Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038362 (stomatitis)
 8,852 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The synthesis and oligosaccharide processing of the glycoproteins of SA11 rotavirus in infected Ma104 cells was examined. Rotavirus assembles in the rough endoplasmic reticulum (RER) and encodes two glycoproteins: VP7, a component of the outer viral capsid, and NCVP5, a nonstructural protein. A variety of evidence suggests the molecules are limited to the ER, a location consistent with the high mannose N-linked oligosaccharides modifying these proteins. VP7 and NCVP5 were shown to be integral membrane proteins. In an in vitro translation system supplemented with dog pancreas microsomes, they remained membrane associated after high salt treatment and sodium carbonate-mediated release of microsomal contents. In infected cells, the oligosaccharide processing of these molecules proceeded in a time-dependent manner. For VP7, Man8GlcNAc2 and Man6GlcNAc2 were the predominant intracellular species after a 5-min pulse with [3H]mannose and a 90 min chase, while in contrast, trimming of NCVP5 halted at Man8GlcNAc2. VP7 on mature virus was processed to Man5GlcNAc2. It is suggested that the alpha-mannosidase activities responsible for the formation of these structures reside in the ER. In the presence of the energy inhibitor carbonyl cyanide m-chlorophenylhydrazone (CCCP), processing of VP7 and the vesicular stomatitis virus G protein was blocked at Man8GlcNAc2. After a 20-min chase of [3H]mannose-labeled molecules followed by addition of CCCP, trimming of VP7 could continue while processing of G protein remained blocked. Thus, an energy-sensitive translocation step within the ER may mark the divergence of the processing pathways of these glycoproteins.
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PMID:Processing of the rough endoplasmic reticulum membrane glycoproteins of rotavirus SA11. 299 4

Lichenoid stomatitis has been reported in the use of a number of drugs. This is a case report of lichenoid stomatitis associated with lithium carbonate. The association between lichenoid stomatitis and lithium carbonate was confirmed by rechallenge in this patient. A number of cutaneous reactions have been reported as adverse effects of lithium therapy. Lichenoid reactions are characterized by an infiltrate of T cells. Lithium has been reported to alter T cell function in vitro.
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PMID:Lichenoid stomatitis associated with lithium carbonate. 393 May 81

2 children with cyclic neutropenia were treated with lithium carbonate. In one patient, fever and stomatitis were ameliorated, but the duration of neutropenia was increased and parotitis occurred. In another patient, aphthous stomatitis disappeared but fever persisted. The duration of neutropenia was prolonged and submaxillaritis and sinusitis occurred. Thus, lithium administration may lead to complications when the duration of neutropenia is prolonged. We recommend discontinuation of the drug, even in the presence of amelioration of symptoms.
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PMID:Lithium therapy for cyclic neutropenia in children. 687 5

Although basic fibroblast growth factor (bFGF/FGF-2) is found outside cells, it lacks a conventional signal peptide sequence; the mechanism underlying its export from cells is therefore unknown. Using a transient COS-1 cell expression system, we have identified a novel membrane-associated transport pathway that mediates export of FGF-2. This export pathway is specific for the 18-kD isoform of FGF-2, is resistant to the anti-Golgi effects of Brefeldin A, and is energy-dependent. In FGF-2-transfected COS-1 cells, this ER/Golgi-independent pathway appears to be constitutively active and functions to quantitatively export metabolically-labeled 18-kD FGF-2. Co-transfection and co-immunoprecipitation experiments, using a vector encoding the cytoplasmic protein neomycin phosphotransferase, further demonstrated the selectivity of this export pathway for FGF-2. When neomycin phosphotransferase was appended to the COOH-terminus of 18-kD FGF-2, the chimera was exported. However, the transmembrane anchor sequence of the integral membrane glycoprotein (G protein) of vesicular stomatitis virus (VSV) blocked export. The chimeric protein localized to the plasma membrane with its FGF-2 domain extracellular and remained cell-associated following alkaline carbonate extraction. Taken together, the data suggest that FGF-2 is "exported" from cells via a unique cellular pathway, which is clearly distinct from classical signal peptide-mediated secretion. This model system provides a basis for the development and testing of therapeutic agents which may block FGF-2 export. Such an intervention may be of considerable use for the treatment of angiogenesis-dependent diseases involving FGF-2.
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PMID:Quantitative export of FGF-2 occurs through an alternative, energy-dependent, non-ER/Golgi pathway. 786 Jun 46

The authors, by means of documental research, study the possibility that the physical and psychic symptoms of Vincent van Gogh may have been due to chronic lead poisoning. The technique and materials used by Van Gogh are analysed as the cause of repeated exposure to lead as well as the possible means of penetration of the metal. Through historical-biographical analysis, the progressive symptoms of the illness are compared with those of lead poisoning. The authors conclude that the excessive and continuous use by Van Gogh of pigments which were highly toxic due to their high lead content, such as white lead (lead carbonate) and yellow chrome (lead chromium), could have penetrated his organism by digestive system (primarily) in minimal daily amounts, giving rise to a clinical condition of chronic lead poisoning. This type of poisoning coincides with the clinical symptoms Van Gogh describes in his autographed letters: initial debilitation, stomatitis with loss of teeth, recurring abdominal pains, anaemia (with a "plumbic" skin tone), neuropathy of the radial and saturnine encephalopathy including epileptic crises, progressive character changes and periods of delirium. The clinical symptoms shown by Van Gogh meet present criteria for diagnosis of Organic Mental Disorder due to cerebral lesion or somatic illness (F.06; CIE-10) (DSM-IV-R), and Organic Character Disorder (F.07; CIE-10) (DSM-IV-R).
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PMID:[Implication of lead poisoning in psychopathology of Vincent van Gogh]. 942 66