High strain rate superplasticity at intermediate temperatures of the Al 7075 alloy severely processed by equal channel angular pressing

The mechanical properties of an overaged Al 7075-O alloy processed by ECAP were examined by tensile tests at intermediate-high temperatures ranging from 250 to 400ºC and strain rates from 10−5 to 10−1 s−1. The influence of the number of ECAP passes on the ductility enhancement was evaluated. Elongation to failure, eF, significantly increased with increasing the number of ECAP passes up to 8 at 130ºC. The alloy processed under these conditions exhibited a maximum value of 322% at 300ºC and an initial strain rate of 10−3 s−1. High strain rate superplasticity was obtained at this temperature, eF=210%, at strain rate as high as 10−2 s−1. The large elongations together with lower stresses and lower stress exponents than those for the start material confirm that grain boundary sliding (GBS) is the operative deformation mechanism. A loss of superplastic behaviour at above temperatures of 350ºC is related to abnormal grain growth and a change of deformation mechanism.Financial support from MICINN (Project MAT2009-14452) is gratefully acknowledged.Peer reviewe

The molecular mechanism and physiological role of silent nociceptor activation

Silent nociceptors are sensory afferents that are insensitive to noxious mechanical stimuli under normal conditions but become sensitized to such stimuli during inflammation. Using RNA-sequencing and quantitative RT-PCR we demonstrate that inflammation selectively upregulates the expression of the transmembrane protein TMEM100 in silent nociceptors and electrophysiology revealed that over-expression of TMEM100 is required and sufficient to un-silence silent nociceptors. Moreover, we show that mice lacking TMEM100 do not develop secondary hyperalgesia, i.e. pain hypersensitivity that spreads beyond the site of inflammation, in a mouse model of knee joint inflammation and that AAV-mediated overexpression of TMEM100 in articular afferents in the absence of inflammation is sufficient to induce secondary hyperalgesia in remote skin regions without causing knee joint pain. Thus, our work identifies TMEM100 as a key regulator of silent nociceptor un-silencing and reveals a physiological role for this hitherto enigmatic afferent subclass in triggering spatially remote secondary hyperalgesia during inflammation

Role of TMEM100 in mechanically insensitive nociceptor un-silencing

Mechanically silent nociceptors are sensory afferents that are insensitive to noxious mechanical stimuli under normal conditions but become sensitized to such stimuli during inflammation. Using RNA-sequencing and quantitative RT-PCR we demonstrate that inflammation upregulates the expression of the transmembrane protein TMEM100 in silent nociceptors and electrophysiology revealed that over-expression of TMEM100 is required and sufficient to un-silence silent nociceptors in mice. Moreover, we show that mice lacking TMEM100 do not develop secondary mechanical hypersensitivity—i.e., pain hypersensitivity that spreads beyond the site of inflammation—during knee joint inflammation and that AAV-mediated overexpression of TMEM100 in articular afferents in the absence of inflammation is sufficient to induce mechanical hypersensitivity in remote skin regions without causing knee joint pain. Thus, our work identifies TMEM100 as a key regulator of silent nociceptor un-silencing and reveals a physiological role for this hitherto enigmatic afferent subclass in triggering spatially remote secondary mechanical hypersensitivity during inflammation