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Kim, Minx2010,Seok,Lee, Geunx2010,Hee,Kim, Yongx2010,Min,Lee, Byoungx2010,Wook,Nam, Hae Yun,Sim, Ux2010,Cheol,Choo, Sukx2010,Jung,Yu, Seongx2010,Woon,Kim, Jae‐,Joong,Kim Kwon, Yunh unknown 2017 Stem cells translational medicine Vol.6 No.6
<P><B>Abstract</B></P><P>Data are limited on the mechanisms underlying memory impairment in heart failure (HF). We hypothesized that angiotensin II (Ang II) may determine the fate of adult hippocampal neural stem cells (HCNs), a cause of memory impairment in HF. HCNs with neurogenesis potential were isolated and cultured from adult rat hippocampi. Ang II decreased HCN proliferation in dose‐ and time‐dependent manners. Moreover, Ang II treatment (1 µM) for 48 hours induced apoptotic death, which was attenuated by pretreatment with Ang II receptor blockers (ARBs). Ang II increased mitochondrial reactive oxygen species (ROS) levels, which was related to mitochondrial morphological changes and functional impairment. Moreover, ROS activated the AMP‐activated protein kinase (AMPK) and consequent peroxisome proliferator‐activated receptor gamma coactivator 1‐alpha (PGC1α) expression, causing cell apoptosis. In the HF rat model induced by left anterior descending artery ligation, ARB ameliorated the spatial memory ability which decreased 10 weeks after ischemia. In addition, neuronal cell death, especially of newly born mature neurons, was observed in HF rat hippocampi. ARB decreased cell death and promoted the survival of newly born neural precursor cells and mature neurons. In conclusion, Ang II caused HCN apoptosis through mitochondrial ROS formation and subsequent AMPK‐PGC1α signaling. ARB improved learning and memory behaviors impaired by neuronal cell death in the HF animal model. These findings suggest that HCN is one treatment target for memory impairment in HF and that ARBs have additional benefits in HF combined with memory impairment. S<SMALL>TEM</SMALL> C<SMALL>ELLS</SMALL> T<SMALL>RANSLATIONAL</SMALL> M<SMALL>EDICINE</SMALL><I>2017;6:1491–1503</I></P>
Effects of 60 Hz 14 µT magnetic field on the apoptosis of testicular germ cell in mice
Kim, Yoonx2010,Won,Kim, Heex2010,Sung,Lee, Jinx2010,Sang,Kim, Youngx2010,Jin,Lee, Sangx2010,Kon,Seo, Jae‐,Nam,Jung, Kyeongx2010,Cheon,Kim, Nam,Gimm, Younx2010,Myoung Wiley Subscription Services, Inc., A Wiley Company 2009 BioElectroMagnetics Vol.30 No.1
<P><B>Abstract</B></P><P>We recently reported that continuous exposure, for 8 weeks, of extremely low frequency (ELF) magnetic field (MF) of 0.1 or 0.5 mT might induce testicular germ cell apoptosis in BALB/c mice. In that report, the ELF MF exposure did not significantly affect the body weight or testicular weight, but significantly increased the incidence of testicular germ cell death. In the present study, we aimed to further characterize the effect of a 16‐week continuous exposure to ELF MF of 14 or 200 µT on testicular germ cell apoptosis in mice. There were no significant effects of MF on body weight and testosterone levels in mice. In TUNEL staining (In situ terminal deoxynucleotidyl transferase‐mediated deoxy‐UTP nick end labeling), germ cells showed a significantly higher apoptotic rate in exposed mice than in sham controls (<I>P</I> < 0.001). TUNEL‐positive cells were mainly spermatogonia. In an electron microscopic study, degenerating spermatogonia showed condensation of nuclear chromatin similar to apoptosis. These results indicate that apoptosis may be induced in spermatogenic cells in mice by continuous exposure to 60 Hz MF of 14 µT. Bioelectromagnetics 30:66–72, 2009. © 2008 Wiley‐Liss, Inc.</P>
Lee, Minx2010,Jae,Jung, Jieun,Na, Kyux2010,Hwan,Moon, Ji Suk,Lee, Heyx2010,Jin,Kim, Jae‐,Hwan,Kim, Gwang Il,Kwon, Sungx2010,Won,Hwang, Seongx2010,Gyu,Kim, Gi Jin Wiley Subscription Services, Inc., A Wiley Company 2010 Journal of cellular biochemistry Vol.111 No.6
