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Talks and Trips, Fall 2012

It’s that time of year when I take stock of how many more times I’ll be away from my family before the semester is through. I’ve pared things down quite a bit this year after traveling too much last year, and so my talks are semi-local, but open to the public. Stay tuned because there may be two more in the works.

September 24-25th, Purdue Conference for Pre-Tenure Women. Obviously I am just an attendee for this conference, but as you probably know I was a huge fan last year. If any of you are going I hope you’ll tell me so we can say hi. I may be a bit battered and bruised because I have a sanctioned scrimmage on the 23rd in Evansville against Sioux Falls (they play Demo City the night before). And incidentally, I’ll be back in West Lafayette the following weekend to play the Lafayette Brawlin’ Dolls. But this is to tell you of my science whereabouts, so onward!

October 5th, Chambana Science Café. Science Cafés are local, casual events where the public and scientists get to engage with each other. The blurb for the one I’m a guest at is: “Kate Clancy is an assistant professor of biological anthropology, blogger of ladybusiness, avenger of bad science, and roller derby athlete. Come hear Dr. Clancy talk about science communication, her research, and how important it is to understand the female body in the face of cultural and political attacks on choice.”

  • Where and when: 5:30pm, Espresso Royale Café (1117 W. Oregon St., Urbana).

October 16th, Bradley University, Peoria, IL “Women in Science” lecture series. My talk title is “The importance of public anthropology to the battle for women’s health.” I’m looking forward to meeting some great women’s studies students earlier that day, and then giving this talk intended for the general public.

The Sports Psychology of Academia: Part II

Writing down all the factors in our sporting or academic lives in which we have no control is a bit disempowering. You mean I’m up against all that, and there isn’t anything I can do?

Except that there is! We are both more and less in control of our lives than we think.

In The Sports Psychology of Academia: Part I on Monday I made two main points:

  • It’s important to recalibrate your understanding of success in the context of your environment.
  • You can only control your own preparation and reaction to external factors.

So in this post we can try and unpack those preparations and reactions, but also identify and rock out on the factors that are in our control.

So how do you prepare for the uncontrollable? Some people find it useful to map out their responses to various scenarios. In athletics we often do visualizations – back when roller derby wasn’t all scrum starts, I often visualized being the first jammer off the line and racing to the back of the pack. I also practiced starts and did plyometrics designed to improve my starts, as a way of maximizing my preparation. So I could imagine scenarios, but also give myself the best possible advantage against any opponent by being at my fastest.

In academia, I try to plan for setbacks or slow progress while keeping a positive outlook. This actually comes from my union organizer days, where we set what we called “high expectations, low bar” for the folks we tried to organize into leaders. So, what journal will I submit to when I don’t get it in Glamor Pub (ok, I’ve never actually submitted to any of the Glamor Pubs, but you might)? If some of my undergrads drift away, how will I get this project completed without them?

But honestly, I’m sure you already do these things. What I find most important to remember about all this is that starting point and environment really matter. Scicurious has a great response to my post where she focuses on this. In particular, she notes:

I often hear about or go to seminars on “mentorship”, or “getting ahead in academia”, or “maximizing your networking potential”. A lot of these seminars are helpful, but a lot of them also actually depend on you having a good beginning position in the first place. “Getting ahead in academia” seminars often assume that you have already worked with some well known people and are already well published and funded. “Mentorship” seminars or “networking” seminars often assume that you are working with people who want to mentor you, or actively work to help you network, or heck, even successful social skills. And if you look around at those seminars, and you do NOT feel as poised and prepared as the others around you…well you start to wonder if this is all your fault.

I think we all understand that an athlete’s current abilities are determined not only by her current effort and resource availability, but the resources she had her entire life. I played soccer for a large public high school, on a team with a ton of raw talent. But few of my teammates had gone to the years and years of summer camps our opponents had had access to. So despite being among many athletes, we didn’t have the right attitude, conditioning or skill level to ever have a winning season in the four years I played.

