Navigating the new, transplanted self: how recipients manage the cognitive risks of organ transplantation.

The physiological risks of organ transplantation are well documented, but more poorly understood are the sociological ways in which organ recipients redefine themselves in reaction to physiological risks and social changes accompanying transplantation. This article analyses transplantation as a procedure that is not only physiologically risky but also poses risk to the social identity of the recipient, and explores how transplant recipients cognitively navigate transplantation surgery from waiting for to recovering after a transplant. It builds on previous sociological exploration of risk as a socially constructed process mediating experiences of health and illness with a focused contribution on explaining how individuals navigate risks posed to their social identities by major biophysical transformations. This article pointedly analyses narratives of fourteen organ recipients and the four dominant phases of identity management that emerged to create what we have coined as the new 'transplanted self', indicating the varied ways the individual social self emerges in response to the social risks of transplantation. We conclude that a better understanding of the recipient experience will contribute to improved care in the transplantation field.

Effect of DNase I treatment and neutrophil depletion on acute limb ischemia-reperfusion injury in mice.

OBJECTIVE: Extracellular traps (ETs) consisting of DNA-protein complexes formed after tissue injury contribute to the inflammatory and thrombosis cascades, thereby exacerbating injury. Exogenous DNase I has been suggested as a therapeutic strategy to limit injury in the brain and myocardium. These studies were designed to evaluate the effects of exogenous DNase I treatment on skeletal muscle injury after acute hindlimb ischemia-reperfusion (IR) injury in mice and to determine whether neutrophils are a major source of ETs in postischemic muscle tissue. METHODS: C57BL6 mice were subjected to 1.5 hours of tourniquet ischemia and 24 hours of reperfusion with and without human recombinant DNase I treatment. A separate set of mice was subjected to neutrophil depletion (ND), followed by the same intervals of IR. Laser Doppler imaging and tissue harvesting were done at 24 hours for assessment of limb perfusion, muscle fiber injury, adenosine triphosphate (ATP) level, markers of inflammation, thrombosis, and formation of ETs. RESULTS: DNase I treatment significantly reduced detection of ETs in postischemic muscle but did not alter skeletal muscle fiber injury, levels of proinflammatory molecules, or ATP level. DNase I treatment did enhance postischemic hindlimb perfusion, decreased infiltrating inflammatory cells, and reduced the expression of thrombin-antithrombin III. ND resulted in a significant yet small reduction in ETs in the postischemic muscle. ND did not alter skeletal muscle fiber injury, hindlimb perfusion, or ATP levels. CONCLUSIONS: These data suggest that neither DNase I treatment nor ND was protective against IR injury, even though both decreased detection of ETs in skeletal muscle after IR. Neutrophils are not the only source of ETs after IR.

Hind limb ischemia-reperfusion injury in diet-induced obese mice.

BACKGROUND: Obesity is a major risk factor for the development of diabetes. Limb ischemia-reperfusion injury (IR) is a common clinical problem in diabetics who have compromised lower extremity perfusion. This study compared the histologic, metabolic, and functional outcomes after hind limb IR in diet-induced obese (DIO) and non-diabetic (ND) mice during the acute and the regenerative phases of IR. METHODS: DIO and ND mice were subjected to 1.5 h unilateral hind limb ischemia followed by 1- or 28-d IR. Muscle morphology, metabolic, and genomic stress were evaluated at days 1 and 28 IR; Acute inflammation and thrombosis were only measured at day-1 IR. At day 28, IR, skeletal muscle contractility, and maturation were also assessed. RESULTS: At day-1 IR, similar levels of acute muscle fiber necrosis were seen in both groups. DIO mice demonstrated substantially greater inflammatory, prothrombotic, and genomic stress responses, which were also associated with a greater reduction in energy substrates and Akt phosphorylation. At 28d, there was no difference in the peak forces generated in the hind limbs for the two groups. DIO mice had reduced fatigue resistance compared with ND and larger areas of fat accumulation although there was no significant difference in muscle fiber maturation. CONCLUSIONS: DIO mice had an exacerbated acute response to IR with enhanced metabolic deficit, fat accumulation, and defective functional recovery during the regenerative phase of IR. These changes in fatigue resistance reflect compromised functional recovery after IR injury and have relevance for the functional recovery of patients with metabolic syndrome and insulin resistance.