A Lifetime of Curiosity

by Robert (Bud) Talbot, PhD

Dr. Talbot’s STEM of choice is Science with a focus on physics education. He now works for The University of Colorado Denver, as an assistant professor of science education in the School of Education and Human Development. Dr. Talbot helps to recruit and train new secondary school science teachers, and does research on teaching and learning science at the university level. In his spare time, outside of work, Dr. Talbot loves to run, work with technology (especially amateur radio!), engage in citizen science projects, and do sciency things with his 6 year old twin daughters. If there was one thing he wished he had known before college about STEM, it would be “how being scientifically literate shapes the way you do anything and everything in the world!”

He studied for many years to get where he is, first at Indiana University for degrees in Geology and science education (BS and MS), then at the University of Colorado Boulder for a PhD in science education, researching how to develop tests and surveys to be used in science teaching and learning.

Introduction

My bio is above, but that is not who I am. Here’s the truth about me: I’m a geek and I’ve always been a geek. I love geeky things like technology, computing, and amateur radio. But I also love to be active. I’m totally obsessed with running and I love to dig deep into all of the data related to my running: GPS tracks, heart rate, power output, pace- lots of numbers! All of this geekery was instilled in me early on. I was lucky enough to grow up in a family where we spent a lot of time outdoors, camping, hiking, taking crazy roadtrips. Did I mention maps? I LOVE maps. They are everywhere in my house. Anyway, back to my childhood. My mom told me that I once went to the public library at the age of 6 and asked for a book on “splitting atoms.” Of course I don’t recall that, but I bet it was a cool book. I didn’t know it at the time, but I was well on my way to being a science teacher.

Materials and Methods

Degrees can only tell you so much about a person’s STEM career, here’s my actual journey: I thought I wanted to be an accountant when I started college. My brother in law was an accountant and I really looked up to him. But the classes turned out to be really boring! Then I discovered Geology. What fun! Maps, rocks, lots of camping and hiking. That was the best. So now I was on my way to being a geologist. Well, I ended up taking a few years off from school before finishing (long story…) during which time I realized that my true passion was trying to help others see how cool science was. I was always asking questions and getting others to geek out with me. So it seemed natural that I should be a teacher!

I went back to school and became a high school physics and Earth science teacher. It was a great experience, and I was fortunate enough to learn a lot and build lasting relationships with many of my students. I know that my work made a difference. After seven years of teaching, I yearned for more learning and to work with teachers, so I went to graduate school in Boulder. It was there that I learned about research on teaching and learning, which prepared me for the job I now have as a professor.

Results

Right now, I am focusing on undergraduate science education at my job as an assistant professor. We help other professors to think about better ways to teach biology, chemistry, and physics at the university, and investigate the impacts of innovative teaching on how students learn. Our main focus is to help students in these courses succeed and become prepared to pursue their future goals. Our work is making a difference!

Discussion

I love science education, and especially physics, and here’s why: it really helps me to see how important it is to have a scientific worldview. I can apply scientific reasoning to any aspect of my life. Not only is that fun, it is useful. Many of the skills and dispositions that we use as scientists (like curiosity, research methods, and writing ability) are useful in all aspects of life. And my interest in physics and Earth sciences lets me do lots of fun things in my spare time, like amateur radio (my callsign is W0RMT), and participating in citizen science projects (check out CoCoRaHS, mPING, CWOP, SETI@home, and LHC@home).

Science is everywhere, and it’s fun and useful. It leads to a lifetime of curiosity!   

Canis lupus familiarus: A ridiculous story of artificial selection

By Dr. Debbie Rook

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“Natural Selection” is a complicated and intricate biological concept that often trips up the most educated and well-read among us. To get to that, we’re first going to start with something we all can relate to and understand- specifically, breeding or “artificial selection”. This means specifically that people are the selecting what traits are passed on to the next generation, instead of nature.

Think of a dog, any dog. You may know a chihuahua down the street or your great aunt’s mastiff. Dogs come in amazingly different varieties, different sizes, weights, strengths, hair, tails, ears, noses… you name it! You probably have heard that the dog came from wild wolves, which even look like a few breeds (huskies and malamutes, mostly). But how did we get there? How is that even possible to get so much change in just a couple of thousand years?

