ObjectiveTo investigate the mechanism by which Notoginsenoside R1 （NGR1） ameliorates hypoxia/reoxygenation （H/R）-induced injury in AC16 human cardiomyocyte cell lines through the regulation of mitophagy. MethodsCommon genes linked to hypoxia/reoxygenation injury and mitophagy were identified by intersecting data from GeneCards and MitoCarta databases. AC16 cell viability was assessed via CCK-8 assay under varying NGR1 concentrations （0， 6.25， 12.5， 25， 50， 100， 200， 300， 400， 500 μmol/L）. AC16 cells were divided into the following groups： control group （Control）， model group （H/R）， and treatment groups （H/R + NGR1 at 100， 200 and 300 μmol/L）. Mitochondrial membrane potential （ΔΨm） was measured using 5，5'，6，6'-tetrachloro-1，1'，3，3'-tetraethylbenzimidazolylcarbocyanine iodide （JC-1） staining. Transcriptional levels of mitophagy-related genes （Parkin， Pink1， P62） were quantified by reverse transcription-quantitative PCR （RT-qPCR）. Protein expression of mitophagy-related markers （Parkin， Pink1， P62， and LC3BⅡ） was evaluated via Western blot analysis. Mitochondrial ultrastructure was visualized by transmission electron microscopy （TEM）. ResultsCompared to the control group， cell viability in the H/R group significantly decreased （P<0.01）. Treatment with NGR1 at concentrations above 100 μmol/L significantly enhanced the cell viability of AC16 cells compared to the H/R group （P<0.01）. H/R induced a significant decrease in mitochondrial membrane potential （P<0.01）， which was restored by NGR1 treatment （P<0.01）. The mRNA levels of Parkin， Pink1， and P62 in the H/R group were upregulated compared to the control group （P<0.05）， while NGR1 intervention downregulated their expression （P<0.05）. Protein expression levels of Parkin， Pink1， and LC3BⅡ in the H/R group significantly increased， while P62 expression decreased compared to the control group （P<0.01）. In contrast， different doses of NGR1 treatment significantly reduced the expression of Parkin， Pink1， and LC3BⅡ while increasing P62 expression （P<0.05）. TEM revealed that the mitochondrial structure in the H/R group was severely disrupted， with fragmented and disorganized cristae， which was alleviated by NGR1. ConclusionNGR1 ameliorates H/R-induced AC16 cell injury， and its mechanism may be associated with modulating the Pink1/Parkin pathway to suppress excessive mitophagy.

Objective:To determine the content of the released nickel ion through the 7 extraction media to extract the Ni-Ti wires and to plot the curve of the released nickel ion so as to identify a leaching medium that can be substituted for blood for in vitro Ni release evaluation. Methods:The release of Ni through microwave digestion/inductively coupled plasma mass spectrometry (ICP-MS) in the goat serum was determined. Because of the high content of Ni release, it could be determined by diluting the extraction medium, and other extraction media could be determined directly. Ni release standard curves were plotted by the release amount and different time point variables. Though the different extraction media Ni release curves confirm the specificity of extraction media instead of blood.Results:By analyzing the Ni release curves of seven leaching media, it was found that none of these seven extraction media was suitable for the evaluation of Ni release in in vitro leaching media. Considering the safety of the leaching medium and the simplicity of preparation, hydrochloric acid solution was chosen as the leaching medium, but the concentration needed to be diluted accordingly. Finally, a hydrochloric acid solution was created as an alternative to blood for the in vitro study of Ni release from Ni-Ti alloy cardiovascular products, with a volume fraction of 0.005%. Conclusions:The in vitro leaching medium that can replace blood was found to be hydrochloric acid for the time being, but its concentration was too high, resulting in too much Ni release as well, which deviated from the actual situation. Therefore, the hydrochloric acid solution was diluted step by step, and the Ni release curve was examined until it was close to the clinical release level, and the actual concentration was determined, thus laying a solid foundation for the subsequent evaluation of the safety and risk.

Objective To summarize the manifestation of pediatric eosinophilic gastroenteritis by ultrasound and discuss the diagnostic value of ultrasonography in pediatric eosinophilic gastroenteritis. Methods The ultrasonic appearances of 31 cases of pediatric eosinophilic gastroenteritis confirmed by clinics and pathology were reviewed and analyzed. Results Nineteen of 31 cases were observed in association with eosinophilic infiltration of other organs which were diagnosed as idiopathic hypereosinophilic syndrome.Eosinophilic cystitis was the most common among the complications(89.4%,17/19).Twelve of 31 cases were diagnosed as eosinophilic gastroenteritis without complications.The endoscopic appearances of eosinophilic gastroenteritis were nonspecific which include erythematous,hyperemia edema,and partiality erosion changes.Endoscopy demonstrates increased numbers of eosinophils in the propria of stomach and the duodenum.Ultrasound features of the gastroenteritis appeared diffuse or the parts of gastrointestinal tract.The most common sites of eosinophilic gastroenteritis were the stomach and duodenum.Involvement of muscle layer and serosal layer showed wall thickening of cyclic annular and uniformity.Ultrasound might show nodular or irregular thickening of the folds in the gastric antrum when the submucosa were thickening.The mucosal layer involvement was not easy to be found by ultrasound.The echo of serous layer and submucosa associated with the disease stage.The thickening of surrounding omentum and mesenteric tissue,echo enhancement and nonspecific hyperplastic mesenteric lymph nodes infiltrated with eosinophils might be present.Eosinophilic ascites could often be detected.Conclusions Ultrasound has obvious advantages in the diagnosis of pediatric eosinophilic gastroenteritis,and the ultrasonic changes of pediatric eosinophilic gastroenteritis are characterized.Ultrasonography can provide the possible diagnosis when combined with inflammatory of other organs,especially cystitis inflammatory changes.