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Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The topographic relationships of platelet membrane glycoprotein IIb and glycoprotein IIIa have been studied in stimulated and unstimulated human platelets using immunoelectron microscopy. An indirect approach with ferritin-conjugated goat anti-rabbit gamma-globulin was used to localize the rabbit antibody to glycoprotein IIIa. The second ultrastructural label was keyhole limpet hemocyanin conjugated directly to antibody to glycoprotein IIb. Using the double labels, it was demonstrated that glycoprotein IIb and glycoprotein IIIa were distributed randomly in the unstimulated platelet membrane. After platelet stimulation with thrombin, large clusters of glycoprotein IIb-glycoprotein IIIa complexes were formed. No complex formation between glycoprotein Ib and glycoprotein IIb was observed in control experiments. These observations suggest that thrombin stimulation initiates the specific glycoprotein IIb-glycoprotein IIIa macromolecular complex formation on the platelet surface, which may act as the active fibrinogen-binding site required for normal platelet aggregation.
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PMID:Thrombin-induced platelet membrane glycoprotein IIb and IIIa complex formation. An electron microscope study. 645 76

The glomerular lesions of focal sclerosis clinically associated with a steroid-resistant nephrotic syndrome, are of unknown origin. IgM and C3 deposits and electron dense material found in areas of sclerosis are not convincing evidence of an immune pathogenesis. These deposits have been studied in a rat model of focal sclerosis induced by uninephrectomy and repeated aminonucleoside administration. Sclerotic lesions closely resembling human disease developed in the remaining kidney. There was a severe progressive proteinuria. Seventy-eight days after initial aminonucleoside injection 65 per cent of glomeruli were sclerotic with IgM, IgG, C3 and fibrinogen deposits, and electron dense deposits by electron microscopy. To study macromolecule in this model of focal sclerosis, ferritin uptake 4 and 24 h after intravenous ferritin given at 77 days was compared in focal sclerosis rats with control rats without sclerosis (uninephrectomy plus saline-only injections). In focal sclerosis rats sclerotic areas contained massive accumulations of ferritin. In unaffected segments of sclerotic glomeruli, and normal glomeruli of focal sclerosis rats, ferritin concentration was no different from controls. Abnormal ferritin trapping in areas of sclerosis suggests that the presence of IgM and C3 may be due to a similar mechanism, and is not indicative of an immune pathogenesis for focal sclerosis.
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PMID:Ferritin deposition in the glomerular deposits of focal glomerular sclerosis in the rat. 648 27

Human and animal sera contain potent inhibitors of saliva-mediated aggregation of oral streptococci. The inhibitors consist of a high-molecular-weight heat-labile factor and a lower-molecular-weight heat-activated factor. The latter appears to be serum albumin. Analyses of purified blood-derived proteins indicated that several high-molecular-weight proteins (fibrinogen, fibronectin, and ferritin) were able to inhibit aggregation at low concentrations. These data suggest that high-molecular-weight proteins may modulate the aggregation process.
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PMID:Inhibition of bacterial aggregation by serum- and blood-derived proteins. 669 Apr 11

When virulent group A streptococci of M type 24 were incubated in fresh heparinized whole blood or in blood reconstituted from cellular elements and plasma, little uptake by neutrophils occurred as determined by light microscopy. When fresh human serum (with or without added heparin) was substituted for plasma, uptake occurred promptly. Uptake in serum could be prevented by adding either plasma or purified human fibrinogen to the incubation mixtures, or by pretreating the organisms with plasma or fibrinogen. Fibrinogen solutions absorbed with purified homologous M protein and centrifuged to remove precipitates lost their inhibitory activity. Uptake in serum depended on heat-labile factors. Immunofluorescent staining of bacteria using fluorescein-labeled antibody to the third component of complement showed that streptococci incubated in fresh serum bound complement evenly over the entire cell surface, whereas streptococci incubated in fresh plasma or in serum plus fibrinogen fluoresced only at some of the cross-walls between adjacent daughter cocci and at occasional terminal cocci. In electron micrographs, the surface fibrillar layer of streptococci treated with plasma or fibrinogen lost its hairlike appearance and became a dark band that stained heavily with ferritin-labeled antifibrinogen. We conclude that the known antiopsonic effect of M protein derives in part from binding of fibrinogen.
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PMID:Antiopsonic activity of fibrinogen bound to M protein on the surface of group A streptococci. 704 54

