Tuesday, March 31, 2009

I Got $500! I Got $500!

Perhaps you remember the scene in Wayne's World in which our heroes, Wayne and Garth, decide to sell the rights to their public access TV program for the tidy sum of $5000. They proceed to dance around Wayne's basement singing, "We got five thousand DOLL-ARS, we got five thousand DOLL-ARS!" and waving the check in the air. Such was the scene at Chez Laura tonight, when I checked the page for the NextBio travel grant that I applied for earlier this month. I won! Although I only got five hundred dollars. Apparently grad students come cheap, even when compared to fictitious metalheads who live with their moms. (Oh, I kid, I kid.)

NextBio, a life science search engine, was offering three $500 travel grants to MS, MD, and PhD students. I heard about this opportunity from the Emory GDBBS mailing list, proving that it pays to read those mass emails from your department. To apply for the grant, I wrote a one-page essay about how I've used NextBio in my research -- to learn more about that, you can click the link to my essay on the NextBio grants page. While I enjoy getting money, I also find NextBio to be a useful resource (and it's even free! we all know how grad students feel about free...), so I don't mind helping to promote their product. And they're helping me attend the scientific conference of my choice with this grant, which is awfully nice of them. I'd love to go to this year's Society for Neuroscience meeting in Chicago, but we'll have to see what my yet-to-be-chosen adviser thinks of that idea ($500 is awesome, but it won't cover the entire cost, so I'll need some additional sponsorship for the conference registration and travel).

As I am but a fledgling scientist, this is actually the first grant I've ever received. I'm pretty psyched about it, and I can't wait to start looking up conferences to attend (which will be another first for me).

If you'd like to support the organization that gave me $500, or to play around with a cool search tool that is way prettier than PubMed, you should check out NextBio. You can create a profile there that's sort of like a science LinkedIn and use it to save searches and bookmarks on your favorite topics, join groups related to your field, upload projects, and do lots of other stuff. It's also a potential avenue for networking and initiating collaborations with other researchers, which is always a good thing.

If you missed out on applying for this travel grant, contact NextBio and ask them to sponsor more students in the future! After all, when they support students, the students can go to conferences, learn new things, come up with exciting research topics, publish their data, submit the data to NextBio, and the circle becomes complete.


Monday, March 30, 2009

Rotation #3 Diary: Week 2

The second week of my rotation was much like the first -- I genotyped, I watched behavioral testing paradigms, I failed to gather helpful data. (Sigh.) Sequencing reports indicate that the two litters of mice I've genotyped are all wild-type, which makes it seem unlikely that this chimera will produce mutant pups. I'll be sequencing some more DNA from a different litter (born to a different chimera) this week, but we're not expecting much from them, either. More chimeras are in the works, so at this point it would almost be a disappointment to find a germ-line mutation in the ones we have (the money has already been spent on making a new batch!). The lack of mutants thus far delays our ability to study the in vivo effects of this mutation, though, which is really what it's all about. So, cross your fingers for my little mice.

During some of my down time this week (while waiting for PCRs to run or enzymes to digest) I went to different talks around campus. I already blogged about the Work/Life Balance Panel. I also went to a presentation in the Environmental Studies department about Gender and the Environment. I know that sounds weird, but the talks, given by Emory undergraduates in the department, were really cool. One was about Sarah Palin and how she fits into the trope of American masculinity embodied by the frontier spirit; another was about the dearth of female leadership in environmentalist organizations. The third talk was supposed to cover intersexuals (whose gender has literally been shaped by the environment, or toxins therein), but the pre-med student who was supposed to deliver it had some lab duties to attend to and couldn't come. I thought this was amusing, since I had left my lab to come listen to her talk. I only left because I didn't have any experiments running at the moment, though. I understand how experiments come to rule your life, but it's a shame that we all missed out on her presentation.

This week I have more genotyping to do, and instead of going to talks during my downtime I'll be studying for Wednesday's Cellular and Developmental Neuroscience exam. I'll be back to blogging after that.

Wednesday, March 25, 2009

Science Blog Gender Drama

If you pay attention to the science blogosphere, you probably heard the commotion yesterday when Sheril Kirshenbaum moved her blog to Discover Magazine. She was welcomed by a bunch of sexist mouth-breathers who drooled over her appearance while simultaneously proclaiming ignorance of anything she's ever written.

