Category Archives: Teaching

Bill Nye the Science Guy meets Vin Can the Science Man

OK, so I need to work on my stage name.

Back in May 2017, I tweeted at Bill Nye:

And it turns out that Bill, and the great writers and producers and everyone else behind Bill Nye Saves the World, were paying attention. Shortly after the tweet I was contacted by a producer of the show and asked if I would like to come on and give a demonstration about the evolution of “super-bugs”, i.e. antibiotic-resistant bacteria.

An opportunity for science outreach involving Bill Nye? Yes, please.

In this post, I first want to talk about the science in my 5 minutes (at the end of Season 2 Episode 3 of Bill Nye Saves the World). Then, I’ll touch on the experience of being on the show.

The Science

I wanted to convey three things in my demo:

  1. Antibiotics work really well!
  2. So does natural selection. In the presence of an antibiotic, bacteria resistant to that antibiotic survive and proliferate more than non-resistant bacteria, leading to the spread of the information conferring that resistance (i.e. the evolution of “super-bugs”).
  3. And that’s why it is important to be judicious about antibiotic use.

all while conveying how scientists can use models of reality to study biology.

So, for my demo I created a model of the evolutionary dynamics of bacterial strains within a person. In this model, bacteria either replicate or die—similar to a common mathematical model used to study evolutionary dynamics called a “birth-death process”. If there is more birth than death, the bacteria grow too big and overflow from the host—the infection spreads to other hosts. If there is more death than birth (as in a typical situation where the immune system does a good job), the bacteria die off —the infection is cleared.

What makes this a model of evolution is that we can introduce two different bacterial strains into the model and observe how the relative abundance of these two strains change within the total bacterial population over time. Let’s say one strain has a mutation in their genome that makes them resistant to antibiotics, and the other strain is still susceptible to antibiotics.

Let’s also assume that the host’s immune system is compromised, all strains are growing more than they are dying. The person goes to their physician, and gets some antibiotics that decrease the birth rate of only the susceptible strain. Growth of the susceptible strain is stopped, but the resistant strain grows and grows, and when the model “overflows” it is the resistant strain that spreads to other hosts.

By continually providing selective pressures favoring resistance, we drive susceptible strains to extinction. As the model suggests, we would expect the spread of antibiotic resistant bacteria to be especially prevalent in areas that have a high concentration of individuals with compromised immune systems that take antibiotics, such as hospitals and nursing homes.

But, there is hope! Many of the mechanisms of resistance are actually costly to bacteria when antibiotics are not present. It may be possible to reverse many of the mechanisms of resistance (select for non-resistant strains) by being extremely judicious about when to apply antibiotics. The original focus of the demo was on how to reverse resistance through exploiting this cost of resistance, however due to time constraints I refocused on the emergence of resistance.

My Experience

Everything was awesome. I had no idea just how much went on behind the scenes to get a show produced. From the props people helping with my demo, to the writers and producers working around the clock anticipating every little thing that will happen. Everyone really cared about being true to the science and explaining the information in an accessible and exciting way. Especially Bill Nye, who was extremely genuine and kind throughout the whole experience. I’m very grateful for the opportunity to help #savetheworld!

20170720_202332

 

P.S.

For those who arrived at my blog curious about my current research: I use mathematical models and simulations to investigate how tumors evolve from our tissues, how evolution has structured our tissues to minimize the risk of cancer, the effects of mutations in growing tumors, and how cancers evolve resistance to chemotherapy. Relating to pathogen evolution, during graduate school, I was part of a team that used mathematical models to study the evolutionary dynamics of pathogens and their hosts.

Generating Biology

I’m taking a Teaching Careers/Methods course and our first assignment was to develop a class we’d like to teach and give a little mini-lesson to convey some learning objectives and outcomes of the class. I proposed a class dubbed “Programming and Quantitative Methods in Biology” (or should it be quantitative methods and programming in biology?). Regardless, it’s meant for upper level undergraduates, and the idea is to give students the means to model and simulate biological systems and interpret the underlying biological phenomena at play. I wanted to turn the teaching of biology on its head a bit, instead of learning words and formulae (for example: drift, selection, p+q=1) and then trying to associate them to some dynamics in your head, you “generate” the biology, observe and manipulate the dynamics, and then learn the corresponding biological concepts. I guess I spent a lot of time in college memorizing terms instead of understanding concepts and I didn’t realize the difference until I was in graduate school. Anyway, I’ll give a synopsis of my mini-lesson below. Please feel free to expand and improve or implement these ideas yourself.