<P><B>Abstract</B></P><P>Translational studies have explored the therapeutic effects of stem cells, raising hopes for the treatment of numerous diseases. Here, we evaluated the therapeutic effect of chorionic plate‐derived mesenchymal stem cells (CP‐MSCs) isolated from human placenta and transplanted into rats with carbon tetrachloride (CCl<SUB>4</SUB>)‐injured livers. CP‐MSCs were analyzed for hepatocyte‐specific gene expression, indocyanine green (ICG) uptake, glycogen storage, and urea production following hepatogenic differentiation. PKH26‐labeled CP‐MSCs were directly transplanted into the livers of rats that had been exposed to CCl<SUB>4</SUB> (1.6 g/kg, twice per week for 9 weeks). Blood and liver tissue were analyzed at 1, 2, and 3 weeks post‐transplantation. The expression of type I collagen (Col I) and matrix metalloproteinases (MMPs) was analyzed in rat T‐HSC/Cl‐6 hepatic stellate cells co‐cultured with CP‐MSCs following exposure to TGF‐β. The expression levels of α‐smooth muscle actin (α‐SMA) and Col I were lower in transplanted (TP) rats than in non‐transplanted (Non‐TP) animals (<I>P</I> < 0.05), whereas the expression levels of albumin and MMP‐9 were increased. TP rats exhibited significantly higher uptake/excretion of ICG than non‐TP rats (<I>P</I> < 0.005). In addition, collagen synthesis in T‐HSC/Cl‐6 cells exposed to TGF‐β was decreased by co‐culture with CP‐MSCs, which triggered the activation of MMP‐2 and MMP‐9. These results contribute to our understanding of the potential pathophysiological roles of CP‐MSCs, including anti‐fibrotic effects in liver disease, and provide a foundation for the development of new cell therapy‐based strategies for the treatment of difficult‐to‐treat liver diseases. J. Cell. Biochem. 111: 1453–1463, 2010. © 2010 Wiley‐Liss, Inc.</P>
Kim, Jae‐,Min,Kim, Sungx2010,Wan,Stewart, Robert,Kim, Seonx2010,Young,Yoon, Jinx2010,Sang,Jung, Sungx2010,Won,Lee, Minx2010,Soo,Yim, Hyeonx2010,Woo,Jun, Taex2010,Youn John Wiley Sons, Ltd. 2011 HUMAN PSYCHOPHARMACOLOGY -CLINICAL AND EXPERIMENTA Vol.26 No.1
<P><B>Abstract</B></P><P><B>Objective</B></P><P>To estimate the 12‐week remission rate of patients with depressive disorders and predictors of this in a naturalistic clinical setting in South Korea.</P><P><B>Methods</B></P><P>For people with DSM‐IV depressive disorders about to receive treatment at 18 hospitals, data on sociodemographic and health status were obtained. A free choice of clinical interventions was allowed and naturalistic follow‐up took place at 1, 2, 4, 8, and 12 weeks later. Remission was defined as a Hamilton Depression Rating Scale score of ≤7 sustained to 12 weeks or last follow‐up, if earlier.</P><P><B>Results</B></P><P>For 723 participants, the 12‐week remission rate was 31.4%. Remission was more likely in women, and in patients without a prior history of suicide attempt, and those with lower baseline anxiety.</P><P><B>Conclusions</B></P><P>Remission associated with unrestricted clinical interventions was comparable to STAR*D estimates for citalopram alone. Comorbid anxiety and a previous suicide attempt were markers of worse outcome. Copyright © 2011 John Wiley & Sons, Ltd.</P>
Thermo‐sensitive nanogel‐laden bicontinuous microemulsion drug‐eluting contact lenses
Lee, Sex2010,Hee,Kim, Hox2010,Joong,Kim, Duckx2010,Hyun,Chang, Wonx2010,Seok,Vales, Temmy Pegarro,Kim, Jae‐,Woo,Kim, Kix2010,Hong,Kim, Jongx2010,Ki John Wiley Sons, Inc. 2019 Journal of Biomedical Materials Research Part B Vol.107 No.4
<P><B>Abstract</B></P><P>The bicontinuous microemulsion contact lens (BMCL) has nanoporous biphasic structures (100–250 nm) that are interconnected via multiple nano‐channels, providing suitable retention of various drugs for glaucoma. Timolol maleate (TM)‐carried thermosensitive poly(<I>N</I>‐isopropylacrylamide) (PNIPAM) nanogel (30–50 nm) was incorporated into BMCLs by soaking or by centrifuging plus soaking. Here, we present drug‐loading and release in silicon‐ or polyethylene oxide‐microemulsion BMCLs under various conditions. Nanoporous BMCLs containing thermosensitive TM‐laden nanogel were capable of potent body‐temperature‐triggered release of TM. Daily drug release was controllable according to the initial volume of drug‐loaded (VDL) and loading method for sustained drug release, making them reduce drug‐loss during transportation or storage. © 2018 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater 107B: 1159–1169, 2019.</P>
