Variations in soil chemical and physical properties explain basin-wide Amazon forest soil carbon concentrations

We investigate the edaphic, mineralogical and climatic controls of soil organic carbon (SOC) concentration utilising data from 147 primary forest soils (0–30 cm depth) sampled in eight different countries across the Amazon Basin. Sampled across 14 different World Reference Base soil groups, our data suggest that stabilisation mechanism varies with pedogenetic level. Specifically, although SOC concentrations in Ferralsols and Acrisols were best explained by simple variations in clay content – this presumably being due to their relatively uniform kaolinitic mineralogy – this was not the case for less weathered soils such as Alisols, Cambisols and Plinthosols for which interactions between Al species, soil pH and litter quality are argued to be much more important. Although for more strongly weathered soils the majority of SOC is located within the aggregate fraction, for the less weathered soils most of the SOC is located within the silt and clay fractions. It thus seems that for highly weathered soils SOC storage is mostly influenced by surface area variations arising from clay content, with physical protection inside aggregates rendering an additional level of protection against decomposition. On the other hand, most of the SOC in less weathered soils is associated with the precipitation of aluminium–carbon complexes within the fine soil fraction, with this mechanism enhanced by the presence of high levels of aromatic, carboxyl-rich organic matter compounds. Also examined as part of this study were a relatively small number of arenic soils (viz. Arenosols and Podzols) for which there was a small but significant influence of clay and silt content variations on SOM storage, with fractionation studies showing that particulate organic matter may account for up to 0.60 of arenic soil SOC. In contrast to what were in all cases strong influences of soil and/or litter quality properties, after accounting for these effects neither wood productivity, above-ground biomass nor precipitation/temperature variations were found to exert any significant influence on SOC stocks. These results have important implications for our understanding of how Amazon forest soils are likely to respond to ongoing and future climate changes

Appendix a la allegación del Doctor D. Thomás Serrano de Paz, en la causa que le mouió el Fiscal Eclesiástico de Ouiedo

Data del texto: Vallisoleti, 1657. -- Sign.: A-B2, C

Por el Doctor don Thomás de Paz ... abogado del Deán y Cabildo de su sancta Iglesia Cathedral ... en el pleyto criminal que le movió D. Francisco de la Pola Argüelles, Fiscal Eclesiástico, imputándole que en vna petición de recusación ... injurió a su Señoría el señor D. Bernardo Cauallero de Paredes, Obispo de dicha Iglesia

Data del texto: Vallisoleti, 1657Sign.: A-R\p2\

Lugares in terminis a favor del Doctor don Thomás Serrano de Paz, que se añaden a su allegación y appendix en la causa con el Fiscal del Obispado de Oviedo

Data del texto: Vallisoleti, 1657. -- Sign.: A

Epigenetics as a mechanism driving polygenic clinical drug resistance

Aberrant methylation of CpG islands located at or near gene promoters is associated with inactivation of gene expression during tumour development. It is increasingly recognised that such epimutations may occur at a much higher frequency than gene mutation and therefore have a greater impact on selection of subpopulations of cells during tumour progression or acquisition of resistance to anticancer drugs. Although laboratory-based models of acquired resistance to anticancer agents tend to focus on specific genes or biochemical pathways, such 'one gene : one outcome' models may be an oversimplification of acquired resistance to treatment of cancer patients. Instead, clinical drug resistance may be due to changes in expression of a large number of genes that have a cumulative impact on chemosensitivity. Aberrant CpG island methylation of multiple genes occurring in a nonrandom manner during tumour development and during the acquisition of drug resistance provides a mechanism whereby expression of multiple genes could be affected simultaneously resulting in polygenic clinical drug resistance. If simultaneous epigenetic regulation of multiple genes is indeed a major driving force behind acquired resistance of patients' tumour to anticancer agents, this has important implications for biomarker studies of clinical outcome following chemotherapy and for clinical approaches designed to circumvent or modulate drug resistance

The pestivirus N terminal protease N(pro) redistributes to mitochondria and peroxisomes suggesting new sites for regulation of IRF3 by N(pro.)

The N-terminal protease of pestiviruses, N(pro) is a unique viral protein, both because it is a distinct autoprotease that cleaves itself from the following polyprotein chain, and also because it binds and inactivates IRF3, a central regulator of interferon production. An important question remains the role of N(pro) in the inhibition of apoptosis. In this study, apoptotic signals induced by staurosporine, interferon, double stranded RNA, sodium arsenate and hydrogen peroxide were inhibited by expression of wild type N(pro), but not by mutant protein N(pro) C112R, which we show is less efficient at promoting degradation of IRF3, and led to the conclusion that N(pro) inhibits the stress-induced intrinsic mitochondrial pathway through inhibition of IRF3-dependent Bax activation. Both expression of N(pro) and infection with Bovine Viral Diarrhea Virus (BVDV) prevented Bax redistribution and mitochondrial fragmentation. Given the role played by signaling platforms during IRF3 activation, we have studied the subcellular distribution of N(pro) and we show that, in common with many other viral proteins, N(pro) targets mitochondria to inhibit apoptosis in response to cell stress. N(pro) itself not only relocated to mitochondria but in addition, both N(pro) and IRF3 associated with peroxisomes, with over 85% of N(pro) puncta co-distributing with PMP70, a marker for peroxisomes. In addition, peroxisomes containing N(pro) and IRF3 associated with ubiquitin. IRF3 was degraded, whereas N(pro) accumulated in response to cell stress. These results implicate mitochondria and peroxisomes as new sites for IRF3 regulation by N(pro), and highlight the role of these organelles in the anti-viral pathway

Desconsuelo del... Doctor y Martyr Ramon Llull... : compuesto en verso Lemori

Copia digital. Madrid : Ministerio de Cultura. Subdirección General de Coordinación Bibliotecaria, 200

Fatal myocarditis in a child with systemic onset juvenile idiopathic arthritis during treatment with an interleukin 1 receptor antagonist

<p>Abstract</p> <p>Background</p> <p>The pathologic diagnosis of isolated myocarditis without pericardial involvement is uncommonly encountered in systemic onset Juvenile Idiopathic Arthritis (soJIA).</p> <p>Case</p> <p>An eleven year-old boy with soJIA died suddenly while being treated with the interleukin 1 (IL-1) receptor inhibitor, anakinra. His autopsy revealed an enlarged heart and microscopic findings were consistent with myocarditis, but not pericarditis. Viral PCR testing performed on his myocardial tissue was negative.</p> <p>Conclusion</p> <p>This case illustrates myocarditis as a fatal complication of soJIA, potentially enabled by anakinra.</p