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최미라 ( Mi Ra Choi ),권인호 ( In Ho Kwon ),김동현 ( Dong Hyun Kim ),김규한 ( Kyu Han Kim ),조소연 ( So Yun Cho ),박귀영 ( Kui Young Park ),이갑석 ( Kap Sok Li ),김범준 ( Beom Joon Kim ),김명남 ( Myeung Nam Kim ),원종현 ( Chong Hy 대한피부과학회 2009 大韓皮膚科學會誌 Vol.47 No.6
Background: Nodular fasciitis presents as a solitary, slightly painful, rapidly growing nodule. It is associated with a reactive, proliferative process of unknown cellular origin and can be misdiagnosed as a sarcoma. Objective: Our study was designed to investigate the process and cellular origin of the disease. Methods: The clinical and histopathologic findings from 28 cases of nodular fasciitis were reviewed. Additional histochemical and immunohistochemical staining was done. Results: The mean age of onset was 29.8 years. A majority of patients with nodular fasciitis had a duration of symptoms of less than 6 months. The upper extremity and face were most frequently involved. Most of the lesions had diameters less than 2 cm. Total excisions were performed in 23 lesions; 3 lesions recurred thereafter. Histopathologically, a subcutaneous plane was most frequently involved. The nodule consisted of numerous large, pleomorphic fibroblasts growing haphazardly in a vascular stroma containing varying amounts of mucoid ground substance, which was confirmed by histochemical stains. In the immunohistochemical stain, most lesions had positive findings for smooth muscle actin (SMA), vimentin and negative findings for CD34 except in a few cases. The stains for desmin and S-100 were negative in all cases. Conclusion: It is suggested that nodular fasciitis is associated with a reactive proliferation of myofibroblasts rather than with a sarcomatous process. (Korean J Dermatol 2009;47(6):649∼657)
Antioxidant Activity of N-hydroxyethyl Adenosine from Isaria sinclairii
Ahn, Mi-Young,Heo, Jung-Eun,Ryu, Jae-Ha,Jeong, Hy-Kyoung,Ji, Sang-Deok,Park, Hae-Chul,Sim, Ha-Sik Korean Society of Sericultural Science 2008 International Journal of Industrial Entomology Vol.17 No.2
The antioxidant activity of Isaria (Paecilomyces) sinclairii was determined by measuring its radical scavenging effect on 1, 1-diphenyl-2-picrylhydrazyl (DPPH) radicals. The n- BuOH extract of P. sinclairii showed strong scavenging activity to DPPH. The anti-oxidant potential of the individual fraction was in the order of ethylacetate> n- BuOH>chloroform>n-hexane. The n-BuOH soluble fraction exhibiting strong anti-oxidant activity was further purified by repeated silica gel column chromatography. N-(2-Hydroxyethyl)adenosine (HEA) was isolated as one of the active principles from the n-BuOH layer. The n-BuOH layer, particularly HEA, did not increase the level of nitric oxide (NO) production in vascular endothelial cells that might be related to vasorelaxation such as the action of viagra. In addition, the vascular endothelial growth factor (VEGF) levels showed little or no increase compared with control group with the treatment of I. sinclairii.
마우스의 급성 DSS 장염 모델에서 편도 유래 중간엽 줄기 세포의 치료 효과
송은미 ( Eun Mi Song ),정성애 ( Sung-ae Jung ),이고은 ( Ko Eun Lee ),장지영 ( Ji Young Jang ),이강훈 ( Kang Hoon Lee ),태정현 ( Chung Hyun Tae ),문창모 ( Chang Mo Moon ),주양희 ( Yang-hee Joo ),김성은 ( Seong-eun Kim ),정혜경 ( Hy 대한소화기학회 2017 대한소화기학회지 Vol.69 No.2
목적: 궤양성 대장염과 크론병으로 대표되는 염증성 장질환은 만성적인 질환으로 재발과 악화를 반복하여 환자의 삶의 질을 악화시킨다. 줄기 세포 치료는 최근 염증성 장질환을 비롯한 다양한 난치성 질환의 잠재적인 치료법으로 각광받고 있다. 새롭게 개발된 편도 유래 중간엽 줄기 세포(tonsil-derived mesenchymal stem cells, T-MSC)는 줄기 세포 고유 기능을 모두 가지며 비교적 채취가 용이하고 여러 기증자로부터 받은 세포가 잘 융화되어 자란다는 장점이 있다. 본 연구에서는 이러한 T-MSC를 dextran sulfate sodium (DSS)로 유도된 만성 장염 마우스 모델에 적용하여 그 효과를 알아보고자 하였다. 방법: C57BL/6 마우스를 각각 정상 대조군, DSS 장염군(DSS+PBS), T-MSC 투여군 (DSS+T-MSC)으로 나눠서 급성장염을 유도하였다. T-MSC 투여군에서는 급성 장염 유도 3일째에 복강 내로 T-MSC 1×106을 투여하였다. 장염의 평가는 임상 증상과 장길이, 조직학적 호전 정도로 평가하였다. 대장조직의 염증성 사이토카인을 측정하여 비교하였다. PKH26으로 표시된 T-MSC의 위치를 생체 내에서 추적하였다. 