Why did Cover the Night fail?

Joseph Kony

Jason Russell (who spearheaded the Invisible Children's Kony 2012 campaign and then single-handedly caused it to fail) should have consulted Randy Olson. 


Randy Olson, author of the book Don't be Such a Scientist, is a scientist-turned-filmaker who believes that the key to communicating complicated or controversial science topics to the public is made up of four principles: [1]

1. Don't be so cerebral:
   
• Just use normal everyday language that everyone can understand and relate to. And don't let your brain be the only organ you rely on (see the "head heart gut groin" concept below).
2. Don't be so literal-minded:
• Use the "arouse and fulfill" method.  Don't just jump straight to the answer. Make them salivate first. 
3. Don't be such a poor storyteller:
• Tell an engaging story without sacrificing accuracy. 
4. Don't be so unlikeable:
• This one explains itself.

Even though Olson was talking about communicating science, the general theory still holds for conveying any idea. The failure of the Cover the Night campaign can also be explained by the "head, heart, gut, groin" concept [1]: 

• head (reason)
• heart (emotion)
• gut (instinct)
• groin (sex appeal)

The lower you go, the more powerful and longer-lasting the connection will be. 


Presenting the plight of the children to the public using facts, figures, and interviews (head) moved people to want to do something to help (heart). 
But when the controversies came out, people had doubts (gut) and moved on. 
Our attention is better held by the concept of hundreds of people spooning simultaneously (groin) instead, on the date that Cover the Night would have taken place [3]. 


The follow-up video "Kony 2012: Part II - Beyond Famous" barely even got any attention. It tried to combat the doubts people had about the campaign by throwing facts and figures at the audience. 
According to The Guardian, the second movie "does not seem to have captured the public's imagination in quite the same way as Invisible Children's earlier video did." In fact, Google statistics show that the second film got less than 2% of the Internet traffic as its predecessor. [4]. Ouch.
I would have seen that outcome a mile away: the second movie stopped at the Head level, while the first movie tapped into the Heart. Everyone's Gut reactions against the first one also played a major role in biasing everyone against any sequels before they were even created.


So not only did viewers find reasons deeper than the Heart level to ignore the Kony 2012 campaign, but Russell just isn't that likable. It's kind of hard to take someone seriously after they have a mental breakdown. [2] Another pointer Russell could have gotten from Olson was that if you want people to listen to what you have to say, then you really ought to get them to like you first.


Now let's look at a more successful piece of advertising.





You may recognize that as a commercial for Nike Free Run+. The reason I call this commercial successful is because it actually made me consider buying a pair of Nike running shoes. (Which is odd, since I don't even like Nike shoes.) 
Don't get me wrong, they look cool and all, but I have never worn a Nike shoe that gave me the arch support I need. 
Those of you who know me understand what a stubborn hard-ass I can be. So saying that I almost bought a pair of shoes from a brand that I don't even like is saying something. Now that's some good advertising!


Looking at the YouTube video's page, it was published April 4, 2012. 
As of April 23, 2012: 

• It has 1,291,411 views. That's an average of almost 68,000 views each day! 
• The video has 6,877 likes and 148 dislikes. That's an average of more than 350 likes each day! Only 2% of the people who voted did not like the video. If 98% of people like a commercial, then I think we can safely say that the general population enjoyed it.

But why is the ad so successful?
The answer is easy; just remember Olson's tips.

1. Don't be so cerebral.
• The actors use the same language we use every day. They don't drone on about burning ATP to mobilize towards each other out of attraction! They say "I love you so I will run to you."
2. Don't be so literal-minded.
• It takes more then a five-second clip of each of them running to meet. As each development happens in each runner's route, we wonder what will happen next, and if they will actually be able to pull it off. (Oh my god, I think that guy really might die!) We are aroused as the runs unfold before we are fulfilled when they meet at the end.
3. Don't be such a poor storyteller.
• The "story" is engaging but still accurate: complications arise during each run that have believable outcomes. The girl asks the guy on the tractor for directions and he points out where she should go. The guy collapses in a puddle of his own vomit and gets rushed to the hospital. These plot points make for a good story because we can easily see those are things that could happen during a run across the country.
4. Don't be so unlikeable.
• Plain and simple: We like the runners. We can all relate to the problems the guy goes through during his run, though probably not quite to that degree of comic destruction. We find ourselves rooting for them to succeed. (Who wouldn't want two lovers to meet after a long and difficult, yet successful, journey?) And let's face it: that girl is smokin' hot. Who on earth doesn't enjoy watching a hot girl running?

The commercial also fulfills all four organs in the "head heart gut groin" concept: 

1. Head:
• The song is catchy and gets stuck in our heads, the rhyming is clever, and the guy makes a very logical point that they could have just flown instead.
2. Heart:
• Two lovers running across the country to meet each other? Dawww...how adorable!
3. Gut:
• We trust the believable outcomes of the obstacles in our guts, and we bust a gut laughing because the guy's fate in hilarious.
4. Groin:
• The girl is hot, and what happens after the commercial ends is "left up to our interpretation".

Moral of the story? Easy:
Aim for the nuts, and don't get caught ranting in public...naked.




[1] Olson, Randy. (2009). Don't be Such a Scientist. Washington, DC: Island Press. ISBN 13# 978-1-59726-563-8. http://www.dontbesuchascientist.com/HTML/SYNOPSIS.html
[2] Wikipedia. Jason Russell breakdown. Retrieved April 20, 2012 from http://en.wikipedia.org/wiki/Jason_Russell#Breakdown_and_hospitalization
[3] NPR. The Social Media Shuffle: From Kony to Spooning. Retrieved April 20, 2012 from http://www.npr.org/2012/04/19/150964208/young-people-turn-from-kony-to-spooning-record?ps=cprs
[4] Reception to Kony 2012: Part II. Wikipedia. Retrieved April 20, 2012 from http://en.wikipedia.org/wiki/Kony_2012#Reception_2

Happy Earth Day!

