收到sci审稿邀请研究方向不同

�皇嵌晕颐钦庑┬〉ノ坏娜司涂嗔耍�蛭�悴蝗鲜端�牵�膊豢赡苁撬�堑难��Ｄ阒挥小⒅荒芡ü�岣咦约何恼轮柿坎鸥�谢�帷；褂芯褪锹���省⑿��,但目前因为杂志生存的原因，较之以前速度可能也都快起来了，也甚至还有些只要给钱就收的杂志，类似于西太平洋大学似的，这是卖文凭，人家就是卖文章的，当然我想大部分杂志还是能够“客观、公正”进行稿源选择吧，但愿吧。 那SCI杂志又是如何审稿呢，相反应该更“客观”，至少不会歧视你是来自无名的单位，就受邀于几个杂志作为其审稿人来说，绝大部分都采用同行审稿（peer-review），也即邀请你审稿的文章多半是与被邀请人所作的研究相似，这就不存在一定是所谓的“牛人”来审了。与你的职称完全没有关系，不是说教授就有资格，而初级就没有资格被SCI杂志邀请审稿杂志社一般都会通过你发表文章找到你的email（我想应该是这样的，所以通讯更牛叉啊，否在人家不会邀请到你的） 当然你也可以拒绝，因为毕竟不是所有的文章我们都有能力去审的，至少我还没那水平，也曾拒绝过一篇关于基因分析的（虽然了解一些，但很难把握）如你接受后，则会自动连接到审稿人页面（如下），除了author centre外，同时也有reviewer centre的页而一般如果没有被邀请审稿，通常进入作者系统后，只会有anthor centre接下来就是审稿了，这篇文章是国内某F教授为通讯的一篇关于血管紧张素在皮肤中作用的综述，毕竟人家在国内还是相当的啊，也是顺便学习了一下，可一下载稿件一看，怎么看怎么不像综述，充其量是个mini review，四个段落，1198个字，26篇参考文献。既然杂志社邀请我审稿，也综述的我所做过的研究，却没引用我的文章，有点“失落”，更重要的是更多文献他们也没有引用，而是引用他们自己的“中文”文章,但还是认真的“分析”了此文。给出审稿意见如下：The review by *** et addresses the interesting and novel topic of the renin-angiotensin-system (RAS), which was originally described as a cardiovascular endocrine system, in skin physiology and Only in recent years, the cutaneous RAS has become an area of scientific interest, and the number of related publications is increasing from year to Therefore, it is indeed time for an article which reviews the existing literature up to However, this review has a number of 中国人语言每次都被审稿人发飙，我的也是，至少部分文章投出去审稿人也是要让我改进，唔，每次让我找个母语的人帮修改，我滴个汗，俺们中国人哪有以说英语母语的，索性每次都“忽悠”过去了，当然也许只是些小杂志的原因吧，语言真的需要提高、再提高。同样该综述，我也提出了我的部分语言意见 - Language editing is - The number of publications dealing with the RAS in skin is still not very Therefore, there is no need to focus this review article on the AT2-receptor (for which data are even more limited) Instead, this review should consider all published data about the cutaneous RAS - Many publications are For example: �6�1Min et , Endocrinology 2004 �6�1Nakai et , J Dermatol Sci 2008 �6�1Rompe et , Hypertension 2010 �6�1Steckelings et , (Exp Dermatol 2004) �6�1Yevdokimova et , J Dermatol Sci 2007 �6�1Morihara et , J Am Acad Dermatol 2006 �6�1Yahata et , J Biol Chem 2006 �6�1Takeda et , Am J Pathol 2004 并逐部分给予我的意见：Abstract:- In the case of AT1R-blockade, AT2R unmasking may indeed be important, but blockade of the AT1R thus interrupting AT1R-mediated actions of Ang II, is at least as The respective passage in the abstract is Introduction: - 3, line 13: “disorders of RAS”: A “disorder” of the RAS has so far only been described for scleroderma (not saying whether the deregulated RAS is a primary cause or only a secondary phenomenon) It is indeed likely that the RAS is deregulated in the other mentioned dermatoses as well, but this is pure speculation and should be discussed as - 3, line 19: “existence of RAS in skin”: References 2 and 3 demonstrate only the existence of receptors, but not of the whole RAS in Adequate references would be: Steckelings et , Exp Dermatol or Philips MI et , In: Saavedra J M, Timmermans P M W M, Angiotensin New York: Plenum Press, 1994: 377– - 3, line 20: “It has been documented…”: It is correct that AT2R upregulation has been demonstrated in skin, and it is also correct that Ang II has been shown to accelerate cutaneous wound However, it has never been shown that acceleration of wound healing by Ang II is mediated by the AT2R In fact, this is rather unlikely, since the AT2R acts anti- - Chapter II 1: Physiological receptor expression should be addressed prior to receptor expression in - p4, line 5 from bottom: “Ang II either…” Please add - chapter II 2: The high expression of Ang II receptors during foetal life indeed suggests a role in However, Ang II receptor knockout mice show no severe developmental deficits, in particular not in Furthermore, there are almost no data about what specifically the role of the AT2R in development may This should be - chapter II 3: This chapter is much too For example, the description of deregulated receptor expression in some dermatoses by Takeda and Kondo (Am J Pathol 2001, Br J Dermatol 2001 and 2002) has not been This chapter may further be the place for some speculations (based on data from non-cutaneous tissues) in which dermatoses the RAS may be - page 5, line 5: “Kawaguchi et al …in SSc fibroblasts, suggesting that… “: This is not a logical What is the causal link between AT2R in SSc fibroblasts and excessive ECM production? Furthermore, expression of AT2R has been shown by several authors for normal - page 5, line 12: Steckelings is a woman (“her” colleagues) - page 5, last section: The impact of AT2R expression on immune cells and of AT2R effects on vascularisation and neuroregeneration with regard to wound healing is not sufficiently - 6, 2 lines from bottom: “…restoring normality not only in the CV system but also in many tissues, such as ” Please provide a reference for the statement that the AT2R has been shown to restore normality in 最后提交时杂志社会有一个勾选表，该文被我拒了该文编辑在结合另一个审稿人意见的情况下还是reject此文了，从投稿到最后给出decision约6个星期，应该说是正常速度了。有意思的是中途，编辑发信催审稿了，估计是作者急着想知道结果，可以理解，想想之前的我们也何尝不是啊，每天都不停得刷屏，也写过催稿信，还以为没有用，甚至有时候也不“敢”写，因为害怕是否会有“反”作用，看来某些时候写信催催也还是可以的。总之，审稿也未必是件好差事，不过倒是可以知己知彼，可以站在审稿人的角度去思考我们自己在写文章的时候应该注意什么，别人文章的有哪些优点、缺点，我们都可以好好去总结，同时我们也获得与最新研究领域的接触也为以后研究，能够写作提供更多的思路。