Ms. Kirshenbaum has written a great post summarizing the resulting brouhaha. She articulately lays the smack down on those who make inappropriate comments about women in a professional setting, and praises the many allies who stepped up to point out that such comments are not okay. You should read her post and click on the links provided there to many other good posts on the subject.

While there were many highs and lows to "mmmmmm, wo-man"-gate, one point that I found especially intriguing was the assumption by some bloggers that the pseudonymous Comrade PhysioProf is a woman. Those who read his blog regularly are aware of his gender, but some who knew him only from his defense of Kirshenbaum's right to blog without being sexually harassed referred to him as a female. Must we automatically assume that anyone who calls someone out for sexist comments is a woman? Plenty of other male bloggers also voiced their outrage about this inexcusable behavior, and I salute them for it. I know plenty of men who consider themselves feminist allies, and I know that it can be uncomfortable for them to speak up about sexism that they witness. Thus, I would like to take this opportunity to thank these men for their contribution to the discussion, and for showing that feminism is not just a mysterious thing that happens to women when they have bad PMS.

When I started this blog, I was conflicted about using my real name and photograph on my posts. Part of this was a concern to maintain a certain level of professionalism within my university and my lab -- I don't want to spread gossip or leak confidential data. But part of it was a fear of being judged not for what I study, but for who I am. If someone reads my blog and sees content that explores issues of women in science as well as articles from issues of Science, will they think I'm whining? Will they not want to hire me, because I might be a trouble-maker? Will they perceive me as less competent because there is a picture of a young blonde woman at the top of the page? Will they be turned off because there's a tag for posts about "feminism?"

The comments directed at Ms. Kirshenbaum have given me still more causes for concern. Thankfully, most people are capable of interacting professionally with women -- even attractive women -- without making the Neanderthal-esque comments that were directed toward this female scientist through the anonymous internet. But who's to say how many people are thinking such things without saying them? I don't mean to accuse everyone who's ever noticed a cute coworker of sexism, but I do wonder about how my scientific work will be perceived as a consequence of my being born female. There are people out there who will never be as impressed by my CV as they are by my T&A, and odds are I'm going to have to work with them eventually. Thinking about this is disheartening, and leaves me feeling rather powerless.

Sheril Kirshenbaum has far more blog readers than I do, with a small army of folks who totally have her back. But, there are people who have my back, too. When things like this start to get me down, I think about my own allies: extraordinary role models, enviably talented classmates, supportive friends, and even total strangers who are enlightened enough to speak up when they see something wrong.

None of us are in this alone. And our numbers are growing.

Tuesday, March 24, 2009

Work/Life Balance

Yesterday, I attended a panel on work/life balance sponsored by Graduate Women in Psychology, the Center for Women at Emory, and Graduate Advocates for Work/Life Balance. This informal panel served as the springboard for a discussion of women scientists in academia and how they achieve balance between career personal life.

The panel consisted of Dr. Lynn Zimmerman, Professor of Biology and Senior Vice Provost for Academic Affairs; Dr. Jessica Sales, Research Assistant Professor in Behavioral Science and Health Education; Dr. Cora MacBeth, Assistant Professor of Chemistry; and Dr. Tanja Jovanovic, Associate in Psychiatry. It was wonderful to see the breadth of academic experiences represented on this panel, and I'm thankful to each of the panelists for donating their time to this important dialogue.

Given the panel's stated focus on work/life balance, a large part of the discussion centered on the compromises one must make when juggling career and family. Three of the four panelists have children, and several of them have faced the two-body problem, in which couples comprised of two academics must find complementary job offers. They generously shared their experiences with us, providing some advice for younger women scientists who will face similar challenges in their own careers.

Because the panel was sponsored by several advocacy groups, we also discussed some of the areas in which institutional reform can lead to better support for working families. Some changes are already in progress at Emory -- for example, the Board of Trustees is soon expected to approve a measure that would allow assistant professors to automatically stop the tenure clock if they have a child (either through birth or adoption). Other goals are yet to be achieved, however. For example, some members of the panel are lobbying for Emory to draft an institutional pregnancy policy. Currently, students who become pregnant are subject to the mercy of their advisers. Professors whose students become pregnant are not bound by any university regulations for arranging family leave, exempting pregnant women from potentially risky tasks, and other issues that can arise in this situation. Other institutions have drafted official pregnancy policies to ensure that everyone is treated fairly when students become pregnant, and Emory should do the same.

