Marathon Diaries: Season Finale

By Elaine To


After hours of toil, pain, and sweat, I am proud to say that this Sunday I finished my first full marathon. I’ll celebrate later; let’s first talk about how you can achieve the same.

So you’ve done it. For months, you ran during your incubation periods and woken up at unimaginably early hours on the weekends just for your long run. It’s now race day and time for you to cross the finish line. When months of training coalesce into that single glorious moment, you don’t want anything to stop you from achieving your goal. How can you ensure that you run the best race ever? It’s not much of a surprise, but the pre-race preparation doesn’t just begin the day before! Here are some tips for preparing:

Days before:

1) Hydrate well in the week leading up to the race. It’s not just something to do a couple days before! Make sure you’re getting 8 glasses of water a day.

2) Your training should have tapered in the 2-3 weeks prior to the race. Any runs should still provide you an adequate workout, but be comfortable. Now is not the time to push your limits!

3) Get a good night’s sleep on the two nights prior. You’re likely to be nervous and unable to sleep well the night before, so build up a buffer with the previous night.

4) On the day immediately before, pick up your race packet and make sure you have 4 safety pins for the bib. Double check your running gear, because if you’re missing anything, the expo that accompanies the packet pick up is the place to buy it.

5) The day before the race is also the time to carbo-load. You want your glycogen stores to be as full as possible, so eat a lot of pizza and pasta. Avoid anything you don’t regularly eat or that has a chance of causing stomach problems.

6) Pin your bib onto your shirt and pack your gear check bag the night before. This isn’t something you want to worry about on the morning of. Good things to put into the gear check bag are warm clothes and granola bars.

7) EAT BREAKFAST. It should be mainly carbohydrate based.

During the race:

1) You can come to the start line wearing extra clothes so that you stay warm until you start. Most races donate clothes that are left behind to charity. If you don’t have anything you’re willing to toss, buy something from a thrift store.

2) Don’t be stressed or nervous! You should be running at a pace that allows you to talk to those around you so don’t be afraid to chat it up with your fellow runners. This will prevent you from trying to run too fast, especially in the beginning. Near the end, your fellow runners are also a great source of encouragement.

3) Do not drink at every water stop unless drinking water every 1.5 miles was normal during your training. If you overhydrate you may deplete your electrolytes, and even if you’re drinking the sports drink, you may get too full. Have faith in your training and follow that. To alleviate the fear of needing water but being far away from the next water stop, I would suggest carrying a bottle that you can refill at each stop. Also make sure you eat during the race, whether its energy gels or provided snacks. Again, be careful to follow what was normal for your training—do not overeat.

4) Make it a goal to high five or thank every single volunteer that you see. They are donating their time so you can run and they are behind you all the way! The morale boost you will get is absolutely crucial for the second half. On this note, you can try to wear something that makes you stand out so you can tell when cheers are directed towards you. Some wear flamboyant clothing such as tutus or hats, many have sentiments on their shirts. In the past my shirts have said “Hopkins,” and supporters have used that. The Virginia Beach bibs actually had our names printed in bold font; it’s an amazing experience to hear “Go Elaine! You’re rocking it!” from complete strangers.

5) If this is your first full marathon, it’s almost guaranteed you will be in pain during the second half. Don’t be afraid to walk and take stretch breaks. Finishing a couple minutes later is better than injuring yourself. On hilly courses, the uphill is particularly painful but reprieve comes during the downhill stretches. Flat courses use the same muscles constantly, so in some ways they are more difficult. I found that even the brief moments spent in a porta-potty revitalized me and helped me come out much stronger and faster.

6) Hopefully your family and friends have signed up for runner tracking so that every time you cross a checkpoint they get a notification. Think about this! Think about all the people who are behind you, wishing for your success, and who will congratulate you in the end! Don’t lose hope!

Crossing the finish line & afterwards:

1) Hold your hands up high, smile, and make sure you get that nice photo finish!

