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

A novel approach for the ultrastructural localization of surface sialic acids is presented. Membrane-bound sialyl residues are chemically modified in situ by the covalent attachment of biotinyl residues, the latter of which are subsequently localized by ferritin-conjugated avidin. In contrast to previous methods, which have been based on electrostatic interactions, the above method does not affect cell surface charge. Consequently, the macromolecular configuration of the labeled sialoglycoconjugates is preserved. The method has been found to be more accurate in the quantitative evaluation and the topographical localization of membrane-based sialic acids both in normal and pathologically induced surface modulations. Modulations in cell surface sialic acid content and/or distribution have been demonstrated in beta-thalassemia and transformed lymphoid cells, and the consequences of such alterations are discussed regarding destruction vs. escape from the immune surveillance system.
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PMID:Ultrastructural modulations of cell surface determinants in pathological processes. 9 32

The auditory function of 75 children affected by homozygous beta0-thalassemia, managed with a low transfusion scheme and treated irregularly with low doses of desferrioxamine, and of 75 controls were examined. In 12 patients a mild bilateral conductive hearing impairment due to bony hypertrophy and/or adenoid hypertrophy was found. In 43 cases a moderate monolateral or bilateral sensory-neural hearing loss at high frequencies with recruitment phenomenon was observed. Ferritin levels were determined in a randomly chosen group of these patients with (14) and without heaing loss (11). In the subjects with sensory-neural hearing loss the mean ferritin levels were significantly higher than in those with no hearing defect. There was no obvious relation between sensory-neural damage on the one hand and Hb levels and unit of blood transfused on the other. The results of this study suggest that iron overload could be a cause of damage in the high frequency elements of the auditory mechanism. Intermittent hypoxia and slow 8th nerve compression due to bony hypertrophy as causes of auditory involvement are also discussed.
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PMID:Auditory involvement in thalassemia major. 10 1

The value of serum ferritin and mean corpuscular volume (MCV) measurement in distinguishing between iron deficient, beta-thalassaemia trait and normal subjects has been studied. Normal subjects had normal ferritin and MCV, iron-deficient ones had low ferritin and low or normal MCV, and thalassaemics had normal ferritin and low MCV. By the combined use of these two measurements it was possible to identify individuals belonging to one of the three categories with an accuracy of over 95%. Although definitive diagnosis of beta-thalassaemia trait requires the demonstration of abnormal haemoglobin A2 levels or reduced beta-chain synthesis, serum ferritin and MCV measurements are useful screening procedures for the initial diagnosis of beta-thalassaemia trait and iron deficiency. Because of the very small amounts of blood required for both of these measurements, they are particularly suitable for surveying large numbers of subjects in populations with a high prevalence of hypochromic-microcytic anaemias.
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PMID:Serum ferritin and mean corpuscular volume measurement in the diagnosis of beta-thalassaemia minor and iron deficiency. 11 17

In view of the reported associations of Hodgkin's disease and ferritin, an electron microscopic study of the peripheral blood lymphocytes of these patients was done. In 5 out of the 6 patients studied intracellular ferritin deposits were seen. No such deposits were seen in the lymphocytes of healthy subjects or in those of a patient with beta-thalassemia. The lymphocyte ferritin accumulation in Hodgkin's disease can arise either from increased synthesis or from phagocytosis.
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PMID:Ferritin deposits in peripheral blood lymphocytes of Hodgkin's disease patients. 12 68

The bone marrow macrophages of patients with homozygous beta-thalassaemia were frequently situated adjacent to collagen fibres and sometimes formed intrasinusoidal cytoplasmic protrusions. They also appeared to phagocytose processes of erythroblast cytoplasm (at times containing precipitated alpha-chains) which projected into them from neighbouring erythroblasts. The cytoplasm of the macrophages included large numbers of heavily-iron-loaded secondary lysosomes of various sizes and shapes in addition to phagocytosed erythroblasts, erythrocytes and extruded erythroblast nuclei. Numerous ferritin molecules were found in the cytoplasmic matrix but there were hardly any in the mitochondria, endoplasmic reticulum or golgi saccules. A small number of ferritin molecules were present within the nucleus. Electron microscope autoradiographs of marrow fragments which had been incubated with [3H]leucine for 1 h revealed the presence of newly-synthesized protein molecules in all types of secondary lysosomes. Light microscope autoradiographs showed the [3H]thymidine labelling index of the bone marrow macrophages was less than 1% and suggested that only a very small proportion of these cells were actively preparing for division.
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PMID:Some features of bone marrow macrophages in patients with homozygous beta-thalassaemia. 20 37

