What is a stem cell?

Tree1You started out as one cell– wicked, right? Now look at you! Brain, skin, blood, all of these can be traced back to that first cell that was you. Since you’re bigger that one cell, this cell had to make more of itself. Since you’re more complicated than a blob of identical cells, they had to specialize to become brain, skin, and blood. These cells that 1) make more of themselves for a long time and 2) can specialize to become other cell types are called stem cells. “Stem cells” is a category more than one specific cell type. Members vary widely, and they differ in the kinds and number of cells they can become.

While people may be familiar with the most controversial kind of stem cells, embryonic stem cells (ESCs), you may not know that you have stem cells in you right now. For just one, you have blood stem cells in your bone marrow. These hematopoietic (blood-forming) stem cells can become every kind of blood cells, red or white. In fact, one true hematopoietic stem cell can remake all of the blood: if you irradiate a mouse such that all the blood cells die (akin to radiation treatment for leukemia), and then you put in one hematopoietic stem cell, this stem cell can remake all of the different kinds of blood cells, and the mouse lives.

If stem cells can go from less specialized to more specialized and remake whole systems, can we go the other way? Can we take a very specialized kind of cell and make it go back to a less specialized stem cell? Yes! Since every cell keeps the same DNA instructions but only uses different subsets, we just have to tell the cell to use a “be a stem cell” subset of DNA instructions. Yeah… just.

It’s hard to do, but you can tell a specialized blood cell to become a any-cell-making stem cell– to make them a “pluripotent” stem cell. This process is a switching-on or “induction” of a subset of DNA instructions that say “be a pluripotent stem cell.” It results in a really powerful bunch of cells that might just hold the ability to repair whole systems– brain, skin, or blood. These are induced pluripotent stem cells. These are iPS cells.

I’m writing this at a stem cell conference. It sounds like the problem has (for now) changed from “how do we make stem cells from specialized cells” to “how do we make specialized cells from stem cells.” It turns out we don’t have a great sense of how you go from that one first cell to all of the different cell types. For example, there are several stages in between fertilized egg and blood that we’re still identifying. But we’re working on it.

Our goal: take a bit of your skin or blood (big pools of cells with easy access), induce the right genes to make them iPS cells, then turn these iPS cells into the kind of cell you need replaced. Maybe we fight Parkinson’s with neurons for your brain, baldness with hair follicle cells for your skin, or HIV with helper T cells for your blood, and each of them from iPS cells.

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What the Ghostbusters Taught Me About Communicating

I was rewatching Ghostbusters II, and Winston Zeddemore taught me something about how to communicate a complex subject effectively.

It was a throwaway scene that looked uncomfortably familiar. There was a problem, and the team needed the help of someone in power. They turned to the mayor, trying to convince him that there was a river of evil, thought-responsive pink slime under the city. Ray (Dan Aykroyd) tried first.

Ray’s plan:
1) Kiss butt.
2) Describe in sciency words (like “psychomagnotheric”) the problem.
3) Expect the mayor to do something.

What was the result? The mayor didn’t get it, and Ray was nearly responsible for the destruction of NYC.

Now the Ghostbusters are four people: two egghead academics (Ray and Egon), one wildcard (Pete), and one regular guy (Winston). Winston saved the day and taught us all an important lesson about communicating a complicated, technical, yet important scientific point.

Winston’s plan:
1) Know his audience is an unfamiliar with this field and might be antagonistic.
2) Explain the essential takeaway of the problem without relying on jargon.
3) Make his audience care by connecting with something they care about.

The mayor is visibly more inclined to think about this version of the story.

So what can we learn from Winston’s technique?

The only hard-fast rule of communication as far as I can tell is KNOW THY AUDIENCE. Ray and Egon use big words that an uninitiated listener wouldn’t know. Would you stop and listen to anyone (even in a lab coat) talking about psychomagnotheric anything? No, because you don’t care. The words important to us as scientists usually mean little to those outside our immediate fields. I know it’s a big deal with someone successfully performs crystallography for an important protein, but try telling that to the mayor of New York City.

Why not say what you would say after “basically…?” When I write something complicated, and can feel myself wording it into knots, I reboot and start the sentence again with “basically.” For some reason, this is especially useful for writing first sentence of paragraphs of science manuscripts. My goal is to write these so that the paper is understandable by reading only these first sentences. Start with the big point.

