What works? Interventions for maternal and child undernutrition and survival

We reviewed interventions that affect maternal and child undernutrition and nutrition-related outcomes. These interventions included promotion of breastfeeding; strategies to promote complementary feeding, with or without provision of food supplements; micronutrient interventions; general supportive strategies to improve family and community nutrition; and reduction of disease burden (promotion of handwashing and strategies to reduce the burden of malaria in pregnancy). We showed that although strategies for breastfeeding promotion have a large effect on survival, their effect on stunting is small. In populations with sufficient food, education about complementary feeding increased height-for-age Z score by 0.25 (95% CI 0.01-0.49), whereas provision of food supplements (with or without education) in populations with insufficient food increased the height-for-age Z score by 0.41 (0.05-0.76). Management of severe acute malnutrition according to WHO guidelines reduced the case-fatality rate by 55% (risk ratio 0.45, 0.32-0.62), and recent studies suggest that newer commodities, such as ready-to-use therapeutic foods, can be used to manage severe acute malnutrition in community settings. Effective micronutrient interventions for pregnant women included supplementation with iron folate (which increased haemoglobin at term by 12 g/L, 2.93-21.07) and micronutrients (which reduced the risk of low birthweight at term by 16% (relative risk 0.84, 0.74-0.95). Recommended micronutrient interventions for children included strategies for supplementation of vitamin A (in the neonatal period and late infancy), preventive zinc supplements, iron supplements for children in areas where malaria is not endemic, and universal promotion of iodised salt. We used a cohort model to assess the potential effect of these interventions on mothers and children in the 36 countries that have 90% of children with stunted linear growth. The model showed that existing interventions that were designed to improve nutrition and prevent related disease could reduce stunting at 36 months by 36%; mortality between birth and 36 months by about 25%; and disability-adjusted life-years associated with stunting, severe wasting, intrauterine growth restriction, and micronutrient deficiencies by about 25%. To eliminate stunting in the longer term, these interventions should be supplemented by improvements in the underlying determinants of undernutrition, such as poverty, poor education, disease burden, and lack of women's empowerment.     

Locus assignment of two alpha-globin structural mutants from the Caribbean basin: alpha Fort de France (alpha 45 Arg) and alpha Spanish Town (alpha 27 Val)

Two alpha-globin structural mutants were mapped to their encoding loci by in vitro translation of hybrid-selected alpha 1- and alpha 2-globin mRNA. The more highly expressed mutant, alpha Spanish Town (alpha 27Val), is encoded at the alpha 2 locus and the less expressed mutant, alpha Fort de France (alpha 45Arg), is encoded at the alpha 1 locus. These results further define the distribution of alpha-globin structural mutations within the alpha-globin gene cluster and substantiate the dominant role of the alpha 2-globin locus in alpha- globin expression.     

Turbulent fluid shear stress induces vascular endothelial cell turnover in vitro.

The effects of hemodynamic forces upon vascular endothelial cell turnover were studied by exposing contact-inhibited confluent cell monolayers to shear stresses of varying amplitude in either laminar or turbulent flow. Laminar shear stresses (range, 8-15 dynes/cm2; 24 hr) induced cell alignment in the direction of flow without initiating the cell cycle. In contrast, turbulent shear stresses as low as 1.5 dynes/cm2 for as short a period as 3 hr stimulated substantial endothelial DNA synthesis in the absence of cell alignment, discernible cell retraction, or cell loss. The results of these in vitro experiments suggest that in atherosclerotic lesion-prone regions of the vascular system, unsteady blood flow characteristics, rather than the magnitude of wall shear stress per se, may be the major determinant of hemodynamically induced endothelial cell turnover.     

A nonlinear quasi-static model of intracranial aneurysms

Abstract

Biomathematical modelsof intracranial aneurysms can provide qualitative and quantitative information on stagesof aneurysm development through elucidationof biophysical interactions and phenomena. However, most current aneurysm models, based on Laplace’s law, are renditionsof static, linearly elastic spheres. The primary goalof this study is to:1. develop a nonlinear constitutive quasi-static model and 2. derive an expression for the critical size/pressureof an aneurysm, with subsequent applications to clinical data. A constitutive modelof an aneurysm, based on experimental dataof tissue specimens available in the literature, was incorporated into a time-dependent setof equations describing the dynamic behaviorof a saccular aneurysm in response to pulsatile blood flow. The setof differential equations was solved numerically, yielding mathematical expressions for aneurysm radius and pressure. This model was applied to clinical data obtained from24 patients presenting with ruptured aneurysms. Aneurysm development and eventu.al rupture exhibited an inverse relationship between aneurysm size and blood pressure. In general, the model revealed that rupture becomes highly probable for an aneurysm diameter greater than 2.0mm and a systemic blood pressure greater than125 mmHg. However, an interesting observation was that the critical pressure demonstrated a minimal sensitivity to the critical radius, substantiating similar clinical and experimental observations that blood pressure was not correlated, to any degree, with aneurysm rupture. Undulations in the aneurysm wall, presented by irregularmultilobulated morphologies, could play an important role in aneurysm rupture. However, dueto the large variation in results, more extensive studies will be necessary for further evaluation and validationof this model.[Neural Res 1997; 19: 489-496]     

Gastric mucosal damage induced by combination of ethanol and lysophosphatidylcholine

The purpose of this study was to determine the effect of lysophosphatidylcholine on the guinea pig stomach after dosing the animal with 20% ethanol by orogastric intubation. We studied four groups of animals; one control group received saline orogastrically followed by buffer and one test group received saline followed by buffer plus 1 mM lysophosphatidylcholine. Two other groups were challenged with 20% ethanol (5 ml) orogastrically followed by buffer or buffer plus 1 mM lysophosphatidylcholine. Compared to other groups, the stomachs of animals given ethanol followed by lysophosphatidylcholine displayed statistically significant increases in the number of gross hemorrhagic lesions, in back-diffusion of hydrogen ion, in net secretion of sodium ion and in morphologic damage. Transmucosal potential differences in this group were also decreased. We conclude that 90 min after dosing with ethanol, the guinea pig stomach is more susceptible to damage by lysophosphatidylcholine. Our data further suggest that these agents cause mucosal damage by different mechanisms and that the combination acts synergistically.This work was supported by funds from the Research Service of the Veterans Administration.These results were presented in part at the Annual Meeting of the Research Society on Alcoholism, Isle of Palms, South Corolina, May 29–June 1, 1985, and were published in abstract form (Alcoholism. Clin Exp Res 9:201, 1985).