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)

This study was performed to investigate modifications in the serum bilirubin forms, hepatobiliary enzymes, and some glycoproteic substances in patients during the course of extrahepatic cholestasis (stage A) and following its clinical resolution (stage B). The series consisted of 16 patients: 11 had main bile duct stones; two, benign stenosis of the main bile duct; and three, main bile duct cancer. Cholestasis resolved spontaneously in one case, under endoscopy in two, and following surgery in 13. Five patients with liver cirrhosis and a picture of intrahepatic cholestasis following anesthesia were also investigated. Serum bilirubin forms were measured using van den Bergh's method and the alkaline methanolysis-HPLC procedure; the mono- and di-conjugated forms were considered together in the overall evaluation of the results. The hepatobiliary enzymes (ALP, GGT, and AST) were increased at stage A and significantly decreased at stage B. Similar patterns were observed in total (TB), unconjugated (UB), and conjugated bilirubin (CB) and in the percentage of CB out of TB (% CB). In the majority of patients, % CB at stage B was lower than at stage A, whereas in subjects with a high initial UB value, a different % CB pattern was observed. The direct bilirubin percentage (% DB), on the other hand, had a different pattern, and the variations between stages A and B were not significant. The pathophysiological bilirubin pattern was similar in patients with intrahepatic cholestasis. At stage A, in a number of patients the levels of glycoproteic substances (CA 19-9, TPA and ferritin) were raised, but at stage B they tended to decrease towards the normal range.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Alterations in bilirubin metabolism during extra- and intrahepatic cholestasis. 160 Mar 31

The authors have studied the distribution of anionic and cationic sites on both luminal and abluminal endothelial aspects of iridial vessels in Macaca mulatta and Macaca fascicularis. With the animals in general anesthesia, anionic ferritin (AF) and cationic ferritin (CF) were either injected intravenam or perfused at known intraocular pressure (15-20 mmHg) through the anterior chamber. AF introduced intravenam was retained in the vessels' lumen. The tight junctions between the endothelial cells were impermeable and the plasmalemmal vesicles did not transport tracer to the iridial stroma. In contrast, when perfused through the anterior chamber, AF was present in the vessels' lumen. Here again the tight junctions between the endothelial cells were impermeable, but AF was contained within a great number of plasmalemmal vesicles. Iridial vessels were impermeable to CF perfused into the lumen, but a continuous layer of CF particles was found to adhere to the luminal plasma membrane. When perfused through the anterior chamber, CF was bound to the proteoglycans associated with collagen fibrils of the iridial stroma and basal laminae of stromal, pericytic, and endothelial cells but was never found in the vessels' lumen. These results indicate that different electrical charges are associated with the plasmalemmal vesicles on the luminal and abluminal fronts of iridial vessels. The authors suggest that in these vessels a unidirectional vesicular transport is responsible for the selective movement of anionic organic substances from the tissues of the eye to the bloodstream.
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PMID:Asymmetric distribution of charged domains on the two fronts of the endothelium of iris blood vessels. 399 13

Studies of iron metabolism were made in 24 patients following surgery under general anaesthesia. No postoperative complications occurred. There was a marked fall in serum iron in all patients on the first postoperative day (P less than 0.001) which remained significantly depressed even at the seventh postoperative day. The total iron binding capacity fell progressively to reach the lowest levels on the third postoperative day, returning to normal levels by the end of the study. Serum ferritin concentration rose significantly in a reciprocal pattern to the changes in serum iron. This study highlights the limitation of iron studies in peripheral blood in postoperative patients.
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PMID:Changes in iron metabolism following surgery. 683 Nov 57

To examine the effect of circulating proteins on the passage of intravenously injected native ferritin across pulmonary capillary endothelium, rats were exchange transfused with FC-43 fluorocarbon emulsion (FCE) under ether anesthesia. Protein concentration was reduced to less than 1.1 mg/ml by exchange transfusion, followed by FCE containing 15, 30, or 60 mg/ml of lyophilized rat serum protein (LRSP). Two minutes after ferritin injection lungs were prepared for ultrastructural morphometry. The diameter and numerical density of vesicles remained unchanged under all experimental conditions; however, at 0.6 mg/ml of circulating protein there was a 5- and 10-fold increase, respectively in percent vesicle (%VL) and basement membrane labeling (BML) by ferritin. This was reversible; at 60 mg/ml of circulating protein %VL and BML was indistinguishable from controls. Following a reduction of circulating protein to less than 1.1 mg/ml, the addition of 15 mg/ml LRSP reduced %VL but had no effect on BML. This suggests that in addition to shuttling vesicles there may be a second mechanism for the transport of ferritin, possibly involving transendothelial chains of vesicles.
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PMID:The bloodless rat: a new model for macromolecular transport studies across lung endothelium. 708 59

