303 research outputs found

    Hypothalamic tanycytes—masters and servants of metabolic, neuroendocrine, and neurogenic functions

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    There is a resurgent interest in tanycytes, a radial glial-like cell population occupying the floor and ventro-lateral walls of the third ventricle (3V). Tanycytes reside in close proximity to hypothalamic neuronal nuclei that regulate appetite and energy expenditure, with a subset sending projections into these nuclei. Moreover, tanycytes are exposed to 3V cerebrospinal fluid and have privileged access to plasma metabolites and hormones, through fenestrated capillaries. Indeed, some tanycytes act as conduits for trafficking of these molecules into the brain parenchyma. Tanycytes can also act as neural stem/progenitor cells, supplying the postnatal and adult hypothalamus with new neurons. Collectively, these findings suggest that tanycytes regulate and integrate important trophic and metabolic processes and possibly endow functional malleability to neuronal circuits of the hypothalamus. Hence, manipulation of tanycyte biology could provide a valuable tool for modulating hypothalamic functions such as energy uptake and expenditure in order to tackle prevalent eating disorders such as obesity and anorexia

    THERMOPLASTIC STARCH/WOOD COMPOSITES: INTERFACIAL INTERACTIONS AND FUNCTIONAL PROPERTIES

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    Thermoplastic starch (TPS)/wood composites were prepared from starch plasticized with 36 wt% glycerol. The components were homogenized by dry-blending, extruded and injection molded to tensile bars. Tensile properties, structure, deformation, water adsorption and shrinkage were determined as a function of wood content, which changed between 0 and 40 vol% in 7 steps. The modification of TPS with wood particles improves several properties considerably. Stiffness and strength increases, and the effect is stronger for fibers with larger aspect ratio. Wood fibers reinforce TPS considerably due to poor ma-trix properties and strong interfacial interactions, the latter resulting in the decreased mo-bility of starch molecules and in the fracture of large wood particles during deformation. Strong interfacial adhesion leads to smaller water absorption than predicted from additivity, but water uptake remains relatively large even in the presence of wood particles. The shrinkage of injection molded TPS parts is very large, around 10 %, and dimensional changes occur on a very long timescale of several hundred hours. Shrinkage decreases to a low level already at 15-20 vol% wood content rendering the composites good dimensional stability

    AKT Signaling Mediates IGF-I Survival Actions on Otic Neural Progenitors

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    Background: Otic neurons and sensory cells derive from common progenitors whose transition into mature cells requires the coordination of cell survival, proliferation and differentiation programmes. Neurotrophic support and survival of post-mitotic otic neurons have been intensively studied, but the bases underlying the regulation of programmed cell death in immature proliferative otic neuroblasts remains poorly understood. The protein kinase AKT acts as a node, playing a critical role in controlling cell survival and cell cycle progression. AKT is activated by trophic factors, including insulin-like growth factor I (IGF-I), through the generation of the lipidic second messenger phosphatidylinositol 3-phosphate by phosphatidylinositol 3-kinase (PI3K). Here we have investigated the role of IGF-dependent activation of the PI3K-AKT pathway in maintenance of otic neuroblasts. Methodology/Principal Findings: By using a combination of organotypic cultures of chicken (Gallus gallus) otic vesicles and acoustic-vestibular ganglia, Western blotting, immunohistochemistry and in situ hybridization, we show that IGF-I-activation of AKT protects neural progenitors from programmed cell death. IGF-I maintains otic neuroblasts in an undifferentiated and proliferative state, which is characterised by the upregulation of the forkhead box M1 (FoxM1) transcription factor. By contrast, our results indicate that post-mitotic p27Kip-positive neurons become IGF-I independent as they extend their neuronal processes. Neurons gradually reduce their expression of the Igf1r, while they increase that of the neurotrophin receptor, TrkC. Conclusions/Significance: Proliferative otic neuroblasts are dependent on the activation of the PI3K-AKT pathway by IGF-I for survival during the otic neuronal progenitor phase of early inner ear development

