The results indicate that a systemic production of free radicals occurs during CPB that may overwhelm the production related to reperfusion of the ischemic heart. This systemic oxidative stress is likely to participate in secondary myocardial damage.

Objective: To assess the mechanisms through which an enlarged aortic root may facilitate right to left shunting through a patent foramen ovale. Patients: 19 patients with the platypnoea-orthodeoxia syndrome (POS) were compared with 30 control patients without platypnoea. Interventions: Multiplane transoesophageal echocardiography. Main outcome measures: The aortic root diameter, atrial septal dimension behind the aortic root, and amplitude of the phasic oscillation of the septum were measured. Four groups of patients were compared: 12 platypnoeic patients with a dilated aortic root (POS-D), 7 platypnoeic patients with a normal aortic root (POS-N), 15 control patients with a dilated aortic root (CONT-D), and 15 control patients with a normal aortic root (CONT-N). Results: In POS-D and CONT-D patients, the apparent atrial septal dimension was 16.3 (2.7) mm and 17.4 (5.9) mm respectively, compared with 24.4 (5.2) mm in POS-N patients and 25 (4) mm in CONT-N (p , 0.005). Furthermore, the amplitude of septal oscillation was 14.7 (2.5) mm in the POS-D group versus 5.8 (2.4) mm in CONT-N (p , 0.001) compared with 23.3 (3) mm in seven patients with an atrial septal aneurysm (p ,0.001). Conclusion: Patients with an enlarged aorta have an apparently smaller dimension and increased mobility of the atrial septum. These findings appear to result from compression by the aortic root and decreased septal tautness. Consequently, a ''spinnaker effect'' with the inferior vena caval flow may take place, opening the foramen ovale and leading to sustained right to left shunting.A patent foramen ovale (PFO) is a defect in the atrial septum that results from incomplete fusion of the septum primum to the septum secundum. The persistence of a PFO into adulthood may lead to several complications, including paradoxical embolism of thrombus, air or tumoural material, and refractory hypoxaemia.Normally, even if a potential channel between the atria remains, the higher left atrial pressure keeps the flap-like valve of the foramen ovale opposed to the septum secundum. Most cases of sustained right to left shunting through a PFO are seen in situations where right atrial pressure exceeds that of the left, forcing open the potentially patent foramen ovale.However, right to left shunting can be less often observed in the absence of any demonstrable pressure gradient between right and left atria. Right to left shunting despite normal right atrial pressure has been reported after right pneumonectomy 1 2 or in association with venous embryonic remnants. 3 4 In these situations, an altered relation between the caval veins and the atrial septum presumably accounts for flow related rather than pressure related shunting.A few cases of aneurysm of the ascending aorta associated with right to left shunting across a PFO have been reported, 5-10 but evidence for a non-fortuitous association is still lacking. Therefore, we conducted a study to further analyse factors facilitating right to left shunting in patients with PFO, with particular attention paid to t...

The animal study showed that electrical impedance measurements reflect morphological changes related to the growth of a cancerous skin lesion. These findings are in agreement with a preliminary clinical study. Electrical Impedance Scanning can therefore be considered as an objective and non-invasive tool for differentiation between benign and malignant skin lesions.

No abstract

Basic ®broblast growth factor (bFGF) was recently shown to promote the survival of neural cells and tissues, raising hopes for its therapeutic potential in degenerative disorders of the CNS. Here we examine the effect of bFGF on the expression of glutamine synthetase, a key enzyme in the detoxi®cation of the neurotransmitter glutamate. Expression of this enzyme is regulated by systemic glucocorticoids and, in chick neural retina tissue, is restricted to Mu È ller glial cells. We report that exogenous supply of bFGF to retinal explants inhibits hormonal induction of glutamine synthetase expression. This inhibition appears to be mediated by the c-Jun protein which accumulated, in response to bFGF, exclusively in Mu È ller glial cells. Ischemic conditions, which reportedly stimulate the release of endogenous bFGF, also led to an increase in c-Jun protein and a decline in glutamine synthetase expression. This decline could be competitively prevented by a soluble ®broblast growth factor receptor but not by a soluble epidermal growth factor receptor. The ®nding that endogenous release of bFGF or its exogenous supply down-regulates glutamine synthetase expression suggests that in addition to its reported neuroprotective effect, bFGF may exacerbate glutamate mediated neurotoxicity through direct down-regulation of glutamine synthetase.