Stimulation of methane oxidation by CH<Subscript>4</Subscript>-emitting rose chafer larvae in well-aerated grassland soil

In this study, the impact of rose chafer (Cetonia aurata L.) larvae on net and gross methane (CH₄) fluxes in soil from an old permanent grassland site (Giessen, Germany) was investigated. Previous studies at this site suggested the existence of Scarabaeidae larvae-induced “CH₄-emitting hot spots” within the soil profile which may subsequently lead to increased CH₄ oxidation. The net (soil + larvae) and gross (soil and larvae separated) CH₄ fluxes were studied in a 3-month laboratory incubation. Addition of larvae changed the soil from a net sink (?330 ± 11 ng CH₄ kg^?1 h^?1) to a net source (637 ± 205 ng CH₄ kg^?1 h^?1). Supply of plant litter to the soil + larvae incubation jars tended to increase CH₄ emissions which was not significant due to large variability. After 11–13 weeks of incubation, the net soil CH₄ oxidation was significantly stimulated by 13–21% in the treatments containing larvae when these were taken out. Analysis of archaeal 16S rRNA genes revealed that the majority of the obtained clones were closely related to uncultured methanogens from guts of insects and other animals. Other sequences were relative to cultivated species of Methanobrevibacter, Methanoculleus, and Methanosarcina. Hence, Scarabaeidae larvae in soils (i) may represent an underestimated source of CH₄ emissions in aerobic upland soils, (ii) may stimulate gross CH₄ consumption in their direct soil environment, and, thus, (iii) contribute to the spatial heterogeneity often observed in the field with closed-chamber measurements. Long-term CH₄-flux balances may be wrongly assessed when “exceptional” net CH₄ flux rates (due to larvae hot spots) are excluded from data sets.     

Expression of adipokines and adipocytokines by epidural adipose tissue in cauda equina syndrome in dogs

BackgroundCompression of epidural adipose tissue (EAT) within the scope of cauda equina syndrome (CES) could lead to an enhanced expression of inflammatory mediators, possibly contributing to pain amplification in dogs.ObjectivesTo analyze expression of inflammatory adipo(‐cyto)kines within the EAT of dogs with CES.AnimalsClient‐owned dogs: 15 dogs with CES and 9 dogs euthanized for unrelated medical reasons (controls).MethodsProspective, experimental study. Epidural adipose tissue and subcutaneous adipose tissue were collected during dorsal laminectomy and used for real‐time quantitative polymerase chain reaction. Tissue explants were cultured for measurements of inflammation‐induced release of cytokines.ResultsResults show a CES‐associated upregulation of the cytokines tumor necrosis factor alpha (TNFα: mean ± SD: 18.88 ± 11.87, 95% CI: 10.90‐26.86 vs 9.66 ± 5.22, 95% CI: 5.29‐14.02, *: P = .04) and interleukin‐ (IL‐) 10 (20.1 ± 9.15, 95% CI: 14.82‐25.39 vs 11.52 ± 6.82, 95% CI: 5.82‐17.22, *: P = .03), whereas the expression of the adipokine leptin was attenuated in EAT of dogs with CES (3.07 ± 2.29, 95% CI: 1.80‐3.34 vs 9.83 ± 8.42, 95% CI: 3.36‐16.30, **: P = .007). Inflammatory stimulation of EAT explant cultures resulted in an enhanced release of IL‐6 (LPS: 5491.55 ± 4438, 95% CI: 833.7‐10 149; HMGB1: 1001.78 ± 522.2, 95% CI: 518.8‐1485; PBS: 310.9 ± 98.57, 95% CI: 228.5‐393.3, ***: P < .001).Conclusion and Clinical ImportanceExpression profile of inflammatory adipo(‐cyto)kines by EAT is influenced from compressive forces acting in dogs with CES and might contribute to amplification of pain.