A GIS tool for flood risk analysis in Flanders (Belgium)

In the past decades, the low-lying region Flanders (Belgium) has fall victim to numerous flood events, causing substantial damage to buildings and infrastructure. In response to this, the Flemish government proposed a new approach which considers the level of risk as a way for safety measurement. Using geographical information systems, this evolution has lead to a comprehensive risk methodology, and more recently to the development of a flood risk assessment tool called LATIS. By estimating the potential damage and the number of casualties during a flood event, LATIS offers the possibility to perform risk analysis in a fast and effective way. This paper presents a brief overview of the currently used methodology for flood risk management in Flanders and its implementation in the LATIS tool. The usefulness of this new tool is demonstrated by a sequence of risk calculations, performed in the framework of climate change impacts on flood risk in Flanders

Blocking elevated p38 MAPK restores efferocytosis and inflammatory resolution in the elderly

Increasing age alters innate immune–mediated responses; however, the mechanisms underpinning these changes in humans are not fully understood. Using a human dermal model of acute inflammation, we found that, although inflammatory onset is similar between young and elderly individuals, the resolution phase was substantially impaired in elderly individuals. This arose from a reduction in T cell immunoglobulin mucin receptor-4 (TIM-4), a phosphatidylserine receptor expressed on macrophages that enables the engulfment of apoptotic bodies, so-called efferocytosis. Reduced TIM-4 in elderly individuals was caused by an elevation in macrophage p38 mitogen-activated protein kinase (MAPK) activity. Administering an orally active p38 inhibitor to elderly individuals rescued TIM-4 expression, cleared apoptotic bodies and restored a macrophage resolution phenotype. Thus, inhibiting p38 in elderly individuals rejuvenated their resolution response to be more similar to that of younger people. This is the first resolution defect identified in humans that has been successfully reversed, thereby highlighting the tractability of targeting pro-resolution biology to treat diseases driven by chronic inflammation

An experimental multiprocessor system for distributed parallel computations.

The availability of low-cost microprocessor chips with efficient instruction sets for specific numerical tasks (signal processors) has been exploited for building a versatile multiprocessor system, consisting of a host minicomputer augmented by a number of joint processors. The host provides a multiuser-multitasking environment and manages system resources and task scheduling. User applications can call upon one or more joint processors for parallel execution of adequately partitioned, computationally intensive numeric operations. Each joint processor has sufficient local memory for storing procedures and data and has access to regions in host memory for shared data. Kernel processes in the host and in the joint processors provide the necessary mechanism for initialization and synchronization of the distributed parallel execution of procedures

Field Production and Functional Evaluation of Chloroplast-Derived Interferon-α2b

Type I interferons (IFNs) inhibit viral replication and cell growth and enhance the immune response, and therefore have many clinical applications. IFN-α2b ranks third in world market use for a biopharmaceutical, behind only insulin and erythropoietin. The average annual cost of IFN-α2b for the treatment of hepatitis C infection is $26 000, and is therefore unavailable to the majority of patients in developing countries. Therefore, we expressed IFN-α2b in tobacco chloroplasts, and transgenic lines were grown in the field after obtaining United States Department of Agriculture Animal and Plant Health Inspection Service (USDA-APHIS) approval. Stable, site-specific integration of transgenes into chloroplast genomes and homoplasmy through several generations were confirmed. IFN-α2b levels reached up to 20% of total soluble protein, or 3 mg per gram of leaf (fresh weight). Transgenic IFN-α2b had similar in vitrobiological activity to commercially produced PEG-Intron™ when tested for its ability to protect cells against cytopathic viral replication in the vesicular stomatitis virus cytopathic effect (VSV CPE) assay and to inhibit early-stage human immunodeficiency virus (HIV) infection. The antitumour and immunomodulating properties of IFN-α2b were also seen in vivo . Chloroplast-derived IFN-α2b increased the expression of major histocompatibility complex class I (MHC I) on splenocytes and the total number of natural killer (NK) cells. Finally, IFN-α2b purified from chloroplast transgenic lines (cpIFN-α2b) protected mice from a highly metastatic tumour line. This demonstration of high levels of expression of IFN-α2b, transgene containment and biological activity akin to that of commercial preparations of IFN-α2b facilitated the first field production of a plant-derived human blood protein, a critical step towards human clinical trials and commercialization

Sestrins induce natural killer function in senescent-like CD8(+) T cells

Aging is associated with remodeling of the immune system to enable the maintenance of life-long immunity. In the CD8⁺ T cell compartment, aging results in the expansion of highly differentiated cells that exhibit characteristics of cellular senescence. Here we found that CD27⁻CD28⁻CD8⁺ T cells lost the signaling activity of the T cell antigen receptor (TCR) and expressed a protein complex containing the agonistic natural killer (NK) receptor NKG2D and the NK adaptor molecule DAP12, which promoted cytotoxicity against cells that expressed NKG2D ligands. Immunoprecipitation and imaging cytometry indicated that the NKG2D-DAP12 complex was associated with sestrin 2. The genetic inhibition of sestrin 2 resulted in decreased expression of NKG2D and DAP12 and restored TCR signaling in senescent-like CD27⁻CD28⁻CD8⁺ T cells. Therefore, during aging, sestrins induce the reprogramming of non-proliferative senescent-like CD27⁻CD28⁻CD8⁺ T cells to acquire a broad-spectrum, innate-like killing activity