Efficient catalytic oxidation of primary and secondary alcohols using a non-heme dinuclear iron complex Ligtenbarg, A.G J; Oosting, P.; Roelfes, Gerard; La Crois, R.M.; Lutz, M; Spek, A.L.; Hage, R.; Feringa, B.L.

A conceptually new class of cationic amphiphiles, Sunfish amphiphiles, designed for the delivery of genes into cells is introduced. Sunfish amphiphiles have two hydrophobic tails, connected at the 4-and the N-position to the cationic pyridinium headgroup. Two extreme morphologies visualised by backfolding and combining of both tails at one site (matching situation) or unfolding of the tails at distinct interaction sites at biological membranes will lead to considerable differences in morphological behaviour. The underlying rationale allows controlled release by using this morphological alteration of

Familial neurohypophyseal diabetes insipidus in humans is a rare disease transmitted as an autosomal dominant trait. Affected individuals have very low or undetectable levels of circulating vasopressin and suffer from polydipsia and polyuria. An obvious candidate gene for the disease is the vasopressin‐neurophysin (AVP‐NP) precursor gene on human chromosome 20. The 2 kb gene with three exons encodes a composite precursor protein consisting of the neuropeptide vasopressin and two associated proteins, neurophysin and a glycopeptide. Cloning and nucleotide sequence analysis of both alleles of the AVP‐NP gene present in a Dutch ADNDI family reveals a point mutation in one allele of the affected family members. Comparison of the nucleotide sequences shows a G‐‐‐‐T transversion within the neurophysin‐encoding exon B. This missense mutation converts a highly conserved glycine (Gly17 of neurophysin) to a valine residue. RFLP analysis of six related family members indicates cosegregation of the mutant allele with the DI phenotype. The mutation is not present in 96 chromosomes of an unrelated control group. These data suggest that a single amino acid exchange within a highly conserved domain of the human vasopressin‐associated neurophysin is the primary cause of one form of ADNDI.

The search for melatonin receptor agonists and antagonists specific towards one of the receptor subtypes will extend our understanding of the role of this system in relaying circadian information to the body. A series of compounds derived from a hit compound discovered in a screening process led to powerful agonists specific for one of the isoform of the melatonin receptor namely, MT2. The compounds are based on a poorly explored skeleton in the molecular pharmacology of melatonin. By changing the steric hindrance of one substituent (i.e., from a hydrogen atom to a tributylstannyl group), we identified a possible partial agonist that could lead to antagonist analogues. The functionalities of these compounds were measured with a series of assays, including the binding of GTPγS, the inhibition of the cyclic AMP production, the β-arrestin recruitment, and the cell shape changes as determined by cellular dielectric spectroscopy (CellKey®). The variations between the compounds are discussed.

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