Land Cover Segmentation with Sparse Annotations from Sentinel-2 Imagery

Land cover (LC) segmentation plays a critical role in various applications, including environmental analysis and natural disaster management. However, generating accurate LC maps is a complex and time-consuming task that requires the expertise of multiple annotators and regular updates to account for environmental changes. In this work, we introduce SPADA, a framework for fuel map delineation that addresses the challenges associated with LC segmentation using sparse annotations and domain adaptation techniques for semantic segmentation. Performance evaluations using reliable ground truths, such as LUCAS and Urban Atlas, demonstrate the technique's effectiveness. SPADA outperforms state-of-the-art semantic segmentation approaches as well as third-party products, achieving a mean Intersection over Union (IoU) score of 42.86 and an F1 score of 67.93 on Urban Atlas and LUCAS, respectively.Comment: 4 pages, short paper. Accepted to IGARSS 202

Land Cover Segmentation with Sparse Annotations from Sentinel-2 Imagery

Land cover (LC) segmentation plays a critical role in various applications, including environmental analysis and natural disaster management. However, generating accurate LC maps is a complex and time-consuming task that requires the expertise of multiple annotators and regular updates to account for environmental changes. In this work, we introduce SPADA, a framework for fuel map delineation that addresses the challenges associated with LC segmentation using sparse annotations and domain adaptation techniques for semantic segmentation. Performance evaluations using reliable ground truths, such as LUCAS and Urban Atlas, demonstrate the technique's effectiveness. SPADA outperforms state-of-the-art semantic segmentation approaches as well as third-party products, achieving a mean Intersection over Union (IoU) score of 42.86 and an F1 score of 67.93 on Urban Atlas and LUCAS, respectively

Epigenetics in paediatric gastroenterology, hepatology, and nutrition: Present trends and future perspectives

Epigenetics can be defined as stable, potentially heritable changes in the cellular phenotype caused by mechanisms other than alterations to the underlying DNA sequence. As such, any observed phenotypic changes including organ development, aging, and the occurrence of disease could be driven by epigenetic mechanisms in the presence of stable cellular DNA sequences. Indeed, with the exception of rare mutations, the human genome-sequence has remained remarkably stable over the past centuries. In contrast, substantial changes to our environment as part of our modern life style have not only led to a significant reduction of certain infectious diseases but also seen the exponential increase in complex traits including obesity and multifactorial diseases such as autoimmune disorders. It is becoming increasingly clear that epigenetic mechanisms operate at the interface between the genetic code and our environment, and a large body of existing evidence supports the importance of environmental factors such as diet and nutrition, infections, and exposure to toxins on human health. This seems to be particularly the case during vulnerable periods of human development such as pregnancy and early life. Importantly, as the first point of contact for many of such environmental factors including nutrition, the digestive system is being increasingly linked to a number of "modern" pathologies. In this review article, we aim to give a brief introduction to the basic molecular principals of epigenetics and provide a concise summary of the existing evidence for the role of epigenetic mechanisms in gastrointestinal health and disease, hepatology, and nutrition

A Celiac Cellular Phenotype, with Altered LPP Sub-Cellular Distribution, Is Inducible in Controls by the Toxic Gliadin Peptide P31-43.

Celiac disease (CD) is a frequent inflammatory intestinal disease, with a genetic background, caused by gliadin-containing food. Undigested gliadin peptides P31-43 and P57-68 induce innate and adaptive T cell-mediated immune responses, respectively. Alterations in the cell shape and actin cytoskeleton are present in celiac enterocytes, and gliadin peptides induce actin rearrangements in both the CD mucosa and cell lines. Cell shape is maintained by the actin cytoskeleton and focal adhesions, sites of membrane attachment to the extracellular matrix. The locus of the human Lipoma Preferred Partner (LPP) gene was identified as strongly associated with CD using genome-wide association studies (GWAS). The LPP protein plays an important role in focal adhesion architecture and acts as a transcription factor in the nucleus. In this study, we examined the hypothesis that a constitutive alteration of the cell shape and the cytoskeleton, involving LPP, occurs in a cell compartment far from the main inflammation site in CD fibroblasts from skin explants. We analyzed the cell shape, actin organization, focal adhesion number, focal adhesion proteins, LPP sub-cellular distribution and adhesion to fibronectin of fibroblasts obtained from CD patients on a Gluten-Free Diet (GFD) and controls, without and with treatment with A-gliadin peptide P31-43. We observed a "CD cellular phenotype" in these fibroblasts, characterized by an altered cell shape and actin organization, increased number of focal adhesions, and altered intracellular LPP protein distribution. The treatment of controls fibroblasts with gliadin peptide P31-43 mimics the CD cellular phenotype regarding the cell shape, adhesion capacity, focal adhesion number and LPP sub-cellular distribution, suggesting a close association between these alterations and CD pathogenesis

