Subject(s)
Deficiency Diseases , Famine , Food , History , Malnutrition , Nutrition Disorders , Nutritional SciencesABSTRACT
Concentrations of As, Ca, Cd, Cl, Co, Cr, Cu, F, Fe, Hg, I, K, Mg, Mn, Mo, Na, Ni, P, Pb, Sb, Se, Sn, V, and Zn were determined in human whole milk samples from Guatemala, Hungary, Nigeria, Philippines, Sweden, and Zaire; in most of these countries, three groups of subjects representing different socioeconomic conditions were studied. Analytical quality control was a primary consideration throughout. The analytical techniques used were atomic absorption spectrophotometry, atomic emission spectrometry with an inductively coupled plasma, colorimetry, electrochemistry, using an ion-selective electrode and neutron activation analysis. The differences between median concentrations of Ca, Cl, Mg, K, Na, and P (minor elements) were lower than 20% among the six countries. Among trace elements, concentrations observed in Filipino milk for As, Cd, Co, Cr, Cu, F, Fe, Mn, Mo, Ni, Pb, Sb, Se, and V were higher than for milk samples from other countries. The remaining five countries showed a mixed picture of high and low values. In the case of at least some elements, such as, F, I, Hg, Mn, Pb, and Se, the environment appears to play a major role in determining their concentrations in human milk. The nutritional status of the mother, as reflected by her socioeconomic status, does not appear to influence significantly the breast milk concentrations of minor and trace elements. Significant differences exist between the actual daily intakes observed in this study and current dietary recommendations made by, for example, WHO and the US National Academy of Sciences. These differences are particularly large (an order of magnitude or more!) for Cr, F, Fe, Mn, and Mo; for other elements, such as, Ca, Cu, Mg, P, and Zn, they amount to at least a factor 2. In the opinion of the present authors, these findings point to the need for a possible reassessment of the dietary requirements of young infants with respect to minor and trace elements, particularly for the elements Ca, Cr, Cu, F, Fe, Mg, Mn, Mo, P, and Zn.
Subject(s)
Milk, Human/chemistry , Trace Elements/analysis , Democratic Republic of the Congo , Female , Guatemala , Humans , Hungary , Infant Nutritional Physiological Phenomena , Infant, Newborn , Nigeria , Philippines , Sweden , Trace Elements/administration & dosageABSTRACT
Cet ouvrage fait le point sur l'ensemble des aspects techniques et pratiques à prendre en considération pour l'élaboration de stratégies directes, efficaces et de faible coût destinées à lutter contre l'anémie ferriprive. Notant que cette affection touche plus de 700 millions de personnes dans le monde, les auteurs se sont efforcés de montrer comment les nouvelles connaissances sur les moyens techniques de prévention et de lutte pouvaient être utilisées pour atteindre le plus grand nombre possible de personnes au moindre coût. Tout au long de cette étude, l'accent est mis sur les problèmes et les écueils dont il faut tenir compte, notamment dans les pays en développement, pour choisir les mesures de lutte les plus appropriées
Subject(s)
Anemia, HypochromicABSTRACT
A guide to the full range of technical and practical considerations required for the design of direct, inexpensive, and effective strategies to combat iron deficiency anaemia. Noting that this condition impairs the lives of over 700 million persons worldwide, the book makes a special effort to show how new knowledge about the technical means for prevention and control can be used to reach the largest numbers at the lowest possible costs. Throughout, emphasis is placed on problems and pitfalls, particularly in developing countries, that need to be considered when selecting the most appropriate measures for control. The opening chapters provide essential background information about the complex causes of iron deficiency anaemia, the many factors that influence its etiology, and the corresponding implications for assessment and treatment. A chapter devoted to etiology and epidemiology includes a thorough explanation of iron requirements, intake, and bioavailability useful in understanding why some individuals are at greater risk than others. Details range from a table indicating recommended daily iron intakes to examples of dietary combinations, commonly found in developing countries, that either enhance or inhibit iron absorption. Against this background, the book turns to the practical problems of assessment, treatment, and prevention. A chapter concerned with anaemia screening and the detection of iron deficiency critically compares available laboratory tests, pointing out advantages and drawbacks likely to be encountered under field conditions in developing countries. Readers are then given detailed information on treatment options using iron tablets, liquid preparations, or tablets including folate or ascorbic acid, on he recommended dosage and duration of therapy, and on side-effects associated with specific preparations and known to cause poor compliance. Information on prevention concentrates on four basic approaches involving supplementation with medicinal iron, education and associated measures to increase dietary iron intake, the control of parasitic and other infections, and the fortification of a staple food with iron. The book concludes with a discussion of the costs and benefits of prevention and a guide to the components, goals, and logistics of an anaemia control programme
Subject(s)
Anemia, HypochromicABSTRACT
Reports about recent famine victims and refugees have described the occurrence of xerophthalmia and resultant blindness related to severe vitamin A deficiency. These populations are subject to high prevalences of childhood protein-energy malnutrition and infectious diseases, pre-existing marginal vitamin A status, and inadequate levels of vitamin A in relief rations. In order to prevent unnecessary morbidity and mortality when any of these risk factors arise, famine victims or refugees should receive vitamin A supplements as an early and essential component of the nutritional support provided by relief agencies. Such supplementation should not await the results of nutrition or blindness surveys but rather should be a standard component of the maternal and child health care provided to the affected population until sufficiency of dietary vitamin A has been clearly established.
