Pre-Excitation Studies for Rubidium-Plasma Generation

The key element in the Proton-Driven-Plasma-Wake-Field-Accelerator (AWAKE) project is the generation of highly uniform plasma from Rubidium vapor. The standard way to achieve full ionization is to use high power laser which can assure the over-barrier-ionization (OBI) along the 10 meters long active region. The Wigner-team in Budapest is investigating an alternative way of uniform plasma generation. The proposed Resonance Enhanced Multi Photon Ionization (REMPI) scheme probably can be realized by much less laser power. In the following the resonant pre-excitations of the Rb atoms are investigated, theoretically and the status report about the preparatory work on the experiment are presented.Comment: 8 pages, 6 figures, submitted to Nucl. Inst. and Meth. in Phys. Res.

Synthesis, Comparative Characterization and Photocatalytic Application of SnO2/MWCNT Nanocomposite Materials

Two different preparation methods were developed to cover successfully multi-walled carbon nanotubes (MWCNT) with tin-dioxide (SnO2) nanoparticles using SnCl2.2H2O as precursor under different solvent conditions. The applied mass ratios of the components were 1:4, 1:8, 1:16, 1:32 and 1:64, respectively. As-prepared tin-dioxide coverages were characterized by TEM, SEM, SEM-EDX, Raman microscopy, BET and X-ray diffraction techniques. Photocatalytic efficiencies of selected composites were investigated in a self-made photoreactor, equipped with UV-A fluorescence lamps. Photocatalytic degradation of phenol solution was followed by using HPLC. Observations revealed that using hydrothermal method we can easily control the layer of SnO2 nanoparticles on the surface of MWCNTs. Using various solvents SnO2 nanoparticles with different morphologies formed. The nanocomposites have low photocatalytic efficiencies under conditions used generally (when lambda>300 nm)

Genetically engineered minipigs model the major clinical features of human neurofibromatosis type 1.

Neurofibromatosis Type 1 (NF1) is a genetic disease caused by mutations in Neurofibromin 1 (NF1). NF1 patients present with a variety of clinical manifestations and are predisposed to cancer development. Many NF1 animal models have been developed, yet none display the spectrum of disease seen in patients and the translational impact of these models has been limited. We describe a minipig model that exhibits clinical hallmarks of NF1, including café au lait macules, neurofibromas, and optic pathway glioma. Spontaneous loss of heterozygosity is observed in this model, a phenomenon also described in NF1 patients. Oral administration of a mitogen-activated protein kinase/extracellular signal-regulated kinase inhibitor suppresses Ras signaling. To our knowledge, this model provides an unprecedented opportunity to study the complex biology and natural history of NF1 and could prove indispensable for development of imaging methods, biomarkers, and evaluation of safety and efficacy of NF1-targeted therapies

The efficacy and safety of cariprazine for the treatment of schizophrenia with negative symptoms with insufficient effectiveness of the previous antipsychotic therapyobservational research (extended abstract)

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Efficient and accurate modeling of electron photoemission in nanostructures with TDDFT

We derive and extend the time-dependent surface-flux method introduced in [L. Tao, A. Scrinzi, New J. Phys. 14, 013021 (2012)] within a time-dependent density-functional theory (TDDFT) formalism and use it to calculate photoelectron spectra and angular distributions of atoms and molecules when excited by laser pulses. We present other, existing computational TDDFT methods that are suitable for the calculation of electron emission in compact spatial regions, and compare their results. We illustrate the performance of the new method by simulating strong-field ionization of C60 fullerene and discuss final state effects in the orbital reconstruction of planar organic molecules

Modulating mitophagy in mitochondrial disease

Mitochondrial diseases may result from mutations in the maternally-inherited mitochondrial DNA (mtDNA) or from mutations in nuclear genes encoding mitochondrial proteins. Their bi-genomic nature makes mitochondrial diseases a very heterogeneous group of disorders that can present at any age and can affect any type of tissue. The autophagic-lysosomal degradation pathway plays an important role in clearing dysfunctional and redundant mitochondria through a specific quality control mechanism termed mitophagy. Mitochondria could be targeted for autophagic degradation for a variety of reasons including basal turnover for recycling, starvation induced degradation, and degradation due to damage. While the core autophagic machinery is highly conserved and common to most pathways, the signaling pathways leading to the selective degradation of damaged mitochondria are still not completely understood. Type 1 mitophagy due to nutrient starvation is dependent on PI3K (phosphoinositide 3-kinase) for autophagosome formation but independent of mitophagy proteins, PINK1 (PTEN-induced putative kinase 1) and Parkin. Whereas type 2 mitophagy that occurs due to damage is dependent on PINK1 and Parkin but does not require PI3K. Autophagy and mitophagy play an important role in human disease and hence could serve as therapeutic targets for the treatment of mitochondrial as well as neurodegenerative disorders. Therefore, we reviewed drugs that are known modulators of autophagy (AICAR and metformin) and may effect this by activating the AMP-activated protein kinase signaling pathways. Furthermore, we reviewed data available on supplements, such as Coenzyme Q and the quinone idebenone, that we assert rescue increased mitophagy in mitochondrial disease by benefiting mitochondrial function