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85Volume 2 Issue 1www.ctsjournal.com Introduction
 

Summary: 85Volume 2 Issue 1www.ctsjournal.com
Introduction
Bacterial infection, trauma, surgery, and biological stressors in
general, induce an acute inflammatory response characterized
by a cascade of events during which multiple cell types are
deployed to locate pathogens, recruit cells, and eventually
eliminate the offenders, thus restoring homeostasis. Under
normal circumstances, this inflammatory response is self-limited,
and once the pathogens are cleared, reparative processes begin
and the response then abates.1,2
Oftentimes pro-inflammatory
responses prevail or anti-inflammatory processes fail, and an
amplified runaway inflammation turns what is normally a
beneficial reparative process into a detrimental physiological
state. One component of the systemic inflammatory response
is a hypermetabolic state which is characterized by significant
alterations in the utilization of amino acids, glucose, and fatty
acids, leading to increased resting energy expenditure, a negative
nitrogen balance, hyperglycemia, and hyperlactatemia. This
results in net muscle protein catabolism with extensive amino

  

Source: Androulakis, Ioannis (Yannis) - Biomedical Engineering Department & Department of Chemical and Biochemical Engineering, Rutgers University

 

Collections: Engineering; Biology and Medicine