Total kallikrein activity and kallikrein activity inhibited by soybean trypsin inhibitor are significantly reduced in the plasma of patients with cystic fibrosis compared to age-matched controls.
The data exclude that ADA belongs to this linkage group while they give weak support for the inclusion of P. There is weak evidence for linkage of cystic fibrosis to PGM3, but none for linkage to HL-A.No new suggestive linkages appeared.
The data exclude that ADA belongs to this linkage group while they give weak support for the inclusion of P. There is weak evidence for linkage of cystic fibrosis to PGM3, but none for linkage to HL-A.No new suggestive linkages appeared.
Immunodiffusion of perchloric acid extracts of CEA-like material from heterozygote carrier blood indicated that the CEA-like material, which was elevated in homozygotes and heterozygotes for CF, showed only partial identity with two separate CEA preparations obtained from colon carcinomas and was not identical to either A, B, or O(H) blood group substances.
Roles for factor XII, prekallikrein and kininogen have been suggested in gouty arthritis, allergic disorders and cystic fibrosis but the evidence is not yet convincing in these disorders.
These results suggest a possible alteration in the carbohydrate moiety of alpha 2-macroglobulin in cystic fibrosis, presumably due to a defective posttranslational process.
These data show for the first time that the diminution in beta cell reserve in CF patients may be of a magnitude similar to that in IDDs in spite of their normal blood glucose and HbA1 concentrations.
alpha 2-Macroglobulin (alpha 2M) is a major plasma protease inhibitor that has been studied because of its suggested role in the pathology of cystic fibrosis (CF).
Although the level of albumin is altered in children with CF, the gene does not segregate with CF, and therefore albumin can be excluded as the site of the basic defect.
The best estimates of the genetic distances are 5 centimorgans between the DNA marker and PON and 15 centimorgans between the DNA marker and the CF locus, meaning that the location of the disease gene has been narrowed to about 1 percent of the human genome (about 30 million base pairs).
Tight linkage with CF was not found with any of the seven markers investigated, and therefore, assuming that the markers (excepting MNS and fibrinogen) are unlinked to one another, approximately half of the total genetic length of chromosome 4 may be excluded.
Tight linkage with CF was not found with any of the seven markers investigated, and therefore, assuming that the markers (excepting MNS and fibrinogen) are unlinked to one another, approximately half of the total genetic length of chromosome 4 may be excluded.
Tight linkage with CF was not found with any of the seven markers investigated, and therefore, assuming that the markers (excepting MNS and fibrinogen) are unlinked to one another, approximately half of the total genetic length of chromosome 4 may be excluded.
Tight linkage with CF was not found with any of the seven markers investigated, and therefore, assuming that the markers (excepting MNS and fibrinogen) are unlinked to one another, approximately half of the total genetic length of chromosome 4 may be excluded.
A collaborative study involving seven research groups provided an opportunity to investigate the linkage relationships between cystic fibrosis and two DNA marker loci, MET and pJ3.11 (D7S8), on an extended sample of 211 tested families.