No abstract

Summary.-The procoagulant activity of cells from some experimental tumours isolated in culture or in single-cell suspensions from ascitic fluid was investigated. Cells from Lewis lung carcinoma (primary and metastasis), Ehrlich carcinoma ascites and JW sarcoma ascites were able to shorten markedly the recalcification time of normal, Factor VIII-and Factor VII-deficient but not of Factor X-deficient human plasma. The same cells generated thrombin when mixed with a source of prothrombin and Factor X, absorbed bovine serum (as a source of Factor V), phospholipid and calcium chloride. Thrombin formation was not influenced by the presence of Factor VII. Cells from Sarcoma 180 ascites were completely inactive in both test systems. It is concluded that cells from some experimental tumours have the capacity to activate Coagulation Factor X directly. These findings suggest the existence of an alternative "cellular" pathway in the initiation of blood clotting distinct from both the intrinsic and extrinsic mechanisms.

Data obtained with time lapse cinemicrographic techniques showed that the distribution of generation times for exponentially proliferating human amnion cells in culture is skewed to the right and that reciprocals of generation times appear normally distributed. As shown for bacteria, the true age distribution is much broader than theoretical distributions which fail to take into account the dispersion of generation times. By means of the technique utilizing autoradiographic detection of tritiated thymidine in cells whose mitotic histories were recorded by time lapse cincmicrography, it was shown that the G1 distribution is similar to the generation time distribution but is more variable. In our experiments, the G2 -tprophase distribution resembled the generation time and G1 distributions. The data suggested two possibilities for S: either it is relatively constant, or it is inversely related to the lengths of G1 and G2 ~ prophasc. Since G1 is more variable than the total cycle, and G2 4-prophase more variable than the computed sum of S n u G2 -t-prophase + mctaphase, it was concluded that the relationships between parts of the cycle are non-random and that compensating mechanisms apparently help regulate the lengths of successive parts of the mitotic cycle in individual cells.

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Mouse fibroblasts were cultured by three different procedures: (a) changing the 0.2 ml/cm2 of growth medium every 2nd d and seeding 1 X 10(5) cells/cm2 after confluency; (b) changing the 0.4 ml/cm2 of growth medium only at subculture performed at confluency by a 1:2 split and keeping the bottles incubated on a rocking platform; (c) the same as Method b but keeping the bottles stationary throughout culture. By Method a no lines were immortalized over 36 experiments whereas Method b gave 1/4 immortalized lines and Method c gave 10:12 immortalized lines. Cells always went into crisis at the 9th to 11th doubling. Immortalized lines had a tetraploid DNA content.