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Background Coronary heart disease (CHD) is the leading cause of death world wide. Coronary angiography is often used as an effective approach for the diagnosis of CHD. However, coronary angiography accounts for relatively low percentagein examination approaches due to the limitation of various conditions in primary care, and more meaningful biomarkers need to be explored to provide a basis for primary care physicians to diagnose and treat CHD. In the previous study of our research group, it is found that early growth response 3 (Egr3) gene may be a susceptibility factor in the heterogeneity of CHD pathogenesis, and there are few reports on the correlation between CHD and Egr3 gene and inflammatory biomarkers. Objective To investigate the correlation between Egr3, interleukin-6 (IL-6) and CHD, as well as their expression levels and the severity of coronary stenosis, so as to provide a favorable laboratory basis for clinical diagnosis and treatment inprimary care. Methods A total of 110 patients who admitted to the Fifth Affiliated Hospital of Xinjiang Medical University for CHD symptoms and completed coronary artery angiography (CAG) during June to December 2021 were collected and divided into the mild stenosis group (group A≤52 points, n=50) , moderate-severe stenosis group (group B>52 points, n=30) and control group (group C, n=30) according to the CAG results and median Gensini score (52 points) . Serum Egr3 and IL-6 levels of the included patients were measured by enzyme-linked immunosorbent assay. Results The IL-6 level in group B was higher than that in group A and group C (P

Objective: To investigate the mechanism of miR-133a in reversing neonatal rat cardiomyocyte hypertrophy induced by phenylephrine., Methods: A miR-133a precursor cDNA was used to construct an adenovirus vector, which was transfected into 293 cells to harvest miR-133a-containing virus. Neonatal rat cardiac myocytes treated by phenylephrine were exposed to miR-133a adenovirus, and the changes in cell area was measured; the expression levels of miR-133a and Acta1, Actc1, Actb, Myh6, Myh7, and BNP mRNAs were detected by quantitative RT-PCR., Results: Phenylephrine treatment increased the area of cardiomyocytes by more than 3 folds and significantly enhanced the expression levels of Acta1, Actc1, Actb, Myh6, Myh7 and BNP mRNAs. All these changes were obviously reverse by miR-133a treatment., Conclusion: miR-133a is an important regulator of phenylephrine-induced cardiomyocyte hypertrophy and negatively regulates this process.

Objective: To estimate the value of blastocyst culture for preimplantation genetic diagnosis (PGD)., Methods: Day 3 embryos were biopsied and analyzed with fluorescence in situ hybridization (FISH) technique. Embryos with normal FISH results were cultured into blastocysts, and the ones with better morphology scores were transferred. Fourteen embryos with abnormal FISH results were cultured into blastocysts. Part of the cells taken from the blastocysts were amplified by whole genomic amplification (WGA) and assessed by array-based comparative genomic hybridization (array-CGH) analysis., Results: Six blastocysts with normal FISH results were transferred in 5 cycles. Four healthy babies of 3 cycles were delivered. Another one was a singleton pregnancy but with embryo growth arrest, whose villus karyotype was normal. Fourteen embryos with abnormal FISH results were cultured into blastocysts and analyzed by array-CGH. Six blastocysts were normal by array-CGH., Conclusion: FISH combined with blastocyst culture may further ensure the accuracy of PGD result. Detection at the blastocyst stage can avoid false positive results and mosaic interferences on Day 3 stage and are therefore more authentic.