Відео

Total energy of the blood falls, including its pressure, due to resistance along the vascular tree. The resistance is largely friction with the vessel walls and the energy is lost as heat. As the vena cava are farthest from the initial pressurization of blood at the heart, the pressure there is very low. Also, according to Bernoulli's equation, due to conservation of energy, as the cross sectional area falls and velocity increases in the large veins (coming from the large total cross sectional area of the capillaries), the pressure must fall to compensate (swapping potential energy for kinetic, essentially)

I don't know what the linkage is between muscle tension, mTor and protein synthesis. I know there are several stimulating factors which, based upon their characteristics must activate mTor in separate ways. Those include mechanical stress (could be a whole variety of potential pathways here), insulin, nutrients, GH, IGF and others.

Prego... glad you found it helpful

Thank you! Glad you found it helpful

If you're looking for specifics of why certain epicardial action potentials are shorter than endocardial ones, I don't think I've ever seen the detailed rationale for the difference in plateau duration. Certainly, it has to do with altered kinetics of the channels involved (I think I recall someone saying it had something to do with the endocardial cells being squashed up against the incompressible blood). If the question is more about why does repolarization occur first in the last regions to depolarize then the answer is in the variation of the action potential duration. If early activated cells (endocardial) have longer action potentials than late activated cells (epicardial) then this can occur. Note that this is absolutely essential and if impeded the heart is apparently far more susceptible to arrhythmias.

There are a variety of mechanisms, but it includes alterations in the kinetics of the voltage-gated channels, changes to their expression (numbers/density) or changes in the electrical properties of the cell itself (e.g., altered cell morphology can alter how electrotonic current flows and, therefore, opens downstream voltage-gated channels). That last one would be altering how a voltage change affects the channels rather than a change to the channels themselves.

glad it helped you out!

Great! glad you are enjoying them/finding them useful

Thanks!

Ha! Glad it is helping her out

Glad you found it helpful!

Thanks! I hope to make more this summer

You're welcome!

Not sure what the question is here. Conotoxins and agatoxins antagonize those channels, inhibiting neurotransmitter release. Depending on if the NT is stimulatory or inhibitory, the downstream effects could be over or under stimulation. In the video I'm using skeletal muscle as the target tissue and ACh is always stimulatory there.

Glad you find this useful!

Professional phagocytes are very good at removing opsonized antigens due to the presence of specific membrane "opsonic" receptors (e.g., receptors for antibodies or complement proteins). Non-professional phagocytes such as fibroblasts or many epithelial cells may also occasionally phagocytose other dead or dying cells using "non-opsonic" receptors that are more generalized.

Does seem a bit odd....but I'm no immunologist. Maybe ask an expert in that specialty.

So glad you find it helpful. More to come this summer.

I can't say positively, but I would assume some do - remember, there is a scale of adaptation rates, not just fast and slow. I assume you are correlating with those fast receptors that fire only at onset and offset of the stimulus. Certainly could be the case and my guess is it would be at least partially due to mechanical "recoil" of the filtering apparatus (e.g., Pacinian corpuscle lamellae).

Glad you found it useful!

So glad to hear it!

you bet!

Glad to hear it!

Quick! Tell my wife! 😜

You bet!

You bet!

Excellent! Glad to hear that.