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- Forzieri, Giovanni, et al.
(författare)
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The Database of European Forest Insect and Disease Disturbances: DEFID2
- 2023
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Ingår i: Global Change Biology. - 1365-2486. ; 29:21, s. 6040-6065
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Tidskriftsartikel (refereegranskat)abstract
- Insect and disease outbreaks in forests are biotic disturbances that can profoundly alter ecosystem dynamics. In many parts of the world, these disturbance regimes are intensifying as the climate changes and shifts the distribution of species and biomes. As a result, key forest ecosystem services, such as carbon sequestration, regulation of water flows, wood production, protection of soils, and the conservation of biodiversity, could be increasingly compromised. Despite the relevance of these detrimental effects, there are currently no spatially detailed databases that record insect and disease disturbances on forests at the pan-European scale. Here, we present the new Database of European Forest Insect and Disease Disturbances (DEFID2). It comprises over 650,000 harmonized georeferenced records, mapped as polygons or points, of insects and disease disturbances that occurred between 1963 and 2021 in European forests. The records currently span eight different countries and were acquired through diverse methods (e.g., ground surveys, remote sensing techniques). The records in DEFID2 are described by a set of qualitative attributes, including severity and patterns of damage symptoms, agents, host tree species, climate-driven trigger factors, silvicultural practices, and eventual sanitary interventions. They are further complemented with a satellite-based quantitative characterization of the affected forest areas based on Landsat Normalized Burn Ratio time series, and damage metrics derived from them using the LandTrendr spectral–temporal segmentation algorithm (including onset, duration, magnitude, and rate of the disturbance), and possible interactions with windthrow and wildfire events. The DEFID2 database is a novel resource for many large-scale applications dealing with biotic disturbances. It offers a unique contribution to design networks of experiments, improve our understanding of ecological processes underlying biotic forest disturbances, monitor their dynamics, and enhance their representation in land-climate models. Further data sharing is encouraged to extend and improve the DEFID2 database continuously. The database is freely available at https://jeodpp.jrc.ec.europa.eu/ftp/jrc-opendata/FOREST/DISTURBANCES/DEFID2/.
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- Frew, Quentin, et al.
(författare)
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Betulin wound gel accelerated healing of superficial partial thickness burns : Results of a randomized, intra-individually controlled, phase III trial with 12-months follow-up
- 2019
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Ingår i: Burns. - : Elsevier. - 0305-4179 .- 1879-1409. ; 45:4, s. 876-890
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Tidskriftsartikel (refereegranskat)abstract
- Objective: Acceleration of wound healing promises advantages for patients and caregivers in reducing the burden of disease, avoiding complications such as wound infections, and improving the long-term outcome. However, medicines that can accelerate wound healing are lacking. The objective of this open, blindly evaluated, randomized, multicenter phase III study was to compare intra-individually the efficacy and tolerability of Oleogel-S10 with fatty gauze dressing versus Octenilin (R) wound gel with fatty gauze dressing in accelerating the healing of superficial partial thickness burn wounds. Methods: Acute superficial partial thickness burn wounds in adults caused by fire, heat burn or scalding were divided into 2 halves and randomly assigned to treatment with Oleogel-S10 or Octenilin (R) wound gel. Photos for observer-blinded analysis of wound healing were taken at each wound dressing change. Percentages of reepithelialization were assessed at defined intervals. Efficacy and tolerability were evaluated based on a 5-point Likert scale. Results: Of 61 patients that were enrolled, 57 received the allocated intervention and 48 completed treatment. The percentage of patients with earlier wound healing was significantly higher for Oleogel-S10 (85.7%, n=30) compared to Octenilin (R) wound gel (14.3%, n= 5, p <0.0001). The mean intra-individual difference in time to wound closure was -1.0 day in favour of Oleogel-S10 (-1.4, -0.6; 95% CI, p <0.0001). Most investigators (87.0%) and patients (84.8%) evaluated the efficacy of Oleogel-S10 to be 'better' or 'much better' than that of Octenilin (R) wound gel. Long-term outcome 3 months and 12 months post injury was improved in some patients. Conclusions: Oleogel-S10 (Episalvan) significantly accelerated the healing of superficial partial thickness burn wounds. It was safe and well tolerated. (C) 2018 Elsevier Ltd and ISBI. All rights reserved.
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- Wang, Lirui, et al.
(författare)
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Nod2 deficiency protects mice from cholestatic liver disease by increasing renal excretion of bile acids
- 2014
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Ingår i: Journal of Hepatology. - : Elsevier. - 0168-8278 .- 1600-0641. ; 60:6, s. 1259-1267
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND & AIMS: Chronic liver disease is characterized by fibrosis that may progress to cirrhosis. Nucleotide oligomerization domain 2 (Nod2), a member of the Nod-like receptor (NLR) family of intracellular immune receptors, plays an important role in the defense against bacterial infection through binding to the ligand muramyl dipeptide (MDP). Here, we investigated the role of Nod2 in the development of liver fibrosis.METHODS: We studied experimental cholestatic liver disease induced by bile duct ligation or toxic liver disease induced by carbon tetrachloride in wild type and Nod2(-/-) mice.RESULTS: Nod2 deficiency protected mice from cholestatic but not toxin-induced liver injury and fibrosis. Most notably, the hepatic bile acid concentration was lower in Nod2(-/-) mice than wild type mice following bile duct ligation for 3weeks. In contrast to wild type mice, Nod2(-/-) mice had increased urinary excretion of bile acids, including sulfated bile acids, and an upregulation of the bile acid efflux transporters MRP2 and MRP4 in tubular epithelial cells of the kidney. MRP2 and MRP4 were downregulated by IL-1β in a Nod2 dependent fashion.CONCLUSIONS: Our findings indicate that Nod2 deficiency protects mice from cholestatic liver injury and fibrosis through enhancing renal excretion of bile acids that in turn contributes to decreased concentration of bile acids in the hepatocyte.
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