In the end, both Ray and Winston failed. This was at least partly because they didn’t know exactly what it is they wanted from mayor. This may have doomed them to fail the first round, but because of Winston’s tactics, the mayor knew to call the Ghostbusters when it all went south.

Thank you for saving the world, Winston Zeddemore, with your superior communication skills.

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Enhancers Are Not Switches – Why We Should Kill a Bad Metaphor

“All models are wrong, but some models are useful.” So said George E.P. Box. Models are mental shortcuts that simplify complex thoughts/events/etc. There’s nothing really wrong with explaining a complex idea using a model– in fact the quality of your model can show how well you understand the full concept. But “enhancers are genomic switches” is an outdated model that is causing us issues in explaining new findings. I’m not going to just bury this metaphor but also suggest a replacement– “Enhancers are genomic boardrooms.”

First, what is the full definition of an “enhancer?” This is trickier than one would guess for a thing that was discovered decades ago. Protein-coding DNA genes get transcribed (photocopied) into mRNA transcripts. Enhancers are also pieces of DNA that “enhance” the transcription of these protein-coding genes. So if you just have the piece of protein-coding DNA in your experiment, it gets transcribed at level X. If you have the protein-coding gene and the enhancer on a piece of DNA, the protein-coding gene gets transcribed more. This is how we used to think of enhancers.

As genomes evolved from simple, circular bacterial DNA to the linear chromosome structure seen in humans, bits of DNA changed or got re-purposed. We can find substantial similarity between the parts of our genomes that code for proteins and the protein-coding genes from our distant ancestors. This is less true of enhancers– they tend to be less “conserved” across evolution. We know many parts of the human genome have certain characteristics of enhancers, but the DNA letters in their spans are tough to find in mice and bacteria. This may mean that, when and where genes are used/transcribed/expressed is the big difference between us and other animals. Gene use/transcription/expression is controlled by enhancers.

Bacteria have one cell type; humans have hundreds. Enhancers in humans control when and where genes are turned on. This is why many researchers and press releases have said that “enhancers are switches.” They can have the effect of some gene or genes being turned on when the enhancer is active. What an “active enhancer” really means is what leads to the breakdown of the metaphor of “enhancers are switches.”

Enhancers are regions of DNA. They don’t have letters in the right order to code for protein though, and enhancers are often hundreds or thousands of letters away from the pieces of DNA that do. So how do enhancers have anything to do with transcription if they can be so far away? Well, DNA is kind of like an old school phone cord. Sure, it twists in the familiar helix shape, but it also loops like string. This way, enhancers can loop toward the genes whose transcription they control in 3D space. What it does when it gets there is only recently starting to be appreciated.

drawing5

Actually, enhancers are like boardrooms. When a meeting is held in a boardroom, decision-makers congregate, and they have some knowledge of the whole system that’s needed to make a decision. The decision-makers of the cell are proteins that bind to DNA to conclude whether or not a gene should be transcribed.

Some protein-coding genes have the right recipe to make proteins that act as signals. (To get technical for a moment, they’re called “transcription factors.”) These signals can mean something about the state of the cell– I’m attacking virus– or the environment the cell is in– it’s hot out– or even something about the type of cell it is– I’m a nerve cell. Production of a certain protein can be the end result of a signal-processing pathway and usually means that some gene needs to be transcribed. So these signalling proteins, whose very existence means something about the cell, bind to enhancers that are responsible for controlling transcription of certain genes. These enhancers get bound by a bunch of other proteins and loop in 3D space to the start of the protein-coding target gene. In this way, enhancers aggregate signals from several information sources to decide whether or not to transcribe given genes.

1) Information-carrying protein binds enhancer
2) Enhancer loops to some target gene
3) Protein-coding gene is transcribed
4) Protein made from transcribed
[Optional] 5) GOTO 1

Why does the “switch” metaphor suck? Calling enhancers “switches” limits the amount of things we can say about the latest findings, the majority of which have to do with what’s going on at/with enhancers. Sure, the end result can be expression of a certain gene, but the switches familiar to a lay audience usually involve only one input and are geographically close to the thing they’re controlling. Enhancers can be really far away in the genome and accumulate decisions made from several bits of information.

