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폐결핵의 조기진단에 있어서 이중중합효소연쇄반응법의 유용성
조성란,최영진,김용훈,이철세,김영창,김휘준 순천향의학연구소 1998 Journal of Soonchunhyang Medical Science Vol.4 No.2
Background: Pulmonary tuberculosis is a great public health problem in Korea. Early detection of Mycobacterium tuberculosis (M. tuberculosis) in clinical samples becomes more and more important in the control of tuberculosis. Recently, molecular methods have been applied to early detection of M. tuberculosis. Methods: To elucidate the effectiveness of nested polymerase chain reaction (PCR) in early diagnosis of pulmonary tuberculosis, we peformed Acid-fast bacilli (AFB) stain, AFB culture, and nested PCR on 84 sputa. Results: 8 (9.5%) specimens were positive by AFB stain, 17 (20.2%) by AFB culture, and 15 (17.9%) by nested PCR. Using AFB culture as standard method, the sensitivity of AFB stain and nested PCR was 47.1% and 82.4%, respectively. The specificity of AFB stain and nested PCR was 100% and 98.5%, respectively. Conclusions: Nested PCR was more sensitive than AFB stain and had shorter processing time(24-48hrs) than AFB culture. So it may be effective to use nested PCR in order to detect M. tuberculosis when AFB smear Is negative.
Lee, Tae-Kyeong,Chen, Bai Hui,Lee, Jae-Chul,Shin, Myoung Cheol,Cho, Jun Hwi,Lee, Hyang-Ah,Choi, Jung Hoon,Hwang, In Koo,Kang, Il Jun,Ahn, Ji Hyeon,Park, Joon Ha,Choi, Soo Young,Won, Moo-Ho SPANDIDOS PUBLICATIONS 2018 MOLECULAR MEDICINE REPORTS Vol.17 No.6
<P>Insulin-like growth factor-I (IGF-I) is a multifunctional protein present in the central nervous system. A number of previous studies have revealed alterations in IGF-I and its receptor (IGF-IR) expression in various regions of the brain. However, there are few reports on age-dependent alterations in IGF-I and IGF-IR expressions in the olfactory bulb, which contains the secondary neurons of the olfactory system. The present study examined the cellular morphology in the olfactory bulb by using cresyl violet (CV) staining at postnatal month (PM) 3 in the young group, PM 6 in the adult group and PM 24 in the aged group in gerbils. In addition, detailed examinations were performed of the protein levels and immunoreactivities of IGF-I and IGF-IR in the olfactory bulb in each group. There were no significant changes in the cellular morphology between the three groups. The protein levels and immunoreactivities of the IGF-I and IGF-IR were the highest in the young group and they decreased with age. He protein levels and immunoreactivities of the IGF-I and IGF-IR were the lowest in the aged group. In brief, our results indicate that IGF-I and IGF-IR expressions are strong in young olfactory bulbs and significantly reduced in aged olfactory bulbs. In conclusion, subsequent decreases in IGF-I and IGF-IR expression with age may be associated with olfactory decline. Further studies are required to investigate the roles of IFG-I and IGF-IR in disorders of the olfactory system.</P>
Lee, Hyang-Ah,Park, Joon Ha,Kim, Dae Won,Lee, Choong-Hyun,Hwang, In Koo,Kim, Hyeyoung,Shin, Myoung Cheol,Cho, Jun Hwi,Lee, Jae-Chul,Noh, Yoohun,Kim, Sung-Su,Won, Moo-Ho,Ahn, Ji Hyeon SPANDIDOS PUBLICATIONS 2018 MOLECULAR MEDICINE REPORTS Vol.17 No.3
<P>Oligodendrocytes are myelin-forming cells in the central nervous system. Research into the effects of aging on oligodendrocyte protein expression remains limited. The present study aimed to determine the alterations in oligodendrocyte-specific protein (OSP) expression in the gerbil hippocampus at 1, 2, 3, 4, 6 and 24 months of age with western blot and immunohistochemistry analyses. OSP expression levels in the hippocampus were highest at 6 months of age. OSP immunoreactivity was identified in numerous cell bodies at 1 month, although the number of OSP immunoreactive cells was different according to hippocampal subregion. The number of OSP immunoreactive cells significantly decreased at 2 months and, thereafter, numbers decreased gradually. The detection of OSP immunoreactive fibers was negligible in all layers in the hippocampal subregions until 4 months. OSP immunoreactive fibers were abundant at 6 and 24 months, although the fiber distribution patterns in the CA1-3 areas and dentate gyrus were different. The results demonstrated that OSP expression in the gerbil hippocampus was age-dependent. The detection of OSP immunoreactive cell bodies and fibers was significantly different according to the layers of hippocampal subregions, indicating that myelination may be continuously altered in the hippocampus during normal aging.</P>