Subject(s)
Refugees , Starvation , Vitamin A Deficiency/etiology , Xerophthalmia/etiology , Child , Child, Preschool , Diet , Humans , Infant , Population Surveillance , Risk Factors , Vitamin A/administration & dosage , Vitamin A/adverse effects , Vitamin A/physiology , Xerophthalmia/prevention & controlSubject(s)
Goiter/epidemiology , Goiter/metabolism , Goiter/prevention & control , Humans , Iodine/urine , Malawi , Thyrotropin/blood , Thyroxine/bloodABSTRACT
Two murine cDNAs (pMIF20/11 and pMIF3/10) coinduced with interferon in mouse cells infected with Newcastle disease virus (NDV) were identified previously. By genomic Southern blot analysis of hamster/mouse somatic cell hybrids, the gene hybridizing with pMIF20/11 has been localized on chromosome 12 and the gene hybridizing with pMIF3/10 on chromosome X.
Subject(s)
Chromosome Mapping , Interferons/genetics , Animals , Cell Line , Collodion , Cricetinae , Electrophoresis, Polyacrylamide Gel , Genetic Markers , Hybrid Cells/metabolism , Interferons/biosynthesis , Mice , Newcastle disease virus/metabolism , PaperABSTRACT
The vast extent and the world wide distribution of vitamin A deficiency is discussed. Its epidemiology is reviewed and sources of vitamin A in diets recorded, along with the high requirements of children. Strategy for prevention is described under three headings--short, medium and long term steps. Strategies in many countries received notice.
PIP: Conservative estimates project over 500,000 cases/year of new active corneal lesions and 6-7 million cases of noncorneal xerophthalmia attributable to vitamin A deficiency on a worldwide basis. Vitamin A deficiency affects growth, the differentiation of epithelial tissues, and immune competence. The most dramatic impact, however, is on the eye and includes night blindness, xerosis of the conjunctiva and cornea, and ultimately corneal ulceration and necrosis of the cornea. Vitamin A deficiency occurs when body stores are exhausted and supply fails to meet the body's requirements, either because there is a dietary insufficiency, requirements are increased, or intestinal absorption, transport and metabolism are impaired as a result of conditions such as diarrhea. Vitamin A deficiency is the single most frequent cause of blindness among preschool children in developing countries. The younger the child, the more severe is the disease and the higher the risk that corneal destruction will be followed by death. The most important step in preventing vitamin A deficiency is ensuring that children's diets include adequate amounts of carotene containing cereals, tubers, vegetables, and fruits. An overall strategy designed to prevent and control vitamin A deficiency, xerophthalmia, and nutritional blindness may be defined in terms of action taken in the short, medium, and long term. A short-term, emergency measure includes the administration to vulnerable groups of single, large doses of vitamin A on a periodic basis. In the medium-term, the fortification of a dietary vehicle (e.g., sugar or monosodium glutamate) with vitamin A can be initiated. Increased dietary intake of vitamin A through home gardening and nutrition education programs comprises the longterm solution to this problem. The World Health Organization plans to launch a 10-year program of support to countries where vitamin A deficiency is a significant public health problem.
Subject(s)
Blindness/prevention & control , Developing Countries , Vitamin A Deficiency/prevention & control , Xerophthalmia/prevention & control , Blindness/epidemiology , Blindness/etiology , Breast Feeding , Child , Child, Preschool , Diet , Female , Health Education , Humans , Infant , Male , Nutritional Sciences/education , Pregnancy , Protein-Energy Malnutrition/complications , Protein-Energy Malnutrition/prevention & control , Vitamin A/administration & dosage , Vitamin A Deficiency/complications , Vitamin A Deficiency/epidemiology , World Health Organization , Xerophthalmia/epidemiology , Xerophthalmia/etiologySubject(s)
Anemia/epidemiology , Adolescent , Adult , Anemia/blood , Child , Child, Preschool , Cross-Cultural Comparison , Cross-Sectional Studies , Developing Countries , Female , Hemoglobinometry , Humans , Infant , Male , Pregnancy , World Health OrganizationABSTRACT
Southern blot analysis with a murine interferon-alpha2 (MuIFN-alpha2) cDNA probe revealed restriction fragment polymorphism of EcoRI- and HindIII-digested C57BL/6 and BALB/cDNA. The inheritance pattern of this polymorphism was examined using DNA from each of the seven recombinant inbred strains derived from C57BL/6 and BALB/c; the strain distribution pattern suggests linkage of INF-alpha genes to two histocompatibility loci on chromosome 4. Southern blot analysis of DNA from six bilinear congenic strains carrying different fragments of the BALB/c chromosome 4 on a C57BL/6 background showed linkage of IFN-alpha genes to the histocompatibility locus H-15. It can therefore be concluded that the IFN-alpha gene cluster is situated on chromosome 4 near the H-15 locus, between loci Mup-1 and b.
