The Factual Enquirer invites you to drop by each Saturday afternoon for a roundup of the week's best science art findings. Scroll down and enjoy!
Saturday, February 4, 2012
Friday, February 3, 2012
Carbon Rehab, Darwin-Style.
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| Photo credit: p.Gordon |
Every living thing is hooked on carbon. And once you're hooked, you're really hooked.
Reason for rehab number one: the carbon cycle.
There has been at least four billion years of organic, biological life on this planet all of which grows, lives and presumably evolves with a carbon addiction. The global carbon cycle shows how producers (photosynthetic plants), consumers (who eat them), and decomposers (like fungi) depend on their carbon fix to function. All of the living matter on Earth has evolved into a system of carbon junkies dealing the miracle drug that gives us that extra special energy boost. There's really nothing like it. Or is there?
A New HIV strategy
Don't work harder, work smarter. This saying is frequently applied in business, schools, and now possibly in science? HIV researchers are testing new ways to make a more effective HIV treatment.
HIV has proven to be one of the trickiest human diseases to treat due to a variety of reasons. For one, it specifically kills immune cells, which eventually allows opportunistic pathogens to infect and kill AIDS patients. More problematically, HIV mutates extremely fast. Mutations are generally thought of as a bad thing, as they are errors in the DNA. However, for HIV having such a high mutation rate is a great thing, because it allows it to change faster than the immune system can recognize and kill it. The high mutation rate is favored, because the immune system will weed out any viral particles that don't mutate and retain the old, "known" form.
Current HIV treatment options focus on trying to both get the body to recognize and destroy the virus, and to try to prevent mutations in HIV as long as possible by throwing lots of different drugs at it.This is known generally as a drug cocktail, or more recently as HAART (Highly Active Antiretroviral Therapy). HAART combines three different classes of HIV medication, each of which targets a different vital component of the virus. Generally, this regimen includes a nucleoside reverse transcriptase inhibitor, a protease inhibitor, and a non-nucleoside inhibitor. Basically, both kinds of the reverse transcriptase inhibitors prevent HIV from copying its genetic material, and the protease inhibitor prevents the complete formation of mature viral proteins. I like to think of this approach as "playing the odds". By targeting more than one component of the virus, HAART increases the number of mutations HIV has to accumulate in order to be successful, which decreases the odds that one HIV viral particle will be able to do so. Now, researchers are proposing a new strategy I like to think of as "go ahead, mutate, we dare you".
A collaboration between researchers at the Ragon Institute, MIT, and Harvard have identified regions of HIV that decrease its fitness when mutated. Basically, if the virus tries to mutate these regions to escape detection by the immune system, it will be unable to survive. If it doesn't mutate these regions, the body will be able to recognize and destroy it. It's rather like being caught between a rock and a hard place for HIV.
While these results were discovered using computer algorithms, more details of which can be found here, the researchers strengthened their findings by comparing to real human data. They found that patients who control HIV on their own without medicine have T cells that target these same regions on HIV, and that strains with mutations in these regions of the virus are extremely rare in nature, indicating that there is strong selection working against such strains. Additionally, because this amino acid sequence is so highly conserved, there's potential for a vaccine to be developed with these regions. Right now, HIV mutates too fast for a vaccine to ever be effective.
Personally, I find this study fascinating because it takes a whole new approach to the HIV problem. Instead of trying to circumvent the problem of HIV's high mutation rate, they are using its mutation rate against it. It is a novel idea, and from my very non-expert point of view, one with a good chance of success.
HIV has proven to be one of the trickiest human diseases to treat due to a variety of reasons. For one, it specifically kills immune cells, which eventually allows opportunistic pathogens to infect and kill AIDS patients. More problematically, HIV mutates extremely fast. Mutations are generally thought of as a bad thing, as they are errors in the DNA. However, for HIV having such a high mutation rate is a great thing, because it allows it to change faster than the immune system can recognize and kill it. The high mutation rate is favored, because the immune system will weed out any viral particles that don't mutate and retain the old, "known" form.
Current HIV treatment options focus on trying to both get the body to recognize and destroy the virus, and to try to prevent mutations in HIV as long as possible by throwing lots of different drugs at it.This is known generally as a drug cocktail, or more recently as HAART (Highly Active Antiretroviral Therapy). HAART combines three different classes of HIV medication, each of which targets a different vital component of the virus. Generally, this regimen includes a nucleoside reverse transcriptase inhibitor, a protease inhibitor, and a non-nucleoside inhibitor. Basically, both kinds of the reverse transcriptase inhibitors prevent HIV from copying its genetic material, and the protease inhibitor prevents the complete formation of mature viral proteins. I like to think of this approach as "playing the odds". By targeting more than one component of the virus, HAART increases the number of mutations HIV has to accumulate in order to be successful, which decreases the odds that one HIV viral particle will be able to do so. Now, researchers are proposing a new strategy I like to think of as "go ahead, mutate, we dare you".
A collaboration between researchers at the Ragon Institute, MIT, and Harvard have identified regions of HIV that decrease its fitness when mutated. Basically, if the virus tries to mutate these regions to escape detection by the immune system, it will be unable to survive. If it doesn't mutate these regions, the body will be able to recognize and destroy it. It's rather like being caught between a rock and a hard place for HIV.
