revised this manuscript and especially paid much attention to your comments and suggestions. We discussed our results only in the structural level, and many previous studies also reported and discussed their observation in the structural level [7, 9-12 also cited in the manuscript] (少量语法问题). The expression profile that is identified to be suitable to verify our observation will be conducted in further work (审稿人并没有强调补试验,故不必画蛇添足). Thank you for you kindly suggestions! (语法问题。不必太多Thank you.惊叹号要慎用).
We have also learned (有点”Chingish”) the paper downloaded from the web site provided by you (http://www.springerlink.com/content/h6q55355q85p4222/). The author provided a 2D-FISH method for visualization of viral nucleotide sequences and expression patterns in the infected interphase nuclei. The method should be applied in further 3D-FISH to study VIRUS A expression. 建议改答 :
Thank you for your careful review and valuable suggestions.
In this study, we addressed the problem on the dynamic reposition of specific chromosomes in VIRUS A infection. It (It所指不明,建议修改)reflects an impact of VIRUS A infection on highly ordered interphase nuclear architecture. Whether or not repositioning of HSA 17 is involved in expression regulation of chromatin, is a problem that we are highly concerned with. Your comments are helpful. The expression profiles for VIRUS A and transcription maps for HSA 17 were initially considered in our study. However, we cannot perform them at present due to the following limitations. Firstly, a causal link between chromatin mobility and gene expression remains to be firmly established [1]. Many human gene clusters or loci move towards the nuclear center for a high-level expression [2-4], whereas the contrary movement towards the nuclear periphery is required for transcriptional activation for other genes according to previous reports [5,6]. Other studies have indicated that repositioning of genetic regions is independent of transcriptional activities [7,8]. Studies on single genes involved in gene reposition and transcription suggested uncertain relationships. The whole chromosomal repositioning in VIRUS A infection is accompanied by gross modifications in the nuclear architecture, involving activation or silencing of specific gene sets at an appropriate time in whole genome. We are not sure how much the expression profiles for VIRUS A or transcription maps for HSA 17 verified our dynamic behavior in CT 17(句子含义不明,建议修改). Secondly, shortage of fund, for example, the expression chips for VIRUS A will cost no less than 100 thousands for 5 stages in infection(语法问题及句子含义不明,建议修改). Due to the above difficulties, we only report our preliminary experiments at present. Nevertheless, We have revised this manuscript and especially paid much attention to your comments and suggestions. We have now discussed our results only at the structural level in the revised manuscript, and cited a few relevant previous studies that also reported and discussed their observation at the structural level [7, 9-12].
We have also downloaded and read the paper you recommended (http://www.springerlink.com/content/h6q55355q85p4222/). The author provided a
2D-FISH method for visualization of viral nucleotide sequences and expression patterns in the infected interphase nuclei. We believe that 3D-FISH method should be applied in the future study on VIRUS A expression. 加注 :
1、这篇论文投稿修稿有些代表性,那就是有些审稿人建议拒稿,而编辑“惜稿”,愿意给作者机会。这点在以前谈过。 2、这篇文章还有个特点就是审稿人在其他的审稿意见中建议补试验,但作者根本无法补做。所以只好尽力用理论描述加文献支持来回复审稿人。是否奏效,真的只能是“听天由命“。可谓“尽人事听天命”! 附
美捷登主编与快乐跑垒手通讯纪录: Dear Dr. XXX
Thanks for your message. I read the comments. Although I am not the expert in your research area, and I haven't had a change to read your full paper, I would like to make a few comments on your situation.
1. Obviously, the reviewer 1 is very nice and gave many constructive comments on how to improve your study and presentation of your manuscript. The reviewer 2 obviously doesn't like your paper (not the idea of study). But he/she also provided some useful comments which will help improve your paper.
2. Fortunately, the editor decided to give you an opportunity to revise your paper. My own experience tells me that over 50% of papers that are rejected by a reviewer but given a chance to revise are accepted eventually, especially when the authors carefully responded to the comments. Therefore, I would encourage you to do your best to revise the paper.
3. When you have done so, you may consider sending your paper to us, ?... 4. If you don't wish to send your paper to us,?. Best wishes, Harry
Dear Dr. XXX
I proofread your paper, with some comments.
I understand that you cannot do any further experiments. Therefore, you have to 听天由命.
