The Biomedical Research Crisis


By Neeley Remmers, PhD


Call it “woman’s intuition” if you will, but all throughout my graduate career I had this persistent voice in the back of my head trying to tell me something. It started as a gentle, lulling whisper in my first year that gradually grew into full-blown fire alarm screeching in my head. What was this alarm? My own growing concern over the sustainability of biomedical science and its job market. I had been exposed, to some degree, of the decline and volatility of research jobs in industry prior to attending graduate school and knew of the ever increasing influx of graduate students entering the biomedical field despite the fact that the number of available faculty and research positions had remained constant. My concerns were fully realized when I went to a career development conference in my 4th year, right about the time I needed to start making more concrete plans as to where I wanted to take my career. The recent article published in PNAS co-authored by Bruce Alberts, Marc W. Kirschner, Shirley Tilghman, and Harold Varmus eloquently highlights some of the concerns I have myself as well as additional faults of the current system used by the biomedical field and gives insightful recommendations as to how to remedy the situation to prevent our field from imploding.


The authors adequately identify the root cause of the looming implosion of biomedical research – the assumption that there will be continual, rapid growth in the field creating job security for those already established and creating a job market rich with opportunity for new scientists. This assumption had been frequently used as bait to persuade me into joining the field even though the NIH budget had already begun to diminish after experiencing a decade of growth by the time I entered college. This decline in available federal funds (thanks to recent economic hardships felt everywhere) has fully opened our eyes to our current situation of having a supply of highly-qualified scientists that surpasses the number of available research positions, more specifically academic research positions. This influx of skilled scientists was the catalyst needed to synthesize a number of other problems that have recently surfaced in biomedical research that hurt everyone in the field, particularly new investigators. I won’t spend time going into detail on these additional problems highlighted by the authors, but I do want to spend a few moments touching on a subject they missed that I feel could also be adding to our current dilemma.


One cause of our problem outlined by the authors is there being too heavy a focus on conducting “translational research.” First, neither the authors nor I are trying to downplay the importance of translational research. After all, for a many of us, advancing medicine is the main reason we decided to enter research. However, it does seem like these days many are over-looking the importance of basic research and that you need solid, basic foundation before you can jump into translational research. By doing quality basic research first, you can gain a firm grasp on the mechanisms that dictate whichever physiological process you are studying and can be more successful in translating that knowledge into clinically relevant studies. Part of the push towards doing more translational research, though, comes from Congress and support from the general public. In this day and age, people like to see immediate results, and translational research can provide the public with results that have a more direct correlation to patient care as opposed to basic science. These results may not always be positive, but even the negative results give a better appearance to the public that something worthwhile is being done with the money they have given us. The problem here is that the general public does not understand the scientific process and the time and effort that goes into discovering new, efficient therapies; a problem easily remedied by educating the public about the research process. Once they realize how important the basic science is to translational research, we can bring some focus back towards awarding investigators who propose long-term, high-quality science rather than on those who propose short-term, translational projects.


Back to the article, the authors give their recommendations for how to rescue biomedical research. I will refrain from commenting too much on how we might remedy the grants review process, selecting review panels, and such as addressed by the authors as I do not have much experience or knowledge in these areas. What I can comment on is their recommendations for altering the way we train new scientists. As mentioned earlier, there has been an inflation of graduate students and post-doctoral researchers in recent years that far surpasses the number of available jobs. This is in part due to the fact that it is cheaper for senior scientists to bring students and post-docs into their labs rather than hire staff scientists and restructuring grant guidelines in terms of salaries, as outlined in the article, could certainly help this. The authors suggest that by prohibiting payment of students from grants and increasing pay of post-docs will help to reduce the numbers of incoming graduate students, promote career advancement of post-docs, and encourage hiring staff scientists all of which can be beneficial in the long-run.


Aside from simply limiting the number of incoming graduate students, I feel it is necessary that graduate programs start implementing career development programs into student training. In the past, one’s career path in science was pretty clear and the apprenticeship scheme used to train current graduate students worked well. However, in today’s world only about 25% of current graduate students will be able to obtain a faculty position leaving the other 75% of current graduate students to find employment elsewhere rendering the apprenticeship scheme no longer a valid training model. Instead, we need to increase efforts to introduce students early on to the many other career options available to them in science by giving them opportunities to meet with professionals in these areas. Students can then begin to make valuable connections to establish relationships with a secondary mentor that can help them get into the fields of patents, policy, scientific writing, etc.


Change in the structure of the biomedical science enterprise is desperately needed to prevent it from collapsing. The reality is that the model currently in use may have worked well in the past but is severely out-of-date for today’s economy. Serious changes are warranted in order to get back to the days of exciting scientific discovery rather than living in the days of scientific survival.

How NOT to Do Your Post Doc Job Search



by Neeley Remmers, PhD

Recently, I have been going through the phase in every scientific career where you transition from student to post-doctoral research associate. The route I took on this journey is definitely not one I would recommend to anyone. My career goal is to become a physician/scientist and attend medical school in a couple of years. In order to do so, I knew I still needed to complete a post-doctoral position and there would be about a 1-2 year delay between graduating with my PhD and starting medical school. I initially saw this as an opportunity to do a post-doc either over-seas or in a different part of the country that I have not yet lived.

Whoops! My Mistakes

  • Mistake #1: I will admit, the initial thought of actually moving over-seas alone scared me and is why I delayed looking for a host lab. Eventually, I researched fellowships I could apply for and began the process of locating a host lab. By the time I found one, I had exactly 3 weeks to complete my fellowship.
  • Mistake #2: I hadn’t considered the lag time between graduating and potentially starting my new position. It wasn’t until AFTER I defended and graduated in August that I learned I would not receive news about the fellowship until late January and even if I got it, I wouldn’t be moving over-seas until February or March giving me almost 6 months of lag time. My graduate advisor told me I could continue to work in his lab to finish up my work, but he could only pay me for 2 months and the rest of the time I would be a “volunteer.”

As you can imagine, it is nearly impossible to find a scientific job if you only guarantee the employer you would only be there for 6 months after which time you MIGHT leave for a different job. I decided to take my advisor’s offer and worked as a volunteer until my work was completed in December and then used the next 2 months to study for the MCAT. During those 6 months, I half-heartedly looked for alternative post-doctoral positions here in the States.

  • Mistake #3: At first, I limited myself to only looking at labs that did pancreatic cancer research on the West Coast. I quickly learned that by restricting yourself that much extremely limits your opportunities. I began to broaden my search and finally came across a couple of positions that could serve as good back-up plans in the event I didn’t get the fellowship. After a long, stressful 5 months of waiting, I finally found out that I did not receive the fellowship and accepted one of the other post-doctoral positions. Ironically, I ended up being in a lab affiliated with my graduate institution. I was a little disappointed that I didn’t get the chance to move somewhere new, but as it turns out I managed to secure a much better position for myself in doing so than had I gone elsewhere. Somehow, I managed to convince my new boss that I am a valuable asset to his team and was able to negotiate a salary much higher than a first-time post-doc would normally receive.

Making Some Adjustments

I have been a part of my new lab for one month now, and am still trying to adjust to my new position and my new lab. Though I am technically at the same institution where I did my graduate research, I am actually at a facility about 1 mile down the road at the local VA hospital officially making me a federal employee. There were a few extra headaches at the beginning that go along with being a federal employee – going through 2 new employee physicals and orientations (one at each institution), mounds of paper work to get clearance into the building and very extensive background checks – but the atmosphere at the VA research facility is much more relaxed compared to that at my graduate institution, which is a nice reprieve after getting a bit burned out during my graduate career.