Towards the end of the semester students are tasked with creating a simulation of an evolving diploid population with constant population size. Ideally, their simulation has input parameters of the initial population size and the initial distribution of genotypes at a particular allele (AA,Aa,aa). It would also be nice to define the relative propensity for specific genotypes to have offspring and the ability for an allele to mutate into another allele at some specified rate. I coded this simulation up myself for the mini-lesson I gave so that the class could play along. You can find the code here:

https://github.com/vcannataro/HW_dynamics

(again, please feel free to expand and improve on this!)

You have to save both .R files into the same folder and then open R, open the HW_dynamics_master.R script, and set the folder you saved the files to as your working directory. Then you can manipulate the parameters, run the whole script, and see the resultant evolutionary dynamics.

What do you think will happen to the genotype distribution if you run the simulation with these initial parameters?

#Number of each genotype in the population initially:
AA <- 0
Aa <- 2000
aa <- 0

#Generations to run the simulation:
Generations <- 50


#Chance of allele mutations per reproduction event:
A.to.a <- 0
a.to.A <- 0

#Some measure of relative fitness. 
AA.fit <- 1
Aa.fit <- 1
aa.fit <- 1

Do you think the population will remain as 100% heterozygote? Do you think any allele will go extinct? Do you think it will continually fluctuate, or reach an equilibrium? Well, here’s an example of what happened for me:

Initial_conditionsAfter a single generation the population snapped in to an equilibrium and remained hovering around that for the rest of the simulation. This is known as the Hardy-Weinberg Equilibrium. (This is a good opportunity to derive the HW formulas on the board and discuss what assumptions are key to maintaining these genotype frequencies). The code spits out the expected HW equilibrium given the initial p and q and the actual average equilibrium after each run, here’s what it looks like for those initial parameters:

"Initial 'p': 0.5"
"Initial 'q': 0.5"
"Expected AA= 0.25 | Expected Aa= 0.5 | Expected aa= 0.25"
"Average AA= 0.26205 | Average Aa= 0.50067 | Average aa= 0.23728       
*(averages after first generation)"

 

Now the fun begins. What would happen if we started violating these “key assumptions” underlying the Hardy-Weinberg principle? Let’s see. What do you think might happen if we started with 20 heterozygotes instead of 2000?

#Number of each genotype in the population initially:
AA <- 0
Aa <- 20
aa <- 0

20_hets

"Initial 'p': 0.5"
"Initial 'q': 0.5"
"Expected AA= 0.25 | Expected Aa= 0.5 | Expected aa= 0.25"
"Average AA= 0.55918 | Average Aa= 0.30918 | Average aa= 0.13163      
 *(averages after first generation)"

 

Woah woah woah, our equilibrium is all off! In fact, an allele went completely extinct after 38 generations. It’s almost like one of the alleles drifted towards fixation in this population.

What if the heterozygote left, on average, twice as many offspring as either homozygote?

#Number of each genotype in the population initially:
AA <- 0
Aa <- 20
aa <- 0

#Generations to run the simulation:
Generations <- 50


#Chance of allele mutations per reproduction event:
A.to.a <- 0
a.to.A <- 0

#Some measure of relative fitness. 
AA.fit <- 1
Aa.fit <- 2
aa.fit <- 1

hets_2xfit

"Initial 'p': 0.5"
"Initial 'q': 0.5"
"Expected AA= 0.25 | Expected Aa= 0.5 | Expected aa= 0.25"
"Average AA= 0.28469 | Average Aa= 0.49898 | Average aa= 0.21633       
*(averages after first generation)"

 

All of the genotypes remain in the population! This is a good spot to bring up fitness, overdominance, and underdominance.

