Febrile rhabdomyolysis of unknown origin in refugees coming from West Africa through the Mediterranean



Odolini S, Gobbi F, Zammarchi L, Migliore S, Mencarini P, Vecchia M, di Lauria N, Schivazappa S, Sabatini T, Chianura L, Vanino E, Piacentini D, Zanotti P, Bussi A, Bartoloni A, Bisoffi Z, Castelli F.


Int J Infect Dis. 2017 Sep;62:77-80. doi: 10.1016/j.ijid.2017.07.018. Epub 2017 Jul 26.


Stroke is a severe neurological disorder characterized by the abrupt loss of blood circulation into the brain resulting into wide ranging brain and behavior abnormalities. The present study was designed to evaluate molecular mechanism by which sesamin (SES) induces neuroprotection in mouse model of ischemic stroke. The results of this study demonstrate that SES treatment (30 mg/kg bwt) significantly reduced infarction volume, lipid per-oxidation, cleaved-caspase-3 activation, and increased GSH activity following MCAO in adult male mouse. SES treatment also diminished iNOS and COX-2 protein expression, and significantly restored SOD activity and protein expression level in the ischemic cortex of the MCAO animals. Furthermore, SES treatment also significantly reduced inflammatory and oxidative stress markers including Iba1, Nox-2, Cox-2, peroxynitrite compared to placebo MCAO animals. Superoxide radical production, as studied by DHE staining method, was also significantly reduced in the ischemic cortex of SES treated compared to placebo MCAO animals. Likewise, downstream effects of superoxide free radicals i.e. MAPK/ERK and P38 activation was also significantly attenuated in SES treated compared to placebo MCAO animals. In conclusion, these results suggest that SES induces significant neuroprotection, by ameliorating many signaling pathways activated/deactivated following cerebral ischemia in adult mouse. CI – Copyright © 2014 Elsevier Inc. All rights reserved.

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Link/DOI: 10.1016/j.ijid.2017.07.018