An injection of viable thymus or thoracic duct lymphocytes was absolutely essential to enable a normal or near-normal 19S liemolysin-forming cell response in the spleens of neonatally thymectomized mice challenged with sheep erythrocytes. Syngeneic thymus lymphocytes were as effective as thoracic duct lymphocytes in this system and allogeneic or semiallogeneic cells could also reconstitute their hosts. No significant elevation of the response was achieved by giving either bone marrow cells, irradiated thymus or thoracic duct cells, thymus extracts or yeast. Spleen cells from reconstituted mice were exposed to anti-H2 sera directed against either the donor of the thymus or thoracic duct cells, or against the neonatally thymectomized host. Only isoantisera directed against the host could significantly reduce the number of hemolysin-forming cells present in the spleen cell suspensions. It is concluded that these antibody-forming cells are derived, not from the inoculated thymus or thoracic duct lymphocytes, but from the host. Thoracic duct cells from donors specifically immunologically tolerant of sheep erythrocytes had a markedly reduced restorative capacity in neonatally thymectomized recipients challenged with sheep erythrocytes. These results have suggested that there are cell types, in thymus or thoracic duct lymph, with capacities to react specifically with antigen and to induce the differentiation, to antibody-forming cells, of hemolysin-forming cell precursors derived from a separate cell line present in the neonatally thymectomized hosts.

The reduced immunological responsiveness of neonatally thymectomized rodents has been reversed far more effectively with cells from spleen, lymph nodes, and thoracic-duct lymph than with cells from either thymus or bone marrow.' In heavily irradiated mice, an inoculum containing a mixture of marrow and thymus cells allowed the production of more hemolysins against sheep erythrocytes than could be accounted for by summating the activities of each cell population alone.2 Some type of interaction must thus take place between thymus cells, bone marrow cells, and antigen. In order to characterize the nature of this interaction one would first have to determine which cell type, thymus or bone marrow, was the immediate precursor of the antibody-forming cell.In thymectomized irradiated mice protected with chromosomally marked bone marrow and grafted with chromosomally marked thymus tissue, both marrowdonor-type and thymus-donor-type cells were found dividing in the lymphoid tissues. The majority of dividing cells were of marrow donor origin,3 but a sharp increase in the proportion of thymus-derived cells occurred for a short period of time after antigenic stimulation.4 An attempt was made to determine the origin of the antibody-forming cell by using a transfer system in which both chromosome and isoantigenic markers were available. The results indicated that, although thymus-graft derived cells responded vigorously to antigenic stimulation by mitosis, the antibody-forming cells had the immunogenetic characteristics of the marrow donor.4 However, it is known that the lymphocyte population of a thymus graft in a marrow-protected irradiated host is entirely replaced within two to three weeks by cells from the inoculated marrow.3 Hence, although antibody-forming cells had the genotypic characteristics of the marrow donor, they could have been derived from cells that had first migrated through the thymus implant which, in these experiments, had been grafted 30 days prior to antigenic stimulation. Such an experimental design therefore failed to establish unequivocally which cell type was the immediate precursor of the antibody-forming cell: thymus or marrow cell.In our laboratory we have attacked the problem by using cell suspensions rather than thymus grafts. A mixture of thymus and bone marrow cells from unrelated strains of mice was inoculated together with sheep erythrocytes into irradiated hosts. Under these conditions no hemolysin response was obtained, I suggesting that interaction does not take place between allogeneic cells immediately upon transfer to irradiated recipients. Neonatally thymectomized mice were then used as hosts of syngeneic or allogeneic thymus cells injected together with sheep erythrocytes. Since the marrow of neonatally thymectomized rodents 296

Feral carp, Cyprinus carpio L., were collected at bimonthly intervals for 12 months from Lake Wellington, where there was no evidence of significant growth of Microcystis aeruginosa. Various blood parameters of these carp were measured to ascertain the normal range values for feral carp in this region. A similar study was conducted at Lake Mokoan, where M. aeruginosa formed a visible scum that contained detectable levels of microcystins for 4 consecutive months. Carp were taken from Lake Mokoan each month, and the histology and blood biochemistry of the fish were examined for indications of microcystin toxicity. During February, March and April, 66% of the carp from Lake Mokoan had livers with widespread hepatocyte atrophy, and 37% of the fish had gills with pinpoint necrosis, epithelial ballooning, folded lamellar tips and exfoliation of the lamellar epithelium. Compared to carp from Lake Wellington, the serum aspartate aminotransferase activity and the serum bilirubin concentrations of carp from Lake Mokoan were elevated during January, February, March and April. The data were consistent with impaired hepatocyte function in some carp from Lake Mokoan. Serum sodium and chloride concentrations in carp from Lake Mokoan were lower than those for carp at Lake Wellington from December to April, indicating that most carp from Lake Mokoan had difficulty maintaining cation‐anion homeostasis during this period. Nevertheless, carp at Lake Mokoan always appeared healthy, and no mortalities were reported.

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