Killing the bear (and other 2014 goals)

Hello friends! So… it’s been a while. It’d be a lie if I didn’t admit that I’m a bit embarrassed and quite disappointed in how long it has taken me to come back to this blog. Last year, when SciFund outreach ended, I made a promise to myself that I would blog at LEAST once a month. And, to put it bluntly, I failed miserably. And for those of you who know me, I’m not really one to accept failure. SO, it’s time to (wo)man up and get back on the right track with this blog! But in order for that to happen, I think it’s time to make some changes. BIG changes. So bring on the personal anecdotes and corny jokes because…

this blog is about to get personal.

In order to understand why I think I need to make changes, let’s take a look back to a lovely evening of sushi and cocktails that I had with my friend, colleague, and importantly, fellow blogger, last month. In between rounds of Jenga and lychee martinis, Albert asked me what sounded like a simple question:

So what happened to your blog?

I remember that I immediately responded with an excuse, something along the lines of, “it’s hard for me to think of good scientific content so frequently, I got busy, I traveled a lot… blah blah blah”. But it was then that I realized I didn’t have a good excuse. There’s no need for my blog to be scientific gold every entry. There’s no need to continuously come up with a fresh take on my research. I just need to WRITE. And write often. This week, Albert posted a new entry into his blog, and so shall I. Thanks for the motivation, Steak Sauce. I owe you one. Oh, and he’s a great blogger, check it out here.

——————————————————-

So I think I’ll start my blogs for 2014 with a quick review of my accomplishments in 2013, and a look ahead to my goals for 2014. I’ve decided to loosely structure my blog around these goals, both personal and professional, to hopefully encourage me to write informally and often.

2013 Accomplishment: Get involved with a nonprofit!

At the beginning of 2013, April, a post-doc in our lab (and a wonderful human being all around), asked me what I wanted to do after I got my Ph.D.. I told her the truth: I’m not exactly sure, but I am really passionate about the mission and motivation behind nonprofit organizations. So she challenged me to find a nonprofit organization in Seattle, and to get involved. REALLY involved. And so I did! For the last year, I have volunteered weekly (and sometimes a bit more), at the Seattle Cancer Care Alliance, where the mission is to offer world-class cancer treatment to the community while supporting the conduct of cutting-edge cancer research. I’ve spent most of my Saturday afternoons at Shine, a retail store housed in the Seattle Cancer Care Alliance house, which provides oncology-related goods, services and support to cancer patients, their families, and the community. While I think I will dedicate a future blog to my love for nonprofits and my experiences with the SCCA, I am proud to say that I have accomplished my 2013 goal of getting involved, and couldn’t be happier about it!

2014 Goal: Kill the bear

Two weeks ago, during dinner with the fantastic Dr. Alex Schier, my training grant cohort asked if he had any advice for young scientists. His advice was simply to “kill the bear”. And, while it didn’t make too much sense at first, I think this advice makes for a GREAT 2014 goal. Let me elaborate…

As scientists, our research isn’t doing anyone any good sitting in notebooks. There are always more experiments we could do, always another question that could be answered. However, we need to stop trying to teach our proverbial “bear” new tricks. Don’t feed our bear any more treats. Don’t pet the bear.

JUST KILL THE BEAR.

And so, my professional goal for 2014 is to publish more! I have two pretty advanced drafts that have been collecting electronic dust on my computer, but I find myself starting new experiments instead of polishing these manuscripts. It’s time to make publishing my number one goal… it’s time to kill the bear!

He may be cute, but it's time to kill the bear!

He may be cute, but it’s time to kill the bear!

I’ll also be working towards killing the bear in my personal life. I’ve come to really enjoy running in the past year or so, but last October, while training for the Dawg Dash 10K, I got a stress fracture in the arch of my foot.  I ended up in a cast for about 2 months, and had to stay away from running until the New Year. Let me promise you, that was NOT FUN. However, I did learn that it is still possible to dress up a cast for a formal function, jump around in the ECS section at a Sounders game, and that the cast can even improve your Halloween costume (at least when you go as Buzz Lightyear, as I did).

