A randomized trial was performed to compare abdominal resection rectopexy and pelvic floor repair (n = 10) with perineal rectosigmoidectomy and pelvic floor repair (n = 10) in elderly female patients with full-thickness rectal prolapse and faecal incontinence. There were no recurrences of full-thickness prolapse following resection rectopexy but one after rectosigmoidectomy. Continence to liquid and solid stool was achieved in nine patients, with faecal soiling reported in only two, after resection rectopexy and in eight, with soiling in six, following rectosigmoidectomy. The median (range) frequency of defaecation was only 1 (1-3) per day following resection rectopexy compared with 3 (1-6) per day after rectosigmoidectomy. There was an increase in the mean(s.d.) maximum resting pressure after resection rectopexy (19.3(15.28) cmH2O) compared with a reduction following rectosigmoidectomy (-3.4(13.75) cmH2O) (P = 0.003). Mean(s.d.) compliance was also greater after resection rectopexy than following rectosigmoidectomy (3.9(0.75) versus 2.2(0.78) ml/cmH2O, P < 0.001). Abdominal resection rectopexy gives better functional and physiological results than perineal rectosigmoidectomy.

Correlation of p53 expression with 5-year survival and histopathological parameters was examined immunohistochemically in two groups of 30 patients with oesophageal carcinoma (5-year survivors versus non-survivors). Tumour type, sex, operative procedure and age were matched. Some 64 per cent of squamous carcinomas and 79 per cent of adenocarcinomas were p53 positive. Normal squamous, normal glandular and metaplastic glandular epithelia were negative. Dysplastic squamous and glandular epithelium adjacent to tumours was positive when the tumour was positive and negative when it was not. Univariate analysis showed that nodal status (P = 0.001), and grade and depth of invasion (both P = 0.01) correlated with outcome. Correlation of tumour grade with outcome, when the most poorly differentiated area is used, is a novel finding for oesophageal carcinoma. The p53 status was not significantly associated with survival or any of these parameters.

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Elastic fibers play a key role in the structure and function of numerous organs that require elasticity. Elastogenesis is a complex process in which cells first produce a microfibrillar scaffold, composed of numerous structural proteins, upon which tropoelastin assembles to be cross-linked into polymeric elastin. Recently, it was demonstrated that low concentrations of free iron upregulate elastin gene expression in cultured fibroblasts. The present studies were conducted to assess whether low-iron diets would affect the deposition of elastic fibers in an in vivo model. One-day-old chicks were fed semipurified diets containing 1.3 (low), 12 (moderate), and 24 (control) mg/kg of iron. After 3 wk, chicks in the low-iron group were underweight and anemic. Their aortas were smaller with significantly thinner walls than control chicks, yet elastin or collagen content did not decrease relative to total protein. They also demonstrated a significantly lower stress-strain resistance than the controls. Electron microscopy demonstrated that aortic and lung smooth muscle cells were vacuolated and surrounded by loose extracellular matrix and disorganized elastic lamellae with diffuse and fragmented networks of elastic fibers and microfibrils. Immunohistology demonstrated that fibrillin-3 (FBN3) was disorganized and markedly reduced in amount in aortas of the low-iron chicks. Elastin messenger RNA levels were not downregulated in the tissues from the low-iron-fed chicks; however, there was a significant reduction in expression of the FBN1 and FBN3 genes compared with control chicks. The studies indicate that iron deficiency had a pronounced negative effect on elastic fiber development and suggests that fibrillin may have an important role in this pathology.

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