Hey, Brian. Yes, I heard the question. Hey, I heard the question very well. So first I want to reiterate what Brian had said about - we were talking about nitrite as an n ion versus nitric oxide. So, nitrite is a precursor and the body’s largest pool of nitric oxide, but it is not directly through or directly just generating nitric oxide. That's really not what's happening when we administer inhaled nebulized nitride. Nitrite has a plasma half-life of about 43 minutes. However, the hemodynamic half-life appears to be much longer. The drug is really - it’s actively in its present form as nitrite. It can result in the generation of nitric oxide particularly as part of hypoxic’s beta signaling. So, hypoxic vascular signaling depends on the generation of nitric oxide as a local invasive dilator in ischemic let’s say, you know, muscle or ischemic areas, because the traditional formation of nitric oxide requires oxygen. So, this bypasses the nitric oxide [indiscernible] pathway and is able to augment local nitric oxide production through reduction of nitride to nitric oxide. But what we're seeing hemodynamically is the hemodynamic effects are much longer than the plasma half-life. We see after repeat dosing that other longer lasting nitrosyl pathway molecules go up like as nitro [indiscernible]. So this has more profound effects on the nitric oxide pathway, but not just to generate nitric oxide. Your question about actually causing stiffening, we've seen the opposite. There are some good animal data looking at aged animals, you know, at aortic stiffening in aged animals who have high cholesterol and high blood pressure. And what we see is that aortic compliance actually gets better using nitrite. In the first study that Brian described that is the ascending dose those study where it's an open label study but we’re giving ascending doses. In that study, we compare directly to nitric oxide. So we have a nitric oxide phase. We have a nitrite phase. And we see differing hemodynamic changes. For instance, nitric oxide alone causes pulmonary capillary wedge pressure to rise, which you don't want to happen because that’s, you know, causing alveolar flooding, increasing left atrial pressures, and back pressures in the lungs, and it actually worsens HFPEF. We see the opposite effect. So, we see venodilation. We see decreases in pulmonary capillary wedge pressure that we feel will result in improved exercise tolerance. So to get your third point, effect on other dissolved gases, we immediately after giving nitrite, we can measure exhaled nitric oxide increase from the lungs. We can measure that, but that effect is around seven minutes. By 15 minutes most of it’s gone and absorbed into the circulatory system. So, we don't have an effect on oxygenation. We don't have an effect on carbon dioxide or other measures like that. Did that answer your question with way too many words?