Lee, Seung-Bin,Shin, Ji-Sun,Han, Hee-Soo,Lee, Hwi-Ho,Park, Jong Cheol,Lee, Kyung-Tae Elsevier 2018 Chemico-biological interactions Vol.284 No.-
<P><B>Abstract</B></P> <P>Kaempferol 7-<I>O</I>-<I>β</I>-D-glucoside (KPG), a natural flavonol isolated from <I>Cudrania tricuspidata</I>, has been reported to exert anti-cancer effects; however, its anti-inflammatory effects have not yet been reported. In this study, we demonstrate the suppressive effect of KPG on the production of nitric oxide (NO), prostaglandin E<SUB>2</SUB> (PGE<SUB>2</SUB>), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) in lipopolysaccharide (LPS)-induced RAW 264.7 macrophages and mouse bone marrow-derived macrophages. KPG downregulated the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) at the protein level and iNOS, COX-2, TNF-α, IL-1β, and IL-6 at the mRNA level in LPS-treated RAW 264.7 macrophages. Moreover, we elucidated the underlying molecular mechanism, demonstrating that KPG attenuated LPS-induced nuclear factor-κB (NF-κB) activation by decreasing p65 nuclear translocation, inhibiting κBα (IκBα) phosphorylation/degradation and IκB kinaseα/β (IKKα/β) phosphorylation. KPG additionally reduced LPS-induced activator protein-1 (AP-1) activity by inhibiting c-Fos expression in the nucleus, though c-Jun was not affected. Furthermore, we revealed that KPG significantly abrogated the LPS-induced phosphorylation of signal transducer and activator of transcription (STAT) 1 (Ser 727, Tyr 701) and STAT3 (Tyr 705) through inhibiting the phosphorylation of Janus kinase (JAK) 1 and JAK2, its upstream activating proteins. Taken together, our data suggest that KPG induces anti-inflammatory activity by blocking NF-κB, AP-1, and JAK-STAT signaling pathways in LPS-treated RAW 264.7 macrophages, thus suppressing inflammatory mediators.</P> <P><B>Highlights</B></P> <P> <UL> <LI> KPG reduces NO and PGE<SUB>2</SUB> production and the expression of iNOS and COX-2. </LI> <LI> KPG attenuates cytokine (TNF-α, IL-1β, and IL-6) production and expression. </LI> <LI> KPG inhibits the activation of AP-1 and NF-κB subunits. </LI> <LI> KPG elicits anti-inflammatory effects via suppressing JAK/STAT and NF-κB/ERK MAPKs. </LI> </UL> </P>
Lee, Jae-Chul,Kim, Yang Hee,Lee, Tae-Kyeong,Kim, In Hye,Cho, Jeong Hwi,Cho, Geum-Sil,Shin, Bich-Na,Park, Joon Ha,Ahn, Ji Hyeon,Shin, Myoung Cheol,Cho, Jun Hwi,Kang, Il Jun,Won, Moo-Ho,Seo, Jeong Yeol SPANDIDOS PUBLICATIONS 2017 MOLECULAR MEDICINE REPORTS Vol.16 No.2
<P>Ischemic preconditioning (IPC) is induced by exposure to brief durations of transient ischemia, which results in ischemic tolerance to a subsequent longer or lethal period of ischemia. In the present study, the effects of IPC (2 min of transient cerebral ischemia) were examined on immunoreactivity of platelet-derived growth factor (PDGF)-BB and on neuroprotection in the gerbil hippocampal CA1 region following lethal transient cerebral ischemia (LTCI; 5 min of transient cerebral ischemia). IPC was subjected to a 2-min sublethal ischemia and a LTCI was given 5-min transient ischemia. The animals in all of the groups were given recovery times of 1, 2 and 5 days and change in PDGF-BB immunoreactivity was examined as was the neuronal damage/death in the hippocampus induced by LTCI. LTCI induced a significant loss of pyramidal neurons in the hippocampal CA1 region 5 days after LTCI, and significantly decreased PDGF-BB immunoreactivity in the CA1 pyramidal neurons from day 1 after LTCI. Conversely, IPC effectively protected the CA1 pyramidal neurons from LTCI and increased PDGF-BB immunoreactivity in the CA1 pyramidal neurons post-LTCI. In conclusion, the results demonstrated that LTCI significantly altered PDGF-BB immunoreactivity in pyramidal neurons in the hippocampal CA1 region, whereas IPC increased the immunoreactivity. These findings indicated that PDGF-BB may be associated with IPC-mediated neuroprotection.</P>
