The dynamics of magnetic ordering in a natural hemo-ilmenite solid solution

We investigated the micromagnetic properties of hemo-ilmenite particles in an alluvial soil. All magnetic accessory minerals except the weathering resistant hemo-ilmenite grains were removed from the soil matrix by chemical treatment with concentrated acid followed by magnetic separation. X-ray diffraction revealed hemo-ilmenite grains with single crystal properties and an ilmenite mole fraction of y = 0.86. Magnetization versus applied magnetic field plots in a temperature range between 6 and 300 K were recorded in order to study the hysteresis and the exchange properties. In addition, field and frequency-dependent AC susceptibility measurements were performed with and without a DC bias field in order to analyse the dynamic magnetization of the sample down to 3 K. The hemo-ilmenite particles are considered as a mixed system with nano-sized cation-ordered areas (COA) and cation-disordered areas (CDA), which differ in their local Fe(III) concentration. Ferrimagnetic single-domain order in the Fe(III)-enriched CDA started at about 220 K. Upon cooling gradual transdomain transformation generates multidomain order. A maximum in the blocking distribution was reached at 44 K, followed by the onset of spin-glass dynamics. At lower temperature, blocking of superparamagnetic clusters in the COA created antiferromagnetic (AFM) ordering, which became more prominent with decreasing temperature. The interaction between the spin-glass like CDA and the AFM areas was documented by the onset of exchange bias at T < 20 K. The occurrence of exchange bias as well as spin-glass dynamics in the hemo-ilmenite grains is probably an effect of the inhomogeneity of the local Fe(III) concentration. This effect leaves a magnetically competitive regime with areas showing ilmenite-like magnetic properties, and Fe(III) rich disordered areas with magnetic long-range ordering up to 220 K and frustration near the ordering temperature of ilmenit

Nitrate leaching from short-hydroperiod floodplain soils

Numerous studies have shown the importance of riparian zones to reduce nitrate (NO&lt;sub&gt;3&lt;/sub&gt;&lt;sup&gt;&amp;minus;&lt;/sup&gt;) contamination coming from adjacent agricultural land. Much less is known about nitrogen (N) transformations and nitrate fluxes in riparian soils with short hydroperiods (1–3 days of inundation) and there is no study that could show whether these soils are a N sink or source. Within a restored section of the Thur River in NE Switzerland, we measured nitrate concentrations in soil solutions as an indicator of the net nitrate production. Samples were collected along a quasi-successional gradient from frequently inundated gravel bars to an alluvial forest, at three different depths (10, 50 and 100 cm) over a one-year period. Along this gradient we quantified N input (atmospheric deposition and sedimentation) and N output (leaching) to create a nitrogen balance and assess the risk of nitrate leaching from the unsaturated soil to the groundwater. Overall, the main factor explaining the differences in nitrate concentrations was the field capacity (FC). In subsoils with high FCs and VWC near FC, high nitrate concentrations were observed, often exceeding the Swiss and EU groundwater quality criterions of 400 and 800 μmol L&lt;sup&gt;−1&lt;/sup&gt;, respectively. High sedimentation rates of river-derived nitrogen led to apparent N retention up to 200 kg N ha&lt;sup&gt;−1&lt;/sup&gt; yr&lt;sup&gt;−1&lt;/sup&gt; in the frequently inundated zones. By contrast, in the mature alluvial forest, nitrate leaching exceeded total N input most of the time. As a result of the large soil N pools, high amounts of nitrate were produced by nitrification and up to 94 kg N-NO&lt;sub&gt;3&lt;/sub&gt;&lt;sup&gt;&amp;minus;&lt;/sup&gt; ha&lt;sup&gt;−1&lt;/sup&gt; yr&lt;sup&gt;−1&lt;/sup&gt; were leached into the groundwater. Thus, during flooding when water fluxes are high, nitrate from soils can contribute up to 11% to the total nitrate load in groundwater

Differential roles of CCL2 and CCR2 in host defense to coronavirus infection.

The CC chemokine ligand 2 (CCL2, monocyte chemoattractant protein-1) is important in coordinating the immune response following microbial infection by regulating T cell polarization as well as leukocyte migration and accumulation within infected tissues. The present study examines the consequences of mouse hepatitis virus (MHV) infection in mice lacking CCL2 (CCL2(-/-)) in order to determine if signaling by this chemokine is relevant in host defense. Intracerebral infection of CCL2(-/-) mice with MHV did not result in increased morbidity or mortality as compared to either wild type or CCR2(-/-) mice and CCL2(-/-) mice cleared replicating virus from the brain. In contrast, CCR2(-/-) mice displayed an impaired ability to clear virus from the brain that was accompanied by a reduction in the numbers of antigen-specific T cells as compared to both CCL2(-/-) and wild-type mice. The paucity in T cell accumulation within the central nervous system (CNS) of MHV-infected CCR2(-/-) mice was not the result of either a deficiency in antigen-presenting cell (APC) accumulation within draining cervical lymph nodes (CLN) or the generation of virus-specific T cells within this compartment. A similar reduction in macrophage infiltration into the CNS was observed in both CCL2(-/-) and CCR2(-/-) mice when compared to wild-type mice, indicating that both CCL2 and CC chemokine receptor 2 (CCR2) contribute to macrophage migration and accumulation within the CNS following MHV infection. Together, these data demonstrate that CCR2, but not CCL2, is important in host defense following viral infection of the CNS, and CCR2 ligand(s), other than CCL2, participates in generating a protective response

The CC chemokine ligand 3 regulates CD11c+CD11b+CD8alpha- dendritic cell maturation and activation following viral infection of the central nervous system: implications for a role in T cell activation.

