1980년대 이후 대만 음식(cuisine)의 형성

마이클 사오(Hsin-Huang Michael Hsiao),메이창(May Yu-Hsin Chang),메이-후이첸(Mei-Hui Chen),권정화(번역자) 서울대학교 아시아연구소 2015 아시아리뷰 Vol.5 No.1

대만 음식의 출현은 대만의 민주화 과정과 1980년대 이래 국가 정체성의 성장과 관련이 깊다. 어떠한 측면에서 대만 음식의 형성은 중국 본토의 장저(江浙) 음식, 쓰촨(四川) 음식, 광둥(廣東) 음식 체계가 우세한 가운데 대만 내 두 개의 주요 민족음식, 즉 민난과 학카 음식이 자유화된 것으로 볼 수도 있다. 한족의 음식으로 알려진 민난과 학카 음식이 대만을 대표하는 요리로 급부상하게 된 것이다. 그러나 한족이 아닌 원주민 음식은 여전히 대만 음식으로 통합되지 않고 있는 점 또한 주목해야 한다. 이 글은 대만 음식의 부상이 정치적 변환과 문화적 변화를 뛰어넘는 사회적 산물이라는 점에 주목하고 있다. 민난과 학카 민족 음식의 소비는 가정의 범주를 넘어 레스토랑에서 볼 수 있는 상품화된 ‘요리’로서 빠르게 자리잡고 있다. 이 글은 민난과 학카 민족 음식의 ‘요리화’와 ‘대중화’의 특징과 변화를 설명하고자 한다. 또한 민난, 학카 음식이 어떻게 ‘표현’되고, 어떠한 ‘위치’에 있고, 대만 국가 음식으로써 ‘어느 정도’ 역할을 하는지도 주목한다. 결론에서는 민주주의, 민족성, 국가정체성이 어떻게 연관되어 있고, 이들의 관계가 대만의 현대 음식에 어떻게 반영되어 있는지를 살펴본다. The emergence of Taiwanese cuisine has much to do with the democratization process and the growth of Taiwan national identity since the 1980s. In one way, the making of Taiwanese cuisine can be seen as the liberalization of two major ethnic foods, Mainan and Hakka, from the dominance of Mainland China’s provincial food customs such as that of Jiang-Zhe, Szechuan, and Guandong. The two ethnic Han food of Minnan and Hakka have thus been ungraded to constitute the new core components of the rising Taiwan’s national cuisine. It is equally important to note that, however, the non-Han aborigine food has not been considered as an integral part of Taiwanese cuisine. This paper intends to argue that the rise of Taiwanese cuisine is the direct social product of the above political transformation and cultural change. The Minnan and Hakka ethnic foods have since then been rapidly commercialized to become the recognized “cuisine” popularly served in restaurants beyond household consumption. The rise of “cuisinization” as well as “popularization” of ethnic Mainnan and Hakka foods will then be discussed in this paper by identifying the main features and changes of each of the ethnic food. Special attention is also paid to how Minnan and Hakka food are being “presented,” “positioned” and “weighted” in the constitution of “Taiwanese national cuisine.”Finally, in the conclusion, the interplay of democracy, ethnicity and national identity and its impact on Taiwan’s contemporary foodscape will be highlighted.

Using Team resource management to improve the execution rate of cardiac rehabilitation exercise

Chen Mei-Jia,Chen Mei-Jia,Yu Chen-Yi,Chou Yi-Ling,Lin Hsin-Yi,Chang Hui-Mei 한국간호과학회 2023 한국간호과학회 학술대회 Vol.2023 No.11

Morphological Characteristics of Granular Starch in Lotus Porridge Flour

Hui-Mei Lin,Jheng-Hua Lin,Yung-Ho Chang,Ming-Jen Sheu,Ting-Jang Lu 한국원예학회 2006 한국원예학회 기타간행물 Vol.- No.-

Sauchinone, a lignan from Saururus chinensis, attenuates neutrophil pro-inflammatory activity and acute lung injury

( Hui Jing Han ),( Mei Li ),( Jong Keun Son ),( Chang Seob Seo ),( Seung Won Song ),( Sang Hyun Kwak ),( Hong Beom Bae ) 영남대학교 약품개발연구소 2014 영남대학교 약품개발연구소 연구업적집 Vol.24 No.0

Previous studies have shown that sauchinone modulates the expression of inflammatory mediators through mitogen-activated protein kinase (MAPK) pathways in various cell types. However, little information exists about the effect of sauchinone on neutrophils, which play a crucial role in inflammatory process such as acute lung injury (ALI). We found that sauchinone decreased the phosphorylation of p38 MAPK in lipopolysaccharide (LPS)-stimulated murine bone marrow neutrophils, but not ERK1/2 and JNK. Exposure of LPS-stimulated neutrophils to sauchinone or SB203580, a p38 inhibitor, diminished production of tumor necrosis factor (TNF)-α and macrophage inflammatory protein (MIP)-2 compared to neutrophils cultured with LPS. Treatment with sauchinone decreased the level of phosphorylated ribosomal protein S6 (rpS6) in LPS-stimulated neutrophils. Systemic administration of sauchinone to mice led to reduced levels of phosphorylation of p38 and rpS6 in mice lungs given LPS, decreased TNF-α and MIP-2 production in bronchoalveolar lavage fluid, and also diminished the severity of LPS-induced lung injury, as determined by reduced neutrophil accumulation in the lungs, wet/dry weight ratio, and histological analysis. These results suggest that sauchinone diminishes LPS-induced neutrophil activation and ALI.

