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1.
Eur Radiol ; 27(8): 3542-3553, 2017 Aug.
Article in English | MEDLINE | ID: mdl-28116518

ABSTRACT

OBJECTIVE: To prospectively compare diagnostic accuracy of fetal post-mortem whole-body MRI at 3-T vs. 1.5-T. METHODS: Between 2012 and 2015, post-mortem MRI at 1.5-T and 3-T was performed in fetuses after miscarriage/stillbirth or termination. Clinical MRI diagnoses were assessed using a confidence diagnostic score and compared with classical autopsy to derive a diagnostic error score. The relation of diagnostic error for each organ group with gestational age was calculated and 1.5-T with 3-T was compared with accuracy analysis. RESULTS: 135 fetuses at 12-41 weeks underwent post-mortem MRI (followed by conventional autopsy in 92 fetuses). For all organ groups except the brain, and for both modalities, the diagnostic error decreased with gestation (P < 0.0001). 3-T MRI diagnostic error was significantly lower than that of 1.5-T for all anatomic structures and organ groups, except the orbits and brain. This difference was maintained for fetuses <20 weeks gestation. Moreover, 3-T was associated with fewer non-diagnostic scans and greater concordance with classical autopsy than 1.5-T MRI, especially for the thorax, heart and abdomen in fetuses <20 weeks. CONCLUSION: Post-mortem fetal 3-T MRI improves confidence scores and overall accuracy compared with 1.5-T, mainly for the thorax, heart and abdomen of fetuses <20 weeks of gestation. KEY POINTS: • In PM-MRI, diagnostic error using 3-T is lower than that with 1.5-T. • In PM-MRI, diagnostic scan rate is higher using 3-T than 1.5-T. • In PM-MRI, concordance with classical autopsy increases with 3-T. • PM-MRI using 3-T is particularly interesting for thoracic and abdominal organs. • PM-MRI using 3-T is particularly interesting for fetuses < 20 weeks' gestation.


Subject(s)
Abortion, Spontaneous/diagnostic imaging , Fetal Diseases/diagnostic imaging , Fetus/diagnostic imaging , Stillbirth , Abortion, Induced , Abortion, Spontaneous/pathology , Autopsy/methods , Brain/diagnostic imaging , Brain/pathology , Diagnostic Errors , Female , Fetal Diseases/pathology , Fetus/pathology , Gestational Age , Heart/diagnostic imaging , Humans , Magnetic Resonance Imaging/methods , Myocardium/pathology , Pregnancy , Prospective Studies , Thorax/diagnostic imaging , Thorax/pathology , Whole Body Imaging/methods
2.
Radiology ; 279(3): 754-61, 2016 Jun.
Article in English | MEDLINE | ID: mdl-26624974

ABSTRACT

Purpose To determine the changes in temperature within the gravid miniature pig uterus during magnetic resonance (MR) imaging at 3 T. Materials and Methods The study received ethics committee approval for animal experimentation. Fiber-optic temperature sensors were inserted into the fetal brain, abdomen, bladder, and amniotic fluid of miniature pigs (second trimester, n = 2; third trimester, n = 2). In the first trimester (n = 2), the sensors were inserted only into the amniotic fluid (three sacs per miniature pig, for a total of six sacs). Imaging was performed with a 3-T MR imager by using different imaging protocols in a random order for animal, each lasting approximately 15 minutes. The first regimen consisted of common sequences used for human fetal MR examination, including normal specific absorption rate (SAR). The second regimen consisted of five low-SAR sequences, for which three gradient-echo sequences were interspersed with two diffusion-weighted imaging series. Finally, a high-SAR regimen maximized the radiofrequency energy deposition (constrained by the 2-W per kilogram of body weight SAR limitations) by using five single-shot turbo spin-echo sequences. Differences in temperature increases between the three regimens and between the three trimesters were evaluated by using one-way analysis of variance. The maximum cumulative temperature increase over 1 hour was also evaluated. Results Low-SAR regimens resulted in the lowest temperature increase (mean ± standard deviation, -0.03°C ± 0.20), normal regimens resulted in an intermediate increase (0.31°C ± 0.21), and high-SAR regimens resulted in the highest increase (0.56°C ± 0.20) (P < .0001). Mean temperature increase in the third trimester was 0.38°C ± 0.27, with no significant differences compared with the first (0.23°C ± 0.27) and second (0.25°C ± 0.32) trimesters (P = .07). The cumulative temperature increase over 1-hour imaging time with high SAR can reach 2.5°C. Conclusion In pregnant miniature pigs, the use of 3-T magnets for diagnostic MR imaging with normal SAR regimens does not lead to temperature increases above 1°C if imaging time is kept below 30 minutes. Longer imaging time, especially with high-SAR regimens, can lead to an increase of 2.5°C. (©) RSNA, 2015 Online supplemental material is available for this article.


