No description available.

No description available.

This parallel randomized control trial study assessed the effect of food-based strategies in improving the haemoglobin level; decreasing anaemia and thus the iron status of pregnant women. The study randomized 195 anaemic women enrolled from four randomly selected health centres in Dire Dawa while attending ANC into two intervention groups and control; and followed for 12weeks. The study intervened diet-based supplementation of 90mg/day vitamin C divided and consumed in three doses; combined with nutrition education intervention in intervention group 1; while only nutrition education intervention in group 2. Dietary diversity was assessed using past 24-hours and 7-days dietary recall approaches and haemoglobin levels were determined at baseline and end-line and compared to analyse treatment effects. By end of the study, intervention group 1 and 2 had significantly increased mean haemoglobin by 0.77 ± 0.11gm/dl and 0.398 ± 0.073gm/dl respectively; however, the control had significant decrease by -0.193 ± 0.05gm/dl. Anaemia prevalence also significantly decreased by 29% and 19.7% in intervention group 1 and 2 respectively. However, all women in the control were anaemic. Intervention group 1 and 2 also had significantly higher dietary diversity, consumption of vitamin C-rich fruits and vegetables, nutritional knowledge and modification practices. The researcher thus concludes that diet-based vitamin C supplementation integrated with nutrition education has a significant effect in improving haemoglobin, decreasing anaemia and thus improving the iron status of pregnant women in Dire Dawa. Based on the findings, the researcher developed a framework for an integrated food-based strategy for improving the iron status of pregnant women in Ethiopia. / Health Studies / D. Litt. et Phil. (Health Studies)

