234ff

Flip-flopping of lipids (and in proteins it is impossible) in plasma membrane is rare due to high energy barrier (video ref). However, it is an important mechanism since it allows asymmetric distribution of lipids in cell membrane. Question: If a specific lipid is flipped E.g. phosphatidylinositol from cytoplasm side to extra-cellular side (E.g. by flippase), what mechanism can the cell do to ensure it will stay towards the extra-cellular fluid side but not flip-flop AGAIN (i.e. establish the asymmetry & enable its function)?

I encountered catalytic hydrogenation recation, where alkene is converted into alkane using Pt/C or Pd/C as catalyst, but I have a question: Bond dissociation energy of H2 = 436kJ/mol. But when H2 is adsorbed on the metal surface, the bond is broken. How come this simple step can break this strong bond? Where does the 436kJ energy come from / what gives this activation energy?

According to my knowledge, negative deviation of the Law is because: - solute-solvent intermolecular attraction is larger in magnitude than both solute-solute & solvent-solvent interactions, so solution reaction is exothermic. With very strong interactions, molecules become less able to escape from the liquid surface and form vapor, hence a lower vapor pressure than Raoult's Law prediction. My question: In terms of intermolecular adhesive force(PE), the above explanation is true. However, the reaction is exothermic (since dH(soln) is negative usually), meaning heat is given out. This increased temperature of the solution hence the KE of molecules. According to the Maxwell-Boltzmann distribution, a higher % of liquid molecules can escape from the liquid surface can into vapor phase. Won't this increase the vapor pressure of the solution instead of a negative deviation? Vice versa, for endothermic dissolution reaction, positive deviation of the Law occurs, but the temperature of the solution drops, won't this pull down the vapor pressure of solution? Thanks a lot in advance and please correct me if I have made any mistakes!

I am learning myology and encountered 2 problems in tetanus and summation: Unfused tetanus is just a continual summation of twitches if I am not mistaken. However, is it a MUST for summation / unfused tetanus to constantly increasing muscle tension from the photo (the graph) i.e. is this the definition? Since we are in unfused tetanus when we hold something, and I can’t feel my biceps are constantly increasing in contraction / tension. (to my understanding, complete tetanus is when we are lifting up very heavy things only as it utilizes too much ATP) Can I say the muscles are in tetanus during contracting (lifting), and also in tetanus during constantly contracted state (keep the thing holding up) Since tetanus is just a frequent action of sliding filaments, which is common in both actions? Also, during tetanus, I don’t need to shorten my muscles anymore (just holding something still), but myosin heads are still power-stroking to shorten the sarcomere/muscle, may I ask how to explain this? Thank you very much.

(I am new to this forum so please tell me how to improve my questions) I am wondering what really powers the myosin head to undergo the power stroke to push the actin filaments towards the M-line. I have 2 thoughts: when ATP in the myosin head gets hydrolyzed, the energy released is stored in the head. This energy powers for the power stroke. when ATP is hydrolyzed, inorganic phosphate and ADP leave accordingly (90deg--> 50deg --> 45deg), the conformational changes of myosin head proteins cause the power stroke. I think (2) is more plausible as the order of actions (moving actin filaments by 6.7nm + 1.3nm in order) is more 'conventional'(wiki), rather than a single action (using energy by ATP hydrolysis, a 1-step boost of energy). However, if (2) is really correct, then may I ask what is the energy released in (1) used for in the myosin head, does it just simply fade away as heat energy? thank you very much :)