April 22 is Earth Day!

Since 1970, today has been a day to raise awareness about protecting the Earth we call home.

There are many easy ways you can help every day by going green:

REDUCE

1. Use less water
• while you're brushing your teeth and shaving.
• This will lower your water bill.
• You really don't need the water running the whole time.
• Take showers instead of baths.
• Plus you won't be sitting in your own filth.



Save water: shower together! ;)
2. Turn off the lights when you will no longer be in the room.
• Less energy used means lower emissions from power plants.
• This will also lower your electric bill.
3. Ride your bike to work, especially during the summer if you live close.



"Other means" = magic spells?

REUSE

1. Many stores sell durable reusable shopping bags for a nominal fee.
• Most have cool pictures or slogans on them, meaning you can express your individuality and help the environment at the same time!



Reusable shopping bags

2. Starbucks sells reusable travel mugs so you can help the environment while you drink your coffee in style!



Awesome Starbucks travel mug with dragon design

3. The Lions Club has a program where you can donate your old eyeglasses to the needy.

RECYCLE

1. Save trees and landfills by using recycling bins for paper and plastic products.
2. Office Max has a discount program based on how many ink cartridges you bring in to be recycled.

REPLENISH

1. Using a composter adds essential nutrients to the soil.
• We put expired leftovers and grass clippings in ours.
• This saves money on fertilizers and by growing some of our own food.
• We get to enjoy home-grown garlic, chives, tomatoes, blackberries, and grapes whenever we want, for free!

RESTORE

1. Volunteer for a local river or pond cleanup group.
• You'll get to keep the environment clean, have fun, and meet new friends!

For more great tips, visit this EPA website.
For more information about Earth Day in general, see the Wikipedia Earth Day page.

If you are reading this, then my blog post has successfully reached you in the future

Cyanide & Happiness, a webcomic by Explosm :)

Now that I have your attention, I can start geeking out. You may or may not know what a neutrino is. For those of you who don't know, a neutrino is an elementary subatomic particle. In English, that means it's “really freakin' tiny”. And by tiny, I mean that the squared radius of an electron neutrino is only 1.0E-33 cm. [1] For comparison, a normal electron has a radius of 2.8E-15 m. (The squared radius of an electron is about 78 million times larger.) And the electron neutrino is the largest of the three flavors – yes, physicists really do refer to the different types as “flavors”.

Before you navigate back to the awesome Hunger Games trailers out of boredom, let me explain why this post is about neutrinos.

Neutrinos are so small that they, logically, have very little mass. This allows them to propagate at speeds approaching the speed of light. (They were thought to be massless until they were found to oscillate.) However, there are some speculative models that show neutrinos as having tachyonic properties, meaning they can travel at the speed of light and possibly back in time. [2]

The prospect of traveling back in time has always been a closet fantasy of mine ever since I was a young child. While all the normal, well-adjusted children were playing tag or maiming each other in dodgeball, I was riding the slide over and over trying to get up enough speed to go back and see the dinosaurs. (I assumed I needed to be moving at least 88 MPH.) The possibility of watching an infinite number of Swat Kats episodes was also a factor.

More recently, however, my desire to travel back in time has deepened, fueled by the desire to stop myself from ever seeing Twilight. In my defense, it was only the last few minutes of the movie.

In the middle of the night, I still wake up screaming in horror, reaching desperately for a bottle of Captain Morgan rum hoping against all hope that I can forget. Unfortunately, as any vet from 'nam will tell you: “What has been seen...cannot be unseen.”

And it only gets worse. A few weeks ago, I heard that the OPERA researchers who did the neutrino-moving-faster-than-light experiment goofed up. I checked this article on Wired Science to find out more. Apparently, there was a loose fiber-optic cable, which made the time stamps from the master clock wrong. The margin of error was so small that the neutrino was only clocked as arriving 60 nanoseconds before it was supposed to [3], so I guess it's true: the size of your margin of error isn't important; it's the motion of your oscillation! HAHAHA! (crickets chirping)

At least that's what people keep telling...my friend. Anyway, another experiment conducted in the same laboratory earlier in March recorded neutrinos as moving at the speed of light. According to this article on BBC News, Antonio Ereditato (the head scientist of the original controversial experiment) has resigned.

Looks like I won't be going back in time anytime soon. Now not only will I never get to see my favorite dinosaur (the ankylosaurus) in action, but to add insult to injury it looks like I've lost my Man Card forever. My dreams of happiness and salvation now lay in shambles around me.

[1] Neutrino. Retrieved April 13, 2012, from http://en.wikipedia.org/wiki/Neutrino.

[2] Tachyon. Retrieved April 13, 2012 from http://en.wikipedia.org/wiki/Tachyon.

[3] Wired Science. Faster than light neutrino results may be due to faulty cables. Retrieved April 13, 2012 from http://www.wired.com/wiredscience/2012/02/neutrinos-faulty-cable/.

[4] BBC News. Neutrino 'faster than light' scientist resigns. Retrieved April 13, 2012 from http://www.bbc.co.uk/news/science-environment-17560379. 

Now on my Bucket List: Run a 4-minute mile.

First off, yes, I have seen the movie. It was great. As I watched the ball drop ushering in 2012, I thought to myself that I should resolve to do something completely badass. For a long time, I had thought about the sheer amount of training, strength, and endurance (and maybe a little bit of insanity) it must take to run a mile in just four minutes. (Random side note: The Four Minute Mile is an awesome movie.)

