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Biomusician
24 February 2009 @ 05:33 pm
This week's article can be found via ScienceDaily here, while the abstract to the actual article from Neuroscience is here.

The Long and Short of It:

Researchers have uncovered another piece of the sleep puzzle by further characterizing the role of adenosine receptors and slow-wave activity (SWA) in sleep.

Background:

Sleep, that mysterious blackmailing blackgard who, in return for a day of alertness and cognitive excellence, demands 7-8 hours or dark unconsciousness, is slowly being understood. Ths article reveals one of the methods used to facilitate our transition from sleepy at night, to bright and alert (or in my case, just as sleepy) in the morning. One of the cogs in the mechanism of sleep has been shown to be a certain adenosine receptor.

Normally, adenosine builds up in the brain during waking hours. Neural adenosine receptors become saturated with adenosine as the day wears on, which increases slow-wave activity in the brain. This causes the organism to feel sleepy. Our favorite anti-sleep ammo, caffeine, is an adenosine antagonist. It works by blocking the neural receptor sites to which adenosine would normally bind, without producing any SWA.

Now, we've known about SWA since the 90s; we knew that SWA directly varied with the time an animal spent awake. This SWA activity, however, remained under the radar until a study was published in 2004 that showed that people performed better on cognitive tests when their SWA response was enhanced. Up until now, it wasn't known how the SWA response was enhanced, or if it was even needed to produce the cognition-enhancing benefits of sleep.

To study the SWA response and to explore its possible relationship with adenosine receptors, the researchers created knockout mice. These mice were engineered so that they conditionally lacked the adenosine receptor-encoding gene. In other words, these mice wouldn't produce any adenosine receptor under certain conditions controlled by the researchers, allowing them to study the effects of the adenosine receptor on sleep, specifically SWA.

Findings and Significance:

The knockout mice produced by the researchers slept for the same amount of time following sleep deprivation, but their SWA activity was significantly lessened. What's more, these mice didn't perform as well as normal mice in navigating a maze to find a piece of chocolate. The researchers made an interesting point: The knockout mice are a good parallel to people acting for an extended period under caffeine; after all, having all of your adenosine receptors blocked is the same as having no receptors at all.

The researchers also showed that SWA was enhanced when sleep-deprived mice slept, presumably to make up for lost time, and restore balance more quickly. For us, this means that you should at least take the time to nap when you're sleep deprived, as a little bit of enhanced SWA goes a long way in maintaining your razor-sharp wit. The researchers' next step is to connect adenosine's role in sleep to its role in metabolism - a daunting study, considering its widespread effects. Sleep well, and see you next week!

 
 
Biomusician
17 February 2009 @ 07:46 pm
Last week, we took a look at making IPSCs from neural progenitor cells. This week, scientists have found out how to go in the other direction - from embryonic stem cells to many different types of neural cells. The cell line is also immortal, which is cool. Take a look at the links for the science. Both Wikipedia and last week's pick will help you with background.

As neat as that is, this week we're following a rabbit trail over to Pharyngula, a blog maintained by P.Z. Meyers. Hit the link for some biographical information, if you desire it; otherwise, we're off for this week's Science Pick of the Week! The two posts of interest are entitled "Francis Collins Will Be So Disappointed," and "Effectively Non-Existent." They're even easier to read than ScienceDaily, so hit 'em up! At the very least, read the first one.

In the first article, PZ addresses a commonly-cited piece of evidence for God: the moral law. Both C.S. Lewis (in Mere Christianity), and Francis Collins (in The Language of God) argue that there is a "moral law" that defines correct human behavior, crossing cultures and producing acts of altruistic behavior. This behavior, they say, cannot be explained by evolution and is evidence of God's intervention in natural affairs (evolution). Some even view human morality as evidence of being created "in the image of God," as Genesis puts it,  or as evidence for a human soul. After all, evolution is all about surviving long enough to pass on your own genes. Surely it cannot explain why a person would put his life at risk for someone else.

Not so fast. There is a sort of "morality" in the animal kingdom, outside of Homo sapiens. For example, check out this article, which details several ways in which monkeys have a sense of morality. For more, check out this article from Stanford on biological altruism.