Aside from the slight change in scenery, there are a number of differences between my new and old labs that I am still trying to get accustomed to since, unfortunately, as a post-doc you don’t have the luxury of completing 6-8 week lab rotations prior to joining a new lab. My old lab was big; we had 16 persons in the lab that included a lab manager, a program coordinator, an administrative assistant, post-docs, and students. My new lab has a total of 4 people including myself with me as the lone post-doc, 2 techs and one surgical fellow. My previous lab was also very social, so much so that you sometimes had to leave entirely or work from home in order to get any computer work done. This most definitely is not the case with my new lab. Now, instead of needing some quiet time at the end of my work day, the first poor soul who says hello to me once I have left work is in for conversational storm with me talking their ear off for a solid 30 minutes before they can get a word in edge-wise…even if they are a complete stranger!

My old lab was predominantly a basic research lab with translational projects whereas my new lab is strictly a translational research lab that is not adequately set up for basic research. The project I was brought in to work on is meant to add a basic research component that will lead to more translational research. This new project is high-risk, high-reward, and my new PI told informed me early on that he (nor anyone else in the lab) will not be of much use in terms of troubleshooting since he has no experience with the techniques I will be utilizing and can really only discuss theory with me. Thus, I am staying in touch with all my contacts from my previous lab to create a support network to help brainstorm around potential road-blocks. Essentially, I’m learning now what it is like to set up your lab, be completely in charge of your project, and deal with administrative tasks such as budgeting and writing IACUC protocols. Though my PI understands that there is a high likely-hood this project will fail, there is still a lot of unsaid pressure to succeed as the lab’s ability to get funding to continue running largely depends on my success. This was daunting at first – and still is – but in the end I know I will gain valuable experience on what it is like to be an independent researcher.

Woulda, Coulda, Shoulda…

Is there anything I wish I would have done differently? Yes, and it all mainly revolves around how I went about handling the international fellowship. I would have started researching international fellowships a solid year or more BEFORE I was planning to graduate to give myself enough time to find a host-lab, write a comprehensive proposal, and create better timing to reduce the lag time between graduating and starting a post-doc to alleviate a lot of unnecessary stress. In the end, I think I will be happy with my new position. So far, he and I seem to work well together, and most importantly he is 100% supportive of my career goals to go to medical school. He has offered to help me get into med school in any way he can AND to keep me on as a paid employee while in med school if I attend our local institution. Even though I didn’t get to move to somewhere new and experience a new culture, I feel like it all worked out in the end and I’m where I’m supposed to be. I suppose I can always move somewhere new for my residency…

Getting the Most Out of Your Heart


By Neeley Remmers

When I was asked to write a post about the new heart rate max calculator and how to use it as a training tool, I was super excited to take on this task. Why? Even though I have been an endurance athlete and road racer for about 6 years now, I have never taken the time to really learn how or why to use your heart rate (HR) as a training tool, and this post has finally forced me to do just that.

Before I delve into the scientific study that finally led to the development of a more accurate hear rate max (HRmax), let me first go into why this is important and how it can help those of you thinking about using your HRmax as a training tool. First, how can monitoring your HR be a useful training tool? Monitoring your HR basically allows you to measure and track the effort you put in to each workout. You might be thinking, like me, that you can simply measure your effort by how you feel during each workout. This method is perfectly fine and sometimes you should just go for a run without constantly monitoring your pace and/or HR, but if you want a more accurate means of measuring your effort that you can log, then monitoring your HR is a great option.

In order to use your HR as an effective training tool, though, you need to first determine your HRmax. There are many means by which you can determine your HRmax and the most accurate way is to make an appointment with a professional trainer who can hook you up to a mask that measures your VO2 or rate of respiration, or you can perform a DIY test as outlined by Runner’s World Magazine in two different articles (article 1 and article 2). Or you can calculate your HRmax using a formula. Previously, the calculation recommended by numerous professionals to calculate your HRmax was simply HRmax = 220 – age. This formula was easy to remember and could be quickly computed in your mind; however, this formula was overly simplified and would almost always produce a HRmax that was ±20 beats from a person’s actual HRmax. Immediately, you can begin to imagine the problems this would create. Being off by that many beats has a huge effect on the HR ranges you use to determine the amount of effort to put into each workout ultimately leading to constantly over-training oneself leading to injuries and burn-out, or not training hard enough causing you to plateau preventing you from achieving the fitness level you are working towards.

Recently, the Karlsen lab in Norway used data collected from the HUNT fitness study that included over 3,000 men and women to develop a more accurate formula for calculating HRmax. This new formula actually takes into account variables that can affect your HR including gender, age, size, and whether or not you are taking beta blockers. Since their formula is more complex, they have conveniently set up a website you can visit to calculate your HRmax as well as your BMI. Although this new formula gives a much closer estimation of your HRmax (emphasis on estimation), it is still to be regarded with a grain of salt. Perhaps the biggest flaw of this formula is that it does not take into account one’s fitness level. I understand this may be difficult to compute with an algorithm unless you could correlate ones resting HR with fitness level and/or HRmax, which may be possible but this is definitely above my current level of understanding on this topic. Being the scientist I am, though, I chose to compare the three DYI methods to calculate my HRmax – the old formula, the new formula, and the method prescribed by Runner’s World (article 1 listed above) to determine my lactate threshold. The old formula gives me a HRmax of: 220-29 = 191 and the new formula gave me a HRmax of 192. However, when I used the method to determine my lactate threshold, my HRmax was more around 180. Unfortunately, I could not get into my friend who is a personal trainer and owes me a free VO2 test to determine what my actual HRmax is, but I would guess it may be between 190-180. Conclusion: I may not have been the best test subject for comparison between the two formulas as I am part of the population that the old formula actually worked for (supposedly), so I cannot give a definite conclusion as to whether or not the new formula is more accurate than the previous. However, I will say that if testing your VO2 at a gym or sports medicine facility is not an option for you but you would like to start using the HR monitor that came with your Garmin or other fitness tracking device, using the new formula to calculate your HRmax would certainly be a good place to start. You can then generate the HR ranges as described in the Runner’s World articles based on the calculated HRmax to guide how much effort you should use for each workout over the next few weeks. After some time has passed (anywhere from 6 weeks to 3 months), it would be wise to try the DYI lactate threshold test to determine your new HRmax as it will have likely increased or decreased as your fitness level decreased or increased over time.

9 Tips for Preparing for a Marathon When in the Lab



Neeley Remmers

This year to celebrate the New Year, I spent New Year’s Eve on my couch studying for the MCAT and waiting until the clock struck 12:01 am so I could quickly get online to register for the Lincoln Marathon before it sold out (which it took less than 12 hours for it to sell all 12,500 spots). Fortunately, I got in and will be running my 3rd marathon this May (yippee!), so I thought what better way to kick off the race season and jump start my marathon prep than to compile a list of marathon do’s and don’ts for anyone looking to tackle the big one this year for the first time or for the 100th time.

1. Find a training program that works for YOU

There are numerous programs available for free online, and they all have three weekly key running workouts that are essential for you to be successful on race day: speed work, a mid-distance tempo run, and the long run.  I recommend following the FIRST training plan which only uses these key runs along with 2 days of cross-training. The thing I LOVE about this program is it is less time-consuming than other plans, which is a huge bonus since most of us spend a lot of time in the lab leaving little down time. Additionally, by cutting out the extra “junk miles” (normally termed “recovery run” in most programs) I found I was less likely to experience burn-out 4-6 weeks before race day.

2. Do your workouts in the morning

This will be a struggle for most since the typical lab day starts around 9:00-9:30 am and hitting the snooze button will seem like a much preferable idea compared to getting up at 5:30 in the morning to go run. But, we all know that lab experiments go awry and our days rarely go as planned. By disciplining yourself to get your run done in the morning, you can avoid making an excuse for yourself not to go run later in the day because it’s 7:00 pm and you’re JUST NOW leaving the lab.

