historian3x

I'm any expert in this field so I apologize ahead of time for my ignorance, but I'm someone who is generally curious about the pathology of obesity for some odd reason. I tend to subscribe to the set point theory(or similar models that entail heavily in the biology of obesity) even if it doesn't explain the social-economical aspects of obesity because it does a good job at modeling biological aspects which tend to be more tangible to me. Usually the current research is around energy homeostasis and the mechanisms that control it such as the metabolic and biochemical processes or neuroendocrine aspects like leptin, inuslin, gerhlin, PPY, NPY, etc and then studying it's effects around energy storage or on over-all metabolism because that approach is the most logical after all. This ends up treats obesity mostly as mostly an endocrine or metabolic disorder. So with that said, I was thinking today about the immune system and started wondering if obesity has been approached as an immune system disease or disorder instead of the former because it's well know to modulate immune system function and the fact that fat cells produce adipokines might mean something much more than simply promoting inflammation. That is to say that maybe the immune system is learning to maintain obese states which ends up modulating metabolic function? For example we know that chronic high circulating leptin(a result of being obese) can increases resistance at the specific neuron group(s) in hypothalamus or other tissue and even can modify the transportation across the blood brain barrier. This is one example of "malfunction" in the syndrome/obesity spectrum. However, has anyone ever approached the effects of high levels of adipokines have on tissues or the immune system and it's learning mechanisms? I really don't know, and would like to see the responses of others here who are probably way smarter than me just to see what they say. Edit* "That is to say that maybe the immune system is learning to maintain obese states which ends up modulating metabolic function" Sorry that part may confuse some people. - I mean this in the fact that obesity is not curable, studies show that people tend to regain the lost weight(hence theories such set points or whatever) and the fact that studies now show that even after liposuction the body will make new adipocytes in different places tends to suggest there is some form of energy homeostasis, along the fact that impaired lipid and glucose metabolism never tend to revert to pre-obese states(although they do improve some what).

So I was reading over at Wikipedia about anorexia nervosa and seen something about epigenetics that had sparked my curiousity. http://en.wikipedia.org/wiki/Anoretic "epigenetics: Epigenetic mechanisms: are means by which genetic mutations are caused by environmental effects that alter gene expression via methods such as DNA methylation, these are independent of and do not alter the underlying DNA sequence. They are heritable, as was shown in the Överkalix study, but also may occur throughout the lifespan, and are potentially reversible. Dysregulation of dopaminergic neurotransmission and Atrial natriuretic peptide homeostasis resulting from epigenetic mechanisms has been implicated in various eating disorders.[74] "We conclude that epigenetic mechanisms may contribute to the known alterations of ANP homeostasis in women with eating disorders."[74][75]" My question is that it says there are mutations caused by environmental factors that alter gene expression, but yet seem not to alter DNA sequence. Can someone please explain to someone who doesn't know much about genetics? Another question is about mutations being reversible. Can someone elaborate on the possibility of mutations being reversible because I was under the impression that it was fixed once it occurs. Is it possible to revert to normal gene expression from mutations? Thanks

Thank you for replying. Well I thought so too. That is what my professor seem to have indicate, as well as every other source I have read in past. However, I recently came across a small book in the library about exercise inducing neurogenesis and wanted confirmation if this was even possible, so I asked here. However, now it seems there may be more it. I was listening to "Brain Science Podcast #87" on aging with brain a couple days ago and that researcher said they now finding that neurogenesis occurs even in older people with aging. This is fascinating to me now since what I believed was wrong.

Hi, I'm studying the nervous system and I have a few questions. I understand that this is a lot, but if you can confirm and answer any of them then I would be very much appreciative. 1) Given two neurons and their relative synaptic cleft, can the neurotransmitters from this given cleft ever leak out of the cleft and effect adjacent/or other neurons? 2) Related to the above question, and if true and neurons can leak out then is it also possible that similar chemicals like norephiephrine and epinephrine can leak out and bind to receptors of non-neuron cells? 3) Are neurons specific in their release of neurotransmitters? What I mean is do neurons have the ability to release more than one type of transmitter? The reason I'm asking is because a) I was listening to an anatomy professor and he mentioned that parasympathetic released acetycholine, and made mention that sympathetic neurons released norepinephrine. As if it wasn't possible for other molecules to be released by these neurons. b) Agouti-related peptide - "Agouti-related protein also called Agouti-related peptide (AgRP) is a neuropeptide produced in the brain by the AgRP/NPY neuron. It is only synthesised in NPY containing cell bodies located in the ventromedial part of the arcuate nucleus in the hypothalamus" - http://en.wikipedia.org/wiki/Agouti-related_peptide 4) Do neurons have receptors for hormones too? Again I know this a lot of questions, but any answer would be appreciated(and any links describing it would be very much appreciated) Thank you for your time

Thank you

Can someone please confirm if the amount of neurons are fixed at birth, as in all that changes throughout life is the neural connections? I ask because topics of neurogenesis keep coming up, and if creating neurons isn't possible then why is the term not simply called synapticgenesis?

I was flipping through my A&P book, couldn't get a direct answer on it. Could someone confirm it? Thanks

Other than converting chemicals via gluconeogenesis, it's to my understanding the only way glucagon can raise blood glucose levels is by signaling the liver to release glucose from glycogen. So is there any other way glucagon can raise blood glucose, and can someone confirm if glucagon can by pull sugar back out of cells via transport through their membranes? If so, what is the mechanism? Thanks

Thank you, I'll buy that book and give it a try, thanks everyone for your time.

Thanks for your input. I was thinking of purchasing something like The Art of Assembly Language because it had great reviews , but then I seen people complaining how it uses HAL and isn't a "true" assembly language. So would something like Introduction to 80x86 Assembly Language and Computer Architecture be a better choice? Thank you again for your replies

I want to better understand CPU architectures, and learn to program at the same time. My goal would be to learn how the CPU manipulates data at the lowest level(I/O, computations, etc), and so I thought maybe learning how to program at lower levels(assembly, or directly on simple micro-controllers) would be a good way to understand. What is your opinion? What would you recommend? I figure someone in the CS field would have the best advice. Thanks