http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
이초아,이경록,조정원 충남대학교 약학대학 의약품개발연구소 2014 藥學論文集 Vol.29 No.-
Skin whitening products are commercially available for cosmetic purposes in order to obtain a lighter skin appearance. They are also utilized for clinical treatment of pigmentary disorders such as melasma or postinflammatory hyperpigmentation. Whitening agents act at diverse levels of melanin synthesis in the skin. Many of them are known as competitive inhibitors of tyrosinase, the key enzyme in melanogenesis. Others inhibit the transformation of this activated enzyme or the transport of melanosomes from melanocytes to surrounding keratinocytes. To avoid systemic absorption, whitening agent is need to create optimal formulation such as liposome, microemulsion, solid lipid nanoparticles (SLN) and NLC (Nanostructure liquid crystal) as well as patch. Functional ingredients and innovative delivery systems are driving the new product development in the field of cosmetics. In this review we present an overview of whitening products that may decrease skin pigmentation by their interference with the pigmentary processes and may formulate cosmetic delivery systems possessing potential as smarter carrier systems.
Aberrant Expression of COT Is Related to Recurrence of Papillary Thyroid Cancer
Lee, Jandee,Jeong, Seonhyang,Park, Jae Hyun,Lee, Cho Rok,Ku, Cheol Ryong,Kang, Sang-Wook,Jeong, Jong Ju,Nam, Kee-Hyun,Shin, Dong Yeob,Lee, Eun Jig,Chung, Woong Youn,Jo, Young Suk Williams & Wilkins Co 2015 Medicine Vol.94 No.6
<▼1><P>Supplemental Digital Content is available in the text</P></▼1><▼2><P><B>Abstract</B></P><P>Aberrant expression of Cancer Osaka Thyroid Oncogene mitogen-activated protein kinase kinase kinase 8 (COT) (MAP3K8) is a driver of resistance to B-RAF inhibition. However, the de novo expression and clinical implications of COT in papillary thyroid cancer (PTC) have not been investigated.</P><P>The aim of this study is to investigate the expression of A-, B-, C-RAF, and COT in PTC (n = 167) and analyze the clinical implications of aberrant expression of these genes.</P><P>Quantitative polymerase chain reaction (qPCR) and immunohistochemical staining (IHC) were performed on primary thyroid cancers. Expression of COT was compared with clinicopathological characteristics including recurrence-free survival. Datasets from public repository (NCBI) were subjected to Gene Set Enrichment Analysis (GSEA).</P><P>qPCR data showed that the relative mRNA expression of <I>A-</I>, <I>B-</I>, <I>C-RAF</I> and <I>COT</I> of PTC were higher than normal tissues (all <I>P</I> < 0.01). In addition, the expression of COT mRNA in PTC showed positive correlation with A- (<I>r</I> = 0.4083, <I>P</I> < 0.001), B- (<I>r</I> = 0.2773, <I>P</I> = 0.0003), and C-RAF (<I>r</I> = 0.5954, <I>P</I> < 0.001). The mRNA expressions of A-, B,- and C-RAF were also correlated with each other (all <I>P</I> < 0.001). In IHC, the staining intensities of B-RAF and COT were higher in PTC than in normal tissue (<I>P</I> < 0.001). Interestingly, moderate-to-strong staining intensities of B-RAF and COT were more frequent in B-RAF<SUP>V600E</SUP>-positive PTC (<I>P</I> < 0.001, <I>P</I> = 0.013, respectively). In addition, aberrant expression of COT was related to old age at initial diagnosis (<I>P</I> = 0.045) and higher recurrence rate (<I>P</I> = 0.025). In multivariate analysis, tumor recurrence was persistently associated with moderate-to-strong staining of COT after adjusting for