734 research outputs found

    Automatic ROI detection and classification of the Achilles tendon ultrasound images

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    Ultrasound (US) imaging plays an important role in medical imaging technologies. It is widely used because of its ease of use and low cost compared to other imaging techniques. Specifically, ultrasound imaging is used in the detection of the Achilles Tendon (AT) pathologies as it detects important details. For example, US imaging is used for AT rupture that affects about 1 in 5,000 people worldwide. Decision support systems are important in medical imaging, as they assist radiologist in detecting probable diagnoses and lesions. The work presented in this paper concerns the development of a software application to detect changes in the AT ultrasound images and subsequently classify them into normal or abnormal. We propose an approach that fully automates the detection for the Region of Interest (ROI) in ultrasound AT images. The original image is divided into six blocks with 1 cm size in each direction. The blocks lie inside the vulnerable area considered as our ROI. The proposed system achieved an accuracy of 97.21%

    Molecular Mechanisms Leading from Periodontal Disease to Cancer

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    Periodontitis is prevalent in half of the adult population and raises critical health concerns as it has been recently associated with an increased risk of cancer. While information about the topic remains somewhat scarce, a deeper understanding of the underlying mechanistic pathways promoting neoplasia in periodontitis patients is of fundamental importance. This manuscript presents the literature as well as a panel of tables and figures on the molecular mechanisms of Porphyromonas gingivalis and Fusobacterium nucleatum, two main oral pathogens in periodontitis pathology, involved in instigating tumorigenesis. We also present evidence for potential links between the RANKL–RANK signaling axis as well as circulating cytokines/leukocytes and carcinogenesis. Due to the nonconclusive data associating periodontitis and cancer reported in the case and cohort studies, we examine clinical trials relevant to the topic and summarize their outcome

    Dynamics of a small neutrally buoyant sphere in a fluid and targeting in Hamiltonian systems

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    We show that, even in the most favorable case, the motion of a small spherical tracer suspended in a fluid of the same density may differ from the corresponding motion of an ideal passive particle. We demonstrate furthermore how its dynamics may be applied to target trajectories in Hamiltonian systems.Comment: See home page http://lec.ugr.es/~julya

    Interruption of torus doubling bifurcation and genesis of strange nonchaotic attractors in a quasiperiodically forced map : Mechanisms and their characterizations

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    A simple quasiperiodically forced one-dimensional cubic map is shown to exhibit very many types of routes to chaos via strange nonchaotic attractors (SNAs) with reference to a two-parameter (A−f)(A-f) space. The routes include transitions to chaos via SNAs from both one frequency torus and period doubled torus. In the former case, we identify the fractalization and type I intermittency routes. In the latter case, we point out that atleast four distinct routes through which the truncation of torus doubling bifurcation and the birth of SNAs take place in this model. In particular, the formation of SNAs through Heagy-Hammel, fractalization and type--III intermittent mechanisms are described. In addition, it has been found that in this system there are some regions in the parameter space where a novel dynamics involving a sudden expansion of the attractor which tames the growth of period-doubling bifurcation takes place, giving birth to SNA. The SNAs created through different mechanisms are characterized by the behaviour of the Lyapunov exponents and their variance, by the estimation of phase sensitivity exponent as well as through the distribution of finite-time Lyapunov exponents.Comment: 27 pages, RevTeX 4, 16 EPS figures. Phys. Rev. E (2001) to appea

    Minimal residual disease negativity by next-generation flow cytometry is associated with improved organ response in AL amyloidosis

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    Light chain (AL) amyloidosis is caused by a small B-cell clone producing light chains that form amyloid deposits and cause organ dysfunction. Chemotherapy aims at suppressing the production of the toxic light chain (LC) and restore organ function. However, even complete hematologic response (CR), defined as negative serum and urine immunofixation and normalized free LC ratio, does not always translate into organ response. Next-generation flow (NGF) cytometry is used to detect minimal residual disease (MRD) in multiple myeloma. We evaluated MRD by NGF in 92 AL amyloidosis patients in CR. Fifty-four percent had persistent MRD (median 0.03% abnormal plasma cells). There were no differences in baseline clinical variables in patients with or without detectable MRD. Undetectable MRD was associated with higher rates of renal (90% vs 62%, p = 0.006) and cardiac response (95% vs 75%, p = 0.023). Hematologic progression was more frequent in MRD positive (0 vs 25% at 1 year, p = 0.001). Altogether, NGF can detect MRD in approximately half the AL amyloidosis patients in CR, and persistent MRD can explain persistent organ dysfunction. Thus, this study supports testing MRD in CR patients, especially if not accompanied by organ response. In case MRD persists, further treatment could be considered, carefully balancing residual organ damage, patient frailty, and possible toxicity