Roger Bannister: 1954 Four-minute mile runner.

You may have already guessed this, but I ran Track and Cross Country in High School. I also regularly run random 5k and 5 mile races, and things like Warrior Dash. I added Parkour to the list when I realized certain objects and buildings on my alma mater's campus could be tricked on and/or scaled at 4am.

So obviously, I have at least some physical ability. But will that be enough? I decided to do a little more research using my good friend Google, and found someone just as nerdy as me who had apparently spent his time finding an answer to the same question. You can read the original article on his blog Gravity and Levity, here.

Basically, his post confirmed my suspicion that as I get closer and closer to my goal of a four-minute mile pace, it will be more and more difficult to get my times down. The basic concept is called the Law of Diminishing Returns. I experienced it first-hand back in Track. Getting my quarter-mile time down ten seconds (and keeping it down) took about three weeks of hard training. But then it took another three weeks to get it down another five seconds. Right now my quarter mile pace is 75 seconds. Assuming I can get my endurance up to run the whole mile at that pace, that would make my mile time 5:00. That's pretty darn close. But of course, I need to shave off another 15 seconds from each quater-mile time. That won't be easy.

Who will win, me or the Law of Diminishing Returns? We shall see.


Source: Gravity and Levity blog post "The fastest possible mile", retrieved Jan 3, 2012; URL = http://gravityandlevity.wordpress.com/2009/04/22/the-fastest-possible-mile/.
Picture from: http://www.worldinsport.com/2010/11/100-greatest-sports-stars-number-91-sir.html.

Cacti read blogs too

So there I was, surfing some blogs, when I came across an interesting article on Southern Fried Science.  It gives ten reasons why dolphins (marine mammals in general, actually) are NOT as cute and innocent as people like to believe.  I especially enjoyed reason number 5.

Follow this link to read the full article:
http://www.southernfriedscience.com/?p=4639

My inaugural post

Hello, my name is Jabby. I am a cactus. Like Patrick, I am very interested in science.

To make up for the fact that I was left in Eastlake AGAIN, Pat decided that I needed a hobby to keep me busy and invited me to post to this sweet blog.

Will I update every day? Of course not, I am a cactus for cryin' out loud!

Did you know that the tallest species of cactus in the world is the Pachycereus pringlei?
Well, you do now.
The tallest one ever recorded was 19.2 meters tall.

To learn more, check out this link:
http://en.wikipedia.org/wiki/Pachycereus_pringlei

70-year fasting feat: Medical miracle or bullshit?

As a biologist-in-training, I have learned that the human body can perform some truly amazing feats. During the Fight-or-Flight Response, our epinephrine (adrenaline) levels can spike, which increases our reaction time, speed, strength, and even dulls sensations of pain. Exposure to a pathogen our body has never encountered before is not a problem the second time around, since our immune system is very efficient at recognition of and response to foreign agents. But this time I noticed an article that sent my Bullshit Detector into overdrive.

According to this article, an 82-year-old man in India named Prahlad Jani has gone 70 years without food or water.

Now, I do understand that meditation can affect metabolism. In the past I have seen documentaries of monks that can dry a wet towel on their back by meditating to increase their body temperature so the water visibly evaporates off like steam. But, come on.

The longest recorded hunger strike I could find lasted only 68 days, and that one ended with Barry Horne's partial blindness and kidney damage.

No matter how long the body can go without food, it will eventually run out of the materials it needs to run normally (glucose, vitamins, minerals, water, etc) and will begin to break itself down to get what it needs.  This directly conflicts with one of the most basic, fundamental principles of biology: the energy requirements to sustain life.

When Prahlad was observed for two weeks by Indian military doctors, nothing seemed out of place, but all that did was prove he can last two weeks without food. Scientists will all agree that it is possible for almost anyone to live for two weeks without food (you'll just be really REALLY hungry). The longest we can live without taking in any water is up to 10 days in optimal conditions.

The human body IS amazing; it can survive for many weeks without food and many days without water.
But it CANNOT survive for 70 straight years without the intake of any food or any water...
It is simply impossible.

Still blogging strong even after all that alcohol

 Even though I am no longer taking Senior Seminar, I have decided to continue posting to our blog. As an avid scientist-in-training, I feel the need to share things about science that I find interesting. As usual, my aim is to try to amuse the average web surfer while teaching a little bit too.

I was sifting through my e-mail when I noticed the link my brother sent me about new pictures NASA obtained of the sun. Four different cameras allow the satellite to look at the sun’s surface, layer by layer.

These pictures, which are 10x better than HD, should help scientists better understand the link between the sun’s activity and the atmosphere (or, more specifically, climate change).

Here is the link.  I would have posted this sooner, but I had Finals to take.  You will have to watch a stupid ad first. I tried to use my mad coding skillset to get around this, but I’m still feeling the effects of partying with my graduating friends so I didn’t try too hard:

http://news.yahoo.com/video/environment-15749659/19271005

Why the Outer Banks will rock your face off

At 5:00 a.m., I was hanging out in the parking lot with my Marine Biology lab notebook and camping gear. I stood there waiting for the rest of my BIO 412 classmates to show up, trying not to move too much because it made the spinning in my head worse. (I knew I would probably be sleeping most of the van ride to North Carolina, so I had gone out and gotten my drink on.) I shivered, wondering vaguely how long it would take for AU Safety Services to investigate a report of a drunkard camping out in the parking lot, when other students began to arrive, yawning and lugging camping gear.  Once all the gear was loaded in the vans, Doctors Posner and Saunders, two of the AU Biology department faculty, began the drive.  We were on our way!

