My bank in LT requires proof of income, and my income is lower than minimum, because I am a student of CS so far only. And i do not need 6 month or more to return it, I may return in a month.
He could have tried injecting senolytics into the weared disks to remove senescent inflammatory phenotypes, as there is some research in senolytics (dasatinib+quercetin) improving arthritic knee joints by removal of senescent inflammatory cells which allows the new cartilage to grow.
Reduced skeletal muscle tone during sleep is pretty much established. If you find out, that there remains some increased muscle tone which correlates with insomnia or reduces the efficiency of PTAS, you could target it. Though you're already targeting it indirectly via delta waves.
That's ok. There just seem to be no explicit mentioning of that, that individual differences in real-time will be taken into account, just some textbook style description.
Have you considered regulating skeletal muscle tone?
There is no information on what do they actually measure in every individual. Without some real-time feedback it seems somewhat not enough basis to deliver the treatment to the intended target. (But if they're hiring...)
If 40 times a second is 40 Hz, than this frequency is pretty high for a deep sleep (in humans), 40Hz would mean some intense pattern recognition/focused attention.
In parallel with Darwin also try more recent advancements,like Don Hoffman's "The case against reality", where they prove that the probability that evolution will equip an organism to see the true reality is Zero.
100x was a demo, not an actual number. But please explain how does intracellular content with DNA, RNA, proteins, structural organoids and all of these metabolic constituents [0] is supposed to be the density of water. You want the cells in an endotelium of a blood vessel to float, allow the blood to get into the wall of the vessel and get hematomas and hemmorhages?
>>how is the intracellular space denser than the extracellular?
Gemini:
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Yes, the intracellular space is denser than the extracellular space:
Here's why:
Packing: Cells are packed with molecules like proteins, carbohydrates, and nucleic acids. These molecules take up a significant amount of space within the cell, leaving little room for just water.
Solutes: The intracellular space contains a higher concentration of dissolved molecules (solutes) compared to the extracellular space. This contributes to a higher density.
Extracellular Matrix: The extracellular space, on the other hand, contains a looser network of connective tissues and fluids like interstitial fluid. This allows for more space between molecules, resulting in a lower density.
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>>Still, trying to really figure out what the 'intention' was all those billions of years ago is hard
With this logic you'll need another billion of years to randomly figure it out. I'd rather focus on how/efficiently does such position contribute to a specific current experimental methodology or results.
All the empirical examples you mentioned pertain to the extracellullar space. So is this stochastic modelling also true in the intracellular space, which is like 100x times denser structurally, biochemically and bioelectrically (given that all biochemistry is effectively a type of electrical process involving very refined transfer/manipulations of charge densities), and allows to explain how do hundreds or thousands of biochemical reaction inside cells happen as required without interfering with each other?
Evolution also "tries" to save energy anywhere possible, so spending energy on the synthesis of endogenous ligands, which eventually will be discarded, seems a bit redundant. There is also a theorem in evolutionary game theory, that probability that natural selection will allow an organism to see reality as it is (=the truth) is exactly zero, as it's enough to make it just "good enough". I was arguing about that with Gemini, and it agreed with me. My point is that "evolution" is just a tool (like ChatGPT) with it's own instrumentally limited pool of empirical data (80% of which was also obtained from macroscopic enough observations rather than reverse engineering or experimentation) to build upon.
I actually want to apply one EE concept, which has some experimental basis. The reason why I am digging this, is that I am searching for some possible explanations of a couple of dozens of experimental studies in bioelectrics/magnetics I found. (though won't discuss in depth on a public forum)
Yea, that's correct. Though I may probably omit proteins and large moelcules, requiring transport vesicles and any specific transport mechanisms.
Stochasticity sounds like there has been performed some theoretical modelling to infer this. But does it imply that there would be some tiny % of any ligand molecules - endogenous or exogenous - which would just by chance get "an empty run" and didn't bind to their receptors (though structurally they're fine ligands with high affinity) and would be removed via waste removal systems? Is there any experimental evidence for this, like some study using radiolabelled high affinity ligand molecules to see what % of them gets into "an empty run"?
The mean free path seems sort of sensible in the extracellular space, though it still seems that the variables affecting mean free path (large amounts of receptors and binding thingys, the very small spaces, and the temperature) may be not enough. But wouldn't mean free path be near zero inside cells, where every nanometer should be occupied by some other biochemical pathway/reaction or bioelectric activity?
>>Neither you nor I will see biology as a mature science.
I personally wouldn't care a lot about proving anything to anybody in some absolute sense, but first of all to prove instrumentally and make stuff work for myself at least. I think that any biology student with the descent understanding should have some mini lab for personalized medicine (as e.g. Sinclair mentioned that his recent research on using 6 chemical compounds for OSK epigenetic reprogramming (rather than bulky viral vectors) can be done by any biology student).
I read one neurosurgeon (developing a theory of quantum biology) tell that mitochondria can develop voltage potentials comparable to a lightning bolt. Then searched a bit in PubMed and found something like still up to a couple of hundreds or a hundred milliVolts.
But I was curious, what do you think about the ways by which ligands find their receptors inside or outside cells in a dense bioelectrical and biochemical environment (as described here [0]). When I asked on stackexchange, they gave me a link about gradients and concentrations, but my question was about the very beginning of ligand's effect when it needs to find and activate at least one receptor. And no receptors seem to be able to "sense" a piece of space with a ligand's concentration, as they need direct binding of a ligand, but before this how does a ligand find a way to the receptor?
This may differ whether its a small or large molecule ligand, but my ligands of interest are ions (Ca/Mg, Na, K ,Cl; Li), peptides, anticancer drugs with metallocomplexes, ion channel drugs and similar drugs.
That's been reiterated by Levin at almost every presentation. Maybe he's overgeneralizing or there's actually a lack of specific experimental context or reference to a specific study. Maybe "anatomy" is a bit too broad of a term, and the thing inferred is some overall macroscopic patterning, so can't say definitely "untrue", as I haven't yet dedicated time to delve into specific articles and been just consuming lectures/presentations.
But I remember he was mentioning some study in left/right asymmetry in DevBio, where they've shown that it's cell potentials/bioelectric signalling and not genes that determine the left/right asymmetry in embryos.
>>When we say voltage gradient, think the traditional ions and the like. But also think of the voltage gradient that a protein can have too, with binding pockets and stuff. Think voltage gradients that are held in place by lipid rafts on the membrane too. Think also the osmotic potential that ion concentration will have, not just the raw total voltage of a voltmeter. There are a lot of components, and therefore gradients, that make up the voltage potential.
It seems that both Claude and you use "voltage gradient" and "ion gradient" interchangeably, which may be not technically correct enough. In electrical engineering voltage = potential = charge difference btw 2 points = the driving force that drives a current to "flow" from a point of bigger potential to a lesser one (typically). Thus it is voltage (or a field) that will drive an ion or any charge gradient.
At least in a specific experimental context and with specific animal models. When they mixed the embryos of a frog and an axolotl, there were no genes in their genome which could predict whether a "frogolotl" will have legs.
When in 18xx FDA or its precursor was being formed, its goal was to confine various "bioelectrical woo" present in medicine and biology at that time. And back then there was Rife's microscope, for example, which was able to accurately image living cells.
Yet no-one tried to account for the cumulative damage/adverse effects done by FDA approved treatments in comparison with a potential or actual damage done by such "woo".
With such apparent speed and quality of research thought we will never have anatomical compiler, let alone electroceutocals and anthrobots, on a routine basis at least in the next couple of hundreds of years.
