Hi. My mom and I both dance. I was trained in ballet, but spent most of my performing years in contemporary and modern dance. My mom was trained in modern, but added some ballet later in her dance life. We are working on a paper together (as research partners) trying to answer the question, "Are we likely to choreograph the same because we are genetically similar as mother/daughter? Or are we not likely to choreograph the same due to our difference in training?" Any insight would be great. Thnx!
So, there are a few problems with the experimental design that I think you described. I’ll get into them and then propose something?
First of all, I don’t think there’s a good measure for similarity in choreography, necessarily. It’s not something like height, weight, or eye color where you can stick a number on it and ask “Are these the same”? It’s not something like handwriting, where you can compare each unit and ask how much they overlap. So you’ll want to spend some time specifying that question: what do you mean when you say “choreograph similarly”?
Secondly, I think most scientists would look askance at your sample size and the design of your experiment. It’s almost impossible for you two to choreograph two pieces without biasing the results in some way, just because you know it’s a study. (The interpretation of whether something is ‘more similar’ or ‘more different’ runs into this same exact problem, which is what I was referring to above.) And even if you could forget that you were choreographing something for a study and just choreograph, with only two people to consider we can’t really generalize in any meaningful way. You’d need more people, with more varying dance backgrounds. (Which was another concern for me: I don’t see much difference between your background - some ballet, but mostly modern and contemporary - and your mother’s background - some ballet, but mostly modern.)
Finally, and possibly most importantly, you need something to compare to. Most geneticists don’t use parent/child pairs as data points in genetic studies because there’s just so much that a parent gives that isn’t DNA. While we can compare genetically identical siblings (identical twins) to genetically non-identical siblings (usually fraternal twins) in order to get a sense of whether something is genetically inherited or not, there’s no perfect control group for a parent/child relationship. That means there’s no other adult who isn’t related to you, but who has the same social/cultural relationship to you as your mother. The best I could think of would be using adoptive parents as a control, but adoptive mother/daughter pairs who both dance seriously has to be a small group of people, and the sad truth is that there are a lot of differences (socially, culturally) between growing up with your birth mother and growing up with your adoptive mother. So even if you found enough non-adopted and adopted mother/daughter pairs to do your study, there would be a host of potentially confounding variables.
One possibility is that you’re considering differences between people who have trained both in ballet and modern, but maybe started in one or the other. If you start in ballet, does it effect your style? You could do a study of that just by examining as many dancers as you can who have trained in both ballet and modern for common stylistic variations. (To be honest, having essentially no dance training, I’m not certain what these would be, but you probably know that part.) This wouldn’t get at genetics necessarily, but it might get at whether style is something that is internal — your style is yours no matter what your background — or external — determined by what, and when, you trained.
Hope that’s helpful!
Somehow, this is more depressing than usual:
I want to extend my congratulations to all of you finishing this year, and wish you luck in the Post Doc and job market. I’m sure someone right now is compiling the numbers of average number of job applications to interview to offer of job ratios, and I’m sure it isn’t looking good. What I’ve heard around the water cooler is that for the biology types the numbers are several 100 applications, less than 5 interviews, and only one offer. Good thing is one is all it takes.
I’m trying to console myself with the fact that other grad students I know have not had that experience (applying for hundreds of postdocs, getting a handful of interviews, and only one offer). They usually get only a handful of interviews, and they usually aren’t accepted everywhere, but they aren’t applying to hundreds of positions, they’re applying to around ten.
It doesn’t help that while I am a reasonably good writer, my skills and patience seem disappear when it comes to the kind of strictly structured writing that does well in grants. And while I have seriously thought about leaving academia in order to pursue other science-related careers, I always come back to academic research as my top choice.
And anyway, I have two papers and a thesis to write. So I should be doing that, not worrying about grant/job applications.
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Drabble lab round four is up on mad art lab! See last week’s winners, write a drabble of your own, and win an illustration!
It’s difficult to tell when it’s appropriate to pontificate on all of the possible ramifications of your research in a conclusion section, and when it’s best to be quieter. On the one hand, I would much rather sound like Watson and Crick at the end of their landmark paper on the structure of DNA, casually underplaying the fact that the double-helical structure suggested a mechanism for DNA replication, than the writers on the ENCODE paper, overstating their conclusions to the point of irrelevancy. On the other hand, I think that Watson and Crick were writing an obviously significant paper - EVERYONE was looking for the structure of DNA, EVERYONE knew that it was a big deal - which isn’t something that most of us experience regularly (if ever). So most of the time you have to go big in order to get anyone to read your paper in the first place.
In particular: I study the placenta, and in particular epigenetics in the placenta. Studying the placenta means that I can draw some kind of hand-wavey link to “curing” pre-eclampsia or premature birth or diseases of pregnancy for every experiment I do, even though my research is such basic science that it won’t have a translational effect for 10 or 20 years (if that). Studying epigenetics means I can do the same thing with cancer. When I was writing grants, there were reaches I could make to say I was studying heart disease, and autism, and schizophrenia, and obesity, and you name it. But none of that seemed honest. I wish we lived in a society that valued basic research more: where I could be honest about why I do my research (to further understanding, because there are cool phenomena that we don’t understand) and still get funded or published. But that’s not where we are right now, so I’m stuck in the bind that every basic researcher is stuck in — how much am I willing to reach to appease others?
Probably, the answer is determined more by what kind of stories you want to tell (read: what kind of researcher you want to be) than by what your data actually says. And right now, I’m hoping that high-quality research with solid conclusions, and a focus on making a story interesting by making it accessible rather than making a story interesting by overstating its importance, will win through in the end.
