Predicting ash dieback severity and environmental suitability for the disease in forest stands

Ash dieback, caused by the ascomycete fungus Hymenoscyphus fraxineus, has been rapidly expanding across Europe during the last two decades, posing a considerable threat to native ash populations. In this study, we applied regression-based models trained by field data, in conjunction with geographic information systems, to produce spatial predictions of ash dieback severity and environmental suitability for the disease in Czech forests. A model of actual ash dieback severity relates disease extent to silvicultural and environmental characteristics of forest stands and their neighbourhood, while a model of environmental suitability for the disease quantifies the relative susceptibility of sites to the disease, independent of the current silvicultural characteristics. The final predictive maps suggested that fertile lowlands and humid areas bordering Poland and Slovakia were the most endangered regions. Areas at the lowest risk of damage were concentrated in dry areas and in highland and mountain areas in the western part of the country, usually with poor soils on acid bedrock. Predictions of actual disease severity are an effective tool for guiding the current management of infested stands whereas predicting environmental suitability is useful for making long-term strategic decisions, e.g. identifying areas where future ash regeneration and cultivation may be unsuccessful.     

Hepatoprotective effect of curcumin in lipopolysaccharide/-galactosamine model of liver injury in rats: relationship to HO-1/CO antioxidant system

This work studied a relationship between HO-1/CO system and lipid peroxidation with consequent effects on liver functions and NOS-2. We focused on curcumin pretreatment in rat toxic model of d-galactosamine and lipopolysaccharide. Hepatocyte viability, lipid peroxidation, antioxidant status, ALT and AST were evaluated. HO-1 and NOS-2 expressions and respective enzyme activity were determined. Curcumin caused decreases in ALT and AST levels as well as in lipid peroxidation. Furthermore, curcumin pretreatment increased liver HO-1 (2.4-fold, p = 0.001), but reduced NOS-2 (4.1-fold, p = 0.01) expressions. In conclusion, the tuning of CO/NO pathways is important in shedding light on curcumin's cytoprotective effects in this model.     

Comment on "A persistent oxygen anomaly reveals the fate of spilled methane in the deep Gulf of Mexico"

Kessler et al. (Reports, 21 January 2011, p. 312) reported that methane released from the 2010 Deepwater Horizon blowout, approximately 40% of the total hydrocarbon discharge, was consumed quantitatively by methanotrophic bacteria in Gulf of Mexico deep waters over a 4-month period. We find the evidence explicitly linking observed oxygen anomalies to methane consumption ambiguous and extension of these observations to hydrate-derived methane climate forcing premature.     

Female scent mobilizes leukocytes to airways in BALB/c male mice

The scent of receptive females as a signal to reproduction stimulates male mice to olfactory search of a potential breeding partner. This searching behavior is coupled with infection risk due to bacterial contamination of the fecal and urine scent marks. We hypothesized that sniffing of female soiled bedding induced the migration of immuno‐competent cells into airways as a possible adaptation to breeding‐related infection. Using bronchoalveolar lavage in a study on mice, we found the number of leukocytes to be significantly higher in male mice that were provided new portions of soiled bedding daily from female cages, in comparison with male mice that were kept in isolation from female scent. The number of leukocytes in blood was equal in both groups. However, monocytes were fewer in number in male mice exposed to female scent than in male mice isolated from female mice. Scent‐induced migration of leukocytes was accompanied by typical behavioral (increased sniffing activity and aggressiveness) and morphological (increase preputial glands and seminal vesicles) responses to olfactory sexual stimulus.     

Similarity of fine specificity of IgA anti-gliadin antibodies between patients with celiac disease and humanized α1KI mice

Gliadins, and primarily α-gliadins containing several sequences such as aa 31-49, aa 56-88 (33-mer), aa 57-68, and aa 69-82, are critical in the induction of immune response or toxic reaction leading to the development of celiac disease (CLD). The role of IgA anti-gliadin antibodies (IgA AGA) is unknown. To this end, we prepared several humanized monoclonal IgA AGA using transgenic α1KI mice. Employing Pepscan with overlapping decapeptides of α-gliadin we observed a robust similarity between the specificity of humanized mouse monoclonal IgA AGA and IgA AGA from patients with florid CLD. The common immunodominant region included several sequential epitopes localized in the N-terminal part of α-gliadin (QFQGQQQPFPPQQPYPQPQPFP, aa 29-50, and QPFPSQQPYLQL, aa 47-58). Notably, IgA AGA produced by clones 8D12, 15B9, 9D12, and 18E2 had significant reactivity against sequences localized in the 33-mer, LQLQPFPQPQ (aa 56-65) and PQLPYPQPQPFL (aa 69-80). Humanized mouse monoclonal IgA AGA that have a known specificity are suitable as standard in ELISAs to detect serum IgA AGA of CLD patients and for studying the AGA pathogenic role in CLD, especially for analyzing the translocation of complex of specific IgA antibodies and individual gliadin peptides through enterocyte barrier.