A series of tris(oxoimidazolyl)hydroborato ligands, which serve as LX [O] donors, have been employed to obtain organometallic zirconium compounds in an uncommon oxygen-rich coordination environment. For example, Cp[To]ZrCl has been synthesized via the reaction of [To]Na with CpZrCl and bears a structural resemblance to the bent metallocene dichloride derivative CpZrCl. In addition, the half-sandwich counterparts [To]ZrCl and [To]ZrCl have been obtained by metathesis of ZrCl with [To]Na and [To]Na, respectively.
View Article and Find Full Text PDFA series of bis- and tris(oxobenzimidazolyl)hydroborato compounds, namely, [Bo]Na and [To]-Na (R = Me, Bu, Ad), which feature uncommon sterically demanding LX [O] and LX [O] donor ligands, have been obtained via the reactions of NaBH with 1-R-1,3-dihydro-2H-benzimidazol-2-ones. Evidence that the alkyl substituents are suitably located to have a significant impact on the coordination environment is provided by the observation that the methyl derivative [To]Na(κ-diglyme) exhibits κ-coordination of the diglyme, whereas the t-butyl and adamantyl derivatives, [To]Na(κ-diglyme) and [To]Na(κ-diglyme), exhibit κ-coordination. The [Bo] and [To] ligands also allow for isolation of discrete mononuclear thallium compounds, [Bo]Tl and [To]Tl, for which the steric demands of the ligands have been quantified in terms of both cone angle and buried volume concepts.
View Article and Find Full Text PDFNeuropsychopharmacology
December 2017
Whereas some rare genetic variants convey high risk for schizophrenia (SZ), common alleles conveying even moderate risk remain elusive. Long interspersed element-1s (L1) are mobile retrotransposons comprising ~17% of the human genome. L1 retrotransposition can cause somatic mosaicism during neurodevelopment by insertional mutagenesis.
View Article and Find Full Text PDFIntroduction: Long interspersed element (LINE)-1 (L1) is a type of retrotransposon capable of mobilizing into new genomic locations. Often studied in Mendelian diseases or cancer, L1s may also cause somatic mutation in the developing central nervous system. Recent reports showed L1 transcription was activated in brains of cocaine-treated mice, and L1 retrotransposition was increased in cocaine-treated neuronal cell cultures.
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