SCI论文投稿cover letter 投稿信模版

SCI论文投稿cover letter 投稿信模版
Dear editorial board of European Journal of Cardiology,
西南票务网>mnccPlease find enclosed the manuscript: “The angiotensin-converting enzyme is not a risk factor for myocardial infarction in French individuals”, by Sarah H., et al., to be submitted as a Short Communication to the European Journal of Neurology for consideration of publication. All co-authors have seen and agree with the contents of the manuscript and there is no financial interest to report. We certify that the submission is original work and is not under review at any other publication.
In this manuscript, we report the results of the first study on the genetic and functional roles of the ACE on the risk of suffering a myocardial infarction in the French population. Indeed, we genotyped the rs4341 polymorphism in 531 IS cases and 549 healthy controls, and then performed functional studies by measuring serum ACE protein level and activity in healthy controls, stroke patients at baseline and stroke patients 24h after stroke symptoms onset. The results from our study did not reveal any association of the ACE variant with myocardia
l infarction, although it affected ACE protein level, and ischemic stroke patients showed lower ACE level than controls in the acute phase but not in the chronic phase.
We believe that our findings could be of interest to the readers of European Journal of Cardiology because they bring new and strong evidence that the ACE gene and protein are not a risk factor for myocardial infarction.
We hope that the editorial board will agree on the interest of this study.
Sincerely yours,
Sarah H. on behalf of the authors.
ifcCorresponding author: Sarah Hamilton at Cardiovascular Research Laboratory, Marie Curie Research Institute, 75000, Paris, France, *****************, phone number: +33582246xxx, fax number: +33582246xxx.
Case 1 
Dear Editor, 
悬崖边的贵族We would like to submit the enclosed manuscript entitled "GDNF Acutely Modulates Neuronal Excitability and A-type Potassium Channels in Midbrain Dopaminergic Neurons", which we wish to be considered for publication in Nature Neuroscience. 
GDNF has long been thought to be a potent neurotrophic factor for the survival of midbrain dopaminergic neurons, which are degenerated in Parkinson’s disease. In this paper, we report an unexpected, acute effect of GDNF on A-type potassium channels, leading to a potentiation of neuronal excitability, in the dopaminergic neurons in culture as well as in adult brain slices. Further, we show that GDNF regulates the K+ channels through a mechanism that involves activation of MAP kinase. Thus, this study has revealed, for the first time, an acute modulation of ion channels by GDNF. Our findings challenge the classic view of GDNF as a long-term survival factor for midbrain dopaminergic neurons, and suggest that the normal function of GDNF is to regulate neuronal excitability, and consequently dopamine release. These results may also have implications in the treatment of Parkinson’s disease. 
Due to a direct competition and conflict of interest, we request that Drs. XXX of Harvard Univ., and YY of Yale Univ. not be considered as reviewers. With thanks for your consideration, I am 
Sincerely yours, 
城市管理执法办法case2 
Dear Editor, 
We would like to submit the enclosed manuscript entitled "Ca2+-binding protein frequenin mediates GDNF-induced potentiation of Ca2+ channels and transmitter release", which we wish to be considered for publication in Neuron. 
We believe that two aspects of this manuscript will make it interesting to general readers of Neuron. First, we report that GDNF has a long-term regulatory effect on neurotransmitter release at the neuromuscular synapses. This provides the first physiological evidence for a role of this new family of neurotrophic factors in functional sy
naptic transmission. Second, we show that the GDNF effect is mediated by enhancing the expression of the Ca2+-binding protein frequenin. Further, GDNF and frequenin facilitate synaptic transmission by enhancing Ca2+ channel activity, leading to an enhancement of Ca2+ influx. Thus, this study has identified, for the first time, a molecular target that mediates the long-term, synaptic action of a neurotrophic factor. Our findings may also have general implications in the cell biology of neurotransmitter release. 
Sincerely yours, 
Case 3 
Sample Cover Letter[the example used is the IJEB] 
Dear Editor of the [please type in journal title or acronym]: 
Enclosed is a paper, entitled "Mobile Agents for Network Management." Please accept it as a candidate for publication in the [journal title]. Below are our responses to your submission requirements. 
1. Title and the central theme of the article. 北京青春
Paper title: "Mobile Agents for Network Management." This study reviews the concepts of mobile agents and distributed network management system. It proposes a mobile agent-based implementation framework and creates a prototype system to demonstrate the superior performance of a mobile agent-based network over the conventional client-server architecture in a large network environment. 
2. Which subject/theme of the Journal the material fits 

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