3. Incorporate a strength training program into your marathon prep

Most assume that strength training will hinder their running ability because it will add bulk in which bulky muscles can make endurance running difficult. However, the right kind of strengthening can help prevent injury and actually improve your running performance. For strengthening, you can do anything from high intensity boot camp style classes to yoga to pilates; the key is to find a program that you find challenging yet enjoyable so you don’t dread these sessions. The more you dread a workout the less likely you are to actually do the workout.

4. Work on flexibility, especially in the hips and legs

Most runners tend to ignore the benefits flexibility can bring to their running performance. First, by keeping the hips loose, you can prevent any number of injuries including IT band flare ups, runner’s knee, and general pain in the knees and ankles. By simply adding 10-15 minutes of stretching at the end of any workout will keep your muscles from getting tight and thus, restricting your range of motion causing unnecessary strain in your joints and muscles.

5. Don't do it alone

The first time you go on a long run that in your mind seems an impossible distance -  find someone to run it with you, ride their bike alongside you, or join you for the last few miles. This distance will be different for everyone, for me it was my first 16 mi run. Fortunately, the week I was slated to go on my first 16 mile run, I had just met a gentleman at the conference I was attending who was an experienced marathoner and offered to run with me. This helped tremendously because he served as my pace setter and provided encouragement towards the end of the run when I started to doubt if I could make it. But he kept me going and an added bonus was I immediately had someone with which to celebrate this huge milestone!

6. Tell your lab mates and mentor that you are training for a marathon

You will be amazed at how supportive they will be and this support system will be huge in keeping you motivated throughout your training and during your race.

7. Get fitted for the proper running shoes

Finding the right running shoes will give you optimal support to prevent pain in your knees and feet. If you want to try barefoot running or running in minimal shoes, do so with caution. Gradually build the distance you run in those shoes to give your body time to adjust.

8. Invest in running clothes

Especially in the clothes to wear during your long runs and on race day. Wearing any old cotton t-shirt will trap the excess heat your body will produce and become insanely heavy from all your sweat making you incredibly uncomfortable. Running clothes are designed to wick away sweat to keep you cool (or warm depending on the weather) and dry so you can have a comfortable run.

9. Come up with a race day nutrition and hydration strategy

Develop this plan weeks in advance so you can try it out on your long runs to see what works best for your body (especially your GI system) and when you should take a gel/salt tab to prevent dehydration, fatigue, and cramping. Your plan should include when and what to eat for breakfast before your run/race (I know this sounds obvious but you would be AMAZED at how many people refuse to eat breakfast before running 26.2 miles), when to take gels and/or sports drinks to boost your blood glucose levels during your run, and when to take salt tabs or electrolytes during your run to maintain hydration.

There are so many more tips I could share with you, but I think I will end it here. For more advice, you can always visit as they are the experts in everything running and they recently published an article giving even more tips for how to run your best marathon, or send me a message via Twitter @TheDrRemmers and I will be happy to share more provide further advice in how to survive the marathon. Good luck and happy running!

Did you ran a marathon or preparing for one? Do you have tips to share?

The Most Scizzling Papers of 2013


The Scizzle Team

Bacteriophage/animal symbiosis at mucosal surfaces

The mucosal surfaces of animals, which are the major entry points for pathogenic bacteria, are also known to contain bacteriophages. In this study, Barr et al. characterized the role of these mucus associated phages. Phages were more commonly found on mucosal surfaces than other environments and adhere to mucin glycoproteins via hypervariable immunoglobulin like domains. Bacteriophage pre-treatment of mucus producing cells provided protection from bacterial induced death, but this was not the case for cells that did not produce mucus. These studies show that there may be a symbiotic relationship between bacteriophages and multicellular organisms which provides bacterial prey for the phages and antimicrobial protection for the animals.


Interlocking gear system discovered in jumping insects

Champion jumping insects need to move their powerful hind legs in synchrony to prevent spinning. Burrows and Sutton studied the mechanism of high speed jumping in Issus coleoptratus juveniles and found the first ever example in nature of an interlocking gear system. The gears are located on the trochantera (leg segments close to the body’s midline) and ensure both hind legs move together when Issus is preparing and jumping. As the insect matures, the gear system is lost, leaving the adults to rely on friction between trochantera for leg synchronization.


HIV-1 capsid hides virus from immune system

Of the two strains of HIV, HIV-1 is the more virulent and can avoid the human immune response, whereas HIV-2 is susceptible. This may be due to the fact that HIV-2 infects dendritic cells, which detect the virus and induce an innate immune response. HIV-1 cannot infect dendritic cells unless it is complexed with the HIV-2 protein Vpx, and even then the immune response isn’t induced until late in the viral life cycle, after integration into the host genome. Lahaye et al. found that only viral cDNA synthesis is required for viral detection by dendritic cells, not genome integration. Mutating the capsid proteins of HIV-1 showed that the capsid prevents sensing of HIV-1 cDNA until after the integration step. This new insight into how HIV-1 escapes immune detection may help HIV vaccine development.


Transcription factor binding in exons affects protein evolution

Many amino acids are specified by multiple codons that are not present in equal frequencies in nature. Organisms display biases towards particular codons, and in this study Stamatoyannopoulos et al. reveal one explanation. They find that transcription factors bind within exonic coding sequences, providing a selective pressure determining which codon is used for that particular amino acid. These codons are called duons for their function as both an amino acid code and a transcription factor binding site.


Chromosome silencing

Down syndrome is caused by the most common chromosomal abnormality in live-born humans: Trisomy 21. The association of the syndrome with an extra (or partial extra) copy of chromosome 21 was established in 1959. In the subsequent fifty years a number of advances have been made using mouse models, but there are still many unanswered questions about exactly why the presence of this extra chromosome should lead to the observed defects. An ideal experimental strategy would be to turn off the extra chromosome in human trisomy 21 cells and compare the “corrected” version of these cells with the original trisomic cells. This is exactly what a team led by Jeanne Lawrence at the University of Massachusetts Medical School has done. Down syndrome is not the only human trisomy disorder: trisomy 13 (Patau syndrome) and trisomy 18 (Edward’s syndrome), for example, produce even more severe effects, with life expectancy usually under one to two years. Inducible chromosome silencing of cells from affected individuals could therefore also provide insights into the molecular and cellular etiology of these diseases.


Grow your own brain

By growing organs in a dish researchers can easily monitor and manipulate the organs' development, gaining valuable insights into how they normally develop and which genes are involved. Now, however, a team of scientists from Vienna and Edinburgh have found a way to grow embryonic “brains” in culture, opening up a whole world of research possibilities. Their technique, published in Nature, has also already provided a new insight into the etiology of microcephaly, a severe brain defect.

[box style="rounded"]Scizzling extra: In general, 2013 was a great year for growing your own kidneyspotentially a limb and liver. What organ will be next? [/box]


Sparking metastatic cell growth

A somewhat controversial paper published in Nature Cell Biology this year showed that the perivescular niche regulates breast tumor cells dormancy. The paper showed how disseminated breast tumor cells (DTC) are kept dormant and how they can be activated and aggressively metastasize. Based on the paper, this is due to the interaction of interaction with the microvascularate, where thrombospondin-1 (TSP-1) induces quiescence in DTC and TGF-beta1 and periosstin induces DTC growth. This work opens the door for potential therapeutic against tumor relapse.


Fear memories inherited epigenetically

Scientists showed that behavioral experiences can shape mice epigenetically in a way that is transmittable to offspring.  Male mice conditioned to fear an odor showed hypomethylation for the respective odor receptor in their sperm; offspring of these mice showed both increased expression of this receptor, and increased sensitivity to the odor that their fathers had been conditioned on.  Does this suggest that memories can be inherited?


