When being mean is actually being nice ... and when it is just being mean

It's a harsh world in here, in academia. We all already know that academic science is not a carebear teaparty, and apparently now things are worse than ever as far as potential jobs for Ph.D.s and funding goes. 

A brief interruption, for an ad:

Use Grammarly's plagiarism checker online because it's better to have a computer criticize you than a person.

 And now back to your regularly scheduled blogramming.

Scicurious has a great post up at Neurotic Physiology about what it is like to be out in the 'real world' and out of academia. She has some fascinating points about how academia has skewed her perspective on things, but one in particular jumped out at me: That now she has to re-learn how to take criticism.

Scicurious says:

"I remember a time when I took criticism well. I did a lot of theater and music, it was something you HAD to take well. I took it, I improved, worked harder, fixed things, and did better. Sometime during grad school, however, criticism began to paralyze me. Every critique felt like a critique of me, as a scientist. Since a scientist was what I WAS, all criticism began to feel like criticism of me, as a person. Sometimes it was indeed phrased that way. You are careless. You are not smart enough, why don't you get this?! You are not focused."

This got me thinking because, honestly, I feel exactly the opposite. I think I learned how to take criticism in grad school partly by learning how to give it.

It's for your own good! (source)

When I am editing a paper or grant for someone, I am trying to help them. The more critical I am the better their paper/grant will be. The paper is headed to peer-review which will determine whether it gets published or not , and the grant is headed to a study section which decides whether it gets funded. Both are grueling and rigorous examinations of quality and scientific merit. These review processes are so important because published papers and funded grants are 'science currency' and will determine your future. In some cases the funding status of a grant can determine whether a lab stays open or a PI gets tenure.

If there is a paragraph that doesn't make sense, or (gasp) a typo, it is obviously better for me to catch it than for someone important to see it and get confused or frustrated.

Understanding this concept, that constructive criticism is the nicest thing a scientist can do for another scientist taught me to take criticism much better than I had previously. I was one of those students who was always 'better enough' than the other students that teachers rarely bothered to push me to true excellence. So I was really not used to criticism, and the initial slings and arrows in graduate school did sting. However at one point it really sunk in that these criticisms were making me better... better at everything: writing, presenting, scientific thinking. 

So that is when being mean is actually being nice.

That said, I never had anyone tell me I wasn't 'smart enough' as Scicurious says. Just because constructive and thorough critique can sound mean, but actually be nice, doesn't mean that there is no such thing as 'meanness' in academia.

Sometimes being mean is really just being mean. A criticism that does not help me improve in any way is just mean. 'you are not smart enough to be a scientist' does not help anyone be a better scientist. It is a completely different kind of criticism than 'you really need to read more about X because you don't understand how X works.' Both are directed at 'you' personally, but one says you can't do it and the other says you can do it and even suggests how you can do it.


© TheCellularScale

Scientizing Art

I've always been fascinated with the way the eye moves around a piece of art.

Andrew Wyeth's "Christina's World" (or as I looked up "that painting of a girl in a field looking at a house")

This piece by Andrew Wyeth is an obvious example of an artist completely controlling your gaze. There are pretty much no options here. You look at the girl and then you follow her gaze to the house. You probably then take a quick glance at that other house/barn to the left, and then maybe follow the edge of the light circle around the houses. (It's my opinion that that is how the eye should go on this painting, but I have no eye tracking data to support it.)

A paper last year in PLoS One really tries to "scientize' this process by testing what factors determine the eye movements, and the 'clusters' where the eye tended to fall. Massaro et al., (2012) compare dynamic and static images and images that contain human subjects or nature subjects. Their cluster analysis overlaying classic paintings makes for quite interesting images:

The next installment at MoMA

This one is a dynamic human image. Each patch of color shows where the parts of the painting where the eye lingers (face, hands, ....crotch...). The authors do all sorts of interesting analysis on this and other paintings, having participants rate the painting for 'movement' or for 'aesthetic value' and since the paper is open access, it is free to people who may not have university access to journal publications. Anyone can read the whole thing here.