Heme oxygenase-1 (HO-1, HSP32) is an early gene that is responsive to an array of pathological conditions including, but not limited to, hypoxia and cerebral ischemia. HO-1 cleaves the heme molecule and produces carbon monoxide (CO) and biliverdin (an antioxidant) and is essential for iron homeostasis. The purpose of this study was to investigate, using transgenic (Tg) mice, whether overexpression of HO-1 in the brain augments or attenuates cellular injury caused by ischemic stroke. Homozygous HO-1 Tg mice that overexpress HO-1 under the control of the neuron-specific enolase promoter (characterized previously) were used. Under halothane anesthesia and normothermic conditions, wild-type nontransgenic (nTg; n = 22) and HO-1 Tg (n = 24) mice were subjected to middle cerebral artery occlusion (MCAo). Six hours after induction of ischemia, Tg and nTg mice developed infarcts that were 39 +/- 6 and 63 +/- 9 mm3, respectively (p < 0.01). No significant difference between the two strains was observed in the values of brain edema (11.3 +/- 4% in Tg vs. 14.6 +/- 5% in nTg; p < 0.1). At 24 h after MCAo, Tg mice exhibited significant neuroprotection as determined by the stroke volumes (41 +/- 2 mm3 in Tg vs. 74 +/- 5 mm3 in nTg; p < 0.01) and values of ischemic cerebral edema (21 +/- 6% in Tg vs. 35 +/- 11% in nTg; p < 0.01). Data suggest that neuroprotection in Tg mice was, at least in part, related to the following findings: (a) constitutively up-regulated cyclic GMP and bcl-2 levels in neurons; (b) inhibition of nuclear localization of p53 protein; and (c) antioxidant action of HO-1, as detected by postischemic neuronal expression of ferritin, and decreases in iron staining and tissue lipid peroxidation. We suggest that pharmacological stimulation of HO-1 activity may constitute a novel therapeutic approach in the amelioration of ischemic injury during the acute period of stroke.
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PMID:Overexpression of heme oxygenase-1 is neuroprotective in a model of permanent middle cerebral artery occlusion in transgenic mice. 1003 92

The purpose of this study was to compare the diagnostic efficacy of single shot fast spin echo sequence (SSh-FSE), and single shot GRASE-sequence (SSh-GRASE) to the conventional T(2)-weighted fast spin echo-sequence (T(2)-FSE) in the imaging of brain disorders. Thirty three patients with high signal intensity lesions on T(2)-weighted images (n = 28), or intracerebral hemorrhage (n = 5), were examined on a 1.0 T MR scanner, with 23 mT/m gradient strength. The scan time for the conventional T(2)-FSE-sequence was 2 min 57 s, the scan time for the single shot-FSE-, and single shot-GRASE-sequences was 11 sec, and 17 sec, respectively. Twenty-one patients remained still during the examination, whereas 12 could not stay still with consecutive marked motion artifacts. Images were reviewed by three radiologists. Lesion conspicuity, image quality, and artifacts were scored on a subjective scale. Signal-to-noise ratios of lesions and normal tissue and contrast-to-noise ratios (CNR) were measured by region of interest (ROI). In the patient group without motion artifacts conspicuity for lesions > or =5 mm did not show a significant difference on conventional T(2)-FSE, single shot-FSE and single shot-GRASE. Detectability of the smaller lesions was significantly inferior on single shot-FSE-, and single shot-GRASE-sequences in artifact free images. For the patient group with motion artifacts SSh-FSE and SSh-GRASE were markedly superior to the conventional T(2)-FSE. Grey-white differentiation was better on conventional T(2)-FSE. Physiologic ferritin as well as pathologic hemosiderin depositions were slightly darker and therefore better visible on SSh-GRASE than on SSh-FSE. Conventional T(2)-FSE showed significantly more artifacts. In conclusion, SSh-FSE and SSh-GRASE imaging can be used for rapid imaging of the brain in those patients who are claustrophobic or in patients with involuntary movements due to extrapyramidal disorders, as well as in children in whom anesthesia is contraindicated or sedation is not possible.
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PMID:Ultrafast magnetic resonance imaging of the brain. 1074 31

