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)

AIMS--To confirm the observation of extremely high concentrations of ferritin in postmortem serum samples in sudden infant death syndrome (SIDS); to examine the factors influencing blood ferritin concentrations postmortem; to determine whether or not these high blood ferritin concentrations are characteristic of SIDS. METHODS--Postmortem samples of cardiac blood were obtained from 58 full term infants who died of SIDS and 14 full-term infants who died of a variety of other causes. Whole blood and serum ferritin concentrations were determined and compared with age at death, liver iron concentration, serum iron concentration, and serum lactate dehydrogenase activity. RESULTS--The median postmortem blood ferritin concentration for all infants was 18,600 micrograms/l, which is about 200 times the concentration found in the serum of normal, live infants. Serum iron concentrations were high and there was a highly significant correlation between serum ferritin and iron concentrations suggesting that much of the serum iron was contributed by ferritin. There was no significant difference between serum and whole blood ferritin concentrations. H to L type ferritin ratios were higher in blood from the left than the right ventricle of the heart but the ferritin was always predominantly L type. Blood ferritin concentrations rose rapidly after death but in samples collected at postmortem examination there was a significant correlation with liver iron concentration and an inverse correlation with age. Median values for blood ferritin were higher in SIDS (22,500; n = 58) than in control cases (6900; n = 7) dying under one year of age; however, in both groups ferritin concentrations decreased with age. CONCLUSIONS--Release of ferritin into the blood postmortem seems to be characteristic of infants dying before the age of one year rather than characteristic of SIDS. Two factors may cause such ferritin release postmortem: tissue breakdown and the high level of storage iron in cells of the reticuloendothelial system (including endothelial cells lining vessel walls). SIDS occurs when tissue iron concentrations are higher than at any other time of life. It is possible that the ready availability of iron enhances free radical damage which might be implicated in SIDS.
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PMID:Postmortem blood ferritin concentrations in sudden infant death syndrome. 756 Feb 6

Liver iron concentrations have been shown to be higher in victims of SIDS than in postmortem controls suggesting that high levels of tissue iron may be implicated in SIDS. To determine whether infants who subsequently die from SIDS are born with greater iron stores than those who do not, the iron stores in newborn infants were assessed retrospectively by measuring blood ferritin concentration in spots from Guthrie cards (collected from almost all infants born in the UK in the first week of life). A method for extracting and measuring ferritin from stored blood spots is described. Eighteen cases of SIDS were identified in South Glamorgan along with four controls for each case. Ferritin concentrations did not differ in SIDS victims and controls suggesting that victims of SIDS are not born with abnormal concentrations of stored iron. If iron stores are found to be higher in SIDS victims than in healthy live infants of the same age then it is more likely that the iron will have been acquired after birth.
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PMID:Blood ferritin concentrations in newborn infants and the sudden infant death syndrome. 865 86

We researched the application of immunohistochemistry for the purpose of establishing forensic pathological diagnoses. In the present study, we examined the induction and expression of heat shock protein (HSP), oxygen regulated protein (ORP), inducible nitric oxide synthase (iNOS), excitatory amino acid transporter 2 (EAAT2) and apolipoprotein E (apo E) in the human brain using forensic autopsy cases as our subjects. Hypoxic/ischemic brain damage. In cases of longer survival and with a history of hypoxic attacks, the proteins HSP and ORP were found in the parieto-occipital lobe and hippocampus. And we are able to observe a weak stain for EAAT2 in almost all asphyxia deaths. Traumatic brain injury (TBI). In traumatic brain injury (TBI), the prolonged induction of iNOS was demonstrated in the neutrophils, microglia/macrophage, and vascular smooth muscle cells in the traumatized brain. Apo E was identified with neurons in the traumatized cortical hemisphere from only a two-hour survival case to long survival cases. To the contrary, there was no positive apo E staining in the contralateral cortical hemisphere at all. In one one-hour survival case, a weak stain for EAAT2 was observed, but intensive expression of EAAT2 was observed from brief to one-day survival cases. Sudden infant death (SID). Numerous ferritin-positive cells were observed in the brain in the cases of pneumonia or myocarditis that we examined. To the contrary, the numbers of ferritin-positive cells were obviously decreased in the cases of sudden infant death syndrome (SIDS). The transferrin-positive cells were in an inverse proportion to the ferritin positive cells in each SIDS case. Also, numerous ORP-150 positive cells were observed in the brain in cases of pneumonia and the SIDS group. In forensic practice, immunohistochemical investigation of these proteins can be a great value for diagnosing not only the cause of death but also the pathophysiological changes and the victims past history.
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PMID:[Application of immunohistochemistry for forensic pathological diagnosis: finding of human brain in forensic autopsy]. 1190 39

We report a child with Sudden Infant Death Syndrome (SIDS), aged 16 months. The histological findings of tonsils, spleen, and bone marrow revealed many hemophagocytic cells. Parainfluenza virus type 2 (PIV2) was cultured in the nasopharynx and detected by reverse-transcription (RT)-PCR in liver tissue and bone marrow. His laboratory data of elevated level of ferritin and IL-6 suggested hemophagocytic syndrome (HPS). It is suspected that PIV2 infection in infants is a risk factor for SIDS.
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PMID:Sudden infant death syndrome due to parainfluenza virus 2 associated with hemophagocytic syndrome. 1584 40

Iron is bound to mobile transferrin (TF) and ferritin in blood. TF receptors (TFRC and TFR2) regulate intracellular iron by delivering iron from TF into the cytoplasm. In this study, we examined the effects of 10 single nucleotide polymorphisms (SNPs) in each of the genes for TF and TF receptors on blood iron concentrations in Japanese subjects. Blood iron levels were determined by microwave plasma-atomic emission spectrometry and the SNPs were analyzed by polymerase chain reaction followed by restriction fragment length polymorphism analysis. Blood iron levels in males were significantly higher than those in females. Therefore, the analysis was performed only in males. Blood iron concentrations did not correlate with age and postmortem intervals in males. Among the 10 SNPs in TF, TFRC, and TFR2 genes, significant associations were observed between TF genotypes (rs12769) and male iron concentrations. Individuals with genotype GG in rs12769 had significantly higher blood iron concentrations than those with GA. Previous studies have shown the association between high tissue iron concentrations and disease, liver iron levels are higher in infants dying from sudden infant death syndrome and decreased blood iron concentrations were observed in critically ill children. Therefore, rs12769 in TF might be related to diseases and mortality risk.
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PMID:Association of SNPs in transferrin and transferrin receptor genes with blood iron levels in human. 3031 34