Uncoupling phosphate deficiency from its major effects on growth and transcriptome via PHO1 expression in Arabidopsis.

Inorganic phosphate (Pi) is one of the most limiting nutrients for plant growth in both natural and agricultural contexts. Pi-deficiency leads to a strong decrease in shoot growth, and triggers extensive changes at the developmental, biochemical and gene expression levels that are presumably aimed at improving the acquisition of this nutrient and sustaining growth. The Arabidopsis thaliana PHO1 gene has previously been shown to participate in the transport of Pi from roots to shoots, and the null pho1 mutant has all the hallmarks associated with shoot Pi deficiency. We show here that A. thaliana plants with a reduced expression of PHO1 in roots have shoot growth similar to Pi-sufficient plants, despite leaves being strongly Pi deficient. Furthermore, the gene expression profile normally triggered by Pi deficiency is suppressed in plants with low PHO1 expression. At comparable levels of shoot Pi supply, the wild type reduces shoot growth but maintains adequate shoot vacuolar Pi content, whereas the PHO1 underexpressor maintains maximal growth with strongly depleted Pi reserves. Expression of the Oryza sativa (rice) PHO1 ortholog in the pho1 null mutant also leads to plants that maintain normal growth and suppression of the Pi-deficiency response, despite the low shoot Pi. These data show that it is possible to unlink low shoot Pi content with the responses normally associated with Pi deficiency through the modulation of PHO1 expression or activity. These data also show that reduced shoot growth is not a direct consequence of Pi deficiency, but is more likely to be a result of extensive gene expression reprogramming triggered by Pi deficiency.

Expression analyses of three members of the AtPHO1 family reveal differential interactions between signaling pathways involved in phosphate deficiency and the responses to auxin, cytokinin, and abscisic acid.

The PHO1 protein is involved in loading inorganic phosphate (Pi) to the root xylem. Ten genes homologous to AtPHO1 are present in the Arabidopsis thaliana (L.) Heyn genome. From this gene family, transcript levels of only AtPHO1, AtPHO1;H1 and AtPHO1;H10 were increased by Pi-deficiency. While the up-regulation of AtPHO1;H1 and AtPHO1;H10 by Pi deficiency followed the same rapid kinetics and was dependent on the PHR1 transcription factor, phosphite only strongly suppressed the expression of AtPHO1;H1 and had a minor effect on AtPHO1;H10. Addition of sucrose was found to increase transcript levels of both AtPHO1 and AtPHO1;H1 in Pi-sufficient or Pi-deficient plants, but to suppress AtPHO1:H10 under the same conditions. Treatments of plants with auxin or cytokinin had contrasting effect depending on the gene and on the Pi status of the plants. Thus, while both hormones down-regulated expression of AtPHO1 independently of the plant Pi status, auxin and cytokinin up-regulated AtPHO1;H1 and AtPHO1;H10 expression in Pi-sufficient plants and down-regulated expression in Pi-deficient plants. Treatments with abscisic acid inhibited AtPHO1 and AtPHO1;H1 expression in both Pi-sufficient and Pi-deficient plants, but increased AtPHO1;H10 expression under the same conditions. The inhibition of expression by abscisic acid of AtPHO1 and AtPHO1;H1, and of the Pi-starvation responsive genes AtPHT1;1 and AtIPS1, was dependant on the ABI1 type 2C protein phosphatase. These results reveal that various levels of cross talk between the signal transduction pathways to Pi, sucrose and phytohormones are involved in the regulation of expression of the three AtPHO1 homologues.

Effectiveness of fused magnesium potassium phosphate for marandu grass

The current high price of KCl and great dependence on importation to satisfy the Brazilian demand indicate the need for studies that evaluate the efficiency of other K sources, particularly those based on domestic raw material. For this purpose, a greenhouse experiment was conducted with samples of a sandy clay loam Typic Haplustox, in a completely randomized 4 x 3 x 2 factorial design: four K rates (0, 60, 120, and 180 mg kg-1), three sources (potassium chloride (KCl), fused magnesium potassium phosphate (FMPP) and a mixture of 70 % FMPP + 30 % KCl) and two particle sizes (100 and 60 mesh), with three replications. Potassium fertilization resulted in significant increases in shoot dry matter production and in K concentrations, both in soil and plants. The K source and particle size had no significant effect on the evaluated characteristics. Potassium critical levels in the soil and the shoots were 1.53 mmol c dm-3 and 19.1 g kg-1, respectively.