* * *

In our roller derby sports psych session, once we had thought about what wasn’t in our control and what we could do about it, Dr. Walker had us list all the factors in our sport that we could control. Then came the scary part: we had to rate ourselves on a scale of 1-10 on each. Here’s what I put down:

  • Nutrition -8
  • Exercise -9
  • Hydration -8
  • Effort -9
  • Strategy -7
  • Communication -6
  • Attitude -5
  • Self-talk -5
  • Focus -8
  • Body language -7
  • Sleep -6
  • Decision-making -8
  • Confidence -7
  • Emotions -6

What he told us to do was take a hard look at these numbers. We all want to focus on the places where we’re already doing well, because that’s what makes us feel good. So for instance, when I want to feel good, I focus on nutrition (8) and off-skates exercise (9) and killing myself at practice (effort -9).

But what Dr. Walker encouraged us to do was make the three or four items where we scored lowest our focus. This means I need to work on attitude, self-talk, sleep, communication, and my emotions.

Me jamming in a roller derby bout in the top photo, me hanging with a teammate in the bottom photo.

To succeed at what I’m doing on the top, I need to do more of what I’m doing on the bottom. Both photos by Alex Wild.

After almost two months of this – and I’m not doing anything especially different in my routine, just making a greater commitment to these things – I am a cooler-headed player. I get more sleep: instead of powering through articles I need to read for a literature review (or, ahem, watching another episode of Justified) I go to bed when I’m tired. As a team, we check in with each other more and are learning to read signs of distress and counteract them. I identify negative self-talk, even if I can’t necessarily stop it. I strive to be ever more generous with my team and referees.

I don’t know that this has changed our ultimate performance – whether our team wins or loses. But I think it has vastly aided my own preparation, my reactions to circumstances during bouts, and given me some confidence in places where I was previously lacking. In the coming months I am going to try and identify evidence-based interventions to actually help me with these factors, rather than just reflect on them passively.

* * *

What can I control as tenure-track faculty? Go on, make your own list of these or other criteria, and rate yourself. Here’s what I came up with:

  • Time -8
  • Effort -9
  • Decision-making -7
  • Confidence -7
  • Attitude -6
  • Self-talk -6
  • Health (in the sense of taking care of myself) -9
  • How I interact with colleagues -9
  • How I mentor my students -7
  • My knowledge of the literature -9
  • My statistical skill set -7
  • My lab skill set -7
  • My writing skill set -8

Looking at this list, some of the same issues plague me as an academic and athlete: confidence, attitude, self-talk are things I need to improve (*cough* impostor syndrome! *cough*). But I also want to be a better mentor, a better statistician, a better lab scientist (to have knowledge of appropriate methods for my research so I can train and support my students). Finally, I want to be better at decision-making: how to allocate my time, what battles to fight, what strategies I should employ for success.

I think my results here reflect my graduate training, which is probably pretty typical. In graduate school, I learned that you have to put in the time, you have to work your ass off, and you have to know the literature. So those come easily. I have a good writing skill set because I taught composition for a year and write this blog. I think I interact with my colleagues fairly well because I try to be generous and fair.

But as many academics have pointed out many times: we aren’t really trained to do our jobs. I have no training in lab management, grantwriting, and personnel management. I have erred several times in my decision-making in the last four years simply because no one warned me about obstacles before I crashed headlong into them.

Moving forward, I want to continue to think about the ways academics beat themselves up for poor performance, which is where the negative self-talk and confidence issues find their way in. Some of the NSF Panels I’ve applied to in the last few years have had a 5% fund rate. Most jobs in my field have over a hundred applicants, which leads to a 1% success rate. And yet we are hard on ourselves when we don’t get the grants or the jobs? This is why it’s so important to parse worth and ultimate performance!

So this exercise brings to light two main issues: 1) ways individuals can work to overcome their weaknesses and thus increase their chances for great academic performance, and 2) ways institutions can better train academics to do their jobs, also increasing their chances for great performance.

How should this look? And what needs to shift for you?

The Sports Psychology of Academia: Part I

Skaters from the Twin City Derby Girls (including Mrs. Myrmecos) have got the opposing jammer's number.

Skaters from the Twin City Derby Girls (including Mrs. Myrmecos) have got the opposing jammer's number. Photo by Alex Wild.