결과: T-MSC의 투여에 의하여 급성 장염 유도 마지막 날DAI가 유의하게 낮아졌으며 (11.3±1.5 vs. 8.3±1.9, p=0.015)장염 증상에 의한 체중의 감소도 완화된 소견을 보였다(-17.1±5.0% vs. -8.1±6.9%, p=0.049). 조직학적 소견을 비교하였을 때 T-MSC 투여군은 염증 세포 침투의 감소, 염증 범위의 감소 및 선와 손상의 완화 등 염증의 호전 소견이 관찰되었다 (22.6±3.8 vs. 17.0±3.4, p=0.039). 염증성 사이토카인인IL-6 and IL-1β 수치 또한 T-MSC 투여에 의하여 의미 있게 감소되었다. T-MSC의 위치를 생체 내에서 추적하였을 때 급성 장염이 유도된 대장 점막에서 T-MSC는 발견되지 않았다. 결론: 급성 장염 모델에서 T-MSC의 투여는 장염의 증상 및 조직학적인 염정 소견을 호전시켰다. 또한, 이러한 효과는 T-MSC의 생체 내 위치와는 무관한 소견으로 향후 T-MSC의 기전에 대한 추가적인 연구가 필요할 것으로 생각된다. Background/Aims: Mesenchymal stem cells (MSCs) are multipotent progenitor cells currently under investigation for its efficacy as the treatment for inflammatory bowel disease. In this study, we evaluated the efficacy of tonsil-derived mesenchymal stem cells (T-MSCs) as a novel source of mesenchymal stem cells and traced their localization in a murine model of acute colitis induced by dextran sulfate sodium (DSS). Methods: C57BL/6 mice were randomly assigned to the following three groups: the normal control group, DSS colitis group (DSS+phosphate buffered saline), and T-MSC group (DSS+T-MSCs, 1x10<sup>6</sup>). The severity of colitis was assessed by determining the severity of symptoms of colitis, colon length, histopathologic grade, and levels of inflammatory cytokines. T-MSCs labeled with PKH26 were traced in vivo. Results: The T-MSC group, compared with the DSS colitis group, showed a significantly lower disease activity index (11.3±1.5 vs. 8.3±1.9, p=0.015) at sacrifice and less reduction of body weight (-17.1±5.0% vs. -8.1±6.9%, p=0.049). In the T-MSC group, the histologic colitis score was significantly decreased compared with the DSS colitis group (22.6±3.8 vs. 17.0±3.4, p=0.039). IL-6 and IL-1β, the pro-inflammatory cytokines, were also significantly reduced after a treatment with T-MSCs. In vivo tracking revealed no PKH26-labelled T-MSCs in the colonic tissue of mice with acute colitis. Conclusions: In the acute colitis model, we demonstrated that the administration of T-MSCs ameliorates inflammatory symptoms and histology. Moreover, the anti-inflammatory activities of T-MSCs were independent of gut homing. (Korean J Gastroenterol 2017;69:119-128)
The adequacy of conization in the management of adenocarcinoma in situ of the uterine cervix(초)
한호섭 ( Ho Suap Hahn ),( Mi La Kim ),( Seok Geun Yoon ),( Woo Chul Kim ),( Hong Jun Choi ),( Sung Ran Hong ),( Hy Sook Kim ),( Yong Soon Kwon ),( In Ho Lee ),( Kyung Taek Lim ),( Ki Heon Lee ),( Jae Uk 대한산부인과학회 2009 대한산부인과학회 학술대회 Vol.95 No.-
Koh, Ara,Lee, Mi Nam,Yang, Yong Ryoul,Jeong, Heeyoon,Ghim, Jaewang,Noh, Jeongeun,Kim, Jaeyoon,Ryu, Dongryeol,Park, Sehoon,Song, Parkyong,Koo, Seung-Hoi,Leslie, Nick R.,Berggren, Per-Olof,Choi, Jang Hy American Society for Microbiology 2013 Molecular and cellular biology Vol.33 No.8
<P>Muscle atrophy occurs under various catabolic conditions, including insulin deficiency, insulin resistance, or increased levels of glucocorticoids. This results from reduced levels of insulin receptor substrate 1 (IRS-1), leading to decreased phosphatidylinositol 3-kinase activity and thereby activation of FoxO transcription factors. However, the precise mechanism of reduced IRS-1 under a catabolic condition is unknown. Here, we report that C1-Ten is a novel protein tyrosine phosphatase (PTPase) of IRS-1 that acts as a mediator to reduce IRS-1 under a catabolic condition, resulting in muscle atrophy. C1-Ten preferentially dephosphorylated Y612 of IRS-1, which accelerated IRS-1 degradation. These findings suggest a novel type of IRS-1 degradation mechanism which is dependent on C1-Ten and extends our understanding of the molecular mechanism of muscle atrophy under catabolic conditions. C1-Ten expression is increased by catabolic glucocorticoid and decreased by anabolic insulin. Reflecting these hormonal regulations, the muscle C1-Ten is upregulated in atrophy but downregulated in hypertrophy. This reveals a previously unidentified role of C1-Ten as a relevant PTPase contributing to skeletal muscle atrophy.</P>
