The synthesis of gold nanoparticles is dependent on both the concentration of trisodium citrate dihydrate and the time that it interacts with tetrachloroauric acid. A wide range of gold nanoparticles with various sizes and dispersity can be produced based on control variables, such as time of reaction and acid concentration, using a similar approach to that of the Turkevich model. In this model, the pH of the solution decreases slightly throughout the reaction (0.005 unit/min) due to the chemical interactions between trisodium citrate dihydrate and tetrachloroauric acid. Dicarboxy acetone is formed during citrate oxidization, resulting in gold nuclei formation over time. In addition, gold nanoparticle nucleation causes pH fluctuation over time based on gold nanoparticle sizes. An inverse correlation (coefficient of smaller than −0.97) was calculated between the pH and reaction time at different ratios of trisodium citrate dihydrate to tetrachloroauric acid. Regression analysis was used to develop a model for the prediction of the size of gold nanoparticles ranging from 18 to 38 nm based on the concentration of trisodium citrate dihydrate and the reaction time.
Staphylococcus aureus is one of the most common opportunistic human pathogens causing several infectious diseases. Ever since the emergence of the first methicillin-resistant Staphylococcus aureus (MRSA) strain decades back, the organism has been a major cause of hospital-acquired infections (HA-MRSA). The spread of this pathogen across the community led to the emergence of a more virulent subtype of the strain, i.e., Community acquired Methicillin resistant Staphylococcus aureus (CA-MRSA). Hence, WHO has declared Staphylococcus aureus as a high-priority pathogen. MRSA pathogenesis is remarkable because of the ability of this “superbug” to form robust biofilm both in vivo and in vitro by the formation of polysaccharide intercellular adhesin (PIA), extracellular DNA (eDNA), wall teichoic acids (WTAs), and capsule (CP), which are major components that impart stability to a biofilm. On the other hand, secretion of a diverse array of virulence factors such as hemolysins, leukotoxins, enterotoxins, and Protein A regulated by agr and sae two-component systems (TCS) aids in combating host immune response. The up- and downregulation of adhesion genes involved in biofilm formation and genes responsible for synthesizing virulence factors during different stages of infection act as a genetic regulatory see-saw in the pathogenesis of MRSA. This review provides insight into the evolution and pathogenesis of MRSA infections with a focus on genetic regulation of biofilm formation and virulence factors secretion.
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