Modulated Rashba interaction in a quantum wire: Spin and charge dynamics

It was recently shown that a spatially modulated Rashba spin-orbit coupling in a quantum wire drives a transition from a metallic to an insulating state when the wave number of the modulation becomes commensurate with the Fermi wave length of the electrons in the wire. It was suggested that the effect may be put to practical use in a future spin transistor design. In the present article we revisit the problem and present a detailed analysis of the underlying physics. First, we explore how the build-up of charge density wave correlations in the quantum wire due to the periodic gate configuration that produces the Rashba modulation influences the transition to the insulating state. The interplay between the modulations of the charge density and that of the spin-orbit coupling turns out to be quite subtle: Depending on the relative phase between the two modulations, the joint action of the Rashba interaction and charge density wave correlations may either enhance or reduce the Rashba current blockade effect. Secondly, we inquire about the role of the Dresselhaus spin-orbit coupling that is generically present in a quantum wire embedded in semiconductor heterostructure. While the Dresselhaus coupling is found to work against the current blockade of the insulating state, the effect is small in most materials. Using an effective field theory approach, we also carry out an analysis of effects from electron- electron interactions, and show how the single-particle gap in the insulating state can be extracted from the more easily accessible collective charge and spin excitation thresholds. The smallness of the single-particle gap together with the anti-phase relation between the Rashba and chemical potential modulations pose serious difficulties for realizing a Rashba-controlled current switch in an InAs-based device. Some alternative designs are discussed.Comment: 20 pages, 6 figure

ВПЛИВ БЛОКАДИ Ш-СИНТАЗИ НА ВАЗОДИЛАТАЦІЙНИЙ ЕФЕКТ ДІЕТИЛОВОГО ЕСТЕРУ 5-АЛКІЛАМІНО-2-{М-[М-БЕНЗОЇЛ-(4-МЕТИЛБЕНЗИЛІДЕН) ГЛІЦИЛ] АМІНОМЕТИЛ}-1,3-ОКСАЗОЛ-4-ІЛФОСФОНОВОЇ КИСЛОТИ НА СЕГМЕНТАХ ІЗОЛЬОВАНОЇ АОРТИ ЩУРІВ

