Numerical simulation of helicon waves current drive in the HL-2M tokamak for the steady-state scenario

Liu Hong Bo,Li Xin Xia,Xiao Zheng Yao,Zhang Ding Zong,Sun Ai Ping 한국물리학회 2021 THE JOURNAL OF THE KOREAN PHYSICAL SOCIETY Vol.79 No.12

The helicon wave heating and current drive in the HL-2M tokamak for the steady-state scenario is studied numerically. Based on the theory of fast wave current drive proposed by Chiu, we analyze the characteristics of helicon waves damping for the HL-2M tokamak. For wave frequencies larger than 420 MHz, strong wave damping occurs, and electron Landau damping is dominant. Moreover, a strong wave absorption region associated with the dimensionless parameters βe and ξe that depend on the wave frequency is obtained. The helicon wave propagation and current drive are simulated using the GENRAY/CQL3D code. The results show that an off-axis current drive with profiles peak at ρ ∼ 0.4 can be generally received at a wave frequency f ∼ 500 MHz and the launched parallel refractive index n∕∕ = 3.8 and that the current drive efficiency reaches up to ∼140 kA/MW. A scan of n∕∕ showed that both the current drive profile peak and the generated current could be adjusted by changing the launched n∕∕ . Finally, a feasible scheme for the helicon wave off-axis current drive in the HL-2M tokamak is proposed.

Cadmium induces apoptosis in primary rat osteoblasts through caspase and mitogen-activated protein kinase pathways

Hong-Yan Zhao,Wei Liu,Yi Wang,Nannan Dai,Jian-Hong Gu,Yan Yuan,Xue-Zhong Liu,Jian-Chun Bian,Zong-Ping Liu 대한수의학회 2015 Journal of Veterinary Science Vol.16 No.3

Exposure to cadmium (Cd) induces apoptosis in osteoblasts (OBs); however, little information is available regarding the specific mechanismsof Cd-induced primary rat OB apoptosis. In this study, Cd reduced cell viability, damaged cell membranes and induced apoptosis in OBs. We observed decreased mitochondrial transmembrane potentials, ultrastructure collapse, enhanced caspase-3 activity, and increasedconcentrations of cleaved PARP, cleaved caspase-9 and cleaved caspase-3 following Cd treatment. Cd also increased the phosphorylationof p38-mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinases (ERK)1/2 and c-jun N-terminal kinase (JNK) in OBs. Pretreatment with the caspase inhibitor, N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone, ERK1/2 inhibitor (U0126), p38 inhibitor(SB203580) and JNK inhibitor (SP600125) abrogated Cd-induced cell apoptosis. Furthermore, Cd-treated OBs exhibited signs of oxidativestress protection, including increased antioxidant enzymes superoxide dismutase and glutathione reductase levels and decreased formationof reactive oxygen species. Taken together, the results of our study clarified that Cd has direct cytotoxic effects on OBs, which are mediatedby caspase- and MAPK pathways in Cd-induced apoptosis of OBs.

N-acetylcysteine protects against cadmium-induced oxidative stress in rat hepatocytes

Jicang Wang,Huali Zhu,Xue-Zhong Liu,Zong-Ping Liu 대한수의학회 2014 JOURNAL OF VETERINARY SCIENCE Vol.15 No.4

Cadmium (Cd) is a well-known hepatotoxic environmentalpollutant. We used rat hepatocytes as a model to studyoxidative damage induced by Cd, effects on the antioxidantsystems, and the role of N-acetylcysteine (NAC) in protectingcells against Cd toxicity. Hepatocytes were incubated for 12and 24 h with Cd (2.5, 5, 10 μM). Results showed that Cd caninduce cytotoxicity: 10 μM resulted in 36.2% mortality after12 h and 47.8% after 24 h. Lactate dehydrogenase, aspartate aminotransferase, and alanine aminotransferase activitiesincreased. Additionally, reactive oxygen species (ROS)generation increased in Cd-treated hepatocytes along withmalondialdehyde levels. Glutathione concentrationssignificantly decreased after treatment with Cd for 12 h butincreased after 24 h of Cd exposure. In contrast, glutathioneperoxidase activity significantly increased after treatmentwith Cd for 12 h but decreased after 24 h. superoxidedismutase and catalase activities increased at 12 h and 24 h. glutathione S-transferase and glutathione reductase activitiesdecreased, but not significantly. Rat hepatocytes incubatedwith NAC and Cd simultaneously had significantly increasedviability and decreased Cd-induced ROS generation. Ourresults suggested that Cd induces ROS generation that leads to oxidative stress. Moreover, NAC protects rat hepatocytes from cytotoxicity associated with Cd.