Walking casts, despite the name, make walking a bit of a challenge.

Walking casts, despite the name, make walking a bit of a challenge.

Even though I’ve always talked about setting running goals, to this day, I’ve never run a race longer than a 5K. So, it’s time to kill the bear! I’m signed up to run the 12th Man 12K (GO HAWKS!) in early April, and am slowly but surely getting back into running shape after my injury. I have some other BIG plans that I’m not quite ready to share with the world yet, but watch out 2014… I’m going to be running circles around you!!!

I hope you guys are excited as I am for Emily’s blog version 2.0. Will there be science? You bet. But will there be a bit more of me? Yeah, I think so. So get ready for many adventures (and some misadventures) as I try to figure out what the HELL I am doing. Toodles!

Top 5 Highlights from WORM2013!

I will always remember June 2013 as a whirlwind month of airports, poster sessions, and far too little sleep. On final count, I took 10 flights out of 8 different airports through 11 states, 4 time zones, and 2 countries! After giving myself a bit of July to recover, I am glad to report that June was a marvelous success, inspiring me with new research ideas and lighting a fire under me to get to writing! I believe my next blog may be a photo tour of June 2013, but until then… let’s talk worms!

My last stop for the month was the 19th International C. elegans Meeting at UCLA in Los Angeles, California! In many ways, this trip was reminiscent of my trip to Cancun (discussed here).

For one, the temperatures were similar:

photo

And secondly, another beautiful location:

photo (4)

While roaming through the rows and rows of posters, it was easy to identify the “unreasonably tan” colleagues who had also attended the ICDB conference in Cancun the previous week. Think of it as Where’s Waldo:

photo (5)

And just like Cancun, I learned a lot about really cool science at WORM2013! So, in the spirit of my last blog post, here are my top 5 highlights from my week in LA at WORM2013:

#1: The hot topic: chromatin remodeling during stress!

I remain a bit partial to this topic, as it is the focus of my own research, but I was extremely excited to see so many fabulous talks and posters focusing on the relationship between chromatin remodeling and stress response! In particular, Christian Riedel from Gary Ruvkun’s lab demonstrated that the SWI/SNF chromatin-remodeling complex is required for DAF-16 (FOXO) gene-activation, and ultimately DAF-16 dependent longevity. This work was recently published in Nature Cell Biology and can be found here. Excitingly, David Fay also described a role for SWI/SNF in stress response, as a mediator of the ethanol and stress-response element (ESRE) pathway. These talks, along with multiple posters (including mine!), really begin to illustrate the critical requirement for chromatin remodeling in a multitude of stress response pathways.

#2: Transdifferentiation… is awesome.

As a trainee in developmental biology, and after recently listening to John Gordun discussing the challenges in transdifferentiation at ISDB2013, Joel Rothman’s talk blew me away. While Gordun’s talk emphasized how removal of chromatin marks specific to differentiated cells is one of the most difficult aspects of transdifferentiation, Rothman described a phenomenon in worms in which this process is not even necessary!  Expressing a single transcription factor, elt-7, resulted in the conversion of differentiated pharynx into endoderm, even in the absence of cell division. This talk was definitely one of the “THAT IS SO COOL” moments of WORM2013 for me.

#3: Memorable talks about teeth, exercise, and sex

Based on the conference twitter feed and the chatter buzzing about the crowd, the next 3 talks were some of the most memorable, as well as the most unique! Mary Ann Royal of the Driscoll lab showed that 30 minutes of swimming a day results in increased pharyngeal pumping later in life, suggesting that “exercising” has health benefits even in worms! Eric Ragsdale of the Sommer lab wowed the crowd with a gruesome video of P. pacificus chowing down on an unsuspecting C. elegans. His talk then went on to focus on the genetic control of a developmental teeth dimorphism in P. pacificus by a sulfatase encoded by eud-1. Finally, Cheng Shi of the Murphy lab pointed out a phenomenon we all felt we should have noticed previously: N2 worms shrink up to 30% after mating! These animals, in addition to a reduction in size, also are less attractive to other males, and live shorter lives. As male seminal fluid contributes to this phenomenon, it may represent an example of male influence on hermaphrodites to maximize their own reproductive success. Overall, Mary Ann, Eric, and Cheng definitely win the “most memorable” superlatives of WORM2013.

