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Objective To discuss the expression and clinical significance of microRNA(miR)- 766 in chil-dren with polyarticular juvenile idiopathic arthritis (poly - JIA). Methods A total of 23 children with poly - JIA who received treatment at the Department of Rheumatology,the Affiliated Children′s Hospital of Capital Institute of Pediat-rics,from November 2014 to September 2016,were enrolled as research group,and 24 healthy children at the same age were selected as healthy control group,while 24 children with oligoarticular juvenile idiopathic arthritis (oligo - JIA) and 19 children with juvenile ankylosing spondylitis (JAS)were selected as case - control groups. The expression lev-els of miR - 766 in plasmas were detected by real - time quantitative polymerase chain reaction (qPCR). The clinical diagnostic values were analyzed by operating characteristic curve (ROC). Correlations between the expression levels of miR - 766 and clinical,laboratory results were analyzed by conducting Pearson correlation coefficient analysis. Results Compared with the healthy control group and case - control group,the expression levels of miR - 766 in poly - JIA group decreased,and the differences were statistically significant (t = 6. 897,6. 446,6. 218,all P < 0. 001). There was no statistical difference of miR - 766 levels in plasma between case - control groups and healthy control group (P >0. 05). Compared with the healthy control group,the area under ROC curve of miR - 766 was 0. 938 (95％ CI:0. 872 -1. 000),and when the cutoff value of miR - 766 was 6. 083 pmol/ L,the sensitivity was 87. 0％ and the specificity was 91. 7％ . Compared with oligo - JIA and JAS,the area under ROC curves of miR - 766 was 0. 908 (95％ CI:0. 819 -0. 996)and 0. 927 (95％ CI:0. 865 - 1. 000),respectively. Correlation analysis indicated that the level of miR - 766 in plasma of poly - JIA children was positively associated with hemoglobin (r = 0. 651,P < 0. 001),but negatively asso-ciated with the 28 - joint Disease Activity Score (DAS28)and the percentage of type 1 helper T cells(Th1％)(r =- 0. 434,P = 0. 038;r = - 0. 417,P = 0. 008). Conclusions The expression levels of plasma miR - 766 in poly - JIA are significantly decreasing. miR -766 may serve as an evaluation indicator for the diagnosis and prognosis of poly - JIA.
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Objective To explore the role of microRNA (miR)-22 and miR-1825 in the diagnosis and differential diagnosis of juvenile systemic lupus erythematous (JSLE).Methods The cases of JSLE hospitalized in Capital Institute of Pediatrics Teaching Hospital Affiliated to Peking University from June 2013 to May 2014 were selected as study group.The cases with systemic juvenile idiopathic arthritis (sJIA),nephrotic syndrome (NS),Kawasaki disease (KD),Henoch-Schonlein purpura(HSP) were selected as patients control group.The healthy children were selected as healthy control group.The expression levels of miR-22 and miR-1825 in the plasma of JSLE,sJIA,NS,KD,HSP and healthy children were detected by using real-time PCR respectively.Receiver operating characteristic curve (ROC) analysis was performed to evaluate the value of miR-22 and miR-1825 miRNA as a biomarker with the sensitivity and specificity.Three data bases,included Targetscan,PicTar and miRanda,were applied to predict the target gene.The target gene was analyzed by adopting Gene Ontology (GO) in terms of molecular function,biological process and cellular component,and by adopting Kyoto Encyclopedia of Genes and Genomes (KEGG) in terms of pathway.Results Compared with healthy children,the amount of miR-22 and miR-1825 in JSLE patients were lower,and there were significant differences(t =-3.076,-9.054,P ＜0.01,0.000 1).The levels of the miR-22 and miR-1825 miRNAs in controls of sJIA,NS,KD,HSP were significantly higher than those of JSLE (t =-4.410,-4.477,-4.494,-2.971,all P ＜ 0.000 1;t =-9.043,-6.045,-10.416,-8.712,all P ＜ 0.000 1),but there was no difference compared with healthy children(all P ＞ 0.05).The area under ROC curve(AUC) of miR-22 between JSLE and healthy children was 0.777.The AUC of miR-1825 between JSLE and healthy children was 1.000.The AUCs between JSLE and controls of sJIA,NS,KD,HSP of miR-22 were 0.731-1.000.The AUCs between JSLE and controls of sJIA,NS,KD,HSP of miR-1825 were 0.939-1.000.There was positive relation between the amount of miR-22 and complement C3 in plasma(r =0.493,P =0.027).Conclusions The amount of miR-22 and miR-1825 in the plasma of JSLE embrace the potential of distinguishing JSLE from healthy children,sJIA,NS,KD,HSP.MiR-22 has the ability to predict the activity of JSLE.
