The effects of acute treatment with Δ9-THC on exploratory behaviour and memory in the rat

The aim of the present study was to evaluate the effects of delta9-tetrahydrocannabinol (delta9-THC) on exploratory behaviour and memory, independent of its locomotor suppressive effects. Dopamine (DA) and noradrenaline (NA) contents were determined in the areas of the brain directly related to such behaviours (hippocampus, striatum and amygdala). An acute dose of delta9-THC led to a decrease in exploratory parameters and motor activity during the holeboard test. The radial arm maze was used to evaluate the effects of this cannabinoid substance on memory. Animals treated with delta9-THC committed more errors in the maze test compared to control, particularly when the retention process was put to test. Furthermore, treatment with delta9-THC led to reduced NA contents in the hippocampus and increased DA contents in the amygdala, without changes in the striatum.     

Soil nutrient fluxes and vegetation changes on molehills

Abstract. The hypothesis that mole burrowing activity alters soil nutrient fluxes and that, as a response to the new conditions, a specialized guild of species develops on the molehills, was tested in an area located in the southwestern Spanish Pyrenees, on a spectrum of montane grassland communities that varies from xeric to temporally waterlogged. Evidence for an association between disturbance and nutrient availability was reported for nitrogen. Mole‐disturbed soils had elevated amounts of inorganic nitrogen compared to soils in surrounding pastures. At the first stages of mound revegetation, changes in nitrate flushes and in species competitive relationships following disturbance appeared to facilitate the establishment of ruderal and non‐mycorrhizal species. The diversity of the whole grassland was enhanced by the existence of these sets of species, abundant on mounds and rarer in the pasture. However, the difference was mainly quantitative, as exclusive colonizers of molehills were not found.     

A Mouse Model Uncovers LKB1 as an UVB-Induced DNA Damage Sensor Mediating CDKN1A (p21WAF1/CIP1) Degradation

Exposure to ultraviolet (UV) radiation from sunlight accounts for 90% of the symptoms of premature skin aging and skin cancer. The tumor suppressor serine-threonine kinase LKB1 is mutated in Peutz-Jeghers syndrome and in a spectrum of epithelial cancers whose etiology suggests a cooperation with environmental insults. Here we analyzed the role of LKB1 in a UV-dependent mouse skin cancer model and show that LKB1 haploinsufficiency is enough to impede UVB-induced DNA damage repair, contributing to tumor development driven by aberrant growth factor signaling. We demonstrate that LKB1 and its downstream kinase NUAK1 bind to CDKN1A. In response to UVB irradiation, LKB1 together with NUAK1 phosphorylates CDKN1A regulating the DNA damage response. Upon UVB treatment, LKB1 or NUAK1 deficiency results in CDKN1A accumulation, impaired DNA repair and resistance to apoptosis. Importantly, analysis of human tumor samples suggests that LKB1 mutational status could be a prognostic risk factor for UV-induced skin cancer. Altogether, our results identify LKB1 as a DNA damage sensor protein regulating skin UV-induced DNA damage response.     

Approaches for Addressing Life Cycle Assessment Data Gaps for Bio‐based Products

There is an increasing need for life cycle data for bio‐based products, which becomes particularly evident with the recent drive for greenhouse gas reporting and carbon footprinting studies. Meeting this need is challenging given that many bio‐products have not yet been studied by life cycle assessment (LCA), and those that have are specific and limited to certain geographic regions. In an attempt to bridge data gaps for bio‐based products, LCA practitioners can use either proxy data sets (e.g., use existing environmental data for apples to represent pears) or extrapolated data (e.g., derive new data for pears by modifying data for apples considering pear‐specific production characteristics). This article explores the challenges and consequences of using these two approaches. Several case studies are used to illustrate the trade‐offs between uncertainty and the ease of application, with carbon footprinting as an example. As shown, the use of proxy data sets is the quickest and easiest solution for bridging data gaps but also has the highest uncertainty. In contrast, data extrapolation methods may require extensive expert knowledge and are thus harder to use but give more robust results in bridging data gaps. They can also provide a sound basis for understanding variability in bio‐based product data. If resources (time, budget, and expertise) are limited, the use of averaged proxy data may be an acceptable compromise for initial or screening assessments. Overall, the article highlights the need for further research on the development and validation of different approaches to bridging data gaps for bio‐based products.     

Principles for life cycle inventories of land use on a global scale

Purpose

To assess the diverse environmental impacts of land use, a standardization of quantifying land use elementary flows is needed in life cycle assessment (LCA). The purpose of this paper is to propose how to standardize the land use classification and how to regionalize land use elementary flows.

Materials and methods

In life cycle inventories, land occupation and transformation are elementary flows providing relevant information on the type and location of land use for land use impact assessment. To find a suitable land use classification system for LCA, existing global land cover classification systems and global approaches to define biogeographical regions are reviewed.

Results and discussion

A new multi-level classification of land use is presented. It consists of four levels of detail ranging from very general global land cover classes to more refined categories and very specific categories indicating land use intensities. Regionalization is built on five levels, first distinguishing between terrestrial, freshwater, and marine biomes and further specifying climatic regions, specific biomes, ecoregions and finally indicating the exact geo-referenced information of land use. Current land use inventories and impact assessment methods do not always match and hinder a comprehensive assessment of land use impact. A standardized definition of land use types and geographic location helps to overcome this gap and provides the opportunity to test the optimal resolution of land cover types and regionalization for each impact pathway.

Conclusions and recommendation

The presented approach provides the necessary flexibility to providers of inventories and developers of impact assessment methods. To simplify inventories and impact assessment methods of land use, we need to find archetypical situations across impact pathways, land use types and regions, and aggregate inventory entries and methods accordingly.

     

Regulation of CC ligand 5/RANTES by acid sphingomyelinase and acid ceramidase

Acid sphingomyelinase (aSMase) generates the bioactive lipid ceramide (Cer) from hydrolysis of sphingomyelin (SM). However, its precise roles in regulating specific sphingolipid-mediated biological processes remain ill defined. Interestingly, the aSMase gene gives rise to two distinct enzymes, lysosomal sphingomyelinase (L-SMase) and secretory sphingomyelinase (S-SMase) via alternative trafficking of a shared protein precursor. Previously, our laboratory identified Ser(508) as a crucial residue for the constitutive and regulated secretion of S-SMase in response to inflammatory cytokines, and demonstrated a role for S-SMase in formation of select cellular Cer species (Jenkins, R. W., Canals, D., Idkowiak-Baldys, J., Simbari, F., Roddy, P., Perry, D. M., Kitatani, K., Luberto, C., and Hannun, Y. A. (2010) J. Biol. Chem. 285, 35706-35718). In the present study using a chemokine/cytokine screen, we identified the chemokine CCL5 (formerly known as RANTES) as a candidate-specific downstream target for aSMase. Regulation of CCL5 by aSMase was subsequently validated using both loss-of-function and gain-of-function models indicating that aSMase is both necessary and sufficient for CCL5 production. Interestingly, cells deficient in acid ceramidase (aCDase) also exhibited defects in CCL5 induction, whereas cells deficient in sphingosine kinase-1 and -2 exhibited higher levels of CCL5, suggesting that sphingosine and not sphingosine 1-phosphate (S1P) is responsible for the positive signal to CCL5. Consistent with this, co-expression of aSMase and aCDase was sufficient to strongly induce CCL5. Taken together, these data identify a novel role for aSMase (particularly S-SMase) in chemokine elaboration by pro-inflammatory cytokines and highlight a novel and shared function for aSMase and aCDase.