AIM: To determine the role of LOX-1/PPAR pathway in regulating expression of adhesion molecules elicited by oxidizing low density lipoprotein(Ox-LDL) through Lectin-like oxidized low-density lipoprotein receptor-1(LOX-1) in human umbilical vein endothelial cells(HUVECs).METHODS: HUVECs were incubated with Ox-LDL,poly(I),carrageenan or 15-deoxy-△12,14-prostaglanding J2(15d-PGJ2).PPAR mRNA and protein were examined by real time RT-PCR and Western blotting.ICAM-1 and E-selectin were detected by RT-PCR and Western blotting respectively.RESULTS: Ox-LDL increased PPAR expression in HUVECs,which was inhibited by pretreatment of HUVECs with LOX-1 blockers.Preincubation of HUVECs with 15d-PGJ2 attenuated the expression of intercellular adhesion molecule-1(ICAM-1) and E-selectin in response to Ox-LDL.Upregulation of ICAM-1 and E-selectin mediated by Ox-LDL were suppressed more significantly by the combination of 15d-PGJ2 and polyinosonic acid as compared to either 15d-PGJ2 or polyinosonic acid alone.CONCLUSION: The results indicate that Ox-LDL exerts a biphasic effects on inflammatory response.It evokes harmful effects by inflammatory injury on one side and protective effects by triggering the LOX-1/ PPAR signaling pathway on the other hand.

Current occupational health and occupational medicine teaching content focused on the detection of harmful factors,and more belonged to validation experiments.Closed-end management of experimental teaching,experimental report-based performance evaluation methods and single model of teaching methods reduced the students' study interesting,lack of problem-solving abilities.Therefore,it is necessary to optimize the experimental curriculum,adopt an open experimental teaching,build a reasonable experimental evaluation system and promote the diversification of teaching model.

AIM: To explore the effect of anthocyanin on cholesterol efflux and elucidate its possible molecular mechanism. METHODS: Mouse Peritoneal macrophages were loaded with 50 mg/L AcLDL to induce macrophage-derived foam cells. Cholesterol efflux from macrophage-derived foam cells induced by anthocyanin was determined by enzymatic methods. PPAR-? mRNA and protein expression in macrophage-derived foam cells was assayed by quantitative PCR and western blotting. RESULTS: Anthocyanins had the capacity of promoting cholesterol efflux from mouse peritoneal macrophage-derived foam cells and increased PPAR-? mRNA and protein expression. CONCLUSION: Anthocyain-induced cholesterol efflux may be related to its enhancing PPAR-? mRNA and protein expression.

Objective To explore the molecular mechanism of blood_stasis syndrome (BSS) by studying the changes of gene expression of endothelin (ET) and constit utive nitric oxide synthase (cNOS) in vascular endothelial cells (VEC) cultured w ith BSS rabbit serum. Methods ET_1 mRNA expression and cNOS mRNA expression were analyzed by semi_quantitative reverse transcription and polymerase chain re action method. Results ET_1 mRNA expression level was increased and cNOS mRN A expression level was decreased in VEC cultured with BSS rabbit serum (Group A) as compared with VEC cultured with normal rabbit serum (Group B) or without rab bit serum (Group C) (P

Objective:To explore the clinical characteristics and pathogenic variant in a child with Cantú syndrome (CS).Methods:A male who was admitted to the Children′s Hospital Affiliated to Zhengzhou University on February 23, 2022 was selected as the study subject. Clinical data of the child was collected. Peripheral blood samples of the child and his parents were collected and subjected to whole-exome sequencing (WES). Candidate variant was verified by Sanger sequencing. This study was approved by Medical Ethics Committee of the Children′s Hospital Affiliated to Zhengzhou University (Ethics No. 2023-K-087).Results:The child, a 3-year-and-2-month-old male, was born with hirsutism, with heavy hair all over the body and peculiar facial features. Routine echocardiography 1 month before had discovered atrial septal defect. Sequencing revealed that the child has harbored a heterozygous c. 2438G>C (p.S813T) variant of the ABCC9 gene, which was de novo in origin. Based on the guidelines from the American College of Medical Genetics and Genomics (ACMG), the c. 2438G>C variant was classified as likely pathogenic (PS2+ PM2_Supporting+ PP3). Conclusion:The heterozygous c. 2438G>C variant of the ABCC9 gene probably underlay the pathogenesis of CS in this child.