Monday, April 30, 2012

Screeeech on the bridge!

No stroll around Allegheny College's campus would be complete without a visit to the 'rustic bridge'.  Last weekend my parents visited and we were fulfilling this requirement when we were stopped by a tour group listening to the history and legend of the bridge (or rather of the romantic 13th plank).  Instead of barging through and disrupting this magical moment for the prospective students we opted to take a closer look at the trees closest to us.  I am sure glad I did because upon closer inspection we spotted four little, puffy owls trying to catch some shut eye. 

Turns out these small fellas were screech owls, three fledglings and their mother.  And when I say small, I mean it- they appeared to be about as tall as your average banana (about 7 in).  This came as a huge surprise to me without a sense of scale the pictures makes them seem much larger.  Additionally, I haven't seen many owls during the day (and when I did they were always flying by confused) and it was too dark to gauge the size of the few owls I've spotted at night. 

Momma screech

Baby screech- all rights reserved
It is moderately acceptable that I haven't spotted many owls at any time of the day because they are masters of disguise.  Their plumage can take on various overall tones but each of those tones are made up of different complex spots and hues of color.  This coloring provides the perfect camouflage during the day  so that even though humans and animals are constantly walking by their napping site they are not often noticed.  This is also advantageous when it comes to finding a meal.  When the unsuspecting small mammal or bird flies under a screech owls perch it is likely to become dinner before even recognizing its lurking predator.

We were lucky enough to see fledglings because screech owls mate earlier than most other birds.  Few have been fortunate enough to witness the elaborate mating display males put on for females so I was unable to find a video but it sounds pretty neat.  It includes mating calls, head and body bobbing and swiveling AND (if the lady owl is lucky) a slow and deliberate wink that says, "How you doin'?" even better than Joey. 

A last tid-bit on screech owls: surely they must make some dreadful screeching sound that led to their current name... turns out no!  Although they have a variety of calls the most common one is a trill or tremolo.  This somewhat eerie noise is familiar from Maine from Texas.

So there you have it: my last entry provides a little background on the somewhat misnamed screech owl along with the reminder to keep your eyes open!  Countless funky creatures are living in right in your backyard-- go check them out!

Friday, April 27, 2012

The Science of Music. Part 2:

Musical structure resembles the human brain's tendency to make patterns out of sound. Tonal music, like most classical music, establishes a pattern or key that will frame the song then dances around and avoids that key or theme until the end restoring order. The brain desperately desires this structure and constantly tries to recreate this order.

Before that pattern can be desired by the brain, it must play hard to get. Music only excites the brain when it makes the auditory cortex struggle to discover the order. If the pattern is too predictable, the music becomes boring. This is why classical musicians introduce the order at the beginning and are dedicated to avoiding it until the end. The longer we are denied the pattern we expect, the greater the emotional response when that order is restored. Harmony logic is the logic of hide of and seek.

As Leonard Meyer shows in his book Emotion and Meaning in Music, music is defined by its flirtation with and not submission to to expectations of order. Earlier theories of music believed that the emotions we find in music were a result of the way noise refers to real world images and experiences we have previously had. But as Meyer and contemporary neuroscientists argue, the emotions come from the unfolding events of the music itself: the patterns music invokes and then ignores.

"For the human mind, such states of doubt and confusion are abhorrent. When confronted with them, the mind attempts to resolve them into clarity and certainty," wrote Meyer. This nervous anticipation and uncertainty to create feeling. Music makes us uncomfortable and we love it.

Next week I'll get into the biology of the emotional quality of music, primarily its connection with dopamine levels.

Evolution, redefined

If you're reading a biology blog, you're probably aware that Charles Darwin was an important dude, and not just for discovering the plant hormone auxin. He also published the theory of evolution, completely revolutionizing our understanding of the world. However, not until the discovery of DNA and genes was it clear how exactly certain physiological traits could be passed from parent to offspring, and how new traits could emerge through mutations. Now, however, disease-causing particles called prions might be redefining what evolution is and how it works.