One interesting thing that the authors find is that pictures containing humans have fewer clusters than pictures of nature. I expect this is because certain aspects of humans (faces, hands ...crotches...) are so salient and the brain focuses directly on them, while all the branches of a tree for example have about equal 'meaning' for a person.

science creates modern art

 Another great image from this paper. The authors show how much gazing was done at different parts of a painting through a heat map. This one is a human static image. The end result is actually quite haunting because the place that you want to look is blanked out (sort of like a Magritte painting).

So here are my questions: If someone looks at a blank page, where does their eye naturally go? Is there some sort of common pattern that most people use just to scan an area? Do chimpanzees use a similar pattern to scan a blank page? Does everyone have their own unique scanning pattern? Or is it just pretty much random? 

And here's an idea for artists: Buy yourself an eye tracker and have customers come use it and stare at a blank page. Trace their eye movements and then create a dynamic painting (or T-shirt, or napkin drawing) that follows the person's natural scanning patterns. This would be the ultimate in commissioned custom art! (Then give me one for free, because I think this sounds like fun.)

© TheCellularScale


Massaro D, Savazzi F, Di Dio C, Freedberg D, Gallese V, Gilli G, & Marchetti A (2012). When art moves the eyes: a behavioral and eye-tracking study. PloS one, 7 (5) PMID: 22624007

SfN Neuroblogging 2012: Implicit and Explicit Gender Bias

Today I am going to talk about just one thing rather than poster highlights from the whole day.
As always, all the SfN Neuroblogging posts can be found here. Other posts on gender and neurosexism can be found here.

Today was the annual "Celebration of Women in Neuroscience Luncheon." This is one of the highlights of SfN for me each year. There is always a fantastic speaker (Phyllis Wise this year) and the lunch is delicious.

Phyllis Wise brought up the 'exact same resume study' in her speech and it got me thinking. The 'exact same resume' study is where researchers construct a fake person and write up their resume, and then submit it in application for various jobs. However, sometimes they put a woman's name at the top and sometimes they put a man's name at the top. 

The study found that the male names received more and higher paying job offers and were judged to be more qualified. And it wasn't just that men thought women less capable. The females who judged the resumes were just as biased as the males who judged resumes. This is pretty depressing. I mean this isn't the middle ages, or even the Victorian era, aren't we past this bias?

But that's exactly the problem. We think we are past this bias. Even though people (both women and men) don't think they have a bias, they actually do. Even you. Just like you probably think you are smarter than average, or a better driver than average, you also probably think that you are less biased than average. That. is. the. problem. People have an implicit bias towards thinking men are smarter, better and more capable even when faced with the exact same description of the person. And they don't acknowledge this bias.

How can you combat or fix a bias that people don't even think they have? A gender blind resume process could be implemented in the initial application process for a jobs. But as soon as the applicant arrives for an interview, the gender bias would rear its ugly head. Should faculty or hiring committees develop an explicit bias towards women in their hiring and salary negotiation process?

I do not know the answer to this question. I can't think of a better way to combat implicit bias than with explicit bias, but it's hard to argue that implementing an explicit bias is 'fair' (It is a bias after all). It would especially seem unfair to those who don't think that they are implicitly biased (which we have established is basically everyone). But is there a fair way to handle this problem?

UPDATE (10/19/12): Thank you to Dario Maestripieri for helping me think about this problem in a new way. Perhaps the best way to start addressing an implicit bias is to make it explicit. When someone makes an idiotic or sexist comment, it should be made public. When someone gets grabby, it should be made public. The whole point of this post is that one of the biggest problems with gender bias in science is that people don't believe it is there. If it is made clear that it is there, people can more easily fight against it.

