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The present study suggests a correlation between concanavalin A-driven blastogenesis and the clinical course of head and neck cancer. Blastogenesis assays were conducted on peripheral blood lymphocytes from controls and from patients with squamous cell carcinoma (SCC) of the head and neck. Our results indicated that 3H-thymidine incorporation in response to concanavalin A and phytohemagglutinin stimulation were significantly lower for patients' than for controls' lymphocytes, whereas PWM stimulation was not statistically different in these two groups. Differences between patients and controls were most notable with concanavalin A stimulation. Five of seventeen patients had a response to concanavalin A stimulation that was in the normal range when expressed as relative to control values. The clinical course of these five patients seems to point to a better prognosis than that of the remaining patients who had below-normal mitogenic responses.

An artificial pancreas consisting of beta cells cultured on synthetic semipermeable hollow fibers was tested in rats with alloxan-induced diabetes. When implanted ex vivo as arteriovenous shunts in the circulatory system these devices lowered concentrations of plasma glucose from 533 to between 110 and 130 milligrams per 100 milliliters, increased concentrations of plasma insulin, and restored intravenous glucose tolerance tests essentially to normal.

The effects of heparin on several in vitro immune functions [blastogenesis, interleukin-2(IL-2) production] were investigated. The addition of heparin to human peripheral mononuclear cells stimulated with phytohemagglutinin or pokeweed mitogen significantly increased the blastogenic response of these cells. Peak IL-2 concentrations in the supernatant of heparin-containing cultures were two- to fourfold higher than in heparin-free cultures. Flow cytometry experiments revealed that Leu-M3-positive cells were the only subset to be significantly affected by heparin, which induced an increase both in number and in fluorescence intensity of Leu-M3-positive cells. In contrast, the expression of DR molecules on monocytes was slightly decreased. It is speculated that the observed antimetastatic effects of heparin may be exerted through local immunomodulation in macrophage-rich tissues.

Approximately two thirds of patients with head and neck cancer have been shown to have peripheral mononuclear cells that exhibit a lowered blastogenic response to the T-cell mitogens, concanavalin A and phytohemagglutinin. To investigate the possible mechanisms of this phenomenon, we measured the amount of activated T-cell lymphokine interleukin-2 present in the supernatant of concanavalin A- or phytohemagglutinin-stimulated peripheral mononuclear cells taken from patients with squamous cell carcinoma of the upper aerodigestive tract. Concentrations were found that were similar to those of healthy subjects. The rate of interleukin-2 consumption and the degree of interleukin-2 receptor expression also were similar for patients and controls. In the course of these experiments, it was noted that differences in blastogenic response between patients and controls were abolished when, 24 hours after the beginning of either concanavalin A or phytohemagglutinin stimulation, the culture supernatant was removed and replaced by fresh medium, containing recombinant interleukin-2 to further sustain cell growth. This suggests that the lower blastogenic response found in patients with head and neck cancer is not due to global immune unresponsiveness, but instead, is caused by selective cell dysfunction(s), which may include the production of a suppressor factor following concanavalin A or phytohemagglutinin stimulation.

Peripheral mononuclear cells of ten patients with oral squamous cell carcinoma (SCC) and ten controls were evaluated for their cell subset composition. Flow cytometry experiments using commercially available subset-specific monoclonal antibodies (of the Leu series) were conducted to determine the percentage and fluorescent pattern of cell subsets. Leu-1+ (total T-cells), Leu-2a+ (T suppressor/cytotoxic cells), Leu-3a+ (T-helper/suppressor-inducer cells), Leu-7+ (natural killer cells), Leu-12+ (B-cells), and Leu-M3+ (monocytes) were analyzed. No significant difference was found between patients and controls in most instances; however, Leu-7+ cells were increased in patients (P less than 0.01). Preliminary experiments (and published evidence) suggest that this increase in Leu-7+ cells reflects an increase in natural killer cells, induced by a soluble factor released by squamous cell carcinoma cells.

Infection with herpes simplex virus often results in a latent infection of local sensory ganglia and a disease characterized by periodic viral reactivation and mucocutaneous lesions. The factors that trigger reactivation in humans are still poorly defined. In our study, five patients with documented histories of recurrent herpes simplex virus infection on the buttocks or sacrum were exposed to three times their minimal erythema dose of ultraviolet light. Site-specific cutaneous herpes simplex virus infection occurred at 4.4 +/- 0.4 days after exposure to ultraviolet light in 8 of 13 attempts at reactivation. We conclude that ultraviolet light can reactivate herpes simplex virus under experimentally defined conditions. This model in humans should prove useful in evaluating the pathophysiology and prevention of viral reactivation.

The treatment of herpes simplex virus (HSV) infections in the past has been largely unsuccessful. Introduction of the drug acyclovir has been a positive development. Acyclovir has been extensively studied in the treatment of a a variety of HSV infections in immunocompromised patients and in otherwise healthy patients. The results have shown it to effectively inhibit HSV replication but to have no effect in preventing or eliminating the latent state of the virus. It has been shown to be very effective in certain instances and not so effective in others.