CharlesOSmith
CharlesOSmith t1_j9a8geg wrote
Reply to Does evolution slow down over time? by AmTheHobo
When an organism is adapted to its environment, and the environmental pressures are not changing, there will appear to be very little evolution going on. In actuality, the alleles of genes will continue to mix and recombine in new ways during sexual reproduction which means that with each new generation the organism is still putting out new versions of itself.
The DNA polymerase is also hardwired with a certain error rate which is very low, but just high enough to allow for a change in DNA here and there. Just rare enough to not really change much, but to allow for change to be possible. These changes too are put out in each new generation.
Typically if the species is excellently adapted to its environment, and the environment doesn't change all, these genetic changes in each new generation aren't likely to provide an improvement so you don't see much change. This is known as stabilizing pressure.
But as soon as a new selective pressure appears, it will become clear that that species never actually retired from the evolution game.
CharlesOSmith t1_j7z8f8w wrote
Reply to Why aren’t there fewer Nodes of Ranvier in a neuron, making the sodium channels even more concentrated? by DoubleZOfficial07
Good question. The point of the nodes is to allow for axonal depolarization to hop over short distances rather than having to move along the entire length of the axon. This speeds up transmission of an electrical impulse along an axon.
Now the Nodes of Ranvier already have the highest concentration of sodium channels anywhere in a neuron. In particular the type of channel is the NAV1.6, which stands for Sodium (Na) and Voltage (V) family 1.6 aka Voltage gated Sodium channel. Importantly for your question, this is also a channel which has an inactivation gate.
Voltage activation means the channel is activated by a strong enough differential in charge across the membrane. This charge is what can "hop" between the Nodes. Inactivation happens after a sodium channel is opened. It has a plug, just like a sink drain. So, when the channel opens and lets in sodium the plug will quickly fill up the channel and stop ion flow. This is useful because it allows for an electrical signal to trigger the sodium channels in a node, allow those channels to respond by opening and allowing sodium ions to cross the membrane thus regenerating the depolarization signal, then quickly and completely turn themselves off.
The critical reason this feature is essential is to prevent retrograde flow of the electrical signal. Each Node is just as far from the next node as it is from the one before it, so the electrical signal can reach the nodes on either side of it, But we only want the next one along the axon to be able to respond to it. By inactivating the sodium channels, a node becomes very temporarily unable to respond, and it turns out that period is just long enough for the signal to traverse down the axon.
Now, there are only so many channels you can fit in a certain membrane space and still have it function as a barrier, so it's possible the Nodes of Ranvier have already achieved that. You might also run the risk of changing the speed or degree to which the sodium current activates which could change how quickly the sodium channels inactivate. This could cause leak of signal backwards, or cause inactivation so strong, the sodium channels are still turned off when the next signal comes along, and the axon accidentally misses messages.
CharlesOSmith t1_j7fm624 wrote
Reply to When does the body store fat? by fappie6
Not a direct answer to your question, but an important addition for consideration: the lecture in this video describes the important differences in how our bodies treat calories derived from different source molecules. The key comparison starts at 45 minutes in, but the whole thing is worth watching.
CharlesOSmith t1_j503c3s wrote
Reply to comment by magicfeistybitcoin in What's the current scientific consensus on resveratrol extending lifespan? by pixeleos
It's also important to know, that in the case of resveratrol, you can't just look up the literature and get an understanding of how effective it is. There was a fairly large scandal in the field around 2012 which was closely followed by the watchdog site retractionwatch. Now while one researcher publishing fraudulent data does not mean the entire field of research is wrong, it does mean each and every paper needs to be carefully scrutinized to see how heavily it relied on background assumptions made by papers that were later shown to be false. In this case in particular, with the researcher publishing over a hundred of papers a year some highly sited that left a pretty big impact. I can't say for sure how strongly this was felt in the longevity research community, but in the field of cardioprotection, which I was in at the time, it was a big deal.
Even a fairly recent review, which is by in large well and fairly balanced regarding the literature still cites papers from this researcher' publications and doesn't mention that aspect of the field's history at all.
CharlesOSmith t1_j18ozq2 wrote
RNA polymerase is the name for a family of protein complexes that use DNA as a template to synthesize complementary RNA. There are eukaryotic and prokaryotic version of this complex, and different versions are recruited in our cells depending on what class of RNA is being made.
