Bernard John Morley

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Two siblings (case 1 and case 2) with homozygous C1q deficiency are described. Both presented with a photosensitive rash, and during follow-up case one developed SLE with nephrotic range proteinuria. Case 2 had microscopic hematuria with a past history of macroscopic hematuria. Renal biopsies revealed mesangioproliferative glomerulonephritis in case 1 and(More)
The molecular basis of hereditary complement factor I deficiency is described in two pedigrees. In one pedigree, there were two factor I-deficient siblings, one of whom was asymptomatic and the other suffered from recurrent pyogenic infections. Their factor I mRNA was analyzed by reverse transcription of fibroblast RNA followed by amplification using the(More)
Acetylcholine receptors that bind nicotine with high affinity but do not bind alpha-bungarotoxin have recently been immunoaffinity purified from brains of chickens and rats (Whiting and Lindstrom, 1986a, b; Whiting and Lindstrom, 1987a). Antisera to these receptors bind to the nicotinic receptors that regulate cation channel opening on chick ciliary(More)
Human autoimmune diseases thought to arise from the combined effects of multiple susceptibility genes include systemic lupus erythematosus (SLE) and autoimmune diabetes. Well-characterised polygenic mouse models closely resembling each of these diseases exist, and genetic evidence links receptors for the Fc portion of immunoglobulin G (FcR) with their(More)
OBJECTIVE To identify intervals containing systemic lupus erythematosus (SLE) susceptibility alleles in the BXSB strain of mice. METHODS We analyzed 286 (B10 x [B10 x BXSB]F1) backcross mice for a range of phenotypic traits associated with the development of SLE in BXSB mice. The mice were genotyped using 93 microsatellite markers, and the linkage of(More)
The BXSB mouse strain is an important model of glomerulonephritis observed in systemic lupus erythematosus (SLE). Linkage studies have successfully identified disease-susceptibility intervals; however, extracting the identity of the susceptibility gene(s) in such regions is the crucial next step. Congenic mouse strains present a defined genetic resource(More)
We describe four cases (from three families) of hereditary factor I deficiency, bringing the total number of cases now reported to 23. In one family there are two affected siblings: one has suffered recurrent pyogenic infections; the other is asymptomatic. In the second family, the patient had recurrent pyogenic infections and a self-limiting vasculitic(More)
OBJECTIVE To describe a new kindred with Clq deficiency and to identify the molecular lesions responsible for complete functional C1q deficiency in this and 2 other previously described kindreds. METHODS The A-, B-, and C-chain genes of C1q were amplified by polymerase chain reaction, cloned, and sequenced. The DNA sequence was checked for mutations. (More)
The C57BL/6 (B6) and C57BL/10 (B10) inbred mouse strains are among the most commonly used in biological research and have provided the genetic background for the construction of many congenic strains (Klein 1989). The two substrains were derived from the parental C57BL stock and were separated prior to 1937. Since then, they have been thought to possess a(More)
BXSB mice spontaneously develop a lupus-like syndrome that is accelerated by the Yaa gene (Y-linked autoimmune accelerator). We studied the phenotype of disease in (B10 x BXSB)F1 and (BXSB x (B10 x BXSB)F1) backcross mice and genotyped 224 backcross animals to allow a microsatellite-based genome-wide linkage analysis to be conducted. In the backcross(More)