Observation of ligand effects during alkene hydrogenation catalysed by supported metal clusters

Homogeneous organometallic catalysts and many enzymes activate reactants through coordination to metal atoms; that is, the reactants are turned into ligands and their reactivity controlled through other ligands in the metal's coordination sphere. In the case of supported metal clusters, catalytic performance is influenced by the support and by adsorbed reactants, intermediates or products. The adsorbates are usually treated as ligands, whereas the influence of the supports is usually ascribed to electronic interactions, even though metal clusters supported on oxides and zeolites form chemical bonds to support oxygen atoms. Here we report direct observations of the structure of supported metal clusters consisting of four iridium atoms, and the identification of hydrocarbon ligands bound to them during propene hydrogenation. We find that propene and molecular hydrogen form propylidyne and hydride ligands, respectively, whereas simultaneous exposure of the reactants to the supported iridium cluster yields ligands that are reactive intermediates during the catalytic propane-formation reaction. These intermediates weaken the bonding within the tetrahedral iridium cluster and the interactions between the cluster and the support, while replacement of the MgO support with gamma-Al2O3 boosts the catalytic activity tenfold, by affecting the bonding between the reactant-derived ligands and the cluster and therefore also the abundance of individual ligands. This interplay between the support and the reactant-derived ligands, whereby each influences the interaction of the metal cluster with the other, shows that the catalytic properties of supported metal catalysts can be tuned by careful choice of their supports.     

Methylmercury sexual dimorphism in the mouse

Summary 5–8 days after a single nontoxic dose of radioactive methylmercury chloride adult male mouse kidneys contain twice as much radioactive mercury per unit wet wt as do kidneys of similarly dosed adult females.This investigation was supported in part by NSF (RANN) grants (GI-30097 and AEN75-14889), by Program Project grant (ES-01248) and Center grant (ES-01247) from the NIEHS, and in part by the US Department of Energy at the University of Rochester Department of Radiation Biology and Biophysics and has been assigned Report No. UR-3490-1308.     

A radiation hybrid map of the zebrafish genome.

Recent large-scale mutagenesis screens have made the zebrafish the first vertebrate organism to allow a forward genetic approach to the discovery of developmental control genes. Mutations can be cloned positionally, or placed on a simple sequence length polymorphism (SSLP) map to match them with mapped candidate genes and expressed sequence tags (ESTs). To facilitate the mapping of candidate genes and to increase the density of markers available for positional cloning, we have created a radiation hybrid (RH) map of the zebrafish genome. This technique is based on somatic cell hybrid lines produced by fusion of lethally irradiated cells of the species of interest with a rodent cell line. Random fragments of the donor chromosomes are integrated into recipient chromosomes or retained as separate minichromosomes. The radiation-induced breakpoints can be used for mapping in a manner analogous to genetic mapping, but at higher resolution and without a need for polymorphism. Genome-wide maps exist for the human, based on three RH panels of different resolutions, as well as for the dog, rat and mouse. For our map of the zebrafish genome, we used an existing RH panel and 1,451 sequence tagged site (STS) markers, including SSLPs, cloned candidate genes and ESTs. Of these, 1,275 (87.9%) have significant linkage to at least one other marker. The fraction of ESTs with significant linkage, which can be used as an estimate of map coverage, is 81.9%. We found the average marker retention frequency to be 18.4%. One cR3000 is equivalent to 61 kb, resulting in a potential resolution of approximately 350 kb.     

Vascular respiratory uncoupling increases blood pressure and atherosclerosis

The observations that atherosclerosis often occurs in non-smokers without elevated levels of low-density lipoprotein cholesterol, and that most atherosclerosis loci so far identified in mice do not affect systemic risk factors associated with atherosclerosis, suggest that as-yet-unidentified mechanisms must contribute to vascular disease. Arterial walls undergo regional disturbances of metabolism that include the uncoupling of respiration and oxidative phosphorylation, a process that occurs to some extent in all cells and may be characteristic of blood vessels being predisposed to the development of atherosclerosis. To test the hypothesis that inefficient metabolism in blood vessels promotes vascular disease, we generated mice with doxycycline-inducible expression of uncoupling protein-1 (UCP1) in the artery wall. Here we show that UCP1 expression in aortic smooth muscle cells causes hypertension and increases dietary atherosclerosis without affecting cholesterol levels. UCP1 expression also increases superoxide production and decreases the availability of nitric oxide, evidence of oxidative stress. These results provide proof of principle that inefficient metabolism in blood vessels can cause vascular disease.     

