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Fang-Hsin Lee,Hsiu-Hung Wang,Yung-Mei Yang,Joh-Jong Huang,Hsiu-Min Tsai 한국간호과학회 2016 Asian Nursing Research Vol.10 No.3
Purpose: This study aimed to explore the factors associated with the intention to receive a Pap test among married immigrant women of Vietnamese origin living in Taiwan. Methods: This was a cross-sectional community-based study.We enrolled 281 women aged 30 years and over in the study, from July 2013 to January 2014. The participants' characteristics, cervical cancer knowledge, Pap test knowledge, attitudes toward cervical cancer, barriers to receiving a Pap test, fatalism, and intention to receive a Pap test, were measured using self-report questionnaires. Hierarchical multiple regression analyses were performed to examine the variables associated with participants' intentions to receive a Pap test. Results: Vietnamese women with low scores on the measures of cervical cancer knowledge and perceived barriers to receiving a Pap test were more willing to receive the test, as were those with high scores on the measures of Pap test knowledge and fatalism. Women who received a Pap test in the previous year were more willing to receive a Pap test within the next 3 years. Conclusions: Preventive healthcare for immigrant women should be a focus of nurses. The development of culturally appropriate health education and strategies should enhance their knowledge of Pap tests and reduce perceived barriers to Pap test participation. This study's results can be a reference for nurses who work with immigrant women.
Monacolin K affects lipid metabolism through SIRT1/AMPK pathway in HepG2 cells
Chia-Hsin Huang,Shin-Mau Shiu,Min-Tze Wu,Wei-Lu Chen,Shyang-Guang Wang,Horng-Mo Lee 대한약학회 2013 Archives of Pharmacal Research Vol.36 No.12
Monacolin K is the secondary metabolite isolatedfrom Monascus spp. It is the natural form of lovastatin,which is clinically used to reduce the synthesis of cholesterolby inhibiting 3-hydroxy-3-methylglutaryl coenzyme Areductase. In the present study, monacolin K increased proteinexpression of SIRT1 and phosphorylation level of AMPactivatedprotein kinase (AMPK) in HepG2 cells. Throughactivation of SIRT1/AMPK pathway, monacolin Kincreased phosphorylation of acetyl CoA carboxylase andcaused nuclear translocation of forkhead box O1. The westernblotting results showed that monacolin K increasedexpression of adipose triglyceride lipase but decreasedabundances of fatty acid synthase (FAS) and sterol regulatory element-binding protein 1 (SREBP1). MonacolinK also decreased the intracellular accumulation of lipids asdemonstrated by Oil Red O staining. In addition, theimmunostaining showed that monacolin K prevented thenuclear translocation of SREBP1, indicating the associationwith down-regulation of FAS. All the demonstrated effectsof monacolin K were counteracted by nicotinamide orcompound C, the inhibitors of SIRT1 orAMPK. In summary,monacolin K reduces the lipid content through SIRT1/AMPK pathway in HepG2 cells, which promotes catabolismand inhibits anabolism of lipid.
( Wei-chen Lin ),( Jen-wei Chou ),( Hsu-heng Yen ),( Wen-hung Hsu ),( Hung-hsin Lin ),( Jen-kou Lin ),( Chiao-hsiung Chuang ),( Tien-yu Huang ),( Horng-yuan Wang ),( Shu-chen Wei ),( Jau-min Wong ) 대한장연구학회 2017 Intestinal Research Vol.15 No.4
Background/Aims: In Taiwan, due to budget limitations, the National Health Insurance only allows for a limited period of biologics use in treating moderate to severe Crohn’s disease (CD). We aimed to access the outcomes of CD patients following a limited period use of biologics, specifically focusing on the relapse rate and remission duration; also the response rate to second use when applicable. Methods: This was a multicenter, retrospective, observational study and we enrolled CD patients who had been treated with adalimumab (ADA) according to the insurance guidelines from 2009 to 2015. Results: A total of 54 CD patients, with follow-up of more than 6 months after the withdrawal of ADA, were enrolled. The average period of treatment with ADA was 16.7±9.7 months. After discontinuing ADA, 59.3% patients suffered a clinical relapse. In the univariate analysis, the reason for withdrawal was a risk factor for relapse (P=0.042). In the multivariate analysis, current smoker became an important risk factor for relapse (OR, 3.9; 95% CI, 1.2-14.8; P=0.044) and male sex was another risk factor (OR, 2.9; 95% CI, 1.1-8.6; P=0.049). For those 48 patients who received a second round of biologics, the clinical response was seen in 60.4%, and 1 anaphylaxis occurred. Conclusions: Fifty-nine percent of patients experienced a relapse after discontinuing the limited period of ADA treatment, and most of them occurred within 1 year following cessation. Male sex and current smoker were risk factors for relapse. Though 60.4% of the relapse patients responded to ADA again. (Intest Res 2017;15:487-494)
Kuo-Feng Hua,A-Ching Chao,Ting-Yu Lin,Wan-Tze Chen,Yu-Chieh Lee,Wan-Han Hsu,Sheau-Long Lee,Hsin-Min Wang,Ding-I. Yang,Tz-Chuen Ju 고려인삼학회 2022 Journal of Ginseng Research Vol.46 No.4
Background: Huntington's disease (HD) is a neurodegenerative disorder caused by the expansion oftrinucleotide CAG repeat in the Huntingtin (Htt) gene. The major pathogenic pathways underlying HDinvolve the impairment of cellular energy homeostasis and DNA damage in the brain. The protein kinaseataxia-telangiectasia mutated (ATM) is an important regulator of the DNA damage response. ATM isinvolved in the phosphorylation of AMP-activated protein kinase (AMPK), suggesting that AMPK plays acritical role in response to DNA damage. Herein, we demonstrated that expression of polyQ-expandedmutant Htt (mHtt) enhanced the phosphorylation of ATM. Ginsenoside is the main and most effectivecomponent of Panax ginseng. However, the protective effect of a ginsenoside (compound K, CK) in HDremains unclear and warrants further investigation. Methods: This study used the R6/2 transgenic mouse model of HD and performed behavioral tests,survival rate, histological analyses, and immunoblot assays. Results: The systematic administration of CK into R6/2 mice suppressed the activation of ATM/AMPK andreduced neuronal toxicity and mHTT aggregation. Most importantly, CK increased neuronal density andlifespan and improved motor dysfunction in R6/2 mice. Conversely, CK enhanced the expression of Bcl2protected striatal cells from the toxicity induced by the overactivation of mHtt and AMPK. Conclusions: Thus, the oral administration of CK reduced the disease progression and markedlyenhanced lifespan in the transgenic mouse model (R6/2) of HD.