Down-regulation of TSPO expression doesn't affect the productions of TNF-α,IL-1β and IL-6 in LPS-stimulated BV-2 microglia

目的研究相对分子质量(Mr)18 000转运蛋白(TSPO)基因表达下调对脂多糖(lPS)诱导bV-2小胶质细胞分泌Tnf-α,Il-1β和Il-6的影响。方法以rnA干扰技术建立TSPO基因表达下调的细胞模型,实时荧光定量PCr(QrT-PCr)和WESTErn blOT法检测转染TSPO SIrnA bV-2细胞TSPO MrnA及蛋白水平表达的效果;用QrT-PCr法检测TSPO基因下调后小胶质细胞bV-2在lPS作用下分泌Tnf-α、Il-1β和Il-6的MrnA水平表达的情况;ElISA检测TSPO基因下调小胶质细胞bV-2在lPS作用下分泌Tnf-α、Il-1β和Il-6的蛋白水平表达的变化。结果成功建立了TSPO基因下调的细胞模型,稳定表达TSPO SIrnA细胞的TSPO MrnA和蛋白水平表达均明显下降,TSPO基因下调后bV-2细胞在lPS作用下分泌Tnf-α、Il-1β和Il-6的量无变化。结论下调TSPO的表达对lPS刺激引起的小胶质细胞Tnf-α、Il-1β和Il-6的分泌无明显影响。Objective To evaluate the effect of translocator protein( TSPO,Mr18 000) on the productions of TNF-α,IL-1βand IL-6 in lipopolysaccharide( LPS)-stimulated BV-2 cells.Methods RNA interference technique was used to decrease TSPO expression in BV-2 cells.Western blotting was performed to assess the level of TSPO protein in BV-2 cells transfected with TSPO siRNA.Then the mRNA and protein levels of TNF-α,IL-1β,and IL-6 were measured in LPS-stimulated BV-2 cells by real-time quantitative PCR( qRT-PCR) and ELISA,respectively.Results The level of TSPO protein obviously decreased in BV-2 cells transfected with TSPO siRNA.However,knockdown of TSPO had no effect on the productions of TNF-α,IL-1βand IL-6 in LPS-stimulated BV-2 cells.Conclusion Down-regulated TSPO is not directly involved in regulating TNF-α,IL-1βand IL-6 productions induced by LPS in microglia.国家自然科学基金(81071182); 福建省医学创新项目(2009-CXB-46); 厦门大学生命科学学院细胞生物和肿瘤工程教育部重点实验室开发基金(2009101); 福建医科大学非直属附属医院科研发展专项基金(2008031

An Information Hiding Algorithm Against the Cropping Attack

提出了一种基于拉丁方阵的抗剪切信息隐藏算法,通过载体图像隐藏容量和秘密信息的大小确定隐藏秘密信息的备份数,根据备份数确定隐藏信息的拉丁方阵模板,对秘密信息进行分组和编号,通过拉丁方阵模板按对应的编号,将秘密信息嵌入到载体图像中,实现信息隐藏.实验结果表明该算法能够实现大容量隐藏并且能够抵抗大面积的剪切攻击,具有较好的应用价值. This paper proposes an anti--cropping steganography scheme based on Latin square. At first, the amount of secret copies is obtained by the cover image＇s hiding capacity and the length of the secret message. According to the amount of copies, a Latin square is confirmed as the template for hiding secret message. The secret message is divided into groups and each group is numbered. Then the secret groups are embedded into the cover image with the corresponding element in the Latin square. Experimental results indicate that the proposed scheme can achieve high capacity, and can be against the cropping attack. It has significant practical value for information security.国家自然基金（61363034,61300109）;广西自然科学基金（2011GXNSFD018026,2012GXNSFBA053166,0832104）;广西科学研究与技术开发计划项目（10123005--8）;重庆市教委科技项目（KJ121310）;涪陵区科技计划项目（FLKJ,2012ABA1056）;广西信息科学实验中心项目（20130204

