Fostering coastal resilience to climate change vulnerability in Bangladesh, Brazil, Cameroon and Uruguay: a cross-country comparison

© 2017, Springer Science+Business Media B.V. This paper describes a comparative study of four different cases on vulnerability, hazards and adaptive capacity to climate threats in coastal areas and communities in four developing countries: Bangladesh, Brazil, Cameroon and Uruguay. Coastal areas are vulnerable to sea-level rise (SLR), storm surges and flooding due to their (i) exposure, (ii) concentration of settlements, many of which occupied by less advantaged groups and (iii) the concentration of assets and services seen in these areas. The objective of the paper is twofold: (i) to evaluate current evidence of coastal vulnerability and adaptive capacity and (ii) to compare adaptation strategies being implemented in a sample of developing countries, focusing on successful ones. The followed approach for the case evaluation is based on (i) documenting observed threats and damages, (ii) using indicators of physical and socioeconomic vulnerability and adaptive capacity status and (iii) selecting examples of successful responses. Major conclusions based on cross-case comparison are (a) the studied countries show different vulnerability, adaptive capacity and implementation of responses, (b) innovative community-based (CBA) and ecosystem-based adaptation (EbA) and (c) early warning systems are key approaches and tools to foster climate resilience. A recommendation to foster the resilience of coastal communities and services is that efforts in innovative adaptation strategies to sea-level rise should be intensified and integrated with climate risk management within the national adaption plans (NAPAs) in order to reduce the impacts of hazards

Curdlan-mediated regulation of human phagocyte-specific chitotriosidase

Human phagocyte-specific chitotriosidase is part of innate immunity and shows anti-fungal activity towards chitin-containing fungi. We investigated the effect of stimulation of the C-type lectin receptor dectin-1 by beta-1,3-glucan (curdlan) on chitotriosidase expression and release by human phagocytes. We observed that curdlan triggers chitotriosidase release from human neutrophils. In addition, we show that curdlan impairs chitotriosidase induction in monocytes. Finally, curdlan temporarily induces chitotriosidase in enzyme-expressing monocyte-derived macrophages, followed by reduction of chitotriosidase expression after prolonged stimulation. These data on regulation of phagocyte-specific chitotriosidase following curdlan recognition support an important role of chitotriosidase in the elimination of chitin-containing pathogens. (C) 2010 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved

The cytosolic B-glucosidase GBA3 does not influence type 1 Gaucher disease manifestation

GBA3, also known as cytosolic ß-glucosidase, is thought to hydrolyze xenobiotic glycosides in man. Deficiency of glucocerebrosidase (GBA), a ß-glucosidase degrading glucosylceramide, underlies Gaucher disease. We examined GBA3, which recently was proposed to degrade glucosylceramide and influence the clinical manifestation of Gaucher disease. Recombinant GBA3 was found to hydrolyze artificial substrates such as 4-methylumbelliferyl-ß-D-glucoside and C6-NBD-glucosylceramide, but hydrolysis of naturally occurring lipids like glucosylceramide and glucosylsphingosine was hardly detected. Consistent with this, inhibition of GBA3 in cultured cells using a novel inhibitor (alpha-1-C-nonyl-DIX) did not result in an additional increase in glucosylceramide as compared to GBA inhibition alone. Examination of the GBA3 gene led to the identification of a common substitution in its open reading frame (1368T¿A), resulting in a truncated GBA3 protein missing the last a-helix of its (ß/a)8 barrel. Both recombinant 1368A GBA3 and 1368A enzyme from spleen of a homozygous individual were found to be inactive. Amongst non-neuronopathic (type 1) Gaucher disease patients, we subsequently identified individuals being wild-type, heterozygous, or homozygous for the GBA3 1368T¿A mutation. No correlation was observed between GBA3 1368A/T haplotypes and severity of type 1 Gaucher disease manifestation. In conclusion, GBA3 does not seem to modify type 1 Gaucher disease manifestatio

The SH3 domain of the Saccharomyces cerevisiae peroxisomal membrane protein Pex13p functions as a docking site for Pex5p, a mobile receptor for the import PTS1-containing proteins

We identified a Saccharomyces cerevisiae peroxisomal membrane protein, Pex13p, that is essential for protein import. A point mutation in the COOH-terminal Src homology 3 (SH3) domain of Pex13p inactivated the protein but did not affect its membrane targeting. A two-hybrid screen with the SH3 domain of Pex13p identified Pex5p, a receptor for proteins with a type I peroxisomal targeting signal (PTS1), as its ligand. Pex13p SH3 interacted specifically with Pex5p in vitro. We determined, furthermore, that Pex5p was mainly present in the cytosol and only a small fraction was associated with peroxisomes. We therefore propose that Pex13p is a component of the peroxisomal protein import machinery onto which the mobile Pex5p receptor docks for the delivery of the selected PTS1 protei