Due to their simple hardware,sensor nodes in IoT are vulnerable to attack,leading to data routing blockages or malicious tampering,which significantly disrupts secure data collection.An Intelligent Active Probing and ...Due to their simple hardware,sensor nodes in IoT are vulnerable to attack,leading to data routing blockages or malicious tampering,which significantly disrupts secure data collection.An Intelligent Active Probing and Trace-back Scheme for IoT Anomaly Detection(APTAD)is proposed to collect integrated IoT data by recruiting Mobile Edge Users(MEUs).(a)An intelligent unsupervised learning approach is used to identify anomalous data from the collected data by MEUs and help to identify anomalous nodes.(b)Recruit MEUs to trace back and propose a series of trust calculation methods to determine the trust of nodes.(c)The last,the number of active detection packets and detection paths are designed,so as to accurately identify the trust of nodes in IoT at the minimum cost of the network.A large number of experimental results show that the recruiting cost and average anomaly detection time are reduced by 6.5 times and 34.33%respectively,while the accuracy of trust identification is improved by 20%.展开更多
The first cell fate choice in the mammalian embryo, the segregation of the inner cell mass （ICM） and trophectoderm （TE）, is regulated by the mutually antagonistic effects of the transcription factors, Oct4 and Cdx...The first cell fate choice in the mammalian embryo, the segregation of the inner cell mass （ICM） and trophectoderm （TE）, is regulated by the mutually antagonistic effects of the transcription factors, Oct4 and Cdx2, while the pluripotency factor, Nanog, is essential to specify the epiblast. We have analyzed the promoters of Nanog and Cdx2, and have found that these two transcription factors are likewise regulated reciprocally. Using an embryonic stem cell line with conditional TE differentiation, we show that Nanog overexpression suppresses the upregulation of TE markers, while Nanog knockdown upregulates the expression of TE markers. We further show that Nanog and Cdx2 bind to and repress each other＇s promoters. However, whereas Nanog knockout results in detectable Cdx2 expression in the ICM, we observe no overt disruption of blastocyst development, indicating that Nanog plays a subservient role to Oct4 in segregation of the ICM and TE.展开更多
Dear Editor Histone deacetylase 6 （Hdac6） is a mostly cytoplasmic class II HDAC. Many proteins have been identified as substrates of Hdac6. Among them, the most well characterized sub- strate of Hdac6 is a-tubulin. ...Dear Editor Histone deacetylase 6 （Hdac6） is a mostly cytoplasmic class II HDAC. Many proteins have been identified as substrates of Hdac6. Among them, the most well characterized sub- strate of Hdac6 is a-tubulin. Through deacetylating acety- lated lysine 40 in a-tubulin, Hdac6 modulates the acetylation of microtubules （Hubbert et al., 2002）.展开更多
Dear Editor, Histone deacetylase 6 （Hdac6） was discovered as a deacetylase of e-tubulin and functions in cell migration, immunity and resistance to virus infection in vitro （Hubbert et al., 2002; Valenzuela-Fernand...Dear Editor, Histone deacetylase 6 （Hdac6） was discovered as a deacetylase of e-tubulin and functions in cell migration, immunity and resistance to virus infection in vitro （Hubbert et al., 2002; Valenzuela-Fernandez et al., 2008）. Overexpression of Hdac6 enhances resistance to virus infection in embryonic stem （ES） cells and in mice （Wang et al., 2015）. Hdac6 also can function to deacetyiate protein and is involved in protein ubiquitination and degradation （Seigneurin-Berny et al., 2001; Zhang et al., 2014）, and self- clearance of misfolded proteins, promoting autophagy and preventing neurodegeneration （Lee et al., 2010; Pandey et al., 2007）. HDAC6 also is implicated in DNA damage response and depletion or inhibition of HDAC6 induces DNA damage and apoptosis （Namdar et al., 2010; Zhang et al., 2014）, suggesting that HDAC6 could be important for DNA repair and integrity maintenance.展开更多
基金supported by the National Natural Science Foundation of China(62072475)the Fundamental Research Funds for the Central Universities of Central South University(CX20230356)。
文摘Due to their simple hardware,sensor nodes in IoT are vulnerable to attack,leading to data routing blockages or malicious tampering,which significantly disrupts secure data collection.An Intelligent Active Probing and Trace-back Scheme for IoT Anomaly Detection(APTAD)is proposed to collect integrated IoT data by recruiting Mobile Edge Users(MEUs).(a)An intelligent unsupervised learning approach is used to identify anomalous data from the collected data by MEUs and help to identify anomalous nodes.(b)Recruit MEUs to trace back and propose a series of trust calculation methods to determine the trust of nodes.(c)The last,the number of active detection packets and detection paths are designed,so as to accurately identify the trust of nodes in IoT at the minimum cost of the network.A large number of experimental results show that the recruiting cost and average anomaly detection time are reduced by 6.5 times and 34.33%respectively,while the accuracy of trust identification is improved by 20%.