Between being subjected to Tom’s awful taste in music approximately seven thousand fifty six times, I managed to take some awesome pictures of our trip. Enjoy!

Camp Awesome: We came here for taxon identification, sleep, and snackage.

At 11:00 p.m. the last night, 30mph gusts came out of nowhere and ripped our tents down.  The poles of two tents were left snapped and useless.

Even 15-foot tall sand dunes are futile attempts to prevent the erosion that barrier islands experience naturally.

We went kayaking in a salt marsh and I spotted a duck. I was able to get close enough to take this sweet pic right as it took off.

The Cape Hatteras Light Station. It is 198 feet tall, and you must climb 257 steps to reach the top!

The view from the top was insane! It took me three minutes just to stop hugging the wall and stand by the edge to take this picture.

The entire climb up, I had a deathgrip on the railing while trying to look like I wasn’t having a claustrophobic / heights freakout.


The Littoraria snails will climb the Spartina marsh grass to escape predation by crabs below. They can hold on even as they sleep by secreting a sticky substance onto the spot and just hang there, sleeping.

We came across this huge fish skeleton in the salt marsh. I took a picture with my hand next to it to set the scale for how huge this thing was.

We wanted such a complete specimen for our lab back in Ohio, so we wrapped it in trash bags and stored it in our lunchmeat cooler.


Once you get the chance, go check out the Outer Banks! But whatever you do, don’t feed the Laughing gulls! They will stalk you forever if you do.

Shower Anyone??

For anyone that has taken a microbiology course, especially here at Ashland you feel completely dirty after finishing up experiments in lab. So what better way of cleansing yourself from a hard days work in the lab, experimenting with bacteria that you are trying to identify for your 25 page lab report. Who doesn’t like waking up and taking a hot shower before school or work to feel clean throughout the day? What people don’t know is that the showerhead is a perfect environment for microbes. It’s moist, warm, dark and frequently replenished with low amounts of nutrients for these microbes to feed on. Who could have thought that these microbes can lead to pulmonary disease and other health risks such as asthma and bronchitis? Believe it or not it is true and studies have proven that microbes do exist.

The common microbe that was found in high levels was Mycobacterium avium, a pathogen that is linked to pulmonary disease. M. avium and related pathogens were seen clumped together on showerheads in slimy biofilms. Studies shown that the showerheads were more than 100 times the background levels of municipal water when compared to the showerhead when they were taken off. "If you are getting a face full of water when you first turn your shower on, that means you are probably getting a particularly high load of Mycobacterium avium, which may not be too healthy," said study leader Norman Pace.


These biofilms were swabbed on interior surfaces of 45 showerheads from nine cities in the United States. Researchers found that nearly a third of the showerheads tested were harboring these pathogens. While it is rarely a problem for most healthy people, those with weakened immune systems, like the elderly, pregnant women or those who are fighting off other diseases, can be susceptible to infection.

One showerhead in the study was found with high loads of the pathogen Mycobacterium gordonae. The showerhead was cleaned with a bleach solution, but later tests on the showerhead showed the bleach treatment had actually caused a three-fold increase in M. gordonae, indicating a general resistance of mycobacteria species to chlorine.
Research at National Jewish Hospital in Denver indicates that increases in lung infections in the United States in recent decades from so-called “non-tuberculosis” mycobacteria species like M. avium may be linked to people taking more showers and few¬er baths, said Pace. Water spurting from showerheads can distribute pathogen-filled droplets that float in the air and can easily be inhaled into the deepest parts of the lungs.







So what should I do about taking showers? I really don’t want to be the smelly kid in class that everyone talks about. Well, fellow readers you can always replace the showerhead. Research shows that that plastic showerheads allow for more bacteria to clump together when compared to the metal showerhead counterpart. You can also allow the water to run at the hottest level for a couple of minutes and then turn the water to a tolerable level. Not welling to give up that 1980’s showerhead? Solution, take a bath.

Falkinham III, Joseph, and Michael Iseman. "Mycobacterium avium in a shower linked to pulmonary disease." Journal of Water and Health. 6.2 (2008): 209-11. Print.

Feazel, Leah, Laura Baumgartner, and Kristin Peterson. "Opportunistic pathogens enriched in showerhead biofilms." Proceedings of the National Academy of Sciences of the United States of America 12.2 (2009): n. pag. Web. 28 Apr 2010.

Can sleep deficiency really kill you?

As I have stated before I am one of the unfortunate 64 million people in America that suffer from insomnia. My dad has it, my brother has it, and I have it. Without insomnia I probably wouldn’t get a whole lot of things done (like this blog post). Fortunately for me having insomnia also has some other perks, such as getting to watch TV shows about insomnia. Earlier tonight I watched a show on the National Geographic channel about a form of insomnia that I was completely unaware of and I am sure I am not the only person who is unaware of it since it affects only 40 families in the entire world. This type of insomnia is called Fatal Familial Insomnia or FFI. I never thought that Insomnia could kill someone, but this form of Insomnia makes every person who is diagnosed with it a victim.

I thought that I would go over the sleep cycle a little bit first to help you understand how sleeping works but since a colleague has already posted a blog about it I will just set up a link to that post here http://fourthirstypandas.blogspot.com/2010/04/sweet-dream-or-beautiful-nightmare.html.

