Exact(1)
Thus, in the presented models, we do not estimate division- or workgroup-level random effects; the parameter estimates from the models that included these random effects were substantively identical to those reported.
Similar(57)
Using this estimated division rate, the age-size distributions corresponding to the Age Model were produced by running the Age & Size Model.
We measure the goodness-of-fit of a model (timer or sizer) by estimating the distance between two distributions: the age-size distribution obtained through simulations of the model with the estimated division rate (as explained above), and the experimental age-size distribution.
The age-size distributions corresponding to the Size Model were produced by running the Age & Size Model (Equation (3) in the main text) using the estimated division rate Bs and an exponential growth function (v(x)= v x) with a rate v directly estimated from the data as the average of single-cell growth rates in the population (e.g. v=0.0274 min −1 for the f1 experiment and v=0.0317 min −1 for s1).
To estimate cell division donor CD8+ T cells were labeled with carboxyfluorescein diacetate succinimidyl ester (CFSE) (Molecular Probes) as previously described [24].
To estimate cell division in vivo, mice received two daily intraperitoneal injections of 1 mg 5-ethynyl-2'-deoxyuridine (EdU) at 12-hour interval for three consecutive days.
Likewise, we estimate the division rate Bs of the Size Model using the size measurements of every cell at every time step.
We estimate the division rate Ba of the Age Model using the age measurements of every cell at every time step.
Nevertheless, these interesting studies were hampered by the scarcity and poor quality of single-cell data as well as the lack of appropriate statistical procedures to estimate the division rate within the models.
Here we overcome these limitations by using high precision measurements of tens of thousands of single bacterial cells combined with recent statistical inference methods to estimate the division rate within the models.
To estimate the division frequency of human HSC subsets, we tracked BrdU incorporation kinetics of phenotypic LT- and ST-HSCs in xenografts and observed, similarly to mouse models, that phenotypic LT-HSCs divide less frequently (1.5- to 1.9-fold) than phenotypic ST-HSCs, whether in expansion or at equilibrium.
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