#4: More disease models in C. elegans

As a scientist working in model organisms, I am always excited to hear about disease models in C. elegans, as it is a great way to study the genetic basis of human disease. Susana Garcia from the Ruvkun lab introduced a worm model designed to investigate the toxicity of CUG repeat-containing RNA, which is commonly associated with the human disease myotonic dystrophy. Garcia discovered that the nonsense mediated decay pathway normally functions to clear these toxic repeats, suggesting that it may be a good target for future myotonic dystrophy research.

Emery-Dreifuss muscular dystrophy is due to mutation in the lamin protein. A.  Mattout from the Gasser lab demonstrated that this mutation, in worms, leads to failed tissue-specific release of heterochromatin and disrupted muscle function. By restoring chromatin organization through genetic manipulation, Mattout was able to fully rescue muscle function in these animals, suggesting that chromatin mislocalization may be of particular importance in human laminopathies.

#5: New insight into everyone’s favorite topic, insulin-like signaling!

It wouldn’t be a worm meeting without several dozen talks and posters about the FOXO transcription factor DAF-16. This year was no exception, but it was great to see some really remarkable new discoveries in a field that has garnered so much interest in the worm community! To highlight just a few, Adrian Wolstenholme from the University of Bath demonstrated the discovery of the sole glutamate transporter in worms, FGT-1! Additionally, Ronald Tepper from the Bussemaker lab at Columbia gave a great talk on the identification of PQM-1, the main regulator of the class II growth and development genes originally thought to be directly activated by DAF-16.

—————————–

As you can tell from the sheer number of talks I’ve mentioned, there was a huge amount of elegant science and interesting discoveries at WORM2013. Visit the meeting’s website for full abstracts and dates of future WORM events!

Top 5 Highlights from ICDB 2013!

It seems that I have neglected my blog a bit this month, but thankfully this is due to an exciting (and exhausting!) month of travel! As of June 1st, I have been to 10 states, 4 time zones, and 2 countries!

I began my whirlwind month in Maryland visiting my family and attending Alumni Weekend at my undergraduate institution, St. Mary’s College of Maryland. This trip was full of crabs, sunshine, and reminiscing with old friends. All in all, it was a great way to get reenergized for conference season!

Speaking of conferences…

A few months ago, I gave a talk at the Northwest Regional Society for Developmental Biology (SDB) meeting, and was beyond excited to win a travel award to attend SDB’s national meeting! Excitingly, this year the national SDB collaborated with other international societies to host the 17th International Congress of Developmental Biology!

The conference was fabulous, and I could blog for hours about all of the amazing science that I got to hear about at the conference. But to save us all some time, here are my top 5 highlights of my trip to ICDB 2013!!

#1: The meeting was held in CANCUN, MEXICO!

Here’s a photograph from my hotel room: IMG_5125

And another from my favorite beach chair:

IMG_5134

Need I say more? The location was absolutely incredible, with a very quick walk to the convention center, seen here across the street from my hotel:

IMG_5177

Located on the top floor of the Cancun Convention Center, the meeting was held in one large room that was easily separated into 3 concurrent sessions for some of the afternoons. The layout of the meeting made it really easy to bounce between rooms, so you could catch talks in all sorts of topics and disciplines. Additionally, posters were constantly on display in the break room, giving attendees plenty of time to scour the 600 excellent posters!

#2: Enhancers play a role in human disease, evolution… and just about everything you could imagine.

