The objective of this thesis was to study the response of Eutrema salsugineum (Yukon) plants to low phosphate (Pi) using seedlings and four- week-old plants grown on media formulated with variable phosphate (Pi). Seedlings showed similar root architecture whether grown with high Pi or without added Pi. Four-week-old plants grown with 0 or 2.5 mM Pi added to the soil had the same shoot biomass and relative growth rates. Confirmation that plants on low Pi were Pi-deficient despite lacking a Pi-starvation phenotype was provided by the increased expression of Pi-starvation-inducible genes (notably EsIPS2) in Pi-deprived plants. We also found that seedling roots on media lacking Pi did not acidify their rhizosphere nor did they show increased phosphatase secretion or phosphatase activity relative to roots of Pi-sufficient seedlings. In soil-grown plants, leaf P remobilization was slower during dark-induced senescence of Eutrema relative to similarly treated, Pi-starved Arabidopsis. Also related to metabolism, in vitro assays showed that the ratio of maximal PPi- and ATP- dependent phosphofructokinase activities approximated 1:1 and 2:1 for Eutrema leaf and root extracts, respectively, with no Pi-responsive changes found and, relative to Arabidopsis, Eutrema phosphoenolpyruvate carboxylase activities were high. The enzyme activities suggest Eutrema operates glycolytic by-passes under Pi sufficient and deficient conditions. Finally, transcripts for the transcription factors Phosphate Starvation Response 1 (PHR1) and WRKY75 were not Pi-starvation-inducible and were more abundant in Eutrema leaves than in leaves of Pi-deprived Arabidopsis. Global gene expression showed the leaf and root transcriptomes to be about 90% similar between 0 and 2.5 mM Pi- treated plants with 2,901 differentially expressed genes detected by DESeq2. In summary, Eutrema displays few Pi-starvation responsive traits whether those traits reflect changes at the level of gene expression or plant morphology, behaviour consistent with a specialist that is continuously primed for Pi starvation. / Thesis / Doctor of Philosophy (PhD)

No description available.

