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Biodiversity indicators are widely-used tools to help determine rates of biodiversity change and the success or failure of efforts to conserve it. However, their sufficiency and suitability in providing information for decision-makers is unclear. Here, we review the indicators brought together under the Biodiversity Indicator Partnership to monitor progress towards the Aichi Targets to determine where there are gaps. Of the 20 Aichi Biodiversity Targets, Targets 2, 3 and 15 are missing indicators entirely. Scoring the indicators in relation to their alignment, temporal relevance and spatial scale shows additional gaps under Targets 1, 13 and 16–20. Predominately, gaps were found to be socio-economic in nature (i.e. benefits, pressures and responses) rather than status-related (i.e. states), principally due to a poor alignment between the indicator and the text of the Aichi Target. Hence, it is critical that existing indicators are properly resourced and maintained and new indicators developed to be able to effectively monitor biodiversity and its influencing factors to 2020 and beyond. This article is protected by copyright. All rights reserved

Cathepsin X (CTSX, also called cathepsin Z/P) is a cysteine protease that still plays an unknown role in human cancer. It has been shown to bind cell surface heparin sulphate proteoglycans and integrins, indicating possible functions of CTSX in cellular adhesion, phagocytosis, and immune response. Our previous studies have shown an association between Helicobacter pylori (H. pylori) infection, a strong up-regulation of CTSX, and development of gastric cancer. In this study, yeast two-hybrid analysis revealed that RPLP0, a ribosomal protein P0, interacts with the human CTSX protein in gastric cancer. The CTSX/RPLP0 interaction was confirmed by co-immunoprecipitation assays. In addition, co-localization studies in cancer cell line N87 and gastric cancer tissue samples were performed. Laserscan microscopy revealed a shuttling of RPLP0 (and CTSX) from cytoplasm to the nucleus after CTSX knockdown. Down-regulation of RPLP0 resulted in G1 arrest of gastric cancer cells, whereas knockdown of CTSX led to G1 arrest and apoptosis after 48 h. Knockdown of both proteins caused increased apoptosis. RPLP0 deficiency could suppress cell growth and cell cycle progression by down-regulating CDK2. It was further demonstrated that RPLP0 affected p21 expression, but did not change the expression of Cyclin E. Down-regulation of both proteins at least through CDK2 suggests an anti-apoptotic effect on gastric cancer cells and opens up new possibilities for apoptotic immune modulation and gastric cancer therapy.

Maes, Joachim... et al.-- 10 pages, 2 figures, 3 tables, supplementary material https://doi.org/10.1016/j.ecoser.2015.10.023, In the EU, the mapping and assessment of ecosystems and their services, abbreviated to MAES, is seen as a key action for the advancement of biodiversity objectives, and also to inform the development and implementation of related policies on water, climate, agriculture, forest, marine and regional planning. In this study, we present the development of an analytical framework which ensures that consistent approaches are used throughout the EU. It is framed by a broad set of key policy questions and structured around a conceptual framework that links human societies and their well-being with the environment. Next, this framework is tested through four thematic pilot studies, including stakeholders and experts working at different scales and governance levels, which contributed indicators to assess the state of ecosystem services. Indicators were scored according to different criteria and assorted per ecosystem type and ecosystem services using the common international classification of ecosystem services (CICES) as typology. We concluded that there is potential to develop a first EU wide ecosystem assessment on the basis of existing data if they are combined in a creative way. However, substantial data gaps remain to be filled before a fully integrated and complete ecosystem assessment can be carried out, Balint Czúcz was supported by the Bolyai Grant of the Hungarian Academy of Sciences under grant number BO/00138/12/8

Death-associated protein kinase (DAPK) is a serine/threonine kinase that contributes to pro-apoptotic signaling on cytokine exposure. The role of DAPK in macrophage-associated tumor cell death is currently unknown. Recently, we suggested a new function for DAPK in the induction of apoptosis during the interaction between colorectal tumor cells and tumor-associated macrophages. Using a cell-culture model with conditioned supernatants of differentiated/activated macrophages (U937) and human HCT116 colorectal tumor cells, we replicated DAPK-associated tumor cell death; this model likely reflects the in vivo tumor setting. In this study, we show that tumor necrosis factor-alpha exposure under conditions of macrophage activation induced DAPK-dependent apoptosis in the colorectal tumor cell line HCT116. Simultaneously, early phosphorylation of p38 mitogen-activated protein kinase (phospho-p38) was observed. We identified the phospho-p38 mitogen-activated protein kinase as a novel interacting protein of DAPK in tumor necrosis factor-alpha-induced apoptosis. The general relevance of this interaction was verified in two colorectal cell lines without functional p53 (ie, HCT116 p53(-/-) and HT29 mutant) and in human colon cancer and ulcerative colitis tissues. Supernatants of freshly isolated human macrophages were also able to induce DAPK and phospho-p38. Our findings highlight the mechanisms that underlie DAPK regulation in tumor cell death evoked by immune cells.

Anne Teller - European Commission, DG Environment. Anne is Biodiversity Policy Officer in the Directorate-General Environment of the European Commission. She has more than twenty years experience in European environmental policy. Her specific domain of interest is the strengthening of the evidence-based approach to environment policy making. Anne is currently coordinating a new initiative on Mapping and Assessment of the state of Ecosystems and of their Services (MAES) in Europe.

Helicobacter pylori are responsible for the induction of chronic gastric inflammation progressing to atrophy, metaplasia, and gastric cancer. The overexpression of Cathepsin X/Z (Ctsz) in H. pylori-infected mucosa and gastric cancer is mediated predominantly by an augmented migration of ctsz(-/-)positive macrophages and the up-regulation of Ctsz in tumor epithelium. To explore the Ctsz-function in the context of chronic inflammation and the development of preneoplastic lesions, we used Ctsz-deficient mice in a H. pylori gastritis model. Ctsz (-/-) and wild-type (wt) mice were infected with H. pylori strain SS1. The mice were sacrificed at 24, 36, and 50 weeks post infection (wpi). The stomach was removed, and gastric strips were snap-frozen or embedded and stained with H&E. Tissue sections were scored for epithelial lesions and inflammation. Ki-67 and F4/80 immunostaining were used to measure epithelial cell proliferation and macrophage infiltration, respectively. The upregulation of compensating cathepsins and cytokines were confirmed by Western blotting and quantitative RT-PCR. SS1-infected wt and ctsz (-/-) mice showed strong inflammation, foveolar hyperplasia, atrophy, and cystically-dilated glands. However, at 50 wpi, ctsz (-/-) mice developed significantly more severe spasmolytic polypeptide-expressing metaplasia (SPEM), showed enhanced epithelial proliferation, and higher levels of infiltrating macrophages. Induction of cytokines was higher and significantly prolonged in ctsz (-/-) mice compared to wt. Ctsz deficiency supports H. pylori-dependent development of chronic gastritis up to metaplasia, indicating a protective, but not proteolytic, function of Ctsz in inflammatory gastric disease.

From 1985 to 1990, the European Commission has realized the CORINE Programme (Coordination of Information on the Environment). The results are essentially of three types, corresponding to the three aims of the Programme

FERN was launched in February 1986 by the European Science Foundation (ESF). The project is to be seen essentially as a coordination and concertation of national research activities already in hand or planned for the near future. It will establish a network of European research groups in the field of forest ecology. An inventory of all participating research teams is in press. The organization of topical workshops results in recommendations aimed at improving the coherence of the overall research carried out in Europe as well as harmonizing the techniques and at establishing common objectives for future investigations.