22 research outputs found
Branched‐Chain Amino Acids in Patients With Hepatic Encephalopathy
Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/142130/1/ncp0097.pd
Oxandrolone Treatment in Adults with Severe Thermal Injury
Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/90285/1/phco.29.2.213.pd
Review of the Refeeding Syndrome
Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/142310/1/ncp0625.pd
Metabolic and Nutritional Aspects of Acute Renal Failure in Critically Ill Patients Requiring Continuous Renal Replacement Therapy
Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/141368/1/ncp0176.pd
Infectious Complications With Nondaily Versus Daily Infusion of Intravenous Fat Emulsions in Non–Critically Ill Adults
Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/141413/1/ncp0737.pd
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. To address the mechanism of this apoptosis, we investigated the effects of parenteral lipid administration on apoptotic signaling in a mouse model. C57BL/6J male mice received physiologic saline and standard chow (control) or standard TPN solution with (TPN+L) or without lipid (TPN-L) emulsion. After 7 days of infusion, apoptosis increased in the TPN+L at a significantly higher rate compared with control and TPN-L groups ( p <0.05). Both TPN, with and without lipids, suppressed the pro-apoptotic signals Bid and Bcl-xs ( p <0.05). In contrast, TPN with lipid increased the expression of Fas and both the pro-apoptotic factor Bad and the anti-apoptotic factor Bcl-xl ( p <0.05). These changes may contribute to TPN-induced hepatocyte injury (apoptosis) or suppress the ability of liver hepatocytes to regenerate.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47162/1/383_2003_Article_1115.pd
Relationship Between Hyperglycemia and Infection in Critically Ill Patients
Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/90178/1/phco.2005.25.7.963.pd
Amino Acid Requirements in Critically Ill Patients with Acute Kidney Injury Treated with Continuous Renal Replacement Therapy
Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/90284/1/phco.28.5.600.pd
Dosing and Monitoring of Trace Elements in Long‐Term Home Parenteral Nutrition Patients
Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/141314/1/jpen0736.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/141314/2/jpen0736-sup-0001.pd