by Shiu Kar Chi. / Thesis (M.Sc.)--Chinese University of Hong Kong, 1998. / Includes bibliographical references (leaves 61-67). / Abstract also in Chinese. / ACKNOWLEDGEMENTS / ABSTRACT / LIST OF TABLES / LIST OF FIGURES / Chapter CHAPTER 1 --- INTRODUCTION --- p.1 / Chapter 1.1 --- Overview --- p.2 / Chapter 1.2 --- Historical perspective --- p.2 / Chapter 1.3 --- Biochemistry of the IgG subclasses --- p.4 / Chapter 1.4 --- IgG subclasses and human diseases --- p.7 / Chapter 1.4.1 --- Glomerulonephritis --- p.7 / Chapter 1.4.2 --- Blistering skin lesions --- p.7 / Chapter 1.4.3 --- Insulin dependent diabetes mellitus (IDDM) --- p.8 / Chapter 1.5 --- Primary antibody deficiencies --- p.8 / Chapter 1.5.1 --- CVID --- p.8 / Chapter 1.5.2 --- X-linked antibody deficiency --- p.8 / Chapter 1.5.3 --- IgG subclass deficiency --- p.10 / Chapter 1.5.4 --- Specific antibody deficiencies --- p.10 / Chapter 1.5.5 --- Selective IgA deficiency --- p.10 / Chapter 1.6 --- IgG subclasses deficiency --- p.10 / Chapter 1.7 --- Clinical manifestation of IgG subclass deficiency --- p.11 / Chapter 1.8 --- Restriction of IgG subclass responses to exogenous antigens --- p.12 / Chapter 1.9 --- Expression of IgG subclasses --- p.14 / Chapter 1.10 --- Mechanisms of IgG subclass deficiency --- p.14 / Chapter 1.10.1 --- Gene deletion --- p.14 / Chapter 1.10.2 --- Immune dysregulation --- p.17 / Chapter 1.10.2.1 --- T-cell receptor defects --- p.18 / Chapter 1.10.2.2 --- Interferon gamma (IFN-y) --- p.18 / Chapter 1.10.2.3 --- Interleukin-4 (IL-4) --- p.19 / Chapter 1.10.2.4 --- Interleukin-6 (IL-6) --- p.19 / Chapter 1.11 --- Prevalence of IgG subclass deficiency --- p.19 / Chapter 1.12 --- Reference intervals for IgG subclass --- p.20 / Chapter 1.13 --- Methods for investigation of IgG subclass deficiency --- p.20 / Chapter 1.13.1 --- Radial-immunodiffusion --- p.21 / Chapter 1.13.2 --- Enzyme linked immunsorbent assay --- p.21 / Chapter 1.13.3 --- Nephelometry/turbidmetry --- p.21 / Chapter 1.14 --- Aim of study --- p.22 / Chapter CHAPTER 2 --- MATERIALS AND METHOD I The Binding Site IgG Subclass Assay --- p.23 / Chapter 2.1 --- Materials --- p.24 / Chapter 2.1.1 --- IgG subclass assay --- p.24 / Chapter 2.1.2 --- Evaluation of patients immune status --- p.24 / Chapter 2.1.3 --- Apparatus and equipment --- p.24 / Chapter 2.2 --- Evaluation of The Binding Site human IgG subclass assay on Beckman Array 360 protein system --- p.25 / Chapter 2.2.1 --- Principle of the Beckman Array Protein System --- p.25 / Chapter 2.2.2 --- Assay preparation and procedure --- p.25 / Chapter 2.2.3 --- Performance characteristic of the IgG subclasses assay --- p.28 / Chapter 2.2.3.1 --- Gain setting --- p.28 / Chapter 2.2.3.2 --- Within batch precision --- p.28 / Chapter 2.2.3.3 --- Interassay precision --- p.28 / Chapter 2.2.3.4 --- Linearity of the assay --- p.29 / Chapter 2.2.3.5 --- Interference of the IgG subclass assay --- p.29 / Chapter 2.2.3.6 --- Recovery experiment --- p.30 / Chapter CHAPTER 3 --- MATERIALS AND METHOD II IgG Subclass Deficiency in Hong Kong --- p.32 / Chapter 3.1 --- Patients and controls --- p.33 / Chapter 3.2 --- Blood samples --- p.33 / Chapter 3.3 --- Serum total haemolytic complement and alternative pathway haemolytic complement assay --- p.34 / Chapter 3.3.1 --- Total haemolytic complement --- p.34 / Chapter 3.3.2 --- Alternative pathway haemolytic complement --- p.34 / Chapter 3.4 --- Statistical analysis --- p.35 / Chapter CHAPTER 4 --- RESULTS I: Evaluation of The Binding Site IgG Subclass Array Kit --- p.36 / Chapter 4.1 --- Gain setting --- p.37 / Chapter 4.2 --- Within batch precision --- p.37 / Chapter 4.3 --- Inter-assay precision --- p.37 / Chapter 4.4 --- Linearity and lowest limit of detection --- p.37 / Chapter 4.5 --- Interference experiments --- p.37 / Chapter 4.6 --- Recovery experiment --- p.37 / Chapter CHAPTER 5 --- RESULTS II: IgG Subclass Deficiency in Hong Kong --- p.45 / Chapter 5.1 --- IgG subclass concentrations and humoral immune status evaluation results of patients and control subjects --- p.46 / Chapter 5.2 --- Statistical tests --- p.45 / Chapter CHAPTER 6 --- DISCUSSION I: The Binding Site IgG Subclass Array Kit --- p.52 / Chapter 6.1 --- IgG subclass assays --- p.53 / Chapter 6.2 --- Within batch and inter-assay precision --- p.53 / Chapter 6.3 --- Lowest limit of detection --- p.53 / Chapter 6.4 --- Interference --- p.54 / Chapter 6.5 --- Recovery of IgG --- p.54 / Chapter 6.6 --- Overall performance of the nephelometric assay --- p.55 / Chapter CHAPTER 7 --- DISCUSSION II: IgG Subclass Deficiency in Hong Kong --- p.56 / Chapter 7.1 --- IgG subclass deficiency in adults --- p.57 / Chapter 7.2 --- Paetiatric patients --- p.59 / Chapter 7.3 --- Recurrent infections and IgG subclass deficiency --- p.59 / Chapter 7.4 --- Summary --- p.60 / REFERENCES --- p.61

