The Experts below are selected from a list of 147873 Experts worldwide ranked by ideXlab platform
Michael J Fulham - One of the best experts on this subject based on the ideXlab platform.
-
primary Lung Tumor segmentation from pet ct volumes with spatial topological constraint
Computer Assisted Radiology and Surgery, 2016Co-Authors: Hui Cui, Xiuying Wang, Jianlong Zhou, Stefan Eberl, Dagan Feng, Michael J Fulham, Weiran LinAbstract:Accurate Lung Tumor segmentation is a prerequisite for effective radiation therapy and surgical planning. However, Tumor delineation is challenging when the Tumor boundaries are indistinct on PET or CT. To address this problem, we developed a segmentation method to improve the delineation of primary Lung Tumors from PET–CT images. We formulated the segmentation problem as a label information propagation process in an iterative manner. Our model incorporates spatial–topological information from PET and local intensity changes from CT. The topological information of the regions was extracted based on the metabolic activity of different tissues. The spatial–topological information moderates the amount of label information that a pixel receives: The label information attenuates as the spatial distance increases and when crossing different topological regions. Thus, the spatial–topological constraint assists accurate Tumor delineation and separation. The label information propagation and transition model are solved under a random walk framework. Our method achieved an average DSC of $$0.848 \pm 0.036$$ and HD (mm) of $$8.652 \pm 4.532$$ on 40 patients with Lung cancer. The t test showed a significant improvement (p value $$<$$ 0.05) in segmentation accuracy when compared to eight other methods. Our method was better able to delineate Tumors that had heterogeneous FDG uptake and which abutted adjacent structures that had similar densities. Our method, using a spatial–topological constraint, provided better Lung Tumor delineation, in particular, when the Tumor involved or abutted the chest wall and the mediastinum.
-
topology polymorphism graph for Lung Tumor segmentation in pet ct images
Physics in Medicine and Biology, 2015Co-Authors: Hui Cui, Xiuying Wang, Jianlong Zhou, Stefan Eberl, Yong Yin, Dagan Feng, Michael J FulhamAbstract:Accurate Lung Tumor segmentation is problematic when the Tumor boundary or edge, which reflects the advancing edge of the Tumor, is difficult to discern on chest CT or PET. We propose a 'topo-poly' graph model to improve identification of the Tumor extent. Our model incorporates an intensity graph and a topology graph. The intensity graph provides the joint PET-CT foreground similarity to differentiate the Tumor from surrounding tissues. The topology graph is defined on the basis of contour tree to reflect the inclusion and exclusion relationship of regions. By taking into account different topology relations, the edges in our model exhibit topological polymorphism. These polymorphic edges in turn affect the energy cost when crossing different topology regions under a random walk framework, and hence contribute to appropriate Tumor delineation. We validated our method on 40 patients with non-small cell Lung cancer where the Tumors were manually delineated by a clinical expert. The studies were separated into an 'isolated' group (n = 20) where the Lung Tumor was located in the Lung parenchyma and away from associated structures / tissues in the thorax and a 'complex' group (n = 20) where the Tumor abutted / involved a variety of adjacent structures and had heterogeneous FDG uptake. The methods were validated using Dice's similarity coefficient (DSC) to measure the spatial volume overlap and Hausdorff distance (HD) to compare shape similarity calculated as the maximum surface distance between the segmentation results and the manual delineations. Our method achieved an average DSC of 0.881 ± 0.046 and HD of 5.311 ± 3.022 mm for the isolated cases and DSC of 0.870 ± 0.038 and HD of 9.370 ± 3.169 mm for the complex cases. Student's t-test showed that our model outperformed the other methods (p-values <0.05).
-
Lung Tumor segmentation in pet images using graph cuts
Computer Methods and Programs in Biomedicine, 2013Co-Authors: Cherry Ballangan, Xiuying Wang, Stefan Eberl, Michael J Fulham, David Dagan FengAbstract:The aim of segmentation of Tumor regions in positron emission tomography (PET) is to provide more accurate measurements of Tumor size and extension into adjacent structures, than is possible with visual assessment alone and hence improve patient management decisions. We propose a segmentation energy function for the graph cuts technique to improve Lung Tumor segmentation with PET. Our segmentation energy is based on an analysis of the Tumor voxels in PET images combined with a standardized uptake value (SUV) cost function and a monotonic downhill SUV feature. The monotonic downhill feature avoids segmentation leakage into surrounding tissues with similar or higher PET tracer uptake than the Tumor and the SUV cost function improves the boundary definition and also addresses situations where the Lung Tumor is heterogeneous. We evaluated the method in 42 clinical PET volumes from patients with non-small cell Lung cancer (NSCLC). Our method improves segmentation and performs better than region growing approaches, the watershed technique, fuzzy-c-means, region-based active contour and Tumor customized downhill.