Grid cells found in humans

Scientists have long studied rats in a maze, but what about humans?  An exciting paper last August demonstrated that we, like out rodent counterparts, navigate in part using hippocampal grid cells.  Initially identified in the entorhinal cortex of rats back in 2005, grid cells have the interesting activity pattern of firing in a hexagonal grid in the spatial environment and as such are thought to underlie the activity of place cells. Since then grid cells have been found in mice, rats, and monkeys, and fMRI data has suggested grid cells in humans.  This paper used electrophysiological recordings to document grid cell activity in humans.


Sleep facilitates metabolic clearance

Sleep is vital to our health, but researchers have never been entirely sure why.  It turns out part of the function of sleep may be washing waste products from the brain, leaving it clean and refreshed for a new day of use.  Exchange of cerebral spinal fluid (CSF), which is the primary means of washing waste products from the brain, was shown to be significantly higher when animals were asleep compared to waking.  This improved flow was traced back to increased interstitial space during sleep, and resulted in much more efficient clearance of waste products.  Thus, sleep may be crucial to flushing metabolites from the brain, leaving it fresh and ready for another day’s work.

[box style = "rounded"] Robert adds: As a college student my friends and I always had discussions about sleep and it was also this mysterious black box of why we actually need to sleep. Studies could show the effects of lack of sleep such as poor cognition and worse memory but this paper linked it to an actual mechanism by which this happens. First of all I found it very impressive that the researchers trained mice to sleep under the microscope. On top of that showing the shrinkage of the neurons and the flow of cerebrospinal fluid which cleans out metabolites finally linked the cognitive aspects of sleep deprivation to the physical brain. [/box]


Poverty impedes cognitive function

People who are struggling financially often find it difficult to escape poverty, in part due to apparently poor decision making.  Investigators demonstrated that part of this vicious cycle may arise from cognitive impairment as a direct result of financial pressures.  The researchers found that thinking about finances reduced performance on cognitive tasks in participants who were struggling, but not in those who were financially comfortable.  Furthermore, farmers demonstrated poorer cognitive performance before harvest, at a time of relative poverty, compared to after harvest when money was more abundant.


Gut Behavior

2013 has definitely been the year of the gut microbiome! Studies have shown that diet affects the composition of trillions of microorganisms in the human gut, and there is also a great deal of evidence pointing towards the gut microbiome affecting an individual's susceptibility to a number of diseases. Recently published in Cell, Hsiao and colleagues report that gut microbiota also affect behavior, specifically in autism spectrum disorder (ASD). Using a mouse model displaying ASD behavioral features, the researchers saw that probiotic treatment not only altered microbial composition, but also corrected gastrointestinal epithelial barrier defects and reduced leakage of metabolites, as demonstrated by an altered serum metabolomic profile. Additionally, a number of ASD behaviors were improved, including communication, anxiety, and sensorimotor behaviors. The researchers further showed that a particular metabolite abundant in ASD mice but lowered with probiotic treatment is the cause of certain behavioral abnormalities, indicating that gut bacteria-specific effects on the mammalian metabolome influence host behavior.

Your skin - their home

A paper published in Nature examined the diversity of the fungal and bacterial communities that call our skin home. The analysis done in this study revealed that the physiologic attributes and topography of skin differentially shape these two microbial communities. The study opens the door for studying how the pathogenic and commensal fungal and bacterial communities interact with each other and how it affects the maintenance of human health.


Discovery of new male-female interaction can help control malaria

A study published in PLOS Biology provided the first demonstration of an interaction between a male allohormone and a female protein in insects.  The identification of a previously uncharacterized reproductive pathway in A. Gambiae has promise for the development of tools to control malaria-transmitting mosquito populations and interfere with the mating-induced pathway of oogenesis, which may have an effect on the development of Plasmodium malaria parasites.

[box style = "rounded"]Chris adds: "My friend chose this paper to present at journal club one week, because he thought it was well written, interesting etc etc. Unbeknownst to him, one of the paper’s authors was visiting us at the time. We sit down for journal club and one of the PIs comes in, sees the guy and exclaims (with mock exasperation) “you can’t be here!” Me and the presenter look at one another, confused. He presents journal club, and luckily enough, the paper is so well written, that he can’t really criticize it!" [/box]


Using grapefruit to deliver chemotherapy

Published in Nature Communications, this paper describes how nanoparticles can be made from edible grapefruit lipids and used to deliver different types of therapeutic agents, including medicinal compounds, short interfering RNA, DNA expression vectors, and proteins to different types of cells. Grapefruit-derived nanovectors demonstrated the ability to inhibit tumor growth in two tumor animal models. Moreover, the grapefruit nanoparticles used in this study had no detectable toxic effects, could be manipulated or modified to target specific cells/ tissues, and were economical to create. Grapefruits may have a bad reputation for interfering with drugs, but perhaps in the future we will be using grapefruit products to deliver drugs more effectively!



In May, a new technique called CLARITY to effectively make tissue transparent through a new fixation technique was published in Nature. This new process has allowed them to clearly see neuron connection networks not possible before because they can now view the networks in thicker tissue sections. This new advancement will help researchers be able to better map the brain, but this new technology can also be to create 3-D images of other tissues such as cancer. This new ability allows us to gain better insight into the macroscopic networks within a specific tissue type.


Crispier genome-editing

This year, the CRISPR technique was developed as an efficient gene-targeting method. The benefit of this method over the use of TALENS or a zinc-finger knockout is it allows for the rapid generation of mice that have multiple genetic mutations in just one step. The following review gives even more information on this new technique and compares its usefulness to that of TALENS and zinc-finger knockouts. Further, just couple of weeks ago, two back-to-back studies in Cell Stem Cell using the CRISPR-Cas9 system to cure diseases in mice and human stem cells.  In the first study the system was used in mice to correct the Crygc gene that causes cataracts; in the second study the CRSPR-Cas9 system was used to correct the CFTR locus in cultured intestinal stem cells of CF patients. These findings serve as a proof-of-concept that diseases caused by a single mutation can be “fixed” with genome editing using the CRISPR-Cas9 system.

What was your favorite paper this year? Let us know! And of course - use Scizzle to stay on top of your favorite topics and authors.

Too Young for Cancer?


Neeley Remmers

Officially, cancer awareness month is over, but honestly where this disease is concerned, we should constantly strive to increase cancer awareness amongst the general public. For this post, I have decided to highlight one area of cancer that gets very little attention, cancer in adolescents and young adults (persons ranging between the ages of 15-39 years) or AYAs for short. Like most, initially I had the bias that cancer in persons under the age of 50 and older than 12 rarely occurred. However, more than 72,000 AYAs learn they have cancer each year in the United States, a number up to seven times larger than the number of children under the age of 15 that are diagnosed with cancer (taken from American Cancer Society’s Facts and Figures). Cancers that are common in AYAs often are rare in the traditional adult oncology clinic—germ cell tumors, leukemias and lymphomas, melanoma, thyroid cancer, and sarcomas, but we are seeing more and more AYAs diagnosed with the more common adult cancers such as breast, colon, ovarian and prostate cancer as well. Unfortunately, AYAs face a number of unique medical issues that adults do not when seeking treatment for cancer. First and foremost, diagnosis often comes late because many physicians rarely think that an AYA displaying the signs and symptoms of cancer could actually have cancer. This alone makes treatment more difficult as cancers typically become more resistant to therapies as they advance.

