I agree that the overall system is probably too large, but we are talking specifically about the flagship university of the UC system. arguably the best public university in the world, and it is getting hurt just as bad as UC Riverside. that's absurd and embarrassing.
this is only getting media attention because twitter is "hip" these days. supernova hunters don't care how they get tipped off about a new burst, and all kinds of avenues result in rapid assessments. i've heard of text messages, emails, you name it. we have a system for rapidly alerting the supernova community based around email, i doubt that twitter will replace it.
the interesting and cool thing about this is that alex happened to be at keck when the news came through, which allowed him to quickly point the monster scope at m51. supernova usually last for months and months, but it is rare for us to get such early data with such powerful machines. it can only really happen randomly.
that's what statistically means. in the long run, in the absence of a selecting force to promote the stability of a beneficial trait, genetic drift will tend to disable neutral traits. this is especially true when 1) the genetic sequences underlying the trait need to be very precise for the trait to function properly (much more important in receptor/effector systems than in gross physical traits) and 2) the sequences are rather long. thus, we can assume that this receptor does not represent a neutral trait, especially because it directly involves a phenotype that is intimately tied to survival (breathing).
if you had read my entire comment, you would have noticed that I said the exact same thing. and not all neurotransmitters are bitter (ie basic), just most. the weird thing is that the neurotransmitters that we know contract the bronchioles (eg acetylcholine) are also predicted to be bitter compounds. strange stuff indeed.
Genetic drift would not explain why it developed in the first place, and would not be sufficient to keep a complicated receptor/effector system intact in a large, heterogeneous population such as ours for very long (in genetic terms). most people misunderstand the term.
I wonder what might be the reasoning behind this system evolving/remaining intact in humans. I can't really think of an exogenous substance that we inhale naturally that would activate such a response and confer an advantage to us. My best guess would be that the natural ligand for these receptors is something that is produced locally in the lungs in scenarios where bronchiodilation is desired (ie sympathetic stimulation). as someone else pointed out, many of the common neuroreceptors are alkaloids, and would probably activate these receptors. From the abstract, it sounds like these receptors are Gq (IP3 and calcium) receptors, which is interesting because the "classic" receptors that dilate the smooth muscle in the lungs are Gs receptors that stimulate increased cAMP. In smooth muscle, more calcium generally leads to stronger, not weaker, contraction. cAMP leads to relaxation, explaining why epinephrine and albuterol have their effects.
didn't have time to read the whole paper. exam on this stuff tomorrow though, wonder if I can use this on an essay question?
talk about a crappy experimental setup. no way to control for all the things that could explain this result.
these kinds of hand-wavy experiments will continue to crop up as our ability to measure the brain outstrips our ability to understand.
it's way to easy to point an fMRI at a region "linked" to a particular behavior or type of thinking, and then wax poetic about what the increased activity may or may not mean. sad coming from a relatively respected lab.
there is a moderate amount of smooth muscle found in the venous system. from what I have been taught (only in my first year of medical school), these muscles are not under the same kind of highly-specific nervous system control that the muscle in arteries is under. ie, your body has a hard time selectively contracting/relaxing specific veins. these muscles are predominantly under hormonal control, meaning that their contraction is regulated at a body-wide level.
the vast majority of control over where blood flows in the body is at the level of arterioles, which are small arteries found before capillary beds.
not always, just when the correction is trivial and doesn't contribute to the understanding at hand. isn't hyperbole ("always") a more dangerous use of language? so much for respect.
to be completely accurate, arteries do indeed 'deliver' blood, as they are responsible for the distribution of the blood to the body. feel free to pop open oed, which I'm sure a doctor of your caliber has at the ready, if you doubt me.
additionally, the elastic quality of the major arteries allows for pumping of blood outside the heart, which more closely fits with your highly specific (but in the context of the discussion at hand, meaningless) definition of deliver. and let's not forget the smooth muscle around arteries which can contract, leading to yet another form of active 'delivery' of blood.
thanks for your career advice, doc. it has been taken to heart.
woah, you're totally right. my professor screwed that one up. we were taught that PDE5 cleaves both cAMP and cGMP, but it looks like only PDE1, 2, and 3 cleave both.
the downstream effects would be almost identical though. both cAMP and cGMP cause myosin light chain kinase to be phosphorylated by their respective kinases (PKA and PKG), leading to lower myosin activity and thus relaxation.
in the context of what the poster was saying, i was pointing out that it is arteries that serve as conduits for blood that is flowing toward the penis (and all other tissues of the body), and veins are what serve as conduits for blood flowing away from the tissues.