While these results were discovered using computer algorithms, more details of which can be found here, the researchers strengthened their findings by comparing to real human data. They found that patients who control HIV on their own without medicine have T cells that target these same regions on HIV, and that strains with mutations in these regions of the virus are extremely rare in nature, indicating that there is strong selection working against such strains. Additionally, because this amino acid sequence is so highly conserved, there's potential for a vaccine to be developed with these regions. Right now, HIV mutates too fast for a vaccine to ever be effective.
Personally, I find this study fascinating because it takes a whole new approach to the HIV problem. Instead of trying to circumvent the problem of HIV's high mutation rate, they are using its mutation rate against it. It is a novel idea, and from my very non-expert point of view, one with a good chance of success.
Janus cats: The trick behind developing two faces
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| Janus kitten, Harvey Dent |
Florida couple Nash Hand and Amanda Forsythe were glad to welcome new kitten, Harvey, into their family even though he suffers from a rare congenital disorder. Harvey, much like his namesake, Harvey Dent, has two faces. This phenomenon can occur in other animals, but two faced cats are referred to as 'Janus cats' because of the Roman God Janus who also had two faces.
Thursday, February 2, 2012
Long live the Krebs cycle
So this is blogging.
Rather than wait around for fanfare, I suppose I'll begin.
If you read the introductory posts by my professor, you'll see that we are aspiring writers, scientists or both. If I'm not mistaken, you'll also see that we have discussed a few of the issues facing science writing and mass communication in general. Today I'd like to expand on the issue of communicating science as it pertains to teachers. I'm sure a good old research paper summary awaits in the near future if that's more your thing. For now, I'd rather take it easy.
This idea has risen in my mind many times before, but it really surfaced when the venerable Robert Krulwich brought it up in a blog for Radiolab: Every kid loves to learn about how the world works. They're crazy about it. They watch bugs go about their chores, sometimes testing their resolve with inconveniently placed sticks and other obstacles. They muck around in mud and ponds looking for snakes, frogs and who-knows-what that they then wrangle with their bare hands for closer examination. Most of all, kids ask questions – endless series of questions. If you let them go, their minds branch off like links on Wikipedia pages that lead you along from subject to wacky subject until you don’t remember where you started.
At some point, for many people, this fascination is lost. Krulwich believes that point is in 9th grade, when most of us are introduced to certain dragons of rote memorization – take the Krebs cycle:
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| Krebs (Citric Acid) cycle: Wikimedia Commons |
I just got chills. This image was introduced to me (in a watered-down form) in middle school. I “learned” it, and promptly forgot it. In AP Biology during my senior year I encountered it again. Same story. Sophomore year of college came around and there it was a third time.
I still don’t know what pyruvate does.
But I’m still standing.
Robert Krulwich’s sentiment, unfairly simplified, is that every kid would be a scientist if only our teachers would inspire them and not scare them away. “Save this ‘Krebs cycle’ stuff for the specialists,” a Krulwich apologist might say.
That would be disastrous, I would reply. Science is hard. Science isn’t always fun. I continue with it because it continues to excite me despite all the chemical names and body parts and processes I’ve learned and forgotten. I’d like to think that if I do become a biologist, I will have earned it. Let us leave science to those who have been through the gauntlet and still have the will to live.
Wednesday, February 1, 2012
Sight for the Blind
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| Flickr Photo by Michael Dawes |
Vision is an amazing process that allows us to do a plethora of things. Most rely on vision to do just about every daily task (like reading this blog). Now imagine that you slowly lost your ability to see things sharply and clearly. Imagine that you could no longer read your own watch or drive to the grocery store. This is reality for people with macular degeneration or dystrophy.
People suffering from macular degeneration (watch animation here) eventually lose most of their independence as their vision deteriorates. However for the first time, Steven Schwartz of UCLA has given a glimpse of hope to those suffering from macular degeneration (the leading cause of blindness in the US) or macular dystrophy (the leading form of pediatric macular degeneration). The preliminary results of this stem cell therapy have recently been published in the Lancet.
Previously human embryonic stem cells (hESCs) have been differentiated into retinal pigment epithelial (RPE) cells. Already, scientists have implanted these hESC-derived RPE in mice and rat models with macular degeneration. This treatment can restore photoreceptor function and prevent loss of vision in these models. Schwartz tested this therapy in two individuals: a 70 year old woman with dry macular degeneration and a 50 year old woman with Stardardt's macular dystrophy. Both of these women had no negative reactions to the treatment and also showed improvement in visual tests, such as the Early Treatment Diabetic Retinopathy Study (ETDRS) visual acuity chart. These improvements were seen in as little as two weeks after the transplantation. Retinal evaluation also showed new growth of cell in the individual with Stardardt's macular dystrophy. Although these results are only from a preliminary study and much work still needs to be done, the prospect of a new therapy to "give sight to the blind" appears promising.
Bill McKibben & the Power of Science Communication
On February 16th, Bill McKibben will be visiting this blog's home, Allegheny College, as a guest speaker and (hopefully) a workshop instructor. Presumably, McKibben will teach students about effective communication, and how to advocate for a cause.
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