The preablation monocyte/ high density lipoprotein ratio predicts the late recurrence of paroxysmal atrial fibrillation after radiofrequency ablation.

BACKGROUND: The monocyte/high-density lipoprotein ratio (MHR) has emerged as a promising alternative biomarker in the fields of cardiovascular disease and atrial fibrillation (AF). This retrospective study was aimed to explore the predictive value of the MHR for the late recurrence of AF after radiofrequency ablation. METHODS: From April 2015 to October 2018, patients with paroxysmal AF who had undergone radiofrequency catheter ablation at Subei People's Hospital of Jiangsu Province were enrolled in our study. All the participants were observed until November 2019 after the procedure. During the postoperative follow up, the patients were categorized into the recurrence group and maintenance of sinus rhythm group based on who had experienced AF recurrence. RESULTS: One hundred twenty-five patients were diagnosed with paroxysmal AF, with an average age of 61.2 ± 9.3 years. Forty-seven patients had developed late recurrence during a mean follow up of 25.1 ± 12.0 months. The AF recurrence event rates were significantly increased in the highest MHR tertile compared with those in the lowest MHR tertile (22.0% vs. 57.1%; P < 0.05). On multivariate logistic regression analysis, the preablation MHR (OR = 1.34; 95% CI = 1.12 ~ 1.60; P = 0.001) and left atrial diameter (LAD) (OR = 1.21, 95% CI = 1.08 ~ 1.35; P = 0.001) were independent risk factors predicting the recurrence of AF after radiofrequency ablation. Furthermore, receiver operating characteristic (ROC) curve analysis revealed that the area under the curve (AUC) of the MHR was 0.712 (95% CI = 0.618 ~ 0.806; P = 0.000) and that of LAD was 0.739 (95% CI = 0.653 ~ 0.814; P = 0.000). Z-test found no significant difference between the MHR and LAD regarding the AUC (Z = 0.451; P = 0.652). CONCLUSION: An elevated preablation MHR was associated with an increased risk of the postoperative recurrence of AF. Additionally, the MHR independently predicted the late recurrence of paroxysmal AF after radiofrequency ablation, with the same predictive value as LAD.

[Expression Changes of Serum Transferrin Receptor and Its Mechanism in Children with Acute Leukemia].

OBJECTIVE: To investigate the expression changes of serum transferrin receptor（sTFR） and its related mechanism in children with acute leukemia（AL）. METHODS: Forty-six children with acute leukemia treated in our hospital from June 2016 to June 2017 were selected and enrolled in the AL group, 40 healthy children were enrolled in the control group. The related clinical data were recorded, including age, sex and CNSL level. RNA interference technology was used to silence TFR genes of KG-1a and TCHu147 cells, MTT method and flow cytometry were used to analyze the effect of TFR gene on proliferation and cell cycle of KG-1a cells and TCHu147 cells. Western blot was used to detect the level of cyclin related to leukemic cells after siRNA interference. RESULTS: The level of sTFR in AL patients was significantly higher than that of healthy people (P<0.05). The mRNA and protein expression levels of TFR in peripheral blood leukemic cells were all higher than those in healthy people (P<0.05). The level of sTFR closely related to the white blood cell（WBC） count, the proportion and absolute number of leukemic cells, hepcidin（Hepc） level, and risk grade in AL patients (P<0.05). The proliferation ability of KG-1a and TCHu147 cells after TFR siRNA interference was significantly inhibited (P<0.05). Fow cytometry showed that after the TFR siRNA interference, the ratio of KG-1a and TCHu147 cells in G0/G1 phase was 62.51%±5.39% and 63.37%±4.27%, respectively, which increased significantly as compared with the blank and negative control group (P<0.05); the ratio of KG-1a and TCHu147 in G2/M phase was 5.74%±1.34% and 7.37%±1.56%, respectively, which significantly decreased as compared with the blank control and the negative control group (P<0.05). CONCLUSION: The peripheral blood leukemic cells of AL patients can synthesize more TFR protein, lead into the increase of sTFR level. It can effectively interfere the division of leukemia cells by downregulating the expression of TFR gene.

ONZIN Upregulation by Mutant p53 Contributes to Osteosarcoma Metastasis Through the CXCL5-MAPK Signaling Pathway.

BACKGROUND/AIMS: Gain-of-function of mutant p53 is associated with a high rate of lung metastasis in osteosarcoma. To investigate the mechanism of mutant p53-induced osteosarcoma metastasis, expression array analysis was performed, comparing non-metastatic osteosarcomas from p53+/- mice with metastatic osteosarcomas from p53R172H/+ mice. Onzin (Plac8) was identified as one of the genes upregulated in p53R172H/+ mouse metastatic osteosarcomas. Accordingly, we investigated the role of ONZIN in human osteosarcoma metastasis. METHODS: ONZIN function and its downstream targets were examined in osteosarcoma cell lines. Assays related to tumorigenesis and metastasis, including cell migration, invasion, clonogenic survival, and soft agar colony formation, were performed in osteosarcoma cells. Additionally, mouse xenograft models were used to examine the role of ONZIN overpression in tumorigenesis in vivo. Lastly, 87 osteosarcoma patients were recruited to investigate the clinical relevance of ONZIN overexpression in metastasis and prognosis. RESULTS: ONZIN overexpression enhanced osteosarcoma cell proliferation, clonogenic survival, migration, and invasion independent of p53 status. Furthermore, ONZIN overexpression induced CXCL5 upregulation and resulted in increased ERK phosphorylation, which contributed to more aggressive osteosarcoma metastatic phenotypes. More importantly, overexpression of ONZIN in human osteosarcoma patients was closely associated with lung metastasis, poor prognoses, and survival. CONCLUSIONS: Overexpression of ONZIN promotes osteosarcoma progression and metastasis, and can serve as a clinical biomarker for osteosarcoma metastasis and prognosis.