Influence of Structural Defects on the Properties of Metamagnetic Shape Memory Alloys

The production of μ-particles of Metamagnetic Shape Memory Alloys by crushing and subsequent ball milling process has been analyzed. The high energy involved in the milling process induces large internal stresses and high density of defects with a strong influence on the martensitic transformation; the interphase creation and its movement during the martensitic transformation produces frictional contributions to the entropy change (exothermic process) both during forward and reverse transformation. The frictional contribution increases with the milling time as a consequence of the interaction between defects and interphases. The influence of the frictional terms on the magnetocaloric effect has been evidenced. Besides, the presence of antiphase boundaries linked to superdislocations helps to understand the spin-glass behavior at low temperatures in martensite. Finally, the particles in the deformed state were introduced in a photosensitive polymer. The mechanical damping associated to the Martensitic Transformation (MT) of the particles is clearly distinguished in the produced composite, which could be interesting for the development of magnetically-tunable mechanical dampers.This research was funded by Projects RTI2018-094683-B-C5 (4,5) (MCIU/AEI/FEDER,UE); ASACTEI Pcia.Santa Fe IO-2017-00138, PID-UNR ING 575 and ING 612 (2018–202

Mechanical Spectroscopy in Fe-Al-Si alloys at Elevated Temperatures

The mechanical spectroscopy response in Fe-25 at.% (Al + Si) and Fe-15 at.% (Al + Si) has been studied in the temperature interval between800 and 1200 K. The solute grain boundary relaxation of aluminium and silicon was strongly dependent of the degree of order in the sample. Adecrease in the order degree allows the development of the solute peak at around 1000K during the cooling from 1200 K. Nevertheless, if the orderdegree is not decreased, the grain boundaries remain locked and consequently the relaxation peak does not appear

Cefditoren: Comparative efficacy with other antimicrobials and risk factors for resistance in clinical isolates causing UTIs in outpatients

<p>Abstract</p> <p>Background</p> <p>To investigate a possible role of Cefditoren, a recently marketed in Greece third-generation oral cephalosporin in urinary infections of outpatients.</p> <p>Methods</p> <p>During a multicenter survey of Enterobacteriaceae causing UTIs in outpatients during 2005–2007, Cefditoren MICs were determined by agar dilution method in a randomly selected sample of uropathogens. Susceptibility against 18 other oral/parenteral antimicrobials was determined according to Clinical and Laboratory Standards Institute methodology.</p> <p>Results</p> <p>A total of 563 isolates (330 <it>Escherichia coli</it>, 142 <it>Proteus mirabilis</it> and 91 <it>Klebsiella</it> spp) was studied; MIC50/MIC90 of Cefditoren was 0.25/0.5 mg/L respectively, with 97.1% of the isolates being inhibited at 1 mg/L. All 12 strains producing ESBLs or AmpC enzymes were resistant to cefditoren. Susceptibility rates (%) for amoxicillin/clavulanic acid, cefuroxime axetil, cefotaxime, ciprofloxacin, trimethoprim/sulfamethoxazole and fosfomycin were 93.1- 94.1- 96.8-93.1-71.9 and 92.8% respectively. Cefditoren MIC was significantly higher in nalidixic/ciprofloxacin non-susceptible strains; resistance to cefditoren was not associated with resistance to mecillinam, fosfomycin nitrofurantoin and aminoglycosides. Multivariate analysis demonstrated history of urinary infection in the last two weeks or three months as risk factors for cefditoren resistance.</p> <p>Conclusions</p> <p>Cefditoren exhibited enhanced in vitro activity against the most common uropathogens in the outpatient setting, representing an alternative oral treatment option in patients with risk factors for resistance to first-line antibiotics.</p

Traumatic brain injury and amyloid-β pathology: a link to Alzheimer's disease?

Traumatic brain injury (TBI) has devastating acute effects and in many cases seems to initiate long-term neurodegeneration. Indeed, an epidemiological association between TBI and the development of Alzheimer's disease (AD) later in life has been demonstrated, and it has been shown that amyloid-β (Aβ) plaques — one of the hallmarks of AD — may be found in patients within hours following TBI. Here, we explore the mechanistic underpinnings of the link between TBI and AD, focusing on the hypothesis that rapid Aβ plaque formation may result from the accumulation of amyloid precursor protein in damaged axons and a disturbed balance between Aβ genesis and catabolism following TBI