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Objective To evaluate the clinical effects of platelet-rich plasma in treatment of DeepⅡburn wounds. Methods Sixty eight cases of inpatients with Deep Ⅱburns were selected, whose age were from 1 to 65 years and their burn areas were between 5%~62%of total body surface area (TBSA). Deep gradeⅡburn of each sample was divided into two parts. Part A was the treatment group and part B was the control group.The burn wounds in the treatment group were treated with platelet-rich plasma and the counterpart in the control group were treated with SD-Ag. Healing time ,recovering rate and the frequency of dressing changes,frequency of changing the most innerlayer gauze and the rate of wound infection were also analyzed. Finally the laboratory abnormalities and adverse effect were monitored regularly. Results The healing time of the treatment group (16.5±3.1 ) d was shorter than that of the control group (19.5±3.8 ) d. The recovering rate of the treatment group was higher than that of the control group on the 14th and 17th day after treatment. There were statistically sig?nificant differences between these two groups (P<0.05). After two weeks’treatment, the internal and external dressing per?meability into wet gauze layers were 20.6 ± 1.7, which were significantly decreased than that in the control group 23.3 ± 5.9. The frequency of dressing changes was(7.2±1.1)times in treatment group versus(9.2±1.4)times in control group and the frequency of changing the inner most layer gauze was( 2.3±0.6)times in the treatment group versus(5.3±1.3)times in con?trol group. There were 5 inflammation reaction cases in the treatment group, but 13 cases in the control group. However, there was no statistic significance between the two group in the outcomes of bacterial culture, the laboratory abnormalities and the adverse effect. Conclusion Platelet-rich plasma can remarkably shorten the healing time,improve healing rate,re?duce frequency of dressing change and promote wound healing for deepⅡburn wound. PRP is a potential safety reagent in treating deepⅡburn wound.
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Objectlve To investigate the inhibition of Coxsackievirus B3(CVB3)infection in cardiac myocytes cultured by small interfering RNA(siRNA)-mediated RNA interference and to evaluate the feasibility of siRNA as the prophylaxis and therapy for CVB3 infection.Methods Cardiac myocytes were prepared in vitro and infected with CVB3,and transfected with siRNA by lipofectamin and electroporation.The numbers of beating cardiac myocytes were counted under the microscope.Neutral red staining was used to evaluate the mortality of cardiac myocytes.Antiviral activities of these siRNAs were estimated by observing cytopathic effect(CPE),plaque reduction assay,Western blot assay and RT-PCR.Results siRNA-3753,which aimed at sequence in 2B section of CVB3 genome,displayed a stronger inhibition of CVB3 infection through screening in HeLa cells,siRNA-3753,chosen to transfect cultured neonatal mice cardiac myocytes,Wag observed to keep a good states of growing and beating at 24 h after CVB3 infection.Whereas the cytopathic signature of controlled cells became stopping beating,round and finally the cell fell off the culture plate.The results showed that siRNA-3753 could protect cells significantly,98.1%inhibition of CVB3 replication with electroporation transfection and 78.2%inhibition of CVB3 with liposome transfection.Transfection efficiencies were 56.0 3%and 9.0%by electroporation and lipofectamin,respectively.Conclusion siRNA,which aims at sequence in 2B section of CVB3 genome,can inhibit CVB3 infection in cultured cardiac myocytes.