Prions are proteins that are usually produced in the human body, but for some reason get misfolded and form aggregates which cause brain tissue to deteriorate. The best-known prion diseases are Mad Cow, Creutzfeld-Jakob, scrapie, and kuru, but there's a prion disease affecting nearly every mammal. Prion diseases are passed by ingesting prion particles. When the normal protein encounters the misfolded prion form, it gets converted into the prion form as well. It's still unclear how exactly this happens, or what causes a previously normal protein to be misfolded into a prion. However, it was previously well-accepted that this prion form was unchangeable. Researchers at Scripps decided to challenge this idea based on a puzzling piece of evidence

They noticed that when you infect mice with a sheep prion, it becomes more virulent over time. An initial spike in virulence from the sheep-to-mouse transfer may have made sense, because it would simply indicate that the mouse brain is more susceptible than the sheep's, but if the prion disease starts killing faster as it infects more mice, this indicates it is adapting to its host to become more successful. So, they decided to test that idea by exposing prions to different conditions and selective pressures, to see if certain variants were more prominent in one situation versus another.

Sure enough, researchers found that different prion particles were present in brain cells versus cell cultures, and that they could get the predominant type to switch if they transferred prions from brain to culture or culture to brain. Also, they exposed prion-infected cells to swainsonine, a compound previously found to have prion-control properties, and found that a drug-resistant form of the prion quickly became the major component of the population. Removing swainsonine returned the population to being mostly susceptible, with less than 1% resistant prions.

The head of the study, Dr. Weissmann, thinks this will have important treatment applications. Because they thought prions couldn't mutate and evolve, the key was going to be finding some way to target the prion and leave the normal, non-problematic cell protein alone. But, if prions can evolve, it's likely that any treatment blocking or removing prions is going to quickly become ineffective, because prion particles resistant to it will quickly take over the population. Instead, Weissmann thinks we should be focusing on finding ways to remove the normal protein from cells, because without a normal protein to convert, the prions will be unable to form large aggregates and cause problems.

Regardless how prion treatments end up looking, it is highly interesting that our ideas of evolution have, once again, expanded. We've been incorrect about a lot of accepted ideas about evolution, for example "silent" mutations. Silent mutations are when there's a mutation, but it doesn't change the protein's building blocks at all, so the rationale was that there was no way that could affect fitness if the protein was the same. However, it turns out that some codes for building blocks are preferable and faster for an organism to make than others, and faster protein assembly may be an advantage. Now, it turns out we might be wrong that the only way a mutation can be passed on is through genetic material, because prions can evolve to fit their environmental conditions better and can pass this along to other members of the population despite being only protein.

Thursday, April 26, 2012

Poop and Destiny

I thought it fitting to spend my last post on this sciencey blog discussing a topic that I first discovered through one of my favorite science communicators, Stephen Jay Gould.  The topic, fitting or not depending on your opinion of my posts, happens to be… guano.  Bird poo.  So come along! 

The species I’d like to discuss is one you may have heard of.  If you have, it’s a name you’re not likely to forget: the Blue-Footed Booby.   

It just fully occurred to me where this post is going, and I’m not sure that I like it.  My apprehension comes not from the mention of “poo” or “Booby,” as you might expect, but rather from the dismal conclusion that could easily be drawn.  Alas, as Dana would attest, writing is about taking leaps, and so I take one now.  I hope to leave you with the notion that nature is both wondrous in its balance and economy, and utterly without human passions, despite what we might hope. 

If you travel to the Galapagos Islands, Blue-Footed Boobies will be among the most obvious of the animals you see.  Not only do they possess, as their name implies, a fairly striking natural pedicure, but many of them seem to be sitting on the bulls-eyes of big, white targets.  Further inspection will reveal that the volcanic landscape has not been modified by a rogue line-painter into some bizarre sporting arena.  Rather, the birds have made the rings themselves – by spraying guano in all directions! 

"This is embarrassing."

