Prediction of return of spontaneous circulation in outof-hospital cardiac arrest with non-shockable initial rhythm using point-of-care testing: a retrospective observational study

BACKGROUND:Out-of-hospital cardiac arrest(OHCA) is a public health concern, and many studies have been conducted on return of spontaneous circulation(ROSC) and its prognostic factors.Rotational thromboelastometry(ROTEM?), a point-of-care testing(POCT) method, has been useful for predicting ROSC in patients with OHCA, but very few studies have focused on patients with non-shockable rhythm. We examined whether the parameters of POCT could predict ROSC in patients with OHCA and accompanying non-shockable rhythm.METHODS:This is a single-center, retrospective observational study. Complete blood count,blood gas, and ROTEM POCT measurements were used. This study included patients with nontraumatic OHCA aged 18 years or older who were transported to the emergency department and evaluated using POCT between January 2013 and December 2021. The patients were divided into the ROSC and non-ROSC groups. Prehospital information and POCT parameters were compared using receiver operating characteristic(ROC) curve analysis, and further logistic regression analysis was performed.RESULTS:Sixty-seven and 135 patients were in the ROSC and non-ROSC groups,respectively. The ROC curves showed a high area under the curve(AUC) for K^(+) of 0.77(95%confidence interval [CI]:0.71–0.83) and EXTEM amplitude 5 min after clotting time(A5) of 0.70(95%CI:0.62–0.77). The odds ratios for ROSC were as follows:female sex 3.67(95%CI:1.67–8.04);K^(+)0.64(95%CI:0.48–0.84);and EXTEM A5 1.03(95%CI:1.01–1.06).CONCLUSION:In OHCA patients with non-shockable rhythm, K^(+) level and the ROTEM parameter EXTEM A5 may be useful in predicting ROSC.

Anti-proliferation and apoptosis-inducing effects of sodium aescinate on retinoblastoma Y79 cells

AIM:To investigate the anti-proliferation and apoptosisinducing effects of sodium aescinate(SA)on retinoblastoma Y79 cells and its mechanism.METHODS:Y79 cells were cultured at different drug concentrations for different periods of time(24,48,and 72 h).The inhibitory effect of SA on proliferation of Y79 cells was detected by the cell counting kit-8(CCK-8)assay,and the morphology of Y79 cells in each group was observed under an inverted microscope.An IC50 of 48 h was selected for subsequent experiments.After pretreatment with SA for 24 and 48 h,cellular DNA distribution and apoptosis were detected by flow cytometry.Real-time qunatitative polymerase chain reaction(RT-qPCR)and Western blot were used to assess changes in related genes(CDK1,CyclinB1,Bax,Bcl-2,caspase-9,caspase-8,and caspase-3).RESULTS:SA inhibited proliferation and induced apoptosis of Y79 cells in a time-dependent and concentrationdependent manner.Following its intervention in the cell cycle pathway,SA can inhibit the expression of CDK1 and Cyclin B1 at the mRNA and protein levels,and block cells in the G2/M phase.In caspase-related apoptotic pathways,up-regulation of Bax and down-regulation of Bcl-2 caused caspase-9 to self-cleave and further activate caspase-3.What’s more,the caspase-8-mediated extrinsic apoptosis pathway was activated,and the activated caspase-8 was released into the cytoplasm to activate caspase-3,which as a member of the downstream apoptotic effect group,initiates a caspase-cascade reaction that induces cell apoptosis.CONCLUSION:SA inhibits the proliferation of Y79 cells by arresting the cell cycle at the G2/M phase,and induces apoptosis via the caspase-related apoptosis pathway,indicating that SA may have promising potential as a chemotherapeutic drug.