Isolation of Acinetobacter calcoaceticus from a cow with mastitis.
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Biomedical subjects
Publications and source records attributed to H Rahman.
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To develop an animal model of the haemolytic-uraemic syndrome during shigellosis, rabbits were injected with lipopolysaccharides (LPS) extracted by the hot phenol-water method from Shigella dysenteriae I and from S. flexneri. Two intravenous injections of LPS spaced by 24 h elicited renal cortical necrosis in a generalized Shwartzman reaction characterized by fibrin deposition in glomerular capillaries and by elevated plasma creatinine concentration. Rabbits rendered leucopenic by busulphan treatment were protected against renal cortical necrosis after injection with LPS derived from S. dysenteriae I. Both LPS preparations derived from Shigella species were also active in producing fever in rabbits, death in rabbits, and gelation of limulus lysate with approximately the same potency as a standard LPS of E. coli 055:B5. These results demonstrated that the LPS of Shigella species given intravenously to rabbits produces renal cortical necrosis, which is caused by leucocyte-mediated intravascular fibrin deposition in renal blood vessels and which resembles histologically the renal lesion in the haemolytic-uraemic during shigellosis in humans.
The major source of aluminum in patients with chronic renal failure treated by hemodialysis is the hemodialysis fluid. The aluminum is derived from both the water and the chemical concentrate used in the preparation of the hemodialysis fluid. Due to the complex physico-chemistry of aluminum in water and dialysis fluid, both the total aluminum concentration and the proportion of aluminum species able to cross the hemodialysis membrane may vary from water supply to water supply and from day to day within a supply. A "safe" level of aluminum in dialysis fluid, which will prevent aluminum transfer from dialysis fluid to blood, and promotes aluminum removal from blood, has yet to be determined.
Ultrafiltration of serum through YM10 membranes showed that 46 per cent of the aluminium in normal subjects and 33 per cent of the aluminium in patients with chronic renal failure is ultrafiltrable, suggesting that the majority of the aluminium is bound to some serum component(s) having molecular weight greater than 10,000 daltons. After desferrioxamine infusion, both the ultrafiltrable and protein-bound aluminium increases significantly, probably due to mobilisation of aluminium from body tissues. Gel filtration on Sephacryl S-300 and affinity chromatography have shown that transferrin is the major aluminium binding protein.
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We describe methods for studying the binding of Al by protein in serum: ultrafiltration, gel filtration, and immuno-affinity chromatography. For ultrafiltration we used an Amicon YM10 cellophane membrane with a nominal cutoff of 10 000 Da to separate ultrafiltrable and non-ultrafiltrable Al. For gel filtration we used Sephacryl S-300, and for immuno-affinity chromatography we used anti-transferrin coupled to CNBr-activated Sepharose to identify the Al-binding protein. For 30 normal subjects 54% of the total Al in serum was non-ultrafiltrable; for 30 patients with chronic renal failure being treated by hemodialysis 67% was non-ultrafiltrable. In both groups transferrin was identified as the major Al-binding protein in the serum. Results of gel-filtration studies should be interpreted with caution: some gel media adsorb "free" Al, which can be subsequently taken up by transferrin or desferrioxamine passing through the column. We find affinity chromatography to be a specific and reliable method, suitable for use in quantitative studies.
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