The Dynamics of Major Species During the First four Year's Restoration from Grazing in Inner Mongolian Grassland

Ying Zhi Gao,Shi Ping Wang,You Neng Yang,De Li Wang,Jie Zhang 한국초지조사료학회 2009 한국초지조사료학회 학술대회논문집 Vol.2009 No.08

Grazing restoration succession of the degraded grassland is an important aspect in community ecology. Field experiment was carried out to examine how major species restore in first four years restoration following 11 consecutive grazing under different stocking rates in Inner Mongolian steppe. A. frigida and P. acaulis are the most important two species in the all treatments (NG, LG, MG and HG) after four years restoration, although they had high fluctuation. The biomasses of these two species account for 40-90% of total biomass. Especially in no grazing area, which was exclosured since 1990, A. frigida and P. acaulis are still the most important two species in the community. These results suggested A. frigida and P. acaulis conununity are quite stable, and will keep long-time if no special measurements were taken during the restoration of the degraded grassland.

Community Productivity and Species Diversity After Four Year's Restoration from Grazing in Inner Mongolian Grassland

Ying Zhi Gao,Shi Ping Wang,De Li Wang,Jie Zhang,Huai Yu Wan 한국초지조사료학회 2009 한국초지조사료학회 학술대회논문집 Vol.2009 No.08

To explore the relationship of species diversity and aboveground productivity in grazing ecosystem is very important to manage grassland. We used the four years' data to check this relationship and to look how abiotic factor affect species diversity and aboveground productivity. We found a good linear relationship between species diversity and aboveground productivity in all previous grazing sites, while no any relationship was found in the no grazing site. From our results, we concluded that drought affects aboveground productivity more than grazing, while heavy grazing affects species diversity more than drought in Inner Mongolian steppe.

Ginsenoside Rg3 in combination with artesunate overcomes sorafenib resistance in hepatoma cell and mouse models

Ying-Jie Chen,Jia-Ying Wu,Yu-Yi Deng,Ying Wu,Xiao-Qi Wang,Amy Sze-man Li,Lut Yi Wong,Xiuqiong Fu,Zhi-Ling Yu,Chun Liang 고려인삼학회 2022 Journal of Ginseng Research Vol.46 No.3

Sorafenib is effective in treating hepatoma, but most patients develop resistance to it. STAT3signaling has been implicated in sorafenib resistance. Artesunate (ART) and 20(R)-ginsenoside Rg3 (Rg3)have anti-hepatoma effects and can inhibit STAT3 signaling in cancer cells. This study aimed to evaluatethe effects of Rg3 in combination with ART (Rg3-plus-ART) in overcoming sorafenib resistance, and toexamine the involvement of STAT3 signaling in these effects. Methods: Sorafenib-resistant HepG2 cells (HepG2-SR) were used to evaluate the in vitro anti-hepatomaeffects of Rg3-plus-ART. A HepG2-SR hepatoma-bearing BALB/c-nu/nu mouse model was used to assessthe in vivo anti-hepatoma effects of Rg3-plus-ART. CCK-8 assays and Annexin V-FITC/PI double stainingwere used to examine cell proliferation and apoptosis, respectively. Immunoblotting was employed toexamine protein levels. ROS generation was examined by measuring DCF-DA fluorescence. Results: Rg3-plus-ART synergistically reduced viability of, and evoked apoptosis in HepG2-SR cells, andsuppressed HepG2-SR tumor growth in mice. Mechanistic studies revealed that Rg3-plus-ART inhibitedactivation/phosphorylation of Src and STAT3 in HepG2-SR cultures and tumors. The combination alsodecreased the STAT3 nuclear level and induced ROS production in HepG2-SR cultures. Furthermore, overactivation of STAT3 or removal of ROS diminished the anti-proliferative effects of Rg3-plus-ART, andremoval of ROS diminished Rg3-plus-ART's inhibitory effects on STAT3 activation in HepG2-SR cells. Conclusions: Rg3-plus-ART overcomes sorafenib resistance in experimental models, and inhibition of Src/STAT3 signaling and modulation of ROS/STAT3 signaling contribute to the underlying mechanisms. Thisstudy provides a pharmacological basis for developing Rg3-plus-ART into a novel modality for treatingsorafenib-resistant hepatoma.

