In search of a dream job: hurdling and vaulting towards a successful postdoc

Side note: I just had to have a track and field reference in the title. It’s been the one extracurricular that has kept me hungry in the world of science.

Five years ago, I had the choice to live and work in one of three places. 1. Dallas, TX where I would have worked in a a so called “postdoc factory;” 2. New York, NY where I would have done a blend of clinical and experimental work, and would’ve had to take out loans in the process since the typical salary for postdocs doesn’t adjust for cost of living; and 3. Atlanta, GA where I had the opportunity to fine tune the three-legged stool of research in a specialized sleep and circadian rhythms program and teaching at a historically black (HBCU), all-male college and medical school. I chose Atlanta.

Honestly, I hated being a postdoc relative to being a PHD student. It’s not that I hated my postdoc; my mentors were unbelievably awesome. I just missed graduate school much more. I did have a certain level of flexibility and autonomy with my National Research Service Award (NRSA). Still, I often felt like a glorified lab technician whom I have mad love and respect for and less like an early career researcher. It’s my own fault though and therefore, I learned many life lessons along the way.

I’m not saying I’m the wisest person, but I am pretty wise and fairly observant. I have been successful at “playing the game” or “climbing up the ivory tower” so to speak. My mentors taught me the ways. So, while your postdoc may be different than mine, I think each of these life lessons learned from my postdoc are critical and imperative to thrive and adapt to the fast-paced, uber competitive enterprise that is academic science.

1. Money is time, time is money.
Money talks. I advise my undergraduates to seek a lab with money over a lab that perfectly fits their research interests. Sure, you want some overlap, but you can’t do science if you don’t have money. During the first year of my postdoc, we were broke. My NRSA didn’t get funded because of this. A year later, I resubmitted my NRSA changing very little of the research strategy except for the fact that my boss had an R01. Needless to say, life was good (and still is) with the R01.
So what if you run into a situation when the lab goes broke? Well, you can still work hard, but you have to work smartly. Focus on the other legs of the stool: teaching, and service. For me, I wrote all my lectures for the neural systems course that I taught for all five years as a postdoc, served on the Board of Directors of the Sleep Research Society, and wrote a popular science book entitled, Meathead: Unraveling the Athletic Brain. You can buy it on Amazon. These activities are what got me my interviews for tenure-track faculty positions at great schools.
2. Have your program officer on speed dial.
I was advised to be in constant contact with my program officers at the NIH early on in graduate school. I’m glad that I listened. I’m a decent grant writer. However, sometimes my specific aims can be too lofty, not terribly hypothesis-driven, and don’t align with fundable research opportunities. This is where constant email and phone communication with your program officer becomes imperative. It’s a win-win. They know what is getting funded and what’s not. They know the literature more than you because they are the ones funding it, for the most part. Plus, if your grant is on the bubble that one phone call with your program officer may be the difference between a job and no job. I’m pretty sure that I got my postdoctoral NRSA because of how often I reach out to my program officer. I still run ideas for future projects by him even with the funded grant.
3. Go to conferences.
This is where you learn science. It’s active learning. Plus, you meet the people who will become your biggest allies, adversaries, and employers for the rest of your life. I never skipped the major conferences of my field and I’m thankful that I didn’t. I have my dream job because of it. A week off from the bench to be social has life-long benefits. And why not just work double-time when you return?
4. Do service work.
Much like the benefit of going to conferences, service work is the easiest and most effective way to meet and become colleagues with leaders in your field. Plus, it’s the easiest and most effective way to ensure that your research agenda and interest has a voice, even if it’s just a small one.
5. Don’t plan your lifestyle around your career, plan your career around your lifestyle.
It’s a life hacking motto, trust me.
It also helps to study research problems that are of interest to your life, for whatever reason.