    Elliptic flow of charged particles in Pb-Pb collisions at 2.76 TeV

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    We report the first measurement of charged particle elliptic flow in Pb-Pb collisions at 2.76 TeV with the ALICE detector at the CERN Large Hadron Collider. The measurement is performed in the central pseudorapidity region (|η\eta|<0.8) and transverse momentum range 0.2< pTp_{\rm T}< 5.0 GeV/cc. The elliptic flow signal v2_2, measured using the 4-particle correlation method, averaged over transverse momentum and pseudorapidity is 0.087 ±\pm 0.002 (stat) ±\pm 0.004 (syst) in the 40-50% centrality class. The differential elliptic flow v2(pT)_2(p_{\rm T}) reaches a maximum of 0.2 near pTp_{\rm T} = 3 GeV/cc. Compared to RHIC Au-Au collisions at 200 GeV, the elliptic flow increases by about 30%. Some hydrodynamic model predictions which include viscous corrections are in agreement with the observed increase.Comment: 10 pages, 4 captioned figures, published version, figures at http://aliceinfo.cern.ch/ArtSubmission/node/389

    Corticofugal Modulation of Initial Neural Processing of Sound Information from the Ipsilateral Ear in the Mouse

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    Background: Cortical neurons implement a high frequency-specific modulation of subcortical nuclei that includes the cochlear nucleus. Anatomical studies show that corticofugal fibers terminating in the auditory thalamus and midbrain are mostly ipsilateral. Differently, corticofugal fibers terminating in the cochlear nucleus are bilateral, which fits to the needs of binaural hearing that improves hearing quality. This leads to our hypothesis that corticofugal modulation of initial neural processing of sound information from the contralateral and ipsilateral ears could be equivalent or coordinated at the first sound processing level. Methodology/Principal Findings: With the focal electrical stimulation of the auditory cortex and single unit recording, this study examined corticofugal modulation of the ipsilateral cochlear nucleus. The same methods and procedures as described in our previous study of corticofugal modulation of contralateral cochlear nucleus were employed simply for comparison. We found that focal electrical stimulation of cortical neurons induced substantial changes in the response magnitude, response latency and receptive field of ipsilateral cochlear nucleus neurons. Cortical stimulation facilitated auditory response and shortened the response latency of physiologically matched neurons whereas it inhibited auditory response and lengthened the response latency of unmatched neurons. Finally, cortical stimulation shifted the best frequencies of cochlear neurons towards those of stimulated cortical neurons

    Rapid Changes in the Light/Dark Cycle Disrupt Memory of Conditioned Fear in Mice

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    Background: Circadian rhythms govern many aspects of physiology and behavior including cognitive processes. Components of neural circuits involved in learning and memory, e.g., the amygdala and the hippocampus, exhibit circadian rhythms in gene expression and signaling pathways. The functional significance of these rhythms is still not understood. In the present study, we sought to determine the impact of transiently disrupting the circadian system by shifting the light/ dark (LD) cycle. Such ‘‘jet lag’ ’ treatments alter daily rhythms of gene expression that underlie circadian oscillations as well as disrupt the synchrony between the multiple oscillators found within the body. Methodology/Principal Findings: We subjected adult male C57Bl/6 mice to a contextual fear conditioning protocol either before or after acute phase shifts of the LD cycle. As part of this study, we examined the impact of phase advances and phase delays, and the effects of different magnitudes of phase shifts. Under all conditions tested, we found that recall of fear conditioned behavior was specifically affected by the jet lag. We found that phase shifts potentiated the stress-evoked corticosterone response without altering baseline levels of this hormone. The jet lag treatment did not result in overall sleep deprivation, but altered the temporal distribution of sleep. Finally, we found that prior experience of jet lag helps to compensate for the reduced recall due to acute phase shifts. Conclusions/Significance: Acute changes to the LD cycle affect the recall of fear-conditioned behavior. This suggests that
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