Long-term follow-up showed that even without spinal fusion, more than half the patients were evaluated as excellent or good. Patients with more than a 10 degrees sagittalrotation angle who need multiple laminectomy, should be given information about the possibility of earlier deterioration of the outcome, and alternative or additional treatment such as concomitant spinal fusion with decompression may be considered.

Cardioprotection by preconditioning is mediated, at least in part, by oxyradicals which are scavenged by SOD or MPG in rabbits.

Oxidative stress is a persistent threat to the genome and is associated with major causes of human mortality, including cancer, atherosclerosis, and aging. Here we established a method to generate libraries of genomic DNA fragments containing oxidatively modified bases by using specific monoclonal antibodies to immunoprecipitate enzyme-digested genome DNA. We applied this technique to two different base modifications, 8-hydroxyguanine and 1,N6-propanoadenine (acrotein-Ade), in a ferric nitrilotriacetate-induced murine renal carcinogenesis model. Renal cortical genomic DNA derived from 10- to 12-week-old male C57BL/6 mice, of untreated control or 6 hours after intraperitoneal injection of 3 mg iron/kg ferric nitrilotriacetate, was enzyme digested, immunoprecipitated, cloned, and mapped to each chromosome. The results revealed that distribution of the two modified bases was not random but differed in terms of chromosomes, gene size, and expression, which could be partially explained by chromosomal territory. In the wild-type mice, low GC content areas were more likely to harbor the two modified bases. Knockout of OGG1, a repair enzyme for genomic 8-hydroxyguanine, increased the amounts of acrolein-Ade as determined by quantitative polymerase chain reaction analyses. This versatile technique would introduce a novel research area as a high-throughput screening method for critical genomic loci under oxidative stress.

Previous studies have shown that preconditioning (PC) with a brief ischemic episode induces heat shock protein (HSP) in cardiac tissue. However, it is unclear when and where in the left ventricle HSP is expressed after PC. Hence, the expression of HSP was studied in rabbit hearts at various time intervals after PC using immunohistochemical methods. Rabbits were preconditioned four times with 5 min of occlusion and 5 min of reperfusion of the coronary artery and then were killed at 0, 3, 24, 48, 72 and 168 h after the PC (n=4, for each time interval). Samples were obtained from the subendocardium and subepicardium of the preconditioned and nonpreconditioned wall and these were processed to 4 m thick cryosections. The sections were immunolabelled with mouse monoclonal IgGs against HSP 72/73. Positive immunoreactivity was observed as early as 3 h after PC, persisting up to 72 h but not detected at 168 h. HSP was expressed not only in the preconditioned myocardium but also in the remote nonpreconditioned myocardium. There was a wide variation in expression among myocytes. Expression was dominant in myocytes compared with vessel walls. It was concluded that PC induced transient and inhomogeneous expression of HSP in rabbit hearts. (Jpn Circ J 1998; 62: 512 -516)