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We would like to thank Nikki Jahnke, Managing Editor of the Cochrane Cystic Fibrosis and Genetic Disorders Group for her support. We would also like to thank Dr Claire Shovlin for providing an in-depth peer review.

While no randomised controlled trials of this treatment are included in this review, a number of observational studies have suggested embolisation therapy has benefits. However, randomised controlled trials are not always feasible on ethical grounds. In the absence of randomised controlled trials, a standardised approach to reporting, as well as long-term follow-up through registry studies can help to improve the safety and outcome of embolisation for pulmonary arteriovenous malformations. Quality of the evidence We have not been able to present any evidence from randomised controlled trials in this version of the review.

Pale, soft, and exudative (PSE) meat has been recognized for decades. Fast glycolysis during early post-mortem stage while the muscle temperature is still high is the cause of PSE meat. To elucidate the molecular mechanism underlying this fast glycolysis in muscle to become PSE meat, post-mortem ATP metabolism, fructose-2,6-diphosphate content, and the activities of AMPK, glycogen phosphorylase, and pyruvate kinase were examined in post-mortem muscle. Earlier and faster post-mortem AMPK activation was responsible for the significantly lower pH and higher lactic acid accumulation (p<0.05) seen in PSE muscle, which resulted in the occurrence of PSE meat. In muscle that became PSE meat, AMPK was activated at 0 h post-mortem and reached maximal activation at 0.5 h post-mortem, whereas AMPK reached maximal activation at 1 h post-mortem in the normal pork loin. Higher fructose-2,6-diphosphate content (p<0.05) was detected in PSE muscle compared to normal muscle at early post-mortem stage. However, no difference in the activities of glycogen phosphorylase and pyruvate kinase, rate-controlling enzymes in glycogenolysis and glycolysis, respectively, was detected between PSE and normal pork loins. Because fructose-2,6-diphosphate is a product of phosphofructokinase-2 (PFK-2), these data suggest that AMPK regulates post-mortem glycolysis through its phosphorylation and activation of PFK-2, which then up-regulates the activity of phosphofructokinase-1 (PFK-1), a key rate-controlling enzyme in glycolysis. Early AMPK activation in PSE muscle is associated with early consumption of ATP, because higher AMP and IMP contents and lower ATP content were detected in PSE meat compared to normal meat. Other mechanisms causing early AMPK activation in PSE meat may exist, which warrants further investigation.

OBJECTIVE

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Background Pulmonary arteriovenous malformations are abnormal direct connections between the pulmonary artery and pulmonary vein which result in a right-to-left shunt. They are associated with substantial morbidity and mortality mainly from the effects of paradoxical emboli. Potential complications include stroke, cerebral abscess, pulmonary haemorrhage and hypoxaemia. Embolisation therapy is a form of treatment based on the occlusion of the feeding arteries to a pulmonary arteriovenous malformation and can prevent many of these debilitating and life-threatening complications. Objectives To determine the efficacy and safety of embolisation therapy in people with pulmonary arteriovenous malformations including a comparison with surgical resection and different embolisation devices. Search methods We searched the Cystic Fibrosis and Genetic Disorders Group's Trials Registers (last searched 07 September 2009). We also searched the following databases: the Australian New Zealand Clinical Trials Registry; ClinicalTrials.gov; International Standard Randomised Controlled Trial Number Register; International Clinical Trials Registry Platform Search Portal (last searched 22 November 2009). We checked cross-references and searched references from review articles. Finally, we contacted manufacturers and specialised centres for unpublished and ongoing trials. Selection criteria Trials in which individuals with pulmonary arteriovenous malformations were randomly allocated to embolisation therapy compared to no treatment, surgical resection or a different embolisation device. Studies identified for potential inclusion were independently assessed for eligibility by two authors, with excluded studies further checked by a third author. Data collection and analysis No trials were identified. As this was the case, no analysis was performed. Main results There were no randomised controlled trials identified.

Background Pulmonary arteriovenous malformations are abnormal direct connections between the pulmonary artery and pulmonary vein which result in a right-to-left shunt. They are associated with substantial morbidity and mortality mainly from the effects of paradoxical emboli. Potential complications include stroke, cerebral abscess, pulmonary haemorrhage and hypoxaemia. Embolisation therapy is a form of treatment based on the occlusion of the feeding arteries to a pulmonary arteriovenous malformation and can prevent many of these debilitating and life-threatening complications. Objectives To determine the efficacy and safety of embolisation therapy in people with pulmonary arteriovenous malformations including a comparison with surgical resection and different embolisation devices. Search methods We searched the Cystic Fibrosis and Genetic Disorders Group's Trials Registers (last searched 07 September 2009). We also searched the following databases: the Australian New Zealand Clinical Trials Registry; ClinicalTrials.gov; International Standard Randomised Controlled Trial Number Register; International Clinical Trials Registry Platform Search Portal (last searched 22 November 2009). We checked cross-references and searched references from review articles. Finally, we contacted manufacturers and specialised centres for unpublished and ongoing trials. Selection criteria Trials in which individuals with pulmonary arteriovenous malformations were randomly allocated to embolisation therapy compared to no treatment, surgical resection or a different embolisation device. Studies identified for potential inclusion were independently assessed for eligibility by two authors, with excluded studies further checked by a third author. Data collection and analysis No trials were identified. As this was the case, no analysis was performed. Main results There were no randomised controlled trials identified.