Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0240066 (iron deficiency)
7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previously, we had identified FOX1 and FTR1 as iron deficiency-inducible components of a high-affinity copper-dependent iron uptake pathway in Chlamydomonas. In this work, we survey the version 3.0 draft genome to identify a ferrireductase, FRE1, and two ZIP family proteins, IRT1 and IRT2, as candidate ferrous transporters based on their increased expression in iron-deficient versus iron-replete cells. In a parallel proteomic approach, we identified FEA1 and FEA2 as the major proteins secreted by iron-deficient Chlamydomonas reinhardtii. The recovery of FEA1 and FEA2 from the medium of Chlamydomonas strain CC425 cultures is strictly correlated with iron nutrition status, and the accumulation of the corresponding mRNAs parallels that of the Chlamydomonas FOX1 and FTR1 mRNAs, although the magnitude of regulation is more dramatic for the FEA genes. Like the FOX1 and FTR1 genes, the FEA genes do not respond to copper, zinc, or manganese deficiency. The 5' flanking untranscribed sequences from the FEA1, FTR1, and FOX1 genes confer iron deficiency-dependent expression of ARS2, suggesting that the iron assimilation pathway is under transcriptional control by iron nutrition. Genetic analysis suggests that the secreted proteins FEA1 and FEA2 facilitate high-affinity iron uptake, perhaps by concentrating iron in the vicinity of the cell. Homologues of FEA1 and FRE1 were identified previously as high-CO(2)-responsive genes, HCR1 and HCR2, in Chlorococcum littorale, suggesting that components of the iron assimilation pathway are responsive to carbon nutrition. These iron response components are placed in a proposed iron assimilation pathway for Chlamydomonas.
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PMID:FEA1, FEA2, and FRE1, encoding two homologous secreted proteins and a candidate ferrireductase, are expressed coordinately with FOX1 and FTR1 in iron-deficient Chlamydomonas reinhardtii. 1766 Mar 59

Iron deficiency anaemia is the most common nutritional disorder in the world. Pregnant women are at especially high risk of iron deficiency and anaemia because of significantly increased iron requirements during pregnancy. Iron supplementation during pregnancy has been recommended for women in the developing world, since usually no basic changes occur in the composition of the diet. This is a retrospective cohort study carried out in Al-Yamamah Hospital, Riyadh, Saudi Arabia, comparing the outcome of haemoglobin levels in 308 pregnant women near term with compliance to iron supplementation during the preceding pregnancy stages. Data were collected using an interview-based questionnaire for assessment of supplementation compliance and the women were divided into three categories: strictly compliant; partially compliant; and non-compliant. Haemoglobin levels were extracted from the medical records for the first antenatal visit (before 13 weeks' gestation) and compared with the level at entrance to the study at 36 weeks' gestation. Both Epi-info 2002 version 3.2 and SPSS version 10 were used for data analysis. Our results show that 49.7% used iron supplements continuously during the second and third trimesters of pregnancy; 38.3% reported partial use and 12.0% used no iron supplements. Haemoglobin levels improved significantly only among strictly compliant pregnant women, by 0.3 g/dl; decreased among partially compliant women by, 0.36 g/dl and significantly decreased among non-compliant, by -1.4 g/dl. Factors associated with non-compliance were education with a simple linear protective effect from being non-compliant. The percentage of anaemic women increased from 29.6% in the first trimester to 34% in the third trimester. Anaemia was significantly associated with non-compliance with iron supplementation, the adjusted OR was 6.19 95% CI 2.55-15.02, p < 0.0001. Strategies to improve compliance and effective iron supplementation among pregnant women should be implemented.
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PMID:Compliance to iron supplementation during pregnancy. 1969 94