© TheCellularScale

Moss-Racusin CA, Dovidio JF, Brescoll VL, Graham MJ, & Handelsman J (2012). Science faculty's subtle gender biases favor male students. Proceedings of the National Academy of Sciences of the United States of America, 109 (41), 16474-9 PMID: 22988126

SfN Neuroblogging 2012: ketamine in neurogenesis and dopamine in obesity

SfN day 3, exhaustion setting in, but the science doesn't quit! Here are some highlights:

ketamine for depression? (source) 

1. Ketamine and the neurogenesis theory of depression. At a nice poster (324.28) R.M. Carter explained that ketamine has fast anti-depressant effects. Some people think that depression is caused by neurodegeneration and cured by neurogenesis (the growth of new neurons). So this group wanted to test whether ketamine could affect the growth of new neurons on the same timescale that ketamine affects depression (a few hours). And it does! Ketamine increased the rate that newly generated neurons in the dentate gyrus became synaptically mature. It will be interesting to see where this theory of depression goes. I would love to see a possible mechanism of action by which an NMDA antagonist could speed up neuron maturity. (Intuitively I would guess it would do the opposite.)

UPDATE 11/5/12: More on mechanisms of ketamine in synaptogenesis.

2. Fat and dopamine. In a nanosymposium (420.06) J. Carlin explained that rats fed a high fat diet from birth had lower dopamine than controls. This goes along with the idea that obesity can be related to a lower sensitivity to reward. The good news is that when the rats were put on a normal diet, the dopamine went back to normal. HOWEVER, this was only true for the males! The female rats did not go back to normal dopamine levels. Yikes, right? Carlin explained that maybe the females do go back to normal dopamine, but just not within the time frame that they tested. As always, more research is necessary.

© TheCellularScale

SfN Neuroblogging 2012: drunk birds, worms, and robot noses

After a distressing night of not having wifi in my hotel, I am finally able to put this post up.  All of the previous "SfN Neuroblogging" posts can be found here.

And now 3 more highlights from day 2 of SfN:

a bird and his beer (source)

1. Can songbirds be a good model organism in which to study the effects of alcohol? Well yes and no. A poster (207.14), presented by C.R. Olson explains that songbirds don't seem to get addicted to alcohol, so they might not make good subjects for alcoholism studies. But alcohol does effect their song learning. Basically when low levels (below the legal human driving limit) of alcohol were maintained in the songbird's bloodstream while the bird was learning its song, the bird crystallized its song earlier.  That is it stopped practicing and settled on a song faster that the sober birds. The meaning of this is still unclear, as the researchers still need to analyze how 'good' the songs are.

2. What can worms tell us about the relationship between voltage and calcium?  A poster (174.03) directly compared a voltage sensitive dye to a calcium sensitive dye it the C. Elegans nematode. H. Shidara's poster explains that the calcium and voltage signals in the AIY neuron do not necessarily correspond. When the voltage was elevated in the soma and dendrites, the calcium was really only elevated in the dendrites, not the soma. I didn't quite catch the putative explanation for this from the researchers, but I suspect the huge surface to volume difference in a cell body compared to a dendrite might have a strong effect on the calcium dye, but not the voltage dye.

3. Finally, a poster (174.06) explains a new method for making an odor sensor. C. Pickford explains that the drosophila larva (commonly referred to as a maggot) has only so many odor receptors but can detect gazillions of different odors (I don't have the exact numbers here). So basically he is trying to make an odor sensor modeled off of the actual larva nose. This would serve two main purposes: 1. to create an odor sensor that can sense many odors and 2. to actually understand how the larva might be processing the information from its few odor receptors to detect many scents. 

© TheCellularScale

SfN Neuroblogging 2012: weird receptors

Day 2 of SfN was so packed with awesome science that I have too much to blog about.

here are two highlights:

NMDA receptor (source)

1. A great special lecture by C. Luscher about drugs and synaptic plasticity introduced me to the concept of a calcium impermeable NMDA receptor. As far as I was concerned, calcium permeability was a defining characteristic of the NMDA receptor. Luscher explained that after cocaine exposure (I don't remember how much or how long an exposure), there was a shift in AMPA receptor type from calcium impermeable to permeable. AND a corresponding shift in NMDA recepter type from calcium permeable to impermeable.