Artificial selection is the answer. Back in the days long ago (around 130,000 years ago), there were likely wolves that hung out around farmers or nomadic tribes because there was easy food to get- whether it be cattle or other farm animals, the rabbits that came to eat crops, or simply leftover scraps that were either discarded or given to the wolves willingly. Over time, the wolves that had a nicer temperament (less biting, better smiles), would be given more scraps (think if a stray dog came up to you at a park- would you share your ham sandwich if it was growling at you or cuddled next to your side?). This was the beginning of a beautiful relationship between the more tame of the wolves and the humans. Now, how was this really selecting? The humans were not breeding these dogs yet, nor were the animals even living with them, so how could that change the population? Simple- food. The nicer dogs are more likely to get scraps from the humans, and therefore more likely to survive the winter and reproduce, while the mean wolves got no scraps and had to fend for themselves. Slowly over time, the scrap-grabbing would change into cohabitation of tame wolves and humans, which would allow those dogs to have even more offspring, because they were being actively cared for by the humans. And that’s how you get dogs! Bring a nice wolf into your house and in a couple (hundred) generations you’ll have yourself a dog (but don’t try this at home…).

So that’s great, a slow change in the population over thousands of years got us from nasty predator wolves to tame live-in dogs. But how did we go from wolf-like dogs (big, sharp teeth, long noses, pointy ears) to all the different kinds today (big/small, variable teeth, long/short/pug noses, pointy/droopy ears)? That is where serious artificial selection comes in, breeding.

Say you are a farmer and need a dog to look after your flock of sheep. You start with the basic wolf-dog and you select for traits that you want. Specifically, you want a dog that is kind to you and your sheep but will scare away other animals. So you take all your dogs and find the ones that meet those criteria best. They won’t be perfect yet, maybe it will sometimes snap at you or a sheep, but otherwise just likes to chase off coyotes. You mate the two together that have the best traits. Those offspring then will have a smaller range of these traits closer to your ideal. It’s possible that in one generation you will have succeeded with at least one of the dogs, but if not you just try again with the next breeding cycle. This also works if you need a dog to pull a sled, or find foxes, or cuddle with your kids, or even carry in your purse. Slowly, over a few generations you can get a lot of change in these animals.

I’ll give you one more example because I think it is so cool. Bull terriers. Bull terriers are known for their noses that are shorter and angled downwards. Here is one:

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This is a very dramatic feature, so you’d think that it would take hundreds or years to get a nose like that from a regular looking dog. BUT…

Here is a bull terrier from 1915.

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And 1918 (for good measure).

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You can see that those noses have changed a lot in the last hundred years. The 1918 picture also shows you a little how this works. If you look at the four dogs, they are all bull terriers and likely related, but there is variation (differences) between the noses. Specifically, the second from the left has a nose that is slightly more downturned than his siblings. If you were trying to make the modern bull terrier, he is the dog you would want to mate to get the next generation.

So you can see that in a few decades you can get dramatic changes in breeds of dog, all by having humans select traits that they like the most. Selective breeding has brought about the multitude of types of dogs that you see today. Hopefully you have a better understanding of this now that you’ve seen it in action!

Next time: nature takes a crack at selecting for different animals, incredible variation, and adaptation occurs.

The Zika Virus (#1)

By Lauren A. R. Tompkins

A collection/series of blog posts entitled:

The Zika virus pandemic – insights from a scientist

The past few weeks (March 2016) have provided major advances in our understanding of Zika virus through publication of several key research studies. In the wake of the global response to the Ebola virus outbreaks, measures to expedite research and prevention strategies for Zika virus are now underway. Emerging infectious diseases, which manifest outbreaks without warning and often without the presence of effective control measures, are dramatically affecting how information is shared between scientists and how prevention strategies, such as vaccines, are regulated. In a time of public health crisis, the scientific community has pulled together with the common goal of a rapid response to combat Zika virus.

 First blog post for this series, entitled: The politics of Zika virus

             On Monday (April 11, 2016), Dr. Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases (NIAID), and Dr. Anne Schuchat, principal deputy director of the Centers for Disease Control and Prevention (CDC), addressed reporters at a White House briefing. The topic of discussion was Zika virus and an appeal for the necessary funds to prepare for mosquito season, when the virus will likely spread to the southern United States. According to the CDC, at least 346 people from the continental United States have been infected with the virus, mainly through travel-related exposure. However, with the summer months approaching, and mosquito populations expanding with warmer weather, local transmission of Zika virus is likely to occur.

A gridlocked Congress is not an unusual concept to the American people. Still, a “public health crisis of international concern”, as stated by the World Health Organization (WHO) in February of this year, should theoretically hold weight if politicians continually claim to have the best interests of Americans in mind, let alone the public health of all inhabitants of our planet. Unfortunately, Congressional Republicans are tightening their wallets and stubbornly resisting the allocation of necessary funds for combating Zika virus. Rather than listening to knowledgeable scientists and public health officials, pleas for appropriations are falling on deaf ears. Indeed, President Obama has asked Congress, again, for the full $1.9 billion dollars that is required to fuel Zika virus research. On Tuesday (April 12, 2016), Congress approved a bill to provide financial incentives to companies to develop treatments for Zika virus infection, although no funding was provided. Currently, roughly $600 million has been diverted from the Ebola virus funds towards Zika virus research.

