Ocular structure in vitamin A deficiency in the monkey

1. The role of vitamin A in the metabolism of cone cells of the retina was investigated, from the morphological angle, by studying their structure in induced deficiency of vitamin A in three monkeys. 2. Unequivocal signs of structural damage were observed in the cone and rod cells of the deficient animals, which also showed the classical signs of vitamin A deficiency in other organs. 3. In vitamin A deficiency, damage to the visual cell layer of the retina occurred in one monkey in the absence of corneal involvement. This finding suggests that chronic vitamin A deficiency in the community may lead to progressive damage to the visual cells in a much larger number of persons than the incidence figures for keratomalacia indicate. 4. Degeneration of pigment epithelium was present in retinal sections from all the deficient animals. The possible role of the pigment epithelium in the pathogenesis of the visual defect in vitamin A deficiency has been discussed. 5. Degenerative changes were noted in Descemet's endothelium. This damage may contribute to the degeneration of the corneal epithelium

Influence of protein deficiency on 19S antibody-forming cells in rats and mice

Influence of protein deficiency on immune response to sheep red blood cells was investigated in rats and mice with Jerne's plaque-forming cell technique. Protein deficiency resulted in a reduction in the number of antibody-producing cells consequent upon a prolongation of cell generation time in rats. Injection of syngeneic thymocytes brings about better improvement in the immune response of the X-radiated protein-deficient mice as compared to the controls. It is suggested that depressed immunity in malnutrition may be partly due to a disturbance in thymic function

Effect of vitamin A and undernutrition on the susceptibility of rodents to a malarial parasite Plasmodium berghei

The ability of vitamin A deficient rats to resist infection with P. berghei was investigated. When 10×106 erythrocytes bearing the parasite/100 g body weight were given to the vitamin A protein energy undernourished rats, parasitemia developed in these animals at a faster pace than the controls. A high number (60% to 95% ) of red blood cells (RBC) carrying the parasite were noticeable within 6 to 7 days after infection, at which time most animals in this group died. The pair-fed controls (protein-energy undernourished but supplemented with vitamin A) fared perceptibly better with an equivalent load of infection. Control ad libitum fed littermates were able to restrict the infection and neither high parasitemia nor death was noted in this group. Oral supplements of retinyl acetate to vitamin A deficient rats enabled the animals to recover from infection. A subclinical dose of 500 parasitized RBC given at an early stage of the vitamin A deficiency precipitated the deficiency symptoms at a faster rate and led to the development of higher order of parasitemia in these rats beginning from the 10th day after infection as compared to pair fed controls. The yield of glass adhering cells obtainable from peritoneal exudates was low in deficient rats. In vitro experiments further suggest a decrease in the capacity of the glass adhering peritoneal exudate cells in vitamin A deficient mice to clear the infection. This capacity was improved by addition of non glass adhering cells from sensitized control mice

Anemia in experimental protein deficiency in the rhesus monkey with special reference to iron metabolism

1. This investigation deals with a study of the anemia of protein deficiency in Rhesus monkeys. 2. Protein deficiency was induced in 17 rhesus monkeys. Seven animals, given a protein-rich diet, served as controls. The diets of both the groups were identical in all respects, except protein. All animals were tube-fed to ensure adequate caloric intake. Hematocrit, hemoglobin, erythroctye count, serum iron, serum iron binding capacity, plasma iron tolerance curves, and iron absorption using the Fe59 fecal recovery method were studied before and at intervals of the experiment in both deficient and control groups. Protein-deficient monkeys consistently developed normocytic normochromic anemia of moderate severity. A striking fall in serum iron binding capacity, total proteins and albumin with a rise in gamma globulin was observed in all deficient animals. A significant and comparable fall in serum iron was also observed. The Fe59 absorption was depressed and there was flattening of plasma iron tolerance curves. Two deficient animals, refed a high protein diet, showed reversal of all these changes. The control animals did not show any of these changes. The mechanism of anemia and decreased iron absorption observed in the protein-deficient animals and the relevance of these findings to those in Kwashiorkor are discussed

Pathophysiology of Himalayan endemic goiter

Goiter prevalence and iodine metabolism were studied in areas of endemic goiter in the Himalayas in India and Nepal. Similar studies were also made in Ceylon. The results are compatible with the hypothesis that severe environmental deficiency of iodide is the primary factor responsible for endemic goiter in these areas. The endemicity was less severe in Ceylon than in India and Nepal. The thyroid glands of persons living in endemic areas show an interesting adaptive response to maintain internal homeostasis in the face of severe iodine deficiency. The mechanism of this adaptation was studied in thyroids of goats raised in endemic and nonendemic areas. Thyroids of goats living in an area of severe iodine deficiency showed higher MIT/DIT and T3/T4 ratios than glands of those in an area of iodine abundance. There was a higher incorporation of 131I in 27S iodoproteins in the iodide-deficient glands. A decrease in iodine concentration of the thyroid and an increase in circulating TSH levels are possibly involved in mediating this response but of the two, the former mechanism seems more likely than the latter

Association between antenatal depression and low birthweight in a developing country

Rahman A, Bunn J, Lovel H, Creed F. Association between antenatal depression and low birthweight in a developing country

Maternal nutritional status, food intake and pregnancy weight gain in Nepal

This is the author's accepted version (version 2) of an article published by SAGE in Journal of Health Management, March 2016. The published version is available at http://pss.sagepub.com/lookup/doi/10.1177/0972063415625537Poor maternal nutrition during pregnancy may predispose to intrauterine growth restriction (IUGR), immunological and metabolic adaptations which manifest as low birth weight and increase the risk of adult non-communicable disease. This study examined the relationships between maternal nutritional status, food intake and pregnancy weight gain (PWG) which may account for risk of low birth weight (LBW) in Nepal

The extent, nature and distribution of child poverty in India

Despite a long history, research on poverty has only relatively recently examined the issue of child poverty as a distinct topic of concern. This article examines how child poverty and well-being are now conceptualized, defined and measured, and presents a portrait of child poverty in India by social and cultural groups, and by geographic area. In December 2006, the UN General Assembly adopted a definition of child poverty which noted that children living in poverty were deprived of (among other things) nutrition, water and sanitation facilities, access to basic health care services, shelter and education. The definition noted that while poverty hurts every human being ‘it is most threatening and harmful to children, leaving them unable to enjoy their rights, to reach their full potential and to participate as full members of the society’. Researchers have developed age-specific and gender-sensitive indicators of deprivation which conform to the UN definition of child poverty and which can be used to examine the extent and nature of child poverty in low and middle-income countries. These new methods have ‘transformed the way UNICEF and many of its partners both understood and measured the poverty suffered by children’ (UNICEF, 2009). This article uses these methods and presents results of child poverty in India based on nationally representative household survey data for India