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( Yu Ah Hong ),( Keum Jin Yang ),( So Young Jung ),( Yoon Kyung Chang ),( Cheol Whee Park ),( Chul Woo Yang ),( Suk Young Kim ),( Hyeon Seok Hwang ) 대한신장학회 2017 Kidney Research and Clinical Practice Vol.36 No.2
Background: Vitamin D is considered to exert a protective effect on various renal diseases but its underlying molecular mechanism remains poorly understood. This study aimed to determine whether paricalcitol attenuates inflammation and apoptosis during lipopolysaccharide (LPS)-induced renal proximal tubular cell injury through the prostaglandin E<sub>2</sub> (PGE<sub>2</sub>) receptor EP4. Methods: Human renal tubular epithelial (HK-2) cells were pretreated with paricalcitol (2 ng/mL) for 1 hour and exposed to LPS (1 μg/mL). The effects of paricalcitol pretreatment in relation to an EP4 blockade using AH-23848 or EP4 small interfering RNA (siRNA) were investigated. Results: The expression of cyclooxygenase-2, PGE<sub>2</sub>, and EP4 were significantly increased in LPS-exposed HK-2 cells treated with paricalcitol compared with cells exposed to LPS only. Paricalcitol prevented cell death induced by LPS exposure, and the cotreatment of AH-23848 or EP4 siRNA offset these cell-protective effects. The phosphorylation and nuclear translocation of p65 nuclear factor-kappaB (NF-κB) were decreased and the phosphorylation of Akt was increased in LPS-exposed cells with paricalcitol treatment. AH-23848 or EP4 siRNA inhibited the suppressive effects of paricalcitol on p65 NF-κB nuclear translocation and the activation of Akt. The production of proinflammatory cytokines and the number of terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling-positive cells were attenuated by paricalcitol in LPS exposed HK-2 cells. The cotreatment with an EP4 antagonist abolished these anti-inflammatory and antiapoptotic effects. Conclusion: EP4 plays a pivotal role in anti-inflammatory and antiapoptotic effects through Akt and NF-κB signaling after paricalcitol pretreatment in LPS-induced renal proximal tubule cell injury.
복지권으로서 교육권 보장을 위한 『장애인 등에 대한 특수교육법』
황정보,이선재,안병주,강경희,김청아 국립특수교육원 2007 특수교육연구 Vol.14 No.2
결핍에서 오는 필요의 개념은 장애인에게 복지권으로서 교육받을 권리를 가장 잘 말해주고 있다. 장애인은 신체적·인지적 손상으로 발생하는 기본적인 생존적 필요의 충족뿐만 아니라 동시에 교육기회 균등이나 개인차의 고려 등을 통해 무지로부터 벗어날 수 있는 보편적 필요가 충족되어야 함을 논의하였다. 장애인들에게 이러한 결핍에 따른 필요를 충족시켜 줄 이론적 근거가 롤즈(J. Rawls)의 정의론이라 할 수 있다. 정의론의 '차등의 원칙'에 따르면, 교육에 있어 비장애인과 장애인 중 먼저 최소 수혜자인 장애인의 교육복지를 우선하여 극대화할 필요성을 제시함으로써, 그들의 교육권 보장을 위한 이론적 근거에 대한 정당화를 논의하였다. 기존의 특수교육진흥법은 '국가가 교육할 권리'를 가지는 국가 주도적 교육이었다면, 「장애인 등에 대한 특수교육법」 제정은 수년간 장애인의 교육권 확보를 위해 애쓴 장애인 교육 주체들이 노력 끝에 '교육받을 권리'를 찾게 된 의미 있는 결실로 평가되어 진다. The concept of need which comes from lack represents well the right to education as welfare rights to individuals with disabilities. It is necessary to meet the universal need of individuals with disabilities such as an equal opportunity for education and the consideration for individual difference as well as their substantial need. The rationale which may satisfy the need associated with the lack can be J. Rawls's a Theory of Justice. The difference principle by Rawls presents the need of the educational welfare of individuals with disabilities(the least advantaged) to take precedence over that of the non-disabled and be maximized, it is considered that he created the rationale that makes secure their right to education. While established Special Education Promotion Law was national-driven education that state had to the education right, the enactment of 'the Special Education Law for the Individuals with Disabilities, etc.' can be a significant fruit which takes back 'the right to education by citizens' by the educational subjects of the individuals with disability who have taken pains to secure their right to education for years.