In addition to receiving late diagnosis, it is becoming evident that cancers in AYAs are genetically different from those seen in either children or adults. This leads to AYA patients receiving treatments that may not be the most effective for their cancer. This is has become most evident in acute lymphoblastic leukemia (ALL) where recent clinical trials indicate that in some cases, AYA patients with ALL may have better outcomes when treated with pediatric regimens versus adult regimens. Work done by Dr. Christine Harrison of Newcastle University in the United Kingdom has shown that some AYAs with ALL have genetic changes that are typical of younger patients, whereas others have previously unknown alterations (Moorman et al., J Clinical Oncology. 2012). Another current, ongoing study done by a team lead by Dr. Cheryl Willman, director of the University of New Mexico Cancer Center, where tumor samples from 500 ALL tumors taken from children, teens, and AYAs has provided some indication that genetic differences do in fact occur in ALL based on patient age. For instance, some AYA tumors have genetic alterations that are often seen in older children with ALL who are at high risk of relapse. (AYAs and high-risk older pediatric patients tend to have worse outcomes than the vast majority of younger children with ALL.)

A similar comparative study has begun for AYAs with colorectal cancer by Dr. Anna Franklin at MD Anderson and her team of colleagues at MD Anderson and Colorado, and preliminary results from this study also indicate that genetic differences occur between tumors from AYAs versus tumors from adults. However, this phenomenon is not seen in all types of tumors affecting AYAs. For example, genetic differences were not seen in breast cancer cases even though AYAs are diagnosed with more aggressive subtype than older patients; however, the reasoning for this discrepancy is not yet fully understood. More research is needed to gain a better understanding of AYA tumor biology. These biological differences may require different treatment strategies in AYAs as compared to children or adults to achieve the best possible outcomes.

Finally, AYAs have more long-term health effects that arise from either latent cancer cells or are a side-effect of their treatment. Some of these health effects include being put at a higher risk for developing cataracts, hearing loss, chronic pain, limb amputation, hypopituitarism, loss of bone mass, and cardiac problems to name a few. Survivors of AYA cancers, like their pediatric counterparts, are also at increased risk for life-threatening problems such as second primary cancers and psychiatric issues such as post-traumatic stress disorder and depression. Unfortunately, many AYA survivors are often unaware of or underestimate their heightened risk for these late health effects; the same is true of many of the doctors and health care providers these survivors see after leaving the confines of active cancer treatment and follow-up.

The reality of AYA cancer is that this is a highly understudied field that is in need of more researchers and clinicians help fill the knowledge gaps to improve treatments for this patient group. Additionally, greater awareness amongst AYAs and physicians alike is needed so we can begin to diagnose their cancers while they are still at an early stage and the importance of realizing that AYA survivors are at a much higher risk for additional health complications later in life.

The information for this post was taken from the NCI website under their page dedicated to cancers in adolescents and young adults.

To Smoke or Not to Smoke?


Neeley Remmers

As I mentioned in my previous post, November is cancer awareness month and in honor of this I promised to highlight different cancers each week throughout November. This week, I have decided to put the spotlight on lung cancer as this particular form has now affected my family twice. Six years ago, my grandfather, who had been a smoker for the majority of his life, died from Stage IIA lung cancer. To refresh your memory, cancers are diagnosed in stages ranging from Stage I to Stage IV based on the size of the primary tumor and degree of metastasis throughout the body. However, non-small cell lung cancer stages are a little different due to its slow-growing nature (see American Cancer Society’s webpage for more in-depth description). My grandfather had a baseball-sized primary tumor in one of his lungs, but we thought he was fortunate because they were able to completely remove the tumor and there were no detectable metastases. However, the tumor came back and he passed away 10 months after diagnosis. More recently, I have an aunt that was diagnosed with metastatic lung cancer (we are still awaiting the official diagnosis) where they were able to remove the metastatic tumor from her brain, but her primary tumor in her lungs has been deemed inoperable. Unlike my grandfather, she was never a smoker and has been relatively healthy her entire life. I’m sharing these personal instances with you because they highlight a common myth associated with lung cancer; many believe that only smokers are susceptible to getting lung cancer and are perplexed when an otherwise healthy, non-smoker is diagnosed with lung-cancer.

The reality is smoking is not the only cause for lung cancer. Repeated exposure to second-hand smoke is another big risk factor along with repeated exposure to such environmental toxins such as diesel car exhaust, radon, asbestos, etc. Basically, if you work or live in an environment where you breathe-in pollutants that your lungs are unable to remove naturally, your risk for developing lung cancer increases. There are two types of lung cancer that arise – small cell lung cancer and non-small cell lung cancer. The difference between these two types is based on the size of the cancer cell and their morphology or how they appear under a microscope. Non-small cell lung cancer (NSCLC) affects 7 of 8 patients as compared to small cell lung cancer, which affects 1 of 8 patients. NSCLC grows at a slower rate than small cell lung cancer and has a different metastatic profile in that it doesn’t spread as rapidly or broadly through the body (information taken from the NCI website). According to the American Cancer Society Facts and Figures, lung cancer is the #1 cause of cancer-related deaths in both men and women, and as you might expect the chances of survival drastically decrease as the disease progresses to metastatic disease.

Two exciting studies were published in 2012 in the New England Journal of Medicine showing how an anti-PD-L1 antibody is an effective immunotherapy strategy to treat both early-stage and advanced stage NSCLC along with other such cancers as melanoma and renal cancer (Brahmer JR et al 2012 N Engl J Med  and Topalian SL et al 2012 N Engl J Med). What makes these studies so exciting is that not only was the antibody able to effectively treat NSCLC regardless of stage, but it also worked in a number of cancer types and it was the first immunotherapeutic agent able to successfully treat NSCLC, which classically had been resistant to immunotherapy. The antibody works by binding to immune-checkpoint protein, PD-L1 (programmed death ligand 1), expressed on the surface of cancer cells thereby preventing it from binding to its receptor on T cells. The PD-1/PD-L1 pathway has been shown to negatively regulate T cell immunity by decreasing the amount of IL-2 secretion and inhibiting T cell proliferation (Carter L et al. 2002 Eur J Immuno). In cancer-bearing mice, blockade of this pathway resulted in increased anti-tumor immunity by increasing the amount of anti-tumorigenic cytokines that were secreted such as IFN-γ and IL-2 thereby reducing tumor burden (Blank C et al 2005 Cancer Res). Essentially, by blocking this pathway we are able to eliminate one method of immune evasion utilized by NSCLC. Clinical trials for this drug are currently ongoing and more information can be found on both the NCI and ACS websites.

Until the development of the PD-L1 antibody, one of the primary methods of treating NSCLC was using targeted drug therapies. There are multiple subtypes of NSCLC such as adenocarcinoma and squamous cell carcinoma that have different molecular signatures and thus respond differently to treatment. Due to this feature, predictive biomarker assays have been developed and are readily used in clinics to determine which patients exhibit mutations in either the epidermal growth factor receptor (EGFR) or anaplastic lymphoma kinase (ALK), which are involved in two major tumor-promoting signaling pathways, and the results of these tests help direct clinicians in determining the best treatment strategy. Additional tests are being developed to determine mutations in other predictive biomarkers such as BRAF, ROS1, MET and PIK3CA all of which are involved in major tumor-promoting signaling pathways and efforts are being made to synthesize agents that directly target these proteins. For information on the current status of targeted drug therapy in NSCLC, Savas P et al. recently published a comprehensive review in Journal of Thoracic Disease last month titled “Targeted therapy in lung cancer: IPASS and beyond, keeping abreast of the explosion of targeted therapies for lung cancer.

To Shave or Not to Shave?


Neeley Remmers

Last week, men all over the US put their razors and shaving cream in storage to grow out their beards and mustaches for No-shave November and bring out their inner lumberjack or Duck Dynasty. But how many people actually know the real reason for No-shave November? No-shave November was started by the American Cancer Society as a fun way to bring about cancer awareness making November officially cancer awareness month. Therefore, I’m going to dedicate my blogs this month to a different cancer or group of cancers each week. For my first entry, though, I want to take the time to discuss a little bit about the ins and outs of cancer in general since not everyone studies this disease.