    Stromelysin-3 over-expression enhances tumourigenesis in MCF-7 and MDA-MB-231 breast cancer cell lines: involvement of the IGF-1 signalling pathway

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    BACKGROUND: Stromelysin-3 (ST-3) is over-expressed in the majority of human carcinomas including breast carcinoma. Due to its known effect in promoting tumour formation, but its impeding effect on metastasis, a dual role of ST-3 in tumour progression, depending on the cellular grade of dedifferentiation, was hypothesized. METHODS: The present study was designed to investigate the influence of ST-3 in vivo and in vitro on the oestrogen-dependent, non-invasive MCF-7 breast carcinoma cell line as well as on the oestrogen-independent, invasive MDA-MB-231 breast carcinoma cell line. Therefore an orthotopic human xenograft tumour model in nude mice, as well as a 3D matrigel cell culture system, were employed. RESULTS: Using both in vitro and in vivo techniques, we have demonstrated that over-expression of ST-3 in MCF-7 and MDA-MB-231 cells leads to both increased cell numbers and tumour volumes. This observation was dependent upon the presence of growth factors. In particular, the enhanced proliferative capacity was in MCF-7/ST-3 completely and in MDA-MB-231/ST-3 cells partially dependent on the IGF-1 signalling pathway. Microarray analysis of ST-3 over-expressing cells revealed that in addition to cell proliferation, further biological processes seemed to be affected, such as cell motility and stress response. The MAPK-pathway as well as the Wnt and PI3-kinase pathways, appear to also play a potential role. Furthermore, we have demonstrated that breast cancer cell lines of different differentiation status, as well as the non-tumourigenic cell line MCF-10A, have a comparable capability to induce endogenous ST-3 expression in fibroblasts. CONCLUSION: These data reveal that ST-3 is capable of enhancing tumourigenesis in highly differentiated "early stage" breast cancer cell lines as well as in further progressed breast cancer cell lines that have already undergone epithelial-mesenchymal transition. We propose that ST-3 induction in tumour fibroblasts leads to the stimulation of the IGF-1R pathway in carcinoma cells, thus enhancing their proliferative capacity. In addition, further different cellular processes seem to be activated by ST-3, possibly accounting for the dual role of ST-3 in tumour progression and metastasis

    Stimulation of MMP-11 (stromelysin-3) expression in mouse fibroblasts by cytokines, collagen and co-culture with human breast cancer cell lines

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    BACKGROUND: Matrix metalloproteinases (MMPs) are central to degradation of the extracellular matrix and basement membrane during both normal and carcinogenic tissue remodeling. MT1-MMP (MMP-14) and stromelysin-3 (MMP-11) are two members of the MMP family of proteolytic enzymes that have been specifically implicated in breast cancer progression. Expressed in stromal fibroblasts adjacent to epithelial tumour cells, the mechanism of MT1-MMP and MMP-11 induction remains unknown. METHODS: To investigate possible mechanisms of induction, we examined the effects of a number of plausible regulatory agents and treatments that may physiologically influence MMP expression during tumour progression. Thus NIH3T3 and primary mouse embryonic fibroblasts (MEFs) were: a) treated with the cytokines IL-1β, IL-2, IL-6, IL-8 and TGF-β for 3, 6, 12, 24, and 48 hours; b) grown on collagens I, IV and V; c) treated with fibronectin, con-A and matrigel; and d) co-cultured with a range of HBC (human breast cancer) cell lines of varied invasive and metastatic potential. RESULTS: Competitive quantitative RT-PCR indicated that MMP-11 expression was stimulated to a level greater than 100%, by 48 hour treatments of IL-1β, IL-2, TGF-β, fibronectin and collagen V. No other substantial changes in expression of MMP-11 or MT1-MMP in either tested fibroblast culture, under any treatment conditions, were observed. CONCLUSION: We have demonstrated significant MMP-11 stimulation in mouse fibroblasts using cytokines, matrix constituents and HBC cell lines, and also some inhibition of MT1-MMP. Our data suggest that the regulation of these genes in the complex stromal-epithelial interactions that occur in human breast carcinoma, is influenced by several mechanisms
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