From memory, organic molecules have rigid structures but also bonds that rotate so macro-molecules can changes shape to envelope a ligand. This is sometimes called the induced-fit model. My general conception of which is a bit like a catcher's mit.

Because of thermal energy equilibrium, a ligand is moving much faster relative to an enzyme. So it'll arrive at break-neck speed and smack into the catcher's mit and then probably bustle around a bit. The ligand and its associated water bubble (closely interacting water molecules) will interact with arms of the enzyme, attracting them to move and grasp the hydrated ligand. Eventually this movement will displace the water molecules, leaving only the chummy direct embrace occuring between the ligand and the protein. They are compatible and decide to make a night of it. So the big one is hugging the little (or the mit is holding the baseball). At this point my dualing metaphors break down because they interact chemically, often with the help of a phosphate molecule to power the little (nano) machines into doing some metabolic magic.

They then decide that they need some time apart to get their heads straight and find themselves, leaving only an ambivalent ADP molecule looking on as they make their separate ways in the endless hustle and bustle (thermal agitation) of the molecular realm.

My metaphor of the catcher's mit seemed to metaphorphose into more of a romantic interlude but you get the idea. Molecules in this situation are basically like ravers in a mosh-pit who are attracted to one another, hug, make out briefly, then realise that they have to find their friends.

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Some ligands will have ionic areas on the molecule (which is what I suppose you mean by charges), such as an amino group (R-NH3+ at physiologic pH) or a carboxyl group (R-COO-). And amino acid side chains within the protein binding site can be like that as well. But the presence of a charged functional group is not necessary for ligand binding. You can have ion-dipole interactions (there would be a charged functional group with that), dipole-dipole (no charged group), hydrogen bonds (no charged group), and hydrophobic van der Waals interactions (no charged group) that all increase binding affinity. There probably are issues regarding the presence of water molecules as well (aqueous solubility), but that's a supposition on my part.

We really don't use the term bonding for the insertion of a ligand into a protein binding site. It's binding, a much more general term. You don't actually form a bond (covalent, ionic), but of course you can have a hydrogen bond, which are transient and reversible. The most important thing for a good fit, however, is a matching of the shape/conformation of the molecules. The hand in a glove analogy is a good one.

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1. Is there an effect of cannabis abuse on brain structure? Evidence is mixed. While there are certainly correlations, it is hard to conclude that it is a causal relationship. While longitudinal evidence supports a causal effect, data from twin and genetic studies show the same genes that are associated with cannabis use are also associated with brain structure (and probably brain development). So we cannot rule out causes besides cannabis use (e.g., behavioral traits associated with a greater likelihood of using cannabis are associated with smaller brain structure). Some recent interesting work has also shown that associations with cannabis are in fact attributable to polysubstance use - not cannabis alone.

2. If there are changes caused by cannabis, are they permanent? As opposed to alcohol, there have been very few studies of cannabis abstinence, though those that exist show some promise that any effects of cannabis on brain structure are probably reversible (provided use is stopped early enough).

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It may be. I haven't read the studies that report this with enough attention to determine if it was 100% well realized or not, but the review article I cited seemed very interesting and comprehensive, citing several papers with different conclusions. Most of them appear to agree that there is a correlation between psychotic alterations and marijuana, but more research is definitely needed to fully understand the mechanisms and possible causality.

If the ligand doesn't fit, it doesn't have to be "kicked away." More like "randomly bounced away." The receptor doesn't have to do anything for the non-ligand molecule to move away. If you look at the wiki for Brownian motion you'll see how molecules are in constant motion. Things suspended in a fluid are not just sitting still... They're bouncing around like a room full of caffeinated 5 year olds.

Or is it that people that are schizophrenic are more prone in % to test drugs than "normal" people, for the lack of a better word?

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I know there’s a lot of conjecture of cause/effect around this, as those in the early stages of developing schizophrenia are much more likely to “self medicate” even unknowingly.

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The superconducting coils that generate the magnetic fields for MRI and NMR spectroscopy systems have zero DC resistance.

They usually operate in persistent mode, meaning that there is no power supply attached to them. As long as you keep them superconducting, you can have hundreds of amps circulating in the coils without any change in the current over several years.

This study from 1979 suggests that there is a decrease in heat tolerance after heat stroke. It’s behind a paywall but the abstract is available. Individuals with and without previous heat stroke performed exercises under different heat conditions. Those with previous heat stroke were unable to complete the exercises under severe heat load, while every individual in the control group completed the exercises. The abstract does not mention how recently the subjects experienced heat stroke.

Cleveland Clinic has an article on heat stroke that also claims individuals who previously had heat stroke were more likely get it in the future, though they don’t reference the research that led to that claim.

This research from the University of Florida doesn’t focus on heat tolerance after heat stroke specifically, but they have found epigenetic changes in mice following heat stroke. They believe this increases the risk of metabolic disorders and weakens the immune system.

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Show me where I specifically said it WILL, for sure. I said it CAN.

I am only half joking when I said at the start of my post that I hope it does, because otherwise I have been wasting my time! It helps a lot when you have occasional bouts of anxiety stemming from trauma, I know that much. A bit of a rewire is no bad thing when what you start with isn't any fun to deal with.

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Got it. Thanks!

The high impedance medium can carry more energy than the low impedance medium. So when a wave goes from high impedance to low impedance some of the energy is reflected back because it can't go forwards.

Sort of yes. They both “block” something but inhibitor is often talked about in reference to enzymes while the latter is normally in reference to a receptor.

Competitive binding means it binds in the same place as the endogenous ligand.

I think the question is more aligned to whether a person's body responds in a different manner after a heat stroke than before. In other words, does the immune system or fight or flight mechanism recognize sooner that the body temperature is getting too high and start causing symptoms of heat exhaustion?