<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>124(7)</volume><submitter>Shah I</submitter><pubmed_abstract>&lt;h4>Background&lt;/h4>High-content imaging (HCI) allows simultaneous measurement of multiple cellular phenotypic changes and is an important tool for evaluating the biological activity of chemicals.&lt;h4>Objectives&lt;/h4>Our goal was to analyze dynamic cellular changes using HCI to identify the "tipping point" at which the cells did not show recovery towards a normal phenotypic state.&lt;h4>Methods&lt;/h4>HCI was used to evaluate the effects of 967 chemicals (in concentrations ranging from 0.4 to 200 μM) on HepG2 cells over a 72-hr exposure period. The HCI end points included p53, c-Jun, histone H2A.x, α-tubulin, histone H3, alpha tubulin, mitochondrial membrane potential, mitochondrial mass, cell cycle arrest, nuclear size, and cell number. A computational model was developed to interpret HCI response</pubmed_abstract><journal>Environmental health perspectives</journal><pagination>910-9</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4937847</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Using ToxCast™ Data to Reconstruct Dynamic Cell State Trajectories and Estimate Toxicological Points of Departure.</pubmed_title><pmcid>PMC4937847</pmcid><pubmed_authors>Kavlock RJ</pubmed_authors><pubmed_authors>Liu J</pubmed_authors><pubmed_authors>Judson RS</pubmed_authors><pubmed_authors>Jack J</pubmed_authors><pubmed_authors>Crofton KM</pubmed_authors><pubmed_authors>Knudsen TB</pubmed_authors><pubmed_authors>Shah I</pubmed_authors><pubmed_authors>Setzer RW</pubmed_authors><pubmed_authors>Houck KA</pubmed_authors><pubmed_authors>Thomas RS</pubmed_authors><pubmed_authors>Martin MT</pubmed_authors><pubmed_authors>Reif DM</pubmed_authors><pubmed_authors>Richard AM</pubmed_authors><pubmed_authors>Dix DJ</pubmed_authors></additional><is_claimable>false</is_claimable><name>Using ToxCast™ Data to Reconstruct Dynamic Cell State Trajectories and Estimate Toxicological Points of Departure.</name><description>&lt;h4>Background&lt;/h4>High-content imaging (HCI) allows simultaneous measurement of multiple cellular phenotypic changes and is an important tool for evaluating the biological activity of chemicals.&lt;h4>Objectives&lt;/h4>Our goal was to analyze dynamic cellular changes using HCI to identify the "tipping point" at which the cells did not show recovery towards a normal phenotypic state.&lt;h4>Methods&lt;/h4>HCI was used to evaluate the effects of 967 chemicals (in concentrations ranging from 0.4 to 200 μM) on HepG2 cells over a 72-hr exposure period. The HCI end points included p53, c-Jun, histone H2A.x, α-tubulin, histone H3, alpha tubulin, mitochondrial membrane potential, mitochondrial mass, cell cycle arrest, nuclear size, and cell number. A computational model was developed to interpret HCI response</description><dates><release>2016-01-01T00:00:00Z</release><publication>2016 Jul</publication><modification>2025-04-19T21:53:15.172Z</modification><creation>2019-03-27T02:17:51Z</creation></dates><accession>S-EPMC4937847</accession><cross_references><pubmed>26473631</pubmed><doi>10.1289/ehp.1409029</doi></cross_references></HashMap>