I'll get to the naturalists in a bit, but until then, I'll deal with the Christians. Alright, Christians. Take a step back. Breathe. Why is it so important to you that Homo sapiens is the only species on earth that behaves "morally?" The Bible says that God created the earth and everything in it "very good." I do not think it is denigrating to think that God created both humans and animals with a crude sense of morality. Science has discovered and characterized ways in which certain animals behave decently toward each other. It's good the for the species as a whole. You may make an argument by degrees, pointing out that humans have a much more developed sense of morality, but such an argument will get you nowhere; you may as well argue that the human brain or human social structure - both impressive, relative to what the rest of the animal kingdom has to offer - as evidence for God.

In the naturalistic view, morality is hypothesized to be a mechanism for the survival of the species. Ants stay out of the nest to hide its presence from predators, dying in the cold. Vampire bats cough up blood meals for less-fortunate hunters, losing out on nutrition. In both cases, ther suffering of few benefits the larger group. More babies are had by all, and the species survives. This brings us to the point on which naturalists and theists can agree: Morality and altruism, whatever their motivation, are good for the species' survival. Portions of the Old Testament law deal with hygiene, mold, and disease, and how to properly deal with them, for the good of the community and the individual. The Christian Old Testament God is concerned with the well-being of people.

So, science has shown that some animals practice basic morality, and that it helps them survive as a species. In turn, many Christians dismiss animal morality as simplistic, clinging to the moral law like a life preserver of Godly proof. Many of you are probably wondering whether I have forgotten what "created in the image of God" means, or whether I even know at all. This particular entry, unfortunately, falls short of my ideal for this blog: To arrive at clear, well-reasoned conclusions regarding important discoveries and questions. Instead of well-constructed paragraphs encasing neatly-reasoned truths, I shall conclude this entry with a list of further ideas that merit thought:

  • Some Christians think that viewing morality in a naturalistic sense degrades morality itself. Why do Christians see most scientific advances that raise nature closer to themselves as degrading, instead of glorifying to God?
  • Other Christians believe that humans have a highly-developed, mature moral sense, while animals only scratch the surface of morality. How then, have the animals managed to keep things in balance for millions of years, while humans, over just 200, have managed to begin potentially-catastrophic global warming? Perhaps there is a distinction of divine responsibility (or, as we Christians like to say, "stewardship") - not just morality - that separates us from the animals. After all, stewardship is something that God gives to humans, exclusive of other species, in Genesis; the human-only gift of moral law is debatable, most often argued from inferred meanings of the "image of God."
  • I have not yet considered at length the eating of the tree of the knowledge of good and evil, which allowed man to know right from wrong ("like God," said the serpent). This may also tie into what makes humans distinctly human, relative to animals.
As a Christian and a scientist, I consider it my duty to thoughtfully and thoroughly consider these questions, and I invite experts on either side to counsel me with truth. For now, I shall enjoy my position as a lonely thinker, risking being branded a heretic by one side, and an irrational mystic by the other.
 
 
Biomusician
10 February 2009 @ 08:24 pm
The second even-numbered posting of the SPoTW is here. This week, we pass up a study on the effects of circadian rhythm on cancer growth to focus on another article about stem cells. The actual article is located here on PubMed, requiring a subscription to Cell Press for full-text access.

The Long and Short of It:

Researchers were able to reprogram neural cells into iPS cells through the activation of just one gene: Oct4.

Background:
This week, we're going to take a look at another advancement in the field of stem cells. The scientific trail to iPS cells has been only recently been blazed: In 2006, iPS cells were created through the activation of 4 genes: Oct4/Sox2/Klf4/c-Myc or Oct4/Sox2/Nanog/LIN28. Unfortunately, stem cells created via this method were prone to causing cancer when injected into host animals, due to overactivation of the oncogenes c-Myc and Klf4. And since the method used to activate the cells was through a viral vector, cancer was also caused by random insertion of viral DNA into the host genome. There was great rejoicing, but there were also problems - which most scientists envisioned us ironing out fairly soon.
Score one for optimism. In November of 2008, a method was published whereby neural progenitor cells - which are fairly undifferentiated cells in the nervous system - could be transformed into iPS cells through the activation of just two genes: Oct4 and Klf4. Because the researchers didn't have to mess with the oncogene c-Myc, cancer incidence went down. But the good news didn't end there; the researchers also outlined a new method for activation of these genes that didn't involve viral vectors. Their method involved the use of two small-molecule compounds, which activated Oct4 and Klf4, inducing the cells to revert to iPS cells.
This small molecule method of gene activation is still fairly new to the scientific community. If it indeed proves to be an efficient, safe alternative to viral vectors, we may hear about it a lot more in the months to come. Still, viral vectors have a large share of the research market; there are a lot of research groups using viral vectors to deliver DNA to host cells. Because of their popularity, we are beginning to understand more about how they work, and are making progress in improving their efficiency and safety in potential clinical applications.