Enhancers really stole the show at this year’s meeting. Many of the talks, a large number of posters, and a lot of coffee break chatter surrounded some fascinating studies into the role of these noncoding regions of DNA in development.

For my developmental biology novices, let’s quickly define enhancers. Our genome consists of long sequences of DNA, in which some regions code for functional proteins, and some regions do not. Enhancers are found within this noncoding region of DNA and are thought to modulate the activity of proteins transcribed from nearby regions of coding DNA.

Schematic of enhancers (green), found upstream of effected genes (blue) (Photo credit: Wikipedia)

Schematic of enhancers (green), found upstream of effected genes (blue) (Photo credit: Wikipedia)

How do we identify enhancers? Chicks are often the best tool for identifying conserved enhancers, as their genome is compact and conserved noncoding regions are likely to contain important regulatory information.

Scientists have long been confused about how mutations in noncoding regions of DNA lead to human disease, but as described at ICDB 2013, many of these mutations are starting to be identified as being located within enhancer regions.

One of my favorite talks of the week was from Harvard’s Cliff Tabin. Many human traits seem to have regressed from the traits found in monkeys (less body hair, shorter fingers, etc.). Regressive traits often come from loss of enhancers upstream of trait-determining genes. Cliff’s lab has demonstrated that the human genome is enriched for deletions in transcription start sites and enhancer regions, suggesting that loss of enhancers did in fact contribute to our regressive loss of monkey-like traits.

For more information on the ICDB enhancer talks, check out the lab websites of Cliff TabinMarianne Bronner, and Alvaro Iglesias!

#3: There was a WHOLE SESSION on how the environment impacts development! 

My particular interest in developmental biology focuses around the long-term impact of environmental stress on phenotype and physiology. I was pleasantly surprised to find an entire session of talks dedicated to this topic!

While many human diseases can be attributed to genetic predisposition, environmental conditions can exaggerate these disease phenotypes.  Sally Dunwoodie gave a great talk discussing how low oxygen conditions (hypoxia) during early development increases the penetrance of genetically heritable scoliosis. Teiya Kijimoto demonstrated that genes involved in classical developmental decisions, including Hedgehog signaling, also control environmentally induced traits, such as horn size in dung beetles!

#4: Improving undergraduate interest in research with projects designed straight from the headlines!

The education section of ICDB 2013 focused on how we can interest students with research projects on current hot topics in the media.  I think this a great idea, as it is so much easier to get excited about science when you know that you are contributing to a relevant and important cause.

Barresi lab uses Deepwater Horizion oil spill as inspiration for undergraduate research (Photo credit: Wikipedia)

Barresi lab uses Deepwater Horizion oil spill as inspiration for undergraduate research (Photo credit: Wikipedia)

For example, Michael Barresi described the upper division research course he designed to investigate the effects of the Deepwater Horizon Oil spill on the development of fish in the Gulf of Mexico. Tyrone Hayes gave an eye-opening talk on the impact of the pesticide atrazine on the sexual behavior and fertility of frogs. Additionally, Tyrone showed correlations between his research on frogs and the decline in fertility of men in close contact with pesticides.

#5: Alternative model organisms are awesome!

As a scientist who works in a commonly used model organism, I am always impressed by the amount of work that goes into the implementation of new and alternative model organisms. This meeting did not disappoint, as I got to hear some really great talks about using tunicates, frogs, and honeybees for scientific research. Many of these tools are being developed to overcome the shortcomings of our current model systems and allow us to address questions that are currently unanswerable.

Nanette Nascone-Yoder introduced the Budgett’s frog- a giant cannibalistic Xenopus alternative that allows for higher resolution of frog development!

Lepidobatrachus_laevis

Budgett’s Frog (Photo credit: wikipedia)

Robert Drewell discussed how DNA methylation in the eusocial honeybee is a new example of genomic imprinting!

Honeybees (Photo credit: NJDEP)

Honeybees (Photo credit: NJDEP)

—————————–

To summarize, the ICDB 2013 meeting was a great experience!