James M Antonini - One of the best experts on this subject based on the ideXlab platform.
-
Lung Tumor production and tissue metal distribution after exposure to manual metal arc stainless steel welding fume in a j and c57bl 6j mice
Journal of Toxicology and Environmental Health, 2011Co-Authors: Patti C Zeidlererdely, Aaron Erdely, Lori A Battelli, Rebecca Salmenmuniz, Michael L Kashon, Petia P Simeonova, James M AntoniniAbstract:Stainless steel welding produces fumes that contain carcinogenic metals. Therefore, welders may be at risk for the development of Lung cancer, but animal data are inadequate in this regard. Our main objective was to examine Lung Tumor production and histopathological alterations in Lung-Tumor-susceptible (A/J) and -resistant C57BL/6J (B6) mice exposed to manual metal arc-stainless steel (MMA-SS) welding fume. Male mice were exposed to vehicle or MMA-SS welding fume (20 mg/kg) by pharyngeal aspiration once per month for 4 mo. At 78 wk postexposure, gross Tumor counts and histopathological changes were assessed and metal analysis was done on extrapulmonary tissue (aorta, heart, kidney, and liver). At 78 wk postexposure, gross Lung Tumor multiplicity and incidence were unremarkable in mice exposed to MMA-SS welding fume. Histopathology revealed that only the exposed A/J mice contained minimal amounts of MMA-SS welding fume in the Lung and statistically increased lymphoid infiltrates and alveolar macrophages....
-
short term inhalation of stainless steel welding fume causes sustained Lung toxicity but no Tumorigenesis in Lung Tumor susceptible a j mice
Inhalation Toxicology, 2011Co-Authors: Patti C Zeidlererdely, Samuel Stone, Bean T Chen, Shihhoung Young, Aaron Erdely, Lori A Battelli, Michael L Kashon, David G Frazer, Ronnee N Andrews, James M AntoniniAbstract:Debate exists as to whether welding fume is carcinogenic, but epidemiological evidence suggests that welders are an at-risk population for development of Lung cancer. Our objective was to expose, by inhalation, Lung Tumor susceptible (A/J) and resistant C57BL/6J (B6) mice to stainless steel (SS) welding fume containing carcinogenic metals and characterize the Lung-inflammatory and Tumorigenic response. Male mice were exposed to air or gas metal arc (GMA)-SS welding fume at 40 mg/m3 × 3 h/day for 6 and 10 days. At 1, 4, 7, 10, 14, and 28 days after 10 days of exposure, bronchoalveolar lavage (BAL) was done. Lung cytotoxicity, permeability, inflammatory cytokines, and cell differentials were analyzed. For the Lung Tumor study, gross Tumor counts and histopathological changes were assessed in A/J mice at 78 weeks after 6 and 10 days of exposure. Inhalation of GMA-SS fume caused an early, sustained macrophage and lymphocyte response followed by a gradual neutrophil influx and the magnitudes of these differed ...
