A few thoughts on reviewers´ conflict of interest

Over the past decade, it has become customary for most peer-review journals (including APS journals) to ask potential reviewers to declare potential conflict of interests. Circumstances that may be perceived as conflict of interest typically include e.g. a close personal or professional relationship between the reviewer and any of the authors, or mutual involvement in a contentious dispute on the topic of the manuscript. However, on a much broader scale, we all (as reviewers and editors) have conflicts of interest, which relate to an ever more precious and scarcer resource: time. When reviewing manuscripts, we extract time from our busy schedules for a task that – by its anonymous nature – constitutes primarily a quiet service to our community by which we pay back what we ourselves receive when our own manuscripts are reviewed by expert reviewers providing – hopefully – meaningful and constructive advice and guidance. Such good citizenship typically yields little-to-no immediate merit for the reviewers themselves. Some reviewers, however, tend to strive for some indirect revenue, by suggesting to authors to reference specific papers which – of course by pure coincidence - happen to be their own. In some instances, this will be entirely justified, as the authors may have missed to take an important piece of literature into consideration which just happens to be authored by the reviewer. In other instances, however, such recommendations will be less motivated by our surge for scientific accuracy but rather by our vanity. Such hijacking of what is essentially a pro bono service for self-promotion constitutes a significant and unacceptable conflict of interest. No-one should be coerced to cite "paper xyz“, unless it serves the purpose to improve the scientific valor and accuracy of a manuscript. Authors submitting manuscripts to AJP-Lung should know that the editorial board and our reviewers work hard to ensure constructive and unbiased reviews of all manuscripts in a fair and timely manner that are based on scientific merit alone. In 2014, the average time to first decision for submitted manuscripts was 22.3 days.

Wolfgang Kuebler, Associate Editor

AJP-Lung will offer CME credit in 2016

The American Physiological Society (APS) is pleased to announce that beginning January 2016 it will offer a manuscript review Continuing Medical Education (CME) activity to the reviewers of the American Journal of Physiology – Lung Cellular and Molecular Physiology (AJP‐Lung) as a benefit of reviewing for the journal. The APS is pleased to be working in collaboration with Washington University School of Medicine, which is administering this CME activity. Washington University School of Medicine is a CME provider accredited by the Accreditation Council for Continuing Medical Education (ACCME) and designates the AMA PRA Category 1 CreditsTM within the American Medical Association Physician Recognition Award (AMA PRA) system.

A participating reviewer may be awarded 3 AMA PRA Category 1 CreditTM per review; a reviewer may claim up to 15 AMA PRA Category 1 CreditTM per year.

Our Associate Editors will be responsible for assigning a score to each review. This score will serve as the measure of acceptability of the review for CME credit. The scoring parameters to receive CME credit are a maximum 14‐day turnaround with a score of "Good" or higher.

Reviewers who indicate an interest in earning CME for their review will receive written notification about whether they earned CME credit based on the quality of the review. This notification will serve as documentation of their earned CME credit. Please note that 1) the CME credit will only be given for first reviews of manuscripts; reviewers will not receive additional credit for revised versions 2) there will be no cost to the reviewer for receiving CME credit as the program is supported by the APS and 3) credit will be awarded annually.

APS Select December 2015

AJP-Lung would also like to recognize one of our papers who was honored with the APSselect selection for December 2015. "DNA damage response at telomeres contributes to lung aging and chronic obstructive pulmonary disease" was written by Jodie Birch and her colleagues. Please click on the link below to access this important article.

http://ajplung.physiology.org/content/309/10/L1124

AJP-Lung submissions on the rise

I am delighted to tell you that AJP-Lung continues to attract high quality manuscripts.  As can be seen from the table below, submission of research manuscripts are 28% higher than last year.  Thank you for sending your best work to AJP-Lung and please continue to do so.