2) Hobble towards the gear check and food lines. Grab your medal(!) on the way. Most races give out mylar sheets so you can stay warm until you get your gear. It’s a good idea to wrap yours securely around yourself before you try to pick up the water and snacks provided.

3) Walk, walk, walk. The more you walk and stretch now, the less pain you’ll have later.

4) Eat a hearty meal that includes both carbs and protein as soon as possible. Rebuild and refuel.

And that’s it! Pat yourself on the back, happily receive the congratulations from your friends and family, take a nap, and then go back to lab. With one big race completed, it’s time to bring that other race to completion: your doctoral thesis!

4 Ways to a Happier Postdoc


By Florence Chaverneff, PhD

Chances are, if you have been a postdoctoral fellow for a little while, you have at some point or another (unless it is constantly) felt like the ‘Desperate man’ in this painting by Gustave Courbet. So, in the aim of trying to help and save you from pulling your hair out of your head, here are a few pointers gathered both from personal experience and that of friends and co-workers which I hope will help you cruise through this particular phase of your career and make the most of it, whichever your next step.

1. Prepare your next step

Certainly, as a postdoctoral fellow, most of your efforts should be concentrated on making advances on your project(s) and getting fabulous data worthy of a 30+ impact factor journal. Equally as important, you should start thinking as early as possible about what your next step should be. If you’re not planning on staying in academia to pursue a tenure track position, which, according to statistics should be the case for about 85% of you, you will need to have a plan B. Some sectors are more popular or should I say, more intuitive as a career alternative (think pharma and biotech sectors). But you shouldn’t limit yourself to those areas, as a whole array of attractive options is available to a postdoctoral fellow seeking to transition outside of academia. What these alternatives are and how to figure out which ones fit(s) you best, as well as how to land a job will be the subject of a future post. Utilize the resources available to you at your current institution as much as you can. If you are as lucky as I am, your university will have a very active office of postdoctoral affairs that organizes a plethora of events aimed at helping fellows with their ‘individual development plan’, a term I only learnt about quite recently I’m afraid to admit.You don’t want to be a postdoc forever. No, really, you don’t. Knowing what’s coming next undoubtedly will help you tackle with poise the many challenges you will be facing during this period. As a side note, international postdocs intending on pursuing their career in the U.S. should also plan on acquiring permanent residency while in academia.

2. Manage your stress

Start to realize that most of the stress you experience is self-imposed. So, make it easy on yourself and go to yoga. Free yoga if you can, cause, you know… Naturally, your PI will most likely be starving for data from everyone in the lab, including you, and knowingly or not, also constitute a sizeable source of stress. Just remember one thing. Your advisor is a whole lot more stressed than you are. And that might have to do with the fact that he/she NEEDS data. No data, no publications. No publications, no grant. No grant, no money. And, well, no money, no lab. It is visibly in everyone’s interest to keep the lab. You know the not so old adage, so I’m not going to repeat it. So, learn to deal with your advisor. This might require a good deal of social and emotional intelligence from you. Developing such skills to the point where they become automatic will be essential throughout your career in dealing effectively with bosses and co-workers. You might find it useful to get acquainted with personality tests such as the well-renowned and widely-used Myers-Briggs. This is a great tool to learn about yourself, of course, but also to use as a complement to social and emotional intelligence to successfully interact and work with any personality type.

3. Ask for help

Another great source of frustration in the professional life of a postdoc is dealing with experiments that either simply fail, are not reproducible, do not yield statistically significant results, or even, contradict your working hypothesis, without even mentioning all kinds of other mishaps that are likely to happen along the way. The best way to deal with these issues is to talk them through with your labmates. They might have great insights about things you wouldn’t think of or notice because you are so involved in your project and experiments. So, don’t hesitate to ask for help. It is not a sign of weakness!