文摘The first cell fate choice in the mammalian embryo, the segregation of the inner cell mass （ICM） and trophectoderm （TE）, is regulated by the mutually antagonistic effects of the transcription factors, Oct4 and Cdx2, while the pluripotency factor, Nanog, is essential to specify the epiblast. We have analyzed the promoters of Nanog and Cdx2, and have found that these two transcription factors are likewise regulated reciprocally. Using an embryonic stem cell line with conditional TE differentiation, we show that Nanog overexpression suppresses the upregulation of TE markers, while Nanog knockdown upregulates the expression of TE markers. We further show that Nanog and Cdx2 bind to and repress each other＇s promoters. However, whereas Nanog knockout results in detectable Cdx2 expression in the ICM, we observe no overt disruption of blastocyst development, indicating that Nanog plays a subservient role to Oct4 in segregation of the ICM and TE.
基金supported by the National Key R&D Program of China (2018YFC1313003)the Fundamental Research Funds for the Central Universities+1 种基金the National Natural Science Foundation of China (21774065 and 31622038)the Natural Science Foundation of Tianjin (18JCQNJC14100 and 18JCJQJC48400)
基金We thank Drs. Xiaohong Zhang, Zhonghua Liu, and Wentao Qiao for help and discussion. This work was supported by the Ministry of Agriculture of China Transgenic Special Program （2009ZX08006-010B, 2009ZX08006-001B）, the National Basic Research Program （973 Program） （Nos. 2011CBA01002 and 2009CB941000）, the National Science and Technology Major Project of China （2012ZX10001-006）, and the Natural Science Foundation of Tianjin, China （No. 14JCYBJC23600）. Dekun Wang, Qingwen Meng, Lihong Huo, Meng Yang, Lingling Wang, Xinyu Chen, Jianchao Wang, Zhiguo Li, Xiaoying Ye, Na Liu, Qiuyan Li, Zhen Dai, Hongsheng Ouyang, Ning Li, Jun Zhou, Lingyi Chen, and Lin Liu declare no conflict of interest. All institutional and national guidelines for the care and use of laboratory animals were followed.
文摘Dear Editor Histone deacetylase 6 （Hdac6） is a mostly cytoplasmic class II HDAC. Many proteins have been identified as substrates of Hdac6. Among them, the most well characterized sub- strate of Hdac6 is a-tubulin. Through deacetylating acety- lated lysine 40 in a-tubulin, Hdac6 modulates the acetylation of microtubules （Hubbert et al., 2002）.
文摘Dear Editor, Histone deacetylase 6 （Hdac6） was discovered as a deacetylase of e-tubulin and functions in cell migration, immunity and resistance to virus infection in vitro （Hubbert et al., 2002; Valenzuela-Fernandez et al., 2008）. Overexpression of Hdac6 enhances resistance to virus infection in embryonic stem （ES） cells and in mice （Wang et al., 2015）. Hdac6 also can function to deacetyiate protein and is involved in protein ubiquitination and degradation （Seigneurin-Berny et al., 2001; Zhang et al., 2014）, and self- clearance of misfolded proteins, promoting autophagy and preventing neurodegeneration （Lee et al., 2010; Pandey et al., 2007）. HDAC6 also is implicated in DNA damage response and depletion or inhibition of HDAC6 induces DNA damage and apoptosis （Namdar et al., 2010; Zhang et al., 2014）, suggesting that HDAC6 could be important for DNA repair and integrity maintenance.
