The thermodynamic properties of sulphonated polystyrene exchanges saturated with a single cation

1955 ◽  
Vol 8 (3) ◽  
pp. 293 ◽  
Author(s):  
JF Duncan

If an ion exchanger is treated as if it were an aqueous electrolyte, it is possible to use several independent experimental data to calculate the osmotic and activity coefficients of the resin phase. Illustrative examples are quoted. The activity coefficient of pure sodium " resinate " is calculated with satisfactory agreement from isopiestic data, and by two methods from the sodium-hydrogen exchange reaction. Activity coefficient curves for lithium, sodium, potassium, rubidium, caesium, copper, and barium " resinates " are given and also activity coefficient data for a number of other divalent cationic " resinates ", at a single value of the ionic strength. These activity coefficients show similar trends to those of aqueous electrolytes.

2013 ◽  
Vol 11 (3) ◽  
pp. 388-393 ◽  
Author(s):  
Mariana Hristova ◽  
Dimitar Damgaliev

AbstractThe flash points of three organic binary mixtures containing alcohols were measured in the present work. The experimental data was obtained using the Pensky-Martens closed cup tester. The experimental data were compared with the values calculated by the Liaw model. Activity coefficients were calculated by the Wilson equation and NRTL equation. The accuracy of predicted flash point values is dependent on the thermodynamic model used for activity coefficient.


1968 ◽  
Vol 14 (9) ◽  
pp. 859-870 ◽  
Author(s):  
Harold Dahms ◽  
Robert Rock ◽  
David Seligson

Abstract Ionic activities of sodium, potassium, and chloride in serums of 26 hospitalized patients were determined with ion-specific electrodes. Comparison of the activities with the corresponding concentrations shows that the two most important parameters influencing the molar activity coefficients of these ions are the water content of serum and the binding between albumin and chloride. Quantitative expressions for activity-concentration conversion factors are given. Calculations show that the conversion factors vary significantly in disease states due to changes in protein.


1994 ◽  
Vol 269 (47) ◽  
pp. 29704-29709
Author(s):  
C Bookstein ◽  
M W Musch ◽  
A DePaoli ◽  
Y Xie ◽  
M Villereal ◽  
...  

2015 ◽  
Vol 309 (4) ◽  
pp. E370-E379 ◽  
Author(s):  
Keeley L. Rose ◽  
Andrew J. Watson ◽  
Thomas A. Drysdale ◽  
Gediminas Cepinskas ◽  
Melissa Chan ◽  
...  

A common complication of type 1 diabetes mellitus is diabetic ketoacidosis (DKA), a state of severe insulin deficiency. A potentially harmful consequence of DKA therapy in children is cerebral edema (DKA-CE); however, the mechanisms of therapy-induced DKA-CE are unknown. Our aims were to identify the DKA treatment factors and membrane mechanisms that might contribute specifically to brain cell swelling. To this end, DKA was induced in juvenile mice with the administration of the pancreatic toxins streptozocin and alloxan. Brain slices were prepared and exposed to DKA-like conditions in vitro. Cell volume changes were imaged in response to simulated DKA therapy. Our experiments showed that cell swelling was elicited with isolated DKA treatment components, including alkalinization, insulin/alkalinization, and rapid reductions in osmolality. Methyl-isobutyl-amiloride, a nonselective inhibitor of sodium-hydrogen exchangers (NHEs), reduced cell swelling in brain slices elicited with simulated DKA therapy (in vitro) and decreased brain water content in juvenile DKA mice administered insulin and rehydration therapy (in vivo). Specific pharmacological inhibition of the NHE1 isoform with cariporide also inhibited cell swelling, but only in the presence of the anion transport (AT) inhibitor 4,4′-diisothiocyanatostilbene-2,2′-disulphonic acid. DKA did not alter brain NHE1 isoform expression, suggesting that the cell swelling attributed to the NHE1 was activity dependent. In conclusion, our data raise the possibility that brain cell swelling can be elicited by DKA treatment factors and that it is mediated by NHEs and/or coactivation of NHE1 and AT.


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