            Sadis Matalon
            Editor  in Chief

	# Research Manuscripts recv thru Oct. 2015	# Research Manuscripts recv thru Oct. 2014	YTD Change No.	YTD Change %
AJP-Cell	275	305	-30	-10%
AJP-Endo	451	490	-39	-8%
AJP-GI&L	340	373	-33	-9%
AJP-Heart	703	695	8	1%
AJP-Regu	413	399	14	4%
AJP-Renal	375	448	-73	-16%
AJP-Lung	350	274	76	28%
Total AJP	2,907	2,984	-77	-3%
Advances	132	121	11	9%
JAPPL	794	872	-78	-9%
JN	905	725	180	25%
PG	95	97	-2	-2%
Physiology	0	0	N/A	N/A
PRV	0	0	N/A	0%
Total	4,833	4,799	34	1%

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Happy Thanksgiving!

AJP Lung has a lot to be thankful for this year.  Our number of submissions and impact factor are up, and time to first decision is down.  We are also thankful for our dedicated editorial board and reviewers, whose hard work and outstanding review efforts have made AJP Lung a top journal to publish basic and translational original articles in the broad field of lung biology.  

We wish all of our reviewers, authors and readers a wonderful holiday!

   

DNA damage response at telomeres contributes to lung aging and chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is a progressive disease characterized by destruction of lung tissue and airflow limitation, with smoking a key risk factor for development of the disease. COPD-induced declines in lung function have been associated with accelerated lung aging and cellular senescence. While it has been accepted that cell senescence generally is associated with shortening of telomeres, recent data has raised questions as to the validity of using telomere length as a biomarker of aging and/or telomere dysfunction. In the recent issue of AJP Lung, Jodie Birch and colleagues at Newcastle University investigated the role of telomere dysfunction in the aging mouse lung and its potential role in cigarette smoke-induced COPD. In lung sections from COPD patients, the authors found that small airways epithelial cells contained more markers of senescence, including increased telomere-associated DNA damage foci (TAF) and reduced SIRT1 expression. Moreover, young mice exposed to cigarette smoke exhibited levels of TAF similar to that observed in the lungs of aged mice, and experiments performed in vitro confirmed that cigarette smoke extract increased TAF in small airways epithelial cells. Interestingly, telomere length was not significantly altered in these studies. While it is possible that small sample size masked an effect on telomere length, taken together, these results suggest that TAF are induced as a consequence of cigarette smoke exposure and may be a more robust signal of lung structural and functional decline in aging and with COPD.

To find out more about this interesting study, please check out the full text of this article. It is available for free on the AJP-Lung website, even for those with no subscription to APS journals:

http://ajplung.physiology.org/content/309/10/L1124

Larrisa Shimoda- Associate Editor

Heterogeneity of pulmonary endothelial cyclic nucleotide response to Pseudomonas aeruginosa ExoY infection

It is well established that cyclic nucleotides function as canonical second messengers. In the lung, these nucleotides exert regulatory influences on a host of cell processes, including endothelial cell barrier permeability. Previous reports demonstrated that Pseudomonas aeruginosa injects host cells with an effector protein, ExoY, the enzymatic activity of which increases cytosolic cAMP, leading to microtubule destabilization and endothelial barrier disruption. Kyle Adam Morrow and colleagues at the University of South Alabama have now published a study showing that inoculation with ExoY caused differential generation of cyclic nucleotides in macro- and microvascular lung endothelial cells (ECs). They found that ExoY increased both purine and pyrimidine cyclic nucleotides, with cGMP exhibiting the largest change. The increase in cyclic nucleotides temporally correlated with endothelial cell monolayer barrier disruption. Intriguingly, the ExoY-induced cyclic nucleotide signature differed in macrovascular and microvascular ECs; in macrovascular ECs ExoY induced a faster and more robust increase in cyclic nucleotides, including cAMP (which was not increased in microvascular ECs), resulting in earlier and more profound barrier disruption. Based on the fact that microvascular ECs are more likely to encounter this bacterium but are apparently more resistant, it is tempting to speculate that pulmonary microvascular ECs have developed host-protective mechanisms to help mitigate the effects of Pseudomonas aeruginosa.

