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Biomedical subjects

D C Candy

Publications and source records attributed to D C Candy.

At least 73 records · Page 4Linked to original sources
PubMed1984

Familial defect of polymorph neutrophil phagocytosis associated with absence of a surface glycoprotein antigen (OKMI).

Two siblings with delayed separation of the umbilical cord, recurrent skin ulceration and dental sepsis were shown to have defective neutrophil phagocytosis of opsonized yeast (S. cerevisiae) and respiratory burst to opsonized and unopsonized zymosan. Increased activity in the NBT reduction test, normal ingestion and killing of S. aureus, and normal spontaneous and directional motility were also demonstrated. These abnormalities of neutrophil phagocytosis were confined to the affected siblings; their healthy parents and brother showed normal neutrophil function. Both children had a polymorph neutrophil leucocytosis, and had normal humoral and cell-mediated immunity. SDS electrophoresis of neutrophil cell membrane preparations showed absence of a glycoprotein band of 175,000 daltons, which was present in the parents' neutrophils in reduced amounts. OKMI monoclonal antibody, which recognized the C3bi receptor (CR3) failed to bind to the affected siblings neutrophils. The findings in these children emphasize the importance of this receptor in phagocytosis, and possibly other neutrophil functions.

Antigens, Surface↗
PubMed1983

Plasmid-mediated adhesion in enteropathogenic Escherichia coli.

A survey of classical serotype enteropathogenic Escherichia coli has been made with respect to their plasmid profile and ability to adhere to HEp-2 cells. Thirty-one of the 32 strains examined contained a 50-70 Md plasmid, and many exhibited HEp-2 adherence. Strain E2348 (0127:H6), which causes diarrhea in volunteers and is HEp-2-adhesive, was chosen for further study. The large 55 Md plasmid in E2348, pMAR2, has been marked with a transposon coding for ampicillin resistance. E2348 that has been cured of pMAR2 loses the ability to adhere to HEp-2 cells, while HB101, a nonadherent E. coli K12, acquires HEp-2 adhesiveness after gaining this plasmid. Plasmid presence was also shown to correlate with in vivo adhesion to intestine, using the colostrum-deprived piglet model.

Animals↗
PubMed1983

Increased adhesion of Escherichia coli to mucosal cells from infants with protracted diarrhoea: a possible factor in the pathogenesis of bacterial overgrowth and diarrhoea.

Mucosal adhesion of bacteria has been studied in eight infants with protracted diarrhoea and malnutrition, using a buccal epithelial cell technique. A known non-adhesive strain of Escherichia coli (O1:K1:H7) adhered to a significantly greater (p less than 0.001) proportion of buccal epithelial cells from patients with protracted diarrhoea, compared with children with acute diarrhoea, healthy infants, and healthy adults. Also, Enterobacteria isolated from the jejunum or stools of patients with protracted diarrhoea adhered to far greater numbers of their own buccal epithelial cells compared with healthy adults. These results suggest that bacterial adhesion may play an important role in the pathogenesis of protracted diarrhoea.

Adhesiveness↗
PubMed1982

Loperamide modifies Escherichia coli, heat-stable enterotoxin-induced intestinal secretion.

We have shown previously that loperamide, an opiate analogue, inhibits cholera-toxin- and prostaglandin E2-induced secretion in the rat small intestine. In these studies loperamide modified secretion induced by partially purified Escherichia coli, heat-stable enterotoxin in infant mice. The drug was effective whether administered before or after established secretion. These experiments provide further suggestive evidence that loperamide has a broad spectrum of antisecretory activity.

Animals↗
PubMed1981

Loperamide: studies on its mechanism of action.