For me, roller derby began with a very steep learning curve. I didn’t know how to skate, I didn’t know the rules, and so every practice left me physically and mentally exhausted. I did bring my own skill set to the sport: I’ve been an athlete my whole life, and played many a contact sport, and so some parts of roller derby – the physical fitness, hitting, body awareness, cross-training and nutrition – came easily.

After a while though, I hit the limit of the edge my athletic performance gave me. And so I had to start reading derby blogs for strategy, increase my off-skates workouts, and learn about roller derby gear to make sure I was using the right materials. I attended some clinics. I tried new moves until spectacular falls became small falls, and small falls became no falls.

I’ve become, I think, a pretty good player. I skate for a young but nationally ranked team, and I have exceptional, talented teammates and coaches (just see a few of them above).

Yet you know enough about sports to know even great teams don’t win every single bout they play, and that when they lose it isn’t always to the more talented team. Most of us understand that in sports, we can’t actually control whether we win or lose. We can only control our preparation leading up to, and our reaction to game conditions.

The best athletes recalibrate their understanding of success: success is less about winning or losing, and more about whether they played their best game. How did they prepare for the event? How did they handle adversity, including bad luck or unfairness? Were they proactive or reactive in the face of their opponents? Did they put in maximum effort?

Success in sport, then, is context-dependent. And to increase your chances of success in the traditional sense (winning), you need to increase your success in the factors that are under your control. You need to get to the point where you can anticipate and handle most contexts.

Academia (heck, most of the jobs of most of you reading today) is the same way. We can control only ourselves and how we react to given situations.

So why are we so hard on ourselves when we fail?

* * *

This summer, my league brought in sports psychologist Dr. Brent Walker to talk to us about how to take the next step in our mental performance. Dr. Walker came as a kindness to a student of his, but was so constructive we would have paid for a million more sessions. Alas, Columbia has just scooped him up from Eastern Illinois University and so now they get to benefit from his wisdom instead.

The first step of our session was to list the factors we cannot control related to performance in roller derby bouts. These included:

  • The floor surface (grippy or slick floors impact our ability to do certain kinds of moves)
  • Referees
  • Fans
  • Attitude of the opposing team
  • Ability of the opposing team
  • Injuries and who we can roster
  • Personal, family, or work stressors
  • Luck

Then we discussed the importance of planning ahead of time for as many of these factors as possible to better control our reactions. So for instance, if we’re skating in an away bout and don’t know anything about the floor, we bring several kinds of wheels to try out during our warmups.

What are those factors for academics, particularly academic scientists? Here are a few that come to mind for me:

  • Whether laboratory materials are delayed, backordered
  • Research participant retention issues
  • My tenure & promotion committee and their decisions
  • My collaborators’ priorities
  • My departmental colleagues’ priorities
  • My students’ priorities, commitments, responsiveness to my mentoring
  • Journals’ manuscript decisions
  • Grant reviewers’ decisions
  • The quality of the pool I am up against for manuscripts and grants
  • My husband’s work priorities
  • My daughter’s health and wellness (to some extent – what I mean here is I cannot control when she gets sick and I have to miss work)
  • My daughter’s school’s days off
  • Crappy luck (things breaking or not working)

What other factors seem to be beyond our control? How do you plan ahead to neutralize or change them?

I’ll have a follow-up post Wednesday on the second part of this exercise. Discuss!


Llama Llama Get With Mama: The Magical Semen Ingredient that Makes the Ladies Swoon (Then Ovulate)

Image of a white llama

Mate with me, and I'll help you ovulate! Oh, yeah. "White Llama" by Petr Kratochvil.

A paper that came out on August 20th in PNAS suggests a factor in semen that could induce ovulation. The idea that this could happen isn’t new, but identification of the factor that might do it certainly is. Ratto et al (2012) contend that they have found The Magical Semen Ingredient That Makes the Ladies Swoon (Then Ovulate), and it is Nerve Growth Factor, or NGF. (Full disclosure: I didn’t notice until I was halfway through writing this post that a collaborator of mine, Roger Pierson, is a co-author on this paper.)