2. A poster (236.14) presented by M. Markham on the weakly electric fish introduced me to the sodium activated potassium channel. I was familiar with calcium activated potassium channels, but a sodium activated potassium channel allows the action potential in the electric fish to repolarize super quickly to facilitate very high frequency firing.  Other species of electric fish do not have these channels and do not use such high frequencies.
But here's the really interesting thing: People (and mammals in general) do have these channels (236.17). In fact a mutation in this channel in humans leads to serious serious central nervous system problems.
And here is the even more interesting part. In humans these channels aren't used to create super fast firing frequencies. It is more likely that they trigger essential intracellular signaling cascades.

UPDATE 11/13/12: for more on the sodium-activated potassium channels (SLICK and SLACK) and how they help the auditory system fire precisely, see this new post.

Again, more details will follow SfN and I will post more highlights from today tomorrow.

© TheCellularScale

SfN neuroblogging 2012: confusion, dopamine, and gay rats

First poster session of SfN. Here are the 3 highlights:

You use too many of them. (source)

1. The worst poster ever. No graphs only words (well one picture of a whole brain) and TABLES! Oh the tables that should have been graphs! But it wasn't just the layout, the presentation was rambly and confusing. I gave them a fair chance to explain their work, asking more than once "what is the main point?" And when they finally got to the point, I said "oh, I see. I didn't get [the main point] until just now." But instead of realizing that the presentation was unclear, they made a bad joke about how neurotransmitter x must not have been working in my brain. um no, just no.

2. Dopamine neurons might not only release dopamine, new research from the Sabatini lab at Harvard suggests that they also release GABA, the main inhibitory neurotransmitter in the brain. This has interesting implications for Parkinson's Disease because the dopamine neurons die. Instead of only thinking about dopamine imbalances, maybe researchers should investigate GABA imbalances in PD.

 UPDATE 10/28/12: Here is a more detailed look at dopamine and GABA

3. Turning rats gay. you heard me right. A group in Mexico can make a male rat gay for another male rat by injecting him with a dopamine D2 agonist Quinpirole when he is around the other male. Eventually the quin-treated male will prefer the  other male even over a 'receptive' female.
The poster I went to today was presenting an extension of this research, inducing same-sex preference in females. This requires oxytocin in addition to quinpirole.
I didn't get a chance to ask about the further implications for this research because the poster was pretty well attended. mostly by young men.

UPDATE 10/23/12: Here is a more detailed look at turning rats gay.

I will post a more detailed analysis of both of these studies after SfN is over. As I've said already, I'll post brief summaries of the daily highlights, and more in-depth posts later.

© TheCellularScale

SfN Neuroblogging 2012: unofficial rules

SfN gives some official rules for presenting posters. These are great and all, but there are some unofficial rules that you should follow as well.

Poster presenting should look like this (source)

Here are the official rules from the SfN website.

• Poster Dimensions Authors scheduled in poster sessions are assigned posterboard space (six feet wide x four feet high or 1.8 m x 1.2 m) for displaying illustrative material (graphs, charts, and tables). Posters cannot exceed these dimensions.
• E-mail Confirmation Authors will receive e-mail confirmation listing session title, session date, and location in late June. Authors will receive another e-mail with board numbers and presentation times in late July. This e-mail will also ask presenters for audiovisual equipment requests.
• Author Presence Presenters are required at poster boards during a scheduled one-hour presentation time, and posters are to be mounted for the duration of a four-hour poster session. No presentation may be given by an individual who is not an author on the abstract.
• Photography
  Photography is prohibited on the poster floor.