Subject(s)
Hot Temperature , Magnetic Resonance Imaging , Pregnancy , Uterus/physiology , Animals , Female , Swine , Swine, Miniature , Uterus/diagnostic imaging
3.
J Immunol ; 177(9): 5912-9, 2006 Nov 01.
Article in English | MEDLINE | ID: mdl-17056515

ABSTRACT

Mucosal immune response depends on the surveillance network established by dendritic cells (DC), APC localized within the epithelium. Bronchial epithelial cells (BEC) play a pivotal role both in the host defense and in the pathogenesis of inflammatory airway disorders. We previously showed that the outer membrane protein A from Klebsiella pneumoniae (KpOmpA), a pathogen-associated molecular pattern (PAMP) derived from Klebsiella pneumoniae, activates BEC. In this study, we evaluated the consequences of this activation on DC traffic and functions. KpOmpA significantly increased the production of CCL2, CCL5, CXCL10, and CCL20 by BEC. Stimulation of BEC increased their chemotactic activity for monocyte-derived DC (MDDC) precursors, through CCL5 and CXCL10 secretion. BEC/MDDC precursor coculture leads to an ICAM-1-dependent accelerated differentiation and enhanced maturation of MDDC. BEC/DC interactions did not affect the capacity of DC to induce T cell proliferation. However, DC preincubated with BEC increased significantly the IL-10 production by autologous T cells. Basolateral and intraepithelial DC differently enhance IL-4 and/or IL-10 synthesis according to the condition of stimulation. In vivo, intranasal injections of KpOmpA into BALB/c mice induced the recruitment of CD11c(+) and I-A(d+) myeloid DC associated with bronchial epithelium activation as evidenced by CCL20 expression. These data show that KpOmpA-exposed BEC participate in the homeostasis of myeloid DC network, and regulate the induction of local immune response.


Subject(s)
Bacterial Outer Membrane Proteins/immunology , Bronchi/immunology , Dendritic Cells/immunology , Administration, Intranasal , Animals , Bacterial Outer Membrane Proteins/administration & dosage , Bronchi/cytology , Bronchi/drug effects , CD11c Antigen/analysis , Cell Movement , Chemokines/metabolism , Coculture Techniques , Cytokines/metabolism , Epithelium/drug effects , Epithelium/immunology , Histocompatibility Antigens Class II/analysis , Humans , Intercellular Adhesion Molecule-1/metabolism , Mice , Mice, Inbred BALB C , Myeloid Cells/immunology , T-Lymphocytes/immunology
4.
J Immunol ; 171(12): 6697-705, 2003 Dec 15.
Article in English | MEDLINE | ID: mdl-14662873

ABSTRACT

Aside from its mechanical barrier function, bronchial epithelium plays an important role both in the host defense and in the pathogenesis of inflammatory airway disorders. To investigate its role in lung defense, the effect of a bacterial cell wall protein, the outer membrane protein A from Klebsiella pneumoniae (kpOmpA) on bronchial epithelial cells (BEC) was evaluated on adhesion molecule expression and cytokine production. Moreover, the potential implication of this mechanism in kpOmpA-induced lung inflammation was also determined. Our in vitro studies demonstrated that kpOmpA strongly bound to BEAS-2B cells, a human BEC line, and to BEC primary cultures, resulting in NF-kappaB signaling pathway activation. Exposure to kpOmpA increased ICAM-1 mRNA and cell surface expression, as well as the secretion of IL-6, CXC chemokine ligand (CXCL)1, CXCL8, C-C chemokine ligand 2, CXCL10 by BEAS-2B cells, and BEC primary cultures (p < 0.005). We analyzed in vivo the consequences of intratracheal injection of kpOmpA to BALB/c mice. In kpOmpA-treated mice, a transient neutrophilia (with a maximum at 24 h) was observed in bronchoalveolar lavage and lung sections. In vivo kpOmpA priming induced bronchial epithelium activation as evaluated by ICAM-1 and CXCL1 expression, associated with the secretion of CXCL1 and CXCL5 in bronchoalveolar lavage fluids. In the lung, an increased level of the IL-6, CXCL1, CXCL5, CXCL10 mRNA was observed with a maximum at 6 h. These data showed that kpOmpA is involved in host defense mechanism by its ability to activate not only APC but also BEC, resulting in a lung neutrophilia.


Subject(s)
Bacterial Outer Membrane Proteins/pharmacology , Bronchi/immunology , Bronchi/metabolism , Klebsiella pneumoniae/immunology , Neutrophil Infiltration/immunology , Respiratory Mucosa/immunology , Respiratory Mucosa/metabolism , Animals , Bacterial Adhesion/immunology , Bacterial Outer Membrane Proteins/administration & dosage , Bacterial Outer Membrane Proteins/metabolism , Bronchi/pathology , Cell Line , Cell Line, Transformed , Cells, Cultured , Chemokines, CXC/biosynthesis , Cytokines/biosynthesis , Cytokines/genetics , Cytokines/metabolism , Drug Synergism , Female , Humans , Inflammation/immunology , Inflammation/metabolism , Inflammation/microbiology , Intercellular Adhesion Molecule-1/biosynthesis , Intercellular Adhesion Molecule-1/genetics , Intercellular Signaling Peptides and Proteins/biosynthesis , Interferon-gamma/pharmacology , Intracellular Fluid/immunology , Intracellular Fluid/metabolism , Intubation, Intratracheal , Klebsiella pneumoniae/physiology , Lung/immunology , Lung/pathology , Mice , Mice, Inbred BALB C , Protein Binding/immunology , RNA, Messenger/biosynthesis , RNA, Messenger/metabolism , Receptors, CCR2 , Receptors, Chemokine/biosynthesis , Respiratory Mucosa/pathology , Signal Transduction/immunology , Tumor Necrosis Factor-alpha/pharmacology , Up-Regulation/immunology
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