CO2 fluxes from wood decomposition represent an important source of carbon from forest ecosystems to the atmosphere, which are determined by both wood traits and climate influencing the metabolic rates of decomposers. Previous studies have quantified the effects of moisture and temperature on wood decomposition, but these effects were not separated from the potential influence of wood traits. Indeed, it is not well understood how traits and climate interact to influence wood CO2 fluxes. selleck kinase inhibitor Here we examined the responses of CO2 fluxes from dead wood with different traits (angiosperm and gymnosperm) to 0%, 35%, and 70% rainfall reduction across seasonal temperature gradients. Our results showed that drought significantly decreased wood CO2 fluxes, but its effects varied with both taxonomical group and drought intensity. Drought-induced reduction in wood CO2 fluxes was larger in angiosperms than gymnosperms for the 35% rainfall reduction treatment, but there was no significant difference between these groups for the 70% reduction treatment. This is because wood nitrogen density and carbon quality were significantly higher in angiosperms than gymnosperms, yielding a higher moisture sensitivity of wood decomposition. These findings were demonstrated by a significant positive interaction effect between wood nitrogen and moisture on CO2 fluxes in a structural equation model. Additionally, we ascertained that a constant temperature sensitivity of CO2 fluxes was independent of wood traits and consistent with previous estimates for extracellular enzyme kinetics. Our results highlight the key role of wood traits in regulating drought responses of wood carbon fluxes. Given that both climate and forest management might extensively modify taxonomic compositions in the future, it is critical for carbon cycle models to account for such interactions between wood traits and climate in driving dynamics of wood decomposition. This article is protected by copyright. All rights reserved.AIMS This study was designed to evaluate the biocontrol of the arbuscular mycorrhizal fungus (AMF) Funnelliformis mosseae and the rhizobium Sinorhizobium medicae on alfalfa (Medicago sativa) wilt caused by Fusarium oxysporum, a severe soil-borne fungal pathogen. METHODS AND RESULTS The effects of co-inoculation of F. mosseae and S. medicae on alfalfa growth, nitrogen, phosphorus uptake, and wilt caused by F. oxysporum were tested. Plant defense related chemicals were measured to reveal the biochemical mechanism by which alfalfa responds to pathogen infection and how it is regulated by AMF and rhizobium. Pathogen infection caused typical yellowing of alfalfa leaflets and significantly reduced plant AMF colonization. AMF or rhizobium alone and the co-inoculation reduced the plant disease index by 83.2%, 48.4%, and 81.8% respectively. Inoculation with AMF or rhizobium alone increased the dry weight of alfalfa by more than 13 and 3 times respectively; it also increased plant chlorophyll content by 65.6% and 16.6%nteractions in the rhizosphere as well as the application of the microbiome in agriculture production. This article is protected by copyright. All rights reserved.Microtubules (MTs) are critical cytoskeletal filaments that exhibit several functions in cell morphogenesis, cell division, vesicle transport, and cytoplasmic separation in the spatiotemporal regulation of eukaryotic cells. MT formation requires the co-interaction of MT nucleation and α-β-tubulins, as well as MT-associated proteins (MAPs). Many key MAPs contributing to MT nucleation and elongation are essential for MT nucleation and regulation of MT dynamics and are conserved in the plant kingdom. Therefore, the deletion or decrease of γ-tubulin ring complex (γTuRC) components and related MAPs, such as the augmin complex, NEDD1, MZT1, EB1, MAP65, etc., in Arabidopsis thaliana results in MT organization defects in the spindle and phragmoplast MTs as well as in chromosome defects. In addition, similar defects in MT organization and chromosome structure have been observed in plants under abiotic stress conditions such as under high UV-B radiation. MTs can sense the signal from UV-B radiation, resulting in abnormal MT arrangement. Further studies are required to determine whether the abnormal chromosomes induced by UV-B radiation are attributed to the involvement of abnormal MT arrays in chromosome migration after DNA damage. This article is protected by copyright. All rights reserved.BACKGROUND Skin patch testing is still seen as the gold standard for the diagnosis of allergic hypersensitivity. For several metals and for patients with a suspected adverse reaction to their medical device implant material, patch testing can be unreliable. The current alternative to metal allergy patch-testing is the in vitro lymphocyte proliferation test (LPT) using tritiated thymidine. This method is well-established but requires handling of radioactive material, often uses heat inactivated allogenic human pooled serum and cannot determine T-cell subsets. OBJECTIVE To develop a radioactive free LPT by using carboxyfluorescein succinimidyl ester (CFSE) and to evaluate the influence of serum source (heat inactivated human pooled serum (HI HPS) versus autologous serum) on the sensitivity and specificity of the nickel specific LPT. METHODS Peripheral blood mononuclear cells derived from nickel allergic patients and healthy controls were collected, labelled with CFSE and cultured in medium containing 10% HI HPSer improved by addition of the cytokine skewing cocktails. CONCLUSIONS Here we describe an optimized and highly accurate flow cytometric LPT which comprises of CFSE labelled cells cultured in autologous serum (not heat inactivated) and without the presence of T-cell skewing cytokines. This article is protected by copyright. All rights reserved.The goal of this study is to investigate the neural correlates of working memory function associated with chemotherapy in pediatric cancer survivors using event-related functional MRI (fMRI) analysis. Fifteen pediatric cancer survivors treated with chemotherapy and 15 healthy controls were studied. Blood oxygenation level dependent (BOLD) fMRI was acquired. A visual n-back task was used to test working memory function during the fMRI scan. Responses were recorded via an MRI compatible button box for analysis. fMRI scans were analyzed using statistical parametric mapping software. All statistics were corrected for multiple comparisons by false discovery rate, with p less then 0.05 as significance. Patients however gave more incorrect responses (p less then 0.05), more no responses (p less then 0.05), and longer response times (p less then 0.05) compared with healthy controls. Correct responses generated significantly lower BOLD responses in the posterior cingulate for pediatric cancer survivors compared with controls (p less then 0.