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tzkcarlos銀蟲 (小有名氣)
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[求助]
自身免疫學(xué)翻譯為中文-幾段話，Autoimmunity Reviews 13 (2014) 108–113
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PLA 2 R1 is a type 1 transmembrane receptor that is expressed by podocytes. Besides a short membrane-spanning intracellular domain, the receptor consists of a long extracellular domain with a cysteine-rich head, a fibronectin type II-like repeat domain and eight repeated carbohydrate-recognition domains [22]. PLA 2 R1 is one of four members of the mannose receptor family [23]. All of them have a conserved domain structure and share common characteristics such as constitutive endocytic recycling at the plasma membrane [24] which may provide a constant source of accessible PLA 2 R1 at the podocyte membrane for immune-complex formation [23]. Further more, the receptors exist in both an extended and a bent conformation conferring distinct ligand binding and oligomerization capacities [25]. Since the anti-PLA 2 R1 autoantibodies in patients with pMN only recognize a conformation-dependent target epitope [21], it is assumed that autoantibody-binding might only occur in one of these two configurations. Therefore, pMN might represent an autoimmune conformational disease (‘conformeropathy’), such as Goodpasture syndrome [1]. Although the exact mechanisms causing pMN are still under investigation, different studies show a strong relationship between antibody levels to podocytic proteins and disease activity. Since the discovery of anti-PLA 2 R1 autoantibodies by Beck et al. in 2009, there has been strong evidence that they are a key player in the pathogenesis [21]. For example, autoantibodies to PLA 2 R1 can not only be eluted from kidney tissue of pMN patients, but also colocalize with PLA 2 R1 in the glomeruli [21]. Therefore, it is widely accepted that upon binding of circulating autoantibodies to PLA 2 R1 on podocytes, subepithelial deposits are formed in situ, leading to complement activation and a cascade of events subsequent to the nephrotic syndrome (in most of the cases) [37]. Interestingly, autoantibodies to PLA 2 R1 have shown to be mainly of the IgG4 subclass, which is regarded as being unable to activate the complement pathway [38,39]. Nevertheless, since the terminal complement compo- nent C5b-9 is detectable in glomeruli and urine of pMN patients [40,41], there is strong evidence for the involvement of the complement system. As most patients with MN have low or undetectable levels of C1q, the classical complement pathway can be excluded. Therefore, either the alternative or the lectin pathway seems to be predominantly involved [42]. This hypothesis is supported by the notion, that mannose binding lectin can be detected in glomeruli of MN patients [43]. |
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ssssllllnnnn 
至尊木蟲 (知名作家)
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【答案】應(yīng)助回帖
★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★
RXMCDM: 金幣+1, 多謝應(yīng)助！ 2014-08-26 00:17:29
tzkcarlos(phu_grassman代發(fā)): 金幣+30, he deserves it. Thanks for your cooperation. 2014-08-26 09:53:38
RXMCDM: 金幣+1, 多謝應(yīng)助！ 2014-08-26 00:17:29
tzkcarlos(phu_grassman代發(fā)): 金幣+30, he deserves it. Thanks for your cooperation. 2014-08-26 09:53:38
本樓樓主要求刪除 我覺得他花了不少時(shí)間和心思的，樓主卻一再挑剔，有點(diǎn)過分哦。  英文這種東西畢竟不是咱中國人的，翻譯過來難免變味，我們理工科的學(xué)生也不是學(xué)文學(xué)的，要達(dá)到“信、達(dá)、雅”也有點(diǎn)難哦。 樓主為何不參照應(yīng)助者提供的信息自己修飾一下呢？  |
2樓2014-08-25 22:24:21
tzkcarlos
銀蟲 (小有名氣)
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3樓2014-08-25 23:21:23
ssssllllnnnn
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4樓2014-08-25 23:36:10
ssssllllnnnn
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5樓2014-08-25 23:41:37
tzkcarlos
銀蟲 (小有名氣)
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6樓2014-08-25 23:50:26
ssssllllnnnn
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- 翻譯EPI: 1690
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- 金幣: 31580.9
- 紅花: 100
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7樓2014-08-25 23:56:53
tzkcarlos
銀蟲 (小有名氣)
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8樓2014-08-26 00:00:00
tzkcarlos
銀蟲 (小有名氣)
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真強(qiáng)必勝: 大家都體諒一下，應(yīng)助者翻譯了也不容易，樓主覺得不恰當(dāng)可用自己推敲補(bǔ)充一下，實(shí)在不行找導(dǎo)師問問 2014-08-26 10:20:02
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不是要求信雅達(dá)，但是有些句子不大通順的情況下，我只是希望回答者再認(rèn)真檢查，看看其他有沒有問題，順便再修飾一下。如果要求很過分的話，自我檢討。至于說我一再挑剔，我想請問，回答者好像就回答了一次，我只是不斷請求他再檢查修飾，因?yàn)檫@個翻譯很重要，但他覺得不用再修改。我也不是說不給他發(fā)金幣，至于斑竹扣發(fā)30金幣，再刪除他的回答，相當(dāng)于罰我30金幣的做法，我不敢茍同。謝謝 |
9樓2014-08-26 10:01:35
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