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Biomedical subjects

B Creamer

Publications and source records attributed to B Creamer.

At least 37 records · Page 2Linked to original sources
PubMed1974

Hyperphagia in intestinal disease.

Six patients with hyperphagia (ingestion of 5-11 000 Kcals/day) associated with severe malabsorption and steatorrhoea are described. The cause of the malabsorption was coeliac disease in three patients, Crohn's disease with ileal resection in two, and carcinoma of the pancreas in one patient. There was no evidence of neurological or endocrine disease (apart from mild diabetes mellitus in the patient with carcinoma of the pancreas) but three patients suffered from severe depression. This association may be commoner than previously realized and be revealed in patients with steatorrhoea of unexplained severity by careful dietary assessment. Its detection has therapeutic implications since restriction of caloric and fat intake decreased steatorrhoea without weight loss in several of the patients described.

Adult↗
PubMed1971

Protein loss and cell loss from the small-intestinal mucosa.

Total protein and deoxyribonucleic acid (dna) were measured in small-intestinal washings from rats with normal and high rates of dna (or cell) loss. There was a significant relationship between the loss of these two substances. Preparations of isolated viable epithelial cells contained much less protein in relation to dna than did the intestinal washings. It was calculated that only 8 to 15% of the protein lost by washing the rat small intestine arose from the intracellular protein of exfoliated epithelial cells. The rest was derived from extracellular sources.Protein and dna loss from small-bowel mucosa was measured in six patients. The ratio of protein to dna was similar to that found in the rats. The mean protein loss from 5 cm of human upper small intestine was 956 mug per min or 1.4 g per 24 hours. By calculation, total protein loss from the whole small intestine of man was about 84 g per day, about 10 g coming from within exfoliated cells and the rest arising from extracellular sources. The normal intestine must reabsorb most of this material.

Animals↗
PubMed1970

Cell loss from small intestinal mucosa: a morphological study.

Large numbers of cells are shed from small intestinal mucosa but they are so rapidly destroyed that there is little direct information about their morphological types. Material obtained by washing the human and rat small intestine was immediately processed and examined by light and electron microscopy. Small intestinal epithelial cells could not be identified by light microscopy but were readily recognized-by the presence of brush borders-using the electron microscope. Eighty to 85% of the cells from both rats and patients with normal small intestinal mucosa were intestinal absorptive cells. This was also the case in four patients with the coeliac syndrome and flat intestinal mucosa. These findings provide further support for the view that measurements of cell loss using intestinal washing techniques and the DNA-loss method, reflect predominantly small intestinal epithelial cell loss and turnover.

Animals↗
PubMed1970

Permeability of the small intestine to substances of different molecular weight.

The permeability of the rabbit small intestine has been studied by measuring the plasma clearances of water-soluble molecules over the molecular weight range 60-33,000. An inverse relationship has been demonstrated between permeability and molecular weight. The significance of these findings in relation to current concepts of the ;pore hypotheses' is discussed, and the possible physiological and pathological implications are considered.

Animals↗