The concentration of ferritin in the serum of normal males (n = 79) was 98 micrograms/l (geometric mean) with a 95% confidence range of 21-447 micrograms/l. In non-menstruating healthy females (n = 39), the concentration was 85 (26-279) micrograms/l. In menstruating females, serum ferritin was less than 30 micrograms/l only when the duration of menstruation was more than or equal to 4 days. Patients with uncomplicated iron-deficiency anemia had a serum ferritin level less than 20 micrograms/l. After oral or parenteral iron therapy, serum ferritin was greater than 20 micrograms/l in 7 to 17 patients. Serum ferritin was greater than 20 micrograms/l in 8 of 12 patients with a simultaneous inflammatory or malignant disease. Of patients with iron-deficiency anemia, 86% had a serum ferritin level lower than 40 micrograms/l. A serum ferritin level less than 40 micrograms/l was only observed in patients with iron-deficiency anemia and not in patients with other forms of anemia. Of patients with iron-deficiency anemia and a hemoglobin concentration lower than 100 g/l, 80% had a serum iron level less than 13 mumol/l and a total iron binding capacity higher than 70 mumol/l. Anemia of chronic disorders was diagnosed with a sensitivity of 0.93 and a specificity of 0.92 in patients with serum iron less than 13 mumol/l, total iron binding capacity less than 60 mumol/l, erythrocyte sedimentation rate greater than 25 mm in the first hour, and serum fibrinogen greater than 4 g/l. Somewhat better was the same combination except with the serum ferritin level greater than 50 micrograms/l instead of the iron binding capacity. However the predictive value using both combinations was too low.
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PMID:[Serum ferritin in differential diagnosis of anemia (author's transl)]. 710 97

Blood concentrations of six acute phase reactants (ESR, neutrophil count, fibrinogen, haptoglobin, alpha 1-antitrypsin, and ferritin), parameters of muscle necrosis (myoglobin, CK, ALT, and AST) as well as hemopexin, iron, and TIBC were determined before and for 7 consecutive days after muscle biopsy in patients and in a control group. A muscle biopsy was chosen as a standardized surgical procedure that induces a mild transient inflammatory response. After muscle biopsy, a significant increase occurred in five (ESR, neutrophil count, fibrinogen, haptoglobin, and alpha 1-antitrypsin) of the six acute phase reactants. The concentration of serum ferritin did not show a significant change. A significant decrease was noted in the serum iron concentration and a significant increase occurred with CK and myoglobin secondary to the muscle biopsy. Thus the inflammation of a muscle biopsy produces a significant acute phase reaction.
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PMID:Quantification of acute phase reactants after muscle biopsy. 711 53

Long term effects of the intracortical implantation of blood and blood products on the electrocorticogram were studied in cats and guinea pigs. Focal epileptiform paroxysmal discharges developed after implantation of whole blood, hemolyzed erythrocytes, methemoglobin, ferritin, ferrous chloride, ferric chloride, fibrinogen, hemin, and cottonoid. In each group recurrent paroxysmal discharges became more prominent and more frequent after several months, suggesting a physiological change caused by a breakdown product of blood. The lesions were characterized by varying degrees of cell loss, iron deposition and glial proliferation. It is thought that posttraumatic epilepsy, which is frequently accompanied by extravasation of blood into the brain, might share a similar physiopathogenesis.
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PMID:Effects of intracortical injection of blood and blood components on the electrocorticogram. 735 64