4. Enjoy your free time

Finally, by all means, try and manage a proper work-life balance. I mentioned yoga earlier, but really, anything that floats your boat and takes you out of the lab, not just outside the door, but literally outdoors. Too many postdocs I have encountered spend most of their awake time in the lab, the rest being spent eating, grocery shopping or doing house chores. If that sounds fun to you, I’m not sure what to tell you. In the opposite case, try and make time to spend on your favorite activity, be it sports, playing guitar or painting. And hang out with your friends and family. Working 24/7 is plain unhealthy and unproductive. So if you feel like you don’t have the time, it most likely is because you’re not managing your time properly. Then, I recommend you learn about time management, be it in a course, a book or on the internet. Also, instead of spending long incubation periods chatting with labmates or surfing the web to whatever websites you favor, do something productive, like catching up on your reading, planning your next experiments, analyzing data…There is plenty to be done and lots of options to pick from. If your project is simply extremely labor-intensive, find yourself an eager undergrad to help lighten the workload. In addition to saving you precious time, you will get practice in mentoring and teaching.

I hope these few tips will help you be a happier postdoc!

Ebola – Closer than You Think


Ebola, the hemorrhagic fever is closer than you think, but there is no reason to panic…yet!

By Jesica Levingston Mac leod, PhD

In case you did not hear about it, the Center of Disease Control (CDC) reported an outbreak of a “more virulent” Ebola virus infections in Guinea, spreading now to Sierra Leone . Ebola virus is the etiological agent of severe hemorrhagic fever. The symptoms? Fever, rash, severe abdominal pain, vomiting, and bleeding, both internally and externally. The fatality rate? Around 90%. Even worse, these outbreaks are occurring with increasing frequency. Some explanations for this are the increased contact between humans and the natural reservoir of the viruses (fruit bats), and fluctuations in viral load and prevalence in this reservoir. The transmission of the virus mostly occurs by contact with infected blood, secretions or organs of either bats, nonhuman primates or humans. This is why you should not eat bats or monkeys if you visit any of the affected areas, or hang around any cemeteries. Not surprisingly, Ebola was named as the most frightening disease in the world. It was documented for the first time in 1976 in the Republic of Congo; one of the sources came from the Ebola River.


In 2012 an outbreak in Uganda found us in a similar medical emptiness: the research of two of the vaccines that were “apparently” going great had been canceled by the department of defense, due to funding constraints.  Therefore, so far we do not have any vaccine or effective treatment available.


Albeit a DNA based vaccine was described in 2003 to fully protected macaques against the fatal virus, it did not continue to further clinical trials.  It was not until 10 years later that a group in the US National Institutes of Health published research about a vaccine consisting of a recombinant vesicular stomatitis virus expressing the ebola glycoprotein which protects macaques from Ebola virus infections, although this method is not licensed for human use.


But, why does the US department of defense care about an African virus? The answer is pretty obvious: it can be used as a bio hazard weapon. On the other hand, no leading pharmaceutical is going to invest in a “very expensive and time consuming” vaccine development to be used in countries that can not afford even a basic level of health care. Some compounds are showing a promising antiviral effect in vitro and/or an inhibition of a variety of viral proteins activities. Sadly, all of them are in an early stage of drug development.


Before freaking out, the best “cure” and prevention method against this scaring virus is knowledge, so check out the updates in the CDC website.

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It's Alive!


How the largest virus ever discovered rose from the dead and taught us a few a lessons about viral latency

By Asu Erden

The first giant DNA virus was discovered only 10 years ago and astounded the scientific community due to its implications for viral biology. How could a virus that lied dormant for thousands of years still be infectious? Last week, scientists from the National Centre of Scientific Research (CNRS) in France published their findings in the Proceedings of the National Academy of Sciences about the 30,000 year-old virus they uncovered from the deeper layers of the Siberian soil. This giant DNA virus, called Pithovirus sibericum, is the largest one ever found. It does not infect humans but Legendre et al. have shown that it can parasitise amoebae.

