Analysis of nutritional adequacy of local foods for meeting dietary requirements of children aged 6-23 months in rural central Tanzania

Background

Under nutrition remains a serious problem among children in Sub-Saharan Africa. Analysing how diets composed of local foods could achieve nutritional goals for infants and young children in low-income settings is essential. The objective of this study was to analyse how local foods can be used rationally and to what extent these foods can be supplemented to achieve nutrient requirements for children aged 6 – 23 months in resource-poor settings.

Methods

A cross-sectional study was carried out to estimate dietary intakes of 400 children aged 6-23 months using a 12-h weighed dietary record, 24-h dietary recalls, and 7-days food records. Anthropometric measurements on each subject were also taken. Analyses were done to establish the level of nutrient intake, and nutritional status of the study population using Microsoft Excel 2013 and ProPAN software version 2.0.

Results

The results showed that the prevalence of stunting, wasting and underweight for children aged 6–23 months was 30–41%, 1.5–3% and 4–9%, respectively. In addition, the results showed that diets that were consumed by the subjects comprised of local foods met vitamin A, vitamin C, protein and energy requirements for children aged 6–23 months. However, the extent of deficit in iron, zinc and calcium in baseline diets was large and difficult to meet under the existing feeding practices.

Conclusions

The study shows that local foods in the study area have a potential to achieve recommended dietary intakes of some essential nutrients, and that interventions are needed to meet the required amount of iron, zinc and calcium for children aged 6–23 months. The interventions we propose here may encourage changes in traditional feeding habits and practices of the target population. Possible intervention options are (1) supplementation of local foods with nutrient-dense foods that are not normally consumed in the locality (2) providing new avenues for increasing the production and wide consumption of local nutrient-dense foods, or optimizing the way local diets are constituted so as to achieve nutrient recommendations for infants and young children.

     

Myelodysplastic syndromes

There has been a remarkable explosion of knowledge into the molecular defects that underlie the acute and chronic leukemias, leading to the introduction of targeted therapies that can block key cellular events essential for the viability of the leukemic cell. Our understanding of the pathogenesis of the myelodysplastic syndromes (MDSs) has lagged behind, at least in part, because they represent a more heterogeneous group of disorders. The significant immunologic abnormalities described in this disease, coupled with the admixture of MDS stem or progenitor cells within the myriad types of dysplastic and normal cells in the bone marrow and peripheral blood, have made it difficult to molecularly characterize and model MDS. The recent availability of several, effective (ie, FDA-approved) therapies for MDS and newly described mouse models that mimic aspects of the human disease provide an opportune moment to try to leverage this new knowledge into a better understanding of and better therapies for MDS.      

Genetic variation in donor CTLA-4 regulatory region is a strong predictor of outcome after allogeneic hematopoietic cell transplantation for hematologic malignancies

Relapse remains a major cause of death after allogeneic hematopoietic cell transplantation (allo-HCT). Graft-versus-tumor effect is primarily mediated by donor T cells. Cytotoxic T lymphocyte antigen-4 (CTLA-4) is a critical inhibitor of T cell proliferation. Single nucleotide polymorphisms (SNPs) in CTLA-4 may affect immune responses. We hypothesized that CTLA-4 SNPs will be associated with disease control after allo-HCT. One hundred sixty-four adult patients with the availability of pretransplantation recipient and donor DNA samples were included in this analysis. Ten tagSNPs of the CTLA-4 gene were identified. Donor CTLA-4 SNP rs4553808 was associated with decreased relapse-free survival (RFS) (P = .019) and overall?survival (OS) (P = .033). In multivariable analysis of an additive genetic model, genotype of CTLA-4 SNP rs4553808 was an independent risk factor for inferior RFS (hazard ratio [HR] = 1.73, 95% confidence interval [CI] 1.10-2.71, P = .017) and OS (HR = 1.84, 95% CI 1.13-3.0, P = .015). CTLA-4 SNPs can be used to identify high-risk patient subsets that may benefit from preemptive immunomodulation to decrease relapse rates and improve survival.     