The “guano rings,” as it turns out, are part of the homes of these ground-nesting birds.  Each mother sits inside her ring, placidly warming her chicks, apparently oblivious to the gawking tourists who snap photographs mere feet from her face.  When Gould was in the Galapagos, he was surprised enough by the Booby behavior that he decided to do a bit of “research.”  He approached a nest with caution, inching toward the circle while the mother stared into space.  Eventually, he toed the line.  Still no response.  Finally, as his toe moved imperceptibly forward, it reached an invisible line within the circle.  The reaction was immediate: frantic squawking, flapping and pecking.  Every time he repeated the toe experiment the same thing would happen. 

The Boobies operate on a very simple strategy of nest protection: if something lies inside the nest, nurture it.  If it is outside, ignore it.   If it crosses the line, attack.  Unfortunately, this applies even to a bird’s own chicks, which have been observed cheeping helplessly mere inches from a guano ring as their mother sits proudly atop the rest of her clutch.  People who have seen such things are incredulous.  How could she be so cruel?  So Stupid?  They want to put the chick back in the nest, but it is forbidden – things in nature tend to happen for a reason. 

A mother Booby lays between one and three eggs per clutch, one-at-a-time.  They hatch in the order that they are laid, so that the oldest is always biggest.  Often, the mother raises all of her chicks to adulthood without a hitch.  Occasionally though, and this is where the post takes a turn for the appalling, the first-born chick will push his or her younger siblings out of the nest, across the short expanse of rock, and over the invisible line, condemning them to death.  The mother will continue to raise the first-born.  She will pay the others no mind at all. 

When I hear things like this, I feel a physical pain in my gut.  The suffering of little, fuzzy creatures is the worst thing I can imagine.  But the world beyond humanity does not share my concepts of justice, good and evil, right and wrong.  The oldest Booby is not a psychopath; his mother is not deranged.  They are two hungry birds in an environment that does not contain enough food to support two or three nestlings, so one of them does what must be done to prevent the death of the entire clutch.   

I admit I hadn’t intended to leave you with such a sobering meditation on the apathy of nature.  Truth be told, I was hoping to make some poop jokes and leave you with a laugh or two.  Alas, what’s done is done.  Besides, it’s sometimes valuable to remember that life isn’t fair.  It helps us to cope when things go wrong in our personal lives.  It also makes watching that chase scene from Planet Earth a little more bearable.  In any case, I hope you’ve enjoyed this Bio 490 project or ours, and I’m sure many of us hope to keep blogging in the future.  Thanks for reading.

New Genetics

Literature classes can teach students to read between the lines, to understand how prose is built beyond the simple linking of nouns and verbs.  The same critical reading skills are required for geneticists to understand how the genome is more than just a long string of letters called DNA.  Rather than reading between the lines, geneticists read above the line in an emerging field called Epigenetics.

To keep a thread from becoming a knotted mess, a seamstress keeps the strands wrapped around a single, large spool.  To keep DNA from becoming tangled, cells wrap the DNA strand around proteins called histones.  Rather than using one large spool, cells wrap the DNA around multiple histones creating a beaded necklace, with histones as the beads and DNA as the chain.  Those histones are more than just simple spools or decorative beads, though.  The structure of those proteins can be altered through the addition and removal of certain chemical groups.  The presence or absence of these alterations is referred to as the epigenetic code because it is genetic information contained "above" the DNA sequence.  Alterations change which portions of the DNA are easily accessible by the cell and which portions are too tightly wrapped up for the cell to read.  If the cell cannot read, or can too easily read, certain portions of the DNA, then the way the cell uses information written on that portion of DNA will change.

Alterations of histone proteins occur at any stage of an individual's life.  Investigating what sorts of stimuli can create those changes and characterizing the results of those changes is the pursuit of Epigenetics.  Research investigating the role of exposure to environmental toxins during gestation has previously indicated that a component of anti-stick coatings like Teflon is correlated with increased rates of obesity in those children when they become adults.  A separate study linked exposure to that same environmental toxin to changes in the histone modifications of newborn infants.  Additionally, resent research indicates the diet and chemical exposure of mothers before and during pregnancy can alter the epigenetic sequence of her offspring, thereby increasing her children's changes of being diagnosed with obesity-related diabetes.  Combining studies of the health effects of environmental toxins with studies of the epigenetic changes caused by those toxins may help investigators explain why certain toxins have certain effects.