The proteins binding to DNA are the managers of different departments that have come to the enhancer boardroom. They have made the decision about if transcription of some gene is right for their purview. If all the department managers bind to DNA, signifying their intent, then transcription happens. They don’t flip switches– they make decision by combining information from many sources.

Some boardrooms are more important than others and decisions made within them can have broad or focused impact. For instance, the enhancers controlling genes whose proteins specify cell type have huge reach and can influence nearly every other gene in the genome. Or, perhaps the decision is more focused on whether or not a certain protein pump needs to be on to get more of chemical X into a cell. Calling enhancers switches makes them too egalitarian.

If you’ve made it this far and hate me for my proposal, fine. But you should also know that enhancers don’t really “enhance” transcription, and the thought-leaders in this field are considering burying the term itself. More on that maybe some other time.

While they live though, enhancers thus are not switches, but they are boardrooms. QED. RIP, bad metaphor.

Tl;dr: Enhancers are DNA segments that bind protein signals and control whether or not a gene is transcribed. Calling enhancers “switches” totally undersells the important part. Protein signals are section managers that meet in the enhancer boardroom to decide to transcribe.

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How We Balance (According to My Girlfriend’s Brain Tumor)

[[Not a medical professional. Not recommending anything here for anyone. This is a story and an explanation of the biology, not a case study or a plan of action.]]

I sat on the sill introducing my work and myself to a 6-foot-intimidating former cop—her father—when she was wheeled back into her hospital room Her hairline was decorated with thumbnail-sized glow-in-the-dark stickers outlined in purple, giving her an oddly Trill-like look. She had been sobbing, and apologized needlessly to her mother, from whom she inherited her forgivably lousy poker face. She hugged her crisply dressed brother, quiet with travel stress and concern. So closed our fourth date and the night before my girlfriend (MGF) had her brain cut into.

Shortly after our first date, her PCP suggested a CT scan to find out what was causing her headaches. This is the same as a CAT (computed [axial] tomography) scan and is essentially a bunch of X-Rays stitched together with computer software. Think of it like bullet-time movie sequences where you take a bunch of simultaneous 2D images from many angles and put them together to get a 3D image. This 3D picture showed that something was definitely amiss in her brain, but it wasn’t detailed enough to pinpoint the cause.

By Life Science Databases(LSDB). [CC-BY-SA-2.1-jp], via Wikimedia Commons

By Life Science Databases(LSDB). [CC-BY-SA-2.1-jp], via Wikimedia Commons

When I think of headaches, I think of Jean-Luc Picard. Specifically one scene where the Captain mentioned his headache to Dr. Crusher, who replied “It may be true that headaches were once quite common, but that was in the days before the brain was charted, before we understood the nature of pain. When we were suffering from such things as the common cold.” The 24th century view of headaches can’t come soon enough. Today, something as common as a headache can come from so many still mysterious causes.

While I was away at a conference, she texted that the CT showed an “asymmetry of the fourth ventricle.” Okay then, Internet, don’t fail me now. I learned that brains really don’t like it when you mess with the the level, flow, and pressure of cerebrospinal fluid (CSF). CSF is a salty fluid that, among other jobs, helps cushion the brain inside the skull. It is salty because salts are the chemicals that make electrical impulses in nerve cells happen. CSF flows through four ventricles in the brain that help maintain CSF at the right levels; the fourth is highlighted on the left in blue. The ventricles are normally symmetric– the left side looks essentially identical to the right. That her ventricle was asymmetric could easily contribute to nasty headaches. That is when I knew she had a growth, though the CT didn’t show where or what kind.

More imaging showed a ping-pong ball-sized growth on her 8th cerebral nerve. An acoustic neuroma.

Holed up in the lab everyday like I am, it’s easy to forget that the samples and cells we work with every day have legacies going back to real people with real diseases. After MGF was diagnosed, I learned that few cell lines– cells that can live essentially forever in a Petri dish– exist for this tumor type, which renders research difficult. I learned, courtesy of the results that popped up from Google’s autocomplete feature, that this is the kind of tumor that people claim, using fuzzy statistics, is linked to cell phone usage. Trying to understand and explain what MGF was going through, I forced myself to remember my anatomy class’s mnemonic device for cranial nerves, completing the decade-long trip from what I once learned in textbooks to a living, breathing patient who is also a person important to me. “On Old Olympus Towering Tall A Finn And German Viewed Some Hops.” The problem was on the “And” nerve.

