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- 저자 : Bruce J. Aronow (검색결과 3 건)
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Kim, Han-Jong,Yoo, Eun-Kyung,Kim, Joon-Young,Choi, Young-Keun,Lee, Hyo-Jeong,Kim, Jeong-Kook,Jeoung, Nam Ho,Lee, Ki-Up,Park, In-Sun,Min, Bon-Hong,Park, Keun-Gyu,Lee, Chul-Ho,Aronow, Bruce J,Sata, Masa The Association 2009 Arteriosclerosis, thrombosis, and vascular biology Vol.29 No.10
<P>OBJECTIVE: Clusterin is induced in vascular smooth muscle cells (VSMCs) during atherosclerosis and injury-induced neointimal hyperplasia. However, its functional roles in VSMCs and endothelial cells remain controversial and elusive. This study was undertaken to clarify the role of clusterin in neointimal hyperplasia and elucidate its mechanism of action. METHODS AND RESULTS: Adenovirus-mediated overexpression of clusterin (Ad-Clu) repressed TNF-alpha-stimulated expression of MCP-1, fractalkine, ICAM-1, VCAM-1, and MMP-9, leading to inhibition of VSMC migration. Both Ad-Clu and secreted clusterin suppressed VSMC proliferation by inhibiting DNA synthesis, but not by inducing apoptosis. Ad-Clu upregulated p53 and p21(cip1/waf1) but downregulated cyclins D and E, leading to suppression of pRb phosphorylation and subsequent induction of G1 arrest in VSMCs. Clusterin deficiency augmented VSMC proliferation in vitro and accelerated neointimal hyperplasia in vivo, but concomitantly impaired reendothelialization in wire-injured murine femoral arteries. Moreover, Ad-Clu significantly reduced neointimal thickening in balloon-injured rat carotid arteries. Clusterin also diminished TNF-alpha-induced apoptosis of human umbilical vein endothelial cells and restored endothelial nitric oxide synthase expression suppressed by TNF-alpha. CONCLUSIONS: These results suggest that upregulation of clusterin during vascular injury may be a protective response against, rather than a causative response to, the development of neointimal hyperplasia.</P>
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Asami Yonekura,Hiroharu Kawanaka,V. B. Surya Prasath,Bruce J. Aronow,Haruhiko Takase 대한의용생체공학회 2018 Biomedical Engineering Letters (BMEL) Vol.8 No.3
In the field of computational histopathology, computer-assisted diagnosis systems are important in obtaining patientspecificdiagnosis for various diseases and help precision medicine. Therefore, many studies on automatic analysis methodsfor digital pathology images have been reported. In this work, we discuss an automatic feature extraction and disease stageclassification method for glioblastoma multiforme (GBM) histopathological images. In this paper, we use deep convolutionalneural networks (Deep CNNs) to acquire feature descriptors and a classification scheme simultaneously. Further,comparisons with other popular CNNs objectively as well as quantitatively in this challenging classification problem isundertaken. The experiments using Glioma images from The Cancer Genome Atlas shows that we obtain 96:5% averageclassification accuracy for our network and for higher cross validation folds other networks perform similarly with a higheraccuracy of 98:0%. Deep CNNs could extract significant features from the GBM histopathology images with highaccuracy. Overall, the disease stage classification of GBM from histopathological images with deep CNNs is verypromising and with the availability of large scale histopathological image data the deep CNNs are well suited in tacklingthis challenging problem.
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Essential role of clusterin in pancreas regeneration
Lee, Song,Hong, Seok‐,Woo,Min, Bon‐,Hong,Shim, Young‐,Jun,Lee, Ki‐,Up,Lee, In‐,Kyu,Bendayan, M.,Aronow, Bruce J.,Park, In‐,Sun Wiley‐Liss, Inc. 2011 Developmental dynamics Vol.240 No.3
<P><B>Abstract</B></P><P>Based on our previous observations that clusterin induction accompanies pancreas regeneration in the rat, we sought to determine if regeneration might be impaired in mice that lacked clusterin. We studied the impact of absent clusterin on morphogenic and functional features of regenerating pancreas. Clusterin induction was accompanied in the regenerating pancreas by a robust development of new lobules with ductules, acini, and endocrine islets in wild type after partial pancreatectomy. In clusterin knock‐out mice, however, pancreatectomy resulted in a poor formation of regenerating lobule. In particular, regeneration of beta‐cells was also significantly reduced and was associated with persistent hyperglycemia. Duct cells obtained from pancreatectomized clusterin knock‐out mice exhibited impaired beta‐cell formation in vitro; this was restored by administration of exogenous clusterin. We suggest that clusterin plays a critical role to promote both exocrine and endocrine regeneration following pancreas injury, as well as for in vitro beta‐cell regeneration. Developmental Dynamics 240:605–615, 2011. © 2011 Wiley‐Liss, Inc.</P>
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