Transmembrane Helix of Novel Oncogene with Kinase-Domain (NOK) Influences Its Oligomerization and Limits the Activation of RAS/MAPK Signaling

Ying-Hua Li,Yin-Yin Wang,Shan Zhong,Zhi-Li Rong,Yong-Ming Ren,Zhi-Yong Li,Shu-Ping Zhang,Zhi-Jie Chang,Li Liu 한국분자세포생물학회 2009 Molecules and cells Vol.27 No.1

Ligand-dependent or independent oligomerization of receptor protein tyrosine kinase (RPTK) is often an essential step for receptor activation and intracellular signaling. The novel oncogene with kinase-domain (NOK) is a unique RPTK that almost completely lacks an ectodomain, expresses intracellularly and activates constitutively. However, it is unknown whether NOK can form oligomer or what function oligomerization would have. In this study, two NOK deletion mutants were generated by either removing the ectodomain (NOKECD) or including the endodomain (NOK-ICD). Co-immunoprecipitation demonstrated that the transmembrane (TM) domain of NOK was essential for its intermolecular interaction. The results further showed that NOK aggregated more closely as lower order oligomers (the dimer- and trimer-sized) than either deletion mutant did since NOK could be cross-linked by both Sulfo-EGS and formaldehyde, whereas either deletion mutant was only sensitive to Sulfo-EGS. Removing the NOK TM domain (NOK-ICD) not only markedly promoted higher order oligomerization, but also altered the subcellular localization of NOK and dramatically elevated the NOK-mediated constitutive activation of extracellular signal-regulated kinase (ERK). Moreover, NOK-ICD but not NOK or NOKECD was co-localized with the upstream signaling molecule RAS on cell membrane. Thus, TM-mediated intermolecular contacting may be mainly responsible for the constitutive activation of NOK and contribute to the autoinhibitory effect on RAS/MAPK signaling.

The Beneficial Effects of Electroacupuncture at PC6 Acupoints (Neiguan) on Myocardial Ischemia in ASIC3 / mice

Ying-Wang,Yi-guo Chen,Wan-shuang Zhao,Di Li,Ya-han Xu,Meng-di Li,Jin Chen,Zhi-jun Kou,Qi-ge Wang,Nsoa dimitri Joseph 사단법인약침학회 2018 Journal of Acupuncture & Meridian Studies Vol.11 No.3

This study aims to investigate the possible mechanisms of electroacupuncture (EA) at PC6to improve myocardial ischemia (MI) by regulating the cardiac transient outward potassiumcurrent channel (Ito). According to the random number table, the mice were dividedinto six groups of six mice each: control group, MI group, PC6, LU7 (Lieque-point), ST36(Zusanli-point), and nonacupoint group. Mice in the control group were injected with saline(20 mg/kg, 24 hours interval), and the other ASIC3 / mice were injected subcutaneouslytwice with isoproterenol (ISO) (20 mg/kg, 24 hours interval). In thepreexperiment, 5 mg/kg, 10 mg/kg, 20 mg/kg, and 30 mg/kg of ISO were used, andthe results showed that 5 mg/kg and 10 mg/kg of ISO both could induce acute MI, butshorter duration of sustained MI. On the other hand, an injection of 30 mg/kg can makethe mice experience arrhythmia or die immediately, and EA was operated at PC6, LU7,ST36 acupoints, and nonacupoint in the mice of PC6, LU7, ST36, and nonacupoint groups,respectively, after injecting twice. Then Western blotting techniques (Western Blot) wereused to analyze the protein expressions of Kv1.4, Kv4.2, Kv4.3, and KchIP2. The results ofthis experiment showed that the protein expressions of Kv1.4, Kv4.2, Kv4.3, and KChIP2 inMI group were significantly lower than those in the control group (p < 0.01). Comparedwith MI group, the results of PC6, LU7, and ST36 groups obviously increased (p < 0.05). Furthermore, the expressions of PC6 group were higher than LU7 group and ST36 group(p < 0.05). And electrocardiogram’s T-waves showed obvious pathological changes inthe MI group compared to the control group (p < 0.01). After EA, the abnormal T-waves voltage of ECG in PC6, LU7, and ST36 groups was improved (p < 0.05). In addition, therate change of PC6 group was larger than that of both LU7 and ST36 groups (p < 0.05). But the T-waves voltage of the nonacupoint group was not significantly different than thatof the MI group (p > 0.05).

