Cell Biology Assignment: Emailing the author of a peer ...
Cell Biology Assignment: Emailing the author of a peer-reviewed journal that is used in your term-paper (10 points)
Peer-reviewed papers are required to have a Primary or Corresponding author, who is responsible for answering questions about the content of a published peer-reviewed paper or a request by you the papers author. They will be indicated in the abstract usually and on the paper itself always. Typically they will include their email address along with the abstract in PubMed, Agricola or which ever search engine you used, although occasionally only a mailing address will be included. Please see the example below for an example see the attached abstract from Pub Med below.
When reading these papers and getting confused about their meaning, we often fail to ask the author what was meant. Asking another biologist/scientist about their paper is a great way to learn about the paper, this is called a “point of clarification”. Asking the author is also a way to ask for a copy of the paper itself (if it is not available as a free-link). Usually in the digital age we ask for an electronic copy of the paper (it costs less to send it this way), this is called a “reprint request”. (Note: reprint requests are the easiest to send and the most likely to get a reply). Point of clarification requests are harder to get reply on, but are often much more informative….shucks you have get a reply from someone with a Nobel Prize.
When you hand in the rough draft to Dr Wilson, you need to include a separate assignment. This is an email reply from an author to one of your requests regarding a paper that is cited in your paper and used in your reference list. The reply needs to include your requested Point of Clarification or Reprint Request (just a copy of your email inquiry), as well as the reply from the author. Be sure to circle the specific paper in your reference list so it is easy to determine which paper you are referring to.
Here are a couple sample emails that could be sent…..
Key things you need…polite language + person you want to send request to + why you are asking + your professional address….
Dear Dr Johnson,
I saw the following paper: Johnson, E. Cell Biology: Aneuploidy and Cancer. Nature 2007, 446:38-39
I am writing a review paper on this same topic and am unable to obtain a copy through our campus interlibrary load system. I am also an undergraduate biology student who lacks the fund to purchase it through the journal itself. Would you be so kind as to send a electronic copy?
Thanks so much for your assistance.
Sincerely,
Dr John Q Student
Dept Biology
Winona State University
Winona, MN 55987
Dear Dr Johnson,
I saw the following paper and spent quite some time reading it and have found it to be quite enlightening. I had one question however, when you discuss aneuploidy in Figure 1, it is unclear to me about whether the process you refer to is aneuploidy in a human cell or a model of a human cell (not actual cell). I looked in the methods and could not determine which system you were working on. Would you be so kind as to clarify what you meant?
Paper: Johnson, E. Cell Biology: Aneuploidy and Cancer. Nature 2007, 446:38-39
Thanks so much for your assistance.
Sincerely,
Dr John Q Student
Dept Biology
Winona State University
Winona, MN 55987
Am J Physiol Lung Cell Mol Physiol. 2009 Apr;296(4):L666-73. Epub 2009 Jan 30.[pic] [pic]Links
Prolonged NO treatment decreases {alpha}-adrenoreceptor agonist responsiveness in porcine pulmonary artery due to persistent soluble guanylyl cyclase activation.
Perkins WJ, Kost S, Danielson M.
Mayo Clinic College of Medicine, 200 First St. SW, Rochester, MN 55905. perkinsw@mayo.edu).
A cultured porcine pulmonary artery (PA) model was used to examine the effects of prolonged nitric oxide (NO) treatment on the response of this vessel to acutely applied NO and to the alpha-adrenoreceptor agonist phenylephrine. Two-hour treatment with the NO donor (Z)-1-[N-(2-aminoethyl)-N-(2-ammonioethyl)amino]diazen-1-ium-1,2-diolate (DETA-NO) decreased both NO and phenylephrine responsiveness. Twenty-four-hour treatment with DETA-NO resulted in a further reduction in NO responsiveness but no further reduction in phenylephrine responsiveness. Acute addition of soluble guanylyl cyclase (sGC) inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) had no effect on phenylephrine responsiveness in PA not treated with DETA-NO. ODQ treatment fully restored phenylephrine responsiveness in PA treated with DETA-NO. sGCbeta(1) subunit protein levels in PA tissue homogenate were 48.6 +/- 6.9, 51.6 +/- 3.5, and 41.3 +/- 2.8 ng/mg total protein for freshly prepared and 2-h and 24-h NO-treated PA, respectively. Steady-state tissue cGMP was not significantly different in control versus NO-treated PA. sGC specific activity in the absence of added NO was measured in PA homogenate and was 0.29 +/- 0.02, 1.38 +/- 0.12, and 0.53 +/- 0.08 mumol cGMP.min(-1).mg sGC(-1), in freshly prepared and 2-h and 24-h NO treated PA, respectively. Ten-minute Hb treatment completely normalized sGC basal activity in homogenates prepared from DETA-NO-treated PA, which was 0.23 +/- 0.02, 0.18 +/- 0.03, and 0.25 +/- 0.04 mumol cGMP.min(-1).mg sGC(-1), in freshly prepared and 2-h and 24-h NO-treated PA, respectively. The kinetics of the Hb reversal of NO-mediated sGC persistent activation do not support sGC covalent modification as the activation mechanism. We conclude that prolonged NO exposure results in a persistently increased sGC specific activity, which accounts for the observed alpha-adrenoreceptor agonist hyporesponsiveness.
PMID: 19181745 [PubMed - in process]
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