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이원하,석경호,이상민,김원정 대한면역학회 2010 Immune Network Vol.10 No.5
APRIL, originally known as a cytokine involved in B cell survival, is now known to regulate the inflammatory activation of macrophages. Although the signal initiated from APRIL has been demonstrated, its role in cellular activation is still not clear due to the presence of BAFF, a closely related member of TNF superfamily, which share same receptors (TACI and BCMA) with APRIL. Methods: Through transfection of siRNA, BAFF-deficient THP-1 cells (human macrophage-like cells) were generated and APRIL-mediated inflammatory activities were tested. The expression patterns of APRIL were also tested in vivo. Results: BAFF-deficient THP-1 cells responded to APRIL-stimulating agents such as monoclonal antibody against APRIL and soluble form of TACI or BCMA. Furthermore, co-incubation of the siBAFF-deficient THP-1 cells with a human B cell line (Ramos) resulted in an activation of THP-1 cells which was dependent on interactions between APRIL and TACI/BCMA. Immunohistochemical analysis of human pathologic samples detected the expression of both APRIL and TACI in macrophage-rich areas. Additionally, human macrophage primary culture expressed APRIL on the cell surface. Conclusion: These observations indicate that APRIL, which is expressed on macrophages in pathologic tissues with chronic inflammation, may mediate activation signals through its interaction with its counterparts via cell-to-cell interaction.
김종헌,석경호,윤성호,장광호,박재찬,한형수,이동익 한국뇌신경과학회 2014 Experimental Neurobiology Vol.23 No.2
Hypothermia is considered a useful intervention for limiting pathophysiological changes after brain injury. Local hypothermia isa relatively safe and convenient intervention that circumvents many of the complications associated with systemic hypothermia. However, successful hypothermia treatment requires careful consideration of several factors including its practicality, feasibility, andassociated risks. Here, we review the protective effects—and the cellular mechanisms that underlie them—of delayed and prolongedlocal hypothermia in rodent and canine brain injury models. The data show that the protective effects of therapeutic hypothermia,which mainly result from the modulation of inflammatory glial dynamics, are limited. We argue that decompressive craniectomycan be used to overcome the limitations of local brain hypothermia without causing histological abnormalities or other detrimentaleffects to the cooled area. Therefore, delayed and prolonged local brain hypothermia at the site of craniectomy is a promisingintervention that may prove effective in the clinical setting.
Comparative Analysis of Protein Tyrosine Phosphatases Regulating Microglial Activation
송견지,석경호,김재홍,김종헌,송승은,박하나,Zhong-Yin Zhang 한국뇌신경과학회 2016 Experimental Neurobiology Vol.25 No.5
Protein tyrosine phosphatases (PTPs) are key regulatory factors in inflammatory signaling pathways. Although PTPs have been extensively studied, little is known about their role in neuroinflammation. In the present study, we examined the expression of 6 different PTPs (PTP1B, TC-PTP, SHP2, MEG2, LYP, and RPTPβ) and their role in glial activation and neuroinflammation. All PTPs were expressed in brain and glia. The expression of PTP1B, SHP2, and LYP was enhanced in the inflamed brain. The expression of PTP1B, TC-PTP, and LYP was increased after treating microglia cells with lipopolysaccharide (LPS). To examine the role of PTPs in microglial activation and neuroinflammation, we used specific pharmacological inhibitors of PTPs. Inhibition of PTP1B, TC-PTP, SHP2, LYP, and RPTPβ suppressed nitric oxide production in LPS-treated microglial cells in a dose-dependent manner. Furthermore, intracerebroventricular injection of PTP1B, TC-PTP, SHP2, and RPTPβ inhibitors downregulated microglial activation in an LPS-induced neuroinflammation model. Our results indicate that multiple PTPs are involved in regulating microglial activation and neuroinflammation, with different expression patterns and specific functions. Thus, PTP inhibitors can be exploited for therapeutic modulation of microglial activation in neuroinflammatory diseases.
북스캔을 이용한 도서 손상 단계에 따른 딥 러닝 기반 도서 복구 방법에 관한 연구
김영모,석경호,이주희,박병찬,김석윤 한국반도체디스플레이기술학회 2023 반도체디스플레이기술학회지 Vol.22 No.4
Recently, with the activation of eBook services, books are being published simultaneously as physical books and digitized eBooks. Paper books are more expensive than e-books due to printing and distribution costs, so demand for relatively inexpensive e-books is increasing. There are cases where previously published physical books cannot be digitized due to the circumstances of the publisher or author, so there is a movement among individual users to digitize books that have been published for a long time. However, existing research has only studied the advancement of the pre-processing process that can improve text recognition before applying OCR technology, and there are limitations to digitization depending on the condition of the book. Therefore, support for book digitization services depending on the condition of the physical book is needed. need. In this paper, we propose a method to support digitalization services according to the status of physical books held by book owners. Create images by scanning books and extract text information from the images through OCR. We propose a method to recover text that cannot be extracted depending on the state of the book using BERT, a natural language processing deep learning model. As a result, it was confirmed that the recovery method using BERT is superior when compared to RNN, which is widely used in recommendation technology.