-
pulmonary inflammation and Tumor induction in Lung Tumor susceptible a j and resistant c57bl 6j mice exposed to welding fume
Particle and Fibre Toxicology, 2008Co-Authors: Patti C Zeidlererdely, Jenny R Roberts, Shihhoung Young, Aaron Erdely, Lori A Battelli, Michael L Kashon, Steven H Reynolds, James M AntoniniAbstract:Welding fume has been categorized as "possibly carcinogenic" to humans. Our objectives were to characterize the Lung response to carcinogenic and non-carcinogenic metal-containing welding fumes and to determine if these fumes caused increased Lung Tumorigenicity in A/J mice, a Lung Tumor susceptible strain. We exposed male A/J and C57BL/6J, a Lung Tumor resistant strain, by pharyngeal aspiration four times (once every 3 days) to 85 μg of gas metal arc-mild steel (GMA-MS), GMA-stainless steel (SS), or manual metal arc-SS (MMA-SS) fume, or to 25.5 μg soluble hexavalent chromium (S-Cr). Shams were exposed to saline vehicle. Bronchoalveolar lavage (BAL) was done at 2, 7, and 28 days post-exposure. For the Lung Tumor study, gross Tumor counts and histopathological changes were assessed in A/J mice at 48 and 78 weeks post-exposure. BAL revealed notable strain-dependent differences with regards to the degree and resolution of the inflammatory response after exposure to the fumes. At 48 weeks, carcinogenic metal-containing GMA-SS fume caused the greatest increase in Tumor multiplicity and incidence, but this was not different from sham. By 78 weeks, Tumor incidence in the GMA-SS group versus sham approached significance (p = 0.057). A significant increase in perivascular/peribronchial lymphoid infiltrates for the GMA-SS group versus sham and an increased persistence of this fume in Lung cells compared to the other welding fumes was found. The increased persistence of GMA-SS fume in combination with its metal composition may trigger a chronic, but mild, inflammatory state in the Lung possibly enhancing Tumorigenesis in this susceptible mouse strain.
Tacconelli S. - One of the best experts on this subject based on the ideXlab platform.
-
miR-574-5p as RNA decoy for CUGBP1 stimulates human Lung Tumor growth by mPGES-1 induction
'FASEB', 2019Co-Authors: Saul, Meike J., Emmerich, Anne C., Ottinger, Sarah M., Bruno A., Wellstein J., Contursi A., Dovizio M., Donnini S., Tacconelli S.Abstract:MicroRNAs (miRs) are important posttranscriptional regulators of gene expression. Besides their well-characterized inhibitory effects on mRNA stability and translation, miRs can also activate gene expression. In this study, we identified a novel noncanonical function of miR-574-5p. We found that miR-574-5p acts as an RNA decoy to CUG RNA-binding protein 1 (CUGBP1) and antagonizes its function. MiR-574-5p induces microsomal prostaglandin E synthase-1 (mPGES-1) expression by preventing CUGBP1 binding to its 3 ' UTR, leading to an enhanced alternative splicing and generation of an mPGES-1 3 ' UTR isoform, increased mPGES-1 protein expression, PGE(2) formation, and Tumor growth in vivo. miR-574-5p-induced Tumor growth in mice could be completely inhibited with the mPGES-1 inhibitor CIII. Moreover, miR-574-5p is induced by IL-1 beta and is strongly overexpressed in human nonsmall cell Lung cancer where high mPGES-1 expression correlates with a low survival rate. The discovered function of miR-574-5p as a CUGBP1 decoy opens up new therapeutic opportunities. It might serve as a stratification marker to select Lung Tumor patients who respond to the pharmacological inhibition of PGE(2) formation.-Saul, M. J., Baumann, I., Bruno, A., Emmerich, A. C., Wellstein, J., Ottinger, S. M., Contursi, A., Dovizio, M., Donnini, S., Tacconelli, S., Raouf, J., Idborg, H., Stein, S., Korotkova, M., Savai, R., Terzuoli, E., Sala, G., Seeger, W., Jakobsson, P.-J., Patrignani, P., Suess, B., Steinhilber, D. miR-574-5p as RNA decoy for CUGBP1 stimulates human Lung Tumor growth by mPGES-1 induction
Patti C Zeidlererdely - One of the best experts on this subject based on the ideXlab platform.
-
Lung Tumor production and tissue metal distribution after exposure to manual metal arc stainless steel welding fume in a j and c57bl 6j mice
Journal of Toxicology and Environmental Health, 2011Co-Authors: Patti C Zeidlererdely, Aaron Erdely, Lori A Battelli, Rebecca Salmenmuniz, Michael L Kashon, Petia P Simeonova, James M AntoniniAbstract:Stainless steel welding produces fumes that contain carcinogenic metals. Therefore, welders may be at risk for the development of Lung cancer, but animal data are inadequate in this regard. Our main objective was to examine Lung Tumor production and histopathological alterations in Lung-Tumor-susceptible (A/J) and -resistant C57BL/6J (B6) mice exposed to manual metal arc-stainless steel (MMA-SS) welding fume. Male mice were exposed to vehicle or MMA-SS welding fume (20 mg/kg) by pharyngeal aspiration once per month for 4 mo. At 78 wk postexposure, gross Tumor counts and histopathological changes were assessed and metal analysis was done on extrapulmonary tissue (aorta, heart, kidney, and liver). At 78 wk postexposure, gross Lung Tumor multiplicity and incidence were unremarkable in mice exposed to MMA-SS welding fume. Histopathology revealed that only the exposed A/J mice contained minimal amounts of MMA-SS welding fume in the Lung and statistically increased lymphoid infiltrates and alveolar macrophages....
