Magnussonmcpherson8964

The theoretical description of the adsorption of surfactants at interfaces between aqueous solutions and oil was based over a very long time on models derived for the solution/air interface. Thus, most of the experimentally observed peculiarities could not be specifically considered but were merely interpreted in terms of a penetration of oil molecules into the alkyl chain layer of the adsorbed surfactant molecules. These penetrating oil molecules enhance the surfactant adsorption as compared to the water/air interface. Later on, for the special situations at water/oil interfaces a competitive adsorption of surfactant and oil molecules was postulated, allowing a much better description of experimental data. This picture, however, was unable to explain why the interfacial tension of the water/oil interface decreases very quickly when extremely small amounts of surfactants are added to the water. This effect cannot be of competitive nature, but a cooperativity of surfactant and oil molecules forming a mixed adsorption layer is required instead. This cooperative effect means that already few surfactant molecules adsorbed at the interface can induce a significant ordering of oil molecules in the interfacial layer. This new interfacial structure, in turn, attracts further surfactant molecules to adsorb. Improving the theoretical description of experimental data was finally achieved by applying suitable adsorption models for the two adsorbing compounds, i.e. a Frumkin adsorption model for the oil molecules and a Langmuir, Frumkin, or reorientation model for the adsorbing surfactant molecules. Here, the progress in modelling surfactant adsorption at water/oil interfaces is discussed mainly for the homologous series of the cationic surfactants CnTAB, of the anionic surfactant SDS, and members of the homologous series of the non-ionic surfactants CnDMPO at water/alkane interfaces. Different 1,3,5-trisubstituted pyrazoline derivatives 2a-c, 3-c, 4a-f, 6a-c, 7a-f and 8a-d were prepared via condensation reaction of the appropriate chalcone 1a-c or 5a-c with various hydrazine derivatives. All compounds were screened for their cytotoxicity against breast MCF-7 cancer cell line and the normal fibroblasts WI-38. Thirteen compounds 2a, 3a, 3c, 4a-d, 6c, 7d, 7e, 8b, 8d and 8f revealed promising cytotoxicity against MCF-7 compared to the reference standard staurosporine and they were safe to the normal fibroblasts WI-38. In addition, compounds 3c, 6c, 7d, 8b and 8d elicited higher cytotoxicity than erlotinib and exhibited promising EGFR inhibitory activity at submicromolar level comparable to that of erlotinib except for compound 8b that may exert its cytotoxicity via another mechanism besides EGFR inhibition. Molecular docking of 3c, 6c, 7d, 8b and 8d in the active site of EGFR confirmed the obtained results. In search for new molecular entities as anti-TB agents, the benzimidazoquinazoline polyheterocyclic scaffold has been designed adopting the scaffold hopping strategy. Thirty-two compounds have been synthesized through an improved tandem decarboxylative nucleophilic addition cyclocondensation reaction of o-phenylenediamine with isatoic anhydride followed by further cyclocondensation of the intermediately formed 2-(o-aminoaryl)benzimidazole with trialkyl orthoformate/acetate. The resultant benzimidazoquinazolines were evaluated in vitro for anti-TB activity against M. tuberculosis H37Rv (ATCC27294 strain). Fourteen compounds exhibiting MIC values in the range of 0.4-6.25 µg/mL were subjected to cell viability test against RAW 264.7 cell lines and were found to be non-toxic ( less then 30% inhibition at 50 µg/mL). The active compounds were further evaluated against INH resistant Mtb strains. The most active compound 6x [MIC (H37Rv) of 0.4 µg/mL] and the compound 6d [MIC (H37Rv) of 0.78 µg/mL] were also found to be active against INH resistant Mtb strain with MIC values of 12.5 and 0.78 µg/mL, respectively. Alkylation of sodium diethyldithiocarbamate with allyl-2-chloroacetate, allyl-3-chloropropionate, chloromethyl-2-(tetrahydrofuran-2-yl)acetate, and 4-(chloromethyl)-1,3-dioxolane in the aqueous medium synthesized functionally substituted esters of N, N-dietyleditiocarbamic acid (M1-M4). Most active compounds were docked into the catalytic active site of the enzyme. We identified that acetate moiety for inhibition of hCA I, hCA II, and α-glycosidase and dioxolane and thiocarbamic acid moieties for inhibition of AChE and BChE enzymes are very important. The hCA I isoform was inhibited by these novel functionally substituted esters based on sodium diethyldithiocarbamate derivatives (M1-M4) in low micromolar levels, the Ki of which differed between 48.03 ± 9.77 and 188.42 ± 46.08 µM. Against the physiologically dominant isoform hCA II, the novel compounds demonstrated Kis varying from 57.33 ± 6.21 to 174.34 ± 40.72 µM. Also, these novel derivatives (M1-M4) effectively inhibited AChE, with Ki values in the range of 115.42 ± 12.44 to 243.22 ± 43.65 µM. For BChE Ki values were found in the range of 94.33 ± 9.14 to 189.45 ± 35.88 µM. For α-glycosidase the most effective Ki values of M4 and M3 were with Ki values of 32.86 ± 7.88 and 37.63 ± 4.08 µM, respectively. A series of six compounds (1a-f) possessing pyridine-pyrazole-benzenethiourea or pyridine-pyrazole-benzenesulfonamide scaffold were synthesized. The target compounds were screened to evaluate their inhibitory effect on human nucleotide pyrophosphatase/phosphodiesterase 1 and -3 (ENPP1 and ENPP3) isoenzymes. Compounds 1c-e were the most potent inhibitors of ENPP1 with sub-micromolar IC50 values (0.69, 0.18, and 0.40 µM, respectively. selleck inhibitor Moreover, compound 1b was the most potent inhibitor of ENPP3 (IC50 = 0.21 µM). They were much more potent than the reference standard inhibitor, suramin (IC50 values against ENPP1 and -3 were 7.77 and 0.89 µM, respectively). Furthermore, all the six compounds were investigated for cytotoxic effect against cancerous cell lines (HeLa, MCF-7, and 1321N1) and normal cell line (BHK-21). Compound 1e was active against all the three cancer cell lines, however, showed preferential cytotoxicity against MCF-7 (IC50 = 16.05 µM), which is comparable to the potency of cisplatin. All the tested compounds exhibited low or negligible cytotoxic effect against the normal cells.