Addition: sometimes, the receptor might not do something directly. Instead, it activates second messenger (intracellular messenger) that may do something, e.g. like what you found on GPCR.

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If you have the same number of atoms and you don't consider any possible subsequent decays, yes.

If you store a sample of initially pure Sr-90 then over a week or so its decay product Y-90 will accumulate until you get one Y-90 decay per Sr-90 decay.

It looks like the study had a multi-pronged approach, but in terms of the mechanism of action, the study was focused more on the brain than the rest of the body, and the authors posit that the areas where the semaglutides are acting are resulting in decreased appetite.

The semaglutides are analogues of GLP-1 (glucagon-like peptide 1) which is released from cells in the intestine, with receptors in the body including in the pancreas, stomach, kidney, lung, heart, skin, immune cells, and the hypothalamus. It is one of the hormones involved in regulating blood sugar and digestion, partially through its regulation of other hormones.

So to sum it up, I don't think they just make you eat less, it seems like there's a hormonal/nervous system/gastrointestinal overlap in mechanism of action.

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Living cells are "factories"for viral replication, and living cells are limited resources.

Hence viruses would be at an advantage if they are able to "control" more hosts by replicating more efficiently and/or modify the hosts' behaviour.

The easiest way is probably to just heat them under dry nitrogen or (even better) vacuum.

Assuming it's not soluble, you could dump in some solvent with a water azeotrope and distill it off.

For samples with the same number of atoms (and undergoing the same type of decay) yes.

The activity means the number of times an atom decays per unit of time and the half-life is the time in which half of the atoms in a sample decay.

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There are two functions happening usually: Binding and Activating, for an agonist.

For an antagonist, you'll have Binding and Blocking. Usually you'll have a greater binding affinity for antagonists that can knock an agonist off of the receptor.

I know you're mentioning messenger proteins, but a chemical example is how Naloxone will knock off morphine from a receptor due to its higher affinity. The naloxone then blocks morphine from activating the receptor.

When an agonist binds, it can change the channel's confirmation allowing influx, or efflux of ions. Depending, this can increase or decrease the chances of an action potential to occur.

Sometimes things get even more complicated. The chloride channel that Valium works on, the GABA receptor, has receptors for GABA and receptors for benzodiazepines (valium-type drugs).

One single channel, or one single neuron may not play a large role, BUT..., When hundreds and thousands and millions of receptors and neurons are affected, you see an overall effect in the subject.

It's more that a certain number of postive centres at a certain distance line up with a number of negative centers at the same distance but, there is definatly the fitting part too proteins fold certain ways and are generally stable unless denatured.There is also the fact that a particle can be Sterically hindred so that there are directions it cannot bond from because of other groups blocking.They don't fit at puzzle pieces but as semisolid clouds of matter where one part of one molecule needs to be the right size and align properly with the right groups on the other molecule.

Please add citations for these studies.

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> OP, the virus mentioned doesn't really represent an organism because it requires the mechanisms of a cell to replicate

There are a slew of obligate parasitic eukarotes that this definition disqualifies as an organism.

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