The effects of loperamide on net solute and water absorption, and prostaglandin E2 (PGE2) and cholera toxin-induced secretion were studied in the rat jejunum using an in vivo steady-state perfusion technique. Loperamide stimulated absorption of fluid, electrolytes, and glucose and reversed PGE2 and cholera toxin-induced secretion to absorption; this opiate analogue had no effect on cholera toxin stimulation of adenylate cyclase activity or the rise of tissue cyclic AMP (cAMP) concentrations. The opiate antagonist, naloxone, reduced the antisecretory effects of loperamide without affecting tissue levels of cAMP. These results indicate that loperamide inhibits PGE2 and cholera toxin-induced secretion, and that this phenomenon is independent of any direct effect that cholera toxin has on the adenylate cyclase system. The action of naloxone suggests, but does not prove, that loperamide exerts its effect via opiate receptors.

Adenylyl Cyclases↗
PubMed1981

A family study of protracted diarrhoea in infancy.

A family study of undiagnosed protracted diarrhoea in infancy was undertaken, based on 67 such patients, seen at The Hospital for Sick Children, London, over a 6-year period. All were fully investigated with the exclusion of those with known cause, such as coeliac disease, cow's milk intolerance, or enteric infections. The families were traced and visited. The material is certainly heterogeneous. In the case of five patients the condition was associated with a syndrome. The remaining 62 index patients could be divided into a group of 15 with severe illness and 47 with a milder illness. Six had onset before one month of age, four died, and in five the diarrhoea lasted more than 12 months and the children persistently failed to thrive. These 15 severe cases had six affected sibs out of 22 (Weinberg proband method) and in all but one of these affected sibs the condition was also severe. Two further sibs had had protracted diarrhoea, but this had not been fully investigated. The 47 index patients with milder disease had 68 sibs of whom only one was affected (this boy was one of the severely affected index patients), and one other sib had protracted diarrhoea which was not fully investigated. It is proposed that the severe group includes one or more autosomal recessive entities, in which the basic defects are not yet known, but are likely to be inborn metabolic errors.

Birth Weight↗
PubMed1980

Short stature as the primary manifestation of coeliac disease.

Thirty-four patients with short stature of undetermined cause and no gastrointestinal symptoms underwent jejunal biopsy for exclusion of coeliac disease. Eight had subtotal or severe partial villous atrophy and seven showed a significant acceleration in height and weight velocity after the introduction of a gluten-free diet. Short stature by itself, in the complete absence of gastrointestinal symptoms, is an indication for jejunal biopsy, particularly if bone age is delayed by more than 4 years and/or there are associated haematological abnormalities.

Adolescent↗
PubMed1980

Yeast opsonisation in children with chronic diarrhoeal states.

Four patients with defective yeast opsonisation and protracted diarrhoea are reported. Plasma infusions improved the opsonising function in all 4 and the diarrhoea in 3. This immunological abnormality was assessed in 100 sequential patients with chronic diarrhoea associated with various gastrointestinal disorders; 52 with protracted diarrhoea and failure to thrive of undetermined cause, 26 with 'toddler diarrhoea', 8 with coeliac disease, 5 with chronic inflammatory bowel disease, and 9 with miscellaneous disorders. 23% of the patients with protracted diarrhoea of undetermined cause had defective opsonisation, a greater proportion (P less than 0.05) than that in 'toddler diarrhoea' or the remaining patients, in whom the frequency (4%) was similar to that (5%) in healthy populations. We suggest that yeast opsonisation be tested in children with protracted diarrhoea, as plasma infusions can be an effective form of treatment.

Child, Preschool↗
PubMed1979

Subcellular fractionation studies of the intestinal mucosa in congenital sucrase--isomaltase deficiency.

1. Jejunal biopsy specimens from three children with congenital sucrase-isomaltase deficiency were assayed for disaccharidase activity and were subjected to analytical subcellular fractionation with enzymic microanalysis. 2. By use of the highly sensitive fluorigenic modification of the disaccharidase assay, brush-border sucrase and isomaltase activities were depressed but nevertheless detectable in each child. 3. Apart from the expected decrease in brush-border alpha-glucosidase activity, the other enterocyte marker-enzyme activities were normal. 4. There were no abnormalities in the enterocytes of any child on analytical subcellular fractionation or on electron microsocopy.

Acetylglucosaminidase↗