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This paper is concerned with the reachable set estimation problem for neutral Markovian jump systems with bounded peak disturbances, which was rarely proposed for neutral Markovian jump systems. The main consideration is to find a proper method to obtain the no-ellipsoidal bound of the reachable set for neutral Markovian jump system as small as possible. By applying Lyapunov functional method, some derived conditions are obtained in the form of matrix inequalities. Finally, numerical examples are presented to demonstrate the effectiveness of the theoretical results.

In this paper, we are concerned with the problem of reachable set estimation for uncertain Markovian jump systems with time-varying delays and disturbances. The main consideration is to find a proper method to obtain the no-ellipsoidal bound of the reachable set of Markovian jump system as small as possible. Based on an augmented Lyapunov–Krasovskii functional, by dividing the time-varying delay into two nonuniform subintervals, more general delay-dependent stability criteria for the existence of a desired ellipsoid are derived. An optimized integral inequality which is based on distinguished Wirtinger integral inequality and reciprocally convex combination inequality is used to deal with the integral terms. Finally, numerical examples are presented to demonstrate the effectiveness of the theoretical results.

Due to the need for numerical calculation and mathematical modelling, this paper focuses on the stability of optimal trajectories for optimal control problems. The basic ideas and techniques are based on the compactness of the optimal trajectory set and set-valued mapping theorem. Through lack of optimal control stability, the result of generic stability for optimal trajectories is obtained under the perturbations of the right-hand side functions of the state equations; in the sense of Baire category, the right-hand side functions of the state equations of optimal control can be approximated by other functions.

Wildlife conservation is crucial to maintaining the stability of ecosystems. Monitoring the population and movement trajectories of endangered species by re-identification (re-ID) is a very promising way for wildlife conservation. The Amur tiger is an endangered species, but there are few studies on Amur tiger re-identification, and the existing methods have deficiencies such as cumbersome processing and low accuracy. In this paper, We introduce a novel locally guided adaptive feature fusion network for the Amur tiger re-ID task, which may help biologists monitor and protect Amur tigers in the wild. The network consists of two parts, global stream and local stream. Especially, The local stream is only used in the training phase, which can not only play the role of pose alignment but also guide and adjust the learning of the Global Stream. In the prediction phase, only global stream is needed, which greatly simplifies the intermediate process compared with the traditional re-ID methods. The experimental results show that our method has achieved high accuracy and efficiency in Amur tiger re-ID task, its performance overtakes the baseline method by a large margin.

In this study, the population pattern intensity of Parapenaeus fissuroides Crosnier in the northeast Fujian sea area was investigated with the negative binomal parameters, average crowding degree and poly block indices. The Paper also further discusses the driving factors of the population pattern intensity. In spring, the population primarily consisted of small patches, population aggregation was low, and individual mean crowding was the lowest of the year. In summer, population aggregation and individual mean was highest. In fall, the population primarily consisted of a small number of large patches. In winter, population aggregation was the lowest. The zooplankton biomass (feed) and water temperature were the major factors affecting population aggregation.

Macroautophagy is an evolutionarily conserved cellular process involved in the clearance of proteins and organelles. Although the autophagy regulation machinery has been widely studied, the key epigenetic control of autophagy process still remains unknown. Here we report that the methyltransferase EZH2 (enhancer of zeste 2 polycomb repressive complex 2 subunit) epigenetically represses several negative regulators of the MTOR (mechanistic target of rapamycin [serine/threonine kinase]) pathway, such as TSC2, RHOA, DEPTOR, FKBP11, RGS16 and GPI. EZH2 was recruited to these genes promoters via MTA2 (metastasis associated 1 family, member 2), a component of the nucleosome remodeling and histone deacetylase (NuRD) complex. MTA2 was identified as a new chromatin binding protein whose association with chromatin facilitated the subsequent recruitment of EZH2 to silenced targeted genes, especially TSC2. Downregulation of TSC2 (tuberous sclerosis 2) by EZH2 elicited MTOR activation, which in turn modulated subsequent MTOR pathway-related events, including inhibition of autophagy. In human colorectal carcinoma (CRC) tissues, the expression of MTA2 and EZH2 correlated negatively with expression of TSC2, which reveals a novel link among epigenetic regulation, the MTOR pathway, autophagy induction, and tumorigenesis.

β-catenin is an evolutionary conserved multifunctional protein, not only with the epithelial cadherin (E-cadherin) combine to form a complex involved in intercellular connections, maintain the normal morphology of epithelial cells, but also as the activation of Wnt signaling pathway in core areas, it plays a critical role in a series of physiological and pathological processes, such as embryogenesis, tumor development, invasion and metastasis. Therefore, the regulation of β-catenin is very important, post-translational modification is an important regulation mechanism of β-catenin. This paper presents a brief review for the research progress of β-catenin post-translational modification and the enzymes.