And here are some unofficial rules:

• Be at your poster the whole time: They say you only need to be there during the one hour that you are scheduled, but it's a good idea to be there basically the whole time. If there really are posters you want to see during your 4 hour poster-slot, then have a co-author stay by your poster during that time. If you're lucky, you will be talking non-stop for the full four hours, and won't have time to even think about leaving.

• Groom yourself: Nothing makes me want to get away from a poster faster that BAD BREATH. You don't need to look like a supermodel and you certainly don't need to wear a suit. But please brush your teeth, and then when you have that all important mid-morning coffee, chew some gum for a minute afterwards (then spit it out, because you don't want to smacking gum in someone's face either).

• Engage your audience: If some one stares at your poster for more than 30 seconds, say something to them.  "Would you like me to take you through it?" or "Do you have any questions?" are perfectly fine things to say. If they say no, then let them read the poster. Though it's their loss. 

• Don't waste your audience's time: If there are only one or two people at a time at your poster, ask them about themselves. "Are you familiar with grid cells?" or "Do you know how the striatum works?" are a great way to get a feel for what you should be telling them. You might have someone who barely knows anything about neuroscience, and for them you should start simple. But it is equally likely that you will be talking to some experts in your field. They will only want to know the newest most interesting aspect of your project. And they are probably busy and don't want to spend more than 5 minutes hearing about your poster. You shouldn't start explaining that a neuron is a cell in your brain to these people.

© TheCellularScale

SfN Neuroblogging 2012: Preparation

So you are going to a big scientific conference, congratulations!

Maybe you are going for the very first time and not presenting anything.  Maybe you are presenting your very own first author poster for the first time.  Maybe you are presenting yet another small update in your ongoing project. Maybe you are presenting a nanosymposiom or minisymposium talk. Maybe you are a PI and have a whole labs worth of posters presented by your students and post-docs. 

Whatever your situation, you need to do some preparation. 


for N00Bs:

If you are just attending the meeting, but not presenting anything, you need to do some pre-planning to get the most out of the conference. We are basically talking about the Society for Neuroscience annual meeting here.  And this conference is HUGE.

There are a ton of presentations and you literally cannot see them all (probably not even a quarter of them). So you have to do some preparation.  You can use the SfN meeting planner to search for topics you want to read about and to make an itinerary. You can also use the Hubbian app (http://hacksfn.org/) to browse abstracts and plan your SfN schedule. 

The absolute worst way to 'do SfN' is to just walk through the posters stopping at whichever ones catch your eye. You will miss the ones you are interested in, and will waste a lot of time.


for the poster presenter:

So you are presenting a poster. You are probably (hopefully)  finished or almost finished creating it at this point in time. If you are still working out the layout, you might want to check out Dr. Zen's blog Better Posters. It gives some helpful insights into those important questions like 'what font should I use?' and 'where should my acknowledgements go?'

Now after your poster is made, you will want to practice actually presenting it.  You can do this alone, just going through the explanation of what you did and why you did it. Or you can present the poster to an actual person. This is a better option because then you can get some feedback and practice answering their questions. But no matter what, PRACTICE your poster presentation.

You took so much time and effort to collect the data, run the simulations, analyze everything and layout out your poster. But all that work will be basically for nothing if you can't quickly and concisely communicate your results. You don't want 'Dr. Big Shot' leaving your poster confused and irritated because she couldn't understand the jumble of words you were throwing at her. 


for those presenting a talk:

It's more obvious to people that they need to practice a talk than that they need to practice the poster presentation. But there are a lot of bad presentations out there, and there is a lot of good advice online. I have proposed one single golden rule for presentations, but others have gone into much greater detail. I highly recommend Scicurious's "And Now, A Powerpoint Presentation" for some excellent tips on presenting scientific findings at a conference. 


For the lab head: (PI):

Not being a PI myself, I turned to twitter, asking 'What is the main role for a PI at a scientific conference?'

