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)

Characteristic cytoplasmic and intranuclear fibrillar bodies were produced, within 24 hours, in epithelial cells of the proximal convoluted renal tubules of rats and mice by injecting a single dose of lead acetate either intraperitoneally (100 mug Pb/g) or into the heart (10 mug Pb/g). The frequency of cytoplasmic fibrillar bodies (CFB) rose during the first 4 days following injection of lead and diminished thereafter. Ten days after intracardiac injection of lead no CFB were found; 10 days after intraperitoneal injection, they were still present, though probably in diminished number. Disappearance of CFB may be related to autophagocytosis. Intranuclear fibrillar bodies did not disappear, perhaps because nuclei lack a lysosomal apparatus. Within the first 3 days after injection of lead, clusters or paracrystalline arrays of ferritin molecules were frequently situated in the immediate vicinity of CRB or abutted against CFB; after the third day, little or no ferritin was found near CFB. Intramuscular injection of iron-dextran complex (50 mg Fe/ml) 24 hours prior to intraperitoneal administration of lead did not increase incidence or size of ferritin clusters in the vicinity of CFB in rats. The presence of ferritin near CFB may have been an indirect consequence of inhibition, by lead, of synthesis of heme prosthetic groups.
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PMID:Evolution of cytoplasmic fibrillar bodies induced by lead in rat and mouse kidneys. 17 27

We report of a 39 years old patient with a large testicular tumor found during an examination for infertility. The tumor consisted of a spermatocytic seminoma (SS) and a differentiated teratoma (TD). Furthermore, two small foci of seminoma were seen in the surrounding testicular tissue, several testicular tubuli contained carcinoma in situ (CIS). The diagnosis was based on the results obtained with various immunohistochemical markers: keratin, vimentin, desmin, LCA, CD3, CD20, CD45R, ferritin, PLAP, AFP. On the basis of the macroscopic and histopathological features, we propose the following etiology: CIS progressed in an earlier phase to the (larger) TD and later to the (smaller) classical seminoma; likewise, in an earlier phase, SS developed from a still unknown precursor stage. Our case of a mixed tumor as well as other cases reported in the last years do not allow the explanation of a differing etiology for SS. On the contrary, it may be presumed that the origins of seminoma and teratoma on the one hand and SS on the other hand are less divergent than hitherto thought.
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PMID:[A combination of spermatocytic and classic seminoma, mature teratoma and carcinoma in situ of the testis. An attempt at an etiologic explanation]. 821 26

We examined three autopsy cases of globoid cell leukodystrophy (GLD) with different survival, using immunohistochemistry and in situ nick end labeling (ISEL). The white matter lesion was pronounced in the corona radiata, corpus callosum and cerebellar peduncles in three cases, where a spongy state developed, in addition to the neuronal loss in the thalamus, cerebellum and inferior olivary nucleus. Ramified microglia, being immunoreactive for ferritin and HLA-DR alpha, were scattered in the white matter, and some of them also had immunoreactivity for TNF-alpha. Both the small-sized and large-sized globoid cells showed immunoreactivity for ferritin KP-1 and NCAM, while some of the small-sized globoid cells were also immunoreactive for HLA-DR alpha and TNF-alpha. As the survival became longer, the occurrence of the globoid cells decreased, however, they were commonly observed in the corpus callosum and cerebellar peduncle in three cases. T lymphocytes immunoreactive for LCA, UCHL-1 and CD3 were increased around the vessels in the white matter. ISEL stained nuclei of mononuclear cells in the white matter in two cases with short survival, although the cell origin was not verified. ISEL also visualized a few nuclei of the small-sized globoid cells in one case. On the other hand, immunostainings against cell death proteins such as bcl-2 family members and p53 failed to identify any significant changes. These data suggest that the immunological step and to a lesser extent the apoptotic process may partly be involved in the myelin breakdown and glial pathology in GLD, as reported in the twitcher mouse, a murine model of GLD.
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PMID:Immunohistological study of globoid cell leukodystrophy. 1214 65

An 82-year-old woman was admitted with fever and anorexia. Aggravated pancytopenia and liver dysfunction suggested the presence of disseminated intravascular coagulation. The serum ferritin level increased to 9,100 ng/ml. Bone marrow aspiration showed an increase of histiocytes with phagocytosis and a diagnosis of hemophagocytic syndrome was made. Symptomatic therapy was performed because of her deteriorated general condition. She died of multiple organ failure, 32 days after admission. Autopsy revealed swollen lymph nodes with proliferation of large neoplastic cells containing rich cytoplasm and pleomorphic and multi-segmented large nuclei. The immunophenotype of the neoplastic cells was LCA-, CD3-, CD5-, CD 20-, CD79a-, UCHL1-, MT1-, CD15-, p80-. Neoplastic cells were positive for CD30, mainly in Golgi apparati, and also positive for EBV-encoded small nonpolyadenylated RNAs (EBER). This case was diagnosed as anaplastic large cell lymphoma (ALCL) associated with hemophagocytic syndrome. It was estimated that Epstein-Barr virus had played an important role in the development of ALCL in the present case.
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PMID:[A case of anaplastic large cell lymphoma associated with Epstein-Barr virus infection, representing clinicopathological features of malignant histiocytosis]. 1457 24