Transfusional iron overload may occur in the lungs. We hypothesized that quantitating siderophages in the bronchoalveolar fluid (BALF) of heavily transfused patients may prove to be a useful tool in determining lung iron overload in transfusion-dependent patients. The study included six patients (7-20 years) with thalassemia major (TM) who had received multiple blood transfusions, one with hereditary spherocytosis (four blood transfusions) and one with sickle cell disease (never transfused); they were compared to three children with idiopathic pulmonary hemosiderosis (IPH) (2.5-7.0 years) as positive controls. Fiberoptic bronchoscopy with bronchoalveolar lavage was performed in seven patients under general anesthesia for elective surgery and the rest were bronchoscoped electively under sedation. Spirometry was also performed in eight patients. There was no significant difference between children with TM and IPH in siderophages as percentage of total count (95% CI -31.0 to 1.5, P = 0.068). There were positive relationships between both mean serum ferritin values during the preceding year and the total number of units of transfused blood, and percent siderophage count among multiply transfused patients (P = 0.010, P = 0.052, respectively); similar findings were noted for the Golde score (P = 0.001, P = 0.031, respectively). None of the patients showed lung function impairment. In conclusion, in this small study, we found that the BALF of multiply transfused patients with benign hematological disorders contain similar numbers of siderophages to that of patients with IPH; this is strongly suggestive of secondary pulmonary hemosiderosis. The correlation between the patients' serum ferritin, and the BALF siderophages suggests that the later may serve as a marker of pulmonary iron overload in patients requiring blood transfusion and appear to be more sensitive than standard pulmonary function tests.
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PMID:Quantification of siderophages in bronchoalveolar fluid in transfusional and primary pulmonary hemosiderosis. 1687 95

Lemurs in captivity progressively accumulate iron deposits in a variety of organs (hemosiderosis) including duodenum, liver, and spleen throughout their lives. When excessive, the toxic effects of intracellular iron on parenchymal cells, particularly the liver, can result in clinical disease and death. The pathogenesis of excessive iron storage in these species has been attributed to dietary factors related to diets commonly fed in captivity. Tissue iron stores can be directly estimated by tissue biopsy and histologic examination, or quantitated by chemical analysis of biopsy tissue, However, expense and risk associated with anesthesia and surgery prevent routine use of tissue biopsy to assess iron status. A noninvasive means of assessing total body iron stores is needed to monitor iron stores in lemurs to determine whether dietary modification is preventing excessive iron deposition, and to monitor potential therapies such as phlebotomy or chelation. Serum ferritin concentration correlates with tissue iron stores in humans, horses, calves, dogs, cats, and pigs. Serum ferritin is considered the best serum analyte to predict total body iron stores in these species and is more reliable than serum iron or total iron binding capacity, both of which may be affected by disorders unrelated to iron adequacy or excess including hypoproteinemia, chronic infection, hemolytic anemia, hypothyroidism, renal disease, and drug administration. We have developed an enzyme-linked immunosorbent assay to measure serum ferritin in lemurs. The assay uses polyclonal rabbit anti-human ferritin antibodies in a sandwich arrangement. Ferritin isolated from liver and spleen of a black and white ruffed lemur (Varecia variegata variegata) was used as a standard. Ferritin standards were linear from 0 to 50 microg/L. Recovery of purified ferritin from lemur serum varied from 95% to 110%. The within-assay variability was 4.5%, and the assay-to-assay variability for three different samples ranged from 10% to 17%. The assay also measures serum ferritin in several other lemur species.
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PMID:Enzyme-linked immunosorbent assay to quantitate serum ferritin in black and white ruffed lemurs (Varecia variegata variegata). 1731 22

Under study were the main regularities of changes in processes of peroxidation and antioxidant defense in patients with different methods of operative hemorrhage replacement. Autohemotransfusion was fulfilled in 33 patients; donor blood was transfused to 33 patients. It was concluded that donor blood transfusion gave rise to activation of lipid peroxidation processes and decrease of antiradical activity. Elevation of the level of nitrogen oxide in the group of patients with transfused donor blood was due to its participation in the mechanisms of antioxidant defense. The content of serum iron was reliably higher on the 10th day of the postoperative period in the group of patients with transfused donor blood. The content of ferritin in the group of patients with transfused donor blood was lower before anesthesia and by the moment of blood replacement. High indices of cortisol in patients with transfused donor blood within 4-6 hours after operation suggest that it has a more pronounced stress-realizing effect than autohemotransfusion.
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PMID:[State of free radical processes, metabolism of nitrogen oxide, iron and cortisol level in autohemotransfusion and transfusion of the donor blood]. 1731 93

We reviewed cardiac T2* assessments from 77 thalassemia major patients between the ages of 2.5 and 18 years to study optimal timing of cardiac iron screening by magnetic resonance imaging. No patient under 9.5 years of age showed detectable cardiac iron in contrast to 36% of patients between the ages of 15-18 years old, corresponding to an odds-ratio of 1.28 (28%) per year. All patients with cardiac iron had received at least 35 grams of transfusional iron. Liver iron and ferritin failed to predict cardiac iron loading. Initiation of cardiac magnetic resonance imaging assessment should be determined according to age and transfusional burden rather than indices of iron overload. When appropriate chelation therapy has been administered since birth, cardiac magnetic resonance imaging can be postponed until 8 years of age when anesthesia is not required. Patients with suboptimal chelation, increased transfusional requirements, or who have initiated transfusions later in life should be tested sooner.
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PMID:Onset of cardiac iron loading in pediatric patients with thalassemia major. 1981 35


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