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Optically Switchable Smart Windows with Integrated Photovoltaic Devices
Kwon, Hyun-Keun,Lee, Kyu-Tae,Hur, Kahyun,Moon, Sung Hwan,Quasim, Malik M.,Wilkinson, Timothy D.,Han, Ji-Young,Ko, Hyungduk,Han, Il-Ki,Park, Byoungnam,Min, Byoung Koun,Ju, Byeong-Kwon,Morris, Stephen M Wiley Blackwell (John Wiley Sons) 2015 Advanced energy materials Vol.5 No.3
The Failure of Redistributive Policy in the Progressive Era Urban Politics
( Byoung Kwon Sohn ) 한국세계지역학회 2006 世界地域硏究論叢 Vol.24 No.2
Although the Progressive reform movement in the United States during the early 20(th) century swept the whole nation, the concrete reform measures taken at various tiers of government were not the same. Depending on the regions and the government types, different social and political needs were paid attention to by different types of reformers. On the other hand, with respect to the levels of governments, different tiers of government addressed different types of social and political issues, and the nature of the reforms driven by those governments were also different. Differentiating the policy responses of various levels of government to social demands, this paper aims at explaining why redistributive policies could hardly be formulated and implemented at the local level of government during the Progressive era. This research question is based on the very premise that the reasons of absence, or failure, of redistributive policies at the municipal level should be different from those at the federal level. With this premise in mind, one of the main arguments of this paper is that the urban business-reform coalition, forged during this Progressive period on the basis of shared interest in efficiency, systematically edged out the redistributive type of policies, such as welfare policy, which were to entail, by nature, new tax imposition on upper-and middle-income groups, massive top-down resource transfer, and the possibility of political mismanagement and corruption. The business-reform coalition invented various institutional schemes such as commission and/or. manager governments to protect their interests, eluding the demands of redistributive nature from the mass.
A MELANOCYTE-SPECIFIC cDNA WHOSE EXPRESSION IS INDUCIBLE BY α-MSH AND IBMX
Kwon, Byoung S,Ruth Halaban,Kim, Gwan Shik,Seymour Pomerantz,Asifa K. Haq 대한구강생물학회 1987 International Journal of Oral Biology Vol.11 No.1
Normal human melanocyte의 λgtll cDNA library를 tyrosinase항체를 이용하여 검 색, 16 cDNA clones을 분리하였다. 이중 albino locus혹은 그인접부위에 존재하는 13clones는 tyrosinase gene으로 여겨지며 나머지 3clones는 상호간 상동성(homology)을 보이고 있으나 tyrosinase gene과 는 상이하였다. 이들 3clones의 대표적인 Pmel 17 - 1에 상응하는 mRNA(cRNA)는 사람과 mouse melanocyte에서만 특이하게 표현되며 크기는 약 2.4kb, 표현도는 melanin양과 비례 하였다. 여러종류의 melanoma cell을 αMSH 또는 IBMX로 자극시 Pmel 17 - 1의 cRNA표현은 증가되었으며 단일항체를 이용한 면역학적 실험으로 Pmel 17 - 1은 tyrosinase와 면역학적 동질성을 갖는 75KD glycoprotein을 합성함이 판명되었다. 또한 genomic DNA blot실험결과 Pmel 17 - 1 cDNA는 mouse albino locus 혹은 인접부위에 위치하지는 않으나 mouse와 사람에 single gene으로 존재하며 evolutionarily conserved gene임을 볼 수 있어 중요한 기능을 가지고 있을 것으로 사료된다.
Kwon, Byoung Soo,Park, Ji Hyun,Kim, Woo Sung,Song, Joon Seon,Choi, Chang-Min,Rho, Jin Kyung,Lee, Jae Cheol The Korean Academy of Tuberculosis and Respiratory 2017 Tuberculosis and Respiratory Diseases Vol.80 No.2
Background: Third-generation tyrosine kinase inhibitors of the epidermal growth factor receptor (EGFR-TKIs) have proved efficacious in treating non-small cell lung cancer (NSCLC) patients with acquired resistance resulting from the T790M mutation. However, since almost 50% patients with the acquired resistance do not harbor the T790M mutation, retreatment with first- or second-generation EGFR-TKIs may be a more viable therapeutic option. Here, we identified positive response predictors to retreatment, in patients who switched to a different EGFR-TKI, following initial treatment failure. Methods: This study retrospectively reviewed the medical records of 42 NSCLC patients with EGFR mutations, whose cancers had progressed following initial treatment with gefitinib or erlotinib, and who had switched to a different first-generation EGFR-TKI during subsequent retreatment. To identify high response rate predictors in the changed EGFR-TKI retreatment, we analyzed the relationship between clinical and demographic parameters, and positive clinical outcomes, following retreatment with EGFR-TKI. Results: Overall, 30 (71.4%) patients received gefitinib and 12 (28.6%) patients received erlotinib as their first EGFR-TKI treatment. Following retreatment with a different EGFR-TKI, the overall response and disease control rates were 21.4% and 64.3%, respectively. There was no significant association between their overall responses. The median progression-free survival (PFS) after retreatment was 2.0 months. However, PFS was significantly longer in patients whose time to progression was ${\geq}10months$ following initial EGFR-TKI treatment, who had a mutation of exon 19, or whose treatment interval was <90 days. Conclusion: In patients with acquired resistance to initial EGFR-TKI therapy, switched EGFR-TKI retreatment may be a salvage therapy for individuals possessing positive retreatment response predictors.
Byoung Kwon Yoo,최지웅,최민식,Mi Kyoung Ryu,박규환,Mi Jin Jeon,고광호 대한약학회 2005 Archives of Pharmacal Research Vol.28 No.8
Peroxynitrite is a potent neurotoxic molecule produced from a reaction between NO and superoxide and induces NO-mediated inflammation under neuropathological conditions. Previously, we reported that glucose deprivation induced ATP depletion and cell death in immunostimulated astrocytes, which was mainly due to peroxynitrite. In this study, the role of MAPKs (ERK1/2, p38MAPK, and JNK/SAPK) signal pathway in the SIN-1/glucose deprivation-induced death of astrocytes was examined. A combined treatment with glucose deprivation and 50 μM SIN-1, an endogenous peroxynitrite generator, rapidly and markedly increased the death in rat primary astrocytes. Also, SIN-1/glucose deprivation resulted in the activation of MAPKs, which was significantly blocked by the treatment with 20 μM MAPKs inhibitors (ERK1/2, PD98059; p38MAPK, SB203580; JNK/SAPK, SP600125). Interestingly, SIN-1/glucose deprivation caused the loss of intracellular ATP level, which was significantly reversed by MAPKs inhibitors. These results suggest that the activation of MAPKs plays an important role in SIN-1/glucose deprivation- induced cell death by regulating the intracellular ATP level.