Leung, Yeung Yeung. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2010. / Includes bibliographical references (leaves 134-154). / Abstracts in English and Chinese. / CONTENTS --- p.i / ACKNOWLEDGEMENTS --- p.iv / ABSTRACT --- p.v / 論文摘要 --- p.viii / LIST OF FIGURES --- p.x / LIST OF TABLES --- p.xiv / LIST OF ABBREVIATIONS --- p.xv / Chapter 1. --- INTRODUCTION --- p.1 / Chapter 1.1 --- Brain iron function and diseases --- p.1 / Chapter 1.1.1 --- Function of iron in the brain --- p.1 / Chapter 1.1.2 --- Iron involved oxidative damage --- p.2 / Chapter 1.1.3 --- Role of iron in neurodegenerative diseases --- p.6 / Chapter 1.1.4 --- Role of iron in Alzheimer's disease --- p.7 / Chapter 1.1.5 --- Deleterious effects of iron in memory function --- p.9 / Chapter 1.2 --- Iron regulation in the brain --- p.10 / Chapter 1.2.1 --- Transport and storage of brain iron --- p.10 / Chapter 1.2.2 --- Iron homeostasis in the brain --- p.14 / Chapter 1.2.3 --- Transport of iron in axon and synapse --- p.17 / Chapter 1.3 --- The hippocampus --- p.19 / Chapter 1.3.1 --- Hippocampus and memory function --- p.19 / Chapter 1.3.2 --- Structure of the hippocampus --- p.20 / Chapter 1.3.3 --- Cell composition in the hippocampus --- p.26 / Chapter 1.3.4 --- Wiring in the hippocampus --- p.28 / Chapter 1.4 --- Synaptic plasticity and long term potentiation --- p.30 / Chapter 1.4.1 --- Basic theory of synaptic plasticity --- p.30 / Chapter 1.4.2 --- Types of synaptic plasticity --- p.30 / Chapter 1.4.3 --- The discovery of long term potentiation --- p.31 / Chapter 1.4.4 --- Long term potentiation --- p.32 / Chapter 1.4.5 --- Cellular mechanism of long term potentiation --- p.33 / Chapter 1.4.6 --- Role of reactive oxygen species in long term potentiation --- p.36 / Chapter 1.5 --- Aim of the study --- p.38 / Chapter 2. --- MATERIALS AND METHODS --- p.39 / Chapter 2.1 --- Rat model of iron overload --- p.39 / Chapter 2.2 --- Multi-electrode field potential measurement --- p.40 / Chapter 2.2.1 --- Acute preparation of hippocampal slices --- p.40 / Chapter 2.2.2 --- Multi-electrode array recording system --- p.41 / Chapter 2.2.3 --- Recording of field excitatory postsynaptic potentials --- p.42 / Chapter 2.2.4 --- Induction of LTP --- p.47 / Chapter 2.2.5 --- Recording of paired-pulse ratio --- p.48 / Chapter 2.3 --- Whole cell patch-clamp recordings --- p.50 / Chapter 2.4 --- Biochemical assays --- p.57 / Chapter 2.4.1 --- Preparation of brain homogenate --- p.57 / Chapter 2.4.2 --- Total iron measurement --- p.57 / Chapter 2.4.3 --- Protein carbonyl measurement --- p.58 / Chapter 2.4.4 --- Determination of reactive oxygen species --- p.60 / Chapter 2.5 --- Drugs and data analysis --- p.61 / Chapter 3. --- RESULTS --- p.62 / Chapter 3.1 --- The acute effects of extracellular iron on synaptic transmission and long-term synaptic plasticity in the hippocampus in vitro --- p.63 / Chapter 3.1.1 --- Effects of ferric ion on basal synaptic transmission --- p.63 / Chapter 3.1.1.1 --- Effect of FAC on basal fEPSPs --- p.63 / Chapter 3.1.1.2 --- Comparison with the effect of AC on basal fEPSPs --- p.69 / Chapter 3.1.2 --- Effects of ferric ion on long-term synaptic plasticity --- p.72 / Chapter 3.1.2.1 --- Effect of acute FAC treatment on LTP --- p.72 / Chapter 3.1.2.2 --- Comparison with the effect of AC on LTP --- p.75 / Chapter 3.1.3 --- Effects of ferric chloride --- p.78 / Chapter 3.1.4 --- Effects of ascorbic acid on the action of FAC --- p.81 / Chapter 3.2 --- "The acute, in vitro effect of extracellular iron on the membrane properties and excitability of hippocampal CA1 neurons" --- p.86 / Chapter 3.2.1 --- Membrane input resistance --- p.86 / Chapter 3.2.2 --- Voltage-Current relationship --- p.88 / Chapter 3.2.3 --- Membrane excitability --- p.90 / Chapter 3.2.3.1 --- Threshold current --- p.90 / Chapter 3.2.3.2 --- Action potential firing frequency --- p.92 / Chapter 3.2.4 --- Action potential characteristics --- p.95 / Chapter 3.2.4.1 --- "Action potential amplitude, area and width" --- p.95 / Chapter 3.2.4.2 --- Rise and decay kinetics of action potential --- p.98 / Chapter 3.3 --- The chronic effects of iron-loading in the brain on hippocampal long-term synaptic plasticity --- p.100 / Chapter 3.3.1 --- Validation of the iron-overload model --- p.100 / Chapter 3.3.1.1 --- Short-term (1 week) treatment --- p.100 / Chapter 3.3.1.2 --- Long-term (4 weeks) treatment --- p.103 / Chapter 3.3.2 --- Effects of chornic iron-overloading on LTP --- p.105 / Chapter 3.3.2.1 --- Short term iron treatment --- p.105 / Chapter 3.3.2.2 --- Long term iron treatment --- p.108 / Chapter 3.3.3 --- Oxidative stress measurement --- p.111 / Chapter 3.3.3.1 --- Protein oxidation --- p.111 / Chapter 3.3.3.2 --- Reactive oxidative species level --- p.116 / Chapter 4. --- DISCUSSION --- p.120 / Chapter 4.1 --- "Acute, in vitro effects" --- p.121 / Chapter 4.2 --- "Chronic, in vivo effects" --- p.125 / Chapter 5. --- REFERENCES --- p.134

Bibliography: leaves 148-163.

Bibliography: leaves 148-163. / xix, 163, [43] leaves : ill. ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis (Ph.D.)--University of Adelaide, Dept. of Public Health, 2001

The aim of this thesis was to study maternal and infant effects of delayed cord clamping (≥180 seconds, DCC) compared to early (≤10 seconds, ECC) in a randomised controlled trial. Practice and guidelines regarding when to clamp the cord vary globally, and different meta-analyses have shown contradictory conclusions on benefits and disadvantages of DCC and ECC. The study population consisted of 382 term infants born after normal pregnancies and randomised to DCC or ECC after birth. The primary objective was iron stores and iron deficiency at 4 months of age, but the thesis was designed to investigate a wide range of suggested effects associated with cord clamping. Paper I showed that DCC was associated with improved iron stores at 4 months (45% higher ferritin) and that the incidence of iron deficiency was reduced from 5.7% to 0.6%. Neonatal anaemia at 2-3 days was less frequent in the DCC group, 1.2% vs. 6.3%. There were no differences between the groups in respiratory symptoms, polycythaemia, or hyperbilirubinaemia. In paper II we demonstrated that DCC versus ECC was not associated with higher risk for maternal post partum haemorrhage and rendered a comparable ratio of valid umbilical artery blood gas samples. In paper III, the Ages and Stages Questionnaire was used to assess neurodevelopment at 4 months. The total scores did not differ, but the DCC group had a higher score in the problem-solving domain and a lower score in the personal-social domain. Immunoglobulin G level was 0.7 g/L higher in the DCC group at 2–3 days, but did not differ at 4 months. Symptoms of infection up to 4 months were comparable between groups. Finally, in paper IV, iron stores and neurodevelopment were similar between groups at 12 months. Gender specific outcome on neurodevelopment at 12 months was discovered, implying positive effects from DCC on boys and negative on girls. We conclude that delaying umbilical cord clamping for 180 seconds is safe and associated with a significantly reduced risk for iron deficiency at 4 months, which may have neurodevelopmental effects at a later age.