Characterization of Atypical Pheochromocytomas with Correlative MRI and Planar/Hybrid Radionuclide Imaging: A Preliminary Study

Pheochromocytomas may show atypical imaging findings leading to diagnostic pitfalls. We correlated the results of magnetic resonance imaging (MRI) with those of radionuclide studies in patients with pheochromocytomas. T2-weighted (-w), T1-w chemical-shift and T1-w dynamic contrast enhanced (DCE) MRI sequences were evaluated to assess tumor structure. 131Iodine metaiodobenzylguanidine (MIBG) scintigraphy, 18fluoro (F) deoxyglucose (FDG) positron emission tomography/computed tomography (PET/CT) or FDG PET/MRI were evaluated for direct comparison. Of a total of 80 adrenal lesions in 73 patients, 20 in 18 patients were pheochromocytomas. More than half (55%) of the pheochromocytomas (n = 11) had the typical increased signal intensity on T2-w and T1-w DCE, while the remaining (n = 9) lesions showed atypical findings; of these nine latter atypical lesions, seven (35%) were cystic (two totally, three predominantly and two partially) and two (10%) were hemorrhagic on MRI. In these atypical lesions, MIBG scintigraphy (n = 5), FDG PET/CT (n = 6) or FDG PET/MRI (n = 2) showed inhomogeneous tracer uptake in the residual viable tissue providing tumor characterization; however, one predominantly cystic pheochromocytoma showed false negative MIBG scan. Our preliminary results show that cystic degeneration may be frequent in pheochromocytoma being so marked that only a thin rim of viable cells may residue to disclose the true nature of the tumor. MRI findings together with those of correlative planar/hybrid radionuclide images are helpful to characterize these atypical pheochromocytomas. In particular, tumor accumulation of MIBG and/or FDG is able to classify these lesions as not simple cysts; in detail, the presence of partial MIBG uptake allows the diagnosis of pheochromocytomas, while the presence of partial FDG uptake generically reflects the presence of viable solid tissue of such cystic tumors

Epigenetics in Paediatric Gastroenterology, Hepatology, and Nutrition: Present Trends and Future Perspectives

Epigenetics can be defined as stable, potentially heritable changes in the cellular phenotype caused by mechanisms other than alterations to the underlying DNA sequence. As such, any observed phenotypic changes including organ development, aging, and the occurrence of disease could be driven by epigenetic mechanisms in the presence of stable cellular DNA sequences. Indeed, with the exception of rare mutations, the human genome-sequence has remained remarkably stable over the past centuries. In contrast, substantial changes to our environment as part of our modern life style have not only led to a significant reduction of certain infectious diseases but also seen the exponential increase in complex traits including obesity and multifactorial diseases such as autoimmune disorders. It is becoming increasingly clear that epigenetic mechanisms operate at the interface between the genetic code and our environment, and a large body of existing evidence supports the importance of environmental factors such as diet and nutrition, infections, and exposure to toxins on human health. This seems to be particularly the case during vulnerable periods of human development such as pregnancy and early life. Importantly, as the first point of contact for many of such environmental factors including nutrition, the digestive system is being increasingly linked to a number of “modern” pathologies. In this review article, we aim to give a brief introduction to the basic molecular principals of epigenetics and provide a concise summary of the existing evidence for the role of epigenetic mechanisms in gastrointestinal health and disease, hepatology, and nutrition

A Celiac Cellular Phenotype, with Altered LPP Sub-Cellular Distribution, Is Inducible in Controls by the Toxic Gliadin Peptide P31-43