Inspired by a recent post by Zuska, I raised my hand during the Q&A portion of the event to ask the panelists if they thought that the problem of work/life balance might be a bit of a red herring in explaining the dearth of women in science. After all, plenty of women in other careers have families. Why is academic science different?

Well, that's kind of a tough question, and I didn't expect anyone to shout "Eureka!" and solve everything. But I did enjoy hearing the response from the panel, which ranged from the fact that everyone's career goals are different, that people may have different family structures that aren't always forgiving of the long hours that academia demands, and that -- perhaps most interestingly -- many young female scientists come into the pipeline feeling that they absolutely don't want to pursue an academic career. While there are many reasons behind this (hostile work environments, the stressful experience of being the only woman in the room...), one point that was brought up during the discussion was that students often see their professors at the worst of times. Some professors seem like workaholic drones: slaving away in the lab, hunching over their desks, furiously writing grants, meeting deadlines, drinking gallons of coffee, and generally suffering. This makes students think, "I don't want that job!" Students may not be as aware of the benefits of an academic career, such as the job security that comes with tenure, flexible hours not often found in the corporate world, and the enjoyment that a scientist derives from doing something really cool for a living. Thus, one way to improve the number of women in academic science might be to humanize the women currently working as academic scientists. If students see their mentors as people who love their jobs, live happy lives, spend time with their families, cultivate hobbies, and occasionally switch to decaf, they might be more inclined to view academic science as an appealing career.

How can we achieve this? More faculty panels! More Emory Women in Neuroscience events! More free snacks! (...Among other things. But it's not a bad way to start.)

Monday, March 23, 2009

MicroRNAs and Mental Illness

ResearchBlogging.orgA paper published in Proceedings of the National Academy of Sciences caught my eye earlier this month. In this paper, Dr. Jannet Kocerha et al. describe the potential link between expression of a micro-RNA (miRNA) and schizophrenia. Because miRNAs are super interesting, and because I'm into understanding the molecular etiology of brain disorders, I thought it would be a good paper to blog about. Then it fell to the bottom of my Google Reader, as tends to happen when one is busy writing rotation proposals, teaching seventh grade science classes, and enjoying spring break. So, I apologize for my tardy reporting. That said, on to miRNAs!

Biochemistry fans will already be familiar with miRNAs, but it's worth explaining them as a preface to this paper because they were discovered relatively recently and tend to fly in the face of traditional biology rules. If you've taken a biology class, you probably learned about The Central Dogma: DNA makes RNA (through transcription) which makes protein (through translation). You may have also learned about the regulation of gene expression, which is a key concept in genetics. Regulated gene expression is what allows the different cells in your body to make different proteins and specialize in different functions, despite the fact that they all contain identical DNA. Depending on the cell, some genes will be turned on and others will be turned off. This allows each cell to focus on its unique function. There are several ways in which gene expression can be regulated, including transcription factors and epigenetic mechanisms. About 15 years ago, scientists discovered that certain RNA molecules can also regulate gene expression (Lee et al., 1993). RNAs that have this function are called "micro-RNAs," because they tend to be much smaller than messenger RNAs (mRNAs; the RNA molecules that carry the message used in protein translation).

miRNAs are freaky because they defy The Central Dogma. These non-coding RNAs (that is, RNAs that do not carry the sequence for translating a protein) arise from parts of the genome often characterized as "junk DNA" due to lack of association with any known protein product. It turns out that some of the "junk" is pretty important -- DNA that codes for miRNAs is essential for proper regulation of gene expression. If you mess with gene expression, all kinds of things can go wrong in a cell. If they regulate important genes, miRNAs can be critical for cellular function.

But how do miRNAs actually work? As I mentioned before, under normal circumstances, DNA makes RNA makes protein. In order for a gene to be expressed, it must be transcribed from DNA to mRNA. To make protein, the mRNA is then translated into a chain of amino acids. miRNAs work by disrupting the translation of mRNA into protein. These pieces of RNA form a sequence that is complementary to a small part of the target mRNA (in other words, where the mRNA has a C, the miRNA has a G; where the mRNA has an A, the miRNA has a U; etc.). When a complementary miRNA encounters its target, it will bind to the mRNA at the site of complementarity. This creates a double-stranded RNA, which prevents the cell's translation machinery from making protein out of the mRNA, and in some cases triggers RNA degradation.