An Information Hiding Method Based on JPEG Images

本文提出一种JPEG图像的信息隐藏算法,根据给定阈值确定隐藏信息的低频DCT系数,对这些低频系数进行编号分组,得到载体信息。将秘密信息每2位分为一组,每组秘密信息转换为十进制数,用这个数确定隐藏到载体中某组系数的位置。根据嵌入方式,对秘密信息进行预处理得到嵌入数据,通过与3的模数修改隐藏信息的低频DCT系数实现信息隐藏。实验结果表明,本文算法有较好的视觉效果。This paper proposes a steganography scheme based on JPEG images. According to a given threshold, the low frequency coefficients are chosen to hide data. Then these low frequency coefficients are divided into groups to get the carrier. Two bits of secret message are taken as a group from the secret information,and converted into a decimal number. This number will be used to determine the hiding po- sition of the coefficients group. According to the hiding scheme,the secret message is preprocessed to get the hidden data,and the low frequency coefficients of the hiding position is modified by model 3 to hide the secret data. Experimental results indicate that the proposed scheme achieves better image quality of stego-images.国家自然科学基金资助项目(61363034,61300109)； 广西自然科学基金资助项目(2011GXNSFD018026,2012GXNSFBA053166,0832104)； 广西科学研究与技术开发计划项目(10123005-8)； 重庆市教委研究项目(KJ121310)； 涪陵区科技计划项目(FLKJ2012ABA1056)； 广西信息科学实验中心项目(20130204

Deficiency in steroid receptor coactivator 3 enhances cytokine production in IgE-stimulated mast cells and passive systemic anaphylaxis in mice

Program for New Century Excellent Talents in University of the Ministry of Education [NCET-10-0718]; Natural Science Foundation of China [31170819]; Fundamental Research Funds for the Central Universities [2012121038]; 111 Project [B12001]Background: Steroid receptor coactivator 3 (SRC-3) is a multifunctional protein that plays an important role in malignancy of several cancers and in regulation of bacterial LPS-induced inflammation. However, the involvement of SRC-3 in allergic response remains unclear. Herein we used passive systemic anaphylaxis (PSA) and passive cutaneous anaphylaxis (PCA) mouse models to assess the role of SRC-3 in allergic response. Results: SRC-3-deficient mice exhibited more severe allergic response as demonstrated by a significant drop in body temperature and a delayed recovery period compared to wild-type mice in PSA mouse model, whereas no significant difference was observed between two kinds of mice in PCA mouse models. Mast cells play a pivotal role in IgE-mediated allergic response. Antigen-induced aggregation of IgE receptor (Fc epsilon RI)on the surface of mast cell activates a cascade of signaling events leading to the degranulation and cytokine production in mast cells. SRC-3-deficient bone marrow derived mast cells (BMMCs) developed normally but secreted more proinflammatory cytokines such as TNF-alpha and IL-6 than wild-type cells after antigen stimulation, whereas there was no significant difference in degranulation between two kinds of mast cells. Further studies showed that SRC-3 inhibited the activation of nuclear factor NF-kB pathway and MAPKs including extracellular signal-regulated kinase (ERK), c-jun N-terminal kinase (JNK), and p38 in antigen-stimulated mast cells. Conclusions: Our data demonstrate that SRC-3 suppresses cytokine production in antigen-stimulated mast cells as well as PSA in mice at least in part through inhibiting NF-kB and MAPK signaling pathways. Therefore, SRC-3 plays a protective role in PSA and it may become a drug target for anaphylactic diseases

Mycoepoxydiene inhibits antigen-stimulated activation of mast cells and suppresses IgE-mediated anaphylaxis in mice

Program for New Century Excellent Talents in University of the Ministry of Education [NCET-10-0718]; Fundamental Research Funds for the Central Universities [2012121038]; Natural Science Foundation of China [31170819]Mycoepoxydiene (MED) is a polyketide isolated from a marine fungus associated with mangrove forest. It has been shown that MED has many kinds of effects such as anti-cancer and anti-inflammatory activities. However, its effects on anaphylaxis are still unknown. Mast cells play a pivotal role in IgE-mediated allergic response. Aggregation of the high affinity IgE receptor (Fc epsilon RI) on the surface of mast cell activates a cascade of signaling events leading to the degranulation and cytokine production in mast cells. Our study showed that MED could significantly suppress antigen-stimulated degranulation and cytokine production in mast cells and IgE-mediated passive cutaneous anaphylaxis (PCA) in mice. Furthermore, we found that MED suppressed antigen-induced activation of Syk, and subsequently inhibited the phosphorylation of PLC gamma 1, Akt, and MAPKs such as extracellular signal-regulated kinase (ERK), c-jun N-terminal kinase (JNK), and p38 in mast cells. Collectively, our study demonstrates that MED can inhibit the activation of mast cells and protect mice from mast cell-mediated allergic response through inhibiting the activation of Syk. These results suggest that MED is a potential compound for developing a promising anti-anaphylaxis drug. (C) 2013 Elsevier B.V. All rights reserved

Mycoepoxydiene induces apoptosis and inhibits TPA-induced invasion in human cholangiocarcinoma cells via blocking NF-kappa B pathway

