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Kim, Hee Man,Kim, Hyun Ki,Lee, Sang Kil,Cho, Jae Hee,Pak, Kyung Ho,Hyung, Woo Jin,Noh, Sung Hoon,Kim, Choong Bai,Lee, Yong Chan,Song, Si Young,Youn, Young Hoon Raven Press 2012 Annals of surgical oncology Vol.19 No.4
<P>The multifocality rate of EGC ranges from 4 to 20%, but there are few data regarding both lymph node metastasis and feasibility of the endoscopic treatment. We investigated the risk of lymph node metastasis with the purpose to evaluate the potential for endoscopic treatment in patients with multifocal EGC.</P>
Chen, Bai Hui,Park, Joon Ha,Ahn, Ji Hyeon,Cho, Jeong Hwi,Kim, In Hye,Lee, Jae Chul,Won, Moo-Ho,Lee, Choong-Hyun,Hwang, In Koo,Kim, Jong-Dai,Kang, Il Jun,Cho, Jun Hwi,Shin, Bich Na,Kim, Yang Hee,Lee, Y Medknow PublicationsMedia Pvt Ltd 2017 Neural regeneration research Vol.12 No.2
<P>Quercetin (QE; 3,5,7,3′,4′-pentahydroxyflavone), a well-known flavonoid, has been shown to prevent against neurodegenerative disorders and ischemic insults. However, few studies are reported regarding the neuroprotective mechanisms of QE after ischemic insults. Therefore, in this study, we investigated the effects of QE on ischemic injury and the expression of antioxidant enzymes in the hippocampal CA1 region of gerbils subjected to 5 minutes of transient cerebral ischemia. QE was pre-treated once daily for 15 days before ischemia. Pretreatment with QE protected hippocampal CA1 pyramidal neurons from ischemic injury, which was confirmed by neuronal nuclear antigen immunohistochemistry and Fluoro-Jade B histofluorescence staining. In addition, pretreatment with QE significantly increased the expression levels of endogenous antioxidant enzymes Cu/Zn superoxide dismutase, Mn superoxide dismutase, catalase and glutathione peroxidase in the hippocampal CA1 pyramidal neurons of animals with ischemic injury. These findings demonstrate that pretreated QE displayed strong neuroprotective effects against transient cerebral ischemia by increasing the expression of antioxidant enzymes.</P>
Chen, Bai Hui,Ahn, Ji Hyeon,Park, Joon Ha,Song, Minah,Kim, Hyunjung,Lee, Tae-Kyeong,Lee, Jae Chul,Kim, Young-Myeong,Hwang, In Koo,Kim, Dae Won,Lee, Choong-Hyun,Yan, Bing Chun,Kang, Il Jun,Won, Moo-Ho Elsevier 2018 Chemico-biological interactions Vol.286 No.-
<P><B>Abstract</B></P> <P>Rufinamide is a novel antiepileptic drug and commonly used in the treatment of Lennox-Gastaut syndrome. In the present study, we investigated effects of rufinamide on cognitive function using passive avoidance test and neurogenesis in the hippocampal dentate gyrus using Ki-67 (a marker for cell proliferation), doublecortin (DCX, a marker for neuroblast) and BrdU/NeuN (markers for newly generated mature neurons) immunohistochemistry in aged gerbils. Aged gerbils (24-month old) were treated with 1 mg/kg and 3 mg/kg rufinamide for 4 weeks. Treatment with 3 mg/kg rufinamide, not 1 mg/kg rufinamide, significantly improved cognitive function and increased neurogenesis, showing that proliferating cells (Ki-67-immunoreactive cells), differentiating neuroblasts (DCX-immunoreactive neuroblasts) and mature neurons (BrdU/NeuN-immunoreactive cells) in the aged dentate gyrus compared with those in the control group. When we examined its mechanisms, rufinamide significantly increased immunoreactivities of insulin-like growth factor-1 (IGF-1), its receptor (IGF-1R), and phosphorylated cAMP response element binding protein (<I>p</I>-CREB). However, rufinamide did not show any increase in immunoreactivities of brain-derived neurotrophic factor and its receptor. Therefore, our results indicate that rufinamide can improve cognitive function and increase neurogenesis in the hippocampus of the aged gerbil via increasing expressions of IGF-1, IGF-1R and <I>p</I>-CREB.</P> <P><B>Highlights</B></P> <P> <UL> <LI> 4-week treatment of rufinamide (Ruf) increases short-term memory in the aged gerbil. </LI> <LI> Ruf increases neurogenesis in the aged hippocampal dentate gyrus (DG). </LI> <LI> Ruf treatment increases IGF-1, IGF-1R, and <I>p</I>-CREB in the aged DG. </LI> <LI> Ruf treatment does not affect expressions of BDNF and TrkB in the aged DG. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>