Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0016632 (Fox)
 1,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A complex of orotate phosphoribosyltransferase and orotidylate decarboxylase has been shown to exist in three molecular weight forms (Brown, G. K., Fox, R. M., and O'Sullivan, W. J. (1975), J. Biol. Chem. 250, 7352). The smallest of these, of molecular weight 62 000, was subjected to further study. On the basis of the inactivation of the enzyme activities, carried out in the presence of low concentrations of guanidine hydrochloride, and of changes in molecular weight of preparations during aging, it was inferred that the enzyme complex contained more than one type of subunit. This was confirmed by chromatography on Sephadex G-75 after preincubation in guanidine hydrochloride or with guanidine hydrochloride in the elution buffer. It was concluded that the enzyme complex consisted of two types of subunits, two decarboxylase units of molecular weight approximately 20 000 and two further subunits of approximately 13 000. The subunits could be separated and reassociated with partial recovery of both activities. A 40 000 molecular weight form had full decarboxylase activity but no phosphoribosyltransferase activity. Restoration of the 62 000 molecular weight form resulted in restoration of both enzymatic activities. An intermediate species of molecular weight 50 000 representing a combination of the decarboxylase dimer with one of the 13 000 subunits was also demonstrated. This form required the presence of dithiothreitol in order to manifest phosphoribosyltransferase activity. A model of the system has been proposed that accounts for both the different molecular weight forms and also for the deficiency of both activities in the rare inborn error of metabolism, hereditary orotic aciduria.
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PMID:Subunit structure of the orotate phosphoribosyltransferase--orotidylate decarboxylase complex from human erythrocytes. 88 98

The structure of foot-and-mouth disease virus (FMDV) strain O1 BFS 1860 has been determined to 2.9 A resolution using the molecular-replacement method [Acharya, Fry, Stuart, Fox, Rowlands & Brown (1989). Nature (London), 337, 709-716]. Crystals of the virus with average dimensions 0.12 x 0.06 x 0.12 mm belong to space group I23, a = 345 A with 1/12 of the icosahedral particle per asymmetric unit giving fivefold noncrystallographic redundancy. Oscillation diffraction photographs were collected at the SERC Synchrotron Radiation Source at Daresbury in accordance with strict disease security regulations. The ambiguity in particle orientation was resolved using a self-rotation function and starting estimates of the phases to 8 A were derived from the known structures of two picornaviruses similarly oriented in the I23 unit cell. The phases were refined and extended using iterative averaging and solvent flattening with the implementation of a simple automatic envelope-determination procedure to increase the phasing power available.
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PMID:Methods used in the structure determination of foot-and-mouth disease virus. 838 28

The author presents an account on different causes of ophthalmological torticollis and rotational nystagmus in paresis of the trochlear nerve and abducent nerve, in Duan's syndrome I or acute Brown's syndrome or in bilateral ptosis combined with paresis of the levators. He recommends different surgical techniques and prefers combined operations performed with a single anaesthesia in pareses of the levators, the abducent nerve and trochlear nerve. For release of the horizontal direct muscles within the framework of paretic affections of the eye he recommends adjustable elongations as described by Gonin-Hollwich. In ptosis he uses frontotarsal suspension as described by Fox, using lyophilized fasciae. The paper contains also a family history of congenital fibrous syndrome.
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PMID:[Ocular torticollis]. 972 81

A conference was held at the State University of New York at Stony Brook in October 1984 to discuss the controversy concerning treatment of a newborn with severe congenital defects that became known as the Baby Jane Doe case. Fox provides some background information on the case to introduce a set of of six articles consisting of papers delivered at the conference. These articles deal with historical aspects of the treatment debate (Stanley J. Reiser), problems of clinical decision making (John M. Freeman), the legal issues involved (John A. Robertson), coverage of the case by the media (Stephen Klaidman and Tom L. Beauchamp), federal efforts to regulate the treatment of handicapped newborns (Lawrence D. Brown), and the alliance that arose between opponents of abortion and advocates of the rights of the handicapped (Constance Paige and Elisa B. Karnofsky).
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PMID:Introduction to the Baby Jane Doe papers. 1164 30

This Society for Medicines Research symposium was held on March 6, 2008, at the National Heart and Lung Institute, London, U.K. The meeting, organized by Kate Brown and David Fox reviewed the state-of-the-art in biotherapeutics. This is an area that is acquiring increasing importance in drug discovery and development portfolios, offering new and alternative ways of treating a wide range of conditions as well as opening up new and exciting areas of science and technology. Presentations ranged from the therapeutic potential of monoclonal and polyclonal antibodies, vaccines and oligonucleotides, through to the scientific basis of the emerging area of RNA interference. In addition, some of the technical aspects of delivering novel therapies and ensuring their quality were also discussed.
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PMID:Biotherapeutics. 1859 94

Developmental stuttering is a speech disorder most likely due to a heritable form of developmental dysmyelination impairing the function of the speech-motor system. Speech-induced brain-activation patterns in persons who stutter (PWS) are anomalous in various ways; the consistency of these aberrant patterns is a matter of ongoing debate. Here, we present a hierarchical series of coordinate-based meta-analyses addressing this issue. Two tiers of meta-analyses were performed on a 17-paper dataset (202 PWS; 167 fluent controls). Four large-scale (top-tier) meta-analyses were performed, two for each subject group (PWS and controls). These analyses robustly confirmed the regional effects previously postulated as "neural signatures of stuttering" (Brown, Ingham, Ingham, Laird, & Fox, 2005) and extended this designation to additional regions. Two smaller-scale (lower-tier) meta-analyses refined the interpretation of the large-scale analyses: (1) a between-group contrast targeting differences between PWS and controls (stuttering trait); and (2) a within-group contrast (PWS only) of stuttering with induced fluency (stuttering state).
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PMID:Stuttering, induced fluency, and natural fluency: a hierarchical series of activation likelihood estimation meta-analyses. 2546 20

TMT (2,5-dihydro-2,4,5-trimethylthiazoline) is known as a component of fox feces inducing fear in rodents. However, no recent chemical analyses of fox feces are available, and few studies make direct comparisons between TMT and fox feces. Fox feces from 3 individuals were used to prepare 24 samples to be analyzed for the presence of TMT using gas chromatography-mass spectrometry (GC-MS). When TMT was added in low amounts (50-2000 nmol/g), TMT was detected in 10 out of 11 samples. When no TMT was added, TMT was detected in only 1 out of 13 samples. In a second experiment, we tested the behavioral response of male Brown Norway (BN) and Wistar rats to either fox feces, a low amount of TMT (0.6 nmol) or 1-hexanol. TMT induced freezing in the rats, but fox feces induced significantly more freezing episodes and longer total duration of freezing in both rat strains. In experiment 3, male BN rats were exposed over several days to fox feces, rat feces, 1-hexanol, cadaverine, 2-phenylethylamine, and TMT, one odor at a time. Fox feces induced significantly more freezing episodes of a longer total duration than any of the other odors, with rat feces and 1-hexanol giving rise to the lowest amount of freezing. This finding, together with our inability to verify the presence of TMT in fox feces, indicates that the concentration of TMT in our fox feces samples was below 50 nmol/g. It may also be that other compounds in fox feces play a role in its fear-inducing properties.
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PMID:Where is the TMT? GC-MS analyses of fox feces and behavioral responses of rats to fear-inducing odors. 2922 18