The kind of tumor that grew in my girlfriend’s brain is called an acoustic neuroma or a vestibular schwannoma; these names themselves say a lot about what this growth is and where it comes from. They’re also tongue-twisting, so her family took to calling it “Norman.” One of my sappier retorts was saying we would take Norman and put her back to Normal.

Of all the nerves that start in the brain– the cranial nerves– the 8th is responsible for transmitting the signals needed for two jobs: processing hearing and sensing balance. This 8th cranial nerve is comprised of individual neurons and has several names that include descriptors like “auditory,” “acoustic”, “cochlear,” and “vestibular.” Auditory, cochlear, and acoustic are terms that refer to processing hearing, while the vestibular system deals with spatial orientation. The vestibulum is in the inner ear and uses a cute trick to help your body sense which way is down. Inside the vestibulum, tiny stones called otoliths are pulled down by gravity. Small hairs sense where the stones are, and send nerve signals to the brain so it can identify which way is down. The nerves have a long tail that is protected by special cells called Schwann cells. Thus, when you screw with the acoustic/auditory/vestibular nerve, you get hearing loss and trouble with balance and orientation. The –oma at the end of the tumor’s name is a convention used for an abnormal mass of cells. Acoustic neuroma = too many Schwann cells pinching the 8th cranial nerve.

By Sunshineconnelly at en.wikibooks [CC-BY-3.0], from Wikimedia Commons

By Sunshineconnelly at en.wikibooks [CC-BY-3.0], from Wikimedia Commons

Balance is a funny thing. We undersell it as one of The Five Senses, but there’s a certain amount of equivalence to balance. Left and right in equal amounts. Even in the time spent on X and Y. Even in the way weight is distributed. Without knowing where down is, it’s easy to lose sense of where you are. To cope with balance issues, we can lean on others just as MGF leaned on her IV pole and on me when she walked during recovery. Even identity has balance– the Trill have to share identity of the host and identity of the symbiont.

Though all tumors are dicks, not all tumors are equally dickish. A tumor is just a lump of cells that’s growing too fast relative to the cells around it. It gets a new term, “cancer,” when it starts to spread beyond the first mass. Not all cancers are the same, just as not all tumors are the same. Since MGF’s schwannoma came from Schwann cells, which live almost exclusively on neurons, there wasn’t a big risk of them breaking off and invading other parts of her body to become full-blown cancer.

Cutting into someone’s brain is always risky. Yet, all of MGF’s doctors recommended surgery. Why bother if the tumor wasn’t going to spread? Well, there’s only so much room in the cranium, and this new growth was messing with things that needed room. When your limbs fall asleep, it’s not because they lose blood flow it is because nerves within them are getting pinched, hindering their ability to carry signals. The cranial nerves on either side of her 8th nerve were getting pinched, causing issues with sensing and controlling her face and tongue– something that needed to be addressed.

Her tears the night before the surgery stemmed from a “legendary” MRI session. The purple spots outlined landmarks on her face to calibrate machines. We slept as best as we could, we woke mere hours later, the prep team came, she was rolled down to the OR, and they cut. The surgeons went in at an angle that permanently severed her 8th cranial nerve. This has good and bad news attached to it. On one hand, they got it all and are confident it didn’t spread. But, on the other hand, she now has to contend with worse balance issues, and is now deaf in her right ear.

The headaches that had been haunting her have yet to return. She has been in physical therapy to cope with her new balance, kicking significant levels of ass along the way (P < 0.05, ASS test). And, perhaps most importantly, the purple spots have washed off and are behind her. Hopefully they’ll never be back.

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The Official List of Dead Cliches in Reaching Audiences of real People (O.L.D.C.R.A.P.) about Genomics

I like doing outreach. I like talking to non-scientists about science, but I’m a relative newbie in science, so the powers-that-be rarely let me give bigger talks to bigger groups. So I frequently find myself watching more senior scientists give talks to non-scientist audiences.

And I am sick of seeing the same trite, tired, ineffective, cliched slides and hearing the same words from each of them.

Henceforth, I propose that we, as concerned scientists, kill and bury the following cliches. This list will never be complete, and I welcome proposals for additions:

1) The Moore’s law slide.