JUNG, JOOHEE,JEONG, SEONG-YUN,PARK, SEOK SOON,SHIN, SEOL HWA,JU, EUN JIN,CHOI, JINHYANG,PARK, JAESOOK,LEE, JAE HEE,KIM, INKI,SUH, YOUNG-AH,HWANG, JUNG JIN,KURODA, SHUN’ICHI,LEE, JUNG SHIN,SONG, SI YEO Spandidos Publications 2015 International journal of oncology Vol.46 No.3
<P>Radiotherapy (RT) is one of the major modalities for non???small cell lung cancer (NSCLC), but its efficacy is often compromised by cellular resistance caused by various mechanisms including the overexpression of epidermal growth factor receptor (EGFR). Although cis???diamminedichloroplatinum(???) (cisplatin, CDDP) has been well characterized as an effective radiosensitizer, its clinical application is limited by its severe nephrotoxic effects. In our current study, we developed a CDDP???incorporated liposome (LP) conjugated with EGFR antibodies (EGFR:LP???CDDP) and evaluated its potential to radiosensitize EGFR???overexpressing cells without exerting nephrotoxic effects. EGFR:LP???CDDP showed higher cytotoxicity than non???targeting liposomal CDDP (LP???CDDP) in the cells expressing EGFR in vitro. In an A549 cell???derived xenograft tumor mouse model, increased delays in tumor growth were observed in the mice treated with a combination of EGFR:LP???CDDP and radiation. Notably, the EGFR:LP???CDDP???treated animals showed no differences in body weight loss, survival rates of nephrotoxicity compared with untreated control mice. In contrast, the use of CDDP caused lower body weights and poorer survival outcomes accompanied by a significant level of nephrotoxicity [e.g., decreased kidney weight, increased blood urea nitrogen (BUN) and creatinine, and pathological change]. These findings suggest the feasibility of using EGFR:LP???CDDP to radiosensitize cells in a targeted manner without inducing nephrotoxic effects. This compound may therefore have clinical potential as part of a tailored chemoradiotherapy strategy.</P>
Hwang, Jung-Suk,Chung, Hye-Kyung,Bae, Eun-Kyong,Lee, Ah-Young,Ji, Hee-Jung,Park, Dong-Woon,Jung, Hwa-Jin,Cho, Chung-Won,Choi, Hyun-Ju,Lee, Dong-Seok,Lee, Kang-Ro,Youn, Hyun-Joo The Pharmaceutical Society of Korea 2003 Archives of Pharmacal Research Vol.26 No.4
A polysaccharide fraction, AIP1, purified from Artemisia iwayomogi was shown to have immunomodulating and anti-tumor activities in mice. In order to determine how the AIP1 fraction exhibits the immunomodulating activity, the effect of the fraction on the apoptosis of mouse spleen cells was investigated. Treatment of the mouse spleen cells with the AIP1 fraction resulted ,in the suppression of apoptotic death and an extension of cell survival in culture, indicating that the fraction might modulate the death of spleen cells. Treatment of the mice with the AIP1 fraction in vivo also resulted in less apoptosis of the spleen cells, which indicates the physiological relevance of the anti-apoptosis effect of the fraction in vitro. A mouse gene array was used to determine the profile of the gene expression change showing a pattern of up- and down-regulated genes by the AIP1 treatment. This study provides preliminary information regarding the immunomodulatory mechanism of the AIP1 fraction.
Jung Ah Yoon,Hee Jung Kang,Soo Jin Hwang,Hyunjung Lim,Haengseok Song 한국발생생물학회 2011 한국발생생물학회 학술발표대회 Vol.30 No.-
In particular, maternal prostacyclin (PGI2) is critical for embryo implantation and the action of PGI2 is not mediated via its G protein-coupled membrane receptor, IP, but its nuclear receptor, peroxisome proliferator-activated receptor δ (PPARδ). Recently, several studies have shown that PGI2 enhances blastocyst development and/or hatching rate in vitro, and subsequently implantation and live birth rates in mice. However, the mechanism by which PGI2 improves preimplantation embryo development in vitro remains unclear. Using molecular, pharmacologic and genetic approaches, we show that PGI2-induced PPARδ activation accelerates blastocyst hatching in mice. mRNAs for PPARδ, RXRs (heterodimeric partners of PPARδ) and PGI2 synthase are temporally induced after zygotic gene activation and their expression reaches maximum levels at the blastocyst stage, suggesting that functional complex of PPARδ can be formed in the blastocyst. Carbaprostacyclin (cPGI, a stable analogue of PGI2) and GW501516 (a PPARδ selective agonist) significantly accelerated blastocyst hatching but did not increase total cell number of cultured blastocysts. Whereas U51605 (a PGIS inhibitor) interfered with blastocyst hatching, GW501516 restored U51605-induced retarded hatching. In contrast to improvement of blastocyst hatching by PPARδ agonists, PPAR antagonists significantly inhibited blastocyst hatching. Furthermore, deletion of PPARδ at early stages of preimplantation mouse embryos caused delay of blastocyst hatching, but did not impair blastocyst development. Taken together, PGI2-induced PPARδ activation accelerates blastocyst hatching in mice.