Magnetic-field dependence of the critical currents in a periodic coplanar array of narrow superconducting strip

We calculate the magnetic-field dependence of the critical current due to both geometrical edge barriers and bulk pinning in a periodic coplanar array of narrow superconducting strips. We find that in zero or low applied magnetic fields the critical current can be considerably enhanced by the edge barriers, but in modest applied magnetic fields the critical current reduces to that due to bulk pinning alone.Comment: 23 pages, 7 figure

МЕТАБОЛИЗМ И МЕХАНИЗМ ТОКСИЧНОСТИ СЕЛЕНСОДЕРЖАЩИХ ПРЕПАРАТОВ, ИСПОЛЬЗУЕМЫХ ДЛЯ КОРРЕКЦИИ ДЕФИЦИТА МИКРОЭЛЕМЕНТА СЕЛЕНА

The work presents a review devoted to the metabolism and the mechanism of toxicity of seleniumcontaining supplements: elemental selenium, sodium selenite, diacetophenonyl selenide, selenopyrane, ebselen, dimethyl dipyrasolyl selenide and selenium-containing amino acids used for correction of selenium deficiency. Elemental selenium penetrating through cell walls, but not through transport channels demonstrates poorly predicted and difficultly regulated bioavailability. Sodium selenate is known to be the most toxic form of selenium in food. The metabolism of xenobiotic diacetophenonyl selenide resembles that of sodium selenide. The xenobiotic reacts with thiols, for instance, with the reduced form of glutathione leading to the formation of hydrogen selenide. Ebselen is not considered to be a well bioavailable form of selenium and thus possesses low toxicity. Xenobiotic selenopyrane eliminates selenium only in processes of xenobiotic liver exchange, and in our investigations - partially in acid-catalyzed hydrolysis. The metabolism of xenobiotic dimethyl dipyrasolyl selenide having low toxicity is poorly investigated. The toxicity of high doses of selenomethionine is determined by the possibility of incorporation in proteins and vitally important enzymes with dramatic changes of protein quaternary structure. The toxicity of high doses of methylselenocysteine seems to be caused by the lack of an exchange pool in the body and quick regeneration of hydrogen selenide from methylselenol which is formed as a result of enzymatic destruction of this amino acid. Also the issue of the most prospect selenium donor is discussed. The physiological compatibility, the low toxicity, the presence of an exchangeable pool in the organism, the antioxidantal properties and the simplicity of production indicate selenocystine as an optimal selenium donor.Приведены обзор литературы и результаты собственных исследований, посвященных метаболизму и механизму токсичности селенсодержащих препаратов: элементного селена, селенита натрия, диацетофенонилселенида, селенопирана, эбселена, диметилдипиразолилселенида и селенсодержащих аминокислот, используемых для коррекции дефицита селена. Элементный селен обладает труднорегулируемой и труднопрогнозируемой биодоступностью, проникая через клеточные стенки, а не по транспортным каналам клетки. Селенит натрия является наиболее токсичным, плохо совестимым с компонентами пищи и малоуправляемым соединением селена. Ксенобиотик диацетофенонилселенид, в целом, имеет схожий с селенитом натрия механизм метаболизма, взаимодействуя с тиолами, например с восстановленным глутатионом, с образованием селеноводорода. Эбселен не является биодоступным источником селена и поэтому малотоксичен. Считается, что ксенобиотик селенопиран может элиминировать селен только в процессах ксенобиотического обмена печени, однако, как показано в наших исследованиях - частично и в процессе кислотно-катализируемого гидролиза. Отмечается малое число исследований, посвященных метаболизму малотоксичного ксенобиотика диметилдипиразолилселенида. Токсичность избытка селенометионина определяется в первую очередь некорректным включением в белки и жизненно важные ферменты, т.е. связана с изменением пространственной структуры белка. Токсичность избытка метилселеноцистеина определяется, по-видимому, отсутствием обменного пула в организме и быстрой генерацией селеноводорода из метилселенола, который образуется при ферментативном расщеплении аминокислоты. Также рассматривается концепция выбора оптимального донора микроэлемента селена. По совокупности таких свойств, как полная физиологическая совместимость, низкая токсичность, наличие обменного пула в организме, антиоксидантных свойств и простота производства, определен оптимальный донор селена -аминокислота селеноцистин

Generation of a localised microwave magnetic field by coherent phonons in a ferromagnetic grating

A high-amplitude microwave magnetic field localized at the nanoscale is a desirable tool for various applications within the rapidly developing field of nanomagnetism. Here, we drive magnetization precession by coherent phonons in a metal ferromagnetic nanograting and generate ac-magnetic induction with extremely high amplitude (up to 10 mT) and nanometer scale localization in the grating grooves. We trigger the magnetization by a laser pulse which excites localized surface acoustic waves. The developed technique has prospective uses in several areas of research and technology, including spatially resolved access to spin states for quantum technologies

METABOLISM AND MECHANISM OF TOXICITY OF SELENIUM-CONTAINING SUPPLEMENTS USED FOR OPTIMIZING HUMAN SELENIUM STATUS

The work presents a review devoted to the metabolism and the mechanism of toxicity of seleniumcontaining supplements: elemental selenium, sodium selenite, diacetophenonyl selenide, selenopyrane, ebselen, dimethyl dipyrasolyl selenide and selenium-containing amino acids used for correction of selenium deficiency. Elemental selenium penetrating through cell walls, but not through transport channels demonstrates poorly predicted and difficultly regulated bioavailability. Sodium selenate is known to be the most toxic form of selenium in food. The metabolism of xenobiotic diacetophenonyl selenide resembles that of sodium selenide. The xenobiotic reacts with thiols, for instance, with the reduced form of glutathione leading to the formation of hydrogen selenide. Ebselen is not considered to be a well bioavailable form of selenium and thus possesses low toxicity. Xenobiotic selenopyrane eliminates selenium only in processes of xenobiotic liver exchange, and in our investigations - partially in acid-catalyzed hydrolysis. The metabolism of xenobiotic dimethyl dipyrasolyl selenide having low toxicity is poorly investigated. The toxicity of high doses of selenomethionine is determined by the possibility of incorporation in proteins and vitally important enzymes with dramatic changes of protein quaternary structure. The toxicity of high doses of methylselenocysteine seems to be caused by the lack of an exchange pool in the body and quick regeneration of hydrogen selenide from methylselenol which is formed as a result of enzymatic destruction of this amino acid. Also the issue of the most prospect selenium donor is discussed. The physiological compatibility, the low toxicity, the presence of an exchangeable pool in the organism, the antioxidantal properties and the simplicity of production indicate selenocystine as an optimal selenium donor