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Three-dimensional cells were infected with either wildtype or SPI-1 Salmonella mutant, fixed 5 mpi, stained with both enterocyte and Salmonella specific antibodies, and the number of bacteria out of ∼50 bacteria localized to the enterocyte marker was quantitated by confocal immunofluorescence (Figure 4B).
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Peripheral venous blood was obtained before and at intervals after exposure, and leukocyte expression of surface markers was quantitated using multiparameter flow cytometry.
CD28 and other phenotypic markers were quantitated within respective CD4+CD28+ and CD4+CD28null subpopulations (Figure 7C).
CD28 and other phenotypic markers were quantitated within respective CD4+CD28+ and CD4+CD28null cell subpopulations, as detailed elsewhere [20].
Paraffin sections were graded for inflammation and histological changes verified by immunohistochemistry. Physiological and inflammatory markers were quantitated by RIA and RT-PCR, respectively.
Activation marker expression was quantitated by flow cytometric analysis.
To assess the cell cycle mechanistic effects the mitotic marker pHH3 was quantitated.
The mRNA level was quantitated by RT-qPCR using designed primers for all the genes of interest (two bone markers and five gut hormone receptors).
FRET was quantitated using an Olympus IX83 inverted fluorescence microscope.
Each sample of cDNA was quantitated and diluted to a similar concentration of 10 ng/mL.
Aortic intimal thickening was quantitated in H&E-stained segments.
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