Findings and Significance:

This study showed that it is possible to reprogram non-stem cells into IPS cells with just one gene: Oct4. This eliminates the cancer gene Klf4, which logically would reduce the incidence of cancer if cells created via this method were injected into mice. The cells that were created via this method passed the tests for pluripotency: They divided into cell types from all three germ layers, and formed teratomas when injected into host mice.
This is exciting, as the article points out, because it shows that we only have to concern ourselves with Oct4 when programming iPS cells. It shows that Oct4 is "head" of reversion, and is necessary and sufficient to cause genetic reprogramming. This potentially simplifies research for others, because they only have to focus on changing one gene, instead of four. Trust me as someone who has done genetic research in the past: It's much easier to work with one gene at a time.
But, as with any other iPS cell study, significant questions remain to be answered. For example, what are the differences, if any, between cells produced by this method, and cells produced by the four or two-gene activation methods? It is becoming increasingly important for stem cell researchers to study the epigenetic characteristics of their generated cells. Induced pluripotent stem cells are great, but there are subtle differences between them, and it is important that we understand them. All iPS cells can form teratomas and tissues from all 3 germ layers, but they cause cancer at different rates when injected into laboratory animals. We need to understand these differences before we penetrate much deeper into the question of how to make iPS cells more like true embryonic stem cells.
I'm sure some researchers are working furiously on answers for these sorts of questions. Until then, it just got easier for everyone who just wants to reprogram (neural) cells into stem cells.

 
 
Current Mood: rushedrushed
 
 
Biomusician
Another week, another Science Pick of the Week. This week, it was a close call between using stem cells to reverse paralysis, the alarming rise of antibiotic-resistant bacteria, and this week's topic: "Skin Cell Into Sperm Or Egg?" I'm still waiting on the full-text, original article to pop up on Pub Med. When it does, I'll post it.

The Long and Short of It:
Researchers at UCLA were able to generate lines of germ line-like cells from induced pluripotent stem cells (iPS cells). These germ cells lacked functionality of "certain vital regulatory processes," including genomic imprinting.
 
Background:
Before we look at iPS cells, we need to briefly go over stem cells. Chances are, you already know what they are. Stem cells have been splattered all over the news ever since embryonic stem cells were derived from human blastocysts in 1998. The reason that stem cells are so special is that they can differentiate into any type of tissue that's present in an adult; they are the unmolded "baby" cells of your body that develop in response to environmental and internal cues, into brain, blood, belly, and everything else. This level of plasticity is called pluripotency. When stem cells were first discovered, the research and medical communities were intrigued; stem cells might be used to regrow damaged tissue of almost any type, if they were guided by the proper molecular cues.

Research on human embryonic stem cells, however, has progressed slowly. Because an embryo is destroyed when the stem cells are taken from a blastocyst, many view human embryonic stem cell research as unethical. And, instead of attacking in vitro fertilization, which produced the thousands of excess embryos destined for destruction, the American public decided to attack stem cell research. Legislation was passed that allowed research only on stem cell lines derived prior to 2001. (As a side note, there was a study published in Nature in 2006, detailing ways of harvesting human embryonic stem cells without destroying the embryo. So far, little has come of it. Many expect President Barack Obama to lift the US ban on stem cell research as soon as this week.)

In 2006, some creative Japanese scientists discovered a way to generate "embryonic stem cell-like" stem cells, by reprogramming skin cells. Eleven months later, sources were still marvelling at this discovery, which was confirmed by other researchers. They accomplished this reprogramming by activating just four genes: Oct-3/4, SOX2, c-Myc, and Klf4. Cells produced by this method passed various tests of pluripotency: teratoma formation, morphology, differentiation into cardiac and neural tissue, and self-renewal among them. The coveted-but-ethically-forbidden human embryonic stem cell was passed over by many, now that we could create our own pluripotent cells from something as plentiful and morally unambiguous as skin.