2) the relaxation I was referring to was of the smooth muscle in the walls of the arteries leading to the penis
3) there isn't much regulation of bloodflow that takes place on the venous side (ie venous drainage is relatively constant). thus if you increase flow inward it will necessarily lead to pooling (ie erection)
the classic ED drugs all work by relaxing the arteries that flow toward the penis by inhibiting PDE5, a phosphodiesterase predominantly found in penis arteries. this increases cAMP levels, leaving to vasodilation and an erection. unfortunately these drugs aren't perfectly specific, and cause small amount of vasodilation throughout the body, along with a corresponding drop in blood pressure. this is why they tell you not to take the ED pills if you take other vasodilators like nitroglycerin.
if you could engineer a Gs (i was wrong in my earlier post when I said Gi, you want more cAMP not less) receptor that was light sensitive, and get it to express only in the penis artery smooth muscle.... and shine light through your skin to activate these receptors, it would work the same way.
obviously not an ideal way to treat a disorder. these light gated channels are probably only good for basic scientific research.
actually, it totally could work.
erections occur because certain smooth muscle in the penis relaxes, allowing blood to flow in the right places. ED drugs block the degradation of a chemical that promotes this relaxation. a light gated receptor of the proper type (Gi) could be designed to do the same thing.
Please note that we have added a consequence for failure. Any contact with the chamber floor will result in an unsatisfactory mark on your official testing record, followed by death.
excellent point. these days, a given professor's field is usually pretty small. they only want to talk shop with people who both understand their niche and show actual intellectual curiosity in it.
If you are trying to find a mentor in any scientific field, you don't go looking for "lists" of interests. I don't even know what that refers to. You find recently published primary literature in areas you have interest in, and speak to those authors. This helps you find people who are actively working in the field you seek to be a part of. Even if the authors themselves aren't right for you, they are more likely to know other people in the field than anyone else.
Frankly, I'm kind of shocked. You are applying to PhD programs, but don't currently know any scientists in the field? What about at your undergraduate institution? How did you get interested in social science without reading any papers?
I would recommend looking into supernova searching. As an undergraduate, I worked in a lab that used a robotic telescope high in the mountains to automatically search for these extremely bright and relatively common phenomena. Given their brightness and longevity, it is relatively simple (in astronomical terms) to design and build a system to look for these objects. check out KAIT, the telescope I worked on.
I took a high-level bio class at UC Berkeley this past semester that concerned exactly this type of genetic therapy. someone brought up the idea of doing this to normals with the pit viper IR heat-sensitive ionic channel gene, tie it to some downstream color of choice.
after a quick look at the paper linked in the article (Identifying photoreceptors in blind eyes caused by RPE65 mutations: Prerequisite for human
gene therapy success), it is clearly not about gene therapy in humans. it is a study of the thickness of the retina in humans homozygous for a mutation in a specific retinal gene. as the title says, it is a prerequisite for gene therapy.
the actual paper, Human gene therapy for RPE65 isomerase deficiency activates the retinoid cycle of vision but with slow rod kinetics, can be found here. It concerns the same gene, incidentally.
Slashdot Mirror
Kin Selection
I agree that the overall system is probably too large, but we are talking specifically about the flagship university of the UC system. arguably the best public university in the world, and it is getting hurt just as bad as UC Riverside. that's absurd and embarrassing.