FFI has been characterized as a genetic disorder caused by a mutation at codon 178 of the prion protein gene. This is also a problem in the condition called “Mad Cow Disease.” Prions are proteins that attack the nervous system and cause the symptoms associated with “Mad Cow Disease.” In FFI the cause of the prion protein is genetic, where a single base pair is coded incorrectly. This is one of 3 billion base pairs known in the human genome. In FFI the prions accumulate in the Thalamus in the brain. The Thalamus was never thought to control sleep, but it does transmit signals to the cortex of the brain. In patients with FFI lesions occurred in the Thalamus and the Cortex of the brain. With FFI 90% of the neurons in the Thalamus have disappeared.

ally sleep has been one of the hardest things to study, but some recent studies using a PET scan and a tagged amino acid may give us some clues as to why we need to sleep. One of the theories is that we need sleep to repair proteins in the cells of the brain, which can’t happen while we are awake because the brain is too busy and has too many processes happening. During a normal day while we are awake we accumulate adenosine in our brain, which signals our bodies to sleep. Sleep would eliminate the adenosine and produce more proteins for repair of the brain cells.

Humans have varying levels of sleep, but so do many animals in nature. A normal human gets somewhere between 7 and 8 hours of sleep per night, but an animal such as a lion gets up to 15 hours a day. A elephant on the other hand gets around 4 hours of sleep. One of the theories about this is that predator species can sleep more because they don’t generally have many predators, while the prey species get much less sleep so they can evade their predators. But what if we could sleep and be awake at the same time. I know this sound ridiculous, but a few animals in nature already have achieved this process. If we could somehow find out how to translate this to humans we could eliminate FFI and other sleep associated disorders.

One of the species in nature that sleeps all the time but we never see it are dolphins. I always think of a dolphin as an animal that is always moving and swimming. A study done in San Diego evaluated if a dolphin lost any mental abilities when forced to stay alert for multiple days. The dolphin was trained to detect a swimmer that was in the bay while the dolphin was detained in a fenced area. When the dolphin detected the swimmer it hit a switch on the dock. The dolphin showed no decline in activity and detected every time the swimmer was in the bay. The dolphin slept throughout the entire experiment. This is possible due to dolphins having something called unihemispheric sleep. Throughout the dolphins life one half of their brain is active while the other is sleeping and then they switch. Another animal that is theorized to do this is many different avian species. Studies have shown that they can sleep while also watching for predators while they are on land, but it is still unclear wheather they can sleep while flying.

So far for all terrestrial mammals, sleep is needed. After several days of sleep deprivation there is a drastic decrease in overall health. One side effect is diabetes, due to insulin resistance that is accumulated. There is also a decrease in lymphocytes which fight bacterial infections in the body. In most mammals if sleep is deprived for 2 weeks death will occur. In patients with FFI death usually occurs from 7 to 36 months, and the unfortunate thing is that once symptoms of FFI start they never go away until the patient dies. The unfortunate thing about this disease is that there is currently no cure. And if one family member is ever diagnosed with FFI there is a 50% chance that their children will be diagnosed with it as well since it is a dominant gene.

So now that I have accumulated a massive amount of adenosine in my brain I think I will go sleep and I encourage everybody else to get sufficient amounts of sleep as well.

References:

1. National Geographic Explorer: “Fatal Insomnia”, aired April 27, 2010

2. Fatal familial insomnia: clinical features and molecular genetics; PIETRO CORTELLI, PIERLUIGI GAMBETTI, PASQUALE MONTAGNA and ELIO LUGARESI; J. Sleep Res. (1999) 8, Suppl. 1, 23-29; European Sleep Research Society

3. Montagna P, Gambetti P, Cortelli P, Lugaresi E (2003). "Familial and sporadic fatal insomnia". Lancet Neurol 2 (3): 167–76. doi:10.1016/S1474-4422(03)00323-5

4. Almer G, Hainfellner JA, Brücke T, et al. (1999). "Fatal familial insomnia: a new Austrian family". Brain 122 ( Pt 1): 5–16. doi:10.1093/brain/122.1.5.

Are tanning beds a cancer risk?

Being the scrawny white nerd that I am, I don’t tan… I burn. This concerned me greatly since I would soon be traveling to the Outer Banks in my Marine Biology class. I wanted to go swimming in the ocean, but that would mean my un-tanned, blinding white-ness would be on display. Not wanting to look completely ridiculous, I contemplated going tanning for the first time ever.

But I was worried. Tanning lotions were out because I don’t like the thought of smearing skin-altering chemicals on myself. And I had heard from many sources that tanning beds cause cancer. So I decided to look into the matter.

According to this study I found [1], exposure to tanning beds actually does increase the risk of developing malignant melanoma (skin cancer).

Where are they getting that from?
Ting and his crew wanted to test the hypothesis that increased exposure to tanning beds was linked to an increased risk of developing malignant melanoma.

To perform the study, surveys were completed by a random sample of 551 patients. The surveys asked questions like:

1. Extent of tanning bed exposure (how much of the body was exposed to the tanning bed),
2. use in the last 12 months (number of tanning sessions in the past year),
3. age at first exposure,
4. season of use (when in the year do they go tanning?),
5. lifetime number of tanning sessions,
6. minutes spent per session,
7. sun protection attitudes and practices (do they usually wear sunscreen?), and
8. leisure and occupational sun exposure (how often are they exposed to natural sunlight?).

The survey also looked at demographic information, such as:

• Gender,
• age,
• race,
• tendency to tan,
• level of education,
• work environment (indoor or outdoor),
• number of sunburns in the past, and
• previous history of various cancers.

Here is a look at the demographic information.

When doing a scientific study, you must always be wary of confounding variables (also known in statistics as a lurking variable). A confounding variable is any variable other than the independent variable that may bear any effect on the behavior of the subject being studied.
An example of a lurking variable would be testing infant memory with a matching game, but waiting too long between tests so that improved results on the second game may be due to the baby’s brain developing and not the baby’s memory. (Wikipedia)

The study took into account confounding variables such as:

• Indoor vs. outdoor occupation and leisure activities,
• Fitzpatrick skin type (numeric scale for skin color),
• history of blistering sunburn, and
• use of sunscreen and sun protective clothing.

