Pulmonary edema associated with increased vascular permeability is a severe complication of Staphylococcus aureus–induced sepsis and an important cause of human pathology and death. We investigated the role of the mammalian acid sphingomyelinase (Asm)/ceramide system in the development of lung edema caused by S. aureus. Our findings demonstrate that genetic deficiency or pharmacologic inhibition of Asm reduced lung edema in mice infected with S. aureus. The Asm/ceramide system triggered the formation of superoxide, resulting in degradation of tight junction proteins followed by lung edema. Treatment of infected mice with amitriptyline, a potent inhibitor of Asm, protected mice from lung edema caused by S. aureus, but did not reduce systemic bacterial numbers. In turn, treatment with antibiotics reduced bacterial numbers but did not protect mice from lung edema. In contrast, only the combination of antibiotics and amitriptyline inhibited both pulmonary edema and bacteremia protecting mice from lethal sepsis and lung dysfunction suggesting the combination of both drugs as novel treatment option for sepsis.Key messagesAntibiotics are often insufficient to cure S. aureus–induced sepsis.S. aureus induces lung edema via the Asm/ceramide system.Genetic deficiency of Asm inhibits lung dysfunction upon infection with S. aureus.Pharmacologic inhibition of Asm reduces lung edema induced by S. aureus.Antibiotics plus amitriptyline protect mice from lung edema and lethal S. aureus sepsis.Electronic supplementary materialThe online version of this article (doi:10.1007/s00109-014-1246-y) contains supplementary material, which is available to authorized users.

While more studies are needed to test for regularity, this study suggests that our modified technique could be a means of getting more accurate quantitative data from dental CBCTs.

No abstract

This study examines upper extremity skin contamination of nuclear medicine and radiation safety staff during 131I-Metaiodobenzylguanidine (MIBG) therapy. Utilizing retrospective data, a methodology for performing a rapid assessment of the radiation dose to the skin of the upper extremities is presented. Using the skin contamination measurements and calculated skin dose for each contamination incident at our facility, a conversion factor (XE) was derived that estimates skin dose (DE) based on the initial contamination measurement. This methodology yields an estimate of the final skin dose accounting for radioactive decay, decontamination and other factors, such as skin sloughing. As a standard practice multiple time-point measurements from initial contamination to background should be used to calculate the total attributable skin dose. However, to provide an early projection of the expected skin dose, the dose can be reasonably estimated to be <0.10% mSv cpm-1 (10% mrem cpm-1) of the initial contamination measurement.