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)

Asbestosis patients have a high cumulative risk of cancer: four of ten asbestosis patients develop cancer. Paraneoplastic involvement of the nervous system, peripheral neuropathy in particular, is often encountered in cancer patients, even at very early stages of the disease. In order to estimate the occurrence of paraneoplastic neuropathy among asbestosis patients, we formed a small cohort (115 asbestosis patients, mean age 56 years, mean duration of exposure to asbestos 21 years) in 1979. Neurological examination revealed slight peripheral neuropathy in 44 (39%) of the patients, 24 (22%) of whom also had central nervous system signs (disturbances in gait and posture, memory and fine movements). The prevalence of peripheral neuropathy among asbestosis patients was higher than among various referent patients (fibrosing alveolitis, diagnosed solvent poisoning and gynaecological carcinoma). No significant differences were found between the patients with and without peripheral neuropathy regarding the following parameters: pulmonary function tests, tumour markers (CEA, ferritin, beta-2-microglobulin), antinuclear antibodies, C3, C4 and circulating immune complexes. Nevertheless, at group level, the asbestosis patients had increased levels of the three tumour markers. Estimates based on the data accumulated so far (10 cancer patients) show that within three years we shall probably have a sufficient number of cancer cases to draw some conclusions about the value of neuropathy in the early diagnosis of occupational cancer.
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PMID:Asbestosis, the nervous system and cancer. 649 37

The aim of this study was to assess the erythropoietic response to hypoxaemia in patients with diffuse idiopathic pulmonary fibrosis (DIPF), and to speculate on the underlying mechanisms. Patients on an established chronic respiratory failure due to DIPF or chronic obstructive pulmonary disease (COPD) were studied. The erythropoietic response to hypoxaemia in both conditions was assessed. We studied 18 patients with DIPF and 29 patients with COPD in respiratory failure in a stable stage, free from acute infection and congestive heart failure. Blood gases, erythrocytic parameters, as well the serum levels of iron, ferritin and erythropoietin were determined. All the DIPF patients studied, apart from two, had normal or subnormal haematocrit values. The patients with COPD had an inconsistant response to hypoxaemia; 12 had normal or subnormal haematocrit values and the remaining 17 were erythraemic. The mean value of erythropoietin (EPO) in both DIPF and COPD patients was significantly higher than normal. In conclusion, patients with DIPF exhibit a lack of erythropoietic response to hypoxaemia, despite the augmented erythropoietin levels. This may reflect a defective bone marrow erythropoietic response in DIPF patients. It is suggested that the pathophysiology of DIPF underlies this mechanism.
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PMID:Erythropoietic response to hypoxaemia in diffuse idiopathic pulmonary fibrosis, as opposed to chronic obstructive pulmonary disease. 1142 4

Heme oxygenase 1 (HO-1) is an inducible enzyme that catalyzes heme to generate bilirubin, ferritin, and carbon monoxide. Because enhanced expression of HO-1 confers protection against many types of cell and tissue damage by modulating apoptotic cell death or cytokine expression profiles, we hypothesized that adenovirus-mediated transfer of HO-1 cDNA and subsequent overexpression of the protein in lung would provide therapeutic benefit in a murine model of bleomycin-induced pulmonary fibrosis. In C57BL/6 mice, HO-1 overexpression clearly suppressed the development of fibrotic changes and was associated with enhanced interferon gamma production in lung and reduced numbers of respiratory epithelial cells with damaged DNA. However, HO-1 overexpression did not prevent pulmonary fibrosis induced by agonistic anti-Fas antibody inhalation in C57BL/6 or ICR mice, a strain known to develop pulmonary fibrosis via the Fas-Fas ligand (FasL) pathway. Consistent with the concept that HO-1 overexpression prevents fibrosis via a pathway independent of Fas-FasL interaction, Ad.HO-1 administration prevented bleomycin-induced pulmonary fibrosis in gld/gld mice, which express nonfunctional FasL. These observations suggest that using HO-1 overexpression strategies to treat idiopathic pulmonary fibrosis, or fibrotic disorders of other target organs, by attenuating apoptotic cell death likely would be effective in clinical situations.
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PMID:Adenovirus-mediated transfer and overexpression of heme oxygenase 1 cDNA in lung prevents bleomycin-induced pulmonary fibrosis via a Fas-Fas ligand-independent pathway. 1244