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Biomedical subjects

A Ghanekar

Publications and source records attributed to A Ghanekar.

6 recordsLinked to original sources
PubMed2001

Small bowel transplantation.

Small bowel transplantation has become the treatment of choice for patients with chronic gut failure whose illness cannot be maintained on home parenteral nutrition. Outcomes have improved as a result of refinements in patient selection, surgical techniques, and the prevention, diagnosis, and treatment of graft rejection. Early listing is important because of the shortage of organ donors. Rejection rates are still 50% or more, despite the use of potent immune suppression. Sepsis rates are also higher for patients who have had small bowel transplantation than for those who have received other organs because of bacterial translocation from the gut secondary to preservation injury and graft rejection. Graft and patient survival rates after small bowel transplantation are comparable to rates after lung transplantation. Successful transplant recipients resume unrestricted oral diets.

Chronic Disease↗
PubMed1997

Rupture of an abdominal aortic aneurysm causes priming of phagocytic oxidative burst.

PURPOSE: The purpose of this investigation was to determine whether rupture and repair of an abdominal aortic aneurysm induced activation of phagocyte oxidant burst, reflecting a systemic inflammatory state, when compared with elective abdominal aortic aneurysm (AAA) repair. METHODS: Blood samples were harvested from 22 patients with elective AAA and 15 patients with ruptured AAA. Phagocyte oxidant activity was measured in response to a panel of activators with luminol and lucigenin as chemiluminescent substrates. Activity of the complement pathways was measured with plasma levels of C3a des arg. RESULTS: Elective AAA repair resulted in significant elevation in phagocyte count and oxidative activity after surgery in response to maximal dose phorbol myristate acetate (PMA) when compared with the baseline sample. In patients with ruptured AAA the oxidative activity of phagocytes was significantly increased in response to both unopsonized zymosan (899.8 +/- 192 ruptured vs 300 +/- 40 elective, p < 0.01) and maximal dose PMA (8769 +/- 2011 vs 3508 +/- 382, p < 0.01) compared with elective cases at the initial sampling. Phagocyte priming has occurred by way of two distinct pathways: receptor-mediated (unopsonized zymosan, CR3 receptor) and receptor-independent (PMA, protein kinase c). CONCLUSIONS: Rupture of an AAA resulted in priming of the phagocyte oxidant capacity before operative repair compared with elective AAA. Phagocyte activation is a critical component of the systemic inflammatory response that may contribute to the high incidence of systemic organ dysfunction and death in this patient group.

Acridines↗