Exact(4)
The next step of the proposed method is the calculation of a correlation coefficient that measures the similarity between a given cell profile and a reference cell profile.
In other words, assuming network size equal N, a total electrical or inhibitory coupling between a given cell and the remaining N-1 cells was made independent of N. With increasing network size, the number of stable patterns expressed increases.
The microarray expression data was analyzed to identify those genes that were differentially expressed between a given cell under differing conditions (−/+ DHT) or between the two cell types WPMY-Vecc vs WPMY-AR) under equivalent conditions.
As the data follows an exponential distribution and only two replicates were sequenced per biological sample, most of the normalized count difference between a given cell line and blood is by chance.
Similar(55)
Unlike FACS, the algorithm used here cannot differentiate between a population of a given cell type that are all homogeneously mildly activated and a population of that cell type that consists of a mixture of some resting cells and some strongly activated cells, since the parameters used to assess activation are merely the total quantity of each gene's mRNA present in the sample.
The relationship between the permissivity of a given cell line to in vitro replication of GLV-1h68 and the in vivo responsiveness of the corresponding xenograft was significant (Fisher exact test p2-value = 0.005) but not absolute.
Further evidence for inter-flagella coupling was obtained by calculating the cross-correlation between pairs of flagella on a given cell.
To identify genes with cell type-specific expression, a two-sample comparison was made between those samples associated with a given cell type and all other samples in the database.
Further work is needed to analyze in details the transformation of sensory neuron precursors into 'intraganglionic hair cells' and demonstrate the suppression of Atoh1 by Neurod1 at the molecular level either within a given cell or between cells via the delta/notch system.
These earlier studies, with the notable exception of the last, have not asked the question of what intrinsic cellular and functional mechanisms might control the change between the two PRC classes in a given cell or in mathematical terms what might cause a transition from one bifurcation class to another.
These results taken together suggest a mechanism in which the relative activities between LARGE and HNK-1ST in a given cell compete to mediate the length of the disaccharide repeat and thus its affinity for ECM ligands.
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