Search PubMed⌕ Search

Biomedical subjects

C A Cain

Publications and source records attributed to C A Cain.

At least 37 records · Page 2Linked to original sources
PubMed1983

Effects of microwaves and hyperthermia on capping of antigen-antibody complexes on the surface of normal mouse B lymphocytes.

Normal mouse B lymphocytes were tested for the ability to cap plasma membrane antigen-antibody complexes following exposure to 2.45-GHz continuous wave (CW) microwaves at power densities up to 100 mW/cm2 (45 W/kg specific absorption rate), at 37, 41, and 42.5 degrees C. After a 30-minute treatment, the irradiated cells and the nonirradiated controls were tested for capping by the direct immunofluorescence technique. First, the cells were incubated for nine minutes at 37 degrees C with fluorescein isothiocyanate-conjugated goat antimouse immunoglobulin. After fixing and washing, the percentage of capped cells was determined under a fluorescence microscope. The results show that for the nonirradiated controls, capping is reduced from 90% at 37 degrees C, to 52% at 41 degrees C, to less than 5% for cells that were pretreated at 42.5 degrees C. There was no significant difference between the microwave-treated cells and the controls when both were maintained at the same temperature. In another experiment, there was no significant difference in the percentage of capping between controls and cells that were exposed to microwave radiation during capping, when the temperature in both preparations was kept at 38.5 degrees C. The results demonstrate that B-lymphocyte capping is sensitive to temperature in the range that is proposed for use in tumor therapy.

Animals↗
PubMed1983

Effects of microwave exposure on the hamster immune system. I. Natural killer cell activity.

Hamsters were exposed to repeated or single doses of microwave energy and monitored for changes in core body temperature, circulating leukocyte profiles, serum corticosteroid levels, and natural killer (NK) cell activity in various tissues. NK cytotoxicity was measured in a 51Cr-release assay employing baby hamster kidney (BHK) targets or BHK infected with herpes simplex virus. Repeated exposure of hamsters at 15 mW/cm2 for 60 min/day had no significant effect on natural levels of spleen-cell NK activity against BHK targets. Similarly, repeated exposure at 15 mW/cm2 over a 5-day period had no demonstrable effect on the induction of spleen NK activity by vaccinia virus immunization, that is, comparable levels of NK were induced in untreated and microwave-treated animals. In contrast, treatment of hamsters with a single 60-min microwave exposure at 25 mW/cm2 caused a significant suppression in induced spleen NK activity. A similar but less marked decrease in spleen NK activity was observed in sham-exposed animals. Moreover, the sham effects on NK activity were not predictable and appeared to represent large individual animal variations in the response to stress factors. Depressed spleen NK activity was evident as early as 4 h postmicrowave treatment and returned to normal levels by 8 h. Hamsters exposed at 25 mW/cm2 showed an elevated temperature of 3.0-3.5 degrees C that returned to normal within 60 min after termination of microwave exposure. These animals also showed a marked lymphopenia and neutrophilia by 1 h posttreatment that returned to normal by 8-10 h. Serum glucocorticosteroids were elevated between 1 aNd 8 h after microwave treatment. Sham-exposed animals did not demonstrate significant changes in core body temperature, peripheral blood leukocyte (PBL) profile, or glucocorticosteroid levels as compared to minimum-handling controls.

Adrenal Cortex Hormones↗
PubMed1983

Effects of microwave exposure on the hamster immune system. II. Peritoneal macrophage function.

