The 5A/6A polymorphism in the promoter of the stromelysin gene is a novel pathogenetic risk factor for AMI.

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Microwave coagulation therapy (MCT) has been widely used, both percutaneously and directly, as effective minimal invasive therapy for liver tumors. To facilitate the use of MCT, we describe the complications we have encountered, and their possible management and prophylaxis. MCT was performed for 42 patients with hepatocellular carcinoma (HCC) and for 29 with metastatic liver tumors, following which complications developed in 14.2% and 20.6% of the HCC and metastatic groups, respectively. The complications included abscess, biloma, bleeding, hepatic failure, and dissemination of cancer cells. In the HCC group, the mean value of tumor size and the clinical stage of patients with complications were significantly larger (P = 0.006) and higher (P = 0.032), respectively, than those of patients without complications. The incidence of complications increased significantly when the tumor size was more than 4cm (P = 0.008). Abscesses and bleeding were successfully treated using percutaneous drainage and interventional angiography, respectively, but as the other serious complications were not able to be treated effectively once induced, prophylaxis is important to facilitate MCT. Transcatheter cooling of the intrahepatic bile duct during MCT and the administration of an anticancer agent into the abdominal cavity are recommended to prevent biloma and dissemination, respectively. MCT is indicated for tumors less than 4 cm in diameter to reduce the risk of complications. The prophylaxis and treatment of these complications enhance the safety of MCT.

Background The retrospectively compared sleeve lobectomy (SL) and pneumonectomy (PN) for lung cancer in terms of surgical complications and postoperative disease‐free survival, as well as incidence and pattern of recurrent disease. Methods From 1977 to 1993, 29 patients with primary lung cancer underwent sleeve resection at our institution. The pneumonectomy group consisted of 29 cases that had been selected during the same period according to the following criteria: (1) in a tumor located in the upper lobe, there was no invasion within 1 cm from both the carina and the orifice of the middle and the lower lobe bronchus, whereas in a tumor located in the middle or lower lobe, there was no invasion within 1 cm of the orifice of the upper bronchus, (2) there was no invasion to the trunks of the pulmonary vessels, (3) there was no invasion to any other lobes, (4) a complete resection was achieved. Results No differences were observed between the two groups regarding stage, histological population, or age. The incidence of postoperative complications was 13.7% in the SL group (2 cases each of pneumonia and arrythmia), and 24.1% in the PN group (3 bronchopulmonary fistula, 2 bleeding, 1 instance each of arrythmia and acute cardiac failure, and 2 operation‐related deaths) (P < 0.05). The 3‐year disease‐free survival was 65.7% in SL, 58.8% in PN (no statistical significance in the log‐rank test). Recurrent disease was observed in the local regions of three patients in the SL group and six patients in the PN group, and at distant organs of six patients in the SL group and seven in the PN group. Conclusions These findings thus suggest that as a curative treatment, lobectomy with bronchoplasty may be a safer procedure than pneumonectomy for lung cancer. J. Surg. Oncol. 64:32–35 © 1997 Wiley‐Liss, Inc.

ilated cardiomyopathy (DCM) is characterized by ventricular dilatation and depressed myocardial contractility, resulting in progressive refractory congestive heart failure and sudden death from ventricular arrhythmias (mainly ventricular tachycardia (VT) and subsequent ventricular fibrillation). 1 A structural increase in ventricular volume (cardiac remodeling) has been viewed as not only an adaptive consequence of initial myocardial damage, but an important determinant of the progression of heart failure. Although risk stratification of cardiac remodeling and ventricular arrhythmias in DCM is an important issue in clinical practice, the factors that lead to cardiac remodeling or induction of VT are not well defined.The adrenergic nervous system, especially through -1-adrenergic receptor ( 1-AR) activation, appears to be of major importance not only in the genesis or progression of cardiac remodeling but also in induction of VT. 2 In transgenic mice, cardiac overexpression of human 1-AR produced an overtly cardiomyopathic phenotype and ultimately chamber dilatation and systolic dysfunction. 3 Clinical evidence has accumulated of the beneficial effect of blockade of 1-AR on cardiac remodeling and prognosis in Circulation Journal Vol.66, August 2002 patients with heart failure caused by DCM or myocardial infarction. 4,5 In the CIBIS-II study, bisoprolol, a highly selective 1-AR blocker, improved the survival rate in patients with heart failure and more importantly, also showed that bisoprolol reduced sudden death most likelycaused by lethal ventricular arrhythmia and hospital admissions for malignant ventricular arrhythmia. 6 The MERIT-HF study showed that metoprolol, a selective 1-AR blocker, also reduced sudden death in patients with heart failure. 7 Accordingly, it seems reasonable to suppose that the signals mediated by 1-AR play an important role in the arrhythmogenesis of heart failure.Beta-1-AR is encoded by a gene comprising a single exon located on chromosome 10q24-26 and consists of 477 amino acids. 8 To date, 18 genetic variants of the single nucleotide chain have been identified. Although 17 of these are located at the coding region, amino acid changes occur only in 7 variants (Ser49Gly, Ala59Ser, Arg389Gly, Arg399Cys, His402Arg, Thr404Ala and Pro418Ala). 9 None of these regions other than the 389 residue have been implicated in the precise function of the 1-AR. The Arg389Gly variant is located at the interface between the last transmembrane helix and the intracellular tail, adjacent to the phosphorylation sites and thought to be critical for Gprotein coupling and subsequent cell signaling. Interestingly, functional studies using transfected fibloblasts indicated that the Arg389 1-AR had approximately 3-fold the adenylyl cyclase activity of the Gly389 1-AR when stimulated by isoproterenol. 10 Therefore, it is quite possible that the Arg389Gly polymorphism functions as either a gene for susceptibility for DCM (role in the emergence of DCM) or a modifier gene (role in the evolution/prognosis Beta-1-ad...

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