463 research outputs found

    Structure, Photophysics and the Order-Disorder Transition to the Beta Phase in Poly(9,9-(di -n,n-octyl)fluorene)

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    X-ray diffraction, UV-vis absorption and photoluminescence (PL) spectroscopy have been used to study the well-known order-disorder transition (ODT) to the beta phase in poly(9,9-(di n,n-octyl)fluorene)) (PF8) thin film samples through combination of time-dependent and temperature-dependent measurements. The ODT is well described by a simple Avrami picture of one-dimensional nucleation and growth but crystallization, on cooling, proceeds only after molecular-level conformational relaxation to the so called beta phase. Rapid thermal quenching is employed for PF8 studies of pure alpha phase samples while extended low-temperature annealing is used for improved beta phase formation. Low temperature PL studies reveal sharp Franck-Condon type emission bands and, in the beta phase, two distinguishable vibronic sub-bands with energies of approximately 199 and 158 meV at 25 K. This improved molecular level structural order leads to a more complete analysis of the higher-order vibronic bands. A net Huang-Rhys coupling parameter of just under 0.7 is typically observed but the relative contributions by the two distinguishable vibronic sub-bands exhibit an anomalous temperature dependence. The PL studies also identify strongly correlated behavior between the relative beta phase 0-0 PL peak position and peak width. This relationship is modeled under the assumption that emission represents excitons in thermodynamic equilibrium from states at the bottom of a quasi-one-dimensional exciton band. The crystalline phase, as observed in annealed thin-film samples, has scattering peaks which are incompatible with a simple hexagonal packing of the PF8 chains.Comment: Submitted to PRB, 12 files; 1 tex, 1 bbl, 10 eps figure

    Acute escitalopram treatment inhibits REM sleep rebound and activation of MCH-expressing neurons in the lateral hypothalamus after long term selective REM sleep deprivation.

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    RATIONALE: Selective rapid eye movement sleep (REMS) deprivation using the platform-on-water ("flower pot") method causes sleep rebound with increased REMS, decreased REMS latency, and activation of the melanin-concentrating hormone (MCH) expressing neurons in the hypothalamus. MCH is implicated in the pathomechanism of depression regarding its influence on mood, feeding behavior, and REMS. OBJECTIVES: We investigated the effects of the most selective serotonin reuptake inhibitor escitalopram on sleep rebound following REMS deprivation and, in parallel, on the activation of MCH-containing neurons. METHODS: Escitalopram or vehicle (10 mg/kg, intraperitoneally) was administered to REMS-deprived (72 h) or home cage male Wistar rats. During the 3-h-long "rebound sleep", electroencephalography was recorded, followed by an MCH/Fos double immunohistochemistry. RESULTS: During REMS rebound, the time spent in REMS and the number of MCH/Fos double-labeled neurons in the lateral hypothalamus increased markedly, and REMS latency showed a significant decrease. All these effects of REMS deprivation were significantly attenuated by escitalopram treatment. Besides the REMS-suppressing effects, escitalopram caused an increase in amount of and decrease in latency of slow wave sleep during the rebound. CONCLUSIONS: These results show that despite the high REMS pressure caused by REMS deprivation procedure, escitalopram has the ability to suppress REMS rebound, as well as to diminish the activation of MCH-containing neurons, in parallel. Escitalopram caused a shift from REMS to slow wave sleep during the rebound. Furthermore, these data point to the potential connection between the serotonergic system and MCH in sleep regulation, which can be relevant in depression and in other mood disorders

    Gene expression during normal and FSHD myogenesis

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    <p>Abstract</p> <p>Background</p> <p>Facioscapulohumeral muscular dystrophy (FSHD) is a dominant disease linked to contraction of an array of tandem 3.3-kb repeats (D4Z4) at 4q35. Within each repeat unit is a gene, <it>DUX4</it>, that can encode a protein containing two homeodomains. A <it>DUX4 </it>transcript derived from the last repeat unit in a contracted array is associated with pathogenesis but it is unclear how.</p> <p>Methods</p> <p>Using exon-based microarrays, the expression profiles of myogenic precursor cells were determined. Both undifferentiated myoblasts and myoblasts differentiated to myotubes derived from FSHD patients and controls were studied after immunocytochemical verification of the quality of the cultures. To further our understanding of FSHD and normal myogenesis, the expression profiles obtained were compared to those of 19 non-muscle cell types analyzed by identical methods.</p> <p>Results</p> <p>Many of the ~17,000 examined genes were differentially expressed (> 2-fold, <it>p </it>< 0.01) in control myoblasts or myotubes vs. non-muscle cells (2185 and 3006, respectively) or in FSHD vs. control myoblasts or myotubes (295 and 797, respectively). Surprisingly, despite the morphologically normal differentiation of FSHD myoblasts to myotubes, most of the disease-related dysregulation was seen as dampening of normal myogenesis-specific expression changes, including in genes for muscle structure, mitochondrial function, stress responses, and signal transduction. Other classes of genes, including those encoding extracellular matrix or pro-inflammatory proteins, were upregulated in FSHD myogenic cells independent of an inverse myogenesis association. Importantly, the disease-linked <it>DUX4 </it>RNA isoform was detected by RT-PCR in FSHD myoblast and myotube preparations only at extremely low levels. Unique insights into myogenesis-specific gene expression were also obtained. For example, all four Argonaute genes involved in RNA-silencing were significantly upregulated during normal (but not FSHD) myogenesis relative to non-muscle cell types.</p> <p>Conclusions</p> <p><it>DUX4</it>'s pathogenic effect in FSHD may occur transiently at or before the stage of myoblast formation to establish a cascade of gene dysregulation. This contrasts with the current emphasis on toxic effects of experimentally upregulated <it>DUX4 </it>expression at the myoblast or myotube stages. Our model could explain why <it>DUX4</it>'s inappropriate expression was barely detectable in myoblasts and myotubes but nonetheless linked to FSHD.</p

    The mental health of populations directly and indirectly exposed to violent conflict in Indonesia

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    Background Large disasters affect people who live both near and far from the areas in which they occur. The mental health impact is expected to be similar to a ripple effect, where the risk of mental health consequences generally decreases with increasing distance from the disaster center. However, we have not been able to identify studies of the ripple effect of man-made disaster on mental health in low-income countries. Objectives The objective was to examine the hypothesis of a ripple effect on the mental health consequences in populations exposed to man-made disasters in a developing country context, through a comparison of two different populations living in different proximities from the center of disaster in Mollucas. Methods Cross-sectional longitudinal data were collected from 510 Internally Displaced Persons (IDPs) living in Ambon, who were directly exposed to the violence, and non-IDPs living in remote villages in Mollucas, Indonesia, who had never been directly exposed to violence in Mollucas. Data were collected during home visits and statistical comparisons were conducted by using chi square tests, t-test and logistic regression. Results There was significantly more psychological distress "caseness" in IDPs than non-IDPs. The mental health consequences of the violent conflict in Ambon supported the ripple effect hypothesis as displacement status appears to be a strong risk factor for distress, both as a main effect and interaction effect. Significantly higher percentages of IDPs experienced traumatic events than non-IDPs in all six event types reported. Conclusions This study indicates that the conflict had an impact on mental health and economic conditions far beyond the area where the actual violent events took place, in a diminishing pattern in line with the hypothesis of a ripple effect
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