Acute exposure to hamsters to microwave energy (2.45 GHz; 25 mW/cm2 for 60 min) resulted in activation of peritoneal macrophages that were significantly more viricidal to vaccinia virus as compared to sham-exposed or normal (minimum-handling) controls. Macrophages from microwave-exposed hamsters became activated as early as 6 h after exposure and remained activated for up to 12 days. The activation of macrophages by microwave exposure paralleled the macrophage activation after vaccinia virus immunization. Activated macrophages from vaccinia-immunized hamsters did not differ in their viricidal activity when the hamsters were microwave- or sham-exposed. Exposure for 60 min at 15 mW/cm2 did not activate the macrophages while 40 mW/cm2 exposure was harmful to some hamsters. Average maximum core temperatures in the exposed (25 mW/cm2) and sham groups were 40.5 degrees C (+/- 0.35 SD) and 38.4 degrees C (+/- 0.5 SD), respectively. In vitro heating of macrophages to 40.5 degrees C was not as effective as in vivo microwave exposure in activating macrophages to the viricidal state. Macrophages from normal, sham-exposed, and microwave-exposed hamsters were not morphologically different, and they all phagocytosed India ink particles. Moreover, immune macrophage cytotoxicity for virus-infected or noninfected target cells was not suppressed in the microwave-irradiated group (25 mW/cm2, 1 h) as compared to sham-exposed controls, indicating that peritoneal macrophages were not functionally suppressed or injured by microwave hyperthermia.

Animals↗
PubMed1983

Immunological effects of amplitude-modulated radio frequency radiation: B lymphocyte capping.

B lymphocytes collected from normal ICR Swiss mouse spleens were exposed in vitro in a Crawford cell to 147-MHz radiofrequency (RF) radiation, amplitude modulated by a 9-, 16-, or 60-Hz sine wave. The power densities ranged between 0.11 and 48 mW/cm2. The irradiated samples and the controls were maintained at 37 degrees C or 42 degrees C, with temperature variations less than 0.1 degrees C. Immediately after a 30-minute exposure, the distribution of antigen-antibody (Ag-Ab) complexes on the cell surface was evaluated at 37 degrees C by immunofluorescence. Under normal conditions (37 degrees C, no RF), Ag-Ab complexes are regrouped into a polar cap by an energy-dependent process. Our results demonstrate that the irradiated cells and the nonirradiated controls capped Ag-Ab complexes equally well after exposure at 37 degrees C. Capping was equally inhibited at 42 degrees C in both the controls and irradiated cells. No statistically significant differences in capping were observed between the RF-exposed and control samples at any of the modulation frequencies and power densities employed as long as both preparations were maintained at the same temperature.

Animals↗
PubMed1983

A role for calcium-activated calmodulin in murine nonspecific cell-mediated cytotoxicity.

The role of Ca++ in mouse nonspecific cell-mediated cytotoxicity was studied using the calcium ionophore A23187, inhibitors of calmodulin activity, and agents which modulate cyclic AMP concentration. A23187 markedly enhanced spleen lymphocyte cytotoxicity against SV3T3 target cells, suggesting that Ca++ influx enhances cytolytic activity. This conclusion was supported by experiments in which verapamil, a Ca++ channel blocker, inhibited normal and ionophore-induced cytotoxicity. A23187 also enhanced cytolysis of YAC-1 cells in a 16-hr 51Cr release assay, but had little effect in the more typical 4-hr assay. Lysis of BHK, a cell line resistant to murine natural cytotoxicity, could not be induced by A23187. However, hamster effector cells, which can lyse xenogeneic target cells, showed increased against either SV3T3 or BHK. This indicates that the effect of the ionophore was not due to nonspecific release of toxic products from the effector cells. Both normal and ionophore-enhanced lysis were also inhibited by the phenothiazines chlorpromazine and trifluoperazine, which block the activity of calmodulin. A more specific calmodulin activity inhibitor, W13, was also shown to profoundly inhibit cytotoxicity induced by A23187. These results suggest that Ca++ acts as a stimulus-response coupler in cell-mediated cytotoxicity, and that calmodulin mediates the effects of the Ca++. Furthermore, cyclic AMP appears to modulate the action of Ca++ since agents which increase cAMP levels reduce the effects of A23187.

Animals↗
PubMed1983

Hyperthermic enhancement of antibody-complement cytotoxicity against normal mouse B lymphocytes and its relation to capping.