A sustainable primary prevention strategy for infant iron deficiency anemia (IDA) was implemented and evaluated in a community with at-risk infants in northern Quebec, Canada. Communication strategies were used to promote iron-rich complementary food rather than iron-fortified formula, which can interfere with breastfeeding practice. This food-based approach has been successfully implemented in developing countries, but has not been applied in an industrialized country setting. / Mass media (i.e., radio dialogues, key messages, print material, point-of-purchase grocery store display) and interpersonal (i.e., homemade baby food cooking activity) communication strategies were developed in collaboration with community members and implemented in partnership with an existing community program. Reach and exposure of the strategies were measured using a questionnaire administered to a post-intervention sample (n = 45). Sales of promoted iron-rich infant food were examined pre- and post-intervention period. A repeat cross-sectional design was used for the impact evaluation. Two groups of mothers with infants, aged 7-10 months at Time 1 (n = 32) and Time 2 (n = 22) were interviewed. Outcome variables were infants' total iron and complementary food iron intakes measured by two 24-hour recalls. Secular trends in infants' hemoglobin values and milk type consumption were examined in the study community and two comparison communities. / Multiple communication channels increased awareness of IDA and influenced self-reported use of iron-rich infant food. Iron-rich infant food sales increased from pre- to post-intervention (p < 0.05). Complementary food intake iron increased between Time 1 (3.2 +/- 0.8 mg) and Time 2 (4.4 +/- 1.1 mg) (p < 0.05). The proportion of infants with anemia (hemoglobin < 110 g/L) significantly decreased from the period before (37.2%) to during (14.3%) the intervention (p < 0.05). No significant difference was found for this variable within the comparison communities. The proportion of infants receiving iron-fortified formula in the study community did not differ between Time 1 and Time 2, but increased from Time 1 (55%) to Time 2 (73%) (p < 0.05) in the comparison communities, indicating an erosion of breastfeeding practice. / These results suggest the effectiveness of communication strategies to improve infant iron nutrition in a community with good access to iron-rich infant food. The potential for this strategy in other communities warrants further investigation.

The objectives of this research were to determine the prevalence of anemia, and identify risk factors for anemia, in 9-month-old Cree infants living in northern Quebec. The prevalence of anemia (hemoglobin <110 g/L) was 25--32%, depending on the study sample. Iron deficiency was present in 28.2% of infants who could be classified and 14.4% had iron deficiency anemia. Fewer than 2% of infants had low birth weight (<2500 g) so most infants should have been born with adequate iron stores. One cause of anemia that was identified was a diet that was low in iron. Only 15.1% of infants were reported by guardians to eat meat daily and 28.5% were reported to never eat meat. Infants who were breastfed or cow's milk fed did not obtain sufficient iron for effective erythropoiesis. Compared with formula that was predominantly iron fortified, the odds ratio (OR) for anemia was 7.9 (95% CI 3.4--18.2) for breast milk and 5.0 (95% CI 2.0--12.7) for cow's milk. When milk type was controlled for, weight gain since birth was significantly associated with microcytic erythrocytes (OR comparing the highest tertile of weight gain to the lowest tertile 2.9, 95% CI 1.2--6.6). This indicates that fast-growing infants were not meeting their iron needs for growth. Another risk factor for anemia that was identified was common childhood infections. The prevalence of anemia among infants reported as recently unwell with an infection was higher than among infants reported as recently well (31.1% vs. 19.0%, chi2 = 4.27, p = 0.039). The prevalence of elevated blood lead was 2.7% and is not a major public health problem. No evidence for vitamin A deficiency was found. Serum retinol was positively associated with all iron status indicators. Cree infants who were given supplements containing vitamin A had a lower prevalence of anemia (hemoglobin <105 g/L) (10.8% vs 23.2%, chi2 = 5.97, p = 0.015). These results suggest a role for vitamin A in iron metabolism. To prevent anemia in aboriginal i

No description available.