Phosphorus Transformations in an Oxisol under contrasting land-use systems: The role of the soil microbial biomass

It is generally assumed that phosphorus (P) availability for plant growth on highly weathered and P-deficient tropical soils may depend more on biologically mediated organic P (Po) turnover processes than on the release of adsorbed inorganic P (Pi). However, experimental evidence showing the linkages between Po, microbial activity, P cycling and soil P availability is scarce. To test whether land-use systems with higher soil Po are characterized by greater soil biological activity and increased P mineralization, we analyzed the partitioning of P among various organic and inorganic P fractions in soils of contrasting agricultural land-use systems and related it to biological soil properties. Isotopic labeling was used to obtain information on the turnover of P held in the microbial biomass. Soil samples were taken from grass-legume pasture (GL), continuous rice (CR) and native savanna (SAV) which served as reference. In agreement with estimated P budgets (+277, +70 and 0 kg P ha−1 for CR, GL and SAV, respectively), available P estimated using Bray-2 and resin extraction declined in the order CR > GL > SAV. Increases in Bray-2 and resin Pi were greater in CR than GL relative to total soil P increase. Organic P fractions were significantly less affected by P inputs than inorganic fractions, but were a more important sink in GL than CR soils. Extractable microbial P (Pchl) was slightly higher in GL (6.6 mg P kg−1) than SAV soils (5.4 mg P kg−1), and significantly lowest in CR (2.6 mg P kg−1). Two days after labeling the soil with carrier free 33P, 25, 10 and 2% of the added 33P were found in Pchl in GL, SAV and CR soils, respectively, suggesting a high and rapid microbial P turnover that was highest in GL soils. Indicators of P mineralization were higher in GL than CR soils, suggesting a greater transformation potential to render Po available. Legume-based pastures (GL) can be considered as an important land-use option as they stimulate P cycling. However, it remains to be investigated whether crops planted in pasture-crop rotations could benefit from the enhanced Po cycling in grass-legume soils. Furthermore, there is need to develop and test a direct method to quantify Po mineralization in these system

Effective action and interaction energy of coupled quantum dots

We obtain the effective action of tunnel-coupled quantum dots, by modeling the system as a Luttinger liquid with multiple barriers. For a double dot system, we find that the resonance conditions for perfect conductance form a hexagon in the plane of the two gate voltages controlling the density of electrons in each dot. We also explicitly obtain the functional dependence of the interaction energy and peak-splitting on the gate voltage controlling tunneling between the dots and their charging energies. Our results are in good agreement with recent experimental results, from which we obtain the Luttinger interaction parameter $K=0.74$.Comment: 5 pgs,latex,3 figs,revised version to be publshed in Phys.Rev.

Biological Nitrification Inhibition—A Novel Strategy to Regulate Nitrification in Agricultural Systems

Human activity has had the single largest influence on the global nitrogen (N) cycle by introducing unprecedented amounts of reactive-N into ecosystems. A major portion of this reactive-N, applied as fertilizer to crops, leaks into the environment with cascading negative effects on ecosystem functions and contributes to global warming. Natural ecosystems use multiple pathways of the N-cycle to regulate the flow of this element. By contrast, the large amounts of N currently applied in agricultural systems cycle primarily through the nitrification process, a single inefficient route that allows much of the reactive-N to leak into the environment. The fact that present agricultural systems do not channel this reactive-N through alternate pathways is largely due to uncontrolled soil nitrifier activity, creating a rapid nitrifying soil environment. Regulating nitrification is therefore central to any strategy for improving nitrogen-use efficiency. Biological nitrification inhibition (BNI) is an active plant-mediated natural function, where nitrification inhibitors released from plant roots suppress soil-nitrifying activity, thereby forcing N into other pathways. This review illustrates the presence of detection methods for variation in physiological regulation of BNI-function in field crops and pasture grasses and analyzes the potential for its genetic manipulation. We present a conceptual framework utilizing a BNI-platform that integrates diverse crop science disciplines with ecological principles. Sustainable agriculture will require development of production systems that include new crop cultivars capable of controlling nitrification (i.e., high BNI-capacity) and improved agronomic practices to minimize leakage of reactive-N during the N-cycle, a critical requirement for increasing food production while avoiding environmental damage

Group 2 innate lymphoid cells exhibit a dynamic phenotype in allergic airway inflammation

