Publications

Wheat germ agglutinin (WGA), previously regarded strictly as a nonmitogenic or anti-mitogenic lectin, can under appropriate conditions markedly stimulate in vitro synthesis and secretion of immunoglobulin (Ig) by human B lymphocytes. Stimulation of Ig production by WGA is 1) confined to a narrow lectin dose range (2 to 10 micrograms/ml; 2) abrogated by the simple sugar N-acetyl-D-glucosamine but not by a variety of other monosaccharides; 3) effective only after early additions of WGA within the initial 72 hr of 12-day cultures; 4) detected in the presence of B and T cells but not B cells alone; and 5) polyisotypic in nature, as indicated by augmented synthetic rates of Ig in each of 3 major classes (IgG, IgA, and IgM). With few exceptions, WGA produces equivalent or greater rates of Ig production as obtained in cultures activated with pokeweed mitogen (PWM), a well-recognized T-dependent polyclonal activator of human B cells. Furthermore, periperal blood lymphocytes from select individuals that respond weakly to PWM are markedly stimulated with WGA. In contrast to these stimulatory effects of WGA on Ig production by lymphocytes exposed to low lectin concentrations, addition of WGA in amounts greater than 15 micrograms/ml to PWM-stimulated human lymphocyte cultures produces marked suppression of the expected level of Ig synthesis. These data indicate that varying doses of WGA can produce contrasting stimulatory and inhibitory effects on human B cell metabolism.

We evaluated 57 patients with modified treadmill exercise testing and angiography early post-infarction (MI) to determine the predictive value of ST segment depression, angina, and an inadequate blood pressure response for multivessel coronary artery disease (MVCAD). ST segment depression alone identified MVCAD stenoses (greater than or equal to 70% diameter narrowing in two or more vessels) with sensitivity 54%, specificity 75%, and accuracy 60%. When ST segment depression and angina were considered a positive treadmill test result, a significant improvement in sensitivity (88%, p less than 0.01) and accuracy (82%, p less than 0.05) for MVCAD was observed. An inadequate blood pressure response was associated with MVCAD (12 of 13 patients) and a significantly reduced average left ventricular (LV) ejection fraction of 39 plus or minus 13% compared to 58 plus or minus 14% for patients without this treadmill abnormality (p less than 0.01). Therefore, we conclude that (1) ST segment depression and angina on early post-MI modified treadmill exercise testing are superior predictors of MVCAD compared to ST segment depression alone and (2) an inadequate blood pressure response during modified exercise testing early following MI is observed in patients with MVCAD and reduced LV performance.