age, sex, extrathyroidal extension, multifocality, T-stage, N-stage, TNM stage, and B-RAF<SUP>V600E</SUP> mutation (odds ratio, 4.662; 95% confidence interval 1.066 − 21.609; <I>P</I> = 0.045). Moreover, moderate-to-strong COT expression in PTC was associated with shorter recurrence-free survival (mean follow-up duration, 14.2 ± 4.1 years; <I>P</I> = 0.0403). GSEA indicated that gene sets related to B-RAF-RAS (<I>P</I> < 0.0001, false discovery rate [FDR] <I>q</I>-value = 0.000) and thyroid differentiation (<I>P</I> = 0.048, FDR <I>q</I>-value = 0.05) scores were enriched in lower COT expression group and gene sets such as T-cell receptor signaling pathway and Toll-like receptor signaling pathway are coordinately upregulated in higher COT expression group (both, <I>P</I> < 0.0001, FDR <I>q</I>-value = 0.000).</P><P>Aberrant expression of A-, B-, and C-RAF, and COT is frequent in PTC; increased expression of COT is correlated with recurrence of PTC.</P></▼2>
GLI1 Transcription Factor Affects Tumor Aggressiveness in Patients With Papillary Thyroid Cancers
Lee, Jandee,Jeong, Seonhyang,Lee, Cho Rok,Ku, Cheol Ryong,Kang, Sang-Wook,Jeong, Jong Ju,Nam, Kee-Hyun,Shin, Dong Yeob,Chung, Woong Youn,Lee, Eun Jig,Jo, Young Suk Williams & Wilkins Co 2015 Medicine Vol.94 No.25
<▼1><P>Supplemental Digital Content is available in the text</P></▼1><▼2><P><B>Abstract</B></P><P>A significant proportion of patients with papillary thyroid cancer (PTC) present with extrathyroidal extension (ETE) and lymph node metastasis (LNM). However, the molecular mechanism of tumor invasiveness in PTC remains to be elucidated.</P><P>The aim of this study is to understand the role of Hedgehog (Hh) signaling in tumor aggressiveness in patients with PTC.</P><P>Subjects were patients who underwent thyroidectomy from 2012 to 2013 in a single institution. Frozen or paraffin-embedded tumor tissues with contralateral-matched normal thyroid tissues were collected. Hh signaling activity was analyzed by quantitative RT-PCR (qRT-PCR) and immunohistochemical (IHC) staining. Datasets from Gene Expression Omnibus (GEO) (National Center for Biotechnology Information) were subjected to Gene Set Enrichment Analysis (GSEA). BRAFT1799A and telomerase reverse transcriptase promoter mutation C228T were analyzed by direct sequencing.</P><P>Among 137 patients with PTC, glioma-associated oncogene homolog 1 (<I>GLI1</I>) group III (patients in whom the ratio of <I>GLI1</I> messenger ribonucleic acid (mRNA) level in tumor tissue to <I>GLI1</I> mRNA level in matched normal tissue was in the upper third of the subject population) had elevated risk for ETE (odds ratio [OR] 4.381, 95% confidence interval [CI] 1.414–13.569, <I>P</I> = 0.01) and LNM (OR 5.627, 95% CI 1.674–18.913, <I>P</I> = 0.005). Glioma-associated oncogene homolog 2 (<I>GLI2</I>) group III also had elevated risk for ETE (OR 4.152, 95% CI 1.292–13.342, <I>P</I> = 0.017) and LNM (OR 3.924, 95% CI 1.097–14.042, <I>P</I> = 0.036). GSEA suggested that higher <I>GLI1</I> expression is associated with expression of the <I>KEGG</I> gene set related to axon guidance (<I>P</I> = 0.031, false discovery rate < 0.05), as verified by qRT-PCR and IHC staining in our subjects.</P><P><I>GLI1</I> and <I>GLI2</I> expressions were clearly related to aggressive clinicopathological features and aberrant activation of GLI1 involved in the axon guidance pathway. These results may contribute to development of new prognostic markers, as well as novel therapeutic targets.</P></▼2>