13 research outputs found
Recommended from our members
Governance in Areas of Limited Statehood: The NGOization of Palestine
In this article we examine the shifting roles played by non-state actors in governing areas of limited statehood. In particular we focus on the emergence of voluntary grassroots organizations in Palestine and describe how regimes of international development aid transformed these organizations into professional non-governmental organizations (NGOs) that created new forms of colonial control. Based on in-depth interviews with 145 NGO members and key stakeholders and a historical analysis of limited statehood in Palestine, we found that social relations became disembedded from the local context and re-embedded in new relations with international donor organizations resulting in a depoliticized public sphere. NGOization of the economy also resulted in new forms of exclusion and inclusion as well as contestations between a new class of urban middle class professionals working in NGOs and the older generation of activists that were involved in grassroots organizations. Our findings have implications for business and human rights and governance in areas of limited statehood, in particular how private actors like NGOs are able to exercise power in the economy
Urine metabolomics reveals novel physiologic functions of human aldehyde oxidase and provides biomarkers for typing xanthinuria
Classical xanthinuria is a rare inherited metabolic disorder caused by either isolated xanthine dehydrogenase (XDH) deficiency (type I) or combined XDH and aldehyde oxidase (AO) deficiency (type II). XDH and AO are evolutionary related enzymes that share a sulfurated molybdopterin cofactor. While the role of XDH in purine metabolism is well established, the physiologic functions of AO are mostly unknown. XDH and AO are important drug metabolizing enzymes. Urine metabolomic analysis by high pressure liquid chromatography and mass spectrometry of xanthinuric patients was performed to unveil physiologic functions of XDH and AO and provide biomarkers for typing xanthinuria. Novel endogenous products of AO, hydantoin propionic acid, N1-methyl-8-oxoguanine and N-(3-acetamidopropyl) pyrrolidin-2-one formed in the histidine, nucleic acid and spermidine metabolic pathways, respectively, were identified as being lowered in type II xanthinuria. Also lowered were the known AO products, N1-methyl-2-pyridone-5-carboxamide and N1-methyl-4-pyridone-5-carboxamide in the nicotinamide degradation pathway. In contrast to the KEGG annotations, the results suggest minor role of human AO in the conversion of pyridoxal to pyridoxate and gentisaldehyde to gentisate in the vitamin B6 and tyrosine metabolic pathways, respectively. The perturbations in purine degradation due to XDH deficiency radiated further from the previously known metabolites, uric acid, xanthine and hypoxanthine to guanine, methyl guanine, xanthosine and inosine. Possible pathophysiological implications of the observed metabolic perturbations are discussed. The identified biomarkers have the potential to replace the allopurinol-loading test used in the past to type xanthinuria, thus facilitating appropriate pharmacogenetic counseling and gene directed search for causative mutations