-
short term inhalation of stainless steel welding fume causes sustained Lung toxicity but no Tumorigenesis in Lung Tumor susceptible a j mice
Inhalation Toxicology, 2011Co-Authors: Patti C Zeidlererdely, Samuel Stone, Bean T Chen, Shihhoung Young, Aaron Erdely, Lori A Battelli, Michael L Kashon, David G Frazer, Ronnee N Andrews, James M AntoniniAbstract:Debate exists as to whether welding fume is carcinogenic, but epidemiological evidence suggests that welders are an at-risk population for development of Lung cancer. Our objective was to expose, by inhalation, Lung Tumor susceptible (A/J) and resistant C57BL/6J (B6) mice to stainless steel (SS) welding fume containing carcinogenic metals and characterize the Lung-inflammatory and Tumorigenic response. Male mice were exposed to air or gas metal arc (GMA)-SS welding fume at 40 mg/m3 × 3 h/day for 6 and 10 days. At 1, 4, 7, 10, 14, and 28 days after 10 days of exposure, bronchoalveolar lavage (BAL) was done. Lung cytotoxicity, permeability, inflammatory cytokines, and cell differentials were analyzed. For the Lung Tumor study, gross Tumor counts and histopathological changes were assessed in A/J mice at 78 weeks after 6 and 10 days of exposure. Inhalation of GMA-SS fume caused an early, sustained macrophage and lymphocyte response followed by a gradual neutrophil influx and the magnitudes of these differed ...
-
pulmonary inflammation and Tumor induction in Lung Tumor susceptible a j and resistant c57bl 6j mice exposed to welding fume
Particle and Fibre Toxicology, 2008Co-Authors: Patti C Zeidlererdely, Jenny R Roberts, Shihhoung Young, Aaron Erdely, Lori A Battelli, Michael L Kashon, Steven H Reynolds, James M AntoniniAbstract:Welding fume has been categorized as "possibly carcinogenic" to humans. Our objectives were to characterize the Lung response to carcinogenic and non-carcinogenic metal-containing welding fumes and to determine if these fumes caused increased Lung Tumorigenicity in A/J mice, a Lung Tumor susceptible strain. We exposed male A/J and C57BL/6J, a Lung Tumor resistant strain, by pharyngeal aspiration four times (once every 3 days) to 85 μg of gas metal arc-mild steel (GMA-MS), GMA-stainless steel (SS), or manual metal arc-SS (MMA-SS) fume, or to 25.5 μg soluble hexavalent chromium (S-Cr). Shams were exposed to saline vehicle. Bronchoalveolar lavage (BAL) was done at 2, 7, and 28 days post-exposure. For the Lung Tumor study, gross Tumor counts and histopathological changes were assessed in A/J mice at 48 and 78 weeks post-exposure. BAL revealed notable strain-dependent differences with regards to the degree and resolution of the inflammatory response after exposure to the fumes. At 48 weeks, carcinogenic metal-containing GMA-SS fume caused the greatest increase in Tumor multiplicity and incidence, but this was not different from sham. By 78 weeks, Tumor incidence in the GMA-SS group versus sham approached significance (p = 0.057). A significant increase in perivascular/peribronchial lymphoid infiltrates for the GMA-SS group versus sham and an increased persistence of this fume in Lung cells compared to the other welding fumes was found. The increased persistence of GMA-SS fume in combination with its metal composition may trigger a chronic, but mild, inflammatory state in the Lung possibly enhancing Tumorigenesis in this susceptible mouse strain.
Saul, Meike J. - One of the best experts on this subject based on the ideXlab platform.