Performance Verification Mechanism for Adaptive Assessment e-Platform and e-Navigation Application

Chang-Shing LEE,Mei-Hui WANG,Cheng-Hao HUANG 국제이네비해양경제학회 2015 International Journal of e-Navigation and Maritime Vol.2 No.1

Sauchinone, a lignan from Saururus chinensis, attenuates neutrophil pro-inflammatory activity and acute lung injury

( Hui Jing Han ),( Mei Li ),( Jong Keun Son ),( Chang Seob Seo ),( Seung Won Song ),( Sang Hyun Kwak ),( Hong Beom Bae ) 영남대학교 약품개발연구소 2013 영남대학교 약품개발연구소 연구업적집 Vol.23 No.0

Previous studies have shown that sauchinone modulates the expression of inflammatory mediators through mitogen-activated protein kinase (MAPK) pathways in various cell types. However, little information exists about the effect of sauchinone on neutrophils, which play a crucial role in inflammatory process such as acute lung injury (ALI). We found that sauchinone decreased the phosphorylation of p38 MAPK in lipopolysaccharide (LPS)-stimulated murine bone marrow neutrophils, but not ERK1/2 and JNK. Exposure of LPS-stimulated neutrophils to sauchinone or SB203580, a p38 inhibitor, diminished production of tumor necrosis factor (TNF)-α and macrophage inflammatory protein (MIP)-2 compared to neutrophils cultured with LPS. Treatment with sauchinone decreased the level of phosphorylated ribosomal protein S6 (rpS6) in LPS-stimulated neutrophils. Systemic administration ofsauchinone to mice led to reduced levels of phosphorylation of p38 and rpS6 in mice lungs given LPS, decreased TNF-α and MIP-2 production in bronchoalveolar lavage fluid, and also diminished the severity of LPS-induced lung injury, as determined by reduced neutrophil accumulation in the lungs, wet/dry weight ratio, and histological analysis. These results suggest that sauchinone diminishes LPS-induced neutrophil activation and ALI. ⓒ2013 Elsevier B.B.All rights reserved.

Association of IgE-mediated allergen sensitivity and promoter polymorphisms of chemokine (C–C motif) ligand 5 gene in Han Chinese patients with allergic skin diseases

Ji-Chang Zhou,Yu-Mei Zhu,Zheng Chen,Shan He,Shi-jie Zheng,Jun-luan Mo,Xiao-Li Liu,Chun-mei Gong,Bin Hou,Hui Yang 한국유전학회 2015 Genes & Genomics Vol.37 No.5

Two single nucleotide polymorphisms (SNPs), rs2280788 (-28C[G) and rs2107538 (-403G[A), in the promoter region of chemokine (C–C motif) ligand 5 (CCL5) was reported to be involved in the immunoglobulin E (IgE) expression and IgE-mediated allergic reactions. This study was to investigate the characteristics of total serum IgE level, specific allergen sensitivities and the two SNPs in the allergic skin disease (ASD) patients. ASD patients visiting the dermatological outpatient department of a local hospital were included with certain criteria, and the fasting venous blood was sampled for analysis. Total serum IgE was assayed with an ELISA kit, and 14 kinds of allergen-specific IgE were tested with an allergen screening system. The polymerase chain reaction–restriction fragment length polymorphism method was used to analyze the two SNPs. Among the finally included 437 patients aged from 16 to 85 years, 68.2 % was positive for the total serum IgE, 49.2 % was positive for at least one of the assayed allergen-specific IgE, and 35.0 % was sensitive to house dust mite. In the SNPs analysis, the GG/(GA?AA) ratio and G/A ratio for the -403G[A locus in the male and/or female C45 years subgroup were significantly lower in the total serum IgE positive patients than in the negative patients (P\0.05). Weak linkage disequilibrium was found between -403A and -28C alleles in male subgroups adjusted by age. Conclusively, house dust mite was the most common allergen in ASD patients, and -403A allele of CCL5 promoter was a risk factor for IgE-mediated sensitization.

