Galectin-3 is a beta-galactoside-binding protein which regulates many biological processes including cell adhesion, migration, cell growth, tumor progression, metastasis, and apoptosis. Although the exact function of galectin-3 in cancer development is unclear, galectin-3 expression is associated with neoplastic progression and metastatic potential. Since studies have suggested that tumor cell survival in microcirculation determines the metastatic outcome, we examined the effect of galectin-3 overexpression in human breast carcinoma cell survival using the liver ischemia/reperfusion metastasis model. While the majority of control cells died by hepatic ischemia/reoxygenation, nearly all of galectin-3 overexpressing cells survived. We showed that galectin-3 inhibits nitrogen free radical-mediated apoptosis, one of the major death pathways induced during hepatic ischemia/reperfusion. Galectin-3 inhibition of apoptosis involved protection of mitochondrial integrity, inhibition of cytochrome c release and caspase activation. Taking these results together with the previous observation that galectin-3 inhibits apoptosis induced by loss of cell adhesion, we propose that galectin-3 is a critical determinant for anchorage-independent and free radical-resistant cell survival during metastasis.

Many recent studies have focused on potential chemopreventive activities of dietary genistein, a natural isoflavonoid compound found in soy products. Genistein has been implicated in anticancer activities, including differentiation, apoptosis, inhibition of cell growth and inhibition of angiogenesis. In previous studies, genistein was shown to induce apoptosis and cell cycle arrest at G(2)/M in several cancer cell lines in vitro, which is associated with induction of p21(WAF1/CIP1), a universal inhibitor of cyclin-dependent kinases. At present, the molecular basis for diverse genistein-mediated cellular responses is largely unknown. In the present study, we investigated whether galectin-3, an anti-apoptotic gene product, regulates genistein-mediated cellular responses. We show that genistein effectively induces apoptosis without detectable cell cycle arrest in BT549, a human breast epithelial cell line which does not express galectin-3 at a detectable level. In galectin-3 transfected BT549 cells, genistein induced cell cycle arrest at the G(2)/M phase without apoptosis induction. Interestingly, genistein induces p21(WAF1/CIP1) expression in galectin-3-expressing BT549 cells, but not in control BT549 cells undergoing apoptosis. Collectively, the results of the present study suggest that galectin-3, at least in part, is a critical determinant for genistein-mediated cell cycle arrest and apoptosis, and genistein induction of p21(WAF1/CIP1) is associated with cell cycle arrest, but not required for apoptosis induction.

Brugada syndrome is characterized by right bundle branch block, ST segment elevation in the precordial leads and sudden death caused by ventricular fibrillation. We present two successful anaesthetic management cases in patients with Brugada syndrome. Accepted for publication 8 May 2004Key words: Brugada syndrome; complications; electrocardiography; sudden death.# Acta Anaesthesiologica Scandinavica 48 (2004) I N 1992 a new syndrome was described consisting of syncope or sudden death in patients with a structurally normal heart and an electrocardiogram (ECG) characteristic of right bundle branch block with ST segment elevation in leads V 1 to V 3 . This condition was named 'Brugada syndrome' (1). The syndrome is genetically determined and caused by mutations in the gene SCN5A on chromosome 3, encoding the human cardiac sodium channel (2).There are few reports of anaesthetic management of patients with Brugada syndrome, and especially regional anaesthesia of patients with Brugada syndrome. Therefore, we report one case of regional anaesthesia and one case of general anaesthesia in patients with Brugada syndrome. Case report Case 1A 33-year-old man was presented for an emergency orthopaedic operation due to open fracture of the patella. One year ago, before admission, Brugada syndrome was diagnosed in routine cardiologic evaluation. He had no past history of syncope and there was no family history of sudden death. On admission, a physical examination revealed no abnormal findings except ECG findings showing the coved-type ST segment elevation in leads V 1 to V 3 with a right bundle branch block (Fig. 1). Echocardiography showed a normal heart with an ejection fraction of 60%. Electrophysiology study revealed normal sinus node function, but non-sustained ventricular tachycardia was induced by electric ventricular stimulation.Having been informed of the associated risks, the patient was taken to the operating room and routine monitors were applied. A radial arterial cannula was inserted under local anaesthetic. Prior to the induction of anaesthesia, an external defibrillator was prepared. Spinal tapping was carried out at the L4/5 space in right lateral position. Afterwards, 0.5% bupivacaine hydrochloride 10 mg was injected intrathecally and satisfactory spinal block was achieved up to the T 10 dermatome.During the operation, ECG and continuous blood pressure were monitored and showed no abnormalities.After a 2-h operation, the patient was transferred to the post anaesthetic care unit (PACU) and postoperative pain was controlled with intravenous patientcontrolled analgesia (PCA) using opioids and NSAID. Postoperative recovery was uneventful. Case 2A 56-year-old male with L 1 vertebral body compression fracture scheduled for spine fusion under general anaesthesia. His preoperative 12-lead ECG showed a complete right bundle branch block and ST segment elevation (Fig. 2). There was no family history of sudden death. Several years ago, before admission, he had one history of syncope attack. Echocardiogram showed no s...