<div><p>Celiac disease (CD) is a frequent inflammatory intestinal disease, with a genetic background, caused by gliadin-containing food. Undigested gliadin peptides P31-43 and P57-68 induce innate and adaptive T cell-mediated immune responses, respectively. Alterations in the cell shape and actin cytoskeleton are present in celiac enterocytes, and gliadin peptides induce actin rearrangements in both the CD mucosa and cell lines. Cell shape is maintained by the actin cytoskeleton and focal adhesions, sites of membrane attachment to the extracellular matrix. The locus of the human Lipoma Preferred Partner (LPP) gene was identified as strongly associated with CD using genome-wide association studies (GWAS). The LPP protein plays an important role in focal adhesion architecture and acts as a transcription factor in the nucleus. In this study, we examined the hypothesis that a constitutive alteration of the cell shape and the cytoskeleton, involving LPP, occurs in a cell compartment far from the main inflammation site in CD fibroblasts from skin explants. We analyzed the cell shape, actin organization, focal adhesion number, focal adhesion proteins, LPP sub-cellular distribution and adhesion to fibronectin of fibroblasts obtained from CD patients on a Gluten-Free Diet (GFD) and controls, without and with treatment with A-gliadin peptide P31-43. We observed a “CD cellular phenotype” in these fibroblasts, characterized by an altered cell shape and actin organization, increased number of focal adhesions, and altered intracellular LPP protein distribution. The treatment of controls fibroblasts with gliadin peptide P31-43 mimics the CD cellular phenotype regarding the cell shape, adhesion capacity, focal adhesion number and LPP sub-cellular distribution, suggesting a close association between these alterations and CD pathogenesis.</p></div

Analysis of LPP levels and sub-cellular distribution in CD and controls fibroblasts before and after P31-43 treatment.

<p>A. Increased focal adhesion localization of LPP in CD fibroblasts with respect to controls, as revealed through paxillin co-staining. a) Confocal immunofluorescence images of fibroblasts from CD patients and controls treated or not with P31-43 for 30 min and stained with antibodies against paxillin (red) and LPP (green); the merge of the red and green fields is shown in yellow. Representative fields. b) Statistical analysis of the number of LPP/paxillin-merged positive focal adhesions per cell. Focal adhesions of 30 fibroblasts from several fields from 3 independent experiments with 5 patients and 5 controls were counted. Columns represent the means, and the bars represent the standard deviations. Student's <i>t</i>-test. * = <i>p</i><0.05;*** = <i>p</i><0.001. B. LPP protein levels were not increased in the fibroblasts from CD patients with respect to the controls and did not vary after 24 h treatment with P31-43. a) Western blot analysis of fibroblasts protein lysates from controls and CD patients treated or not with P31-43. The upper line was stained for LPP, and the lower line was stained for tubulin. Representative experiment. b) Densitometric analysis of western blots stained for LPP in fibroblasts from 5 CD patients and 5 controls treated or not with P31-43. LPP levels were normalized to tubulin levels. Columns represent the means, and the bars represent the standard deviations. Student's <i>t</i>-test. C. Decreased localization of LPP in the nuclear fraction of CD fibroblasts. a) Western blot analysis of LPP after separating the nuclear and cytosolic protein fractions. The upper lines were stained for LPP, and the lower lines were stained for tubulin and lamin A/C, which were used as loading controls for the cytosol and nuclear fractions, respectively. Representative experiment. b) Densitometric analysis of western blots stained for LPP in fibroblasts from 5 CD patients and 5 controls. The LPP levels were normalized in each protein fractions to the loading controls. Columns represent the means, and the bars represent the standard deviation. Student's <i>t</i>-test. * = p<0.05; ** = <i>p</i><0.01.</p

Cell shape and area of fibroblasts from CD patients and controls before and after P31-43 treatment.

<p>A. Cell shape and area are altered in fibroblasts from CD patients with respect to controls (CTR). Confocal immunofluorescence images of fibroblasts from CD patients and controls stained with Phalloidin-FITC to highlight F-actin. White lines identify the cell area. Representative fields. B. Treatment with P31-43 alters the shape and area of control fibroblasts. Confocal immunofluorescence images of fibroblasts from CD patients and controls treated with P31-43 for 30 min and stained with Phalloidin-FITC to highlight F-actin. White lines identify the cell area. Representative fields. C. Statistical analysis of 30 fibroblasts from several fields of 3 independent experiments from 6 patients and 6 controls. The area of the cells was analyzed using LSM-Zeiss confocal software. Columns represent the means, and the bars represent the standard deviation of the fibroblasts area. The area of the cells was analyzed using LSM-Zeiss confocal software. Columns represent the means, and the bars represent the standard deviation. Student's <i>t</i>-test. * = <i>p</i><0.05; ** = <i>p</i><0.01.</p