Down with Glam; Up with Fast & Cheap

Apr 03 2013 Published by under Publication, Research issues

A lot of folks are trying to reinvent the way we share research. I cannot remember the last time I read a paper journal; even with traditional publishing models, the dead tree format ends up in the recycling. When I need to know something, I search online via PubMed or Google Scholar. Topics I want to keep up-to-date at all times have shared searches that update me periodically.

Some journals will now be online-only, either with a fairly traditional publishing model or a more liberal acceptance policy (PLoS One, for example). Platforms such as Figshare allow investigators to make raw data publicly available and citable, even if not included in the final paper for a study. Recently, Beyond the PDF 2 took place in Amsterdam where visionaries gathered to once again discuss the printing press of this century. More information can be found about this conference and conversation here.

PeerJAfter scanning this discussion, I began playing around with PeerJ. The model is intriguing; you pay a lifetime fee up front. You can freely pre-publish works (PeerJ PrePrints) and get public feedback . With a mouse-click, you can send your manuscript to peer review which will be based on scientific soundness of the research without attention to impact or "sex-appeal" factor of the work. The goal here is PLoS One without the high publication fees. For $99 you can become a basic lifetime member, able to submit unlimited public "pre-publications" and publish one peer-reviewed article for life. Of course, you will be expected to also review at least one article for life. All authors on the article must have memberships; if you wait until article acceptance to join, fees will be ~30% greater. Right now, content in PeerJ is limited to biomedical science and health issues. PeerJ only publishes research articles. Literature review articles, commentaries, case reports and other works may instead be submitted to PeerJ PrePrints.

My biggest concern took some digging about the web site:

PeerJ will be indexed in all major Abstracting & Indexing databases, including for example PubMed, PubMedCentral, GoogleScholar, and Microsoft Academic Search. We will also be applying for indexed status in services such as MedLine and Web of Science.

This model certainly has the right price; $99 runs less than the page fees for my last journal submission. As a senior professor, this site may be perfect for some of my less impressive results that I just want to get out there. When I was early in my career, PeerJ would have let me get some new data peer-reviewed and published and still make my grant deadline.

What other new-wave publishing services deserve exploration? Any Whizbangers have experience with PeerJ or similar platforms?

Share

3 responses so far

#EB2012: Renal Section Honors

Apr 24 2012 Published by under EB2012 Meeting, [Biology&Environment]

Untitled

Di Feng makes an award-winning presentation

Every year the Renal Section of the American Physiological Society grants awards to undergraduate and post-doctoral trainees for work they submit and present at the meeting. A committee selects 5 finalists based on the abstract submitted, and their presentations are judged during the Posters and Professors Session that was held on Sunday, April 22.

Undergraduate Finalists

  • Justine Abais, Virginia Commonwealth University
  • Di Feng, Medical College of Wisconsin
  • Teresa Kennedy-Lydon, Roya Veterinary College
  • Jacob Richards, University of Floriday
  • Ryan Cornelius, University of Nebraska

The award went to Di Feng for her work :

Genetic regulation and functional relevance of the p67phox gene in salt-sensitive hypertension
Di Feng1, Chun Yang1, Jozef Lazar2, David Mattson1, Paul O'Connor1, Allen W. Cowley, Jr. 1,3. 1Physiology Department, 2Human and Molecular Genetics Center, 3Cardiovascular Center, Medical College of Wisconsin, Milwaukee, WI