Subject(s)
Chromosome Mapping , Genetic Linkage , Histocompatibility Antigens/genetics , Interferon Type I/genetics , Polymorphism, Genetic , Animals , Crosses, Genetic , DNA Restriction Enzymes , Mice , Mice, Inbred BALB C , Mice, Inbred C57BL , Species SpecificityABSTRACT
Two histocompatibility loci, H-23 and H-28, and an interferon locus, If-1, are shown linked to matted, ma, and varitint-waddler, Va, on chromosome 3 of the mouse. The gene order (from centromere) with intervening percent recombination is: ma-19.1(+/- 4.9)-H-23-12.0(+/- 4.0)-VaJ-7.7(+/- 2.2)-H-28-5.9(+/- 2.2)-If-1.
Subject(s)
Histocompatibility , Interferons/genetics , Mice/genetics , Animals , Chromosome Mapping , Genetic LinkageABSTRACT
A cDNA library was constructed from polysomal poly(A)+RNA from Newcastle disease virus (NDV)-induced mouse C243 cells, and screened with a human interferon-alpha (HuIFN-alpha) cDNA probe. A cDNA clone for one of the murine interferon-alpha (MuIFN-alpha) genes was isolated, and sequencing analysis revealed that it was a partial copy which is almost identical to the published sequence for the MuIFN-alpha 2 gene. This partial cDNA clone represents a virus-induced message as seen by Northern blot analysis of RNA from NDV-induced C243 cells, and Southern blot analysis of DNA from BALB/c mouse revealed the presence of a multiple IFN-alpha gene family. The MuIFN-alpha genes were mapped to chromosome 4 by Southern blot analysis of hamster/mouse somatic cell hybrid DNAs.
Subject(s)
Genes , Interferon Type I/genetics , Mice/genetics , Animals , Base Sequence , Chromosome Mapping , Cloning, Molecular , Cricetinae , DNA/genetics , Hybrid Cells/metabolismABSTRACT
Production of circulating interferon (IFN) was measured in inbred mouse strains following intravenous injection of herpes simplex virus type 1 (HSV-1). IFN titres reached maximal levels 2 to 3 h after injection of virus and a 10-fold difference was found between C57BL/6 mice and BALB/c, as high and low producers respectively. Mendelian analysis revealed that HSV-induced IFN production is governed by several loci, one of which is X-linked. The strain distribution pattern obtained from results in recombinant inbred lines and the results obtained in the congenic B6-C-H-28c-If-1(1) strain furthermore indicated an absence of close linkage to If-1. It is concluded that the levels of HSV-induced early IFN production are influenced by several autosomal loci and one X-linked locus.
Subject(s)
Genes , Interferons/biosynthesis , Sex Chromosomes , Simplexvirus/physiology , X Chromosome , Animals , Crosses, Genetic , Female , Genetic Linkage , Male , Mice , Mice, Inbred BALB C , Mice, Inbred C57BL , Recombination, Genetic , Species SpecificityABSTRACT
C57BL/6 (B6) mice are relatively resistant to infection with herpes simplex virus type 1 (HSV-1). Paradoxically, B6 mice were resistant to 250 LD50 (50% lethal dose) of HSV-1 but were killed by 25 or 2.5 LD50 of HSV-1 injected intraperitoneally. At the injection site 250 LD50 of virus induced high titers of interferon (IFN) (greater than 1,000 international units) that reached maximal levels 2-4 hr after inoculation, whereas 25 or 2.5 LD50 of HSV-1 generated only borderline levels of IFN (15-40 international units). Simultaneous inoculation of 250 LD50 of HSV-1 and antiserum to mouse IFN (MuIFN) rendered B6 mice susceptible to infection; however, treatment with antiserum to MuIFN did not increase susceptibility to 1 LD50 of virus. Injections of MuIFN given 2 hr before and 2 hr after inoculation with virus protected B6 mice against 25 LD50 of virus. Thus, endogenous IFN induced after injection with 250 LD50 of HSV-1 protects B6 mice, whereas low doses of virus kill the animals because they do not generate a detectable IFN response at the infection site.
Subject(s)
Herpes Simplex/immunology , Interferons/physiology , Animals , Brain/microbiology , Herpes Simplex/microbiology , Immunity, Innate , Interferons/biosynthesis , Male , Mice , Mice, Inbred C57BL , Simplexvirus/isolation & purificationSubject(s)
Anemia, Hypochromic/therapy , World Health Organization , Adult , Child , Child, Preschool , Community Health Services , Delayed-Action Preparations , Developing Countries , Female , Food, Fortified , Humans , Industry , Infant , Iron/administration & dosage , Nutritional Requirements , Patient Compliance , PregnancyABSTRACT
The iron losses/requirements of children, adolescents, adult men and women, pregnant and lactating women are presented and interpreted in the light of present information concerning the intestinal iron absorption. This helps to explain the high frequency of iron deficiency during childhood and in fertile women. The problems affecting treatment as well as the various approaches to iron deficiency prevention are also discussed.