Tomorrow, I am off to the International Caenorhabditis elegans meeting at UCLA! Follow me on twitter @em_fawcett and look for my live tweets with #worm2013!

And look forward to another top 5 blog post next week!

 

You work with WHAT?! Common misconceptions about studying nematodes

We are all worms, but I do believe I am a glow-worm”- Winston Churchill

Well, if Mr. Churchill is right, and we are all worms, I am most definitely a nematode.

Now you may be thinking, “Emily, you’ve lost it. A nematode? A toad is most definitely NOT a worm”.  Don’t worry; I haven’t totally lost it (in this instance, anyways). Nematode is another name for the roundworm, which account for over 80% of the individual animals on the planet! In our lab at the University of Washington and at labs all around the world, the nematode is very close to our hearts. This is because we study one particular species of nematode called Caenorhabditis elegans. Scientific names can often be a mouthful, so most shorten it to simply C. elegans.

When I tell people that I work on worms, I usually get a look of disgust, confusion, or skepticism.  But let’s get something straight- C. elegans are not what you are picturing. They don’t look like this:

Source: fir0002 | flagstaffotos.com.au

Source: fir0002 | flagstaffotos.com.au

Or this:

100toys76

And unfortunately, they don’t look like this either:

1540

In fact, C. elegans are very hard to see without a microscope. Adults are only about 1 millimeter long. To put that into perspective, a single C. elegans worm could be picked up by a single eyelash! Having a hard time picturing it? Here are a couple of views of C. elegans:

Crawling C. elegans hermaphrodite worm

Crawling C. elegans hermaphrodite worm (Photo credit: Wikipedia)

Caenorhabditis elegans

Caenorhabditis elegans (Photo credit: AJC1)

Ok, ok… but who in their right mind decided studying these tiny worms was a good idea?

Well, studying diseases in larger animals like mice and rats isn’t easy: they take a long time to develop and grow, are expensive to maintain, and are complicated in design. In the 1960’s, a scientist named Sydney Brenner suggested that studying C. elegans would improve on a lot of these problems: C. elegans only live for a few weeks in the lab, are cheap and easy to maintain, and it is easy to manipulate their genes! To put the simplicity of C. elegans into perspective, while the human body has trillions of cells, C. elegans only have around 1000 cells! Today, along with fruit flies, C. elegans is frequently used as a model organism for studying disease and cellular processes.

In the 40+ years that C. elegans have been used in scientific research, they have greatly contributed to the advancement of science, particularly in the study of aging. Many genes that make C. elegans live longer in the laboratory have been identified as important in the aging process in humans and other mammals. Additionally, C. elegans are a great model  for studying human disease, as more than half of the genes known to be involved in human disease are also found in C. elegans. For example, models of neurodegenerative diseases including Parkinson’s and Alzheimer’s have been developed, and are currently being utilized to better understand and development treatments for these diseases.

In the last 15 years, THREE Nobel Prizes have been awarded to scientists for their work in C. elegans!

Hopefully, the next time that you hear a scientist mention that they study worms, you will not necessarily picture them digging around in the dirt and looking at earthworms. While we have all been known to dig in the dirt from time to time, C. elegans researchers are tackling tough research problems from behind a microscope, using this tractable and inexpensive model organism!

——————————————–

And now for some great references to find out more about C. elegans!

A Short History of C. elegans Research

Worms in SPACE?!

Wormatlas: A bit dense for the nonscientist, but great images!

Introduction to C. elegans

 

When peer review meets the press

How do scientific ideas progress from being a project at my lab bench to being the headline story on your nightly news? The process, while all-too-familiar to research scientists, can be a bit of a black box to everyone else. In the last few weeks, this process has reached the front-page news more than once, so let’s talk about the scientific process (and some of its’ flaws)!

The first thing to realize? Science takes a very, very long time. The grant review process, the actual science, the publication process: all are notoriously slow, albeit crucial, steps in the world of science.

