簡介：中文中文12萬字萬字出處出處REITSMAS,SLAAFDW,VINKH,ETALTHEENDOTHELIALGLYCOCALYXCOMPOSITION,FUNCTIONS,ANDVISUALIZATIONJPFLüGERSARCHIVEUROPEANJOURNALOFPHYSIOLOGY,2007,4543345359內(nèi)皮細胞糖萼組成，功能及可視性內(nèi)皮細胞糖萼組成，功能及可視性REITSMAS,SLAAFDW,VINKH,ETAL摘要本文旨在提出關(guān)于內(nèi)皮細胞糖萼構(gòu)成與功能的最新知識。內(nèi)皮糖萼是一個覆蓋于管腔內(nèi)皮、與細胞膜連接，由蛋白多糖及糖蛋白等構(gòu)成的網(wǎng)絡(luò)。其中包含內(nèi)皮源性及血源性的可溶性分子。近十年來,人們對血管內(nèi)皮糖萼在各種生理、病理過程中作用的認識在不斷增加,其中包括細胞膜的機械運輸、止血、信號傳導以及血細胞與血管壁的相互作用。本文就內(nèi)皮細胞糖萼在糖尿病、缺血/再灌注組織損傷、動脈粥樣硬化中的起到的作用進行綜述。從微觀和宏觀的實驗數(shù)據(jù)揭示內(nèi)皮細胞糖萼對心血管系統(tǒng)的保護作用。為評估內(nèi)皮細胞糖萼的確切作用，將這一細微結(jié)構(gòu)可視化，是一個巨大的挑戰(zhàn)。已有綜述列舉目前為止將內(nèi)皮細胞糖萼可視化的不同方法，其中包括通過雙光子顯微鏡成像技術(shù)，及通過該項技術(shù)獲得的第一數(shù)據(jù)。關(guān)鍵詞內(nèi)皮細胞糖萼。內(nèi)皮細胞表面層。硫酸乙酰肝素。透明質(zhì)酸。血管疾病。光學成像。雙光子顯微成像。簡介40年前，LUFT通過電子顯微鏡成像技術(shù)使得內(nèi)皮細胞糖萼可視化成為可能。至今，我們對內(nèi)皮細胞糖萼層組成和功能了解仍然較少。在過去的幾十年里，人們高度認可內(nèi)皮細胞糖萼在血管生理、病理過程中的重要作用。在2000年P(guān)RIES等人的綜述以及其他最近的評論中都有描述。人們對內(nèi)皮細胞糖萼在病、生理中作用的關(guān)注始于人們發(fā)現(xiàn)血管系統(tǒng)的代謝水平和藥理活性水平的不同決定了毛細血管內(nèi)血細胞比容的不同。一方面代謝水平與激動劑誘作用，提高紅細胞流動速率。另一方面，管內(nèi)紅細胞比容的關(guān)系可部分由FAHRAEUS效應(yīng)的延伸血漿撇清原理解釋。然而,由于肝素酶可分解內(nèi)皮細胞糖萼上硫酸乙酰肝素，應(yīng)用肝素酶進行的微血管的局部治療可破壞這種關(guān)系。這一發(fā)現(xiàn)與用理論估計預(yù)測的蛋白多糖（粘蛋白）蛋白多糖被普遍認為是內(nèi)皮細胞糖萼中最重要的“支柱”分子，由一個核心蛋白組成，有一條或多條糖胺聚糖鏈與之相連。蛋白多糖核心蛋白之間有著明顯的不同，區(qū)別于分子量大小、連接糖胺聚糖鏈的數(shù)量以及是否與細胞膜相連。多配體（蛋白）聚糖及磷脂酰肌醇（蛋白）聚糖的核心蛋白組通過跨膜區(qū)域（多配體（蛋白）聚糖）或糖基化磷脂酰肌醇錨（磷脂酰肌醇（蛋白）聚糖）與細胞膜緊密連接。其他蛋白多糖，例如MIMECAN、基底膜蛋白多糖、二聚糖，在他們聚集、糖胺聚糖鏈被修改之后被分泌。這領(lǐng)導了存在于內(nèi)皮細胞糖萼及血流中的可溶性蛋白多糖的生成。蛋白多糖與糖胺聚糖鏈的連接非?；祀s，這說明了，一種核心蛋白可包含不同種類型的糖胺聚糖鏈。不同糖胺聚糖鏈之間的組成比例因周圍環(huán)境及刺激的不同而變化。因此，不能根據(jù)一種糖胺聚糖鏈而命名這種蛋白多糖。例如，多配體（蛋白）聚糖1蛋白多糖通常被稱為硫酸乙酰肝素蛋白多糖。實際上，他包含的硫酸乙酰肝素的數(shù)量與硫酸軟骨素鏈的數(shù)量很相近。有五種類型的糖胺聚糖鏈硫酸乙酰肝素、硫酸軟骨素、硫酸皮膚素、硫酸角質(zhì)素及透明質(zhì)酸。他們是線性聚合物，由于硫酸化、（去）乙酰化程度的不同，具有長度可變的二聚糖。每一個二聚糖都由一個質(zhì)酸和氨基己糖組成。糖胺聚糖分類取決于包含何種質(zhì)酸或是氨基己糖，以及是否被硫酸化。五種糖胺聚糖中每一種都已被仔細的調(diào)查與廣泛的研究過。硫酸皮膚素常常被認為是單獨一類糖胺聚糖，盡管它是B型硫酸軟骨素。兩者之間的差異可能是由于硫酸皮膚素中，GLUCURONIC葡糖醛酸通過差向異構(gòu)轉(zhuǎn)變成艾杜糖醛酸。這對最終的功能有著重要的影響。只要有可能，我們會盡可能的區(qū)分兩者，或者以下，我們將以硫酸軟骨素|硫酸皮膚素命名。在血管系統(tǒng)中，硫酸乙酰肝素蛋白多糖大約占目前已發(fā)現(xiàn)的內(nèi)皮細胞糖萼中蛋白多糖的5090。然而，這個數(shù)字是可變的，內(nèi)皮細胞表達蛋白多糖取決于不同的刺激。例如，多配體（蛋白）聚糖的表達程度與內(nèi)皮細胞激活及化學因子刺激的不同而不同。在內(nèi)皮細胞糖萼中，第二常見的糖胺聚糖是硫酸軟骨素|硫酸皮膚素。據(jù)報道，在血管內(nèi)皮，硫酸乙酰肝素與硫酸軟骨素的表達有一個經(jīng)典的比例41。在血管系統(tǒng)中，硫酸角質(zhì)素糖胺聚糖的表達和其在（?。┥碇械闹匾赃€不明確。在內(nèi)皮細胞糖萼中另一個重要的糖胺聚糖是透明質(zhì)酸。這種長的聚合物分子（可長達104KDA）與其他糖胺聚糖不同，他不與核心蛋白

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簡介：中文中文1萬字萬字出處出處MEDAF,FOLCIM,BACCARELLIA,ETALTHEEPIGENETICSOFAUTOIMMUNITYJCELLULARMOLECULARIMMUNOLOGY,2011,83226236自身免疫表觀遺傳學自身免疫表觀遺傳學摘要摘要自身免疫性疾病的病因始終不為人們所知。同卵雙生子的疾病共顯率低于50，然而全基因組關(guān)聯(lián)研究只在一小部分病人發(fā)現(xiàn)了顯著關(guān)聯(lián)性。這個證據(jù)強烈支持了還有其他的補充機制涉及到了基因表達的調(diào)節(jié)過程最終導致了顯著的自身免疫病。組蛋白翻譯后修飾以及DNA甲基化是兩個主要的表觀遺傳學機制可能導致免疫耐受的下降以及自身免疫疾病的持續(xù)。在最近幾年對臨床以及實驗的研究中提出了表觀遺傳學可能使我們更容易理解自身免疫病的起病和疾病的持續(xù)。更特殊的是，數(shù)據(jù)顯示表觀遺傳學的改變在系統(tǒng)性紅斑狼瘡，風濕性關(guān)節(jié)炎，多發(fā)性硬化以及其他自身免疫病的影響，在某些病例是基于機械的觀察。在這篇文章，我們討論一下目前所知道的以及我們對未來的展望。最后，表觀遺傳學的治療已經(jīng)被用于腫瘤學，也可能在自身免疫病的治療中有良好的作用。為何研究表觀遺傳學為何研究表觀遺傳學自身免疫病通常被認為是一種復雜的疾病。遺傳背景使得人們對疾病有一定的易感性或抵抗性，但是它并不能成為疾病發(fā)展的使動原因。許多發(fā)病時環(huán)境的相似性已經(jīng)證實了，但是自身免疫性疾病的病因還不為人們所知。全基因組關(guān)聯(lián)研究已經(jīng)證實了強烈的遺傳背景的存在，但是這個研究并沒有證實免疫耐受下降的單基因機制，并且強烈的基因關(guān)聯(lián)性也只在一小部分人中被證實。在同卵雙生子自身免疫性疾病的不完全共顯率強烈的支持其他補充機制可能涉及到基因表達的調(diào)節(jié)，最終導致自身免疫疾病?；谶@些觀察，用一些新的方法來分析組蛋白修飾和DNA甲基化支持了表觀遺傳學可能在引起自身免疫性疾病中起了重要的作用這一概念。表觀遺傳學研究的機制即決定和維持基因組的功能，不伴有DNA序列的改變。表觀遺傳基因組和表觀遺傳基因型被認為是細胞通過表觀遺傳學機制誘導基因表大的特異的和穩(wěn)定的模式。在功能上，表觀遺傳學機制，確實在細胞分化過程中占重要的角色，它能夠誘導基因穩(wěn)定的表達和抑制。表觀遺傳學也能夠干預(yù)細胞的代謝，以此使細胞適應(yīng)周圍環(huán)境的改變。表觀遺傳學對環(huán)境和基因相互作用中扮演的角色，已經(jīng)在一些有趣的實驗中證實，當環(huán)境改變，會對基因表達產(chǎn)生修飾。首先，一項生殖的研究調(diào)查食物成分的改變對其影響，食物中富含甲基供體，為了改變懷孕刺鼠到的毛色，與喂養(yǎng)普通食物組對比，這些特殊食物所謂養(yǎng)出來的刺鼠后代毛色有特殊的改變。這個現(xiàn)象被證實有很明顯的DNA甲基化的改變，這就是非常徹底的表觀遺傳學的研究機制。這個過程是IAP逆轉(zhuǎn)錄病毒插入元件靜息，最終限制了刺鼠等位基因的表現(xiàn)。另一個典型的例子就是荷蘭人在二戰(zhàn)期間在子宮內(nèi)和兒童時期挨餓，對于胰島素樣生長因子表達調(diào)節(jié)區(qū)DNA甲基化分析，證明暴露組與非暴露組相比存在一個高度保守的低甲基化狀態(tài)。最近的觀察研究已經(jīng)證實，DNA甲基化與一些遺傳因素有關(guān)，包括懷孕前吸煙，酒精攝入，環(huán)境污染物。基于這些觀察，表觀遺傳學機制應(yīng)該被視為是環(huán)境和基因組作用的先驅(qū)。這樣就結(jié)合了那句老話“壞基因，壞運氣”。這個被實驗證據(jù)所支持，DRFRAGA和其同事證明了表觀遺傳學也許能夠解釋同卵雙生子自生免疫疾病非共顯率的問題。隨著年齡的增長，表型的異常顯著的增加，被稱為“表觀遺傳學流”，它是基于不同環(huán)境暴露所產(chǎn)生的。500個堿基對組成，CG的含量超過過55，CPG島有一個關(guān)鍵的調(diào)節(jié)功能，它存在于啟動子區(qū)域并占了大部分的區(qū)域。改變CPG島的甲基化狀態(tài)，也許能改變?nèi)旧|(zhì)結(jié)構(gòu)，最終能調(diào)節(jié)啟動轉(zhuǎn)錄因子與轉(zhuǎn)錄機制的相互作用。作為結(jié)果，在大多數(shù)的例子中，這種獲得性的和遺傳性的的甲基化狀態(tài)能夠?qū)е禄虮磉_的抑制，另外，CPG島甲基化狀態(tài)能與一種叫甲基CPG結(jié)合域的蛋白相互作用，盡管他們在不同細胞，不同位點的不同作用還不為大家所知，MBP蛋白被認為通過結(jié)合甲基化的DNA來抑制基因的表達，這個過程將會導致染色質(zhì)的修飾和重塑。DNA甲基化在基因表達中的重要性，通過性染色體的平衡呈現(xiàn)出來，女性X染色體的轉(zhuǎn)錄被部分抑制，這個事實通過對特異性的序列甲基化來實現(xiàn)的。哺乳動物的基因包含分散的基因簇，他從親代繼承的甲基化狀態(tài)決定了他某些特異性基因的表達機體繼承了這些表達了的或為表達的富含CPG的基因序列，被稱為基因印跡。因此，這些基因印跡甲基化過程的錯誤能夠使這些基因表達被繼承下來。從臨床的角度，DNA甲基化的重要性，尤其是甲基化損傷，是體現(xiàn)在兩個疾病，SILVERRUSSEL不對稱身材矮小性發(fā)育異常綜合征和BECKWITHWIEDEMANN。這兩種狀況都來自于11號染色體上基因印跡甲基化的錯誤，這種錯誤發(fā)生在編碼IGFF2以及母源基因表達（H19）。在生理情況系這些基因只在父源等位基因發(fā)生甲基化。BECKWITHWIEDEMANN綜合征由于父源母源的等位基因都發(fā)生甲基化而過多表達IGF2，然而，如果是這兩個印跡中心甲基化消失會導致IGF2位點的抑制以及H19表達增加最終導致SILVERRUSSEL綜合征。MICRORNAMICRORNA是翻譯后的調(diào)節(jié)因子，它涉及很多生理的過程，包括生長，分化，增殖、凋亡。MIRNA是一個22NT長非編碼RNA，他通過結(jié)合互補MRNA來抑制翻譯，并導致特定的RNA的降解。MIRNAS是基因編碼MRNA并且通過RNA聚合酶Ⅱ翻譯，與普通的編碼蛋白質(zhì)的RNA一樣，最近在自身免疫疾病和慢性炎癥中發(fā)現(xiàn)了他們。最著名的表觀遺傳學調(diào)節(jié)就是MIRNADNA相互作用，其代表就是女性X染色體的靜息。事實，兩條X染色體有一條在女性通過表觀遺傳學調(diào)節(jié)而處于靜息，導致X染色體的會存在劑量補償。這種平衡是通過X染色體靜息中心的X染色體靜息基因的轉(zhuǎn)錄來調(diào)節(jié)，這就使女性的基因表達與男性相適應(yīng)。XIST編碼一個非編碼MRNA包裝X染色體以此過程使得一大群在X染色體上的基因序列靜息。組蛋白抑制性標記物和DNA甲基化是這種靜息變得很穩(wěn)定，因為這些發(fā)生在X染色體上表觀遺傳學的錯誤能夠涉及到某些疾病的發(fā)病機制，包括自身免疫疾病。這確實是富有吸引人的假說，這就能夠解釋某些自身免疫病女性占優(yōu)勢的原因。自身免疫疾病和表觀遺傳修飾自身免疫疾病和表觀遺傳修飾表觀遺傳學對在所有復雜疾病中的影響里在快速的提高，并很快會在我們對醫(yī)學的理解中占重要的地位，我們也許可以假想表觀遺傳學將填補在特定情況下疾病發(fā)病機制中關(guān)于基因和環(huán)境因素的之間關(guān)系的空白。在某些自身免疫性疾病，免疫細胞的表觀遺傳學調(diào)節(jié)過程中出現(xiàn)的特異性損害可能會導致免疫耐受下降，這個過程涉及到基因低甲基化和轉(zhuǎn)錄抑制。在自身免疫性疾病中，表觀遺傳學主要是通過人類外周血單核細胞核或用動物模型來研究。在體和體外研究模型已經(jīng)證實，表觀基因組的變異也許可以導致自身反應(yīng)性T細胞克隆的發(fā)生，特異性的表觀遺傳學缺陷與某些自身免疫性疾病是有關(guān)的。例如，通過表觀遺傳學的調(diào)控，輔助性T細胞分化成TH1細胞亞群并產(chǎn)生IFN?并能夠?qū)辜毦?，TH2細胞產(chǎn)生IL4和IL13。TH1細胞有的IFNΓ啟動子區(qū)域去甲基化，

