The decrease in hemoglobin A (HbA, α2β2) synthesis in the erythroid cells of patients with β-thalassemia is due to a selective defect in β-chain synthesis. Since α-chains continue to be formed at a normal rate in these cells, this results in a marked relative excess of α-chain synthesis over β- and γ-chain synthesis. The α-chains uncombined with β- or β-like-chains (δ, γ) will be referred to as free α-chains. The experiments presented in this paper show that these free α-chains are capable of combining with β-chains to form HbA and are, therefore, structurally normal. Alternatively, in the absence of added β-chains, α-chains aggregates of various sizes are formed.
Arthur Bank
Usage data is cumulative from August 2024 through August 2025.
Usage | JCI | PMC |
---|---|---|
Text version | 185 | 20 |
56 | 10 | |
Scanned page | 325 | 14 |
Citation downloads | 67 | 0 |
Totals | 633 | 44 |
Total Views | 677 |
Usage information is collected from two different sources: this site (JCI) and Pubmed Central (PMC). JCI information (compiled daily) shows human readership based on methods we employ to screen out robotic usage. PMC information (aggregated monthly) is also similarly screened of robotic usage.
Various methods are used to distinguish robotic usage. For example, Google automatically scans articles to add to its search index and identifies itself as robotic; other services might not clearly identify themselves as robotic, or they are new or unknown as robotic. Because this activity can be misinterpreted as human readership, data may be re-processed periodically to reflect an improved understanding of robotic activity. Because of these factors, readers should consider usage information illustrative but subject to change.