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RISS 인기검색어
- 검색키워드
- 저자 : Chris Jackson (검색결과 3 건)
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Compensatory Neural Reorganization in Tourette Syndrome
Jackson, Stephen ,R.,Parkinson, Amy,Jung, Jeyoung,Ryan, Suzanne ,E.,Morgan, Paul ,S.,Hollis, Chris,Jackson, Georgina ,M. Cell Press 2011 Current biology Vol.21 No.7
<P><B>Summary</B></P><P>Children with neurological disorders may follow unique developmental trajectories whereby they undergo compensatory neuroplastic changes in brain structure and function that help them gain control over their symptoms [1–6]. We used behavioral and brain imaging techniques to investigate this conjecture in children with Tourette syndrome (TS). Using a behavioral task that induces high levels of intermanual conflict, we show that individuals with TS exhibit enhanced control of motor output. Then, using structural (diffusion-weighted imaging) brain imaging techniques, we demonstrate widespread differences in the white matter (WM) microstructure of the TS brain that include alterations in the corpus callosum and forceps minor (FM) WM that significantly predict tic severity in TS. Most importantly, we show that task performance for the TS group (but not for controls) is strongly predicted by the WM microstructure of the FM pathways that lead to the prefrontal cortex and by the functional magnetic resonance imaging blood oxygen level-dependent response in prefrontal areas connected by these tracts. These results provide evidence for compensatory brain reorganization that may underlie the increased self-regulation mechanisms that have been hypothesized to bring about the control of tics during adolescence.</P>
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이유진,정재교,설재원,Meilang Xue,Chris Jackson,박상열 생화학분자생물학회 2013 Experimental and molecular medicine Vol.45 No.2
Activated protein C (APC) is a cytoprotective anticoagulant that can promote cutaneous healing. We examined the effect of APC on viability and differentiation of the osteoblastic line, MG63, in the presence and absence of bisphosphonates (BPs). Osteoblasts were cultured and treated for 24 or 48 h with Alendronate (Aln), Zoledronate (Zol) or Pamidronate (Pam) at concentrations ranging from 104 to 106 M. Cell differentiation was measured using type 1 collagen production, Alizarin red staining and alkaline phosphatase activity, whereas cell viability was assessed using MTT and crystal violet assays. All three BPs induced MG63 cell death in a dose- and time-dependent manner. Pam- and Zol-related cell death was prevented by APC treatment; however, cell death induced by Aln was accelerated by APC. APC induced MG63 cell differentiation that was enhanced by Aln, but inhibited by Pam or Zol. Endothelial protein C receptor (EPCR) was expressed by MG63 cells and mediated the protective effect of APC on Zol-induced viability. In summary, we have demonstrated that (1) APC favorably regulates MG63 viability and differentiation toward bone growth, (2) APC differentially regulates the effects of specific BPs and (3) at least part of the effects of APC is mediated through EPCR. These findings highlight the potential importance of the PC pathway in bone physiology and provide strong evidence that APC may influence bone cells and has potential to be a therapeutic drug for bone regeneration, depending on concurrent BP treatment.
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Protective effect of hypoxia on bisphosphonate?related bone cell damage.
Moon, Myung-Hee,Seol, Jae-Won,Seo, Jae-Suk,Jeong, Jae-Kyo,Lee, You-Jin,Kim, In-Shik,Jackson, Chris,Sambrook, Philip,Park, Sang-Youel D. A. Spandidos 2010 MOLECULAR MEDICINE REPORTS Vol.3 No.5
<P>Bisphosphonates (BPs) are widely used for the prevention and treatment of osteoporosis. However, there have been numerous reports of side effects of BPs, including osteonecrosis of the jaw. In the present study, we investigated whether hypoxia inhibits BP-induced apoptosis, and examined the mechanisms of this inhibition. The cell viability of the MG 63 human osteoblast-like cell line treated with the nitrogen-containing (N)-BPs alendronate, risedronate and zoledronate was investigated, and hypoxia was assessed by crystal violet staining and the MTT assay, and by observing cell morphology. The effect of N-BPs and hypoxia on apoptotic cell signaling was evaluated using Western blotting, immunocytochemistry and the TUNEL assay. The results of crystal violet staining and the MTT and TUNEL assays showed that the N-BPs inhibited proliferation and induced apoptosis in MG?63 cells. Hypoxia significantly prevented N-BP-induced MG 63 cell apoptosis, and also attenuated BP-induced c-Jun N-terminal kinase (JNK) phosphorylation and BCL-xL reduction. Hypoxia prevented BP-induced cell damage by blocking JNK phosphorylation and by regulating the BCL-xL protein. Thus, hypoxia or hypoxia-related genes, including hypoxia-inducible factor 1α, may be a potential therapy for BP-related side effects such as osteonecrosis of the jaw.</P>
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