Intestinal atresia and necrotizing enterocolitis: Embryology and anatomy.

The primitive gut originates at week 3 of gestation from the endoderm, with posterior incorporation of the remaining embryo layers. Wnt, Notch and TLR4 pathways have been shown to play central roles in the correct development of the intestine. The classical hypothesis for intestinal atresia development consists of failure in bowel recanalization or a vascular accident with secondary bowel reabsorption. These have been challenged due to the high frequency of associated malformations, and furthermore, with the discovery of molecular pathways and genes involved in bowel formation and correlated defects producing atresia. Necrotizing enterocolitis (NEC) has a multifactorial pathogenesis with prematurity being the most important risk factor; therefore, bowel immaturity plays a central role in NEC. Some of the same molecular pathways involved in gut maturation have been found to correlate with the predisposition of the immature bowel to develop the pathological findings seen in NEC.

Anionic and Cationic Silver Nanoparticle Binding Restructures Net-Anionic PC/PG Monolayers with Saturated or Unsaturated Lipids.

We have examined the interactions between polymer-coated anionic (Ag-COOH) and cationic (Ag-NH) silver nanoparticles, and net-anionic lipid monolayers using dynamic surface pressure measurements. Monolayers composed of saturated or monounsaturated mixtures of anionic phosphatidylglycerol (PG) and zwitterionic phosphatidylcholine (PC) lipids (3:1 molar ratio) were used to determine how lipid packing and monolayer phase state influence the extent of nanoparticle binding and the monolayer response. Anionic Ag-COOH inserted into saturated dipalmitoyl-PC/PG (DPPC/DPPG) and dioleoyl-PC/PG (DOPC/DOPG) monolayers at a low initial surface pressure (10 mN m-1) and caused lipid condensation at high initial surface pressures (20 and 30 mN m-1). Hydrophobic interactions were responsible for insertion, while electrostatic and charge-dipole interactions with PCs were responsible for condensation. In contrast, cationic Ag-NH inserted only into saturated DPPC/DPPG monolayers and otherwise led to lipid condensation. For Ag-NH, adsorption was driven primarily by electrostatic interactions with PGs. Analysis of the subphase Ag and phosphorus concentrations confirmed that Ag-NH had a higher degree binding compared to Ag-COOH, and that the monolayer response was not due to lipid extraction.