And now for the bad.
1. Sexism is pervasive.
Like many med schools, there are more mustaches than females in our department. For the record, I don’t tout myself as a feminist. My teammates call me their “browife.” I’m that kind of gal. I’m also kind of a narcissist and look good naked; these are relevant to this story. My point is that if I’m being told by colleagues that “I shouldn’t wear white pants because they aren’t slimming enough,” and that I should “host a luncheon with the other (few) females in the department to discuss issues of confidence,” then I can’t imagine how females who may not be as self-assertive and absorbed as me feel when these types of remarks are made.
So how do you combat this? You don’t perpetuate any preconceived stereotypes. You don’t overreact, you don’t get defensive, and you answer matter-of-factly. It’s difficult, trust me. But, these actions help to prevent from being told “your problem is that you are highly aggressive and overly emotional.”
2. Racism is real, for all races.           I work at a historically black college. Before that, I did my undergraduate and graduate work at two of the most liberally progressive and diverse schools in the US. I’ve always been open-minded about race. I grew up in a city that is mostly black and many of my cousins are biracial. However, I have never felt so discriminated or profiled in my entire life as I have working for an HBCU. It took one of my closest friends in Atlanta (a black male) for me to recognize this fact, but once I became aware, I listened and observed a bit more. I’ve heard talk of me being the “privileged white girl with an Ivy League education,” when I’m sorry, I’m one of the most selfless, courteous, and appreciative staff members there. Just ask the administrative assistants. They are awesome peeps by the way who do amazing behind the scenes grunt work that we as scientists should be very grateful for. Anyway, it’s interesting and always will be that it took being at an HBCU for me to recognize that racism is a real problem and affects everyone of every color.

Aside from the sexism and racism that I’ve experienced, I have loved every minute of my postdoc. Sure I wouldn’t do it over again (much like I wouldn’t get my PHD again). I didn’t just have a successful postdoc because of me and my doings though. There are many folks who made it possible for me to grow as a scientist, a colleague, a person, and someday, the ability to mentor young people in science, so thank y’all. You know who you are.

Neuroblogging, sightseeing, and exhibit halling at SfN

First off, I am honored to be selected as an official blogger of the annual Society for Neuroscience meeting for the 7th year. My blog was evolved immensely since 2009. Although, most of my posts are housed on Fitness Cult Chronicles to promote my popular science book, Meathead: Unraveling the Athletic Brain. As for SfN, posts related to Theme E (neuroendocrine and homeostatic systems) can be found here. I’ll also have shorter commentary and musings via Twitter and Instagram @beastlyvaulter. I promise not to upset the @sfnpolice.

Get it now on Amazon and Barnes and Noble Book cover

As far as sightseeing, I am excited about the many ethnic foods of Chicago (i.e. pierogis) and to see beautiful lakefront. I will be getting a bag of Garrett’s as soon as I land in O’Hare. And a thick Midwestern steak at some point. As far as the meeting goes, it is in your best interest to take advantage of as many nightlife socials as possible. It’s not for the free booze but rather networking. You never know who you will meet and what commonalities you’ll have in science for collaboration and beyond. Also, this social is gonna be #onfleek. It’s a sell out crowd every year. Plus, it is the perfect opportunity to meet the faces of social media behind the meeting.

Be ready.

As for the non-empirical portions of SfN (i.e., navigating the exhibit hall), I have a bit of advice.

  1. Do not go at lunch time. Do not go at lunch time. Early morning is best if you are looking to speak to someone about troubleshooting and new products not lunch time.
  2. Get your free stuff with your promo cards early. Stuff runs out by Monday!
  3. The exhibit hall is a great place to spend time if you are on the job hunt or junior faculty. You want to go into an interview knowing how much startup $$ you need with actual numbers on hand. Nearly all sales reps will give you printouts (or emailed) quotes on the spot. It will save you at least a week’s worth of work.

Safe travels, y’all!!

Neury Thursday: Modeling disrupted sleep in Angelman Syndrome

It has been a minute since I have done a Neury Thursday post where I highlight an article from the most current issue of Journal of Neuroscience. Well this week I am pleased to say that there is very familiar research, names, labs, and institutions in one of the featured articles. We started this project 2.5 years ago and have generated handfuls of interesting data from it. As you may recall, there are two biological processes that govern daily amounts and timing of sleep. There is a classic homeostatic process known as Process S which basically “encourages” us to sleep more if we get a night of insufficient sleep. There is also Process C which is governed by the ticking and speed of our internal biological clock located in the hypothalamus. In the present study, we aimed to study both of these processes in an animal model of Angelman Syndrome. Angelman Syndrome is a genetically-determined neurological disorder. It is characterized by severe motor and mental impairments, seizures, and sleep distrubances.