정화영 ( Hwa Young Jung ),김미리 ( Mi Ri Kim ),박영민 ( Young Min Park ),박철종 ( Chul Jong Park ),김진우 ( Jin Woom Kim ),김경문 ( Kyung Moon Kim ),이정덕 ( Jeong Deuk Lee ),강훈 ( Hoon Kang ),조백기 ( Baik Kee Cho ),박현정 ( Hy 대한피부과학회 2015 대한피부과학회지 Vol.53 No.1
Background: Rosacea is characterized by erythema of the central face that persists for several months or longer. Reports of the histological changes in rosacea are scarce, and few attempts have been made to correlate suchchanges with clinical findings and pathophysiology. Objective: This study aimed to elucidate the clinical manifestations of rosacea and investigate its histologicalfeatures. Methods: We performed a retrospective analysis of 278 patients with histologically confirmed rosacea who visitedthe Department of Dermatology at the Catholic Medical Center between January 2008 and May 2013. Clinicalsubtypes, disease severity, and precipitating factors were evaluated. In 115 randomly selected patients, histopathologicalfeatures were evaluated as well. Results: The ratio of males to females was 1:1.8. The age distribution showed a peak incidence in the fifthdecade. The most common subtype was papulopustular rosacea (52.9%) followed by erythematotelangiectatic rosacea(34.9%), ocular rosacea (4.0%), and phymatous rosacea (2.9%). Granulomatous rosacea accounted for 5.4% ofrosacea cases. Precipitating factors included hot weather (54.7%), stress (51.8%), sun exposure (37.4%), alcohol(37.4%), and hot baths (33.1%). Histological analysis of skin biopsies from 115 patients revealed solar elastosis in62 patients (53.9%) and telangiectasia in 85 patients (73.9%).Conclusion: In this study, Korean rosacea patients were predominantly female with a peak age in the fifth decadeand the majority suffered from the papulopustular and erythematotelangiectatic types of rosacea. Histologicalobservations pertaining to each rosacea type were also discussed. (Korean J Dermatol 2015;53(1):1∼9)
Park, Jin‐,Sil,Lim, Mi‐,Ae,Cho, Mi‐,La,Ryu, Jun‐,Geol,Moon, Young‐,Mee,Jhun, Joo‐,Yeon,Byun, Jae‐,Kyeong,Kim, Eun‐,Kyung,Hwang, Sue‐,Yun,Ju, Ji Hy Wiley Subscription Services, Inc., A Wiley Company 2013 Vol.65 No.4
<P><B>Abstract</B></P><P><B>Objective</B></P><P>To investigate the connection between p53 and interleukin‐17–producing Th17 cell/Treg cell balance in rheumatoid arthritis (RA).</P><P><B>Methods</B></P><P>Th17 cell and Treg cell frequencies were analyzed by flow cytometry, and cytokine levels in the supernatant were determined using enzyme‐linked immunosorbent assays. The expression of transcription factors was analyzed by immunostaining and Western blotting, and the interactions between p53 and STAT‐3 or STAT‐5 were determined by immunoprecipitation–Western blot analysis. A p53 agonist was administered in the collagen‐induced arthritis (CIA) model, and the effects in vivo were determined.</P><P><B>Results</B></P><P>CD4+ T cells from p53<SUP>–/–</SUP> mice decreased the activity of STAT‐5, lowered the level of phosphorylated STAT‐5, and compromised Treg cell differentiation. The protein p53 bound STAT‐5 directly, and this interaction was enhanced with increasing p53 activity. Under inflammatory conditions, p53 suppressed Th17 cell differentiation and skewed T cells toward Treg cell differentiation through the activation of STAT‐5 signaling cascades. In mice with CIA, injection of a p53 overexpression vector or an antagonist of Mdm2 had the effect of controlling arthritis development in vivo. The regulatory effect of p53 was recapitulated in the cells of RA patients, with more pronounced suppression due to the repressed status of p53 in RA.</P><P><B>Conclusion</B></P><P>We demonstrated a link between p53‐mediated and STAT‐mediated regulation of Th17 cells/Treg cells in RA. Our results suggest that factors involved in this pathway might constitute novel therapeutic targets for the treatment of RA.</P>