Whaley K
Western Infirmary
Network
Latest external collaboration on country level. Dive into details by clicking on the dots.
Publication
Featured researches published by Whaley K.
The Lancet | 1970
Whaley K; R. B. Goudie; John Williamson; George Nuki; W.Carson Dick; W W Buchanan
Abstract The prevalence of liver disease in patients with rheumatoid arthritis, Sjogrens syndrome with rheumatoid arthritis, and Sjogrens syndrome without rheumatoid arthritis, has been studied, using mitochondrial antibody as a marker. Clinical and/or biochemical evidence of liver disease was found in 6% of patients with Sjogrens syndrome without rheumatoid arthritis, 1·5% of patients with Sjogrens syndrome and rheumatoid arthritis, and 0·66% with rheumatoid arthritis alone. It is suggested that liver disease is a feature of Sjogrens syndrome.
Human Genetics | 1992
A. Theriault; E. Boyd; Whaley K; James M. Sodetz; J.M. Connor
SummaryThe genes encoding the α and β subunits of human complement protein C8 previously mapped to chromosome 1 have been further localised to 1p32 by in situ hybridisation using biotinylated 2.4-kb human cDNA clones encoding the α and β subunits of human complement protein C8 as probes.
Human Genetics | 1991
Z. Siddique; A.R. McPhaden; David F. Lappin; Whaley K
SummaryRestriction fragment length polymorphism analysis, the polymerase chain reaction and nucleotide sequencing have been used to characterise a single base substitution (G→T) at nucleotide 8863 in the C1-inhibitor gene. This destroys the 5′ donor splice site recognition motif of the sixth intron. Family studies suggest that the mutation is responsible for type I hereditary angio-oedema in a studied kindred.
Clinical Genetics | 2008
A. R. McPhaden; G. D. Birnie; Whaley K
Four out of 12 kindreds with Type I hereditary angio‐oedema (HAE) were shown to have unique disease‐related restriction fragment length polymorphism (RFLPs) in one allele of the C1‐inhibitor gene. These RFLPs were used to localise the gene mutations responsible for them in each family. The four mutations affected exon 4, exon 6, exon 7 and exon 8, respectively. Mutations in exon 6 and exon 8 have not been described previously in Type I HAE. The other two mutations which comprised an exon 4 deletion and an exon 7 deletion have already been documented by other investigators. In each family the mutation was seen to cosegregate with the disease. Detection of a disease‐related RFLP in 30% of the Type I HAE kindred tested is higher than other published studies, and reflects the larger number of restriction enzymes employed. These results suggest that Type I HAE is likely to be associated with a multiplicity of gene mutations as is seen in other genetic diseases. A new C1‐inhibitor gene‐related RFLP in the normal population was also characterised. This may be useful as an indirect marker of the mutant C1‐inhibitor allele in certain families with Type I HAE.
International Archives of Allergy and Immunology | 1981
David F. Lappin; Whaley K
The production of the second complement component (C2) by human monocytes in culture was inhibited by increasing their intracellular concentrations of cAMP following the addition to the culture medium of dibutyryl-cyclic AMP, 8-bromo-cyclic AMP, theophylline, isobutylmethylxanthine, cholera toxin or adenosine. The effects were not due to cytotoxicity or loss of cells from the monolayers, and therefore must reflect a decreased synthesis of section of C2. Although dibutyryl-cyclic GMP enhanced C2 production, 8-bromo-cyclic GMP, ascorbic acid and sodium nitroprusside did not have this effect. These observations suggest that the action of dibutyryl-cyclic GMP is not due to elevation of cyclic GMP levels and that cyclic GMP levels do not play a major role in C2 production by monocytes.
Scottish Medical Journal | 1980
A. E. El-Ghobarey; D. J. P. Sloane; Whaley K
During the two-year period (1st October 1974–30th September 1976), 2979 sera were tested for DNA antibodies by the Farr test. One thousand six hundred and ninety-five of these were tested because they had high ANA titres (1/256 or greater). In this group 285 sera were found to have raised DNA binding capacities (DNA-bc), 86 of which were found in patients having diagnoses other than SLE. When the diagnoses were reviewed following the finding of a raised DNA-bc, 55 of these patients were found to be suffering from SLE. Of the 1284 sera tested for DNA antibodies without the prior ANA screening procedures, 288 were positive, 36 of which came from patients not considered to have SLE; 30 of these patients were subsequently shown to have SLE. Thus the DNA-bc test is an important tool in the diagnos is of SLE, and the ANA test appears to be a valuable screening procedure. The level of DNA-bc was not of any diagnostic value.
Biochemical Journal | 1992
David F. Lappin; D Guc; A Hill; T McShane; Whaley K
Seminars in Liver Disease | 1997
Whaley K; Wilhelm J. Schwaeble
Nature | 1981
Whaley K; David F. Lappin; T. Barkas
Biochemical Journal | 1987
A O Hamilton; L Jones; L Morrison; Whaley K