Genetic Toolkit for Assessment and Prediction of Population-Level Impacts of Bridge Construction on Birds

Recent studies have highlighted alarming rates of declines in bird populations across the country. The State of California is home to over 650 resident and migrant avian species. Legislation for protecting these species has existed for over a century now, yet tools for identifying populations and understanding seasonal movement remain limited. Recently, genetic and genomic tools have provided a method for understanding population structure, allowing for more informed delineation of management units. The goal of this project was to create a genetic toolkit for identifying breeding populations and assigning individuals to those populations. Ultimately, such tools could be used to assess population-level impacts when there are conflicts with birds at infrastructure construction sites. As a test case, we sequenced entire genomes for 40 individual Anna’s hummingbirds (Calypte anna) from across the state. Based on this initial data, we found low levels of differentiation between sampled locations, suggesting that C. anna in California are not subdivided into different population units. However, there was a weak signal of geography suggesting there may be localized genetic differences in a small proportion of the genome. Follow-up work will focus on a broader sampling across the state of California to clarify any possible population subdivision or geographical patterns of differentiation.View the NCST Project Webpag

Reductive cleavage of sulfones and sulfonamides by neutral organic super electron-donor (S.E.D.) reagent

The sulfonyl group finds extensive applications in organic and medicinal chemistry both in sulfonamides, popular as robust protecting groups for amines, and in sulfones. Frequently, sulfones are introduced into synthetic schemes to assist particular transformations; further progress along the synthetic route can later require the removal of a sulfone group, and this can be achieved by reductive desulfonylation or, in the special cases of α-halo- or ß-acyloxysulfones, by elimination to an alkene

Predicting the reducing power of organic super electron donors

The utilization of computational methods to predict reactivity is an increasingly useful tool for chemists to save time and materials by screening compounds for desirable reactivity prior to testing in the laboratory. In the field of electron transfer reactions, screening can be performed through the application of Marcus Hush theory to calculate the activation free energy of any potential reaction. This work describes the most accurate and efficient approach for modelling the electron transfer process. In particular, the importance of using an electron transfer complex to model these reactions rather than considering donor and acceptor molecules as separate entities is highlighted. The use of the complex model is found to produce more accurate calculation of the electron transfer energy when the donor and acceptor spin densities are adequately localised

In-situ monitoring for CVD processes

Aiming towards process control of industrial high yield/high volume CVD reactors, the potential of optical sensors as a monitoring tool has been explored. The sensors selected are based on both Fourier transform infrared spectroscopy (FTIR) and tunable diode laser spectroscopy (NIR-DLS). The former has the advantage of wide spectral capability, and well established databases. NIR-DLS spectroscopy has potentially high sensitivity, laser spatial resolution, and the benefits of comparatively easier integration capabilities-including optical fibre compatibility. The proposed technical approach for process control is characterised by a 'chemistry based' feedback system with in-situ optical data as input information. The selected optical sensors continuously analyze the gas phase near the surface of the growing layer. The spectroscopic data has been correlated with process performance and layer properties which, in turn establish data basis for process control. The new process control approach is currently being verified on different industrialised CVD coaters. One of the selected applications deals with the deposition of SnO2 layers on glass based on the oxidation of (CH3)2SnCl2, which is used in high volume production for low-E glazing

Influence of solvent in controlling peptide−surface interactions

Protein binding to surfaces is an important phenomenon in biology and in modern technological applications. Extensive experimental and theoretical research has been focused in recent years on revealing the factors that govern binding affinity to surfaces. Theoretical studies mainly focus on examining the contribution of the individual amino acids or, alternatively, the binding potential energies of the full peptide, which are unable to capture entropic contributions and neglect the dynamic nature of the system. We present here a methodology that involves the combination of nonequilibrium dynamics simulations with strategic mutation of polar residues to reveal the different factors governing the binding free energy of a peptide to a surface. Using a gold-binding peptide as an example, we show that relative binding free energies are a consequence of the balance between strong interactions of the peptide with the surface and the ability for the bulk solvent to stabilize the peptide

Enzymatically activated emulsions stabilised by interfacial nanofibre networks

We report on-demand formation of emulsions stabilised by interfacial nanoscale networks. These are formed through biocatalytic dephosphorylation and self-assembly of Fmoc(9-fluorenylmethoxycarbonyl)-dipeptide amphiphiles in aqueous/organic mixtures. This is achieved by using alkaline phosphatase which transforms surfactant-like phosphorylated precursors into self-assembling aromatic peptide amphiphiles (Fmoc-tyrosine-leucine, Fmoc-YL) that form nanofibrous networks. In biphasic organic/aqueous systems, these networks form preferentially at the interface thus providing a means of emulsion stabilisation. We demonstrate on-demand emulsification by enzyme addition, even after storage of the biphasic mixture for several weeks. Experimental (Fluorescence, FTIR spectroscopy, fluorescence microscopy, electron microscopy, atomic force microscopy) and computational techniques (atomistic molecular dynamics) are used to characterise the interfacial self-assembly process

Impairment of enzymatic antioxidant defenses is associated with bilirubin-induced neuronal cell death in the cerebellum of Ugt1 KO mice

Severe hyperbilirubinemia is toxic during central nervous system development. Prolonged and uncontrolled high levels of unconjugated bilirubin lead to bilirubin-induced encephalopathy and eventually death by kernicterus. Despite extensive studies, the molecular and cellular mechanisms of bilirubin toxicity are still poorly defined. To fill this gap, we investigated the molecular processes underlying neuronal injury in a mouse model of severe neonatal jaundice, which develops hyperbilirubinemia as a consequence of a null mutation in the Ugt1 gene. These mutant mice show cerebellar abnormalities and hypoplasia, neuronal cell death and die shortly after birth because of bilirubin neurotoxicity. To identify protein changes associated with bilirubin-induced cell death, we performed proteomic analysis of cerebella from Ugt1 mutant and wild-type mice. Proteomic data pointed-out to oxidoreductase activities or antioxidant processes as important intracellular mechanisms altered during bilirubin-induced neurotoxicity. In particular, they revealed that down-representation of DJ-1, superoxide dismutase, peroxiredoxins 2 and 6 was associated with hyperbilirubinemia in the cerebellum of mutant mice. Interestingly, the reduction in protein levels seems to result from post-translational mechanisms because we did not detect significant quantitative differences in the corresponding mRNAs. We also observed an increase in neuro-specific enolase 2 both in the cerebellum and in the serum of mutant mice, supporting its potential use as a biomarker of bilirubin-induced neurological damage. In conclusion, our data show that different protective mechanisms fail to contrast oxidative burst in bilirubin-affected brain regions, ultimately leading to neurodegeneration. \ua9 2015 Macmillan Publishers Limited All rights reserved