992 resultados para tumor classification
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The growing importance and influence of new resources connected to the power systems has caused many changes in their operation. Environmental policies and several well know advantages have been made renewable based energy resources largely disseminated. These resources, including Distributed Generation (DG), are being connected to lower voltage levels where Demand Response (DR) must be considered too. These changes increase the complexity of the system operation due to both new operational constraints and amounts of data to be processed. Virtual Power Players (VPP) are entities able to manage these resources. Addressing these issues, this paper proposes a methodology to support VPP actions when these act as a Curtailment Service Provider (CSP) that provides DR capacity to a DR program declared by the Independent System Operator (ISO) or by the VPP itself. The amount of DR capacity that the CSP can assure is determined using data mining techniques applied to a database which is obtained for a large set of operation scenarios. The paper includes a case study based on 27,000 scenarios considering a diversity of distributed resources in a 33 bus distribution network.
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Ovarian cancer is within the most lethal gynecological malignancies in woman. Therefore, many investigators study its biological aspects with the purpose of discovering more rapid diagnostic methods and efficient treatment. Resembling many other tumors, in ovarian cancer, aberrant glycosylation occurs with the appearance of novel or altered carbohydrate structures. These can be terminal motifs, such as the Lewis determinants, or entire carbohydrate sequences, which have been related to tumorigenesis and its outcome.(...)
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Febs Journal (2009)276:1776-1786
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Signal Processing: Algorithms, Architectures, Arrangements, and Applications (SPA), 2013
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Quality of life is a concept influenced by social, economic, psychological, spiritual or medical state factors. More specifically, the perceived quality of an individual's daily life is an assessment of their well-being or lack of it. In this context, information technologies may help on the management of services for healthcare of chronic patients such as estimating the patient quality of life and helping the medical staff to take appropriate measures to increase each patient quality of life. This paper describes a Quality of Life estimation system developed using information technologies and the application of data mining algorithms to access the information of clinical data of patients with cancer from Otorhinolaryngology and Head and Neck services of an oncology institution. The system was evaluated with a sample composed of 3013 patients. The results achieved show that there are variables that may be significant predictors for the Quality of Life of the patient: years of smoking (p value 0.049) and size of the tumor (p value < 0.001). In order to assign the variables to the classification of the quality of life the best accuracy was obtained by applying the John Platt's sequential minimal optimization algorithm for training a support vector classifier. In conclusion data mining techniques allow having access to patients additional information helping the physicians to be able to know the quality of life and produce a well-informed clinical decision.
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In the last few years the number of systems and devices that use voice based interaction has grown significantly. For a continued use of these systems the interface must be reliable and pleasant in order to provide an optimal user experience. However there are currently very few studies that try to evaluate how good is a voice when the application is a speech based interface. In this paper we present a new automatic voice pleasantness classification system based on prosodic and acoustic patterns of voice preference. Our study is based on a multi-language database composed by female voices. In the objective performance evaluation the system achieved a 7.3% error rate.
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Background: Tumor necrosis factor alpha (TNFα) antagonists are effective in treating several immune-inflammatory diseases, including psoriasis and inflammatory bowel disease. The paradoxical and unpredictable induction of psoriasis and psoriasiform skin lesions is a recognized adverse event, although of unclear aetiology. However, histological analysis of these eruptions remains insufficient, yet suggesting that some might constitute a new pattern of adverse drug reaction, rather than true psoriasis. Case report: The authors report the case of a 43-year-old woman with severe recalcitrant Crohn disease who started treatment with infliximab. There was also a personal history of mild plaque psoriasis without clinical expression for the past eight years. She developed a heterogeneous cutaneous eruption of psoriasiform morphology with pustules and crusts after the third infliximab infusion. The histopathological diagnosis was of a Sweet-like dermatosis. The patient was successfully treated with cyclosporine in association with both topical corticosteroid and vitamin D3 analogue. Three weeks after switching to adalimumab a new psoriasiform eruption was observed, histologically compatible with a psoriasiform drug eruption. Despite this, and considering the beneficial effect on the inflammatory bowel disease, it was decided to maintain treatment with adalimumab and to treat through with topicals, with progressive control of skin disease. Discussion: Not much is known about the pathogenesis of psoriasiform eruptions induced by biological therapies, but genetic predisposition and Koebner phenomenon may contribute to it. Histopathology can add new facets to the comprehension of psoriasiform reactions. In fact, histopathologic patterns of such skin lesions appear to be varied, in a clear asymmetry with clinical findings. Conclusion: The sequential identification in the same patient of two clinical and histopathologic patterns of drug reaction to TNFα antagonists is rare. Additionally, to the authors’ knowledge, there is only one other description in literature of a TNFα antagonist-induced Sweet-like dermatosis, emphasizing the singularity of this case report.
