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Association of air pollution and body composition in obstructive sleep apnea

為了解決Yang Ming Line HK Lt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.

探討經紋球藻萃取物對口腔癌細胞株抑制作用的機制

為了解決Yang Ming Line HK Lt的問題，作者黃政諺 這樣論述：

口腔癌為全球前十大癌症之一，名列台灣男性常見癌症的第四位。口腔癌中有超過90％的患者被確定為所謂的口腔鱗狀細胞癌(Oral Squamous Cell Carcinoma；OSCC)，主要造成的原因為長期嚼食檳榔、抽菸、飲酒，或是人類乳突病毒的感染。多數患者就診時已進入第三或四期，此時的癌細胞已經逐漸轉移至其他部位，造成五年存活率低下，所以新藥物的開發及探討誘導癌病變之檳榔成分益顯重要。而微藻已被發現具抗發炎及抗癌活性，成為新藥物開發的新目標。本研究所使用的材料為微藻中經紋球藻屬(Coelastrella)之經紋球藻C. F50，是於台灣南部新鑑定出的品種，其有機萃取物，以不同濃度分別處理

OC2和OCSL二株國內建立的口腔癌細胞株，並於處理後不同的時間點透過MTT試驗來測試細胞生長情況，結果發現C. F50萃取物能降低二株細胞株的生存率，其IC50皆約為500 μg/ml。在細胞侵入試驗(Cell invasion assay)中也發現C. F50萃取物處理後確實可以抑制OC2和OCSL的侵入能力。另外，也測試臨床上用來治療口腔癌常見的第一線的化療藥物Cisplatin和C. F50萃取物一同處理之效果，結果顯示兩者一同添加處理比個別單一藥物處理更能夠抑制癌細胞株生長。此外，為進一步探討此抑制作用的機制，以實驗室先前發現活性氧化物質(Reactive Oxygen Specie

s, ROS)和內質網壓力(ER stress)啟動未摺疊蛋白反應(Unfolded Protein Respond, UPR)所造成的一系列訊息傳遞途徑為主要目標，因為C. F50萃取物處理OC2和OCSL後其UPR相關的p-PERK、IRE1α、GRP78等標記蛋白之量皆有下降的現象，但ROS卻有上升的情況，所以推測C. F50萃取物可能使ROS堆積過量，而抑制UPR的作用，進而造成細胞壞死。我的初步實驗結果也顯示:與細胞增殖、生長和遷移相關的蛋白p-Akt (Akt)和p-mTOR (mTOR) 在以C. F50萃取物處理時均有被下調的情形。另外，因先前有文獻指出mTOR本身會抑制細胞自

噬的發生，所以我也透過LC3的表現來評估C. F50是否會造成細胞自噬，發現C. F50處理後的LC3的量並無明顯變化，以Acridine orange染色結果亦是如此，故推測細胞自噬並非C. F50造成細胞死亡的主因。 另外，本實驗室先前的研究中發現檳榔水萃取物中有誘發細胞核固縮壞死(pyknotic necrosis)的能力，其核固縮壞死發生時會先造成細胞的腫脹，這樣的現象跟臨床上有檳榔嚼食患者的病理組織切片觀察相當類似，故我們想要更進一步的去分析檳榔水萃取物中主要造成這種現象的成分為何。以HPLC (高效液相層析儀)從檳榔水萃取物中初步分離出幾個波峯，分別處理細胞並觀察是否造成細胞

核固縮，目前有發現數個波峯段之成分是具有效果的，未來希望找出造成細胞核固縮的有效成分。