Honestly, I am not sure of the fate of your revised manuscript since I am not an expert in your area. Based on your reply letter, I would assume that there are also many language problems in your manuscript, in addition to being unable to add required experiments.
However, if you are confident, then you may re-submit the revised manuscript as it is now. I wish to know the outcome. Let me know if you have any questions, Good luck, Harry
尊敬的夏老师
我非常非常感谢您的无私帮助,改的很细致,很好。我的文章就是我自己写的,的确很差,我是这么想的如果内容没有问题的话,杂志想要的时候还会给我修改语言的机会,到时候我再想办法修改一下。我对这个文章更没有信心,反正我老板就是死活不补实验,还没有什么钱。听天由命吧。无论有怎样的结果,我都会及时通报给您的。 再一次感谢您的帮助!占用了您的宝贵时间 快乐跑垒手如果能早半年读到夏老师的帖子,我的文章可能不会这么凄惨了。向夏老师致敬!I already replied to your PM. Good luck!受益匪浅,期望这次回修能够有好运!向夏老师致敬!难得有这么高水平而又热心的老师举办讲座,读后受益良多!夏老师一语道破,读起来颇有心得。
恰巧最近自己手头也有这样的例子,拿出来跟大家分享一下,班门弄斧,希望夏老师多多指导。 论文题目
:Loss of enteric neurons accompanied by ...... 所投杂志
:Neurogastroenterology and Motility 结果
:大修(major revision),修回意见后接受(accept)。 Editor's Comments to Author:
One reviewer is now satisfied with this paper, but the other (Rev 1), recommends one more experiment to be added, unless you feel you can address this point. I am pleased for you to do either as I like this paper and look forward to seeing it in the journal. I look forward to seeing the revision. 【编辑“惜稿”,给作者机会,让大修】 审稿人1内容(有删节):
In this revised version the authors have addressed most of the original criticisms. However, still some issues remain to be addressed in order to support the proposed hypothesized link between a reduction in GDNF expression, pAkt and neuronal loss. In particular, the reported reduced expression of pAkt could be due to the fact that fewer neurons are present (as the data suggests). If the authors are suggesting that a decrease in GDNF is responsible for the reduction in pAkt then they will need to show total Akt expression and determine whether the ratio pAkt/Akt is changed. This is particularly important as the figures show that pAkt stain is completely absent at 12 weeks of diabetes while PGP9.5 is still visible. 作者原答:
We very much appreciate the reviewer’s comments and good suggestions.
In our paper, we reported a reduction in GDNF expression, pAkt and neuronal loss induced by diabetes in rat model. Then we concluded that the enteric neuropathy may be partly mediated via a reduction of GDNF and its main downstream signaling pathway PI3K/Akt, which is based on PI3K/Akt is a survival signal for enteric neurons. As suggested by the reviewer, detecting the ratio pAkt/Akt will help to further confirm our conclusion.
However, as the specimens for this experiment have been stored for more than one year, we are afraid that it’s difficult to get a satisfactory result or whether the possible result will be convincing. Moreover, there may be not enough time for
us to establish the model of diabetic rats for the second time to get fresh specimens and add the additional experiment. Hence, here we try to use another way to further confirm our conclusion. Anitha and Brami-Cherrier tested the percentage of pAkt/neurons (% of p-Akt positive neurons) to show changes of Akt phosphorylation in their papers. (Journal of Clinical Investigation 2006, 116: 344-356; references 8. J Neurosci, 2002, Oct 22: 8911-8921.) I think p-Akt/neurons could be used as a substitute for p-Akt/Akt, but I agree with you that p-Akt/Akt is better. In my revision I tested the protein of p-Akt/neurons (see figure below) and showed decrease along with disease course. As you said that pAkt stain is completely absent at 12 weeks of diabetes while PGP9.5 is still visible. In accordance with my figure the ratio almost decreased to zero at 12 weeks. It may due to there are also other signaling pathways to maintain survival of neurons besides Akt associated pathway.
Anitha M et al in their literature have well demonstrated that diabetic mice exhibit enteric neuronal apoptosis using the Ret/TUNEL method and the over-expressed GDNF could prevent diabetic neuronal apoptosis (Journal of Clinical Investigation, 2006, 116: 344-356; references 8 ). As our paper is only a preliminary study for diabetic colon dysfunction, we will do more work in our further research with your helpful suggestions. 我的建议改答 : Thank you for your critical comments and we totally agree with your suggestions which might be of great help to improve the quality of our manuscript.
