Search for Charged Higgs Bosons in e+e- Collisions at \sqrt{s} = 189 GeV

A search for pair-produced charged Higgs bosons is performed with the L3 detector at LEP using data collected at a centre-of-mass energy of 188.6 GeV, corresponding to an integrated luminosity of 176.4 pb^-1. Higgs decays into a charm and a strange quark or into a tau lepton and its associated neutrino are considered. The observed events are consistent with the expectations from Standard Model background processes. A lower limit of 65.5 GeV on the charged Higgs mass is derived at 95 % confidence level, independent of the decay branching ratio Br(H^{+/-} -> tau nu)

Current challenges in software solutions for mass spectrometry-based quantitative proteomics

This work was in part supported by the PRIME-XS project, grant agreement number 262067, funded by the European Union seventh Framework Programme; The Netherlands Proteomics Centre, embedded in The Netherlands Genomics Initiative; The Netherlands Bioinformatics Centre; and the Centre for Biomedical Genetics (to S.C., B.B. and A.J.R.H); by NIH grants NCRR RR001614 and RR019934 (to the UCSF Mass Spectrometry Facility, director: A.L. Burlingame, P.B.); and by grants from the MRC, CR-UK, BBSRC and Barts and the London Charity (to P.C.

Measurement of Triple-Gauge-Boson Couplings of the W Boson at LEP

We report on measurements of the triple-gauge-boson couplings of the W boson in $\mathrm{e^+e^-}$ collisions with the L3 detector at LEP. W-pair, single-W and single-photon events are analysed in a data sample corresponding to a total luminosity of 76.7~pb$^{-1}$ collected at centre-of-mass energies between 161~GeV and 183~GeV. CP-conserving as well as both C- and P-conserving triple-gauge-boson couplings are determined. The results, in good agreement with the Standard-Model expectations, confirm the existence of the self coupling among the electroweak gauge bosons and constrain its structure

Effect of support of Co-Na-Mo catalysts on the direct conversion of CO2 to hydrocarbons

This study of the effect of support of Co-Na-Mo based catalysts on the direct hydrogenation of CO2 into hydrocarbons (HC) provides guidelines for the design of catalysts for CO2 conversion. We demonstrate that the surface area of the support and the metal-support interaction have a key role determining the cobalt crystallite size and consequently the activity of the system. Cobalt particles with sizes <2 nm supported on MgO present low reverse water gas shift conversion with negligible Fischer-Tropsch activity. Increasing the cobalt particle size to ∼15 nm supported on SiO2 and ZSM-5 supports not only substantially increases the CO2 conversion but it also provides high HC selectivities. Further increase of the cobalt particle size to 25–30 nm has a detrimental effect on the global CO2 conversion with HC:CO ratios below 1, however, lower methane selectivity and enhanced formation of unsaturated HC products are achieved. Additionally, the metal-support interaction potentially also has a strong effect on the growth chain probability of the formed hydrocarbons, increasing as the metal-support interaction increases. These evidences demonstrate that CO2 conversion and hydrocarbon distribution can be tuned towards desired products by controlled catalyst design

Biodegradable polymer‐Metal‐Organic Framework (MOF) composites for controlled and sustainable pesticide delivery

Due to high surface area, loading capacity, and selectivity, Metal-Organic Frameworks (MOFs) have shown much promise recently for potential applications in extraction and delivery of agrochemicals for environmental remediation and sustainable release, respectively. However, application of MOFs for pesticide delivery in wider agricultural context can be restricted by their granular form. Herein, an alternative approach is studied using biodegradable polymer-MOF composites to address this limitation. The loading and release of a widely used pesticide, 2,4-dichloropheoxycetic acid (2,4-D), is studied using two MOFs, UiO-66 and UiO-66-NH2, and the 2,4-D-loaded MOFs are incorporated into biodegradable polycaprolactone composites for convenient handling and minimizing runoff. The MOFs are loaded by in-situ, and post-synthetic methods, and characterised thoroughly to ensure successful synthesis and loading of 2,4-D. The pesticide release studies are performed on the MOFs and composites in distilled water, and analysed using UV-Vis spectroscopy, demonstrating sustained-release of 2,4-D over 16 days. The loaded MOF samples show high loading capacity, with up to 45 wt% for the in-situ loaded UiO-66. Release kinetics show more sustained release of 2,4-D from UiO-66-NH2 compared to UiO-66, which can be due to supramolecular interactions between the NH2 group of UiO-66-NH2 and 2,4-D. This is further supported by computational studies

Gata3 Acts Downstream of β-Catenin Signaling to Prevent Ectopic Metanephric Kidney Induction

Metanephric kidney induction critically depends on mesenchymal–epithelial interactions in the caudal region of the nephric (or Wolffian) duct. Central to this process, GDNF secreted from the metanephric mesenchyme induces ureter budding by activating the Ret receptor expressed in the nephric duct epithelium. A failure to regulate this pathway is believed to be responsible for a large proportion of the developmental anomalies affecting the urogenital system. Here, we show that the nephric duct-specific inactivation of the transcription factor gene Gata3 leads to massive ectopic ureter budding. This results in a spectrum of urogenital malformations including kidney adysplasia, duplex systems, and hydroureter, as well as vas deferens hyperplasia and uterine agenesis. The variability of developmental defects is reminiscent of the congenital anomalies of the kidney and urinary tract (CAKUT) observed in human. We show that Gata3 inactivation causes premature nephric duct cell differentiation and loss of Ret receptor gene expression. These changes ultimately affect nephric duct epithelium homeostasis, leading to ectopic budding of interspersed cells still expressing the Ret receptor. Importantly, the formation of these ectopic buds requires both GDNF/Ret and Fgf signaling activities. We further identify Gata3 as a central mediator of β-catenin function in the nephric duct and demonstrate that the β-catenin/Gata3 pathway prevents premature cell differentiation independently of its role in regulating Ret expression. Together, these results establish a genetic cascade in which Gata3 acts downstream of β-catenin, but upstream of Ret, to prevent ectopic ureter budding and premature cell differentiation in the nephric duct