Is this critically ill patient immunocompromised?

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Fractional volume of fluid method for free boundary dynamics

The volume of fluid (VOF) technique is presented as a simple and efficient means for numerically treating free boundaries embedded in a calculational mesh of Eulerian or Arbitrary-Lagrangian-Eulerian cells. It is particularly useful because it uses a minimum of stored information, treats intersecting free boundaries automatically, and can be readily extended to three-dimensional calculations

Nivolumab plus interferon-γ in the treatment of intractable mucormycosis

SCOPUS: le.jinfo:eu-repo/semantics/publishe

Street canyon ventilation: Combined effect of cross‐section geometry and wall heating

Understanding the dynamics ofmass exchange between a street canyon and the overlying atmosphere is crucial to predict air quality in urban areas. Despite the large number of studies on this topic, there are many aspects that still need to be clarified. Among these, one is certainly the role of thermal stratification in street canyon ventilation. In order to fill this gap, this study evaluates how the combined effect of street canyon geometry, wall roughness and differential heating of the building facades influences pollutant dispersion within the canyon and out of it. The study was carried out in a wind tunnel, adopting an idealized urban geometrymade up of square bars placed normal to thewind direction. The boundary conditions inside the canyon were modified by heating its windward and leeward walls, by changing its aspect ratio and by introducing roughness elements at the walls. A passive scalar was injected from a line source at ground level. The flow and concentration fields were measured in a cross-section of the canyon. Characteristic exchange velocities within the canyon and towards the external flow were estimated comparing the experimental data with an analytical model for the cavity wash-out. Results show that the transition from one recirculating cell to two counter-rotating cells inhibits canyon ventilation, with a consequent increase in pollutant concentration at the pedestrian level. This transition occurs as the cavity aspect ratio increases and is facilitated by adding roughness elements at the windward wall. Heating the leeward wall has negligible effects on canyon ventilation. Heating the windward wall accelerates pollutant removals in square cavities, while it contributes to a worsening of air quality in narrow cavities. Finally, the wash-out times of the cavity are discussed in terms of a relative contribution of the mean advectivemotion and its turbulent counterpart

Staphylococcus aureus alpha-toxin induces apoptosis in peripheral blood mononuclear cells:role of endogenous tumour necrosis factor-alpha and the mitochondrial death pathway

Staphylococcus aureus infections can result in septic and toxic shock with depletion of immune cells and massive cytokine production. Recently, we showed that, in S. aureus-infected Jurkat T cells, alpha-toxin is the major mediator of caspase activation and apoptosis. Here, we investigated the mechanisms of cell death induced by alpha-toxin in peripheral blood mononuclear cells (MNC). We show that alpha-toxin is required and sufficient for S. aureus-induced cell death not only in transformed Jurkat T cells but also in MNC. Low alpha-toxin doses (3-30 ng ml-1) dose- and time-dependently induced apoptosis in both cell types, which was completely blocked by the caspase inhibitor zVAD-fmk. In Jurkat T cells and MNC, alpha-toxin induced the breakdown of the mitochondrial membrane potential and the intrinsic activation of caspase-3, -8 and -9. Interestingly, unlike in Jurkat T cells, apoptosis in MNC was additionally mediated by a caspase-9-independent component. MNC, but not Jurkat T cells, produced tumour necrosis factor (TNF)-alpha upon alpha-toxin stimulation. Blocking endogenous TNF-alpha with a TNF-alpha receptor antagonist partially decreased apoptosis in MNC. Our data therefore suggest that, whereas in Jurkat T cells apoptosis is solely mediated by the mitochondrial pathway, in MNC endogenous TNF-alpha and a death receptor-dependent pathway are also involved, which may contribute to depletion of immune cells during S. aureus infection