"Soft and rigid" dithiols and Au nanoparticles grafting on plasma-treated polyethyleneterephthalate

Surface of polyethyleneterephthalate (PET) was modified by plasma discharge and subsequently grafted with dithiols (1, 2-ethanedithiol (ED) or 4, 4'-biphenyldithiol) to create the thiol (-SH) groups on polymer surface. This "short" dithiols are expected to be fixed via one of -SH groups to radicals created by the plasma treatment on the PET surface. "Free" -SH groups are allowed to interact with Au nanoparticles. X-ray photoelectron spectroscopy (XPS), Fourier transform infrared spectroscopy (FTIR) and electrokinetic analysis (EA, zeta potential) were used for the characterization of surface chemistry of the modified PET. Surface morphology and roughness of the modified PET were studied by atomic force microscopy (AFM). The results from XPS, FTIR, EA and AFM show that the Au nanoparticles are grafted on the modified surface only in the case of biphenyldithiol pretreatment. The possible explanation is that the "flexible" molecule of ethanedithiol is bounded to the activated PET surface with both -SH groups. On the contrary, the "rigid" molecule of biphenyldithiol is bounded via only one -SH group to the modified PET surface and the second one remains "free" for the consecutive chemical reaction with Au nanoparticle. The gold nanoparticles are distributed relatively homogenously over the polymer surface

Comparative Lipidomics in Clinical Isolates of Candida albicans Reveal Crosstalk between Mitochondria, Cell Wall Integrity and Azole Resistance

Prolonged usage of antifungal azoles which target enzymes involved in lipid biosynthesis invariably leads to the development of multi-drug resistance (MDR) in Candida albicans. We had earlier shown that membrane lipids and their fluidity are closely linked to the MDR phenomenon. In one of our recent studies involving comparative lipidomics between azole susceptible (AS) and azole resistant (AR) matched pair clinical isolates of C. albicans, we could not see consistent differences in the lipid profiles of AS and AR strains because they came from different patients and so in this study, we have used genetically related variant recovered from the same patient collected over a period of 2-years. During this time, the levels of fluconazole (FLC) resistance of the strain increased by over 200-fold. By comparing the lipid profiles of select isolates, we were able to observe gradual and statistically significant changes in several lipid classes, particularly in plasma membrane microdomain specific lipids such as mannosylinositolphosphorylceramides and ergosterol, and in a mitochondrial specific phosphoglyceride, phosphatidyl glycerol. Superimposed with these quantitative and qualitative changes in the lipid profiles, were simultaneous changes at the molecular lipid species levels which again coincided with the development of resistance to FLC. Reverse transcriptase-PCR of the key genes of the lipid metabolism validated lipidomic picture. Taken together, this study illustrates how the gradual corrective changes in Candida lipidome correspond to the development of FLC tolerance. Our study also shows a first instance of the mitochondrial membrane dysfunction and defective cell wall (CW) in clinical AR isolates of C. albicans, and provides evidence of a cross-talk between mitochondrial lipid homeostasis, CW integrity and azole tolerance