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955 results for “Phosphates”
Effects of Soluble Phosphate in Humans
ClinicalTrials.gov study NCT02095392. IPD Sharing: Not stated. Countries: 1. Publications: 2.
PD Study to Assess Phosphate Binding Characteristics of K2CG Chewing Gum
ClinicalTrials.gov study NCT01319578. IPD Sharing: Not stated. Countries: 1. Publications: 1.
The Effects of Preconditioning on Intramuscular High-Energy Phosphate Levels During Ischemia
ClinicalTrials.gov study NCT00883467. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Enteral Supplementation With Sodium Dihydrogen Phosphate and Disodium Hydrogen Phosphate Granules for the Treatment of Hypophosphatemia.
ClinicalTrials.gov study NCT07233889. IPD Sharing: YES. Countries: 1. Publications: 12.
Raw data for: Phosphate deprivation-induced changes in tomato are mediated by an interaction between brassinosteroid signaling and zinc
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Synchrotron imagery of phosphatized eggs in Waptia cf. W. fieldensis from the middle Cambrian (Miaolingian; Wuliuan) Spence Shale of Utah
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Data from: Dissecting nutrient-related co-expression networks in phosphate starved poplars
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Effects of Chlorella vulgaris on P release from ferric phosphate sediment by consecutive cultivation
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Data from: Onychophoran-like musculature in a phosphatized Cambrian lobopodian
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Data from: Regeneration of glycocalyx by heparan sulfate and sphingosine 1-phosphate restores inter-endothelial communication
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Data from: Apolipoprotein M-bound sphingosine-1-phosphate regulates blood-brain barrier paracellular permeability and transcytosis
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An experimental study on the separation of lanthanides from phosphate ore by organic and inorganic acids
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Cruise measurements (temperature, salinity, density, chlorophyll, C14, phosphate, silicate, nitrate, nitrite) collected from CTD casts aboard CalCOFI cruises in the California Current, and averaged annually and by cruise, from 1984 - 2019 (updated periodically).
Water column bottle sample data averaged across up to 46 standard stations (inshore and offshore) per cruise and then averaged over a varying number of cruises in any one year to give an annual average.
Data from: Glucose-6-phosphate dehydrogenase deficiency and stroke outcomes
<p><span><b>Objective: </b>To ascertain whether G6PD deficiency affects outcomes at 3 months after stroke, we recruited 1251 patients with acute ischemic stroke and detected erythrocyte-G6PD activity.</span></p> <p><span><b>Methods:</b> The prospective study participants consisted of 1,251 patients with ischemic stroke within 2 weeks of onset from four clinical centers in South China. Patients were individually categorized into the G6PD-deficiency group and non-G6PD-deficiency group according to erythrocyte-G6PD activity upon admission. Baseline characteristics and clinical outcomes (modified Rankin Scale score [mRS], poor functional outcome [mRS ≥ 2] at 3 months, and death) were compared between the two groups. The associations of G6PD deficiency with outcomes were evaluated using Cox proportional hazards and logistic regression analyses.</span></p> <p><span><b>Results: </b>Among 1251 patients,<b> </b>150 (12.0 %) were G6PD deficient; patients with G6PD deficiency had higher proportions of large-artery atherosclerosis (56.7% vs. 46.0% in non-G6PD-deficiency; odds ratio [OR] 1.53, 95% confidence interval [CI] 1.09-2.17) and stroke history (23.3% vs. 13.6% in non-G6PD-deficiency; OR 1.93, 95% CI 1.26-2.90). Multivariable logistic regression analysis showed the G6PD-deficiency and non-G6PD-deficiency group differed significantly in their overall distribution of mRS scores (adjusted common OR 1.57, 95% CI 1.14-2.17). Patients with G6PD deficiency had higher rates of poor functional outcome at 3 months (61.9% vs. 50.0% in non-G6PD-deficiency; adjusted OR 1.73, 95% CI 1.08-2.76). The hazard ratio of in-hospital death for patients with G6PD-deficiency was 1.46 (95% CI 1.37-1.84).</span></p> <p><span><b>Conclusions: </b>G6PD deficiency is associated with the risk of poor functional outcome at 3 months after ischemic stroke, and may increase the risk of in-hospital death.</span></p>
Data from: Gene amplification of 5-enol-pyruvylshikimate-3-phosphate synthase in glyphosate-resistant Kochia scoparia
The widely used herbicide glyphosate inhibits the shikimate pathway enzyme 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS). Globally, the intensive use of glyphosate for weed control has selected for glyphosate resistance in 31 weed species. Populations of suspected glyphosate-resistant Kochia scoparia were collected from fields located in the US central Great Plains. Glyphosate dose response verified glyphosate resistance in nine populations. The mechanism of resistance to glyphosate was investigated using targeted sequencing, quantitative PCR, immunoblotting, and whole transcriptome de novo sequencing to characterize the sequence and expression of EPSPS. Sequence analysis showed no mutation of the EPSPS Pro106 codon in glyphosate-resistant K. scoparia, whereas EPSPS genomic copy number and transcript abundance were elevated three- to ten-fold in resistant individuals relative to susceptible individuals. Glyphosate-resistant individuals with increased relative EPSPS copy numbers had consistently lower shikimate accumulation in leaf disks treated with 100 μM glyphosate and EPSPS protein levels were higher in glyphosate-resistant individuals with increased gene copy number compared to glyphosate-susceptible individuals. RNA sequence analysis revealed seven nucleotide positions with two different expressed alleles in glyphosate-susceptible reads. However, one nucleotide at the seven positions was predominant in glyphosate-resistant sequences, suggesting that only one of two EPSPS alleles was amplified in glyphosate-resistant individuals. No alternatively spliced EPSPS transcripts were detected. Expression of five other genes in the chorismate pathway was unaffected in glyphosate-resistant individuals with increased EPSPS expression. These results indicate increased EPSPS expression is a mechanism for glyphosate resistance in these K. scoparia populations.
