SYNTHESIS, CHARACTERIZATION AND ANTIBACTERIAL STUDIES OF SOME METAL COMPLEXES WITH THE SCHIFF BASE OF A HETEROCYCLIC ALDEHYDE

Metal complexes of Co(II), Ni(II), Cu(II), Zn(II), Cd(II) and Hg(II) with a new Schiff base derived from 3-aminodibenzofuran and 2-furancarboxaldehyde are reported. The complexes have been characterized using chemical analysis, spectroscopic methods (IR, UV-vis, 1H NMR and ESR), conductometric and magnetic data. According to these data, we propose an octahedral geometry for Co(II), Ni(II) and Cu(II) complexes and a tetrahedral geometry for Zn(II), Cd(II) and Hg(II) complexes. Antibacterial activity of the ligand and its complexes were studied against selected bacteria: Escherichia coli, Staphylococcus aureus and Pseudomonas aeruginosa. It has been found that all the complexes are antimicrobially active and show higher activity than the free ligand.KEY WORDS: Schiff base, Metal complexes, Antibacterial activityBull. Chem. Soc. Ethiop. 2009, 23(1), 63-68

Mesoporous silica functionalized with 1-furoyl thiourea urea for Hg(II) adsorption from aqueous media

International audienceNew organic–inorganic hybrid materials were prepared by covalently anchoring 1-furoyl thiourea on mesoporous silica (SBA-15). By means of various characterization techniques (X-ray diffraction, nitrogen adsorption–desorption, thermogravimetric analysis, and FTIR spectroscopy) it has been established that the organic groups were successfully anchored on the SBA-15 surfaces and the ordering of the inorganic support was preserved during the chemical modifications. The hybrid sorbents exhibited good ability to remove Hg(II) from aqueous solution. Thus, at pH 6, the adsorption capacity of mercury ions reached 0.61mmolg−1

Modified SBA-15 mesoporous silica for heavy metal ions remediation

International audienceN-Propylsalicylaldimino-functionalized SBA-15 mesoporous silica was prepared, characterized and used as an adsorbent for heavy metal ions. The organic–inorganic hybrid material was obtained using successive grafting procedures of SBA-15 silica with 3-aminopropyl-triethoxysilane and salicylaldehyde, respectively. For comparison an amorphous silica gel was functionalized using the same procedure. The structure and physicochemical properties of the materials were characterized by means of elemental analysis, X-ray diffraction (XRD), nitrogen adsorption–desorption, thermogravimetric analysis and FTIR spectroscopy. The organic functional groups were successfully grafted on the SBA-15 surfaces and the ordering of the support was not affected by the chemical modification. The behavior of the grafted solids for the adsorption of heavy metals ions from aqueous solutions was investigated. The hybrid materials showed high adsorption capacity and high selectivity for copper ions. Other ions, such as nickel, zinc, and cobalt were adsorbed by the modified SBA-15 material. The adsorbent can be regenerated by acid treatment without altering its properties

Haploinsufficiency of BAZ1B contributes to Williams syndrome through transcriptional dysregulation of neurodevelopmental pathways

Williams syndrome (WS) is a neurodevelopmental disorder caused by a genomic deletion of ∼28 genes that results in a cognitive and behavioral profile marked by overall intellectual impairment with relative strength in expressive language and hypersocial behavior. Advancements in protocols for neuron differentiation from induced pluripotent stem cells allowed us to elucidate the molecular circuitry underpinning the ontogeny of WS. In patient-derived stem cells and neurons, we determined the expression profile of the Williams-Beuren syndrome critical region-deleted genes and the genome-wide transcriptional consequences of the hemizygous genomic microdeletion at chromosome 7q11.23. Derived neurons displayed disease-relevant hallmarks and indicated novel aberrant pathways in WS neurons including over-activated Wnt signaling accompanying an incomplete neurogenic commitment. We show that haploinsufficiency of the ATP-dependent chromatin remodeler, BAZ1B, which is deleted in WS, significantly contributes to this differentiation defect. Chromatin-immunoprecipitation (ChIP-seq) revealed BAZ1B target gene functions are enriched for neurogenesis, neuron differentiation and disease-relevant phenotypes. BAZ1B haploinsufficiency caused widespread gene expression changes in neural progenitor cells, and together with BAZ1B ChIP-seq target genes, explained 42% of the transcriptional dysregulation in WS neurons. BAZ1B contributes to regulating the balance between neural precursor self-renewal and differentiation and the differentiation defect caused by BAZ1B haploinsufficiency can be rescued by mitigating over-active Wnt signaling in neural stem cells. Altogether, these results reveal a pivotal role for BAZ1B in neurodevelopment and implicate its haploinsufficiency as a likely contributor to the neurological phenotypes in WS