http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
P247 : A study on use of complementary and alternative medicine for acne
( Sook Kyung Lee ),( Taek Geun Lee ),( Hyun Hwang Bo ),( Tae Gwang Kwon ),( Se Won Jung ),( Young Seok Lee ) 대한피부과학회 2013 대한피부과학회 학술발표대회집 Vol.65 No.2
Background: Complementary and alternative medicine (CAM) is any practice that has healing effects, but is not based on evidence demonstrated by scientific method. Recently, CAM has been used in various diseases including acne. However, there have been no studies on CAM for acne in Korea. Objectives: The purpose of this study was to analyze the use of CAM in acne patients. Methods: A total of 159 patients with acne were enrolled on the study, and filled out a questionnaire about use of CAM. Results: Overall 87.4% (139/159) of the patients reported the previous or current use of at least one more type of CAM. Cosmetics for acne (100, 22.9%) was most frequently used, followed by diet therapy (81, 18.5%), spa and bath therapies (77, 17.6%), health food supplement (67, 15.3%), skin care shop (64, 14.6%), oriental medicine (38, 8.7%), and aromatherapy (9, 2.1%). The most common reason for using CAM was ``wish to try everything`` (28.6%), and the most common source of information was internet (40.5%). The therapeutic effect of CAM was best with diet therapy (32.1%). The most common side effect of CAM was aggravation of symptoms. The most common monthly cost for CAM was between 50,000 and 100,000 won/person. Conclusion: As our results, we can predict that the use of various types of CAM for acne will become more common. Therefore, dermatologists need to study about benefits and adverse effects of CAM for acne.
Hwang, Joo-Yeon,Lee, Seung-Hun,Go, Min-Jin,Kim, Beom-Jun,Kim, Young-Jin,Kim, Dong-Joon,Oh, Ji-Hee,Koo, Hee-Jo,Cha, My-Jung,Lee, Min-Hye,Yun, Ji-Young,Yoo, Hye-Sook,Kang, Young-Ah,Oh, Ki-Won,Kang, Moo- Korea Genome Organization 2011 Genomics & informatics Vol.9 No.2
Osteoporotic fracture (OF), along with bone mineral density (BMD), is an important diagnostic parameter and a clinical predictive risk factor in the assessment of osteoporosis in the elderly population. However, a genome-wide association study (GWAS) on OF has not yet been clarified sufficiently. To identify OF-associated genetic variants and candidate genes, we conducted a GWAS in a population-based cohort (Korean Association Resource [KARE], n=1,427 [case: 288 and control: 1139]) and performed a de novo replication study in hospital-based individuals (Asan and Catholic Medical Center [ACMC], n=1,082 [case: 272 and control: 810]). In a combined meta-analysis, a newly identified genetic locus in an intergenic region at 10p11.2 (near genes FZD8 and ANKRD30A ) showed the most significant association (odd ratio [OR] = 2.00, 95% confidence interval [CI] = 1.47~2.74, p=$1.27{\times}10^{-6}$) in the same direction. We provide the first evidence for a common genetic variant influencing OF and genetic information for further investigation in bone metabolism.
Hepatic Iron, Serum Ferritin, <i>HFE</i> Mutation, and Hepatic Fibrosis in Chronic Hepatitis C
Won, Ji-Eon,Jeong, Sook-Hyang,Chung, Jae Il,Lee, Ji Hye,Hwang, Sung Ho,Kim, Jin-Wook,Lee, Sang Hyub,Kim, Nayoung,Park, Young Soo,Lee, Dong Ho,Kim, Haeryoung S. Karger AG 2009 Intervirology Vol.52 No.5
<P><I>Objectives:</I> We studied the status of hepatic iron deposition and its relationship with blood iron indices, liver histology, and <I>HFE </I>gene mutations in Korean patients with chronic hepatitis C (CH-C). <I>Methods:</I> 105 patients with CH-C who underwent pretreatment liver biopsy were consecutively enrolled. The hepatic iron deposition, histological activity and fibrosis were assessed by appropriate pathological scoring systems, clinical data including serum iron indices, and <I>HFE</I> gene mutation. <I>Results:</I> Hepatic iron deposition was found in 37 patients (35%), which was not significantly associated with degree of hepatic fibrosis or steatosis. The serum ferritin level was elevated in 27% of the patients and was an independent factor associated with hepatic iron deposition by logistic regression; however, it was not significantly associated with hepatic fibrosis either. Only H63D heterozygote was found in 6 out of 48 patients (12.5%), which was not different from the prevalence of H63D mutation in the Korean population (8.5%). <I>Conclusions:</I> Hepatic iron deposition was uncommon and mild in Korean CH-C. Neither hepatic iron deposition nor serum ferritin were significantly related to the severity of hepatic fibrosis, which does not support the significant role of iron in the progression of hepatic fibrosis.</P><P>Copyright © 2009 S. Karger AG, Basel</P>
