I'm a pretty firm believer that just about every single aspect of an individual, from their personality/tendencies to appearance and everything in between, is gene-regulated. That being said, I don't think I ever considered the possibility that you're born with a predisposition to be either Conservative or Liberal.
DRD4, the gene that codes for dopamine receptor 4 in humans, has recently been linked to a tendency for individuals to be politically liberal. A medical genetics professor at UC San Diego, in reference to the new finding, asserts that "we hypothesize that individuals with a genetic predisposition toward seeking out new experiences will tend to be more liberal - but only if they had a number of friends growing up." Being more open to new experiences is only one aspect of having a "more liberal personality", if it is at all.
Whether you consider yourself to be a Republican, a Democrat, Libertarian, or even a member of the Rent is Too Damn High Party (see video below), you're only one to a certain degree. Political ideology is on a spectrum, due to the amalgam of platforms and issues. Can we really associate an individual's propensity to try new things with being politically liberal? Are there any personality traits we can really link to voting one way or the other? I personally think political views are one of those things that are mostly influenced by environmental factors (SES, upbringing, friends, etc.) rather than genotype, which could explain why/how an individual's political views can shift with age/environment.
October 31, 2010
October 26, 2010
when is it no longer "just a fluke"?
This is a screen shot I took from the NHL website a few days ago, when the New York Islanders were leading the Eastern Conference, and League, in points:
The Islanders, who finished 26th (out of 30) in the league last season, and who have been less than impressive for the better part of the decade, seem to be holding their own. Even without their "best" players who were injured in preseason or signing any big time players during the off-season, the Isles are managing points in almost every game. How is this happening?
According to Rangers and Leafs fans, of course it's a fluke. But how many games will the Isles have to win to shut 'em up? In a season of 80 games, will we have to wait for 20 games? 40? Or is it about consistently pulling out W's against the "hardest hittin' teams in the league"? Or will we have to wait and see who scoops up the coveted playoff spots? It's usually a fan's defense mechanism to put down a rival team's success by calling it a "fluke", but how long do I have to wait before I can legitimately remind Rangers fans how much more money they spend per year on "star" players that always seem to disappoint?
In the same token, I think the 5-1 record has finally proven to be enough to stop Giants fans from calling the Jets season a "fluke"? Given the season is only 16 games long in comparison to the NHL's 80...
The Islanders, who finished 26th (out of 30) in the league last season, and who have been less than impressive for the better part of the decade, seem to be holding their own. Even without their "best" players who were injured in preseason or signing any big time players during the off-season, the Isles are managing points in almost every game. How is this happening?
According to Rangers and Leafs fans, of course it's a fluke. But how many games will the Isles have to win to shut 'em up? In a season of 80 games, will we have to wait for 20 games? 40? Or is it about consistently pulling out W's against the "hardest hittin' teams in the league"? Or will we have to wait and see who scoops up the coveted playoff spots? It's usually a fan's defense mechanism to put down a rival team's success by calling it a "fluke", but how long do I have to wait before I can legitimately remind Rangers fans how much more money they spend per year on "star" players that always seem to disappoint?
In the same token, I think the 5-1 record has finally proven to be enough to stop Giants fans from calling the Jets season a "fluke"? Given the season is only 16 games long in comparison to the NHL's 80...
October 23, 2010
a spray of DNA keeps the bad guys away?
Some businesses in Holland have been using a new burglary system - one that sprays synthetic DNA on robbers as they walk out the door. The spray is deployed by an employee without the knowledge of the robber - it's odorless and invisible - and alerts the local police department. The synthetic DNA (which doesn't even cost that much to produce) is specific to the store from which it's deployed, and is meant to help cops link burglars to the scene of the crime. Businesses that have used this system (usually installed by the police departments) have reported declines in crime rate, although there is no current data as of yet.
What could be causing this decline? The synthetic DNA alarm system hasn't been used yet to identify a criminal, but it has been triggered accidentally many times, which would allude to it being used as a scare tactic more than anything else. Businesses that have this system installed are required to have a sign posted outside alerting consumers. Even if it weren't required, it'd be a good move. The appearance of "DNA" on a sign outside of stores definitely deters prospective burglars. I don't see how synthetic DNA spray is any more effective than using UV ink, but fear of the unknown is daunting enough for most people. Even by glancing at readers' comments below the NYTimes article, I'm surprised at how little people actually understand about the use of DNA. Some worry about the prospect of being sprayed by "hybrid-human DNA", without realizing synthetic DNA is completely inactive and would cause no harm to the individual it's been sprayed on. On a more general level, I think criminals tend to associate "DNA" with "getting caught", which is enough to dissuade them.