Pharmacology of GPR55 in yeast and identification of GSK494581A as a mixed-activity glycine transporter subtype 1 inhibitor and GPR55 agonist

GPR55 is a G protein-coupled receptor activated by L-α-lysophosphatidylinositol and suggested to have roles in pain signaling, bone morphogenesis, and possibly in vascular endothelial cells. It has affinity for certain cannabinoids (molecules that interact with the cannabinoid CB(1) and CB(2) receptors), but investigation of its functional role in cell-based systems and in tissue has been limited by a lack of selective pharmacological tools. Here, we present our characterization of GPR55 in the yeast Saccharomyces cerevisiae and in human embryonic kidney (HEK293) cells. We describe GSK494581A (1-{2-fluoro-4-[1-(methyloxy)ethyl]phenyl}-4-{[4'-fluoro-4-(methylsulfonyl)-2-biphenylyl]carbonyl}piperazine), a selective small-molecule ligand of GPR55 identified through diversity screening. GSK494581A is one of a series of benzoylpiperazines originally identified and patented as inhibitors of the glycine transporter subtype 1 (GlyT1). The structure-activity relationship between GPR55 and GlyT1 is divergent across this series. The most GPR55-selective example is GSK575594A (3-fluoro-4-(4-{[4'-fluoro-4-(methylsulfonyl)-2-biphenylyl]carbonyl}-1-piperazinyl)aniline), which is approximately 60-fold selective for GPR55 (pEC(50) = 6.8) over GlyT1 (pIC(50) = 5.0). Several exemplars with activity at GPR55 and GlyT1 have been profiled at a broad range of other molecular targets and are inactive at cannabinoid receptors and all other targets tested. The benzoylpiperazine agonists activate human GPR55 but not rodent GPR55, suggesting that the relatively low level of sequence identity between these orthologs (75%) translates to important functional differences in the ligand-binding site.     

Different indices of fetal growth predict bone size and volumetric density at 4 years of age

We have demonstrated previously that higher birth weight is associated with greater peak and later‐life bone mineral content and that maternal body build, diet, and lifestyle influence prenatal bone mineral accrual. To examine prenatal influences on bone health further, we related ultrasound measures of fetal growth to childhood bone size and density. We derived Z‐scores for fetal femur length and abdominal circumference and conditional growth velocity from 19 to 34 weeks' gestation from ultrasound measurements in participants in the Southampton Women's Survey. A total of 380 of the offspring underwent dual‐energy X‐ray absorptiometry (DXA) at age 4 years [whole body minus head bone area (BA), bone mineral content (BMC), areal bone mineral density (aBMD), and estimated volumetric BMD (vBMD)]. Volumetric bone mineral density was estimated using BMC adjusted for BA, height, and weight. A higher velocity of 19‐ to 34‐week fetal femur growth was strongly associated with greater childhood skeletal size (BA: r = 0.30, p < .0001) but not with volumetric density (vBMD: r = 0.03, p = .51). Conversely, a higher velocity of 19‐ to 34‐week fetal abdominal growth was associated with greater childhood volumetric density (vBMD: r = 0.15, p = .004) but not with skeletal size (BA: r = 0.06, p = .21). Both fetal measurements were positively associated with BMC and aBMD, indices influenced by both size and density. The velocity of fetal femur length growth from 19 to 34 weeks' gestation predicted childhood skeletal size at age 4 years, whereas the velocity of abdominal growth (a measure of liver volume and adiposity) predicted volumetric density. These results suggest a discordance between influences on skeletal size and volumetric density. © 2010 American Society for Bone and Mineral Research     

Self‐reported weight at birth predicts measures of femoral size but not volumetric BMD in eldery men: MrOS

The mechanism whereby poor intrauterine growth increases risk of adult hip fracture is unclear. We report the association between birth weight and proximal femoral geometry and density in community‐dwelling elderly men. We used self‐reported birth weight, measured adult height and weight and proximal femoral quantitative computed tomography (QCT) measurements of femoral neck axis length, cross‐sectional area, and volumetric BMD (vBMD) among the participants in the Osteoporotic Fractures in Men (MrOS), a cohort study of community‐dwelling US men aged 65 and older. We compared men with birth weight <7 pounds (lower birth weight [LBW]; n = 501) and ≥9 pounds (higher birth weight [HBW]; n = 262) with those weighing 7–8.9 pounds (medium birth weight [MBW], referent group; n = 1068) using linear regression adjusting for current age, height, and BMI. The mean age of the 1831 men who had both birth weight and QCT measurements was 73 years (SD 5.9). Compared with the referent MBW, HBW men had concordantly longer femoral neck (+0.16 SD; p = .028) and cross‐sectional area (+0.24 SD, p = .001). LBW men had a smaller cross‐sectional (–0.26 SD, p < .001) but longer femoral neck for their height (+0.11 SD, p = .05). Neither cortical nor trabecular vBMD at the femoral neck was associated with birth weight. These findings support the hypothesis that the skeletal envelope, but not density, is set, in part, at birth. Further research exploring the association between early developmental factors and lifetime fracture risk is needed and may inform primary preventative strategies for fracture prevention. © 2011 American Society for Bone and Mineral Research