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Background: The laparoscopic repair of non-midline ventral hernia (LNM) has been debated. The aim of this study is to analyze our experience performing the laparoscopic approach to non-midline ventral hernias (NMVHs) in Northwest Italy for 6 years., Methods: A total of 78 patients who underwent LNM between March 2008 and March 2014 in the selected institutions were analyzed. We retrospectively analyzed the peri- and postoperative data and the recurrence rate of four subgroups of NMVHs: subcostal, suprapubic, lumbar, and epigastric. We also conducted a literature review., Results: No difference was found between the four subgroups in terms of demographic data, defect characteristics, admission data, and complications. Subcostal defects required a shorter operating time. Obesity was found to be a risk factor for recurrence., Conclusions: In our experience, subcostal defects were easier to perform, with a lower recurrence rate, lesser chronic pain, and faster surgical performance. A more specific prospective randomized trial with a larger sample is awaited. Based on our experience, however, the laparoscopic approach is a safe treatment for NMVHs in specialized centers., (Copyright © 2016 IJS Publishing Group Ltd. Published by Elsevier Ltd. All rights reserved.)

Through the genotype/phenotype cosegregation analysis of an F(2) intercross, from the crossbreeding of stroke-prone spontaneously hypertensive rats (SHRSP) and stroke-resistant spontaneously hypertensive rats (SHR), we previously identified a quantitative trait locus for stroke on rat chromosome 5 (STR2) that colocalized with the genes encoding atrial and brain natriuretic peptides (ANP and BNP) and conferred a stroke-delaying effect. To further characterize ANP and BNP as candidates for stroke, we performed additional studies. Comparative sequence analysis revealed point mutations in both the coding and regulatory regions of ANP, whereas no interstrain differences were found for BNP. In in vitro studies in COS-7 and AtT-20 cells that were performed to test the relevance of a G-->A substitution at position 1125, a Gly-->Ser transposition in the SHRSP pro-ANP peptide resulted in different posttranslational processing of the SHRSP ANP gene product that was also associated with higher cGMP production (P<0.05). Furthermore, an analysis of a 5' end mutation affecting a PEA2 regulatory binding site in the 5' untranslated regulatory sequence of SHRSP ANP demonstrated a significantly lower ANP promoter activation in endothelial cells (P<0.05 versus the SHR ANP). In addition, the expression of ANP was significantly reduced in the brain, but not in the atria, of SHRSP compared with SHR (P<0.0001). No differences were detected with regard to BNP expression. The present results reveal substantial differences in ANP, but not BNP, structure and product among SHR and SHRSP, which supports a role of ANP in the pathogenesis of stroke in the SHRSP animal model.