It was hitherto believed that giant DNA viruses belonged to two widely different families: the Megaviridiae and the Pandoraviruses. The former have smaller particle sizes and genomes and replicate in the host cell’s cytoplasm, which means that they do not need to hijack the cell machinery to make copies of themselves. The Pandoraviruses, on the other hand, have larger particle sizes and genomes and need to enter the host nucleus to replicate. The newly discovered Siberian virus belongs to a new category, called Pithoviruses, that combines features from both of the formerly described giant virus families. It exhibits a large particle size, a small genome, and has entirely cytoplasmic replication. This means that the biology of giant viruses is much more diverse than previously imagined. It seems that many different features can allow a virus to survive freezing temperatures and to rise still fully functional after thirty millennia of hibernation.

While scientists keep virus stocks at freezing temperature for long-term storage, the idea that viruses can survive for tens or hundreds of millennia in ice remains a contentious issue in the field. In their study, Legendre et al. combined microscopy techniques and infection assays in amoebae to identify putative DNA viruses from Siberian deep soil samples. Using amoebae as bait for putative pathogens from soil samples, they observed that these eukaryotic organisms started to die. This is when Legendre et al. knew they were onto something. The infection assay allowed them to identify and characterise Pithovirus sibericum as a rod-shaped virus of approximately 1.5 μm making it bigger than many bacteria. Infection “symptoms” within the amoebae appeared after 4 to 6 hours. A few hours later, viral particles were ready to bud out of their host cells and continue their infectious cycle.

The French team was somewhat helped by the geochemical and geophysical properties of the Siberian deep soil, also called permafrost. Indeed, this frozen soil layer has a neutral pH and provides an anaerobic environment to the organisms it imprisons. Previous studies have shown that these non-fluctuating frozen conditions are ideal for long-term DNA preservation. As such, the credible threat posed by the thawing of such viruses remains unclear. However, it seems like this undead prehistoric pathogen can teach us a few lessons about viruses of current relevance to public health.

Many of the viruses infecting humans have a latent phase during which they continue to infect cells but do not replicate and therefore do not circulate within their hosts. They therefore remain invisible to our immune system and are extremely difficult to monitor. Such viruses include the varicella zoster virus (VZV) responsible for chicken pox during childhood and shingles later in life, cytomegalovirus, which infects over 60% of us, and most infamously the human immunodeficiency virus (HIV).

While the discovery of P. sibericum from thawed Siberian permafrost is a relevant harbinger of the many long-term destructive effects of global warming, it should also be lauded as a reminder of the ongoing scientific challenge that viral latency poses to researchers, physicians, and most importantly patients. Just like the features that allow some pathogens to survive for thousands of years in the ice before they are unleashed into the wild, the precise factors that lead to the reactivation of a latent virus remain elusive. As Legendre et al. put it, “an entire world of viruses [remains] to be unraveled.” Let this new viral discovery be a humbling memo that there is still plenty that we do not understand about these microorganisms and that they will continue to fascinate and challenge us for years to come.

Got allergies? Try worms


By Amanda Keener

If you have allergies, it may be because you don’t have worms. At least, that is, according to the “hygiene hypothesis” and its more recent cousin, the “old friends hypothesis.”  Both of these suggest that the absence of pathogens and microorganisms in our environment somehow promotes atopic allergic diseases and are supported by the rise of allergies in Western cultures throughout the 20th century.  The “old friends hypothesis” suggests that the type of microorganisms we come in contact with matter; those that humans as a population have grown accustomed to offer benefits that are lost as sanitation increases.  Tiny worm-like parasites called helminthes have been the case-in-point for this idea.  Helminth infection can re-program the immune response by promoting the production of regulatory T cells and B cells. These cells balance their inflammatory counterparts and the worms create an environment for themselves where the immune system is dulled and incapable of clearing the invaders.

Epidemiologically, helminth infection is inversely related to allergic and autoimmune diseases.  Some studies, however, have found that helminthes actually aggravate allergies.  In a recent issue of PLoS Neglected Tropical Diseases, Layland et al took a closer look at this relationship in mice.  They used the blood fluke, Schistosoma mansoni to ask whether the stage of the parasitic infection would influence how the immune response responded to allergic airway inflammation.

