Self-gripping Covidien™ ProGrip™ mesh versus polypropylene mesh in open inguinal hernia repair: multicenter short term results.

The purpose of this study was to compare clinical outcomes following sutureless ProGrip™ mesh repair to traditional Lichtenstein repair with polypropylene mesh secured with sutures. Data were collected prospectively and were analyzed for 57 male and 3 female patients with 60 inguinal hernias. All patients included underwent open surgical repair for inguinal hernia with polypropylene mesh or ProGrip mesh. In our two centres study sixty patients were operated; 30 were treated with Lichtenstein repair with polypropylene mesh (L group) and 30 with ProGrip mesh (P group) with or without fixation. The primary parameter measured was intensity of postoperative pain using visual analogue scale (VAS); other outcomes included assessment of early and late complication. VAS was assessed in 7 days and 4 months of the postoperative period. Our results show that VAS scored at the 7th postoperative day was 1.5 for the ProGrip mesh versus 4.4 in Lichtenstein repair group. The difference between groups was statistically significant (P=0.001). Surgery duration was significantly shorter in the P group (24.9 vs. 58.3 min; P=0.001). No recurrence was observed at 3 months in both groups. The 3-months follow-up has shown that time necessary to return to daily routine activity was significantly lower in the P group during the (P=0.001). Surgery duration, early and late postoperative, pain and return to daily routine activity rates were significantly reduced with self-gripping ProGrip mesh compared to Lichtenstein repair with polypropylene mesh.

17Beta-estradiol modulates endothelin-1 expression and release in human endothelial cells.

OBJECTIVE: In this study the role of 17beta-estradiol (E2) in the regulation of endothelin-1 (ET-1) mRNA expression and secretion was investigated in cultured human umbilical vein endothelial cells (HUVECs). METHODS: Endothelial cells were either deprived of or treated with 17beta-estradiol (10(-9), 10(-7) M) for 48 h. After the incubation, the effect of E2 on ET-1 gene expression was evaluated by Northern blot analysis. ET-1 release into the media was measured by radioimmunoassay after 6 h of incubation under basal conditions and upon stimulation with thrombin (4 U/ml). In addition, the cyclic guanosine 5'-monophosphate (cGMP) content of cells was assayed by immunoassay. In order to exclude the role of nitric oxide (NO) in E2-induced effects on endothelin-1 gene expression and secretion, nitric oxide synthase (NOS) inhibitor, N-nitro L-arginine methyl ester (1 mM) (L-NAME) was added to the media of some cultures. RESULTS: Incubation of HUVECs with 10(-9) and 10(-7) M E2 for 48 h resulted in a 30 and 47% inhibition of ET-1 mRNA expression, respectively. Incubation with E2 also decreased the basal and thrombin-stimulated ET-1 release while increasing the cGMP content of cells significantly. NOS inhibitor L-NAME increased the release of ET-1 from E2-incubated cells but did not alter the ET-1 release from hormone-deprived cells. However, ET-1 secretion of E2-treated cells were significantly less than the deprived ones. Northern blot analyses also demonstrated that inhibition of NOS only partly attenuated the effect of E2 on ET-1 gene expression. In the presence of L-NAME, treatment with 10(-7) M E2 caused a 12% decrease in ET-1 gene expression. CONCLUSION: The results demonstrate that E2 may play both direct and indirect role in regulation of ET-1 gene expression and production in human endothelial cells. E2-induced increase in NO but decrease in ET-1 production may partly explain the mechanism of the protective effects of the hormone on the cardiovascular system.