MHC-B variation in maternal and paternal synthetic lines of the Argentinian Campero INTA chicken

The Campero-INTA chicken of Argentina was developed to provide a robust bird that can survive under Argentinian pasture conditions with no significant additional nutrition, producing a source of animal protein for small producers or low-income families. In previous work we described the AH paternal line of Campero and its Major Histocompatibility Complex B region (MHC-B) variation. In this work we analyzed the three remaining synthetic lines used to produce the Campero-INTA production bird: lines AS, A and E. Because of the association between variation within the MHC of chickens and disease resistance, MHC variation within this breed is of particular interest. MHC variability within the lines used to produce the Campero-INTA chicken was examined using a 90 SNP panel encompassing the chicken MHC-B region plus the VNTR, LEI0258, located within the chicken MHC. Across all four lines 12 haplotypes were found, with 7 of these being previously reported in North America/European breeds, reflecting the original breed sources for these birds. Three Campero unique haplotypes were found, two of which likely originated from MHC recombination events. MHC-B variation for all lines involved with production of the final Campero-INTA bird have now been determined.EEA PergaminoFil: Iglesias, Gabriela M. Universidad Nacional de Río Negro. Sede Alto Valle y Valle Medio. Escuela de Veterinaria y Producción Agroindustrial. Cátedra de Genética; ArgentinaFil: Beker, María P. Universidad Nacional de Río Negro. Sede Alto Valle y Valle Medio. Escuela de Veterinaria y Producción Agroindustrial. Cátedra de Genética; ArgentinaFil: Remolins, José S. Universidad Nacional de Río Negro. Sede Alto Valle y Valle Medio. Escuela de Veterinaria y Producción Agroindustrial. Cátedra de Genética; ArgentinaFil: Canet, Zulma Edith. Instituto Nacional de Tecnología Agropecuaria (INTA). Estación Experimental Agropecuaria Pergamino. Sección Avicultura; ArgentinaFil: Canet, Zulma Edith. Universidad Nacional de Rosario. Facultad de Ciencias Veterinaria. Cátedra de Genética; ArgentinaFil: Librera, José. Universidad Nacional de Rosario. Facultad de Ciencias Veterinarias. Cátedra de Genética; ArgentinaFil: Cantaro, Horacio Luis. Instituto Nacional de Tecnología Agropecuaria (INTA). Estación Experimental Agropecuaria Alto Valle; ArgentinaFil: Cantaro, Horacio Luis. Universidad Nacional de Río Negro. Sede Alto Valle y Valle Medio. Escuela de Veterinaria y Producción Agroindustrial. Cátedra de Genética; ArgentinaFil: Maizon, Daniel Omar Instituto Nacional de Tecnología Agropecuaria (INTA). Estación Experimental Agropecuaria Anguil; ArgentinaFil: Fulton, Janet E. Hy-Line International; Estados Unido

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Calciotropic hormones and nephrolithiasis.

In recurrent calcium stone formers interfering factors or changes in receptor sensitivity may alter the interrelationships among calcium-regulating hormones, and hormonal behavior often does not fit with the theoretical assumptions. The vitamin D system appears to have the most important metabolic and clinical effects. Abnormal up-regulation of the synthesis of calcitriol and the consequent parathyroid hormone (PTH) suppression can induce hypercalciuria. Consequently, the hypocalciuric effect of thiazide would be caused by an enhanced response to PTH and by a reduction in 1,25(OH)2-vit D. A negative role of vitamin D on the skeleton has been observed in the presence of a negative calcium balance. Moreover, vitamin D also plays a role in urine oxalate excretion. PTH seems not to be directly stimulated in hypercalciuria and recurrent calcium nephrolithiasis, and patients with hyperparathyroidism and recurrent calcium nephrolithiasis show a similar degree of bone demineralization, irrespective of the presence of absence of the so-called 'primary hyperparathyroidism.' Calcitonin plays a contributory role in the pathogenesis of recurrent calcium nephrolithiasis that seems to be strictly related to dietary calcium intake. A higher sensitivity of thyroid C cells, particularly in absorptive hypercalciuric patients, could be related to the pathogenesis of hypercalciuria and contribute to its persistence