Development,plasticity and evolution of butterfly eyespot patterns

The developmental and genetic bases for the formation, plasticity and diversity of eyespot patterns in butterflies are examined. Eyespot pattern mutants, regulatory gene expression, and transplants of the eyespot developmental organizer demonstrate that eyespot position, number, size and colour are determined progressively in a developmental pathway largely uncoupled from those regulating other wing-pattern elements and body structures. Species comparisons and selection experiments suggest that the evolution of eyespot patterns can occur rapidly through modulation of different stages of this pathway, and requires only single, or very few, changes in regulatory genes.     

Behaviour and habitat of Neohela monstrosa (Boeck, 1861) (Amphipoda: Corophiida) in Norwegian Sea deep water

There are few in situ observations of deep-sea macrofauna, due to the remoteness of this ecosystem. Visual surveys conducted for marine management by MAREANO, (marine area database for Norwegian waters) and the petroleum industry (by SERPENTS, scientific and environmental remotely operated vehicle partnership using existing industrial technology) have provided unique material of visual information from large areas in the Norwegian Sea. The distribution, density and behaviour of the deep-sea amphipod Neohela monstrosa (Boeck, 1861) is described based on videos and samples from the Norwegian Sea. This amphipod is common on mud bottoms at 200–2181 m depth in the area. Dense communities were found in stands of the arctic sea pen Umbellula encrinus at more than 1000 m depth where temperatures were below 0° C. The mean density of N. monstrosa observed for larger areas was 4/100 m² but densities of 15–36 individuals per m² were found in local patches. It is domicolous which is characteristic of the superfamily Corophiida and digs burrows in soft muddy bottoms primarily by using large shovel-like gnathopods to scoop the sediment out. The amphipod was observed pushing and rolling sediment balls out of its burrow, which were probably held together with amphipod silk. It digs out an upper 3 to 4 cm wide burrow with a horizontal side burrow a couple of centimetres down. Neohela monstrosa appears to feeds on newly settled detritus that it collects from the surface sediment through the use of its long antennae while the burrow is mainly used for protection against predators such as demersal fish. Newly released juveniles are probably kept in the burrow for protection. Based on the local high density of N. monstrosa together with its habit of making long burrows, we suggest that there is significant bioturbation associated with the presence of N. monstrosa in deep sedimentary habitats of the Norwegian Sea, which likely provides an important ecosystem function.     

Kainate receptors are involved in synaptic plasticity

The ability of synapses to modify their synaptic strength in response to activity is a fundamental property of the nervous system and may be an essential component of learning and memory. There are three classes of ionotropic glutamate receptor, namely NMDA (N-methyl-D-aspartate), AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole-4-propionic acid) and kainate receptors; critical roles in synaptic plasticity have been identified for two of these. Thus, at many synapses in the brain, transient activation of NMDA receptors leads to a persistent modification in the strength of synaptic transmission mediated by AMPA receptors. Here, to determine whether kainate receptors are involved in synaptic plasticity, we have used a new antagonist, LY382884 ((3S, 4aR, 6S, 8aR)-6-((4-carboxyphenyl)methyl-1,2,3,4,4a,5,6,7,8,8a-decahydro isoquinoline-3-carboxylic acid), which antagonizes kainate receptors at concentrations that do not affect AMPA or NMDA receptors. We find that LY382884 is a selective antagonist at neuronal kainate receptors containing the GluR5 subunit. It has no effect on long-term potentiation (LTP) that is dependent on NMDA receptors but prevents the induction of mossy fibre LTP, which is independent of NMDA receptors. Thus, kainate receptors can act as the induction trigger for long-term changes in synaptic transmission.