Transcobalamin II and the membrane receptor for the transcobalamin II-cobalamin complex.

Transcobalamin II is a plasma protein that binds vitamin B12 (cobalamin) as it is absorbed in the terminal ileum and distributes it to tissues. The circulating transcobalamin II-cobalamin complex binds to receptors on the plasma membrane of tissue cells and is then internalized by receptor-mediated endocytosis. A number of genetic abnormalities are characterized either by a failure to express transcobalamin II or by synthesis of an abnormal protein.

Iron protoporphyrin IX (hemin) but not tin or zinc protoporphyrin IX can stimulate gene expression in K562 cells from enhancer elements containing binding sites for NF-E2.

Many genes whose transcription is erythroid-specific contain enhancer or promoter elements that bind the transcription factor NF-E2. Hemin induction increases the expression of globin genes in the human erythroleukemia cell line K562, and increases the expression of reporters gene regulated by an enhancer elements containing binding sites for NF-E2. The failure of metalloporphyrins other than hemin to stimulate the transient expression of a CAT reporter gene linked to an enhancer element containing a binding site for NF-E2 was correlated with their failure to induce benzidine-positive K562 cells and increase the steady-state level of gamma-globin mRNA.

Assessment of quality of life before and after surgery for severe obesity.

Quality of life is poor in obese people because of poor physical health and mental well-being and impaired psychosocial functioning. Obese people perceive discrimination and prejudice against them as their heaviest burden. Reports of absence of psychopathology in obese people reflect adaptation to chronic disease or failure of assessment instruments to detect disturbances.

Endothelial cells are required for inhibition of contractile responses induced by reduction in extracellular magnesium and sodium ions in rat aortic smooth muscle [corrected].

The possible importance of facilitation of sodium-calcium (Na(+)-Ca2+) exchange by removal of extracellular magnesium ions ([Mg2+]o) in expression of endothelium-dependent relaxation was investigated in aortic rings isolated from female rats. Simultaneous [Mg2+]o withdrawal (0 mM Mg2+) and reduction in extracellular Na+ (Total [Na+]o = 84 mM), by replacement of NaCl with isosmolar amounts of sucrose in normal Krebs-Ringer bicarbonate (NKRB), induced significant increases of basal tone of denuded rat aortic rings, but not in tissues with intact endothelium. These vascular effects were not affected by indomethacin, phentolamine or atropine in any of the tissues tested.

A single point mutation of Ala-25 to Asp in the 14,000-Mr envelope protein of vaccinia virus induces a size change that leads to the small plaque size phenotype of the virus.

The molecular defect responsible for a structural and functional abnormality of the 14,000-molecular-weight (14K) envelope protein of vaccinia virus has been identified. Through DNA sequence analysis of the entire 14K gene from wild-type vaccinia virus and three vaccinia virus mutants, a single base change of C to A was found that resulted in the substitution of Asp for Ala-25. This mutation is responsible for protein size abnormality, as documented by cell-free translation in a rabbit reticulocyte lysate of in vitro mRNA transcripts.