Clinical Significance of Thrombosis in an Intracardiac Blind Pouch After a Fontan Operation

The univentricular heart after the Fontan operation may have a blind pouch formed by the pulmonary stump or rudimentary ventricle according to the anatomy before surgery. Thrombosis in an intracardiac blind pouch of patients with a univentricular heart is a hazardous complication. Because only a few reports have described this complication, the authors evaluated the clinical significance of thrombosis in an intracardiac blind pouch of a univentricular heart. They performed a retrospective review of medical records from August 1986 to December 2007. Four patients were confirmed as having thrombosis in a pulmonary artery stump and one patient as having thrombosis in a rudimentary ventricle shown by cardiac computed tomography (CT). This represents 1.85% (5/271) of patients with ongoing regular follow-up evaluation after the Fontan operation. The median age at diagnosis was 14.2 years. Two of the five patients were taking aspirin and one patient was taking warfarin when they were identified for the development of thrombosis. None of the patients demonstrated thrombosis in the Fontan tract or venous side of the circulation. Brain magnetic resonance imaging (MRI) showed that three patients had cerebral infarction and one patient had suggestive old ischemia. Three patients with thrombus in the pulmonary stump underwent pulmonary artery stump thrombectomy and pulmonary valve obliteration. One patient with thrombus in the rudimentary ventricle underwent ventricular septal defect (VSD) closure with thrombectomy. Thrombus in a blind pouch could cause systemic thromboembolism despite little blood communication. Therefore, surgical modification of the pulmonary stump and VSD closure of the rudimentary ventricle are required to reduce the risk of later thrombus formation. Clinicians should not overlook the possibility of thrombus in a ligated pulmonary artery stump or a rudimentary ventricle after the Fontan operation, which may increase the risk of embolic stroke for patients with single-ventricle physiology

Laboratories, laws, and the career of a commodity

Unlike most foods, milk is produced fresh at least twice every day, thus recreating, over 700 times a year, a commodity ‘designed’ by the combination of nature, commerce, and law. The paper is a study of the ontogenesis of this commodity in Britain since 1800, stressing the emergence of two new objectivities: dairy science and the law on adulteration. In the words of Christopher Hamlin, what mattered was the “manufacture of certainty, however flimsy that certainty might later be shown to be.'' This was achieved by the collection of samples, the generation of facts by the deployment of the laboratory technologies of physics and chemistry, and a semimonopoly over the truth-power of dairy science that was gradually built up by the large commercial companies. A foundation of state-sponsored regulation provided an official legitimation of compositional standards that suited the interests of capital but ignored ‘natural’ variations in quality and often pilloried innocent producers. The public eventually became accustomed to the regulated quality of the milk in its ‘pinta’ and assumed it to be natural. Even the standardization of composition since 1993 has caused very little disquiet among the consuming public, although milk is now a fully constructed commodity like any other dairy product. Mechanical modernity has at last triumphed over a century of ‘milk as it came from the cow’

Promotion of plasma membrane repair by vitamin E

Severe vitamin E deficiency results in lethal myopathy in animal models. Membrane repair is an important myocyte response to plasma membrane disruption injury as when repair fails, myocytes die and muscular dystrophy ensues. Here we show that supplementation of cultured cells with α-tocopherol, the most common form of vitamin E, promotes plasma membrane repair. Conversely, in the absence of α-tocopherol supplementation, exposure of cultured cells to an oxidant challenge strikingly inhibits repair. Comparative measurements reveal that, to promote repair, an anti-oxidant must associate with membranes, as α-tocopherol does, or be capable of α-tocopherol regeneration. Finally, we show that myocytes in intact muscle cannot repair membranes when exposed to an oxidant challenge, but show enhanced repair when supplemented with vitamin E. Our work suggests a novel biological function for vitamin E in promoting myocyte plasma membrane repair. We propose that this function is essential for maintenance of skeletal muscle homeostasis