SCI论文投稿coverletter投稿信模版.pdf
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1、SCISCI 论文投稿论文投稿 cover lettercover letter 投稿信模版投稿信模版Dear editorial board of European Journal of Cardiology,Please find enclosed the manuscript:“The angiotensin-converting enzyme is not a risk factor formyocardial infarction in French individuals”,by Sarah H.,et al.,to be submitted as a ShortCommunica
2、tion to the European Journal of Neurology for consideration of publication.Allco-authors have seen and agree with the contents of the manuscript and there is no financialinterest to report.We certify that the submission is original work and is not under review at anyother publication.In this manuscr
3、ipt,we report the results of the first study on the genetic and functional roles ofthe ACE on the risk of suffering a myocardial infarction in the French population.Indeed,wegenotyped the rs4341 polymorphism in 531 IS cases and 549 healthy controls,and thenperformed functional studies by measuring s
4、erum ACE protein level and activity in healthycontrols,stroke patients at baseline and stroke patients 24h after stroke symptoms onset.Theresults from our study did not reveal any association of the ACE variant with myocardial infarction,although it affected ACE protein level,and ischemic stroke pat
5、ients showed lower ACE level thancontrols 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 Cardiologybecause they bring new and strong evidence that the ACE gene and protein are not a risk factorfor myocardial inf
6、arction.We hope that the editorial board will agree on the interest of this study.Sincerely yours,Sarah H.on behalf of the authors.Corresponding author:Sarah Hamilton at Cardiovascular Research Laboratory,Marie CurieResearch Institute,75000,Paris,France,phone number:+33582246xxx,fax number:+33582246
7、xxx.Case 1Dear Editor,We would like to submit the enclosed manuscript entitled GDNF Acutely Modulates NeuronalExcitability and A-type Potassium Channels in Midbrain Dopaminergic Neurons,which we wishto be considered for publication in Nature Neuroscience.GDNF has long been thought to be a potent neu
8、rotrophic factor for the survival of midbraindopaminergic neurons,which are degenerated in Parkinsons disease.In this paper,we report anunexpected,acute effect of GDNF on A-type potassium channels,leading to a potentiation ofneuronal excitability,in the dopaminergic neurons in culture as well as in
9、adult brain slices.Further,we show that GDNF regulates the K+channels through a mechanism that involvesactivation of MAP kinase.Thus,this study has revealed,for the first time,an acute modulation ofion channels by GDNF.Our findings challenge the classic view of GDNF as a long-term survivalfactor for
10、 midbrain dopaminergic neurons,and suggest that the normal function of GDNF is toregulate neuronal excitability,and consequently dopamine release.These results may also haveimplications in the treatment of Parkinsons disease.Due to a direct competition and conflict of interest,we request that Drs.XX
11、X of Harvard Univ.,and YY of Yale Univ.not be considered as reviewers.With thanks for your consideration,I amSincerely yours,case2Dear Editor,We would like to submit the enclosed manuscript entitled Ca2+-binding protein frequeninmediates GDNF-induced potentiation of Ca2+channels and transmitter rele
12、ase,which we wishto be considered for publication in Neuron.We believe that two aspects of this manuscript will make it interesting to general readers ofNeuron.First,we report that GDNF has a long-term regulatory effect on neurotransmitter releaseat the neuromuscular synapses.This provides the first
13、 physiological evidence for a role of thisnew family of neurotrophic factors in functional synaptic transmission.Second,we show that theGDNF effect is mediated by enhancing the expression of the Ca2+-binding protein frequenin.Further,GDNF and frequenin facilitate synaptic transmission by enhancing C
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