First, let’s get down to some of the major molecular events that occur in cancer. In 2000, Dr. Hanahan and Dr. Weinberg published an article in Cell describing the 6 hallmarks of cancer, which include the ability to sustain proliferation, evade growth suppressors, activate invasion and metastasis, enable replicative immortality, induce angiogenesis, and evade cell death (Hanahan and Weinberg Cell 2000). These hallmarks are driven by a number of molecular events leading to genetic mutations that inactivate tumor suppressor genes and activate tumor promoting genes. The most commonly mutated genes, at least in solid tumors, are the cell cycle inhibitor p53, the oncogenic Akt kinase, and oncogenic K-ras protein. Indeed, there are literally thousands of mutations found in each cancer type; however, few of these mutations are actual drivers of oncogenesis (the process of developing cancer). In fact, only a handful of driver mutations such as those described above are actually necessary to initiate oncogenesis. The multitudes of other mutations found in cancers are referred to as passenger mutations because they play a secondary part in initiating and maintaining oncogenesis. Genetic mutations have long been the focus of cancer research, but they are not the only molecular events that occur and drive oncogenesis. In the past decade, it has become very apparent that changes in the post-translational modifications of proteins (such as changes in glycosylation, sumoylation, and ubiquitylation) and epigenetic changes (such as methylation and acetylation) to DNA also play very important roles in oncogenesis.

The literature on the molecular events behind oncogenesis of any one particular cancer is too vast to cover in this small post, but you can easily create a feed for that on the Scizzle website to read articles in any of these fields.

The events discussed above drive oncogenesis from the cancer cell; however, tumorigenesis or the formation of the tumor as a whole is more complex and involves the actions of hundreds of different cell types that surround the tumor. These cells make up what is called the tumor microenvironment. I am not going to go into much detail about the microenvironment as I wrote a post back in July called “A Lannister Always Pays His Debts,” which you can read to gain more insight into the tumor microenvironment. But I could not write a comprehensive cancer blog without at least mentioning the tumor microenvironment because it is such a huge factor in the survival of the tumor.

I’m going to change gears a bit and talk about the clinical aspect of cancer. I’m sure many of you have heard about Stage I cancer Stage IV cancer, but you know what the stages mean? Cancer staging is a method of describing the severity of one’s cancer in terms of its size and extent of its reach meaning is it localized to the site of the original tumor (primary tumor), has it metastasized to the regional lymph nodes (the lymph nodes adjacent to the primary tumor), or has it metastasized to adjacent or distant organs. The stages refer to the TNM grade of the tumor which scores the size of the primary tumor (T), number of regional lymph nodes that have metastasis (N), and number of distant metastatic sites (M). For example, Stage I breast cancer means that there is detectable tumor within the breast tissue but there likely isn’t any metastasis to either the regional lymph nodes or distant organ sites. Stage IV breast cancer indicates that the primary tumor is rather large and metastasis can be detected in a number of distant organ sites. For more information on tumor staging, you can visit the NCI’s website.

This brings me to my next topic – metastasis. We have all heard the word and immediately associate it with a sense of foreboding and rightly so. Metastasis is the process by which a cancer cell from the primary tumor detaches from the tumor, enters the lymphatics or the peripheral blood system to travel to distant organs where it can then extravasate from the blood vessels to enter the tissue bed of the distant organ. This whole process is referred to as epithelial to mesenchymal transition (EMT) as the detached cancer cell actually changes its phenotype to that of a mesenchymal cell in order to survive traveling through the blood system to reach its final destination. It’s not entirely known at this point how these cells decide which organ to invade, but there is a common theme in terms of which organs are the most frequent sites of metastasis for solid tumors. These organs include the bone, liver and lungs. The metastatic process itself is rather complicated, but the NCI has a fairly good summary page. Typically, if a patient has extensive distant metastases, they are ineligible for surgical treatment (which involves surgical removal of the tumors) and tend to have a poorer prognosis as once a tumor has gained this extensive invasive capacity, the tumors become highly resistant to therapy, which brings me to my next point of discussion: cancer treatment strategies.

Cancer therapy is constantly evolving so that we can become more effective at treating patients while limiting their discomfort. The types of therapy fall into basically 4 broad types: surgical resection, radiation, chemotherapy, and immunotherapy, which can be used singularly or (more commonly) in combination with each other. The first two are pretty self-explanatory while chemotherapy and immunotherapy are more broad and complex. Chemotherapy basically involves using a small molecule inhibitor or neutralizing antibody that blocks a specific signaling cascade. However, these types of treatments come with severe side-effects which have been pretty well advertised. Immunotherapy involves utilizing one’s own immune system to fight the tumor. In fact, when healthy, our immune system is the most effective at destroying cancer cells; that is until the cancer cell becomes smart enough to evade our immune system through various means. Thus, the concept of re-triggering the patient’s best defense mechanism to fight cancer is simple and brilliant, but not exactly easy. It has been a long struggle in this field, but recent advancements have shown that immunotherapy is effective and is part of the current surge towards personalized treatment. The NCI’s website has a plethora of information about current therapeutic options for patients involving both chemotherapy and immunotherapy and highlights some of the current publications in these fields.

New Spin on Pancreatic Cancer Diagnostics

Neeley Remmers

Recently, 15-year old Jack Andraka made national headlines for the diagnostic assay he created to detect pancreatic cancer. Before I get into discussing the science behind his assay, let me first give Jack a major shout-out for having the courage to pursue his idea in the first place. He gave a presentation of his theory to 200 professors at Johns Hopkins University, a feat that would terrify most of us even after having graduated with our PhD let alone at the age of 15. He impressed Dr. Anirban Maitra, a world-renowned pathologist and scientist in pancreatic cancer, and gained an invitation into Dr. Maitra’s lab to work on his idea. Jack’s motivation to design a diagnostic assay for pancreatic cancer because his uncle died from the disease.

For those of you who don’t know the field, there currently is no effective way to diagnose pancreatic cancer, especially when it is in its earliest stages. There are a number of reasons for this – clinical symptoms do not present themselves until the disease has progressed to metastasis at which point makes it very hard to treat, most symptoms are typically any combination of abdominal pain, back pain,  jaundice and weight loss which can be the cause of any number of diseases, and due to the anatomical position of the pancreas it is very hard to image making it difficult to use standard imaging techniques to screen for early lesions like you can with breast cancer. As you can see, the need for a blood-based or other bodily-fluid based screening test is huge to adequately diagnose pancreatic cancer. Many scientists and physicians have been diligently working on this issue for a number of years, myself included, and have generated multiple platforms to use for early diagnosis including Dr. Brian Haab’s antibody-lectin arrays (the most recent publication being Cao Z et al. Mol Cell Proteomics 2013), Dr. Clausen and Dr. Blixt’s glycopeptide arrays to detect auto-antibodies (Pedersen JW et al. Int J Cancer  2011, Blixt O et al J Proteome Res 2010), and conjugating antibodies to Qdots, sphero beads, nanotubes and other fluorescent tags. The reasoning behind conjugating the antibody that recognizes your biomarker of choice is that fluorescence provides greater sensitivity than colorimetric assays that rely on the enzymatic cleavage of DAB or ABTS, for example. All these platforms are innovative and effective in their own right, but the real trick to designing an efficacious diagnostic assay is choosing the right biomarker to detect. This is where things get messy in the field of pancreatic cancer diagnostics.