They infected mice with S. mansoni and during different stages of the parasite’s life cycle, they sensitized the mice to egg ovalbumin, a protein commonly used for studying antigen-specific immune cells.  Repeated exposures to the OVA essentially make the mice allergic to it, so that when they are challenged with the aerosolized protein many weeks late, they get an allergic airway inflammatory response, much like asthma.  If the mice were sensitized to the allergen during the time that the parasites were actively producing eggs, then the immune response to the allergen was significantly reduced.  This protection against lung inflammation was absent if sensitization to the allergen took place during the early stages of infection.

To understand how the egg-producing stage of the infection prevented airway inflammation, the researchers looked to the regulatory T cell (Treg) population, which had been known to expand during helminth infection.  The late stage infected mice did in fact have greater numbers of Tregs in the lymph nodes draining the lungs.  If the researchers depleted the Tregs during the allergen sensitization, the mice responded to OVA challenge with lung inflammation whether or not they were infected with the parasite.  So, the Tregs were vital in mediating the anti-allergic effect of the S. mansoni eggs.

It would be interesting to know how the Treg population changed during the course of the infection—were they only expanded during the late, egg-producing stage and not the earlier stages?  The group didn’t compare the cellular immune responses of the mice sensitized during early and late stage infection, so it’s unclear whether eggs direct better Treg expansion than worms.  What is clear is that the stage the helminth infection is at during allergen sensitization does matter and this study may help explain the variability in the way that helminthes direct allergic responses.  It may also direct researchers to potentially useful antigens expressed only by the eggs that could be explored as therapies to treat or prevent allergies.

Amanda Keener is a freelance science writer and a PhD candidate in Microbiology and Immunology.  She writes about immunology research on her blog ImmYOUnology.

Can a Mutation Protect You From Diabetes?


Evelyn Litwinoff

For the first time in diabetes research history, researchers have found mutations in a gene that is associated with a 65% decrease in risk of developing type 2 diabetes (T2D).  What’s even more astounding is that only one copy of the gene has to be mutated to show this protection.  The gene of interest is SLC30A8, which encodes a zinc transporter in pancreatic islet cells.  (A quick brush up on your cellular anatomy: Pancreatic islet cells produce insulin, which the body uses to uptake glucose into cells.  Zinc plays an important role in the uptake, secretion, and structure of insulin.) This study found not 1, not 2, but 12(!) different loss-of-function mutations, all in SLC30A8 and all predicted to result in a shortened protein, that associates with protection from T2D risk.


Most of this study is based upon sequencing genes that were previously associated with a risk of developing T2D.  Overall, the authors looked at about 150,000 individuals from various ethnic populations in order to obtain statistical significance for their associations.  Their results are surprising since previous studies had linked mutations in SLC30A8 with an increased risk of T2D.


However, this study does not address how a decrease in function of the zinc transporter, named ZnT8, could lead to protection from a disease state.  The authors did conduct one mechanistic-ish experiment, but this was only to see if the mutations in ZnT8 actually affect the activity of the protein.  To this end, the authors overexpressed 4 different mutated versions of ZnT8 in HeLa cells and saw a decrease in protein levels in 2 out of the 4 versions.  Furthermore, they showed that the increased protein degradation could be part of the reason for the observed decrease in amount of protein.  Their main conclusion from these cell experiments show that some of the mutations in ZnT8 result in an unstable protein, which would help us understand how the zinc transporter is not working, but it does not explain why the dysfunctional protein protects from T2D.  Hopefully, this paper will spark others to investigate a mechanism for the associated protection.


Currently, Pfizer and Amgen are starting to develop drugs that mimic this mutation to see if they can replicate the protection.  Although a new diabetes drug based on this study could be 10-20 years down the road, this study still makes a big splash in the diabetes research community.