These reprogrammed cells were dubbed "induced pluripotent stem cells" (iPS cells), and while they have proven to be quite pluripotent, they aren't quite like embryonic stem cells. The scientific community is still working out just how to influence differentiation into specific tissues, and how to overcome certain problems associated with using iPS cells. For example, there was a 20% incidence of cancer in mice produced by blastocysts in which there were iPS cells. The reason is that c-Myc is an oncogene, and unusually high expression levels cause cancer. Also, there is concern that the viral method of activating the four "pluripotency genes," can cause instability in the host's genetic code. There are ways to work around these problems, but the current methods of doing so sacrifice efficiency for safety, rendering them almost useless as therapeutic methods.

Findings and Significance:
This brings us to this week's study: UCLA researchers found that placing iPS cells among fetal gonadal cells sparked development into germ cells, which normally differentiate further into sperm or egg cells. That is neat. These germ cells, however, did not behave as normal germ cells do, lacking "certain vital regulatory processes." Unfortunate. If we had access to this paper, we might know exactly what went wrong, but it is unclear how exactly these germ cells are different from normally-derived germ cells. It seems likely to assume that methylation patterns, which are not immediately changed by transfection, may be playing a factor here. There is probably a different complement of activated genes in normally-derived germ cells, which mediate the regulatory process. Also, the researchers point out the problem of genomic imprinting, which is something that would have to be emulated in iPS germ cell development.

As the differences between the cells are discovered and further characterized (which is likely the researchers' next step), we will come closer to actually producing germ cells, and many other types of cells to boot. As things are now, we know that if we put iPS cells in an environment where normal pluripotent stem cells would differentiate into germ cells, we get almost germ cells.

Despite our current imperfect knowledge of the precise differences between iPS cells and embryonic stem cells, this article is a step in the right direction because it demonstrates, once again, the plasticity of iPS cells, and helps direct future research in looking for similarities and differences between the natural and induced stem cell. This is one of the main veins of current research, so expect more news on this front soon!

 
 
Biomusician
27 January 2009 @ 10:00 pm
Back again for its second week in a row is the Science Pick of the Week.

This week's article is titled "Rethinking the Genetic Theory of Inheritance: Heritability May Not Be Limited to DNA," and can be found here. The abstract of the actual publication from Nature Genetics is located here. Read up!

The Long and Short of It:
Epigenetics is a burgeoning field in biology that studies mechanisms of inheritance that aren't directly related to DNA sequence. This field has been around for a while, but research on the subject is just now picking up steam.

Background:
In our survey of epigenetics, we'll begin with the word itself: The prefix "epi" means "above," or "outside." So, molecular mechanism of heritability that isn't based on DNA sequence is outside the realm of traditional genetics, and is thus epi-genetic. Lost? Here's a metaphor: I want to send a package of cleaning supplies to a friend. The post office, however, will not allow me to send them through the postal service. I must therefore use an "epipostal" means of delivering my package to my friend - perhaps by means of another friend, or a private delivery service.

So, epigenetics describes any way of delivering information from parents to offspring, apart from the ATGC base sequence of DNA. The first, most well-known epigenetic method of heritability is DNA methylation and histone remodeling. To help us understand methylation and histones, I'm going to use a metaphor. Imagine you are employed at a large warehouse, full of boxes stacked to shoulder height. All of the boxes have latches, and each box is linked to two adjacent boxes to form one continuous chain. The warehouse manager will want access to the contents of certain boxes at certain times, and it is your job to unstack, re-stack, and unlatch the requested boxes when called.

Now, to translate our metaphor to science: The warehouse is the nucleus of a cell and the boxes are histones, which package portions of your DNA. When that DNA is needed for transcription, it must often be unpacked. The latches on the boxes are methyl groups, which hinder effective transcription by binding the DNA closely to the histones and interfering with replication machinery. These methyl groups must be removed from the DNA before it can be read by RNA polymerases, which carry the information from the DNA, from the nucleus, to the cytoplasm or endoplasmic reticulum, to create proteins. Going back to the metaphor, by unhooking the latches from a box, you would be serving as a methyltransferase, an enzyme that removes the methyl group from the DNA, allowing the DNA to pull away from the histone enough to be read by an RNA polymerase.

DNA methylation and histone remodeling are necessary for arranging the DNA in the nucleus, and these methylation patterns are transmitted to daughter DNA strands when the DNA is replicated. Thus, if a gene is turned off by a series of methylations, each of the two DNA strands resulting from replication will have roughly the same methylation pattern, and the gene will likely be turned off in both these strands. In this way, a predisposition toward certain genes being turned off or on can be passed to offspring.