Yes, the cost of sequencing DNA has gone down. It’s gone down fast. It’s gone down faster than it “should.” Why in the world do we care? This ain’t no economics lecture. It used to matter because of the mythical $1000 genome and how close we were to that. We hit it; there were no parades. How about we instead show the rate of production of DNA sequence in hard drives? Or terabytes? Or petabytes? As an aside, the government is good at some things, and quality slide aesthetics seems to not be one of them.

2) “Junk DNA.”
Call it the Jason Voorhees of genomics metaphors for the number of times it’s been killed and revived only to be killed again. Whoever decided that, just because we didn’t know what this DNA was doing, it meant it was junk ought to feel shame. So very much shame. Your mother gave you this DNA, and it was important to her that you have it, so it should be important to you. People who call it “junk DNA” don’t love their mothers.

3) “Dark Matter of the Genome.”

BPaKNFqCUAAkO9R

Photo Credit to @ErinPodolak


This is tied up in the recently departed junk DNA accusation. As “junk DNA” gets zombified, a new term has cropped up to admit that, okay, it’s not junk, but we don’t know what it does. Biologists have borrowed a highly defined term from cosmology to describe pieces of the genome with unknown function but known presence. It’s at least better than “junk DNA,” so it’s more like hating your great aunt than hating your mother.

4) The GWAS SNP slide.
GWAS_2012-12
There. Is. No. Information. In. This. Presentation. It used to be cute when you could see that you’re pointing out stuff on chromosomes. It used to be cute when there were only a couple colors and a couple regions you cared about. It used to be cute before Calibri. Now, it looks like someone spilled sprinkles on their mom’s team-building memos. What’s the point? There are exact counts of SNPs. There are bar charts that show how many pieces of DNA are correlated with a disease. If you need to rely on a confusing slide to express that genomics is confusing, you miiiight be a scientist.

Okay, end rant. Who’s got more OLDCRAP for me to hate on?

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Asari Sex & Genes 101: How We Do It Like Liara

Copyright ideonexus under Creative Commons Attribution License

Copyright ideonexus under Creative Commons Attribution License

The Asari are near the top of list of uber-powerful galactic babes, alongside Leia and Twi’leks. Yet, if you’ve played Mass Effect, you know that they’ve got a peculiar way of ensuring the stable beauty of their species. Asari can and do mate with many other species, but the offspring is always wholly Asari and pretty much always gorgeous.

In human-human mating, half of your genes come from your mom and half from your dad. In humans and many other species, this halving is accomplished by chromosomes– big chunks of DNA that break the encyclopedia set of all your genes into 23 pairs of books. Half of these chromosomes come from the sperm cell and half come from the egg cell. The cell that results when the sperm meets the egg then has two copies of each chromosome.4.0.4

Asari, supposing they also use DNA for their parent-to-offspring inheritance, pass on their genes in a slightly different way. When an Asari and a member of another species do it, apparently all of the DNA containing all the genes come from the Asari parent and none from the other one.

Wait, doesn’t this make each Asari an exact genetic duplicate of its mother? Wouldn’t that mean there are gobs of Asari clones walking around? Since there is some variation between Asari individuals, there must be something different than this.

It turns out that one of the two copies of the genes gets “shuffled.” So each Asari daughter gets one, unshuffled set of chromosomes from her mom; the other chromosome copy has source DNA material from her mom, but it gets shuffled. The shuffling happens based on the thought patterns of the mate.

So this gene “shuffling,” does that happen in human mating? We learn in school that you get one of each chromosome from mom and one from dad, but do you end up with exactly the same chromosomes your parents have? Nope!
Meiosis_overview

When sperm cells and egg cells form– a process called meiosis– there is something like Asari shuffling. In humans, we don’t shuffle one copy of each chromosome’s genes by thought patterns, but instead there is a shuffling-like step called “crossing over.”

During meiosis, there is a point where either your mom’s cell or your dad’s cell divvy up chromosomes between two egg or sperm cells. (Each egg or sperm is supposed to have only one copy of the chromosomes, so we *have to* split the chromosomes.) It turns out you can take chunks of a given chromosome along with chunks of the one its paired with and make a combined chromosome. You’re not getting exactly the same chromosome that your grandparents had or your parents had. It’s not exactly like Asari shuffling, but it keeps our diversity spicy.

