159 research outputs found

    Dependence of Giant Tunnel Magnetoresistance of Sputtered CoFeB/MgO/CoFeB Magnetic Tunnel Junctions on MgO Barrier Thickness and Annealing Temperatur

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    We investigated the dependence of giant tunnel magnetoresistance (TMR) on the thickness of an MgO barrier and on the annealing temperature of sputtered CoFeB/MgO/CoFeB magnetic tunnel junctions deposited on SiO2/Si wafers. The resistance-area product exponentially increases with MgO thickness, indicating that the quality of MgO barriers is high in the investigated thickness range of 1.15-2.4 nm. High-resolution transmission electron microscope images show that annealing at 375 C results in the formation of crystalline CoFeB/MgO/CoFeB structures, even though CoFeB electrodes are amorphous in the as-sputtered state. The TMR ratio increases with annealing temperature and is as high as 260% at room temperature and 403% at 5 K.Comment: 12 pages, 5 figure

    Autonomic Dysreflexia during a Bowel Program in Patients with Cervical Spinal Cord Injury.

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    The purpose of the present study was to investigate the relationship between bowel maneuvers and autonomic dysreflexia (AD) in patients with cervical spinal cord injuries (CSCI). Fifteen consecutive, clinically stable patients with CSCI participated. We evaluated changes in blood pressure (BP), pulse rate (PR) and classic symptoms of AD before, during and after a bowel program involving the manual removal of stool in lateral recumbency. The insertion of rectal medication induced a significant increase in systolic BP, which persisted during additional digital rectal stimulation. Furthermore, the manual removal of stool induced AD, with maximal increases of systolic BP (169.1(+-)19.5 mmHg, mean(+-)SD). However, the insertion of a finger into the anus after the end of stool flow did not cause a further increase in systolic BP. Systolic BP recovered to pre-program values within 5 min after defecation. Our study demonstrated that the combined effects of rectal and/or anal sphincter distension and uninhibited rectal contraction in response to the manual removal of stool might induce AD. We recommend avoiding, if at all possible, the manual removal of stool in order to prevent AD in patients with CSCI

    抗原および Ca ionophore A23187 刺激時におけるアトピー型気管支喘息末梢血好塩基球の運動能

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    We examined histamine release and morphological changes in basophilic granulocytes from atopic subjects, in response to stimulation with antigen and Ca ionophore A23187. 1. Histamine release and a reduction in the rumber of basophils were more rapid and greater in extent at an early stage of antigen stimulation compared with Ca ionophore A23187 stimulation. 2. Morphological changes in basophils, represented by increased motility, in terms of an increased ratio of short to long axis diameter (L/S ratio), as well as the increased frequency of basophils with localized granules and those with pseudopods, were more often observed antigen stimulation than with Ca ionophore A23187 stimulation. In contrast, morphogical changes in which basophils appeared swollen, showing an increased mean cell diameter and an increased frequency of cells with 5 vacuoles or more were more predominant with Ca ionophore A23187 than with antigen stimulation. The results obtained here show that bridging of IgE receptors is essential to activate basophils and induce increased motility in these cells.アトピー型気管支喘息末梢血好塩基球を用い,抗原および Ca ionophore A23187 刺激時のヒスタミン遊離およびその形態的変化について比較検討した。1.抗原刺激時には, Ca ionophore A23187 刺激時に比べ,好塩基球からのヒスタミン遊離および好塩基球数の減少の程度は,より急激でかつ高度であった。2.好塩基球の形態的変化,すなわち,長経/短経比の増大,限局性顆粒あるいは偽足を有する好塩基球の出現頻度の増加などの運動能の亢進を示唆する好塩基球の形態的変化は, Ca ionophore A23187 に比べ抗原刺激時により高度であった。一方,平均直径の増大,5個以上の空砲を有する好塩基球の出現頻度の増加などの,むしろ膨化傾向を示唆する好塩基球の形態的変化は,抗原刺激時に比べ, Co ionophore A23187 刺激時により高度であった。これらの結果より,抗原刺激によるIgE受容体のbridgingが,好塩基球を活性化し,運動能の亢進をひき起こすものと判断された

    Improvement in the productivity of xylooligosaccharides from waste medium after mushroom cultivation by hydrothermal treatment with suitable pretreatment

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    The effective xylooligosaccharides (XOs) production from the waste medium after mushroom cultivation (WM) was investigated. The WM contains rich nutrients (protein, etc.) which induce Maillard reaction with reducing sugars under hydrothermal conditions. To improve the productivity of XOs, the suitable pretreatment combined with washing and grinding was investigated, and subsequently hydrothermal treatment was demonstrated with batch type and continuous flow type reactor. The washing pretreatment with hot water of 60 degrees C was effective to remove nutrients from the WM, and it led to prevent brownish discoloration on the hydrothermal treatment. On the basis of experimental data, industrial XOs production processes consisting of the pretreatment, hydrothermal treatment and purification step was designed. During the designed process, 2.3 kg-dry of the purified XOs was produced from 30 kg-wet of the WM (15% yield as dry basis weight). Theoretical yield of XOs attained to 48% as xylan weight in the WM.ArticleBioresource Technology. 101(15):6006-6011 (2010)journal articl

    Adenovirus E4orf6 targets pp32/LANP to control the fate of ARE-containing mRNAs by perturbing the CRM1-dependent mechanism

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    E4orf6 plays an important role in the transportation of cellular and viral mRNAs and is known as an oncogene product of adenovirus. Here, we show that E4orf6 interacts with pp32/leucine-rich acidic nuclear protein (LANP). E4orf6 exports pp32/LANP from the nucleus to the cytoplasm with its binding partner, HuR, which binds to an AU-rich element (ARE) present within many protooncogene and cytokine mRNAs. We found that ARE-mRNAs, such as c-fos, c-myc, and cyclooxygenase-2, were also exported to and stabilized in the cytoplasm of E4orf6-expressing cells. The oncodomain of E4orf6 was necessary for both binding to pp32/LANP and effect for ARE-mRNA. C-fos mRNA was exported together with E4orf6, E1B-55kD, pp32/LANP, and HuR proteins. Moreover, inhibition of the CRM1-dependent export pathway failed to block the export of ARE-mRNAs mediated by E4orf6. Thus, E4orf6 interacts with pp32/LANP to modulate the fate of ARE-mRNAs by altering the CRM1-dependent export pathway
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