Group 2 innate lymphoid cells (ILC2) are implicated in allergic asthma as an early innate source of the type 2 cytokines IL-5 and IL-13. However, their induction in house dust mite (HDM)-mediated airway inflammation additionally requires T cell activation. It is currently unknown whether phenotypic differences exist between ILC2s that are activated in a T cell-dependent or T cell-independent fashion. Here, we compared ILC2s in IL-33-and HDM-driven airway inflammation. Using flow cytometry, we found that surface expression levels of various markers frequently used to identify ILC2s were dependent on their mode of activation, highly variable over time, and differed between tissue compartments, including bronchoalveolar lavage (BAL) fluid, lung, draining lymph nodes, and spleen. Whereas in vivo IL-33-activated BAL fluid ILC2s exhibited an almost uniform CD25+CD127+T1/ST2+ICOS+KLRG1+ phenotype, at a comparable time point after HDM exposure BAL fluid ILC2s had a very heterogeneous surface marker phenotype. A major fraction of HDM-activated ILC2s were CD25lowCD127+T1/ST2low ICOSlowKLRG1low, but nevertheless had the capacity to produce large amounts of type 2 cytokines. HDM-activated CD25low ILC2s in BAL fluid and lung rapidly reverted to CD25high ILC2s upon in vivo stimulation with IL-33. Genome-wide transcriptional profiling of BAL ILC2s revealed ~1,600 differentially expressed genes: HDM-stimulated ILC2s specifically expressed genes involved in the regulation of adaptive immunity through B and T cell interactions, whereas IL-33-stimulated ILC2s expressed high levels of proliferation-related and cytokine genes. In both airway inflammation models ILC2s were present in the lung submucosa close to epithelial cells, as identified by confocal microscopy. In chronic HDM-driven airway inflammation ILC2s were also found inside organized cellular infiltrates near T cells. Collectively, our findings show that ILC2s are phenotypically more heterogeneous than previously thought, whereby their surface marker and gene expression profile are highly dynamic

Critical exponents and equation of state of the three-dimensional Heisenberg universality class

We improve the theoretical estimates of the critical exponents for the three-dimensional Heisenberg universality class. We find gamma=1.3960(9), nu=0.7112(5), eta=0.0375(5), alpha=-0.1336(15), beta=0.3689(3), and delta=4.783(3). We consider an improved lattice phi^4 Hamiltonian with suppressed leading scaling corrections. Our results are obtained by combining Monte Carlo simulations based on finite-size scaling methods and high-temperature expansions. The critical exponents are computed from high-temperature expansions specialized to the phi^4 improved model. By the same technique we determine the coefficients of the small-magnetization expansion of the equation of state. This expansion is extended analytically by means of approximate parametric representations, obtaining the equation of state in the whole critical region. We also determine a number of universal amplitude ratios.Comment: 40 pages, final version. In publication in Phys. Rev.

Epithelial IL-6 trans-signaling defines a new asthma phenotype with increased airway inflammation

Background: Although several studies link high levels of IL-6 and soluble IL-6 receptor (sIL-6R) to asthma severity and decreased lung function, the role of IL-6 trans-signaling (IL-6TS) in asthmatic patients is unclear. Objective: We sought to explore the association between epithelial IL-6TS pathway activation and molecular and clinical phenotypes in asthmatic patients. Methods: An IL-6TS gene signature obtained from air-liquid interface cultures of human bronchial epithelial cells stimulated with IL-6 and sIL-6R was used to stratify lung epithelial transcriptomic data (Unbiased Biomarkers in Prediction of Respiratory Disease Outcomes [U-BIOPRED] cohorts) by means of hierarchical clustering. IL-6TS-specific protein markers were used to stratify sputum biomarker data (Wessex cohort). Molecular phenotyping was based on transcriptional profiling of epithelial brushings, pathway analysis, and immunohistochemical analysis of bronchial biopsy specimens. Results: Activation of IL-6TS in air-liquid interface cultures reduced epithelial integrity and induced a specific gene signature enriched in genes associated with airway remodeling. The IL-6TS signature identified a subset of patients with IL-6TS-high asthma with increased epithelial expression of IL-6TS-inducible genes in the absence of systemic inflammation. The IL-6TS-high subset had an overrepresentation of frequent exacerbators, blood eosinophilia, and submucosal infiltration of T cells and macrophages. In bronchial brushings Toll-like receptor pathway genes were upregulated, whereas expression of cell junction genes was reduced. Sputum sIL-6R and IL-6 levels correlated with sputum markers of remodeling and innate immune activation, in particular YKL-40, matrix metalloproteinase 3, macrophage inflammatory protein 1 beta, IL-8, and IL-1 beta. Conclusions: Local lung epithelial IL-6TS activation in the absence of type 2 airway inflammation defines a novel subset of asthmatic patients and might drive airway inflammation and epithelial dysfunction in these patients.Peer reviewe