Screening of Nitrosamine Impurities in Sartan Pharmaceuticals by GC-MS/MS

Shu-Han Chang,Hui-Yu Ho,Chi-Zong Zang,Ya-Hui Hsu,Mei-Chih Lin,Su-Hsiang Tseng,Der-Yuan Wang 사단법인 한국질량분석학회 2021 Mass spectrometry letters Vol.12 No.2

Probable human carcinogenic compounds nitrosamines, have been detected as by-product impurities in sartan phar- maceuticals in recent years which has drawn worries for medication safety. To provide a sensitive and effective method for the quality control of sartan pharmaceuticals, this study established a feasible gas chromatography–tandem mass spectrometry (GC– MS/MS) method for simultaneous determination of 13 nitrosamines. The target analytes were separated on a DB-WAX Ultra Inert column (30 m × 0.25 mm; i.d., 0.25 µm) and were then subjected to electron impact ionization in multiple reaction moni- toring mode. The established method was validated and further employed to analyze authentic samples. Limits of detection (LODs) and limits of quantification (LOQs) of the 13 nitrosamines were 15-250 ng/g and 50-250 ng/g, respectively, which also exhibited intra-day and inter-day accuracies of 91.4-104.8%, thereby satisfying validation criteria. Five nitrosamines, viz., N- nitrosodiethylamine, N-nitrosodimethylamine, N-nitrosodiphenylamine, N-nitrosomorpholine, and N-nitrosopiperidine were detected at concentrations above their LODs in 68 positive samples out of 594 authentic samples from seven sartans.

Transient Knock Down of Grp78 Reveals Roles in Serum Ferritin Mediated Pro-inflammatory Cytokine Secretion in Rat Primary Activated Hepatic Stellate Cells

Wang, Chi-Mei,Li, Shan-Jen,Wu, Chi-Hao,Hu, Chien-Ming,Cheng, Hui-Wen,Chang, Jung-Su Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.2

Chronic liver diseases, including cancer, are characterized by inflammation and elevated serum ferritin (SF). However, the causal-relationship remains unclear. This study used primary rat hepatic stellate cells (HSC) as a model to investigate effects of physiological SF concentrations (10, 100 and 1000 pM) because HSCs play a central role in the development and progression of liver fibrosis. Physiological concentrations of SF, either horse SF or human serum, induced pro-inflammatory cytokine $IL1{\beta}$, IL6 and $TNF{\alpha}$ secretion in rat activated HSCs (all p<0.05). By contrast, treatment did not alter activation marker ${\alpha}SMA$ expression. The presence of SF markedly enhanced expression of Grp78 mRNA (p<0.01). Furthermore, transient knock down of Grp78 by endotoxin EGF-SubA abolished SF-induced $IL1{\beta}$ and $TNF{\alpha}$ secretion in activated HSCs (all p<0.05). In conclusion, our results showed that at physiological concentrations SF functions as a pro-inflammatory mediator in primary rat HSCs. We also provide a molecular basis for the action of SF and identified Grp78-associated ER stress pathways as a novel potential therapeutic target for resolution of fibrosis and possible prevention of liver cancer.

VHL Gene Mutation Analysis of a Chinese Family with Non-Syndromic Pheochromocytomas and Patients with Apparently Sporadic Pheochromocytoma

Zhang, Bin,Qian, Jing,Chang, De-Hui,Wang, Yang-Min,Zhou, Da-Hai,Qiao, Gou-Mei Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.5

Objective: The Von Hippel-Lindau syndrome (VHLD), an inherited neoplastic syndrome predisposing to central nervous system hemangioblastoma (CNS), pheochromocytoma (PCC), renal cell carcinoma(RCC), retinal hemangioma (RA) and renal cysts, is caused by mutations or deletions of the VHL tumor-suppressor gene. To assess VHL genotype-phenotype correlations with function of pVHL a gene mutation analysis of members in a Chinese family with non-syndromic PCCs and individuals with apparently sporadic pheochromocytoma (ASP) was performed. Materials and Methods: DNA samples of 20 members from the Chinese family with non-syndromic PCCs and 41 patients with ASP were analyzed by polymerase chain reaction and direct sequencing, confirmed by Taqman probe. Results: Three novel mutations (H125P, 623(^TTTGTtG) and R120T) were identified in the Chinese family and in 3 among 41 ASP patients. The mutations were all located in exon 2 of VHL gene encoding ${\beta}$-domain of pVHL. The tumor type in H125P carriers and R120T carriers was VHL type 2C. And 623(^TTTGTtG) carriers presented VHL type 2B or type 2C. Conclusions: VHL gene abnormalities were identified in the Chinese family with non-syndromic PCCs and patients with APS, resulting in dysfunction of pVHL. H125P and R120T could be associated with VHL type 2C, while 623(^TTTGTtG) might be linked with VHL type 2B or type 2C. Not only is the genetic analysis helpful for early diagnosis and treatment of patients with VHLD, it is also benefitial for research intoVHLD pathogenesis.