簡介：中文中文4000字出處出處KACZY?SKAA,KOSTRUBIECM,CIURZY?SKIM,ETALBTYPENATRIURETICPEPTIDEINACUTEPULMONARYEMBOLISMJCLINICACHIMICAACTA,2008,398214BNP在急性肺動脈栓塞預(yù)后中的意義在急性肺動脈栓塞預(yù)后中的意義ANNAKACZY?SKA,MACIEJKOSTRUBIEC,MICHA?CIURZY?SKI,PIOTRPRUSZCZYK【摘要】急性或慢性左心室功能不全時心肌擴張會導致心房利鈉肽的釋放。然而，有證據(jù)表明，B型利鈉肽（BNP）和N端片段（NTPROBNP）可能來源于右心室，當急性肺栓塞尤其存在右心功能不全（RVD）時它們的濃度會升高。近來，急性肺栓塞（APE）嚴重程度評估以及危險分層受到關(guān)注，治療方案的選擇是基于對患者的血流動力學狀態(tài)、心肌損傷標志物以及右心功能不全。BNP的和NTPROBNP是有助于識別存在右心功能不全的APE患者，在新興的超聲心動圖作為輔助工具的前提下，BNP或NTPROBNP水平升高也顯著的預(yù)測APE死亡和/或復雜的臨床過程?！娟P(guān)鍵字】急性肺栓塞，BNP，NTPROBNP水平，右心室功能不全，預(yù)后眾所周知，急性或慢性左心室功能不全時心肌擴張會導致心房利鈉肽的釋放。然而，有證據(jù)表明，B型利鈉肽（BNP）和N端片段（NTPROBNP）可能來源于右心室，當急性肺栓塞尤其存在右心功能不全（RVD）時它們的濃度會升高。最近強調(diào)指出，急性肺栓塞（APE）以及嚴重程度評估的風險分層和治療方案的選擇是基于對患者的血流動力學狀態(tài)、心肌損傷標志物和右心功能不全（RVD）。右心室功能，可直接由超聲心動圖和/或增強螺旋CT評估。由于血漿腦利鈉肽濃度反映右心功能不全的嚴重程度，因此，它的作用在APE危險分層中也被探討。針對B型利鈉肽，尤其是對于右心功能不全的檢測和臨床過程的嚴重程度預(yù)測。筆者進行了探討。1文獻選擇通過檢索“肺栓塞”，“BNP”和“NTPROBNP”，從1997年至2008年3月，共檢索到49篇文章。32兩篇文獻被排除，因為它們是病例報告、評論文章、社論或信件。他們沒有結(jié)束點，或沒有提供的生物標志物的濃度值。最終，17個有關(guān)BNP和NTPROBNP濃度升高影響短期死亡率，結(jié)果不良事件（死亡，心源性休克，需要溶栓，導管或外科手術(shù)取栓術(shù)，使用升壓藥，需要氣管插管和機械通氣，心肺復蘇），右心室功能不全的研究被選擇（表1）。2BNP和NTPROBNP含量測定B型利鈉肽前肽（PROBNP）可裂解為相同分子量的B型利鈉肽（BNP）和N末端片段（NTPROBNP）。BNP具有生理活性。BNP可由幾種放射免疫學或熒光免疫方法來測定濃度，而對于NTPROBNP，只有電化學發(fā)光免疫分析（ECLIA）測定。因此，BNP和NTPROBNP水平評估的結(jié)果是很難進行比較。3BNP和NTPROBNP水平在右心室功能不全檢測中的意義第一份關(guān)于APE中B型利鈉肽意義的報告來自2001年1。雖然患者數(shù)量較少，但是該研究證明，APE患者血漿BNP水平急性期較對照組顯著升高，在年齡和性別匹配的情況下。右室擴大的患者中最高的BNP濃度為（235（341628）PMOL/L），放射免疫學方法測定，APE相關(guān)死亡只發(fā)生在本組。相同的結(jié)果在庫徹等人研究的73例患者中被證實在2。懇求主要作者在分析截止90皮克/毫升作為BNP值用于排除充血性心臟衰竭。在大多數(shù)BNP升高的患者中，不同程度的RVD是由經(jīng)胸超聲心動圖觀察到的。此外，在克魯格等3的研究中，BNP90CUTOFF值皮克/毫升這個時候，作為ROC分析時計算所用，這是一個有意義的預(yù)測值，在不伴左心室功能障礙的亞組分析中（AUC07895％CI064092，敏感性64％，特異性94％）。在一項67例患者的研究中，200皮克/毫升被報道可預(yù)究中，分析評估預(yù)測致命的結(jié)果和/或后靜脈血栓栓塞在3個月內(nèi)復發(fā)的BNP濃度15。其計算截止點為125PMOL/L，靈敏度為60％，特異性為60％，陽性預(yù)測值為57％（AUC06395％CI為056070）。下面觀察老年患者（65歲），有臨床并發(fā)癥的患者BNP濃度顯著高于無并發(fā)癥的患者（274（142581）VS78（33230）PG/ML，P100皮克/毫升4。在TULEVSKI等的研究中，一半的患者入院時BNP濃度升高（10PMOL/L）。2例死亡患者的BNP濃度10PMOL/L17。從庫徹等人的關(guān)于NTPROBNP對于APE意義的的首份報73例患者中，發(fā)生并發(fā)癥的患者NTPROBNP水平顯著高于未發(fā)生不良結(jié)果（4250（8049,607）VS121（1634,802）PG/ML，P1000PG/ML為發(fā)生復雜臨床事件的陰性預(yù)測值為95％，死亡率為100。1相同的值，在另一個研究中被證實（AUC0809）20。NTPROBNP1000的PG/ML被用于預(yù)測不利的結(jié)果（OR117995％CI為16527，P0007）。NTPROBNP1000PG/ML的患者比7500PG/ML和24小時內(nèi)濃度下降小于50％的患者30天亡率為61％（95％CI39％84％）18。正如之前提到的，無LV充血性心力衰竭的右心功能不全患者，沒有已經(jīng)確定的分界點。ROC分析BNP濃度范圍從90到200PG/ML5,14,3,4。對于NTPROBNP，一個分析報告得出500PG/ML為分界點6（表2）。較低的閾值90100皮克/毫升有較高的靈敏度和中度的特異性，而采取更高的閾值科提高檢查出RVD的特異性。也有幾個分界點預(yù)測APE的不利結(jié)果。RIA法BNP提出了3個值125PMOL/L，25PMOL/L和10PMOL/L15,17,12。后兩個有類似的敏感性，但特異性較高的為10PMOL/L（表3）。對于由免疫方法測定的BNP的閾值范圍為50PG/ML和487PG/ML14,3,16,4,2。建議預(yù)測不良預(yù)后的分界值有高靈敏性及中度的特異性。只有一個研究3沒有確定BNP在預(yù)測APE不良預(yù)后中的作用。NTPROBNP閾值介于500至1000PG/M，他們有很高的陰性預(yù)測值20,7,6,19一項研究顯示7600PG/ML預(yù)測APE發(fā)生死亡有較高的特異性8。5結(jié)論根據(jù)研究，B型鈉尿肽可起源于右心室，對APE患者進行危險分層有重要的意義。BNP和NTPROBNP作為超聲心動圖的輔助工具也有助于確定患者是否發(fā)生右心功能不全。然而，仍需要包括大樣本患者、建立標準化的閾值，排除急性右心功能不全的患者研

簡介：ORIGINALPAPEREFFECTSOFDISTALPROTECTIONONLEFTVENTRICULARFUNCTIONINACUTEANTERIORMYOCARDIALINFARCTIONADOPPLERECHOCARDIOGRAPHICSTUDYYUNYANDUAN?HAIBINZHANG?LIWENLIU?XIAODONGZHOU?CHENGXIANGLI?JUNLI?TINGZHU?HAILISU?YONGSHENGZHU?HONGLINGLI?JUNZHANGRECEIVED14JANUARY2009/ACCEPTED16SEPTEMBER2009/PUBLISHEDONLINE4OCTOBER2009?SPRINGERSCIENCEBUSINESSMEDIA,BV2009ABSTRACTWHETHERDISTALPROTECTIONDEVICESDPDSDURINGPERCUTANEOUSCORONARYINTERVENTIONPCICANIMPROVEMYOCARDIALFUNCTIONINPATIENTSWITHACUTEMYOCARDIALINFARCTIONAMIISSTILLUNDERDEBATEUSINGTISSUEDOPPLERIMAGINGTDI,WEEVALUATETHEGLOBALANDREGIONALLEFTVENTRICULARSYSTOLICANDDIASTOLICFUNCTIONSINPATIENTSWITHANTERIORAMIUSINGDPDSCOMPAREDWITHCONVENTIONALPCININETYSIXPATIENTSWITHANTERIORAMIWERERANDOMLYASSIGNEDTOEITHERPCIWITHDPDSDPD,N46ORTRADITIONALPCICONTROL,N50GROUPSATTHE3AND6MONTHFOLLOWUPS,THEDPDGROUPHADAHIGHERLEFTVENTRICULAREJECTIONFRACTIONTHANTHECONTROLGROUP516±36VS493±53AND530±37VS508±52,RESPECTIVELYBOTHP\005MOREOVER,PEAKSYSTOLICSAANDEARLYDIASTOLICEAMITRALANNULARVELOCITIESOBTAINEDBYTDIWERESIGNIFICANTLYHIGHERINTHEDPDGROUPTHANINTHECONTROLGROUPSA757±053VS712±062CM/SAND771±063VS732±059CM/SEA723±078VS689±086CM/SAND749±069VS704±085CM/S,RESPECTIVELYALLP\005HOWEVER,SYSTOLICANDDIASTOLICREGIONALMYOCARDIALVELOCITIESSIGNIFICANTLYIMPROVEDINTHEDPDGROUPFROMTHE1MONTHFOLLOWUPCOMPAREDWITHTHOSEINTHECONTROLGROUPALLP\005PATIENTSWHORECEIVEDTREATMENTWITHDPDSEXPERIENCEDENHANCEDIMPROVEMENTOFCARDIACFUNCTIONTHUS,ANTERIORAMIPATIENTSCANBENEFITFROMDPDSDURINGPCIKEYWORDSECHOCARDIOGRAPHY?TISSUEDOPPLERIMAGING?DISTALPROTECTIONDEVICESABBREVIATIONSAPEAKFLOWVELOCITYDURINGLATEDIASTOLEAMIACUTEMYOCARDIALINFARCTIONDPDSDISTALPROTECTIONDEVICESEPEAKFLOWVELOCITYDURINGEARLYDIASTOLEEAPEAKEARLYDIASTOLICMITRALANNULARVELOCITIESEMPEAKEARLYDIASTOLICMYOCARDIALVELOCITIESLADLEFTANTERIORDESCENDINGCORONARYARTERYLVLEFTVENTRICLE/VENTRICULARPCIPERCUTANEOUSCORONARYINTERVENTIONRWMSIREGIONALWALLMOTIONSCOREINDEXSAPEAKSYSTOLICMITRALANNULARVELOCITIESYUNYANDUANANDHAIBINZHANGCONTRIBUTEDEQUALLYTOTHISSTUDYYYDUAN?HBZHANG?LWLIU?XDZHOU?JLI?TZHU?HLSU?YSZHU?HLLI?JZHANGFLOWGRADE3WITHINTHEVESSELWASCONSIDEREDTOBENORMALTHEPOSTINTERVENTIONANDFOLLOWUPTHERAPYSTRATEGIESWERESIMILARINTHETWOGROUPSECHOCARDIOGRAPHICEXAMINATIONECHOCARDIOGRAPHYWASPERFORMEDBEFOREPCIANDAT1,3,AND6MONTHSAFTERPCITHEOBSERVERWASBLINDTOALLCLINICALANDANGIOGRAPHICDATAALLECHOCARDIOGRAMSWEREPERFORMEDWITHANULTRASOUNDSYSTEMHDI5000ATL,PHILIPSMEDICALSYSTEM,USATHELVVOLUMESANDEJECTIONFRACTIONSWERECALCULATEDUSINGTHEMODIFIEDBIPLANESIMPSON’SFORMULAWITHIMAGESOBTAINEDFROMTHEAPICALFOURANDTWOCHAMBERVIEWSASRECOMMENDEDBYTHEAMERICANSOCIETYOFECHOCARDIOGRAPHY16PULSEDDOPPLERMEASUREMENTSOFLVFILLINGWEREOBTAINEDINTHEAPICALFOURCHAMBERVIEW,WITHTHESAMPLEVOLUMEPLACEDATTHELEVELOFTHEMITRALTIPSWEOBTAINEDPEAKFLOWVELOCITIESDURINGEARLYEANDLATEADIASTOLICFILLING,ANDTHEDIASTOLICTRANSMITRALE/AVELOCITYRATIOTHEPULSEDWAVETDIWASACQUIREDFROMAPICALFOURCHAMBER,TWOCHAMBER,ANDLONGAXISVIEWSA5MMSAMPLEVOLUMEOFTDIWASPOSITIONEDINSIXPOINTSOFTHEMITRALANNULUS,ANDTHEPEAKSYSTOLICSAANDPEAKEARLYDIASTOLICEAVELOCITIESWEREMEASUREDTOASSESSGLOBALLVSYSTOLICANDDIASTOLICFUNCTIONSTHERESULTSAREREPORTEDASAMEANOFTHESIXSAMPLESOFTHEMITRALANNULUSMEASUREMENTSOFTHEREGIONALMYOCARDIALVELOCITIESWERESAMPLEDINBASAL,MIDLEVEL,ANDAPICALSEGMENTSOFTHELVANTERIORWALLSFROMAPICALTWOCHAMBERVIEWSPEAKSYSTOLICMYOCARDIALVELOCITIESSMANDEARLYDIASTOLICMYOCARDIALVELOCITIESEMWEREOBTAINEDTHELVANTERIORWALLMOTIONWASSEMIQUANTITATIVELYGRADEDFROM1TO4ASFOLLOWS1NORMAL,2HYPOKINESIS,3AKINESIS,AND4DYSKINESISTHEREGIONALWALLMOTIONSCOREINDEXRWMSIOFTHEANTERIORWALLWASDERIVEDFROMTHEMEANOFTHETHREESEGMENTSCORES16WEPREVIOUSLYREPORTEDTHEMETHODSANDREPRODUCIBILITYOFTDIINDICESINOURLABORATORY17,18INTRAOBSERVERVARIABILITYWAS42±22FORSA,44±22FOREA,38±18FORSM,AND40±23FOREMTHECORRESPONDINGVALUESFORINTEROBSERVERVARIABILITYWERE49±27,55±29,46±25,AND52±24,RESPECTIVELYSTATISTICALANALYSISVALUESAREEXPRESSEDASTHEMEANS±STANDARDDEVIATIONS,WHENAPPROPRIATEGROUPDIFFERENCESWEREDETECTEDBYTHESTUDENT’STTESTORANALYSISOFVARIANCEANOVAFORCONTINUOUSVARIABLESANDV2TESTFORDISCRETEVARIABLESAPVALUE\005WASCONSIDEREDSTATISTICALLYSIGNIFICANTALLSTATISTICALANALYSESWEREPERFORMEDUSINGSTANDARDSTATISTICSSOFTWARESPSSVERSION100RESULTSGENERALCLINICALCHARACTERISTICSDURINGTHEENROLLMENTPERIOD,178PATIENTSWITHTHEIRFIRST,ANTERIORAMIWERESCREENEDOFTHESEPATIENTS,96WEREELIGIBLEFORRANDOMIZATIONFIFTYPATIENTSWERERANDOMLYASSIGNEDTOTHECONTROLGROUPAND46TOTHEDPDGROUPFIG1THEAGESOFTHESEPATIENTS81MALESWEREBETWEEN31AND75YEARSWITHAMEANAGEOF56±7YEARSBASELINECLINICALANDANGIOGRAPHICFEATURESWEREWELLMATCHEDBETWEENTHETWOSTUDYGROUPSTABLE1INTJCARDIOVASCIMAGING201026125–133127123

簡介：ULTRASOUNDSCREENINGOFPERIARTICULARSOFTTISSUEABNORMALITYAROUNDMETALONMETALBEARINGSTAKASHINISHII,MD,PHD,TAKASHISAKAI,MD,PHD,YMASAKITAKAO,MD,PHD,YHIDEKIYOSHIKAWA,MD,PHD,YANDNOBUHIKOSUGANO,MD,PHDABSTRACTALTHOUGHMETALHYPERSENSITIVITYORPSEUDOTUMORSARECONCERNSFORMETALONMETALMOMBEARINGS,DETAILEDPATHOLOGIESOFPATTERNS,SEVERITY,ANDINCIDENCEOFPERIPROSTHETICSOFTTISSUELESIONSAREINCOMPLETELYUNDERSTOODWEEXAMINEDTHEPOTENTIALOFULTRASOUNDFORSCREENINGOFPERIARTICULARSOFTTISSUELESIONSAROUNDMOMBEARINGSULTRASOUNDEXAMINATIONSWERECONDUCTEDIN88HIPS79PATIENTSWITHMOMHIPRESURFACINGSORMOMTOTALHIPARTHROPLASTIESWITHALARGEFEMORALHEADFOURQUALITATIVEULTRASOUNDPATTERNSWERESHOWN,INCLUDINGNORMALPATTERNIN69HIPS,JOINTEXPANSIONPATTERNIN11HIPS,CYSTICPATTERNIN5HIPS,ANDMASSPATTERNIN3HIPSHIPSWITHTHELATTER3ABNORMALPATTERNSSHOWEDSIGNIFICANTLYHIGHERFREQUENCYOFCLINICALSYMPTOMS,WITHOUTSIGNIFICANTDIFFERENCESOFSEX,DURATIONOFIMPLANTATION,HEADSIZES,ANDCUPABDUCTION/ANTEVERSIONANGLES,COMPAREDWITHHIPSWITHNORMALPATTERNULTRASOUNDEXAMINATIONPROVIDESSENSITIVESCREENINGOFSOFTTISSUEREACTIONSAROUNDMOMBEARINGSANDMAYBEUSEFULINMONITORINGPROGRESSIONANDDEFININGTREATMENTFORPERIARTICULARSOFTTISSUEABNORMALITIESKEYWORDSMETALONMETAL,ULTRASOUND,MRIMAGING,SOFTTISSUEREACTION,BEARINGS?2012ELSEVIERINCALLRIGHTSRESERVEDINTHE2000S,RENEWEDMETALONMETALMOMHIPRESURFACINGANDTOTALHIPARTHROPLASTYTHAWITHALARGEFEMORALHEADGAINEDGREATPOPULARITYWITHTHEEXPECTATIONOFLOWBEARINGWEAR,HIGHFUNCTIONANDACTIVITYOFPATIENTS,ANDLOWINCIDENCEOFPOSTOPERATIVEDISLOCATION13ASMOMHIPARTHROPLASTIESHAVEBECOMEMOREWIDESPREAD,INCREASINGABNORMALREACTIONSINPERIARTICULARSOFTTISSUEREACTIONSTHATPRESENTASCYSTS,FLUIDCOLLECTION,ENHANCEDBURSAE,SOLIDMASS,ANDINFLAMMATORYMASSESHAVEBEENREPORTED410SOMEOFTHESECASESWERERELATEDTOSEVEREPAININTHEHIPORGROIN,PALPABLEHUGEMASSES,OREXTENSIVEPERIPROSTHETICBONELOSSLEADINGTOREVISIONSURGERYWITHRESECTIONOFSOFTTISSUELESIONS,ANDALTERATIONINBEARINGSWITHOTHERMATERIALS9FROMANALYSESOFRETRIEVEDTISSUEANDCOMPONENTS,ADELAYEDTYPEHYPERSENSITIVEREACTIONSPECIFICALLYTERMEDASEPTICLYMPHOCYTICVASCULITIS–ASSOCIATEDLESIONSORRESPONSETOEXCESSIVEWEARPARTICLESOFMOMBEARINGSWASSUSPECTEDASTHEMAINCAUSEOFTHESOFTTISSUEREACTIONS5,1113HOWEVER,THEDETAILEDPATHOLOGIESOFPATTERNS,SEVERITY,INCIDENCE,ANDNATURALCOURSEOFPERIPROSTHETICSOFTTISSUELESIONSHAVENOTYETBEENELUCIDATEDONEOFTHEDIFFICULTIESENCOUNTEREDININVESTIGATIONOFPERIARTICULARSOFTTISSUEREACTIONSAROUNDARTIFICIALJOINTSISTHEABSENCEOFSENSITIVEIMAGINGMODALITIESPLAINRADIOGRAPHYANDCOMPUTEDTOMOGRAPHYARELESSSENSITIVEFORTHEEVALUATIONOFSOFTTISSUEDISORDERSBECAUSEOFPOORIMAGINGCONTRASTBETWEENNORMALANDABNORMALSTRUCTURESMAGNETICRESONANCEIMAGINGMRIHASTHEADVANTAGESOFSUPERIORIMAGINGCONTRASTFORSOFTTISSUEABNORMALITIESANDTHEREADYAVAILABILITYOF3DIMENSIONALASSESSMENTOFABNORMALLESIONSHOWEVER,THEASSESSMENTOFSOFTTISSUEREACTIONSADJACENTTOTHEIMPLANTWASDIFFICULTBECAUSEOFMETALSUSCEPTIBILITYARTIFACTSEVENWHILEUSINGSOPHISTICATEDMETALARTIFACTREDUCTIONTECHNIQUES9,14,15ULTRASOUNDASSESSMENTAROUNDTHEHIPARTHROPLASTYHASSEVERALADVANTAGESOVEROTHERIMAGINGMODALITIESTHESEINCLUDETHEABSENCEOFIONIZINGRADIATION,ABSENCEOFMETALARTIFACTSINTRODUCEDBYIMPLANTS,ANDRELATIVELYLOWCOST16THEREFORE,ULTRASOUNDASSESSMENTMAYBESUITABLEFORTHESCREENINGOFPERIARTICULARSOFTTISSUEREACTIONSAFTERHIPARTHROPLASTYSOMEREPORTSDEMONSTRATEDTHEUSEOFULTRASOUNDFORTHEEVALUATIONOFPERIARTICULARSOFTTISSUEREACTIONSINMOMBEARINGS6,17,18FROMTHEDEPARTMENTOFORTHOPAEDICMEDICALENGINEERING,OSAKAUNIVERSITYGRADUATESCHOOLOFMEDICINE,22YAMADAOKA,SUITA,OSAKA,JAPANANDYDEPARTMENTOFORTHOPAEDICSURGERY,OSAKAUNIVERSITYGRADUATESCHOOLOFMEDICINE,22YAMADAOKA,SUITA,OSAKA,JAPANSUBMITTEDAPRIL4,2011ACCEPTEDSEPTEMBER16,2011THECONFLICTOFINTERESTSTATEMENTASSOCIATEDWITHTHISARTICLECANBEFOUNDATDOI101016/JARTH201109015REPRINTREQUESTSTAKASHINISHII,MD,DEPARTMENTOFORTHOPAEDICMEDICALENGINEERING,OSAKAUNIVERSITYGRADUATESCHOOLOFMEDICINE,22YAMADAOKA,SUITA,OSAKA5650871,JAPAN?2012ELSEVIERINCALLRIGHTSRESERVED08835403/270600123600/0DOI101016/JARTH201109015895THEJOURNALOFARTHROPLASTYVOL27NO62012COMPONENTAND4“MASSPATTERN”WITHALARGEMASSEXTENDINGANTERIORTOTHEFEMORALCOMPONENTTHEREWERE69HIPSWITHTHENORMALPATTERN,11HIPSWITHTHEJOINTEXPANSIONPATTERN,5HIPSWITHTHECYSTICPATTERN,AND3HIPSWITHTHEMASSPATTERNWHENTHEJOINTEXPANSION,CYSTIC,ANDMASSPATTERNSWERECLASSIFIEDINTOTHEABNORMALPATTERNONULTRASOUND,THEFREQUENCYOFCLINICALSYMPTOMSWASSIGNIFICANTLYHIGHERINHIPSWITHTHEABNORMALPATTERN63THANINHIPSWITHTHENORMALPATTERN25TABLE1THEREWASNOSIGNIFICANTLYDIFFERENCEREGARDINGOTHERPATIENTSPROFILES,DURATIONOFIMPLANTINSITU,TYPESOFOPERATIONANDBEARINGS,CUPANDHEADSIZES,RADIOLOGICPARAMETERSOFTHEIMPLANTPLACEMENT,ANDPRESENCEOFOSTEOLYSIS,BETWEENTHEHIPWITHNORMALANDABNORMALPATTERNSALLOFTHE3PATIENTSSHOWINGMASSPATTERNONULTRASOUNDWEREWOMENWITHMTHAOPERATIONSANDHADONLYSLIGHTPAINORDISCOMFORTINTHEHIPTABLE2FIG1CLASSIFICATIONOFPERIARTICULARSOFTTISSUEREACTIONSONANTERIORLONGITUDINALORTRANSVERSEULTRASOUNDIMAGESNORMALPATTERNA,JOINTEXPANSIONPATTERNB,CYSTICPATTERNC,ANDMASSPATTERNDARROWSINDICATEANTERIORCAPSULEANDARROWHEADSINDICATEMASSLESIONULTRASOUNDSCREENINGOFPERIARTICULARABNORMA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簡介：INVITEDCRITICALREVIEWBTYPENATRIURETICPEPTIDEINACUTEPULMONARYEMBOLISMANNAKACZY?SKA,MACIEJKOSTRUBIEC,MICHA?CIURZY?SKI,PIOTRPRUSZCZYK?DEPARTMENTOFINTERNALMEDICINEANDCARDIOLOGY,MEDICALUNIVERSITYOFWARSAW,POLANDABSTRACTARTICLEINFOARTICLEHISTORYRECEIVED14MAY2008RECEIVEDINREVISEDFORM25JUNE2008ACCEPTED19JULY2008AVAILABLEONLINE24JULY2008KEYWORDSACUTEPULMONARYEMBOLISMBNPNTPROBNPRIGHTVENTRICLEDYSFUNCTIONPROGNOSISMYOCARDIALSTRETCHLEADSTOTHENATRIURETICPEPTIDESRELEASEINACUTEORCHRONICLEFTVENTRICULARDYSFUNCTIONHOWEVER,THEREISANACCUMULATINGEVIDENCETHATBTYPENATRIURETICPEPTIDEBNPANDITSNTERMINALFRAGMENTNTPROBNPMAYORIGINATEFROMRIGHTVENTRICLEANDTHEIRCONCENTRATIONSAREELEVATEDINPATIENTSWITHACUTEPULMONARYEMBOLISMAPEESPECIALLYWHENRESULTINGINRIGHTVENTRICULARDYSFUNCTIONRVDRECENTLYITISUNDERLINEDTHATSEVERITYASSESSMENTOFAPEASWELLASTHERISKSTRATIFICATIONANDTHERAPYSELECTIONISBASEDBOTHONPATIENTSHEMODYNAMICSTATUSANDMARKERSOFMYOCARDIALINJURYANDRVDBNPANDNTPROBNPAREHELPFULINIDENTIFYINGPATIENTSWITHRVDINAPE,EMERGINGASANADJUNCTIVETOOLTOECHOCARDIOGRAPHYELEVATEDBNPORNTPROBNPLEVELSAREALSOSIGNIFICANTPREDICTORSOFDEATHAND/ORCOMPLICATEDCLINICALCOURSEINAPE?2008ELSEVIERBVALLRIGHTSRESERVEDCONTENTS1STUDIESSELECTION12BNPANDNTPROBNPASSAYS13BNPANDNTPROBNPINTHEDETECTIONOFRVD24PROGNOSTICVALUEOFBNPANDNTPROBNPINAPE25CONCLUSIONS4REFERENCES4ITISWELLKNOWNTHATMYOCARDIALSTRETCHLEADSTOTHENATRIURETICPEPTIDESRELEASEINACUTEORCHRONICLEFTVENTRICULARDYSFUNCTIONHOWEVER,THEREISANACCUMULATINGEVIDENCETHATCONCENTRATIONSOFBTYPENATRIURETICPEPTIDEBNPANDITSNTERMINALFRAGMENTNTPROBNPAREELEVATEDINPATIENTSWITHACUTEPULMONARYEMBOLISMAPEESPECIALLYWHENRESULTINGINRIGHTVENTRICULARDYSFUNCTIONRECENTLYITISUNDERLINEDTHATSEVERITYASSESSMENTOFACUTEPULMONARYEMBOLISMAPEASWELLASTHERISKSTRATIFICATIONANDTHERAPYSELECTIONISBASEDBOTHONPATIENTSHEMODYNAMICSTATUSANDMARKERSOFMYOCARDIALINJURYANDRIGHTVENTRICULARDYSFUNCTIONRVDRIGHTVENTRICULARFUNCTIONCANBEDIRECTLYASSESSEDATECHOCARDIOGRAPHYAND/ORCONTRASTENHANCEDSPIRALCOMPUTEDTOMOGRAPHYSINCEPLASMACONCENTRATIONOFBRAINNATRIURETICPEPTIDEREFLECTSTHESEVERITYOFRVDITSASSESSMENTWASIMPLOREDINAPERISKSTRATIFICATIONASWELLWEPERFORMEDASYSTEMATICREVIEWAIMEDONBTYPENATRIURETICPEPTIDESINAPEESPECIALLYFORTHERVDDETECTIONANDCLINICALCOURSEPREDICTION1STUDIESSELECTIONOVERALL49ARTICLESWEREFOUNDSEARCHINGPUBMEDBYTERMS‘PULMONARYEMBOLISM’,‘BNP’AND‘NTPROBNP’FROM1997TOMARCH2008THIRTYTWOPAPERSWEREEXCLUDEDFROMCURRENTREVIEWBECAUSETHEYWERECASEREPORTS,REVIEWPAPERS,EDITORIALSORLETTERSTHEYDIDNOTREPORTONENDPOINTSORDIDNOTPROVIDEVALUESOFBIOMARKERSCONCENTRATIONEVENTUALLY,17STUDIESCONCERNINGTHEINFLUENCEOFELEVATEDBNPANDNTPROBNPONSHORTTERMMORTALITY,ADVERSEOUTCOMEEVENTSDEATH,CARDIOGENICSHOCK,NEEDFORTHROMBOLYSIS,CATHETERORSURGICALEMBOLECTOMY,USEOFVASOPRESSORS,NEEDFORENDOTRACHEALINTUBATIONANDMECHANICALVENTILATION,CARDIOPULMONARYRESUSCITATIONANDRVDWERESELECTEDTABLE12BNPANDNTPROBNPASSAYSPROPEPTIDEFORBTYPENATRIURETICPEPTIDEPROBNPISCLEAVEDTOEQUIMOLARAMOUNTSOFBTYPENATRIURETICPEPTIDEBNPANDNTERMINALFRAGMENTNTPROBNPBNPISPHYSIOLOGICALLYACTIVEBNPCONCENTRATIONISASSESSEDUSINGSEVERALRADIOIMMUNOLOGICASSAYSORIMMUNOFLUOROMETRICASSAYS,WHILEFORNTPROBNPONETESTISCLINICACHIMICAACTA39820081–4?CORRESPONDINGAUTHORDEPARTMENTOFINTERNALMEDICINEANDCARDIOLOGY,MEDICALUNIVERSITYOFWARSAW,ULLINDLEYA402005WARSAW,POLANDTEL48225021144FAX48225022142EMAILADDRESSPIOTRPRUSZCZYKAMWAWEDUPLPPRUSZCZYK00098981/–SEEFRONTMATTER?2008ELSEVIERBVALLRIGHTSRESERVEDDOI101016/JCCA200807020CONTENTSLISTSAVAILABLEATSCIENCEDIRECTCLINICACHIMICAACTAJOURNALHOMEPAGEWWWELSEVIERCOM/LOCATE/CLINCHIMCOMPLICATEDCLINICALCOURSEWITHOR8095CI13–501,P0026INTERESTINGLYAUTHORSALSOATTEMPTEDTOIDENTIFYTHEMOSTSENSITIVEBNPCUTOFFLEVELFORIDENTIFYINGLOWRISKAPEPATIENTSITTURNEDTOBEB50PG/MLWITHITSNEGATIVEPREDICTIVEVALUEOF972ELEVATEDBNPWASALSOFOUNDTOBEAPREDICTOROFALLCAUSEASWELLASAPERELATEDMORTALITYINGROUPOF110PATIENTS12THREEMONTHMORTALITYWAS10INTERESTINGLYALLDEATHSOCCURREDINPATIENTSWITHBNPCONCENTRATIONINSECONDANDTHIRDTERTILEIEEXCEEDING25PMOL/LAND217PMOL/L,RESPECTIVELYINTHESTUDYBYKRüGERETAL3,HOWEVER,BNPCUTOFFVALUEOFN90PG/ML,ASCALCULATEDFROMROCANALYSIS,WASNOTDIRECTLYASSOCIATEDNEITHERWITHINHOSPITALCOMPLICATEDCOURSENORWITHSHORTTERMMORTALITYHOWEVER,ASMENTIONEDEARLIERITWASREPORTEDTOBEUSEFULINRVDPREDICTIONIMPORTANTLY,ASEXPECTED,HIGHERINCIDENCEOFCOMPLICATIONSASWELLASTRENDTOWARDHIGHERMORTALITYWASOBSERVEDINPATIENTSWITHRVDCONVERSELY,ASMALLSTUDYONUNSELECTEDGROUPOF17PATIENTSWITHAPE,INCLUDINGPATIENTSBOTHWITHANDWITHOUTRVDREPORTEDSIGNIFICANTLYHIGHERCONCENTRATIONOFBNPINPATIENTSWHODIEDOFPETHANINTHOSEWHOSURVIVED916775–3362VS144119–274PMOL/L,P00213THEFOLLOWINGSTUDYCOMPRISING61INITIALLYHEMODYNAMICALLYSTABLEPATIENTSREPORTEDHIGHERBNPCONCENTRATIONONADMISSIONINPATIENTSWITHSUBSEQUENTCOMPLICATEDCLINICALCOURSETHANWITHFAVORABLEOUTCOME950±314VS296±353PG/ML,PB0000114IMPORTANTLYALL4INHOSPITALDEATHSAND11COMPLICATIONSOBSERVEDINTHISSTUDYOCCURREDINPATIENTSWITHBNPINTHEHIGHESTTERTILE,NAMELY527–1300PG/MLROCANALYSISCONFIRMEDCUTOFFPOINTOF487PG/MLASINDICATINGPATIENTSWITHHIGHERRISKOFCOMPLICATIONSAUC09895CI096–099,SENSITIVITY86,SPECIFICITY100INTHE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簡介：EFFECTOFTOTALKNEEARTHROPLASTYIMPLANTPOSITIONONFLEXIONANGLEBEFOREIMPLANTBONEIMPINGEMENTHIDEKIMIZUUCHI,MD,PHD,YCLIFFORDWCOLWELLJR,MD,SHUICHIMATSUDA,MD,PHD,YCESARFLORESHERNANDEZ,BS,YUKIHIDEIWAMOTO,MD,PHD,YANDDARRYLDDLIMA,MD,PHDABSTRACTWEGENERATEDPATIENTSPECIFICCOMPUTERMODELSOFTOTALKNEEARTHROPLASTYFROM10PATIENTSTOCOMPUTEMAXIMUMFLEXIONANGLEBEFOREIMPLANTBONEIMPINGEMENTMOTIONWASSIMULATEDFOR5DIFFERENTFEMORALIMPLANTPOSITIONSAND11DIFFERENTTIBIALINSERTPOSITIONSAT4DIFFERENTTIBIALPOSTERIORSLOPESINTHENEUTRALPOSITION,THEMEANMAXIMUMFLEXIONANGLEWAS1363°THERANGEBECAUSEOFANATOMICALVARIATIONAMONGPATIENTSWAS130°ACOMBINATIONOF2MMPOSTERIORTRANSLATIONOFTHEFEMORALCOMPONENTWITHA10MMANTERIORTRANSLATIONOFTHEINSERTANDA7°POSTERIORSLOPEINCREASEDFLEXIONBYAMEANOF14°RELATIVETOTHENEUTRALPOSITIONTHERATEOFCHANGEINFLEXIONANGLEWAS04°/MMTO15°/MMWITHRESPECTTOIMPLANTPOSITIONAND15°/MMINCREASEINTHEPOSTERIORCONDYLAROFFSETKEYWORDSTOTALKNEEARTHROPLASTY,KNEEFLEXIONANGLE,COMPUTERSIMULATION,COMPONENTPOSITION,ANATOMICALVARIATION?2011ELSEVIERINCALLRIGHTSRESERVEDTOTALKNEEARTHROPLASTYTKAHASBECOMEONEOFTHEMOSTSUCCESSFULORTHOPEDICPROCEDURESWITHREPORTEDSURVIVALRATESOFGREATERTHAN90AFTER15YEARS1,2WITHTHEIMPROVEMENTOFLONGTERMOUTCOMES,THEREISRENEWEDINTERESTINMAXIMIZINGRANGEOFMOTIONAFTERTKA310THERANGEOFMOTIONINFLEXIONISEXTREMELYIMPORTANTINASIANCOUNTRIESANDFORPATIENTSWITHLIFESTYLESTHATINVOLVESITTINGONTHEFLOORINDEEPFLEXION3EVENINNORTHAMERICANPATIENTS,UPTO75IDENTIFIEDTHATACTIVITIESREQUIRINGDEEPERKNEEFLEXIONANGLESUCHASSQUATTING,KNEELING,ANDGARDENINGWEREPERFORMEDWITHGREATERDIFFICULTYAFTERTKA4MANYCLINICALSTUDIESHAVEINVESTIGATEDFACTORSAFFECTINGPOSTOPERATIVERANGEOFMOTION5,6,10,11PATIENTRELATEDFACTORSSUCHASPREOPERATIVERANGEOFMOTION,BODYMASSINDEX,DISEASE,AGE,ANDSEXGREATLYINFLUENCETHEPOSTOPERATIVERANGEOFMOTIONSIMILARLY,SURGICALTECHNIQUESCANALSOAFFECTTHEPOSTOPERATIVERANGEOFMOTIONEXAMPLESINCLUDETHEHEIGHTOFJOINTLINE,PATELLARTRACKING,APPROPRIATEGAPBALANCING,RELEASEOFPOSTERIORCAPSULE,ANDREMOVALOFTHEOSTEOPHYTESANOTHERIMPORTANTFACTORISTHEPOSTERIORCONDYLAROFFSETPCO,WHICHHASBEENASSOCIATEDWITHPOSTOPERATIVERANGEOFMOTIONINFLUOROSCOPICANALYSISINVIVO5PREVIOUSSTUDIESHAVEANALYZEDTHEEFFECTOFIMPLANTALIGNMENTANDRELATIVEPOSITIONONPOSTOPERATIVERANGEOFMOTION1215WALKERETAL12REPORTEDTHATPOSTERIORANDPROXIMALFEMORALPLACEMENTANDAGREATERPOSTERIORTIBIALSLOPEINCREASEDMAXIMUMFLEXIONANGLEINPLASTICMODELSOFTHEFEMURANDTIBIAMASSINANDGOURNAY13DEMONSTRATEDTHATGREATERPCOINCREASEDTIBIALPOSTERIORSLOPE,ANDAMOREPOSTERIORFEMOROTIBIALCONTACTPOINTCANINCREASEFLEXIONINASTUDYTHATUSED2DIMENSIONALTEMPLATESOFPROSTHETICCOMPONENTSONLATERALKNEERADIOGRAPHSHOWEVER,THECOMBINEDEFFECTOFTHE3DIMENSIONALANATOMYOFTHEPATIENTANDTHEIMPLANTPOSITIONHASNOTBEENSTUDIEDWEGENERATEDPATIENTSPECIFICANATOMICALMODELSOFIMPLANTBONEIMPINGEMENTTOEVALUATETHEEFFECTOFIMPLANTPOSITIONANDANATOMICALVARIATIONONFLEXIONANGLEOURPRIMARYHYPOTHESISWASTHATIMPLANTPOSITIONWOULDSIGNIFICANTLYAFFECTMAXIMUMKNEEFLEXIONANGLEBEFOREBONEPROSTHESISIMPINGEMENTOURSECONDARYHYPOTHESISWASTHATTHEPCOWOULDCORRELATESIGNIFICANTLYWITHMAXIMUMFLEXIONANGLEFROMTHESHILEYCENTERFORORTHOPAEDICRESEARCHANDEDUCATIONATSCRIPPSCLINIC,LAJOLLA,CAANDYDEPARTMENTOFORTHOPAEDICSURGERY,GRADUATESCHOOLOFMEDICALSCIENCES,KYUSHUUNIVERSITY,FUKUOKA,JAPANSUBMITTEDAPRIL19,2010ACCEPTEDAUGUST1,2010NOBENEFITSORFUNDSWERERECEIVEDINSUPPORTOFTHESTUDYREPRINTREQUESTSDARRYLDDLIMA,MD,PHD,SHILEYCENTERFORORTHOPAEDICRESEARCHANDEDUCATIONATSCRIPPSCLINIC,11025NTORREYPINESROAD,SUITE140,LAJOLLA,CA92037?2011ELSEVIERINCALLRIGHTSRESERVED08835403/260500113600/0DOI101016/JARTH201008002721THEJOURNALOFARTHROPLASTYVOL26NO52011INSERTACONSTANTMASSWASAPPLIEDATAFIXEDDISTANCE300MMFROMTHECLINICALEPICONDYLARAXISOFTHEFEMURTOGENERATEAFLEXIONMOMENTBECAUSEOFGRAVITYTHEFEMURWASTHENALLOWEDTOFLEX,ANDTHEMAXIMUMFLEXIONWASRECORDEDBEFOREIMPINGEMENTBETWEENTHEPOSTERIORCORTEXOFTHEFEMURANDTHETIBIALINSERTFIG2PEAKFLEXIONANGLESWERERECORDEDASTHEINSERTWASMOVEDAT2MMINTERVALSRANGINGFROM10MMANTERIORTO10MMPOSTERIORFOREACHOFTHE5FEMORALIMPLANTPOSITIONSNEUTRAL,2MMANTERIOR/POSTERIOR,AND2MMPROXIMAL/DISTALFROMTHENEUTRALTHISPROCESSWASTHENREPEATEDFOREACHOF4TIBIALPOSTERIORSLOPEANGLES0°,3°,5°,AND7°TOTHEMECHANICALAXISOFTHETIBIAWEALSOMEASUREDTHEPCOFOREACHOFTHEDIFFERENTFEMORALIMPLANTPOSITIONSASDEPICTEDINFIG1BPOSTERIORCONDYLAROFFSETWASMEASUREDASTHEMAXIMUMDISTANCEBETWEENTHEPOSTERIORSURFACEOFTHEDISTALFEMURANDTHEPOSTERIORCONDYLE5VALIDATIONOFTHECOMPUTERMODELFOURFRESHFROZENHUMANCADAVERKNEESWERETESTEDTOVALIDATETHECOMPUTERMODELCOMPUTEDTOMOGRAPHICSCANSWEREOBTAINEDAFTERIMPLANTINGFIDUCIALMARKERSINEACHTIBIAANDFEMUR3TITANIUMSCREWSINEACHBONEKNEEARTHROPLASTYWASPERFORMEDUSINGASURGICALNAVIGATIONSYSTEMSTRYKERNAVIGATION,FREIBURG,GERMANYCOMPONENTALIGNMENTWASSIMILARTOTHATDESCRIBEDFORTHECOMPUTATIONALMODELSCORPIOCRSTRYKERORTHOPAEDICSTIBIALANDFEMORALCOMPONENTSWEREUSEDTHEPATELLAWASNOTRESURFACEDALLSOFTTISSUESAROUNDTHEKNEEJOINTWEREREMOVEDASMUCHASPOSSIBLEEXCEPTTHEPOSTERIORCRUCIATELIGAMENT,THEMEDIALANDLATERALCOLLATERALLIGAMENTS,ANDTHEEXTENSORMECHANISMAFTERARTHROPLASTYTHETIBIAWASMOUNTEDVERTICALLYONACUSTOMRIG,ANDTHEFEMURWASALL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簡介：CARDIACTROPONINIRELEASEINACUTEPULMONARYEMBOLISMINRELATIONTOTHEDURATIONOFSYMPTOMSGOPIKRISHNAPUNUKOLLUA,IJAZAKHANB,,RAMESHMGOWDAA,GAURAVLAKHANPALA,BALENDUCVASAVADAA,TERRENCEJSACCHIAADIVISIONOFCARDIOLOGY,LONGISLANDCOLLEGEHOSPITAL,BROOKLYN,NY,USABDIVISIONOFCARDIOLOGY,UNIVERSITYOFMARYLANDSCHOOLOFMEDICINE,22SOUTHGREENESTREETS3B06,BALTIMORE,MD21201,USARECEIVED24JUNE2003RECEIVEDINREVISEDFORM5JANUARY2004ACCEPTED8JANUARY2004AVAILABLEONLINE2APRIL2004ABSTRACTPURPOSETOEVALUATETHERELEASEOFCARDIACTROPONINIINNORMOTENSIVEPATIENTSWITHACUTEPULMONARYEMBOLISMINRELATIONTOTHEDURATIONOFSYMPTOMSMETHODSFIFTYSEVENNORMOTENSIVEPATIENTSWITHACUTEPULMONARYEMBOLISMWEREINCLUDEDINTHESTUDYPATIENTSWEREDIVIDEDINTOTWOGROUPSBASEDONTHEDURATIONOFSYMPTOMSATPRESENTATIONSYMPTOMSOFV72H,GROUPASYMPTOMSOF72H,GROUPBSERUMCARDIACTROPONINILEVELSWEREMEASUREDATPRESENTATIONRESULTSMEANAGEWAS63F18YEARSAND2340PATIENTSWEREMALESTHIRTYTHREE58PATIENTSHADSYMPTOMSOFV72HGROUPAAND2442HADSYMPTOMSOF72HGROUPBBOTHGROUPSHADSIMILARPREVALENCEOFRIGHTVENTRICULARDYSFUNCTIONONECHOCARDIOGRAPHY55N18INGROUPAVS42N10INGROUPB,PNSSIXTEENPATIENTSHADELEVATEDSERUMCARDIACTROPONINIMEANFSD33F23NG/ML,RANGE06–83NG/MLELEVATEDSERUMCARDIACTROPONINIWASSTRONGLYASSOCIATEDWITHRIGHTVENTRICULARDYSFUNCTIONP0015ALLPATIENTSWITHELEVATEDSERUMCARDIACTROPONININ16WEREINGROUPAP72HGROUPBTABLE2THEREWASNODIFFERENCEINTHESEVERITYOFPULMONARYEMBOLISMBETWEENTHETWOGROUPSANDBOTHGROUPSHADSIMILARPREVALENCEOFRIGHTVENTRICULARDYSFUNCTION55N18INGROUPAVS42N10THEPREVALENCEOFCARDIOVASCULARFACTORSWASSIMILARINBOTHGROUPSSIXTEENPATIENTSHADELEVATEDSERUMCARDIACTROPONINIMEANFSD33F23NG/ML,RANGE06–83NG/MLELEVATEDCARDIACTROPONINIWASSTRONGLYASSOCIATEDWITHRIGHTVENTRICULARDYSFUNCTIONP0015ALLPATIENTSWITHELEVATEDSERUMCARDIACTROPONINILEVELSN16WEREINGROUPANONEOFTHEPATIENTSINGROUPBHADELEVATEDSERUMCARDIACTROPONINILEVELSP00001AMONGGROUPA,12OF1867PATIENTSWITHP00005AND4OF1527PATIENTSWITHOUTPNSRIGHTVENTRICULARDYSFUNCTIONHADELEVATEDSERUMCARDIACTROPONINITHIRTEENOF1681PATIENTSWITHELEVATEDSERUMCARDIACTROPONINIHADDURATIONOFSYMPTOMSV24HATPRESENTATIONTABLE3INPATIENTSPRESENTINGWITHIN8HAFTERSYMPTOMONSETN7,THEPEAKSERUMTROPONINILEVELSWEREFOUNDATCLINICALPRESENTATIONIN50N4OFTHEPATIENTS4DISCUSSION41BACKGROUNDCARDIACTROPONINELEVATIONINACUTEPULMONARYEMBOLISMISASSOCIATEDWITHBOTHMASSIVEANDSUBMASSIVEPULMONARYEMBOLISMPACOURETETAL15INITIALLYREPORTEDTHATCARDIACTROPONINILEVELSWEREELEVATEDINSUBMASSIVEPULMONARYEMBOLISMSUBSEQUENTSTUDIESCONFIRMEDTHATSERUMCARDIACTROPONINIANDTLEVELSCOULDBEELEVATEDINBOTHMASSIVEANDSUBMASSIVEPULMONARYEMBOLISMWITHASTRONGCORRELATIONWITHRIGHTVENTRICULARDYSFUNCTION5,6,11,12,16–18THEELEVATEDCARDIACTROPONINSHAVEINDEPENDENTPROGNOSTICVALUEFORINHOSPITALDEATH,HYPOTENSIONANDCARDIOGENICSHOCKINPATIENTSWITHPULMONARYEMBOLISM5,11SIMILARRELATIONWASREPORTEDBYKONSTANTINIDESETAL12WHEREELEVATEDCARDIACTROPONINILEVELSWEREASSOCIATEDWITHINCREASEDOVERALLMORTALITYANDCOMPLICATEDINHOSPITALCOURSETHERISKOFCOMPLICATEDINHOSPITALCOURSEWASREPORTEDTOBEFIVETIMESHIGHERINTHEHIGHCARDIACTROPONINIGROUPCOMPAREDWITHPATIENTSWITHMODERATECTNIELEVATION42CARDIACTROPONINIFORRISKSTRATIFICATIONINPULMONARYEMBOLISMEVENTHOUGHELEVATEDLEVELSOFCARDIACTROPONINIANDTHAVEPROGNOSTICSIGNIFICANCEINACUTEPULMONARYEMBOLISM,THECLINICALUTILITYOFELEVATEDCARDIACTROPONINLEVELSINTHERISKSTRATIFICATIONOFHEMODYNAMICALLYSTABLEPATIENTSISUNKNOWNANDITISAPPEALINGTOSPECULATETHATTROPONINSCOULDFUNCTIONASADISCRIMINATORFORTHROMBOLYTICTHERAPYINPULMONARYEMBOLISMPATIENTSWHOAREHEMODYNAMICALLYSTABLEBUTHAVERIGHTVENTRICULARDYSFUNCTIONLARGEMULTICENTERSTUDIESARENEEDEDTOPROVETHATELEVATEDLEVELSOFCARDIACTROPONINSMAYBEUSEFULINTHERAPEUTICTRIAGEOFNORMOTENSIVEPATIENTSWITHRIGHTVENTRICULARDYSFUNCTIONINACUTEPULMONARYEMBOLISM,WHEREASEQUALLYIMPORTANTWOULDBETOEVALUATETHERELEASEOFTROPONINSINACUTEPULMONARYEMBOLISMESPECIALLYINRELATIONTODURATIONOFSYMPTOMSASTHEWINDOWPERIODFORTHROMBOLYTICTHERAPYINACUTEPULMONARYEMBOLISMCANEXTENDUPTO14DAYS19–2143RELEASEKINETICSOFCARDIACTROPONINITHEMAJORITYOFCARDIACTROPONINSAREBOUNDTOMYOFILAMENTS,ANDTHEREMAINDERISFREEINTHECYTOSOLINACUTEMYOCARDIALINFARCTIONSUFFICIENTMYOCARDIALNECROSISOCCURSTOSUSTAINANABNORMALLYELEVATEDLEVELSOFTROPONINS,WHICHBEGINTORISEIN4–6HANDPEAKATABOUT24HAFTERTHEONSETOFSYMPTOMSTOREACHLEVELSOFABOUT20–50TIMESTHEUPPERREFERENCELIMITTHECONCENTRATIONOFTHESESUBUNITSREMAINELEVATEDINBLOODFORMANYDAYS,ABOUT4–7DAYSFORCARDIACTROPONINIAND10–14DAYSFORCARDIACTROPONINT,DUETOPROTRACTEDRELEASEFROMSTORESBOUNDTODETERIORATINGMYOFILAMENTS22,23ITISESTIMATEDTHAT3–4OFCARDIACTROPONINIAND6–8OFCARDIACTROPONINTISFOUNDASFREECYTOPLASMICCOMPONENTS24,25INMICROINFARCTIONSANDINITIALSTAGESOFMYOCARDIALINJURY,ITHASBEENTHOUGHTTHATRELEASEOFTHECYTOPLASMICTROPONINOCCURSWITHTHEDETECTABLELEVELSOFCARDIACTROPONINSINPERIPHERALBLOOD22INADDITION,OTHERFORMSOFCARDIACTROPONINIANDTHAVEBEENSHOWNTOBERELEASEDINTOTHEBLOODAFTERMYOCARDIALINFARCTION26SOTHERELEASEANDCLEARANCEMECHANISMSOFCARDIACTROPONINIANDTARESTILLINCOMPLETELYUNDERSTOODTHEREARENOSTUDIESWHERECARDIACTROPONINSHAVEBEENEVALUATEDINRELATIONTOTHEONSETOFSYMPTOMSINACUTEPULMONARYEMBOLISM,ALTHOUGHSTUDIESHAVEEVALUATEDTHESE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簡介：THEPOTENTIALROLEOFMICRORNA146INALZHEIMER’SDISEASEBIOMARKERORTHERAPEUTICTARGETLILINGWANGA,YUEHUANGB,GANGWANGA,?,SHENGDICHENA,C,?ADEPARTMENTOFNEUROLOGY2THEMECHANISMSUNDERLYINGTHERELATIONSHIPBETWEENMIR146AALTERATIONSANDTHEPATHOLOGICALPROGRESSIVEPROCESSINADSIMILARQUESTIONSALSOARISEINTHEINVESTIGATIONSOFMIRINSTROKESANDOTHERNEUROLOGICALDISORDERS36,37CONCLUSIONANDPERSPECTIVEINORDERTODETERMINETHEPHYSIOLOGICALFUNCTIONSOFMIR146AANDB,ITISNECESSARYTORECOGNIZETHEIRPOTENTIALTARGETSMIR146INHIBITSAGROUPOFGENESINCLUDINGIRAK1,TRAF6,CFH,ANDTSPAN12WEPROPOSEDTHATBOTHMIR146AANDBAREINVOLVEDINADPATHOGENESISVIASUPPRESSINGTHEABOVEGENESANDALTERINGTHEIRDOWNSTREAMSIGNALINGPATHWAYSINITIALLY,MIR146WASIDENTIFIEDASANEGATIVEFEEDBACKREGULATORINTHECONTROLOFTOLLLIKERECEPTORSANDCYTOKINESIGNALING,YET,THESUPPRESSIONOFIRAK1NFJBSIGNALINGMEDIATEDBYMIR146AEVENTUALLYCAUSEDSTRONGACTIVATIONOFTHEIRAK2NFJBSIGNALINGPATHWAY,RESULTINGINENHANCEDINFLAMMATORYRESPONSETHROUGHANUNKNOWNMECHANISM31INADDITION,THETARGETGENESOFMIR146,SUCHASROCK1,EGFRANDNOTCH1,ALLPLAYCRUCIALROLEINCANCERWHETHERMIR146MEDIATEDINHIBITIONOFTHOSEGENESISINVOLVEDINTHEPATHOGENESISOFADREMAINSTOBEELUCIDATEDINORDERTOEXPANDTHEKNOWLEDGEONTHEFUNCTIONOFMIR146INAD,ITISESSENTIALTOANALYZETHEPHENOTYPEOFMICEWITHTARGETEDDELETIONOFMIR146AORMIR146BINSUMMARY,THEFUNCTIONSOFMIR146INDICATEDTHATITWOULDHAVEAPPLICABLEPOTENTIALSONATLEASTTWOASPECTSTHEFIRSTISASABIOMARKERFORTHEEARLYCLINICALDETECTIONOFAD,ASITSPRESENCEINCIRCULATINGMONOCYTESINADULTBLOODENABLESEASYCOLLECTIONWITHMINIMUMINVASIONINTHISCONTEXT,CLINICALLYCONFIRMEDADCOHORTWITHSUFFICIENTCASENUMBERSHOULDBEUSEDTOEVALUATEITSPOTENTIALTHEOTHERISASAPOTENTIALTHERAPEUTICTARGETDUETOTHEIMPLICATIONSOFMIR146AINADTREATMENTADANDSTRESSEDBRAINCELLSASSOCIATEDWITHASIGNIFICANTDOWNREGULATIONINMIR146ATARGETS,ENCODINGIRAK1,CFHANDTSPAN1214,31THEUSEOFANTIMIR146ATOREPRESSTHEEFFECTSOFUPREGULATEDMIR146AMAYBEAPOTENTIALTHERAPEUTICAPPROACHAPPLYINGANTIMIR146ATOADTRANSGENICMOUSEMODELSISTHEIMMEDIATESTEPTOWARDSANTIMIR146ACLINICALTRIALSFORADCONFLICTOFINTERESTNONEDECLAREDACKNOWLEDGEMENTSTHISSTUDYWASSUPPORTEDBYTHENATIONALBASICRESEARCHDEVELOPMENTPROGRAMOFCHINANO2010CB945200,SHANGHAIKEYDISCIPLINEPROGRAMNOS30202,SHANGHAIKEYPROJECTOFBASICSCIENCERESEARCHNO09DZ1950400ANDTHEPROGRAMFOROUTSTANDINGMEDICALACADEMICLEADERNOLJ06003REFERENCES1DUYCKAERTSC,DELATOURB,POTIERMCLASSIFICATIONANDBASICPATHOLOGYOFALZHEIMERDISEASEACTANEUROPATHOL20091185–362MORALESI,FARIASG,MACCIONIRNEUROIMMUNOMODULATIONINTHEPATHOGENESISOFALZHEIMER’SDISEASENEUROIMMUNOMODULATION201017202–43BOUTAJANGOUTA,QUARTERMAIND,SIGURDSSONEIMMUNOTHERAPYTARGETINGPATHOLOGICALTAUPREVENTSCOGNITIVEDECLINEINANEWTANGLEMOUSEMODELJNEUROSCI20103016559–664JONESL,HOLMANSPA,HAMSHEREML,HAROLDD,MOSKVINAV,IVANOVD,ETALGENETICEVIDENCEIMPLICATESTHEIMMUNESYSTEMANDCHOLESTEROLMETABOLISMINTHEAETIOLOGYOFALZHEIMER’SDISEASEPLOSONE20105E139505VOLLMARP,KULLMANNJS,THILOB,CLAUSSENMC,ROTHHAMMERV,JACOBIH,ETALACTIVEIMMUNIZATIONWITHAMYLOIDBETA142IMPAIRSMEMORYPERFORMANCETHROUGHTLR2/4DEPENDENTACTIVATIONOFTHEINNATEIMMUNESYSTEMJIMMUNOL20101856338–476LULF,LISTONAMICRORNAINTHEIMMUNESYSTEM,MICRORNAASANIMMUNESYSTEMIMMUNOLOGY2009127291–87XIAOC,RAJEWSKYKMICRORNACONTROLINTHEIMMUNESYSTEMBASICPRINCIPLESCELL200913626–368SABAR,GOODMANC,HUZAREWICHRL,ROBERTSONC,BOOTHSAMIRNASIGNATUREOFPRIONINDUCEDNEURODEGENERATIONPLOSONE20083E36529WANGWX,RAJEEVBW,STROMBERGAJ,RENN,TANGG,HUANGQ,ETALTHEEXPRESSIONOFMICRORNAMIR107DECREASESEARLYINALZHEIMER’SDISEASEANDMAYACCELERATEDISEASEPROGRESSIONTHROUGHREGULATIONOFBETASITEAMYLOIDPRECURSORPROTEINCLEAVINGENZYME1JNEUROSCI2008281213–2310PONOMAREVED,VEREMEYKOT,BARTENEVAN,KRICHEVSKYAM,WEINERHLMICRORNA124PROMOTESMICROGLIAQUIESCENCEANDSUPPRESSESEAEBYDEACTIVATINGMACROPHAGESVIATHEC/EBPALPHAPU1PATHWAYNATMED20111764–7011TAGANOVKD,BOLDINMP,CHANGKJ,BALTIMOREDNFKAPPABDEPENDENTINDUCTIONOFMICRORNAMIR146ANINHIBITORTARGETEDTOSIGNALINGPROTEINSOFINNATEIMMUNERESPONSESPROCNATLACADSCIUSA200610312481–612NAKASAT,MIYAKIS,OKUBOA,HASHIMOTOM,NISHIDAK,OCHIM,ETALEXPRESSIONOFMICRORNA146INRHEUMATOIDARTHRITISSYNOVIALTISSUEARTHRITISRHEUM2008581284–9213ARONICAE,FLUITERK,IYERA,ZUROLOE,VREIJLINGJ,VANVLIETEA,ETALEXPRESSIONPATTERNOFMIR146A,ANINFLAMMATIONASSOCIATEDMICRORNA,INEXPERIMENTALANDHUMANTEMPORALLOBEEPILEPSYEURJNEUROSCI2010311100–714LUKIWWJ,ZHAOY,CUIJGANNFKAPPABSENSITIVEMICRORNA146AMEDIATEDINFLAMMATORYCIRCUITINALZHEIMERDISEASEANDINSTRESSEDHUMANBRAINCELLSJBIOLCHEM200828331315–2215PERRYMM,WILLIAMSAE,TSITSIOUE,LARNERSVENSSONHM,LINDSAYMADIVERGENTINTRACELLULARPATHWAYSREGULATEINTERLEUKIN1BETAINDUCEDMIR146AANDMIR146BEXPRESSIONANDCHEMOKINERELEASEINHUMANALVEOLAREPITHELIALCELLSFEBSLETT20095833349–5516CAMERONJE,YINQ,FEWELLC,LACEYM,MCBRIDEJ,WANGX,ETALEPSTEINBARRVIRUSLATENTMEMBRANEPROTEIN1INDUCESCELLULARMICRORNAMIR146A,AMODULATOROFLYMPHOCYTESIGNALINGPATHWAYSJVIROL2008821946–5817CHANGTC,YUD,LEEYS,WENTZELEA,ARKINGDE,WESTKM,ETALWIDESPREADMICRORNAREPRESSIONBYMYCCONTRIBUTESTOTUMORIGENESISNATGENET20084043–5018SONKOLYE,WEIT,JANSONPC,SAAFA,LUNDEBERGL,TENGVALLLINDERM,ETALMICRORNASNOVELREGULATORSINVOLVEDINTHEPATHOGENESISOFPSORIASISPLO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簡介：中文中文7700字出處出處WENTZELJJ,CHATZIZISISYS,GIJSENFJ,ETALENDOTHELIALSHEARSTRESSINTHEEVOLUTIONOFCORONARYATHEROSCLEROTICPLAQUEANDVASCULARREMODELLINGCURRENTUNDERSTANDINGANDREMAININGQUESTIONSJCARDIOVASCULARRESEARCH,2012,96223443本科外文翻譯內(nèi)皮剪切力在冠狀動脈粥樣硬化斑塊和血管重內(nèi)皮剪切力在冠狀動脈粥樣硬化斑塊和血管重建進展中的作用機制當前的理解和存在的問建進展中的作用機制當前的理解和存在的問題ENDOTHELIALSHEARSTRESSINTHEEVOLUTIONOFCORONARYATHEROSCLEROTICPLAQUEANDVASCULARREMODELLINGCURRENTUNDERSTANDINGANDREMAININGQUESTIONS學部（院）電子信息與電氣工程學部專業(yè)生物醫(yī)學工程學生姓名學號指導教師完成日期內(nèi)皮剪切力在冠狀動脈粥樣硬化斑塊和血管重建進展中的作用機制當前的理解和存在的問題–2–位的內(nèi)側(cè)緣，這些部位存在紊亂的血流和低ESS。相反，乳溝動脈是暴露在生理狀態(tài)下的ESS是抗粥樣硬化的。早期對ESS和斑塊位置之間聯(lián)系的觀察主要是在尸體解剖材料上，因此，不能觀察到ESS對動脈粥硬化的影響?；谘茉煊昂脱軆?nèi)超聲的在體動脈血管三維重建的優(yōu)點開辟了新的觀察途徑來研究ESS在動脈粥樣硬化自然進程中的作用（圖1）。這些三維重建技術(shù)已經(jīng)得到了在體驗證并且在全世界很多的中心得到了應(yīng)用。通過這些技術(shù)，已經(jīng)發(fā)現(xiàn)了低ESS區(qū)域和動脈粥樣硬化斑塊，以及低ESS區(qū)域和冠狀動脈患者、實驗動物的支架內(nèi)再狹窄之間的位置關(guān)聯(lián)。而且，通過一系列的測量顯示低ESS環(huán)境在斑塊的進展，斑塊向有破裂傾向的斑塊發(fā)展中也起到了作用。另一個觀察發(fā)現(xiàn)是，開始向官腔內(nèi)侵入的成熟（ADVANCED）斑塊回暴露在高水平ESS，這可能參與到急性斑塊的破裂。圖1基于雙平面血管造影和血管內(nèi)超聲融合三維（3D）重建人體冠狀動脈。中央面板顯示用相同的方向作為正向和側(cè)向雙平面血管造影描繪左前降支（LAD）三維重建，右冠狀動脈（RCA），左回旋（LCX）。左面板和右面板分別顯示正向和側(cè)向雙平面血管造影的冠狀動脈。早期損傷發(fā)展到暴露在官腔內(nèi)的成熟（ADVANCED）高危斑塊或是出現(xiàn)管腔狹窄的高危斑塊的病理生理機制尚不明確。局部ESS環(huán)境，血管重建和血管生物學之間的動態(tài)

