Wednesday, December 17, 2014

The Ebola Epidemic: Does it ever end?

The Ebola outbreak has been in the forefront of the news this year. Please take a moment to read our editorial, “Ebola: History, treatmentand lessons from a new emerging pathogen.”
on this very deadly disease by Dr. Kevin S. Harrod, a prominent member of our Editorial Board with significant expertise in virology.  Within this article you will see two highlighted tables on the etiology, transmission and clinical outcome of Ebola infection.  Ebola is another example of a zoonotic disease (like AIDS) but its natural reservoir has not been identified. 

During the last two years we have published at least 14 articles on viral infections {Pubmed search using the following terms: am j physiol lung cell mol physiol. AND viral infections AND (2014 OR 2013)}.  Please submit your research manuscripts on viral infections to AJP-Lung.  They will be reviewed promptly and fairly and the reviews will improve the quality of your paper.

With best wishes for the holidays

Sadis Matalon, PhD, Sc.D. (Hon.)
Editor in Chief, AJP-Lung

Amy McEver,
Administrative Assistant, AJP-Lung

Friday, December 12, 2014

Chlorine Gas Exposure in the News

December 7th, 2014
Chicago Tribune

A recent article published in the Chicago Tribune described an incident in which the entire Rosemont Hyatt Regency Hotel in Chicago was evacuated due to the intentional release of chlorine gas. The evacuation of the hotel resulted in the hospitalization of 19 people. Fortunately, there were no deaths associated with this incident probably due to the lower doses of the toxic gas involved. Immediate symptoms due to chlorine inhalation can range from a burning sensation in the nose, coughing, chest tightness and shortness of breath. Upon inhalation of higher doses of chlorine gas, the long term consequences of lung injury can lead to lung edema, respiratory distress and even death. A recent study published in the ‘American Journal of Physiol Lung Cell Mol Physiol’ demonstrated that chlorine inhalation caused sloughing of bronchial epithelium one day after chlorine exposure, which can cause pneumonitis and bronchial hyper-reactivity (1). Surprisingly, health screenings for individuals located within one mile of a 54 metric ton release of liquid chlorine following a 16 tanker car train derailment on 6 January, 2005 in Graniteville, South Carolina, USA demonstrated that even 8-10 months after the event, patients still had abnormal lung function and some even developed new pulmonary symptoms (2).

 However, there are no immediate counter-measures available to date to mitigate chlorine toxicity. Current treatment regimes consist of providing supportive medical care in a hospital setting. For effective treatment, first responders and hospitals need compounds that are easily administered for the purpose of halting the cascade of events that lead to future respiratory complications. Recent work being conducted at the University of Alabama at Birmingham in the labs of Drs. Sadis Matalon and Rakesh Patel have shown that the administration of aerosolized heparin can reduce lung injury, and an intramuscular injection of nitrite can reduce mortality after chlorine exposure (3,4). The research was supported by the Counter Act Network, and therefore many will potentially benefit from the work being done at UAB and other institutions under the Counter Act umbrella. 

Author: Dr. Saurabh Aggarwal MD., Ph.D. Instructor, Department of Anesthesiology, UAB, Birmingham, Al

Saturday, November 22, 2014

Looking forward with AJP-Lung

It is hard to believe but I have completed my first term as Editor in Chief of AJP Lung.  It has been a wonderful and highly rewarding experience.  Please see the editorial published on line in the November issue on the “state-of-the art” of the American Journal of Physiology-Lung Cellular and Molecular Physiology.  Our impact factor is above four and we are the leading respiratory journal publishing basic and translational science articles based on the H-factor.  More important, we have received a lot of positive comments from authors who are very pleased with the feedback from reviewers and Associate Editors and feel that their papers always become better after review.  There will be some new faces among the Associate and Consulting editors, as well as among the Editorial Board members.   I promise our contributors and readers that the best is yet to come. 

Sadis Matalon, Editor in Chief for three more years.

Monday, November 17, 2014

Does exposure of a developing, immature mouse lung to high levels of oxygen impact antiviral immunity?

From our esteemed  associate editor Dr. Rory Morty:

