An Unbiased Look At Rucaparib

albicans cells were phagocytosed by PMN, #ALPI randurls[1|1|,|CHEM1|]# whereas only 4% C. albicans cells were phagocytosed by monocytes. Furthermore, PMN play a major role in the immune response, because these phagocytes are associated with 97% of all killed C. albicans cells (see Supplementary Figure 2A). This is achieved either directly, via phagocytosis and intracellular killing (66.5%) of the pathogen, or indirectly by the release of antimicrobial peptides on a pathogen's first event of phagocytosis (30.5%) (see Supplementary Figure 2H). Four hours post-infection, most C. albicans cells were killed (89%) while a minority of 11% cells were extracellular and became resistant against killing and phagocytosis. These results are in quantitative agreement with those obtained previously for the P-SBM (H��nniger et al., 2014). Figure 6 Comparison of the time-evolution for the combined units from the experimental whole-blood infection assay (dotted lines as a guide for the eye) with the PI-SBM in (A,B), and the ABM in (C,D). In (A,B), the thickness of the solid lines represents the standard ... 3.2. Predictions on monocytopenia and neutropenia from PI-SBM The state-based model PI-SBM opens the possibility to study the dependence of the immune response against C. albicans on the number of PMN and monocytes in blood. Simulating the virtual infection scenario with the previously estimated parameters (see Supplementary Table 3), we considered various cases of immune cell deficiencies. The model predictions at 4 h post-infection and for gradual decreases in the immune cell numbers are presented in Figure ?Figure77 for the cases of monocytopenia and neutropenia separately. Figure 7 Simulation results of the PI-SBM with different immune cell numbers at 4 h post-infection for the conditions (A) monocytopenia and (B) neutropenia. The relative numbers of C. albicans cells of killed cells (CK), phagocytosed cells in monocytes (CM) and ... We found, as expected from the above quantification of the immune response, that monocytopenia is not a critical condition with regard to C. albicans infections: deficiency of monocytes and even their complete absence was fully compensated by PMN-mediated killing. In fact, patients with monocytopenia have not been reported to develop systemic candidiasis to date (Lionakis, 2014). The situation is extremely different in the case of neutropenia. In the absence of PMN, the number of killed C. albicans cells is predicted to decrease from about 89% under physiological conditions down to 45%, i.e., CK = 89% for 5 �� 106 PMN and CK = 45% for ��5��103 PMN (see Figure ?Figure7B).7B). Monocytes compensated PMN deficiency by phagocytosis of C. albicans cells only partly, where the fraction increased from 3% under physiological conditions up to 48%. However, 42% of the C.