It basically came down to:

1. Communicate your research as a whole, as in: "Tell your lab's science story" (@Oldsjames) or "talk up lab work" (@GertyZ)

2. Networking, as in: "being the honey bee in the pollen-rich garden" (@neuropolarbear)

3. Help your students out, as in: "Introducing peeps to folks" (@GertyZ) or "pay for lab dinner" (@jsnsndr)

You also might want to take a stroll down 'NIH row' to do some schmoozing as recommended by Drugmonkey. 

So there you have it, tips for SfN attendees at all levels. Now go prepare, people!

© TheCellularScale

SfN Neuroblogging 2012: Introduction

SfN

The Cellular Scale is one of the official NeuroBloggers of the Society for Neuroscience annual meeting this year. You might have some questions, so let me answer them:

What is the Society for Neuroscience meeting?

The Society for Neuroscience annual meeting is the biggest neuroscience conference ever.  It is attended by about 30,000 people each year, and there are about 20,000 presentations (including posters).  It's like a gigantic science fair. 

one tiny corner of SfN

How often will I be blogging?

I am planning to post at least once a day about interesting posters or talks I see or events I attend during the actual meeting (October 13th-17th). These posts won't be super in-depth in terms of the science, but I plan to write a whole bunch of follow up posts after the meeting delving deeper into the most interesting science.

What will I be blogging about? 

SfN is divided up into themes. I don't know about you, but I have never put much thought into the 'theme' I wanted to visit during the meeting. In fact I am not quite certain which theme my own poster is in.  But regardless, the official bloggers are also organized by theme and The Cellular Scale will be covering themes B and D.

Theme B: Neural Excitability, Synapses, and Glia: Cellular Mechanisms.
   This is a good match for this blog because I've already discussed many of the sub-topics in this theme, such as synaptic plasticity, glia-neuronal interactions, and other weird things about cells.

Theme D: Sensory and Motor Systems
    This is also a good match because I love to blog about the senses at a cellular level. See these links for posts about the cells involved in vision, hearing, taste and smell.

So these themes are what I am 'officially' covering, but I plan to blog about the most interesting science even if it falls under another category.

What else?

I am going to index all the "SfN Neuroblogging" posts in a tab at the top of the page so you can easily get to all of them.

I will also be tweeting the meeting as they say, so follow me @cellularscale on twitter for up-to-the-minute updates.

If you have any questions that I didn't answer here, add a comment and I will try to answer it.

© TheCellularScale

A little stress goes a long way

.... toward preventing PTSD symptoms.

Post Traumatic Stress Disorder

This may surprise you as the S in PTSD stands for STRESS.  How on earth could stress prevent it? But you heard correctly. A new paper by Rao et al., (2012) from Biological Psychiatry shows that a little stress in the form of glucocorticoids, prior to an acute stress event actually prevents PTSD-like symptoms in rats.

First of all how do you tell if a rat has PTSD?
This study uses two measures: one behavioral and one cellular.

To test anxiety in a rat, you can put in on an Elevated Plus Maze (EPM). Rats don't love heights, and they do love dark corners. But, they are also somewhat naturally curious. The EPM makes use of these rat characteristics to test how anxious the rat is.

Elevated Plus Maze (source)

The EPM has four arms, two are open (but far enough off the ground that the rat can't just step off the maze) and two are enclosed with walls. Normal rats tend to explore all the arms of the maze roughly equally, but anxious rats tend to strongly avoid the open arms. The amount of time spent in the open arm area is a generally accepted measure of how anxious the rat is.

An earlier paper from the same lab, found that rats who had undergone the single stress event were more anxious (spent less time in the open arms of the EPM) 10 days after the event, but NOT 1 day after the event.  The single event stress and the delay of symptom onset are why this study is more relevant for PTSD than for chronic stress. 

Rao et al., 2012 Fig 4B

As interesting as the behavioral experiments are, the cellular level experiments are where it gets really cool (The Cellular Scale is not biased or anything). They used the Golgi stain to visualize neurons in the Amygdala. They measured how long the dendrites were and also how many spines they had on them. (Spines are the little protrusions that come of dendrites to receive synaptic inputs).


