381 research outputs found

    Coherent oscillations of electrons in tunnel-coupled wells under ultrafast intersubband excitation

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    Ultrafast intersubband excitation of electrons in tunnell-coupled wells is studied depending on the structure parameters, the duration of the infrared pump and the detuning frequency. The temporal dependencies of the photoinduced concentration and dipole moment are obtained for two cases of transitions: from the single ground state to the tunnel-coupled excited states and from the tunnel-coupled states to the single excited state. The peculiarities of dephasing and population relaxation processes are also taken into account. The nonlinear regime of the response is also considered when the splitting energy between the tunnel-coupled levels is renormalized by the photoexcited electron concentration. The dependencies of the period and the amplitude of oscillations on the excitation pulse are presented with a description of the nonlinear oscillations damping.Comment: 8 pages, 12 figure

    Trion dynamics in coupled double quantum wells. Electron density effects

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    We have studied the coherent dynamics of injected electrons when they are either free or bounded both in excitons and in trions (charged excitons). We have considered a remotely doped asymmetric double quantum well where an excess of free electrons and the direct created excitons generate trions. We have used the matrix density formalism to analyze the electron dynamics for different concentration of the three species. Calculations show a significant modification of the free electron inter-sublevel oscillations cWe have studied the coherent dynamics of injected electrons when they are aused by electrons bound in excitons and trions. Based on the present calculations we propose a method to detect trions through the emitted electromagnetic radiation or the current density.Comment: 14 pages, 13 figure

    Papers for Task Force Meeting on Future and Impacts of Artificial Intelligence, 15-17 August 1983

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    IIASA's Clearinghouse activity is oriented towards issues of interest among our National Member Organizations. Here, in the forefront, are the issues concerning the promise and impact of science and technology on society and economy in general, and some selected branches in particular. Artificial Intelligence (AI) is one of the most promising research areas. There are many indications that the long predicted upswing of this discipline is finally in the making. A recent survey had Nobel-laureates predict that the most influence in the next century will be made by computers, AI, and robotics. Already, at present, "expert" systems are emerging and applied; natural language understanding systems developed; AI principles are used in robots, flexible automation, computer aided-design, etc. All this will have an, as yet, unspecified social and economic impact on the activity of human beings, both at work and leisure. It certainly takes interdisciplinary and cross-culturally based studies to enhance the understanding of this complex phenomenon. This is the aim of our endeavors in the field which is in excess of our duty to pass useful knowledge to our constituency. We think that IIASA, cooperating in this respect with the Austrian Society for Cybernetic Studies (ASCS), can develop some comparative advantage here. This publication contains papers written by leading personalities, both East and West, in the field of artificial intelligence on the future and impact of this emerging discipline. We hope that the meeting, where the papers will be discussed, will not only identify important areas where the impact of artificial intelligence will be felt most directly, but also find the most rewarding issues for further research

    Inhomogeneous broadening of tunneling conductance in double quantum wells

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    The lineshape of the tunneling conductance in double quantum wells with a large-scale roughness of heterointerfaces is investigated. Large-scale variations of coupled energy levels and scattering due to the short-range potential are taken into account. The interplay between the inhomogeneous broadening, induced by the non-screened part of large-scale potential, and the homogeneous broadening due to the scattering by short-range potentials is considered. It is shown that the large inhomogeneous broadening can be strongly modified by nonlocal effects involved in the proposed mechanism of inhomogeneity. Related change of lineshape of the resonant tunneling conductance between Gaussian and Lorentzian peaks is described. The theoretical results agree quite well with experimental data.Comment: 11 pages, 5 figure

    Implications of Ape1 in reactive oxygen signaling response following cisplatin treatment of dorsal root ganglion neurons

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    Peripheral neuropathy is one of the major side-effects of the anticancer drug, cisplatin. Although previous work suggests that this neuropathy correlates with formation of DNA adducts in sensory neurons, growing evidence suggests that cisplatin also increases the generation of reactive oxygen species (ROS), which could cause DNA damage. Apurinic/apyrimidinic endonuclease/redox factor-1 (Ape1/Ref-1) is a multifunctional protein involved in DNA base excision repair (BER) of oxidative DNA damage and in redox regulation of a number of transcription factors. Therefore, we asked whether altering Ape1 functions would influence cisplatin induced neurotoxicity. Sensory neurons in culture were exposed to cisplatin for 24 hrs and several endpoints of toxicity were measured including production of ROS, cell death, apoptosis, and release of the immunoreactive calcitonin gene-related peptide (iCGRP). Reducing expression of Ape1 in neuronal cultures using siRNA enhances cisplatin-induced cell killing, apoptosis, ROS generation and the cisplatin-induced reduction in iCGRP release. Overexpressing wild-type (WT)-Ape1 attenuates all the toxic effects of cisplatin in cells containing normal endogenous levels of Ape1 and in cells with reduced Ape1 levels following Ape1siRNA treatment. Overexpressing the redox deficient/repair competent C65-Ape1 provides partial rescue, while the repair deficient Ape1 (N226A+R177A) does not protect neurons from cisplatin toxicity. We also observe an increase in phosphorylation of p53 following a decrease in Ape1 levels in sensory neuronal cultures. These results strongly support the notion that Ape1 is a potential translational target such that protecting Ape1 levels and particularly its DNA repair function could reduce peripheral neuropathy in patients undergoing cisplatin treatment

    DNA damage mediates changes in neuronal sensitivity induced by the inflammatory mediators, MCP-1 and LPS, and can be reversed by enhancing the DNA repair function of APE1

