James Ross
Case Western Reserve University, OH·Medicine & Clinical Research·Early-career
Trauma is a leading cause of death and long-term disability in the United States. Nearly one in four survivors of severe injury develops serious complications such as organ failure, blood clots or infection.
- Fields
Medicine & Clinical Research
Physiology
Biochemistry
- Topics
trauma
hemolysis
free hemoglobin
- Grants
- 1 known grant, through Jun 2031
What they work on
- Define how free hemoglobin lowers nitric oxide availability and triggers endothelial injury in human endothelial cell models, and test whether haptoglobin, a hemoglobin-binding protein, reduces these effects.
- Use a multicenter observational trauma cohort to determine how haptoglobin genotype relates to hemolysis markers, endothelial dysfunction and clinical outcomes after injury.
- Evaluate in a prospective study of injured patients how hemolysis affects nitric oxide signaling, vascular function and tissue perfusion, using biospecimens, transcriptomics and near-infrared spectroscopy.
More about the research
One possible cause is hemolysis, the bursting of red blood cells, which releases free hemoglobin into the blood. Free hemoglobin may soak up nitric oxide, a gas that keeps blood vessels relaxed, and cause oxidative stress. This could damage the endothelium, the thin layer of cells lining blood vessels.
Why it matters
Patients who survive severe injury could benefit if doctors could predict who is likely to develop organ failure, clots or infection. Identifying haptoglobin genotype and hemolysis markers as risk factors may yield predictive biomarkers, and clarifying how free hemoglobin harms blood vessels could point to new strategies to prevent these life-threatening complications.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Jamie Meegan
University of South Alabama, AL·Physiology·Early-career
Test whether cell-free hemoglobin released from fragile red blood cells during sepsis disrupts the lung microvascular endothelial cell barrier by oxidizing low-density lipoprotein to oxidized LDL.
Kenneth Remy
Case Western Reserve University, OH·Medicine & Clinical Research
Measure how plasma proteins bind heme, the iron core of hemoglobin, during sepsis and after red blood cell transfusion compared with chronic hemolytic diseases and healthy conditions, using human patient samples.
Pooneh Bagher
University of Nebraska Medical Center, NE·Physiology
Determine whether hemoglobin alpha in artery-lining endothelial cells becomes glycated in a mouse model of diabetes, including at sites within its putative eNOS-binding domain.
The school
Case Western Reserve University: 34 labs on PI Pages, $643M a year on research, 213 research doctorates a year.
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