Maybe it has something to with the fact that the state of california has cannibalized the funding for my beloved alma mater.
this is only getting media attention because twitter is "hip" these days. supernova hunters don't care how they get tipped off about a new burst, and all kinds of avenues result in rapid assessments. i've heard of text messages, emails, you name it. we have a system for rapidly alerting the supernova community based around email, i doubt that twitter will replace it.
the interesting and cool thing about this is that alex happened to be at keck when the news came through, which allowed him to quickly point the monster scope at m51. supernova usually last for months and months, but it is rare for us to get such early data with such powerful machines. it can only really happen randomly.
my guess is that you have something along the lines of calcium carbide in those rocks
that's what statistically means. in the long run, in the absence of a selecting force to promote the stability of a beneficial trait, genetic drift will tend to disable neutral traits. this is especially true when 1) the genetic sequences underlying the trait need to be very precise for the trait to function properly (much more important in receptor/effector systems than in gross physical traits) and 2) the sequences are rather long. thus, we can assume that this receptor does not represent a neutral trait, especially because it directly involves a phenotype that is intimately tied to survival (breathing).
if you had read my entire comment, you would have noticed that I said the exact same thing. and not all neurotransmitters are bitter (ie basic), just most. the weird thing is that the neurotransmitters that we know contract the bronchioles (eg acetylcholine) are also predicted to be bitter compounds. strange stuff indeed.
Genetic drift would not explain why it developed in the first place, and would not be sufficient to keep a complicated receptor/effector system intact in a large, heterogeneous population such as ours for very long (in genetic terms). most people misunderstand the term.
/degree in genetics and genomics
i use reasoning in an abstract sense to mean "biological driving force." but you already knew that.
I wonder what might be the reasoning behind this system evolving/remaining intact in humans. I can't really think of an exogenous substance that we inhale naturally that would activate such a response and confer an advantage to us. My best guess would be that the natural ligand for these receptors is something that is produced locally in the lungs in scenarios where bronchiodilation is desired (ie sympathetic stimulation). as someone else pointed out, many of the common neuroreceptors are alkaloids, and would probably activate these receptors. From the abstract, it sounds like these receptors are Gq (IP3 and calcium) receptors, which is interesting because the "classic" receptors that dilate the smooth muscle in the lungs are Gs receptors that stimulate increased cAMP. In smooth muscle, more calcium generally leads to stronger, not weaker, contraction. cAMP leads to relaxation, explaining why epinephrine and albuterol have their effects.
/med student
didn't have time to read the whole paper. exam on this stuff tomorrow though, wonder if I can use this on an essay question?
talk about a crappy experimental setup. no way to control for all the things that could explain this result.
these kinds of hand-wavy experiments will continue to crop up as our ability to measure the brain outstrips our ability to understand.
it's way to easy to point an fMRI at a region "linked" to a particular behavior or type of thinking, and then wax poetic about what the increased activity may or may not mean. sad coming from a relatively respected lab.
there is a moderate amount of smooth muscle found in the venous system. from what I have been taught (only in my first year of medical school), these muscles are not under the same kind of highly-specific nervous system control that the muscle in arteries is under. ie, your body has a hard time selectively contracting/relaxing specific veins. these muscles are predominantly under hormonal control, meaning that their contraction is regulated at a body-wide level.
the vast majority of control over where blood flows in the body is at the level of arterioles, which are small arteries found before capillary beds.
not always, just when the correction is trivial and doesn't contribute to the understanding at hand. isn't hyperbole ("always") a more dangerous use of language? so much for respect.
to be completely accurate, arteries do indeed 'deliver' blood, as they are responsible for the distribution of the blood to the body. feel free to pop open oed, which I'm sure a doctor of your caliber has at the ready, if you doubt me.
additionally, the elastic quality of the major arteries allows for pumping of blood outside the heart, which more closely fits with your highly specific (but in the context of the discussion at hand, meaningless) definition of deliver. and let's not forget the smooth muscle around arteries which can contract, leading to yet another form of active 'delivery' of blood.
thanks for your career advice, doc. it has been taken to heart.
woah, you're totally right. my professor screwed that one up. we were taught that PDE5 cleaves both cAMP and cGMP, but it looks like only PDE1, 2, and 3 cleave both.
the downstream effects would be almost identical though. both cAMP and cGMP cause myosin light chain kinase to be phosphorylated by their respective kinases (PKA and PKG), leading to lower myosin activity and thus relaxation.
nice catch!
that's semantics.
