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1.
J Magn Reson Imaging ; 2018 Mar 08.
Artigo em Inglês | MEDLINE | ID: mdl-29517831

RESUMO

BACKGROUND: Lung T1 is a potential translational biomarker of lung disease. The precision and repeatability of variable flip angle (VFA) T1 mapping using modern 3D ultrashort echo time (UTE) imaging of the whole lung needs to be established before it can be used to assess response to disease and therapy. PURPOSE: To evaluate the feasibility of regional lung T1 quantification with VFA 3D-UTE and to investigate long- and short-term T1 repeatability in the lungs of naive mice. STUDY TYPE: Prospective preclinical animal study. POPULATION: Eight naive mice and phantoms. FIELD STRENGTH/SEQUENCE: 3D free-breathing radial UTE (8 µs) at 4.7T. ASSESSMENT: VFA 3D-UTE T1 calculations were validated against T1 values measured with inversion recovery (IR) in phantoms. Lung T1 and proton density (S0 ) measurements of whole lung and muscle were repeated five times over 1 month in free-breathing naive mice. Two consecutive T1 measurements were performed during one of the imaging sessions. STATISTICAL TESTS: Agreement in T1 between VFA 3D-UTE and IR in phantoms was assessed using Bland-Altman and Pearson 's correlation analysis. The T1 repeatability in mice was evaluated using coefficient of variation (CV), repeated-measures analysis of variance (ANOVA), and paired t-test. RESULTS: Good T1 agreement between the VFA 3D-UTE and IR methods was found in phantoms. T1 in lung and muscle showed a 5% and 3% CV (1255 ± 63 msec and 1432 ± 42 msec, respectively, mean ± SD) with no changes in T1 or S0 over a month. Consecutive measurements resulted in an increase of 2% in both lung T1 and S0 . DATA CONCLUSION: VFA 3D-UTE shows promise as a reliable T1 mapping method that enables full lung coverage, high signal-to-noise ratio (∼25), and spatial resolution (300 µm) in freely breathing animals. The precision of the VFA 3D-UTE method will enable better design and powering of studies. LEVEL OF EVIDENCE: 1 Technical Efficacy: Stage 2 J. Magn. Reson. Imaging 2018.

2.
Clin Sci (Lond) ; 125(12): 565-74, 2013 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-23789621

RESUMO

A significant number of clinical asthma exacerbations are triggered by viral infection. We aimed to characterize the effect of virus infection in an HDM (house dust mite) mouse model of asthma and assess the effect of oral corticosteroids. HDM alone significantly increased eosinophils, lymphocytes, neutrophils, macrophages and a number of cytokines in BAL (bronchoalveolar lavage), all of which were sensitive to treatment with prednisolone (with the exception of neutrophils). Virus infection also induced cell infiltration and cytokines. RSV (respiratory syncytial virus) infection in HDM-treated animals further increased all cell types in BAL (except eosinophils, which declined), but induced no further increase in HDM-elicited cytokines. However, while HDM-elicited TNF-α (tumour necrosis factor-α), IFN-γ (interferon-γ), IL (interleukin)-2, IL-5 and IL-10 were sensitive to prednisolone treatment, concomitant infection with RSV blocked the sensitivity towards steroid. In contrast, influenza infection in HDM- challenged animals resulted in increased BAL lymphocytes, neutrophils, IFN-γ, IL-1ß, IL-4, IL-5, IL-10 and IL-12, but all were attenuated by prednisolone treatment. HDM also increased eNO (exhaled NO), which was further increased by concomitant virus infection. This increase was only partially attenuated by prednisolone. RSV infection alone increased BAL mucin. However, BAL mucin was increased in HDM animals with virus infection. Chronic HDM challenge in mice elicits a broad inflammatory response that shares many characteristics with clinical asthma. Concomitant influenza or RSV infection elicits differing inflammatory profiles that differ in their sensitivity towards steroids. This model may be suitable for the assessment of novel pharmacological interventions for asthmatic exacerbation.


Assuntos
Asma/complicações , Glucocorticoides/uso terapêutico , Infecções por Orthomyxoviridae/imunologia , Prednisolona/uso terapêutico , Infecções por Vírus Respiratório Sincicial/imunologia , Animais , Peso Corporal , Modelos Animais de Doenças , Feminino , Pulmão/química , Pulmão/virologia , Camundongos , Camundongos Endogâmicos BALB C , Infecções por Orthomyxoviridae/tratamento farmacológico , Pyroglyphidae/imunologia , Infecções por Vírus Respiratório Sincicial/tratamento farmacológico
3.
Pest Manag Sci ; 73(3): 546-553, 2017 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-27158946

RESUMO

BACKGROUND: A 2 year study was conducted to determine whether western bean cutworm (Striacosta albicosta Smith) (WBC) larval feeding damage increases severity of the fungal disease Gibberella ear rot [Fusarium graminearum (Schwein.) Petch] in field corn (Zea mays L.). The effect of a quinone-outside inhibiting fungicide, pyraclostrobin, on Gibberella ear rot severity and mycotoxin production, both with and without WBC pressure, was also evaluated. The impact of each variable was assessed individually and in combination to determine the effect of each upon ear disease severity. RESULTS: There was a positive correlation between the presence of WBC larvae in field corn and Gibberella ear rot severity under inoculated conditions in the 2 years of the experiment. An application of pyraclostrobin did not impact Gibberella ear rot development when applied at corn growth stage R1 (silks first emerging). CONCLUSION: Feeding damage from WBC larvae significantly increases the development of F. graminearum in field corn. We conclude that an effective integrated management strategy for Gibberella ear rot should target the insect pest first, in an effort to limit disease severity and subsequent mycotoxin production by F. graminearum in kernels. © 2016 Society of Chemical Industry.


Assuntos
Gibberella/fisiologia , Mariposas/fisiologia , Doenças das Plantas/microbiologia , Zea mays/microbiologia , Animais , Comportamento Alimentar , Gibberella/crescimento & desenvolvimento , Indiana , Larva/fisiologia , Mariposas/crescimento & desenvolvimento , Zea mays/fisiologia
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