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Yang, Zhi Hong,Gu, Li Juan,Zhang, Dong Liang,Li, Zheng,Li, Jing Jie,Lee, Mi-Ra,Wang, Chun Yan,Wang, Zhen,Cho, Jeong-Hee,Sung, Chang-Keun Asian Australasian Association of Animal Productio 2012 Animal Bioscience Vol.25 No.5
In order to investigate and evaluate the effects of red deer antlers on hair growth in the full-thickness wound healing model, Sprague-Dawley rats were given incision wounds through the full thickness of their dorsal skin and deer antler was applied for 40 days. At specified intervals thereafter (4, 8, 16, 32 and 40 days), the animals were sacrificed and the wound site skins were excised, processed, and sectioned. At post-injury days 16, 32 and 40, longer and more active new hair appeared around the healing wound of antler-treated skin. Histological studies showed that the antler extract markedly increases the depth, size, and number of hair follicles. Expression of IGF-I (insulin-like growth factor) mRNA was detected by RT-PCR and real time RT-PCR. The result showed that the expression of IGF-I (days 16, 32, and 40) was obviously up-regulated in antler-treated skins compared to control skins. Similar results were seen in the ELISA analysis to quantify the IGF-I expression. These results support the notion that wound healing can cause hair growth by enhancing the expression of IGF-I. Deer antler extract appears to have the potential to promote hair growth and could be used in hair growth products.
Sun, Qi-Chang,Liu, Mi-Bo,Shen, Hong-Jie,Jiang, Zhi,Xu, Lan,Gao, Li-Ping,Ni, Jian-Long,Wu, Shi-Liang Asian Pacific Journal of Cancer Prevention 2013 Asian Pacific journal of cancer prevention Vol.14 No.4
Objective: To study changes of tumor associated carbohydrate antigen (TACAs) expression and mRNA levels for tumor associated glycosyltransferases, and assess subcellular localizations of N-acetyl galactosyltransferases (GalNAc-Ts) in the K562 leukemia cell line after imatinib treatment. Methods: RT-PCR was performed to analyze the expression of glycosyltransferases which synthesize O-glycan in tumor-associated carbohydrate antigens (TCTAs). The expression of Tn antigen, T antigen and sialyl T antigen on K562 cell membranes was measured by flow cytometry after treatment with different concentrations of imatinib. Co-localization of GalNAc-Ts and ER (endoplasmic reticulum) was determined by confocal laser scanning microcopy. Results: Transcript expression levels of several glycosyltransferases related to TCTAs were decreased after imatinib ($0-0.3{\mu}M$) treatment. Expression of Tn antigen and T antigen was increased while that of sialyl T antigen was decreased. Co-localization of GalNAc-Ts and ER was reduced by $0.2{\mu}M$ of imatinib. Conclusion: Imatinib inhibited the expression of O-glycan related TACAs and several related glycosyltransferases, while decreasing the co-localization of GalNAc-Ts and ER and normalizing O-glycosylation in the K562 human leukemia cell.
Song, Li-Jie,Zhang, Wei-Jie,Chang, Zhi-Wei,Pan, Yan-Feng,Zong, Hong,Fan, Qing-Xia,Wang, Liu-Xing Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.9
Invasion and metastasis is the major cause of tumor recurrence, difficulty for cure and low survival rate. Excavating key transcription factors, which can regulate tumor invasion and metastasis, are crucial to the development of therapeutic strategies for cancers. PU.1 is a master hematopoietic transcription factor and a vital regulator in life. Here, we report that, compared to adjacent non-cancerous tissues, expression of PU.1 mRNA in metastatic hepatocellular carcinoma (HCC), but not primary HCC, was significantly down-regulated. In addition, levels of PU.1 mRNA in metastatic hepatoma cell lines MHCC97L and MHCC97H were much lower than in non-metastatic Hep3B cells. Transwell invasion assays after PU.1 siRNA transfection showed that the invasion of hepatoma cell lines was increased markedly by PU.1 knockdown. Oppositely, overexpression of PU.1 suppressed the invasion of these cells. However, knockdown and overexpression of PU.1 did not influence proliferation. Finally, we tried to explore the potential mechanism of PU.1 suppressing hepatoma cell invasion. ChIP-qPCR analysis showed that PU.1 exhibited a high binding capacity with miR-615-5p promoter sequence. Overexpression of PU.1 caused a dramatic increase of pri-, pre- and mature miR-615-5p, as well as a marked decrease of miR-615-5p target gene IGF2. These data indicate that PU.1 inhibits invasion of human HCC through promoting miR-615-5p and suppressing IGF2. These findings improve our understanding of PU.1 regulatory roles and provided a potential target for metastatic HCC diagnosis and therapy.
