Nasal carriage of Staphylococcus aureus treated with topical mupirocin (pseudomonic acid) in a children's hospital

2% mupirocin ointment applied intra-nasally for 5 days was assessed for elimination of nasal carriage of Staphylococcus aureus in 31 staff members in a children's hospital. Three volunteers failed to complete the trial because of side effects, i.e. buccal reddening and swelling, and unpleasant taste. During treatment staphylococcal nasal carriage was not found in any case; of the 24 post-treatment nasal swabs taken 4 days after treatment 22 were still negative. Re-colonization with S. aureus of different phage types occurred in the remaining two cases

Sulphur deposition on the Italian area: a trajectory model study

2nonenoneCALORI G.; FINZI G.Calori, G.; Finzi, Giovann

Ataxin-2 modulates the levels of Grb2 and Src but not Ras signaling

Ataxin-2 (ATXN2) is implicated mainly in mRNA processing. Some ATXN2 associates with receptor tyrosine kinases (RTK), inhibiting their endocytic internalization through interaction of proline-rich domains (PRD) in ATXN2 with SH3 motifs in Src. Gain of function of ATXN2 leads to neuronal atrophy in the diseases spinocerebellar ataxia type 2 (SCA2) and amyotrophic lateral sclerosis (ALS). Conversely, ATXN2 knockout (KO) mice show hypertrophy and insulin resistance. To elucidate the influence of ATXN2 on trophic regulation, we surveyed interactions of ATXN2 with SH3 motifs from numerous proteins and observed a novel interaction with Grb2. Direct binding in glutathione S-transferase (GST) pull-down assays and coimmunoprecipitation of the endogenous proteins indicated a physiologically relevant association. In SCA2 patient fibroblasts, Grb2 more than Src protein levels were diminished, with an upregulation of both transcripts suggesting enhanced protein turnover. In KO mouse embryonal fibroblasts (MEF), the protein levels of Grb2 and Src were decreased. ATXN2 absence by itself was insufficient to significantly change Grb2-dependent signaling for endogenous Ras levels, Ras-GTP levels, and kinetics as well as MEK1 phosphorylation, suggesting that other factors compensate for proliferation control. In KO tissue with postmitotic neurons, a significant decrease of Src protein levels is prominent rather than Grb2. ATXN2 mutations modulate the levels of several components of the RTK endocytosis complex and may thus contribute to alter cell proliferation as well as translation and growth