• Title/Summary/Keyword: chao

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History of Symptom Discrimination based on Theory of Triple Energizers(三焦) before Tang Dynasty(唐代) (당대(唐代) 이전(以前)의 '삼초이론(三焦理論)에 기초한 변증(辨證)'의 연혁(沿革))

  • Jo, Hak-Jun
    • Journal of Korean Medical classics
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    • v.28 no.2
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    • pp.87-102
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    • 2015
  • Objectives : I intended to find out the origin and development of symptom discrimination based on theory of triple energizers before Tang Dynasty(唐代). Methods : I extracted the topic-related contents from books in this era. After arraying them in a chronological order, I analyzed the materials. Results : The author in Zhong Zang Jing(中藏經) first mentioned that symptom of Huo Luan(霍亂) was deeply related with triple energizers. Ge Hong(葛洪) did not only come out with some symptoms and mechanisms for Shang Han(傷寒) and Za Bing(雜病), but also applied them to their usages for herb medicine. Chao Yuan Fang(巢元方) suggested its symptoms were more closely related with Shang Han and Za Bing than before. For the first time, Chao subdivided its symptoms to both cold-heat and weakness-strength sides. Sun Sai Miao(孫思邈) supplemented its discrimination invented by Chao(巢元方), adding more symptoms and prescriptions for triple energizers. Wang Tao(王燾) showed more prescriptions for triple energizers than before, and initially designed the discrimination for Huo Luan, diabetes(消渴), and epidemic Wen Bing(溫病). Conclusions : Before Tang dynasty, the symptom discrimination based on theory of triple energizers had been originated and developed for the purpose of repairing Za Bing, not just treating Wen Bing.

Study on classification of diseases in oriental medicine (한의학(韓醫學)의 질병분류(疾病分類)에 관한(關) 소고(小考))

  • Kim, Sung-Hoon
    • Journal of Haehwa Medicine
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    • v.8 no.1
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    • pp.97-114
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    • 1999
  • By studying disease classifications of oriental medicine from Nei-Ching, Chao's-Bing-Yuan, Dong-Yi-Bao-Jian and Korea-standard classification of causes of disease & death. The results were obtained as follows : 1. In Nei-Ching 181 kinds, Chao's-Bing-Yuan 1729 kinds, Dong-Yi-Bao-Jian 966 kinds, and Korea-standard classification of causes of disease & death 2519 kinds of diseases, which suggested more diseases as time flew. 2. In classical books such as Nei-Ching, Chao's-Bing-Yuan, and Dong-Yi-Bao-Jian most of diseases and their names were originated from six kinds of pathogenic factors, Zang-Fu, Jung-Qi-Blood-Fluid, soul, and outer-body-signs, while Korea-standard classification of causes of disease & death classified diseases according to oriental medical departments. 3. Symptoms of Cold-Heat-Excess-Deficiency and pathogenic factors, body parts, Zang-Fu were applied to names of diseases in oriental medicine. 4. In oriental medicine, some symtoms, many intermal diseases were used as disease name, but it is necessary for us to select exact name of diseases in modem clinical treatment. 5. We should consider disease names in Korea-standard classification of causes of disease & death in relations with western medical terms of diseases.

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m6A in the Signal Transduction Network

  • Jang, Ki-Hong;Heras, Chloe R.;Lee, Gina
    • Molecules and Cells
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    • v.45 no.7
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    • pp.435-443
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    • 2022
  • In response to environmental changes, signaling pathways rewire gene expression programs through transcription factors. Epigenetic modification of the transcribed RNA can be another layer of gene expression regulation. N6-adenosine methylation (m6A) is one of the most common modifications on mRNA. It is a reversible chemical mark catalyzed by the enzymes that deposit and remove methyl groups. m6A recruits effector proteins that determine the fate of mRNAs through changes in splicing, cellular localization, stability, and translation efficiency. Emerging evidence shows that key signal transduction pathways including TGFβ (transforming growth factor-β), ERK (extracellular signal-regulated kinase), and mTORC1 (mechanistic target of rapamycin complex 1) regulate downstream gene expression through m6A processing. Conversely, m6A can modulate the activity of signal transduction networks via m6A modification of signaling pathway genes or by acting as a ligand for receptors. In this review, we discuss the current understanding of the crosstalk between m6A and signaling pathways and its implication for biological systems.

Effect of Embelin on TRAIL Receptor 2 mAb-induced Apoptosis of TRAIL-resistant A549 Non-small Cell Lung Cancer Cells

  • Jiang, Lei;Hao, Jin-Li;Jin, Mu-Lan;Zhang, Yun-Gang;Wei, Ping
    • Asian Pacific Journal of Cancer Prevention
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    • v.14 no.10
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    • pp.6115-6120
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    • 2013
  • Introduction: Some non-small cell lung cancer (NSCLC) tumor cells are insensitive to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) -based therapy. This study was conducted to examine the effect of embelin on the sensitivity of the A549 NSCLC cell line to TRAIL receptor2 (TRAILR2) monoclonal antibodies and to investigate the potential mechanisms. Materials and Methods: A549 cells were treated with embelin, TRAILR2 mAb or a combination of both. Cell viability was measured using ATPlite assay and apoptosis rates were determined by flow cytometry with AnnexinV-FITC and propidium iodide staining, with the expression levels of proteins analyzed by Western blotting. Results: The cell survival rate of separate treatments with 100 ng/ml TRAILR2 antibody or 25 uM embelin were $81.5{\pm}1.57%$ and $61.7{\pm}2.84%$, respectively. Their combined use markedly decreased cell viability in A549 cells to $28.1{\pm}1.97%$ (P<0.05). The general caspase inhibitor Z-VAD-FMK could inhibit the embelin-enhanced sensitivity of A549 cells to TRAILR2 mAb ($75.97{\pm}3.17%$)(P<0.05). Both flow cytometry and cell morphological analysis showed that embelin was able to increase TRAIL-induced apoptosis in A549 cells. Combined treatment with embelin and TRAILR2 mAb augmented the activation of initiator caspases and effector caspase. In addition, A549 cells showed increasing levels of TRAILR2 protein and decreasing levels of Bcl-2, survivin and c-FLIP following the treatment with embelin+TRAILR2 mAb. Conclusions: Embelin could enhance TRAIL-induced apoptosis in A549 cells. The synergistic effect of the combination treatment might be due to modulation of multiple components in the TRAIL receptor-mediated apoptotic signaling pathway, including TRAILR2, XIAP, survivin, Bcl-2 and c-FLIP.