










Ross Zafonte: Traumatic Brain Injury Clinical Trials from the Past for the Future
Experts Discuss Mass Casualty Incident Response
Researchers discuss advances in battlefield medicine
Doctors discuss challenges of traumatic brain injury
Carl Hauser, MD, FACS, FCCM:
BIDMC, HMS
Alfred Ayala, PhD:
Rhode Island Hospital/Brown University
Wolfgang Junger, PhD:
BIDMC, HMS
(No Video Available)
Presenters at the Oct. 16 Forum at Simches Research Center of Massachusetts General Hospital reported on their work involving the body’s reaction to shock.
Dr. Carl Hauser is a visiting professor of surgery at Beth Israel Deaconess Medical Center, and Harvard Medical School. He spoke on “Post-resuscitation Injury: Translational Approaches to Cell Signaling in Shock and Resuscitation.”
He said that trauma causes about 150,000 civilian deaths per year in the U.S. and is the leading cause of death up to age 45. More than 50,000 preventable deaths occur per year when trauma, hemorrhage, sepsis or shock triggers the systemic inflammatory response syndrome (SIRS). SIRS is a clinical descriptor for the body’s immune activation in response to the dead and dying tissues injured by trauma.
His lab studies neutrophils (PMN), the most common circulating white blood cells. After injury PMN can attack vital organs causing critical illness and death. To study such human illness as directly as possible, the lab assays the effects of substances released from clinical tissue injury sites on PMN.
Dr. Hauser said, “PMN activating substances often act by increasing the concentration of calcium in the cell. These events occur via a complex pathway of signals that lead from cell surface receptors to intracellular calcium storage organs, and then back to calcium channels on the cell surface.
“Injury radically changes the dynamics of such post-receptor PMN calcium mobilization, in part by altering the fatty composition of cell membranes. All these changes alter PMN stimulus-response coupling and cell function (for example, migration and bacterial killing).
“Since cellular calcium entry is a key regulator of PMN activity and is abnormally regulated after injury, we are developing strategies to modulate PMN-mediated inflammation after shock and trauma by modulating calcium signals.”
Also speaking was Wolfgang Junger, PhD, visiting professor of surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Department of Surgery. His topic was “Autocrine Regulation of Immune Cell Function.”
Dr. Junger said immune cells can play important roles in the defense of the host after trauma. He is studying chemotaxis, the ability of cells, such as neutrophils, to detect and move towards the source of chemoattractant signals.
He outlined some of the lab’s research, and said, “Our findings could lead to the development of novel therapeutic approaches that target PMN chemotaxis and thereby reduce the risk of host tissue damage caused by PMN in inflammatory diseases such as colitis, arthritis, asthma, and acute lung injury.”
Alfred Ayala, PhD, Division of Surgical Research/Department of Surgery, Rhode Island Hospital/Warren Alpert School of Medicine at Brown University, spoke on the topic of, “The Role of Systemic Immune Cell Signaling in While Body Ischemia/Reperfusion (I/R) Injury (Hemorrhagic Shock).”
Post a comment / start a discussion on the Forum Blog regarding this Forum.
![]()
Wikipedia
Start or edit a Shock and Resuscitation encyclopedia article on Wikipedia.
You can link to this page from the article using the following URL:
http://www.cimit.org/forum/forum-trauma-10.16.17.html
Learn more about Wikipedia.
![]()