Won, Hee Yeon,Jang, Eun Jung,Lee, Kihyun,Oh, Sera,Kim, Hyo Kyung,Woo, Hyun Ae,Kang, Sang Won,Yu, Dae-Yeul,Rhee, Sue-Goo,Hwang, Eun Sook The American Association of Immunologists, Inc. 2013 JOURNAL OF IMMUNOLOGY Vol.191 No.8
<P>Peroxiredoxin (Prx) II is an intracellular antioxidant molecule that eliminates hydrogen peroxide, employing a high substrate-binding affinity. PrxII deficiency increases the levels of intracellular reactive oxygen species in many types of cells, which may increase reactive oxygen species–mediated inflammation. In this study, we investigated the susceptibility of PrxII knockout (KO) mice to experimentally induced colitis and the effects of PrxII on the immune system. Wild-type mice displayed pronounced weight loss, high mortality, and colon shortening after dextran sulfate sodium administration, whereas colonic inflammation was significantly attenuated in PrxII KO mice. Although macrophages were hyperactivated in PrxII KO mice, the amount of IFN-γ and IL-17 produced by CD4<SUP>+</SUP> T cells was substantially reduced. Foxp3<SUP>+</SUP> regulatory T (Treg) cells were elevated, and Foxp3 protein expression was increased in the absence of PrxII in vitro and in vivo. Restoration of PrxII into KO cells suppressed the increased Foxp3 expression. Interestingly, endogenous PrxII was inactivated through hyperoxidation during Treg cell development. Furthermore, PrxII deficiency stabilized FoxO1 expression by reducing mouse double minute 2 homolog expression and subsequently activated FoxO1-mediated Foxp3 gene transcription. PrxII overexpression, in contrast, reduced FoxO1 and Foxp3 expression. More interestingly, adoptive transfer of naive CD4<SUP>+</SUP> T cells from PrxII KO mice into immune-deficient mice attenuated T cell–induced colitis, with a reduction in mouse double minute 2 homolog expression and an increase in FoxO1 and Foxp3 expression. These results suggest that inactivation of PrxII is important for the stability of FoxO1 protein, which subsequently mediates Foxp3<SUP>+</SUP> Treg cell development, thereby attenuating colonic inflammation.</P>
Hwang, Ki-Jun,Lee, Tae-Suk,Kim, Ki-Won,Kim, Beam-Tae,Lee, Chul-Min,Park, Eun-Young,Woo, Ran-Sook The Pharmaceutical Society of Korea 2001 Archives of Pharmacal Research Vol.24 No.4
Bioisostere approach has been shown to be useful to augment potency or to modify certain physiological properties of a lead compound. Based upon well documented bioisosterism, an isosteric replacement of benzene ring of 4-hydroxy-2-quinolone compound (L-695902) with a thiophene moiety was carried out to prepare the title compounds, 4-hydroxy-6-oxo-6,7-dihydro-thieno[2,3-b] pyrimidines 15. The resulting bioisosteric compounds 15 were evaluated for their antagonistic activity (birding assay) for NMDA receptor glycine site.
Enhancement of Allergen-induced Airway Inflammation by NOX2 Deficiency
Won, Hee-Yeon,Jang, Eun-Jung,Min, Hyun-Jung,Hwang, Eun-Sook The Korean Association of Immunobiologists 2011 Immune Network Vol.11 No.3
Background: NADPH oxidase (NOX) modulates cell proliferation, differentiation and immune response through generation of reactive oxygen species. Particularly, NOX2 is recently reported to be important for regulating Treg cell differentiation of CD4+ T cells. Methods: We employed ovalbumin-induced airway inflammation in wild-type and NOX2-deficient mice and analyzed tissue histopathology and cytokine profiles. Results: We investigated whether NOX2-deficiency affects T cell-mediated airway inflammation. Ovalbumin injection which activates T cell-mediated allergic response increased airway inflammation in wild-type mice, as evidenced by increased immune cell infiltration, allergic cytokine expression, and goblet cell hyperplasia in the lung. Interestingly, NOX2 knockout (KO) mice were more susceptible to allergen-induced lung inflammation compared to wild-type mice. Immune cells including neutrophils, lymphocytes, macrophages, and eosinophils were drastically infiltrated into the lung of NOX2 KO mice and mucus secretion was substantially increased in deficiency of NOX2. Furthermore, inflammatory allergic cytokines and eotaxin were significantly elevated in NOX2 KO mice, in accordance with enhanced generation of inflammatory cytokines interleukin-17 and interferon-${\gamma}$ by CD4+ T cells. Conclusion: These results indicate that NOX2 deficiency favorably produces inflammatory cytokines by T cells and thus increases the susceptibility to severe airway inflammation.