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    Although inflammation-induced peripheral sensitization oftentimes resolves as an injury heals, this sensitization can be pathologically maintained and contribute to chronic inflammatory pain. Numerous inflammatory mediators increase the production of reactive oxygen (ROS) and nitrogen species (RNS) during inflammation and in animal models of chronic neuropathic pain. Our previous studies demonstrate that ROS/RNS and subsequent DNA damage mediate changes in neuronal sensitivity induced by anticancer drugs and by ionizing radiation in sensory neurons, thus we investigated whether inflammation and inflammatory mediators also could cause DNA damage in sensory neurons and whether that DNA damage alters neuronal sensitivity. DNA damage was assessed by pH2A.X expression and the release of the neuropeptide, calcitonin gene-related peptide (CGRP), was measured as an index of neuronal sensitivity. Peripheral inflammation or exposure of cultured sensory neurons to the inflammatory mediators, LPS and MCP-1, elicited DNA damage. Moreover, exposure of sensory neuronal cultures to LPS or MCP-1 resulted in changes in the stimulated release of CGRP, without altering resting release or CGRP content. Genetically enhancing the expression of the DNA repair enzyme, apurinic/apyrimidinic endonuclease (APE1) or treatment with a small-molecule modulator of APE1 DNA repair activity, both which enhance DNA repair, attenuated DNA damage and the changes in neuronal sensitivity elicited by LPS or MCP-1. In conclusion, our studies demonstrate that inflammation or exposure to inflammatory mediators elicits DNA damage in sensory neurons. By enhancing DNA repair, we demonstrate that this DNA damage mediates the alteration of neuronal function induced by inflammatory mediators in peptidergic sensory neurons

    THE EFFECT OF THE ANISOTROPY DRILLING INDEX ON THE DEVIATION OF THE WELL AXIS FROM THE DESIGN PROFILE

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    Analytical studies of the interaction of the  load on the bottom and the bottom hole assembly of the drill string with the bottom itself and the wall of the well during drilling tilted formations have been  carried out. The correlation interrelation among the drilling index of anisotropy, zenith angle, the slope of the seams, geometric characteristics of the well, the bottom hole assembly of the drill string and the axial load on the bit has been proved.Analytical studies of the impact of bottom hole  assembly  of the drill string containing a centralizer on the bottom itself and the borehole wall have been performed. It has been found  that with an increase in the axial load on the bit and the gap between  the loaded drill pipes and the borehole wall from the bit to the point of contact, the column with the borehole wall distance decreases, and the centralizer in the bottomhole assembly of the drill string increases this distance, thus  increasing bit  load without the risk of the zenith angle deviation.Keywords: borehole wall, zenith angle, drill string, bit load, bottom hole assembly of the drill string, centralizer, dispersion index anisotropy, reservoir angle.кандидат технічних наук, доцент, Кочкодан Я. М., Васько А. І., Добруцький Р. Л. Вплив бурового індексу анізотропії на відхилення осі свердловини від проектного профілю/ Івано-Франківський національний технічний університет нафти і газу, Україна, Івано-ФранківськПроведено аналітичні дослідження взаємодії навантаження на вибій та компоновки низу бурильної колони з вибоєм та стінкою свердловини при бурінні у похило залеглих пластах. Показано взаємозв’язок між буровим індексом анізотропії, зенітним кутом, кутом нахилу пластів, геометричними характеристиками свердловини, компоновкою низу бурильної колони та осьовим навантаженням на долото.Аналітично  досліджено вплив нижньої частини бурильної колони з вибоєм та стінкою свердловини при наявності центратора. Встановлено, що зі збільшенням осьового навантаження на долото та зазору між обважненими бурильними трубами і стінкою свердловини відстань від долота до точки дотику колони зі стінкою свердловини зменшується, а наявність в компоновці низу бурильної колони центратора збільшує цю відстань, що дозволяє збільшити навантаження на долото без небезпеки росту зенітного кута.Ключові слова: стінка свердловини, зенітний кут, бурильна колона, навантаження на долото,компоновка низу бурильної колони, центратор, буровий індекс анізотропії, кут нахилу пласта

    The repair function of the multifunctional DNA repair/redox protein APE1 is neuroprotective after ionizing radiation

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    Although exposure to ionizing radiation (IR) can produce significant neurotoxicity, the mechanisms mediating this toxicity remain to be determined. Previous studies using neurons isolated from the central nervous system show that IR produces reactive oxygen species and oxidative DNA damage in those cells. Because the base excision DNA repair pathway repairs single-base modifications caused by ROS, we asked whether manipulating this pathway by altering APE1 expression would affect radiation-induced neurotoxicity. In cultures of adult hippocampal and sensory neurons, IR produces DNA damage as measured by phosphorylation of histone H2A.X and results in dose-dependent cell death. In isolated sensory neurons, we demonstrate for the first time that radiation decreases the capsaicin-evoked release of the neuropeptide CGRP. Reducing APE1 expression in cultured cells augments IR-induced neurotoxicity, whereas overexpressing APE1 is neuroprotective. Using lentiviral constructs with a neuronal specific promoter that selectively expresses APE1s different functions in neurons, we show that selective expression of the DNA repair competent (redox inactive) APE1 constructs in sensory neurons resurrects cell survival and neuronal function, whereas use of DNA-repair deficient (redox active) constructs is not protective. Use of an APE1 redox-specific inhibitor, APX3330, also facilitates neuronal protection against IR-induced toxicity. These results demonstrate for the first time that the repair function of APE1 is required to protect both hippocampal and DRG neuronal cultures—specifically neuronal cells—from IR-induced damage, while the redox activity of APE1 does not appear to be involved
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