INFLUENCE OF NO - SYNTHASE BLOCKADE ON VASODILATORY EFFECT OF DIETHYL ESTER OF 5-ALKILAMINE-2-{N-[N-BENZOYL-(4-METHYLBENZILIDEN) GLYCYL] AMINOMETHYL}- 1,3 - OXASOL-4-YLPHOSPHONIC ACID ON RAT’S ISOLATED AORTA I.V. Nizhenkovska1, A.V. Romanenko1, K.V. Sedko1, M.М. Grusha1, V.S. Brovarets2, A.V. Golovchenko21 Bogomolets National Medical University2 Institute of Bioorganic Chemistry and Petrochemistry at NAS of Ukraine Essential hypertension, hypertensive heart disease, secondary hypertension and related diseases caused by them are the result of a lot of pathological changes in the cardiovascular system. One of the main mechanisms which affects the blood pressure is increasing of the tone of smooth muscle vascular wall component.A significant number of endogenous vasodilators exert their activity by mechanisms which are directly or indirectly related to the production of nitric oxide by endothelial cells, so the effects associated with its release, is a target for pharmacological correction of muscle tone in clinical practice.Previously, it was found that phosphorylated peptidomimetics, which are derivatives of 1,3-oxazole, have vasodilatative effects. However, the contribution of mechanisms of NO production and its release on vasotropic action of these compounds was not researched. That`s why the aim of our experiment was to study the vasodilatative effects of new synthesized derivative of 1,3-oxazole - diethyl ester of 5-alkilamine-2-{N-[N-benzoyl-(4-methylbenziliden) glycyl] aminomethyl}- 1,3 - oxasol-4-ylphosphonic acid (oxazole containing peptidomimetic) on rat’s isolated aorta on the background of the NO-synthase blockade.For experiment it was used isolated segments (n=5) of the thoracic descending aorta of Wistar rats with average weight 200-250 g. Received aortic segments before the experiment were kept at least 30 minutes at a temperature 35-37 °C in Krebs solution. To register the tone of aortic segments it was used installation consisting of a flow chamber (volume - 2 ml) at 36,5 °C.Vasodilatative activity of the compound was estimated by the effect on basal tone and amplitude of smooth muscle contraction of blood vessels in response to the including of α1-adrenoreceptor agonist -adrenalin (5•10-6 M) in the incubation medium. In assessing the effectiveness of vasoactive impact of the researched substance as 100% was taken the amplitude of tonic contraction of muscle in control in response to adrenaline (5•10-6 M) application for 10 sec.Average amplitude of adrenoreaction in control was 3,34 ± 1,07 mN. Adding of NO-synthase blocker - L-NAME (1•10-4 M) to Krebs solution had not an effect on basal tone of smooth muscles isolated segment of the thoracic descending aorta. However, the adding of L-NAME (1•10-4 M) to perfusate caused increasing the amplitude of adrenoreaction on 71% from baseline on 90th minute. The received changes in the amplitude are probably related to the blockade by L-NAME of NO production and release, and reducing the effect of vasodilatative component in providing the vascular reactivity to the action of α1-adrenergic receptors agonist - adrenaline (5•10-6 M).Additional including of oxazole containing peptidomimetic (1•10-5 M) to perfusate, after 30 minutes from beginning of application caused the amplitude reduction of adrenoreaction by 33% comparatively with its amplitude in conditions of only L-NAME (1•10-4 M) presence in the perfusate.The effect, which was caused by the including of oxazole containing peptidomimetic (1•10-5 M) to Krebs solution, was reversible. Within 30 min after removing of the last substance of perfusate, amplitude of adrenoreaction increased by 26% comparatively with its amplitude in conditions of simultaneous presence both of these compounds in solution. L-NAME removing of Krebs solution lead to regular amplitude decreasing of adrenoreaction.Experiments, conducted by using isolated segments of the rat`s thoracic descending aorta give reason to consider that diethyl ester of 5-alkilamine-2-{N-[N-benzoyl-(4-methylbenziliden) glycyl] aminomethyl}- 1,3 - oxasol-4-ylphosphonic acid (1•10-5 M) is able to keep its vasodilatative properties in conditions of NO-synthase blockade. The fact of saving of oxazole containing peptidomimetic effective action on the background of NO-synthase blockade by L-NAME (1•10-4 M) shows that vasodilatative effect of these two compounds is realized through various targets. Therefore, further study of vasodilatative mechanism of test compound, which can be used as potential antihypertensive medicine, is perspective for next researches.Literature:International Classification of Diseases 10th revision [Electron resource]. - Access: httpHYPERLINK "http://mkb-10.com/"://HYPERLINK "http://mkb-10.com/"mkbHYPERLINK "http://mkb-10.com/"-10.HYPERLINK "http://mkb-10.com/"comHYPERLINK "http://mkb-10.com/"/.Nizhenkovskaya I.V. The influence of sufan on myocardial energetic metabolism in case of  adriamycin-induced heart failure. / Nizhenkovskaya I.V. // Research Trends. Current Topics in Pharmacology. Short Communication. SCOPUS. – 2013. - 17, 1. – P. 103-108.Mishichnie tkani: uchebnoe posobie dlya vuzov / U.S. Chentsov, Е.А. Shubnicova, N.А. Yurina, N.B. Gusev.  - М.: Medicina, 2001. -  256 s.Ryabov G.А. Rol` oxida azota kak regulyatora kletochnih protsessov pri formirovanii poliorgannoy nedostatochnosti / Ryabov G.А., Аzizov Yu.М. // Аnesteziologia I reanimatologia. – 2008. - №1. – S. 8-13.I.N. Yakovenko. The synthesis and investigation of vasoactive properties of new phosphorylated peptidomimetics / I.N. Yakovenko, O.I. Lukashuk, K.M. Kondratyuk, A.V. Golovchenko, V.V. Zhyrnov, V.S. Brovarets // Journal of Organic and Pharmaceutical Chemistry. – 2013. - V. 11, Iss. 3 (43). – Р. 43-50.Doclinichni doslidzhennya likarskih zasobiv (metodichni rekomendacii) / Za red. О.V. Stefanova. – К.: VD «Аvicena», 2002. – 527 s.Blattner R. Experimenti na isolirovannih preparatah gladkih mishts / Blattner R., Klassen H., Denert H. i dr. - М. : Мir, 1983.- 206 s.Lukiantseva G.V. Dinamika sokratitelnoy aktivnosti isolirovannogo kolcevogo preparata aorti kris pod vliyaniem amilina/ Lukiantseva G.V., Sergeev I.U., Pastuhova V.А., Gunina L.M. // Ukrainskiy morfologichniy almanah. – 2013. – Т. 11, №1. - S. 77-78.Paulis L. Regression of L-NAME-induced hypertension: the role of Nitric oxide and endothelium-derived constricting factor / Paulis L., Zicha J., Kunes J. and others // Hipertension research. – 2008. - № 31. – P. 793-803.Moslemi F. Inhibition of Nitric oxide synthase by L-NAME in male rats / Moslemi F., Nematbakhsh M. and others // Intarnational scholarly research notices: Toxicology. – 2013. – V. 2013. – P. 227-232