ResearchBlogging.orgAs an attempt to model Angelman Syndrome in mice, we used transgenic mice lacking expression of the maternal Ube3a gene in the brain. The paternal Ube3a gene is typically silenced. In the first set of experiments, we characterized daily activity and molecular rhythms in the central biological clock–the suprachiasmatic nucleus–of the hypothalamus.


No disruption in circadian timekeeping in mice lacking Ube3a   No disruption to the molecular biological clock in mice lacking Ube3a

Interestingly, there was no disruption to general circadian timekeeping (Process C) at the level of behavior and the brain. Mice lacking maternal Ube3a were equally as active as mice expressing Ube3a and responded and adapted to an intermittent light pulse presented early or late in the night at similar rates compared to mice expressing Ube3a. Despite this, if you look closer at the activity plots in (A) you’ll notice that the distribution of daily activity looks different. Well, it is different.

Additional analyses revealed that mice lacking maternal Ube3a do not nap during the mid-dark period like most normal mouse strains. They keep running on their wheels right through it!

Mice lacking Ube3a do not have a siesta

From here, we examined the impact of Ube3a on daily amounts of sleep and responsiveness and adaptation to short-term sleep loss. Like many of our studies, we deprive mice of sleep for the first six hours of the light-phase when the propensity to sleep is at its highest. In looking at daily amounts of sleep and wakefulness under undisturbed, baseline conditions, EEG  indeed confirmed that mice lacking maternal Ube3a are active through the siesta.

EEG confirms that mice lacking Ube3a sleep through the siesta

This reorganization of sleep and wake carried over into how the mice responded to short-term sleep deprivation. Not only did the mice lacking maternal Ube3a not recover as much sleep after sleep deprivation as mice expressing Ube3a, but their EEGs were less saturated with slow wave activity which is an electrophysiological correlate of sleepiness. In all, we can conclude that the brains of mice lacking Ube3a are wired differently favoring states of arousal and wakefulness. This likely explains the sleep disturbances common in individuals suffering from Angelman Syndrome.

Ehlen, J., Jones, K., Pinckney, L., Gray, C., Burette, S., Weinberg, R., Evans, J., Brager, A., Zylka, M., Paul, K., Philpot, B., & DeBruyne, J. (2015). Maternal Ube3a Loss Disrupts Sleep Homeostasis But Leaves Circadian Rhythmicity Largely Intact Journal of Neuroscience, 35 (40), 13587-13598 DOI: 10.1523/JNEUROSCI.2194-15.2015

In case you wonder about the hiatus.

I try to post once a month. Well, I have been. Except it isn’t here but rather part of my new blogging endeavors with Fitness Cult Chronicles. They obviously have much more readership than me and rightfully so. If you feel like you have been missing out on some posts, below are a few posts that I have written for them. The first is geared toward getting psyched up for competition. The second has become one of my most popular posts: the benefits of sleeping naked. But don’t fret. Dormivigilia is not retiring. I’ll be blogging about my experiences at Paleo FX in Austin, Texas this weekend.

Enjoy spring, y’all! And don’t forget to purchase Meathead on Amazon or Barnes and Noble!


Check out Fitness Cult Chronicles

Embrace your inner meathead



A Continuation in the Search for the Function of Sleep: Commentary from On Your Mind Podcast

This morning, I had the pleasure on being a guest host for one of the more entertaining, informative neuroscience podcasts of today’s smart technology society: On Your Mind. We talked about the job market, my new book–Meathead: Unraveling the Athletic Brain, and wrapped up with discussion of some peer-reviewed literature.

ResearchBlogging.orgIt turned out that I gave the show hosts–Kathryn Vaillancourt and Liam Crapper–the wrong but related paper out of the same collaboration. I meant to give them this one which focused on sleep deprivation, while the one that I sent was actually more focused on disease: insomnia. It worked out beautifully  though because there was much overlap in the results, presentation of data, and technique as this is where my initial confusion actually arose.

The group of researchers used a very sophisticated form of magnetic resonance imaging that we have yet to fully comprehend. The three of us–Kathryn, Liam, and myself–decided that this technology known as “31-Phosphorus Magnetic Resonance Spectroscopy Study at 4 Tesla” is basically a hybrid of MRI and PET imaging coupled with analysis similar to mass spectrometry to quantify amounts of phosphorus-containing compounds. I think Figure 1 of both papers nicely helps the reader visualize the technique.