Histone methyltransferase G9a has critical roles in promoting cancer-cell growth and gene suppression, but whether it is also associated with the DNA damage response is rarely studied. Here, we report that loss of G9a impairs DNA damage repair and enhances the sensitivity of cancer cells to radiation and chemotherapeutics. In response to DNA double-strand breaks (DSBs), G9a is phosphorylated at serine 211 by casein kinase 2 (CK2) and recruited to chromatin. The chromatin-enriched G9a can then directly interact with replication protein A (RPA) and promote loading of the RPA and Rad51 recombinase to DSBs. This mechanism facilitates homologous recombination (HR) and cell survival. We confirmed the interaction between RPA and G9a to be critical for RPA foci formation and HR upon DNA damage. Collectively, our findings demonstrate a regulatory pathway based on CK2–G9a–RPA that permits HR in cancer cells and provide further rationale for the use of G9a inhibitors as a cancer therapeutic.

Suppressor of variegation 3–9 homolog 1 (SUV39H1), a histone methyltransferase, catalyzes histone 3 lysine 9 trimethylation and is involved in heterochromatin organization and genome stability. However, the mechanism for regulation of the enzymatic activity of SUV39H1 in cancer cells is not yet well known. In this study, we identified SET domain-containing protein 7 (SET7/9), a protein methyltransferase, as a unique regulator of SUV39H1 activity. In response to treatment with adriamycin, a DNA damage inducer, SET7/9 interacted with SUV39H1 in vivo, and a GST pull-down assay confirmed that the chromodomain-containing region of SUV39H1 bound to SET7/9. Western blot using antibodies specific for antimethylated SUV39H1 and mass spectrometry demonstrated that SUV39H1 was specifically methylated at lysines 105 and 123 by SET7/9. Although the half-life and localization of methylated SUV39H1 were not noticeably changed, the methyltransferase activity of SUV39H1 was dramatically down-regulated when SUV39H1 was methylated by SET7/9. Consequently, H3K9 trimethylation in the heterochromatin decreased significantly, which, in turn, led to a significant increase in the expression of satellite 2 ( Sat2 ) and α-satellite ( α-Sat ), indicators of heterochromatin relaxation. Furthermore, a micrococcal nuclease sensitivity assay and an immunofluorescence assay demonstrated that methylation of SUV39H1 facilitated genome instability and ultimately inhibited cell proliferation. Together, our data reveal a unique interplay between SET7/9 and SUV39H1—two histone methyltransferases—that results in heterochromatin relaxation and genome instability in response to DNA damage in cancer cells.

The ataxia-telangiectasia mutated (ATM) protein is a key signaling molecule that modulates the DNA damage response. However, the exact mechanism by which ATM regulates DNA damage repair has not yet been elucidated. Here, we report that ATM regulates the DNA damage response by phosphorylating lysine-specific demethylase 2A (KDM2A), a histone demethylase that acts at sites of H3K36 dimethylation. ATM interacts with KDM2A, and their interaction significantly increases in response to DNA double-stranded, but not single-stranded, breaks. ATM specifically phosphorylates KDM2A at threonine 632 (T632) following DNA damage, as demonstrated by a mutagenesis assay and mass spectrometric analysis. Although KDM2A phosphorylation does not alter its own demethylase activity, T632 phosphorylation of KDM2A largely abrogates its chromatin-binding capacity, and H3K36 dimethylation near DNA damage sites is significantly increased. Consequently, enriched H3K36 dimethylation serves as a platform to recruit the MRE11 complex to DNA damage sites by directly interacting with the BRCT2 domain of NBS1, which results in efficient DNA damage repair and enhanced cell survival. Collectively, our study reveals a novel mechanism for ATM in connecting histone modifications with the DNA damage response.

In this paper, we define the fitting energy by a new kernel function, which is to do in the range of an image what traditional filters do a small neighborhood of the same location. We combine the advantages of the LBF model and our model by taking domain and range kernel functions into account. The new level set method with domain and range kernel functions has been tested and assessed on different modalities of medical images. Experiments prove our simulation results demonstrate that our model has better segmentation results compared with the LBF model.

In this paper, on the basis of techniques of curve evolution, we propose a novel variational level set model for segmentation of intensity inhomogeneity images. The model is integrated with some advantages of fitting statistical model and region-based active contour model to the intensity in each of a set of regions. Furthermore, the experimental results show the validity of this model for various image modalities. All of these results may be useful in the study of the image segmentation.

This paper investigates the robust stability of uncertain neutral system with time-varying delay. By using Lyapunov method and linear matrix inequality technology, new delay-dependent stability criteria are obtained and formulated in terms of linear matrix inequalities (LMIs), which can be easy to check the robust stability of the considered systems. Numerical examples are given to indicate significant improvements over some existing results.

