Browsing by Author "Chen, Huei-Wen"

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A method for measuring two-dimensional refractive index distribution with the total internal reflection of p-polarized light and the phase-shifting interferometry
(2006-12-01)
Jian, Zhi-Cheng
;
Hsieh, Po-Jen
;
Hsieh, Hung-Chih
;
Chen, Huei-Wen
;
Su, Der-Chin
Based on the total internal reflection of p-polarized light and the phase-shifting interferometry, an alternative method for measuring the two-dimensional refractive index distribution of a material is presented. The p-polarized light is incident on the boundary between a right-angle prism and a tested material. When the total internal reflection occurs at the boundary, and the p-polarized light has a phase variation. It depends on the refractive index of the tested material. Firstly, the two-dimensional phase variation distribution of the p-polarized light at the boundary is measured by the four-step phase shifting interferometric technique. Then, substituting the data into the special equations derived from Fresnel equations, the two-dimensional refractive index distribution of the tested material can be obtained. (c) 2006 Elsevier B.V. All rights reserved.
Landscape of Mitochondria Genome and Clinical Outcomes in Stage 1 Lung Adenocarcinoma
(2020-03-01)
Raghav, Lovely
;
Chang, Ya-Hsuan
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Hsu, Yi-Chiung
;
Li, Yu-Cheng
;
Chen, Chih-Yi
Risk factors including genetic effects are still being investigated in lung adenocarcinoma (LUAD). Mitochondria play an important role in controlling imperative cellular parameters, and anomalies in mitochondrial function might be crucial for cancer development. The mitochondrial genomic aberrations found in lung adenocarcinoma and their associations with cancer development and progression are not yet clearly characterized. Here, we identified a spectrum of mitochondrial genome mutations in early-stage lung adenocarcinoma and explored their association with prognosis and clinical outcomes. Next-generation sequencing was used to reveal the mitochondrial genomes of tumor and conditionally normal adjacent tissues from 61 Stage 1 LUADs. Mitochondrial somatic mutations and clinical outcomes including relapse-free survival (RFS) were analyzed. Patients with somatic mutations in the D-loop region had longer RFS (adjusted hazard ratio, adjHR = 0.18, p = 0.027), whereas somatic mutations in mitochondrial Complex IV and Complex V genes were associated with shorter RFS (adjHR = 3.69, p = 0.012, and adjHR = 6.63, p = 0.002, respectively). The risk scores derived from mitochondrial somatic mutations were predictive of RFS (adjHR = 9.10, 95%CI: 2.93-28.32, p < 0.001). Our findings demonstrated the vulnerability of the mitochondrial genome to mutations and the potential prediction ability of somatic mutations. This research may contribute to improving molecular guidance for patient treatment in precision medicine.
Proteogenomics of Non-smoking Lung Cancer in East Asia Delineates Molecular Signatures of Pathogenesis and Progression
(2020-07-09)
Chen, Yi-Ju
;
Roumeliotis, Theodoros, I
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Chang, Ya-Hsuan
;
Chen, Ching-Tai
;
Han, Chia-Li
Lung cancer in East Asia is characterized by a high percentage of never-smokers, early onset and predominant EGFR mutations. To illuminate the molecular phenotype of this demographically distinct disease, we performed a deep comprehensive proteogenomic study on a prospectively collected cohort in Taiwan, representing early stage, predominantly female, non-smoking lung adenocarcinoma. Integrated genomic, proteomic, and phosphoproteomic analysis delineated the demographically distinct molecular attributes and hallmarks of tumor progression. Mutational signature analysis revealed age- and gender-related mutagenesis mechanisms, characterized by high prevalence of APOBEC mutational signature in younger females and over-representation of environmental carcinogen-like mutational signatures in older females. A proteomics-informed classification distinguished the clinical characteristics of early stage patients with EGFR mutations. Furthermore, integrated protein network analysis revealed the cellular remodeling underpinning clinical trajectories and nominated candidate biomarkers for patient stratification and therapeutic intervention. This multi-omic molecular architecture may help develop strategies for management of early stage never-smoker lung adenocarcinoma.
The difference in myocardial injuries and mitochondrial damages between asphyxial and ventricular fibrillation cardiac arrests
(2012-10-01)
Tsai, Min-Shan
;
Huang, Chien-Hua
;
Tsai, Shang-Ho
;
Tsai, Chia-Ying
;
Chen, Huei-Wen
Introduction: Ventricular fibrillation (VF) and asphyxia account for most cardiac arrests but differ in cardiac arrest course, neurologic deficit, and myocardial damage. In VF resuscitation, cardiac mitochondria were known to be damaged via excess generation of reactive oxygen species. This study evaluated the difference of cardiac mitochondrial damages between VF and asphyxial cardiac arrests. Methods: In the VF + electrical shock (ES) group, VF was induced and untreated for 5 minutes, followed by 1 minute of cardiopulmonary resuscitation (CPR) and 1 ES of 5 J. Animals were killed immediately after ES. In the asphyxia group, cardiac arrest was induced by airway obstruction, and then pulselessness was maintained for 5 minutes, followed by 1 minute of CPR. The animals were killed immediately after CPR. The histology and ultrastructural changes of myocardium and complex activities and respiration of mitochondria were evaluated. The mitochondrial permeability transition pore opening was measured based on mitochondrial swelling rate. Results: The histopathologic examinations showed myocardial necrosis and mitochondrial damage in both cardiac arrests. Instead of regional damages of myocardium in the VF + ES group, the myocardial injury in the asphyxia group distributed diffusely. The asphyxia group demonstrated more severe mitochondrial damage than the VF + ES group, which had a faster mitochondrial swelling rate, more decreased cytochrome c oxidase activity, and more impaired respiration. Conclusions: Both VF and asphyxial cardiac arrests caused myocardial injuries and mitochondrial damages. Asphyxial cardiac arrest presented more diffuse myocardial injuries and more severe mitochondrial damages than VF cardiac arrest. (c) 2012 Elsevier Inc. All rights reserved.