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Expression data from total knee arthroplasty patients

ABSTRACT: Ischaemic preconditioning is a method of protecting tissue against ischaemia-reperfusion injury. It is an innate protective mechanism that increases a tissue's tolerance to prolonged ischaemia when it is first subjected to short burst of ischaemia and reperfusion. It is thought to provide this protection by increasing the tissue's tolerance to ischaemia, therby reducing oxidative stress, inflammation and apoptosis in the preconditioned tissue. We used microarrays to investigate the genomic response induced by ischaemic preconditioning in muscle biopsies taken from the operative leg of total knee arthroplasty patients in order to gain insight into the ischaemic preconditioning mechanism.

ORGANISM(S): Homo sapiens

PROVIDER: GSE21164 | GEO | 2010/04/02

SECONDARY ACCESSION(S): PRJNA126619

REPOSITORIES: GEO

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Expression data from total knee arthroplasty patients

Project description:Ischaemic preconditioning is a method of protecting tissue against ischaemia-reperfusion injury. It is an innate protective mechanism that increases a tissue's tolerance to prolonged ischaemia when it is first subjected to short burst of ischaemia and reperfusion. It is thought to provide this protection by increasing the tissue's tolerance to ischaemia, therby reducing oxidative stress, inflammation and apoptosis in the preconditioned tissue. We used microarrays to investigate the genomic response induced by ischaemic preconditioning in muscle biopsies taken from the operative leg of total knee arthroplasty patients in order to gain insight into the ischaemic preconditioning mechanism. Patients undergoing primary knee arthroplasty were randomised to control and treatment (ischaemic preconditioning) groups. Patients in the treatment group received a preconditioning stimulus immediately prior to surgery. The ischaemic preconditioning stimulus consisted of three five-minute periods of tourniquet insufflation on the lower operative limb, interrupted by five minute periods of reperfusion. All patients had a tourniquet applied to the lower limb after the administration of spinal anaesthesia, as per normal protocol for knee arthroplasty surgery. Muscle biopsies were taken from the quadriceps muscle of the operative knee at the immediate onset of surgery (T0) and at 1 hour into surgery (T1). Total RNA was extracted from biospies of four control and four treatment patients and hybridised to the Affymetrix Human U133 2.0 chip.

2010-04-12 | E-GEOD-21164 | biostudies-arrayexpress

Expression data from intact and ventilation-preconditioned murine lungs

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Coral thermal tolerance: tuning gene expression to resist thermal stress

Project description:Thermal history plays a role in the response of corals to subsequent heat stress. Prior heat stress can have a profound impact on later thermal tolerance, but the mechanism for this plasticity is not clear. The understanding of gene expression changes behind physiological acclimatization is critical in forecasts of coral health in impending climate change scenarios. Acropora millepora fragments were preconditioned to sublethal bleaching threshold stress for a period of 10 days; this prestress conferred bleaching resistance in subsequent thermal challenge, in which non-preconditioned coral bleached. Using microarrays, we analyze the transcriptomes of the coral host, comparing the bleaching-resistant preconditioned treatment to non-preconditioned and control treatments. This experiment compared host gene expression of Acropora millepora across control, non-preconditioned, and preconditioned treatments. Fragments were sampled prior to preconditioning (Day 4), following 10 days of thermal preconditioning (Day 20), and after two (Day 23), four (Day 25), and eight days (Day 29) of 31M-BM-0C thermal challenge. The analysis implements 45 arrays, representing 5 sampling points of three treatments (n=3).

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Project description:Recombinant tissue-type plasminogen activator (tPA) is the fibrinolytic drug of choice to treat stroke patients. However, a growing body of evidence indicates that besides its beneficial thrombolytic role, tPA can also have a deleterious effect on the ischaemic brain. Although ageing influences stroke incidence, complications and outcome, age-dependent relationships between endogenous tPA and stroke injuries have not been investigated yet. Here, we report that ageing is associated with a selective lowering of brain tPA expression in the murine brain. Moreover, our results show that albumin D site-binding protein (DBP) as a key age-associated regulator of the neuronal transcription of tPA. Additionally, inhibition of DBP-mediated tPA expression confers in vitro neuroprotection. Accordingly, reduced levels of tPA in old mice are associated with smaller excitotoxic/ischaemic injuries and protection of the permeability of the neurovascular unit during cerebral ischaemia. Likewise, we provide neuroradiological evidence indicating the existence of an inverse relationship between age and the volume of the ischaemic lesion in patients with acute ischaemic stroke. Together, these results indicate that the relationship among DBP, tPA and ageing play an important role in the outcome of cerebral ischaemia.

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Muscle transcriptome analysis following Total Knee Arthroplasty with Tourniquet

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Succinate accumulation drives ischaemia-reperfusion injury during organ transplantation

Project description:During heart transplantation, storage in cold preservation solution is thought to protect the organ by slowing metabolism; by providing osmotic support; and by minimising ischaemia-reperfusion (IR) injury upon transplantation into the recipient. Despite its widespread use, our understanding of the metabolic changes prevented by cold storage and how warm ischaemia leads to damage is surprisingly poor. Here, we compared the metabolic changes during warm ischaemia (WI) and cold ischaemia (CI) in hearts from mouse, pig, and human. We identified common metabolic alterations during WI and those affected by CI, thereby elucidating mechanisms underlying the benefits of CI, and how WI causes damage. Succinate accumulation is a major feature within ischaemic hearts across species, and CI slows succinate generation, thereby reducing tissue damage upon reperfusion caused by the production of mitochondrial reactive oxygen species (ROS). Importantly, the inevitable periods of WI during organ procurement led to the accumulation of damaging levels of succinate during transplantation, despite cooling organs as rapidly as possible. This damage was ameliorated by metabolic inhibitors that prevented succinate accumulation and oxidation. Our findings suggest how WI and CI contribute to transplant outcome and indicate new therapies for improving the quality of transplanted organs.

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