Much of the online conversation I’ve seen about this paper begins with an implication that the research was on or related to humans, then a quick switcheroo to reveal they were, in fact, talking about llamas.

Yes, llamas.

Which are an admittedly cool species, one which my generation of Sesame Street watchers no doubt remembers from this song:

And that same generation now reads to their own children Llama Llama Red Pajama, Llama Llama Mad at Mama, and the rest of the Llama Llama series by Anna Dewdney (we have nearly all, and my daughter can recite most from memory). It’s fun to say, it rhymes with a lot of stuff, and they can spit at you. What’s not to love?

But, well, llamas aren’t humans. So I’m going to explain why this distinction is important, why this research is still really cool, and the reasons I can see that make NGF interesting in humans after all.

Bet you can’t make me ovulate!

Some animals ovulate with the act of intercourse – either the physical act stimulates it, or there is some factor in the semen that signals that it’s time to pop out that egg. Such an animal is called an induced ovulator, and this group includes llamas, the rest of the camelids (camels, alpacas), but also cats, minks, voles, and a few others.

The other kind of ovulator is the spontaneous ovulator. This is far more common and this is how we primates ovulate. Spontaneous ovulation is when ovulation is triggered spontaneously and internally via the suite of hormones that nourish and mature egg follicles. This is why you often see a distinction in the infertility literature between “spontaneous” cycles that occur naturally, and “stimulated” cycles that are brought about using fertility drugs (which are just synthetic versions of the hormones we produce).

So there is room for an external mechanism to influence ovulation, even in spontaneous ovulators. We have scores of papers showing that energetic stressors (particularly not eating enough) can delay or cease ovulation. Issues with insulin, thyroid hormone or androgens (take your pick, it’s a murky mechanism) can make too many follicles ripen at once then struggle to ovulate, leading to a diagnosis of polycystic ovarian syndrome (PCOS).

But that’s not quite the same thing as The Magical Semen Ingredient That Makes the Ladies Swoon (Then Ovulate).

Oh, the things NGF could do that are good for you

In llamas, the discovery of NGF and its abilities supports the hypothesis many have held that there is something in semen whose specific purpose is to stimulate ovulation… among induced ovulators. And the discovery that it’s NGF, and not some newer, whacked-out chemokine that had never before been identified, suggests we are looking at a fairly conserved (evolutionarily old and passed on among many modern species) feature.

This alone is striking and important.

What else does NGF do, and why would this be the trigger for ovulation in llamas and their fellow induced ovulators? NGF has a lot of other jobs, mostly related to in utero development of the central and peripheral nervous system, and neuroendocrine or immune tasks once born (Levi-Montalcini, 1987).

But NGF has also already been examined for a possible role in ovarian function. And its role is quite interesting!

NGF appears to facilitate ovulation. In the hour leading up to egg release, trkA (tyrosine kinase receptor) and NGF gene expression increase in the ovary (Mayerhofer et al., 1996). What seems to happen is that NGF activates trkA receptors in a way that eventually leads to a degradation of the follicular wall, which aids in follicular rupture from the ovary. Breaking down the ovary’s last arguments about why the egg shouldn’t get to go out that night, NGF is like a feisty aunt that encourages troublemaking.

If this aunt spoils the egg too much, or doesn’t see enough of her, problems can arise. In one sample of women seeking assisted reproductive technology, NGF was found to be higher among women with diminished ovarian reserve, but lower among those with PCOS (Buyuk and Seifer, 2008). Yet a different study found NGF associated with PCOS in a mouse model, and high NGF in women with PCOS (Dissen et al., 2009). Both studies measured NGF in follicular fluid in women during assisted cycles to try to get pregnant: the Buyuk and Seifer (2008) collected during egg retrieval, but the Dissen et al (2009) doesn’t say when (it would make sense to assume the same time-point, though).

Follicular fluid NGF is higher in women with low ovarian reserve, and lower in women with PCOS, in this sample (Buyuk and Seifer 2008).