We greatly accept the reviewer’s suggestions that the ratio pAkt/Akt be used to strongly support our hypothesis that a decrease in GDNF is responsible for the reduction in pAkt. According to the reviewer’s suggestions, we performed some modifications in our manuscript. First, we precluded that p-Akt/neurons could be used as a substitute for p-Akt/Akt to show changes of Akt phosphorylation, at least partly, as suggested by Anitha and Brami-Cherrier ((Journal of Clinical Investigation 2006, 116: 344; J Neurosci, 2002, 22: 8911). Therefore, in our revised manuscript, we performed the protein of p-Akt/neurons (see figure below) again. The figure showed that the ratio of p-Akt/neurons decreased and then almost to zero at 12 weeks, which is in accordance with the fact that pAkt stain is completely absent at 12 weeks of diabetes while PGP9.5 is still visible. It also suggested that there might be some other signaling pathways to maintain survival of neurons besides Akt associated pathway. Second, we have made also some modifications in the discussion part according to the reviewer’s suggestions, which have been underlined with red color:
“In our manuscript, we draw the conclusion that the loss of enteric neuropathy may due to reduction of GDNF and its main downstream signaling pathway PI3K/Akt, at least partly. The conclusion was made as it might be PI3K/Akt is a survival signal for enteric neurons. However, there are still some limitations in this present study. First, p-Akt/Akt might be more effective index that should be substitute for p-Akt/neurons; ?... “
心得感悟:
1.只要有机会,就要抓住;
2.直面问题,不要顾左右而言它,能解决一点的解决一点,突出说明....其它不明说明的,呵呵,放在discussion中又何妨..今晚有幸拜读了美捷登主编夏老师的半月谈专题,受益匪浅!
我的文章刚补完实验准备给编辑回信,请帮忙看看编辑来信,解读一下文章的命运。另:是否有时间帮忙修改回信。谢谢!
http://www.dxy.cn/bbs/post/view?bid=45&id=14886256&sty=1太不错啦!本来对自己实验存在老多问题,但是可以把其中的讨论以及放limition!很受启发,希望可以抽空谢谢!!!向夏老师学习,真正的传道解惑!!支持啊一直没来感谢夏老师,那时候我第一次投稿被拒了,开始想申诉,中间咨询过夏老师,给了我不少建议。跟老板商量后后来放弃了,结合意见投向另一个3分多的杂志,在8月底接受了。
再次感谢夏老师!!!非常高兴看到yeyang1222这样的帖子。它无异于国庆、中秋节送给我的厚礼!
没有什么比看到DXYers的文章被接受更让人欣慰的了。 我也要感谢**战友对我的信任和尊重,这也是我再忙碌也要每天花上至少1个小时在**的原因。我最喜欢这个地了,呵呵,每天必逛**。祝夏老师及各位战友国庆中秋双节快乐!!好贴留名先向夏老师表示由衷的感谢 今天集中读了很多您的帖子 有很多感触和收获
现在再看自己写的东西真是稚嫩啊
要去重新写回复编辑和reviewer的意见了 越写越觉得复杂了,呵呵
先谢谢啦正需要中,谢谢!努力学习审稿人的意见,不知这样回答可否?
How reproducible was cartilage in animal model? - In my experience there can be development of spontaneous cartilage defects in healthy animals (even when quite young) independent of treatment which can skew results 我的回答:
We do not rule out the possibility, but the data set has a total eight samples used in the experiment不知前后文,只能根据提供的信息稍作改进。
We thank the reviewr to share his/her experience. We accept the comment and have addressed this point in the Duscussion, by adding a sentence \this result was consistently observed in a total of eight animals in the present study, the possibility that spontaneous cartilage defects may develope in healthy animals\If there is a reference provided by the reviewer, you can add \when quite young) independent of treatment\
Make sure you add the sentence in the Discussion of the revised version of the manuscript.最近我大修论文的点对点回答上传,请夏老师和广大战友提出宝贵意见。 Reviewer #1: Overall I found this article very interesting, however I feel that some parts require further information.
In particular I was unable to clearly establish from the article why pH6.0 was used as the experimental condition? What was the rationale for this pH and not any other pH lower than pH 7.4. Also the composition of the acidic solution is not specified
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