So Many Planets, So Little Telescope Time



By Knicole Colon


NASA’s Kepler mission just celebrated its fifth anniversary on March 6th, and it certainly has a lot to be proud of!  Since launching into space in 2009, the Kepler telescope has revolutionized the field of extrasolar planet research.  By monitoring the brightness of  some 150,000 stars over several years, Kepler has been able to detect the tiny dip in brightness caused by a planet that periodically transits (or passes in front of) a star.   With the recent announcement of 715 (!) new transiting planets by the Kepler team, Kepler has increased its total number of planet discoveries to 961 (discoveries that are documented here and here).  That is remarkable, considering that prior to this announcement the number of known extrasolar planets was hovering around 1000.  This recent announcement therefore nearly doubled the number of known extrasolar planets.  Amazing.


How did the Kepler team pull off a bulk discovery like this?  Nominally, each planet candidate that is detected (by any technique) must be confirmed by various methods.  This includes measuring the mass of the planet and determining the properties of the host star (since the derived planetary properties are highly dependent on the properties of the star).  The short story is that confirming that a planet is real requires a lot of additional data, and to get that data you need time on various telescopes.  Given that there are a finite number of telescopes suitable for confirming planets, and that there are a finite (actually quite small) number of nights a year when you can use these telescopes, there simply is not enough telescope time available to confirm every single known planet candidate.


To answer the question posed above, we have to look to statistics.  An important aspect of Kepler’s recent discovery is that the 715 newly-confirmed planets are all in multiple-planet systems.  This means that for the 305 stars that these planets orbit, a given star has more than one transiting planet that is orbiting around that star.  The statistical technique used to confirm these planets relies on this fact.  Given the few thousand planet candidates Kepler has detected by observing some 150,000 stars, logically one might think that on average most stars host just one (if any) planet.  However, that is assuming that planets are evenly distributed among different stars.  Clearly this is not the case, since the Kepler team identified a significant number of multiple-planet candidate systems.  Based on this observation, it is now logical to think that the probability of a planet in a multiple-planet candidate system not being real is very small (because what are the odds that you get multiple false signals from a single star?).  The Kepler team employs rigorous techniques to validate this logic, and they ultimately conclude that more than 99% of these systems are composed of real planets.


Another exciting aspect of this discovery is that nearly 95% of these 715 planets are smaller than Neptune (which is about four times larger than Earth).  A majority of the first extrasolar planets discovered were approximately the same size as Jupiter (which is the largest planet in our solar system, being about 11 times the size of Earth).   It is not surprising that astronomers used to think that Jupiter-size planets were the most common type of planet and because of this, our solar system was unique (as it is composed primarily of many small planets).  It turns out that with the various techniques astronomers have for detecting extrasolar planets, large, massive planets like Jupiter were simply the easiest to detect.  Improved observing techniques and data analysis eventually allowed for the discovery of an increasing number of small planets, but Kepler really hit a home run by providing definitive evidence that small planets are extremely common.  It looks like the solar system is not so unique anymore, which is a good thing!  It means that as astronomers continue to search for and discover new planets, it is safe to conclude that they will eventually find planetary systems that are very similar to our solar system.


The best part is, Kepler isn’t finished.  Its nominal mission is over, due to the failure of a wheel that was used to stabilize the pointing of the telescope.  But, there is now a secondary “K2” mission that is actively studying a new set of stars.  Plus, there are still thousands of planet candidates that need to be confirmed (with possibly more on the way, as the Kepler team has not finished analyzing the available four+ years of data).  This does not even include findings from other active planet-hunting surveys.  Given that there are so many planets, but there is so little telescope time, statistical techniques may become the key to future breakthroughs in extrasolar planet research.


DIY Organs: Healing and Regeneration Through Printing

By Susan Sheng

3D printers are the latest trend in the recent “Do it yourself” movement that has seen the increase in popularity of spaces such as TechShop, FabLab, and MakerSpace. 3D printing is an additive process, where materials such as plastics are progressively layered to create different shapes, based on a digital model. Printers can be small enough to sit on a desk, or large enough to be able to build parts for turbines.