Data from: Effect of arsenate substitution on phosphate repository of cell: a computational study
The structural analogy with phosphate derives arsenate into various metabolic processes associated with phosphate inside the organisms. But it is difficult to evaluate the effect of arsenate substitution on the stability of individual biological phosphate species, which span from a simpler monoester form like pyrophosphate to a more complex phosphodiester variant like DNA. In this study, we have classified the physiological phosphate esters into three different classes on the basis of their structural differences.This classification has helped us to present a concise theoretical study on the kinetic stability of phosphate analogue species of arsenate against hydrolysis. All the calculations have been carried out using QM/MM methods of our Own N-layer Integrated molecular Orbital molecular Mechanics. For quantum mechanical region we have used M06-2X density functional with 6-31+G(2d,2p) basis set and for molecular mechanics region AMBER force field. The calculated rate constants for hydrolysis show that none of the phosphate analogue species of arsenate has a reasonable stability against hydrolysis.
The 1.1 Å Structure of the Periplasmic Phosphate-Binding Protein from Stenotrophomonas maltophilia - a crystallisation contaminant identified by molecular replacement using the entire protein database (X-ray diffraction images).
<p>During efforts to crystallise the enzyme 2,4-dihydroxyacetophenone dioxygenase (DAD) from <em>Alcaligenes</em> sp. 4HAP, a small number of strongly diffracting protein crystals were obtained after two years of crystal growth in one condition. The crystals diffracted synchrotron radiation to almost 1.0 Å resolution and were, until recently, assumed to be formed by the DAD protein. However, when another crystal form of this enzyme was eventually solved at lower resolution, molecular replacement using this structure as the search model did not give a convincing solution with the original atomic resolution dataset. Hence we considered that these crystals might be due to a protein impurity, although molecular replacement using the structures of common crystallisation contaminants as search models again failed. A script to perform molecular replacement using MOLREP (Vagin, A. & Teplyakov, A. (2010). Acta Crystallogr. D 66, 22-25.) in which the first chain of every structure in the PDB was used as a search model was run on a multi-core cluster. This identified a number of prokaryotic phosphate binding proteins as scoring highly in the MOLREP peak lists. Calculation of an electron density map at 1.1 Å resolution allowed most of the amino acids to be identified visually and built into the model. A BLAST search then indicated that the molecule was most probably a phosphate binding protein from <em>Stenotrophomonas maltophilia</em> (UniProt ID: B4SL31; gene ID: Smal_2208) and fitting of the corresponding sequence to the atomic resolution map fully corroborated this. Proteins in this family have been linked with the virulence of antibiotic resistant strains of pathogenic bacteria and with biofilm formation. The structure has been refined to an R-factor of 10.15 % and an R-free of 12.46 % at 1.1 Å resolution. The molecule adopts the type-II periplasmic binding protein fold with a number of extensively elaborated loop regions. A fully-dehydrated phosphate anion is bound tightly between the two domains of the protein and interacts with conserved residues and a number of helix dipoles. </p>
Figure 5 in A new species of Halisaurus from the Late Cretaceous phosphates of Morocco, and the phylogenetical relationships of the Halisaurinae (Squamata: Mosasauridae)
Figure 5. Halisaurus arambourgi sp. nov. A, MNHN PMC 15, referred specimen, disarticulated cranium, Late Cretaceous (Maastrichtian), Oulad Abdoun Basin, Morocco; B, OCP DEK/GE 100, referred specimen, incomplete disarticulated skeleton, Late Cretaceous (Maastrichtian), Oulad Abdoun Basin, Morocco, interpretative drawings. Abbreviations as in Fig. 3. Scale bars = 10 cm.
Diffsuion of ferrocene through vanadyl phosphate by DFT
<p>We are using CI-NEB method to simulate Ferrocene diffusion through Vanadyl phosphate. </p>
Crystallization of Calcium Carbonate and Calcium Phosphate Phases in Silica Hydrogel: Morphological and Compositional Characterization
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Allen Brain Atlas
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Annotated Behaviour and Observability Dataset (ABODe)
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