by Xiao Gang. / Thesis (M.Sc.)--Chinese University of Hong Kong, 1998. / Includes bibliographical references (leaves 91-99). / Abstract also in Chinese. / ACKNOWLEDGEMENTS --- p.i / SUMMARY --- p.1 / Chapter 1 --- LITERATURE REVIEW / Chapter 1.1 --- MAGNESIUM --- p.3 / Chapter 1.1.1 --- GENERAL FUNCTION OF MAGNESIUM --- p.3 / Chapter 1.1.2 --- ABSORPTION AND METABOLISM OF MAGNESIUM --- p.6 / Chapter 1.1.3 --- CLINICAL ASPECTS --- p.8 / Chapter 1.1.4 --- METHODS OF DETERMINATION OF MAGNESIUM --- p.11 / Chapter 1.2 --- ZINC --- p.13 / Chapter 1.2.1 --- GENERAL FUNCTION OF ZINC --- p.13 / Chapter 1.2.2 --- ABSORPTION AND METABOLISM OF ZINC --- p.14 / Chapter 1.2.3 --- CLINICAL ASPECTS --- p.16 / Chapter 1.2.4 --- ASSESSMENT OF THE BODY ZINC STATUS --- p.19 / Chapter 1.2.5 --- METHODS OF DETERMINATION OF ZINC --- p.20 / Chapter 1.3 --- COPPER --- p.21 / Chapter 1.3.1 --- GENERAL FUNCTION OF COPPER --- p.21 / Chapter 1.3.2 --- ABSORPTION AND METABOLISM OF COPPER --- p.21 / Chapter 1.3.3 --- CLINICAL ASPECT --- p.25 / Chapter 1.3.4 --- LABORATORY ASSESSMENT OF COPPER STATUS --- p.28 / Chapter 1.3.5 --- METHODS FOR THE DETERMINATION OF COPPER --- p.29 / Chapter 1.4 --- SELENIUM --- p.31 / Chapter 1.4.1 --- GENERAL FUNCTION OF SELENIUM --- p.31 / Chapter 1.4.2 --- ABSORPTION AND METABOLISM OF SELENIUM --- p.31 / Chapter 1.4.3 --- CLINICAL ASPECTS --- p.34 / Chapter 1.4.4 --- ASSESSMENT --- p.36 / Chapter 1.4.5 --- METHODS OF DETERMINATION OF SELENIUM --- p.37 / Chapter 1.5 --- INTRODUCTION TO ATOMIC ABSORPTION SPECTROPHOTOMETRY --- p.38 / Chapter 1.5.1 --- PRINCIPLE OF AAS --- p.38 / Chapter 1.5.2 --- INSTRUMENTATION --- p.39 / Chapter 2 --- INTRODUCTION --- p.43 / Chapter 2.1 --- TRACE ELEMENT DEFICIENCY IN HOSPITAL PATIENT --- p.43 / Chapter 2.2 --- MICRONUTRIENT DEFICIENCY AMONG PATIENTS WITH ACUTE MYOCARDIAL INFARCTION --- p.44 / Chapter 2.2.1 --- MAGNESIUM DEFICIENCY --- p.44 / Chapter 2.2.2 --- CHANGE OF ZINC AND COPPER IN AMI --- p.47 / Chapter 2.2.3 --- SELENIUM DEFICIENCY --- p.50 / Chapter 2.3 --- OBJECTIVES OF THIS PROJECT --- p.52 / Chapter 3 --- MATERIALS AND METHODS / Chapter 3.1 --- PATIENTS SELECTION --- p.53 / Chapter 3.1.1 --- CONTROL GROUP --- p.53 / Chapter 3.1.2 --- AMI GROUP --- p.53 / Chapter 3.1.3 --- DIGOXIN TREATMENT GROUP --- p.54 / Chapter 3.2 --- ANALYTIC METHODS --- p.55 / Chapter 3.2.1 --- DETERMINATION OF SERUM Magnesium --- p.55 / Chapter 3.2.2 --- DETERMINATION OF SERUM ZINC --- p.57 / Chapter 3.2.3 --- DETERMINATION OF SERUM COPPER --- p.60 / Chapter 3.2.4 --- DETERMINATION OF SERUM SELENIUM --- p.63 / Chapter 4 --- RESULTS --- p.68 / Chapter 4.1 --- RESULTS OF EVALUATION OF ANALYTICAL --- p.68 / Chapter 4.1.1 --- RESULTS OF METHODS EVALUATION OF SERUM ZINC ASSAY --- p.68 / Chapter 4.1.2 --- RESULTS OF METHODS EVALUATION OF SERUM COPPER ASSAY --- p.71 / Chapter 4.1.3 --- RESULTS OF METHODS EVALUATION OF SERUM SELENIUM ASSAY --- p.73 / Chapter 4.2 --- RESULTS OF PATIENTS STUDY --- p.76 / Chapter 4.2.1 --- CONTROL GROUP --- p.76 / Chapter 4.2.2 --- PATIENTS WITH ACUTE MYOCARDIAL INFARCTION I DEMOGRAPHIC DATA --- p.77 / Chapter 4.2.3 --- DIGOXIN GROUP --- p.83 / Chapter 5 --- DISCUSSION --- p.85 / Chapter 5.1 --- AMI PATIENTS AND TRACE ELEMENT STATUS --- p.85 / Chapter 5.2 --- MAGNESIUM AND ZINC STATUS IN PATIENTS RECEIVING DIGOXIN TREATMENT --- p.88 / REFERENCE --- p.91 / LIST OF TABLES --- p.99 / LIST OF TABLES --- p.102 / TABLES & FIGURES

