Dr Eugenia Rose Aylmer Cooper (1898-1991): Manchester's renowned female anatomist and neurohistologist.

Having excelled in histology, Dr Eugenia Cooper, following graduation in medicine in Manchester, embarked on a career spanning 44 years in anatomy and histology at Manchester University. Her inimitable character was readily remembered by those she had taught. She was the first female graduate to gain an MD with gold medal for her thesis on the histology of the endocrine organs. However, her main study was the development of the human brainstem from the early weeks of gestation, which remains the basis for anatomical understanding today. More controversial was her theory on circulation and absorption of the cerebrospinal fluid. On retiring as Reader in Histology, she expressed disappointment at not being appointed a professor, which she considered was due to her gender. Possibly to compensate for this, she had studied law as an additional interest. She continued in research for a further 10 years in reproductive pharmacology. After retirement she donated her medals to the University, three to be awarded in medicine and histology, which have now lapsed, but the medals in computer science and music continue to be important rewards.

William Roentgen's (1845-1923) influence: contrasts and comparisons.

William Roentgen's discovery of X-rays in 1895 influenced two students from Manchester who first met in 1899. They developed an interest in radiology of the gastrointestinal tract through which they maintained a long association. Sir Arthur Hurst, after qualifying in Oxford in 1904, became a renowned physician at Guy's Hospital, London, and founder of what was to become the British Society of Gastroenterology. Dr Alfred Barclay qualified in Cambridge in 1904 and subsequently became the first Consultant Radiologist in Manchester and doyen of gastrointestinal radiology. He moved to Cambridge in 1928 to sustain the DMRE course. In 1937 he was invited to join the Nuffield Institute of Medical Research in Oxford at an age when many would have considered retiring. In 1939 Hurst also returned to Oxford where he taught at the medical school and consulted at the Radcliffe Infirmary, bringing his path and Barclay's together once more.

Walter Max Dale (formerly Deutsch) (1894-1969): pioneer and eminent radiobiochemist at the Christie Hospital and Holt Radium Institute, Manchester.

The political upheaval in Germany in 1933 and subsequent movement of medical scholars with the support of the Rockefeller Foundation allowed Manchester to benefit from the arrival of Dr Walter Deutsch, later known as Dr Walter Dale. His research background enabled him to develop a radiobiochemistry laboratory at the Christie Hospital and Holt Radium Institute where he became a world authority on the effects of X-rays on enzymes and also the protective effect of additional solutes. In 1959 he initiated and then edited the International Journal of Radiation Biology. By the time of his retirement in 1962 the strength of his research resulted in his laboratory being recognized by the Medical Research Council.

Dr Arnold Renshaw (1885-1980): Manchester pathologist and forensic pathologist with a clinical interest in rheumatoid arthritis.

Dr Arnold Renshaw trained in both dentistry and medicine in Manchester, being actively involved in the University student organisations. He followed a career in pathology and bacteriology that was interrupted by serving in the RAMC during World War I. Bacteriological interest in the antiseptic properties of aniline dyes followed. His main interest, however, was in pathology where he was associated with the Pathology Society of Manchester for more than twenty years. He was also actively involved in the founding of the Association of Clinical Pathologists. The Association led to the formation of the Royal College of Pathologists and to Renshaw being elected one of the Founding Fellows. He also developed a special expertise in forensic pathology which he pioneered in northwest England. His later years witnessed an interest in rheumatoid arthritis to investigate a possible cause and suggest a unique treatment consisting of the small intestinal enzymes, erepsin.

Faecal calprotectin: a marker of inflammation throughout the intestinal tract.

OBJECTIVE: To assess the potential of measuring the calcium-binding protein calprotectin in faeces as a method of screening for alimentary inflammation and neoplasia. SETTING: Hospital day services unit for endoscopy and faecal analysis in the clinical biochemistry department. PARTICIPANTS: Consented patients attending for routine endoscopy were requested to provide faeces. Seventeen of the initial 30 patients provided faeces before and 1 week after endoscopy. After this, 116 patients for planned endoscopy provided faeces before endoscopy. The group comprised 43 patients with upper-gastrointestinal lesions, seven patients with inflammatory bowel disease, seven patients with irritable bowel syndrome, 31 patients with colonic disorders, and 28 normal people. A final 18 patients with known inflammatory bowel disease (seven patients), gastric carcinoma (one patient), colorectal cancer (eight patients) and colorectal adenoma (two patients) had faeces analysed. METHOD: Faeces were analysed by the Nycotest PhiCal enzyme-linked immunosorbent assay (ELISA) (Nycomed, Oslo, Norway), and the final 18 patients were analysed by the newer version marketed as Calprest. RESULTS: No definite differences between pre- and post-endoscopy calprotectin were found, but it was considered preferable in the subsequent patients to analyse pre-endoscopy faeces. Upper-gastrointestinal disorders showed little difference in calprotectin levels, Barrett's oesophagus (median 6.8 mg/l), gastric ulcer (median 6.5 mg/l) or gastritis/duodenitis (median 5.2 mg/l), but these levels were all higher than the median calprotectin level of normal subjects (4.5 mg/l). The oesophageal and gastric carcinoma median was elevated significantly at 30 mg/l. Inflammatory bowel disease was also associated with marked elevation (Crohn's disease, 31.2 mg/l; ulcerative colitis, 116.2 mg/l). Colorectal polyps (median 3.7 mg/l) and adenoma (median 3.8 mg/l) showed no elevated levels in contrast to colorectal carcinoma (median 53.4 mg/l). The elevated calprotectin in inflammatory bowel disease and colorectal carcinoma combined gave a sensitivity of 81.8% and a specificity of 73.2%. CONCLUSIONS: Calprotectin levels are elevated in inflammation and cancer but are not helpful in differentiating between these disorders. In our series, calprotectin was not elevated in colonic polyps or adenomata. Calprotectin could be helpful as a screening method in a general gastroenterology population for inflammatory bowel disease and those with carcinoma, as well as assessing and monitoring disease activity in inflammatory bowel disease.