Untitled

Feng receives her plaque while Jacob Richards looks on

A narrow region on rat Chr 13 was identified to harbor salt- sensitive genes. p67phox, a cytosolic subunit of NAD(P)H oxidase, is located in this region. We have previously found that on a high salt diet, the renal outer medulla (OM) of Dahl salt-sensitive (SS) rats exhibited higher levels of p67phox expression and NAD(P)H oxidase activity than salt-resistant congenic rats that contain the p67phox allele from the salt-resistant Brown Norway rat. We generated the first p67phox null mutant (p67phox-/-) SS rat in which we observed significantly reduced salt-sensitive hypertension. In our present study, we sequenced a 1650 bp promoter region and found that the SS allele of p67phox had a 204 bp deletion and four SNPs compared to the BN allele. The activity of the SS p67phox promoter was 1.7 fold higher than that of the BN p67phox promoter. We further characterized p67phox-/- rats and showed that they had a 40% reduction in OM H2O2 levels measured from interstitial fluid collected by microdialysis. Respiratory burst responses of peritoneal macrophages to phorbol 12-myristate 13-acetate were abolished in p67phox-/- rats. p67phox-/- rats also showed reduced renal injury, including reduced OM fibrosis, infiltrated T cells and macrophages, and glomerulosclerosis. These data provide new insights into the genetic regulation and functional relevance of p67phox in salt-sensitive hypertension. (HL-82798; HL-29587)

Postdoctoral finalists included:

  •  Krishna Boini, Virginia Commonwealth University
  • Richard Grimm, University of Mryland
  • Elena Mironova, University of Texas-San Antonio
  • Ann Riquier-Brison, University of Southern California
  • Ankita Roy, University of Pittsburgh
Untitled

Dr. Grimm gives me a guided tour of his work

Richard Grimm took home the award for this submission:

SPAK, OSR1 and Cab39/MO25 form an Interdependent Signaling system which Regulates Thiazide-Sensitive Salt- transport, Distal Tubule Mass and Blood Pressure
P Richard Grimm1, Tarvinder Taneja1, Jie Liu1, Richard Coleman1, Yang-Yi Chen1, Eric Delpire2, James B Wade1, Paul A Welling1. 1Physiology, University of Maryland School of Medicine, Baltimore, MD, 2Anesthesiology, Vanderbilt School of Medicine, Nashville, TN

STE20/SPS-1-related proline-alanine-rich protein kinase (SPAK) and, Oxidative Stress Related Kinase (OSR1), co-localize at the apical membrane of the Thick ascending Limb (TAL) and Distal Convoluted Tubule (DCT) and both regulate the potassium- dependent sodium-chloride co-transporter, NKCC2, thiazide- sensitive sodium-chloride cotransporter, NCC in vitro. Yet genetic ablation of SPAK in mice causes a salt-wasting nephropathy that is restricted to the DCT, reminiscent of Gitelman’s syndrome. Here, we explore why proper DCT function is especially SPAK- dependent. In the TAL of SPAK-/- mice, OSR1 and Cab39/MO25, a newly described OSR1/SPAK regulatory protein, remain at the apical membrane where they function with a compensatory increase in the AMP-activated kinase (AMPK) to hyper- phosphorylate NKCC2. By contrast, the OSR1/SPAK/M025 signal transduction apparatus is completely disrupted in the DCT. OSR1 and MO25 become largely displaced from the thiazide-sensitive sodium-chloride cotransporter, NCC, and the apical membrane. OSR1 redistributes to dense punctate structures within the cytoplasm. These changes are paralleled by a dramatic decrease in NCC abundance and phosphorylation. Without SPAK and the proper localization of OSR1 and MO25, phosphorylation- dependent regulation of NCC by dietary sodium restriction is lost. SPAK-/- mice also exhibit a decrease in the mass of the distal convoluted tubule, exclusive to DCT1. As a result of the interdependent nature of OSR1 and MO25 on SPAK in the DCT, SPAK-/- mice are highly sensitive to dietary salt-restriction, displaying prolonged negative sodium balance and hypotension.

Untitled

Dr. Grimm wins

 

Share

No responses yet

#EB2012: A Pendrin for Your Thoughts

Apr 23 2012 Published by under EB2012 Meeting, [Biology&Environment]

Pendrin, also known as SLC26A4, is a luminal anion transporter. Anions, molecules with a negative charge, include chloride, bicarbonate, iodide, and others. The family of similar transporters (see figure) have some functional overlap, although knock-out studies confirm some individual transport specificities.

A child that lacks pendrin has Pendred Syndrome. This usually occurs as a monogenic recessive disorder (both parents have a mutation in the pendrin gene) although a few families have a digenic inheritance where the mutation occurs in a gene that controls the creation or function of pendrin. The major manifestation of the syndrome is progressive hearing loss; this syndrome may produce as much as 10% of congenital familial deafness. The syndrome also causes enlargement of portions of the inner ear and an enlarged thyroid gland (or goiter). The function of the thyroid remains normal, but it accumulates material and grows.