The aims of the present studies were to determine the magnitude of iron deficiency anemia among preschool children in Northern Ethiopia and to evaluate different control strategies. The cross-sectional study showed that anemia was highly prevalent (42%) and that iron deficiency was the commonest cause of anemia. However, the iron deficiency was not due to lack of iron in the diet but to its poor availability and to other non-dietary risk factors. Unsafe water, mother's illness, older child (24--60 months), family not having food reserves and family income below poverty-line were predictors of anemia. Hookworm and malaria were rare and did not account for the anemia. In the iron pot study three types of Ethiopian foods were cooked in three types of pots (iron, aluminum and clay) and assessed for their total and available iron. After adjusting for cooking time and moisture, there were significantly higher total and available iron in all the three types of foods when cooked in iron pots compared to the aluminum or clay pots. The study also showed that the hemoglobin status and length of children improved significantly when they consumed food cooked in iron pots. In the third study, a randomized, placebo-controlled, and double-blind trial, both iron and vitamin A supplemented children showed increased hemoglobin levels. Combined iron and vitamin A supplementation showed the highest rise. Iron-supplemented children showed increase in length, but no increase in weight. They also showed lower rates of c-reactive protein positivity and decreases in the prevalence and frequency of diarrhea. A single dose of vitamin A did not result in any increase in length or weight but a decrease in the prevalence and frequency of diarrhea was observed. Children supplemented with iron only or vitamin A only showed higher ARI rates, but those children who received combined iron and vitamin A showed significantly lower ARI rates. Iron supplementation did not have any effect on either zinc

No description available.

Anemia and micronutrient deficiencies in infancy are common in low-income settings. These are partly due to maternal malnutrition and may impair child health and development. We studied the impact of maternal food and micronutrient supplementation, duration of exclusive breastfeeding (EBF), growth and infection on infant anemia and micronutrient status. In the MINIMat trial in Matlab, Bangladesh, pregnant women were randomized to Early or Usual promotion of enrolment in a food supplementation program and to one of three daily micronutrient supplements. Capsules containing 400µg folic acid and (a) 30 mg iron (Fe30Fol), (b) 60 mg iron (Fe60Fol), (c) 30 mg iron and other micronutrients (MMS) were provided from week 14 of gestation. Capsule intake was assessed with the eDEM device recording supplement container openings. Blood samples (n=2377) from women at week 14 and 30 were analyzed for hemoglobin (Hb). Duration of EBF and infant morbidity was based on monthly maternal recalls. Infants were weighed and measured monthly. Blood samples (n=1066) from 6-months-old infants were analyzed for Hb and plasma ferritin, zinc, retinol, vitamin B12 and folate. In women, Hb increase per capsule reached a plateau at 60 Fe60Fol capsules, indicating that nine weeks of daily supplementation produced maximum Hb response. Anemia was common (36%) at capsule intakes >60 indicating other causes of anemia than iron deficiency. In infants, vitamin B12 deficiency prevalence was lower in the MMS (26.1%) than in the Fe30Fol group (36.5%), (p=0.003) and zinc deficiency prevalence was lower in the Usual than in the Early group. There were no other differential effects of food or micronutrient supplementation on infant anemia or micronutrient status. Infants exclusively breast-fed for 4-6 months had a higher mean plasma zinc concentration (9.9±2.3 µmol/L) than infants exclusively breast-fed for <4 months (9.5±2.0 µmol/L), (p< 0.01). No other differences in anemia, iron or zinc status were observed between EBF categories. Infection, low birth weight and iron deficiency were independent risk factors for infant anemia. Regardless of studied interventions, prevalence of anemia (43%), deficiency of zinc (56%), vitamin B12, vitamin A (19%) and iron (22%) in infancy was high and further preventive strategies are needed. / MINIMat

Call number: LD2668 .T4 1964 A55 / Master of Science

No description available.

published_or_final_version / Biochemistry / Doctoral / Doctor of Philosophy