82 research outputs found
Photo-enhanced antinodal conductivity in the pseudogap state of high-T-c cuprates
A major challenge in understanding the cuprate superconductors is to clarify the nature of the fundamental electronic correlations that lead to the pseudogap phenomenon. Here we use ultrashort light pulses to prepare a non-thermal distribution of excitations and capture novel properties that are hidden at equilibrium. Using a broadband (0.5-2 eV) probe, we are able to track the dynamics of the dielectric function and unveil an anomalous decrease in the scattering rate of the charge carriers in a pseudogap-like region of the temperature (T) and hole-doping (p) phase diagram. In this region, delimited by a well-defined T*(neq)(p) line, the photoexcitation process triggers the evolution of antinodal excitations from gapped (localized) to delocalized quasiparticles characterized by a longer lifetime. The novel concept of photo-enhanced antinodal conductivity is naturally explained within the singleband Hubbard model, in which the short-range Coulomb repulsion leads to a k-space differentiation between nodal quasiparticles and antinodal excitations. \ua9 2014 Macmillan Publishers Limited. All rights reserved
The Actin-Binding Protein Capulet Genetically Interacts with the Microtubule Motor Kinesin to Maintain Neuronal Dendrite Homeostasis
BACKGROUND: Neurons require precise cytoskeletal regulation within neurites, containing microtubule tracks for cargo transport in axons and dendrites or within synapses containing organized actin. Due to the unique architecture and specialized function of neurons, neurons are particularly susceptible to perturbation of the cytoskeleton. Numerous actin-binding proteins help maintain proper cytoskeletal regulation. METHODOLOGY/PRINCIPAL FINDINGS: From a Drosophila forward genetic screen, we identified a mutation in capulet--encoding a conserved actin-binding protein--that causes abnormal aggregates of actin within dendrites. Through interaction studies, we demonstrate that simultaneous genetic inactivation of capulet and kinesin heavy chain, a microtubule motor protein, produces elongate cofilin-actin rods within dendrites but not axons. These rods resemble actin-rich structures induced in both mammalian neurodegenerative and Drosophila Alzheimer's models, but have not previously been identified by loss of function mutations in vivo. We further demonstrate that mitochondria, which are transported by Kinesin, have impaired distribution along dendrites in a capulet mutant. While Capulet and Cofilin may biochemically cooperate in certain circumstances, in neuronal dendrites they genetically antagonize each other. CONCLUSIONS/SIGNIFICANCE: The present study is the first molecularly defined loss of function demonstration of actin-cofilin rods in vivo. This study suggests that simultaneous, seemingly minor perturbations in neuronal dendrites can synergize producing severe abnormalities affecting actin, microtubules and mitochondria/energy availability in dendrites. Additionally, as >90% of Alzheimer's and Parkinson's cases are sporadic this study suggests mechanisms by which multiple mutations together may contribute to neurodegeneration instead of reliance on single mutations to produce disease
La délocalisation des pratiques pour la mise en valeur des territoires: L'exemple des événements de glisse en zone urbaine
Cytotoxic Leaf Essential Oils from Neotropical Lauraceae: Synergistic Effects of Essential Oil Components
Antibacterial Activity of Anti-Aphthous Spray and Oral Drop: Two Thymus Commercial Products
Residual amounts of glycoproteins IIb and IIIa may be present in the platelets of most patients with Glanzmann's thrombasthenia
Immunochemical characterization of the platelet-specific alloantigen Leka: a comparative study with the PlA1 alloantigen
The human platelet membrane glycoprotein complex GP IIb-IIIa expresses antigenic sites not exposed on the dissociated glycoproteins
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