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)

Small cell lung cancer (SCLC) is one of the most malignant tumors, especially often associated with nonmetastatic neurological disorders, corresponding to paraneoplastic neurological syndromes. The pathogenesis of which is unknown, however, mostly attributed to autoimmune processes. The aim of the study was to determine the pattern of the peripheral nervous system damage in SCLC. To provide further data contributing to the pathomechanism underlying these syndromes, immunocytochemical studies were initiated. Autopsy material was collected from 47 cases of SCLC. All these patients were examined clinically. The sections from the cervical, thoracic and lumbosacral segments of the spinal cord with spinal roots and dorsal root ganglia were taken. For immunohistochemistry following antisera were used: GFAP, MBP, IgG, IgM, ferritin, ubiquitin, alpha 1-antichymotrypsin, alpha 2-macroglobulin, C3 and C5b9 complement fractions. In 18 patients peripheral nervous system disturbances were diagnosed neurologically, 21 of cases presented neuromuscular disorders by emg. Among the nonmetastatic lesions most often a damage of dorsal root ganglia was observed (in 33 cases). Degeneration of the spinal roots was absent only in 8 cases. In 21 cases degenerative changes of motor neurons within anterior horn were present. In no case ubiquitin-positive inclusion bodies within the motor neurons could be found. In 8 cases extravasation of the IgG with diffuse labeling of the grey matter was observed. IgM immunoreactivity was markedly less frequently present, C5b9 complement fraction immunoreactivity was also confined only to cases with peripheral nervous system disturbances. Therefore, our preliminary data seem to confirm the participation of humoral immunity in paraneoplastic syndrome pathogenesis.
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PMID:Peripheral nervous system alterations in small cell lung cancer. Clinico-pathological study. 133 75

In this study we investigated the effects of severe hypothermia (cryoinjury) on oligodendrocyte (OL) cell marker expression and morphological features. We used a chemically defined cell culture medium, glial development medium (GDM), which favored the optimal expression of the OL phenotype in CG4 cells. Experiments using CG4 cells cultured in 2% serum or in GDM were conducted in parallel. After severe hypothermia, cells were reanimated at 37 degrees C and 4.5% CO(2) and cultured in either GDM or in medium supplemented with 2% serum. In either medium, around 70% of the total number of cells detached within 2 to 4 hours following reanimation. Oligodendroglial markers such as A2B5, O4, Tf, ferritin, tubulin, and MBP were examined by double and triple immunofluorescence. All of these markers except MBP re-appeared at different times during the recovery period for up to 48 hours. Glial fibrillary acidic protein (GFAP) and heat shock protein 60 (HSP-60) were used as injury markers. The presence of serum induced HSP-60 expression, while GDM did not. All CG4 cells expressed HSP-60 in response to hypothermia independently of the cell culture medium used. Cryoinjury induced a spectrum of morphological changes in CG4 cells. The expression of OL specific markers was also influenced by hypothermia. Moreover both, serum and cryoinjury induced the expression of HSP-60 that colocalized with OL and myelin markers. The expression of GFAP by injured cells but not by normal cells corroborated the state of injury of CG4 cells.
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PMID:In vitro injury model for oligodendrocytes: development, injury, and recovery. 1127 24

We have used a model of iron deficiency in the rat to analyze the effects of a disruption in iron availability on oligodendroglial cell (OLGc) maturation and myelinogenesis and to explore the possible beneficial influence of an intracranial injection (ICI) of apotransferrin (aTf) at 3 days of age on this process. Studies carried out on postnatal days 17 and 24 showed that iron deficiency produced a decrease in myelin proteins and lipids at 24 days of age. Immunohistochemistry showed that in untreated iron-deficient (ID) rats, the immunoreactivity of anti-adenomatous polyposis coli (APC) and anti-MBP antibodies decreased markedly with reference to normal controls, whereas in ID rats treated with an ICI of aTf, the immunoreactivity of these markers increased. A similar situation occurred with the immunoreactivity of H-ferritin. In primary OLGc cultures from ID rats, there was a high number of cells positive to the antibody against the polysialylated form of the cell surface glycoprotein NCAM (PSA-NCAM) compared with in OLGc cultures prepared from normal controls or from ID animals treated with aTf. The number of MBP+ cells in cultures from ID rats increased after treatment with aTf. The presence of lipid rafts evaluated with a specific anti-protein prion cellular (PrPc) antibody showed a smaller number of PrPc-positive structures in ID rat cultures. Treatment of the ID animals with a single ICI of aTf stimulated myelination, producing a significant correction in the different biochemical parameters affected by ID.
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PMID:Effect of transferrin on hypomyelination induced by iron deficiency. 1845 35