Abstract: Spinal cord injury affects a large number of young individuals with a significant cost to affected persons, families and societies both in terms of economic and non-economic costs. To date, our interventions have been limited to prevention, good initial resuscitation, modest pharmacotherapy and nursing care. This review examines the role of surgery in spinal cord injury. The pathophysiology of spinal cord injury is reviewed. The compelling animal data for early decompression is discussed as well as evidence for improved neurological outcome with early decompression in humans. Finally, the impact of early surgery on non-neurological outcome and overall complication rates is examined with the concept of "damage control" discussed with relevance to spinal cord injury. It appears that favourable outcomes are achieved with early surgery, with reduced morbidity/mortality, but definitive data is still pending.

Abstract: Cervical arthroplasty after anterior decompression with insertion of a prosthetic total disc replacement has been suggested as an alternate to anterior cervical fusion. Currently there are four cervical arthroplasty devices available on the market whose results in clinical use have been reported. Each device varies in terms of materials, range of motion, insertion technique and constraint. It is not known which device is ideal. Early studies suggest that in the short term, the complication rate and efficacy is no worse than fusion surgery. Long-term results have not yet been reported. This review examines the current prostheses available on the market as well as discussing issues regarding indications and technique. Pitfalls are discussed and early experiences reviewed. In time, it is hoped that a refinement of cervical arthroplasty occurs in terms of both materials and design as well as in terms of indications and clinical outcomes as spinal surgeons enter a new era of the management of cervical spine disease.

Abstract: The EMS1 and CCND1 genes at chromosome 11q13 are amplified in about 15% of primary breast cancers but appear to confer different phenotypes in ER positive and ER negative tumours. Since there are no published data on EMS1 expression in large series of breast cancers we examined the relationship of EMS1 expression with EMS1 gene copy number and expression of mRNAs for cyclin D1 and ER. In a subset of 129 patients, where matched tumour RNA and DNA was available, EMS1 mRNA overexpression was associated predominantly with gene amplification (P = 0.0061), whereas cyclin D1 mRNA overexpression was not (P = 0.3142). In a more extensive series of 351 breast cancers, there was no correlation between cyclin D1 and EMS1 expression in the EMS1 and cyclin D1 overexpressors (P = 0.3503). Although an association between EMS1 mRNA expression and ER positivity was evident (P = 0.0232), when the samples were divided into quartiles of EMS1 or cyclin D1 mRNA expression, the increase in the proportion of ER positive tumours in the ascending EMS1 mRNA quartiles was not statistically significant (P = 0.0951). In marked contrast there was a significant stepwise increase in ER positivity in ascending quartiles of cyclin D1 mRNA (P = 0.030). A potential explanation for this difference was provided by the observation that in ER positive breast cancer cells oestradiol treatment resulted in increased cyclin D1 gene expression but was without effect on EMS1. The relationship between EMS1 expression and clinical outcome was examined in a subset of 234 patients with median follow-up of 74 months. High EMS1 expression was associated with age > 50 years (P = 0.0001), postmenopausal status (P = 0.0008), lymph node negativity (P = 0.019) and an apparent trend for worse prognosis in the ER negative subgroup. These data demonstrate that overexpression of EMS1 mRNA is largely due to EMS1 gene amplification, is independent of cyclin D1 and ER expression and, in contrast to cyclin D1, is not regulated by oestrogen. Independent overexpression of these genes may confer different phenotypes and disease outcomes in breast cancer as has been inferred from recent studies of EMS1 and CCND1 gene amplification.