Multidimensional Scaling of Cognitive Ability and Academic Achievement Scores

Multidimensional scaling (MDS) was used as an alternate multivariate procedure for investigating intelligence and academic achievement test score correlations. Correlation coefficients among Wechsler Intelligence Scale for Children, Fifth Edition (WISC-5) and Wechsler Individual Achievement Test, Third Edition (WIAT-III) validity sample scores and among Kaufman Assessment Battery for Children, Second Edition (KABC-II) and Kaufman Test of Educational Achievement, Second Edition (KTEA-2) co-norming sample scores were analyzed using multidimensional scaling (MDS). Three-dimensional MDS configurations were the best fit for interpretation in both datasets. Subtests were more clearly organized by CHC ability and academic domain instead of complexity. Auditory-linguistic, figural-visual, reading-writing, and quantitative-numeric regions were visible in all models. Results were mostly similar across different grade levels. Additional analysis with WISC-V and WIAT-III tests showed that content (verbal, numeric, figural) and response process facets (verbal, manual, paper-pencil) were also useful in explaining test locations. Two implications from this study are that caution may be needed when interpreting fluency scores across academic areas, and MDS provides more empirically based validity evidence regarding content and response mode processes

Simultaneous high-speed measurement of temperature and lifetime-corrected OH laserinduced fluorescence in unsteady flames

A means of performing simultaneous, high-speed measurements of temperature and OH lifetime-corrected laser-induced fluorescence (LIF) for tracking unsteady flames has been developed and demonstrated. The system uses the frequency-doubled and frequency-tripled output beams of an 80 MHz mode-locked Ti:sapphire laser to achieve ultrashort laser pulses (order 2 ps) for Rayleigh-scattering thermometry at 460 nm and lifetime-corrected OH LIF at 306.5 nm, respectively. Simultaneous, high-speed measurements of temperature and OH number density enable studies of flame chemistry, heat release, and flame extinction in unsteady, strained flames where the local fluorescence-quenching environment is unknown

An apodizing phase plate coronagraph for VLT/NACO

We describe a coronagraphic optic for use with CONICA at the VLT that provides suppression of diffraction from 1.8 to 7 lambda/D at 4.05 microns, an optimal wavelength for direct imaging of cool extrasolar planets. The optic is designed to provide 10 magnitudes of contrast at 0.2 arcseconds, over a D-shaped region in the image plane, without the need for any focal plane occulting mask.Comment: 9 pages, 5 figures, to appear in Proc. SPIE Vol. 773

C-terminal phosphorylation of NaV1.5 impairs FGF13-dependent regulation of channel inactivation

International audienceVoltage-gated Na(+) (NaV) channels are key regulators of myocardial excitability, and Ca(2+)/calmodulin-dependent protein kinase II (CaMKII)-dependent alterations in NaV1.5 channel inactivation are emerging as a critical determinant of arrhythmias in heart failure. However, the global native phosphorylation pattern of NaV1.5 subunits associated with these arrhythmogenic disorders and the associated channel regulatory defects remain unknown. Here, we undertook phosphoproteomic analyses to identify and quantify in situ the phosphorylation sites in the NaV1.5 proteins purified from adult WT and failing CaMKIIδc-overexpressing (CaMKIIδc-Tg) mouse ventricles. Of 19 native NaV1.5 phosphorylation sites identified, two C-terminal phosphoserines at positions 1938 and 1989 showed increased phosphorylation in the CaMKIIδc-Tg compared with the WT ventricles. We then tested the hypothesis that phosphorylation at these two sites impairs fibroblast growth factor 13 (FGF13)-dependent regulation of NaV1.5 channel inactivation. Whole-cell voltage-clamp analyses in HEK293 cells demonstrated that FGF13 increases NaV1.5 channel availability and decreases late Na(+) current, two effects that were abrogated with NaV1.5 mutants mimicking phosphorylation at both sites. Additional co-immunoprecipitation experiments revealed that FGF13 potentiates the binding of calmodulin to NaV1.5 and that phosphomimetic mutations at both sites decrease the interaction of FGF13 and, consequently, of calmodulin with NaV1.5. Together, we have identified two novel native phosphorylation sites in the C terminus of NaV1.5 that impair FGF13-dependent regulation of channel inactivation and may contribute to CaMKIIδc-dependent arrhythmogenic disorders in failing hearts

Hepatic effects of tartrazine (E 102) after systemic exposure are independent of oestrogen receptor interactions in the mouse

Tartrazine is a food colour that activates the transcriptional function of the human oestrogen receptor alpha in an in vitro cell model. Since oestrogens are cholestatic, we hypothesised tartrazine will cause periportal injury to the liver in vivo. To test this hypothesis, tartrazine was initially administered systemically to mice resulting in a periportal recruitment of inflammatory cells, increased serum alkaline phosphatase activity and mild periportal fibrosis. To determine whether an oestrogenic effect may be a key event in this response, tartrazine, sulphonated metabolites and a food additive contaminant were screened for their ability to interact with murine oestrogen receptors. In all cases, there were no interactions as agonists or antagonists and further, no oestrogenicity was observed with tartrazine in an in vivo uterine growth assay. To examine the relevance of the hepatic effects of tartrazine to its use as a food additive, tartrazine was orally administered to transgenic NF-κB-Luc mice. Pre- and concurrent oral treatment with alcohol was incorporated given its potential to promote gut permeability and hepatic inflammation. Tartrazine alone induced NF- κB activities in the colon and liver but there was no periportal recruitment of inflammatory cells or fibrosis. Tartrazine, its sulphonated metabolites and the contaminant inhibited sulphotransferase activities in murine hepatic S9 extracts. Given the role of sulfotransferases in bile acid excretion, the initiating event giving rise to periportal inflammation and subsequent hepatic pathology through systemic tartrazine exposure is therefore potentially associated an inhibition of bile acid sulphation and excretion and not on oestrogen receptor-mediated transcriptional function. However, these effects were restricted to systemic exposures to tartrazine and did not occur to any significant effect after oral exposure