David Negro : un judío cortesano en la coyuntura portuguesa de 1383-1385

Aportación al estudio de los judíos cortesanos portugueses, en especial, el caso de Don David Negro. Consejero y funcionario regio del Rey Don Fernando y, más tarde, rabí de Castilla, en el reinado de Juan I. Don David participó en la rebelión política de 1383 - 1385 que culminó en la ascensión al trono de Mestre de Avis, Don João I de Portugal.Contribution to the study of Portuguese Judaic courtiers, in particular of Don David Negro. King Fernando's councilor and royal servant, and the later rabbi in Castilla, during the reign of Juan I. Don David took part in the political rebellion of 1383 - 1385 which resulted in the rise of the Master of Avis to the throne of Portugal - D. João I

Implications of Sediment Geochemistry and Diet Habits in Fish Metal Levels and Human Health Risk

In this study the concentration of Cd, Cu, Fe, Ni, Pb, and Zn in muscle and liver tissues was compared between four estuarine fish species (Centropomus parallelus, Genidens genidens, Diapterus rhombeus, and Mugil liza) to assess contamination levels and the influence of eating habits on metal distribution and human health risk by consumption. In general, liver tissue showed higher metal contents than muscle. Between metals, Fe and Zn contents were relatively higher for both tissues in all analyzed populations. Based on the observations, the variability of metal levels between species is associated with their transfer from the contaminated sediments, where diet habits associated with the substrate result in higher metal accumulation in fish, exerting great influence than bioaccumulation by trophic level. The estimated daily intake (EDI), target hazard quotients (THQ) and the total target hazard quotients (TTHQ), below 1 for all metals on muscle tissues, are suggested the absence of health hazard for the human population. However, high levels of Pb and Zn in liver tissue may endanger predators

Resistance to recombinant human erythropoietin therapy in haemodialysis patients: Focus on inflammatory cytokines, leukocyte activation, iron status and erythrocyte damage

Anaemia is a common complication in haemodialysis patients. This condition is associated to a decreased bone marrow production of erythrocytes, mainly due to the inability of the failing kidneys to secrete erythropoietin (EPO). The introduction of recombinant human EPO (rhEPO) therapy led to a significant reduction in anaemia and improved patients’ quality of life. However, there is a marked variability in the sensitivity to rhEPO, with up to 10-fold variability in dose requirements to achieve correction of anaemia. Approximately 5-10% of the patients show a marked resistance to rhEPO therapy. rhEPO resistance is associated to an increased morbidity and mortality of haemodialysis patients. In this paper a revision of the mechanisms underlying resistance to rhEPO therapy will be performed, with particular emphasis on inflammatory cytokines, leukocyte activation, iron status, and erythrocyte damage

The HIF System Response to ESA Therapy in CKD‐Anemia

Anemia is a common complication of chronic kidney disease (CKD) associated with disease progression and increased mortality. This anemia is mainly due to inadequate production of erythropoietin (EPO) by the failing kidneys, resulting from the reduction in renal EPO‐producing cells (REPC) or from dysregulation of the hypoxia‐inducible factor (HIF) system that regulates several genes related to hypoxia, angiogenesis, fibrosis and glucose metabolism, among others. In this chapter, we present a review on the HIF system in CKD‐anemia, the HIF response to erythropoiesis‐stimulating agents (ESA) therapy and its potential involvement in the development of ESA resistance by enhancing kidney fibrosis and inflammation. Due to concerns related to ESA use, new drugs to correct anemia are under study, being the prolyl hydroxylase inhibitors the most promising candidates

Hereditary spherocytosis and the (TA)nTAA polymorphism of UGT1A1 gene promoter region: a comparison of the bilirubin plasmatic levels in the different clinical forms

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