scholarly journals A Method to Rapidly and Accurately Compare the Relative Efficacies of Non-invasive Imaging Reporter Genes in a Mouse Model and its Application to Luciferase Reporters

2011 ◽  
Vol 14 (4) ◽  
pp. 462-471 ◽  
Author(s):  
Jose S. Gil ◽  
Hidevaldo B. Machado ◽  
Harvey R. Herschman
Keyword(s):  
Mouse Model ◽  
Reporter Genes ◽  
Non Invasive ◽  
Luciferase Reporters

scholarly journals Non-invasive imaging using reporter genes altering cellular water permeability

2016 ◽  
Vol 7 (1) ◽  
Author(s):  
Arnab Mukherjee ◽  
Di Wu ◽  
Hunter C. Davis ◽  
Mikhail G. Shapiro
Keyword(s):  
Water Permeability ◽  
Reporter Genes ◽  
Non Invasive ◽  
Cellular Water

scholarly journals A Mouse Model of Acute Q Fever Following Infection Via A Non-Invasive Intratracheal Inoculation Method

2019 ◽  
Author(s):  
Xueyuan Hu ◽  
Yonghui Yu ◽  
Junxia Feng ◽  
Mengjiao Fu ◽  
Lupeng Dai ◽  
...  
Keyword(s):  
Mouse Model ◽  
Low Dose ◽  
Q Fever ◽  
Pulmonary Delivery ◽  
Delivery Device ◽  
Inflammatory Infiltration ◽  
Pathological Lesions ◽  
Non Invasive ◽  
Therapeutic Drugs ◽  
Acute Q Fever

Abstract Background: Q fever is a worldwide zoonosis caused by Coxiella burnetii and mainly transmitted by aerosols. This study aims at establishing a systematic and efficient mouse model of acute Q fever via intratracheal (IT) inoculation of aerosolized C. burnetii. Methods: BALB/c mice were infected with C. burnetii via IT route using a non-invasive aerosol pulmonary delivery device to directly place the living C. burnetii organisms into their tracheas. The bacterial loads, pathological lesions, and serological responses were analyzed in mice, and compared with those of mice infected via intraperitoneal (IP) route. Results: As early as at day three post-infection (pi) with a low dose of C. burnetii (1×10⁴ per mouse), a large amount of C. burnetii organisms were determined in blood, lungs, hearts, livers, and spleens of the mice. The inflammatory infiltration was observed in hearts and lungs of mice. Compared with mice infected via IP route, the mice infected via IT route exhibited a higher level of bacterial loads and more severe pathological lesions in hearts and lungs at day 3 and day 7 pi. Conclusions: These data indicated that IT route is more efficient than IP route to cause acute C. burnetii infection in mice. Overall, we successfully established a mouse model of C. burnetii infection via IT route, which is useful for investigations of pathogenesis and immunity of acute C. burnetii infection as well as evaluation of therapeutic drugs and preventive vaccines of Q fever.

scholarly journals Cervical epithelial damage promotes Ureaplasma parvum ascending infection, intrauterine inflammation and preterm birth induction in mice

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Ioannis Pavlidis ◽  
Owen B. Spiller ◽  
Gabriella Sammut Demarco ◽  
Heather MacPherson ◽  
Sarah E. M. Howie ◽  
...  
Keyword(s):  
Preterm Birth ◽  
Mouse Model ◽  
Bacterial Load ◽  
Preterm Births ◽  
Intrauterine Infection ◽  
Cervical Injury ◽  
Epithelial Damage ◽  
Ureaplasma Parvum ◽  
Non Invasive ◽  
Ascending Infection

AbstractAround 40% of preterm births are attributed to ascending intrauterine infection, and Ureaplasma parvum (UP) is commonly isolated in these cases. Here we present a mouse model of ascending UP infection that resembles human disease, using vaginal inoculation combined with mild cervical injury induced by a common spermicide (Nonoxynol-9, as a surrogate for any mechanism of cervical epithelial damage). We measure bacterial load in a non-invasive manner using a luciferase-expressing UP strain, and post-mortem by qPCR and bacterial titration. Cervical exposure to Nonoxynol-9, 24 h pre-inoculation, facilitates intrauterine UP infection, upregulates pro-inflammatory cytokines, and increases preterm birth rates from 13 to 28%. Our results highlight the crucial role of the cervical epithelium as a barrier against ascending infection. In addition, we expect the mouse model will facilitate further research on the potential links between UP infection and preterm birth.

Determining the Signal Source in Magnetic Resonance Imaging of Myelofibrotic Bone Marrow

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 3140-3140
Author(s):  
Shinobu Matsuura ◽  
Shenia Patterson ◽  
Hector Lucero ◽  
Aaron Grant ◽  
Victoria L. M. Herrera ◽  
...  
Keyword(s):  
Magnetic Resonance Imaging ◽  
Bone Marrow ◽  
Magnetic Resonance ◽  
Mouse Model ◽  
Conflicts Of Interest ◽  
Integrative Approach ◽  
Histological Findings ◽  
Resonance Imaging ◽  
Non Invasive ◽  
Lipid Signal

Abstract Magnetic resonance imaging (MRI) is a promising diagnostic method for evaluation of bone marrow myelofibrosis for offering non-invasive, wider-area coverage over conventional histology. Although the most striking feature in histology of myelofibrotic bone marrow is the proliferation of reticulin fibers, the spectrum of findings involves abnormalities in cell number and composition, vessel proliferation, as well as possible pre-fibrotic abnormalities in matrix such as inflammation/edema. Correlation of MRI observations with such histological findings to accurately define the pathogenic phases of myelofibrosis has been challenging. Here, we present the first MRI analysis of myelofibrosis in a mouse model (Gata-1low mice) in an attempt to correlate MRI signal observations with histological findings. T2-weighted MRI images of femur bone marrow of Gata-1low animals at different ages (12 to 46 weeks) showed high MR signal intensity, absent in age-matched wild-type controls, that is detected as early as 12 weeks of age, before onset of histologically-defined fibrosis in this mouse model. MRI acquisitions employing fat suppression, a technique that suppresses signals from lipids, together with the absence of chemical shift artifacts in the images, excluded the possibility of lipids as the source of the prominent MR signal. To determine the source of this prominent non-lipid signal in Gata-1low bone marrow, cellular composition, vascularization and vascular permeability were tested. Our findings demonstrate a multi-source nature of MRI signals in bone marrow, which evolves from young (12 weeks) to old (40 weeks) Gata-1low bone marrow consistent with the pathologic progression of myelofibrosis. Data support the importance of an integrative approach to further the development of this non-invasive modality for following the dynamics and progression of this multifactorial pathology in humans. Disclosures No relevant conflicts of interest to declare.

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