Why is ATP used as the energy source in all living cells?
All scientists and students studying science know ATP is the "energy molecule." But ask them why, and they probably cannot tell you the answer. ATP is made up of the adenosine base, a sugar, and three phosphate groups bound together like so: O-P-O-P-O-P-O (other oxygens are left out for clarity). Cells cannot use ADP or AMP for release of energy, so I will only focus on the bond connecting the second phosphate to the third phosphate: Phosphorous is a very large atom compared to oxygen. When you have to phosphorous atoms straddling an oxygen atom, it is almost as if that oxygen atom is not there. Bound to each phosphorous is a double bonded oxygen. Due to the size of the phosphorous atom, these double bonded oxygens are so close together, yet they want to repel each other due to the lone pairs of electrons associated with them. This intense repulsion puts immense steric hindrance on the bond between the phosphorous and the oxygen; therefore, this bond carries a lot of energy (-7.3 kcal/mol of ATP). This is why ATP is known as the energy molecule.
Why is some of the energy from glucose "lost" during the formation of ATP through glycolysis, TCA, and the electron transport chain?
If you were to look at the energy stored as ATP from the breakdown of one mole of glucose, it would be around -277.4 kcal/mol. However, the actual energy stored in a mole of glucose is -686 kcal/mol. Where does that difference in energy go? This energy is released as heat during the breakdown of glucose in glycolysis, TCA, and the ETC. The human body must be kept near 98.6 °F for optimal enzyme operation. In other words, this heat is needed to maintain homeostasis.
What changes to the outer membrane of gram negative bacteria can cause a nosocomial organism to resist last resort antibiotics?
There are a few mechanisms that have been recently identified in Acinetobacter baumannii and Enterobacter cloacae. Both of these organisms are nosocomial. This means they are only found in hospitals and resist many first line and last line antibiotics. In A. baumannii, reinforcement of Lipid A acylation has been identified as a mechanism by which this bacteria can resist colistin. Colistin is known as a drug of last resort for gram negative infections due to the failure of more common antibiotics such as tetracycline, ciprofloxacin, etc. This reinforcement occurs when a new fatty acid chain is added to the Lipid A molecule sometimes increasing the number of fatty acid chains to 7 per Lipid A in the outer membrane. In E. cloacae, Lipid A is also altered but in a slightly different way. Instead of altering the fatty acid chains, the hydrophilic sugar portion of lipid A is modified. 4-amino-4-deoxy-L-arabinose is added to the lipopolysaccharide region of the Lipid A molecule. These mechanisms have been recently identified as reasons why these bacteria resist colisitin (polymixin e) treatment.