Let me pause here to let the following concept sink in: now that Ebola is no longer a potential threat to the United States, it is assumed that the rest of the world can handle the fallout itself…but, that doesn’t seem to be the case. Dr. Margaret Chan, WHO director-general, announced in January that although all known chains of transmission in West Africa had stopped, including the most recent outbreak in Liberia, new flare-ups are likely to occur. This will require a sustained response for prevention of future outbreaks. Indeed, Sylvia Mathews Burwell, U.S. Health and Human Services Secretary, told reporters, “We face two global health challenges, Ebola and Zika, and we don’t have an option to set one aside in the name of the other.” The decision to pull money from the Ebola fund is somewhat analogous to withdrawing military troops from countries where the United States has intervened and then pulled out, for one reason or another, hoping for sustainable change in those regions. Historically, this system doesn’t seem to work, and furthers the global opinion that Americans don’t care about non-Americans.

There is a comical phrase among infectious disease scientists: “ATM diseases” get the money. Essentially, the majority of funding is allocated to AIDS/HIV, tuberculosis, and malaria research, which some say are “sexy diseases” as they engender public attention. We know that these diseases are incredibly important to study and combat, but when funding is limited, research on other diseases stalls. Why don’t we know that much about Zika virus? It didn’t cause outbreaks until recently. This is the problem with emerging pathogens: they burst forth rapidly when we don’t have the tools to control them. The scientific community is now scrambling, working around the clock to learn as much as possible, as quickly as possible. $600 million sounds like a great deal of money, but it is nowhere near enough to fight Zika virus, as Dr. Fauci reiterated on Monday.

Pull-quote: “When the president asked for $1.9 billion, we needed $1.9 billion.” – Dr. Fauci, NIAID

One day several years ago, as a novice virologist, I was star struck when I met Dr. Fauci during one of his routine visits to the laboratories of the NIAID. The first thing I noticed was Dr. Fauci’s notorious New York accent, the second, his calm demeanor, humility, and compassion. His lectures inspired me, giving me great faith in the leaders of our scientific community. Why this faith is lacking in our Congressional leaders is nonsensical to me. If we cannot trust those we have appointed to run programs ethically and passionately, then what is the point of having these leaders?

Pull-quote: “Everything we look at with (Zika) virus seems to be a bit scarier than we initially thought.” – Dr. Schuchat, CDC

The NIAID and CDC, institutions that preserve public health in America, are not the only scientific leaders voicing the urgency of combating infectious disease outbreaks before they become uncontrollable pandemics. The WHO has also emphasized the potential consequences of a Zika virus pandemic. Indeed, although Zika virus is an old virus (it was discovered in 1947), it emerged as a rapidly spreading pathogen causing sizeable outbreaks in recent years. In the span of about one year, 440,000 to 1.3 million Brazilians have been infected with Zika virus, which has spread to at least 33 countries. At this point, the association between Zika virus infection during pregnancy and microcephaly, a condition among infants resulting in a smaller than normal head size, has essentially reached causality. That is, scientists can definitively and causally link the virus to microcephaly. [In subsequent posts, I will present some of the important research rocketing into publication regarding this issue.] In addition to microcephaly, the WHO acknowledges that Zika virus infection likely causes Guillain-Barré syndrome, an autoimmune disorder in which a person’s immune system attacks his/her own nerves.

Science is not devoid of political influence. Granted, financial resources are not endless, but history has shown the rapidity with which infectious diseases can spread and the devastation that follows. We were not prepared for Ebola virus, which claimed the lives of over 11,000 people. Will the necessary funding come for Zika virus research, or are we destined to continually ignore potential public health crises until it’s too late to combat them?

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Hot and Spicy Chemicals

By Dr. Doris Kimbrough

You grab a bag of corn chips and a bowl of salsa out of the refrigerator and settle in to watch TV. The salsa is hotter than you expected and after about five chips, your mouth is on fire. Big gulps of ice water don’t help, so you head back to the kitchen to look for sour cream or a glass of milk. What is going on in your mouth? How can cold salsa from the fridge burn your mouth? Why doesn’t cold water help the way it would for hot soup or hot tea? How does the sour cream or whole milk solve the problem?

To answer these questions we have to look at some special nerve cells (neurons) and the chemicals found in hot peppers. In addition to the nerve cells that help you move (motor) and control body functions (autonomic) you have lots of different kinds of sensory nerve cells. Sensory neurons are responsible vision and hearing and all your other senses. There are many different types of neurons involved in touch. Some can detect pain; others respond to pressure, heat, cold, or itchiness to name a few. The nerve cells that detect heat are the ones we need to focus on for this story.

