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1.
Sensors (Basel) ; 19(18)2019 Sep 14.
Article in English | MEDLINE | ID: mdl-31540098

ABSTRACT

Soil electrical conductivity (EC) maps obtained through proximal soil sensing (i.e., geophysical data) are usually considered to delineate homogeneous site-specific management zones (SSMZ), used in Precision Agriculture to improve crop production. The recent literature recommends the integration of geophysical soil monitoring data with crop information acquired through multispectral (VIS-NIR) imagery. In non-flat areas, where topography can influence the soil water conditions and consequently the crop water status and the crop yield, considering topography data together with soil and crop data may improve the SSMZ delineation. The objective of this study was the fusion of EC and VIS-NIR data to delineate SSMZs in a rain-fed vineyard located in Northern Italy (Franciacorta), and the assessment of the obtained SSMZ map through the comparison with data acquired by a thermal infrared (TIR) survey carried out during a hot and dry period of the 2017 agricultural season. Data integration is performed by applying multivariate statistical methods (i.e., Principal Component Analysis). The results show that the combined use of soil, topography and crop information improves the SSMZ delineation. Indeed, the correspondence between the SSMZ map and the CWSI map derived from TIR imagery was enhanced by including the NDVI information.

2.
Oncotarget ; 6(12): 9908-23, 2015 Apr 30.
Article in English | MEDLINE | ID: mdl-25839161

ABSTRACT

Interleukin (IL)-21 triggers inflammatory signals that contribute to the growth of neoplastic cells in mouse models of colitis-associated colorectal cancer (CRC). Because most CRCs are sporadic and arise in the absence of overt inflammation we have investigated the role of IL-21 in these tumors in mouse and man. IL-21 was highly expressed in human sporadic CRC and produced mostly by IFN-γ-expressing T-bet/RORγt double-positive CD3+CD8- cells. Stimulation of human CRC cell lines with IL-21 did not directly activate the oncogenic transcription factors STAT3 and NF-kB and did not affect CRC cell proliferation and survival. In contrast, IL-21 modulated the production of protumorigenic factors by human tumor infiltrating T cells. IL-21 was upregulated in the neoplastic areas, as compared with non-tumor mucosa, of Apc(min/+) mice, and genetic ablation of IL-21 in such mice resulted in a marked decrease of both tumor incidence and size. IL-21 deficiency was associated with reduced STAT3/NF-kB activation in both immune cells and neoplastic cells, diminished synthesis of protumorigenic cytokines (that is, IL-17A, IL-22, TNF-α and IL-6), downregulation of COX-2/PGE2 pathway and decreased angiogenesis in the lesions of Apc(min/+) mice. Altogether, data suggest that IL-21 promotes a protumorigenic inflammatory circuit that ultimately sustains the development of sporadic CRC.


Subject(s)
Colonic Neoplasms/immunology , Colonic Neoplasms/pathology , Interleukins/immunology , Animals , Carcinogenesis , Cell Growth Processes/immunology , Cell Transformation, Neoplastic/immunology , Cell Transformation, Neoplastic/pathology , Female , HT29 Cells , Humans , Inflammation/immunology , Inflammation/pathology , Interferon-alpha/immunology , Interleukins/biosynthesis , Male , Mice , Mice, Inbred C57BL , Mice, Knockout , NF-kappa B/immunology , STAT3 Transcription Factor/biosynthesis , STAT3 Transcription Factor/immunology , Signal Transduction
3.
Hepatology ; 58(4): 1436-50, 2013 Oct.
Article in English | MEDLINE | ID: mdl-23564603

ABSTRACT

UNLABELLED: Fulminant hepatitis (FH) is a disease characterized by massive destruction of hepatocytes with severe impairment of liver function. The pathogenesis of FH is not fully understood, but hyperactivity of T cells and macrophages with excessive production of cytokines are important hallmarks of the condition. In this study, we investigated the role of interleukin (IL)-25 in FH. IL-25 expression was evaluated in patients with FH and in livers of mice with FH induced by D-galactosamine (D-Gal) and lipopolysaccharide (LPS). Mice were treated with IL-25 before D-Gal/LPS-induced FH and before or after concanavalin A (ConA)-induced FH. Mononuclear cells were isolated from livers of mice treated with or without IL-25 and analyzed for GR1(+) CD11b(+) cells. CFSE-labeled T cells were cocultured with GR1(+) CD11b(+) cells and their proliferation was evaluated by flow cytometry. Mice were also treated with a depleting anti-GR1 antibody before IL-25 and D-Gal/LPS administration. IL-25 was constitutively expressed in mouse and human liver and down-regulated during FH. IL-25 prevented D-Gal/LPS-induced FH and this effect was associated with increased infiltration of the liver with cells coexpressing GR1 and CD11b. In vitro studies showed that GR1(+) CD11b(+) cells isolated from mice given IL-25 inhibited T-cell proliferation. Consistently, in vivo depletion of GR1(+) cells abrogated the protective effect of IL-25 in experimental D-Gal/LPS-induced FH. IL-25 was both preventive and therapeutic in ConA-induced FH. CONCLUSIONS: IL-25 expression is markedly reduced during human and experimental FH. IL-25 promotes liver accumulation of GR1(+) CD11b(+) cells with immunoregulatory properties.


Subject(s)
Chemical and Drug Induced Liver Injury/drug therapy , Chemical and Drug Induced Liver Injury/prevention & control , Hepatocytes/pathology , Interleukins/therapeutic use , Myeloid Cells/pathology , T-Lymphocytes/pathology , Animals , CD11b Antigen/metabolism , Cell Proliferation/drug effects , Chemical and Drug Induced Liver Injury/metabolism , Coculture Techniques , Concanavalin A/adverse effects , Disease Models, Animal , Down-Regulation/drug effects , Galactosamine/adverse effects , Hepatitis/metabolism , Hepatitis/pathology , Hepatocytes/metabolism , Humans , Interleukin-17/metabolism , Interleukins/metabolism , Interleukins/pharmacology , Lipopolysaccharides/adverse effects , Male , Mice , Mice, Inbred BALB C , Myeloid Cells/metabolism , Receptors, Chemokine/metabolism , T-Lymphocytes/drug effects , T-Lymphocytes/metabolism
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