Other elusive biological questions of interest to Epigeneticists include why inheriting a certain gene from one parent rather than the other can produce different effects, the causes of diseases including schizophrenia and colon cancer, and why identical twins are not perfectly identical.

Wednesday, April 25, 2012

Misfolded Proteins

Proteins are present throughout our bodies and are involved in virtually every cell function.  Proteins enable movement by allowing muscle contraction, speed up chemical reactions, and defend against foreign cells.  Proteins are made up of a chain of compounds called amino acids, which interact with each other in a specific way causing the amino acid chain to fold.  The folding of a protein is essential for its function.  However if the protein isn't folded correctly, then they can be destructive to our bodies.  For instance, Huntington's disease, Alzheimer's disease, type 2 diabetes, sickle cell disease and prion disease are all proteopathies, or diseases caused by protein misfolding.

What if these incorrectly folded proteins were capable of replicating themselves to further damage the body?  Well prions do just that.  Prions are defined as infectious agents comprised of a misfolded protein.  Unlike other disease-causing agents like viruses and bacteria, prions contain no genetic material (DNA or RNA); however, they have the ability to convert properly folded proteins into incorrectly folded one like themselves.  The improperly folded proteins then accumulate in tissue causing tissue damage and cell death.  This chain reaction occurs in prion diseases like mad cow disease and its human counterpart, Creutzfeldt-Jakob disease (CJD), the degenerative neurological disorder.

Prion diseases have always been considered untreatable because it is difficult to target these misfolded protein because proteins are all throughout our bodies.  A recent study published in the Journal of Biological Chemistry this month found a way to inhibit their ability to produce more prions.  They used luminescent conjugated polymers (LCPs) to detect the presence of prions in mice brains.  However, they noticed that the number of prions, toxicity, and infectibility decreased in the process.  Most likely, the interaction with the LCP's stabilizes the prions, inhibiting their propagation.  However, LCP's contain many chemical subgroups.  When eight different subgroups were tested, all of them had significant decrease in the toxicity of the prions.

These results are the first that provide the possibility of treating prion diseases.  Also if the LCP's can interact with other misfolded proteins that cause other proteopathies, then the application of these results may be applied to other diseases, like Alzheimer's disease and Huntington's disease.    

Read more about this research here.

Mad Cow Disease in the U.S.

A random test has demonstrated that mad cow disease has infected a cow in California.  This is the first case (out of four, total) of the disease in the United States since 2006 in Alabama.  South Korea, an importer of U.S. beef, is not pleased

Mad cow disease is officially known as Bovine Spongiform Encephalopathy (BSE).  BSE outbreaks in the past have been attribute to feeding cows, which are natural herbivores, with supplements that include the meat and litter of other animals - including cattle. 

BSE is the result of proteins, called prions, becoming misshapen and resistant to degradation.  There are normally prions in the brain, deemed PrP-sen, that do not cause harmful symptoms.  The "broken" prions that cause disease are called PrP-res, for "resistant."  When a PrP-res is passed to a healthy organism, it comes in contact with PrP-sen, and converts the PrP-sen into the dangerous PrP-res.  As the number of PrP-sen grows, the bad prions tend to cluster together, forming amyloid fibers.  The amyloid fibers kill surrounding cells.  As the dead cells are digested, substantial holes are left in the brain, to the detriment of the organism.  Eventually, it will lead to loss of control of the body (ataxia), and subsequent death.

A timeline and explanation regarding prion-based disease can be found here.

Prion diseases like BSE (or the human manifestation called Creutzfeldt-Jakob disease) are incurable once a person is infected with a PrP-res.  As well, due to the nature of PrP-res being a protein and not a living pathogen, meat from a BSE cow cannot be destroyed by heating it. 

Luckily, 40,000 cows per year are selected for BSE checks.  Hopefully, this is the only current case of BSE, and it can be taken care of effeciently.