So what does this mean? Well, it adds another possible layer of regulation for gene expression. Imagine a cell expresses Gene X. Some other process might control the expression of the complementary miRNA Y. So, in cases where Gene X is switched on but miRNA Y is switched off, Gene X leads to the production of Protein X. If miRNA Y does get switched on, though, Protein X doesn't get made -- even if Gene X is still being transcribed! All sorts of complicated feedback cycles can be created in this way, especially when certain miRNAs impact the production of other miRNAs, and on ad infinitum.

After that lengthy preface, I will now discuss the paper. Its main points and key criticisms can all be gleaned from the commentary by Dr. Joseph Coyle in the same issue of PNAS, but I will attempt to summarize the article in my own words. It's good practice for me!

Kocerha et al. were investigating a mouse model of schizophrenia in which a certain class of neurotransmitter receptor (the NMDA receptor) does not function properly. This model is based on work done in humans that has implicated decreased NMDA-receptor-mediated signaling in many brain disorders, including schizophrenia. For their paper, the researchers modeled NMDA hypofunction in several ways: they treated mice with a drug called dizocilpine, which is an NMDA receptor antagonist, and they examined mice with a mutation in a gene called Grin1, which is crucial for the formation of normal NMDA receptors. In either case, the mice exhibited "schizophrenia-like deficits" in motor behavior due to the experimental manipulations.

To identify which miRNAs might be associated with decreased NMDA receptor function, the scientists used a microarray. This technique allows us to measure whether any of a large number of RNAs are upregulated or downregulated by experimental conditions. In this case, microarray data showed that expression of a miRNA called miR-219 was significantly reduced by a single dizocilpine treatment. The researchers did not observe the same changes in mice chronically treated with dizocilpine, which is problematic because chronic treatment is considered by some to be a better model of schizophrenia than acute treatment. Still, the fact that dizocilpine had an effect on miR-219 expression made the miRNA worthy of further investigation. A similar effect to dizocilpine was seen in mice that possess a mutation in Grin1. These mice experience a 90% reduction in functional NMDA receptors that leads to locomotor behavior reminiscent of schizophrenic humans. The mutant mice were also found to have significantly decreased miR-219 in their brains.

To see whether the observed miRNA expression changes were indeed brought about specifically by the schizophrenia-like symptoms of dizocilpine treatment and Grin1 mutation, Dr. Kocerha and colleagues repeated their experiments after pre-treating the test subjects with haloperidol, an antipsychotic drug. They found that haloperidol effectively suppressed both the schizophrenia-like behaviors of the mice and the associated decrease in miR-219.

Thus convinced that miR-219 plays a role in NMDA receptor function, the researchers sought its mRNA target. Using bioinformatics, they looked for genes with RNA sequences complementary to the sequence of miR-219. One of the best candidates was CaMKIIγ, a crucial regulator of NMDA signaling. They tested miR-219's regulatory effect on CaMKIIγ by seeing whether miR-219 could inhibit the expression of the CaMKIIγ gene in cultured cells. The cells contained either normal CaMKIIγ (which has a sequence complementary to miR-219) or mutant CaMKIIγ (with mutations that made the sequence no longer complementary) connected to a reporter gene (luciferase). The reporter gene made it easy to quantify the amount of CaMKIIγ expressed in the cultured cells. These experiments showed that CaMKIIγ containing the normal miR-219 complementarity sequence was decreased by about 40% compared to CaMKIIγ that could not form double-stranded RNA with miR-219. Then, to test whether this effect was miR-219-dependent, the scientists used an antisense version of miR-219 to inhibit the reduction of CaMKIIγ. "Antisense" means the complementary sequence to the "sense" RNA that is normally found in the cell. In a way, they made a miRNA against the miRNA -- the antisense RNA binds to miR-219 perfectly, which prevents the miR-219 from binding to its complementary site on the CaMKIIγ mRNA. This antisense experiment restored a significant amount of CaMKIIγ expression, providing evidence that CaMKIIγ expression is indeed inhibited by miR-219. These results were further confirmed by measuring endogenous CaMKIIγ protein in cortical neuron cultures made to overexpress miR-219 and seeing a reduction in CaMKIIγ compared to controls.

