The epidemiology mid histology of Hodgkin's disease in Cali, Colombia is reported on the basis of data from the Cancer Registry and a review of slides from several of the city's departments of pathology. Comparison of the results with incidence data published by UICC and with other reports on histologic subclassification has led to the identification of several epidemiologic patterns. Pattern I is characterized by high rates in children and predominance of histologic subtypes associated with poor prognosis. Pattern III is characterized by high rates in young adults and predominance of histologic subtypes associated with better prognosis. Pattern II is intermediate. These patterns are related to the economic stratification of the communities studied, and it is suggested that many of the epidemiological variegations of Hodgkin's disease may be explained on the basis of the interplay of environmental and host etiologic factors.

Mixed infection with simian virus 40 (SV40) and adenovirus 1 2 can occur in African green monkey kidney (AGMK) cells in vitro, and electron micrographs demonstrating both viruses within the nucleus of a single cell have been presented ( 1 ) . Variable degrees of partial exclusion were produced by altering the time interval between inoculation of SV40 and adenovirus 12, and approximately 40% of the cells contained both viruses when the adenovirus was inoculated 24 hours after SV40(1). Further studies of AGMK cultures infected with both viruses compared with cultures infected with adenovirus 12 only have shown that SV40 enhances the growth of the adenovirus. A similar enhancement of growth of adenovirus 5 has been found when AGMK cultures were infected with SV40 and adenovirus 5.Materials and methods. Cell Cultures: Primary AGMK cell cultures were obtained from Microbiological Associates, Inc., Bethesda, Md., and primary human embryo kidney cell cultures (HEK) from the Virology Research Resources Branch, National Cancer Institute, through the kindness of Drs. Robert E. Stevenson and Theodore Malinin. Roller tube cultures maintained in a medium composed of 2 % fetal bovine serum and 98% mixture 199 and incubated at 36.5"C were used in all experiments.Viruses: SV40 and adenovirus 12 strains were the same as those previously described (1). Adenovirus 5 was obtained from the American Type Culture Collection. SV40 was grown and titrated in AGMK cell cultures, and adenoviruses 12 and 5 were grown and titrated in HEK cultures. Viruses were titrated by serial 10-fold dilutions with 3 to 5 tubes per dilution. Titrations were observed for 2 1 days and titers were calculated by the Reed-Muench method.The amount of adenovirus in the AGMK cultures after infection with both SV40 and adenovirus 12 or adenovirus 5 was determined by titration in HEK cell cultures in which a typical adenovirus-type CPE was produced. Although Shein and Enders have shown that SV40 can produce an incomplete CPE in HEK cell cultures after more than 17 days (2), the cellular degeneration described by them did not resemble the CPE produced by adenovirus 12 and 5, and the inocula they used contained considerably more SV40 than could have been present in the terminal dilutions in our titrations.Experiments and results. In the first experiment, AGMK cell cultures infected with adenovirus 12 only were compared with similar cultures infected simultaneously with both SV40 and adenovirus 12 (Table I). After 48 hours' incubation, clusters of rounded refractile cells were observed in both the singly and doubly infected cultures although the changes were more extensive in the doubly infected cultures. Uninfected control cultures showed no changes. At 72 and 122 hours, the CPE had progressed in all infected tubes; however, it continued to be more severe and extensive in the doubly infected cultures.Electron microscopic studies at 72 and 122 hours showed a significant difference between the singly and doubly infected cultures. In the singly infected cultures, althou...

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Sera from 813 patients were examined independently by 3 test centers for the presence of alpha‐fetoprotein (AFP). The sera were collected at 5 different African centers and 2 non‐African centers. There was disagreement in the serologic results among the 3 test laboratories in only 27, or 3.3%, of cases. A clinical and/or histologic diagnosis of primary liver cancer had been made in 231 of the cases in which there was serologic agreement, and 151, or 65.4%, of these were positive for AFP. If only those cases with histologic confirmation of liver cell cancer were included, the percentage of cases with AFP increases to 75%. Analysis of the results from each collection center has been made, and the basis for “false‐positives” and serologic disagreements is discussed. The test has proven to be highly specific for primary liver cell cancer and may be used with advantage in differential diagnosis of this disease and in epidemiologic studies.