New Safrole Oxide Derivatives: Synthesis and in vitro Antiproliferative Activities on A549 Human Lung Cancer Cells

Wang, Li-Ying,Wang, Xiu-Hua,Tan, Jia-Lian,Xia, Shuai,Sun, Heng-Zhi,Shi, Jin-Wen,Jiang, Ming-Dong,Fang, Liang,Zuo, Hua,Dupati, Gautam,Jang, Kiwan,Shin, Dong-Soo Korean Chemical Society 2012 Bulletin of the Korean Chemical Society Vol.33 No.11

A number of novel small molecules, safrole oxide derivatives 4a-c, 6a-c, 9a-h, were synthesized by the reaction of safrole oxide with anilines 3 and 5, or its alkyl allyl ether derivative 7 with alkyl bromide 8 in moderate yields. The antiproliferative effects of all the target molecules on A549 cell growth were investigated and it was found that the 14 novel compounds could suppress A549 lung cancer cell growth. Among them, compound 6b was the most effective compound in inhibiting the proliferation of A549 cells.

Sputum Metabolomic Profiling Reveals Metabolic Pathways and Signatures Associated With Inflammatory Phenotypes in Patients With Asthma

Liu Ying,Zhang Xin,Zhang Li,Oliver Brian G,Wang Hong Guang,Liu Zhi Peng,Chen Zhi Hong,Wood Lisa,Hsu Alan Chen-Yu,Xie Min,McDonald Vanessa,Wan Hua Jing,Luo Feng Ming,Liu Dan,Li Wei Min,Wang Gang 대한천식알레르기학회 2022 Allergy, Asthma & Immunology Research Vol.14 No.4

Purpose: The molecular links between metabolism and inflammation that drive different inflammatory phenotypes in asthma are poorly understood. We aimed to identify the metabolic signatures and underlying molecular pathways of different inflammatory asthma phenotypes. Methods: In the discovery set (n = 119), untargeted ultra-high-performance liquid chromatography-mass spectrometry (UHPLC-MS) was applied to characterize the induced sputum metabolic profiles of asthmatic patients with different inflammatory phenotypes using orthogonal partial least-squares discriminant analysis (OPLS-DA), and pathway topology enrichment analysis. In the validation set (n = 114), differential metabolites were selected to perform targeted quantification. Correlations between targeted metabolites and clinical indices in asthmatic patients were analyzed. Logistic and negative binomial regression models were established to assess the association between metabolites and severe asthma exacerbations. Results: Seventy-seven differential metabolites were identified in the discovery set. Pathway topology analysis uncovered that histidine metabolism, glycerophospholipid metabolism, nicotinate and nicotinamide metabolism, linoleic acid metabolism as well as phenylalanine, tyrosine and tryptophan biosynthesis were involved in the pathogenesis of different asthma phenotypes. In the validation set, 24 targeted quantification metabolites were significantly expressed between asthma inflammatory phenotypes. Finally, adenosine 5′-monophosphate (adjusted relative risk [adj RR] = 1.000; 95% confidence interval [CI] = 1.000–1.000; P = 0.050), allantoin (adj RR = 1.000; 95% CI = 1.000–1.000; P = 0.043) and nicotinamide (adj RR = 1.001; 95% CI = 1.000–1.002; P = 0.021) were demonstrated to predict severe asthma exacerbation rates. Conclusions: Different inflammatory asthma phenotypes have specific metabolic profiles in induced sputum. The potential metabolic signatures may identify therapeutic targets in different inflammatory asthma phenotypes.

New Safrole Oxide Derivatives: Synthesis and in vitro Antiproliferative Activities on A549 Human Lung Cancer Cells

Li-Ying Wang,Xiu-Hua Wang,Jia-Lian Tan,Shuai Xia,Heng-Zhi Sun,Jin-Wen Shi,Ming-Dong Jiang,Liang Fang,Hua Zuo,Gautam Dupati,장기완,신동수 대한화학회 2012 Bulletin of the Korean Chemical Society Vol.33 No.11

A number of novel small molecules, safrole oxide derivatives 4a-c, 6a-c, 9a-h, were synthesized by the reaction of safrole oxide with anilines 3 and 5, or its alkyl allyl ether derivative 7 with alkyl bromide 8 in moderate yields. The antiproliferative effects of all the target molecules on A549 cell growth were investigated and it was found that the 14 novel compounds could suppress A549 lung cancer cell growth. Among them, compound 6b was the most effective compound in inhibiting the proliferation of A549 cells.

