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The antibiotic treatment led to altering and/or misreading of genetic code for fatty acids and lipid biosynthesis and resulted in disappearance of some fatty acids and induction of others.
These differing conditions at the substrate led to altering of the coating's chemical as well as phase composition.
It can be concluded that antibiotic treatment at certain antibiotic concentrations led to altering and/or misreading of genetic code for fatty acids and lipid biosynthesis which led to the disappearance of some fatty acids and induction of others [ 25].
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Finally, we found only 2 reviews in which quantitative changes much greater than 50% led to altered conclusions.
Quantitative changes in accumulated 5' Hox may have led to altered onset of Shh expression, resulting in enlargement of endoskeletal elements during fin evolution (Fig. 6).
It is possible that the higher BDI score in the de novo patients led to altered response monitoring (Nc) although the Ne amplitude is significantly reduced in the de novo patients, compared to controls.
This led to altered heterodimerization of the podocin protein.
The structural modification led to altered secondary structure elements, accompanied by an increased hydrodynamic radius.
KDAC inhibitor treatment of HeLa cells led to altered splicing of nearly 700 human genes.
However, disturbed TH levels led to altered hepatic fatty acid composition and glycogen accumulation.
Disruption of these interactions led to altered transcription termination and decreased polyadenylation efficiency [ 12, 13].
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