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Paragangliomas are rare tumors, with a reported incidence of 2–8 per million. They are chromaffin cell tumors that develop from the neural crest cells and may be divided in tumors derived from the parasympathetic or sympathetic ganglia. We report a case a of a 32-year-old nulliparous woman, referred to our Infertility Clinic. Abdomino-pelvic ultrasound identified a large abdominopelvic tumor, without ovarian origin (both ovaries were identified and had normal morphology). Magnetic Resonance Imaging suggested a right adnexal multicystic, vascularized mass close to iliac vessels and questioning an ovarian origin. At exploratory laparotomy, a 10 cm encapsulated and vascularized mass was found beginning just below right renal artery and extending to the level of the broad ligament. This mass was totally excised and histopathology was consistent with Paraganglioma.
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Introduction. This study aims to compare the molecular gene expression during ischemia reperfusion injury. Several surgical times were considered: in the beginning of the harvesting (T0), at the end of the cold ischemia period (T1), and after reperfusion (T2) and compared with graft dysfunction after liver transplant (OLT). Methods. We studied 54 patients undergoing OLT. Clinical, laboratory data, and histologic data (Suzuki classification) as well as the Survival Outcomes Following Liver Transplantation (SOFT) score were used and compared with the molecular gene expression of the following genes: Interleukin (IL)-1b, IL-6, tumor necrosis factor-a, perforin, E-selectin (SELE), Fas-ligand, granzyme B, heme oxygenase-1, and nitric oxide synthetase. Results. Fifteen patients presented with graft dysfunction according to SOFT criteria. No relevant data were obtained by comparing the variables graft dysfunction and histologic variables. We observed a statistically significant relation between SELE at T0 (P ¼ .013) and IL-1b at T0 (P ¼ .028) and early graft dysfunction. Conclusions. We conclude that several genetically determined proinflammatory expressions may play a critical role in the development of graft dysfunction after OLT.
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Grasslands in semi-arid regions, like Mongolian steppes, are facing desertification and degradation processes, due to climate change. Mongolia’s main economic activity consists on an extensive livestock production and, therefore, it is a concerning matter for the decision makers. Remote sensing and Geographic Information Systems provide the tools for advanced ecosystem management and have been widely used for monitoring and management of pasture resources. This study investigates which is the higher thematic detail that is possible to achieve through remote sensing, to map the steppe vegetation, using medium resolution earth observation imagery in three districts (soums) of Mongolia: Dzag, Buutsagaan and Khureemaral. After considering different thematic levels of detail for classifying the steppe vegetation, the existent pasture types within the steppe were chosen to be mapped. In order to investigate which combination of data sets yields the best results and which classification algorithm is more suitable for incorporating these data sets, a comparison between different classification methods were tested for the study area. Sixteen classifications were performed using different combinations of estimators, Landsat-8 (spectral bands and Landsat-8 NDVI-derived) and geophysical data (elevation, mean annual precipitation and mean annual temperature) using two classification algorithms, maximum likelihood and decision tree. Results showed that the best performing model was the one that incorporated Landsat-8 bands with mean annual precipitation and mean annual temperature (Model 13), using the decision tree. For maximum likelihood, the model that incorporated Landsat-8 bands with mean annual precipitation (Model 5) and the one that incorporated Landsat-8 bands with mean annual precipitation and mean annual temperature (Model 13), achieved the higher accuracies for this algorithm. The decision tree models consistently outperformed the maximum likelihood ones.
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Aberrant blood vessels enable tumor growth, provide a barrier to immune infiltration, and serve as a source of protumorigenic signals. Targeting tumor blood vessels for destruction, or tumor vascular disruption therapy, can therefore provide significant therapeutic benefit. Here, we describe the ability of chimeric antigen receptor (CAR)-bearing T cells to recognize human prostate-specific membrane antigen (hPSMA) on endothelial targets in vitro as well as in vivo. CAR T cells were generated using the anti-PSMA scFv, J591, and the intracellular signaling domains: CD3ζ, CD28, and/or CD137/4-1BB. We found that all anti-hPSMA CAR T cells recognized and eliminated PSMA(+) endothelial targets in vitro, regardless of the signaling domain. T cells bearing the third-generation anti-hPSMA CAR, P28BBζ, were able to recognize and kill primary human endothelial cells isolated from gynecologic cancers. In addition, the P28BBζ CAR T cells mediated regression of hPSMA-expressing vascular neoplasms in mice. Finally, in murine models of ovarian cancers populated by murine vessels expressing hPSMA, the P28BBζ CAR T cells were able to ablate PSMA(+) vessels, cause secondary depletion of tumor cells, and reduce tumor burden. Taken together, these results provide a strong rationale for the use of CAR T cells as agents of tumor vascular disruption, specifically those targeting PSMA. Cancer Immunol Res; 3(1); 68-84. ©2014 AACR.
