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)

A retrospective study of the 99 surviving heart and lung transplant (HLT) recipients at one center showed that 31% had significant anemia (hemoglobin less than 100g/L) six months after transplantation. Chronic anemia persisted in 18% of HLT recipients two years posttransplantation. A similar study of 100 heart transplant recipients showed no unexplained anemic patients. The prevalence of anemia after HLT was unrelated to the original diagnosis, immunosuppression, or acute rejection. All HLT recipients appeared to be unduly sensitive to the myelosuppressive effects of azathioprine. Detailed studies in 16 representative patients showed a normochromic, anisocytotic anemia with normal reticulocyte counts, B12 and folate levels, and haptoglobin levels and appropriate erythropoietin levels--but increased ESRs, low/normal iron levels and low/normal total iron binding capacity, normal or raised ferritin levels, and autoantibodies in 4 (25%). Bone marrow aspirates in 10 patients showed dyshemopoiesis out of proportion to the degree of anemia and colonies of activated lymphoid cells. The cause for this anemia appears to be a combination of anemia of chronic disease and dyshemopoiesis, both of uncertain etiology.
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PMID:The prevalence, course, and characteristics of chronic anemia after heart and lung transplantation. 160 80

1. Exercise-induced haemolysis has been implicated in the sub-optimal iron status of endurance-trained athletes. Accordingly, erythrocyte survival studies using 51Cr were performed on male and female distance runners (n = 20) and sedentary control subjects (n = 10) in order to determine whether the rate of erythrocyte destruction was altered as a consequence of repetitive exercise training. 2. The chromium half-disappearance time of the male (25.4 +/- 3.6 days, mean +/- SD) but not the female (28.3 +/- 4.6 days) athletes was significantly lower than that of the male (33.1 +/- 4.5 days) and female (32.3 +/- 2.6 days) control subjects (P less than 0.01). The mean erythrocyte lifespan of the male and female distance runners (67.2 +/- 22.2 and 72.4 +/- 26.0 days, respectively) was significantly shorter than that of the non-exercising male and female subjects (113.4 +/- 31.0 and 114.1 +/- 29.0 days, respectively) (P less than 0.01). 3. There was no correlation between the mean erythrocyte lifespan and the haemoglobin concentration, serum ferritin levels, body mass, weekly training distance, number of years running or daily protein intake. The mean cell volume and reticulocyte count measured in the same athletes before and after completing a standard 42 km marathon race were within the normal range, whereas the plasma haemoglobin levels were elevated (77.0 +/- 50.5 mg/l) and the serum haptoglobin levels were decreased (0.89 +/- 0.4 g/l) at rest, with a further significant decrease after running (0.69 +/- 0.4 g/l) in the latter measurement (P less than 0.05). 4. It is concluded that the demonstrated increase in erythrocyte turnover may be sufficient to precipitate an iron deficiency in endurance athletes when dietary intake or absorption does not meet the accelerated erythropoietic demands.
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PMID:Haemolytic effects of exercise. 165 57

The blood iron status of 44 male runners of various running specialties (18 sprinters, 13 middle- and 13 long-distance runners) is evaluated by measuring serum ferritin (SF), serum iron (Si), hemoglobin concentration (Hb), hematocrit (Ht), red blood cells content (RBC) and haptoglobin concentration (Hp). The results of these analyses (except Hp) are compared to those obtained in sedentary male subjects (control group) of the same mean age. Mean SF, SI, Hb and Ht measured in athletes are significantly lower than in control group. The remarkably low Hp values obtained in athletes suggests the occurrence of hemolysis. Using unpaired t test, it appears that the blood iron status of these runners does not depend on their running specialty.
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PMID:Iron status in runners of various running specialties. 169 84