Since very few patients are diagnosed in the early stages of pancreatic cancer, there is a very limited supply of samples from the early lesions, which are called PanINs. In fact, a large portion of the PanINs actually studied were pulled out of tumors from patients that had advanced disease, so you have to be really careful with conclusions drawn from these “PanINs” since we don’t know if they behave the same as true PanINs that arise prior to malignancy. Therefore, at this point in time, we are limited to studying the vast number of secreted proteins that can be found in blood, plasma, or urine of advanced pancreatic cancer patients. There are a limited number of studies (I know of 2 done in the UK) where blood samples were collected from patients over 20+ years in which a portion of these patients developed pancreatic cancer, and these samples are available for use in retrospective studies to see if the protein chosen to be used as a biomarker for pancreatic cancer is found in these patients early on when they would have presumably had early-stage disease. As you can see, there are a lot of challenges in this field that can make it rather daunting, and more often than not the biomarkers chosen to be used for diagnosis end up failing.

What did Jack Andraka do, other than being a 15-year old studying this challenging field, to make such a splash in the headlines? The platform Jack designed is unique in that he chose to attach his nanotube-conjugated antibodies to nothing other than filter paper making his platform the cheapest one yet. The biomarker he has chosen to detect in the bodily-fluids from patients is mesothelin. Mesothelin has been investigated as a potential biomarker of pancreatic cancer since at least 2004, but has yet to be shown to truly be better than all the other potential pancreatic cancer biomarkers. Jack’s test is still in preliminary stages so we have yet to see how efficacious it really is at diagnosing pancreatic cancer early on. Additionally, utilizing nanotubes conjugated to antibodies is not new either. In fact, a student in one of our collaborating labs at my university was doing the exact same thing 5 years ago; however, because we did not have an instrument on campus that would allow him to detect the nanotubes, he had to drop the project. What does make Jack’s platform unique is he linked his nanotubes to nothing more than filter paper instead of a more expensive spotted plate making his assay the cheapest one yet. The biggest flaw in Jack’s design is that it relies entirely on the detection of a single biomarker. It is pretty well-known and accepted in the field that in order to have a highly specific, effective diagnostic test you need to assay for a panel of established biomarkers that can distinguish pancreatic cancer from other benign and malignant diseases. Thus, he may need to go back to the drawing board to determine which panel of biomarkers perform the best in detecting pancreatic cancer. However, I do think his platform shows promise and will soon turn into a clinically useful early diagnostic assay.


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Who Was Stung – Open Access or Peer-Review?

Neeley Remmers

You may have noticed this week that the Science world is abuzz with talk about Open Access Journals and the dangers of publishing in these journals versus traditional. The debate about whether or not to publish in Open Access journals is not new, but the debate has escalated due to the sting article published in Science written by John Bohannon. After reading the article, instead of questioning the credibility of Open Access Journals I was left questioning the failed peer review process that resulted in the acceptance of the fake articles. If you are unaware of the controversy behind the Open Access movement, here is a brief synopsis. As you may have noticed, online publishing is the hottest thing since sliced bread in the world of publication (just think of the huge sales brought in by the invention of tablets and e-readers). This has led to the creation of online scientific journals that earn a profit through authorship fees rather than relying on subscription fees like most magazines, and they publish their articles online so that the general public can read them for free. Those who favor traditional magazines (think Science, Nature, Cell) that require an active subscription or require you to purchase the article before you can read it, claim that the Open Access movement has led to the increased publication of poor-quality science. Some take it even further to say that by publishing in Open Access journals, you effectively drive your career into the dumpster as these journals are a “dumping-ground” for articles that are rejected at the “more prestigious” traditional journals.

Personally, I commend the Open Access movement for making research articles more readily available. I cannot count the number of times I would run into a road block with literature searches because my library did not have a subscription to a journal that published an article that had useful information for my projects. And let’s face it, unless you are a full-time professor with a couple R01 grants supporting your salary, it simply isn’t feasible for most to pay $30+ for an article that may or may not be entirely useful for your project.

Getting back to the sting, here is a brief summary of what went down for those who have not read the article yet. Bohannon composed an article containing data so inaccurate he claimed that anyone with a high school level knowledge of chemistry could recognize the lack of scientific soundness. He chose to submit this falsified paper to over 300 Open Access journals where just over 50% of the journals accepted the paper after asking for trivial revisions. In an article written by Curt Rice reflecting on this sting, you will find a more in-depth explanation of the sting itself and Open Access movement than what I provided here, a look into the peer review system, the corruption that comes with heightened pressure to publish, and flaws with the current publication process. Rice points out that what this sting really brings to light is the corruption that has ensued in the last few years in publishing by charging overpriced author fees, which can be seen in both Open Access and traditional journals, and the flaws in the current peer-review system that allows bad science to get published and how all journals are vulnerable to this. This in turn, is in-part facilitated by the increased pressure on scientists to publish and increased work-load of reviewers struggling to keep up (see Celine’s recent blog for more thoughts on the current state of scientific communication).

Personally, I agree with Rice in that this sting does not point a bad finger at Open Access (even though it was written in that context), but rather points out the flaws in the current scientific publication system and calls for changes to be made. Moral of the story, this sting really enforces the practice of critically reading articles to evaluate their scientific soundness on your own before accepting the results and conclusions

Taking the Reigns - Part II

Neeley Remmers

In the previous post we discussed why knowing your type is so important, in this post we'll discuss how  knowing your personality traits and that of your mentor help improve your mentorship? Let me go back to the workshop I attended this summer. For each personality pair, we the participants divided into the categories we fell into, and as we went through each pairing we went through a series of exercises that helped us teach each other why we act the way we do and how we can bridge the communication gap between the dividing personality traits. I found out that I am an ENTP or I’m an extroverted, intuitive, thinking perceiver. As an extrovert, I learned that introverts prefer to communicate via email, want us extroverts to come to meetings more prepared, and simply to shut-up and listen every now and then. Now, think about what personality trait your mentor might have. Perhaps you, like me, are extroverted while your mentor is introverted. The best way to begin communication with your mentor to discuss your project would be to first email them to set up an appointment (that is if you don’t have regularly scheduled individual meetings with your mentor, in which case you should be active in frequently setting up meetings with them on a weekly or every-other week basis). In this email, give them an idea of what you want to discuss by sending them either an outline or experimental plan that you want to pursue for your project. At the meeting, print off a copy of your experimental plan, data, etc so you can stay on topic and have an effective meeting. This same approach works wonderfully if your mentor is extroverted as well because it gives him/her direction to prevent him/her from going off on random tangents and getting completely off subject. Now say that you are a sensor (in which statistics will be an ideal area for you!) whereas your mentor is intuitive. You likely get frustrated when talking with your mentor because they tend to look at the bigger picture and leave out the little steps and details that help you get to the big picture. This is where you will need to use your communication skills to draw them back to remember you need help drawing out the experiments that will ultimately allow you to answer the big picture question. In my opinion, the next personality pair thinking versus feeling can have a major effect on your relationship with your mentor, especially if you two are on opposite sides of the spectrum. Studies presented to us at the MBTI workshop I attended showed an overwhelming majority of scientists are thinkers, and if you are a feeler you can begin to see where this may cause some major problems between you and your mentor. If this is the case, my best advice to you is to remember that if at any point in your interactions it seems as if your mentor is personally attacking you, remember that he/she is not. They treat everyone in the lab the same way (if they are a thinker) and that any harsh judgment IS NOT a reflection on you as a person, but instead they are criticizing your work. Yes, they recognize you have worked hard to get the data you have, but just keep in mind that sometimes the data simply doesn’t fall in line with your hypothesis and projects fail. After all, about 90% of science is about failure and you learn more from failing than you do from succeeding. A tough fact to swallow, but perhaps that is why so many scientists are thinkers or have adapted to become thinkers.  Finally, if your mentor is a hard-core perceiver meaning they leave everything to the last minute, the best advice I can give you is to remember that your mentor will edit your fellowship in time for you to submit it even though he/she may get it back to you with one hour to spare. It may be good policy to start telling them deadlines are a few days earlier than they actually are so you don’t have to be up all night putting the finishing touches on a proposal and hitting the submission button with 59 seconds before the call closes.