The role of CC chemokine ligand 3 (CCL3) in activation of dendritic cells (DCs) following mouse hepatitis virus (MHV) infection of the central nervous system (CNS) was examined. The results indicate that CCL3 participates in an effective host response to MHV infection by contributing to CD11c+CD11b+CD8alpha- DC maturation, activation, and migration to cervical lymph nodes (CLN). Diminished CD8alpha- DC activation correlated with reduced IFN-gamma expression by virus-specific T cells accompanied by increased IL-10 production suggesting that CCL3 contributes to an effective host response to viral infection by enhancing the T cell activation potential of DC

CXCL10 Can Inhibit Endothelial Cell Proliferation Independently of CXCR3

CXCL10 (or Interferon-inducible protein of 10 kDa, IP-10) is an interferon-inducible chemokine with potent chemotactic activity on activated effector T cells and other leukocytes expressing its high affinity G protein-coupled receptor CXCR3. CXCL10 is also active on other cell types, including endothelial cells and fibroblasts. The mechanisms through which CXCL10 mediates its effects on non-leukocytes is not fully understood. In this study, we focus on the anti-proliferative effect of CXCL10 on endothelial cells, and demonstrate that CXCL10 can inhibit endothelial cell proliferation in vitro independently of CXCR3. Four main findings support this conclusion. First, primary mouse endothelial cells isolated from CXCR3-deficient mice were inhibited by CXCL10 as efficiently as wildtype endothelial cells. We also note that the proposed alternative splice form CXCR3-B, which is thought to mediate CXCL10's angiostatic activity, does not exist in mice based on published mouse CXCR3 genomic sequences as an in-frame stop codon would terminate the proposed CXCR3-B splice variant in mice. Second, we demonstrate that human umbilical vein endothelial cells and human lung microvascular endothelial cells that were inhibited by CXL10 did not express CXCR3 by FACS analysis. Third, two different neutralizing CXCR3 antibodies did not inhibit the anti-proliferative effect of CXCL10. Finally, fourth, utilizing a panel of CXCL10 mutants, we show that the ability to inhibit endothelial cell proliferation correlates with CXCL10's glycosaminoglycan binding affinity and not with its CXCR3 binding and signaling. Thus, using a very defined system, we show that CXCL10 can inhibit endothelial cell proliferation through a CXCR3-independent mechanism

PD-1 Blockade in Chronically HIV-1-Infected Humanized Mice Suppresses Viral Loads

An estimated 34 million people are living with HIV worldwide (UNAIDS, 2012), with the number of infected persons rising every year. Increases in HIV prevalence have resulted not only from new infections, but also from increases in the survival of HIV-infected persons produced by effective anti-retroviral therapies. Augmentation of anti-viral immune responses may be able to further increase the survival of HIV-infected persons. One strategy to augment these responses is to reinvigorate exhausted anti-HIV immune cells present in chronically infected persons. The PD-1-PD-L1 pathway has been implicated in the exhaustion of virus-specific T cells during chronic HIV infection. Inhibition of PD-1 signaling using blocking anti-PD-1 antibodies has been shown to reduce simian immunodeficiency virus (SIV) loads in monkeys. We now show that PD-1 blockade can improve control of HIV replication in vivo in an animal model. BLT (Bone marrow-Liver-Thymus) humanized mice chronically infected with HIV-1 were treated with an anti-PD-1 antibody over a 10-day period. The PD-1 blockade resulted in a very significant 45-fold reduction in HIV viral loads in humanized mice with high CD8+ T cell expression of PD-1, compared to controls at 4 weeks post-treatment. The anti-PD-1 antibody treatment also resulted in a significant increase in CD8+ T cells. PD-1 blockade did not affect T cell expression of other inhibitory receptors co-expressed with PD-1, including CD244, CD160 and LAG-3, and did not appear to affect virus-specific humoral immune responses. These data demonstrate that inhibiting PD-1 signaling can reduce HIV viral loads in vivo in the humanized BLT mouse model, suggesting that blockade of the PD-1-PD-L1 pathway may have therapeutic potential in the treatment of patients already infected with the AIDS virus

An Immunofluorescence Assay to Detect Urediniospores of \u3ci\u3ePhakopsora pachyrhizi\u3c/i\u3e

An indirect immunofluorescence spore assay (IFSA) was developed to detect urediniospores of Phakopsora pachyrhizi, utilizing rabbit polyclonal antisera produced in response to intact nongerminated (SBR1A) or germinated (SBR2) urediniospores of P. pachyrhizi. Both antisera were specific to Phakopsora spp. and did not react with other common soybean pathogens or healthy soybean leaf tissue in enzyme-linked immunosorbent assay (ELISA). SBR1A and SBR2 bound to P. pachyrhizi and P. meibomiae urediniospores were detected with goat anti-rabbit Alexa Fluor 488-tagged antiserum using a Leica DM IRB epifluorescent microscope with an I3 blue filter (excitation 450 to 490 nm, emission 515 nm). The assay was performed on standard glass microscope slides; double-sided tape was superior to a thin coating of petroleum jelly both in retaining spores and in immunofluorescence. The IFSA was used to confirm the identity of P. pachyrhizi urediniospores captured on glass slides from passive air samplers from Georgia, Kentucky, and Ohio during 2006