They found that the stressed rats had more dendritic spines on the amygdala neurons than the non-stressed rats.  Not only that, but this increase in spine density was apparent 10 days after the stress event, but not 1 day after.  


You might think dendritic spine growth is a good thing, and likely signifies synaptic plasticity and pathway strengthening... but remember this is the amygdala, a structure critical for FEAR learning, more spines here may not be beneficial. Stronger pathways to these amygdala neurons likely means that they fire more easily.


Now that we understand how PTSD is measured in a rat, we can move on to how they 'cured' it in this paper.  

Rao et al found that when they injected vehicle (a fancy science term for 'nothing' or 'placebo' or 'saline') into the rat 30 minutes before the 2 hour stress event, the rat no longer showed either the increased in anxiety (fewer open arm entries on the EPM) or the increase in dendritic spine density.

Pretty weird, considering they were injecting vehicle prior to the stress event.  How could inactive saline (essentially nothing) cure PTSD symptoms?

They figured out that the actual injection process was stressing the rat out a little bit. When animals (including humans) are stressed, they release a hormone called cortisol.

Rao et al., 2012 Fig 1C,D,E

They found that the 2 hour stress event caused a huge rise in corticosterone (right and left panels), while the injection (vehicle) alone caused a small rise (middle panel). 

Because they were injecting nothing, they hypothesized that the corticosterone produced by the small stress of being injected was somehow protecting against the large 2 hour stress event.

The rest of their paper is basically confirming this. They add corticosterone to the water of the rats and this also prevents the PTSD-like symptoms.  They find that all their manipulations isolating the corticosterone confirm that this is what is protecting the rats from the delayed impact of the stress event.  

Interestingly there is evidence that 'small stress' can help prevent 'big stress' in humans too. They cite clinical studies reporting that intensive care unit (ICU) patients who receive injections of stress-level cortisol during treatment are less likely to develop ICU-related PTSD symptoms.

It is a puzzling paradox at the moment, but the next step is to figure out how exactly this little stress can reduce big stress.


Epilogue: 

I was lucky enough to see Dr. Chattarji, the principle investigator of this study, give a talk at a conference a few months ago.  And one interesting piece of information that you can get from a talk, but will never read in a paper is how the scientists originally stumbled upon their finding.  In this case, Chattarji's lab didn't start their study by injecting vehicle. They were actually testing a real drug that they thought might help alleviate PTSD.  They had a beautiful result showing that when you injected "drug X" before the 2 hour stress event, you eliminated the PTSD symptoms. The natural conclusion is to think that "drug X" is a new cure for PTSD.

 But therein lies the importance of the control group. To control for any effects of simply injecting the rat, they injected vehicle. When they saw that the vehicle prevented the PTSD symptoms just like the actual drug, they were crushed! This is the ultimate demise of an experiment.  The control group shows the same thing as the drug group, which means that the drug does not work! Luckily they were flexible and smart enough to investigate what they did see, that the injection alone could protect against the PTSD symptoms.

Also, if someone would like to explain the difference between cortisol and corticosterone, please do. I clearly do not have a full understanding here.

© TheCellularScale




Rao RP, Anilkumar S, McEwen BS, & Chattarji S (2012). Glucocorticoids Protect Against the Delayed Behavioral and Cellular Effects of Acute Stress on the Amygdala. Biological psychiatry PMID: 22572034

Mitra R, Jadhav S, McEwen BS, Vyas A, & Chattarji S (2005). Stress duration modulates the spatiotemporal patterns of spine formation in the basolateral amygdala. Proceedings of the National Academy of Sciences of the United States of America, 102 (26), 9371-6 PMID: 15967994

Science + Art at Artomatic

As much as I may complain about misrepresentations of literature in science or misrepresentation of science in entertainment, I love artwork inspired by science. Which is why I was delighted by the many science and art connections to be seen at Artomatic this year. 

