215 research outputs found

    Follicular thyroid lesions: Is there a discriminatory potential in the computerized nuclear analysis?

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    Background: Computerized image analysis seems to represent a promising diagnostic possibility for thyroid tumors. Our aim was to evaluate the discriminatory diagnostic efficiency of computerized image analysis of cell nuclei from histological materials of follicular tumors. Methods: We studied paraffin-embedded materials from 42 follicular adenomas (FA), 47 follicular variants of papillary carcinomas (FVPC) and 20 follicular carcinomas (FC) by the software ImageJ. Based on the nuclear morphometry and chromatin texture, the samples were classified as FA, FC or FVPC using the Classification and Regression Trees method. Results: We observed high diagnostic sensitivity and specificity rates (FVPC: 89.4% and 100%; FC: 95.0% and 92.1%; FA: 90.5 and 95.5%, respectively). When the tumors were compared by pairs (FC vs FA, FVPC vs FA), 100% of the cases were classified correctly. Conclusion: The computerized image analysis of nuclear features showed to be a useful diagnostic support tool for the histological differentiation between follicular adenomas, follicular variants of papillary carcinomas and follicular carcinomas.This study received financial support from Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP; process number 2014/10028-2), and PIBIC/PROPE-Unesp (process number 33347). The authors thank to Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP; process number 2014/10028-2), and PIBIC/PROPE-Unesp (process number 33347) for the research support and to Marcos Roberto Franchi and Luiz Fernando Franchi for the help in processing the histological material

    Ginzburg-Landau vortex dynamics with pinning and strong applied currents

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    We study a mixed heat and Schr\"odinger Ginzburg-Landau evolution equation on a bounded two-dimensional domain with an electric current applied on the boundary and a pinning potential term. This is meant to model a superconductor subjected to an applied electric current and electromagnetic field and containing impurities. Such a current is expected to set the vortices in motion, while the pinning term drives them toward minima of the pinning potential and "pins" them there. We derive the limiting dynamics of a finite number of vortices in the limit of a large Ginzburg-Landau parameter, or \ep \to 0, when the intensity of the electric current and applied magnetic field on the boundary scale like \lep. We show that the limiting velocity of the vortices is the sum of a Lorentz force, due to the current, and a pinning force. We state an analogous result for a model Ginzburg-Landau equation without magnetic field but with forcing terms. Our proof provides a unified approach to various proofs of dynamics of Ginzburg-Landau vortices.Comment: 48 pages; v2: minor errors and typos correcte

    Central Santa Catarina coastal dunefields chronology and their relation to relative sea level and climatic changes

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    During the past decades, there have been contrarian explanations for the formation and stabilization of coastal dunefields: while many authors believe the dunes formation would be enhanced by falling sea level, others argue that a rising or stable sea level context would be favorable. For Brazilian coastal dunefields, the second hypothesis seems to be more consistent with the luminescence ages found so far; however, most of these data were obtained without using the SAR protocol. Another point of concern is the role of climate change in the aeolian system, which is still not very clear. The aim of this paper is to try to clarify these two questions. To this end, five coastal dunefields were selected in central Santa Catarina coast. The remote sensing and dating results allowed the discrimination and mapping of at least four aeolian generations. Their age distribution in relation to the global curve of relative sea level variation during the Late Pleistocene allows us to suggest that the formation of Aeolian dunefields in the coastal context is supported by stable relative sea level. However, relative sea level is not the only determinant for the formation and preservation of the aeolian coastal dunes. Evidences of climatic control indicate that the initiation of dunefields would be favored by periods of less humidity while their stabilization would occur preferably during the periods of rain intensification, connected to monsoon activity

    Early and extensive CD55 loss from red blood cells supports a causal role in malarial anaemia