If a patient had a family history of malignant melanoma, he was not assessed because of the potential for inaccuracy. (If their family is genetically more likely to get skin cancer without ever having used a tanning bed, than if they use tanning beds and get cancer it is impossible to determine the cause of the cancer.)

The answers to the survey were compared to those patients’ medical records. Of the 501 records available, 194 of the patients had been diagnosed with some kind of skin cancer (see Table 1).

Tables 2 and 3 below show the data that links exposure to tanning beds and risk for developing malignant melanoma.  Click on them to make them larger.

“Most modern tanning units produce mainly UV-A and less than 5% UV-B, although this amount of UV-B irradiation exceeds that in natural sunlight, and is sufficient to cause immunosuppression.” [1]
Ummm…yikes.

Interestingly, (according to Ting) this was the first study that accounted for confounding factors, and considered the frequency or duration of tanning bed exposure.
Yeah, that might help.

After they did a bunch of calculations that I won’t go into, they found that their hypothesis was correct. Increased exposure to tanning beds increased the risk of developing malignant melanoma.
Most of the patients that went tanning the most were young women under 45 years old, which meant that they were at the greatest risk of developing skin cancer.


Since exposure to tanning beds would increase my risk for developing cancer, I guess I better find a safer way to get a tan.
Of course, all of this is a moot point now that I’m already back from our OBX trip.
And yes, I did get sunburned after only an hour of kayaking.



[1]
Ting, W., Schultz, K., Cac, N. N., Peterson, M., & Walling, H. W. (2007). Tanning bed exposure increases the risk of malignant melanoma. International Journal of Dermatology, 46(12), 1253-1257.

DOI: 10.1111/j.1365-4632.2007.03408.x

Journal article LINK

Preventing Parasitic Infection

Nearly one third of the people that will die this year will die from an Infectious disease worldwide. So what exactly is an Infectious disease? An infectious disease is an illness derived from a pathogenic microbe. A pathogenic microbe can range from bacteria, a virus, a fungus, or a parasite. Current research is focused on preventative and medicinal treatments that can attack the microbe before it can invade the host body. One way a drug can disrupt the microbe from invading the host cell is to use small-molecules to prevent the pathogen from invading the host cell.

Invading pathogens have proteins on their outer shell that can be used to identify the pathogen or the proteins can be used to attach to a host cell. These proteins can also be used to locate and disable a foreign microbe from invading your body. This study focuses on identifying small-molecules that can disrupt the ability of a certain pathogen, Toxoplasma gondii. T. gondii is the causative agent in toxoplasmosis, and is related to Plasmodium which causes malaria.  ¹Toxoplasmosis is a parasite that can infect humans, but is transmitted to humans by the common housecat.  ²People and animals can become infected by being exposed to contaminated meat, fecal matter of an infected cat, or from a mother to her fetus. Roughly one third of the world is estimated to be carrying the Toxoplasma parasite. Symptoms of infection are mild flu like symptoms. However, if you have a weakened Immune System or are pregnant, the infection may cause more serious symptoms such as swelling of the brain and neurological disease, or it can be fatal especially to the fetus.

T. gondii has two distinct phases in its lifecycle. The first phase is the sexual stage. The sexual stage takes place in humans and in cats, the pathogen invades a cell and produce bradyzoites (form of the pathogen).  Bradyzoites most commonly found in muscle or in the brain, are continually being produced until the host cell bursts from the infection. The burst cell releases the replicated bradyzoites which are now called tachyzoites.  Tachyzoites are the mobile form of the pathogen that can infect new cells or pass into the small intestine. The tachyzoites can be killed off by the host immune system once the host cell has burst. However, if the tachyzoites reach the small intestine, the tachyzoites produce oocytes which get excreted in fecal matter. The production of the oocytes is the sexual phase of the T. gondii life cycle. The shed oocytes can then be passed onto humans by consuming unwashed vegetables or eating infected meat.

The molecular mechanism by which T. gondii invades cell is still unknown, but is crucial to survival of the pathogen. Although the ³mechanism by which cells are invaded isn’t known, it is known that small-molecules can inhibit the invasion of host cells by the parasite T. gondii. The current experiment tested 12,160 small molecules for their ability to prevent the pathogen from invading cells. The experiment was carried out by placing equal amounts of the differing small-molecules into wells with possible host cells and one invading parasite (T. gondii) and one non-invasive parasite. The invasive T. gondii pathogens were labeled with a yellow fluorescent protein that allows the parasite to be visualized using a microscope. The effectiveness of the small-molecules on preventing the Toxoplasma pathogen from invading host cells was determined visually by looking to see if any Toxoplasma pathogens made it into the cell. If yellow specks were seen in the cell, the cell was invaded by the pathogen and the small-molecule did not prevent the pathogen from entering the cell.

Of the 12,160 small-molecules tested, only twenty-four molecules non-cytotoxic prevented invasion by the Toxoplasma parasite. After identifying the twenty-four inhibitory small-molecules, nineteen of the small-molecules effects could be reversed. That leaves five small-molecules that cause irreversible effects to the Toxoplasma pathogen.  

