The Aguablanca Ni–(Cu) sulfide deposit, SW Spain: geologic and geochemical controls and the relationship with a midcrustal layered mafic complex

The Aguablanca Ni–(Cu) sulfide deposit is hosted by a breccia pipe within a gabbro–diorite pluton. The deposit probably formed due to the disruption of a partially crystallized layered mafic complex at about 12– 19 km depth and the subsequent emplacement of melts and breccias at shallow levels (<2 km). The ore-hosting breccias are interpreted as fragments of an ultramafic cumulate, which were transported to the near surface along with a molten sulfide melt. Phlogopite Ar–Ar ages are 341– 332 Ma in the breccia pipe, and 338–334 Ma in the layered mafic complex, and are similar to recently reported U–Pb ages of the host Aguablanca Stock and other nearby calcalkaline metaluminous intrusions (ca. 350–330 Ma). Ore deposition resulted from the combination of two critical factors, the emplacement of a layered mafic complex deep in the continental crust and the development of small dilational structures along transcrustal strike-slip faults that triggered the forceful intrusion of magmas to shallow levels. The emplacement of basaltic magmas in the lower middle crust was accompanied by major interaction with the host rocks, immiscibility of a sulfide melt, and the formation of a magma chamber with ultramafic cumulates and sulfide melt at the bottom and a vertically zoned mafic to intermediate magmas above. Dismembered bodies of mafic/ultramafic rocks thought to be parts of the complex crop out about 50 km southwest of the deposit in a tectonically uplifted block (Cortegana Igneous Complex, Aracena Massif). Reactivation of Variscan structures that merged at the depth of the mafic complex led to sequential extraction of melts, cumulates, and sulfide magma. Lithogeochemistry and Sr and Nd isotope data of the Aguablanca Stock reflect the mixing from two distinct reservoirs, i.e., an evolved siliciclastic middle-upper continental crust and a primitive tholeiitic melt. Crustal contamination in the deep magma chamber was so intense that orthopyroxene replaced olivine as the main mineral phase controlling the early fractional crystallization of the melt. Geochemical evidence includes enrichment in SiO2 and incompatible elements, and Sr and Nd isotope compositions (87Sr/86Sri 0.708–0.710; 143Nd/144Ndi 0.512–0.513). However, rocks of the Cortegana Igneous Complex have low initial 87Sr/86Sr and high initial 143Nd/144Nd values suggesting contamination by lower crustal rocks. Comparison of the geochemical and geological features of igneous rocks in the Aguablanca deposit and the Cortegana Igneous Complex indicates that, although probably part of the same magmatic system, they are rather different and the rocks of the Cortegana Igneous Complex were not the direct source of the Aguablanca deposit. Crust–magma interaction was a complex process, and the generation of orebodies was controlled by local but highly variable factors. The model for the formation of the Aguablanca deposit presented in this study implies that dense sulfide melts can effectively travel long distances through the continental crust and that dilational zones within compressional belts can effectively focus such melt transport into shallow environments

A laboratory study of the transfer of U-234 and U-238 during water-rock interactions in the Carnmenellis granite (Cornwall, England) and implications for the interpretation of field data

Laboratory time-scale experiments were conducted on gravels from the Carnmenellis granite, Cornwall, England, with the purpose of evaluating the release of natural uranium isotopes to the water phase. The implications of these results for the production of enhanced U-234/U-238 activity ratios in Cornish groundwaters are discussed. It is suggested that the U-234/U-238 lab data can be used to interpret activity ratios from Cornwall, even when the observed inverse relationship between dissolved U and U-234/U-238 in leachates/etchates is taken into account. (C) 2001 Elsevier B.V. Ltd. All rights reserved

Predictors of trend in CD4-positive T-cell count and mortality among HIV-1-infected individuals with virological failure to all three antiretroviral-drug classes

Background Treatment strategies for patients in whom HIV replication is not suppressed after exposure to several drug classes remain unclear. We aimed to assess the inter-relations between viral load, CD4-cell count, and clinical outcome in patients who had experienced three-class virological failure. Methods We undertook collaborative joint analysis of 13 HIV cohorts from Europe, North America, and Australia, involving patients who had had three-class virological failure (viral load &gt;1000 copies per mL for &gt;4 months). Regression analyses were used to quantify the associations between CD4-cell-count slope, HIV-1 RNA concentration, treatment information, and demographic characteristics. Predictors of death were analysed by Cox's proportional-hazards models. Findings 2488 patients were included. 2118 (85%) had started antiretroviral therapy with single or dual therapy. During 5015 person-years of follow-up, 276 patients died (mortality rate 5.5 per 100 person-years; 3-year mortality risk 15.3% (95% Cl 13.5-17.3). Risk of death was strongly influenced by the latest CD4-cell count with a relative hazard of 15.8 (95% CI 9.28-27.0) for counts below 50 cells per muL versus above 200 cells per muL. The latest viral load did not independently predict death. For any given viral load, patients on treatment had more favourable CD4-cell-count slopes than those off treatment. For patients on treatment and with stable viral load, CD4-cell counts tended to be increasing at times when the current viral load was below 10 000 copies per mL or 1.5 log(10) copies per mL below off-treatment values. Interpretation In patients for whom viral-load suppression to below the level of detection is not possible, achievement and maintenance of a CD4-cell count above 200 per muL becomes the primary aim. Treatment regimens that maintain the viral load below 10 000 copies per mL or at least provide 1.5 log(10) copies per mL suppression below the off-treatment value do not seem to be associated with appreciable CD4-cell-count decline

Predictors of trend in CD4-positive T-cell count and mortality among HIV-1-infected individuals with virological failure to all three antiretroviral-drug classes

Background Treatment strategies for patients in whom HIV replication is not suppressed after exposure to several drug classes remain unclear. We aimed to assess the inter-relations between viral load, CD4-cell count, and clinical outcome in patients who had experienced three-class virological failure. Methods We undertook collaborative joint analysis of 13 HIV cohorts from Europe, North America, and Australia, involving patients who had had three-class virological failure (viral load >1000 copies per mL for >4 months). Regression analyses were used to quantify the associations between CD4-cell-count slope, HIV-1 RNA concentration, treatment information, and demographic characteristics. Predictors of death were analysed by Cox's proportional-hazards models. Findings 2488 patients were included. 2118 (85%) had started antiretroviral therapy with single or dual therapy. During 5015 person-years of follow-up, 276 patients died (mortality rate 5·5 per 100 person-years; 3-year mortality risk 15·3% (95% CI 13·5-17·3). Risk of death was strongly influenced by the latest CD4-cell count with a relative hazard of 15·8 (95% CI 9·28-27·0) for counts below 50 cells per μL versus above 200 cells per μL. The latest viral load did not independently predict death. For any given viral load, patients on treatment had more favourable CD4-cell-count slopes than those off treatment. For patients on treatment and with stable viral load, CD4-cell counts tended to be increasing at times when the current viral load was below 10 000 copies per mL or 1·5 log10copies per mL below off-treatment values. Interpretation In patients for whom viral-load suppression to below the level of detection is not possible, achievement and maintenance of a CD4-cell count above 200 per μL becomes the primary aim. Treatment regimens that maintain the viral load below 10 000 copies per mL or at least provide 1·5 log10copies per mL suppression below the off-treatment value do not seem to be associated with appreciable CD4-cell-count decline