The potential impacts of changes in bear hunting policy for hunting organisations in Croatia

The brown bear (Ursus arctos) in Croatia is currently being managed through trophy hunting, with quotas allocated to local hunting organisations. Human-bear conflict is present at a low level, but any losses are compensated by the hunting organisations that benefit from bear hunting. Attitudes towards bears are generally positive, and the bear population appears stable, or even increasing. Croatia's current bear hunting policy relies upon both the ecological sustainability of the quotas and the economic sustainability of the hunting organisations. To address the first of these pillars of current policy, we used a two-sex matrix model of the bear population to investigate the biological sustainability of current hunting levels. The model suggests that if the annual allocated quota were fully realised, the population would suffer a considerable decrease over 10 years. A likely explanation for the mismatch between this result and the observed stability of the population is that the bear population size is underestimated. To address the second pillar, we quantified the current structure, costs and benefits of bear hunting to hunting organisations through an interview survey with hunting managers. We found that bear hunting is a substantial component of hunting organisations' income, supporting the other activities of the organisation. Croatia's recent accession to the EU will require changes in their bear management system, potentially stopping bear trophy hunting. Therefore, we assessed the changes in hunting organisations' budgets in the absence of bear hunting. Our results demonstrate that a loss of bear trophy hunting would result in a substantial loss of income to the hunting organisations. Moving bear hunting and compensation mechanisms from local management and responsibility to a more centralised system without trophy hunting, as suggested by EU legislation, will lead to considerable uncertainties. These include how to make centralised decisions on population targets and offtake levels for population control, given the uncertainty around population estimates, and on compensation payments given the loss of the current system which relies heavily on local income from trophy hunting, local relationships and informal monetary and non-monetary compensation

Strain measurement of medical textile using 2d digital image correlation method

Medical textile plays an important role in the technical textiles sector as one of the most rapidly growing sectors in the technical textile market. The textile materials should have some adequate mechanical properties to be useful as medical textile. Tensile strength presents one of the basic mechanical properties used to describe textile specimens. Standardized tensile testing procedures on textile specimens were commonly used in the past. The aim of this paper was to measure in-plane strain field on the tensile medical textile specimen using 2D Digital Image Correlation method (2D-DIC). 2D-DIC is a non-contact optical method for accurate displacement and strain full-field measurement. In this study, two medical cotton textiles, with density 120 and 130 g/m2, were used to create three specimens for each material. Each specimen was placed in the tensile testing machine and measured until the break. During the tensile testing, camera was automatically recording full-field displacement in X and Y directions. Textile 1 and Textile 2 showed significant differences in point distance values, despite the small deviation in densities (less than 10%). Mean value of the elongation for Textile 1 is more than a double than the elongation for Textile 2, although the difference for mean value of Maximum force if negligible. Also, it has been showed that 2D-DIC can play significant role for measurement in textile mechanical properties measurement

Association of SOD2 (Rs4880) and GPX1 (rs1050450) gene polymorphisms with risk of Balkan endemic nephropathy and its related tumors

© 2019 by the authors. Licensee MDPI, Basel, Switzerland. T. Background: Experimental data show that superoxide dismutase 2 (SOD2) is involved in ochratoxin (OTA)-induced nephrotoxicity, whereas clinical data indicate the role of SOD2 rs4880 or glutathione peroxidase 1 (GPX1) rs1050450 polymorphisms in end-stage renal disease and urothelial carcinoma risk, known to be the major complications of Balkan endemic nephropathy (BEN). Therefore, we hypothesized that SOD2 and GPX1 gene polymorphisms would influence the risk of BEN and its associated tumors. Materials and Methods: The study was conducted in 207 BEN patients and 86 controls from endemic areas. Results: Individuals with both copies of variant SOD2 allele, known for lower mitochondrial antioxidant protection, are at a significantly higher BEN risk (OR = 2.6, p = 0.021). No association was observed between GPX1 gene polymorphism and BEN risk. Combining SOD2 and GPX1 genotypes did not alter the risk of BEN development. Regarding the risk of urothelial tumors in BEN patients, none of the polymorphisms studied was significantly associated with the risk of these tumors. Conclusions: Polymorphism in SOD2 rs4880 gene affects the risk of BEN development. Hence, SOD2 genotyping could, together with a panel of other enzymes, be used as a biomarker of susceptibility in BEN areas

Abnormalities of mitochondrial dynamics and bioenergetics in neuronal cells from CDKL5 deficiency disorder

CDKL5 deficiency disorder (CDD) is a rare neurodevelopmental disorder caused by pathogenic variants in the Cyclin-dependent kinase-like 5 (CDKL5) gene, resulting in dysfunctional CDKL5 protein. It predominantly affects females and causes seizures in the first few months of life, ultimately resulting in severe intellectual disability. In the absence of targeted therapies, treatment is currently only symptomatic. CDKL5 is a serine/threonine kinase that is highly expressed in the brain, with a critical role in neuronal development. Evidence of mitochondrial dysfunction in CDD is gathering, but has not been studied extensively. We used human patient-derived induced pluripotent stem cells with a pathogenic truncating mutation (p.Arg59*) and CRISPR/Cas9 gene-corrected isogenic controls, differentiated into neurons, to investigate the impact of CDKL5 mutation on cellular function. Quantitative proteomics indicated mitochondrial defects in CDKL5 p.Arg59* neurons, and mitochondrial bioenergetics analysis confirmed decreased activity of mitochondrial respiratory chain complexes. Additionally, mitochondrial trafficking velocity was significantly impaired, and there was a higher percentage of stationary mitochondria. We propose mitochondrial dysfunction is contributing to CDD pathology, and should be a focus for development of targeted treatments for CDD