Nagoya Institute of Technology

About: Nagoya Institute of Technology is a education organization based out in Nagoya, Japan. It is known for research contribution in the topics: Thin film & Turbulence. The organization has 10766 authors who have published 19140 publications receiving 255696 citations. The organization is also known as: Nagoya Kōgyō Daigaku & Nitech.

Multiple Incremental Decremental Learning of Support Vector Machines

Abstract: We propose a multiple incremental decremental algorithm of support vector machines (SVM). In online learning, we need to update the trained model when some new observations arrive and/or some observations become obsolete. If we want to add or remove single data point, conventional single incremental decremental algorithm can be used to update the model efficiently. However, to add and/or remove multiple data points, the computational cost of current update algorithm becomes inhibitive because we need to repeatedly apply it for each data point. In this paper, we develop an extension of incremental decremental algorithm which efficiently works for simultaneous update of multiple data points. Some analyses and experimental results show that the proposed algorithm can substantially reduce the computational cost. Our approach is especially useful for online SVM learning in which we need to remove old data points and add new data points in a short amount of time.

Chromatin regulator PRC2 is a key regulator of epigenetic plasticity in glioblastoma

Abstract: Tumor cell plasticity contributes to functional and morphologic heterogeneity. To uncover the underlying mechanisms of this plasticity, we examined glioma stem-like cells (GSC) where we found that the biologic interconversion between GSCs and differentiated non-GSCs is functionally plastic and accompanied by gain or loss of polycomb repressive complex 2 (PRC2), a complex that modifies chromatin structure. PRC2 mediates lysine 27 trimethylation on histone H3 and in GSC it affected pluripotency or development-associated genes (e.g., Nanog, Wnt1, and BMP5) together with alterations in the subcellular localization of EZH2, a catalytic component of PRC2. Intriguingly, exogenous expression of EZH2-dNLS, which lacks nuclear localization sequence, impaired the repression of Nanog expression under differentiation conditions. RNA interference (RNAi)-mediated attenuation or pharmacologic inhibition of EZH2 had little to no effect on apoptosis or bromodeoxyuridine incorporation in GSCs, but it disrupted morphologic interconversion and impaired GSC integration into the brain tissue, thereby improving survival of GSC-bearing mice. Pathologic analysis of human glioma specimens revealed that the number of tumor cells with nuclear EZH2 is larger around tumor vessels and the invasive front, suggesting that nuclear EZH2 may help reprogram tumor cells in close proximity to this microenvironment. Our results indicate that epigenetic regulation by PRC2 is a key mediator of tumor cell plasticity, which is required for the adaptation of glioblastoma cells to their microenvironment. Thus, PRC2-targeted therapy may reduce tumor cell plasticity and tumor heterogeneity, offering a new paradigm for glioma treatment.