The aim of this study is to elucidate the change in serum levels of gynecological tumor markers throughout the period from the early gestational stage to puerperium. We measured eight tumor markers of--CA 125, TPA, SCC, AFP, haptoglobin, ferritin, CA19-9 and CEA--in 17 healthy women with a normal course of pregnancy, delivery and puerperium, and obtained the following results: 1) Profiles of change in serum levels of CA125, SCC, haptoglobin and ferritin were similar during pregnancy, with those levels being the highest at 4-15 weeks of gestation and declining gradually from 16 to 27 weeks. Serum levels of these four markers decreased significantly (p less than 0.01) at 16-27 and 28-40 weeks of gestation, respectively. 2) A significant (p less than 0.01) increase in CA125 and SCC was observed 2 hours after delivery compared with the levels in the first stage of delivery. However, these two markers decreased to the normal range after the fifth day postpartum. 3) Serum TPA decreased significantly (p less than 0.05) in 16-27 weeks of gestation, comparing with those of 4-15 weeks. Serum CA19-9 and CEA remained almost unchanged within the normal range throughout the period from pregnancy to puerperium. 4) Tumor markers of CA125, TPA, SCC, haptoglobin, ferritin and CEA of which serum levels decreased during the course of pregnancy and puerperium might be a clue to judge whether gynecological tumors in pregnant women are malignant or benign.
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PMID:[Changes in serum levels of gynecological tumor markers throughout the period from early gestation to puerperium]. 170 31

1. It has been suggested that the physiological consequences of strenuous exercise are analogous to those of the acute-phase response. 2. In 70 male and 20 female competitive distance runners, a marked, but transient, neutrophil leucocytosis occurred immediately after these athletes completed a standard (42 km) marathon race. Concomitant significant increases were noted in the plasma cortisol levels, creatine kinase activity, C-reactive protein level, total protein level and albumin level (P less than 0.01). 3. The plasma fibrinogen, C-reactive protein and total protein concentrations were markedly increased both 24 h and 48 h after exercise (P less than 0.01). The serum haptoglobin level was significantly decreased after exercise (P less than 0.01), and increased 48 h later (P less than 0.05). There was no change in the serum iron level, total iron-binding capacity, per cent saturation of transferrin and serum ferritin level. 4. A significant increase in interleukin-1-type activity was demonstrated immediately and 24 h after exercise (P less than 0.01). 5. It is concluded that the metabolic sequelae of sustained exercise are similar, but not analogous, to the acute-phase response, and interleukin-1, probably plays a significant role in linking the haematological and immunological changes observed after sustained strenuous exercise.
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PMID:Strenuous exercise: analogous to the acute-phase response? 172 63

We measured the level of serum haptoglobin, transferrin, alfa-I antitrypsin, orosomucoid, beta-2-microglobulin, ferritin in the case of 30 children (aged 11-16 years) with juvenile chronic arthritis. We divided the patients into two groups. In the first group there were 15 patients with active disease under continuous treatment and in clinical remission (We 20 mm/hour). In the second group there were 15 patients without active disease and they were not given continuous treatment for two Years. These groups were studied, by a control one. If we measure more phase-proteins together, they are suitable for the demonstration of the inflammatory activity in juvenile chronic arthritis. We made a points system for the evaluation of activity.
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PMID:Measurement of the inflammatory activity by the help of serum acute-phase proteins in juvenile chronic arthritis. 172 74

The aim of the present study was to compare the iron status of 19 top-level soccer players and 20 male control subjects. All players showed no impairment of physical performance and had a dietary iron intake adequate to cover the iron losses. Serum iron, TIBC, % transferrin saturation and serum ferritin were not significantly different in athletes and controls: serum haptoglobin was significantly lower in the former than in the latter, the result probably indicating an increase in resting intravascular hemolysis. Since the formed Hb-Hp complex is taken up and metabolized by hepatocytes, it has been suggested that in soccer players a redistribution of iron stores occurs among tissue compartments. A multiparametric hematological monitoring of iron metabolism, just as in runners, is therefore necessary in these athletes, too, in order to detect subjects at risk of real iron deficiency. The pharmacological iron supplementation should be limited to these subjects and only when clinical evidence of reduced tissue iron supply is present.
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PMID:Hematological comparison of iron status in trained top-level soccer players and control subjects. 175 10

