Large two-level magnetoresistance effect in doped manganite grain boundary junctions

We performed a systematic analysis of the tunneling magnetoresistance (TMR) effect in single grain boundary junctions formed in epitaxial La(2/3)Ca(1/3)MnO(3) films deposited on SrTiO(3) bicrystals. For magnetic fields H applied parallel to the grain boundary barrier, an ideal two-level resistance switching behavior with sharp transitions is observed with a TMR effect of up to 300% at 4.2 K and still above 100% at 77 K. Varying the angle between H and the grain boundary results in differently shaped resistance vs H curves. The observed behavior is explained within a model of magnetic domain pinning at the grain boundary interface.Comment: 4 pages, 3 figures, to appear in Phys. Rev. B (Rapid Comm.

Large two-level magnetoresistance effect in doped manganite grain boundary junctions

We performed a systematic analysis of the tunneling magnetoresistance (TMR) effect in single grain boundary junctions formed in epitaxial La(2/3)Ca(1/3)MnO(3) films deposited on SrTiO(3) bicrystals. For magnetic fields H applied parallel to the grain boundary barrier, an ideal two-level resistance switching behavior with sharp transitions is observed with a TMR effect of up to 300% at 4.2 K and still above 100% at 77 K. Varying the angle between H and the grain boundary results in differently shaped resistance vs H curves. The observed behavior is explained within a model of magnetic domain pinning at the grain boundary interface.Comment: 4 pages, 3 figures, to appear in Phys. Rev. B (Rapid Comm.

Antiglucocorticoid RU38486 reduces net protein catabolism in experimental acute renal failure

BACKGROUND: In acute renal failure, a pronounced net protein catabolism occurs that has long been associated with corticoid action. By competitively blocking the glucocorticoid receptor with the potent antiglucocorticoid RU 38486, the present study addressed the question to what extent does corticoid action specific to uremia cause the observed muscle degradation, and does inhibition of glucocorticoid action reduce the protein wasting? METHODS: RU 38486 was administered in a dose of 50 mg/kg/24 h for 48 h after operation to fasted bilaterally nephrectomized (BNX) male adult Wistar rats and sham operated (SHAM) controls. Protein turnover was evaluated by high performance liquid chromatography (HPLC) of amino acid efflux in sera from isolated perfused hindquarters of animals treated with RU 38486 versus untreated controls. RESULTS: Administration of RU 38486 reduces the total amino acid efflux (TAAE) by 18.6% in SHAM and 15.6% in BNX and efflux of the indicator of net protein turnover, phenylalanine (Phe) by 33.3% in SHAM and 13% in BNX animals as compared to the equally operated, but untreated animals. However, the significantly higher protein degradation observed in BNX (0.6 ± 0.2 nmol/min/g muscle) versus SHAM (0.2 ± 0.1 nmol/min/g muscle) rats, as demonstrated by the marker of myofribrillar proteolytic rate, 3-Methylhistidine (3 MH) remains unaffected by administration of RU 38486 (0.5 ± 0.1 v. 0.2 ± 0.1 nmol/min/g muscle in BNX v. SHAM). CONCLUSION: RU 38486 does not act on changes of muscular protein turnover specific to uremia but reduces the effect of stress- stimulated elevated corticosterone secretion arising from surgery and fasting. A potentially beneficial effect against stress- induced catabolism in severe illness can be postulated that merits further study

Role of Innate Immunity in the Pathogenesis of Chronic Rhinosinusitis: Progress and New Avenues

Chronic rhinosinusitis is a heterogeneous and multifactorial disease with unknown etiology. Aberrant responses to microorganisms have been suggested to play a role in the pathophysiology of the disease. Research has focused on the presence, detection, response to, and eradication of these potential threats. Main topics seem to center on the contribution of structural cells such as epithelium and fibroblasts, on the consequences of activation of pattern-recognition receptors, and on the role of antimicrobial agents. This research should be viewed not only in the light of a comparison between healthy and diseased individuals, but also in a comparison between patients who do or do not respond to treatment. New players that could play a role in the pathophysiology seem to surface at regular intervals, adding to our understanding (and the complexity) of the disease and opening new avenues that may help fight this incapacitating disease