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Association of air pollution and body composition in obstructive sleep apnea

為了解決Fx678 gold的問題，作者NGUYEN THANH TUNG 這樣論述：

A relationship between exposure to ambient air pollution and obstructive sleep apnea (OSA) severity was reported in epidemiological studies. Exposure to air pollution may result in increased oxidative stress, inflammation, epithelial barrier disruption, and permeability in the upper airway, which c

ould all predispose to OSA. However, there is paucity of data on the biological mechanism of this hyperpermeability. Furthermore, the overnight changes in body composition after exposure to air pollution and how they affected the severity of OSA is still unclear.To investigate the associations of bo

dy composition changes with OSA, pre- and post-sleep body composition of 1584 patients with OSA were collected. We observed that increases in limb fat deposition and visceral fat level were associated with increased OSA severity. Each increase in total fat deposition and segmental fat deposition was

associated with increased odds ratio of positional OSA. In patients with positional OSA, an increase in the fat distribution of the limbs was associated with increases in the total arousal index, especially in the non-rapid eye movement (NREM) stage.To examine the association of air pollutant expos

ure with nocturnal body composition changes and OSA, we measured pre- and post-sleep body composition of 197 subjects from a sleep center and their individual air pollution exposure (particulate matter (PM) less than 2.5 µm in aerodynamic diameter (PM2.5), ozone (O3), and nitric dioxide (NO2)). We o

bserved that exposure to air pollutants was associated with total muscle mass and leg fat percentage changes. We found an association between PM deposition in lung regions, especially in the alveolar region, and body fat accumulation in OSA. The leg fat deposition and total muscle mass changes was f

ound to be associated with the apnea-hypopnea index (AHI). These findings implied that air pollution was associated with increases in the leg fat percentage and total muscle mass changes, thus aggravating OSA severity.We then collected road dust PM2.5 from 20 cities in China and treated to human pha

ryngeal epithelial (FaDu) cells. We observed that road dust PM2.5 exposure led to declines in cell viability and increases in lactate dehydrogenase (LDH) and interleukin (IL)-6. PM2.5, especially the inorganic elemental components, led to decreases in E-cadherin and occludin and increases in EGFR an

d phosphorylated (p)-EGFR on FaDu cells, later confirmed by the knockdown of E-cadherin. The findings indicate that PM2.5 may induce the inflammation, disrupt the epithelial barrier integrity, and increase the permeability in human upper airway through the regulation of occludin, E-cadherin, EGFR, a

nd p-EGFR.Together, the air pollution-induced hyperpermeability could increase overnight fluid shift and body composition changes, thus aggravating OSA. Air pollution, particularly the PM2.5, had the potential to increase the severity of OSA through body composition changes and upper airway hyperper

meability. Our study shed light on the etiology of OSA and positional OSA. Decreasing the total fat mass and fat percentage may reduce OSA severity. Finally, measures to decrease air pollution in urban areas could be beneficial for OSA patients.

以類傑夫法製備電極用於臨床尿液檢體之肌酸酐電位式感測

為了解決Fx678 gold的問題，作者胡毅 這樣論述：

肌酸酐為肌酸 (creatine) 與磷酸肌酸 (creatine phosphate) 之代謝廢物，為人體血液與尿液中作為評估腎臟功能的重要指標之一，臨床上常使用傑夫呈色法 (Jaffé reaction)，利用苦味酸 (picric acid) 與肌酸酐之呈色反應進行檢測。本研究期望以電化學方法結合傑夫呈色法以達到更快速且便利之定量手段。以3,5-二硝基苯甲酸 (3,5-dinitrobenzoic acid, DNB) 取代苦味酸，透過分光光度計、螢光光度計和紅外線光譜儀分析DNB與肌酸酐之呈色反應，本研究簡稱為類傑夫呈色法 (modified Jaffé reaction)。

本研究擬將DNB固定於以poly(Pyr-P3CA) 高分子膜修飾的工作電極上，poly(Pyr-P3CA) 是以吡咯 (pyrrole, Pyr) 與吡咯-3-羧酸 (pyrrole-3-carboxylic acid, P3CA) 經由電聚合方式形成的共聚膜。文中除了以分光光度計、螢光光度計和紅外線光譜儀分析確認DNB與肌酸酐之反應性，乃是以電化學電位式進行肌酸酐濃度的校正與檢測。此外不同的電極製備參數亦將於本研究中進行探討，同時，亦以本研究開發的肌酸酐感測器對尿液檢體進行感測與比對，以確認開發的感測器在臨床應用的可行性。