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Objective To discuss the effect of the bedside shielding protection on the first and second operators against position radiation in percutaneous coronary intervention.Methods The surface entrance dosage rate for the first and second operators at 125 cm height with and without radiation protection shielding (provided separately) were measured.The t-test was used for statistical analysis of arithmetic mean values of dosage rates.And the effect of bedside shielding protection was calculated.Results The position radiation dosage rate at which the first operator exposed was significantly higher than that for the second in the case of no bedside protection (t =97.1-2 263.0,P ＜ 0.05),whereas the dosage rate at which the first operator (except for the left foot position) exposed was significantly lower than that for the second in the case of no bedside protection (t =-80.9-275.1,P ＜ 0.05).The shielding effect of bedside protection on the first and second operators was in the range of 92.26％-99.36％ and 27.83％-97.90％,respectively.Conclusions The bedside protection may effectively reduce position radiation dose to patients and the use of bedside protection changed the trends in the dose distribution in operators' standing region.Attention should be focused on the radiation protection of the second operators in daily work by making full use of bedside protection.
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Objective To determine the protective effects and potential mechanism of activating retinoid X receptor (RXR) on rat cardiomyocytes H9c2 against hypoxia/reoxygenation (H/R) induced oxidative injury.Methods The model of H-/R injury was established with hypoxia for 2 hours and reoxygenation for 4 hours in cardiomyocytes of H9c2,and 9-cis-retinoic acid (c-RA) was obtained as RXR agonist,and HX531 as RXR antagonist.Cultured cardiomyocytes were randomly (random number) divided into four groups:sham group,H/R group,H/R + c-RA-pretreated group (100 nmol/L c-RA) and H/R +c-RA + HX531-pretreated group (2.5 μmol/L HX531).We measured the cell viability by MTT (methyl thiazolyl tetrazolium),apoptosis rate of cardiomyocytes by using flow cytometry,and mitochondrial membrane potential by JC-1 fluorescent probe,protein levels of Bcl-2,Bax and cleaved Caspase-9 with Western blot.All measurement data were expressed as (-x ± s),and statistically analyzed using One-way ANOVA and Dunnett-t test.Differences were considered significant when P ＜ 0.05.Results Pretreatment with RXR agonist enhanced cell viability,reduced apoptosis ratio,stabilized mitochondrial membrane potential.Dot blotting experiments demonstrated that under H/R stress conditions,Bcl-2 protein level decreased,while Bax and cleaved Caspase-9 increased.The c-RA administration prior to H/R stress prevented these effects,however,overall protective effects of activating RXR on rat cardiomyocytes against H/R induced oxidative injury were abolished when pretreated with RXR pan-antagonist HX531.Conclusions Activating RXR has the protective effects against H/R injury in rat cardiomyocytes H9c2 through attenuation of mitochondria apoptosis signaling pathway.