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Enzymatic transamination consists of the enzyme catalyzed reversible transfer of the alpha amino nitrogen of an amino acid to an alpha-keto acid with the synthesis of a second amino acid and a second alpha-keto acid. Enzymes catalyzing different transamination reactions are found widely distributed in animal tissues and have been shown to change in activity in some tissues during disease (1-3). These observations prompted the present study to determine if transaminase activity could be demonstrated in human serum and blood cellular elements and, if so, to study any variations in activity of this enzyme in the blood of normal and diseased man. METHODS AND MATERIALSThe two transaminases found most active in animal tissues are:1. "Glutamic-oxalacetic transaminase" Aspartate + alpha-keto glutarate = glutamate + oxalacetate 2. "Glutamic-pyruvic transaminase"Alanine + alpha-keto glutarate = glutamate + pyruvate When aspartate or alanine are incubated with alphaketo glutarate and a source of enzyme, the rate of production of glutamate may be taken as a measure of transaminase activity. The amount of glutamate produced after a given incubation period under standardized conditions was measured by quantitative paper chromatographic analysis (4).One-tenth molar solutions of I-aspartate, I-alanine, and alpha-keto glutarate were prepared in 0.06 M phosphate buffer and the pH of the solutions adjusted to pH 7.6. For serum transaminase determinations, 0.5 ml. of clear, non-hemolyzed serum, 1.5 ml. of 0.06 M phosphate buffer, pH 7.6, and 0.5 ml. of either the alanine or aspartate solutions were incubated for ten minutes at 37°C. At this time, 0.5 ml. of the alpha-keto glutarate solution was added and the incubation continued for 18 hours. For whole blood hemolysate transaminase determinations, equal volumes of blood and distilled water were shaken together for ten minutes, 1.0 ml. of the hemolysate was added to 1.0 ml. of the phosphate buffer, and the substrates added as above. The time of incubation of the hemolysate substrate mixture was three hours.At the end of the incubation period, proteins were separated by adding 7.0 ml. of absolute ethyl alcohol, centrifuging for ten minutes, and washing the precipitate with 5 ml. of 70 per cent ethanol. The supernatant was evaporated to dryness over a water bath and the residue dissolved in 1.0 ml. of 0.06 M phosphate buffer. Aliquots of 0.05 ml. were then applied to Whatman No. 1 filter paper and chromatographed by the descending method for 18 hours, using phenol saturated with water as solvent and water saturated with phenol to saturate the atmosphere of the tank. The papers were then removed and dried in air at room temperature (5). The position of the amino acids was located by spraying the paper with a 0.1 per cent solution of ninhydrin in butanol and heating gently with an infra-red lamp.The areas of paper corresponding to glutamate were cut out, rolled, and placed in test tubes. Elution of the amino acid from the paper and quantitative color development with ninhydrin were perf...

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The incidence found at autopsy of cardiac metastases in patients who died of cancer is reported in the literature to be less than 4%.1 Pollia and Gogol2 found involvement of the heart by metastatic disease in 29 cases among 1,450 autopsies of patients dying of cancer; Scott and Garvin,3 101 among 1,085; Ritchie,4 16 in 857; and Prichard,5146 of 4,375 cancer autopsies. The disproportionate frequency of serial changes in the electrocardiograms of patients dying of cancer at Memorial Center led us to review the clinical and postmortem data of 500 consecutive cancer deaths observed between 1948 and 1950. METHOD AND MATERIALThe incidence of cardiac metastases in the various neoplastic diseases encountered was tabulated, and the exact site of the metastases, as well as the degree of cardiac involvement, was noted. The clinical, electrocardiographic, and roentgenographic findings were correlated, insofar as possible, with the pathological changes described at autopsy. No primary heart tumors were encountered in this series, and therefore discussion of these rare tumors will not be included. Data are based on 124 patients dying of leukemia, 69 of lymphoma, and 307 of other tumors. For the purposes of this study we include under the heading of lymphoma the following conditions: Hodgkin's disease, Hodgkin's sarcoma, Hodgkin's granuloma, lymphosarcoma (all types), and reticulum cell sarcoma. The leukemias were represented by acute and chronic lymphatic, acute and chronic myelogenous, acute monocytic, acute micromyeloblastic, and stem cell leukemia. RESULTSThe over-all incidence of cardiac infiltration in 119 patients with leukemia of various types was 44% (52 patients). A slightly greater frequency of myocardial infiltration was noted in lymphatic leukemia (58%) than in myelogenous (40%). In acute myelogenous leukemia, occurring in 53 persons, the incidence was 42% (22 patients with cardiac involvement) as opposed to 35% (7 of 20 persons) in the chronic form, and the incidence was 59% (10 of 17) and 57% (8 of 14), respectively, for chronic and acute lymphocytic leukemia.Cardiac infiltration was found in 23% (3 of 13) of pa¬ tients with stem cell leukemia and in the one patient each with acute monocytic and acute micromyeloblastic leu¬ kemia. No postmortem evidence of cardiac involvement was found in five patients with multiple myeloma. The cardiac involvement in all instances was characterized by interstitial and perivascular infiltration of the heart with leukemia cells. Occasional microscopic areas of fibrosis and myocardial necrosis were encountered.The frequency of cardiac infiltration in 69 patients who died from lymphomas of various types was estab¬ lished, with an over-all incidence of 24% (17 patients). No significant differences were found among Hodgkin's disease (29%, or 4 of 14), Hodgkin's sarcoma (31%, or 4 of 13), and reticulum cell sarcoma (30%, or 7 of 23). Cardiac infiltration was found in only 13% (2 of 15) of the patients with lymphosarcoma and in none of the four cases of Hodgkin's granuloma. The type of ...