Iron is essential for life, but iron overload is toxic and potentially fatal. The liver is a major site of iron storage and is particularly susceptible to injury from iron overload, especially when (as in primary hemochromatosis) the iron accumulates in hepatocytes. Iron can be taken up by the liver in several forms and by several pathways including: (1) receptor-mediated endocytosis of diferric or monoferric transferrin or ferritin, (2) reduction and carrier-facilitated internalization of iron from transferrin without internalization of the protein moiety of transferrin, (3) electrogenic uptake of low molecular weight, non-protein bound forms of iron, and (4) uptake of heme from heme-albumin, heme-hemopexin, or hemoglobin-haptoglobin complexes. Normally, pathway 2 is probably the major one for uptake of iron by hepatocytes. Iron is stored in the liver in the cores of ferritin shells and as hemosiderin, an insoluble product derived from iron-rich ferritin. Iron in hepatocytes stimulates translation of ferritin mRNA and represses transcription of DNA for transferrin and transferrin receptors. The major pathologic effects of chronic hepatic iron overload are: (1) fibrosis and cirrhosis, (2) porphyria cutanea tarda, and (3) hepatocellular carcinoma. Although precise pathogenetic mechanisms remain unknown, iron probably produces these and other toxic effects by increasing oxidative stress and lysosomal lability. Vigorous efforts at diagnosis and treatment of iron overload are essential since the pathologic effects of iron are totally preventable by early vigorous iron removal and prevention of iron re-accumulation.
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PMID:Iron and the liver. 184 76

Serum iron deficiency has a high incidence in female athletes. We investigated the effects of a daily oral iron supplement, (160 mg) administered during an intensive 7-week physical training programme, on body iron status, and the maximal aerobic capacity (VO2max) of 13 women (group A) compared to 15 who took a placebo (group B). The subjects were 19 years old. Blood samples were obtained before training began and on days 1, 7, 21 and 42 of training. They were analysed for packed cell volume (PVC) and for haemoglobin (Hb), 2,3-diphosphoglycerate (2,3-DPG), haptoglobin, iron and ferritin concentrations. The VO2max was measured on days 0, 21 and 42 of training. Following 21 days of training Hb, PCV and ferritin were significantly higher (P less than or equal to 0.01) in group A compared to group B. Over the training period Hb rose by 9.3% and 2.4% in groups A and B, respectively. At the end of training 66% of group B exhibited ferritin concentrations below 10 ng.ml-1, while none of group A had such low values. Mean VO2max of group A had increased by 7.5% following 21 days of training (P less than or equal to 0.01) and by 15.3% after 42 days. No appreciable increase in VO2max had occurred in group B by day 21 (significantly lower than VO2max of group A; P less than or equal to 0.05), however by day 42 it had increased by 14.3% (P less than or equal to 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of an iron supplement on body iron status and aerobic capacity of young training women. 187 36

Yersinia pestis is one of many microorganisms responding to environmental iron concentrations by regulating the synthesis of proteins and an iron transport system(s). In a number of bacteria, expression of iron uptake systems and other virulence determinants is controlled by the Fur regulatory protein. DNA hybridization analysis revealed that both pigmented and nonpigmented cells of Y. pestis possess a DNA locus homologous to the Escherichia coli fur gene. Introduction of a Fur-regulated beta-galactosidase reporter gene into Y. pestis KIM resulted in iron-responsive beta-galactosidase activity, indicating that Y. pestis KIM expresses a functional Fur regulatory protein. A cloned 1.9-kb ClaI fragment of Y. pestis chromosomal DNA hybridized specifically to the fur gene of E. coli. The coding region of the E. coli fur gene hybridized to a 1.1-kb region at one end of the cloned Y. pestis fragment. The failure of this clone to complement an E. coli fur mutant suggests that the 1.9-kb clone does not contain a functional promoter. Subcloning of this fragment into an inducible expression vector restored Fur regulation in an E. coli fur mutant. In addition, a larger 4.8-kb Y. pestis clone containing the putative promoter region complemented the Fur- phenotype. These results suggest that Y. pestis possesses a functional Fur regulatory protein capable of interacting with the E. coli Fur system. In Y. pestis Fur may regulate the expression of iron transport systems and other virulence factors in response to iron limitation in the environment. Possible candidates for Fur regulation in Y. pestis include genes involved in ferric iron transport as well as hemin, heme/hemopexin, heme/albumin, ferritin, hemoglobin, and hemoglobin/haptoglobin utilization.
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PMID:Identification and cloning of a fur regulatory gene in Yersinia pestis. 189 28


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