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The Analysis of Nonstandard English Grammar Used in the Chinese NNS-NNS Interaction
Haibo Zhang,Chan Kyoo Min 한국영어교과교육학회 2016 영어교과교육 Vol.15 No.3
With the rapid development of Asian English language teaching (ELT), studies on how nonnative speakers use English varieties when communicating with other nonnative speakers have drawn attention. China English used by Chinese speakers of English is attracting great interest from English educators. Adopting the methods such as error analysis and conversation analysis, this study aims to analyze the nonstandard grammar items of China English which has appeared in peer-peer interactions among Chinese college interlocutors. This study also aims to check the intelligibility of the nonstandard grammar forms and to find out which types of triggers may cause communication difficulties in China English. The results of the study show that nonstandard grammar items are widely used in Chinese college students’ peer-peer interactions. This study also shows that the nonstandard grammar items seldom lead to communication difficulties. Based on the analysis, pedagogical implications and suggestions are made for the improvement of teaching nonstandard forms of China English.
Haibo Zhang,Junkoo Yi,윤두학,류재웅,In Kyu Lee,김명옥 대한암예방학회 2020 Journal of cancer prevention Vol.25 No.4
Hepatocellular carcinoma (HCC) is the most common primary liver cancer and is one of the leading causes of cancer-related deaths worldwide. Imatinib and GNF-5 are breakpoint cluster region-Abelson murine leukemia tyrosine kinase inhibitors which have been approved for the treatment of chronic myeloid leukemia and various solid tumors. However, the effect and underlying mechanisms of imatinib and GNF-5 in HCC remain poorly defined. In this study, we investigated the anticancer activity and underlying mechanisms of imatinib and GNF-5 in HepG2 human hepatocarcinoma cells. Cell proliferation and anchorage-independent colony formation assays were done to evaluate the effects of imatinib and GNF-5 on the growth of HepG2 cells. The cell cycle was assessed by flow cytometry and verified by immunoblot analysis. Gene overexpression and knockdown assays were conducted to evaluate the function of S-phase kinase-associated protein 2 (Skp2). Imatinib and GNF-5 significantly inhibited the growth of HepG2 cells. Imatinib and GNF-5 induced G0/G1 phase cell cycle arrest by downregulating Skp2 and upregulating p27 and p21. Overexpression of Skp2 reduced the effect of imatinib and GNF-5 on HepG2 cells. Knockdown of Skp2 suppressed the proliferation and induced G0/ G1 phase arrest. Furthermore, knockdown of Skp2 enhanced the effect of imatinib and GNF-5 on growth of HepG2 cells. In conclusion, imatinib and GNF-5 effectively suppress HepG2 cell growth by inhibiting Skp2 expression. Skp2 promotes the cell proliferation and reverse G0/G1 phase cell cycle arrest and it represents a potential therapeutic target for HCC treatment. Key Words Hepatocellular carcinoma, Cell cycle, S-phase kinase-associated protein 2, Imatinib, GNF-5
Survival Association and Cell Cycle Effects of B7H3 in Neuroblastoma
Zhang, Haibo,Zhang, Jinsen,Li, Chunjie,Xu, Hao,Dong, Rui,Chen, Clark C.,Hua, Wei The Korean Neurosurgical Society 2020 Journal of Korean neurosurgical society Vol.63 No.6
Objective : The function of B7H3, a member of the B7 family of proteins, in neuroblastoma (NB) remains poorly characterized. Here we examine the expression pattern of B7H3 in clinical NB specimens and characterize the phenotype of B7H3 knock-down in NB cell line. Methods : Immunohistochemical (IHC) staining was carried out to assess the expression of B7H3 in clinical NB specimens. Survival association was analyzed using five Gene Expression Omnibus (GEO) datasets (GSE85047, GSE45480, GSE62564, GSE16476, GSE49710). Clonogenic survival and flow cytometry were performed after B7H3 knockdown to assess the cellular proliferation and cell survival in vitro. Impact of B7H3 silencing on NB growth was examined in vivo using the SH-SY5Y xenograft model. Results : On IHC staining, B7H3 was widely expressed in clinical NB specimens. Analysis of the transcriptional profiles of five GEO datasets clinically annotated NB specimens revealed that decreased B7H3 expression was associated with improved overall survival. B7H3 knockdown suppressed the proliferation of the SH-SY5Y NB model in vitro and in vivo. Cell cycle analysis revealed that B7H3 silencing induced G1/S arrest. This arrest was associated with the suppression of E2F1 expression and induction of Rb expression. Conclusion : Our results demonstrate that B7H3 expression correlate with clinical survival in NB patients. Preliminary studies suggest that B7H3 may mediate the G1/S transition.