A 71 year-old man with adult onset Still's disease was admitted to our hospital because of fever, sore throat, myalgia and macular nonpruritic salmon pink eruption. He was treated with prednisolone, 40 mg daily and these symptoms disappeared. When the dose of prednisolone was reduced to 30 mg daily, he began to notice fever. 5 days later he developed adult respiratory distress syndrome (ARDS). The dose of prednisolone was increased to 50 mg daily and oxygen administration was started. All symptoms began to improve immediately and the dose of prednisolone was decreased to 40 mg daily. 10 days later he noticed fever and skin rash. Laboratory investigation showed platelet counts of 69,000/mm3, a ferritin of 37,000 ng/ml, and increased fibrinogen degradation product, indicating increased activity of adult onset Still's disease associated with disseminated intravascular coagulation (DIC). The dose of prednisolone was again increased to 60 mg daily, and 100 mg of nafamostat mesilate was administrated intravenously. All above symptoms associated with adult onset Still's disease and DIC disappeared. The dose of prednisolone was gradually decreased and the clinical course was uneventful with daily administration of 10 mg of prednisolone. Although there are a couple of case report which described the association of adult onset Still's disease with either ARDS or DIC, the association of adult onset Still's disease with both ARDS and DIC have not been reported yet.
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PMID:[A case of adult onset Still's disease complicated with adult respiratory distress syndrome and disseminated intravascular coagulation]. 755 55

We have investigated the effect of cytokines, including interleukin-6 (Il-6), interleukin-1 alpha (Il-1 alpha), and tumor necrosis factor-alpha (TNF-alpha), on the inducible expression of cytochrome P450s (CYP) CYP1A1, CYP1A2, and CYP3A4 in human hepatocytes in primary culture. The ability of these cultures to mimic the acute phase response when stimulated with cytokines was evaluated using immunoblotting to measure the production of albumin, ferritin, fibrinogen, and ceruloplasmin. The cytokines exhibited specific patterns of action on the production of these proteins. Albumin was depressed by all the cytokines. In contrast to Il-6 and Il-1 alpha, TNF-alpha reduced the production of fibrinogen and ceruloplasmin but stimulated the production of ferritin. When cells were treated with the CYP inducer alone, large increases in the expression of CYP1A1 and CYP1A2 by beta-naphthoflavone and of CYP3A4 by rifampicin were observed at messenger RNA (mRNA) and protein levels, by ribonuclease protection and immunoblotting, respectively. When the cells were treated with the inducer plus cytokines, the induction of mRNA was greatly reduced. Again, specific patterns of action were revealed: Il-6 had the most potent effect on CYP3A4, whereas TNF-alpha was the most potent with CYP1A genes. In all cases, changes at the protein levels paralleled changes at the mRNA levels. In cells preinduced with beta-naphthoflavone or rifampicin, the decay with time of the levels of the CYP1A2 or CYP3A4 proteins, after the removal of the inducer, was not affected by cytokines. We conclude that cytokines strongly repress the inducibility of CYP1As and CYP3A4 genes at a transcriptional or a posttranscriptional level, but affect neither the rate of translation of CYP mRNAs nor the rate of degradation of the CYP proteins in these cultures.
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PMID:Differential effects of cytokines on the inducible expression of CYP1A1, CYP1A2, and CYP3A4 in human hepatocytes in primary culture. 755 64

A case of granulosa cell tumor of the ovary associated with hepatocytic differentiation is reported in a 45-year-old patient with a torsioned ovarian tumor. Serum alpha-fetoprotein (AFP) levels were normal 6 days postoperatively. Histopathologically, the granulosa cell tumor was typically trabecular. Its cells had nuclear grooves and were positive only for vimentin. Scattered diffusely throughout the tumor were small groups of regular polygonal cells, the cytoplasm of which secreted bile and was strongly positive for keratin, carcinoembryonic antigen (CEA), alpha-1-antitrypsin (A1AT), and ferritin and moderately positive for fibrinogen and ceruloplasmin. These results unequivocally identified them as hepatic cells. The AFP negativity of the hepatic cells was interpreted as a sign of terminal hepatocytic differentiation. The scattered arrangement of the hepatocytes simulated stromal luteinization. As neither a primary liver tumor nor any associated germ cell tumor was found, the histogenesis of the hepatic cells was thought to be metaplastic.
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PMID:Granulosa cell tumor of the ovary with diffuse true hepatic differentiation simulating stromal luteinization. 768 May 45


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