I would like to draw your attention to an interesting paper published last week in AJP-Lung “Articles in Press”. In their study titled “Neonatal hyperoxia leads topersistent alterations in NK cell responses to influenza A virus infection” (DOI: 10.1152/ajplung.00233.2014, published on 7th November 2014), Reilly et al. address the question of whether exposure  of a developing, immature mouse lung to high levels of oxygen would impact antiviral immunity in later life. There is currently much interest in the long-terms of exposure to hyperoxia, since exposure of immature, developing lungs to high levels of oxygen is a life-saving intervention in pre-term infants that have a limited gas-exchange capacity. Whether or not exposure of developing, immature lungs to high oxygen concentrations has an impact on lung function that extends into later life, and thus, may predispose prematurely born infants to respiratory disease and complications in later life, is currently a matter of much interest and investigation. The study by Reilly et al. makes some interesting inroads into this little-explored area of lung developmental biology. Focusing on natural killer (NK) cell dynamics and function, Reilly et al. report that in adult mice that had been exposed to 100% oxygen for 96 hours immediately after birth and then returned to room air, that number of gamma-interferon-positive and granzyme B-positive NK cells were elevated seven days after influenza virus exposure. Additionally, as early as day five post-influenza virus infection, fewer NK cells produced interleukin (IL)-22 in mice that had been exposed to an hyperoxic environment as neonates. Thus, early life exposure to a high-oxygen environment resulted in a persistent “skewing” of the NK cell population from a regulatory to a classical cytotoxic NK cell population. The authors went on to demonstrate, using bone-marrow transplantation studies, that neonatal oxygen supplementation influences both the inherent properties of hematopoietic cells as well dynamically developing extra-hematopoietic environments, in this case, the lung. These studies highlight the need to better understand how early-life oxygen exposure may disrupt both the pulmonary and extra-pulmonary systems, which have important functional consequences for lung health in later life. The entire Editorial team looks forward to receiving more manuscripts that experimentally address the question of how perturbed late lung development per se, as well as the strategies that we employ to correct this important pediatric intensive care problem, may predispose prematurely-born infants to respiratory and other diseases in later life.

Wednesday, October 22, 2014

Nominations are now being accepted for these prestigous awards...

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 2s012-2014 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  (<>) with a copy to Ms. McEver (<>) by February 1st, 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 2015 meeting.

The Hermann Rahn Award for Excellence in Pulmonary Research (sponsored by Dr. Sadis Matalon)

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 February 1st, 2015, to Dr. Sadis Matalon, ( with a copy to Ms. McEver (<>).  The three winners will receive $250 each and a certificate of appreciation at the EB 2015 meeting.

 The Usha (which means dawn in Sankrit) Awards (sponsored by D. Prakash YS)
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 February 1st, 2015. The TWO winners will receive $500 and a certificate of appreciation at the EB 2015 meeting.

Monday, October 20, 2014

TG2 in Pulmonary Hypertension

Penumatsa KC, Toksoz D, Warburton RR, Hilmer AJ, Liu T, Khosla C, Comhair SA, Fanburg BL.Am J Physiol Lung Cell Mol Physiol. 2014 Oct 1;307(7):L576-85. doi: 10.1152/ajplung.00162.2014. Epub 2014 Aug 15.

Penumatsa KC, Fanburg BL.Am J Physiol Lung Cell Mol Physiol. 2014 Feb 15;306(4):L309-15. doi: 10.1152/ajplung.00321.2013. Epub 2013 Dec 27. Review.

Hello everyone,

I wanted to bring your attention to two recent papers in AJP Lung by Barry Fanburg’s group at Tufts University on tissue transglutaminase (TG2) in pulmonary hypertension (Penumatsa KC et al. AJPL Oct 1 2014 and Penumatsa and Fanburg BL AJPL Feb 14 2014). These very interesting papers highlight the role of TG2 in mediating and modulating the effects of hypoxia in the pulmonary vasculature in the context of PH. TG2 is a calcium-dependent enzyme that is expressed ubiquitously in multiple cell types including smooth muscle cells. TG2 is famous (or is it infamous?) for its role in celiac disease, but given its presence in other cell types, and its calcium dependency, there is much interest in its role in other diseases. TG2 is quite appealing in terms of both pathophysiology and a targetable mechanism given availability of blockers of this enzyme. (My personal interest in TG2 further lies in the fact that my uncle worked with Laszlo Lorand at Northwestern who was instrumental in our understanding of transglutaminases such as TG2 and factor XIII of the coagulation cascade). 

The Fanburg group has previously found that TG2 is increased by hypoxia while conversely blocking  TG2 prevents pulmonary hypertension in mouse models. The relevance to humans lies in increased serotonylated fibronectin (that results from increased TG2 activity) in patients with PH. In the Oct 1 paper, these authors explored the role of TG2 in mediating/modulating hypoxia effects on pulmonary artery smooth muscle cell proliferation (an aspect of vascular remodeling in PH that is in need of targeted therapies). Hypoxia was found to increase TG2 expression: an effect blocked by inhibition of HIF1a transcription factor. Separately, inhibition of the plasma membrane calcium sensing receptor blocked TG2 activity. The relevance of this latter mechanism lies in emerging evidence that the CaSR (also well known in other organ systems, particularly the parathyroid) is involved in vascular smooth muscle calcium regulation and cell proliferation. Furthermore, activators and inhibitors of CaSR are available (calcimimetics and calcilytics) and are probably being tested in the pulmonary artery. These types of studies (albeit in vitro) point to the complexity of interactions between calcium sensing/responsive pathways and proliferative/remodeling mechanisms in the pulmonary artery that likely contribute to the overall difficulty of alleviating structural and functional vascular changes in pulmonary hypertension. On the other hand, they are also exciting in terms of helping us understand how such interactions may play a role in other diseases that also involve both structural and functional changes at the level of smooth muscle (e.g. asthma). 

Y.S. Prakash