Then came some really exciting stuff. After showing that miR-219 and CaMKIIγ interact in vitro, Kocerha et al. wanted to see if they could improve the schizophrenia-like symptoms of their mouse model by treating them with antisense miR-219. After infusing the brains of dizocilpine-treated mice with this miR-219 inhibitor (a tricky technique to master, because RNA degrades so easily), the team observed "markedly altered hyperlocomotion and stereotypy 30 min after dizocilpine administration ... when compared with mice receiving the LNA mismatch or saline." The mice treated with antisense miR-219 had less pronounced schizophrenia-like motor symptoms, although the effect of the drug was not completely eliminated. This seems to indicate that a significant portion of the behavioral effect of dizocilpine is mediated by miR-219.

Of course, we should take such experiments with a grain of salt, especially when animal models are being used to represent a complex psychiatric disorder like schizophrenia. Dr. Coyle points out one especially intriguing point in his commentary in PNAS: "It seems counterintuitive that reduction in miR-219 appears to be responsible for hyperactivity in the acute dizocilpine paradigm but reducing miR-219 levels with antisense infusion reverses dizocilpine-induced hyperactivity." Hopefully further research will be able to explain this apparent inconsistency. As for the broader implications of this study for schizophrenia patients, it's difficult to assess whether mice are experiencing hallucinations or mood disorders, so all of the results observed here are based on the motor symptoms of decreased NMDA receptor function (hypermobility, stereotyped repetitive movements). We already have drugs that can mimic the beneficial effect of miR-219 inhibition in these animal models, so at this point no one is advocating RNA interference as a potential treatment for psychiatric patients. This research does show a new mechanism by which schizophrenia symptoms and the drugs that relieve them may be interacting, however, which could lead to new avenues of drug development as we further elucidate the players in this biochemical pathway.

For those without subscriber access to PNAS, other reviews of the paper can be found at The Scripps Research Institute and Schizophrenia Research Forum.


Lee R.C., Feinbaum R.L., Ambros V. The C. elegans heterochronic gene lin-4 encodes small RNAs with antisense complementarity to lin-14. Cell 75(5): 843–54. (1993) DOI: 10.1016/0092-8674(93)90529-Y

Kocerha, J., Faghihi, M., Lopez-Toledano, M., Huang, J., Ramsey, A., Caron, M., Sales, N., Willoughby, D., Elmen, J., Hansen, H., Orum, H., Kauppinen, S., Kenny, P., & Wahlestedt, C. MicroRNA-219 modulates NMDA receptor-mediated neurobehavioral dysfunction Proceedings of the National Academy of Sciences 106(9): 3507-3512 (2009) DOI: 10.1073/pnas.0805854106

Sunday, March 22, 2009

University Budget Crises: Who Suffers?

The article that inspired this post doesn't directly affect me, since I'm currently a fairly well-funded graduate student at a private university in Georgia. But I think the topic of university budget crises brings up a lot of points that are universal. Universities around the country (including my alma mater) are facing budget cuts and hard choices about how to restructure themselves in this economic climate. Thus, I thought this was worth writing about.

I spent part of my spring break this year visiting my hometown of Gainesville, FL. While I was in town, I read this article in the local newspaper about one way in which the University of Florida is trying to adjust its budget. UF, like most educational institutions in Florida, was having financial problems even before the current economic downturn, and they're in for some hard times. I was accepted by a graduate program at UF, but I decided not to attend for several reasons, one of them being the blatant disregard for education funding that the State of Florida seems to have. And I was especially disheartened to read about UF's decision to cut back on undergraduate programs in education and nursing to compensate for some of these financial woes.

The college might still admit undergraduates but have the expectation that they would continue their educations by entering graduate school, [College of Nursing Dean Kathleen Long] said. The college plans to phase out master's degrees, so nursing students would eventually be expected to get doctorates, she said.

Undergraduate students in early childhood and elementary education programs already are asked to take a fifth year to earn their master's degrees. College of Education Dean Catherine Emihovich said the undergraduate programs might admit fewer students while others would need to take other routes that required even more graduate classes.

