The influence of weathering and organic matter on heavy metals lability in silicatic, Alpine soils

We investigated the effect of organic matter and weathering on the lability and solid phase speciation of heavy metals (Cd, Cr, Cu, Ni, Pb, Zn) in two contrasting subalpine regions in the Italian Alps. Cr, Ni and Cu could be linked to weathering. This was not the case for Pb. Since organic matter (OM) influences the solid phase speciation of heavy metals, the total organic C and N content, the C and N content of different density fractions of OM and also of the labile (oxidised by H2O2) and stable (H2O2-resistant) fractions were determined. Soil OM stocks were high and soils on north-facing slopes had more OM than the south-facing sites to which they were paired. Density measurements and the H2O2 fractionation indicated that the higher OM content on north-facing sites was due to an accumulation of weakly degraded organic material. Due to higher weathering intensity on north-facing sites, the abundance of the EDTA-extractable heavy metals was higher than on south-facing sites. All EDTA-extractable heavy metals showed a good correlation to the water-soluble phenolic concentrations which indicates that the metals were probably translocated as metalorganic complexes. Pb and Cu correlate not only to the light (density b1 g/cm3) and labile, organic fraction but also to the heavy (densityN2g/cm3) and stable fraction. High-mountain ecosystems like the Alps are sensitive to changing environmental conditions such as global warming. A warmer climate and the more favourable conditions it brings for biological activity, especially at cooler sites, will probably lead in the short- to mid-term to an increased loss of accumulated, weakly degraded OM. As the Pb and Cu content is significantly related to the labile organic matter pools, the risk exists that an increase in OM mineralisation could affect the storage capacity and mobility of these metals in soils

A transcriptional network in polycystic kidney disease

Mutations in cystic kidney disease genes represent a major genetic cause of end-stage renal disease. However, the molecular cascades controlling the expression of these genes are still poorly understood. Hepatocyte Nuclear Factor 1β (HNF1β) is a homeoprotein predominantly expressed in renal, pancreatic and hepatic epithelia. We report here that mice with renal-specific inactivation of HNF1β develop polycystic kidney disease. We show that renal cyst formation is accompanied by a drastic defect in the transcriptional activation of Umod, Pkhd1 and Pkd2 genes, whose mutations are responsible for distinct cystic kidney syndromes. In vivo chromatin immunoprecipitation experiments demonstrated that HNF1β binds to several DNA elements in murine Umod, Pkhd1, Pkd2 and Tg737/Polaris genomic sequences. Our results uncover a direct transcriptional hierarchy between HNF1β and cystic disease genes. Interestingly, most of the identified HNF1β target gene products colocalize to the primary cilium, a crucial organelle that plays an important role in controlling the proliferation of tubular cells. This may explain the increased proliferation of cystic cells in MODY5 patients carrying autosomal dominant mutations in HNF1β

A highly virulent variant of HIV-1 circulating in the Netherlands

We discovered a highly virulent variant of subtype-B HIV-1 in the Netherlands. One hundred nine individuals with this variant had a 0.54 to 0.74 log10 increase (i.e., a ~3.5-fold to 5.5-fold increase) in viral load compared with, and exhibited CD4 cell decline twice as fast as, 6604 individuals with other subtype-B strains. Without treatment, advanced HIV-CD4 cell counts below 350 cells per cubic millimeter, with long-term clinical consequences-is expected to be reached, on average, 9 months after diagnosis for individuals in their thirties with this variant. Age, sex, suspected mode of transmission, and place of birth for the aforementioned 109 individuals were typical for HIV-positive people in the Netherlands, which suggests that the increased virulence is attributable to the viral strain. Genetic sequence analysis suggests that this variant arose in the 1990s from de novo mutation, not recombination, with increased transmissibility and an unfamiliar molecular mechanism of virulence