<i>Chd7</i> Is Critical for Early T-Cell Development and Thymus Organogenesis in Zebrafish

Liu, Zhi-Zhi,Wang, Zi-Long,Choi, Tae-Ik,Huang, Wen-Ting,Wang, Han-Tsing,Han, Ying-Ying,Zhu, Lou-Yin,Kim, Hyun-Taek,Choi, Jung-Hwa,Lee, Jin-Soo,Kim, Hyung-Goo,Zhao, Jian,Chen, Yue,Lu, Zhuo,Tian, Xiao-L Elsevier 2018 The American journal of pathology Vol.188 No.4

<P>Coloboma, heart defect, atresia choanae, retarded growth and development, genital hypoplasia, ear anomalies/deafness (CHARGE) syndrome is a congenital disorder affecting multiple organs and mainly caused by mutations in CHD7, a gene encoding a chromatin-remodeling protein. Immunodeficiency and reduced T cells have been noted in CHARGE syndrome. However, the mechanisms underlying T lymphopenia are largely unexplored. Herein, we observed dramatic decrease of T cells in both chd7knockdown and knockout zebrafish embryos. Unexpectedly, hematopoietic stem and progenitor cells and, particularly, lymphoid progenitor cells were increased peripherally in nonthymic areas in chd7-deficient embryos, unlikely to contribute to the T-cell decrease. Further analysis demonstrated that both the organogenesis and homing function of the thymus were seriously impaired. Chd7 might regulate thymus organogenesis through modulating the development of both neural crest cell-derived mesenchyme and pharyngeal endoderm-derived thymic epithelial cells. The expression of faxn1, a central regulator of thymic epithelium, was remarkably down-regulated in the pharyngeal region in chd7-deficient embryos. Moreover, the T-cell reduction in chd7-deficient embryos was partially rescued by overexpressingfoxnl, suggesting that restoring thymic epithelium may be a potential therapeutic strategy for treating immunodeficiency in CHARGE syndrome. Collectively, the results indicated that chd7 was critical for thymic development and T-lymphopenia in CHARGE syndrome may be mainly attributed to the defects of thymic organogenesis. The current finding may benefit the diagnosis and therapy of T lymphopenia and immunodeficiency in CHARGE syndrome.</P>

The WNT/Ca2+ pathway promotes atrial natriuretic peptide secretion by activating protein kinase C/transforming growth factor-β activated kinase 1/activating transcription factor 2 signaling in isolated beating rat atria

Li Zhi-yu,Liu Ying,Han Zhuo-na,Li Xiang,Wang Yue-ying,Cui Xun,Zhang Ying 대한약리학회 2022 The Korean Journal of Physiology & Pharmacology Vol.26 No.6

WNT signaling plays an important role in cardiac development, but abnormal activity is often associated with cardiac hypertrophy, myocardial infarction, remodeling, and heart failure. The effect of WNT signaling on regulation of atrial natriuretic peptide (ANP) secretion is unclear. Therefore, the purpose of this study was to investigate the effect of Wnt agonist 1 (Wnta1) on ANP secretion and mechanical dynamics in beating rat atria. Wnta1 treatment significantly increased atrial ANP secretion and pulse pressure; these effects were blocked by U73122, an antagonist of phospholipase C. U73122 also abolished the effects of Wnta1-mediated upregulation of protein kinase C (PKC) β and γ expression, and the PKC antagonist Go 6983 eliminated Wnta1-induced secretion of ANP. In addition, Wnta1 upregulated levels of phospho-transforming growth factor-β activated kinase 1 (p-TAK1), TAK1 banding 1 (TAB1) and phospho-activating transcription factor 2 (p-ATF2); these effects were blocked by both U73122 and Go 6983. Wnta1-induced ATF2 was abrogated by inhibition of TAK1. Furthermore, Wnta1 upregulated the expression of T cell factor (TCF) 3, TCF4, and lymphoid enhancer factor 1 (LEF1), and these effects were blocked by U73122 and Go 6983. Tak1 inhibition abolished the Wnta1-induced expression of TCF3, TCF4, and LEF1 and Wnta1-mediated ANP secretion and changes in mechanical dynamics. These results suggest that Wnta1 increased the secretion of ANP and mechanical dynamics in beating rat atria by activation of PKC–TAK1–ATF2–TCF3/LEF1 and TCF4/LEF1 signaling mainly via the WNT/Ca2+ pathway. It is also suggested that WNT–ANP signaling is implicated in cardiac physiology and pathophysiology.