Normal mouse B lymphocytes were exposed to water-bath hyperthermia in vitro and examined for susceptibility to antibody-complement (Ab-C) cytotoxicity. Enhancement of Ab-C cytotoxicity was observed during heat treatment at 42 or 43 degrees C. Sensitivity to Ab-C cytotoxicity returned to normal levels by 2-3 hr post exposure to 42 degrees C. No such recovery was observed when cells were preheated at 43 degrees C for 40 min. The mechanism responsible for heat-induced enhancement of Ab-C cytotoxicity may be related to the way heat affects the redistribution of membrane-bound antigen-antibody (Ag-Ab) complexes. To investigate this possibility, cells were preheated at 37, 42, or 43 degrees C. The Ab-C assay was then performed at 37 degrees C immediately or 2.5 hr after hyperthermia. The distribution of Ag-Ab complexes was evaluated by immunofluorescence. A direct correlation was found between the hyperthermic enhancement of Ab-C cytotoxicity and the hyperthermic inhibition of capping, a process where membrane-bound Ag-Ab complexes coalesce into a polar cap on the cell surface. Sensitivity to Ab-C cytotoxicity returned to normal levels when cells restored the ability to cap Ag-Ab complexes following 42 degrees C hyperthermia. Cells heated at 43 degrees C were still sensitive to Ab-C cytotoxicity and did not recover the capping ability even 2.5 hr after heat treatment.

Animals↗
PubMed1982

Local tumor hyperthermia using a computer-controlled microwave system.

A minicomputer-based system was designed to control the microwave (2.45-GHz) power to four local hyperthermia applicators. Errors in temperature measurement, due to electromagnetic field interactions with small thermocouple probes, are minimized by sampling the temperature only when the microwave power is off. The programmable controller can regulate the temperature in tumors in 0.1 degree C increments from 30 to 60 degrees C. This technique reduces temperature differences throughout the tumor at steady state to less than 0.4 degrees C and prevents skin burns.

Animals↗
PubMed1982

An annular focus ultrasonic lens for local hyperthermia treatment of small tumors.

A system for applying local hyperthermia employing ultrasonic transducers with annular focusing lenses gave better temperature uniformity in small fibrosarcomas than conventional unfocused transducers. The lenses were designed for ultrasonic frequencies of 3, 4, 5 and 9 MHz for tumors approximately 6 mm dia. Tests in degassed water indicated that the focusing lenses concentrated approx. 80% of the ultrasonic energy into an annular-shaped focus of 6 mm dia. located at a distance of 3 cm in front of the lens. These transducers were used to heat subcutaneous PARA-7 fibrosarcomas in hamsters. Steady-state temperature measurements indicated temperature gradients within tumors of 0.5-1.0 degree C when transducers employing annular-focused lenses were used, versus gradients of 2.0-2.3 degree C with 10 mm dia. unfocused transducers.

Animals↗
PubMed1981

Biological effects of oscillating electric fields: role of voltage-sensitive ion channels.

An alternating component of potential across the membrane of an excitable cell may change the membrane conductance by interacting with the voltage-sensing charged groups of the protein macromolecules that form voltage-sensitive ion channels. Because the probability than a voltage sensor is in a given state is a highly nonlinear function of the applied electric field, the average occupancy of a particular state will change in an oscillating electric field of sufficient magnitude. This "rectification" at the level of the voltage sensors could results in conformational changes (gating) that would modify channel conductance. A simplified two-state model is examined where the relaxation time of the voltage sensor is assumed to be considerably faster than the fastest changes of ionic conductance. Significant changes in the occupancy of voltage sensor states in response to an applied oscillating electric field are predicted by the model.

Electrophysiology↗
PubMed1981

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.

Antibodies, Neoplasm↗
PubMed1980

Development of alcoholism in adoptees raised apart from alcoholic biologic relatives.

Male adoptees raised apart from alcoholic biologic parents were followed up and compared with adoptees of nonalcoholic biologic parents. Significant associations were found between adoptee alcoholism and an alcoholic biologic background and between childhood conduct disorder and the development of alcoholism as an adult. None of the environmental factors--psychiatric or alcohol problems in adoptive family, socioeconomic status of the adoptive family, or exposure to discontinuous mothering as an infant--predicted adoptee alcoholism. These findings suggest the importance of a genetic factor in alcoholism and are in accord with previous work that failed to show an independent effect of an alcoholic environment in development of adoptee alcoholism.

Adolescent↗