-
miR-574-5p as RNA decoy for CUGBP1 stimulates human Lung Tumor growth by mPGES-1 induction.
2019Co-Authors: Saul, Meike J., Baumann Isabell, Bruno Annalisa, Emmerich, Anne C., Wellstein Julia, Ottinger, Sarah M., Contursi Annalisa, Dovizio Melania, Donnini Sandra, Tacconelli StefaniaAbstract:MicroRNAs (miRs) are important posttranscriptional regulators of gene expression. Besides their well-characterized inhibitory effects on mRNA stability and translation, miRs can also activate gene expression. In this study, we identified a novel noncanonical function of miR-574-5p. We found that miR-574-5p acts as an RNA decoy to CUG RNA-binding protein 1 (CUGBP1) and antagonizes its function. MiR-574-5p induces microsomal prostaglandin E synthase-1 (mPGES-1) expression by preventing CUGBP1 binding to its 3'UTR, leading to an enhanced alternative splicing and generation of an mPGES-1 3'UTR isoform, increased mPGES-1 protein expression, PGE formation, and Tumor growth in vivo. miR-574-5p-induced Tumor growth in mice could be completely inhibited with the mPGES-1 inhibitor CIII. Moreover, miR-574-5p is induced by IL-1β and is strongly overexpressed in human nonsmall cell Lung cancer where high mPGES-1 expression correlates with a low survival rate. The discovered function of miR-574-5p as a CUGBP1 decoy opens up new therapeutic opportunities. It might serve as a stratification marker to select Lung Tumor patients who respond to the pharmacological inhibition of PGE formation.-Saul, M. J., Baumann, I., Bruno, A., Emmerich, A. C., Wellstein, J., Ottinger, S. M., Contursi, A., Dovizio, M., Donnini, S., Tacconelli, S., Raouf, J., Idborg, H., Stein, S., Korotkova, M., Savai, R., Terzuoli, E., Sala, G., Seeger, W., Jakobsson, P.-J., Patrignani, P., Suess, B., Steinhilber, D. miR-574-5p as RNA decoy for CUGBP1 stimulates human Lung Tumor growth by mPGES-1 induction
-
miR-574-5p as RNA decoy for CUGBP1 stimulates human Lung Tumor growth by mPGES-1 induction
'FASEB', 2019Co-Authors: Saul, Meike J., Emmerich, Anne C., Ottinger, Sarah M., Bruno A., Wellstein J., Contursi A., Dovizio M., Donnini S., Tacconelli S.Abstract:MicroRNAs (miRs) are important posttranscriptional regulators of gene expression. Besides their well-characterized inhibitory effects on mRNA stability and translation, miRs can also activate gene expression. In this study, we identified a novel noncanonical function of miR-574-5p. We found that miR-574-5p acts as an RNA decoy to CUG RNA-binding protein 1 (CUGBP1) and antagonizes its function. MiR-574-5p induces microsomal prostaglandin E synthase-1 (mPGES-1) expression by preventing CUGBP1 binding to its 3 ' UTR, leading to an enhanced alternative splicing and generation of an mPGES-1 3 ' UTR isoform, increased mPGES-1 protein expression, PGE(2) formation, and Tumor growth in vivo. miR-574-5p-induced Tumor growth in mice could be completely inhibited with the mPGES-1 inhibitor CIII. Moreover, miR-574-5p is induced by IL-1 beta and is strongly overexpressed in human nonsmall cell Lung cancer where high mPGES-1 expression correlates with a low survival rate. The discovered function of miR-574-5p as a CUGBP1 decoy opens up new therapeutic opportunities. It might serve as a stratification marker to select Lung Tumor patients who respond to the pharmacological inhibition of PGE(2) formation.-Saul, M. J., Baumann, I., Bruno, A., Emmerich, A. C., Wellstein, J., Ottinger, S. M., Contursi, A., Dovizio, M., Donnini, S., Tacconelli, S., Raouf, J., Idborg, H., Stein, S., Korotkova, M., Savai, R., Terzuoli, E., Sala, G., Seeger, W., Jakobsson, P.-J., Patrignani, P., Suess, B., Steinhilber, D. miR-574-5p as RNA decoy for CUGBP1 stimulates human Lung Tumor growth by mPGES-1 induction