This paper investigates the problem of absolute stability and robust stability of a class of Lur-e systems with neutral type and time-varying delays. By using Lyapunov direct method and linear matrix inequality technique, new delay-dependent stability criteria are obtained and formulated in terms of linear matrix inequalities (LMIs) which are easy to check the stability of the considered systems. To obtain less conservative stability conditions, an operator is defined to construct the Lyapunov functional. Also, the free weighting matrices approach combining a matrix inequality technique is used to reduce the entailed conservativeness. Numerical examples are given to indicate significant improvements over some existing results., {"references":["J. K. Hale, S. M. & Verduyn Lunel Introduction to functional differential\nequation. New York: Springer 1993:292-293","S. Boyd, L.El. Ghaoui, E. Feron, &V. Balakrishnan, Linear matrix\ninequalities in systems and control theory. Philadelphia: SIAM 1994.","H. Miyagi, K. Yamashita, Stability studies of control systems using\na non-Lur-e type Lyapunov function. IEEE Trans. Automat. Control\n1986;31:970-972.","T. Li, J.J. Yu, Z. Wang, Delay-range-dependent synchronization criterion\nfor Lure systems with delay feedback control. Communications in\nNonlinear Science and Numerical Simulation 2009;14;1796-1803.","S.M. Lee, Ju H. Park, Delay-dependent criteriaforabsolutestabilityof\nuncertain time-delayedLuredynamicalsystems. Journal of the Franklin\nInstitute 2010;347:146-153.","Q.-L. Han, A new delay-dependent absolute stability criterion for a class\nof nonlinear neutral systems. Automatica 2008;44:272-277.","S. M. Lee, O. M. Kwon, Ju H. Park, Novel robust delay dependent\ncriterion for absloute stability of Lur-e of neutral type. Modern Physics\nLetters B (MPLB) 2009;23:1641-1650.","Y. He, M. Wu, Absolute stability for multiple delay general Lur-e\ncontrol systems with multiple nonlinearities. Journal of Computational\nand Applied Mathematics 2003;159:241-248.","Y. He, M. Wu, J.-H. She, Guo-Ping Liu, Robust stability for delay Lur-e\ncontrol systems with multiple nonlinearities. Journal of Computational\nand Applied Mathematics 2005;176:371-380.\n[10] J.F. Gao, H.Y. Su, Xiaofu Ji, Jian Chu, Stability analysis for a class\nof neutral systems with mixed delays and sector-bounded nonlinearity.\nNonlinear Analysis: Real World Applications 2008;9:2350-2360.\n[11] S.J. Choi, S.M. Lee, S.C. Won, Ju H. Park, Improved delay-dependent\nstability criteria for uncertain Lur-e systems with sector and slope\nrestricted nonlinearities and time-varying delays. Applied Mathematics\nand Computation 2009;208:520-530.\n[12] K. Gu, V.L. Kharitonov, J. Chen, Stability of Time-Delay Systems.\nBirkhauser, Boston, 2003.\n[13] K.Q. Gu, S.I. Niculescu, Additional dynamics in transformed time-delay\nsystems. IEEE Trans. Autom. Control 2000;45:572-575.\n[14] D.Y. Liu, X.Z. Liu, S.M. Zhong, Delay-dependent robust stability and\ncontrol synthesis for uncertain switched neutral systems with mixed\ndelays. Applied Mathematics and Computation 2008;202:828-839.\n[15] J.H. Park, Novel robust stability criterion for a class of neutral systems\nwith mixed delays and nonlinear perturbations. Appl. Math. Comput.\n2005;161;413-421.\n[16] W.-H. Chen, W. X. Zheng. Delay-dependent robust stabilization for uncertain\nneutral systems with distributed delays. Automatica 2007;43:95-\n104.\n[17] X.H. Nian, Delay dependent conditions for absolute stability of Lurie\ntype control systems. Acta Automatica Sin. 1999;25:564-566.\n[18] B. Yang, J.C. Wang, Delay-dependent criterion for absolute stability of\nneutral general lurie systems, Acta Automatica Sin. 2004;30:261-264.\n[19] L. Yu, Q.L. Han, S.M. Yu, J.F. Gao, Delay-dependent conditions for\nrobust absolute stability of uncertain time-delay systems. Proceedings\nof the 42nd IEEE Conference on Decision and Control 2003:6033-6037.\n[20] Q.L. Han, Absolute stability of time-delay systems with sector-bounded\nnonlinearity. Automatica 2005;41:2171-2176.\n[21] F. Qiu, B.T. Cui, Y. Ji, Novel robust stability analysis for uncertain\nneutral system with mixed delays, Chaos, Solitons and Fractals 42\n(2009) 1820-1828 .\n[22] L.L. Xiong, S.M. Zhong, J.K. Tian, Novel robust stability criteria of\nuncertain neutral systems with discrete and distributed delays, Chaos,\nSolitons and Fractals 40 (2009) 771-777."]}

DNA damage is a relatively common event in eukaryotic cell and may lead to genetic mutation and even cancer. DNA damage induces cellular responses that enable the cell either to repair the damaged DNA or cope with the damage in an appropriate way. Histone proteins are also the fundamental building blocks of eukaryotic chromatin besides DNA, and many types of post-translational modifications often occur on tails of histones. Although the function of these modifications has remained elusive, there is ever-growing studies suggest that histone modifications play vital roles in several chromatin-based processes, such as DNA damage response. In this review, we will discuss the main histone modifications, and their functions in DNA damage response.