Les biomarqueurs dans la maladie de Fabry: relation entre Sphingosine-1 phosphate et Lyso-Gb3

Problématique : La maladie de Fabry est une maladie métabolique à stockage lysosomal. C'est une maladie héreditaire à transmission récessive qui concerne l'enzyme alpha-Galactosidase A. Le gène de l'alpha-Galactosidase A (GLA) se trouve au niveau du bras long du chromosome X «carté en Xq21.33-Xq22 ». L'enzyme muté ne recouvre plus son rôle catabolisateur et il ne métabolise pas le substrat globotriaosylceramide (Gb3). Par conséquence le Gb3 s'accumule dans tous les tissus. Dans les parois des vaisseaux sanguins le Gb3 s'accumule dans l'endothelium, la tunique interne des vaisseaux sanguins. Ce déficit métabolique se traduit par l'épaississement de la paroi vasculaire, des processus d'infarctus et ischémies du tissu cardiaque, rénal et cérébral. L'implication cardiaque de la maladie de Fabry est décrite chez plus de 78% des patients affectés par la maladie et se manifeste par une hypertrophie cardiaque du ventricule gauche. Toutefois, il n'existe pas de relation étroite entre hypertrophie cardiaque et le Gb3. La sphingosine 1-phosphate à été identifiée dans notre laboratoire et proposée comme facteur de croissance à l'origine du remodelage cardiovasculaire. De plus, la Globotriaosylsphingosine (Lyso-Gb3) à été aussi proposée comme facteur vasoactif chez les patients Fabry. Objectif : L'identification d'un biomarqueur pour le diagnostic et le suivi thérapeutique de la maladie de Fabry représente une domaine d'investigation active en recherche scientifique. Le Gb3 plasmatique ou dans les urines, la biopsie rénale ou cardiaque qui est mis en évidence grâce à la microscopie électronique sous forme de corps concentrique lamellaires, constituent les biomarqueurs classiques de la maladie de Fabry. Dernièrement, le Lyso-Gb3 et le Sphingosine-1 phosphate (S1P) ont été proposés comme marqueurs du remodelage cardiovasculaire. Le but de ce travail est de rassembler et de discuter la littérature concernant ces nouveaux marqueurs et, d'étudier une possible interaction entre Lyso-Gb3 et le S1P. Méthodologie : Rassembler la littérature scientifique et analyser l'implication de ces marqueurs dans la maladie de Fabry et leur effets cardiovasculaires. De plus, un travail expérimental est effectué. Ce travail consiste en l'identification d'une relation possible entre le Lyso-Gb3 et le S1P. Résultats : Avec ce travail on a cherché à actualiser et mettre à jour les notions concernant les biomarqueurs qui prennent place dans cette pathologie et les connaissances qu'on possède à ce jour sur les manifestations cardiovasculaires et neurologiques.La recherche d'un biomarqueur prime par le fait qu'un nombre considerable de patients est sous-diagnostiqués pour la maladie de Fabry et que entre les taux de substrat enzymatique accumulé dans les tissus et l'hypertrophie cardiaque, on peut constater une discordance. Grâce à ce travail expérimental, on a exclue la possibilité d'un effet précurseur du lyso-Gb3 pour le S1P. Nous avons montré que le Lyso-Gb3 est reconnu par les récepteurs du S1P avec des effets commun pour les S1P1-3 et différents pour le S1P2. Les taux du Lyso-Gb3 et du S1P doivent être mesuré chez les patients Fabry et une stratégie thérapeutique doit prendre en compte le rapport S1P/Lyso-Gb3.

Mobility of inorganic and organic phosphorus forms under different levels of phosphate and poultry litter fertilization in soils

The eutrophication of aquifers is strongly linked to the mobility of P in soils. Although P mobility was considered irrelevant in a more distant past, more recent studies have shown that P, both in organic (Po) and inorganic forms (Pi), can be lost by leaching and eluviation through the soil profile, particularly in less weathered and/or sandier soils with low P adsorption capacity. The purpose of this study was to determine losses of P forms by leaching and eluviation from soil columns. Each column consisted of five PVC rings (diameter 5 cm, height 10 cm), filled with two soil types: a clayey Red-Yellow Latosol and a sandy loam Red-Yellow Latosol, which were exposed to water percolation. The soils were previously treated with four P rates (as KH2PO4 ) to reach 0, 12.5, 25.0 and 50 % of the maximum P adsorption capacity (MPAC). The P source was homogenized with the whole soil volume and incubated for 60 days. After this period the soils were placed in the columns; the soil of the top ring was mixed with five poultry litter rates of 0, 20, 40, 80, and 160 t ha-1 (dry weight basis). Treatments consisted of a 4 x 5 x 2 factorial scheme corresponding to four MPAC levels, five poultry litter rates, two soils, with three replications, arranged in a completely randomized block design. Deionized water was percolated through the columns 10 times in 35 days to simulate about 1,200 mm rainfall. In the leachate of each column the inorganic P (reactive P, Pi) and organic P forms (unreactive P, Po) were determined. At the end of the experiment, the columns were disassembled and P was extracted with the extractants Mehlich-1 (HCl 0.05 mol L-1 and H2SO4 0.0125 mol L-1) and Olsen (NaHCO3 0.5 mol L-1; pH 8.5) from the soil of each ring. The Pi and Po fractions were measured by the Olsen extractant. It was found that under higher poultry litter rates the losses of unreactive P (Po) were 6.4 times higher than of reactive P (Pi). Both the previous P fertilization and increasing poultry litter rates caused a vertical movement of P down the soil columns, as verified by P concentrations extracted by Mehlich-1 and NaHCO3 (Olsen). The environmental critical level (ECL), i.e., the P soil concentration above which P leaching increases exponentially, was 100 and 150 mg dm-3 by Mehlich-1 and 40 and 60 mg dm-3 by Olsen, for the sandy loam and clay soils, respectively. In highly weathered soils, where residual P is accumulated by successive crops, P leaching through the profile can be significant, particularly when poultry litter is applied as fertilizer.

