Suppression of Ehrlich ascites tumor growth by immunization with ganglioside GT1b of its origin, its IgM antibody or anti-idiotype of the anti-GT1b IgM.

Ehrlich tumor expresses the ganglioside GT1b. The plasma of mice with Ehrlich ascites tumor burden also contains GT1b. The structural identity of plasma GT1b was ascertained by a series of enzymatic degradation and mass spectral analysis. Mice were vaccinated with purified plasma GT1b admixed with Freund's adjuvant (FA). Sixty nine percent suppression of Ehrlich ascites tumor growth was observed in vaccinated mice. The suppression was dose-dependent. It is hypothesized that the tumor growth-suppression is a result of immune response to GT1b Humoral immune response to GT1b was demonstrated by passive hemagglutination assay of the sera of vaccinated mice. To test the hypothesis, the mice were administered with rabbit polyclonal anti-GT1b IgM antibody in varying doses and challenged with Ehrlich tumor. A significant reduction in tumor growth (65%) was observed in mice administered with anti-GT1b IgM antibody. Again, the suppression was dose-dependent. To verify further, another batch of mice was immunized with anti-idiotypic antibodies to rabbit anti-GT1b IgM raised in rat. The polyclonal anti-idiotype antibody is expected to carry the structural image of GT1b. In a dose-dependent manner, a maximum of 82% suppression of tumor growth was observed in mice immunized with the anti-idiotype antibody. This observation further strengthened the hypothesis that ganglioside mediated suppression of tumor growth may be a result of immunogenicity of the target ganglioside. This was also supported by positive reaction of the sera of anti-idiotype vaccinated mice with both anti-idiotype antibody and ganglioside GT1b in passive hemagglutination assay. The results favour the therapeutic potential of immunogenic tumor-associated gangliosides.

Seguimiento de hepatis aguda tipo A en 60 niños / Follow up of acute hepatitis A of 60 children

Se realizo un estudio de 60 niños deagnosticados como hepatitis viral tipo A, en edades comprendidas entre 18 meses y 14 años. Se confirmó el daignostico clínico epidemiológico con la presencia de la IgM anti HAV por el método ELISA. El grupo de edad más frecuente fue entre 10 a 14 años (53,3 porciento), predominando la forma clínica ictérica ( 68,3 porciento). La remisión de los síntomas clínicos ocurrió antes de los 30 días en el 83,5 porciento. Las cifras de aminotrasferasas predominaron entre 100-500 U/L (58,3 porciento) en el momento del diagnóstico inicial. el tiempo de curación dado por la normalización de las aminotransferasas resultó de más de 12 semanas en 33 (55 porciento). Nuestra serie demuestra que la evolución clínica de la hepatitis por virus A en la infancia, aunque no evoluciona a la cronicidad no es de curso tan benigno, ni de evlución tan corta como se señala en la literatura, ya que dos evolucionaron con hepatonecrosis (3,3 porciento) confirmada por endoscopia y el 55 porciento tuvo un curso prolongado entre 3 y 6 meses.