http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Poster Session 2 : Characterization of neural cell types expressing peroxiredoxins in mouse brain
( Mei Hua Jin ),( Young Ho Lee ),( Jin Man Kim ),( Hu Nan Sun ),( Eon Yi Moon ),( Min Ho Shong ),( Sun Uk Kim ),( Sang Ho Lee ),( Tae Hoon Lee ),( Dae Yeul Yu ),( Dong Seok Lee ) 한국생화학분자생물학회 (구 한국생화학회) 2005 생화학분자생물학회 춘계학술발표논문집 Vol.2005 No.-
Jin, Mei Hua,Nam, Ah-Rong,Park, Ji Eun,Bang, Ju-Hee,Bang, Yung-Jue,Oh, Do-Youn American Association for Cancer Research 2017 Molecular cancer therapeutics Vol.16 No.6
<P>Trastuzumab in combination with chemotherapy is the standard of care for patients with human epidermal growth factor receptor 2 (HER2)-positive breast and gastric cancers. Several resistance mechanisms against anti-HER2 therapy have been proposed. Src activation has been suggested to be responsible for the resistance of HER2-positive breast cancer. In our study, we generated four trastuzumab-resistant (HR) cancer cell lines from HER2-amplified gastric and biliary tract cancer cell lines (SNU-216, NCI-N87, SNU-2670, and SNU-2773). Elevated Src phosphorylation was detected in SNU2670HR and NCI-N87HR cell lines, but not in SNU216HR or SNU2773HR cell lines. In SNU216HR and SNU2773HR cell lines, phospho-FAK (focal adhesion kinase) was elevated. Bosutinib as a Src inhibitor suppressed growth, cell-cycle progression, and migration in both parental and HR cell lines. Specifically, Src interacted with FAK to affect downstream molecules such as AKT, ERK, and STAT3. Bosutinib showed more potent antitumor effects in Src-activated HR cell lines than parental cell lines. Taken together, this study suggests that Src inhibition may be an effective measure to overcome trastuzumab resistance in HER2-positive cancer. (C) 2017 AACR.</P>
Hua, Jin Mei,Moon, Tae-Chul,Hong, Tae-Gyun,Park, Kyong-Min,Son, Jong-Keun,Chang, Hyeun-Wook 대한약학회 2008 Archives of Pharmacal Research Vol.31 No.5
5-Methoxy-8-(2-hydroxy-3-buthoxy-3-methylbutyloxy)-psoralen (MP) is a medicinal herbal product isolated from Angelica dahurica that inhibits the cyclooxygenase-2 (COX-2)-dependent phase of prostaglandin $D_2 (PGD_2)$ generation in bone marrow-derived mast cells ($IC_{50}$, $23.5\;{\mu}M$). Western blotting with specific anti-COX-2 antibodies showed that the decrease in $PGD_2$ production was accompanied by a decrease in COX-2 protein levels. In addition, this compound consistently inhibited the production of leukotriene $C_4$ in a dose dependent manner, ($IC_{50}$, $2.5\;{\mu}M$). These results demonstrate that MP inhibits both cyclooxygenase-2 and 5- lipoxygenase activity. Furthermore, this compound also inhibited the degranulation reaction $(IC_{50}$, $4.1\;{\mu}M$). Therefore, this compound might provide a basis for novel anti-inflammatory drug development.
Jin, Mei Hua,Hong, Chang Hee,Lee, Hye Young,Kang, Hyo Jin,Han, Sang Won Wiley Subscription Services, Inc., A Wiley Company 2010 Environmental toxicology Vol.25 No.1
<P>2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a potent endocrine disruptor compound and induces multiple organ dysfunctions. The effect of TCDD exposure both in adults and in utero has been well established. However, little is known about the effects of TCDD acquired through mother's milk on the development of the male reproductive system. The aim of this study was to investigate the effects and mechanisms of TCDD from lactational exposure. TCDD (1 μg/kg) was administered to C57BL/6 mouse mothers for 4 days from the day of delivery. On postnatal day 30 (PND 30) and postnatal day 60 (PND 60), body weight, body length, and anogenital distance (AGD) of male offspring were measured. The weights of the testes and epididymides were also measured. Epididymides were used for sperm counts, and testes were used to measure the activity of antioxidant enzymes (SOD, CAT, GPX, GR), the parameters of oxidative stress (hydrogen peroxide, MDA), and testosterone. In addition, expression of p53 and the proapoptotic protein, Bax, were analyzed by Western blot. TCDD exposure decreased body weight, body length, and AGD in both PND 30 and PND 60 groups compared with the control group. The activity of all antioxidant enzymes at PND 60 was decreased after TCDD treatment. TCDD treatment decreased testicular testosterone levels in both the PND 30 and PND 60 groups. The expression of p53 and Bax were also upregulated by TCDD and did not return to normal levels by PND 60. These data suggest that TCDD affects development of male offspring when the mother is exposed to TCDD during lactation. In addition, oxidative stress is a major mediator of TCDD-induced adverse effects, and p53 may play an important role in this mechanism. © 2008 Wiley Periodicals, Inc. Environ Toxicol, 2010.</P>