After Richard J. H. Smith reviewed the features and genetics of the syndrome, Philene Wangemann showed the role of pendrin in ear development in mice.

Click to enlarge

Using conditional knock-outs of the gene, her group has established a critical 2-day period in gestation where lack of pendrin results in deafness. The mice also develop enlargement of the cochlea, just like humans. For her review on pendrin in ear development click here (PDF is free!).

So why does the thyroid enlarge in this syndrome? For those of you who are not endocrinologists (I may not be one, but I do sleep with one), thyroid hormone contains iodine.That's why a low iodine diet so profoundly affects growth and development (AKA cretinism). Since this family of transporters helps move iodine about, the thyroid can enlarge, even though its ability to make and release the hormone is intact. This topic was addressed by Peter Kopp.

Finally (saving the best for last?) Vladimir Pech reviewed the role of pendrin in blood pressure regulation. Pendrin resides in the type B intercalated cells of the cortical collecting duct where it exchanges chloride and bicarbonate between the lumen and the cell. Pendrin knock-out mice have normal blood pressures; however, during states where aldosterone would be activated (low sodium and low volume), pendrin mice are unable to conserve sodium as avidly as those with the transporter.

Huh? Most aldosterone-dependent sodium reabsorption occurs via the ENaC channel in the principal cell. How does a lack of pendrin tell another cell to behave differently? It does so by decreasing the activation of ENaC which requires a cleavage step to work. Perhaps this occurs via altered luminal pH or bicarbonate concentration, or some other signal that impairs the milieu for sodium channel activation. More to come; click here for a nice review (unfortunately not available freely online).

Ear and kidney abnormalities often occur together in children. Pendrin may provide one link to explain some of these issues.

Share

No responses yet

#EB2012 #Navar: Reflections on the Work of a Lifetime

Apr 23 2012 Published by under EB2012 Meeting, [Biology&Environment]

Untitled

Dr. Navar and his entourage, pre-lecture

The final official event of Saturday actually provided the official opening of the meeting for the American Physiological Society (APS). Current president Joey Granger walked us through 125 years of the APS, including the founding of the umbrella organization FASEB (Federation of American Societies for Experimental Biology) 100 years ago. He then introduced the speaker, Gabby Navar, who presented his lifetime of work in renal physiology and the role of the kidney in hypertension (click here for more background).

Science takes place in baby-steps. Even a paper in a glamour journal with years of data, like a toddler's first efforts, is just as likely to lead to falling back on a full diaper as a movement forward. Take enough of these steps, and you can eventually get somewhere. You may always risk a trip and a fall, but with time you move forward.

Dr. Navar's contributions to science brought to mind two major observations. First, hypertension is not a disease. A disease has a cause and an effect. While the effect may be a single physiological measurement such as blood pressure, its causes clearly involve multiple genes and environmental factors. We should think of it as a syndrome.

Syndrome generally means a cluster of symptoms; the origins of the word signify concurrence. For example, a microangiopathic hemolytic anemia with kidney damage leads to a diagnosis of hemolytic uremic syndrome. This syndrome may be the result of several known diseases as well as some not yet characterized. I propose that hypertension, while not a cluster of abnormalities, is a syndrome in  a similar sense. Multiple diseases, defined and not, can cause high blood pressure as their sole manifestation.

The other point I considered overnight was how essential animal research has been in our advances in hypertension. We simply would not be able to tease out the complex relationships between neural, renal, and other mechanisms in blood pressure control without the use of animals.

Congratulations to Gabby Navar for a great talk and a good start to a great meeting.

Share

No responses yet

#EB2012 #apsACE: My First Storify

Apr 22 2012 Published by under EB2012 Meeting, [Biology&Environment]

I attended an excellent session on the need to increase transparency and public outreach in animal experimentation. I tweeted throughout the session, and I have assembled the highlights using Storify. I had hoped to include original observations from others in the room, but most of the other tweets were retweets of me (or the others tweeting forgot to use the hashtag).

