Prophylactic intraperitoneal mesh placement to prevent incisional hernia after stoma reversal: a feasibility study

Background

Incisional hernias in old stoma wounds occur in one-third of former stoma patients and pose a significant clinical problem. Parastomal hernias can be prevented by prophylactic mesh placement; however, no trial results are available for incisional hernia prevention after stoma reversal. In this feasibility study, we explore the safety of placing an intraperitoneal mesh to prevent incisional herniation after temporary stoma reversal.

Methods

Ten patients who underwent a low anterior resection with a deviating double-loop stoma for rectal cancer received an intraperitoneal parastomal mesh at the time of stoma formation. At stoma reversal, laparoscopy was performed and adhesions were scored. After reversal, the mesh defect was closed. Mesh and stoma complications were closely monitored. Incisional herniation was assessed at the 2-year follow-up after stoma reversal using ultrasonography.

Results

No infections occurred after mesh placement. After a median of 6 months, stomas were reversed. Laparoscopy could be performed in seven patients; all patients had adhesions (median of 25 % of mesh surface). In three patients, the bowel was involved; one required a laparotomy for bowel mobilization during stoma reversal. No adhesion-related morbidity was noted at any time. Except for one superficial wound infection after stoma reversal, no infectious complications were observed. After a median follow-up of 26 months, no incisional herniations were demonstrated.

Conclusions

Prophylactic mesh placement in temporary stoma formations seems safe and feasible and prevents incisional herniation 2 years after stoma reversal.     

Growth factor–heparan sulfate “switches” regulating stages of branching morphogenesis

The development of branched epithelial organs, such as the kidney, mammary gland, lung, pancreas, and salivary gland, is dependent upon the involvement and interaction of multiple regulatory/modulatory molecules, including soluble growth factors, extracellular matrix components, and their receptors. How the function of these molecules is coordinated to bring about the morphogenetic events that regulate iterative tip-stalk generation (ITSG) during organ development remains to be fully elucidated. A common link to many growth factor-dependent morphogenetic pathways is the involvement of variably sulfated heparan sulfates (HS), the glycosaminoglycan backbone of heparan sulfate proteoglycans (HSPG) on extracellular surfaces. Genetic deletions of HS biosynthetic enzymes (e.g., C5-epimerase, Hs2st), as well as considerable in vitro data, indicate that variably sulfated HS are essential for kidney development, particularly in Wolffian duct budding and early ureteric bud (UB) branching. A role for selective HS modifications by enzymes (e.g., Ext, Ndst, Hs2st) in stages of branching morphogenesis is also strongly supported for mammary gland ductal branching, which is dependent upon a set of growth factors similar to those involved in UB branching. Taken together, these studies provide support for the notion that the specific spatio-temporal HS binding of growth factors during the development of branched epithelial organs (such as the kidney, mammary gland, lung and salivary gland) regulates these complex processes by potentially acting as “morphogenetic switches” during the various stages of budding, branching, and other developmental events central to epithelial organogenesis. It may be that two or more growth factor-selective HS interactions constitute a functionally equivalent morphogenetic switch; this may help to explain the paucity of severe branching phenotypes with individual growth factor knockouts.     

Covariance adjustment for batch effect in gene expression data

Batch bias has been found in many microarray gene expression studies that involve multiple batches of samples. A serious batch effect can alter not only the distribution of individual genes but also the inter‐gene relationships. Even though some efforts have been made to remove such bias, there has been relatively less development on a multivariate approach, mainly because of the analytical difficulty due to the high‐dimensional nature of gene expression data. We propose a multivariate batch adjustment method that effectively eliminates inter‐gene batch effects. The proposed method utilizes high‐dimensional sparse covariance estimation based on a factor model and a hard thresholding. Another important aspect of the proposed method is that if it is known that one of the batches is produced in a superior condition, the other batches can be adjusted so that they resemble the target batch. We study high‐dimensional asymptotic properties of the proposed estimator and compare the performance of the proposed method with some popular existing methods with simulated data and gene expression data sets. Copyright © 2014 John Wiley & Sons, Ltd.     

Structure-Guided Rescaffolding of Selective Antagonists of BCL-XL

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