Sequences surrounding the transcription start sites of <i>Mef2C</i>, <i>Nkx2-5</i>, and <i>Gata4</i> genes in R1 mouse ESCs subjected to oxidative stress.

<p>Sequences surrounding the transcription start sites of <i>Mef2C</i>, <i>Nkx2-5</i>, and <i>Gata4</i> genes in R1 mouse ESCs subjected to oxidative stress.</p

G∙C to C∙G transversions at exon 1 of the <i>Tbx5</i> gene in R1 mouse ESCs subjected to oxidative stress.

<p>G∙C to C∙G transversions at exon 1 of the <i>Tbx5</i> gene in R1 mouse ESCs subjected to oxidative stress.</p

Occupancy of Ogg1 at the <i>Tbx5</i> promoter.

ChIP-qPCR results showed specific reduced occupancy by Ogg1 (white bars) at the Tbx5 promoter in oxidative stressed R1 mouse ESCs while occupancy by histone H3 did not change. Mean ± standard deviation (SD), ***p < 0.001, one-sided t-test.</p

Primer sequences for biomarker genes of cardiac specification.

Primer sequences for biomarker genes of cardiac specification.</p

Establishment of the Hoogsteen base pairing-mediated PCR-Sequencing assay for 8-oxoG lesions in DNA.

<p>(A) pUC19oxoG(+) was prepared by site-directed mutagenesis, (B) 8-oxoG lesion was identified by Hind III resistance, and (C) Hoogsteen base pairing-mediated 8-oxoG to T transversion. T4: T4 DNA ligase, HIII: Hind III restriction enzyme.</p

Effects of oxidative stress on R1 mouse ESC proliferation and differentiation.

<p>(A) Proliferation of ESCs after oxidative stress induced for two days by removing 2-mercaptoethanol (2ME) from ESC medium. *<i>p</i> < 0.05, Welch t-test. Means of fold changes with standard errors were presented. (B) Different EB morphologies from (+)2ME and (-)2ME media (bar = 100 μm) and (C) the percentages of beating EBs were observed from oxidative-stressed ESCs vs. controls (**<i>p</i> < 0.01, one-sided t-test).</p

Differential expression levels of 8-oxoG repair genes <i>Ogg1</i> and <i>PolB</i> in ESCs induced by oxidative stress.

<p>Relative mRNA levels of (A) <i>Ogg1</i> mRNA and (B) <i>PolB</i>. Gapdh was used as an internal control. Mean ± SD, **<i>p</i> < 0.01, ***<i>p</i> < 0.001, one-sided t-test. (C) Levels of Ogg1 and PolB proteins by Western blotting. α-tubulin was used as an internal control.</p

Delta neutrophil index as a predictor of mortality and neurologic outcomes at 30 days after out-of-hospital cardiac arrest.

<p>The technique of Contal and O’Quigley based on the log-rank test was used to assess prognostic value of the delta neutrophil index (DNI) by considering time to event. Cut-off points for DNI measured on day 1 were (A) DNI >8.4 (p = 0.01), HR = 3.227 (95% CI, 1.495–6.967; p = 0.001) for 30-day mortality and (B) DNI >8.4 (p = 0.01) HR = 2.718 (95% CI, 1.508–4.899; p<0.001) for neurologic outcomes at 30 days. Cut-off points for DNI measured on day 2 were (C) DNI >12.9 (p<0.001), HR = 3.292 (95% CI, 1.662–6.519; p<0.001) for 30-day mortality and (D) DNI >10.5 (p = 0.004), HR = 1.709 (1.051–2.778; p = 0.02) for neurologic outcomes at 30 days. Duration: Days after out-of-hospital cardiac arrest.</p

Univariate Cox proportional analysis for 30-day mortality and neurologic outcomes.

<p>CPC: cerebral performance category, ACS: acute coronary syndrome, ROSC: return of spontaneous circulation, CPR: cardiopulmonary resuscitation, BUN: blood urea nitrogen, Cr: creatinine, RDW: red cell distribution width, APACHE II: Acute Physiology and Chronic Health Evaluation II, DNI: delta neutrophil index</p><p>*: <i>p</i><0.05.</p><p>Univariate Cox proportional analysis for 30-day mortality and neurologic outcomes.</p

Multivariate Cox proportional hazard model for 30-day mortality and neurologic outcomes.

<p>*: <i>p</i><0.05.</p><p>Multivariate Cox proportional hazard model for 30-day mortality and neurologic outcomes.</p