http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Ruth E. Propper,Alexis Grant,Ryan King,Stephen D. Christman 서울대학교 인지과학연구소 2019 Journal of Cognitive Science Vol.20 No.3
Individual differences in handedness in episodic memory have been demonstrated across a wide variety of stimuli and protocols, with inconsistent-handers (ICH) having superior memory relative to consistent-right-handers (CRH). The current study looks at the question of whether ICH also report better subjective memory. Prior work shows that objective and subjective memory performance are generally unrelated, but the current study found that ICH indeed report better subjective memory, as measured by the Cognitive Failures Questionnaire. Given evidence for associations between personality factors and subjective memory, the current study also looked at the Behavioral Inhibition Scale (BIS) and found (i) no handedness differences on the BIS, but (ii) a negative association between neuroticism and cognitive failures in CRH.
P. Le Cloirec,R. M. Lelacheur. J. D,R. F. Christman 慶星大學校 環境問題硏究所 1991 環境硏報 Vol.1 No.1
시료 용액이 pH=2일 경우 XAD-8 수지와 XAD-4 수지의 연속 흡착에 의해 염소처리된 용액중의 부식물질 분리와 논축의 좋은 결과값을 얻었다. 각 수지에 흡착된 물질의 추출은 NaOH 용액과 ether soxhlet 추출에 의하여 추출하였으며, 이 실험결과 칼럼에 존재하는 TOC와 A254, TOX의 회수율이 높았다. 전체 과정에 대한 물질 수지의 계산은 model compound나 염소 처리된 수용성 부식물질에 의하여 가능하였다.
Jung, Jae-Woo,Choi, Jae-Chol,Kim, Jae-Yeol,Park, In-Won,Choi, Byoung-Whui,Shin, Jong-Wook,Christman, John William The Korean Academy of Tuberculosis and Respiratory 2011 Tuberculosis and Respiratory Diseases Vol.70 No.2
Background: Macrophages are one of the most important inflammatory cells in innate immunity. PU.1 is a macrophage-specific transcription factor. Ubiquitins are the ultimate regulator of eukaryotic transcription. The ubiquitination process for PU.1 is unknown. This study investigated the lipopolysaccharide (LPS)-induced activation of PU.1 and its relation to ubiquitins in the macrophages. Methods: Raw264.7 cells, the primary cultured alveolar, pulmonary, and bone marrow derived macrophages were used. The Raw264.7 cells were treated with MG-132, $NH_4Cl$, lactacytin and LPS. Nitric oxide and prostaglandin D2 and E2 were measured. Immunoprecipitation and Western blots were used to check ubiquitination of PU.1. Results: The PU.1 ubiquitination increased after LPS ($1{\mu}g$/mL) treatment for 4 hours on Raw264.7 cells. The ubiquitination of PU.1 by LPS was increased by MG-132 or $NH_4Cl$ pretreatment. Two hours of LPS treatment on macrophages, PU.1 activation was not induced nor increased with the inhibition of proteasomes and/or lysosomes. The ubiquitination of PU.1 was increased in LPS-treated Raw264.7 cells at 12- and at 24 hours. LPS-treated cells increased nitric oxide production, which was diminished by MG-132 or $NH_4Cl$. LPS increased the production of $PGE_2$ in the alveolar and peritoneal macrophages of wild type mice; however, $PGE_2$ was blocked or diminished in Rac2 null mice. Pretreatment of lactacystin increased $PGE_2$, however it decreased the $PGD_2$ level in the macrophages derived from the bone marrow of B57/BL6 mice. Conclusion: LPS treatment in the macrophages ubiquitinates PU.1. Ubiquitination of PU.1 may be involved in synthesis of nitric oxide and prostaglandins.
Choi, Jun-Young,Kwun, Min Jung,Kim, Kyun Ha,Lyu, Ji Hyo,Han, Chang Woo,Jeong, Han-Sol,Ha, Ki-Tae,Jung, Hee-Jae,Lee, Beom-Joon,Sadikot, Ruxana T.,Christman, John W.,Jung, Sung-Ki,Joo, Myungsoo Hindawi Publishing Corporation 2012 Evidence-based Complementary and Alternative Medic Vol.2012 No.-
<P>The fruit hull of <I>Gleditsia sinensis</I> (FGS) has been prescribed as a traditional eastern Asian medicinal remedy for the treatment of various respiratory diseases, but the efficacy and underlying mechanisms remain poorly characterized. Here, we explored a potential usage of FGS for the treatment of acute lung injury (ALI), a highly fatal inflammatory lung disease that urgently needs effective therapeutics, and investigated a mechanism for the anti-inflammatory activity of FGS. Pretreatment of C57BL/6 mice with FGS significantly attenuated LPS-induced neutrophilic lung inflammation compared to sham-treated, inflamed mice. Reporter assays, semiquantitative RT-PCR, and Western blot analyses show that while not affecting NF-<I>κ</I>B, FGS activated Nrf2 and expressed Nrf2-regulated genes including GCLC, NQO-1, and HO-1 in RAW 264.7 cells. Furthermore, pretreatment of mice with FGS enhanced the expression of GCLC and HO-1 but suppressed that of proinflammatory cytokines in including TNF-<I>α</I> and IL-1<I>β</I> in the inflamed lungs. These results suggest that FGS effectively suppresses neutrophilic lung inflammation, which can be associated with, at least in part, FGS-activating anti-inflammatory factor Nrf2. Our results suggest that FGS can be developed as a therapeutic option for the treatment of ALI.</P>
( Jae Woo Jung ),( Jae Chol Choi ),( Jae Yeol Kim ),( In Won Park ),( Byoung Whui Choi ),( Jong Wook Shin ),( John William Christman ) 대한결핵 및 호흡기학회 2011 Tuberculosis and Respiratory Diseases Vol.70 No.2
Background: Macrophages are one of the most important inflammatory cells in innate immunity. PU.1 is a macrophage-specific transcription factor. Ubiquitins are the ultimate regulator of eukaryotic transcription. The ubiquitination process for PU.1 is unknown. This study investigated the lipopolysaccharide (LPS)-induced activation of PU.1 and its relation to ubiquitins in the macrophages. Methods: Raw264.7 cells, the primary cultured alveolar, pulmonary, and bone marrow derived macrophages were used. The Raw264.7 cells were treated with MG-132, NH4Cl, lactacytin and LPS. Nitric oxide and prostaglandin D2 and E2 were measured. Immunoprecipitation and Western blots were used to check ubiquitination of PU.1. Results: The PU.1 ubiquitination increased after LPS (1ug/mL) treatment for 4 hours on Raw264.7 cells. The ubiquitination of PU.1 by LPS was increased by MG-132 or NH4Cl pretreatment. Two hours of LPS treatment on macrophages, PU.1 activation was not induced nor increased with the inhibition of proteasomes and/or lysosomes. The ubiquitination of PU.1 was increased in LPS-treated Raw264.7 cells at 12- and at 24 hours. LPS-treated cells increased nitric oxide production, which was diminished by MG-132 or NH4Cl. LPS increased the production of PGE2 in the alveolar and peritoneal macrophages of wild type mice; however, PGE2 was blocked or diminished in Rac2 null mice. Pretreatment of lactacystin increased PGE2, however it decreased the PGD2 level in the macrophages derived from the bone marrow of B57/BL6 mice. Conclusion: LPS treatment in the macrophages ubiquitinates PU.1. Ubiquitination of PU.1 may be involved in synthesis of nitric oxide and prostaglandins.