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This paper presents an overview of depth averaged modelling of fast catastrophic landslides where coupling of solid skeleton and pore fluid (air and water) is important. The first goal is to show how Biot-Zienkiewicz models can be applied to develop depth integrated, coupled models. The second objective of the paper is to consider a link which can be established between rheological and constitutive models. Perzyna´s viscoplasticity can be considered a general framework within which rheological models such as Bingham and cohesive frictional fluids can be derived. Among the several alternative numerical models, we will focus here on SPH which has not been widely applied by engineers to model landslide propagation. We propose an improvement, based on combining Finite Difference meshes associated to SPH nodes to describe pore pressure evolution inside the landslide mass. We devote a Section to analyze the performance of the models, considering three sets of tests and examples which allows to assess the model performance and limitations: (i) Problems having an analytical solution, (ii) Small scale laboratory tests, and (iii) Real cases for which we have had access to reliable information

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Murine mAbs reactive with the surface of Mycobacterium tuberculosis were assayed for their ability to affect the course of infection in mice challenged with virulent organisms. An IgG3 mAb (9d8) specific for arabinomannan and reactive with purified antigen from a clinical isolate of M. tuberculosis conferred partial protection on mice after respiratory challenge (30–60% survival >75 days; P ≤ 0.05). Control mice pretreated with an irrelevant mAb of the same isotype succumbed to tuberculosis within 30 days. Mice with gene disruptions in interferon γ and major histocompatibility complex Class II also were partially protected from challenge. The protective mAb was neither bactericidal nor inhibitory of infection or bacterial replication. Nevertheless, it profoundly altered the nature of the granulomas in the infected lungs. Mice treated with mAb 9d8 and challenged with M. tuberculosis localized the pathogen within granuloma centers, suggesting that the mAb conferred protection by enhancing a cellular immune response.