At a time when Florida is experiencing a shortage of nurses and qualified teachers in many subjects, the largest public university in the state will require students to take more classes before entering the workforce. I can only assume this is because they will be guaranteed more tuition money and more cheap graduate student labor by asking the students to stay in school longer. (Some students are offered scholarships, but graduate programs in nursing and education are not as generously funded as PhD programs in the life sciences.) Even so, how does it make sense to force such changes on the programs that produce much-needed nurses and teachers? Wouldn't it be a better idea to focus on departments that are less vital to meeting Florida's needs in healthcare and education?

Especially reprehensible is this theory:

[Education professor Dorene Ross] questioned why education and nursing, which have mostly women students, were targeted for possible elimination. In 2008, undergraduate nursing had 98 percent female students and early childhood and elementary education had 95 percent female students.

"There is a question whether these programs are being targeted ... because there will be less push back," Ross said.

Say it ain't so, UF. Consider this post to be just one drop in the many bucketloads of "push back" that you will incur if this turns out to be true.

Saturday, March 21, 2009

Rotation #3 Diary: Week 1

A new rotation brings a new series of blog posts! I finished my first week today, and I think things went well. I started off pretty helpless, as is the case with any new lab position. It's interesting to see how different labs perform common tasks like PCR and westerns, because everyone has their own favorite reagents, special protocols, and secret tricks for optimizing the results. Once I learned some of this lab's quirks, I was set free to start doing my experiments.

I started off genotyping mice. Woo, thrilling. But, I'm actually quite interested in what the results will be (I should know on Monday, when my sequencing data comes in). The lab is generating a new line of mice, and I'm testing the first litters born to a couple of chimeras. When making genetically engineered mice, you have to start with regular mice and make these blended embryos from normal mouse cells and mouse cells that you have messed with. If these embryos survive, they grow up to be chimeras (usually you choose mice of two different colors, so that the chimeras will be obvious because they come out all patchy). Then you have to hope that at least some of the germ cells (eggs or sperm -- the chimeras are normally male, but we have one female, who is probably XO rather than the normal XX due to some quirks of the mouse-making process) from those chimeras are mutant cells, so that they will produce offspring that contain your desired genetic modification. If you don't get any germ-line chimeras, you have to make more chimeras, which quickly gets expensive. So, we have a vested interest in seeing if these baby mice are mutants or not.

Thus, I did some PCRs, then purified my PCR product and sent it off for sequencing. Apparently this is easier, more reliable, and perhaps even cheaper than doing an enzyme digest to see whether my mice are mutants or not. (The mutant gene contains a restriction site that isn't found in the normal gene, thus if you digest the DNA with a restriction enzyme, the mutant DNA is cut into two pieces while the wild-type DNA remains whole. You can see the different sized pieces of DNA if you run them out on a gel.) It costs about $8/sample, which seems ridiculously cheap to me. Of course, I'm only sequencing an amplified piece of DNA that's around 300 base pairs long. For reference, your genome is a million times bigger than that -- that's three billion base pairs. And I would not pay $8 million to have my genome sequenced. So, it might not be such a great deal, after all...

In between my genotyping experiments, I got to learn some new mouse-related skillz. This lab identifies individual mice with numbered ear tags, which I have not used before. To tag the mice you use a little pliers-type thing that punches a small metal tab through the ear flap and puts the tag in place. It's basically like getting your ears pierced by the piercing gun at a Claire's in the mall. I had never done this before (previous labs used toe-cutting -- which is pretty barbaric, but it's the only way to ID very small newborn mice -- and ear punches). So, I got to practice tagging a few mice. I have to say, they seem much more upset about being picked up and gently restrained than they do about having their ears pierced.

The lab also does a fair number of behavioral assays, which I have no experience with. On Friday, my labmates were testing a drug treatment on some of the mice, so I got to watch them administer the drug and give the mice a behavioral score reflecting the severity of the drug's effects every 10 minutes. It was pretty interesting, but I can see how it would get old after doing it over many trials. Since you're observing every 10 minutes, it would be hard to get anything else done during the trial, and staring at mice is not the most fun thing in the world. A video recording system would allow the experimenter to walk away during the trial and review the film later (with the added benefit of blinding the experimenter to the amount of time elapsed since drug administration, if the film could be chopped up into segments and rearranged), but since this system is intended to be high-throughput, they just suck it up and spend a few boring hours running lots of mice as needed.

