By Magne K. Fagerhol, Diane Wilson Cox (auth.), Harry Harris, Kurt Hirschhorn (eds.)

ISBN-10: 1461583039

ISBN-13: 9781461583035

ISBN-10: 1461583055

ISBN-13: 9781461583059

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Further data will be required to ensure that this unusual finding is not due to chance. Several possible explanations for heterogeneity were proposed by Gedde-Dahl et at. (1975). There is no evidence for more than one Pi locus. The specific amino acid substitutions in Pi Sand Z types of

One direct proof of the origin of the plasma {X , AT is the observation (Sharp, 1971) that after liver transplants to {X,AT-deficient patients, their plasma {X,AT levels returned to normal and converted to the Pi M type of the donors. , 1977). Eriksson et at. (1978) have shown that alAT synthesis in vitro by cultured fetal human liver cells is sensitive to alAT in the medium. The release of alAT from the cells was suppressed by increasing concentrations of alAT in the medium. , 1979). The studies by Bagdasarian and Colman (1978) included platelets from one patient with the Pi type Z and one with absolute alAT deficiency (Pi type null) and suggest that the alAT in the granular and soluble subcellular fractions may be synthesized by the platelets while membranebound alAT may be adsorbed from plasma.

There is a wide range of clinical variation in lung disease among individuals with u , AT deficiency. , 1976). Smoking has a pronounced effect on the development of lung disease. The onset of emphysema is from 13-15 years earlier in Pi Z individuals who smoke (Black and Kueppers, 1978; Larsson, 1978). Nonsmokers can live into their sixth and seventh decades. The extent of clinical variation is not entirely accounted for by smoking history, and other factors, possibly genetic, must be involved (Black and Kueppers, 1978).

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Advances in Human Genetics 11 by Magne K. Fagerhol, Diane Wilson Cox (auth.), Harry Harris, Kurt Hirschhorn (eds.)

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