Interestingly, salinity increases NO production selectively in mesophyll cells of sorghum leaves, where photosynthetic

C-4 phosphoenolpyruvate carboxylase (C-4 PEPCase) is located. PEPCase is regulated by a phosphoenolpyruvate carboxylase-kinase (PEPCase-k), which levels are greatly enhanced by salinity in sorghum. This work investigated whether NO is involved in this effect. NO donors (SNP, SNAP), the inhibitor of NO synthesis NNA, and the NO scavenger cPTIO were used for long- and short-term treatments. Long-term treatments had multifaceted consequences on both PPCK gene expression and PEPCase-k activity, and they also decreased photosynthetic gas-exchange parameters and plant growth. Nonetheless, selleck products it could be observed that SNP increased PEPCase-k activity, resembling salinity effect. Short-term treatments with NO donors, which did not change

photosynthetic gas-exchange parameters and PPCK gene expression, increased PEPCase-k activity both in illuminated leaves and in leaves kept at dark. At least in part, these effects were independent on protein synthesis. PEPCase-k activity was not decreased by short-term treatment TGF-beta inhibitor with cycloheximide in NaCl-treated plants; on the contrary, it was decreased by cPTIO. In summary, NO donors mimicked salt effect on PEPCase-k activity, and scavenging of NO abolished it. Collectively, these results indicate that NO is involved in the complex control of PEPCase-k activity, and it may mediate some of the plant responses to salinity.”
“Shiga toxin-producing Escherichia coli-associated haemolytic uraemic syndrome (STEC-HUS) is

one of the most important causes of acute kidney injury in patients of all ages, especially in children. It can occur sporadically or in outbreaks. STEC-HUS is a systemic illness caused CT99021 in vitro by toxin-mediated injury to the vascular endothelium and a generalized inflammatory response. The kidney and the brain are the two primary target organs. Nearly 40% of patients with STEC-HUS require at least temporary renal replacement therapy and up to 20% will have permanent residual kidney dysfunction. Neurological injury can be sudden and severe and is the most frequent cause of acute mortality in patients with STEC-HUS. Over the past 30 years, a wide range of inflammatory mediators have been linked to the pathogenesis of STEC-HUS and associated renal and neurological complications. Recently, evidence has accumulated that abnormal activation of the alternative pathway of complement occurs in patients with STEC-HUS. In the large outbreak of STEC-HUS caused by E. coli O104:H4 that occurred in Germany in May 2011, a large number of patients received eculizumab, a monoclonal antibody directed against C5, in an open-label manner. We describe the experience with eculizumab under these emergent circumstances at one large centre.