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Inflammation can promote or inhibit cancer progression. In this study we have addressed the role of the proinflammatory cytokine thymic stromal lymphopoietin (TSLP) during skin carcinogenesis. Using conditional loss- and gain-of-function mouse models for Notch and Wnt signaling, respectively, we demonstrate that TSLP-mediated inflammation protects against cutaneous carcinogenesis by acting directly on CD4 and CD8 T cells. Genetic ablation of TSLP receptor (TSLPR) perturbs T-cell-mediated protection and results in the accumulation of CD11b(+)Gr1(+) myeloid cells. These promote tumor growth by secreting Wnt ligands and augmenting β-catenin signaling in the neighboring epithelium. Epithelial specific ablation of β-catenin prevents both carcinogenesis and the accumulation of CD11b(+)Gr1(+) myeloid cells, suggesting tumor cells initiate a feed-forward loop that induces protumorigenic inflammation.
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The 2009 International Society of Urological Pathology consensus conference in Boston made recommendations regarding the standardization of pathology reporting of radical prostatectomy specimens. Issues relating to the substaging of pT2 prostate cancers according to the TNM 2002/2010 system, reporting of tumor size/volume and zonal location of prostate cancers were coordinated by working group 2. A survey circulated before the consensus conference demonstrated that 74% of the 157 participants considered pT2 substaging of prostate cancer to be of clinical and/or academic relevance. The survey also revealed a considerable variation in the frequency of reporting of pT2b substage prostate cancer, which was likely a consequence of the variable methodologies used to distinguish pT2a from pT2b tumors. Overview of the literature indicates that current pT2 substaging criteria lack clinical relevance and the majority (65.5%) of conference attendees wished to discontinue pT2 substaging. Therefore, the consensus was that reporting of pT2 substages should, at present, be optional. Several studies have shown that prostate cancer volume is significantly correlated with other clinicopathological features, including Gleason score and extraprostatic extension of tumor; however, most studies fail to demonstrate this to have prognostic significance on multivariate analysis. Consensus was reached with regard to the reporting of some quantitative measure of the volume of tumor in a prostatectomy specimen, without prescribing a specific methodology. Incorporation of the zonal and/or anterior location of the dominant/index tumor in the pathology report was accepted by most participants, but a formal definition of the identifying features of the dominant/index tumor remained undecided.
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NKG2D is an activation receptor that allows natural killer (NK) cells to detect diseased host cells. The engagement of NKG2D with corresponding ligand results in surface modulation of the receptor and reduced function upon subsequent receptor engagement. However, it is not clear whether in addition to modulation the NKG2D receptor complex and/or its signaling capacity is preserved. We show here that the prolonged encounter with tumor cell-bound, but not soluble, ligand can completely uncouple the NKG2D receptor from the intracellular mobilization of calcium and the exertion of cell-mediated cytolysis. However, cytolytic effector function is intact since NKG2D ligand-exposed NK cells can be activated via the Ly49D receptor. While NKG2D-dependent cytotoxicity is impaired, prolonged ligand exposure results in constitutive interferon gamma (IFNgamma) production, suggesting sustained signaling. The functional changes are associated with a reduced presence of the relevant signal transducing adaptors DNAX-activating protein of 10 kDa (DAP-10) and killer cell activating receptor-associated protein/DNAX-activating protein of 12 kDa (KARAP/DAP-12). That is likely the consequence of constitutive NKG2D engagement and signaling, since NKG2D function and adaptor expression is restored to normal when the stimulating tumor cells are removed. Thus, the chronic exposure to tumor cells expressing NKG2D ligand alters NKG2D signaling and may facilitate the evasion of tumor cells from NK cell reactions.
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Retroviral transfer of T cell antigen receptor (TCR) genes selected by circumventing tolerance to broad tumor- and leukemia-associated antigens in human leukocyte antigen (HLA)-A*0201 (A2.1) transgenic (Tg) mice allows the therapeutic reprogramming of human T lymphocytes. Using a human CD8 x A2.1/Kb mouse derived TCR specific for natural peptide-A2.1 (pA2.1) complexes comprising residues 81-88 of the human homolog of the murine double-minute 2 oncoprotein, MDM2(81-88), we found that the heterodimeric CD8 alpha beta coreceptor, but not normally expressed homodimeric CD8 alpha alpha, is required for tetramer binding and functional redirection of TCR- transduced human T cells. CD8+T cells that received a humanized derivative of the MDM2 TCR bound pA2.1 tetramers only in the presence of an anti-human-CD8 anti-body and required more peptide than wild-type (WT) MDM2 TCR+T cells to mount equivalent cytotoxicity. They were, however, sufficiently effective in recognizing malignant targets including fresh leukemia cells. Most efficient expression of transduced TCR in human T lymphocytes was governed by mouse as compared to human constant (C) alphabeta domains, as demonstrated with partially humanized and murinized TCR of primary mouse and human origin, respectively. We further observed a reciprocal relationship between the level of Tg WT mouse relative to natural human TCR expression, resulting in T cells with decreased normal human cell surface TCR. In contrast, natural human TCR display remained unaffected after delivery of the humanized MDM2 TCR. These results provide important insights into the molecular basis of TCR gene therapy of malignant disease.