After the death of a 12-year old girl with newly discovered insulin-dependent diabetes mellitus, we used monoclonal antibodies in an effort to identify the cells invading the pancreas. The majority of infiltrating lymphocytes were of the T cytotoxic/suppressor phenotype, but other T-cell subpopulations were present. Some of the T cells were "activated" (positive for HLA-DR antigen, and the interleukin-2 receptor). Immunocytes bearing IgG were scattered in the gland, and complement-fixing IgG antibodies were deposited in some islets. Increased expression of Class I (HLA-A, B, and C) molecules was observed in the affected islet cells, and in damaged islets showing scant lymphocytic infiltration, some beta cells (still producing insulin), but not glucagon or somatostatin cells, were HLA-DR positive. The capillary endothelium was markedly dilated and strongly HLA-DR positive. These findings may contribute to an understanding of the sequence of events leading to the destruction of beta cells in classic Type I diabetes mellitus.

SummaryEarlier studies have demonstrated an unexplained depletion of the epidermal growth factor receptor (EGFR) protein expression in prostatic cancer. We now attribute this phenomenon to the presence of a variant EGFR (EGFRvIII) that is highly expressed in malignant prostatic neoplasms. In a retrospective study, normal, benign hyperplastic and malignant prostatic tissues were examined at the mRNA and protein levels for the presence of this mutant receptor. The results demonstrated that whilst EGFRvIII was not present in normal prostatic glands, the level of expression of this variant protein increased progressively with the gradual transformation of the tissues to the malignant phenotype. The selective association of high EGFRvIII levels with the cancer phenotype underlines the role that this mutant receptor may maintain in the initiation and progression of malignant prostatic growth, and opens the way for new approaches in the management of this disease including gene therapy. © 2000 Cancer Research Campaign Keywords: tumour marker; stromal-epithelial interaction; EGFR; prostate/prognostic factors; hormone resistance 186British Journal of Cancer (2000) 82(1), 186-194 © 2000 Cancer Research Campaign Article no. bjoc.1999 Received 24 These results were presented in part at

. de J. (1978). Thorax, 33,[335][336][337][338][339][340][341][342][343][344] Structural basis for the changing physical properties of human pulmonary vessels with age. Circumferential strips of pulmonary vessel wall were obtained at necropsy from the major arterial and venous branches at the lung hilum in patients aged 7-87 years.The extensibility of these strips was measured using the tension balance method of Harris et al. (British Heart Journal, 1965, 27, 651-659). The vessels were then bisected, and half of each strip was submitted for structural analysis using morphometric methods on paraffin sections stained to show the collagen, elastin, and muscle content. The other halves of the formalin-fixed vessel strips were examined chemically to determine their collagen content by estimation of the total hydroxyproline content. The thickness of the vessel media was measured microscopically on all of the sections examined.Quantitative measurements were made on 42 arteries and 37 veins. Contrary to expectation, there was a steady fall in medial collagen content with increasing age in arteries and veins. The decrease in collagen content was similar in the morphometric and chemical studies and was statistically significant. The thickness of the vessel media did not change significantly with age.The pulmonary artery and vein strips were less extensible in the older age groups, the main change occurring in the elastic phase of the vascular stress/strain curves. It is suggested that changes in the elastic tissue at a molecular and lamellar level are responsible for the increasing stiffness of pulmonary vessels rather than changes in the medial collagen content.

Background-Flat adenomas are nonexophytic with a flat top or central depression and histologically the depth of dysplastic tissue is never more than twice the mucosal thickness. Flat adenomas frequently contain severely dysplastic tissue, and may progress rapidly through the adenoma-carcinoma sequence. Flat lesions have never been described in a British asymptomatic population. Aims-To determine whether flat adenomas exist in an asymptomatic population participating in a large randomised controlled trial of flexible sigmoidoscopy screening. Patients-A total of 3000 subjects (aged 55-64 years) underwent screening by flexible sigmoidoscopy. Methods-All polyps were removed and sent for histology. The number of polyps with endoscopic and histological features of flat adenomas was recorded. Results-Three subjects had a total of four flat lesions-that is, one per 1000 people screened. Three contained severely dysplastic tissue, one a focus of adenocarcinoma. Three of the four lesions were less than 5 mm in size and the fourth was 15 mm in diameter. Conclusions-Flat lesions with severe dysplasia exist in the asymptomatic population. This has major implications for gastroenterologists who should be trained to identify them. Their existence is of importance to molecular biologists and epidemiologists investigating the aetiology of colorectal cancer. (Gut 1998;43:229-231)