170 research outputs found

    Subaqueous soils: Pedogenesis in a submersed environment.

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    ABSTRACT and sediment parameters is difficult to determine. To apply a new approach, a pedological approach, it is Proposals for the inclusion of permanently submersed materials necessary to demonstrate that shallow water sediments in soil taxonomic systems have periodically been put forth since some can be described by a pedological paradigm. time in the mid 1800s. The proposals were largely conceptual in nature, relying more on subjective reasoning rather than analytical and field Since the inception of pedological research, debate data. Advances in computer and global positioning technology, and concerning the inclusion of subaqueous materials in soil the continuing development of the discipline of pedology provided taxonomic systems has arisen periodically (v.Post, 1862; the opportunity to examine shallow water estuarine sediments within a pedological framework. Morphological and analytical data from 85 The question at the center of the debate seems to be 1.5-to 2.0-m profiles from Sinepuxent Bay, Maryland, indicate that related to the concepts of the "upper limit" of soil and the four pedogenic processes of additions, losses, transformations

    Manganese-coated IRIS to document reducing soil conditions

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    Iron-coated indicatorof reduction in soils (IRIS) devices have been used for nearly two decades to help assess and document reducing conditions in soils, and official guidance has been approved for interpreting these data. Interest in manganese (Mn)-coated IRIS devices has increased because Mn oxides are reduced under more moderately reducing conditions than iron (Fe) oxides (which require strongly reducing conditions), such that they are expected to be better proxies for some important ecosystem services like denitrification. However, only recently has the necessary technology become available to produce Mn-coated IRIS, and the need is now emerging for guidance in interpreting data derived from Mn IRIS. Ninety-six data sets collected over a 2-yr period from 40 plots at 18 study sites among eight states were used to compare the performance of Mn-coated IRIS with Fe-coated IRIS and to assess the effect of duration of saturation and soil temperature as environmental drivers on the reduction and removal of the oxide coating. It appears that the current threshold prescribed by the National Technical Committee for Hydric Soils for Fe-coated IRIS is appropriate for periods when soil temperatures are warmer (\u3e11 °C), but is unnecessarily conservative when soil temperatures are cooler (5–11 °C). In contrast, Mn-coated devices are particularly useful early in the growing season when soil temperatures are cool. Our data show that when using a threshold of 30% removal of Mn oxide coatings there is essentially 100% confidence of the presence of reducing soil conditions under cool (\u3c11 °C) conditions

    Interrelationship between TP53 gene deletion, protein expression and chromosome 17 aneusomy in gastric adenocarcinoma

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    Background: This study evaluates the existence of numerical alterations of chromosome 17 and TP53 gene deletion in gastric adenocarcinoma. the p53 protein expression was also evaluated, as well as, possible associations with clinicopathological characteristics.Methods: Dual-color fluorescence in situ hybridization and immunostaining were performed in twenty gastric cancer samples of individuals from Northern Brazil.Results: Deletion of TP53 was found in all samples. TP53 was inactivated mainly by single allelic deletion, varying to 7-39% of cells/case. Aneusomy of chromosome 17 was observed in 85% of cases. Chromosome 17 monosomy and gain were both observed in about half of cases. Cells with gain of chromosome 17 frequently presented TP53 deletion. the frequency of cells with two chr17 and one TP53 signals observed was higher in diffuse than in intestinal-type GC. Immunoreactivity of p53 was found only in intestinal-type samples. the frequency of cells with two chr17 and two TP53 signals found was higher in samples with positive p53 expression than in negative cases in intestinal-type GC.Conclusion: We suggest that TP53 deletion and chromosome 17 aneusomy is a common event in GC and other TP53 alterations, as mutation, may be implicated in the distinct carcinogenesis process of diffuse and intestinal types.Financiadora de Estudos e Projetos (FINEP CT-INFRA/FADESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Fed Univ Para, Inst Biol Sci, Humans Cytogenet Lab, BR-66075900 Belem, Para, BrazilUniv Fed Piaui, Dept Biol, Campus Minist Reis Velloso Parnaiba, Teresina, PI, BrazilUniversidade Federal de São Paulo, Dept Morphol, Div Genet, São Paulo, BrazilUniv Fed Ceara, Sch Med, Dept Pathol, Mol Genet Lab, Fortaleza, Ceara, BrazilFed Univ Para, Joao de Barros Barreto Univ Hosp, BR-66075900 Belem, Para, BrazilUniversidade Federal de São Paulo, Dept Morphol, Div Genet, São Paulo, BrazilFinanciadora de Estudos e Projetos (FINEP CT-INFRA/FADESP): 0927-03. RRBWeb of Scienc

    Malignant inflammation in cutaneous T-cell lymphoma: a hostile takeover

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    Cutaneous T-cell lymphomas (CTCL) are characterized by the presence of chronically inflamed skin lesions containing malignant T cells. Early disease presents as limited skin patches or plaques and exhibits an indolent behavior. For many patients, the disease never progresses beyond this stage, but in approximately one third of patients, the disease becomes progressive, and the skin lesions start to expand and evolve. Eventually, overt tumors develop and the malignant T cells may disseminate to the blood, lymph nodes, bone marrow, and visceral organs, often with a fatal outcome. The transition from early indolent to progressive and advanced disease is accompanied by a significant shift in the nature of the tumor-associated inflammation. This shift does not appear to be an epiphenomenon but rather a critical step in disease progression. Emerging evidence supports that the malignant T cells take control of the inflammatory environment, suppressing cellular immunity and anti-tumor responses while promoting a chronic inflammatory milieu that fuels their own expansion. Here, we review the inflammatory changes associated with disease progression in CTCL and point to their wider relevance in other cancer contexts. We further define the term "malignant inflammation" as a pro-tumorigenic inflammatory environment orchestrated by the tumor cells and discuss some of the mechanisms driving the development of malignant inflammation in CTCL

    CEBPA-mutated leukemia is sensitive to genetic and pharmacological targeting of the MLL1 complex

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    The gene encoding the transcription factor C/EBP alpha is mutated in 10-15% of acute myeloid leukemia (AML) patients. N-terminal CEBPA mutations cause ablation of full-length C/EBP alpha without affecting the expression of a shorter oncogenic isoform, termed p30. The mechanistic basis of p30-induced leukemogenesis is incompletely understood. Here, we demonstrate that the MLL1 histone-methyltransferase complex represents a critical actionable vulnerability in CEBPA-mutated AML. Oncogenic C/EBP alpha p30 and MLL1 show global co-localization on chromatin and p30 exhibits robust physical interaction with the MLL1 complex. CRISPR/Cas9-mediated mutagenesis of MLL1 results in proliferation arrest and myeloid differentiation in C/EBP alpha p30-expressing cells. In line, CEBPA-mutated hematopoietic progenitor cells are hypersensitive to pharmacological targeting of the MLL1 complex. Inhibitor treatment impairs proliferation and restores myeloid differentiation potential in mouse and human AML cells with CEBPA mutations. Finally, we identify the transcription factor GATA2 as a direct critical target of the p30-MLL1 interaction. Altogether, we show that C/EBP alpha p30 requires the MLL1 complex to regulate oncogenic gene expression and that CEBPA-mutated AML is hypersensitive to perturbation of the MLL1 complex. These findings identify the MLL1 complex as a potential therapeutic target in AML with CEBPA mutations
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