Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02794 (ferritin)
17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To help elucidate the general rules of globular protein folding, computer simulations of the conformational transition in model proteins having the left-handed, four-helix bundle motif in which the helices are joined by one or two long loops, as in apoferritin and somatotropin, respectively, have been undertaken. In the context of simple tetrahedral lattice protein models, these unique native helix bundle motifs can be obtained by a set of interactions similar to those found in previous simulations of the folding of four-member alpha-helical bundles with tight bends and beta-barrel proteins including the Greek key motif. The essential features sufficient to produce the four-helix bundle motif with long loops are as follows: (i) a general pattern of hydrophobic and hydrophilic type residues which differentiate the interior from the exterior of the molecule; (ii) the existence of hydrophilic regions in the amino acid sequence that, on the basis of short-range interactions, are indifferent to loop formation but that interact favorably with all the exterior residues of the helix bundle. Thus, these simulations indicate that, to reproduce all varieties of the left-handed four-helix bundle motif, site-specific interactions are not required.
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PMID:Monte Carlo simulation of equilibrium globular protein folding: alpha-helical bundles with long loops. 270 42

Caisson disease of bone, which may affect compressed air workers and divers, is characterized by regions of bone and marrow necrosis that may lead to secondary osteoarthrosis of the hip and shoulder joints. A review of the pathologic, radiologic, and clinical aspects demonstrated uncertainties in the exact etiology. Early diagnosis is often not possible because of the delayed appearance of radiologic abnormalities. Research into these two aspects of this condition was carried out by the Medical Research Council Decompression Sickness Research Team in Newcastle upon Tyne over a ten-year period (1972 to 1982). Because no suitable animal model exists for the study of this condition, bone and marrow necrosis was produced by embolism of bone blood vessels with glass microspheres. With this model, it was shown that the presence of bone and marrow necrosis could be detected by bone scintigraphy using 99mTc-MDP and by measuring changes in serum ferritin concentration at a much earlier stage than was possible by radiography. However, only the former method has proved useful in clinical practice. Investigations into the etiology of caisson disease of bone have shown evidence for an increase in marrow fat cell size resulting from hyperoxia. This phenomenon may play a role in the production and localization of gas bubble emboli, which are thought to be the cause of the bone and marrow necrosis.
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PMID:Caisson disease of bone. 375 75

The ultrastructure of the blood-bubble interface has been studied in rats decompressed experimentally. Subsequent to staining with ruthenium red there was detected by electron microscopy a continuous envelope like layer about 20 nm thick at the bubble-facing surface of the interface. The envelope like structure was visualized also by concanavalin A-ferritin, a glycosyl- and mannosyl residue-recognizing lectin coupled with an electron-dense probe, but the structure was not at all seen by the use of the conventional stains used in electron microscopy, uranyl acetate and lead citrate. No electron-dense layer was discernible on the application of only osmium tetroxide without further staining. The results indicate that material stainable by ruthenium red, and binding concanavalin A (probably a glycoprotein), is concentrated at the blood-bubble interface upon decompression. It is suggested that it plays a role in stabilization of the bubble and in the hematological alterations that are frequently observable in decompression sickness.
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PMID:Ruthenium red staining of blood-bubble interface in acute decompression sickness in rat. 616 82

Serum ferritin levels were determined in six U.S. Navy divers during a 29d helium-oxygen saturation dive. Progressive increases in serum ferritin were observed during compression. These increases were maintained during decompression and for 1 week postdive. No relationship was found between serum ferritin increases and the development of decompression sickness (DCS). However, the two divers who subsequently developed DCS had significantly higher serum ferritin levels than those divers who remained free of DCS. These findings indicate that DCS does not result in differential serum ferritin variability and may, therefore, not be involved directly in aseptic bone necrosis (ABN) as postulated earlier by others. However, high baseline levels of serum ferritin may be involved in both DCS and ABN.
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PMID:Serum ferritin increases during deep saturation dives. 715 Jan 52