Heat detecting neurons don’t work at or below normal body temperature; think of them as sleeping until you touch a hot stove when they wake up and tell you “Ouch, pull back! Pull back!” Hot peppers like jalapeños contain a chemical called capsaicin (cap-SAY-shin) that fools these nerve cells. The capsaicin binds to the nerve cells and wakes them up. Your brain gets signals that something is burning you even though nothing that is actually hot (in temperature) is involved. There are other chemicals that can do this: piperine and sabinene are chemicals found in ground pepper and curry spices.

So why doesn’t a nice cold drink of water help with the burning? Capsaicin is a chemical that is hydrophobic—literally: “water fearing”. Capsaicin doesn’t really fear water; it can’t because it is a molecule, which cannot have feelings. However hydrophobic compounds, like capsaicin, do not dissolve in water. Other hydrophobic substances are vegetable oil, wax and gasoline. So when you gulp cold water because spicy salsa is “burning” your mouth, the capsaicin stays bound to your neuron and your brain still gets signals that your mouth is burning. Hydrophobic compounds do dissolve in other hydrophobic substances, like oils or fats. You may have heard the expression, “like dissolves like”. The fat in sour cream and whole milk will dissolve the capsaicin and remove it from the nerve cell. This turns off the signaling to the brain and lets you get on with your life.

About the author: Doris Kimbrough is a chemistry professor at CU Denver. She grew up in Atlanta, GA, and went to college at the College of William and Mary in Virginia and to graduate school at Cornell University in Ithaca, New York. She has loved science and chemistry since she was a little girl when her chemist father let her play (safely!) with stuff in his lab.

For the Love of Derby…I mean Biology

By Abena Watson-Siriboe

Who I really am-

I grew up in a family of scientists. My grandmother obtained her pharmacy degree when few women or even women of color were involved in the field. My grandfather was a Korean War vet and dentist deeply entrenched in his community. My mother is a biologist and father a chemical engineer. You can say that science was in my blood. Growing up, my family made sure to foster my interests by providing me with science kits and even a rat to dissect when I was too young to handle a scalpel. In middle school, I received a microscope that probably dated to the late 60s, but I loved it. I searched my house for things to inspect and was even tempted to take my own blood sample but eventually chickened out. Little did I know that as an adult, I would be inspecting and showing off x-rays of my ankle broken during a roller derby game. Not only am I a scientist, I’m a roller derby player who goes by the name Norah P Neffrin. You can take the nerd out of the lab but you can’t take the science nerd out of the girl.

How I got here-

When I first started my undergraduate degree, I was a philosophy major with aspirations of going to medical school. As my studies progressed and I took courses such as cellular biology and neuroscience, I realized that medical school wasn’t in the cards. I wanted to be a researcher. So, much to my parent’s pleasure, I changed my major to Biological Sciences and decided on a minor in neuroscience. One of my teachers expressed to her class that she was looking for students to conduct research in her neuroscience lab. I immediately jumped at the chance and was immediately smitten. My research involved the response of a brain region called the Supra Optic Nucleus (SON) to dehydration in rats. Most of my days were spent treating, sacrificing and preparing rat brain tissue. I would go home and my mother complained that I smelled like rat, but I loved every minute of it.

My time conducting research during undergrad inspired me to get a Masters degree, but it also required moving across the country away from family. I continued to work in the neuroscience field but my work focused on a smaller scale. My work focused on a transporter responsible for sequestering molecules such as serotonin and norepinephrine into vesicles. Small changes in the genetic script of this protein have been linked to mental conditions such as bipolar disorder. It was my hope to provide some insight into the role this protein plays in such a complicated condition. During my MS, is when I started roller derby, hence the derby name, a play on norepinephrine. Oddly, most people don’t get it.

What I do now-

Currently, I work in a biophysical laboratory at CU, Denver. My lab examines membrane binding proteins, some of which are present in the brain and or pancreas. We use varying techniques to determine what parts and under what conditions does the protein bind to the membrane. Some of the proteins we work with contribute to membrane fusion whilst others prevent it. My protein of interest prevents vesicles that contain insulin from being released by specialized pancreatic cells, potentially playing a role in diabetes. By understanding how this protein works, our work can inform potential drug targets. In addition to my work in the lab, I still play roller derby with a league ranked #9 in the world. But these days I skate under my legal name.

Passion for the subject-

As a kid, I was obsessed with how things worked, especially the natural world. It still amazes me that we’re made of atoms, molecules, cells, organs that all work together mostly in harmony. Even more amazing is how small changes can disrupt an equilibrium and result in conditions such as bipolar disorder or diabetes. It’s this wonder and hunger for answers that keeps me motivated and impassioned.