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Dysregulated phosphate metabolism is a common consequence of chronic kidney disease, and is characterized by a high circulating level of fibroblast growth factor (FGF)-23, hyperparathyroidism, and hyperphosphataemia. Kidney transplantation can elicit specific alterations to phosphate metabolism that evolve over time, ranging from severe hypophosphataemia (<0.5 mmol/l) to hyperphosphataemia (>1.50 mmol/l) and high FGF-23 levels. The majority of renal transplant recipients develop hypophosphataemia during the first 3 months after transplantation as a consequence of relatively slow adaptation of FGF-23 and parathyroid hormone levels to restored renal function, and the influence of immunosuppressive drugs. By 3-12 months after transplantation, phosphate homeostasis is at least partially restored in the majority of recipients, which is paralleled by a substantially reduced risk of cardiovascular-associated morbidity and mortality compared with the pre-transplantation setting. Many renal transplant recipients, however, exhibit persistent abnormalities in phosphate homeostasis, which is often due to multifactorial causes, and may contribute to adverse outcomes on the cardiovascular system, kidney, and bone. Dietary and pharmacologic interventions might improve phosphate homeostasis in renal transplant recipients, but additional insight into the pathophysiology of transplantation-associated abnormalities in phosphate homeostasis is needed to further optimize disease management and improve prognosis for renal transplant recipients.

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El fosfato es la forma principal en que se encuentra el elemento fósforo en el organismo. Participa en procesos como el metabolismo energético, la transducción de señales y el control de actividad enzimática. Es esencial para el desarrollo y la mineralización del esqueleto. Su homeostasis es compleja y está regulada principalmente por la acción conjunta de la hormona paratiroidea, la vitamina D y el recientemente identificado FGF23, los cuales actúan de manera coordinada sobre intestino, riñón y hueso. En este trabajo se revisan los conceptos conocidos de la fisiología normal del fosfato y se describe el rol del FGF23 en su homeostasis. Además, se refieren algunos desórdenes asociados a variaciones en los niveles circulantes de este factor.

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The survival of plants, as sessile organisms, depends on a series of postembryonic developmental events that determine the final architecture of plants and allow them to contend with a continuously changing environment. Modulation of cell differentiation and organ formation by environmental signals has not been studied in detail. Here, we report that alterations in the pattern of lateral root (LR) formation and emergence in response to phosphate (Pi) availability is mediated by changes in auxin sensitivity in Arabidopsis thaliana roots. These changes alter the expression of auxin-responsive genes and stimulate pericycle cells to proliferate. Modulation of auxin sensitivity by Pi was found to depend on the auxin receptor TRANSPORT INHIBITOR RESPONSE1 (TIR1) and the transcription factor AUXIN RESPONSE FACTOR19 (ARF19). We determined that Pi deprivation increases the expression of TIR1 in Arabidopsis seedlings and causes AUXIN/INDOLE-3-ACETIC ACID (AUX/IAA) auxin response repressors to be degraded. Based on our results, we propose a model in which auxin sensitivity is enhanced in Pi-deprived plants by an increased expression of TIR1, which accelerates the degradation of AUX/IAA proteins, thereby unshackling ARF transcription factors that activate/repress genes involved in LR formation and emergence.

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The effect of phosphate (Pi) deficiency on starch accumulation was studied in bean (Phaseolus vulgaris). After 3 weeks of Pi deprivation total Pi concentration in root and shoot was reduced by 68% and 42%, respectively; however, only shoot growth was affected. In leaves, Pi deprivation induced glucose, fructose and starch accumulation. Pi deficiency did not affect starch synthesis, but it reduced its mobilization during the dark period. At the same time, starch produced by Pi deficient plants have fewer Pi bound and was also less susceptible to beta-amylase hydrolysis. R1 protein is the protein responsible of phosphorylating C3 and C6 glucosyl residues of the polyglucan, increasing the hydration capacity and the interaction with amylolytic enzymes. Pi deprivation did not change the amount of R1 protein detected in total extracts but decreased its association with starch granules.

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Arabidopsis (Arabidopsis thaliana) plants display a number of root developmental responses to low phosphate availability, including primary root growth inhibition, greater formation of lateral roots, and increased root hair elongation. To gain insight into the regulatory mechanisms by which phosphorus (P) availability alters postembryonic root development, we performed a mutant screen to identify genetic determinants involved in the response to P deprivation. Three low phosphate-resistant root lines (lpr1-1 to lpr1-3) were isolated because of their reduced lateral root formation in low P conditions. Genetic and molecular analyses revealed that all lpr1 mutants were allelic to BIG, which is required for normal auxin transport in Arabidopsis. Detailed characterization of lateral root primordia (LRP) development in wild-type and lpr1 mutants revealed that BIG is required for pericycle cell activation to form LRP in both high (1 mm) and low (1 microm) P conditions, but not for the low P-induced alterations in primary root growth, lateral root emergence, and root hair elongation. Exogenously supplied auxin restored normal lateral root formation in lpr1 mutants in the two P treatments. Treatment of wild-type Arabidopsis seedlings with brefeldin A, a fungal metabolite that blocks auxin transport, phenocopies the root developmental alterations observed in lpr1 mutants in both high and low P conditions, suggesting that BIG participates in vesicular targeting of auxin transporters. Taken together, our results show that auxin transport and BIG function have fundamental roles in pericycle cell activation to form LRP and promote root hair elongation. The mechanism that activates root system architectural alterations in response to P deprivation, however, seems to be independent of auxin transport and BIG.

