Data-driven finite elements for geometry and material design

Crafting the behavior of a deformable object is difficult---whether it is a biomechanically accurate character model or a new multimaterial 3D printable design. Getting it right requires constant iteration, performed either manually or driven by an automated system. Unfortunately, Previous algorithms for accelerating three-dimensional finite element analysis of elastic objects suffer from expensive precomputation stages that rely on a priori knowledge of the object's geometry and material composition. In this paper we introduce Data-Driven Finite Elements as a solution to this problem. Given a material palette, our method constructs a metamaterial library which is reusable for subsequent simulations, regardless of object geometry and/or material composition. At runtime, we perform fast coarsening of a simulation mesh using a simple table lookup to select the appropriate metamaterial model for the coarsened elements. When the object's material distribution or geometry changes, we do not need to update the metamaterial library---we simply need to update the metamaterial assignments to the coarsened elements. An important advantage of our approach is that it is applicable to non-linear material models. This is important for designing objects that undergo finite deformation (such as those produced by multimaterial 3D printing). Our method yields speed gains of up to two orders of magnitude while maintaining good accuracy. We demonstrate the effectiveness of the method on both virtual and 3D printed examples in order to show its utility as a tool for deformable object design.National Science Foundation (U.S.) (Grant CCF-1138967)United States. Defense Advanced Research Projects Agency (N66001-12-1-4242

Splenic CD11c(+) cells derived from semi-immune mice protect naive mice against experimental cerebral malaria

Background: Immunity to malaria requires innate, adaptive immune responses and Plasmodium-specific memory cells. Previously, mice semi-immune to malaria was developed. Three cycles of infection and cure (\u27three-cure\u27) were required to protect mice against Plasmodium berghei (ANKA strain) infection. Methods: C57BL/6 J mice underwent three cycles of P. berghei infection and drug-cure to become semi-immune. The spleens of infected semi-immune mice were collected for flow cytometry analysis. CD11c(+) cells of semiimmune mice were isolated and transferred into naive mice which were subsequently challenged and followed up by survival and parasitaemia. Results: The percentages of splenic CD4(+) and CD11c(+) cells were increased in semi-immune mice on day 7 post-infection. The proportion and number of B220(+)CD11c(+)low cells (plasmacytoid dendritic cells, DCs) was higher in semi-immune, three-cure mice than in their naive littermates on day 7 post-infection (2.6 vs 1.1% and 491,031 vs 149,699, respectively). In adoptive transfer experiment, three months after the third cured P. berghei infection, splenic CD11c(+) DCs of non-infected, semi-immune, three-cure mice slowed Plasmodium proliferation and decreased the death rate due to neurological pathology in recipient mice. In addition, anti-P. berghei IgG1 level was higher in mice transferred with CD11c(+) cells of semi-immune, three-cure mice than mice transferred with CD11c(+) cells of naive counterparts. Conclusion: CD11c(+) cells of semi-immune mice protect against experimental cerebral malaria three months after the third cured malaria, potentially through protective plasmacytoid DCs and enhanced production of malaria-specific antibody

Unique T Cells with Unconventional Cytokine Profiles Induced in the Livers of Mice during Schistosoma mansoni Infection

During infection with Schistosoma , serious hepatic disorders are induced in the host. The liver possesses unique immune systems composed of specialized cells that differ from those of other immune competent organs or tissues. Host immune responses change dramatically during Schistosoma mansoni infection; in the early phase, Th1-related responses are induced, whereas during the late phase Th2 reactions dominate. Here, we describe unique T cell populations induced in the liver of mice during the period between Th1- and Th2-phases, which we term the transition phase. During this phase, varieties of immune cells including T lymphocytes increase in the liver. Subsets of CD4+ T cells exhibit unique cytokine production profiles, simultaneously producing both IFN-γ and IL-13 or both IFN-γ and IL-4. Furthermore, cells triply positive for IFN-γ, IL-13 and IL-4 also expand in the S. mansoni-infected liver. The induction of these unique cell populations does not occur in the spleen, indicating it is a phenomenon specific to the liver. In single hepatic CD4+ T cells showing the unique cytokine profiles, both T-bet and GATA-3 are expressed. Thus, our studies show that S. mansoni infection triggers the induction of hepatic T cell subsets with unique cytokine profiles