Reversible control of free energy and topography of nanostructured surfaces.

We describe a facile method for the formation of dynamic nanostructured surfaces based on the modification of porous anodic aluminum oxide with poly(N-isopropyl acrylamide) (PNIPAAm) via surface-initiated atom transfer radical polymerization. The dynamic structure of these surfaces was investigated by atomic force microscopy (AFM), which showed dramatic changes in the surface nanostructure above and below the aqueous lower critical solution temperature of PNIPAAm. These changes in surface structure are correlated with changes in the macroscopic wettability of the surfaces, which was probed by water contact angle measurements. Principal component analysis was used to develop a quantitative correlation between AFM image intensity histograms and macroscopic wettability. Such correlations and dynamic nanostructured surfaces may have a variety of uses.

Effects of microwave exposure on the hamster immune system. IV. Spleen cell IgM hemolytic plaque formation.

Microwave exposure has been reported to affect various components of the immune system. In this study, we examined the effect of a single whole-body exposure of hamsters to microwave (mw) energy (2.45 GHz; 5-25 mW/cm2; 1 h) on the IgM antibody (Ab) response of spleen cells to sheep red blood cells (SRBC). MW-exposed, sham-exposed, and cage-control hamsters were immunized with SRBC and plaque-forming cells (PFC) in spleens assayed using the direct hemolytic plaque assay. In cage-control hamsters the Ab response was highest between days 4 and 5, returning to baseline by day 9. MW exposure (25 mW/cm2 for 1 h) significantly augmented PFC response only on days 4 and 5 postimmunization, causing approximately a 4.3- and 3.5-fold increase over controls, respectively. Exposure to 15 mW/cm2 caused a lesser, but significant increase in PFC. Exposure to intensities below 15 mW/cm2 for 1 h did not produce any increase in Ab response. Immunization with different concentrations of SRBC following 1 h of 25 mW/cm2 MW exposure revealed a stimulation in PFC at all concentrations ranging from 5 X 10(7) to 5 X 10(8) SRBC. Pretreatment of hamsters with MW radiation prior to immunization showed that the animals retained an increased sensitivity to SRBC for as long as 4 days after MW exposure. In contrast, exposure of hamsters to MW energy on different days after immunization showed an effect of the PFC response only if given between 0 and 1 day after immunization. These results suggest that MW exposure augments the primary IgM response to SRBC by affecting some early event in the immune response process. The various possible explanations for this phenomenon are discussed.

Hyperthermia enhancement of antibody-complement cytotoxicity for human colon tumor cells.

HCT-8R human colon tumor cells heated for 60 minutes at 37-44.5 degrees C showed an increased sensitivity to lysis by rabbit anti-HCT-8R antibodies and complement (Ab-C) at the higher temperatures. As compared to the 51Cr release assay, the colony formation (CF) assay was a more sensitive measure of hyperthermia-induced cell damage and sensitization to Ab-C lysis. Also the CF assay was more efficient than the 51Cr assay in detecting effects of low-temperature heating (41.5 degrees C) on Ab-C cytotoxicity. The direct toxicity of heating alone was minimal. Because heating did not influence the pH of the medium, the pH of our assay system did not appear to be factor in the enhanced sensitivity of heated cells to Ab-C cytotoxicity. Significantly smaller amounts of antibodies were capable of lysing heated cells as compared to unheated cells, but heated cells did not bind more antibodies than did unheated cells. This suggests that the hyperthermia effect on the cell occurs at some stage of the lytic event after antibody binding. Hyperthermia treatment at 43.5 degrees C enhanced cytotoxicity by antibodies monospecific to carcinoembryonic antigen, which is expressed on the surface of these cells. Thus hyperthermia may be an effective tool in augmenting specific immune reactions against tumor-associated cell membrane antigens.