So far, so good. Everyone in the lab has been really friendly to me, and they seem like a fun bunch of people. Plus, we get free lunch at lab meetings! (This is a crucial point to consider when choosing a lab.) Mouse work is not my favorite thing, as maintaining a mouse colony gets tedious (not to mention smelly), but the mouse is a pretty good model system if you want to do clinically relevant research. I may have to just resign myself to the task.

More updates next week!

Thursday, March 12, 2009

Brain Awareness Week

Yesterday I spent the morning and part of the afternoon teaching seventh graders at Sutton Middle School about neuroscience as part of Brain Awareness Month. A classmate and I partnered up for this outreach activity, which required us to create a lesson plan that met Georgia Performance Standards for Science and covered some of the Society for Neuroscience's Core Concepts. We chose to talk about neurotoxins, specifically those found in some poisonous species of native Georgia wildlife (the Eastern coral snake and the black widow spider).

My partner (fellow first-year neuroscience Ph.D. student Karen Murray) and I worked together to design our lesson. I made a PowerPoint presentation that covered the basic concepts of neurons, synapses, and the neuromuscular junction, as well as neurotoxins and their effects. Karen created a worksheet that contained questions for the students to answer as they listened to our lesson, as well as some more in-depth "thinking questions" to do for homework. We also collaborated to design an in-class activity in which students acted out synaptic transmission at the neuromuscular junction by throwing Jolly Rancher candies (representing the neurotransmitter acetylcholine) into decorated shoeboxes (receptors). I've uploaded
the PowerPoint presentation to my Emory webspace and created a globally-accessible Google Documents version, as well. (The Google version contains some errors caused by the change in file format, and it doesn't include additional the notes I made for each slide in PowerPoint.) If you're interested in using any of this material for a similar activity, please let me know and I'd be happy to send along all of my notes.

Overall, I think the lesson went quite well. The kids seemed engaged and attentive. We tried to do a lot of interactive teaching -- asking the kids what they thought "neuroscience" was before we defined it ourselves, helping them to break down tricky words like "neurotransmitter," and constantly reinforcing the material we had just covered ("So, the neurotransmitter at the neuromuscular junction is called acetylcholine. And which cell has the neurotransmitter? Is it the neuron, or is it the muscle cell?"). I think this teaching style paid off, because by the end of the lesson all of the students had filled out their in-class worksheets perfectly. We also structured the lesson such that every ten minutes or so, we were acting out neurotransmission under different conditions (normal, in the presence of coral snake venom, and in the presence of black widow spider venom). Getting out of their seats and watching their classmates act a bit goofy (we had one student play the muscle in each skit, and they were great at flexing their biceps and doing their best bodybuilder impressions) seemed to keep the students entertained, and we never spent long blocks of time just lecturing.

Here I am in the classroom, talking about neurotoxins. (I've cropped out Karen, in case she doesn't want silly pictures of herself on the internet. I've also cropped out students who were facing the camera or in profile; hopefully the parents of the students pictured won't be upset that I'm showing the backs of their heads here. If you are such a parent, please contact me.) I was impressed with the questions that students came up with on this subject, like "Why does a black widow spider need to use a neurotoxin to catch its food?" I'm not sure anyone knows the definitive answer to that question, so I talked about how different animals have evolved different strategies for survival, and this spider happens to use venom as a strategy. We talked about other strategies that predators use, such as being bigger, faster, and stronger than their prey (like a lion). Perhaps using a neurotoxin to catch prey allows the spider to devote less resources to being big and strong and more resources into things like making baby spiders.

We also got some great questions about the kinds of jobs a neuroscientist can do (I explained the different between neuroscience and neurology/neurosurgery -- we're not medical doctors, although a lot of us do research on clinically relevant subjects). One student even came up to me after class and said that he wants to be a scientist and would love to learn more about what it's like to do scientific research. I talked to him for a few minutes and encouraged him to email me if he had any more questions. My heart pretty much melted at that point. But then, another student came up to me after class and asked if he could buy some Jolly Ranchers off of us! I guess they can't all be future scientists.

I had a great time doing this outreach activity, and I would definitely go back to public schools in the future. Several students asked if we go to lots of other schools talking about neuroscience, and we explained that this was our first year in the neuroscience program and thus our first time participating in Brain Awareness Month. I hope that the questions we got about this imply that students couldn't
tell that it was our first time, and thus that we did a pretty good job. All in all, it was a great experience for me, and hopefully for the students, too.