In this case, the fear of the unknown appears to be effective enough to discourage robbers. It'll be interesting to see raw data pertaining to crime rates though...
What could be causing this decline? The synthetic DNA alarm system hasn't been used yet to identify a criminal, but it has been triggered accidentally many times, which would allude to it being used as a scare tactic more than anything else. Businesses that have this system installed are required to have a sign posted outside alerting consumers. Even if it weren't required, it'd be a good move. The appearance of "DNA" on a sign outside of stores definitely deters prospective burglars. I don't see how synthetic DNA spray is any more effective than using UV ink, but fear of the unknown is daunting enough for most people. Even by glancing at readers' comments below the NYTimes article, I'm surprised at how little people actually understand about the use of DNA. Some worry about the prospect of being sprayed by "hybrid-human DNA", without realizing synthetic DNA is completely inactive and would cause no harm to the individual it's been sprayed on. On a more general level, I think criminals tend to associate "DNA" with "getting caught", which is enough to dissuade them.
In this case, the fear of the unknown appears to be effective enough to discourage robbers. It'll be interesting to see raw data pertaining to crime rates though...
October 20, 2010
overgeneralizing results
I was reading an article for my Neuroscience seminar about how the uncoupling protein UCP2 is required for the exercise-induced changes that occur in the hippocampi of mice (Dietrich, Andrews & Horvath, 2008). In comparison to UCP2ko mice, the researchers found that only wildtype mice showed increases in both oxygen consumption during mitochondrial respiration and in the number of synapses in the CA1 region of the hippocampus. The methods used in this paper were very straight forward and the researchers appeared to control very well for potential biases. It would be very difficult to argue the validity of these results. Therefore I will accept, as Dietrich, Andrews and Harvath conclude, that voluntary exercise in mice increases mitochondrial respiration, mitochondria number, and spine synapse density in the dentate gyrus and the CA1 region of the hippocampus, all of which are dependent on UCP2.
Just when I thought I had finally read a paper for my seminar that hadn't bothered me in some way, I came across this in the conclusion: "Our data illustrate the role of uncoupling proteins in promoting brain plasticity and their participation in physiological and pathological adaptations of the brain." Isn't that statement a tad bit broad for this relatively straight-forward study which really only assessed the importance of UCP2? Furthermore, multiple times throughout the paper, the researchers assert that they did not monitor the effects or levels of UCP3 or UCP5, two other predominant uncoupling proteins. What about UCP1? It has been found to have implications in generating heat in hibernating mammals - how would this come into play in exercise-induced brain function, if at all?
Overgeneralization of results in science can be problematic for the directions of future research. The conclusion of this paper would lead one to believe that all uncoupling proteins have been found to have the same implications on these processes as UCP2 did, when in fact they may not in the least. This concept got me thinking about a trade-off, between overgeneralization and over-specificity, which was perceptively blogged about a few days ago. In Science papers, overgeneralizing can mislead future research, and lead to oversight. On the other hand, being too specific about something could lead to frivolous research, wasting time and resources.
Perhaps for this paper, an appropriate way to conclude this paper would be to assert that UCP2 has been implicated in these mechanisms, but further research is required to determine whether or not all uncoupling proteins produce the same results.
Just when I thought I had finally read a paper for my seminar that hadn't bothered me in some way, I came across this in the conclusion: "Our data illustrate the role of uncoupling proteins in promoting brain plasticity and their participation in physiological and pathological adaptations of the brain." Isn't that statement a tad bit broad for this relatively straight-forward study which really only assessed the importance of UCP2? Furthermore, multiple times throughout the paper, the researchers assert that they did not monitor the effects or levels of UCP3 or UCP5, two other predominant uncoupling proteins. What about UCP1? It has been found to have implications in generating heat in hibernating mammals - how would this come into play in exercise-induced brain function, if at all?
Overgeneralization of results in science can be problematic for the directions of future research. The conclusion of this paper would lead one to believe that all uncoupling proteins have been found to have the same implications on these processes as UCP2 did, when in fact they may not in the least. This concept got me thinking about a trade-off, between overgeneralization and over-specificity, which was perceptively blogged about a few days ago. In Science papers, overgeneralizing can mislead future research, and lead to oversight. On the other hand, being too specific about something could lead to frivolous research, wasting time and resources.