When the chromosome pairs don’t separate correctly in sex cells, we get disorders like Down syndrome and Klinefelter syndrome. These are caused by the fertilized egg having the wrong number of chromosomes and giving all other cell types too many copies of certain chromosomes. This makes me wonder: do Asari always get the right number of chromosomes? Does that mean that there is no possibility of these types of disorders happening among Asari? Does anyone Citadel-centric know?

Reference: http://masseffect.wikia.com/wiki/Asari

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Things I Learned at #scio14 – Building the Network

Scio14_Together_big

This above all, know thy audience. It is amazing how frequently these words were uttered, have to be uttered, and should be uttered to all who communicate. Beyond this, the most important thing I got out of Scio14 was the community, the network.

I went to my first ScienceOnline event in the form of the dearly departed scioBeantown. This group, alas, was destined for failure because hashtags-plus-nicknames-longer-than-city-name doesn’t work. Through this group, I realized the potential for awesome in the ScioX meeting and vowed to go. I refreshed the registration page gobs as soon as it was scheduled to open to guarantee a spot for myself. (As an aside, we [read: Erin Podolak and Haley Bridger] rebranded as scioBoston and will start kicking tail as soon as the tundra thaws.)

The chronological first thing I learned at Scio14 was that no one’s a vegetarian because there are irremovable numbers of tardigrades in pretty much all the plants. Thanks, Meg Lowman.

I learned that we need to form a roving band of friendly scientists to put their faces in front of people who treat scientists like endangered species. I had a great talk with Emily Finke to this effect and really want to rope in AAAS/@MeetAScientist. Let’s Howard Dean this stuff.

Dave Wescott‘s self PR (#scioSelfPR) talk might have been my favorite. I am a great follower of instructions, and his were salient and succinct: know your audience, get where they are, tell them what they want to hear.

I learned that there is a man named Todd whose job it is to control bird populations at LAX via Justin Kiggins.

I learned that, dammit, I need to make swag with my Twitter handle on it.

I learned that there are two rules governing tweeting something and understanding it:
1) If you can’t tweet it, you don’t understand it. ~Janet Stemwedel
2) Even if you can tweet it, it doesn’t mean you understand it. ~Pascale Lane

I learned that PowerPoint karaoke will DEFINITELY be atop my suggested events for the institute retreat.

I learned that there are many hats and varying numbers of people to wear them in the world of “helping useful people help others.” Mentors, sponsors, advocates, cheerleaders all describe some subset of these people, but we lack a Venn diagram describing their overlap. The conversation should continue on #scioMentor

I learned that there is power in this community. I covered my feelings of distraction previously, but it was so powerful to see important problems addressed head-on by those most affected.

I learned that, if I must depart this world sometime, I would prefer to be drowned in coconut cream.

The Network:
I wanted to capture the connections made at Scio14, and I am a computer geek. I decided to parse Twitter hashtags for who used them and create a network based on the ScienceOnline logo.

1) To parse Twitter, I installed the R package twitteR.
2) I found the most recent 500 tweets using each of the session hashtags.
3) I used igraph to plot the edge list where each edge/line connects a tweeter to a hashtag.

The output image is a PDF and can be searched by your username. There’s a certain amount of randomness in the layout, so apologies if you’re behind someone– nothing nefarious there. I myself am behind the #scioHope node.

The Code:
library(twitteR)
library(igraph)

### Convince Twitter you’re legit
reqURL <- “https://api.twitter.com/oauth/request_token”
accessURL <- “https://api.twitter.com/oauth/access_token”
authURL <- “https://api.twitter.com/oauth/authorize”
consumerKey <- “c0nsum3rk3y” ### Replace with your own OAuth data
consumerSecret <- “c0nsum3r5ecr37″ ### Replace with your own OAuth data
twitCred consumerSecret=consumerSecret,
requestURL=reqURL,
accessURL=accessURL,
authURL=authURL)
twitCred$handshake()
registerTwitterOAuth(twitCred)

