Giant Magnetoresistance Oscillations Induced by Microwave Radiation and a Zero-Resistance State in a 2D Electron System with a Moderate Mobility

The effect of a microwave field in the frequency range from 54 to 140 $\mathrm{GHz}$ on the magnetotransport in a GaAs quantum well with AlAs/GaAs superlattice barriers and with an electron mobility no higher than $10^6$ $\mathrm{cm^2/Vs}$ is investigated. In the given two-dimensional system under the effect of microwave radiation, giant resistance oscillations are observed with their positions in magnetic field being determined by the ratio of the radiation frequency to the cyclotron frequency. Earlier, such oscillations had only been observed in GaAs/AlGaAs heterostructures with much higher mobilities. When the samples under study are irradiated with a 140-$\mathrm{GHz}$ microwave field, the resistance corresponding to the main oscillation minimum, which occurs near the cyclotron resonance, appears to be close to zero. The results of the study suggest that a mobility value lower than $10^6$ $\mathrm{cm^2/Vs}$ does not prevent the formation of zero-resistance states in magnetic field in a two-dimensional system under the effect of microwave radiation.Comment: 4 pages, 2 figur

Generation of recombinant adenoviral vectors encoding neural cell adhesion molecules ncam1, ncam2 and l1cam

To succed in gene therapy it is necessary to observe few basic conditions, such as targeted delivery of the therapeutic gene into the target organ and its effective expression. Nowadays targeted delivery of therapeutic genes is one of the critical problems of gene therapy. Delivery of recombinant genes using cell carriers (vectors), expressing tissue-specific cell adhesion molecules, allows us to move toward solving this problem. Using Gateway cloning technology (Invitrogen) we have created recombinant expression constructs pAd-NCAM1, pAd-NCAM2 and pAd-L1CAM, encoding neural cell adhesion molecules. Expression of recombinant proteins has been confirmed by immunofluorescent analysis. Based on these genetic constructs recombinant adenoviruses (serotype 5) were generated and titered. Obtained viral vectors encoding neural cell adhesion molecules may be subsequently used to modify cells carrying additional therapeutic genes to increase the efficiency of gene-cell therapeutics delivery to target organ. © Human stem cells institute, 2013

Superconductivity on the localization threshold and magnetic-field-tuned superconductor-insulator transition in TiN films

Temperature- and magnetic-field dependent measurements of the resistance of ultrathin superconducting TiN films are presented. The analysis of the temperature dependence of the zero field resistance indicates an underlying insulating behavior, when the contribution of Aslamasov-Larkin fluctuations is taken into account. This demonstrates the possibility of coexistence of the superconducting and insulating phases and of a direct transition from the one to the other. The scaling behavior of magnetic field data is in accordance with a superconductor-insulator transition (SIT) driven by quantum phase fluctuations in two-dimensional superconductor. The temperature dependence of the isomagnetic resistance data on the high-field side of the SIT has been analyzed and the presence of an insulating phase was confirmed. A transition from the insulating to a metallic phase is found at high magnetic fields, where the zero-temperature asymptotic value of the resistance being equal to h/e^2.Comment: 5 pages, 4 eps figures, RevTeX4, Published versio

Generation of recombinant adenoviruses and lentiviruses expressing angiogenic and neuroprotective factors using Gateway cloning technology

The critical aspect in gene and gene-cell therapy is to find an optimal vector - a carrier of genetic information. Viruses represent a natural biological system for gene transfer into eukaryotic cells. One of the most effective and proven vectors for delivery of recombinant nucleic acids into mammalian cells are adenoviruses and lentiviruses. In this study using the Gateway cloning we have constructed adenoviral and lentiviral vectors encoding angiogenic and neuroprotective factors: various isoforms of vascular endothelial growth factor vegf121, vegf165, vegf189; basic fibroblast growth factor fgf2; glial cell-derived neurotrophic factor gdnf. The efficiency of transduction of HEK293A cell line with generated recombinant viruses and expression of recombinant proteins were confirmed by immunofluorescent analysis

Modulation of neurotransmitter release by carbon monoxide at the frog neuro-muscular junction

Carbon monoxide (CO) is an endogenous gaseous messenger, which regulates numerous physiological functions in a wide variety of tissues. Using extracellular microelectrode recording from frog neuro-muscular preparation the mechanisms of exogenous and endogenous CO action on evoked quantal acetyl-choline (Ach) release were studied. It was shown that CO application increases Ach-release in dose-dependent manner without changes in pre-synaptic Na+ and K+ currents. The effect of exogenous CO on Ach-release was decreased by prior application of guanylate cyclase inhibitor ODQ and prevented by application of a cyclic guanylate monophospate (cGMP) analog 8Br-cGMP. Pre-treatment of the preparation with adenylate cyclase inhibitor MDL-12330A has completely abolished the effect of CO, whereas elevation of intracellular level of cyclic adenosine monophospate (cAMP) mimicked and eliminated CO action. Application of cGMP-activated phosphodiestherase-2 inhibitor EHNA did not prevent CO action, whereas inhibition of cGMP-inhibited phosphodiestherase-3 by quazinone has partially blocked the effect of CO. Utilizing immuno-histochemical methods CO-producing enzyme heme-oxygenase-2 (HO-2) was shown to be expressed in skeletal muscle fibers, mostly in subsarcolemmal region, karyolemma and sarcoplasmic reticulum. Zn-protoporphirin-IX, the selective HO-2 blocker, has depressed Ach-release, suggesting the tonic activating effect of endogenous CO on pre-synaptic function. These results suggest that facilitatory effect of CO on Ach-release is mediated by elevation of intracellular cAMP level due to activation of adenylate cyclase and decrease of cAMP breakdown. As such, endogenous skeletal muscle-derived CO mediates tonic retrograde up-regulation of neuro-transmitter release at the frog neuro-muscular junction. © 2007 Bentham Science Publishers Ltd