The thermal decomposition behaviours of oxovanadium(IV)hydroxamate complexes of composition [VO(Q)2−n(HL1,2)n]: [VO(C9H6ON)(C6H4(OH)(CO)NHO)] (I), [VO(C6H4(OH)(CO)NHO)2] (II), [VO(C9H6ON)(C6H4(OH)(5-Cl)(CO)NHO)] (III), and [VO(C6H4(OH)(5-Cl)(CO)NHO)2] (IV) (where Q = C9H6NO− 8-hydroxyquinolinate ion; HL1 = [C6H4(OH)CONHO]− salicylhydroxamate ion; HL2 = [C6H3(OH)(5-Cl)CONHO]− 5-chlorosalicylhydroxamate ion; n = 1 and 2), which are synthesised by the reactions of [VO(Q)2] with predetermined molar ratios of potassium salicylhydroxamate and potassium 5-chlorosalicylhydroxamate in THF + MeOH solvent medium, have been studied by TG and DTA techniques. Thermograms indicate that complexes (I) and (III) undergo single-step decomposition, while complexes (II) and (IV) decompose in two steps to yield VO(HL1,2) as the likely intermediate and VO2 as the ultimate product of decomposition. The formation of VO2 has been authenticated by IR and XRD studies. From the initial decomposition temperatures, the order of thermal stabilities for the complexes has been inferred as III > I > II > IV.
Thermal behaviour of newly synthesized niobium(V) aryloxides of composition [NbCl5−n(OC6H4CH(CH3)2-4)n] (where n = 1 → 5) synthesized by the reactions of niobium pentachloride with 4-isopropylphenol in predetermined molar ratios in carbon tetrachloride has been studied by thermogravimetric (TG) and differential thermal analysis (DTA) techniques. The results showed that thermal decomposition of complex of composition [NbCl4(OC6H4CH(CH3)2-4)] resulted in the formation of NbOCl3 as the ultimate decompositional product while all other complexes yielded Nb2O5 as the final product of thermal decomposition. From the mathematical analysis of TG data, the kinetic and thermodynamic parameters viz. energy of activation, frequency factor, entropy of activation, etc. have been evaluated using Coats–Redfern equation.
The thermal decomposition behavior of oxovanadium(IV)hydroxamate complexes of composition [VO(acac)(C6H5C(O)NHO)] (I), [VO(C6H5C(O)NHO)2] (II), [VO(acac)(4-ClC6H4C(O)NHO)] (III), [VO(4-ClC6H4C(O)NHO)2] (IV) (where acac = (CH3COCHCOCH3–) synthesized from the reactions of VO(acac)2 with equi- and bimolar amounts of potassium benzohydroxamate and potassium 4-chlorobenzohydroxamate in THF + MeOH solvent medium has been studied by TG and DTA techniques. TG curves indicated that complexes I, II, and IV undergo decomposition in single step to yield VO2 as the final residue, while complex III decomposes in two steps to yield VO(acac) as the likely intermediate and VO2 as the ultimate product of decomposition. The formation of VO2 has been authenticated by IR and XRD studies. From the initial decomposition temperatures, the order of thermal stability for the complexes has been inferred as IV > I > III > II.
Pathogenic yeasts from the genus
can cause serious infection in humans particularly, in immunocompromised patients and are now recognized as major agents of hospital acquired (nosocomial) infections. In the recent years, there has been a marked increase in the incidence of treatment failures in candidiasis patients receiving long-term antifungal therapy, which has posed a serious problem in its successful use in chemotherapy.
cells acquire drug resistance (MDR) during the course of the treatment. The mechanisms of resistance to azole antifungal agents have been elucidated in
species and can be mainly categorized as (i) changes in the cell wall or plasma membrane, which lead to impaired drug (azole) uptake; (ii) alterations in the affinity of the drug target Erg11p (lanosterol 14∝-demethylase) especially to azoles or in the cellular content of Erg11p due to target site mutation or overexpression of the
gene; and (iii) the efflux of drugs mediated by membrane transport proteins belonging to the ATP-binding cassette (ABC) transporters, namely
or to the major facilitator superfamily (MFS) transporter,
. Many such manifestations are associated with the formation of
biofilms including those occurring on devices like indwelling intravascular catheters. Biofilm-associated
show uniform resistance to a wide spectrum of antifungal drugs. A combination of different resistance mechanisms is responsible for drug resistance in clinical isolates of