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國防醫學院 生命科學研究所 高森永所指導 陳淑芬的 婦癌病人接受化學治療期間症狀群集、復原力與其相關因素探討 (2021),提出Pilot Road 4 SC關鍵因素是什麼,來自於婦癌、症狀群集、復原力。

而第二篇論文臺北醫學大學 國際醫學研究博士學位學程 莊 校奇、劉 文德所指導 NGUYEN THANH TUNG的 Association of air pollution and body composition in obstructive sleep apnea (2021),提出因為有 Apnea–hypopnea index (AHI)、Body fluid、Fat distribution、Muscle distribution、Particulate matter、Nitrogen dioxide、Ozone、Road dust、Upper airway的重點而找出了 Pilot Road 4 SC的解答。

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婦癌病人接受化學治療期間症狀群集、復原力與其相關因素探討

為了解決Pilot Road 4 SC的問題,作者陳淑芬 這樣論述:

背景與目的 病人在化學治療過程中會同時經歷許多症狀,衝擊到病人的疾病適應與復原力,國內鮮少研究探討婦癌病人症狀群集與復原力的關係。本研究旨在探討婦癌病人接受化學治療期間症狀群集、復原力與相關因素之相關性。研究方法 本研究採前瞻性重複測量研究設計,以方便取樣方法在北部某醫學中心婦科病房收案,收案標準為初次診斷婦癌接受手術治療後輔助化學治療的婦女,年齡在18歲以上,需接受化學治療6次、沒有認知障礙;其排除標準為認知功能惡化的患者如譫妄或腦轉移或沮喪病史,共選取124位婦癌病人為研究對象,資料收集共4次時間點,分為婦癌病人接受手術治療後準備要進行化學治療前、第一次化療後、第三次化療後與

第六次化療後。研究工具包括基本資料、疾病特性、身體功能量表、症狀群集量表和復原力量表。以SPSS 22.0版進行描述性與推論性統計分析。研究結果壹、婦癌病人在化學治療前歷經症狀經驗,嚴重度高為「難以入睡」、「疼痛」與「精力缺乏」;而接受化學治療後症狀困擾嚴重度高為「掉髮」、「手腳麻木與刺痛」與「難以入睡」。貳、在婦癌病人接受化學治療前出現三個症狀群集,分為情緒症狀群集、疲憊症狀群集、身體心像症狀群集,而在化學治療後三次追蹤的時間點,其症狀群集包括與情緒症狀群集、疲憊症狀群集、身體心像症狀群集及腸胃症狀群集等四個因素。參、身體功能狀態是影響婦癌病人在化學治療期間「疲憊症狀群集」重要預測因子,隨著

治療時間的變化,身體功能降低愈多,在疲憊症狀群集與腸胃症狀群集愈增加。肆、年齡影響婦癌病人在化學治療期間「腸胃症狀群集」的因素,隨著治療時間的變化,年齡愈長,在腸胃症狀群集分數減少。伍、婦癌病人復原力總分由接受化學治療前的141.41分下降至第六次化療後的124.21分,隨著時間趨勢變化,達統計顯著意義。陸、以廣義方程式多變量迴歸分析結果影響復原力的因素為職業、化療藥物與「情緒症狀群集」,隨著時間的變化,控制職業與化學藥物後,「情緒症狀群集」是影響復原力主要因素,情緒症狀群集分數愈高,復原力下降愈多。結論與建議本研究發現情緒症狀群集是影響婦癌病人復原力的主要因子。據此,在化學治療前提供婦癌病人

症狀群集的認知,並定時評估與症狀管理,提供適當的介入措施與適時轉介跨領域專業人員,以緩解不適的症狀發生,進而提升復原力,協助病人適應疾病。

Association of air pollution and body composition in obstructive sleep apnea

為了解決Pilot Road 4 SC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.