4 Tesla technology



The researchers were interested in specific cellular energy metabolites that have long been forgotten about or fully considered in the field of sleep–ATP, ADP, phosphocreatine–as well as constituents of the cell membrane like phosphocholine. In the insomnia paper, these cellular constituents were examined in a group of individuals with clinically diagnosed insomnia. In the sleep deprivation paper, changes in these cellular constituents were quantified before and after a brief bout of sleep deprivation as well as across a two day recovery period from sleep deprivation. The researchers also dissected differences in these cellular constituents between the grey and white matter of the brain which are very different in architectural makeup: the former containing the nerve cells with the latter containing glia.

In both papers, there was a decrease in phosphocreatine which is required to keep up with energy demands in individuals diagnosed with insomnia or after a night of sleep deprivation. This was specific to the grey matter.

PCr changes in the grey matter


This is basically the most important and consistent finding of the two papers. In discussing the presentation of data, we all agreed that the data could have been presented better to separate out tissue-specific differences as well as interactions. The biggest hiccup is this general fitting curve to show the direction of change for both tissues regardless if one had a significant effect (grey matter) or not (white matter). This is a bit disingenuous. We also agreed that the title would have been perfectly fine up until the placement of the colon and mention of the technique. Sure, the technology adds to the attention grabbiness of the paper but is it really necessary? Anyways, I don’t want to take away from the impact of these two studies by focusing on minute details. It is awesome that we now have human data to support the animal work from 2010 in regards to how cellular energy metabolites change across a protocol of sleep deprivation or spontaneous sleep and wake. Truly there is more than just one function of sleep. Even more reason as to why we should take advantage of a good night’s sleep.

Harper, D., Plante, D., Jensen, J., Ravichandran, C., Buxton, O., Benson, K., O’Connor, S., Renshaw, P., & Winkelman, J. (2013). Energetic and Cell Membrane Metabolic Products in Patients with Primary Insomnia: A 31-Phosphorus Magnetic Resonance Spectroscopy Study at 4 Tesla SLEEP DOI: 10.5665/sleep.2530

Plante, D., Trksak, G., Jensen, J., Penetar, D., Ravichandran, C., Riedner, B., Tartarini, W., Dorsey, C., Renshaw, P., Lukas, S., & Harper, D. (2014). Gray Matter-Specific Changes in Brain Bioenergetics after Acute Sleep Deprivation: A 31P Magnetic Resonance Spectroscopy Study at 4 Tesla SLEEP DOI: 10.5665/sleep.4242



Meathead, now available!

I have been working on this book for over three years. It combines athletic anecdotes with scientific discoveries in a very under appreciated field of exercise physiology. Whether you are looking for  motivation to continue working out or want to bring your athletic training to the next level, this book can help you accomplish both. One of my pet peeves as a scientist is when scientists resist in making complex information understandable to the general public. This is our civic duty yet many scientists fail at doing this. I hope that this book has inspired the lives of many; whether it means it got you off the couch or to train smarter. Also, the foreword is really touching and written by a very talented and strong woman of sport and life. The book is available in all e-book platforms as well as a soft and hardcover edition. However, I receive more royalties if you order it directly from the publisher:


Humans in the Wild.

This recent publication comes out of the lab of my graduate mentor. Adam, DG, and a group of undergrads sorted through the power grid of the Northwest Pacific which is easily and freely available online. After importing this data into Clocklab which is used in circadian research to track and collate daily rhythms of ResearchBlogging.orgbehavior (wheel running) and physiology (core body temperature), I present to you an activity record of humans in their natural habitat (in January).

You may be surprised to know (or not) that the length of the night becomes progressively shorter as the summer approaches and longer as winter approaches. I doubt this means that humans are going to bed earlier and waking up later– therefore getting more sleep–but perhaps this is true : )

At any rate, this is a really simplistic and cool way to think about human behavior and how lifestyle and climate shapes our environment. I wonder how different this power grid would be for Europe? Or Africa? You should know that this power grid data does not differentiate between city and rural areas.

humans in the wild, changes in light use

Stowie, A., Amacarelli, M., Crosier, C., Mymko, R., & Glass, J. (2014). Circadian analysis of large human populations: Inferences from the power grid Chronobiology International, 1-7 DOI: 10.3109/07420528.2014.965316


6 years of Dormivigilia and how to get that Science paper

It’s hard to believe that Dormivigilia is going six years strong. Sure, I don’t post as often as I did in graduate school, but hopefully my readers haven’t given up total hope. From being selected as the official neuroblogger of the neuroendocrine and homeostatic section at the annual Society for Neuroscience meeting five times in a row to having more than 10,000 viewed posts in the past year alone, I am honored. So thank y’all!

