PubMed Health⌕ Search

Biomedical subjects

E A Ahmed

Publications and source records attributed to E A Ahmed.

6 recordsLinked to original sources
PubMed1998

The need for revised standards for skinfold thickness in infancy.

Skinfold standards provide a useful indication of subcutaneous fat. To evaluate skinfold thickness of 252 Cambridge infants over the first 2 years of age, SD scores relative to the Tanner standards were calculated, taking account of skewness in the standards. Cambridge SD scores were low, varying according to age from -1.2 to -1.8 for triceps and -0.6 to -1.2 for subscapular skinfolds. The Tanner skinfold standards were last revised 30 years ago, at a time of high prevalence of infantile obesity, and the present and other studies indicate that infants are now thinner. There is a need for new skinfold standards to reflect this change. Since the Cambridge infants contributed to the recent British height and weight references, it is suggested that their skinfold measurements could also serve as reference points.

Age Factors↗
PubMed1997

Allelic polymorphisms at the H-2A and HLA-DQ loci influence the response of murine lymphocytes to the Mycoplasma arthritidis superantigen MAM.

Mycoplasma arthritidis, an agent of rodent arthritis, produces a potent superantigen (SAg), MAM. Previous work established that MAM is presented to T cells by murine H-2E or the homologous human HLA-DR molecules and that lymphocytes lacking a functional H-2E molecule fail to respond to MAM. Recently, more potent and purified preparations of MAM of known protein content have become available. This enabled us to more effectively compare the response of MAM with that of other SAgs by using lymphocytes from mice whose cells express different H-2A and HLA-DQ molecules. Here we demonstrate that cells from some H-2E-negative mouse strains respond to higher concentrations of MAM. By use of inbred, congenic, and recombinant mice, we show that these differences are, in fact, exercised at the level of the major histocompatibility complex (MHC) and that allelic polymorphisms at H-2A influence reactivity to MAM. In addition, polymorphisms at HLA-DQ, the human homolog of H-2A, also influence responsiveness to MAM. Cells expressing DQw6 (HLA-DQA1*0103 and DQBI*0601 chains) gave much higher responses to MAM than did cells expressing DQw8 (DQA1*0301 and DQB1*0302 chains). In fact, responses of lymphocytes expressing DQB1*0601 chains homozygously were as high as those observed for cells expressing a functional H-2E molecule. Murine lymphocytes responded less well to staphylococcal enterotoxin B (SEB) and SEA, but mouse cells expressing human MHC molecules gave much higher responses. The patterns of reactivity observed with cells expressing the various murine and human alleles differed for MAM, SEB, and SEA, suggesting that each of these SAgs interacts with different regions or residues on MHC molecules. It has been hypothesized that SAgs might play a role in susceptibility to autoimmune disease. Allelic polymorphisms at MHC loci might therefore influence susceptibility to autoimmune disease by affecting immunoreactivity to specific superantigens.

Alleles↗
PubMed1997

Expression of the superantigen Mycoplasma arthritidis mitogen in Escherichia coli and characterization of the recombinant protein.

Mycoplasma arthritidis mitogen (MAM), is a soluble protein with classical superantigenic properties and is produced by an organism that causes an acute and chronic proliferative arthritis. Unfortunately, the process of obtaining purified MAM from M. arthritidis culture supernatants is extremely time-consuming and costly, and very little material is recovered. Thus, our laboratory has expressed MAM in Escherichia coli by using a protein fusion expression system. The construction and expression of recombinant MAM (rMAM), as well as a comparison of the biological properties of rMAM to those of native MAM, are discussed. Briefly, conversion of the three UGA codons to UGG codons was required to obtain full-length expression and mitogenic activity of rMAM. Antisera to native MAM recognized both rMAM and the fusion protein. The T-cell receptor Vbeta and major histocompatibility complex class II receptor usages by rMAM and the fusion protein were identical to that of native MAM. In addition, the ability to induce suppression and form the superantigen bridge could also be demonstrated with rMAM. Importantly, dose-response experiments indicated that homogeneous native MAM and rMAM were of equal potency. Thus, MAM has been successfully expressed in E. coli, thereby creating a viable alternative to native MAM.

Antigens↗
PubMed1993

Genomic composition and allelic polymorphisms influence V beta usage by the Mycoplasma arthritidis superantigen.

The Mycoplasma arthritidis superantigen (MAM) is produced by an organism that causes systemic disease in rodents leading to chronic proliferative arthritis. MAM is a typical superantigen that requires presentation to T cells by MHC molecules without processing and T cell recognition of MAM occurs through the V beta chains of the TCR. Several major findings are presented here. First, different MAM-MHC class II isotype complexes may engage different sets of V beta TCR. Thus, activation of V beta 6- and V beta 8.3-bearing T cells is more dependent upon the I-E molecule of the murine H-2 MHC than is activation of cells bearing the V beta 5.1, 8.1, and 8.2 TCR. Secondly, both genomic composition and allelic polymorphisms at the V beta chain segment of the TCR exert profound effects upon the pattern of V beta that are used by MAM. Thus, in V beta b haplotype mice, MAM engages V beta 5.1, 6, and the V beta 8 family of TCR whereas in V beta a (C57BR) and V beta c (RIIIS) haplotype mice that lack various combinations of these V beta, activation of cells bearing V beta 1, 3.1, 7, and 16 can be demonstrated. These differences in V beta usage by MAM appear to be caused by both differences in the avidity of MAM for the various V beta s and to structural allelic polymorphisms in these V beta. Clonal expansion of specific V beta in vivo after injection of MAM is also dependent upon the genomic composition of the mice, because expansion of the V beta 8 TCR seen in V beta b haplotype mice (B10.RIII) whereas marked expansion of V beta 6 is seen in V beta a mice (C57BR). In as much as these TCR have been implicated in a number of experimental autoimmune diseases, MAM may represent an ideal model to evaluate the role of superantigens in the triggering of autoimmune disease.

Alleles↗
PubMed1986

Weaning practices in the United Kingdom and variations in anthropometric development.

The influence of different weaning practices on the dietary energy intake and growth of Cambridge infants has been investigated. Bottle fed children were in general given solid foods sooner, 10.6 weeks for boys and 13.9 weeks with girls: among breast-fed babies the average age was 14.9 weeks in the case of boys and 17.4 weeks for girls. All four groups of children exhibited different growth patterns from those of the NCHS and Tanner reference curves. Over the first three months both boys and girls exhibited a faster velocity of growth in weight, length and weight-for-length. After this time, however, growth velocity was slower than that of the reference children particularly among breast-fed boys who were not given solids until after 16 weeks. For most of infancy triceps and subscapular skinfold thicknesses remained around the 10th centile of the corresponding Tanner reference children, although again the babies weaned later had the lower values. Bottle-fed infants had growth patterns similar to those of the earlier weaned breast-fed babies for all parameters. It is concluded that babies grow differently now that infant feeding patterns have changed.

Breast Feeding↗