Perhaps for this paper, an appropriate way to conclude this paper would be to assert that UCP2 has been implicated in these mechanisms, but further research is required to determine whether or not all uncoupling proteins produce the same results.
October 11, 2010
mirror-guided body inspection is not an adequate measure of self-awareness in animals
Numerous comparative psychology and biology studies have utilized mirror-guided body inspection to answer the age-old question of whether or not animals possess the ability to self-recognize. Studies have used animals ranging from dolphins (Reiss & Marino, 2001) to primates. While one would think that repeated positioning in front of a mirror after a mark has been visibly put on the subjects would confer that the organism was recognizing oneself. However, I think this method is largely flawed and I find it tough to buy into any hard results researchers deduce from mirror-guided experiments.
First and foremost, the (hopefully) double-blinded observers are forced into subjectively anthropomorphizing the behaviors of subjects. And although I am aware I am being ironically anthropomorphic in my reasoning, animals’ usage of mirrors can be attributed to a variety of justifications.
The mirror itself is a novel object in the animal’s environment, and without a proper baseline assessment, researchers may attribute behavior at a mirror to be due to self-awareness fallaciously. The subjects simply be curious by the introduction of a novel stimulus, and perhaps decreased presence in the mirror as the experiment progresses is attributed to desensitization to the stimulus rather than by the presence of self-recognition. By the same token, animals may not have any reaction to experimental marks if they do not in fact resemble anything that might cause for concern in a normal environment. For example, if the mark on the animal resembles a parasite or blood, the animal could potentially be more interested in pursuing its removal. However, if the animal has seen similar marks on other individuals around him and is no cause for concern, the animal could simply be ignoring its presence. This does not mean that the animal does not possess self-recognition; it is simply not displaying the behaviors we are looking for in our assessment of self-recognition. This potential explanation is of course largely anthropomorphic, and I am implying a first- or even second-order intentionality system to provide an alternate interpretation, but I think it is feasible for primates, especially chimpanzees.
Self-recognition is, in my opinion, largely mental and is close to impossible to assess in organisms who are unable to provide personal accounts. As seen in humans, one can possess a mental state without displaying it, and without a sufficient motive or cause for concern, animals may simply not display the behaviors we are looking for. That being said, mirror-guided body inspection can provide us with some valid information about the possibility of non-human self-recognition – but it’s simply not the whole picture.
October 7, 2010
is memory reorganization during labile states evolutionarily adaptive?
There are two labile states of fear memories. The first occurs shortly after learning, before the consolidation process, during which short-term memories are vulnerable for disruption whereas long-term memories are impervious. After consolidation, with the exposure to the proper environmental cues, such a memory can be retrieved in the brain. Following this retrieval, the second labile stage occurs. During this stage, the aforementioned memory is susceptible to alterations once again. Evidence (Nader, et al. 2000; Kaang, et al. 2009) has illustrated that protein-synthesis dependent reconsolidation processes are required to maintain the original memory. Administering a protein synthesis inhibitor before or immediately after memory retrieval (not quite sure how they elicited the retrieval, or how they measured when exactly it occurred, which would be interesting to know) disrupted the original memory.
Kaang, et al. (2009) hypothesized that these reconstruction processes induced by memory retrieval provide opportunities for memory update or reorganization. Furthermore, they found that new information (stimuli) must be necessary to trigger the destabilization process after memory retrieval. When I first read this, I automatically figured this made sense evolutionarily. Wouldn't we want the opportunity to modify our memories if our environmental stimuli are changing around us? Especially as humans, who live for a much longer time than do rodents, it would be important for our memories to adapt to new technologies and experiences. No question about it. But then as I thought further - I thought about all the downsides this could potentially have.
Let's say as a child you develop a taste aversion to dairy products because you have gotten sick from them on multiple occasions. If your memory serves you right, hopefully you have learned to stay away from dairy. But what happens if one day you have dairy by accident and you don't happen to get sick? Does that mean that single experience should remodel the existing memory you already have of dairy-induced discomfort? This example could be applied throughout species - especially since taste aversions are much more imperative to survival of rodents and less complex animals than humans. Anyway...my point being - if memory reorganization occurs each time a long-term memory is retrieved, how drastic does the changed stimulus have to be to alter the existing memory? Does it have to occur more than once? Does it matter how long the memory has been encoded for, or how many times it has previously been retrieved (strength of memory)? It just doesn't seem like it would make evolutionary sense to have all long-term memories susceptible to disruption each time it is retrieved, does it? Would it make more sense to just form new memories in response to new stimuli rather than modify pre-existing ones? Or would that just require more (ugh, don't make me say it) neural plasticity/neurogenesis than our brains are capable of?
