Objective To analyze the risk factors of paroxysmal atrial fibrillation (PAF) in very olderly hypertensive patients. Methods According to the electrocardiograph (ECG) and history data, two hundred and six older old-hypertensive patients were divided into PAF group (n=66) and sinus rhythm (SR) group (n=140). Data of age, gender, body mass index (BMI), the use of angiotension-converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs) and statin drug history, 24-hour ambulatory blood pressure monitoring (ABPM), echocardiography, pulse wave velocity (PWV), blood lipid profile and renal function were recorded in two groups. Logistic regression analyses of the relevant factors were compared between groups. Results Data of age, the diameter of the left atrium (LAD), the 1eft ventricular mass index (LVMI) and the PWV were significantly higher in PAF group than those of SR group [(88.92±3.42) years old vs. (86.36±4.67) years old, (39.00±6.66) mm vs. (33.54±7.77) mm, (132.49±14.83) g vs. (119.00±11.35) g, (13.45±4.85) m/s vs. (9.89±2.74) m/s, respectively]. Values of three acyl glycerin (TG), blood pressure smoothing index (SI) were lower in PAF group than those of SR group [(1.33±0.91) mmol/L vs. (1.95±1.29) mmol/L, 0.75±0.06 vs. 0.79±0.04, respectively]. Results of two classification Logistic regression analyses showed that the reduced SI, the enlarged LAD and LVMI and the increased PWV were the risk factors of PAF in very olderly hypertensive patients. Conclusion Unstable blood pressure, left atrial enlargement, left ventricular hypertrophy and arterial stiffness are the risk factors of PAF in very olderly hypertensive patients.

This study examined the possible role of p120ctn in the pathogenesis and development of pancreatic cancer. PANC-1 cells, a kind of human pancreatic carcinoma cell line, were cultured in this study. p120ctn was immunocytochemically detected in PANC-1 cells. The recombinant lentivirus vector was constructed to knock down the p120ctn expression of PANC-1 cells. Real-time quantitative PCR (RQ-PCR) and Western blotting were used to determine the expression of p120ctn and E-cadherin in PANC-1 cells after p120ctn knockdown. The adhesion, invasion and migration capacity of PANC-1 cells after p120ctn knockdown was detected by cell adhesion, invasion and migration assays. Cell growth was measured by the MTT method. Cell cycle and apoptosis were analyzed by fluorescence-activated cell sorting. The results showed that p120ctn knockdown led to significantly down-regulated E-cadherin and a reduced cell-to-cell adhesion ability in PANC-1 cells. shRNA-mediated knockdown of p120ctn reduced invasion and migration capacity of PANC-1 cells, inhibited cell growth, caused a significant decrease in the percentage of cells in G(1), an increase in S, and promoted apoptosis of PANC-1 cells. It was concluded that p120ctn plays a pivotal role in the proliferation and metastasis of pancreatic carcinoma, suggesting that p120ctn is a novel target for pancreatic carcinoma treatment.

This study examined the possible role of p120ctn in the pathogenesis and development of pancreatic cancer. PANC-1 cells, a kind of human pancreatic carcinoma cell line, were cultured in this study. p120ctn was immunocytochemically detected in PANC-1 cells. The recombinant lentivirus vector was constructed to knock down the p120ctn expression of PANC-1 cells. Real-time quantitative PCR (RQ-PCR) and Western blotting were used to determine the expression of p120ctn and E-cadherin in PANC-1 cells after p120ctn knockdown. The adhesion, invasion and migration capacity of PANC-1 cells after p120ctn knockdown was detected by cell adhesion, invasion and migration assays. Cell growth was measured by the MTT method. Cell cycle and apoptosis were analyzed by fluorescence-activated cell sorting. The results showed that p120ctn knockdown led to significantly down-regulated E-cadherin and a reduced cell-to-cell adhesion ability in PANC-1 cells. shRNA-mediated knockdown of p120ctn reduced invasion and migration capacity of PANC-1 cells, inhibited cell growth, caused a significant decrease in the percentage of cells in G(1), an increase in S, and promoted apoptosis of PANC-1 cells. It was concluded that p120ctn plays a pivotal role in the proliferation and metastasis of pancreatic carcinoma, suggesting that p120ctn is a novel target for pancreatic carcinoma treatment.
Catenins ; genetics ; Cell Line, Tumor ; Gene Silencing ; Humans ; Pancreatic Neoplasms ; genetics