In science and medicine, 3D printing has had many applications. Recently at the University of Louisville, cardiothoracic surgeons used CT images to print a model of patient’s heart. The patient was born with 4 congenital heart defects and required a complex operation to repair the defects. The 3D printed model allowed the surgeons to study the heart defects that needed to be repaired and come up with a complete surgical plan before even picking up a scalpel.


Another recent application of 3D printing in medicine was the announcement of a collaboration between Ekso Bionics and 3D Systems. Ekso Bionics is a California-based company which builds exoskeletons both for military use and for medical purposes in the rehabilitation of patients who have lost the ability to walk. Up until now, their exoskeletons have essentially been a “one-size-fits all,” but on Feb 19, 2014, at a Singularity University conference in Budapest, Ekso Bionics unveiled their first customized exoskeleton suit. The advantage of such a suit is that it can be shaped to the contours of the user’s body, reducing the likelihood of bruising or abrasions from an ill-fitting suit. Given that the patient population using these suits includes paraplegics or stroke patients who may have lost sensation in their lower limbs, such bruising or abrasions may go unnoticed and result in infections.


In the spirit of the DIY movement, a recent story in CNET discussed one man’s year-long work in creating a prosthetic fingertip. The man, Christian Call, lost his right index finger tip through a work-related accident and was unable to afford a professional prosthetic. Given his background and interests in machining and mechanics, he decided to try making his own prosthetic. One and half years and several prototypes later, Call has created a prosthetic that behaves much like a real fingertip, complete with a magnetic tip to assist with picking up metal objects. He has been contacted by other people searching for fingertip prosthetics and has even started his own 3D-printing/design business.


As 3D printing technology becomes more advanced, the potential applications for 3D printing in science and in daily life are limited only by our imagination. 3D printing could be used to create customized lab equipment for specialized experiments, potentially at a fraction of the cost of purchasing from a commercial company. If bioprinting (printing with living cells) becomes more viable, miniature organs could be created for research and drug development purposes, or possibly combined with stem cell technology to grow whole organs in the lab for transplant purposes.

Mice are Not Men

On the use of rodent models in neuroscience research

By Franchesca Ramirez

We depend on animal models for biomedical research. In so doing we work diligently under the assumptions that these animal models will provide us insight into the development of novel treatment approaches. Specifically, the rodent is become flagship of animal research. We gleened a great deal from the study of rodent models that seem to recapitulate the symptoms of psychiatric diseases and yet not consistently been led to clear therapeutic insight as a result. Essentially, clinical trials are necessary because animal studies do not predict the efficacy of treatment in human populations with sufficient certitude.

Let us consider what we ask of our rodent models. We expect for such animals to model the etiology of psychiatric disorders, confer some congruence with molecular markers confirmed in humans and ideally to respond to available treatment. Indeed, we are witness to robust mouse models of disorders like, Rett syndrome, fragile X and Down’s syndrome to name a few. However, these human brain disorders have discrete and recognizable genetic  causes. Why then do behaviorally induced animal models of other neurocognitive disorders, like depression or schizophrenia fall short, one may ask. The thing that makes an animal model bad is that perhaps we should not be modelling a psychiatric disorder with cerebral and cognitive diagnostic criteria in a bottom-up fashion. That is to say by focusing on the details of complex biological systems in animals we can not know the landscape of cognition in humans.

Perhaps neuroscientists must be reticent to draw analogies between animals showing symptoms of psychiatric illness without knowledge of the cognitive process underlying the behavior, agrees neuroscientist, Erik Klann at New York University in NYC. Individual humans do not at all display identical symptomatology so how then do the animal symptoms add up to a recognizable human psychiatric disorder? How would we model hallucinations, sadness and guilt in animals, says Klann. These are legitimate concerns for the future of biomedical neuroscience research. We cannot know what it is like to experience the conscious state of another organism, we may however, ask what brain systems are conserved across taxa and how do they work to elicit behaviors that mimic symptoms of psychiatric disorders.