Dissen et al 2009 Figure 1 showing PCOS women have higher NGF in follicular fluid and granulosa cell culture medium

Different results despite a similar sample population and sampling methods? It might mean we don’t understand the mechanism that well yet. It could also point to the fact that PCOS is a hugely variable syndrome, likely with multiple origins, and so you could potentially get different samples with different NGF concentrations by chance and still have both studies be meaningful. Either way, NGF seems like a very important factor to consider in PCOS, since in some PCOS women we are seeing maturation of many follicles but no ovulation.

So how else might NGF be stimulating ovulation?

Maybe NGF stimulates luteinizing hormone!

This is the pathway the authors of this paper propose (Ratto et al 2012). Rather than NGF acting in some paracrine (cell to cell) manner, they contend NGF zooms over to the anterior pituitary (in your brain), which makes luteinizing hormone (LH), and the LH then zips to the ovary and tells it to put the finishing touches on the egg and let it go.

If we’re talking about locally produced (by the woman) NGF, this all makes sense to me because it would be part of her own spontaneous cycle regulation. Here’s what I don’t get. If semen-derived NGF were to induce ovulation it probably wouldn’t happen in time for that ejaculate’s sperm to have a follicle to fertilize. So this would really only work if someone was having sex regularly so that an earlier episode could prime a later fertilization. In a promiscuous species, which is somewhere in our ancestry, this seems like a terrible idea. You might be wasting your mating effort ripening a female’s eggs so that some other schmo gets to fertilize them! This is why to me, semen-derived NGF is currently in the “may not help, but doesn’t hurt” category for now when it comes to spontaneous ovulators like us.

Maybe NGF stimulates mast cells!

Or perhaps the mechanism is an inflammatory one? NGF activates mast cells, which degranulate (release histamine) and start the inflammatory process. Mast cells in the endometrium produce tryptase which induces angiogenesis and neovascularization (making new blood vessels). But endometrial mast cells are the most activated just before menstruation (Salamonsen and Lathbury, 2000). In fact, tryptase activates matrix metalloproteinases (MMPs), which break stuff down, which is why they are so important to menstruation. However, some think histamine could be a paracrine signal involved in decidualization and implantation (Noskova et al., 2006). So… NGF could facilitate menstruation if timed towards the end of the cycle, or implantation, if timed during the implantation window.

Llama Llama Ovarian Drama

Intra-ovarian NGF is an important component of the mechanism of ovulation in spontaneous ovulators, and seminal NGF is important for ovulation in induced ovulators. It’s entirely possible the seminal NGF is also important to women’s reproductive function in some way. My big questions – and I really hope someone does follow-up work on this – are what is a physiologically relevant concentration of NGF in spontaneous ovulators (so, how much you need to actually do anything), and what produces variation in intra-ovarian NGF? I’m very curious whether gonadotropins, hormones, or external factors influence any of this stuff. Considering intra- and extra-ovarian sources of variation in ovulation just made lady parts that much more interesting!


Buyuk E, Seifer DB. 2008. Follicular-fluid neurotrophin levels in women undergoing assisted reproductive technology for different etiologies of infertility. Fertility and Sterility 90(5):1611-1615.
Dissen GA, Garcia-Rudaz C, Paredes A, Mayer C, Mayerhofer A, Ojeda SR. 2009. Excessive ovarian production of nerve growth factor facilitates development of cystic ovarian morphology in mice and is a feature of polycystic ovarian syndrome in humans. Endocrinology 150(6):2906-2914.
Levi-Montalcini R. 1987. The nerve growth factor 35 years later. Science 237(4819):1154-1162.
Mayerhofer A, Dissen G, Parrott J, Hill D, Mayerhofer D, Garfield R, Costa M, Skinner M, Ojeda S. 1996. Involvement of nerve growth factor in the ovulatory cascade: trkA receptor activation inhibits gap junctional communication between thecal cells. Endocrinology 137(12):5662-5670.
Noskova V, Bottalico B, Olsson H, Ehinger A, Pilka R, Casslén B, Hansson SR. 2006. Histamine uptake by human endometrial cells expressing the organic cation transporter EMT and the vesicular monoamine transporter-2. Molecular human reproduction 12(8):483-489.
Salamonsen LA, Lathbury LJ. 2000. Endometrial leukocytes and menstruation. Human Reproduction Update 6(1):16-27.
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