Natural Science Foundation of Fujian Province of China [2010D015]; China Postdoctoral Science Foundation [20100480713]; Youth Foundation of Health Department of Fujian Province [2010-2-84]; Natural Science Foundation of China [81071182]; Medical Innovation Foundation of Fujian of China [2009-00-46]Human cholangiocarcinoma (CCA) is a chemoresistant bile duct carcinoma with a poor prognosis. Conventional chemotherapy and radiotherapy have not been reported to be effective in improving long-term survival. Mycoepoxydiene (MED), a polyketide isolated from the marine fungal strain Diaporthe sp. HLY-1 associated with mangroves, has been shown to be an agent capable of inducing apoptosis in MCF-7 and Hela cell lines. However, little is known about the effect of MED in CCA. Herein, we investigated the effect of MED on CCA cells proliferation and invasion. The results demonstrated that MED induced apoptosis in CCA cells such as SK-ChA-1 and Mz-ChA-1 through inhibiting the expression of antiapoptotic proteins such as BcI-XL and Bcl-2, two targets of NF-KB. In addition, MED significantly inhibited 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced CCA cells invasion in a dose-dependent manner by reducing the expression of matrix metalloelastase 9 (MMP-9). Moreover, MED inhibited TPA-induced NF-KB activation via blocking phosphorylation and degradation of hcBct and phosphorylation of IKB kinase (IKK). MED had no effect on the activation of extracellular signal-regulated kinase (ERK), c-jun N-terminal kinase (INK) and p38, which are also involved in regulating the MMP-9 expression. Collectively, MED significantly suppressed proliferation and invasion of CCA cells such as SK-ChA-1 and Mz-ChA-1, suggesting that MED is a potential lead compound for the development of novel drugs for therapy of CCA. (C) 2014 Elsevier Masson SAS. All rights reserved

Mycoepoxydiene inhibits activation of BV2 microglia stimulated by lipopolysaccharide through suppressing NF-kappa B, ERK 1/2 and toll-like receptor pathways

National Natural Science Foundation of China [81071182]; Medical Innovation Foundation of Fujian, China [2009-CXB-46]; Natural Science Foundation of Fujian Province of China [2010D015]; Youth Foundation of Health Department of Fujian Province [2010-2-84]Mycoepoxydiene (MED) is a polyketide isolated from the marine fungal Diaporthe sp. HLY-1 associated with mangroves. Although MED has been shown to have various biological effects such as antimicrobial, anticancer, and anti-inflammatory activities, its activities and cellular mechanisms during microglial activation have yet to be elucidated. In the present study, we assessed the anti-inflammatory effect of MED on the production of inflammatory mediators in lipopolysaccharide (LPS)-stimulated murine BV2 microglia. MED significantly inhibited LPS-induced production of pro-inflammatory mediators such as tumor necrosis factor a (INF-alpha), interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6), interferon-gamma (INF-gamma), and nitric oxide (NO), whereas it increased anti-inflammatory interleukin-10 (IL-10) and transforming growth factor-beta (TGF-beta 1) production in BV2 microglia in a concentration-dependent manner without causing cytotoxicity. Moreover, MED suppressed NF-kappa B activation by blocking IkappaB-alpha (I kappa B-alpha) degradation and inhibited the phosphorylation of ERK 1/2 and toll-like receptor 4 (TLR4) expression, but had no effect on the phosphorylation of JNK, and p38. Our results demonstrate that the inhibitory and promotion effect of MED on LPS-stimulated inflammatory mediators and anti-inflammatory factor production in BV2 microglia is associated with the suppression of the NF-kappa B, ERK 1/2 and TLR signaling pathways. Therefore, MED may have therapeutic potential for neurodegenerative diseases by inhibiting inflammatory mediators and enhancing anti-inflammatory factor production in activated microglia. (C) 2014 Elsevier B.V. All rights reserved

JUNO Sensitivity on Proton Decay p→νˉK+p\to \bar\nu K^+ Searches

The Jiangmen Underground Neutrino Observatory (JUNO) is a large liquid scintillator detector designed to explore many topics in fundamental physics. In this paper, the potential on searching for proton decay in $p\to \bar\nu K^+$ mode with JUNO is investigated.The kaon and its decay particles feature a clear three-fold coincidence signature that results in a high efficiency for identification. Moreover, the excellent energy resolution of JUNO permits to suppress the sizable background caused by other delayed signals. Based on these advantages, the detection efficiency for the proton decay via $p\to \bar\nu K^+$ is 36.9% with a background level of 0.2 events after 10 years of data taking. The estimated sensitivity based on 200 kton-years exposure is $9.6 \times 10^{33}$ years, competitive with the current best limits on the proton lifetime in this channel