mechanism by which miR-186/SKP2 axis modulates pituitary tumor cell proliferation through $p27^{Kip1}$-mediated cell cycle alternation.
Yin Bin Chen,Yu Fang Wang,Wei Hou,Ying-Ping Wang,Sheng-Yuan Xiao,Yang Yang Fu,Jia Wang,Si Wen Zheng,Pei-He Zheng 고려인삼학회 2017 Journal of Ginseng Research Vol.41 No.2
Background: Both ginsenoside Re and B-complex vitamins are widely used as nutritional supplements. They are often taken together so as to fully utilize their antifatigue and refreshing effects, respectively. Whether actually a drugenutrient interaction exists between ginsenoside Re and B-complex vitamins is still unknown. The objective of this study was to simultaneously investigate the effect of B-complex vitamins on the antifatigue activity and bioavailability of ginsenoside Re after their oral administration. The study results will provide valuable theoretical guidance for the combined utilization of ginseng and B-complex vitamins. Methods: Ginsenoside Re with or without B-complex vitamins was orally administered to mice to evaluate its antifatigue effects and to rats to evaluate its bioavailability. The antifatigue activity was evaluated by the weight-loaded swimming test and biochemical parameters, including hepatic glycogen, plasma urea nitrogen, and blood lactic acid. The concentration of ginsenoside Re in plasma was determined by liquid chromatographyetandem mass spectrometry. Results: No antifatigue effect of ginsenoside Re was noted when ginsenoside Re in combination with Bcomplex vitamins was orally administered to mice. B-complex vitamins caused to a reduction in the bioavailability of ginsenoside Re with the area under the concentrationetime curve from zero to infinity markedly decreasing from 11,830.85 2,366.47 h$ng/mL to 890.55 372.94 h$ng/mL. Conclusion: The results suggested that there were pharmacokinetic and pharmacodynamic drugenutrient interactions between ginsenoside Re and B-complex vitamins. B-complex vitamins can significantly weaken the antifatigue effect and decrease the bioavailability of ginsenoside Re when simultaneously administered orally.
Yin Yang,Qian Li,Qi-Hua He,Ji-Sheng Han,Li Su,You Wan 생화학분자생물학회 2018 Experimental and molecular medicine Vol.50 No.-
Activation of the cholecystokinin type B receptor (CCKBR) by cholecystokinin octapeptide (CCK-8) inhibits opioid analgesia. Chronic opiate treatment leads to an increase in the CCK-8 concentration and thus enhances the antagonism of CCK-8 against opioid analgesia; the underlying molecular mechanisms remain of great interest. In the present study, we validated the colocalization of the μ-opioid receptor (MOR) and CCKBR in pain signal transmissionrelated spinal cord dorsal horn and dorsal root ganglion neurons of rats. Co-immunoprecipitation (Co-IP) and fluorescence lifetime-imaging-microscopy-based fluorescence resonance energy transfer (FLIM-FRET) assays showed that MOR heteromerized with CCKBR directly in transfected HEK293 cells. Combined with MOR mutant construction, the third transmembrane domain of MOR (TM3MOR) was demonstrated to participate in heteromerization with CCKBR. Receptor ligand binding, ERK phosphorylation and cAMP assays showed that MOR heteromerization with CCKBR weakened the activity of MOR. A cell-penetrating interfering peptide consisting of TM3MOR and TAT (a transactivator of HIV-1) sequences from the N terminal to the C terminal disrupted the MOR–CCKBR interaction and restored the activity of MOR in transfected HEK293 cells. Furthermore, intrathecal application of the TM3MOR-TAT peptide alleviated CCK-8-injection-induced antagonism to morphine analgesia in rats. These results suggest a new molecular mechanism for CCK-8 antagonism to opioid analgesia in terms of G-protein-coupled receptor (GPCR) interaction through direct heteromerization. Our study may provide a potential strategy for pain management with opioid analgesics.