Dr. Chen, Chien-Chang ’s Lab陳建璋 博士 實驗室

國立陽明大學

國際研究生分子醫學學程

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國立中興大學

生物科技學研究所

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國立中興大學

生命科學研究所

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國立成功大學

Taiwan International Graduate Program Interdisciplinary Neuroscience (TIGP-INS)

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國立成功大學

Taiwan International Graduate Program Interdisciplinary Neuroscience (TIGP-INS)

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PhD candidate, Graduate Program of Translational Medicine, Tzu Chi University and Academic Sinica, Taiwan 

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國防醫學院

生命科學研究所

Postdoctoral researcher at Genomic Research Center, Academia SINICA

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國立陽明大學

國際研究生分子醫學學程

The central machenism of chronic pain using mouse model. My focus is studying the function of a brain region, PVA, in pain circuitry: how PVA neurons response to noxious peripheral imputs, how it mediates chronic pain developement. Hopefully this will be a step to the better pain management.

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國立陽明大學

國際研究生分子醫學學程

My study interest is in the field of cardiac hypertrophy. Cardiac hypertrophy can be classified by the cardiac function, causes and molecular mechanism into two categories: physiological and pathological cardiac hypertrophy. For example, the fetal gene reprograming is a distinct feature of pathological cardiac hypertrophy; however, we find those fetal genes, such as atrial natriuretic factor (ANF), β-myosin heavy chain (β-MHC), are not expressed on every cardiomyocyte in the pathological hypertrophic heart. I desire to know what makes cardiomyocytes from a single heart have different phenotype. Taking advantage of the transgenic mouse line which can express yellow fluorescent protein (YFP) tagged β-MHC fusion protein, I am trying to analyze the gene or protein expression pattern to characterize the YFP positive and negative cardiomyocytes. I am using transverse aortic banding (TAB) and neurohumoral infusion to induce pathological cardiac hypertrophy in YFP-β-MHC transgenic mice. Meanwhile, I will use several approaches and techniques, such as fluorescence activated cell sorting (FACS), next generation sequencing (NGS), immunofluorescence assay, western blot and qPCR to analyze the gene/protein expression. This study can help us to understand more mechanism in cellular level, and hopefully may help us to discover a better way to treat the cardiovascular disease.

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國立陽明大學

國際研究生分子醫學學程

Platelets play important role in hemostasis and thrombus formation. Increased intracellular calcium concentration leads to activation of platelets followed by aggregation. Previous studies have shown that elevation in [Ca²⁺]_I  occurs through the release of ca²⁺ from intracellular stores and entry of extracellular ca²⁺ from different calcium channels. However, role of T type calcium channel in platelets activation is not yet known. Preliminary study involving FeCl₃ induced carotid artery thrombosis showed lesser thrombosis in Ca_v3.2 (KO) mice compared to wild type and Ca_v3.1. Therefore, we hypothesize that T type calcium channel, especially Ca_v3.2, is present in platelets and somehow influences either adhesion, activation or aggregation of platelets.

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