By conventional linkage analysis this eliminates a minimum of 10.4 cM including and surrounding the SAA gene cluster as the site of the FMF mutation although SAA proteins are prominent physiologic markers of the acute attacks.
By conventional linkage analysis this eliminates a minimum of 10.4 cM including and surrounding the SAA gene cluster as the site of the FMF mutation although SAA proteins are prominent physiologic markers of the acute attacks.
Sera samples of 168 patients with familial Mediterranean fever (FMF) and their 184 first degree relatives were analyzed for the presence of autoantibodies to ssDNA, dsDNA, poly (I), poly (G), cardiolipin, histones, RNP and Ro(SSA), using an enzyme linked immunosorbent assay (ELISA).
Sera samples of 168 patients with familial Mediterranean fever (FMF) and their 184 first degree relatives were analyzed for the presence of autoantibodies to ssDNA, dsDNA, poly (I), poly (G), cardiolipin, histones, RNP and Ro(SSA), using an enzyme linked immunosorbent assay (ELISA).
To examine critically whether there is linkage between FMF and the immunogenetic region (major histocompatibility complex-MHC) on chromosome 6, including the HLA, BF, and GLO1 loci, blood samples from members of 13 nuclear Armenian families were tested for these genetic markers.
To examine critically whether there is linkage between FMF and the immunogenetic region (major histocompatibility complex-MHC) on chromosome 6, including the HLA, BF, and GLO1 loci, blood samples from members of 13 nuclear Armenian families were tested for these genetic markers.
Renal amyloidosis (RA) and recurrent fever of unknown origin (RFUO) are characteristics of familial Mediterranean fever (FMF), a human disorder inherited as an autosomal-recessive trait.
Localizing MEF more precisely on the basis of homozygosity rates alone would be difficult, for two reasons: First, the high FMF carrier frequency increases the chance that inbred offspring could have the disease without being homozygous by descent at MEF.
Localizing MEF more precisely on the basis of homozygosity rates alone would be difficult, for two reasons: First, the high FMF carrier frequency increases the chance that inbred offspring could have the disease without being homozygous by descent at MEF.
Using DNAs from affected Israeli families, we have recently mapped the gene causing FMF (designated MEF) to the short arm of chromosome 16, with two-point lod scores in excess of 20.
Using DNAs from affected Israeli families, we have recently mapped the gene causing FMF (designated MEF) to the short arm of chromosome 16, with two-point lod scores in excess of 20.
Recently, linkage was demonstrated between FMF and the VNTR probes 3'HVR and 5'HVR of the alpha-globin complex at 16p13.3 (theta = 0.06-0.10, Lodmax = 9.76-14.47) and the insertion/deletion polymorphism detected by the probe CMM65 of D16S84 (theta = 0.04, Lodmax = 9.17).
Recently, linkage was demonstrated between FMF and the VNTR probes 3'HVR and 5'HVR of the alpha-globin complex at 16p13.3 (theta = 0.06-0.10, Lodmax = 9.76-14.47) and the insertion/deletion polymorphism detected by the probe CMM65 of D16S84 (theta = 0.04, Lodmax = 9.17).
Using a combination of cosmid walking and screening for P1, PAC, BAC, and YAC clones, we have generated a contig of genomic clones spanning approximately 1050 kb that contains the FMF critical region.