(A very cellular scale) "Portrait of a Human" by Artologica

The work I was most excited to see was from Artologica. Michele Banks makes gorgeous water color paintings of neurons and microbes. I love how she brings out the natural beauty of bacteria. It reminds me how beautiful and sufficient the natural world is.

Another fantastic exhibit was by Sarah Noble, a research scientist at NASA and artist.

"Our Earth" Sarah Noble

She has some amazing portraits of planets and abstract rockets, but I really love her 'earth from space' series. Especially "our earth" shown above.  I love the stark whites, the hint of blue on the earth, and the feeling of loneliness it evokes. It reminds me of the scene in Ursula LeGuin's The Left Hand of Darkness, where two characters are traveling alone on a glacier which extends as far as the eye can see.

The 30 Computers Project uses discarded computer parts to make large 3D models of viruses and molecules and other exciting science things!

Adeno cd virus

You can go HERE to see how they made this large sculpture. 

Another favorite was Erika Rubel's Had Matter kitchen bugs: 

Kitchen Spatula Bug

These insects made with salvaged vintage kitchen utensils remind me of the little steampunk robots in Girl Genius. The only thing that could make them cooler is if they were controlled by rat neurons. 

Another delightful exhibit was from Duncan Guthery, quite possibly the coolest 11 year old ever.
He makes lego mosaics of familiar characters, like this streetfighter:

pixels made with legos

Also on exhibit were the Beatle's Yellow Submarine and a big Totoro. Not exactly science related, but turning legos into pixels is pretty cool.

And finally, the great Peep Diorama Contest submissions were all on display.  Although the "OccuPeepDC" diorama won the contest, my favorite was the peep CERN lab. 

Peep CERN lab

close up of marshmallow Peep CERN lab

There was so much more at Artomatic than I can possibly cover here. I was there for 4 hours or so and still only managed to see 3 of the 11 floors full to bursting of art exhibits. I am sure I missed some amazing science-related art. If you were there or are a science-related artist, please comment or email to let me know about your work. 


© TheCellularScale 
(I took all of the pictures here except "our earth" which I got from Sarah Noble's website)

How to Tell a Story: Science Edition

Recently I watched a really great Ph.D. dissertation defense, and it got me thinking:
What was so great about it?

While there are many factors that go into a good presentation (and you can read all about them at Neurodojo: the Zen of Presentations parts 1-1bazillion), but I think there is a single golden rule after which all other rules are secondary.

Use as few words as possible.  

(source)

This doesn't mean 'say as little as possible'.
It means say a lot, but make your points using the minimum number of words necessary.

Aside from the obvious cutting out 'ummms' and 'likes' that can be distracting, simply saying what you are going to say without caveats and without extra phrases is always the best way to go.

Here's a secret about me: In my pre-neuroscience life, I spent 2 years teaching special education at an elementary school.  This job involved herding distracted children and trying to teach them things in the most interesting and engaging way possible. The idea being that if the students are engaged with the lesson they will be less likely to throw their pencil box across the room or knock their desk over (both unfortunately frequent occurrences).

One infinitely transferable lesson I learned was 'how to tell a story'. 

The method was something like this:

1.  Read the story to yourself.
2. Write the story down in 10 sentences.
3. Write the story down in 5 sentences.
4. Write the story down in 1 sentence.
5. Tell the story at the level of detail appropriate for the situation. 

 Simple, right? And obviously applicable to scientific communication. This is a step by step method for crafting a good elevator story.  It is also something everyone should do before they make a poster, give a presentation, or even write a paper.  In fact, you should stop what you are doing right now and try to write down your dissertation or current project in 10, 5 and 1 sentence.

Becoming an expert on something is not simply knowing all the details about it.  It's also knowing which ones are critical to the main point and which ones are not.

© TheCellularScale