Objective:To develop a luminescent oxygen channeling immunoassay for pregnancy associated plasm a protein A.Methods:The monoclonal antibody of PAPP-A was labeled with biotin ,the polyclonal antibody of PAPP-A was coated on receptor particles.The LOCI reagents also contained sensitizer particles coated with streptavidin.The optimal test conditions and analytical per-formance of the method were studied.Results:The within-run and the between-run coefficients of variation were 5.91%-7.94% and 6.14%-9.69%,respectively;the analytical sensitivity was 2.8 mU/L and the function sensitivity was 4.6 mU/L,good linear in 2.8 mU/L-8 000 mU/L range;the recovery rate was 96.7%-100.3%.The interference rate of hemolysis , icterus and triglycerides were less than 10%; there is no Hook effect of PAPP-A concentrations up to 8 000 mU/L;the correlation coefficient between clinical samples detection results and Time resolved fluoroimmunoassay analysis results was 0.974.Conclusion:This LOCI can be used for the quantitative of serum PAPP-A,and detection performance in line with the requirements of clinical diagnostic reagents .

Objective:To explore the efficacy of breaking blood expelling stasis method accelerates hematoma resolution after intracerebral hemorrhage (ICH) and its potential mechanism.Methods:63 ICH patients confirmed by computer tomography (CT) scan from August 2019 to February 2020 were selected as the research objects and randomly divided into control group ( n=29, routine treatment plus placebo) and observation group ( n=34, routine treatment plus breaking blood expelling stasis granules). The changes of neurological function and hematoma volume were observed before and after treatment. At the same time, the ICH rat model was constructed to observe the changes of neurobehavior and hematoma volume after the intervention of breaking blood expelling stasis granules. The expressions of peroxidase proliferator-activated-receptor γ(PPARγ), CD11b and CD36 in the surrounding tissues of hematoma were detected by Western blot on the third day after the intervention. Results:After two weeks of treatment, the National Institutes of Health Stroke Scale (NIHSS) score and hematoma volume of the two groups decreased (all P<0.05), and the NIHSS score and hematoma volume of the observation group were significantly lower than those of the control group (all P<0.05). In addition, the changes of NIHSS score and hematoma volume in the observation group before and after treatment were significantly greater than those in the control group ( P<0.01). In animal experiments, the hematoma volume in the breaking blood expelling stasis group on the 14th day after ICH was significantly smaller than that in the ICH group [(9.8±4.9)mm 3 vs (17.6±6.4)mm 3,P<0.05], and the reduction of hematoma in the breaking blood expelling stasis group on the 7th and 14th day was significantly larger than that in the ICH group [(4.6±2.9)mm 3 vs (-2.1±1.6)mm 3, (14.3±3.8)mm 3 vs (4.2±2.8)mm 3, all P<0.01]. The percentage of right turn on 3rd, 7th and 14th day and the modified Neurological Severity Score (mNSS) on 7th and 14th day in the breaking blood expelling stasis group were lower than those in the ICH group (all P<0.05). Western blot analysis showed that the expressions of CD11b, CD36 and PPARγ in the breaking blood expelling stasis group on the third day after ICH were significantly higher than those in the ICH group (CD11b: 0.78±0.12 vs 0.49±0.11, P<0.05; CD36: 1.16±0.16 vs 0.80±0.11, P<0.05; PPARγ: 0.78±0.11 vs 0.37±0.10, P<0.01). Conclusions:Breaking blood expelling stasis can effectively accelerate intracerebral hematoma clearance and improve neurological outcome after ICH, and the mechanism maybe probably mediated by activating PPARγ and enhanced CD36, CD11b upregulation on microglia/macrophages, which resulting in facilitating erythrocyte endogenous phagocytosis.

Objective To explore the mechanism underlying ITGB1-induced drug resistance in gastric cancer based on the circRNA-miRNA-ITGB1 regulatory network.Methods Tumor tissue samples were collected from 21 patients with gastric cancer.The ITGB1 gene expression levels were determined using real-time fluorescent quantitative polymerase chain reaction,and circRNA sequencing was performed to compare the differences in circRNAs between patients with low and high ITGB1 expression.BGC-823 cells were trans-fected with si-circ_0027189,si-miR-455,or si-NC and divided into the si-circ_0027189,si-miR-455,or si-NC groups,respectively.The circ_0027189,miR-455,and ITGB1 expression levels in each group and the sensitivity to oxaliplatin were measured.Results The circRNA regulatory network showed that circ_0027189 regulated ITGB1 expression through miR-455.Compared to the si-NC group,the si-circ_0027189 group exhibited decreased expression levels of circ_0027189 and ITGB1,increased expression levels of miR-455,and reduced sensitivity to oxaliplatin.In contrast,the si-miR-455 group showed decreased expression levels of miR-455,increased expression levels of ITGB1,and enhanced sensitivity to oxaliplatin compared to the si-NC group.Conclusion circ_0027189 can increase ITGB1 expression levels by targeting miR-455 expression,ultimately increasing drug resistance in gastric cancer cells.