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Park, Jinbong,Jeon, Yong-Deok,Kim, Hye-Lin,Lim, Hara,Jung, Yunu,Youn, Dong-Hyun,Jeong, Mi-Young,Kim, Hyun-Ju,Kim, Sung-Hoon,Kim, Su-Jin,Hong, Seung-Heon,Um, Jae-Young Hindawi Publishing Corporation 2013 Evidence-based Complementary and Alternative Medic Vol.2013 No.-
<P>Obesity has become a major health threat in developed countries. However, current medications for obesity are limited because of their adverse effects. Interest in natural products for the treatment of obesity is thus rapidly growing. Korean Medicine (KM) is characterized by the wide use of herbal formulas. However, the combination rule of herbal formulas in KM lacks experimental evidence. According to <I>Shennong's Classic of Materia Medica</I>, the earliest book of herbal medicine, <I>Veratrum nigrum</I> (VN) has antagonistic features against <I>Panax ginseng</I> (PG), and the PG-VN pair is strictly forbidden. In this study, we have shown the effects of PG, VN, and their combination on obesity in high-fat (HF) diet-induced obese mice and in 3T3-L1 cells. PG, VN, and PG-VN combination significantly reduced weight gain and the fat pad weight in HF diet-induced obese mice. They also significantly decreased lipid accumulation and the expressions of two major adipogenesis factors, PPAR<I><I>γ</I></I> and C/EBP<I><I>α</I></I>, in 3T3-L1 cells. In addition, the PG-VN combination had synergistic effects compared with the mixture of extracts of PG and VN on inhibition of PPAR<I><I>γ</I></I> and C/EBP<I><I>α</I></I> expressions at lower doses. These results indicate a new potential anti-obese pharmacotherapy and also provide scientific evidence supporting the usage of herbal combinations instead of mixtures in KM.</P>
( Chul Ju Hwang ),( Dong Young Choi ),( Yu Yeon Jung ),( Young Jung Lee ),( Jae Suk Yun ),( Ki Wan Oh ),( Sang Bae Han ),( Seikwan Oh ),( Mi Hee Park ),( Jin Tae Hong ) 영남대학교 약품개발연구소 2016 영남대학교 약품개발연구소 연구업적집 Vol.26 No.-
Approximately, 7-10 million people in the world suffer from Parkinson``s disease (PO), Recently, increasing evi-dence has suggested the protective effect of estrogens against nigrostriatal dopaminergic damage in PD. In this study, we investigated whether estrogen affects l-methyl-4-phenyl-l,2,3,6-tetrahydropyridine (MPTP)-induced behavioral impairment in estrogen receptor alpha (ERa)-deficient mice. MPTP (15 mg/kg, four times with l.5-h interval)-induced dopaminergic neurodegeneration was evaluated in ERα wild-type (WT) and knockout (KO) mice. Larger dopamine depletion, behavioral impairments (Rotarod test, Pole test, and Gait test), activation of mi-croglia and astrocytes, and neurointlammation after MPTP injection were observed in ERα KO mice compared to those in WT mice.Immunostaining for tyrosine hydroxylase (TH) after MPTP injection showed fewerTH-positive neurons in ERα KO mice than WT mice. Levels of dopamine and 3,4-<lihydroxyphenylacetic acid (OOPAC, metab-olite of dopamine) were also lowered in ERα KO mice after MPTP injection. Interestingly, a higher immunoreac-tivity for monoamine oxidase (MAO) B was found in the substantia nigra and striatum of ERα KO mice after MPTP injection. We also found an increased activation of p38 kinase (which positively regulates MAO B expression) in ERα KO mice. In vitro estrogen treatment inhibited neuroinflammation in l-methyl-4-phenyl pyridium (MPP +)-treated cultured astrocyte cells; however, these inhibitory effects were removed by p38 inhibitor. These results indicate that ERα might be important for dopaminergic neuronal survival through inhibition of p38 pathway.