PA21, a New Iron-Based Noncalcium Phosphate Binder, Prevents Vascular Calcification in Chronic Renal Failure Rats.

Chronic renal failure (CRF) is associated with the development of secondary hyperparathyroidism and vascular calcifications. We evaluated the efficacy of PA21, a new iron-based noncalcium phosphate binder, in controlling phosphocalcic disorders and preventing vascular calcifications in uremic rats. Rats with adenine-diet-induced CRF were randomized to receive either PA21 0.5, 1.5, or 5% or CaCO3 3% in the diet for 4 weeks, and were compared with uremic and nonuremic control groups. After 4 weeks of phosphate binder treatment, serum calcium, creatinine, and body weight were similar between all CRF groups. Serum phosphorus was reduced with CaCO3 3% (2.06 mM; P ≤ 0.001), PA21 1.5% (2.29 mM; P < 0.05), and PA21 5% (2.21 mM; P ≤ 0.001) versus CRF controls (2.91 mM). Intact parathyroid hormone was strongly reduced in the PA21 5% and CaCO3 3% CRF groups to a similar extent (1138 and 1299 pg/ml, respectively) versus CRF controls (3261 pg/ml; both P ≤ 0.001). A lower serum fibroblast growth factor 23 concentration was observed in the PA21 5%, compared with CaCO3 3% and CRF, control groups. PA21 5% CRF rats had a lower vascular calcification score compared with CaCO3 3% CRF rats and CRF controls. In conclusion, PA21 was as effective as CaCO3 at controlling phosphocalcic disorders but superior in preventing the development of vascular calcifications in uremic rats. Thus, PA21 represents a possible alternative to calcium-based phosphate binders in CRF patients.

Audit report on Highway Safety Projects administered by The Integer Group Midwest for the year ended September 30, 2007

Audit report on Highway Safety Projects administered by The Integer Group Midwest for the year ended September 30, 2007

Audit report on Highway Safety Projects administered by The Integer Group Midwest for the year ended September 30, 2008

Audit report on Highway Safety Projects administered by The Integer Group Midwest for the year ended September 30, 2008

Audit report on Highway Safety Projects administered by The Integer Group Midwest for the year ended September 30, 2009

Audit report on Highway Safety Projects administered by The Integer Group Midwest for the year ended September 30, 2009

Different PTH response to oral peptone load and oral calcium load in patients with normocalcemic primary hyperparathyroidism, primary hyperparathyroidism, and healthy subjects.

BACKGROUND: Normocalcemic primary hyperparathyroidism (PHPT-N) is a condition that may have similar long-term implications to primary hyperparathyroidism (PHPT); however, differential diagnosis and treatment for parathyroid disorders are not clearly defined. We investigated the effect of an oral peptone and an oral calcium load on calcium-regulating hormones in PHPT-N compared with PHPT and healthy controls to provide a new potential diagnostic tool. DESIGN: Case-control study. METHODS: We evaluated serum gastrin, PTH, ionized calcium, and phosphate responses to oral calcium (1 g) and peptone (10 g) load in 22 PHPT and 20 PHPT-N patients matched for PTH serum values. Moreover, 30 healthy subjects were enrolled as controls. In 12 patients for each group, we also performed the oral peptone test adding aluminum hydroxide (AH) to suppress phosphate absorption. RESULTS: In PHPT patients, PTH increased significantly 30 min after the oral peptone load, while no significant increase was found in PHPT-N and controls. After oral calcium load, PTH remained stable in PHPT while it decreased dramatically in PHPT-N patients, and ionized calcium increased significantly in each of the three groups. Peptones plus AH induced a blunted PTH increase in the three groups. CONCLUSIONS: Considering the marked difference in PTH response elicited by peptones in PHPT compared with PHPT-N, we suggest that the oral peptone test could be added to the diagnostic evaluation of PHPT patients. In case of absent response to peptones, patients should have their serum calcium levels assessed twice a year in accordance with recent guidelines.

Audit report on Highway Safety Projects administered by The Integer Group Midwest for the year ended September 30, 2010

Audit report on Highway Safety Projects administered by The Integer Group Midwest for the year ended September 30, 2010