I am reminded of the following facts:

  • People are programmed to want the world to make sense
  • Nature abhors a vacuum
  • If there is no story to make sense of something, people will supply their own
  • If you want the truth to be known, you should supply the story

Until scientists supply the stories to justify their research on both scientific and ethical grounds, people will remain suspicious of our intentions. We must reach out to the public and let them see and feel and hear our stories; not hide in a vivarium-bunker.

 

Share

No responses yet

Meeting & Greeting

Apr 09 2012 Published by under [Education&Careers]

An interesting post at Science News addresses the costs of conferences. All sorts of issues arise, including shrinking travel budgets, environmental costs of all that air travel, preliminary work that becomes "permanent", and even the number of trees used to generate program books. Having been in the biomedical science biz for 20+ years now, I have survived several waves of "let's quit meeting and just do this online." Conferences will never go away for one reason: we like them.

Bumping into new contacts in the Exhibit Hall

Oh, I hear people complaining about taking time away from their work and family. We all gripe about time spent in airports. Yet we all keep submitting and accepting and going because nothing replaces face-to-face interactions for us human beings.

There is value in meeting potential colleagues and reviewers. Some of the best ideas and collaborations get built around informal conversations when you toss a group of people with something in common together. Big keynote addresses could just as easily be done via the net, but those do not keep me on the road. No, it's the chance to meet new people who will help me think about things in a new way. I always consider a meeting successful if I get one new idea to explore.

Last month my department had a panel discussion about working a meeting, directed at our trainees and junior faculty. Those of us on the panel all agreed that networking (there's that word again) was why we paid for attendance. You never know who may be important in reviewing your work or getting you hired sometime down the line. Even if you really only connect with other trainees, you will learn more stuff about what other programs are like (you may be in nirvana and not know it). You may meet someone who will be hiring when you are ready for a second job. You may meet someone who will be reviewing you on their first study-section assignment. You will learn something from everyone you meet. Think of it as being mentored by a hive of "E-Bees".

There are some tips we gave our n00bs to make their networking easier. First, get a professional non-university email. You do not want all your job offers and conversations going through your university accounts. You also do not want to use an address that is too personal; "lovesbeer@yahoo.com" or "partygirl@gmail.com" will not impress potential colleagues. If it does, you probably do not want that job. Figure out some permutation of your name and/or science and get that gmail account set up now. As someone who recently changed jobs, it was wonderful to have a "permanent" email to use as my university account went dead.

Next we suggested business cards. Even in the age of the electronic frontier, the humble piece of dead tree remains the most accepted method of exchanging contact information. You're a trainee and they don't make cards for you? Do it yourself! Anyone with a computer and printer can buy a pack at the office store and have reasonable cards in less than an hour. Yes, some people will exchange cards and then throw yours out in the airport. Some new acquaintances will put you in their contacts. That's the way it works. You will do the same.

Finally, consider starting an online presence. If you aren't up to a full-fledged website, at least start on LinkedIn (this link takes you to my public profile as an example). The networking site for professionals essentially puts your resume into your profile. Upload a nice photo of your face, and you're in business. Eventually, you will make connections on the site. Some of us even get the odd job offer via LinkedIn (wrong place, wrong time, but otherwise something I would have jumped at). It will not yet replace emailing your CV, but it does give you an online presence that should not provide any embarrassing personal details. Eventually you will find useful information here via interest groups and discussions.

Finally, remember that the real meeting takes place away from the microphone. Casual discussions in hallways and restaurants and bars are more important than plenary sessions (unless you are on the platform, and even then...).

Share

2 responses so far

Countdown to EB: 14 Days

Apr 06 2012 Published by under [Education&Careers]

Two weeks from today I board a plane and fly to San Diego for Experimental Biology. As one of the official bloggers for the American Physiological Society I find myself doing more prep work than any other year. The Online Itinerary Builder is now live, allowing attendees to search the program by track, presenter, society, keywords...or any combination of the above.

I have identified a few sessions, and some suggestions have been made by you, my loyal readers.