The Tooth as a Model for Organ Development
Jung, Han-Sung,Kim, Jae-Young,Kim, Eun-Jeung,Song, Soo-Jin,Park, Mi-Jin Korean Academy of Oral Biology and the UCLA Dental 2001 International Journal of Oral Biology Vol.26 No.2
To investigate tooth organ development, it very important to understand how the epithelial and mesenchymal cells accommodate the growing embryos. Embryonic induction is a process by which the fate of the responsive tissues is altered following tissue interactions. It is a gradual process composed of many steps. Recently, many studies have shown the mutual interactions, as well as antagonistic systems, of several genes expressed in the process of tooth bud development. Also, craniofacial abnormalities resulting from defective genes also have been reported in many cases. We would like to revisit how muchwe have learned by studying tooth bud development in embryogenesis and propose further possible further possible studies in which we may move forward in our knowledge and understanding of embryogenesis.
Novel Transcription Coactivator Complex Containing Activating Signal Cointegrator 1
Jung, Dong-Ju,Sung, Hee-Sook,Goo, Young-Wha,Lee, Hyun Mi,Park, Ok Ku,Jung, Sung-Yun,Lim, Janghoo,Kim, Han-Jong,Lee, Soo-Kyung,Kim, Tae Sung,Lee, Jae Woon,Lee, Young Chul 전남대학교 약품개발연구소 2002 약품개발연구지 Vol.11 No.-
Human activating signal cointegrator 1 (hASC-1) was originally isolated as a transcriptional coactivator of nuclear receptors. Here we report that ASC-1 exists as a steady-state complex associated with three polypeptides, P200, P100, and P50, in HeLa neclei; stimulates transactivation by serum response factor (SRF), activating protein 1 (AP-1), and nuclear factor κB (NF-κB) through direct binding to SRF, c-Jun, p50, and p65; and relieves the previously described transrepression between nuclear receptors and either AP-1 or NF-κB. Interestingly, ectopic expression of Caenorhabditis elegans ASC-1 (ceASC-1), an ASC-1 homologue that binds P200 and P100, like hASC-1, while weakly interacting only with p65, in HeLa cells appears to replace endogenous hASC-1 from the hASC-1 complex and exerts potent dominant-negative effects on AP-1, NF-κB, and SRF transactivation. In addition, neutralization of endogenous P50 by single-cell microinjection of a P50 antibody inhibits AP-1 transactivation; the inhibition is relieved by coexpression of wild-type P50, but not of P50△KH, a mutant form that does not interact with P200. Overall, these results suggest that the endogenous hASC-1 complex appears to play an essential role in AP-1, SRF, and NF-κB transactivation and to mediate the transrepression between nuclear receptors and either AP-1 or NF-κB in vivo.
( Sang Youn Hwang ),( Seon-mi Lee ),( Jung Woo Im ),( Ki Jeong Jeon ),( Cheol-won Choi ),( Kyung-su Kim ),( Wan Jeon ) 대한간암학회 2019 대한간암학회지 Vol.19 No.1
Sorafenib is a well-known approved systemic therapeutic agent used in patients with advanced hepatocellular carcinoma (HCC). Regorafenib and nivolumab are approved as second-line therapeutic drugs in patients showing disease progression after sorafenib therapy. However, there is no established third- or fourth-line therapy in patients with progression after regorafenib or nivolumab treatment. Recently, the combination of tyrosine kinase inhibitors (TKIs) and immune checkpoint inhibitors (ICPIs) has been attempted as a firstline treatment strategy in advanced HCC patients based on the hypothesis that combination therapy may overcome resistance in ICPI monotherapy. On the basis of this suggestion, we herein describe the case of an HCC patient demonstrating macrovascular invasion, whereby partial remission was achieved via the combination of sorafenib and nivolumab following disease progression after nivolumab therapy. Further studies on the combination of TKIs and ICPIs are necessary to determine ways to manage HCC patients showing disease progression after ICPI therapy. (J Liver Cancer 2019;19:74-78)