ABSTRACT
Objective@#To explore the mediating effect and gender difference of mobile phone use in the association between different types of childhood abuse experiences and sleep quality of medical students, so as to provide reference for promoting sleep quality of medical students.@*Methods@#A longitudinal study design method was used to select freshmen and sophomores in two medical colleges in Anhui Province from November to December 2019, follow up data were collected from May to June 2020, and a total of 6 879 students were included in this study. Spearman correlation was used to analyze the association between baseline childhood abuse experiences, baseline mobile phone use and follow up sleep quality. Bootstrap program and Process software were applied to test the mediating effect of mobile phone use in the relationship between childhood abuse and sleep quality.@*Results@#Childhood abuse experiences were positively correlated with mobile phone use and sleep quality score ( r = 0.27 , 0.24, P <0.01), and mobile phone use was positively correlated with sleep quality score ( r =0.31, P <0.01). In the total sample, after adjusting for confounding factors, mobile phone use played a partial mediating role in childhood abuse experiences (including emotional abuse, physical abuse, sexual abuse) and sleep quality, and the mediating effect was 18.08% (18.12%, 17.15%, 24.09%). The mediating effect of mobile phone use on the relationship between childhood emotional abuse, sexual abuse, childhood abuse and sleep quality in girls(18.32%, 28.05%, 18.24%) was higher than in boys(17.81%, 18.94%, 17.63%).@*Conclusion@#Mobile phone use has a mediating effect on the relationship between childhood abuse and sleep quality, controlling mobile phone overuse may contribute to improving the sleep quality for those who have experienced childhood abuse.
ABSTRACT
<p><b>OBJECTIVE</b>To evaluate the change of endothelin-1 (ET-1) in the mini-swine model of acute myocardial infarction (AMI) and reperfusion and the effect of Tongxinluo (TXL) on it, and to explore the possible mechanism of no-reflow.</p><p><b>METHODS</b>Forty mini-swines were randomized into 5 groups: the model group, the small,middle and large dose of TXL groups and the sham-operated group, 8 in each group. The AMI reperfusion model was established by coronary ligation for 3 hrs followed with relaxation for 1 hr. Plasma ET-1 content before and after AMI, and after reperfusion was determined respectively by radioimmunoassay. The ET-1 mRNA expression in myocardial tissue of normal, ischemic and no-reflow area were respectively quantified by reverse transcription-polymerase chain reaction.</p><p><b>RESULTS</b>(1) Compared with before AMI, levels of plasma ET-1 at the time points of 5 min and 3 hrs after AMI, 5 min and 1 hrs after reperfusion in the model group were significantly raised, showing an increasing tendency (all P < 0.01). But the increment in the middle and large dose of TXL groups were all lower than that in the model group (P < 0.05). (2) In the model and the TXL groups, levels of ET-1 in myocardial tissue of ischemic and no-reflow area were significantly higher than those in the normal area, and the increment in no-reflow area was higher than that in ischemic area (all P < 0.01). Compared with the model group, significant lowering of ET-1 in ischemic area was only shown in the middle and large dose of TXL groups (P < 0.01). (3) In the model and the TXL groups, ET-1 mRNA expression in ischemic area was significantly higher (all P < 0.01), while it in no-reflow area was significantly lower than that in the normal area respectively (all P < 0.01). The raised ET-1 mRNA expression in the middle and large dose TXL groups was significantly lowered when compared with that in the model group (P < 0.01).</p><p><b>CONCLUSION</b>The endothelium injury might be one of the important mechanisms for no-reflow phenomenon. TXL might reduce the no-reflow by protecting endothelium cells. was significantly higher (all P < 0.01), while it in no-reflow area was significantly lower than that in the normal area respectively (all P < 0.01). The raised ET-1 mRNA expression in the middle and large dose TXL groups was significantly lowered when compared with that in the model group (P < 0.01). Conclusion The endothelium injury might be one of the important mechanisms for no-reflow phenomenon. TXL might reduce the no-reflow by protecting endothelium cells.</p>