Objective:To establish a candidate reference procedure for the enumeration of cell particles in urine and applied to the multi-center performance evaluation of an automated urine formed elements analyzer.Methods:According to the standardized mannual microscopic examination of fresh non-centrifuged urine samples and the recommended reference method for enumeration of cell particles in urine published by ISLH, we established a candidate reference procedure for the enumeration of cell particles in urine. From four class A tertiary hospitals′ clinical laboratories, three rigorous trained technicians per hospital tested the same specimen respectively using the reference procedure. Each specimen was repeatedly counted 5 times, obtaining the quantitative results of cell particles were obtained in urine. Four hospitals used the established candidate reference measurement procedure and the automated urine formed elements analyzer to detect 40 to 60 urine specimens from September 2020 to January 2021, and evaluate the established reference method, meanwhile evaluate the accuracy and consistency of the each count from automated urinalysis analyzer.Results:Using the candidate reference measurement procedures, the coefficient of variation of results derived from three trained technicians per hospital was less than 6.98% (red blood cells), 6.99% (white blood cells), 13.94% (epithelial cells) and met the quality requirements. The performance evaluation results of automated urine formed elements analyzer showed that the accuracy of red blood cells, white blood cells and epithelial cells met the requirements (bias≤4.98%) and was well consistent with the reference measurement procedure ( R2≥0.989). Conclusions:A candidate reference measurement procedure for the enumeration of urine cell particles was successfully established with satisfactory precision and accuracy. This procedure was applied to multicenter performance evaluation of an automated urine formed elements analyzer with good accuracy and consistency.

Objective:To investigate the protective effect and mechanism of isorhamnetin on myocardial injury in rats with acute myocardial infarction (AMI).Methods:The AMI rat model was established by coronary artery left anterior descending ligation. The SD rats were divided into sham-operated group, model group, Fasudil group (30 mg/kg) and low-, medium-, and high-dose (25, 50, 100 mg/kg) groups. Each group had 5 rats. They were administrated intragastric, once a day, and were treated for 14 d. Color Doppler ultrasonography was used to detect cardiac function by measuring left ventricular end-systolic diameter (LVESd), left ventricular end-diastolic diameter (LVEDd), and left ventricular long-axis shortening fraction (FS). Myocardial infarct size was detected by TCT staining. Superoxide dismutase (SOD), malondialdehyde (MDA), interleukin (IL)-6, IL-1β, and tumor necrosis factor-α (TNF-α) levels in rat serum were detected by ELISA and TUNEL assay for the cardiomyocyte apoptosis index. Cysteinyl aspartate specific proteinase-3 (Caspase-3) activity in myocardial tissue was detected by the Caspase-3 activity assay kit, and the expression of Bcl-2 associated X protein (Bax) and B-cell lymphoma-2 (Bcl-2) proteins in myocardial tissue was detected by Western Blot.Results:Compared with the sham operation group, the FS, SOD content, and expression levels of Bcl-2 protein in the model group were significantly decreased (all P<0.05), and LVEDd, LVESd, myocardial infarct size, MDA content, IL-6 content, TNF-α content, IL-1β content, apoptosis index, Caspase-3 activity, and Bax protein expression level were significantly increased (all P<0.05). There was no significant difference between the low concentration of isorhamnetin and the model group (all P>0.05). However, the above changes caused by the construction model after treatment with Fasudil and medium- and high-concentrations of isorhamnetin significantly reversed (all P<0.05). Conclusions:Isorhamnetin can improve cardiac function and protect myocardial injury in AMI rats by reducing oxidative stress and inflammatory damage to cardiomyocytes and inhibiting cardiomyocyte apoptosis.