Round two of drabble lab is up at Mad Art Lab! Go see the winner from last week and contribute a drabble for this one!
Guys. Hey, guys. There’s a new feature at Mad Art Lab. Write a drabble, and win an illustration! There are already some great ones up there; go see what other people have written, and write your own! 100 words doesn’t take very long!
It is taking all my restraint not to post this entire comic. But I want you to visit The Oatmeal and experience all its riches, so: Why The Mantis Shrimp Is My New Favorite Animal.
If you haven’t clicked through yet, let me add a little incentive: a later panel of this comic contains the line “The mantis shrimp is the harbinger of blood-soaked rainbows.”
And if you would like to know even MORE about these miraculous creatures, we have a Radiolab episode for you, complete with a Mantis Shrimp choir.
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If we listen to Rebecca Schuman, who recently updated Pannapacker’s screed for 2013 in Slate, [people stay in academia] because we were too stupid to heed his message, suggesting that the original article “convinced no one.” And, as Schuman writes, “It certainly didn’t convince me! Why? Because Pannapacker is a tenured professor. He pulled it off, so why can’t you? After all, someone has to get these jobs.” Yes, perhaps we are stupid and optimistic and blind. In some situations, like when the world is going to shit, sometimes these aren’t the worst things to be. But I don’t think it’s that we’re all just sitting unaware that the sky is falling and hoping it won’t fall on us. Some of us, as Tressie McMillan Cottom suggests on her blog, are trying our best to be “brave” and we are trying to stick around in this shitstorm of terrible labor practices, endless competition for scarce jobs, nasty administrative choices (like the president of CUNY calling grad students “roaches” or, even worse, pepper spraying our undergraduates who have dared to question the vision for higher education in this country) because we care and we want to change it. Or, because even if the university succeeds in chasing us out, we haven’t failed by completing a PhD.
A very thoughtful response to the typical “Never go to graduate school” article that comes out every so often. I sincerely believe that academia is, in certain ways, fundamentally broken - but that it will only be changed by people willing and able to work from the inside. If tenure is a lottery (and it probably is), then this is just a numbers game. We can move the numbers in our favor by having more graduate students and faculty applicants who actually do care, who are braving it, who want to change the system. Read the whole thing!
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can you describe the evolution of a phenotype trait and what kind of environment is it adaptive for in that environment, example: skin color
I’m not entirely sure where you’re going with this, necessarily, or how wedded you are to understanding skin color. Skin color, especially in humans, is a very complex trait with many genes involved. But there are some pretty obvious selective advantages for both pale skin and dark skin that vary based on geographical location, so I’ll definitely get to that. I wanted to start with something genetically simpler, however, so I’m going to start by talking about sickle cell anemia and malaria risk.
(All of the geneticists who follow me are now rolling their eyes, because that is just about the most obvious example to use. But it’s obvious for a reason, as you’ll see.)
In tropical areas, where malaria is endemic, it’s a very serious health risk. Malaria is a disease caused by a parasite (Plasmodium) that lives in mosquitos and in humans. In humans, it lives in the liver for a while, and then in red blood cells. It doesn’t cause that much trouble in the liver, but in red blood cells it can wreak a lot of havock - causing malaria. Because malaria is so dangerous, there’s a strong selective pressure towards essentially anything that will make the parasite less likely to infect you. One of those things is changing the shape of red blood cells so that they get degraded and recycled more quickly. If any specific red blood cell is only in the blood stream for a short time, the parasite doesn’t have time to multiply, and the disease isn’t as dangerous. This is referred to as sickle cell trait. It’s controlled by a single allele of hemoglobin (the molecule that carries oxygen in blood), and it’s very prevalent in western Africa (up to 25% of the population has sickle cell trait). That’s because in western Africa, where malaria is an issue, sickled cells are an advantage.
However, as soon as you leave the tropics, malaria isn’t so much an issue. In northern Europe, for instance, malaria is rare. In that situation, another trait of sickled cells comes out: they aren’t as effective at transporting oxygen, especially when someone has two copies of the sickle-form hemoglobin. That’s when you run into cases of sickle-cell anemia, or sickle-cell disease. And it’s a serious disease as well.
So you have two competing pressures: one against sickle-cell disease (and hence the S form of hemoglobin), and one against malaria (and hence for the S form of hemoglobin). In climates where malaria is prevalent, the latter takes over and the S form is selected for. In climates where malaria isn’t prevalent, the former takes over and the S form is selected against. We can see this by population genetics: people whose ancestors came from northern climes don’t have the S form, people whose ancestors came from the tropics much more often have some allele that makes them more resistant to malaria (such as the S form, or several others, most of which also have similar trade-offs).
How does that fit in with skin color? Well, your skin makes an essential vitamin: vitamin D. It only does that when you’re out in the sun, though, so in northern climes it’s hard to make as much vitamin D. If you don’t get enough vitamin D, you can wind up with a host of health problems - such as rickets, where you don’t get enough calcium into your bones. One way to more efficiently grab vitamin D from the sunlight is to have lighter skin. So in northern climes, lighter skin is an advantage.
On the other hand, sunlight also has some negative health effects. Like skin cancer. In the tropics, therefore, it’s an advantage to have darker skin.
I can’t point to any specific alleles that have been selected for or against, because like I said skin color in human populations is an enormously complicated trait. But hopefully that summary helps you understand why different skin colors may have evolved, and why different climates require different genes, both pigment-related and not.
