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Articles by X Dai
Total Records ( 3 ) for X Dai
  X Dai , O Yli Harja and A. S. Ribeiro

Motivation: Gene regulatory networks (GRNs) are stochastic, thus, do not have attractors, but can remain in confined regions of the state space, i.e. the ‘noisy attractors’, which define the cell type and phenotype.

Results: We propose a gamma-Bernoulli mixture model clustering algorithm (BMM), tailored for quantizing states from gamma and Bernoulli distributed data, to determine the noisy attractors of stochastic GRN. BMM uses multiple data sources, naturally selects the number of states and can be extended to other parametric distributions according to the number and type of data sources available. We apply it to protein and RNA levels, and promoter occupancy state of a toggle switch and show that it can be bistable, tristable or monostable depending on its internal noise level. We show that these results are in agreement with the patterns of differentiation of model cells whose pathway choice is driven by the switch. We further apply BMM to a model of the MeKS module of Bacillus subtilis, and the results match experimental data, demonstrating the usability of BMM.

  S Wang , H Zhang , X Dai , R Sealock and J. E. Faber

Collaterals are arteriole-to-arteriole anastomoses that connect adjacent arterial trees. They lessen ischemic tissue injury by serving as endogenous bypass vessels when the trunk of 1 tree becomes narrowed by vascular disease. The number and diameter ("extent") of native (preexisting) collaterals, plus their amount of lumen enlargement (growth/remodeling) in occlusive disease, show remarkably wide variation among inbred mouse strains (eg, C57BL/6 and BALB/c), resulting in large differences in tissue injury in models of occlusive disease. Evidence suggests similar large differences exist among healthy humans.


To identify candidate loci responsible for genetic-dependent collateral variation.

Methods and Results:

Cerebral collateral number and diameter were determined in 221 C57BL/6xBALB/c F2 progeny, followed by linkage analysis to identify quantitative trait loci (QTL) for collateral number and diameter. Four QTL were obtained for collateral number, including epistasis between 2 loci. A QTL that was identical to the strongest QTL for collateral number on chromosome 7 (logarithm of the odds [LOD]=29, effect size=37%) was also mapped for collateral diameter (LOD=17, effect size=30%). Chromosome substitution strain analysis confirmed this locus. We also obtained a unique QTL on chromosome 11 for collateral remodeling after middle cerebral artery occlusion. Association mapping within the chromosome 7 QTL interval using collateral traits measured for 15 inbred strains delineated 172-kbp (P=0.00002) and 290-kbp (P=0.0004) regions on chromosome 7 containing 2 and 7 candidate genes, respectively.


We conclude that collateral extent and remodeling are unique, highly heritable complex traits, with 1 QTL predominantly affecting native collateral number and diameter.

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