I will not be "live" blogging. I attempted that a couple of times, and I just do not have that skill set. Watch my twitter feed in the right column (or follow me on twitter; you really should, you know) for real-time updates on what I am attending. Some sessions will get full coverage a bit later; others may not.

Some sessions will be covered with twitter feeds via Storify. This web-based service will let me collect tweets, facebook updates, photos, videos, and other thoughts on various sessions to tell a more completes version. The first session I will use for this technique is on Saturday, April 21, at 3 pm in Room 25C of the San Diego Convention Center. The APS Communications Committee has convened a discussion about the use of social media to communicate about physiology. James Hicks will chair the symposium, while the panel is staffed by Dr. Isis, Jason Goldman, Danielle Lee, and yours truly. Since I am on the platform participating, I will look to the audience for thoughts and impressions.

So how can I track down your thoughts and impressions? Hashtags. On twitter, thoughts can be mapped to topics via #keyword. We can use those same hashtag/keywords on other platforms to mark relevant content. Here are the ones I will be following for Saturday events:

  • #apsACE          Animal Research: A Toolkit for Investigators (Sat, Apr 21, 1pm, 25B)
  • #apsComm    Using Social Media to Communicate About Physiology and You (Sat, Apr 21, 3pm, 25C)
  • #Navar              Physiology in Perspective: The Walter B. Cannon Memorial Award Lecture (Sat, Apr 21, 5:45pm, Ballroom 20A)
  • #apsParty       APS Beach Party (Sat, Apr 21, 7pm, North Embarcadero)

Since I cannot be everywhere at once, some sessions will not get my blog treatment. If anyone wants to see a session immortalized online, just let me know what hashtag you and your colleagues are using; I will be glad to assemble coverage here!

For photos and video, you can also add your stuff to a Flickr group (http://www.flickr.com/groups/eb2012/).

Don't be shy; consider this your scientific outreach!

Share

No responses yet

Poison by Any Other Name

Apr 05 2012 Published by under [Medicine&Pharma]

Evil chemicals! Click for source

What image springs to mind when you see the word...

nicotine?

If you smoke, you may have a warm, fuzzy feeling, but for a lot of us, poison comes to mind. Nicotine makes tobacco products addictive, so it cannot be good. See the diagram at right; it's used as an insecticide! It kills bugs! It must be bad!

Of course, nicotine is merely a chemical. But chemicals are bad, right? Even a natural one that comes from a plant (like tobacco)? Even one with a short, pronounceable name?

So nicotine is bad...except when it isn't.

Renoprotective effects of long-term oral nicotine in a rat model of spontaneous proteinuria.
Agarwal et al. Am J Physiol Renal Physiol 302:F895, 2012
DOI:  10.1152/ajprenal.00507.2011

Nicotine has demonstrated beneficial effects in a number of inflammatory disorders, including inflammatory bowel disease, sepsis, and hypersensitivity pneumonitis. In animal models of ischemia-reperfusion kidney injury results are more variable, depending on the model and route of nicotine administration. It seems that macrophages (immune white blood cells) and capillaries in the kidney have alpha-7 nicotinic acetylcholine receptors which modulate these anti-inflammatory effects.

This study used a rat model of spontaneous proteinuria, Munich-Wistar-Fromter rats. As these rats age, they develop proteinuria. As protein is reabsorbed by the peritubular capillaries in the kidney, filtered agents such as cytokines and growth factors can promote inflammation and further kidney damage. At the time proteinuria begins in this model (24 weeks, a middle-aged rat), animals were begun on one of three doses of nicotine in drinking water along with an untreated control group. Saccharine in the water in all groups masked the taste of nicotine (yes, the control rats were drinking diet soda, circa 1970). Every 4 weeks they measured blood pressure, glomerular filtration rate, and proteinuria. They examined kidney structure in a number of ways after 28 weeks of study, when the rats reached one year of age.

Kidney function (upper panel) & proteinuria (lower panel)

The control rats showed the typical course for the MWF model, with glomerular filtration rates less than half of baseline after 28 weeks of study (see figure at left). This effect on clearance of waste products was blunted by nicotine ingestion. Protein excretion increased in all groups of rats, but, once again, nicotine treatment reduced the level of protein spill.

