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Biomedical subjects

A P Read

Publications and source records attributed to A P Read.

100 records · Page 6Linked to original sources
PubMed1981

Matching for properdin factor B (Bf) in renal transplantation.

Forty-five donor and recipient primary cadaveric kidney transplant pairs were phenotyped for the properdin factor B (Bf) polymorphism. Graft survival was analyzed on the basis of Bf matching between donor and recipient. Patients receiving a Bf-identical kidney had significantly better graft survival than those receiving a Bf-incompatible kidney (P = 0.045). It is postulated that Bf, which maps in the major histocompatibility system, is a marker for genes of importance in kidney transplant survival.

Complement Factor B↗
PubMed1981

Apparent prevention of neural tube defects by periconceptional vitamin supplementation.

An earlier preliminary paper is expanded. Women who had given birth to one or more infants with a neural tube defect were recruited into a trial of per conceptional vitamin supplementation. Two hundred mothers attending five centres were fully supplemented (FS), 50 were partially supplemented (PS), and 300 were unsupplemented (US). Neural tube defect recurrences in the study pregnancies were 1 (0.5%), in FS, none in PS, and 13 (4%) in US mothers. The difference in outcome between FS and US mothers is significant. The most likely explanation is that supplementation has prevented some neural tube defects, but further studies are needed.

Adolescent↗
PubMed1980

Comparison of pregnancy outcome after amniocentesis for previous neural tube defect or raised maternal serum alphafetoprotein.

Amniocentesis was performed in 219 pregnancies because a previous pregnancy produced a fetus with neural tube defect (NTD) and in 212 pregnancies in which the indication for amniocentesis was a high maternal serum alphafetoprotein (AFP) level. The proportion of abnormal fetuses, the frequency of low birth weight infants, and the frequency of undesired fetal loss were significantly greater in the group with high maternal serum AFP, in which there was also a significant excess of male births. It is concluded that maternal serum AFP screening defines a group of high risk pregnancies. The greater fetal loss and low birth weight associated with high maternal serum AFP levels were not the result of amniocentesis but were an inherent feature of these pregnancies.

Adult↗
PubMedDate not supplied

A transcription factor involved in skeletal muscle gene expression is deleted in patients with Williams syndrome.

Williams-Beuren syndrome (WS) is a developmental disorder caused by a hemizygous microdeletion of approximately 1.4MB at chromosomal location 7q11.23. The transcription map of the WS critical region is not yet complete. We have isolated and characterised a 3.4 kb gene, GTF3, which occupies about 140 kb of the deleted region. Northern blot analysis showed that the gene is expressed in skeletal muscle and heart, and RT-PCR analysis showed expression in a range of adult tissues with stronger expression in foetal tissues. Part of the conceptual GTF3 protein sequence is almost identical to a recently reported slow muscle-fibre enhancer binding protein MusTRD1, and shows significant homology to the 90 amino-acid putative helix-loop-helix repeat (HLH) domains of the transcription factor TFII-I (encoded for by the gene GTF2I). These genes may be members of a new family of transcription factors containing this HLH-like repeated motif. Both GTF3 and GTF2I map within the WS deleted region, with GTF2I being positioned distal to GTF3. GTF3 is deleted in patients with classic WS, but not in patients we have studied with partial deletions of the WS critical region who have only supravalvular aortic stenosis. A feature of WS is abnormal muscle fatiguability, and we suggest that haploinsufficiency of the GTF3 gene may be the cause of this.

Amino Acid Sequence↗