Lee, Jae-Chul,Park, Chan Woo,Shin, Myoung Cheol,Cho, Jun Hwi,Lee, Hyang-Ah,Kim, Young-Myeong,Park, Joon Ha,Ahn, Ji Hyeon,Cho, Jeong Hwi,Tae, Hyun-Jin,Hwang, In Koo,Lee, Tae-Kyeong,Won, Moo-Ho,Kang, Il Elsevier 2018 Neurochemistry International Vol.118 No.-
<P><B>Abstract</B></P> <P>Tumor Necrosis Factor-α (TNF-α) is a proinflammatory cytokine implicated in neuronal damage in response to cerebral ischemia. Ischemic preconditioning (IPC) provides neuroprotection against a subsequent severer or longer transient ischemia by ischemic tolerance. Here, we focused on the role of TNF-α in IPC-mediated neuroprotection against neuronal death following a subsequent longer transient cerebral ischemia (TCI). Gerbils used in this study were randomly assigned to eight groups; sham group, TCI operated group, IPC plus (+) sham group, IPC + TCI operated group, sham + etanercept (an inhibitor of TNF-a) group, TCI + etanercept group, IPC + sham + etanercept group, and IPC + TCI + etanercept group. IPC was induced by a 2-min sublethal transient ischemia, which was operated 1 day prior to a longer (5-min) TCI. A significant death of neurons was found in the stratum pyramidale (SP) in the CA1 area (CA1) of the hippocampus 5 days after TCI; however, IPC protected SP neurons from TCI. We found that TNF-α immunoreactivity was significantly increased in CA1 pyramidal neurons in the TCI and IPC + TCI groups compared to the sham group. TNF-R1 expression in CA1 pyramidal neurons of the TCI group was also increased 1 and 2 days after TCI; however, in the IPC + TCI group, TNF-R1 expression was significantly lower than that in the TCI group. On the other hand, we did not detect TNF-R2 immunoreactivity in CA1 pyramidal neurons 1 and 2 days after TCI; meanwhile, in the IPC + TCI group, TNF-R2 expression was significantly increased compared to TNF-R2 expression at 1 and 2 days after TCI. In addition, in this group, TNF-R2 was newly expressed in pericytes, which are important cells in the blood brain barrier, from 1 day after TCI. When we treated etanercept to the IPC + TCI group, IPC-induced neuroprotection was significantly weakened. In brief, this study indicates that IPC confers neuroprotection against TCI by TNF-α signaling through TNF-R2 and suggests that the enhancement of TNF-R2 expression by IPC may be a legitimate strategy for a therapeutic intervention of TCI.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Ischemic preconditioning (IPC) protects CA1 pyramidal neurons from ischemic damage. </LI> <LI> IPC attenuates TNF-α and TNF-R1 expressions in ischemic CA1 pyramidal neurons. </LI> <LI> IPC increases TNF-R2 expressions in pericytes in CA1 area after ischemic insult. </LI> <LI> IPC-mediated neuroprotective effect is reversed by etanercept (an inhibitor of TNF-a) treatment. </LI> </UL> </P>
Effects of Proto-oncogene Protein DEK on PCAF Localization
Lee, In-Seon,Lee, Seok-Cheol,Lee, Jae-Hwi,Seo, Sang-Beom The Korean Society of Applied Pharmacology 2007 Biomolecules & Therapeutics(구 응용약물학회지) Vol. No.
The proto-oncogene protein DEK is a nuclear binding phosphoprotein that has been associated with various human diseases including leukemia. Histone acetylation is an important post-translational modification which plays important role in transcriptional regulation. Auto-acetylation of histone acetyltransferase PCAF results in increment of its HAT activity and facilitation of its nuclear localization. In this study, we report that DEK inhibits PCAF auto-acetylation through direct interaction. The C-terminal acidic domains of DEK are responsible for the interaction with PCAF. Using confocal microscopy, we have shown that nuclear localization of PCAF is severely inhibited by DEK. Taken together, our results suggest that DEK may be involved in various cellular signal transduction pathways accommodated by PCAF through the regulation of PCAF auto-acetylation.