The second currently-known mechanism of epigenetic inheritance are RNA transcripts. Many genes produce a product that influence the future expression of that gene. This product (either RNA or a protein) can also be transmitted to neighboring cells, influencing gene expression there. In the case of inheritance, the mother donates a lot of RNA and protein during the formation of the egg. The fertilizing sperm also contributes a small amount or RNA and protein, which may also play a role in epigenetic inheritance.

This leaves us two final mechanisms of epigenetic inheritance: prions and structural inheritance. Prions are malformed proteins that can cause correctly-formed proteins of the same kind to form dysfunctional clumps. Think of it like peer pressure: Prions are the charismatic bad boys, leading hopeless hordes of functional proteins astray. These protein clumps form other, bigger clumps, interfering with the work of that protein, and often causing damage to the cell. How bad is that? Well, mad cow disease is caused by prions. If a parent is suffering from a prion disease, chances are, some of those malformed protein clumps are going to make it into the germ cells of the next generation, which make prions an epigenetic carrier of disease - if the offspring survives long enough to notice.

Structural inheritance is the last a least well-known mechanism of epigenetics. This method of inheritance is inferred from studies done on ciliates. In these studies, the researchers experimentally altered the pattern of cila on the organism, and observed that the changes they made were transmitted, more or less, to offspring. There isn't a lot of information out there yet about how this works. It boils down to, "We changed something, without changing the DNA, and the changes were inherited." It seems reasonable to assume that when cells divide, existing structures in the cell are used as templates for new structure.

Findings and Significance:
Now, those of you who are mildly acquainted with science may be thinking, "Wow, this is really neat! To think that there's something other than DNA that influences our natural development! And to think we just now figured it out, a century-and-a-half after Mendel laid the foundation for genetic research!" But, if everything that I just wrote about had been figured out in one study, there would have been more than a ScienceDaily article about it. Those of you who have been in science for a while know that this article is written to be a lot more sensational than it really is. Epigenetics is nothing very new in science. Papers about it were being published way back in the late 80s and early 90s. I was taught about it in my undergraduate genetics course.

This study is significant for two reasons: It supports previously-established scientific theory, and makes an attempt to catalogue differences in DNA methylation between monozygotic and dizygotic twins. Another, very similar study was completed back in 2005 ("Epigenetic Differences Arise during the Lifetime of Monozygotic Twins" full text), though in that study the researchers did not characterize methylation patterns as extensively.

This article is old news. For all the excitement and cutting-edge language used in the article and by Dr. Petronis (the author of the referenced study), most of he found had been found 3 years earlier. Why did ScienceDaily run this article now? Maybe Dr. Petronis has some sway, or is more well-known than the 2005 researchers. Perhaps the article writer just wasn't familiar with epigenetics. Whatever the case, it gave us a good opportunity to briefly explore one of the modern offshoots of heritability and genetics. My hat is off to Dr. Petronis for scientific rigor and for bringing new data regarding DNA methylation patterns. See you next week!


 
 
 
Biomusician
20 January 2009 @ 01:41 pm
Every week, I read articles from Science Daily and Science Now. Though most of them are fairly mundane, many are exciting and worth fleshing out. So, in an effort to keep you, my fellow science aficionados and friends, in the scientific know, I've started the Science Pick of the Week. Expect an update every Saturday. Unfamiliar terms or jargon will be explained here or in links to supplementary material. When possible, I will provide a link to the full-text journal article. This week's pick, sadly, requires a subscription to the journal Circulation. Now, on to the science!

This week's article is titled "Gene Therapy Reversed Heart Damage in Rats with Heart Failure." A link to the Science Daily article can be found here, while the abstract of the actual publication from Circulation is located here.

The Long and Short of It:
Researchers reversed heart failure in rat models by injecting an gene-carrying adenovirus into the heart tissue. This virus carried a working copy of a gene called beta ARKct into the DNA of the heart tissue (transfection), and it was expressed. Over a 12-week period, the expressed beta ARKct protein inhibited the action of an over-expressed G protein-coupled receptor kinase. This put the heart tissue on the road to recovery, restoring normal beta-adrenergic signaling and "rescuing" heart function.