The twenty-four small molecules were then examined to determine how they exerted their effects on the parasite.  There are five ways that the parasite can be inhibited, but only three were examined. The first mechanism studied was the motility of the Toxoplasma pathogen. Of the 24 inhibitory molecules, 21 prevented the parasite from becoming mobile by inhibiting slime trail formation which helps the parasite glide across a surface. A second mechanism that was studied was the formation of a conoid extension. A conoid extension extends and retracts repeatedly as the parasite moves across a cell. None of the inhibitory small-molecules caused a conoid extension, while three inhibited extension but did not affect motility of the parasite. The final mechanism studied was the secretion of microneme. Micronemes are secretory organelles that help the parasite attach to the host cell.  18 of the 24 small-molecules inhibited the secretion of a certain microneme protein. However, the effect of inhibiting microneme protein secretion on parasite-host relationships was not studied.

The study found 24 out of 12,160 small molecules inhibited the invasion of T. gondii into a host cell.  The 24 molecules that inhibited invasion of a pathogen into a host cell can be used to study how the parasite infects the host cell. Further characterization of the inhibitory molecules can be used to help determine how each of the molecules prevents the invasion into a host cell. By studying Toxoplasma gondii, the molecular mechanism by which the parasite infects cells can be studied. By identifying the mechanism of invasion, further infections of the Toxoplasma pathogen and other pathogens related to it can be prevented.

¹http://en.wikipedia.org/wiki/T._gondii  

²http://en.wikipedia.org/wiki/Toxoplasmosis

³Carey, K et al. “A Small-Molecule approach to studying invasive mechanisms of Toxoplasma gondii.” Proceedings of the National Academy of Sciences in the United States of America. Doi. 10.1073

Welcome to the Future!

In general, there are two main forms of “being sick”—a bacterial infection which most know can be treated through use of antibiotics and a viral infects in which case…just go back to bed because there’s nothing you can do. Well, welcome to 2010 America! A recent publication in PNAS, the Proceedings of the National Academy of Sciences in the United States of America explains current research being performed using bacterial vectors as a mechanism to deliver RNase P-based ribozymes into specific human cells and inhibit viral infections (1).

In a nutshell a virus is an infectious agent that hijacks the cellular mechanisms of another type of cell. Most every organism can be infected by viruses including plants, bacteria, animals and humans. The basic structure of a virus is simple: protein coat and genetic material (hence the big controversy of whether or not they’re “living”) however some may contain an envelope of membranous material and surface proteins that often act in antigen-recognition of immunological responses. The genetic material of viruses is perhaps one of the reasons they’re so difficult to treat. Many viruses contain DNA, however some crazies out there have RNA and either of these can be single stranded, double stranded, linear or circular on top of the many recombinations, horizontal gene transfers, reassortments and mutations.
Viruses do not perform their own metabolism but, as mentioned earlier, hijack the host’s cellular machinery through the same basic process: Attachment to the outer membrane of the cell, penetration of the membrane into the cell’s interior, uncoating in which the viral protein coat, called a capsid, is removed to avoid immune defenses and inject the viral genome; Replication in which the genes injected are transcribed and translated via the host cell and the subsequent proteins assist in viral replication and finally release in which the host cell cannot continue producing viral proteins and burst, thus spreading the virus to surrounding cells (2).

Because the virus eliminated its protein coat, targeting the problem becomes especially hard. Also because it is host cells producing the viral proteins and subsequent virus for spread, eliminating host cells is the ideal, however not really an option (you can’t go off killing all your cells….Bad news Bears!) So for a while there, people just slept until their immune systems could “kick in” and get the job done. For some, however, that was not a possibility and the flu virus meant certain death. Sure there were some basic antiviral drugs that could target and prevent DNA replication, but often were not site-specific and ended in very gruesome side effects. Vaccines also help in which attenuate (dead or weakened) virus was pre-introduced before a nature infection could take place so the immune system could build antibodies before a real problem him. That’s really convenient…until the strain isn’t actually weakened or dead and you just infected an innocent human being with polio, THANKS CUTTER LABORATORIES! (3) Regardless most viral infections cannot truly be “cured” or even treated for that matter…until February 2010.

Yong Bai, Hongjian Li, Gia-Phong Vu, Hao Gong, Sean Umamoto, Tianhong Zhou, Sangwei Lu and Fenyong Liu recently published their research on Salmonella-mediated delivery of RNase P-based ribozymes for inhibition of viral gene expression and replication in human cells (1).

According to Bai et al, the main challenge of gene therapy is finding approached to deliver nucleic-acid based gene interfering agents like interfering RNAs and ribozymes. Interfering RNAs are small single stranded RNAs that are complementary to a sequence of mRNA. Upon being delivered, these single stranded RNAs find and bind with mRNA preventing translation and tagging it for destruction via the RNA-induced silencing complex (RISC) (4). Ribozymes (or RNA enzymes) are RNA molecules capable of catalyzing a reaction. These reactions are more than often hydrolysis of phosphodiester bonds including those in the backbones of complementary sequences, thus preventing translation of mRNA (I don’t know like maybe that of VIRAL INFECTIONS?! Hmmm) (5).


Anywho, back to the research. In the article mentioned above, human cytomegalovirus (HCMV) was used as the target virus for study. A functional RNase P ribozyme called M1GS was constructed which targets the mRNA essential in synthesizing capsid proteins: the scaffolding protein and assembling which are required for the protein coat of the HCMV. This ribozyme was expressed using Salmonella strains and up to 90% of viral protein expression as well as about 5,000-fold reduction in viral growth was seen in the treated cells and NOT in untreated.

