Dr. C. D. Forbes, University Department of Medicine, Royal Infirmary, Glasgow. Dr. I. Markova, University of Stirling, Department of Psychology, Stirling. Professor J. Stuart, Department of Haematology, Queen Elizabeth Hospital, Edgbaston, Birmingham. Dr. P. Jones Director Haemophilia Centre, Royal Victoria Infirmary, Newcastle upon Tyne.
Immunocytochemistry of gastric mucosal blood groupsWe read with interest the findings of the detailed study by Kapadia et all on the immunocytochemistry of gastric mucosal blood groups.We studied gastric carcinoma and agree that only a minority of these cases show loss of blood group antigens.2We were staining the alcohol-soluble glycolipid blood group substance present on the endothelial cells of all subjects, regardless of secretor status like Kovarik et al3 and Davidsohn et a!4 1971 and suppose that Kapadia et al were staining the water-soluble glycoprotein compo- nent-no mention is made of small vessel staining.We found changes in some tumours involving loss of A or B sub- stance and persistence of H (loss of terminal residue).The peroxidase tech- nique is more sensitive and we are presumably staining a different antigen but would suggest that non-secretors may express certain blood group antigens in gastric mucosa.The exploration of the hypotheses suggested on page 3341 will require a comprehensive study of all types of A, B, H antigens.
Energy production by oxidative metabolism in kidney, stomach, and heart, is primarily expended in establishing ion gradients to drive renal electrolyte homeostasis, gastric acid secretion, and cardiac muscle contraction, respectively. In addition to orchestrating transcriptional control of oxidative metabolism, the orphan nuclear receptor, estrogen-related receptor gamma (ERRgamma), coordinates expression of genes central to ion homeostasis in oxidative tissues. Renal, gastric, and cardiac tissues subjected to genomic analysis of expression in perinatal ERRgamma null mice revealed a characteristic dysregulation of genes involved in transport processes, exemplified by the voltage-gated potassium channel, Kcne2. Consistently, ERRgamma null animals die during the first 72 h of life with elevated serum potassium, reductions in key gastric acid production markers, and cardiac arrhythmia with prolonged QT intervals. In addition, we find altered expression of several genes associated with hypertension in ERRgamma null mice. These findings suggest a potential role for genetic polymorphisms at the ERRgamma locus and ERRgamma modulators in the etiology and treatment of renal, gastric, and cardiac dysfunction.
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