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1. The mucoprotein from pig gastric mucus has been purified by equilibrium centrifugation in a CsCl gradient. 2. This procedure removes the non-covalently bound protein, which is closely associated with the mucoprotein and not easily removed from it by gel filtration. 3. The purified mucoprotein is separable by gel filtration into a high-molecular-weight mucoprotein A (mol.wt. 2.3x10(6)) and a low-molecular-weight mucoprotein B/C (mol.wt. 1.15x10(6)). 4. These two mucoproteins have the same chemical analysis namely fucose 11.3%, galactose 26%, glucosamine 19.5%, galactosamine 8.3% and protein 13.6%. 5. Mucoprotein A contains 3.1% ester sulphate. 6. These mucoproteins are isolated without enzymic digestion and have a higher protein content than the blood-group-substance mucoproteins from proteolytic digestion of gastric mucus. Detailed amino acid analysis shows that the extra protein in the non-enzymically digested material is composed of amino acids other than serine and threonine. 7. Mucoproteins A and B/C contain respectively 130 and 9 half-cystine residues per molecule of which about 78 and 6 residues are involved in disulphide linkages. 8. Cleavage of these disulphide linkages by mercaptoethanol splits both mucoproteins into four equally sized subunits of mol.wt. 5.2x10(5) for mucoprotein A and 2.8x10(4) for mucoprotein B/C. 9. The sole N-terminal amino acid of mucoprotein A is aspartic acid, whereas mucoprotein B/C has several different N-terminal amino acid residues.

SUMMARYWe measured the concentration of bile acids in gastric aspirates from patients who had had operations for peptic ulcer. Some patients were asymptomatic and some had postoperative symptoms of the type that have been attributed to duodenogastric reflux. Samples were obtained via a nasogastric tube when the patients were fasting, after food, after pentagastrin, and overnight. We related the concentration and amount of bile acid and the volume aspirated to the presence or absence of symptoms and compared the results with radiological and endoscopic assessments of duodenogastric reflux. The most useful index to discriminate between symptomatic and asymptomatic patients was the amount of bile reflux in half an hour's aspiration from the fasting stomach; this we have termed 'fasting bile reflux' (FBR) and expressed as ,umol bile acids refluxing/hour. A figure greater than 120 ,umol/h was present in 17 of 22 symptomatic patients and in all who complained of bile regurgitation or bile vomiting. The FBR was less than 120 ,tmol/h in all of 20 asymptomatic patients, although some of them had reflux detected radiologically and endoscopically.

SUMMARY.We describe a simple, sensitive assay for oxalate in urine or plasma. Acidified urine is pretreated by dilution with neutral phosphate buffer and passage through a C,8 cartridge. Stabilized plasma is diluted with neutral acetate buffer and oxalate extracted using a strong anion exchange cartridge. Treated samples are applied to an ion-paired chromatographic system and oxalate detected electrochemically. Recovery of oxalate from augmented samples exceeded 97% from both urine and plasma. Within-and between-assay coefficients of variation assessed at three concentrations were, respectively, better than 4.1% and 8.4% for urine and 3.9% and 5.2% for plasma. The reference range for urinary oxalate excretion is 109-497 pmo1/24 h. The range for plasma oxalate concentration is 0.6-2.8 pmol/L or 0.7-3.9 pmol/L after an overnight fast or without dietary restriction, respectively. Urine and plasma oxalate concentrations from this method, gave correlation coefficients (r) of 0.97 and 0.98, respectively, when compared with those from established oxalate oxidase based assays.

Background: The increase in creatinine in patients on fibrate therapy is well-recognized, but its mechanism is not clearly understood. A study by Hottelart et al. suggested that fibrate-induced creatininaemia was due to the effect of fibrates on creatinine metabolism as opposed to a decline in renal function. To address this hypothesis, we have monitored renal function in a group of hyperlipidaemic patients before commencing fibrate treatment and after three months of therapy. Methods: We studied 12 subjects (10 men, 2 women), median age 43.5 y (range 33-70 y). Serum creatinine, cystatin C, creatine kinase and fasting lipids were measured. Results: We observed statistically significant increases in concentrations of serum creatinine (P , 0.005) and cystatin C (P , 0.01). Concentrations of both analytes increased in 10 (83.3%) of the patients. In these patients, the median increases were 15.1% (range 5.5 -23.2%) for creatinine and 9.9% (range 1.1 -26.1%) for cystatin C. Conclusions: These results suggest that the decrease in estimated glomerular filtration rate, observed in patients undergoing fibrate therapy, is a genuine effect on kidney function rather than a change in creatinine metabolism as previously postulated, since the rises in serum creatinine concentration were reflected by rises in cystatin C, an independent marker of renal function.

The general availability of potent sulphonylurea preparations and the ease with which they can be taken, may explain the increase in both the iatrogenic and factitious hypoglycaemia caused by them (Refs 1,2). Whereas insulin‐induced hypoglycaemia is relatively easy to diagnose in the laboratory, that caused by a sulphonylurea may not be, mainly because its biochemical features in many respects resemble those observed in insulinoma. In both conditions plasma insulin and C‐peptide concentrations are inappropriately high during hypoglycaemia and B‐hydroxybutyrate levels are low. The only sure way to distinguish between them in the absence of a positive history of ingestion, is by detection of sulphonylurea in the patient's blood. We describe here a typical case presentation and a preliminary assessment of the incidence of sulphonylurea‐induced factitious hypoglycaemia from a survey of 151 cases of “spontaneous” hypoglycaemia.

Colorectal cancer (CRC) causes 20 000 deaths per annum in the UK alone. Screening has been shown to reduce mortality but debate exists as to which approach to use. Direct visualization of the colorectum has the advantage that it detects lesions most effectively and is required at less frequent intervals, but the procedure is invasive and at present too costly for screening purposes. Faecal occult blood measurement, despite its limitations, is currently the recommended screening method, with follow-up of positive tests by colonoscopy or other visualization techniques. This strategy has been shown to reduce mortality from CRC by about 20% and screening trials directed towards individuals in the over 50 years age group are underway in the UK and elsewhere. Future developments in CRC screening include colorectal visualization by computed colonography -- a less-invasive alternative to colonoscopy. Developments in stool analysis are also occurring. Examination of faecal samples for cellular products derived from neoplasms (e.g. calprotectin) may prove more sensitive and specific than faecal occult blood measurements. In addition, detection of altered DNA in faeces is being investigated by molecular biology techniques. Using a multi-target assay panel to detect point mutations and other neoplasia-associated DNA abnormalities may be an effective strategy for CRC screening in the future.

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