In order to fund, perform, and publish scientific research, scientists rely on one very important group: our peers. First, a panel of other scientists reviews our grant proposals. Once the grant is funded, collaborations are critical for the success of a research project. Finally, when the research is completed and submitted for publication, our colleagues review the manuscript for content and clarity. Involving our peers in every step of the process, in theory, ensures the funding of only the best grants and the publication of only the best scientific papers.

Peer-Review-Nick-Kim-cartoon3-resize (1)

Peer review can be a long, hard road for any scientist                                               (Cartoon credit: Nick D Kim, strange-matter.net)

As the title of my post suggests, the peer review process has come under scrutiny as of late. Let’s do a quick rundown of the recent headlines about the scientific process!

1) The battle over open access

If I were to give you a list of 10 influential scientific articles from the last 20 years and ask you to find full versions of them, you would have a very hard time. In fact, when you reach the website of the appropriate journal, you’d probably be asked to pay the reasonable fee of only 50-100 dollars to view the article.

Wait… $100 to read ONE article?!

The reason? Most research journals charge steep subscription fees to access their articles (current or archived). However, as a large number of these articles are from publicly funded research labs, many believe that this research should be free for anyone to read.

The good news? We have seen a rise in the number of journals with “open access” policies over the last few years. As of 2011, 12% of articles were available open access, with this number rising all the time. The availability of academic research to the public is increasing, and this is definitely a good thing!

Read more: Nature News tackles the topic of Open Access 

2) Is the peer review process in grant selection unsatisfactory?

The National Science Foundation (NSF) is a government agency that provides a large amount of funding to science and engineering research. NSF grants are selected, you guessed it, through a peer review process. After an intensive review of grants that received funding from the NSF over the last few years, some lawmakers believe that the selected grants are not always “groundbreaking” research.

To “fix” this apparent problem, Representative Lamar Smith (R-TX) drafted a bill last month to implement Congress-selected funding criteria on the grant selection process. Many scientists believe that this funding criteria, which requires grants to “answer questions or solve problems that are of utmost importance to society at large”, undermines the peer review process and would negatively impact the advancement of basic research.  Basic research, as opposed to being aimed at curing a particular disease or illness, focuses on understanding the fundamental principles of the world. While this work may not directly “advance the national health, prosperity, or welfare”, it is important an building block for our understanding of the human world. The bill, which has not been formally introduced to Congress, has sparked a large amount of debate within the scientific and political realm. How should we decide who gets funded, when the amount of funding keeps dwindling?

Read more: Science Insider on the NSF Grant Bill

3) Are timeliness and thoroughness in peer review mutually exclusive?

When something BIG happens in science, the authors want to get it out fast with as big of a splash as possible. But where do we find the balance between rushing to publish big results and allowing the peer review process to be effective?

One of those BIG things in science happened this month: Shoukhrat Mitalipov, a US researcher, reported that he had cloned human stem cells from skin cells. The research was published in the journal Cell, a prestigious journal in the scientific community. In the last few days, concerns from anonymous readers began pouring in on potential errors  in the publication. Figures were labeled incorrectly, and an image was duplicated and reused in a different section of the paper. These are the type of errors that are usually caught during the tedious peer review process. So why weren’t they corrected before the publication of such a big story?

To put it simply, this paper went through review at an incomprehensibly fast rate. To give you a framework, a case study of 2,000 manuscripts submitted to a journal in 2010 reported that the average submission took 6.8 weeks from submission to editorial decision. Mitalipov’s submission was reviewed and accepted in only 3 days. Additionally, the paper was published just 12 days after acceptance.

Cell went on to defend the speediness of their review process, stating: “It is a misrepresentation to equate slow peer review with thoroughness or rigor or to use timely peer review as a justification for sloppiness in manuscript preparation”. Thankfully, it appears that the errors in the manuscript do not impact the findings of the research. However, the negative publicity from these errors certainly detracts from the impressive and innovative science performed by Mitalipov and colleagues.