Network Intrusion Detection Based on Directed Acyclic Graph and Belief Rule Base
Bang-Cheng Zhang,Guan-Yu Hu,Zhi-Jie Zhou,You-Min Zhang,Pei-Li Qiao,Lei-Lei Chang 한국전자통신연구원 2017 ETRI Journal Vol.39 No.4
Intrusion detection is very important for network situation awareness. While a few methods have been proposed to detect network intrusion, they cannot directly and effectively utilize semi-quantitative information consisting of expert knowledge and quantitative data. Hence, this paper proposes a new detection model based on a directed acyclic graph (DAG) and a belief rule base (BRB). In the proposed model, called DAG-BRB, the DAG is employed to construct a multi-layered BRB model that can avoid explosion of combinations of rule number because of a large number of types of intrusion. To obtain the optimal parameters of the DAG-BRB model, an improved constraint covariance matrix adaption evolution strategy (CMA-ES) is developed that can effectively solve the constraint problem in the BRB. A case study was used to test the efficiency of the proposed DAG-BRB. The results showed that compared with other detection models, the DAG-BRB model has a higher detection rate and can be used in real networks.
Actinorugispora endophytica gen. nov., sp. nov., an actinomycete isolated from Daucus carota.
Liu, Min-Jiao,Zhu, Wen-Yong,Li, Jie,Zhao, Guo-Zhen,Xiong, Zhi,Park, Dong-Jin,Hozzein, Wael N,Kim, Chang-Jin,Li, Wen-Jun Society for General Microbiology 2015 International journal of systematic and evolutiona Vol.65 No.8
<P>An actinomycete strain, designated YIM 690008T, was isolated from Daucus carota collected from South Korea and its taxonomic position was investigated by using a polyphasic approach. The strain grew well on most media tested and no diffusible pigment was produced. The aerial mycelium formed wrinkled single spores and short spore chains, some of which were branched. The whole-cell hydrolysates contained meso-diaminopimelic acid, glucose, mannose, ribose, galactose and rhamnose. The predominant menaquinones were MK-10(H4), MK-10(H6), MK-10(H8) and MK-10(H2). The polar lipids were diphosphatidylglycerol, phosphatidylcholine, phosphatidylinositol, phosphatidylinositol mannosides, some unknown phospholipids, glycolipids and polar lipids. The major fatty acids were i-C16?:?0, ai-C17?:?0 and C18?:?1ω9c. The DNA G+C content of the genomic DNA was 63.1?mol%. Phylogenetic analysis indicated that the isolate belongs to the family Nocardiopsaceae. However, based on phenotypic, chemotaxonomic and genotypic data, it was concluded that strain YIM 690008T represents a novel genus and novel species of the family Nocardiopsaceae, for which the name Actinorugispora endophytica gen. nov., sp. nov. (type strain YIM 690008T?=?DSM 46770T?=?JCM 30099T?=?KCTC 29480T) is proposed.</P>
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 (NOKECD) 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 NOKECD 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 Effects of Ginsenoside Rb1 on JNK in Oxidative Injury in Cardiomyocytes
Chun-Su Yuan,Jing Li,Zuo-Hui Shao,Jing-Tian Xie,Chong-Zhi Wang,Srinivasan Ramachandran,Jun-Jie Yin,Han Aung,Chang-Qing Li,Gina Qin,Terry Vanden Hoek 대한약학회 2012 Archives of Pharmacal Research Vol.35 No.7
Reactive oxygen species (ROS) can induce oxidative injury via iron interactions (i.e. Fenton chemistry and hydroxyl radical formation). Our prior work suggested that American ginseng berry extract and ginsenoside Re were highly cardioprotective against oxidant stress. To extend this study, we evaluated the protective effect of protopanaxadiol-type ginsenoside Rb1 (gRb1)on H2O2-induced oxidative injury in cardiomyocytes and explored the ROS-mediated intracellular signaling mechanism. Cultured embryonic chick cardiomyocytes (4-5 day) were used. Cell death was assessed by propidium iodide and lactate dehydrogenase release. Pretreatment with gRb1 (0.01, 0.1, or 1 μM) for 2 h and concurrent treatment with H2O2 (0.5 mM) for 2 h resulted in a dose-dependent reduction of cell death, 36.6 ± 2.9% (n = 12, p < 0.05), 30.5 ± 5.1% (n = 12, p < 0.05) and 28.6 ± 3.1% (n = 12, p < 0.01) respectively, compared to H2O2-exposed cells (48.2 ± 3.3%, n = 12). This cardioprotective effect of gRb1 was associated with attenuated intracellular ROS generation as measured by 6-carboxy-2’, 7’-dichlorodihydrofluorescein diacetate, preserved the mitochondrial membrane potential as determined using JC-1. In the ESR study, gRb1 exhibited the scavenging DPPH and hydroxyl radical activities. Furthermore, our data showed the increased JNK phosphorylation (p-JNK) in H2O2-exposed cells was suppressed by the pretreatment with gRb 1 (1 μM) (p < 0.01). Co-treatment of gRb1 with a specific inhibitor of JNK SP600125 (10 μM) further reduced the p-JNK and enhanced the cell survival after H2O2exposure. Collectively, our results suggest that gRb1 conferred cardioprotection that was mediated via attenuating ROS and suppressing ROS-induced JNK activation.
