29 research outputs found

    Magnetic Resonance Microscopy (MRM) images at 14 Tesla and 25°C of human meningioma brain tumor sample showing the different contrasts obtained using different image sequences (A–F) and compared to correlative histopathology (G).

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    <p>A) T1-weighted spin echo image; B) T2-weighted spin echo image; C) T2*-weighted gradient echo image; D) proton density weighted image; E) Apparent Diffusion Coefficient (ADC) map calculated from multi-slice multi-b-values image sequence; F) R2 map calculated from multi-slice multiecho image sequence; G) Hematoxylin and eosin (HE) stain at low magnification power of human meningioma brain tumor sample with two zoomed regions showing microhemorrhages (a) and collagen pattern (b).</p

    Scheme showing the protocol followed in this study.

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    <p>Tissue samples coming from the surgery room are fixed at the Anatomopathology Department. There, a reference cut is performed on the sample for geometrical referencing purposes. The sample is then submerged in an agarose matrix in the MRM tube at the MR Imaging lab to minimize sample motion and magnetic susceptibility artifacts. The MRM tube containing the sample is then introduced in the MR 14 Tesla magnet and MRM images are obtained at high resolution. Finally, the agarose matrix is dissolved and the samples are washed with formalin and embedded in paraffin for histopathology analysis at the Anatomopathology Department.</p

    Relative MRM intensity of selected ROIs in brain tumor tissue.

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    <p>Qualitative MRM region of interest (ROI) signal intensity trend relative to dominant tissue signal intensity for different areas as selected by expert pathologists and defined by correlation with respect histopathology images.</p

    Magnetic Resonance Microscopy (MRM) images at 14 Tesla and 25°C of different human brain excised tissue showing different structural details in the different image sequences and brain tissues.

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    <p>A) Proton density spin echo image of a human cerebral cavernous malformation (CCM) lesion biopsy showing the potential honeycomb region enclosed in a white square; B) T2-weighted spin echo image of a human fibroblastic meningioma brain tumor; C) T2-weighted spin echo image of a human meningothelial meningioma brain tumor biopsy; D) T2-weighted spin echo image of a human gliosarcoma brain tumor biopsy; E) ADC map of a human oligoastrocytoma showing the change in water diffusion between the tumoral (high ADC) and peritumoral (low ADC, white arrows) regions; F) T1-weighted spin echo image of human healthy brain showing the differences between gray (hyper-intense) and white (hypo-intense) matter.</p

    Development and characterization of an experimental model of diet-induced metabolic syndrome in rabbit

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    <div><p>Metabolic syndrome (MetS) has become one of the main concerns for public health because of its link to cardiovascular disease. Murine models have been used to study the effect of MetS on the cardiovascular system, but they have limitations for studying cardiac electrophysiology. In contrast, the rabbit cardiac electrophysiology is similar to human, but a detailed characterization of the different components of MetS in this animal is still needed. Our objective was to develop and characterize a diet-induced experimental model of MetS that allows the study of cardiovascular remodeling and arrhythmogenesis. Male NZW rabbits were assigned to control (n = 15) or MetS group (n = 16), fed during 28 weeks with high-fat, high-sucrose diet. We measured weight, morphological characteristics, blood pressure, glycaemia, standard plasma biochemistry and the metabolomic profile at weeks 14 and 28. Liver histological changes were evaluated using hematoxylin-eosin staining. A mixed model ANOVA or unpaired t-test were used for statistical analysis (P<0.05). Weight, abdominal contour, body mass index, systolic, diastolic and mean arterial pressure increased in the MetS group at weeks 14 and 28. Glucose, triglycerides, LDL, GOT-AST, GOT/GPT, bilirubin and bile acid increased, whereas HDL decreased in the MetS group at weeks 14 and 28. We found a 40% increase in hepatocyte area and lipid vacuoles infiltration in the liver from MetS rabbits. Metabolomic analysis revealed differences in metabolites related to fatty acids, energetic metabolism and microbiota, compounds linked with cardiovascular disease. Administration of high-fat and high-sucrose diet during 28 weeks induced obesity, glucose intolerance, hypertension, non-alcoholic hepatic steatosis and metabolic alterations, thus reproducing the main clinical manifestations of the metabolic syndrome in humans. This experimental model should provide a valuable tool for studies into the mechanisms of cardiovascular problems related to MetS, with special relevance in the study of cardiovascular remodeling, arrhythmias and SCD.</p></div

    Energy intake in the experimental groups.

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    <p>Panel (A) illustrates the evolution of weekly intake during the 28 weeks of the experimental period. In panel (B), mean caloric intake is displayed. The relative intake in percentage of kcal from high-fat chow and the drinking solution can be observed in panel (C). Control (n = 6), MetS (n = 8), *p<0.05 <i>vs</i>. control, error bars display SEM.</p
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