Read more: Nature News: “Human stem cells created by cloning

Read more: Nature News on Errors in Mitalipov Stem Cell Paper

Read more: 2010 Case Study on average length of peer review

Conclusions

In summary, these three stories have brought the scientific process and peer review into the spotlight. Peer review has a lot of benefits, improving the caliber of the science we deliver to the public and lowering the rate of publication of unethical scientific practices. However, the question now remains: how do we improve the peer review process to keep up with the rapid speed of scientific discovery while still yielding the high quality publications we expect?

——–

Some suggested reading for more information:

Nature tackles the Peer Review Debate

Nature: How are funded grants chosen?

Change the world? Challenge accepted

Graduate students are angsty. It’s true, don’t try and deny it. We are sleep-deprived and grumpy and covered in emotional bruises from being knocked down so many times. One of my friends posted this all-too-familiar sentiment to social media last week:

 “Ya know, I became a scientist because I wanted to help people. Because I wanted to cure a disease, or find a therapy, or make a discovery that changes the world. And as I sit here reading papers for class I can’t help but think there are much better ways to truly help people, and that this is all just a big joke.”

I can nearly guarantee you that every graduate student has had this thought at one point or another. We came in with such aspirations, such dreams to do something good, but as the seemingly neverending PhD continues, we start to lose our faith in this ideal. In a city like Seattle, many people our age are employed by Microsoft or Amazon, working better hours for more than twice the salary. Knowing that, it’s hard not to question our decision to go to grad school. We make very little money, see very little progress in our grueling day-to-day science, and are constantly bombarded with the premise that we are simply not as smart as everyone else. I am about to start the twentieth grade, for goodness’ sake! What am I doing here?!

177377_631228287443_2045552082_oSometimes, planning out my future feels more like drawing cartoons.

But what I’ve started to learn is this: grad school isn’t supposed to be about changing the world. It’s about changing you first.

As first years, we are as prepared to cure cancer as we are to fly a spaceship to Mars. So, we read mountains of scientific literature that we only occasionally care about (or understand, for that matter). We sit through lecture after lecture of successful scientists, sometimes understanding what they are talking about. We do an exorbitant number of experiments that fail three-quarters of the time… on a good day. But through all of that, we learn how to think. We learn how to problem solve. We learn how to be a scientist. And that’s the point of being a graduate student. At my committee meeting yesterday, my boss told me I needed to start making the transition from thinking of myself as a student to thinking of myself as a colleague. Three years ago, I would have been terrified of that transition, but after three years of grad school, I’ve changed.

Writing this blog, it’s hard to find a middle ground between the angsty overworked graduate student and the motivated inspired scientist. I’m not here to convince you that graduate school doesn’t suck. It does! But I’m also not here to convince you that it’s a worthless waste of time, because I don’t think that’s true, either. I think I am mostly trying to reaffirm that what we are doing, while not immediately changing the world, will make us the people we want to be. The people who cure cancer, who change policies, who reimagine the way science will work in 15 years.

If you were to ask my classmates, I’m sure they’d tell you that I love grad school more than most. I do. I started working in a lab at 16. I’m pretty sure my mom thought I was crazy when I walked into her room and said I wanted to give up my summer and most of my senior year to drive to Frederick and work on cancer. And, to be honest, as cliché as it all sounds, I fell in love with science that year. And until my second year of graduate school, 6 years later, I never once questioned the path I was going to take: college, research, grad school, academic researcher, rounding off my career by curing cancer.

Recently, my goals have changed a bit. I know this may come as a surprise to many, but

I probably won’t be the one to cure cancer.

I may not even be behind a microscope in 10 years (guess I’ll have to change my blog title at that point)! I do know that I love talking to people. I love engaging students who never knew that being a scientist was a possibility. I love trying to fix the Grand Canyon-sized gap between research scientists and the public. I don’t think that I would have realized these things, or been able to formulate a plan to incorporate them into a career, if I didn’t walk the long and terrifying path of graduate school.