In any event, these are all genes, that are transcribed and translated like any other.
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CharlesOSmith t1_ivz03yb wrote
Reply to comment by tt1702y in Does malnourished parents effect how tall your final adult height would be? by [deleted]
That's not accurate. If the parents are malnourished, that is the trigger for epigenetic markings on their gametes. It doesn't have to be population wide.
CharlesOSmith t1_ivxzaqz wrote
You are asking about epigenetics.
The general idea is that our exposure to our environment can shape our genomes.
In particular there are some types of environmental exposures that can directly indicate health, and living quality, things like starvation, exposure to chronic stress, habitual use of drugs, or exposure to toxins. On an evolutionary scale the system allows the nourished adult to pass that information on to its gametes which then have information saying "things are good, so let's allow for the best growth for which our genes allow", and the malnourished adult to pass that information on to its gametes which then have information saying "things aren't that good, so let's limit growth to the minimum our genes allow."
Its not fully decoded yet, and the generational influence appears to be more extended than just parent to offspring. Its also a highly tunable and modular modification to the genome so there are lots of gradations to the overall outcome.
So you can think of your final height being a range that is possible given your specific combination of genes. Epigenetic markers on those genes may indicate what height in that range is considered to be the target, and your own environment, and nutrition status will influence where your final height lands relative to the target within your range.
CharlesOSmith t1_iuj1wyg wrote
Reply to comment by FunnymanDOWN in What is the actual mechanism by which the body generates a fever? by Pheophyting
according to NPR the record is:
115 degrees: On July 10, 1980, 52-year-old Willie Jones of Atlanta was admitted to the hospital with heatstroke and a temperature of 115 degrees Fahrenheit. He spent 24 days in the hospital and survived. Jones holds the Guinness Book of World Records honor for highest recorded body temperature.
CharlesOSmith t1_iui6voe wrote
Reply to comment by Agouti in What is the actual mechanism by which the body generates a fever? by Pheophyting
That's part of resetting the internal thermostat, so I didn't include it as one of the biochemical mechanisms for generating the heat, but its a good point.
CharlesOSmith t1_iuhrqly wrote
You are right, it is surprisingly difficulty to find the type of information you are asking about when you include the word "fever" in your search.
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Our body heat is regulated by our body's ability to balance of how much heat we generate and how much heat we lose to the environment.
Here are some examples of heat production (notice how many are simply the result of normal metabolims):
-Basal metabolism
-Muscle activity, by shivering and muscle contractions
-Extra metabolism caused by the effect of sympathetic stimulation and norepinephrine, -epinephrine on the cells
-Extra metabolism caused by increased chemical activity in the cells, especially when the cell -temperature increases
-Extra metabolism caused by thyroid hormone and, to a lesser extent, testosterone and -growth hormone on the cells
-Extra metabolism needed for digestion, absorption, and storage of food
-Most of the heat produced in the body is generated in the liver, brain, heart, and skeletal -0--muscles during exercise.
And we balance that by also regulating mechanisms of heat Loss which is determined almost entirely by:
-How rapidly heat transfers from the skin to the surroundings
-How rapidly heat is conducted from where it is produced in the body core to the skin
https://www.ncbi.nlm.nih.gov/books/NBK499843/
A fever triggers an adjustment of where that balance is, so as metabolic processes are triggered to run hotter, our circulatory system is triggered to allow less heat loss through our skin, and we don't sweat.
The term "a fever broke" is referring to a person who after a fever has begun to sweat to allow for the rapid loss of all that heat.
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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4786079/
Fever induction and signal transmission
CharlesOSmith t1_j9ud7ak wrote
Reply to How does adenosine accumulate in brain and cause sleep? by Lojcs
This is a pretty dense review, but it covers your topic extensively. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4544655/
To briefly state one point they examine; the changes in glycogen levels observed in the sleep/wake transition, may be more diagnostic of that transition happening, and not actually a causative agent of that transition.
Similarly two other reviews examining the role of adenosine in sleep found that while adenosine does have a role in sleep, it is much more specific in its function, not a master "go to sleep" signal https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2769007/, and that the role adenosine takes changes depending on where in the brain, and what receptors it is working on https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6650574/
Looking around for publications, its clear that there is a lot of work being done and different camps with different models they are testing. I don't think their is a complete mechanism that everyone agrees on.