Plasticization-resistant glassy polyimide membranes for CO2/CH4 separations

It is known that CO2 acts as a plasticizer in CO2/CO4 membrane separations at elevated pressures. The polymer matrix swells upon sorption of CO2, accelerating the permeation of CH4. As a consequence, the polymer membrane loses its selectivity. To overcome this effect, plasticization should be minimized. We succeeded in stabilizing the polymer membrane by a thermal treatment. For this purpose the polyimide Matrimid 5218 is used as model polymer. In single gas experiments with CO2, the untreated membrane normally shows a minimum in its pressure dependence on permeability, whereas the treated membranes do not. Membrane performances for CO2/CO4 gas mixtures showed that the plasticizing effect indeed accelerates the permeation of methane. The heat treatment clearly suppresses this undesired methane acceleration. Additionally to the pure and mixed gas permeation results, process calculations reveal valuable information as to what extent the stabilized membranes show improved membrane performance. The favourable performance of the stabilized membrane can be attributed to less methane loss and therefore a higher recovery, resulting in higher profit from gas sales

Shrinkage effects during polmer phase separation on microfabricated molds

Phase separation microfabrication (PSμF) is a fabrication method that allows the preparation of membranes having micropattern surface topologies. PSμF entails the phase separation of a polymer solution cast onto structured supports. The polymer solution wets the features and upon phase separation and solidification the polymer replicates the underlying microstructure. Shrinkage of the solidifying polymer solution influences the replication precision. Through the systematic study of a PES/PVP/NMP/water system, the relation between polymer concentration and replication performance was assessed. Normal shrinkage (thickness) is found to be dependent on polymer concentration, with pore sizes varying between two limits. Outside these limits, the pore size does not vary with polymer concentration and shrinkage scales inversely with it. Lateral shrinkage proceeds according to the same mechanism. Yet, its extent is lower. Influence of the mold features on the shrinkage of the replicas and the deformation of the overlying film is explained in terms of feature size and distribution, along with the porosity of the film

Micropatterned polymer films by vapor-induced phase separation using permeable molds

Microstructured polymeric films are fabricated by a novel replication method. A polymer solution is applied and contained between two substrates, of which at least one is a patterned PDMS mold. The ensemble is then put in an atmosphere containing water vapor, which diffuses through the PDMS. The absorption of water into the polymer solution causes the precipitation (phase separation) of the polymer while in contact with the microstructured molds. The thickness of the PDMS slab can be exploited to tune the water vapor transport and hence the phase separation kinetics and resulting polymer morphology. Removal of excess polymer solution from between two PDMS slabs, followed by vapor induced phase separation, can also result in microperforated polymer films with great control over the dimensions

Barbiturates inhibit ATP-K+ channels and voltage-activated currents in CRI-G1 insulin-secreting cells.

1. Patch-clamp recording techniques were used to examine the effects of barbiturates upon the ATP-K+ channel, and voltage-activated channels present in the plasma membrane of CRI-G1 insulin-secreting cells. 2. Thiopentone inhibited ATP-K+ channel activity when applied to cell-attached patches or the intracellular or extracellular surface of cell-free patches. Secobarbitone and pentobarbitone were also effective inhibitors of ATP-K+ channels in cell-free patches, whereas phenobarbitone was ineffective. 3. The diabetogenic agent, alloxan, which is structurally related to the barbiturates also produced an inhibition of ATP-K+ channel activity in outside-out patches. 4. Whole-cell ATP-K+ currents were used to quantify the effects of the barbiturates: concentration-inhibition curves for thiopentone, secobarbitone and pentobarbitone resulted in IC50 values of 62, 250 and 360 microM respectively. Phenobarbitone at a concentration of 1 mM was virtually ineffective. 5. Calculation of the apparent membrane concentrations for these drugs indicate that for a given degree of ATP-K+ channel inhibition a similar concentration of each barbiturate is present in the membrane. This suggests that hydrophobicity plays a primary role in their mechanism of action. The pH-dependence and additive nature of barbiturate block also indicates a membrane site of action. 6. Thiopentone, (100 microM) was also found to inhibit differentially voltage-activated whole-cell currents. The relative potency of thiopentone at this concentration was 0.64, 0.38 and 0.12 for inhibiting Ca2+, K+ and Na+ currents respectively when compared with its ability to inhibit the ATP-K+ channel