Clinical trial: Inhibitory effect of revaprazan on gastric acid secretion in healthy male subjects
Kim, Hyungx2010,Keun,Park, Soox2010,Heon,Cheung, Daex2010,Young,Cho, Youngx2010,Seok,Kim, Jinx2010,Il,Kim, Sungx2010,Soo,Chae, Hiunx2010,Suk,Kim, Jae‐,Kwang,Chung, Inx2010,Sik Blackwell Publishing Asia 2010 Journal of gastroenterology and hepatology Vol.25 No.10
<P><B>Abstract</B></P><P><B>Background and Aim: </B> Revaprazan is a novel acid pump antagonist. The aim of this study was to investigate the inhibitory effect of revaprazan on gastric acid secretion in healthy male subjects.</P><P><B>Methods: </B> In a double‐blind, three‐way cross‐over study, 30 healthy male volunteers were randomized to 100, 150 or 200 mg of oral revaprazan daily for 7 days. Serum gastrin concentration was measured, and 24‐h intragastric pH was recorded at baseline and on days 1 and 7 of each administration period. Serial blood samples were processed for pharmacokinetics.</P><P><B>Results: </B> Median intragastric pH over 24 h and mean percentage time that pH was > 4 increased in a dose‐dependent manner and were significantly higher on days 1 and 7 compared with baseline in all groups (<I>P</I> < 0.05). The antisecretory effect of revaprazan was rapid and nearly maximal on day 1 in all groups. Serum gastrin levels were rapidly normalized by 100 and 150 mg/day of revaprazan on days 1 and 7, but were significantly higher in the 200 mg/day revaprazan group. The pharmacokinetic effect was rapidly absorbed and eliminated on days 1 and 7 in all groups.</P><P><B>Conclusions: </B> Revaprazan rapidly and effectively inhibits gastric acid secretion in healthy male subjects. Therefore, revaprazan can be used as an effective drug for acid‐related disease.</P>
Kim, Dong Ha,Choi, Yun Jung,Sung, Ki Jung,Yoo, Seonx2010,A,Sung, Young Hoon,Kim, Jeong Kon,Choi, Changx2010,Min,Yun, Miyong,Lee, Eun Yong,Jin, Yong Suk,Cook, Seungho,Rho, Jin Kyung,Lee, Jae Cheol John Wiley and Sons Inc. 2018 Molecular Oncology Vol.12 No.12
<P>Central nervous system (CNS) metastasis is one of the serious complications of epidermal growth factor receptor (EGFR)‐mutant lung cancer, which arises due to poor penetration of the brain–blood barrier by EGFR‐tyrosine kinase inhibitors (EGFR‐TKIs). Although osimertinib, a third‐generation EGFR‐TKI, has efficacy against CNS metastases, further treatment modalities are still needed as some of these lesions do not respond to osimertinib, or undergo progression after an initial response to this drug if radiotherapy has already been conducted. Here, we investigated the efficacy of water‐soluble erlotinib (NUFS‐sErt) against these metastases. This agent was synthesized using a nano‐particulation platform technology utilizing fat and supercritical fluid (NUFS™) to resolve the low solubility problem that typically prevents the creation of injectable forms of EGFR‐TKIs. The average NUFS‐sErt particle size was 236.4 nm, and it showed time‐dependent dissolution in culture media. The effects of NUFS‐sErt were similar to those of conventional erlotinib in terms of inhibiting the proliferation of EGFR‐mutant lung cancer cells and suppressing EGFR signaling. In an intraperitoneal xenograft model of HCC827 cells, intraperitoneal administration of NUFS‐sErt produced a dose‐dependent inhibition of tumor growth and enhanced survival rate. Notably, the injection of NUFS‐sErt into the brain ventricle caused significant tumor growth inhibition in an intracranial xenograft model. Hence, our current findings indicate that NUFS‐sErt is a novel, water‐soluble form of erlotinib that can be administered using intraventricular or intrathecal injections. The target cases would be patients with a progressive CNS metastasis and no other therapeutic options. This drug could also be given intravenously to patients with swallowing difficulties or an inability to ingest due to a medical condition.</P>