簡介：ASSESSMENTOFVASOMOTOROSCILLATIONSWITHFOURIERANALYSISOFBIOLOGICALTISSUEIMPEDANCEANESTEROV,IGAVRILOV,LSELECTOR,IMUDRAYAANDSREVENKO1NATIONALCARDIOLOGYCENTER,RESEARCHINSTITUTEOFUROLOGY,MOSCOW,RUSSIAEMAILS_REVENKOMAILRUABSTRACTFOURIERANALYSISREVEALEDANUMBEROFPERIODICITIESINSMALLVARIATIONSOFBIOIMPEDANCEOFHUMANFINGERINCLUDINGTHEMAJORSPECTRUMPEAKSATTHEFREQUENCIESOFHEARTBEATS,RESPIRATION,ANDMAYERWAVE01HZTHESEPERIODICVARIATIONSOFBIOIMPEDANCEWEREDETECTEDUNDERTHENORMALCONDITIONSANDDURINGBLOODFLOWARRESTINTHEHANDBYAPNEUMATICCUFFPLACEDONTHEARMTHEYAREEXPLAINEDBYPERIODICVARIATIONSINSYSTEMICBLOODPRESSUREANDBYOSCILLATIONSOFREGIONALVASCULARTONERESULTEDFROMNEURALVASOMOTORCONTROLDURINGNORMALBLOODFLOW,THEGREATESTVARIATIONSINBIOIMPEDANCEWEREOBSERVEDATTHEHEARTRATE,ANDTHEIRAMPLITUDESURPASSEDBYANORDEROFMAGNITUDETHEAMPLITUDESOFRESPIRATORYOSCILLATIONSANDMAYERWAVEINCONTRAST,DURINGBLOODARREST,THELARGESTAMPLITUDEOFRHYTHMICALCHANGESOFTHEIMPEDANCECHARACTERIZEDTHEOSCILLATIONSATRESPIRATIONRATE,WHILETHEAMPLITUDEOFOSCILLATIONSATTHEHEARTRATEWASTHESMALLESTDURINGNORMALRESPIRATIONANDCIRCULATION,TWOSIDECARDIACPEAKSWEREREVEALEDINBIOIMPEDANCEAMPLITUDESPECTRUMWHICHDISAPPEAREDDURINGRESPIRATIONARRESTANDTHOUGHTTOREFLECTTHEAMPLITUDERESPIRATORYMODULATIONOFTHECARDIACOUTPUTVIASYMPATHETICINFLUENCESDURINGNORMALBREATHING,THESECONDANDTHETHIRDHARMONICSOFTHECARDIACSPECTRUMPEAKWERESPLITREFLECTINGFREQUENCYRESPIRATORYMODULATIONOFTHEHEARTRATEBYPARASYMPATHETICINFLUENCESTHERESULTSFAVOURAPPLICABILITYOFFOURIERANALYSISOFBIOIMPEDANCEVARIATIONSINASSESSMENTOFREGIONALNEURALINFLUENCESANDNEUROGENICMODULATIONOFCARDIACACTIVITY1INTRODUCTIONASPECTACULARPROGRESSINMICROELECTRONICSRESULTEDINAPPEARANCEOFLOWNOISECHIPSANDPOWERFULCOMPUTERSWHICHMADEITPOSSIBLETOMEASUREANDANALYZESMALLBIOIMPEDANCEVARIATIONSWITHALABORATORYMADEHIGHRESOLUTIONIMPEDANCECONVERTERANDORIGINALSOFTWAREWEANALYZEDBIOIMPEDANCEVARIATIONSINHUMANFINGERWITHFOURIERTRANSFORMINTHEFREQUENCYBANDOF008150HZUNDERTHENORMALCONDITIONSANDDURINGCIRCULATIONARRESTINTHEARMOPTIONALLYCOMBINEDWITHEXPIRATORYDELAYFOR40SECTHEAIMWASTOASSESSTHENEUROGENICCONTRIBUTIONTOBIOIMPEDANCEVARIATIONS,WHICHPROBABLYRESULTFROMVASOMOTORACTIVITYOFSYMPATHETICNERVESYSTEM2METHODSBIOIMPEDANCEWASMEASUREDWITHORIGINALIMPEDANCECONVERTERBASEDONSYNCHRONOUSDETECTIONPRINCIPLERESULTINGINTOTAL“BASIC”REALPARTOFIMPEDANCEINTHEFREQUENCYBANDOF0–15HZRANDTHEVARIABLECOMPONENTOFTHISREALPARTINTHEFREQUENCYBANDOF008–15HZRTHEMEASURING1TOWHOMANYCORRESPONDENCESHOULDBEADDRESSEDINTERNATIONALCONFERENCEONELECTRICALBIOIMPEDANCEIOPPUBLISHINGJOURNALOFPHYSICSCONFERENCESERIES2242010012125DOI101088/17426596/224/1/012125C?2010IOPPUBLISHINGLTD1FIGURE2AMPLITUDESPECTRUMOFBIOIMPEDANCEVARIATIONSINHUMANFINGEROVERBROADFREQUENCYRANGEWITHMAYER’SPEAK1,RESPIRATORYPEAK2,FOURCARDIACHARMONICS3TO3’’’’,ANDTHESIDEPEAKS3L,3R,ETCNOTETHEBREAKINORDINATEANOTHERIMPORTANTOBSERVATIONISSPLITTINGOFHIGHERHARMONICSOFTHECARDIACPEAKOBSERVEDUNDERNORMALCONDITIONSINSOMECASESFIGURE3,ASUCHSPLITTINGWASFARLESSPRONOUNCEDUNDERRESPIRATIONDELAYFIGURE3,BSPLITTINGOFAPEAKCANBEEXPLAINEDBYFREQUENCYMODULATIONOFBASICOSCILLATORYPROCESSWITHANOTHERPROCESSGOINGONATASMALLERRATEINTHISCASE,SPLITTINGCANRESULTFROMVAGALMODULATIONOFTHEHEARTRATEATTHERESPIRATIONFREQUENCYINTHISEXPERIMENT,THEOSCILLATIONSWERECUTOFFBELOW03HZ,SONOMAYERPEAKISSEENINFIGURE3FIGURE3THERESPIRATORY2ANDSIDECARDIACPEAKSLANDRAREOBSERVEDUNDERNORMALCONDITIONSABUTDISAPPEAREDDURINGEXPIRATORYDELAYBINORDERTOASSESSTHECHANGESINBIOIMPEDANCEOFNONPULSATILENONCARDIACORIGIN,WECOMPAREDTHEBIOIMPEDANCESPECTRADURINGNORMALCIRCULATIONFIGURE4,AANDDURINGBLOODARRESTINTHEARMSFIGURE4,BCIRCULATIONARRESTDIDNOTELIMINATEOSCILLATIONSOFBIOIMPEDANCEALTHOUGHDIMINISHEDTHEIRAMPLITUDEFIGURE4,BUNDERTHESECONDITIONS,THEPERIODICBIOIMPEDANCEOSCILLATIONSCOULDBEPRODUCEDEITHERBYNEUROGENICVASOMOTORINFLUENCESORBYSPONTANEOUSVASOMOTIONSTHELATTERARECHARACTERIZEDWITHABROADRANGEATTHELOWFREQUENCIESOF0008–011HZ4THENARROWSHAPEOFALLPEAKSINFIG4DOESNOTFAVOURTHEHYPOTHESISOFSPONTANEOUSNATUREOFTHECORRESPONDINGBIOIMPEDANCEOSCILLATIONSTHUS,ALLTHEPEAKSINFIGURE4,BAREPROBABLYNEUROGENICANDVASOMOTORINNATUREARRESTOFCIRCULATIONDRAMATICALLYREDUCEDTHECARDIACPEAK,WHICHISATRIVIALCONSEQUENCEOFTHEFACTTHATDURINGNORMALCIRCULATIONTHEMAJORVARIATIONSINBIOIMPEDANCEAREPRODUCEDBYPUMPINGACTIONOFTHEHEARTSURPRISINGLY,THERESPIRATORYPEAK2ANDMAYER’SPEAK1DECREASEDBYNOMORETHAN2FOLDITMEANSTHATDURINGNORMALCIRCULATION,THEHEARTANDSYSTEMICBLOODPRESSUREARENOTTHEMAJORPLAYERSWHOCONTROLTHESERHYTHMICVARIATIONSOFBIOIMPEDANCEDURINGCIRCULATIONARREST,THEINTERNATIONALCONFERENCEONELECTRICALBIOIMPEDANCEIOPPUBLISHINGJOURNALOFPHYSICSCONFERENCESERIES2242010012125DOI101088/17426596/224/1/0121253

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簡介：中文中文2020字，字，1560單詞，單詞，8800英文字符英文字符出處出處NESTEROVA,GAVRILOVI,SELECTORL,ETALASSESSMENTOFVASOMOTOROSCILLATIONSWITHFOURIERANALYSISOFBIOLOGICALTISSUEIMPEDANCEC//JOURNALOFPHYSICSCONFERENCESERIESIOPPUBLISHING,2010,22410121251使用生物組織阻抗傅里葉分析使用生物組織阻抗傅里葉分析評估血管舒縮振幅評估血管舒縮振幅ASSESSMENTOFWASOMOTOROSCILLATIONSWITHFOURIERANALYSISOFBIOLOGICALTISSUEIMPEDANCETHETITLEOFFOREIGNLANGUAGE學部（院）電子信息與電氣工程學部專業(yè)生物醫(yī)學工程使用生物阻抗諧波分析為診斷工具評估局部循環(huán)和神經(jīng)活動3譜做平均。將阻抗變換器與人的中指（N14）的近端指骨連接，將兩個輸出電流和兩個輸出電壓與兩個AG/AGCL電銀絲（直徑為04MM）電極連接起來，電極表面包裹沾有生理鹽水的窄紗布。電極之間的距離是2CM。為了減弱心臟和肺部引起的機械振動，將手臂固定起來。暫時用充氣袖帶把手臂血流阻斷，至少是2倍收縮壓來阻斷手臂的液壓波動。3結(jié)果如圖1所示，在正常情況（A）和阻斷左臂血流過程中（C）測量基本阻抗R（B）和可變阻抗成分R。心臟的抽吸作用導致了（A，B）的生物阻抗的大振幅，可以在心臟循環(huán)未阻斷時觀察到更小的一個（C），這反映了血管舒縮的神經(jīng)活動。圖1，人手指的可變分量（A）和基本生物阻抗（B）。（C）手臂循環(huán)阻斷時的可變分量。另外一個重要的觀察是心臟波峰的高次諧波的分離，它是在某些正常情況下（圖3，B）觀察到的。波峰的分離可以解釋為另外一個基礎(chǔ)震蕩過程的調(diào)頻速率更?。辉谶@種情況下，分離可由心臟迷走神經(jīng)呼吸作用的速率引起。在這個實驗中，震動被切割成低于3HZ的片段，所以圖3中沒有邁爾波。