Plus, you can play with the mutation rate between alleles (what happens if the whole population is AA but there is some chance of a spontaneous A–>a mutation? What happens if this ‘a’ allele confers some fitness advantage?)

#Number of each genotype in the population initially:
AA <- 1000
Aa <- 0
aa <- 0

#Generations to run the simulation:
Generations <- 100


#Chance of allele mutations per reproduction event:
A.to.a <- 0.0001
a.to.A <- 0

#Some measure of relative fitness. 
AA.fit <- 1
Aa.fit <- 2
aa.fit <- 2.5

 

muts

Chances are that whatever resultant dynamics you observe from the model have already been described by population geneticists. And that’s the point-  you generate the biology, figure out what’s going on to lead you to the dynamics you observe, and learn how these biological phenomena have been previously described. There will also be a focus on the limitations of models and simulations.

 

Anyway, that’s my idea. Your thoughts are appreciated!

 

 

 

January 2015 fun facts

Woah, I’m way backlogged on blog posts! Don’t worry, I have some cool stuff in the works and I’ll share soon. In the meantime check out some of the science I’ve been starting my classes off with this month.

Aging research: blood to blood – scientists can splice animals together by creating a wound in each animal and sewing them together- their natural wound healing mechanisms join their bodies and their blood (it’s called parabiosis)! If you splice an old animal to a young one the tissue in the old animal gets “rejuvenated” by the young animal’s blood.  Sounds like the premise for a horror movie.

Scientists have discovered a new antibiotic that kills pathogens without detectable resistance.

Scientists have discovered that tumor cells can actually acquire previously lost DNA (in this case mitochondrial) from “normal” cells, and that the newly acquired DNA restores missing function. Think about that. Somatic cells (or cells that were once deemed somatic but now have become tumor cells) can horizontally transfer DNA. Biology textbooks get rewritten every day.

And, of course, I can’t introduce metabolic scaling and not discuss the invariance of heartbeats.

Enjoy!

Mind controlling parasites- how sci-fi are zombies anyway?

 

Halloween weekend is drawing to a close, and as I type this (looking out a coffee shop window) I can still see the zombie makeup on the faces of those passing by. It’s understandable why the whole zombie thing can be pretty terrifying. In the movies the protagonist usually watches their once fully autonomous friends and loved ones fall prey to some microscopic parasite and become a mindless vessel, obeying the will of their neural captors, tasked with ensuring the survival of the parasite and oblivious to their own health. Good thing it’s science fiction! Right? Well, anyone studying parasitology can tell you that in some cases it’s less fiction and more science.

Whenever I teach the lab on species interaction I always spend a good bit of time on mind controlling parasites. First off- they’re just cool. Plus, there’s a lot of captivating videos out there! One of my favorite being:

(p.s. larva emerging from a caterpillar body below, viewer discretion advised!)

Great music and sound effects aside, it’s always interesting and sort of mind-blowing to see the caterpillar actively defend the larva that just busted through its skin. It really gives you a sense of just how possessed an organism can become at the whim of a parasite. Another zombie-state-inducing parasite infects snails:

And another favorite, the inspiration for the zombie-survival game The Last of Us, infects and alters the behavior of entire forests full of insects:

 

Ok, so mind controlling parasites might actually be all around us, but at least they only infect invertebrates. Right?! Well, no.

Rats have a natural (and understandable) aversion to cats. When they smell cat urine they feel fear and head in the other direction. However, rats infected with the protozoan Toxoplasma gondii, which only reproduces in the cat intestine, are actually drawn to cat urine. The parasite hijacks the sexual arousal pathway in the rat brain, and instead of feeling fear the rat feels sexual attraction to the cat odor. So, just like the snails in the video above, the rats search out their natural predators for the benefit of their parasite.

