Serum carotenoids reveal poor fruit and vegetable intake among schoolchildren in Burkina Faso

The health benefits of fruits and vegetables are well-documented. Those rich in provitamin A carotenoids are good sources of vitamin A. This cross-sectional study indirectly assessed fruit and vegetable intakes using serum carotenoids in 193 schoolchildren aged 7 to 12 years in the Western part of Burkina Faso. The mean total serum carotenoid concentration was 0.23 +/- 0.29 mu mol/L, which included alpha- and beta-carotene, lutein, and beta-cryptoxanthin, and determined with serum retinol concentrations in a single analysis with high performance liquid chromatography. Serum retinol concentration was 0.80 +/- 0.35 mu mol/L with 46% of children (n = 88) having low values <0.7 mu mol/L. Total serum carotene (the sum of alpha- and beta-carotene) concentration was 0.13 +/- 0.24 mu mol/L, well below the reference range of 0.9-3.7 mu mol carotene/L used to assess habitual intake of fruits and vegetables. Individual carotenoid concentrations were determined for beta-carotene (0.01 +/- 0.05 mu mol/L), beta-carotene (0.17 +/- 0.24 mu mol/L), beta-cryptoxanthin (0.07 +/- 0.06 mu mol/L), and lutein (0.06 +/- 0.05 mu mol/L). These results confirm the previously measured high prevalence of low serum vitamin A concentrations and adds information about low serum carotenoids among schoolchildren suggesting that they have low intakes of provitamin A-rich fruits and vegetables

CLARIT Experiments in Batch Filtering: Term Selection and Threshold Optimization in IR and SVM Filters

The Clairvoyance team participated in the Filtering Track, submitting two runs in the Batch Filtering category. While we have been exploring the question of both topic modeling and ensemble filter construction (a

CLARIT Experiments in Batch Filtering:

Introduction The Clairvoyance team participated in the Filtering Track, submitting two runs in the Batch Filtering category. While we have been exploring the question of both topic modeling and ensemble filter construction (as in our previous TREC filtering experiments [5]), we had one distinct objective this year, to explore the viability of monolithic filters in classification-like tasks. This is appropriate to our work, in part, because monolithic filters are a crucial starting point for ensemble filtering, and it is possible for them to contribute substantially in the ensemble approach. Our primary goal in experiments this year, thus, was to explore two issues in monolithic filter construction: (1) term count selection and (2) filter threshold optimization. In fact, our pre-TREC experiments were conducted in a brief period and we were unable to complete all the tests we had planned. Our official submissions reflect essentially our first, baseline results. They are overall poor i

Differential diagnosis of vitamin D‐related hypercalcemia using serum vitamin D metabolite profiling

International audienceGenetic causes of vitamin D-related hypercalcemia are known to involve mutation of 25-hydroxyvitamin D-24-hydroxylase CYP24A1 or the sodium phosphate co-transporter SLC34A1; which result in excessive 1,25-(OH)2 D hormonal action. However, at least 20% of idiopathic hypercalcemia (IH) cases remain unresolved. In this case-control study, we used precision vitamin D metabolite profiling based on LC-MS/MS of an expanded range of vitamin D metabolites - to screen German and French cohorts of hypercalcemia patients, to identify patients with altered vitamin D metabolism where involvement of CYP24A1 or SLC34A1 mutation had been ruled out, and possessed normal 25-OH-D3 :24,25-(OH)2 D3 ratios. Profiles were compared to those of hypercalcemia patients with hypervitaminosis D, Williams-Beuren syndrome (WBS), CYP24A1 mutation, and normal subjects with a range of 25-OH-D levels. We observed that certain IH and WBS patients exhibited a unique profile comprising 8-10-fold higher serum 23,25,26-(OH)3 D3 and 25-OH-D3 -26,23-lactone than normals; as well as very low serum 1,25-(OH)2 D3 (2-5 pg/mL) and elevated 1,24,25-(OH)3 D3 , which we interpret implies hypersensitive expression of vitamin D-dependent genes, including CYP24A1, as a general underlying mechanism of hypercalcemia in these patients. As serum 25-OH-D3 and 24,25-(OH)2 D3 remained normal, we excluded the possibility that the aberrant profile was caused by hypervitaminosis D, but instead points to an underlying genetic cause that parallels the effect of Williams Syndrome Transcription Factor deficiency in WBS. Furthermore, we observed normalization of serum calcium and vitamin D metabolite profiles at follow up of an IH patient where 25-OH-D was reduced to 9 ng/mL, suggesting that symptomatic IH may depend on vitamin D nutritional status. Other hypercalcemic patients with complex conditions exhibited distinct vitamin D metabolite profiles. Our work points to the importance of serum vitamin D metabolite profiling in the differential diagnosis of vitamin D-related hypercalcemia that can rationalize expensive genetic testing, and assist healthcare providers in selecting appropriate treatment

Differential diagnosis of vitamin D–related hypercalcemia using serum vitamin D metabolite profiling

International audienceGenetic causes of vitamin D-related hypercalcemia are known to involve mutation of 25-hydroxyvitamin D-24-hydroxylase CYP24A1 or the sodium phosphate co-transporter SLC34A1; which result in excessive 1,25-(OH)2 D hormonal action. However, at least 20% of idiopathic hypercalcemia (IH) cases remain unresolved. In this case-control study, we used precision vitamin D metabolite profiling based on LC-MS/MS of an expanded range of vitamin D metabolites - to screen German and French cohorts of hypercalcemia patients, to identify patients with altered vitamin D metabolism where involvement of CYP24A1 or SLC34A1 mutation had been ruled out, and possessed normal 25-OH-D3 :24,25-(OH)2 D3 ratios. Profiles were compared to those of hypercalcemia patients with hypervitaminosis D, Williams-Beuren syndrome (WBS), CYP24A1 mutation, and normal subjects with a range of 25-OH-D levels. We observed that certain IH and WBS patients exhibited a unique profile comprising 8-10-fold higher serum 23,25,26-(OH)3 D3 and 25-OH-D3 -26,23-lactone than normals; as well as very low serum 1,25-(OH)2 D3 (2-5 pg/mL) and elevated 1,24,25-(OH)3 D3 , which we interpret implies hypersensitive expression of vitamin D-dependent genes, including CYP24A1, as a general underlying mechanism of hypercalcemia in these patients. As serum 25-OH-D3 and 24,25-(OH)2 D3 remained normal, we excluded the possibility that the aberrant profile was caused by hypervitaminosis D, but instead points to an underlying genetic cause that parallels the effect of Williams Syndrome Transcription Factor deficiency in WBS. Furthermore, we observed normalization of serum calcium and vitamin D metabolite profiles at follow up of an IH patient where 25-OH-D was reduced to 9 ng/mL, suggesting that symptomatic IH may depend on vitamin D nutritional status. Other hypercalcemic patients with complex conditions exhibited distinct vitamin D metabolite profiles. Our work points to the importance of serum vitamin D metabolite profiling in the differential diagnosis of vitamin D-related hypercalcemia that can rationalize expensive genetic testing, and assist healthcare providers in selecting appropriate treatment