Evidence of carrier‐mediated transport in the penetration of donepezil into the rat brain
Kim, Mix2010,Hwa,Maeng, Hanx2010,Joo,Yu, Kyungx2010,Ha,Lee, Kyeongx2010,Ryoon,Tsuruo, Takashi,Kim, Daex2010,Duk,Shim, Changx2010,Koo,Chung, Sukx2010,Jae Wiley Subscription Services, Inc., A Wiley Company 2010 Journal of Pharmaceutical Sciences Vol.99 No.3
<P><B>Abstract</B></P><P>The objective of this study was to characterize the mechanism that controls the transport of donepezil into the brain. The apparent brain uptake clearance (CL<SUB>app,br</SUB>) was decreased as a function of the dose of donepezil, suggesting an involvement of a saturable transport process via transporter(s) in the penetration across the blood–brain barrier (BBB). Consistent with <I>in vivo</I> results, the uptake of substrates for organic cation transporters was significantly reduced by donepezil in both MBEC4 cells (i.e., a model for BBB) and HEK 293 cells expressing the transporters found in the brain, indicative of the involvement of organic cation transporters in the transport of the drug. Furthermore, donepezil transport was enhanced (<I>p</I> < 0.01) in HEK 293 cells expressing rOCNT1, rOCTN2, or rCHT1. The CL<SUB>app,br</SUB> was reduced up to 52.8% of the control in rats that had been pretreated with choline, while the CL<SUB>app,br</SUB> was unaffected with pretreatments with organic cations other than choline, suggesting that choline and donepezil share a common transport mechanism in the penetration across the BBB <I>in vivo</I>. Taken together, these observations suggest that the transport of donepezil across the BBB is mediated by organic cation transporters such as choline transport system(s). © 2009 Wiley‐Liss, Inc. and the American Pharmacists Association J Pharm Sci 99: 1548–1566, 2010</P>
Lee, Kimoon,Oh, Min Suk,Mun, Sungx2010,jin,Lee, Kwang H.,Ha, Tae Woo,Kim, Jae Hoon,Park, Sangx2010,Hee Ko,Hwang, Chix2010,Sun,Lee, Byoung H.,Sung, Myung M.,Im, Seongil WILEY‐VCH Verlag 2010 Advanced Materials Vol.22 No.30
<P><B>Direct quantitative mapping of the density‐of‐states</B>, named the photo‐excited charge‐collection technique, for the interface traps at the n‐ZnO and/or p‐pentacene thin‐film transistor channel is implemented by using monochromatic photons which are carried by optical fibers and are probed onto thin‐film transistors. </P>
Hwang, Ihx2010,Yeon,Sun, Eunx2010,Sun,An, Ji Hak,Im, Hana,Lee, Sunx2010,Ho,Lee, Joox2010,Yong,Han, Pyungx2010,Lim,Koh, Jae‐,Young,Kim, Yangx2010,Hee Blackwell Publishing Ltd 2011 Journal of Neurochemistry Vol.118 No.5
<P> <I>J. Neurochem.</I> (2011) <B>118</B>, 855–863.</P><P><B>Abstract</B></P><P>Tissue plasminogen activator (tPA) is necessary for hippocampal long‐term potentiation. Synaptically released zinc also contributes to long‐term potentiation, especially in the hippocampal CA3 region. Using cortical cultures, we examined whether zinc increased the concentration and/or activity of tPA. Two hours after a 10‐min exposure to 300 μM zinc, expression of tPA and its substrate, plasminogen, were significantly increased, as was the proteolytic activity of tPA. In contrast, increasing extracellular or intracellular calcium levels did not affect the expression or secretion of tPA. Changing zinc influx or chelating intracellular zinc also failed to alter tPA/plasminogen induction by zinc, indicating that zinc acts extracellularly. Zinc‐mediated extracellular activation of matrix metalloproteinase (MMP) underlies the up‐regulation of brain‐derived neurotrophic factor (BDNF) and tropomyosin receptor kinase (Trk) signaling. Consistent with these findings, co‐treatment with a neutralizing antibody against BDNF or specific inhibitors of MMPs or Trk largely reversed tPA/plasminogen induction by zinc. Treatment of cortical cultures with <I>p</I>‐aminophenylmercuric acetate, an MMP activator, MMP‐2, or BDNF alone induced tPA/plasminogen expression. BDNF mRNA and protein expression was also increased by zinc and mediated by MMPs. Thus, an extracellular zinc‐dependent, MMP‐ and BDNF‐mediated synaptic mechanism may regulate the levels and activity of tPA.</P>