Background:
To put this study in perspective, it's helpful to understand how a healthy heart's adrenergic signaling pathway works. The adrenergic signaling pathway is activated under strain or stress ( "fight-or-flight") by a group of signaling molecules called the catecholamines, which include familiar molecules like dopamine and epinephrine (adrenaline). In the movies or on TV, you've probably seen good-looking actors and actresses stab other actors and actresses in the chest with EpiPens, in attempts to restore cardiac function -that's epinephrine, a catecholamine. In any case, when these molecules are released from the adrenal glands into the bloodstream, they bind to adrenergic receptors in many different body tissues. This causes fight-or-flight effects like pupil dilation, insulin release from the pancreas, and dilation of blood vessels that lead to muscle tissue, to name a few. When this signaling pathway is activated in the heart, it begins to beat faster, and to eject more blood per beat (ejection volume).

An improperly-functioning beta-adrenergic pathway can cause an irregular heartbeat and contribute to heart failure. This is where the G protein-coupled receptor kinase 2 (GRK2, for sho, talked about in this article, comes in. If GRK2 is upregulated (produced in excess) in the heart, it causes irregularities in the beta-adrenergic pathway, leading to heart failure. Unfortunate. But that's not the whole story: The beta ARKct protein can come to the rescue, inhibiting the function of GRK2 and restoring regular beta-adrenergic signaling, thus reversing the damage caused by the over-expressed GRK2.

Theoretically, the researchers began on firm ground, as all of the above had already been established prior to their beginning their experiment. Previous studies had introduced the beta ARKct gene into the organism in one of two ways: by injecting the beta ARKct-containing DNA into the nucleus of a fertilized embryo and comparing its development to an organism that hadn't received the new gene, or by injecting it into an adult organism using a viral vector, and examining the results. The germ-line method, when accomplished successfully, results in gene expression levels that are, in general, much more stable compared to the expression levels conferred by the viral vector method.

This is because it is difficult to efficiently infect adult cells with most viral vectors, due to a variety of factors, including interference by the host immune system, and poor recombination efficiency of the vector with the host DNA. Inefficient viral DNA transfer usually produces little or no effect in the host organism, because the gene that the virus carries is not being expressed at sufficient levels. Other times, the gene may be expressed, but only transiently; as the cell divides, the gene is lost or inactivated and expression ceases.

Findings and Significance:
So, if the theory behind the study was already known, then why did I pick this article for my first SPOTW? The answer lies in the method of delivering the beta ARKct gene to the cardiac tissue. In their study, the researchers successfully introduced an exogenous gene into their target organism, whose expression continued into the 12th week of their study. They successfully designed a viral vector that overcame many of the difficulties of that method of gene transfer. This, along with the affirmation that beta ARKct inhibition of GRK2 can indeed reverse heart failure, is where the true value of the paper lies.

Our knowledge of the genetic mechanisms of disease is growing exponentially. Oftentimes, we even know the specific, base-pair mutations that are responsible for causing the disease. Now, many researchers are trying to discover and design mechanisms of getting healthy, mutation-free genes to replace the mutated genes, restoring normal function.

Viral vectors are promising candidates for this, but as mentioned before, there are problems. The four principal difficulties are efficient transfection, persistent expression, localization of the vector to specific tissues, and cancer, which may result when the viral gene is inserted in the middle of another gene. Nevertheless, these difficulties can be surmounted, and have been; gene therapy studies have been conducted, and are giving promising results. And though the long-term effects of these therapies is still unknown - We don't know if the rats will develop cancer after a few years -, studies like this are exciting in their potential benefit to those suffering from genetic disorders.

 
 
Current Location: Veolia ES
Current Mood: accomplishedaccomplished
 
 
Biomusician
10 September 2008 @ 03:55 pm
Dream, try, think, act, then all hope-wracked,
Make that hard pact: get college-trained.
Read, learn, write; pass each great, grand class;
Add to large mass of knowledge gained.
Search, find, talk, start; job first seems smart,
Just a small part of giant’s team.
Work, weigh, think, trudge, through each day’s sludge,
Yet this one drudge keeps science dream.

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Current Mood: determineddetermined
 
 
Biomusician
08 November 2007 @ 03:14 am
In researching for my senior seminar paper (eugenics!), I've discovered a disturbing paradox. The more important a topic is, and the closer one gets to the real issue at hand, the larger the mountains of information grow, and the smaller the jeweled deposits of quality thought become. Bigger mountains, smaller yields.

