How accurate are pedotransfer functions for bulk density for Brazilian soils?

The aim of this study was to evaluate the predictive capability of PTFs available in the literature to estimate soil pb in different regions of Brazil, using different metrics (mean absolute error (MAE), root mean squared error (RMSE), mean error (ME) and regression error characteristic (REC) curve)

Effects of bromopride on expression of metalloproteinases and interleukins in left colonic anastomoses : an experimental study

Anastomotic dehiscence is the most severe complication of colorectal surgery. Metalloproteinases (MMPs) and interleukins (ILs) can be used to analyze the healing process of anastomosis. To evaluate the effects of bromopride on MMP and cytokine gene expression in left colonic anastomoses in rats with or without induced abdominal sepsis, 80 rats were divided into two groups for euthanasia on the third or seventh postoperative day (POD). They were then divided into subgroups of 20 rats for sepsis induction or not, and then into subgroups of 10 rats for administration of bromopride or saline. Left colonic anastomosis was performed and abdominal sepsis was induced by cecal ligation and puncture. A colonic segment containing the anastomosis was removed for analysis of gene expression of MMP-1α, MMP-8, MMP-13, IL-β, IL-6, IL-10, tumor necrosis factor-α (TNF-α), and interferon-γ (IFN-γ). On the third POD, bromopride was associated with increased MMP-1α, MMP-13, IL-6, IFN-γ, and IL-10 gene expression. On the seventh POD, all MMP transcripts became negatively modulated and all IL transcripts became positively modulated. In the presence of sepsis, bromopride administration increased MMP-8 and IFN-γ gene expression and decreased MMP-1, TNF-α, IL-6, and IL-10 gene expression on the third POD. On the seventh POD, we observed increased expression of MMP-13 and all cytokines, except for TNF-α. In conclusion, bromopride interferes with MMP and IL gene expression during anastomotic healing. Further studies are needed to correlate these changes with the healing process

Human biomonitoring health surveillance for metals near a waste-to-energy incinerator: The 1-year post-operam study

This human biomonitoring (HBM) follow-up survey, within the SPoTT project, assessed the temporal and spatial trends of exposure to 18 metals in a cohort living around the waste-to-energy (WTE) incinerator of Turin (Italy) before (T0, 2013) and after 1-year of plant activity (T1, 2014). Urine of 380 adult individuals (186 exposed and 194 unexposed subjects, classified on fallout maps) were analyzed by sector field inductively coupled mass spectrometry. A decrease trend of the majority of metals in all subjects indicates that the overall air quality of the studied sites was not significantly compromised, also in proximity of the WTE plant, as corroborated also by air monitoring data of the regional agency. The only relevant exception was the higher Cr levels found at T1 than T0 in exposed subjects, suggesting a possible contribution from the WTE plant. Chromium, Mn and Pt urine levels were also higher in the site far from the WTE, in relation to other sources as vehicular traffic, industrial and civil activities. Whilst, As and Cd were influenced by fish intake and tobacco smoke. A very small number of individuals at T1, equally distributed in both areas, exceeded the health-based guidance values and so, at current knowledge, living near the Turin incineration did not significantly influence the exposure status of the population

Hypoxia-inducible factor 2α drives nonalcoholic fatty liver progression by triggering hepatocyte release of histidine rich glycoprotein

Mechanisms underlying progression of non-alcoholic fatty liver disease (NAFLD) are still incompletely characterized. Hypoxia and hypoxia inducible factors (HIFs) have been implicated in the pathogenesis of chronic liver diseases but the actual role of HIF-2α in the evolution of NAFLD has never been investigated in detail. In this study, we show that HIF-2α is selectively overexpressed in the cytosol and the nuclei of hepatocytes in a very high percentage (> 90%) of liver biopsies from a cohort of NAFLD patients at different stage of the disease evolution. Similar features were also observed in mice with steatohepatitis induced by feeding a methionine/choline-deficient (MCD) diet. Experiments performed in mice carrying hepatocyte-specific deletion of HIF-2α and related control littermates fed with either choline-deficient L-amino acid-refined (CDAA) or MCD diets showed that HIF-2α deletion ameliorated the evolution of NAFLD by decreasing parenchymal injury, fatty liver, lobular inflammation and the development of liver fibrosis. The improvement in NAFLD progression in HIF-2α deficient mice was related to a selective down-regulation in the hepatocyte production of Histidine-Rich Glycoprotein (HRGP), recently proposed to sustain macrophage M1 polarization. In vitro experiments confirmed that the up-regulation of hepatocyte HRGP expression was hypoxia- and HIF-2α-dependent. Finally, analyses performed on specimens from NAFLD patients indicated that HRGP was overexpressed in all patients showing hepatocyte nuclear staining for HIF-2α and revealed a significant positive correlation between HIF-2α and HRGP liver transcripts levels in these patients

The role of T cell subsets and cytokines in the regulation of intracellular bacterial infection

Cellular immune responses are a critical part of the host's defense against intracellular bacterial infections. Immunity to Brucella abortus crucially depends on antigen-specific T cell-mediated activation of macrophages, which are the major effectors of cell-mediated killing of this organism. T lymphocytes that proliferate in response to B. abortus were characterized for phenotype and cytokine activity. Human, murine, and bovine T lymphocytes exhibited a type 1 cytokine profile, suggesting an analogous immune response in these different hosts. In vivo protection afforded by a particular cell type is dependent on the antigen presented and the mechanism of antigen presentation. Studies using MHC class I and class II knockout mice infected with B. abortus have demonstrated that protective immunity to brucellosis is especially dependent on CD8+ T cells. To target MHC class I presentation we transfected ex vivo a murine macrophage cell line with B. abortus genes and adoptively transferred them to BALB/c mice. These transgenic macrophage clones induced partial protection in mice against experimental brucellosis. Knowing the cells required for protection, vaccines can be designed to activate the protective T cell subset. Lastly, as a new strategy for priming a specific class I-restricted T cell response in vivo, we used genetic immunization by particle bombardment-mediated gene transfer