What I want to discuss now is advice for those struggling postdocs feeling the pressure to get that Science, Nature, or Cell paper. I’m with you. Since being on the job market, I thought that I was competitive with my sustained NIH funding and 10+ original research publications in respectable journals–broad and/or field-specific–but nope! Funding is tight and job search committees want you to have that “R”-equivalent grant coupled with an “S” “N” or “C” paper. Well, I’d like to think that the project that I have been working on since starting my postdoc and one that was already five years in the works is close to being an “SNC” paper. But to be totally sure, I contacted a colleague of mine in chronobiology who recently got a beautifully designed study published in Science without using any gee whiz techniques that most scientists seem to think is a priori for funding and high-impact publication nowadays. You’re wrong. Here is a paraphrased email exchange between myself and the last author. Basically, you have to be committed to getting an SNC paper on many levels. It’s not just about the science, but the writing and making it clearly understandable to a skeptic/curmudgeon (ie, reviewer) outside of your field.

“I spent a long time thinking about what I wanted to say, and then wrote the first draft in an hour.  The paper then went through about 10 full revisions with my collaborator.  We nitpicked over every word, period, comma, etc.  Long talks on the phone going over it together.  Sleepless nights, etc.  I sent it in, without any supplementary materials, and was shocked when they actually sent it out for review.  The important point there is that your cover letter really matters.  They rejected the paper.  One reviewer loved it, the other hated it.  The hater was rather angry that we didn’t have any electrophysiology or molecular biology.  Predictable.  Healso listed several things that he felt we should have done.  Those things were already in the paper, however.  I emailed the editor, pointed out the fact that he was not being responsible, and she said, too bad, go elsewhere.  I protested again, and she took the issue to her colleagues.  They offered to send it out for arbitration, which I didn’t know even existed outside of labor unions.  I was then invited to rewrite it and resubmit, i.e., start all over.  So, I incorporated the helpful comments and resubmitted.”

“Three single-spaced pages of comments came back from the arbitrator, and a single paragraph from a new reviewer, who thought it was fine as is.  The arbitrator clearly had no background in rhythms or learning and memory.  I spent 6 weeks 24/7 doing nothing but generating all of the data in the supplementary materials, writing it up, and calling ex-students to see if they could locate information that we usually don’t keep track of.  My cover letter in the reply was 15 single spaced pages with 25 references going back to the 1970’s.  I had to explain the history of SCN lesions, detailed discussions of statistics, and so on.  That letter and the supp materials went through at least 8 revisions each.  It was accepted 4 days after submission, at the end of a 5 month process.”
So yes the bottom line is that if you want to dream big, you have to be willing to put in the work and time.

A decade’s worth of data on alcohol and circadian rhythms

Many of you may recall that I spent five years in graduate school investigating how alcohol acts on the circadian timing system- behaviorally and physiologically. This was the basis of my dissertation and a research direction that has been pursued by my graduate school mentors for almost a decade. As Drs. Dave Glass and Rebecca Prosser can attest to, it was not an easy journey. Both of them had no formal training in the alcohol field which as we have discovered can be cliquish, placing a HUGE emphasis on pedigree. Hey, I get it. The sleep field is no different and I’m very much part of that pedigree trajectory. However, they both overcame this barrier by proposing and doing fantastic, mechanistic science that has resulted in over 10 original research articles on how long-term and binge-like consumption of alcohol affects circadian timekeeping on many levels.

ResearchBlogging.orgTheir research has combined in vivo (live animal) and in vitro (isolated tissue) experiments that have produced overlapping results, strengthening the body of evidence that alcohol severely disrupts circadian timekeeping. And so, let’s go over this decade of findings.

1. One-time and high (binge-like) doses  of alcohol block the ability of behavioral rhythms to adjust/adapt to unanticipated light. The mechanism involves glutamate. 

