Welfare and environment in Rural Uganda: Results from a small-area estimation approach

This study combines census, survey and bio-physical data to generate spatially disaggregated poverty/biomass information for rural Uganda. It makes a methodological contribution to small area welfare estimation by exploring how the inclusion of bio-physical information improves small area welfare estimates. By combining the generated poverty estimates with national bio-physical data, this study explores the contemporaneous correlation between poverty (welfare) and natural resource degradation at a level of geographic detail that has not been feasible previously. The resulting estimates of poverty measures were improved by the inclusion of bio-physical information and the poverty estimates appear to be more robust, as the standard errors show a decline of up to 40 percent in some cases. The coefficients of variation (i.e., the ratio of the standard error and the point estimate) decline in general as well. Overall, we conclude that the estimates of the poverty measures are more robust when bio-physical information is taken into account. One of the outputs of this study is a series of maps showing poverty and biomass overlays for Uganda. These maps can be used as a planning tool and for targeting purpose

High CD33-antigen loads in peripheral blood limit the efficacy of gemtuzumab ozogamicin |(Mylotarg®) treatment in acute myeloid leukemia patients

Gemtuzumab ozogamicin (Mylotarg®) induces remission in approximately 30% of relapsed AML patients. We previously demonstrated that gemtuzumab infusion results in near-complete CD33 saturation in peripheral blood, and that saturating gemtuzumab levels result in continuous binding and internalization of gemtuzumab due to renewed CD33 expression. We now demonstrate that a high CD33-antigen load in peripheral blood is an independent adverse prognostic factor, likely due to peripheral consumption of gemtuzumab. Indeed, CD33 saturation in bone marrow is significantly reduced (40-90% saturation) as compared with CD33 saturation in corresponding peripheral blood samples (>90%). In vitro, such reduced CD33 saturation levels were strongly related with reduced cell kill. Apparently, high CD33-antigen loads in blood consume gemtuzumab and thereby limit its penetration into bone marrow. Consequently, CD33 saturation in bone marrow is reduced, which hampers efficient cell kill. Therefore, gemtuzumab should be administered at higher or repeated doses, or, preferably, after reduction of the leukemic cell burden by classical chemotherapy

Tagged IDS causes efficient and engraftment-independent prevention of brain pathology during lentiviral gene therapy for Mucopolysaccharidosis type II

Mucopolysaccharidosis type II (OMIM 309900) is a lysosomal storage disorder caused by iduronate 2-sulfatase (IDS) deficiency and accumulation of glycosaminoglycans, leading to progressive neurodegeneration. As intravenously infused enzyme replacement therapy cannot cross the blood-brain barrier (BBB), it fails to treat brain pathology, highlighting the unmet medical need to develop alternative therapies. Here, we test modified versions of hematopoietic stem and progenitor cell (HSPC)-mediated lentiviral gene therapy (LVGT) using IDS tagging in combination with the ubiquitous MND promoter to optimize efficacy in brain and to investigate its mechanism of action. We find that IDS tagging with IGF2 or ApoE2, but not RAP12x2, improves correction of brain heparan sulfate and neuroinflammation at clinically relevant vector copy numbers. HSPC-derived cells engrafted in brain show efficiencies highest in perivascular areas, lower in choroid plexus and meninges, and lowest in parenchyma. Importantly, the efficacy of correction was independent of the number of brain-engrafted cells. These results indicate that tagged versions of IDS can outperform untagged IDS in HSPC-LVGT for the correction of brain pathology in MPS II, and they imply both cell-mediated and tag-mediated correction mechanisms, including passage across the BBB and increased uptake, highlighting their potential for clinical translation.</p

Total Zinc Intake May Modify the Glucose-Raising Effect of a Zinc Transporter (SLC30A8) Variant

Objective: Many genetic variants have been associated with glucose homeostasis and type 2 diabetes in genome-wide association studies. Zinc is an essential micronutrient that is important for β-cell function and glucose homeostasis. We tested the hypothesis that zinc intake could influence the glucose-raising effect of specific variants. Research Design and Methods: We conducted a 14-cohort meta-analysis to assess the interaction of 20 genetic variants known to be related to glycemic traits and zinc metabolism with dietary zinc intake (food sources) and a 5-cohort meta-analysis to assess the interaction with total zinc intake (food sources and supplements) on fasting glucose levels among individuals of European ancestry without diabetes. Results: We observed a significant association of total zinc intake with lower fasting glucose levels (β-coefficient ± SE per 1 mg/day of zinc intake: −0.0012 ± 0.0003 mmol/L, summary P value = 0.0003), while the association of dietary zinc intake was not significant. We identified a nominally significant interaction between total zinc intake and the SLC30A8 rs11558471 variant on fasting glucose levels (β-coefficient ± SE per A allele for 1 mg/day of greater total zinc intake: −0.0017 ± 0.0006 mmol/L, summary interaction P value = 0.005); this result suggests a stronger inverse association between total zinc intake and fasting glucose in individuals carrying the glucose-raising A allele compared with individuals who do not carry it. None of the other interaction tests were statistically significant. Conclusions: Our results suggest that higher total zinc intake may attenuate the glucose-raising effect of the rs11558471 SLC30A8 (zinc transporter) variant. Our findings also support evidence for the association of higher total zinc intake with lower fasting glucose levels

Updating poverty maps with panel data

This paper extends the methodology of Elbers, C., Lanjouw, J. O., & Lanjouw, P. (2003). Micro level estimation of poverty and inequality. Econometrica 71(1), 355-364 and presents a low cost approach to arriving at small area welfare estimates for non-census years. The approach requires panel data and the estimation of a relation between per capita consumption from the year of interest and household characteristics from the census year. The method is illustrated for Uganda. It is shown that with the exception of the North progress in rural poverty reduction was broadly shared during 1992-99. Areas with high initial levels of poverty appear to have benefited less from growth

Slim, snel en sociaal. Versnellen en verrijken. Maar wanneer en hoe?

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Teacher attitudes toward academic acceleration and accelerated students in the Netherlands

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Jonge, versnelde leerlingen in het voortgezet onderwijs

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Self-concept of accelerated and non-accelerated students in their first, second and last year of secondary school in the Netherlands

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