Nicotine treatment also reduced scarring in the glomeruli, the filtering units of the kidneys. Macrophages, those pesky blood cells that promote inflammation and scarring, were also reduced by nicotine treatment. Production of scar materials by the kidney was also reduced with the nicotine treatment.

So proteinuric patients should smoke? Or at least wear those patches?

Not exactly.

Smoking is a major risk factor for the development and progression of all sorts of kidney diseases. We ABSOLUTELY DO NOT WANT ANYONE SMOKING EVER FOR ANY REASON!

Like most molecules, nicotine has many faces. In this case, we examined its perky, anti-inflammatory side. Nicotine also has other effects that may not be desirable. Short-term ingestion raises blood pressure and heart rate via stimulation of the adrenergic system; these effects were not detected with long-term ingestion in this rat model. Nicotine also affects a number of systems that modulate blood flow (and can therefore affect function) of the kidney. Changes in these systems were not assessed in the present study.

Also, prior studies show that what happens in rats does not necessarily happen in mice when it comes to nicotine. Why? We really do not know. Do these species metabolize nicotine differently? Or is there some other reason for these differences? When it comes to nicotine, are people more like rats or mice or neither?

Nicotine has another danger: addiction. Can we come up with a modified nicotine (with a longer, scarier, more chemically name) that would provide anti-inflammatory effects without producing undesirable vascular or behavioral effects? Anything is possible, but this molecule is still in the future.

The bottom line: nicotine from a natural, plant-based source like tobacco can be a killer. Pure nicotine from the lab may be a healer. Only time and more experiments will tell.

Share

2 responses so far

Waltzing Matilda Needs to Run!

Apr 03 2012 Published by under Women in Science

I posted over at another of my sites about an interesting paper I read on the Matilda Effect in STEM awards.

Not this Matilda

Who is Matilda? She's related to Matthew of biblical fame. Lines from this gospel essentially state that the rich get richer and the poor get poorer. In STEM disciplines, this means that more successful senior people get more grants, awards, and accolades, even if younger, less-known investigators propose similar ideas. Matilda refers to the tendency of people to recognize the work of men (like Watson and Crick) but marginalize the contributions of women (like Rosalind Franklin).

So click on over and read about this study of awards to men and women in a variety of STEM fields from 1991-2010. People still blame the lack of women in the pipeline, but this work suggests that hypothesis is wrong!

 

Share

No responses yet

42 Days and Counting

Mar 09 2012 Published by under Societies and Meetings, [Biology&Environment]

In just over a month thousands of life scientists will gather in San Diego for Experimental Biology, the meeting formerly known as FASEB. In addition to being the annual gathering of the American Physiological Society, this year also celebrates the 125th anniversary of the APS.

Yes, I am proud to be a physiologist!

Of course, I am also honored to be one of the APS's official meeting bloggers! I have access to the press room (I don't suppose that includes a hot tub and wet bar?). This status means I am looking at the meeting in a whole new light. Instead of focusing on my own interests (and using the down-time to relax at the Marriott's poolside bar), I want to communicate things that my audience will appreciate as well.

What things will I definitely cover?

  • APS Communications Committee Symposium: Using Social Media to Communicate About Physiology and You (I'm on the panel, so I have to be there)
  • Physiology in Perspective: The Walter B. Cannon Memorial Award Lecture (Gabriel Navar, a renal physiologist, is the speaker at this opening event)
  • Renal Section Awards Banquet (Another I-have-to-be-there)

I will also likely attend and blog some of the teaching of physiology sessions. As I transition from physician-scientist to physician-educator-administrator (with physiology research as more of a hobby), these sessions have become important for me.

What would you, my loyal readers, like to hear about? I cannot guarantee that I will cover it, but you never know...

Use the links to the meeting sites above to explore the program and exhibits and activities. Provide suggestions in the comments, and I will see how it all fits together.

If you have a student presenting, let me know. I may want to blog their science!

 

Share

One response so far

Older posts »