This hypothesis was first investigated in hamsters which have very robust rhythms of wheel running and are highly responsive and adaptive to unexpected presentations of light. From here, the same experiments were conducted in mice since this is the “preferred” model of biomedical research given the ability to manipulate its genome. Regardless of the species of study, alcohol inhibited the ability of hamsters and mice to either advance (for hamsters) or delay (for mice) their rhythms to light. These experiments were undertaken by my lab mates and me.

Alcohol dose-dependently prevents animals from adapting to unanticipated light

Dr. Prosser’s lab found that the reason alcohol blocks this adaptation to light is because alcohol blocks glutamate signaling which has been known for over 20 years to affect this adaptation to light.

2. Long-term consumption of alcohol destabilizes daily rhythms of activity. 

These experiments were the most intriguing to me because our hamsters and mice could tolerate drinking a 20% (for hamsters) or 15% (for mice) concentrated alcohol solution and ONLY this alcohol solution for months on end. The deleterious effects of alcohol on daily activity rhythms were striking and present early on. It doesn’t take an expert in circadian rhythms to notice differences in the intensity of daily activity levels between these activity records of mice drinking water (bottom) or drinking alcohol (top) for months on end.

Long-term alcohol intake (top) results in sporadic activity

3. Exercise is an effective substitute for alcohol

Our hamsters inspired us to undertake this experiment because they love to run, running anywhere from 3-5 miles every day, and they love to drink alcohol, drinking 50x as much as the average human male every day. So what we did was to give these “booze-soaked fur balls” access to alcohol in the presence of a locked or unlocked running wheel. When the wheel was unlocked, they ran more and drank less. When the wheel was locked, they drank more. They were also extremely cantankerous during this time, making it very difficult to clean their cages.

Hamsters who run more, drink less

4. Genetic disruption to circadian rhythms (via Per2) increases binge-like, compulsive drinking. 

This work was the most time-consuming for me for several reasons. First, it involved the study of drinking in over 300 mice across 3 years and many, many rounds of microdialysis collection which is one of the more physiologically revealing techniques in neuroscience, but yet very cumbersome because of the low success rate. However, largely thanks to the fact that Kent State University does not charge per diem for animal care, I was able to breed many animals at once to complete this experiment in a timely manner. While this may have taken 3 years at Kent, per diem at most universities could have pushed this project to take 6 years to complete. At any rate, we found that the reason that mice lacking Per2 (in protein form) drink more is because they are awake for two, additional hours during the night and are heavily drinking during this time. This is reflected in the left-side panels of these activity (top) and drinking (bottom) records in comparison to wild-type mice (right-side panels).

Per2 mutant mice are awake more and therefore drink more

5. Acamprosate (market name: Campral) acts in reward-processing and (surprisingly) circadian areas of the brain to reduce alcohol intake

Acamprosate has been on the market for years and yet little attention has been paid to how it acts in the brain. So we used a relatively simple yet under-appreciated and undervalued approach to see where acamprosate acts in the brain. The simplicity resided in mixing up the acamprosate in wax and then popping these tiny wax pellets into the edges of brain areas regulating rewarding behavior and circadian timekeeping. This was complex because these brain areas are relatively small and so our coordinates had to be very precise. Actually, it was through missed targets that we discovered that some brain areas like the hippocampus are not responsive to acamprosate. This figure took over 60 hours to make (seriously) and does a nice job of detailing where in the brain and how effectively acamprosate acts.

Brain areas where acamprosate acts


And that’s a wrap. This research direction is far from complete but golly, we sure made an impact on the alcohol field in just ten short years.

Prosser RA, & Glass JD (2014). Assessing ethanol’s actions in the suprachiasmatic circadian clock using in vivo and in vitro approaches. Alcohol (Fayetteville, N.Y.) PMID: 25457753

Best of 2014: #pandanation #allbridgers #rabs #SfN #cashmoneyscience

I can’t believe that I am approaching my 7th year of neuroblogging. This year was so so. There were some good parts in the middle but it started and ended on crappier moments. However, I’m looking forward to some promising moments in 2015, including the publishing of Meathead: Unraveling the Athletic Brain–a book that I have been working on for a few years–as well as competing in the 2015 Reebok Crossfit Games with #pandanation.

January: I went to an awesome workshop on visual presentation of scientific data taught by Edward Tufte. The bottom line is less is more.

