Phosphates concentration factor

The formation of tricalcium phosphate in a cooling system is primarily a net result of system pH, calcium concentration, temperature, and phosphate concentration factors. An increase in any of these factors leads to an increased risk of phosphate deposition. 

For both coordinated and congruent control, the pH depends upon the phosphate concentration and the sodium to phosphate ratio. Generally, however, phosphates are unsuitable for use at boiler pressures above 100 bar as their low solubility and high concentration factors developed lead to corrosive conditions. 

Several factors can influence metal uptake by stream autotrophic biofllms in fluvial systems. These include chemical factors (pH, saUnity, phosphate concentration) which affect metal bioavailabiHty by either altering the speciation of the metal or by complexing it at the biotilm s matrix and cell surfaces [18, 40], and also other biological and physical factors. 

When cyanoacetylene (5), which is produced when an electric discharge is passed through a mixture of methane and nitrogen, is dissolved in a phosphate buffer a stable enol-phosphate (6) is formed. Pyrophosphate is produced when neutral aqueous solutions of (6) and orthophosphate are heated, and the phosphorylation of UMP has been achieved. However, from a study of the rate of phosphorylation and a consideration of environmental factors, especially the likely phosphate concentration in oceans, it is suggested that (6) is not an important intermediate in prebiotic phosphorylation. The conversion of the 3 -phosphate of 0 2 -cyclocytidine (7) into 2, 3 -cyclic CMP under mild conditions in aqueous solution has... 

The first phosphatase step is very important FBPase converts fructose,1-6-bisphos-phate into fructose-6-phosphate under allosteric control of several factors but during fasting, glucagon-induced regulation is crucial. One effect of glucagon stimulation of liver cells is to reduce the concentration of fructose-2,6-bisphosphate, an isomer that activates PFK-1 and is itself synthesized by PFK-2 when fructose-6-phosphate concentration rises... 

FIGURE 1.4 Dependencies of retention factors k on counterion (i.e., phosphate) concentration [X]. Experimental conditions Mobile phase, methanol-sodium dihydrogenphosphate buffer (50 50 v/v) (pHa 6.5 adjusted in the mixture with sodium hydroxide) flow rate, 1 mLmin temperature, 25°C CSP, 0-9-[3-(triethoxysilyl)propylcarbamoyl]-quinine bonded to silica [30] column dimension, 150 x 4 mm ID. 

We realize that there are a number of factors in addition to temperature that influence the % alcohol response of the wine sugar content, pressure, magnesium concentration in the fruit, phosphate concentration in the fruit, presence of natural bacteria, etc. Although we strive to keep as many of these factors as controlled and therefore as constant as we can (e.g., pressure), we have no control over many of the other factors, especially those associated with the fruit (see Section 1.2). However, even though we do not have control over these factors, it is nonetheless reasonable to expect that whatever the % alcohol response is at 23°C, the % alcohol response at 27°C should increase for each of the fruits in our study if temperature has a significant effect. That is, if we are willing to make the assumption that there are no interactions between the factor of interest to us (temperature) and the other factors that influence the system, the differences in responses at 27°C and 23°C should be about the same for each pair of experiments carried out on the same fruit. 

In this experiment, tap water with added phosphate was used as influent. Concentration of phosphate was adjusted to an adequate range from 2 to 23 mg/jg. Calcium chloride and sodium hydroxide solution were added to maintain calcium concentration from 70 to 100 mg/jg and pH of the effluent from 9.0 to 9.5. Using this equipment, we performed experiments to obtain efficiency of phosphate removal, relationship between phosphate concentration, and crystallization rate and factors affecting phoshate removal. 

The changes in calvarial phosphatase activities observed in animals treated with 25-(OH)D3 are totally different from those obtained with either 1.25-(OH)2D3 or 24.25—(OH)2D3. This fact indicates that physiological doses of 25-(OH)D3 may have an effect on cellular activity, independent of the conversion of this metabolite into these dihydroxyderivatives. The various effects of these vitamin D3 metabolites cannot be correlated with changes in serum calcium and/or phosphate concentrations. Among those factors other than serum calcium and phosphate concentrations that may be involved in the mechanism of action of vitamin D3 metabolites on bone phosphatase activities, the parathyroid hormone is of importance. This hormone is known to be a potent activator of bone phosphatases223,224,228. Parathormone increases the content of alkaline, neutral and acid phosphatases in mouse calvaria in vitro. Calcitonin does not prevent the increase of those enzymes while dichloromethylene diphosphonate causes a decrease in acid phosphatase and pyrophosphatase226. ... 

Fig. 22. Mixed mode retention. Logarithmic retention factor for oligoriboadenylic acids vs. phosphate concentration in the mobile phase, pH 6.3. The figures at the curves indicate the number of adenylyl phosphate residues in the samples. (From Ref. 74) with permission)...

Both the active and passive modes of calcium transport are increased during pregnancy and lactation. This is probably due to the increase in calbindin and serum PTH and 1,25-dihydroxyvitamin D concentrations that occur during normal pregnancy. Intestinal calcium absorption is also dependent on age, with a 0.2% per year decline in absorption efficiency starting in midlife. The fractional absorption of calcium depends on the form and dietary source. Absorption rates are 29% for the calcium in cow s milk, 35% for calcium citrate, 27% for calcium carbonate, and 25% for tricalcium phosphate. Other factors that limit the bioavailability of calcium in the intestine are oxalates and phy-tates, which are found in high quantities in vegetarian diets and which chelate calcium. 

Amorphous aluminum oxide has recently been proved to extract lithium from brines and bitterns having lithium concentrations of 0.83 and 13.1 mg/1, respectively. The sorption may be explained by the formation of hydrous lithium aluminum oxide. The sorption capacity of amorphous hydrous aluminum oxide was found to be 4.0 mmol/g. For brines and bitterns the lithium concentration factors on the sorbent attained values of 370 and 130, respectively equilibrium was reached after 7 days. The desorption of lithium ions was carried out with boiling water yielding a maximum concentration factor of lithium in the eluate of 46 in reference to the initial lithium concentration of the brines. Lithium was separated from the eluates by solvent extraction with cyclohexane containing thenoyltrifluoracetone and trioctyl-phosphine oxide, subsequent back extraction with hydrochloric acid, and precipitation of lithium phosphate by addition of K3P04. The purity of the precipitate amounted to at least 95% I7 21). 

In contrast to the calcium-conserving effect of PTH on the kidneys, PTH increases renal phosphate excretion at the proximal tubule by directly lowering the renal phosphate threshold. Approximately 6.5 g (210 mmol) of phosphate is filtered by the kidneys each day. Normally, 85% to 90% is reabsorbed by the renal tubules (proximal and distal convoluted tubule). PTH is one of the most important factors regulating the renal phosphate threshold and hence the serum phosphate concentration. 

ED (BGE optimization). Three-level fnll factorial design. Factors SDS concentration, pH, phosphate concentration. Response resolntion and migration time. 

A wide range of plasma phosphorus concentration has been observed by other workers in primary hyperparathyroidism (C7) and explained in terms of diet and renal excretion. Unlike the calcium concentration, which is normally very constant regardless of dietary intake and urinary excretion, the concentration of inorganic phosphate in plasma is the resultant of the rate of phosphorus absorption from the gut and protein catabolism, on the one hand, and of renal excretion, on the other. Although the parathyroid hormone promotes phosphorus excretion, this is only one of the factors governing plasma phosphate concentration. Plasma phosphate in cases of hyperparathyroidism on a relatively high phosphorus intake may therefore not be distinguishable from that in normal subjects on a lower intake. 

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