285 research outputs found
Waterwinning in de duinen: aantasting en regeneratiemogelijkheden van het abiotisch milieu
Wetensch. publicatieInstitute of Environmental Science
Evolution of the Munali Intrusive Complex: host to a carbonate-rich Ni-(Cu-PGE) sulfide deposit
The Munali Intrusive Complex is hosted within supracrustal metasedimentary rocks located along a major structural lineament within the Zambezi Belt in southern Zambia. The complex comprises unmineralised gabbro surrounded by a marginal heterogeneous mafic–ultramafic breccia unit that is host to Ni-Fe sulfide. This marginal unit comprises a range of variably evolved brecciated mafic–ultramafic rocks that include gabbro, olivine-gabbro and dolerite, alongside younger, pegmatitic, apatite-magnetite-bearing clinopyroxenite, wehrlite and dunite. The magmatic evolution is most consistent with a model whereby early mafic rocks interact with hot, MgO- and volatile-rich melts along gabbro contacts, causing localised metasomatism of gabbro and pyroxenites, and progressively replacing pyroxene-rich rocks with olivine, forming pegmatitic ‘replacive dunites’. Sulfide mineralisation is characterised by a carbonate-rich apatite-magnetite-bearing assemblage predominately present as lenses of semi-massive to massive sulfide ore. The complex is enveloped almost entirely within a unit of marble, yet C and O isotope signatures of carbonate at Munali have revealed a clear mantle signature for some of the carbonate associated with sulfide, alongside a more dominant, crustally derived component. The carbonate occurring alongside sulfide displays micro to macro textures signifying the presence of carbonate melts formed from anatectic melting of the country rocks. The presence of fracture sets that define coarse breccia clasts (>1 m) indicate that the host rock was significantly crystallised and brittly deformed prior to carbonate and sulfide melt infiltration. Both carbonate and sulfide melts appear to have independently utilised these pre-existing weaknesses producing a pseudobreccia, and accounting for the seemingly chaotic nature of the orebody. The indication of sulfide being a significantly later phase suggests that the sulfide did not form in situ and was mobilised from elsewhere to be subsequently emplaced late within the Munali system
Leukocyte TLR5 deficiency inhibits atherosclerosis by reduced macrophage recruitment and defective T-cell responsiveness
Toll-like receptors (TLR) provide a critical link between innate and adaptive immunity, both important players in atherosclerosis. Since evidence for the role of TLR5 is lacking, we aimed to establish this in the immune axis of atherosclerosis. We assessed the effect of the TLR5-specific ligand Flagellin on macrophage maturation and T-cell polarisation. Next, we generated TLR5-/-LDLr-/- chimeras to study the effect of hematopoietic TLR5 deficiency on atherosclerosis formation. Flagellin stimulation did not influence wildtype or TLR5-/- macrophage maturation. Only in wildtype macrophages, Flagellin exposure increased MCP-1 and IL6 expression. Flagellin alone reduced T-helper 1 proliferation, which was completely overruled in the presence of T-cell receptor activation. In vivo, hematopoietic TLR5 deficiency attenuated atherosclerotic lesion formation by ≈25% (1030*103 ± 63*103 vs. 792*103 ± 61*103 μm2; p = 0.013) and decreased macrophage area (81.3 ± 12.0 vs. 44.2 ± 6.6 μm2; p = 0.011). In TLR5-/- chimeric mice, we observed lower IL6 plasma levels (36.4 ± 5.6 vs. 15.1 ± 2.2 pg/mL; p = 0.003), lower (activated) splenic CD4+ T-cell content (32.3 ± 2.1 vs. 21.0 ± 1.2%; p = 0.0018), accompanied by impaired T-cell proliferative responses. In conclusion, hematopoietic TLR5 deficiency inhibits atherosclerotic lesion formation by attenuated macrophage accumulation and defective T-cell responsiveness
Microscale data to macroscale processes: A review of microcharacterization applied to mineral systems
Microanalysis can provide rapid, quantitative characterization of mineral systems that complements the field- and core-scale observations traditionally made in ore deposits. We review recent innovations in microanalytical procedures and their application to studies of ore deposits. Case studies are presented examining how microanalysis can provide constraints on macroscopic processes within mineral systems. Synchrotron X-ray fluorescence shows centimetre-scale chemical variations associated with proximity to mineralization in samples from Sunrise Dam Gold Mine, Western Australia. Pseudomorphs of igneous plagioclase and chemically driven recrystallization interpreted from electron backscatter diffraction suggest that the system was dominated by fluid-driven brecciation with very little shearing. Both the fluid chemistry and fluid pressure evolved during a protracted sequence of vein formation and alteration accompanying gold mineralization. A second case study of sulphide mineralogy at the Mt Keith nickel sulphide deposit, Western Australia demonstrates how X-ray computed tomography combined with trace element mapping can constrain the chemistry and dynamics of magmatic systems. Large-scale interaction between silicate and sulphide melts, shown by homogenous palladium enrichment in pentlandite, leads to a large proportion of globular ores with a high nickel content. Increasing use of microanalysis in ore deposit geology is resulting in the constant reassessment of established models for ore genesis though a combination of micro- and macroscale datasets.This research was undertaken on the X-ray fluorescence microscopy beamline at the Australian Synchrotron, Victoria, Australia and was funded by AngloGold Ashanti. LS acknowledges support from a CSIRO Mineral
Resources Flagship Internship to support this work
Increased circulating IgG levels, myocardial immune cells and IgG deposits support a role for an immune response in pre- and end-stage heart failure
The chronic inflammatory response plays an important role in adverse cardiac remodelling and the development of heart failure (HF). There is also evidence that in the pathogenesis of several cardiovascular diseases, chronic inflammation is accompanied by antibody and complement deposits in the heart, suggestive of a true autoimmune response. However, the role of antibody-mediated immune responses in HF progression is less clear. We assessed whether immune cell infiltration and immunoglobulin levels are associated with HF type and disease stage, taking sex differences into account. We found IgG deposits and increased infiltration of immune cells in the affected myocardium of patients with end-stage HF with reduced ejection fraction (HFrEF, n = 20). Circulating levels of IgG1 and IgG3 were elevated in these patients. Furthermore, the percentage of transitional/regulatory B cells was decreased (from 6.9% to 2.4%) compared with healthy controls (n = 5). Similarly, increased levels of circulating IgG1 and IgG3 were observed in men with left ventricular diastolic dysfunction (LVDD, n = 5), possibly an early stage of HF with preserved EF (HFpEF). In conclusion, IgG deposits and infiltrates of immune cells are present in end-stage HFrEF. In addition, both LVDD patients and end-stage HFrEF patients show elevated levels of circulating IgG1 and IgG3, suggesting an antibody-mediated immune response upon cardiac remodelling, which in the early phase of remodelling appear to differ between men and women. These immunoglobulin subclasses might be used as marker for pre-stage HF and its progression. Future identification of auto-antigens might open possibilities for new therapeutic interventions
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