Hepatocellular carcinoma (HCC) is a common human malignancy. In this study, we aimed to investigate the serum levels of visfatin and miR-21 in HCC patients, to analysis the relationship between the pathological features and the plasma level of visfatin or miR-21, and to explore the roles of visfatin and miR-21 in migration of HCC cells. Our results showed that the serum levels of visfatin and miR-21 were significant higher in HCC patients than healthy subjects. The diagnostic sensitivity of serum visfatin was 82.5% and the specificity was 65.0%. The serum visfatin was significantly associated with the histology and metastasis. Visfatin induced miR-21 expression and cell migration in HepG2 cells. Transfection of miR-21 inhibitor suppressed the visfatin-induced migration in HCC cells. These results suggested that visfatin induced HCC cell migration via upregulation of miR-21, which provides a novel basis for the diagnosis of HCC.

The present study was conducted to investigate the effects of visfatin on the activation of hepatic stellate cells (HSC) and the possible underlying mechanism. HSC were isolated from the livers of Sprague‑Dawley rats by in situ perfusion of collagenase and pronase and a single‑step density Nycodenz gradient. The culture‑activated cells were serum‑starved and incubated with different concentrations of recombinant visfatin (0, 25, 50, 100 or 200 ng/ml) for 24 h. The expression of α‑smooth muscle actin (α‑SMA), collagen types I and III and connective tissue growth factor (CTGF) were then measured by reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and western blot analysis. The results demonstrated that 100 and 200 ng/ml concentrations of visfatin induced the expression of α‑SMA in culture‑activated rat HSC, which was accompanied by a significant increase in collagen types I and III, as confirmed by western blot and RT‑qPCR analyses. In addition, treatment of the HSC with certain concentrations of visfatin upregulated the expression of CTGF. These findings suggested that visfatin activated HSC and induced the production of collagen types I and III.

To compare the Stretta procedure with proton pump inhibitors for the treatment of nonerosive reflux disease (NERD). From July 2018 to April 2019, patients diagnosed with NERD and referred for treatment were enrolled. They were treated with either Stretta procedure or proton pump inhibitor (PPI) medication and followed-up for 6 months. The symptom control, quality of life, lower esophageal sphincter (LES) pressure, 24-hour pH parameters, PPI usage and satisfaction rate were evaluated. The complications were assessed. The outcomes of the 2 groups were analyzed and compared. Twenty-eight patients in the Stretta group and 21 patients in the PPI group completed the 6-month follow-up. No severe adverse events occurred in both groups. Both interventions were effective in improvement of symptom and quality of life. The symptom score improvement was significantly superior in the Stretta group compared to the PPI group (6.3 ± 3.4 vs 8.5 ± 4.1, P = .03). LES pressure increased significantly in the Stretta group compared to the PPI group (14.2 ± 4.4 mm Hg vs 10.0 ± 4.0 mm Hg, P < .01). Although both interventions improved 24-hour pH parameters, including number of acid episodes (P = .27), acid exposure time (P = .39), and DeMeester score (P = .28), no difference was found between the 2 groups. Complete PPI cessation rate (82% vs 52%, P = .03) as well as satisfaction rate (89% vs 57%, P = .02) was much higher in Stretta group than those in the PPI group The Stretta procedure was safe and effective in the short term for the management of NERD. The Stretta procedure resulted in higher LES pressure and achieved better improvement of symptom control and PPI cessation than did PPI in the short term.