Acidithiobacillus ferrooxidans is an acidophilic chemolithoautotroph that is important in biomining and other biotechnological operations. The cells are able to oxidize inorganic iron, but the insolubility and product inhibition by Fe(3+) complicates characterization of these cultures. Here we explore the growth kinetics of A. ferrooxidans in iron-based medium in a pH range from 1.6 to 2.2. It was found that as the pH was increased from 1.6 to 2.0, the maintenance coefficient decreased while both the growth kinetics and maximum cell yield increased in the precipitate-free, low Fe(2+) concentration medium. In higher iron media a similar trend was observed at low pH, but the formation of precipitates at higher pH (2.0) hampered cell growth and lowered the specific growth rate and maximum cell yield. In order to eliminate ferric precipitates, chelating agents were introduced into the medium. Citric acid was found to be relatively non-toxic and did not appear to interfere with iron oxidation at a maximum concentration of 70 mM. Inclusion of citric acid prevented precipitation and A. ferrooxidans growth parameters resumed their trends as a function of pH. The addition of citrate also decreased the apparent substrate saturation constant (KS ) indicating a reduction in the competitive inhibition of growth by ferric ions. These results indicate that continuous cultures of A. ferrooxidans in the presence of citrate at elevated pH will enable enhanced cell yields and productivities. This will be critical as these cells are used in the development of new biotechnological applications such as electrofuel production.
The chemolithoautotroph Acidithiobacillus ferrooxidans has been proposed as a potential electrofuel synthetic platform, and its growth medium is engineered to increase its conductivity and energy density, thereby improving viability of the process. The ion V 31 is used as an indirect electron supplier together with Fe 21 to grow A. ferrooxidans to increase the energy density of the medium, overcoming the Fe 31 solubility limit. A medium containing 10 mM Fe 21 with 60 mM V 31 was able to support cell growth to a final cell concentration very similar to medium of 70 mM Fe 21 . Integration of the biological process with an electrochemical reactor requires, for economical operation, a medium with high ionic conductivity. This is achieved by the addition of salt, and Mg 21 was found to be least toxic to the bacterium. A concentration of 500 mM Mg 21 is optimal considering constraints on bacterial growth and electrochemistry.
Sars-Cov-2 binds to ACE-2 receptor, resulting in excess amount of ACE-1 dependent angiotensin production. Sars-Cov-2 has four stages of symptoms, 80% if symptomatic patients have been shown to only suffer a “mild” disease course, meanwhile 20% endure stage 3, which is characterized by conditions such as ARDS, shock, and multiorgan failure. The binding of Covid to ACE receptors promotes the conversion of angiotensin 1 to angiotensin 2, constricting blood vessels, leading to thrombosis, lack of oxygen, and Ischemia. In Cardiac injury, the Covid receptor becomes represented in the heart, inducing in a pro-inflammatory increase, high cytokine concentrations, myocyte cardiac apoptosis, cardiac arrythmia, cardiac fibrotic tissue, myocarditis, and Heart failure. Cytokine storms associated with production of S1P, TNF activation of MMPs prompts myocardial depression, dilation of LV, and Heart failure. Covid-induced Sepsis corresponds with dysregulated host immune responses, increased pro-inflammatory mediators, fluid leakage, increase in cGMP, LV dysfunction, and arrythmia. Blood clots in the capillaries surrounding the kidneys generate renal impairment. Progression of renal impairment generates a state of systemic inflammation. Increased sodium content in the body results in elevated plasma blood and uncontrolled hypervolemia. Emotional and physical stresses during Sars-Cov-2 induce blood gas changes, angiotensin converting enzyme imbalance, and immune/inflammatory factors. Overactivation of the SNS induces Takotsubo syndrome. In ARDS, fluid leak in the membrane gas exchange region of the lung results in vascular remodeling. Inducing further vascular remodeling as part of the body’s response to hypoxia. The constant vascular remodeling triggers RHF.
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