/medical student
in the context of what the poster was saying, i was pointing out that it is arteries that serve as conduits for blood that is flowing toward the penis (and all other tissues of the body), and veins are what serve as conduits for blood flowing away from the tissues.
thanks for your deep insight though.
1) veins don't deliver blood, arteries do
2) the relaxation I was referring to was of the smooth muscle in the walls of the arteries leading to the penis
3) there isn't much regulation of bloodflow that takes place on the venous side (ie venous drainage is relatively constant). thus if you increase flow inward it will necessarily lead to pooling (ie erection)
the classic ED drugs all work by relaxing the arteries that flow toward the penis by inhibiting PDE5, a phosphodiesterase predominantly found in penis arteries. this increases cAMP levels, leaving to vasodilation and an erection. unfortunately these drugs aren't perfectly specific, and cause small amount of vasodilation throughout the body, along with a corresponding drop in blood pressure. this is why they tell you not to take the ED pills if you take other vasodilators like nitroglycerin.
if you could engineer a Gs (i was wrong in my earlier post when I said Gi, you want more cAMP not less) receptor that was light sensitive, and get it to express only in the penis artery smooth muscle.... and shine light through your skin to activate these receptors, it would work the same way.
obviously not an ideal way to treat a disorder. these light gated channels are probably only good for basic scientific research.
actually, it totally could work. erections occur because certain smooth muscle in the penis relaxes, allowing blood to flow in the right places. ED drugs block the degradation of a chemical that promotes this relaxation. a light gated receptor of the proper type (Gi) could be designed to do the same thing.
Please note that we have added a consequence for failure. Any contact with the chamber floor will result in an unsatisfactory mark on your official testing record, followed by death.
I have to ask... what made you want to pursue a PhD if you weren't acquainted with papers and research? General interest?
I'm not shocked he doesn't have an advisor. I'm shocked that he thought going to university websites would be the way to go.
excellent point. these days, a given professor's field is usually pretty small. they only want to talk shop with people who both understand their niche and show actual intellectual curiosity in it.
If you are trying to find a mentor in any scientific field, you don't go looking for "lists" of interests. I don't even know what that refers to. You find recently published primary literature in areas you have interest in, and speak to those authors. This helps you find people who are actively working in the field you seek to be a part of. Even if the authors themselves aren't right for you, they are more likely to know other people in the field than anyone else.
Frankly, I'm kind of shocked. You are applying to PhD programs, but don't currently know any scientists in the field? What about at your undergraduate institution? How did you get interested in social science without reading any papers?
I would recommend looking into supernova searching. As an undergraduate, I worked in a lab that used a robotic telescope high in the mountains to automatically search for these extremely bright and relatively common phenomena. Given their brightness and longevity, it is relatively simple (in astronomical terms) to design and build a system to look for these objects. check out KAIT, the telescope I worked on.
I took a high-level bio class at UC Berkeley this past semester that concerned exactly this type of genetic therapy. someone brought up the idea of doing this to normals with the pit viper IR heat-sensitive ionic channel gene, tie it to some downstream color of choice.
sign me up.
after a quick look at the paper linked in the article (Identifying photoreceptors in blind eyes caused by RPE65 mutations: Prerequisite for human gene therapy success), it is clearly not about gene therapy in humans. it is a study of the thickness of the retina in humans homozygous for a mutation in a specific retinal gene. as the title says, it is a prerequisite for gene therapy.
the actual paper, Human gene therapy for RPE65 isomerase deficiency activates the retinoid cycle of vision but with slow rod kinetics, can be found here. It concerns the same gene, incidentally.