It's important to take into consideration that the studies i've read largely deal with fear-conditioned memories. It would be compelling to study and determine whether or not there are differences in the appearance of labile states in other types of memories (e.g. olfactory aversions, conditioned taste aversions, object/social recognition memory, spatial memory). Would it make sense for some of these to be more susceptible to disruptions more or less routinely?
Kaang, et al. (2009) hypothesized that these reconstruction processes induced by memory retrieval provide opportunities for memory update or reorganization. Furthermore, they found that new information (stimuli) must be necessary to trigger the destabilization process after memory retrieval. When I first read this, I automatically figured this made sense evolutionarily. Wouldn't we want the opportunity to modify our memories if our environmental stimuli are changing around us? Especially as humans, who live for a much longer time than do rodents, it would be important for our memories to adapt to new technologies and experiences. No question about it. But then as I thought further - I thought about all the downsides this could potentially have.
Let's say as a child you develop a taste aversion to dairy products because you have gotten sick from them on multiple occasions. If your memory serves you right, hopefully you have learned to stay away from dairy. But what happens if one day you have dairy by accident and you don't happen to get sick? Does that mean that single experience should remodel the existing memory you already have of dairy-induced discomfort? This example could be applied throughout species - especially since taste aversions are much more imperative to survival of rodents and less complex animals than humans. Anyway...my point being - if memory reorganization occurs each time a long-term memory is retrieved, how drastic does the changed stimulus have to be to alter the existing memory? Does it have to occur more than once? Does it matter how long the memory has been encoded for, or how many times it has previously been retrieved (strength of memory)? It just doesn't seem like it would make evolutionary sense to have all long-term memories susceptible to disruption each time it is retrieved, does it? Would it make more sense to just form new memories in response to new stimuli rather than modify pre-existing ones? Or would that just require more (ugh, don't make me say it) neural plasticity/neurogenesis than our brains are capable of?
It's important to take into consideration that the studies i've read largely deal with fear-conditioned memories. It would be compelling to study and determine whether or not there are differences in the appearance of labile states in other types of memories (e.g. olfactory aversions, conditioned taste aversions, object/social recognition memory, spatial memory). Would it make sense for some of these to be more susceptible to disruptions more or less routinely?
October 6, 2010
"everything's better in moderation" - neural plasticity can't be the exception to that rule.
My neuroscience and behavior seminar, required for all us lucky (or not-so-lucky) neuroscience majors at Vassar, has been molded around one of the most broad and frankly irritating topics of all time: plasticity. Like, I get it. Plasticity's important. New synapses, changes in dendritic spines, pruning - all clearly vital to a functioning brain. And it's definitely necessary for someone studying neuroscience - or any science for that matter - to understand that the brain is capable of changing, even after the so-called "critical period".
Environmental conditions, both intra- and extra-cellularly, have the potential to impact the structure of synapses in the brain. Behaviors can even be re-delegated to new brain regions after an injury (dependent on age and other factors of course). While this all sounds great, there is no way that neural plasticity is always a positive thing. It doesn't make sense that something that can change relatively often would be beneficial to most organisms. Perhaps one can make the argument that as the average life span of a species increases, it could be more favorable (over a century, a lot of environmental stimuli can change dramatically), but often times, plasticity studies are done on mice and rats, both of which do not have a long life span at all. What would be the advantage of neural plasticity after the critical period in development in a mouse that only lives for a few months? Could it possibly be more advantageous for the mouse to have strengthened synapses and stable dendritic branches throughout its lifetime? Is it possible that an organism undergoing neuronal plasticity is actually being diverted from stimuli it should be paying attention to?
It's week 5 of my neuroscience seminar. I have read 17 articles on how neuronal plasticity occurs at different levels of an individual's biology (chromatin remodeling all the way up to cortical neurons being remodeled), and how a thousand different neuronal processes are altered by synaptic plasticity and dendritic changes. After discussing all 17 articles, never has one student questioned the real benefits of these changes occurring in post-developmental subjects. Admittedly, neither have I. I don't know if I can attribute my own hesitation to challenge my Professor's apparent deep affection for neurogenesis and plasticity to my fellow classmates, but there is no way they're not also feeling this frustration. Nothing in science is ever good all the time. In fact, most of the time, eventually we find out that things we think are beneficial turn out to have colossal downsides. So when is it too much when it comes to plasticity?