Zhang, Kan,Li, Ping,Guo, Shiying,Jeong, Jong Yeob,Jin, Bingjun,Li, Xiaoming,Zhang, Shengli,Zeng, Haibo,Park, Jong Hyeok The Royal Society of Chemistry 2018 Journal of Materials Chemistry A Vol.6 No.45
<P>In this paper, we precisely controlled the <I>d</I>-spacing of vertically aligned MoS2 arrays ranging from 6.2 to 10 Å <I>via</I> heating-controlled deintercalation of NH4<SUP>+</SUP> ions. The finely controllable interlayer nanoarchitecture resulted in an optimal <I>d</I>-spacing of 7.3 Å, which on nitrogenous reduced graphene oxide (N-RGO) delivered a reversible capacity of 295 mA h g<SUP>−1</SUP> after 2000 cycles at 1 A g<SUP>−1</SUP> for Na<SUP>+</SUP> intercalation.</P>
Haibo Zhang,Junkoo Yi,휘앙하이,Si Jun Park,권욱봉,김은경,So-Young Jang,Si-Yong Kim,최성균,Du-Hak Yoon,Sung-Hyun Kim,Kangdong Liu,Zigang Dong,Zae Young Ryoo,Myoung Ok Kim 고려인삼학회 2022 Journal of Ginseng Research Vol.46 No.3
Colorectal cancer (CRC) has a high morbidity and mortality worldwide. 20 (S)-ginsenosideRh2 (G-Rh2) is a natural compound extracted from ginseng, which exhibits anticancer effects in manycancer types. In this study, we demonstrated the effect and underlying molecular mechanism of G-Rh2 inCRC cells in vitro and in vivo. Methods: Cell proliferation, migration, invasion, apoptosis, cell cycle, and western blot assays wereperformed to evaluate the effect of G-Rh2 on CRC cells. In vitro pull-down assay was used to verify theinteraction between G-Rh2 and Axl. Transfection and infection experiments were used to explore thefunction of Axl in CRC cells. CRC xenograft models were used to further investigate the effect of Axlknockdown and G-Rh2 on tumor growth in vivo. Results: G-Rh2 significantly inhibited proliferation, migration, and invasion, and induced apoptosis andG0/G1 phase cell cycle arrest in CRC cell lines. G-Rh2 directly binds to Axl and inhibits the Axl signalingpathway in CRC cells. Knockdown of Axl suppressed the growth, migration and invasion ability of CRCcells in vitro and xenograft tumor growth in vivo, whereas overexpression of Axl promoted the growth,migration, and invasion ability of CRC cells. Moreover, G-Rh2 significantly suppressed CRC xenografttumor growth by inhibiting Axl signaling with no obvious toxicity to nude mice. Conclusion: Our results indicate that G-Rh2 exerts anticancer activity in vitro and in vivo by suppressingthe Axl signaling pathway. G-Rh2 is a promising candidate for CRC prevention and treatment.
Rhein suppresses colorectal cancer cell growth by inhibiting the mTOR pathway in vitro and in vivo
Haibo Zhang,Zae Young Ryoo,Myoung Ok Kim 한국실험동물학회 2021 한국실험동물학회 학술발표대회 논문집 Vol.2021 No.7
Background: Rhein has demonstrative exerts therapeutic effects in different cancer models. However, the effects and the underlying mechanisms of rhein in colorectal cancer (CRC) remain poorly elucidated. We investigated the potential anticancer activity and underlying mechanisms of rhein in CRC in vitro and in vivo. Methods: Cell proliferation and anchorage-independent colony formation were performed to examine the effects of rhein on cell growth. Wound healing assay and transwell migration and invasion assay were conducted to detect cell migration and invasion. Cell cycle and apoptosis were investigated by flow cytometry and verified by immunoblotting. Tissue microarray was used to detect mTOR expression in patients with CRC. Gene overexpression and knockdown were implemented to analyze the function of mTOR in CRC. The effect of rhein on tumor growth was assessed in a xenograft mouse model. Results: Rhein significantly inhibited CRC cell growth by inducing S phase cell cycle arrest and apoptosis. Rhein inhibited CRC cell migration and invasion ability through EMT process. mTOR was highly expression in CRC cancer tissues and cells. Overexpression of mTOR promoted cell growth, migration, and invasion ability, whereas mTOR knockdown diminished these phenomena of CRC cells in vitro. Moreover, rhein directly targeted mTOR and suppressed the mTOR signaling pathway in CRC cells. Intraperitoneal administration of rhein inhibited CRC cell HCT116 xenograft tumor growth through the mTOR pathway. Conclusions: Rhein exerted anticancer activity in vitro and in vivo through inhibiting mTOR signaling pathway in CRC. Rhein is a potent anticancer agent that could be useful for the prevention or treatment of CRC.