Wednesday, March 4, 2009

Psychedelic Medicine

I received an email this afternoon with the subject "2-book set: Psychedelic Medicine," from an email address I didn't recognize. I wasn't sure what this referred to, at first, but my spam filters are pretty good; unless a mysterious message mentions H3RB4L VI4GR4 in the subject, I usually read it.

The email turned out to be from Dr. Thomas B. Roberts. He included some information about his book Psychedelic Medicine: New Evidence for Hallucinogenic Substances as Treatments, and a line suggesting that I might like to request a copy for my library. I can only assume that he discerned my interest in the subject from my post about DMT's action on the sigma-1 receptor, which reviews the recent article by Fontanilla et al. on a newly-discovered role for hallucinogens/entheogens in the brain. Because there was little information in the email not related to promoting the book, I did feel a bit spammed. However, I doubt that these emails are sent out in mass quantities to people who haven't indicated that they would appreciate more information on psychedelics. So I decided to post about it, in case some of my blog readers (all seven of you, according to Blogger's subscriber statistics!) would be interested.

I haven't actually seen Dr. Roberts' book, but the table of contents makes it seem like informative reading that would be suitable for non-scientists. I don't feel right asking my library to buy the book, given that I'm not doing any real research on hallucinogens. But, if you liked my previous post and want to learn more about how these drugs can affect the brain, you might want to track down a copy.

Monday, March 2, 2009

Book Review: Microcosm

Microcosm: E. coli and the New Science of Life Microcosm: E. coli and the New Science of Life by Carl Zimmer

Rating: 4 of 5 stars

I'm a big fan of Carl Zimmer. His blog, The Loom, is a great way to keep up with the latest scientific developments in words that a layperson can understand. His other books (I've read Parasite Rex, At the Water's Edge, and Soul Made Flesh) have been quite good. His newest book, on the bacterium E. coli, was also an enjoyable and educational read.

I find I get the most out of science writing when it's on a subject outside of my expertise. I loved Parasite Rex for this reason, because parasitology, despite being utterly fascinating, is often overlooked in general biology classes. I'm training to be a neuroscientist, so I don't really study bacteria (although, they are handy when I need to produce vast quantities of DNA for use in experiments on organisms that actually have a nervous system). Therefore, I learned a lot from this book about the complicated genetic circuits that can exist in such a simple organism.

I knew some basic facts about E. coli from my genetics classes (operons, phages, plasmids, bacterial sex...), but I had never studied the mechanisms by which the germ senses chemicals in its environment and chooses its method of locomotion accordingly. These little bacteria, with only the most rudimentary of sensory organs, manage to locate food sources and move toward them, or move away from noxious chemicals. This is really pretty amazing when you think about it. I mean, I have a fully functional brain and have still been known to accidentally drink sour milk. The bacteria also form complicated bacterial "cities," called biofilms, in which they seem capable of cooperation and even altruism, sacrificing themselves for the good of the colony. All this, without so much as a nucleus! They are some pretty impressive little cells.

The little details about scientists that get thrown into this book really add a lot of flavor to the potentially dull retelling E. coli biology's history. People writing "Hooray!" in their notebooks when an experiment works, husband-and-wife teams cracking the genetic code of bacteria, experiments testing just how long an E. coli colony can live that span multiple generations of researchers... these touches make the stories seem more real to me. I can picture the labs, the distinctive red graph paper notebooks, the begloved grad students. I can almost smell the Luria broth.

Some of the later chapters tackle genetic engineering and synthetic biology, both hot-button scientific issues with E. coli inspiring their biggest advances. While Zimmer covers some of the controversy, I would have enjoyed more discussion on this, and perhaps a little less of the basic genetics that I already knew. I'm a pretty specialized reader, though, and can appreciate how important that background knowledge is if one isn't already a biologist. I can also appreciate that the book should not be allowed to grow indefinitely long, and debating the ethical issues in full detail is probably a book in and of itself.

Overall, I'd say that Microcosm makes enlightening reading for anyone who's already a biology enthusiast, but perhaps might be a hard sell for non-bacteria fans. I still think Parasite Rex is Zimmer's most jaw-droppingly fascinating book (perhaps because parasites can become so creepily entwined with brain function -- I love that stuff!), but I'd probably rate this one as his second best. Give it a read, why don't you?

(Cross-posted from my GoodReads page. View all of my book reviews.)