Environmental conditions, both intra- and extra-cellularly, have the potential to impact the structure of synapses in the brain. Behaviors can even be re-delegated to new brain regions after an injury (dependent on age and other factors of course). While this all sounds great, there is no way that neural plasticity is always a positive thing. It doesn't make sense that something that can change relatively often would be beneficial to most organisms. Perhaps one can make the argument that as the average life span of a species increases, it could be more favorable (over a century, a lot of environmental stimuli can change dramatically), but often times, plasticity studies are done on mice and rats, both of which do not have a long life span at all. What would be the advantage of neural plasticity after the critical period in development in a mouse that only lives for a few months? Could it possibly be more advantageous for the mouse to have strengthened synapses and stable dendritic branches throughout its lifetime? Is it possible that an organism undergoing neuronal plasticity is actually being diverted from stimuli it should be paying attention to?
It's week 5 of my neuroscience seminar. I have read 17 articles on how neuronal plasticity occurs at different levels of an individual's biology (chromatin remodeling all the way up to cortical neurons being remodeled), and how a thousand different neuronal processes are altered by synaptic plasticity and dendritic changes. After discussing all 17 articles, never has one student questioned the real benefits of these changes occurring in post-developmental subjects. Admittedly, neither have I. I don't know if I can attribute my own hesitation to challenge my Professor's apparent deep affection for neurogenesis and plasticity to my fellow classmates, but there is no way they're not also feeling this frustration. Nothing in science is ever good all the time. In fact, most of the time, eventually we find out that things we think are beneficial turn out to have colossal downsides. So when is it too much when it comes to plasticity?
using a 31-gene profile to predict the occurrence of breast cancer metastasis
So I know it's been a while since I've posted, but the first month of senior year has been a little hellish. Turns out I don't know nearly enough biochemistry for molecular bio, or enough about random brain regions for my neuroscience seminar, but maybe it'll just motivate me to keep up with my genomics readings and blog posts.
This semester, I'm taking a class about the biopolitics of breast cancer. While the class itself is, by and large, one large women studies-fueled (don't even get me started...) debate, it has propelled me to look a little bit more into breast cancer in the US. I happened to stumble across an article on GenomeWeb that really sparked interest - there is now a way for patients diagnosed with breast cancer to find out the likelihood and time it would take for the cancer to metastasize, based on a 31-gene signature.
This time-to-an-event breast cancer gene panel can be seen as a totally new type of diagnostic paradigm, that essentially has the potential to alter clinical management of breast cancer. On one hand, if accurate, individuals affected by breast cancer can avoid drastic treatment options if this gene panel predicts a very low chance of metastasis. On the other, patients can seek earlier therapies if they find out there is a good chance of their cancer metastasizing. Of course, the accuracy of this method would have to be just about 100% - I can't even imagine the legal liability that would come along with this kind of technology. But the prospects of this type of test could completely revolutionize a breast cancer diagnosis. Maybe then I wouldn't have to hear about how mastectomies "objectify women" because of some silly conspiracy theory about male doctors trying to take over the world... but I digress - we all know how I feel about vassar college feminazis...
This semester, I'm taking a class about the biopolitics of breast cancer. While the class itself is, by and large, one large women studies-fueled (don't even get me started...) debate, it has propelled me to look a little bit more into breast cancer in the US. I happened to stumble across an article on GenomeWeb that really sparked interest - there is now a way for patients diagnosed with breast cancer to find out the likelihood and time it would take for the cancer to metastasize, based on a 31-gene signature.
This time-to-an-event breast cancer gene panel can be seen as a totally new type of diagnostic paradigm, that essentially has the potential to alter clinical management of breast cancer. On one hand, if accurate, individuals affected by breast cancer can avoid drastic treatment options if this gene panel predicts a very low chance of metastasis. On the other, patients can seek earlier therapies if they find out there is a good chance of their cancer metastasizing. Of course, the accuracy of this method would have to be just about 100% - I can't even imagine the legal liability that would come along with this kind of technology. But the prospects of this type of test could completely revolutionize a breast cancer diagnosis. Maybe then I wouldn't have to hear about how mastectomies "objectify women" because of some silly conspiracy theory about male doctors trying to take over the world... but I digress - we all know how I feel about vassar college feminazis...
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