This study establishes the prevalence and distribution of an MCV less than 80 fl by review of the Coulter indices of 7887 samples. Retrospectively, 146 patients are studied and the relationships between the low MCV, film microscopy, iron status, and clinical diagnosis assessed. Plasma ferritin measured radioisotopically in 100 patients is compared to serum iron and iron binding capacity values and some of the problems of assessing iron stores are discussed. The discriminant formulae devised to differentiate between the microcytosis of thalassaemia trait and that or iron deficiency are found to be of limited value when applied to the red cell indices of a hospital population.
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PMID:The low mean cell volume in routine haematology. 54 44

Homozygous beta-thalassaemia is a disease in which there is a progressive iron overload from infancy to death in early adulthood. Liver biopsies from 10 patients in various stages of this disease were examined by electron microscopy. A number of round or oval lysosomal structures, containing lamellae different from myelin figures, were seen in all patients, including those with minimal iron overload. Ferritin molecules were seen either in relationship with the lamellae forming arrays, or in paracrystalline arrangement, or with no organized form. There were practically no ferritin molecules in sub-cellular compartments other than cell sap and lysosomes. The density of cell sap ferritin was constant beyond infancy, but the number of iron-laden lysosomes increased with age. The stages in the process of iron seclusion, seen even in advanced phases of iron overload, are described. Ferritin is thought to accumulate in lysosomes by a transmembraneous movement, but other explanations are considered.
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PMID:Ferritin in human liver cells of homozygous beta-thalassaemia: ultrastructural observations. 60 78

The diagnostic value of serum ferritin measurements in discriminating iron-deficiency anemia from thalassemia trait has been studied. In contrast to serum iron, percent transferrin saturation and total iron-binding capacity, where a high degree of overlap existed between the two groups, a clear-cut difference in serum ferritin levels was found between iron deficiency and thalassemia trait. The best separation of iron deficiency, thalassemia and normal controls was given by the combination of mean corpuscular volume and serum ferritin. Although definitive diagnosis of beta-thalassemia trait requires the demonstration of abnormal Hb A2 levels or beta-chain synthesis, serum ferritin is a useful screening test for the initial diagnosis of thalassemia trait. Because of the very small amounts of serum required for the measurement of ferritin, it is particularly suitable for surveying populations with a high prevalence of hypochromic-microcytic anemias.
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PMID:Serum ferritin in beta-thalassemia trait. 75 May 37

The blood counts of 187 non-anaemic children who attended hospital with minor illnesses and who were between the ages of 12 months and 6 years were studied retrospectively. As many as 76-8% of these children were found to have MCVs below the normal adult range. A prospective study of a further 28 non-anaemic children in the same age group showed that the majority of children with low MCVs have normal haemoglobin A2 and F levels and have serum ferritin levels within the normal adult range. These findings indicate that microcytosis is an intrinsic feature of erythropoiesis in early childhood and that in most instances this feature cannot be attributed to iron deficiency or beta-thalassaemia syndromes.
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PMID:Red cell indices and serum ferritin levels in children. 84 65

During a study of pathogenetic mechanisms in the hepatic cirrhosis of thalassaemia major, 16 liver biopsies were examined by electron microscopy. Previous ultrastructural studies of liver cells during iron overload have shown electron-dense iron as lysosomal haemosiderin, and as lysosomal and cell-sap ferritin. In this study, all biopsies, regardless of the patient's age, showed ferritin molecules within lysosomes in a specific pattern in relationship with regularly arranged lamellae. This membrane-associated lysosomal ferritin is considered to be a stage in the segregation of iron seen in iron overload. The dimensions and electron density of individual ferritin molecules indicate differences between cell sap and lysosomal ferritin. Intracellular ferritin transport and iron-seclusion mechanisms are reconsidered in view of these findings. The liver biopsies of thalassaemic infants also provide information about the causal relationship between iron overload and collagen deposition. Since the collagen deposition precedes any morphological evidence of cellular injury (other than the increased iron content), the primary cirrhotogenic factor in thalassaemia is apparently not cell necrosis but possibly excessive collagen deposition induced by iron.
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PMID:The liver in thalassaemia major: ultrastructural observations. 105 35


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