Synthesis, characterisation and catalytic activity of dithiocarbazate Schiff base complexes in oxidation of cyclohexane

Schiff base complexes of transition metals can be used for catalytic oxidation of hydrocarbons in the presence of tert-butyl hydroperoxide (TBHP). In this work, metal complexes of dithiocarbazate Schiff bases (abbreviated as NiSBdiAP, CuSBdiAP, CoSBdiAP, FeSBdiAP, MnSBdiAP and ZnSBdiAP, in which SBdiAP represents the Schiff base) were synthesized and characterized using several techniques; Fourier transforms infrared spectroscopy, nuclear magnetic resonance, 1H NMR and 13C NMR, magnetic susceptibility measurements, molar conductivity, ultraviolet-visible spectroscopy, and inductively coupled plasma spectrometry. The oxidation of cyclohexane by the prepared metal complexes as catalysts was investigated in the presence of TBHP as an oxidative source under mild conditions. The product was analyzed using gas chromatography. It was found that cyclohexanol and cyclohexanone were the main products of the oxidation reaction. The iron complex of Schiff base derived from 2,6-diacetyl pyridine and S-benzyldithiocarbazate showed the highest activity during the screening studies towards cyclohexane oxidation. The results showed that the time of the reaction, temperature, and the concentration of TBHP and the catalyst type influenced the selectivity and conversion of cyclohexane oxidation. The selectivity of the reaction was 96% indicating the significance of the work toward industrial oxidation of cyclohexane

Catalytic oxidation of cyclohexane using transition metal complexes of dithiocarbazate schiff base

Metal complexes of dithiocarbazate Schiff bases (abbreviated as NiSMdiAP, CoSMdiAP, FeSMdiAP, MnSMdiAP and ZnSMdiAP, where SMdiAP represents the Schiff base) were synthesized and characterized using techniques including Fourier transform infrared spectroscopy, nuclear magnetic resonance, 1H NMR, 13C NMR, magnetic susceptibility measurements, molar conductivity, ultraviolet–visible spectroscopy, and inductively coupled plasma-optical emission spectrometry. The study focused on the oxidation of cyclohexane by using the metal complexes as catalysts with hydrogen peroxide as the oxidative source under special conditions. These catalysts showed good conversion and high selectivity compared to other Schiff base complexes. The conditions of the oxidation reaction catalysed by these complexes were investigated. Gas chromatography was used to analyse the products of the oxidation reaction of cyclohexane and it showed that cyclohexanol and cyclohexanone are the main products. A copper complex of Schiff base formed from 2,6-diacetyl pyridine and S-methyldithiocarbazate, [CuIISMdiAP] showed the highest level of activity during the screening studies towards cyclohexane oxidation. The time of reaction, temperature, and the concentration of H2O2 as an environmentally friendly oxidant and the catalyst type played an important role in the selectivity and conversion of cyclohexane oxidation. The selectivity of the reaction was 98%

Phenotype-specific effect of chromosome 1q21.1 rearrangements and GJA5 duplications in 2436 congenital heart disease patients and 6760 controls

Recurrent rearrangements of chromosome 1q21.1 that occur via non-allelic homologous recombination have been associated with variable phenotypes exhibiting incomplete penetrance, including congenital heart disease (CHD). However, the gene or genes within the ∼1 Mb critical region responsible for each of the associated phenotypes remains unknown. We examined the 1q21.1 locus in 948 patients with tetralogy of Fallot (TOF), 1488 patients with other forms of CHD and 6760 ethnically matched controls using single nucleotide polymorphism genotyping arrays (Illumina 660W and Affymetrix 6.0) and multiplex ligation-dependent probe amplification. We found that duplication of 1q21.1 was more common in cases of TOF than in controls [odds ratio (OR) 30.9, 95% confidence interval (CI) 8.9-107.6); P = 2.2 × 10−7], but deletion was not. In contrast, deletion of 1q21.1 was more common in cases of non-TOF CHD than in controls [OR 5.5 (95% CI 1.4-22.0); P = 0.04] while duplication was not. We also detected rare (n = 3) 100-200 kb duplications within the critical region of 1q21.1 in cases of TOF. These small duplications encompassed a single gene in common, GJA5, and were enriched in cases of TOF in comparison to controls [OR = 10.7 (95% CI 1.8-64.3), P = 0.01]. These findings show that duplication and deletion at chromosome 1q21.1 exhibit a degree of phenotypic specificity in CHD, and implicate GJA5 as the gene responsible for the CHD phenotypes observed with copy number imbalances at this locu

Phenotype-specific effect of chromosome 1q21.1 rearrangements and GJA5 duplications in 2436 congenital heart disease patients and 6760 controls

Recurrent rearrangements of chromosome 1q21.1 that occur via non-allelic homologous recombination have been associated with variable phenotypes exhibiting incomplete penetrance, including congenital heart disease (CHD). However, the gene or genes within the ∼1 Mb critical region responsible for each of the associated phenotypes remains unknown. We examined the 1q21.1 locus in 948 patients with tetralogy of Fallot (TOF), 1488 patients with other forms of CHD and 6760 ethnically matched controls using single nucleotide polymorphism genotyping arrays (Illumina 660W and Affymetrix 6.0) and multiplex ligation-dependent probe amplification. We found that duplication of 1q21.1 was more common in cases of TOF than in controls [odds ratio (OR) 30.9, 95% confidence interval (CI) 8.9–107.6); P = 2.2 × 10−7], but deletion was not. In contrast, deletion of 1q21.1 was more common in cases of non-TOF CHD than in controls [OR 5.5 (95% CI 1.4–22.0); P = 0.04] while duplication was not. We also detected rare (n = 3) 100–200 kb duplications within the critical region of 1q21.1 in cases of TOF. These small duplications encompassed a single gene in common, GJA5, and were enriched in cases of TOF in comparison to controls [OR = 10.7 (95% CI 1.8–64.3), P = 0.01]. These findings show that duplication and deletion at chromosome 1q21.1 exhibit a degree of phenotypic specificity in CHD, and implicate GJA5 as the gene responsible for the CHD phenotypes observed with copy number imbalances at this locus