HCMV is an opportunistic pathogen which can lead to death in immunocompromised, neonates, AIDS patients and transplant recipients. In these patients the HCMV infests macrophages and monocytes resulting in lysis and spreading of the infection. To combat infections like this, Nucleic-acid based gene interference (the ribozymes and RNAi mentioned earlier) are used for specific targeting of infected cells. The problem with these mechanisms is getting them to the cells. Many of the vectors used now-a-days are attenuated or modified viruses which have many problems previously described. The research done here used the invasive bacteria Salmonella which has the ability to enter human cells and transfer genetic material. These bacteria have been used for anti-tumor small hairpin RNAs in cancer therapy due to their ability to specifically target dendritic cells, macrophages and epithelial cells. Using these bacteria to deliver ribozyme plasmids to macrophages infected with HCMV, it was seen that not only are capsid-scaffolding proteins and assmeblin necessary for viral replication but also that delivery of ribozyme via Salmonella to HCMV-infected cells resulted in effective inhibition of gene expression and replication and may demonstrate a novel method for ribozyme delivery and treatment of viral diseases.







1. Bai, Yong, et al. "Salmonella-mediated delivery of RNase P-based ribozymes for inhibition of viral gene expression and replication in human cells ." Proceedings of the National Academy of Sciences in the United States of America . 107.16 (2010): 7269-7274. Print.
2. http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/V/Viruses.html
3. http://en.wikipedia.org/wiki/Polio_vaccine
4. http://en.wikipedia.org/wiki/RNA_interference
5. http://en.wikipedia.org/wiki/Ribozyme#Activity

Michael Specter: The danger of science denial | Video on TED.com

Michael Specter: The danger of science denial | Video on TED.com

I just though I would post this video on science denial since we touched on it earlier in the semester. It is very interesting. The man speaking in the video is Michael Specter. He is a staff writer for the New Yorker and has recently written a new book called "Denialism" touching on some major issues of why we have begun to fear science instead of accept all the advances that we have.

Oh those poor bats...

As summer approaches, I can't help but think of going caving again. Crawling through tight spaces and climbing down cliffs is such an adrenaline rush; plus it's a great way to learn some pretty cool science. Please allow me to encourage you to go!

I hear people saying all the time that being short has its perks, but I know of one situation in which it's a curse. While at Mammoth Cave, our guide took us to a drop which they call the Lion's Head. As you can see, I'm (yes, that's me!) hanging on for dear life (actually I'm having the time of my life)! Even though the floor is about 5 feet under me I still don't want to fall. Plus there's a huge stalagmite below not pictured prepared to attack, giving the formation the title of the Lion's Head. However, the tour guides there are helpful and make sure that you get down safely. Anyway, aside from the crazy expeditions, you can learn many things from going on a tour like this. You can learn about the glittering water in the cave that contains many organisms and certain minerals. You can also learn about certain epidemics that are affecting certain native species. For example, bats living in the caves are starting to contract a particular fungus. This fungus grows on their noses, killing them and affecting their natural behavior. This is known as the white nose syndrome and has effected many bats. It can be transferred to bats via humans. The syndrome also spreads amongst bats. I find this interesting and important because the bat population is steadily decreasing due to this malicious killer. Since the introduction of the white nose syndrome, the bat population in 2 New York caves was found to be reduced by 75% [1]. This disease has spread to other caves in North America and researchers are studying this more to gain more of an insight into what it is and how to treat it.

I did a little more research on the subject because I want to know more about it. I found one paper by Courtin et al titled "Pathologic Findings and Liver Elements in Hibernating Bats With White-Nose Syndrome" that discussed this disease. The paper gave a great overview of the disease and did a nice job This malicious disease first appeared in 2006 in a New York cave and then spread throughout the Northeast during the winters of 2007 and 2008. By 2009 it had found its way to Pennsylvania and Virginia [1]. The bats most commonly affected are the little brown, northern-long eared, and big brown species. When they examined some of the bats, they found lesions on the muzzle and wings. Geomyces destructans, a white fungus, was found around these lesions. Behavioral differences were also seen. Some of the bats flew out of the caves in the middle of winter during hibernation and some even flew during the day. What is interesting about this study is that they analyzed the lesions and looked to see if there were any metals or minerals at abnormal levels. This could correlate to the disease [1].

For this experiment, they collected dead or almost-dead bats with the disease. They collected two groups: one for microbiological examination and the other for metal and mineral analysis. In the examination group they found that the dead bats had fungus that started to penetrate the basement membrane of the root sheaths and into surrounding tissues, but this was not the case in the almost-dead bats. They also found that the body weights of the bats were on the low side. They found that the fungal hyphae grew along the hair follicles and also went along the surface of the skin in hairless places such as on the wings. One interesting thing Courtin et al discussed was that this type of fungus is that it can extend into the epidermis, near the noncorneal layers as well as the sebaceous glands [1]. While examining the bats, they also found that there was fungus growing, as well as gram-negative bacteria, in the dermal-epidermal interface. They also found no organ failure in these bats.

In the second group, they analyzed the livers for different metals. They found that most metal levels varied and were not consistent. Courtin et al collected several different species of bats (they are listed above). They found, along with other labs, that the little brown bat is more commonly afflicted with the fungus, whereas the the big brown bats are not. They believe this could be due to the areas in which the big brown bats hibernate. They hibernate in drier, ventilated areas whereas the little brown bats do not. So, in conclusion, their home choice could have an effect on their susceptibility to this fungus [1].

I don't know about you, but I can't help but think of these poor bats. So, if you do go caving, please, don't touch the bats. Even though the Mammoth Cave bats have not seen this fungus as of now, there is still the potential that it could be introduced.

[1] Courtin, F., Stone, W. B., Risatti, G., Gilbert, K., & Van Kruiningen, H. (2010). Pathologic findings and liver elements in hibernating bats with white-nose syndrome. Veterinary pathology, 47(2), 214-219.

Photo of bat from Courtin et al, (2010).