I have given you a lot to think about, but if you can derive anything from this post I hope it is this: be more active in your mentorship, you have more control in your relationship with your mentor than you may think. Be forthcoming with your expectations of your mentor, actively set up regular meetings if your mentor doesn’t already hold that policy, and clear communication on both your parts is key to getting everything you need from your mentor to help you become a quality scientist. Mentoring, like any relationship, is a two-way street and its effectiveness is dependent on both parties involved.

Taking the Reigns - Part I

Neeley Remmers

Today I’m going to talk about a topic that affects everyone – from graduate students to post-docs to mentors. Mentoring. Mentoring is a key component in developing new scientists, yet as scientists embark on the faculty career pathway, no one takes the time to really teach effective mentorship even though this will become a significant aspect of one’s career as they develop into a primary investigator. Instead, the common theme throughout scientific history has simply been to train young scientists into clones that resemble their mentors. However, in today’s scientific world, we now have more scientists than ever before thanks to the increase in funding and admittance into graduate programs seen in the earlier part of this millennium and unfortunately, simply training young scientists to become clones of their mentors is no longer an effective mentoring strategy as there are many different job opportunities available for scientists today aside from the standard academic route.

Fortunately, there are scientists out there who are studying effective mentoring strategies and are trying to put together resources to teach effective mentoring strategies, but until this becomes an integral part in training young scientists, we as students and post-docs all are going to have to take a more active role our mentorship. After all, our mentors are only human and unfortunately lack the skill to read our minds to find out what kind of help we need and what is the best way to help each of us. The number one tool that can make an immediate impact in improving your relationship with your mentor is effective communication. However, before we get into effective communication strategies, we need to take a step back to be sure we first understand our own personalities, goals, and the personality of our mentor.

A couple weeks ago, I wrote a blog describing the many careers available to scientists and utilizing the MyIDP tool created by Science Careers. First, I highly recommend you make use of this tool so you can begin to visualize the career path you want to make for yourself. Once you know what area of science you want to build your career, you need to do a little research to find out what you can do while still in graduate school or your first post-doc position that can set you up to get an introductory position in that field. Once you have a plan worked out, you then should convey your career goals with your mentor so they can help you attain your goals in any way they can because regardless of what you may currently believe, your mentor really wants you to succeed…even if they use “tough love” to show it.

Now that you have completed step one and defined a career path, now it’s time to learn about your personality traits and how this may affect your communication skills with others and your success in the workforce. A very good tool for this is to take the Myers-Briggs personality test. This is not a test you can simply do online by yourself, but you need to either contact a MBTI center or suggest to your GSA or post-doc society to hold a workshop by a MBTI professional to administer the test and explain each of the personality traits. I recently attended one and it was like a HUGE lightbulb went off in my head. I was able to easily recognize the traits that applied to me, my mentor, and my colleagues and learned skills to better communicate with people who had opposite traits as me. Before I go farther, let me briefly explain the personality traits central to the MBTI personality types. There are four personality pairs: extroversion and introversion, intuition and sensing, thinking and feeling, and judging and perceiving. First, it is essential that I state that these personality traits are considered to be preferences meaning at this stage in your life you might test to be an introvert, but as you grow over the next 5 years your preferences may change to make you more of an extrovert. Additionally, you might always remain an introvert in nature; however, you may develop the skills of an extrovert to help you in certain situations. The easiest to understand is the first pair – extroversion and introversion – describes how one derives their energy and interacts with the world. As you can imagine, extroverts love to socialize with others, prefer to be around other people, and derive their energy from social interactions whereas an introvert gets their energy from being left alone to think things through. The second pair – intuition and sensing – relates to how one takes in information. For example, a sensor will look at an abstract picture and focus on the details that they can see within the picture whereas someone who is intuitive will look for hidden meanings and tends to think in terms of seeing the bigger picture. The third pair – thinking and feeling – relates to how you make decisions. A thinker relies on the facts regardless of the specific situation whereas a feeler treats each situation differently. For example, in terms of mentorship, a thinking mentor will treat everyone the same way whereas a feeling mentor will look at each person in their lab individually and tailor their interactions to each individual’s personality. The last pair – judging and perceiving – relate to how you live your outer life. For example, when planning a vacation, a judger will make a detailed itinerary listing what you will do each day and leave no room for spontaneity whereas the only plans a perceiver will make is to book the plane tickets and accommodations in advance and determine what they want to do each day as the day comes. For more thorough definitions of each personality trait, please visit the Myers Briggs Foundation website at:

In the next post, I'll discuss how knowing your personality traits can help you improve your mentorship.

Piled Higher and Deeper: Bioinformatics

Neeley Remmers

I was perusing the table of contents of the current issue of Clinical Cancer Research, and saw an abstract for a paper entitled “Uncovering the Molecular Secrets of Inflammatory Breast Cancer Biology: An Integrated Analysis of Three Distinct Affymetrix Gene Expression Datasets” by Steven J Van Laere  et al. This particular paper looks at molecular signatures distinct to inflammatory breast cancer (IBC) by means of analyzing Affymetrix microarray data from 137 patients compared to 232 control patients that did not have IBC. After doing a lot of data mining with the help of the PAM50 algorithm, they did find a molecular signature unique to IBC versus normal patients though they would need to do similar comparisons to other forms of breast cancer to see if there are distinctions that set them apart. My initial reaction after reading this abstract and seeing how many patients they had to analyze and compare was a sense of being overwhelmed. In order to do clinical or translational research, you have to work with these large data sets to account for all the many variances that come with studying human samples, which means you also need to have a good understanding of and willingness to do bioinformatics.

Personally, I think it takes a special kind of person to do bioinformatics and, for that matter, biostatistics. If you are fortunate enough to work in an institution that has a bioinformatics and biostatistics core, consider yourself lucky. I recently have been honing my bioinformatics skills by analyzing RNA-sequencing data trying to figure out which activation and chemotaxis pathways in leukocytes are turned on upon treating them with my protein of interest. I had an appreciation for those who make a living in this field, but after countless hours in front of my computer creating different gene lists and analyzing them with Ingenuity I have an even greater appreciation for what bioinformaticians and biostatisticians do. My brain was not wired to understand or generate the many algorithms now available to help us perform these complex analyses and generate the statistics needed to validate the findings, but I applaud those who can. Personally, I think there should be a national bioinformatician/biostatistician appreciation day.

Using Your Spidey-Sense to Network

Neeley Remmers

As I am going through the process of solidifying my first position post-graduation, I am realizing more and more the value of networking. I had always had a general appreciation for networking even during undergraduate school and knew that in the professional world, the success of your career can be influenced by knowing the right people. In fact, I used networking to get my two internships in the pharmaceutical industry while still in undergrad.  Thanks to my undergraduate advisor having ingrained in me the importance of networking, I knew the importance of making an impact when meeting people for the first time at the various conferences I attended throughout my graduate career. I also jumped at the opportunity to take invited speakers to breakfast, dinners, or lunches, even if their research area was outside my interests, Read more

5 Ways to Make the Most Out of Your Grad School Experience

Welcome to grad school, you are on your way to adding 3 magical letters at the end of your name. As we'd like y'all to start well-informed and be prepared, our brilliant contributors share their wisdom and best advice on making the most our of your grad school (and beyond) experience!

That's our top 5:

  1. Run while you still can! Just kidding....
  2. Learn new things and learn all the time and it will all come together at the end, we promise!
  3. Take a careful look of the PI personality and lab's dynamics when choosing a lab.
  4. Keep it balanced, as in stay healthy!
  5. Diversify your experience at the bench and beyond it.

Now read on:Read more