Adverse events associated with resuscitation and thrombolysis.

<p>14 of 104 patients could be discharged with good neurological outcome.</p

Effect of the time until thrombolysis onset on outcome.

<p>(A) Time dependent ROSC, (B) time dependent successful hospital discharge.</p

Time-outcome relation.

<p>Time of thrombolysis onset, CPR time after thrombolysis and total CPR duration in patients with and without successful CPR (A), in patients with hospital discharge vs. those who died (B), and in patients with hospital discharge versus those with secondary lethality after initially successful CPR.</p

KCR1 suppresses spontaneous action potential activity.

<p>(A) Representative original recordings of spontaneous action potentials of control neonatal rat ventricular cardiomyocytes. (B) KCR1 infection suppressed spontaneous beating activity in neonatal cells. Action potential artificially induced by a depolarizing pulse in a quiescent neonatal cardiocyte. (C) KCR1^siRNA infection accelerated spontaneous beating activity in neonatal cells. (D) Overexpression and knock-down of endogenous KCR1 resulted in a significant (_*, p<0.001) decrease and increase of the beating rate, respectively. For data see text.</p

Effect of KCR1 and KCR1^siRNA on single native I_f channel gating in one-channel patches.

<p>(A) Comparison between single native I_f channels of control neonatal ventriculocytes (left), KCR1-infected (middle) and KCR1^siRNA-infected cells (right). Recording technique as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0001511#pone-0001511-g003" target="_blank">Figure 3</a>. Scale bars, 50 ms, 3 pA for unitary current traces, and 1 s, 20 fA for ensemble average current. (B) Enhanced expression and knock-down of KCR1 significantly shifted the half-maximal activation of I_f to more negative and more positive potentials, respectively. Channel activation was measured by the parameter availability, plotted against the test potential and then determined by using the Boltzmann function. For data see text. (C) Open-time histograms: KCR1 exhibited no effect on the number of native I_f open states, whereas KCR1^siRNA induced an increase of the number of open states. Number of open events (square root) were plotted against the logarithmically binned open time durations for I_f alone and with exogenous KCR1 or KCR1^siRNA (pooled one- and multi [n≤3]-channel experiments). (D) Closed-time histograms: KCR1 did not affect the number of native I_f closed states, while KCR1 knock-down resulted in a loss of one closed state. Number of closed events (square root) were plotted against the logarithmically binned closed time durations for I_f alone and with exogenous KCR1 or KCR1^siRNA (pooled one-channel experiments only).</p

Single-channel parameters of native I_f in adult and neonatal cardiomyocytes modulated by KCR1 and KCR1^siRNA

<p>Modulation of single-channel parameters of native I_f (control) by KCR1 overexpression (KCR1-infected) and knock-down of endogenous KCR1 (KCR1^siRNA-infected) in adult and neonatal cardiomyocytes. Holding potential −35 mV, test potential −90 mV. I_peak was measured from ensemble average currents. For closed time and latency analysis, only experiments containing just one detected open level were used for calculation. Numbers of experiments given in parentheses indicate number of experiments with only one channel in the patch. Pooled data are presented as mean±SEM.</p>*<p>p<0.05 vs. control;</p>#<p>p<0.05 vs. KCR1-infected.</p

Effect of KCR1 on single native I_f channel gating in one-channel patches.

<p>(A) Comparison between single native I_f channels of control adult ventriculocytes (left) and KCR1-infected cells (right). Recording technique as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0001511#pone-0001511-g003" target="_blank">Figure 3</a>. Scale bars, 50 ms, 2.5 pA for unitary current traces, and 1 s, 60 fA for ensemble average current. (B) KCR1 significantly shifted I_f activation to more negative potentials. Channel activation was measured by the parameter availability, plotted against the test potential and then determined by using the Boltzmann function. For data see text. (C) Open-time histograms: KCR1 exhibited no effect on the number of native I_f open states. Number of open events (square root) were plotted against the logarithmically binned open time durations for I_f alone and with exogenous KCR1 (pooled one- and multi [n≤3]-channel experiments). (D) Closed-time histograms: KCR1 did not affect the number of native I_f closed states. Number of closed events (square root) were plotted against the logarithmically binned closed time durations for I_f alone and with exogenous KCR1 (pooled one-channel experiments only).</p

A high MELD-XI score identified sicker patients with multiple preconditions.

<p>Normally distributed data points are expressed as mean ± standard deviation.</p

Gating of single recombinant HCN2 and KCR1-cotransfected I_HCN2

<p>Single-channel parameters of HCN2 (control) and KCR1-cotransfected I_HCN2 channels in CHO-cells. Holding potential −35 mV, test potential −90 mV. I_peak was measured from ensemble average currents. For closed time and latency analysis, only experiments containing just one detected open level were used for calculation. Numbers of experiments given in parentheses indicate number of experiments with only one channel in the patch. Pooled data are presented as mean±SEM.</p>*<p>p<0.05 vs. control.</p>1)<p>in this case n = 12 experiments were taken for conductance calculation.</p

KCR1 reduces current size of native I_f in neonatal rat cardiomyocytes.

<p>(A–C) Original whole-cell recordings of I_f in neonatal rat cardiocytes: (A) control, (B) KCR1-infected and (C) KCR1^siRNA-infected. (D) Mean current densities of I_f in neonatal cells show that KCR1 overexpression reduced I_f, while suppression of endogenous KCR1 by KCR1^siRNA significantly increased native I_f(_*, p<0.001). For data see text.</p