To find out more about this interesting study, please check out the full text of this article. It is available for free on the AJP-Lung website, even for those with no subscription to APS journals:

http://ajplung.physiology.org/content/309/10/L1199

-Larissa Shimoda, Associate Editor

The Hermann Rahn Award for Excellence in Pulmonary Research

Dr. Sadis Matalon, Editor-in-Chief of the American Journal of Physiology-Lung Cellular and Molecular Physiology, is soliciting nominations for the 2015 Hermann Rahn Awards, in honor of the 36th APS President (1963-1964), a leader in the field of respiration physiology. The nominees must be either first or senior author in a paper published in the American Journal of Physiology-Lung Cellular and Molecular Physiology since 2012 and must have been  a trainee (graduate student or post-doctoral fellow), or junior faculty (Instructor or Assistant Professor) when the paper was submitted.  Criteria for selection include the importance of the work to the field, the contribution of the nominee to this project and his trajectory as a research scientist. Please submit nominations by December 1, 2015, to Dr. Sadis Matalon, (sadis@uab.edu) with a copy to Ms. McEver (amcever@emory.edu).  The three winners will receive $250 each and a certificate of appreciation at the EB 2016 meeting.

Peer Review

Many years ago, I created a fake Yahoo email address in order to play a practical joke on a colleague.  While it was all in good fun then, many journals are now finding the prank is on them.  Authors, and in some cases editors, found a way to circumvent the traditional peer-review system by supplying fake email addresses for recommended reviewers, allowing them to review the paper themselves. Not surprisingly, these “reviewers” returned glowing evaluations in record time.  A spate of retractions highlights the problem of fake “reviewers” that has plagued the scientific peer-review system: http://retractionwatch.com/2015/08/19/17-retractions-from-sage-journals-bring-total-fake-peer-review-count-to-250/

The disturbing issue of review falsification was further emphasized in a recent commentary published in the New England Journal of Medicine (http://www.nejm.org/doi/full/10.1056/NEJMp1512330 ). 

Fraudulent peer-review, whether perpetrated by authors, editors or journals, undermines the hard work of the scientific community and tarnishes the reputation of the entire biomedical research enterprise in the eyes of the public.  The Editors at AJP-Lung are committed to providing peer review of the highest quality.  When selecting reviewers for manuscripts, we utilize a series of safeguards to ensure the validity of the process. Editors assign reviewers from: 1) their own wide network of colleagues within the field; 2) the Editorial Board, members of which undergo rigorous vetting by the Editors and journal staff prior to appointment; and 3) the large APS reviewer database, which provides verified contact information as well as links to each reviewer’s publications.  In cases where authors recommend reviewers that are not already known to the editor, the recommended reviewer is carefully scrutinized before being added to the potential reviewer list, typically involving verification of institution and email address and a Pubmed search to guarantee appropriate expertise and prevent conflict of interest.

Fair peer review requires trust on the part of all involved parties.  At AJP-Lung, we promise to remain vigilant in securing the most qualified reviewers for your manuscripts. 

-Larissa Shimoda, Associate Editor

-Wolfgang Kuebler, Associate Editor

Call for Applications- Usha Awards

The Usha (which means dawn in Sankrit) Awards

Dr. Prakash YS, Deputy Editor of the American Journal of Physiology-Lung Cellular and Molecular Physiology, is soliciting nominations for the Usha awards. The nominee must be a promising trainee (undergraduate or graduate student, or a research fellow (5 years since being granted the terminal degree (e.g. PhD, MD, DO, DVM), and should have contributed a 1st author abstract to the Respiration Section of the APS for presentation at the APS. Criteria for selection will include the level of excitement regarding the nominee's future, contribution by the nominee to the work, and the importance of the work to the field. Nominees are to be selected by the Respiration Section of the APS. All applications must be submitted by December 1, 2015. The TWO winners will receive $500 and a certificate of appreciation at the EB 2016 meeting.

To apply online, follow this link:  http://www.the-aps.org/mm/awards/sections/Resp.aspx

A Change is Coming

We want to make sure our authors are aware that the APS has approved a restructuring of Journal Publication Costs. What does this mean for our authors? Well, effective January 1, 2016, changes to the APS research journals’ author fees include:

• Submission fees will be eliminated.
• Page charges for AuthorChoice (program allowing articles to be freely available on publication) will be eliminated. Fees for participating in the program remain.
• Color fees for non-members will be reduced from $400 to $200 per figure.
• Increase of page charges from $75 to $85 per page.

