Factors associated with survival in infants with congenital diaphragmatic hernia requiring extracorporeal membrane oxygenation: a report from the Congenital Diaphragmatic Hernia Study Group.

Objective: To identify factors associated with survival in patients with congenital diaphragmatic hernia (CDH) treated with extracorporeal membrane oxygenation (ECMO).

Methods: We retrospectively analyzed the data on 3100 patients with CDH in the Congenital Diaphragmatic Hernia Study Group from 82 participating pediatric surgical centers (1995-2004). Covariates considered included prenatal and perinatal clinical information, specifics of surgical repair, and the duration of extracorporeal support.

Total parenteral nutrition leads to alteration of hepatocyte cell cycle gene expression and proliferation in the mouse.

Total parenteral nutrition (TPN) is correlated with progressive liver injury. Such injury may be associated with either an increase or decrease in hepatocyte growth. The goal of these experiments was to determine TPN-related alterations in intrahepatic genes, as they relate with the cell cycle, using microarray techniques.

Effects of lipid administration on liver apoptotic signals in a mouse model of total parenteral nutrition (TPN).

Lipids are an important component of total parenteral nutrition (TPN), contributing the largest caloric load per volume of solution and providing essential fatty acids necessary for survival. However, lipids are known to be causative factors in oxidative stress, which are expressed via the Bcl-2 family of proteins and/or Fas-mediated apoptosis in several tissues. Interestingly, we have recently observed an increase in hepatocyte apoptosis with administration of TPN.

Hepatic P-glycoprotein changes with total parenteral nutrition administration.

Background: The mechanism(s) responsible for the development of parenteral nutrition-associated liver disease (PNALD) is unknown. Recently, a number of bile canalicular transport proteins have been identified that transport bile components out of hepatocytes. One group of these genes, multidrug resistance 1 (mdr1) and mdr2, encode P-glycoproteins.

Interleukin-6 changes tight junction permeability and intracellular phospholipid content in a human enterocyte cell culture model.

Proinflammatory cytokines and secretory phospholipase A(2) (sPLA(2)) are elevated in patients with inflammatory bowel disease (IBD). We previously reported that the proinflammatory cytokine IL-6 increased the expression of sPLA(2) (a hydrolyzer of phosphatidylcholine) and decreased membrane integrity in an intestinal epithelial cell culture model. To determine the physiological effects of the IL-6 mediated increase in sPLA(2) on decreased epithelial layer integrity, we investigated alterations of intracellular/secretory phospholipid (PL) composition in a cell culture model.

Effect of a high fat diet on lipid absorption and fatty acid transport in a rat model of short bowel syndrome.

Long chain fatty acids (LCFAs) appear to be powerful stimulants for small bowel adaptation in patients with short bowel syndrome (SBS). However, the dietary lipid content may alter intestinal lipid transport. The aim of this study was to investigate the effects of a high fat diet (HFD) on in vivo lipid absorption and molecular and cellular mechanisms of LCFAs uptake by the remaining bowel.

Lysophosphatidylcholine alters enterocyte monolayer permeability via a protein kinase C/Ca2+ mechanism.

The activity of phospholipase A(2) (PLA(2)) is elevated in the intestinal epithelia of patients with inflammatory bowel disease. We recently reported that PLA(2) mediates the hydrolysis of phosphatidylcholine (PC) to lysophosphatidylcholine (L-PC) when both are applied to the apical surface of cultures enterocyte monolayers, resulting in increased bacterial translocation (BT) and decreased transepithelial electrical resistance (TEER). However, the mechanism by which the converted L-PC affects tight-junction permeability (TJP) as reflected by decreased TEER is unknown.

The effect of mucin on bacterial translocation in I-407 fetal and Caco-2 adult enterocyte cultured cell lines.

Although the intestinal mucosa forms a crucial barrier between the host and the environment, bacterial translocation (BT) occurs frequently in neonates and may be a source of sepsis. The intestinal mucous gel layer is thought to be a vital component of the gut barrier and is composed, in part, of a family of glycoproteins known as mucins. Our aim was to study the effects of mucin on BT in an enterocyte cell-culture model using a fetal (I-407) and an adult (Caco-2) intestinal cell line.

The effect of phospholipids and mucin on bacterial internalization in an enterocyte-cell culture model.

A primary component of the intestinal mucous layer that functions as a barrier to luminal bacteria is mucin, a high-molecular-weight glucoprotein. In addition, the mucous layer also contains other important elements such as phospholipids (PLs), which may effect bacterial translocation (BTL). It has been reported that mucin inhibits Escherichia coli translocation; however, the effect of PLs on intestinal permeability is still controversial.