Surface tension--area relations.
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Biomedical subjects
Publications and source records attributed to S Schurch.
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While infecting a vertebrate host, blood flukes (Schistosoma mansoni) must continually resist adhesions by immune effector cells. However, the male and female schistosomes must adhere to one another in order to establish and maintain the sexual pairing process after 4 wk postinfection. Using a contact angle method, the relative adhesiveness of male and female parasites were determined. Results indicate that schistosomes restrict effector cell adhesion through developmental, sexual, and regional differences in adhesive properties.
The ability of the synthetic leukotrienes LTB4, LTC4, LTD4 and LTE4 to stimulate porcine AM was compared with that of two known AM stimuli: zymosan, a particulate stimulus and phorbol myristate acetate (PMA), a soluble stimulus. The criteria for AM stimulation were: increased generation of superoxide anion (O2-), the release of the lysosomal enzymes N-acetyl-beta-D-glucosaminidase (NABG) and arylsulfatase and an increase in surface free energy. Whereas zymosan and PMA both stimulated AM according to each of the three criteria, the effect of leukotrienes was relatively minor. LTB4 (10(-6) M) and LTD4 (10(-6) M) caused a modest reduction in spontaneous O2- release by AM. LTD4 (10(-6) M) also caused a small (18%), but significant (p less than 0.05), reduction in the additional O2- release induced by PMA. LTC4 and LTE4 did not alter spontaneous O2- release. Neither spontaneous nor stimulated enzyme release was systematically altered by any of the leukotrienes. LTD4 caused a cysteine-inhibitable, dose-dependent increase in surface free energy with a plateau at concentrations above 10(-8) M. The increased surface free energy induced by LTD4 may be a consequence of binding to a surface dipeptidase.
Hypoxia affects the biochemistry of mammalian cells and thus alters their sensitivity to subsequent chemo- and radiotherapy. When V79 Chinese hamster lung fibroblasts were grown under conditions of extreme hypoxia (less than 10 ppm O2) there was a significant shift in the membrane glycoprotein composition. Scanning electron microscopy revealed altered cell surface morphology including loss of pseudopodial projections. Experiments to determine changes in interfacial free energy of these cells using equilibrium two phase systems of poly(ethylene glycol) (PEG) and dextran were carried out. Test fluid droplets of the denser dextran-rich phase were formed on layers of cells in the PEG-rich phase as the bathing medium, and the contact angles the droplets made with the cell layers were measured from photomicrographs. The contact angles on cells in the plateau phase increased significantly with time of exposure to hypoxia, from 25 degrees (zero time) to 35 degrees (6 h) to 60 degrees (9 h). Contact angles on cells in the exponential phase increased from 80 degrees (zero time) to 150 degrees after 20 h of hypoxia. It appears that the altered contact angles reflect changes in cell surface hydrophobicity that may, in part, reflect alterations in the membrane glycoprotein composition.
Porcine alveolar macrophages (AM) metabolize leukotriene D4 (LTD4) to leukotriene E4 (LTE4). In the present study, the ability of a fluid-phase AM stimulus (A23187) and a phagocytic stimulus (opsonized zymosan) to augment LTD4 metabolism was examined. Both stimuli increased the release of superoxide (O-2) anions. However, whereas zymosan caused a consistent reduction in surface free energy, the effect of A23187 was variable. Similarly, zymosan induced release of the lysosomal enzymes N-acetyl-beta-D-glucosaminidase and arylsulphatase (mean net release, 14.9% and 12.0%, respectively), whereas release induced by A23187 was smaller (mean net release 1.42% and 1.31%, respectively) and of marginal statistical significance. Zymosan, but not A23187, caused a significant (P less than 0.005) augmentation of LTD4 inactivation: from 93 +/- 7 pM/10(7) cells (69 +/- 5% of added LTD4) at 60 min by control AM, to 117 +/- 3 pM/10(7) cells (88 +/- 2% of added LTD4) at 60 min by zymosan-treated AM. Zymosan also induced the release of LTD4 inactivating capacity (128 +/- 21 pM LTD4/10(7) AM/60 min) into the supernatant. Conversion of LTD4 to LTE4 by zymosan-treated AM and their supernatants was confirmed chromatographically. In addition, LTD4 inactivation by AM and their supernatants was inhibited by 10 mM L-cysteine. These data suggest that zymosan released a dipeptidase, possibly of lysosomal origin, which catalysed the conversion of LTD4 to LTE4.
Tissue culture cells incubated at 43 degrees C show a dramatic decrease in cell survival compared with cells incubated at lower temperatures; the effect is termed hyperthermic cell death (HCD). Replacing water in the culture medium with deuterium oxide produces a dose-dependent reduction in HCD. On the basis of this and other evidence it is concluded that the mechanism of HCD involves a hydration-dependent phase transition in membrane lipids.