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Biomedical subjects

J F Soothill

Publications and source records attributed to J F Soothill.

At least 109 records · Page 6Linked to original sources
PubMed1976

Progressive restriction of antigen binding by human foetal thymus lymphocytes.

The proportion of foetal thymus lymphocytes (FTL) that binds the bacterial antigens beta-galactosidase and flagellin is high in early foetal life. Binding of beta-galactosidase, and the response by FTL in mixed lymphocyte culture falls during gestation. Some FTL bound both antigens, suggesting that immature lymphocytes are not fully restricted in their capacity to recognize antigens. Such findings have been reported in foetal lymphocytes from other species. We suggest that cellular diversity may partly be generated by progressive restriction of antigen recognition by individual lymphocytes, which may result from progressive stabilization of genetic repression during lymphocyte multiplication.

Antibody Specificity↗
PubMed1976

The effect of amino acid restricted diets on the clearance of 125I-labelled polyvinyl pyrrolidone in mice.

Impaired overall phagocytic function, as measured by clearance of radio-labelled polyvinyl pyrrolidone from the blood (KPVP), has been demonstrated in mice whose dietary intake of the essential amino acids phenylalanine and tryptophan was reduced to less than a quarter of that in a standard diet which supported optimal growth. This was associated with loss in weight of body, liver, spleen and thymus and an increase in the phagocytic index, alphaPVP.

Amino Acids↗
PubMed1975

IgA deficiency, epilepsy, and phenytoin treatment.

In a prospective study of thirty-two children with seizures treated with phenytoin (diphenylhydantoin), five had low levels of serum-IgA before treatment. All of these were among the fifteen who had had febrile convulsions in infancy. IgA levels fell significantly during 6 months treatment in the fourteen patients studied sequentially. Treated children with low serum-IgA had normal numbers of lymphocytes with surface IgA. This suggests that phenytoin causes failure of terminal differentiation of B lymphocytes, and is the first known cause of this, the commonest mechanism of immunoglobulin deficiency.

Adolescent↗
PubMed1975

Cyclophosphamide treatment in steroid-sensitive nephrotic syndrome of childhood.

An 8-week course of 3 mg. per kg. body-weight per day of cyclophosphamide was administered to eighty-two children with steroid-senstitive nephrotic syndrome. One died, and of the remainder, 69% were in remission after 1 year and 44% after 4-years. Older children and those in whom cyclophosphamide was given during a steroid-maintained remission fared better.

Administration, Oral↗
PubMed1975

Leukaemia in children and their grandparents: studies of immune function in six families.

Seven of 500 children with acute leukaemia seen over a 15-year period were known to have a close relative with leukaemia or lymphoma. In each case the affected relative was a grandparent of the child, six of the seven being paternal grandparents. Investigation of thses six families showed that the fathers, who had two affected first-degree relatives, had lower lymphocyte counts and higher serum IgA concentrations than paired controls. Atopy, repeated infections and rheumatic disease were common amongst the parents and their sibs. The findings suggest a possible immunodeficiency basis for leukaemia in these families and perhaps also for acute lymphoblastic leukaemia of childhood in general. In the only family in which three generations, including both leukaemic patients, were available for HL-A typing, the affected grandson had not inherited either of his affected grandmother's haplotypes.

Adolescent↗
PubMed1975

Immunodeficiency and infantile bone and joint infection.

Fifteen patients with infantile bone and joint infections were studied immunologically and clinically, 3 at the time of illness and 12 later. Abnormality of immunoglobulins, or complement, or phagocytes was found in 9 patients; 6 were within normal limits for the tests undertaken. Immunodeficiency is probably responsible for the subdued clinical signs of infection and for delayed diagnosis in some patients. It was also related to the extent of femoral head damage in infective arthritis of the hip and to the incidence of wound infection in late elective surgery.

Adolescent↗
PubMed1975

Familial opsonization defect associated with fatal infantile dermatitis, infections, and histiocytosis.

Members of four generations of a family had a defect of serum opsonization for yeast phagocytosis consistent with dominant inheritance. 2 were healthy, one had chronic osteomyelitis, and the fourth developed a fatal illness in infancy characterized by exfoliative dermatitis, diarrhoea, multiple bacterial infections, and failure to thrive, which resembled the two prevously reported cases with this opsonization defect. At necropsy the infant also had lymphoid depletion, which was possibly secondary, and massive histiocytic infiltration.

Adult↗
PubMed1975

The inhibition of complement-dependent lymphocyte rosette formation by the sera of children with steroid-sensitive hephrotic syndrome and other renal diseases.

Sera from patients with steroid-sensitive nephrotic syndrome (SSNS) in relapse, Henoch-Schonlein purpura with nephritis (HSP) and acute post-strptococcal glomerulonephritis inhibited EAC rosette formation by normal human lymphocytes; a similar effect was seen in some patients with focal glomerulosclerosis, but not in patients with congenital neophrotic syndrome. There was significantly less inhibition by sera of SSNS and HSP patients in remission. There were fewer EAC rosette-forming cells (EAC-RFC) in the blood of three patients with SSNS in relapse, suggesting that such blockade occurred in vivo. These findings, interpreted as evidence of circulating activated C3 in the sera, provide further indirect evidence of the immunopathogenesis of these diseases. Sera of healthy adults inhibited EAC rosette formation to a small extent which correclated inversely with the numbers of EAC-RFC in their blood. The EAC rosette inhibition test may be sensitive enough to detect normal variations of complement activation in healthy individuals.

Adenoids↗