 

Ok, so mind controlling parasites can infect and manipulate the behavior of mammals as well. But, certainly humans, with their giant and complex brains, don’t have to worry about being influenced and controlled by the whims of a tiny microscopic organism. Right?! Well…

I have a habit of bringing up the universe that exists within multicellular organisms. It’s easy to think of this as a one way interaction- a large organism goes about their business and the little organisms tag along for the ride. But the survival and wellbeing of the microbiome is extremely important- so important that hosts even synthesize food for their microbiome during periods of illness to ensure that their microbial friends stay happy.

Is it possible that some of our microbial friends could be manipulating our behavior for their benefit? Some scientists have recently suggested that might be the case- we might be at the whims of a microbial puppet master. More research is needed to test these hypotheses, but I look forward to the day where taking a microbe-filled pill can change my appetite for the better and bolster my microbiome.

Outside of our bacterial microbiome, we also house a vast virome. Research published in PNAS this week has shown that humans can be infected with an algal virus, and this virus was associated with a 10% decrease in performance on visual processing exams. Additionally, mice infected with the virus took about 10% longer to navigate a maze and explored 20% less.

So, maybe we’re not so autonomous after all. Spooky! Happy Halloween!

Awesome camouflage

Staying in the lab is tough when you live in the sunshine state. I mean, at SUNY Geneseo it was easier- the lab served as a warm refuge against those Western NY winds and clouds. So every once and again I’ll find a break in the Floridian sunshowers and bring my work outside. However, as any biologist can tell you, work is impossible outside because you always get distracted by some cool critter crawling by your laptop. Case in point: last time I tried this I noticed a little pile of moss moving across the table…

20140711_150819

… so of course I flipped it over…

lacewing1_5

…and found legs! (Woah, I need to find out what this is.) Further investigation revealed impressive mandibles and a set of sticky spines:

lacewing2

It looked very similar to an antlion, which is the larval form of a certain family of lacewing. Antlions are awesome in their own right, they form little trenches in the sand and eat ants that fall into their trap. I teach an intro bio lab on the spatial distribution of organisms, and I always take the students outside to hunt for antlions (they are typically (spoiler) clumped together in sandy spots under the eaves of buildings). And I always show this video:

Anyway, it turns out that critter I found was also a larval lacewing! Certain species have sticky spines on their back that trap debris and help the larva blend in with their environment. This isn’t a new tactic- scientists have found a 110 million year old larval lacewing trapped in amber that has fern trichomes stuck on its back. How cool is that?! (Another spoiler: very)

And such is the curse of the biologist- go outside to write and in minutes you are a few Wikipedia pages deep classifying insects.

Fun Fact Experiment

I tried something new with my Intro Bio lab students this semester. Every week I would have a new “Fun science fact of the week”- something relatively contemporary that I found exciting and had a (sometimes admittedly weak) connection to the current lab. I remember when I took intro bio lab things could feel a little stale and cookie-cutter, so I incorporated this as a way to spice things up.

For example- The week Voyager 1 left our solar system we were dissecting fetal pigs. I used this as an opportunity to show the slides of human anatomy stored on the Voyager 1 and describe just how similar pigs and humans are on the inside. This turned into a really fun discussion about space travel and genetic engineering. When we were discussing photosynthesis I went into some fun properties of light and the speed of light… which turned into a discussion about relative velocity and time dilation

When we discussed niche space I brought up the Radiotrophic Fungi discovered in Chernobyl. We then started discussing evolution and the “speed” of evolution. See, the fun facts naturally transitioned into a back-and-forth discussion among the students and myself. This set the pace and mood for the lab, and what might have been a stale lecture started off on the right foot as a passionate discussion about something fun.

The original plan on my end was that I would also blog about these facts every week and share them here… but it turns out grad school is pretty darn time consuming and my time allocation skills need refinement. There is always next semester!

Well, the results are in. According to my teaching evaluations the fun facts of the week were a big hit! Students looked forward to what the fact would be every week and share them with their friends after lab. In fact, after a few weeks I even had students emailing me with facts (“Hey, did you see this cool science video? Did you hear about this new research?” etc.) So, I would say the fun fact experiment was a success- and not just from the student’s perspective. I would get excited to see students excited about the fun facts, and looking forward to teaching every week certainly made preparations and grading less of a hassle!

 

More fun facts on here soon, I promise.