Much research into the fundamentals of membrane formation and separation has been performed in order to improve the efficiency of the manufacture of ultrafiltration membranes. Determination of the membrane characteristics is a key problem in these investigations. In this paper, we report on a study of membrane morphology by fractional rejection measurements, using low molecular weight saccharides as the test solute, and by electron microscopy. Using a simple model for solute/solvent transport through cylindrical pores, a “characteristic pore size” was derived from saccharide rejection data. This pore size of a hypothetical isoporous membrane, interpreting the measured separation characteristics, provides a promising means of describing differences between membranes with respect to pore size and pore size changes caused by solute adsorption. From high resolution electron micrographs, information was obtained on the skin layer morphologies and, for some membranes the sizes of the larger pores could be estimated.

The aim of this study was to define as possible abnormality of interleukin 2 (IL2) production by PHA-stimulated peripheral blood lymphocytes (PBL) in systemic lupus erythematosus (SLE). Thirty-four SLE PBL samples were stimulated to produce IL2 and compared with PBL from healthy (age- and sex-matched) controls. A significant defect in IL2 production was observed in SLE patients. This defect was not restricted to corticosteroid-treated patients and was not correlated with the presence of lymphotoxic antibodies or with clinical disease activity.Although 5-day responsiveness to phytohaemagglutinin (PHA) decreased in SLE, the SLE PHA-blasts responded as well as control blasts to semipurified IL2, suggesting that the receptor for IL2 was normally expressed on SLE blasts. In 9 cases, the effect of addition of indomethacin (2 μg/ml) or of an optimal amount of IL1 on PHA-induced IL2 production was studied. Indomethacin increased (22%) the IL2 yield of healthy individual PBL. In SLE, indomethacin (but not IL1) was able to completely restore (41% increase) the IL2 production of lectin-stimulated PBL (P<0.01). These data suggest that, in SLE, the inhibition of IL2 production is mediated by prostaglandin, possibly produced by monocytes.Le but de ce travail était de définir la capacité de production d'interleukine 2 (IL2) par les lymphocytes périphériques stimulés par la phytohémagglutinine (PHA) des malades atteints de lupus érythémateux disséminé (LED). Les malades atteints de LED (n=34) ont été comparés à des sujets sains (n=24). Les lymphocytes des malades produisent significativement moins d'IL2 que ceux des sujets témoins; ce défaut n'est lié ni au traitement, ni à la présence d'anticorps lymphocytotoxiques ni à l'activité de la maladie. Alors que la réponse mitogénique induite par la PHA (5è jour) est diminuée chez les lupiques, leurs lymphoblastes répondent comme ceux des témoins à l'addition d'IL2 semi-purifiée, ce qui suggère que les récepteurs pour l'IL2 sont normaux sur les lymphoblastes de LED. Dans neuf cas, on a pu étudier le rôle de l'adjonction d'IL1 ou d'indométhacine (2 μg/ml) sur la production de l'IL2 induite par la PHA. Chez les sujets atteints de LED, l'indométhacine (mais non l'IL1) est capable de restaurer complètement (41% d'augmentation) la production d'IL2 des lymphocytes stimulés (P<0,01). Ces résultats suggèrent que, chez les sujets atteints de LED, l'inhibition de la production d'IL2 est sous le contrôle des prostaglandines, vraisemblablement produite par les monocytes.