Perhaps the effort should be devoted to research on humans to map the progression and symptomatology of psychiatric disease to then probe the neural circuitry in our beloved rodent models, says Yadin Dudai, a neuroscientist at Weizmann Institute of Science in Rehovot, Israel. It is logical to conclude that it is not the fault of the model in question but rather the approach we take to probe the system for answers to our research questions. One approach Dudai endorses is to start with the human components of a disorder but not the entire spectrum. In this case the top-down approach is key- let us study humans as models for our animal systems. Just so, this is largely how we attained such robust disease animal models in the first place.

Unraveling the Mystery: Tips for Giving an Effective Chalk Talk


By Elizabeth Ohneck

The chalk talk is perhaps the most enigmatic form of oral presentation, the most mysterious, unpredictable, and nerve-wracking part of interviewing for a faculty position. While your CV and manuscripts get you interviews, your chalk talk plays a major role in whether you are offered a job. However, as these presentations often take place behind doors closed to graduate students and postdocs, few of us know what a chalk talk actually is, much less how to give one. The following is a collection of advice from new faculty members and postdocs currently undergoing the interview process to help you prepare and present an effective chalk talk.

What is a chalk talk, anyway?

While your seminar shows off all of the hard work you have done, your chalk talk should focus on what you will do in your future lab. However, the chalk talk should not present the master plan for your entire career. Rather, it should be a focused, specific plan for the first 2 – 3 years of your lab. Think of it as a verbal grant application for your start-up package – what are you going to do to start your research and put together your first R01 (or other grant application)? It’s also important to keep in mind that the chalk talk is a chance for you to get a feel for the department. Observing how the members of the department interact with you and with each other will provide an idea of the types of relationships among faculty, an important consideration in choosing a department in which you will feel comfortable.

How can I prepare?

You should be informed of the format of the chalk talk before your interview. If not, don’t be afraid to ask. Some departments may allow you to use a few introductory slides or handouts, but for the most part, you should be prepared to give your talk without such visual aids. To help you organize and plan your talk, you can write an NIH format specific aims page, instructions for which can be found online. Ask people to read this summary to make sure it is clear and logical. Additionally, the hiring committee will want to know if you have permission to take the research outlined in your aims with you to start your lab, so discuss with your PI the scope and specifics of the research you can take. Finally, practice! Gather your peers, your PI, or other faculty who might be willing to help and get comfortable discussing your research plan and presenting without slides. Choose people who will not be afraid to interrupt you and ask tough questions, and who can offer constructive criticism about your presentation style, including pace, clarity, and body language, as these stylistic details contribute to engaging your audience.

How do I use chalk in a talk?

You should be given some time to prepare before your talk. Use this time to write your specific aims on the board. Having your specific aims easily visible will help keep you organized, and if you don’t get through your entire talk in the allotted time, the committee can see the full scope of your research plan. You should also draw any models or pathways relevant to your research, to help your audience follow along. During your talk, you can draw generalized graphs, blots, etc. to help depict important trends.

Other tips:

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  • Be focused and specific. Present a plan for a reasonable amount of work to accomplish in the first 2 – 3 years of your lab. Indicate particular projects appropriate for graduate students and postdocs who join your lab.
  • Know your audience and tailor your talk accordingly. What is the primary focus of the department? In what backgrounds are the members experts? Highlight areas that will be most exciting to the audience, and provide extra details in subjects with which they may not be as familiar.
  • Highlight what makes you unique. What techniques and background do you bring to the department? How is your research unique to the field? What distinguishes your lab from other labs with similar research interests?
  • Be flexible. You will get interrupted with questions, and you may not get through everything you planned to discuss. Answer questions to the best of your ability, but if someone becomes argumentative over the same point for an extended period of time, know when and how to graciously disengage to keep the presentation moving.
  • Present work you are truly excited about doing. Your enthusiasm will engage your audience, keep you motivated, and convey your passion for your research.