發問時間: 社會與文化語言 · 6 年前

求英文paper翻譯(睡眠醫學方面)

Diminished endothelial function is an important consequence of OSA and is frequently measured as impaired endotheliumdependent vasodilatation .Different studies show lower levels of circulating NO in OSA, for example, by the reduced levels of serum nitrite/nitrate (by-products of normal NO metabolism) in OSA subjects (38.9 lMvs. 63.1 lMin controls) . This was confirmed in other studies where nitrate/nitrite levels were significantly lower in OSA patients (35.6 lM) when compared to control (72.6 lM) . Many mechanisms have been suggested for endothelial dysfunction because of OSA or IH, including (1) interaction of NO and ROS forming peroxynitrite, (2) uncoupling of endothelial nitric oxide synthase (eNOS), and (3) decreased endothelial expression of eNOS and increased levels of endogenous eNOS inhibitors . Because of its short half-life and large volume of distribution, peroxynitrite is hard to measure and these factors explain the lack of difference in nitrotyrosine levels between OSA and healthy subjects. However, Jelic et al. found an increased expression of nitrotyrosine in endothelial cells derived from OSA patients.In all the forms of NOS, including the endothelial one, enzymatic activity requires five cofactor groups to incorporate oxygen into the amino acid L-arginine to produce NO. Those cofactors include flavin adenine dinucleotide (FAD), flavin mononucleotide (FMN), heme, tetrahydrobiopterin (BH4), and Ca2+-calmodulin. If NOS lacks L-arginine or any of these cofactors, it will produce superoxide anion instead of NO through an uncoupled state of NOS . Antoniades et al. showed that increased ROS production during hypoxia could lead to BH4 oxidation and increased levels of arginase II that degrades L-arginine, leading to further eNOS uncoupling. Patients with OSA have increased levels of asymmetrical dimethylarginine (ADMA), a competitive inhibitor of NOS .

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  • 6 年前
    最佳解答

    減少內皮功能是OSA的一個重要後果,並經常測量為受損endotheliumdependent血管舒張。不同的研究表明,在OSA的循環編號,例如較低水平,血清亞硝酸鹽/硝酸鹽的水平降低(副產物的正常NO代謝)在OSA患者(38.9 lMvs。63.1 LMIN控制)。這在其他研究中被證實在哪裡時,與對照組相比(72.6 LM)硝酸鹽/亞硝酸鹽的含量均顯著降低OSA患者(35.6 LM)。許多機制已被建議用於血管內皮功能障礙,因為OSA或IH的,包括(1)相互作用NO和ROS形成過氧亞硝酸鹽,內皮型一氧化氮合酶(eNOS)的(2)脫開,和eNOS(3)降低內皮表達和增加內源性eNOS的抑製劑水平。由於其半衰期短和分佈容積大的,過氧亞硝酸鹽是難以測量和這些因素解釋缺乏在OSA和健康受試者間硝基酪氨酸水平的差異。然而,耶利奇等。發現硝基酪氨酸在從OSA patients.In衍生NOS的所有形式,包括血管內皮1內皮細胞的增加的表達,酶活性需要五個輔助因子基團,其中包含的氧氣進入氨基酸L-精氨酸產生NO。這些輔因子包括黃素腺嘌呤二核苷酸(FAD),黃素單核苷酸(FMN),血紅素,四氫生物蝶呤(BH4)和Ca2 + - 鈣調蛋白。如果一氧化氮合酶缺乏L-精氨酸或任何這些輔助因子,它會通過一氧化氮合酶的耦合狀態下產生超氧陰離子,而不是沒有。 Antoniades等。表明增加的ROS產生缺氧可導致BH4氧化和精氨酸酶II降解L-精氨酸水平的增加,從而導致進一步的eNOS解偶聯。 OSA患者增加了非對稱二甲基精氨酸(ADMA),NOS的競爭性抑製劑的水平。

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