Dissociating object familiarity from linguistic properties in mirror word reading-1

<p><b>Copyright information:</b></p><p>Taken from "Dissociating object familiarity from linguistic properties in mirror word reading"</p><p>http://www.behavioralandbrainfunctions.com/content/3/1/43</p><p>Behavioral and brain functions : BBF 2007;3():43-43.</p><p>Published online 20 Aug 2007</p><p>PMCID:PMC1995209.</p><p></p>as a function of their lexical category

Dissociating object familiarity from linguistic properties in mirror word reading-0

<p><b>Copyright information:</b></p><p>Taken from "Dissociating object familiarity from linguistic properties in mirror word reading"</p><p>http://www.behavioralandbrainfunctions.com/content/3/1/43</p><p>Behavioral and brain functions : BBF 2007;3():43-43.</p><p>Published online 20 Aug 2007</p><p>PMCID:PMC1995209.</p><p></p>as a function of their lexical category

Mean P-wave duration measured in a single lead over all sectors (95% CI).

<p>The two sectors which comprise the manoeuvres are shaded grey. We observed significant differences for ITH and MM vs BL during the manoeuvre (both p<0.001). The P-wave duration did not change during the course of the BL (p = 0.99) and AP (p = 0.94) manoeuvre. All analyses were adjusted for PAF status, heart rate, age, BMI, and sex. BL = baseline (normal breathing). ITH = inspiration through a threshold load (simulating an obstructive hypopnea). MM = Mueller manoeuvre (simulating an obstructive apnea). AP = end-expiratory breath holding (simulating central apnea).</p

Simulated Obstructive Sleep Apnea Increases P-Wave Duration and P-Wave Dispersion

<div><p>Background</p><p>A high P-wave duration and dispersion (Pd) have been reported to be a prognostic factor for the occurrence of paroxysmal atrial fibrillation (PAF), a condition linked to obstructive sleep apnea (OSA). We tested the hypothesis of whether a short-term increase of P-wave duration and Pd can be induced by respiratory manoeuvres simulating OSA in healthy subjects and in patients with PAF.</p><p>Methods</p><p>12-lead-electrocardiography (ECG) was recorded continuously in 24 healthy subjects and 33 patients with PAF, while simulating obstructive apnea (Mueller manoeuvre, MM), obstructive hypopnea (inspiration through a threshold load, ITH), central apnea (AP), and during normal breathing (BL) in randomized order. The P-wave duration and Pd was calculated by using dedicated software for ECG-analysis.</p><p>Results</p><p>P-wave duration and Pd significantly increased during MM and ITH compared to BL in all subjects (+13.1ms and +13.8ms during MM; +11.7ms and +12.9ms during ITH; p<0.001 for all comparisons). In MM, the increase was larger in healthy subjects when compared to patients with PAF (p<0.05).</p><p>Conclusion</p><p>Intrathoracic pressure swings through simulated obstructive sleep apnea increase P-wave duration and Pd in healthy subjects and in patients with PAF. Our findings imply that intrathoracic pressure swings prolong the intra-atrial and inter-atrial conduction time and therefore may represent an independent trigger factor for the development for PAF.</p></div

Differences in P-wave mean and Pd in ms during breathing manoeuvres in all patients (n = 57).

<p>Differences in P-wave mean and Pd in ms during breathing manoeuvres in all patients (n = 57).</p

Clinical characteristics by study population.

<p>Clinical characteristics by study population.</p

DataSheet1_Regulation of cellular contractile force, shape and migration of fibroblasts by oncogenes and Histone deacetylase 6.docx

The capacity of cells to adhere to, exert forces upon and migrate through their surrounding environment governs tissue regeneration and cancer metastasis. The role of the physical contractile forces that cells exert in this process, and the underlying molecular mechanisms are not fully understood. We, therefore, aimed to clarify if the extracellular forces that cells exert on their environment and/or the intracellular forces that deform the cell nucleus, and the link between these forces, are defective in transformed and invasive fibroblasts, and to indicate the underlying molecular mechanism of control. Confocal, Epifluorescence and Traction force microscopy, followed by computational analysis, showed an increased maximum contractile force that cells apply on their environment and a decreased intracellular force on the cell nucleus in the invasive fibroblasts, as compared to normal control cells. Loss of HDAC6 activity by tubacin-treatment and siRNA-mediated HDAC6 knockdown also reversed the reduced size and more circular shape and defective migration of the transformed and invasive cells to normal. However, only tubacin-mediated, and not siRNA knockdown reversed the increased force of the invasive cells on their surrounding environment to normal, with no effects on nuclear forces. We observed that the forces on the environment and the nucleus were weakly positively correlated, with the exception of HDAC6 siRNA-treated cells, in which the correlation was weakly negative. The transformed and invasive fibroblasts showed an increased number and smaller cell-matrix adhesions than control, and neither tubacin-treatment, nor HDAC6 knockdown reversed this phenotype to normal, but instead increased it further. This highlights the possibility that the control of contractile force requires separate functions of HDAC6, than the control of cell adhesions, spreading and shape. These data are consistent with the possibility that defective force-transduction from the extracellular environment to the nucleus contributes to metastasis, via a mechanism that depends upon HDAC6. To our knowledge, our findings present the first correlation between the cellular forces that deforms the surrounding environment and the nucleus in fibroblasts, and it expands our understanding of how cells generate contractile forces that contribute to cell invasion and metastasisis.</p

Correlation between the RET receptor expression and RET transcripts on four different cell lines.

<p>(A) Flow cytometric histogram graphs showing the MFI levels of expression of RET receptor (black line) of 4 different cell lines. Gray shaded histograms represent the isotype controls. (B) Histogram bar graph showing the number of RET mRNA copies produced by the same cell lines displayed in panel A and analyzed within the same time-frame in culture. Values are normalized on SK-N-MC cell line of one experiment and are reported as fold increased in expression (2^−ΔCt) as mean of three independent experiments. Of note, the level of RET receptor expressed on cell membrane significantly correlated with the amount of RET transcripts, as assessed by the Spearman rank test for correlation.</p

Modulation of RET-independent genes.

<p>Histogram bar graph showing the relative transcript levels of genes that, regardless of treatment with GDNF and GFRα1, are differently modulated in PBMCs from healthy donors and HSCR patients. The amounts of mRNA either in freshly purified (left part of the graph) or treated (right part of the graph) of PBMCs of healthy donors (white bars) and HSCR patients (black bars) were detected by Taqman Low Density Array (TLDA) card.</p

Levels (pg/ml) and standard deviation (SD) of soluble inflammatory cytokines and chemokines measured in the supernatant of PBMCs either in the absence (italic) or in the presence (bold italic) o treatment with GDNF and GFRα1.

<p>Levels (pg/ml) and standard deviation (SD) of soluble inflammatory cytokines and chemokines measured in the supernatant of PBMCs either in the absence (italic) or in the presence (bold italic) o treatment with GDNF and GFRα1.</p