I also presented an article in journal club about the athletic consequences of game day travel across time zones. The bottom line is that if you have Vegas stakes on the line and a West Coast team is playing an East Coast team in Sunday, Monday, or Thursday night football at home, bet on the West Coast team even if it is the San Diego Chargers. Trust me.

February: The “road to the fittest on earth” (i.e., Crossfit season) began once again. Our very own #pandanation at Crossfit Terminus made an appearance in the commercial. And I got to begin participating in an exercise physiology study at Kennesaw State University that focused on cardiorespiratory fitness in elite Crossfitters.

I also blogged about the very disturbing research field of plant neurobiology. It is true that plants experience adapt and respond to stressors, but to say they have an intact nervous system is a bit too much.

Finally, the world record in men’s pole vault set by Sergei Bubka of the Ukraine was broken by Renaud Lavillenie of France in Bubka’s home country of Ukraine. Unbelievable.

March: March was cool. I attended the first Gordon Research Conference on Sleep Regulation in Galveston, TX and met some cool dudes and peeps who will be lifelong friends and colleagues. I also worked my ass off to qualify as an individual in the Reebok Crossfit Regionals after a very disappointing opener workout. With Montegraphia’s vast, statistical knowledge, I was able to figure out what I needed to place in each week’s workouts to be in the top 48. And I did it! I crawled back from 292nd to 43rd in the Southeast (FL, GA, SC, AL) region with the final two workouts clutching this spot.

April: April was a month of grueling training in preparation for the Southeast Crossfit Regionals. In the blogging world, this infographic went viral in regards to the pathetic, academic job market for newly minted PhDs in science. I also presented this article in our quarterly journal club with the cardiovascular institute that finally did an impressive empirical investigation on risks for cardiovascular events around Daylight Savings.

May: The first half of the month was spent preparing for the Reebok Crossfit Regionals while the second half was spent recovering from the “shoulder annihilation” of Regionals. Check out 3:07:00 onward in this video:

But the greatest part of the weekend was seeing my long-time training partner qualify for the 2014 Reebok Crossfit Games after years of hard work and patience. Also, my most popular post of the year was in response to this egotistical, conceited fitness brat.

June: I spent most of the month on the road traveling to professional society meetings. The first half of the month was spent in Minneapolis attending SLEEP. From there, I went to Big Sky, Montana for SRBR which was absolutely stunning in scenery and science. We saw moose trek into our yard every day, snow-capped mountains, and lots of Glass lab shenanigans, mostly involving “Turn Down for What.”

After Montana, I traveled to Berkeley to give a talk and to spend a week in Napa with the in-laws. It started out beautifully and ended poorly when I got my most sentimental shit stolen, including my wedding ring, Crossfit Games gear and general Crossfit gear as well as my most sentimental possession which was my four-year varsity jacket from Brown track and field.

July: This was the month of the World Cup as well as Em’s debut in the Crossfit Games. To address the former, I re-blogged about a research article that first appeared in the Journal of Neuroscience. I also went to a phenomenal grant writing workshop on writing R grants. But I’m not about to publicly reveal those secrets ; ) Lastly, I went home to Ohio for the funeral of my younger cousin who tragically died from a motorcycle accident. It had been a very stressful two years for our family.

August: Blood made a comeback in neuroscience research. From genomic screens of blood to how donating blood taken from one mouse affects the brain of another, it looks like we are back to where we started hundreds of years ago.

September: This month I attended one of the most enlightening conferences in research ever. It was basically a science camp for grant writing, research ethics, and new technologies at the edge of the San Bernardino mountain range in Lake Arrowhead, California. I also competed in a grueling three-day Crossfit competition in Pensacola, FL.

October: Blood control of brain function continued to make an appearance in peer-reviewed journals. I also griped about gender inequality in academia in regards to respect for women scientists, not representation of women scientists. This post was my second most popular post aside from the Erin Simmons one. Also, my young adult fictional book that I wrote ten years ago was re-released in a second edition and became an e-book! Buy it NOW for $1.99.


November: This month was busy prepping for upcoming job interviews as well as for the annual neuroscience meeting which was held in DC this year. For the sixth year in a row I was selected as a neuroblogger. I also traveled to Southern Mexico at the end of the month but came back with Montezuma’s revenge a few days before some on-campus interviews.

December:  I spent a good portion of the month interviewing (unsuccessfully) for jobs but gained some important insight for future job prospects (hopefully).

Happy New Year and blogging in 2015!


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