### Hashtags to retrieve
toGet<-c(“scioSafe”, “scioMentor”, “scioWomen”, “scioWiseup”, “scioBoundaries”, “scioLaw”, “scioCritSci”, “sciSciLit”, “scioSciBiz”, “scioLang”, “scioDesign”, “scioAlt”, “scioDiversity”, “scioTools”, “scioSciAll”, “scioSociety”, “scioCollab”, “scioProcess”, “scioSelfPR”, “scioReview”, “scioTradLit”, “scioHope”, “scioPsych”, “scioPress”,”scioBigSci”, “scioBeyond”, “scioAble”, “scioNews”, “scioBeltway”, “scioSciComm”, “scioMOOC”, “scioSuccess”, “scioLive”, “scioResearch”, “scioVirtual”, “scioParasite”, “scioImprove”, “scioVidBrand”, “scioVisual”, “scioDigLit”, “scioJSE”, “scioBlogNet”, “scioPlatforms”, “scioComments”, “scioMentor”, “scioBootstrap”, “scioSchoolTools”, “scioUncertainty”, “scioCommunity”, “scioStandards”, “scioImagine”, “scioEthics”)

edges<-matrix(nrow=0, ncol=2)

### Retrieve 500 tweets per hashtag
for(i in 1:length(toGet)) {
tweets<-searchTwitter(paste(“#”, toGet[i], sep=””), n=500)
df <- do.call(“rbind”, lapply(tweets, as.data.frame))

newEdges<-matrix(ncol=2,nrow=length(unique(df$screenName)))
newEdges[,1]<-unique(df$screenName)
newEdges[,2]<-toGet[i]

edges<-rbind(edges, newEdges)
Sys.sleep(30) # because Twitter doesn’t like it without
}

### Do some prettying up
theGraph<-graph.edgelist(edges)
V(theGraph)$color<-”orange”
V(theGraph)$frame.color<-”orange” V(theGraph)$size=2 V(theGraph)$vertex.label.color=”black” V(theGraph)[degree(theGraph)>40]$color<-”black” V(theGraph)[degree(theGraph)>40]$frame.color=”black”
V(theGraph)[degree(theGraph)>40]$size=5
V(theGraph)[degree(theGraph)>40]$label.color=”orange”

plot(theGraph, vertex.label.cex=.05, edge.width=0.001, edge.arrow.mode=0, layout=layout.kamada.kawai)

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My Offline Contribution to #scioSelfPR

Hi, I’m TSS, my website is TheSnarkyScientist.com, and I am a previous karaoke contest winner.

My audience is grown-ups who vote and who had their last science class years ago. People get busy, so I can forgive them for not knowing what a gene is.

My question is a bit self-deprecating: I’m not as good a writer as a lot of the people in this room right now. I have found my strength is more in face-to-face communication. How can I find ways to get my target audience in front of me or in an AV situation where I get to talk to them and it isn’t a classroom.

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On The Lingering Issue of Harassment at #scio14

I am a relative newbie to the ScienceOnline community. I have partaken in ScioBeantown in its previous iteration and hope to continue as part of ScioBoston. Through this group, I have met some wonderful people that are hurting right now. My status as a newbie affords me less of the in-community baggage that’s accumulated. That I am unabashed affords me the opportunity to be blunt.

The first breakout session of Scio14 had selections focused on women in science and ways to be an ally to all “minorities.” According to the stream, attendance at these sessions was highly slanted toward women. Apparently the males (myself included, hypocrisy noted) chose poorly and went to a less-weighty law session. Following the tweets from the other session (#sciowomen and #scioboundaries) made me feel horrible for not attending the other sessions, and not being an active contributor to addressing and solving this problem.

Why were there so many sessions focusing on women in science and harassment? Well, Bora Zivkovich, a godfather of science communication, was an extensive, repeat [alleged (added 3/2)] harasser of women. This has been covered elsewhere, and, Dear Newbies, a google search will give you the lay of the land. This led to a conceptualization of “ripples of doubt” wherein female communicators couldn’t separate his favoritism and assistance from their own ability to succeed without his help. Tl;dr, A guy named Bora was powerful and [allegedly (added 3/2)] harassed a bunch of female science communicators.

This elephant in the room needed to be addressed here, because Bora was a big part of ScienceOnline. This led to the session selection. But this wasn’t enough. Friends I’ve made early in this community went to the sessions that tap danced around the subject of Bora [allegedly (added 3/2)] harassing members of the community. Friends were left shaken by the fact that these sessions covered nothing substantially and didn’t really address Bora by name.