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    BACKGROUND\ud \ud Levels of complement regulatory proteins (CrP) on the surface of red blood cells (RBC) decrease during severe malarial anaemia and as part of cell ageing process. It remains unclear whether CrP changes seen during malaria contribute to the development of anaemia, or result from an altered RBC age distribution due to suppressive effects of malaria on erythropoiesis.\ud \ud METHODS\ud \ud A cross sectional study was conducted in the north-east coast of Tanzania to investigate whether the changes in glycosylphosphatidylinositol (GPI)-anchored complement regulatory proteins (CD55 and CD59) contributes to malaria anaemia. Blood samples were collected from a cohort of children under intensive surveillance for Plasmodium falciparum parasitaemia and illness. Levels of CD55 and CD59 were measured by flow cytometer and compared between anaemic (8.08 g/dl) and non- anaemic children (11.42 g/dl).\ud \ud RESULTS\ud \ud Levels of CD55 and CD59 decreased with increased RBC age. CD55 levels were lower in anaemic children and the difference was seen in RBC of all ages. Levels of CD59 were lower in anaemic children, but these differences were not significant. CD55, but not CD59, levels correlated positively with the level of haemoglobin in anaemic children.\ud \ud CONCLUSION\ud \ud The extent of CD55 loss from RBC of all ages early in the course of malarial anaemia and the correlation of CD55 with haemoglobin levels support the hypothesis that CD55 may play a causal role in this disorder

    The RAG1 N-terminal region regulates the efficiency and pathways of synapsis for V(D)J recombination

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    Immunoglobulin and T cell receptor gene assembly depends on V(D)J recombination initiated by the RAG1-RAG2 recombinase. The RAG1 N-terminal region (NTR; aa 1-383) has been implicated in regulatory functions whose influence on V(D)J recombination and lymphocyte development in vivo is poorly understood. We generated mice in which RAG1 lacks ubiquitin ligase activity (P326G), the major site of autoubiquitination (K233R), or its first 215 residues (Δ215). While few abnormalities were detected in R1.K233R mice, R1.P326G mice exhibit multiple features indicative of reduced recombination efficiency, including an increased Igκ+:Igλ+ B cell ratio and decreased recombination of Igh, Igκ, Igλ, and Tcrb loci. Previous studies indicate that synapsis of recombining partners during Igh recombination occurs through two pathways: long-range scanning and short-range collision. We find that R1Δ215 mice exhibit reduced short-range Igh and Tcrb D-to-J recombination. Our findings indicate that the RAG1 NTR regulates V(D)J recombination and lymphocyte development by multiple pathways, including control of the balance between short- and long-range recombination

    IL-26 is overexpressed in chronically HCV-infected patients and enhances TRAIL-mediated cytotoxicity and interferon production by human NK cells

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    Objective Interleukin-26 (IL-26) is a member of the IL-10 cytokine family, first discovered based on its peculiar expression by virus-transformed T cells. IL-26 is overexpressed in chronic inflammation (rheumatoid arthritis and Crohn’s disease) and induces proinflammatory cytokines by myeloid cells and some epithelial cells. We thus investigated the expression and potential role of IL-26 in chronic HCV infection, a pathology associated with chronic inflammation.Design IL-26 was quantified in a cohort of chronically HCV-infected patients, naive of treatment and its expression in the liver biopsies investigated by immunohistochemistry. We also analysed the ability of IL-26 to modulate the activity of natural killer (NK) cells, which control HCV infection. Results The serum levels of IL-26 are enhanced in chronically HCV-infected patients, mainly in those with severe liver inflammation. Immunohistochemistry reveals an intense IL-26 staining in liver lesions, mainly in infiltrating CD3+ cells. We also show that NK cells from healthy subjects and from HCV-infected patients are sensitive to IL-26. IL-26 upregulates membrane tumour necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) expression on CD16− CD56bright NK cells, enabling them to kill HCV-infected hepatoma cells, with the same efficacy as interferon (IFN)-α-treated NK cells. IL-26 also induces the expression of the antiviral cytokines IFN-β and IFN-γ, and of the proinflammatory cytokines IL-1β and TNF-α by NK cells. Conclusions This study highlights IL-26 as a new player in the inflammatory and antiviral immune responses associated with chronic HCV infection
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