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Los elementos bioquímicos constitutivos del organismo humano están sujetos a sufrir variaciones cuantitativas provocadas por múltiples procesos fisiológicos, patológicos y genéticos, así como por factores extrínsecos. Para establecer una interpretación racional de los análisis de laboratorio para estos elementos se hace necesario e indispensable el conocimiento de sus variaciones en individuos o grupos adecuadamente definidos que permitan establecer comparaciones adecuadas a nuestras características particulares propias como población. Los resultados de los análisis de laboratorio se han interpretado clínicamente por comparación tradicional con los inadecuadamente llamados valores normales, los cuales no conocemos su procedencia ni cómo fueron obtenidos. Como alternativa se han establecido los valores de referencia, los que permiten realizar comparaciones confiables e interpretaciones adecuadas a nuestras características particulares. Por las razones antes referidas se seleccionó un grupo de jóvenes de ambos sexos (n=80) de diversos entornos del estado Mérida, a fin de determinar los niveles de fosforo inorgánico y fosfatasas alcalinas. Las determinaciones se realizaron en suero por métodos fotocolorimétricos. Los resultados obtenidos para fósforo inorgánico (x=3.53 mg/dL y 58.27 mg/dL) y para fosfatasa alcalina fueron tratados estadísticamente, lo que permite establecer valores de referencia orientativos para este grupo etareo a ser utilizados en nuestro laboratorio en análisis de rutina, así como en estudios posteriores sobre cambios fisiológicos, detección temprana de alteraciones en el metabolismo óseo, diagnóstico diferencial, monitoreo de terapias, así mismo establecer métodos de evaluación del estado de salud, identificación de personas con riesgos a enfermedades del metabolismo óseo y en el pronóstico de pacientes en fases específicas de una enfermedad en nuetra región

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The effects of acidic pH on the kinetics of Ca2+-ATPase isoforms from intracellular membranes of skeletal muscle, cardiac muscle, cerebellum and blood platelets were studied. At neutral pH, all four Ca2+-ATPase isoforms exhibited similar Ca2+-concentration requirements for half-maximal rates of Ca2+ uptake and ATP hydrolysis. A decrease in the pH from 7.0 to 6.0 promoted a decrease in both the apparent affinity for Ca2+ [increasing half-maximal activation (K0.5)] and the maximal velocity (Vmax) of Ca2+ uptake. With skeletal muscle vesicles these effect were 5 to 10 times smaller than those observed with all the other isoforms. Acidification of the medium from pH 7.0 to 6.5 caused the release of Ca2+ from loaded vesicles and a decrease in the amount of Ca2+ retained by the vesicles at the steady state. With the vesicles derived from skeletal muscle these effects were smaller than for vesicles derived from other tissues. The rate of passive Ca2+ efflux from skeletal and cardiac muscle vesicles, loaded with Ca2+ and diluted in a medium containing none of the ligands of Ca2+-ATPase, was the same at pH 7.0 and 6.0. In contrast, the rate of Ca2+ efflux from cerebellar and platelet vesicles increased 2-fold after acidification of the medium. The effects of DMSO, Mg2+ with Pi and arsenate on the rate of Ca2+ efflux varied among the different preparations tested. The differences became more pronounced when the pH of the medium was decreased from 7.0 to 6.0. It is proposed that the kinetic differences among the Ca2+-ATPase isoforms may reflect different adaptations to cellular acidosis, such as that which occurs during ischaemia.

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Os autores estudaram 99 amostras de L.A. obtido por amniocentese em gestantes no último trimestre de gestaçäo no qual dosaram zinco e fosfato. Foi calculada a relaçäo fosfato/zinco e classificadamostras em bactericidas, bacteriostáticas e näo inibidoras conforme a relaçäo fosse respectivamente menor que 100, entre 100 e 200 e maior que 200. A concentraçäo de zinco variou de 0,022 a 0,74 microng/ml com média de 0,11 microng/dl e näo mostrou relaçäo com a idade gestacional e com a presença de infecçäo. A concentraçäo de fosfato variou de 1,67 a 9,89 microng/ml con concentraçäo média de 14,64 ng/ml e foi maior nos casos com infecçäo. A relaçäo fosfato-zinco menor que 100(L.A. bactericida) ocorreu em 38.03%) ocorreu em 38,03% e neste grupo a incidência de infecçäo foi de 33,3%; 25,35% dos L.A. tinham relaçäo fosfato-zinco 100-200 (L.A. bacteriostático) e a incidência de infecçäo foi de 16,7%; 36,62% dos L.A. Apresentaram relaçäo fosfato-zinco maior que 200 (L.A. näo inibidor) com incidência de 69,2% de infecçäo

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