This leaves me with a question: why bother having the sessions on harassment and inclusion if 1) the right people didn’t attend and 2) if you aren’t going to address the actual issue.

This matter is hanging like a fart in the air over the conference and needs to be addressed head-on. It should have been the first thing mentioned in a plenary session. The hard truth should not be opted into. It is the only way to build community with newbies like myself. They need to know how we got to where we are today. We all need to know what to look for. And, above all others, we all need to know how to be allies to each other.

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How and Why Journals Should Respond To Retractions

Litmus_paper

This picture is of a litmus test. It’s a paper strip with various dyes on it that can be used to detect the pH (acidity or alkalinity) of a liquid.

According to two papers that were published late January, if you take cells that have committed to being a certain cell type and put them in a certain pH environment for a certain time, these cells behave as though they haven’t made that decision. That is, a cell that has committed to being a blood cell can be coaxed back to being a stem cell.

This did not pass my litmus test for how I understand biology to work.

Imagine my complete lack of surprise when irregularities were reported in the papers.

When the papers originally came out, I was in the middle of taking an NIH-mandated course on research ethics. A lot of the subject matter centered on publishing good research and being a good academic citizen. A lot of the punishment for not doing these things was “oh, you’ll have to retract your papers.” (As a side note, I don’t know if these papers will end up being retracted, nor is it what I’m arguing for at this point.)

In academic circles, having your paper retracted is an embarrassing issue. You only do this if you’re proven wrong in your findings or methods. Since your paper was published (root word “public”), this has to be done in the public eye.

Science is quality-controlled by peer review. This is the process by which fellow scientists read your paper and double-check that you didn’t get anything wrong or misrepresent your results. There’s another party involved in peer review that scientists tend to forget about: the journal itself. In negotiations to get research article published, journals are represented by editors that solicit peer reviews from other masters of the field, since they themselves cannot be masters of all paper subjects. The editor then reads the reviews and gives a final decision about whether the paper gets to be published in the journal.

What happens to the journal when someone’s paper gets retracted? At worst, nothing; at best, double the hits on their website for those checking the article and then the retraction reason. Nature isn’t going to take it on the chin for, if the allegations hold, publishing bunk science. No, they’re going to publicize the investigation and make a big deal about taking down this researcher’s career– not that I’m defending publishing bunk science.

When a journal publishes a scientific paper, they have chosen to publicize a certain finding over all the other findings they could have. There is no one holding journals to a standard that this science be right. Journals are in the business of selling ads and magazines, not in the business of publishing good science. Oftentimes, the best science IS the most engaging and interesting article. Oftentimes, it is not. The editor is responsible for weighing the quality of the science (as analyzed by peer review) with the sexiness factor that will move the journal’s product.

Journals have to worry about their bottom line, and this bottom line is not always aligned with good science. So they paradoxically can benefit from publishing total crap science. Thus, I propose that, if a paper is retracted from a given journal, the underlying peer review process needs to be made public. This disclosure will help the readers of the original article understand how bunk science made it out in the first place. Did the peer reviewers voice these concerns and they were overruled? Did the editor do everything he or she could to address problems with the manuscript?

Why does this matter? Journals like Nature are taste-makers. As soon as these papers were published, I know of at least two other labs a stone’s throw from my own who tried this acid experiment. Think of the time and resources collectively wasted if this result was based on bad science. Keeping up with something interesting enough to be published in Nature is kind of an academic necessity, so of course we’re going to try replicating the results.

My favorite thing about the irregularities in the stem-cell-acid-bath papers coming to light is the timing: it took a mere 2.5 weeks for the papers to be published, get a ton of press, and then be picked apart by post-publication reviewers on the internet. If it only took such a short time for mere interested parties to find the holes, shouldn’t dedicated peer reviewers have picked them out too? Something has clearly gone pear-shaped here.

I really want to know who fails to keep bad science behind the gates. Journals have no legal imperative to do so if it’s going to sell, even if it wastes taxpaper dollars in the form of research funding. Peer reviewers names are usually kept blinded. And the writers of the article are of course going to do everything they can to get into Nature– it’s a big deal to get your paper published there.

TL;DR: because journals of a certain tier have no incentive to keep bad science unpublished, they should make the peer review process for retracted papers public.

And what’s the carrot for the journals? More transparency, invested peer reviewers, and, of course more pageviews.

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