312401_650330606243_1490617681_n

The realization that your scope has taught you more than it’s taught you…

As graduate students, we are, by most definitions, adults. We pay rent, we buy our own groceries, we can vote, drive cars (if we can afford the gas), pay taxes, get married, have children, buy houses. There is a quote from an early season of Grey’s Anatomy that I think describes it best:

“Four years of high school, four years of college, four years of med school. By the time we graduate we’re in our late 20s and we’ve never done anything except go to school and think about science. Time stops… And Meredith, she’s 17 years old, we’re all 17 years old”.

So, here I am, a 24-year-old graduate student, still contemplating what I want to be when I grow up. The answer currently: Who knows! That is the answer of most graduate students these days, especially with an increasing number of Ph.D.s and a diminishing resource of jobs and funding (that’s a topic for another day). But I do know that going through graduate school will be one of the biggest and best accomplishments of my life. And mark my words, I will change the world one day. I just have to work on changing myself first.

Hydrogen sulfide: A smelly, deadly gas… but could it save lives?

asdf

Take a moment and imagine a street in Paris in the 18th century, much like this depiction of “Place du Havre, Paris, Rain” by Camille Pissarro. The first things you’ll notice: it’s beautiful, romantic, bustling. But what you might not notice is that is also very, VERY smelly.

Back then, sewer systems were extremely unsophisticated, and the smell of rotten eggs spilled into the streets. Even more, if a person were to go too far below ground, they would likely find themselves dead in minutes. The culprit? Hydrogen sulfide, a gas that smells of rotten eggs and is produced when bacteria breakdown the organic material found in sewage.

Thankfully for us, modern-day sewers have come a long way since the 18th century, but so has our understanding of this smelly, toxic gas. In the last 10-15 years, scientists have found that hydrogen sulfide is important for cell-to-cell communication in our bodies. Additionally, exposure to low levels of hydrogen sulfide has beneficial effects on many different organisms. For example, plants exposed to hydrogen sulfide grow  better, and worms grown in hydrogen sulfide are long-lived! Remarkably, in rats and mice, treatment with hydrogen sulfide also protects against damage from devastating injuries including stroke, heart attack, and severe blood loss. With so many recent discoveries highlighting the benefits of hydrogen sulfide, you may be asking yourself:

How can something that is so deadly also be beneficial?

The answer lies in the dosage. While scientists are still working on understanding HOW the gas functions in the body, we do know that hydrogen sulfide has beneficial effects at low levels, but toxic effects at high levels. The importance of dosage on human health is not just specific to smelly hydrogen sulfide. In fact, just about every substance that we come in contact with throughout the day has different effects depending on the dosage: even drinking water can be harmful if you consume too much! (Water intoxication: it’s a real thing! Read about it here.)

An easy way to think about dosage effects is the common saying (and the Kelly Clarkson pop hit):

What Doesn't Kill You, Makes You Stronger

In other words, exposure to low doses can activate cellular responses that provide protection to the cell, making it “stronger”. However, these cellular responses may be insufficient at higher doses, ultimately resulting in damage and death. 

There is a lot to learn about hydrogen sulfide before we begin using it regularly as a therapeutic. For those who work in environments where hydrogen sulfide poses a serious occupational threat, utilizing the gas for medical treatment still sounds extremely dangerous and irresponsible. By improving our understanding of the cellular effects of hydrogen sulfide at different doses, scientists can minimize potential dangers of hydrogen sulfide as a therapeutic. Ultimately, the potential benefits of hydrogen sulfide in agriculture and human health make it an important and exciting research field for the future.

If you’re interested in learning more about hydrogen sulfide, you can visit our lab’s website here!

This blog post originated as an exercise for my SciFund Challenge Outreach course, but I liked it so much that I thought it’d make a great first blog post! Let me know what you think!