It makes sense, I suppose. Keeping the mountain metaphor, let us suppose the heart of the mountain represents a perfect analysis of the subject, and the top of the mountain represents a cursory analysis. Many cursory analyses are carried out, adding considerable mass to the mountain, but few people take the time to bury their way through the mountain to get at the valuable information inside. Even fewer pull a Neo ("There is no mountain."), think things through completely by themselves, and get to the center of the mountain. I considered it, but decided that since I need to cite sources for my thesis anyway, I might as well dig through a few hundred thousand words.

It's too bad the wheat/chaff metaphor doesn't apply; wind is a lot easier than work.

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Current Location: mineshaft #6
Current Mood: determineddetermined
Current Music: Nickel Creek
 
 
Biomusician
27 July 2007 @ 05:07 am
Let such an adverb describe the manner in which this entry is given: infrequently, unexpectedly, expressed such that the sun can't read over my shoulder (nocturnally, if the single adverb is preferred or brevity valued). Therefore, let this sabbatical-ending blog commence.

This summer, like most summers, I've not found that equilibrium of activity which could truthfully be embraced as 'normal.' Work in lab and at the Old Spaghetti Factory gives predictable hours, but while the work itself remains unchanging in principle and purpose, methods and expectations are changing. Work (as a career, certainly, but also any effort toward an end to which such a label might be applied) constitutes a large part of life, but it is no backbone. Work is flesh, intimately connected to the mind of a person - their thoughts, ambitions - who he or she is choosing to be. The bones of a person give a person their basic shape while the muscles give further definition and even beauty to the form underneath.

Normally, summers serve as as my x-ray. I hope one day to serve as an x-ray technician instead of the disappointed patient. X-rays are dangerous, and no one likes to see broken bones (unless you play rugby, or are the team doctor, paid on commission). Yet I know that if I am to live in a manner worthy of my creator and his calling, such doctor's appointments are essential. For how am I to see clearly, run fastly, handle gently, or live wonderfully adverbially otherwise?

I desire no normal normal. The normal I desire is perfection - a most abnormal thing to us. From this 'normal' spring confidence, purpose, and power - and all these in purest profound essence.

Yet the slope of my life continues to change, the derivative rarely constant, the integral (I hope) always increasing (Forgive me; such puns, are, after all, normal for me.). For though the slope may change, the bones will reform and regrow, and my life's experience bar will continue to be filled.
So! With medical school on the horizon, my final year of college the mountain before it, and my friends with me at its foot, I stand (fidgeting a bit, maybe). Until a focused, energizing idea floods my mind and demands to overflow into such a container (as can be expected normally, given the passage of time), I bid this stretch of internet beach and its surfers a temporary farewell.

I might even return to give a few "this is what I've been doing all this time" facts, like, "I read Jane Eyre and HP7!" Au-revoir!

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Current Location: in front of a fan
Current Mood: okayokay
Current Music: birds
 
 
Biomusician
30 May 2007 @ 08:51 am
Bloodshot means red,
Bruises are blue:
One in and one under
My tired eyes two.

My duty confines my limp mind to a book,
While my booty (asleep) gloats in what I’ve forsook.
To read with my eyes closed, to run in my sleep!
To somehow (in God’s name) my sanity keep!
To harvest plowed pages all age and love-yellowed!
To revel in meaning, with Sleep my bedfellow!
What’s mellow?

My classes define me and many of mine,
Our homework intoxicates more than fine wine.
Broken backs pull the weight of impossible dreams,
While the feelings of many lead only to “seems.”
We stumble about with our eyes crusty-caked:
Small sight to see greatness with eyes half-awaked.
Will I break?

“Alas! There’s not time to pursue all the good
“Quite as much as I’d like; I must settle for “could.”
“As much as I can to bless my chaps and dames,
“To longboard, to hike and to play video games.
“To honor what beauty there is that I see,
“And to look for still more that now hidden may be.
Where is glee?”

I wonder and work, try to love, try to live,
Such big words, ill-used, must like water-filled sieves
Hold meaning for which I must struggle and hunt,
While lurking, encircling, prowl my favorite shunts.
A hand through the water, a voice through the trees,
Gasping air, all root-tripped. “A little rest please?”
Wisdom’s keys?

Wisdom’s no gate, nor a door, nor a path,
But a stone that to some feels like undeserved wrath.
I am dashed over edges and torn flesh from bone.
The blood-keys seep into the rare living stone.
A rare run, then a stagger, next limp and soon fall,
“Is o’ chem important?” I ask as I crawl?
What is tall?

Pains are blood-red,
Bruises sky-blue,
A life torn asunder,
Will try to renew.

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