Butyric Acid

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/142237/1/jpen0443.pd

Research in Jeopardy

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/142292/1/jpen1075.pd

Tumour necrosis factor‐α‐induced loss of intestinal barrier function requires TNFR1 and TNFR2 signalling in a mouse model of total parenteral nutrition

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/99095/1/jphysiol.2013.253518.pd

Effects on Varying Intravenous Lipid Emulsions on the Small Bowel Epithelium in a Mouse Model of Parenteral Nutrition

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/141978/1/jpen0775.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/141978/2/jpen0775-sup-0001.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/141978/3/jpen0775-sup-0002.pd

Total Body Sodium Depletion and Poor Weight Gain in Children and Young Adults With an Ileostomy

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/141860/1/ncp0397.pd

Changes to the Intestinal Microbiome With Parenteral Nutrition

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/142098/1/ncp0798.pd

Intestinal Microbial Diversity and Perioperative Complications

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/141018/1/jpen0392-sup-0001.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/141018/2/jpen0392.pd

Dissociation of E-cadherin and Β-catenin in a mouse model of total parenteral nutrition: a mechanism for the loss of epithelial cell proliferation and villus atrophy

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/65985/1/jphysiol.2008.162719.pd

Clinical Research: Establishing a Comprehensive Database for Home Parenteral Nutrition: Six Years of Data

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/141734/1/ncp0279.pd

Distraction-Induced Intestinal Growth: The Role of Mechanotransduction Mechanisms in a Mouse Model of Short Bowel Syndrome

Novel strategies are needed to address the problem of patients with short bowel syndrome. We previously demonstrated a three-fold lengthening of pig bowel after 2 weeks of applied distractive forces, but we have not elucidated the mechanisms facilitating this growth. We used a mouse model of distraction-induced enterogenesis. High molecular weight polyethylene glycol (PEG) osmotically stretched an isolated small bowel segment (PEG-stretch). Significant increases in villus height and crypt depth and in intestinal epithelial cell length and numbers suggested epithelial remodeling in addition to proliferation during enterogenesis. LC-MS/MS analysis showed a two-fold upregulation of α-actinin-1 and -4. We also demonstrated that p-focal adhesion kinase (FAK), FAK, α-actinin, and Rac1 were significantly upregulated and that F-actin was relocalized in PEG-stretch versus controls. Blockade of the phosphotidyl inositol 3? kinase pathway failed to influence the increase in proliferation or decline in apoptosis after stretch, suggesting alternative signaling pathways are used, including MEK and P38MAPK, which were both upregulated during enterogenesis. Our data suggests that several known mechanotransduction pathways drive distraction-induced enterogenesis.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/140227/1/ten.tea.2013.0383.pd