Why are noble gases unreactive?
Elements react with one another for many different reasons, but one of the main reasons is because the unfilled and unbalanced number of electrons they possess. All elements, besides those of the noble gases, contain unfilled electron orbitals. The inner most orbital for every atom contains at most two electrons and if the atom contains anymore electrons they are filled in other orbitals further from the nucleus. Each orbital after the inner most orbital can contain a maximum of eight electrons and again if the next orbital fills its orbital with eight electrons and still has more remaining, they go to the next outer orbital until all the electrons have a place to reside respectively. Noble gases are special in that all their orbitals that contain electrons are fully filled. Neon for example has a total of ten electrons per atom in its neutral state. The first orbital, which can only contain two electrons, is fully filled with its two electrons and since there are a total of ten there are still eight electrons remaining. These eight electrons are filled in the next orbital out and as mentioned before, each orbital after the first can hold eight electrons so therefore the remaining eight electrons from neon fully fill the orbital. Since the two orbitals neon atoms use are fully filled, there is no room for electrons to be added into the atomic structure and since being fully filled is most stable for the atom, the atom most certainly won't want to give up its electrons as well. Since there are no electron transfers going on, they are almost never reactive since their electron orbitals are completely satisfied and are content with keeping and not gaining anymore electrons.
Describe how the renin-angiotensin system works in the body and explain why ACE inhibitors are used in individuals who have high blood pressure.
When blood reaches the kidneys, it enters into a renal corpuscle to be filtered. Some of the components within the blood are reabsorbed into the body while others are excreted out by the process of urination. There is a very special component of the renal corpuscle however that checks the sodium content of the blood and determines whether or not it is low and needs to reabsorb sodium or high and needs to be excreted during the filtration process. Upon entering into the renal corpuscle, the blood passes through the juxtaglomerular apparatus. The specific structure known as the macula densa determines the concentration of sodium and whether or not it needs to be reabsorbed or excreted. The macula densa is a set of specialized cells that hug a port of the ascending limb of the same nephron and determine the concentration of sodium. In the event that the sodium concentration is low, the cells within the macula densa send a signal to the juxtaglomerular cells signaling the release of renin. Renin then enters into blood circulation and targets angiotensinogen and acts on this protein by cleaving a small portion of its amino acids. Angiotensinogen is a zymogen, meaning an inactive substance, until it is cleaved by renin into what is now angiotensin I. Angiotensin I is then converted into angiotensin II by an enzyme known as angiotensin converting enzyme or ACE for short. Angiotensin II works by constricting the arterioles causing blood pressure to increase. At the same time, angiotensin II also acts on the adrenal cortex in the adrenal gland to produce aldosterone. Aldosterone then is able to target the distal convoluted tubule located near the collecting duct of each nephron to cause the re-absorption of sodium back into the blood and out of the filtrate of the nephron that would otherwise be later held in the bladder for excretion. Since now there is more sodium in the blood then in the filtrate, water follows the sodium into the blood as well by a simple understanding of concentration gradients. With more water now back in the blood, the pressure of the blood is allowed to increase. This whole process produces a result of an increase in blood pressure whether it is by acting directly on the constriction of arterioles or by the process of adolsterone. This poses an issue for individuals with high blood pressure. This process further increases blood pressure so if something is inhibited in the pathway, it can stop the increase of blood pressure. One of the initial steps in this system is the conversion of angiotensin I to angiotensin II. Without angiotensin II present, neither arteriole constriction or aldosterone release will occur. The enzyme mandatory in this conversion as previously stated is angiotensin converting enzyme or ACE so by inhibiting the functionality of this enzyme, the renin-angiotensin system is blocked altogether and thus blood pressure cannot be increased. This is how many individuals regulate their high blood pressure and is an effective target in doing so.
Please explain why the antiderivative of e^x is e^x, but why the antiderivative of e^2x is not e^2x.
Most students struggle with the derivative and anti derivative of e. If you simply understood the root of how e works, all the other problems you encounter with it are easy. The anti derivative of e^x is simple. Start by looking at the exponent, in this case it is just x. In order to find the anti derivative all you need to do is divide the original function of e, so in this case, e^x, but the derivative of the exponent. The exponent in this example is simply just x and the derivative of x is 1. So now take the original function e^x and divide by 1. The anti derivative therefore is still e^x because anything divided over 1 is just itself. Now let us take a look at e^2x. Look at the exponent, in this case it is 2x. What is the derivative of 2x? It is 2. So the original function divided by the derivative of the exponent in this case is (e^(2x))/2.