The number of childhood adverse life events affects relative telomere length at adult age.

<p>Relative telomere length is adjusted for age and sex. Each bar presents group mean (± standard error of the mean).</p

Telomere length as a function of age.

<p>Anxiety disorder core and subthreshold cases (N = 321) are shown with red dots and controls (N = 653) with blue dots, each dot representing one individual. Regression lines for both groups are shown with the same color coding.</p

Telomere length is affected by childhood adverse life events but not by anxiety disorder diagnosis or recent psychological stress.

1<p>Difference in standardized telomere length for one unit or category change in each independent variable.</p>2<p>Standard error of the mean.</p>3<p>Sum score of the 12-item General Health Questionnaire.</p>4<p>Categorized to 0 adversities, 1 adversity, 2 or 3 adversities, and 4 or more adversities.</p><p>Results from three independent regression models are shown in which sex and age adjusted telomere length was explained by either anxiety disorder status, GHQ-12 score, or number of childhood adversities.</p

Several differentially expressed genes show significant clustering in around on mouse chromosome 4, and might therefore be coregulated

The probesets for Ppt1 were excluded from the dataset and thus Ppt1 is shown in gray. The genes participating in the regulated loci or being independently regulated are shown, together with their location in base pairs in mouse chromosome 4. Genes that exhibit expression differences in both mouse models are indicated with *. Expression changes only in the mouse are indicated with **.<p><b>Copyright information:</b></p><p>Taken from "Brain gene expression profiles of and deficient mice unravels common molecular pathways underlying neuronal degeneration in NCL diseases"</p><p>http://www.biomedcentral.com/1471-2164/9/146</p><p>BMC Genomics 2008;9():146-146.</p><p>Published online 28 Mar 2008</p><p>PMCID:PMC2323392.</p><p></p

Western blot analysis of cytoplasmic and membrane bound fractions of cytoskeletal, growth-cone and synapse assembly proteins

Antibodies: β-tubulin, synapsin 1, synapsin 1&2, Rab3 and Gap43.<p><b>Copyright information:</b></p><p>Taken from "Brain gene expression profiles of and deficient mice unravels common molecular pathways underlying neuronal degeneration in NCL diseases"</p><p>http://www.biomedcentral.com/1471-2164/9/146</p><p>BMC Genomics 2008;9():146-146.</p><p>Published online 28 Mar 2008</p><p>PMCID:PMC2323392.</p><p></p

Indomethacin: New Polymorphs of an Old Drug

This study reports the appearance and characterization of multiple new polymorphic forms of indomethacin. Considering the interest in amorphous suspensions for toxicology studies of poorly water-soluble drugs, we sought to investigate the crystallization behavior of amorphous indomethacin in aqueous suspension. Specifically, the effect of pH and temperature on crystallization behavior was studied. Quench cooled amorphous powder was added to buffered media at different pH values (1.2, 4.5, and 6.8) at 5 and 25 °C. Both the solid and the solution were analyzed at different time points up to 24 h. Attenuated total reflection Fourier transform infrared (ATR-FTIR) spectroscopy (with principal component analysis) was used to study solid-phase transformations and ultraviolet (UV) spectroscopy used to probe solution concentration. The crystallization onset time decreased and rate of crystallization increased with increasing pH and temperature. Diverse polymorphic forms were observed, with three new forms being identified; these were named ε, ζ, and η. At 25 °C, the amorphous form recrystallized directly to the α form, except at pH 6.8, where it initially converted briefly into the ε form. At 5 °C, all three new polymorphic forms were observed sequentially in the order ε, ζ, and then η, with the number of these forms observed increasing sequentially with decreasing pH. The three new forms exhibited distinct X-ray powder diffraction (XPRD), differential scanning calorimetry (DSC), and FTIR and Raman spectroscopy profiles. The solution concentration profiles suggest that the relative physical stabilities of the polymorphs at 5 °C from lowest to highest is ε < ζ < η < α. The appearance of new polymorphs in this study suggests that amorphous suspensions are worth considering when performing polymorphic screening studies

Multimodal Nonlinear Optical Imaging for Sensitive Detection of Multiple Pharmaceutical Solid-State Forms and Surface Transformations

Two nonlinear imaging modalities, coherent anti-Stokes Raman scattering (CARS) and sum-frequency generation (SFG), were successfully combined for sensitive multimodal imaging of multiple solid-state forms and their changes on drug tablet surfaces. Two imaging approaches were used and compared: (i) hyperspectral CARS combined with principal component analysis (PCA) and SFG imaging and (ii) simultaneous narrowband CARS and SFG imaging. Three different solid-state forms of indomethacinthe crystalline gamma and alpha forms, as well as the amorphous formwere clearly distinguished using both approaches. Simultaneous narrowband CARS and SFG imaging was faster, but hyperspectral CARS and SFG imaging has the potential to be applied to a wider variety of more complex samples. These methodologies were further used to follow crystallization of indomethacin on tablet surfaces under two storage conditions: 30 °C/23% RH and 30 °C/75% RH. Imaging with (sub)­micron resolution showed that the approach allowed detection of very early stage surface crystallization. The surfaces progressively crystallized to predominantly (but not exclusively) the gamma form at lower humidity and the alpha form at higher humidity. Overall, this study suggests that multimodal nonlinear imaging is a highly sensitive, solid-state (and chemically) specific, rapid, and versatile imaging technique for understanding and hence controlling (surface) solid-state forms and their complex changes in pharmaceuticals

Association results of SNPs associated at a significance value of 0.05 or less in the individual genotyping stage, along with their pooling stage results.

<p>SNPs written in bold are significant after correcting for multiple testing.</p

Graphical summary of association results from the genome-wide screen of pooled samples.

<p>X-axis represents the chromosome position; y-axis shows -log10 of the P-value obtained for each SNP.</p

15 SNPs chosen for individual genotyping with the P-values from the pooling stage.

a<p>Indicates SNPs that did not survive quality control measures to be included in the association validation analysis.</p