Balance decompression of orbit at endocrine ophthalmopathy. First experience

The publication presents the methodology of the combined approach to decompression of the orbit in the endocrine ophthalmopathy. The analysis of our own results of surgical interventions on the orbit was performed by resection of its bone walls. Patients underwent transethmoidal decompression of the orbit by endonasal access and resection of the lateral orbital wall by the external access. The technique of operations, postoperative patient management and treatment outcomes were analyzed. The study showed high efficacy of a combined surgical approach to decompression operations on the orbit in relation to the exophthalmos regression

Expression of NF-L protein in the sensorimotor cortex during the modeling of transient ischemia against the background of sensitization by brain antigen and immunocorrection of the changes

Abstract Aim. To study the levels of NFР-L protein expression in the sensorimotor cortex of rats in the simulation of transient ischemia against the background of sensitization by the brain antigen and immunocorrection of the resulting changes by imunofan. Materials and methods. The study was conducted on 185 male mature white rats from Wistar line weighted 260–290 g, in which the damage of the brain was modulated. The brain for study was taken on the 1st, 3rd, 10th, 30th and 90th days after the start of the experiment. The histological, immunehistochemical, morphometric and statistical methods were used. Results. Observations have shown that sensitization with the brain antigen causes diffuse degenerative changes in the cerebral cortex and a decrease in NFP-L expression. This background leads to an increase in the severity of brain damage in acute circulatory disturbances compared with when no sensitization was performed. After transient ischemic attack, the recovery period was significantly less than in the absence of sensitization, rounded corpuscles with a relatively high level of expression of NFР-L, which we qualified as nerve growth flasks (cones). This allows us to say that sensitization by the brain antigen delays the regeneration of nerve fibers, which is an important component of compensatory-recovery processes in the cerebral cortex after ischemic attack. Imunofan under the conditions of modeling of combined immune-vascular lesions of the brain had protective properties and reduced the severity of the decrease in NFР-L expression. We attribute these effects of imunofan, especially in the recovery period after brain damage in the first place, to its immunomodulatory effect which is confirmed by comparing the dynamics of the restoration of NFР-L expression in the affected and contralateral hemispheres, where the latter experienced immune damage in the absence of ischemia. Conclusions. Sensitization by the brain antigen leads to diffuse degenerative changes in the cerebral cortex, which are accompanied by a decrease in the expression of NFР-L. Previous sensitization by brain antigen in acute impairment of cerebral circulation leads to increased severity of brain damage and decreased expression of NFР-L, slows and changes the dynamics of its recovery. The effect of immunophan use is to reduce changes in NFР-L expression in the sensorimotor cortex caused by both sensitization with the brain antigen and in combination with transient impairment of cerebral blood flow