1988 ◽  
Vol 10 (3) ◽  
pp. 1-12 ◽  
Author(s):  
I. Darnton-Hill ◽  
F. Sibanda ◽  
M. Mitra ◽  
M. M. Ali ◽  
A. E. Drexler ◽  
...  

1998 ◽  
Vol 19 (2) ◽  
pp. 137-148 ◽  
Author(s):  
Martin W. Bloem ◽  
Saskia de Pee ◽  
Ian Darnton-Hill

Even mild to moderate vitamin A deficiency is now recognized as an important factor in child health and survival. This has given increased emphasis to the goal of virtually eliminating vitamin A deficiency and its consequences, including blindness, by the end of the decade. The implications of vitamin A deficiency, however, vary according to the group at risk, and this needs to be addressed when looking at ways to achieve the goal. In pre-school children, vitamin A deficiency can lead to increased risk of mortality and morbidity and to blindness. In pregnant and lactating women, it can lead to night-blindness and appears to have implications for maternal morbidity and mortality. Although the immediate health consequences for schoolchildren and adolescents are not completely known, they are probably less dramatic. Nevertheless, it is clear that there is a cross-generational cycle leading to and perpetuating vitamin A deficiency in affected communities. This also has implications when addressing prevention and control strategies. The existing, somewhat successful approach has been to target children aged six months to six years; it is implicit that this criterion is used to measure progress towards the end-of-decade goals. A broader, complementary, life-cycle approach to vitamin A deficiency is now appropriate in many countries. There is increasing emphasis on such approaches, i.e., fortifying foods with vitamin A and improving the diet, which address the whole population at risk. A mix of interventions will give governments the chance to shift from a subsidized vitamin A capsule programme to more sustainable, non-subsidized, consumer-funded vitamin A interventions, although in an appreciable number of countries, supplementation with vitamin A will be a necessity for some years to come. Guidelines to assist governments in such transitions are a high priority.


2002 ◽  
Vol 132 (9) ◽  
pp. 2845S-2850S ◽  
Author(s):  
Alfred Sommer ◽  
Frances R. Davidson

Development ◽  
1997 ◽  
Vol 124 (23) ◽  
pp. 4749-4758 ◽  
Author(s):  
P. Kastner ◽  
N. Messaddeq ◽  
M. Mark ◽  
O. Wendling ◽  
J.M. Grondona ◽  
...  

Knock-out of the mouse RXRalpha gene was previously shown to result in a hypoplastic heart ventricular wall, histologically detectable in 12.5 dpc fetuses. We show here that a precocious differentiation can be detected as early as 8.5 dpc in ventricular cardiomyocytes of RXRalpha(−/−) mutants. This precocious differentiation, which is characterized by the presence of striated myofibrils, sarcoplasmic reticulum and intercalated disks, is found after 9.5 dpc in about 50% of RXRalpha(−/−) subepicardial myocytes. In contrast, wild-type subepicardial myocytes remain morphologically undifferentiated up to at least 16.5 dpc. A similar precocious differentiation was observed in 9.5 dpc subepicardial myocytes of several RXRbeta(−/−) and RARalpha(−/−) mutants, as well as in vitamin A-deficient embryos. The proportion of differentiated subepicardial myocytes almost reached 100% in RXRalpha/RXRbeta double null mutants, indicating a partial functional redundancy between RXRalpha and RXRbeta. This differentiation defect was always paralleled by a decrease in the mitotic index. In addition, subepicardial myocytes of RXRalpha(−/−), RXRalpha(−/−)/RXRbeta(−/−) or vitamin A deficient, but not of RXRbeta(−/−) and RARalpha(−/−) embryos, were often flattened and more loosely connected to one another than those of WT embryos. Thus, retinoids are required at early stages of cardiac development to prevent differentiation, support cell proliferation and control the shape of ventricular myocytes, and both RXRs and RARs participate in the mediation of these functions.


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