Characterization of the Methylation Status of Pax7 and Myogenic Regulator Factors in Cell Myogenic Differentiation

Chao, Zhe,Zheng, Xin-Li,Sun, Rui-Ping,Liu, Hai-Long,Huang, Li-Li,Cao, Zong-Xi,Deng, Chang-Yan,Wang, Feng Asian Australasian Association of Animal Productio 2016 Animal Bioscience Vol.29 No.7

Epigenetic processes in the development of skeletal muscle have been appreciated for over a decade. DNA methylation is a major epigenetic modification important for regulating gene expression and suppressing spurious transcription. Up to now, the importance of epigenetic marks in the regulation of Pax7 and myogenic regulatory factors (MRFs) expression is far less explored. In the present study, semi-quantitative the real-time polymerase chain reaction (RT-PCR) analyses showed MyoD and Myf5 were expressed in activated and quiescent C2C12 cells. MyoG was expressed in a later stage of myogenesis. Pax7 was weakly expressed in differentiated C2C12 cells. To further understand the regulation of expression of these genes, the DNA methylation status of Pax7, MyoD, and Myf5 was determined by bisulfite sequencing PCR. During the C2C12 myoblasts fusion process, the changes of promoter and exon 1 methylation of Pax7, MyoD, and Myf5 genes were observed. In addition, an inverse relationship of low methylation and high expression was found. These results suggest that DNA methylation may be an important mechanism regulating Pax7 and MRFs transcription in cell myogenic differentiation.

Regulation of matrix metalloproteinase-9 protein expression by 1α , 25-(OH)2D3 during osteoclast differentiation

Jian-Hong Gu,Xi-Shuai Tong,Guohong Chen,Xue-Zhong Liu,Jian-Chun Bian,Yan Yuan,Zong-Ping Liu 대한수의학회 2014 Journal of Veterinary Science Vol.15 No.1

To investigate 1α,25-(OH)2D3 regulation of matrixmetalloproteinase-9 (MMP-9) protein expression duringosteoclast formation and differentiation, receptor activator ofnuclear factor κB ligand (RANKL) and macrophagecolony-stimulating factor (M-CSF) were administered toinduce the differentiation of RAW264.7 cells into osteoclasts. The cells were incubated with different concentrations of1α,25-(OH)2D3 during culturing, and cell proliferation wasmeasured using the methylthiazol tetrazolium method. Osteoclast formation was confirmed using tartrate-resistantacid phosphatase (TRAP) staining and assessing bone lacunarresorption. MMP-9 protein expression levels were measuredwith Western blotting. We showed that 1α,25-(OH)2D3inhibited RAW264.7 cell proliferation induced by RANKLand M-CSF, increased the numbers of TRAP-positiveosteoclasts and their nuclei, enhanced osteoclast boneresorption, and promoted MMP-9 protein expression in aconcentration-dependent manner. These findings indicatethat 1α,25-(OH)2D3 administered at a physiological relevantconcentration promoted osteoclast formation and couldregulate osteoclast bone metabolism by increasing MMP-9protein expression during osteoclast differentiation.

Involvement of the Ca2+ signaling pathway in osteoprotegerin inhibition of osteoclast differentiation and maturation

Ying-Xiao Fu,Jian-Hong Gu,Yi Wang,Yan Yuan,Xue-Zhong Liu,Jian-Chun Bian,Zong-Ping Liu 대한수의학회 2015 Journal of Veterinary Science Vol.16 No.2

The purpose of this study was to determine whether the Ca2+ signaling pathway is involved in the ability of osteoprotegerin (OPG) to inhibit osteoclast differentiation and maturation. RAW264.7 cells were incubated with macrophage colony-stimulating factor (M-CSF) + receptor activator of nuclear factor-κB ligand (RANKL) to stimulate osteoclastogenesis and then treated with different concentrations of OPG, an inhibitor of osteoclast differentiation. The intracellular Ca2+ concentration [Ca2+]i and phosphorylation of Ca2+/calmodulin-dependent protein kinase II (CaMKII) in the different treatment groups were measured by flow cytometry and Western blotting, respectively. The results confirmed that M-CSF + RANKL significantly increased [Ca2+]i and CaMKII phosphorylation in osteoclasts (p < 0.01), and that these effects were subsequently decreased by OPG treatment. Exposure to specific inhibitors of the Ca2+ signaling pathway revealed that these changes varied between the different OPG treatment groups. Findings from the present study indicated that the Ca2+ signaling pathway is involved in both the regulation of osteoclastogenesis as well as inhibition of osteoclast differentiation and activation by OPG.

Inhibitory effects of osteoprotegerin on osteoclast formation and function under serum-free conditions

Ying-Xiao Fu,Jian-Hong Gu,Yi-Ran Zhang,Xi-Shuai Tong,Hong-Yan Zhao,Yan Yuan,Xue-Zhong Liu,Jian-Chun Bian,Zong-Ping Liu 대한수의학회 2013 Journal of Veterinary Science Vol.14 No.4

The purpose of this study was to determine whether osteoprotegerin (OPG) could affect osteoclat differentiation and activation under serum-free conditions. Both duck embryo bone marrow cells and RAW264.7 cells were incubated with macrophage colony stimulatory factor (M-CSF) and receptor activator for nuclear factor κB ligand (RANKL) in serum-free medium to promote osteoclastogenesis. During cultivation, 0,10, 20, 50, and 100 ng/mL OPG were added to various groups of cells. Osteoclast differentiation and activation were monitored via tartrate-resistant acid phosphatase (TRAP) staining,filamentous-actin rings analysis, and a bone resorption assay. Furthermore, the expression osteoclast-related genes, such as TRAP and receptor activator for nuclear factor κB (RANK),that was influenced by OPG in RAW264.7 cells was examined using real-time polymerase chain reaction. In summary,findings from the present study suggested that M-CSF with RANKL can promote osteoclast differentiation and activation,and enhance the expression of TRAP and RANK mRNA in osteoclasts. In contrast, OPG inhibited these activities under serum-free conditions.