Lin Fang,Fei-Hu Yan,Chao Liu,Jing Chen,Dan Wang,Chun-Hui Zhang,Chang-Jie Lou,Jie Lian,Yang Yao,Bo-Jun Wang,Rui-Yang Li,Shu-Ling Han,Yi-Bing Bai,Jia-Ni Yang,Zhi-Wei Li,Yan-Qiao Zhang 대한암학회 2021 Cancer Research and Treatment Vol.53 No.1
Purpose Systemic inflammatory response is a critical factor that promotes the initiation and metastasis of malignancies including pancreatic cancer (PC). This study was designed to determine and compare the prognostic value of neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), monocyte-to-lymphocyte ratio (MLR), and fibrinogen-to-albumin ratio (FAR) in resectable PC and locally advanced or metastatic PC. Materials and Methods Three hundred fifty-three patients with resectable PC and 807 patients with locally advan-ced or metastatic PC were recruited in this study. These patients were classified into a training set (n=758) and a validation set (n=402). Kaplan-Meier survival plots and Cox proportional hazards regression models were used to analyze prognosis. Results Overall survival (OS) was significantly better for patients with resectable PC with low preoperative PLR (p=0.048) and MLR (p=0.027). Low FAR, MLR, NLR (p < 0.001), and PLR (p=0.003) were significantly associated with decreased risk of death for locally advanced or metastatic PC patients. FAR (hazard ratio [HR], 1.522; 95% confidential interval [CI], 1.261 to 1.837; p < 0.001) and MLR (HR, 1.248; 95% CI, 1.017 to 1.532; p=0.034) were independent prognostic factors for locally advanced or metastatic PC. Conclusion The prognostic roles of FAR, MLR, NLR, and PLR in resectable PC and locally advanced or metastatic PC were different. FAR showed the most prognostic power in locally advanced or metastatic PC. Low FAR was positively correlated with OS in locally advanced or metastatic PC, which could be used to predict the prognosis.
Fan, Fang-Tian,Shen, Cun-Si,Tao, Li,Tian, Chao,Liu, Zhao-Guo,Zhu, Zhi-Jie,Liu, Yu-Ping,Pei, Chang-Song,Wu, Hong-Yan,Zhang, Lei,Wang, Ai-Yun,Zheng, Shi-Zhong,Huang, Shi-Le,Lu, Yin Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.5
Pyruvate kinase isozyme type M2 (PKM2) was first found in hepatocellular carcinoma (HCC), and its expression has been thought to correlate with prognosis. A large number of studies have demonstrated that epithelial-mesenchymal transition (EMT) is a crucial event in hepatocellular carcinoma (HCC) and associated metastasis, resulting in enhanced malignancy of HCC. However, the roles of PKM2 in HCC EMT and metastasis remain largely unknown. The present study aimed to determine the effects of PKM2 in EGF-induced HCC EMT and elucidate the molecular mechanisms in vitro. Our results showed that EGF promoted EMT in HCC cell lines as evidenced by altered morphology, expression of EMT-associated markers, and enhanced invasion capacity. Furthermore, the present study also revealed that nuclear translocation of PKM2, which is regulated by the ERK pathway, regulated ${\beta}$-catenin-TCF/LEF-1 transcriptional activity and associated EMT in HCC cell lines. These discoveries provide evidence of novel roles of PKM2 in the progression of HCC and potential therapeutic target for advanced cases.