The Editors hope that the elimination of submission fees and reductions in color fees will encourage authors to submit their best work to AJP-Lung!

Reminder- Best Research Paper by a Junior Investigator Nominations

Reminder: Call for Nominations

Best Research Paper published in AJP-Lung by a Junior Investigator (sponsored by the American Physiological Society)

The American Journal of Physiology-Lung Cellular and Molecular Physiology invites nominations for the “Best original research paper published in AJP-Lung between 2012-2014 by a junior author (Assistant Professor, Instructor, Post-doctoral fellow or graduate student.)  The nominee must be either first or senior author and in the opinion of the nominator, contributed significantly in the inception and conduct of this project.  Please submit a nomination stating the importance of this paper in the field as well as the contributions of the first author to Dr. Sadis Matalon, Editor AJP-Lung  (sadis@uab.edu) with a copy to Ms. McEver (amcever@emory.edu) by December 1, 2015.  All applications will be reviewed by the Editor and Associate Editors who will chose the winner by secret ballot.  The winner will receive $500 and a certificate of appreciation at the EB 2016 meeting.

APSselect November 2015

AJP-Lung would also like to recognize another APSselect selection for November 2015. " The H2S-generating enzymes cystathionine β-synthase and cystathionine γ-lyase play a role in vascular development during normal lung alveolarization" was written by Alicia Madurga and her colleagues. Please click on the link below to access this important article.

http://ajplung.physiology.org/content/309/7/L710

APSselect November 2015

 










AJP-Lung would like to recognize Dr. Laura Fredenburgh, Dr. Bryan Kraft and their colleagues on the selection of their article “Effects of inhaled CO administration on acute lung injury in baboons with pneumococcal pneumonia” for APSselect in November.

This terrific article can be accessed here: http://ajplung.physiology.or/content/309/8/L834

Respiration Section Fall Newsletter

The role that neutrophils play in regulating inflammatory cell influx and immunopathology

Pseudomonas aeruginosa is an important Gram-negative pathogen for both hospital-acquired infections and patients with lung diseases like Cystic Fibrosis.  One thing to note about P. aeruginosa is that this bacterial infection often causes a significant influx of neutrophils.  Certainly these innate immune cells play an important role in helping to ingest and kill the pathogen, but it is also appreciated that neutrophils can promote tissue damage, and may contribute to the pathogenesis of some autoimmune diseases.  Exactly how neutrophils promote the “immunopathology” that can occur following some infections is not clear.  A new article in AJP Lung this month provides compelling new evidence for the importance of neutrophils in producing the cytokine, interleukin (IL)-1β and the mechanism for how they are activated.  IL-1β production is critical for initiating inflammatory cell recruitment and activation, but prolonged IL-1β production can lead to immunopathology.  What is most intriguing about this paper is the observation that the molecular signaling mechanisms that lead to IL-1β production in macrophages vs. neutrophils are completely different despite the fact that these are both innate immune cell types responsible for initial engagement with bacterial pathogens.  Macrophages generally secrete IL-1β following activation of the inflammasome containing NLRC4, ASC and caspase-1.   Given this, one would have predicted that mice deficient in ASC, one of the NLRC4 inflammasome components, would be prevented from IL-1β secretion in response to P. aeruginosa infection. However, Patankar et al. in this issue (American Journal of Physiology - Lung Cellular and Molecular Physiology, 2015; 309:L902) demonstrated that ASC-deficient mice still produce abundant IL-1β in response to infection.  Interestingly, these authors demonstrate that neutrophils are able to produce IL-1β independently of ASC, but still dependent on caspase 1.  These interesting results shed new light on the role that neutrophils play in regulating inflammatory cell influx and immunopathology, but as all good science does, these results also raise new questions.  Exactly how caspase 1 regulates IL-1β cleavage and activation in the absence of the cannonical NLRC4-ASC-containing inflammasome will be the subject of future investigations.

Associate Editor AJP-Lung, Beth Moore