[Calculation of Steel's cell loss factor and cell kinetic parameters for a population with exponential growth of cell number and cell death in the G1 and/or G0 phase with probabilities less than 1].

The method of calculation of the proliferative pool and of the Steel's loss factor was shown to be the same for the exponential growth state with cell death at the G1-phase and/or at the G0-phase with propabilities less than one (the model of F type), and for the exponential growth state model of C type. A method is proposed for calculation of the number of the cell kinetics parameters on the data of percentage of labeled cells cultivated with 3H-thymidine. An unsatisfactory agreement between the exponential growth state model of F type with the interpretation of the experimental of Drewinco e.

[Calculation of Steel's cell loss factor and of the parameters of cellular kinetics for a population with an exponential growth of the cell number and cell death at G0 phase with a probability equal to 1].

The method of calculation of three cell kinetics parameters (the Steel's cell loss factor phi, the proliferative pool Pc, and the mean number m of the proliferating cells after mitotic division of one cell) was shown to be the same for the exponential growth state of cell number with cell death at the G0-phase, and for the exponential growth state with cell death occurring immediately after mitosis. The value of the mean number delta of non-proliferating cells that appeared after mitotic division of one cell is different for these two models of the exponential growth state with the equal values of the other three parameters (phi, Pc, and m). A method is proposed for calculating the parameter delta on the data of the percentage of labeled cells obtained in the experiments with continuous cultivation of cells in the nutrient medium containing 3H-thymidine.

[Effect of long-term adaptation of rats to hypoxia on the proliferation of bone marrow erythroid cells. I. An increase in cell flows and a decrease in the duration of mitosis].

A 60 day adaptation of Wistar rats to hypoxia (six times a week, 6 hours a day) leads to: (1) the increase in cell flow from any phase of the erythroid cell life cycle to the next phase; (2) the change in the duration of the life cycle phases, corresponding to erythroblasts, basophilic normoblasts, and polychromatophilic normoblasts of the third type, (3) the shortening of the duration of all the mitotic phases by, in average, 1.8 times, and (4) the shortening of the radiation G2-block from 60 to 10 minutes. The changes in the mitotic index within a 24 hour period may be explained by non-periodic changes in the value of the cell flow from phase G2 to the mitosis every 6 hours, provided the duration of mitosis being constant.

[Exponential growth of cell numbers. II. Cell death immediately after mitosis].

A mathematical model was examined of the exponential growth state of the cell number (N) with the proliferative pool Pc greater than or equal to 1, the non-zero variability of the phase duration of the mitotic cycle and with the cell death immediately after mitosis. At this state it is impossible to calculate the cell loss factor phi from Steel's formula (1968). A method was proposed for calculation of phi, Pc and the potential doubling time (tDpot) of N (and the mean duration of mitosis, tM), provided the doubling time of N, the indexes of S- and M-phase, the mean durations of mitotic cycle and of S, G2- and M-phases (or G2 + 0.

Study of kinetics of epithelial cell populations in normal tissues of the rat's intestines and in carcinogenesis. III. Changes in kinetics of enterocyte populations in the course of experimental intestinal tumour induction in rats.

A stage-by-stage study of disturbances in enterocyte proliferation in the ileum and descending colon in the course of tumour induction by treatment with 1,2-dimethylhydrazine was performed. Even at early stages, an expansion of the zone of epithelial cell proliferation in the crypts and migration of dividing cells as far as to the crypt mouth, which is a manifestation of enterocyte differentiation disturbances, were observed. Enterocytes of the crypts chiefly proliferated through a short cycle, the mean duration of which was slightly greater than in normal intestinal tissue.

[Exponential growth status of the cell number. I. The independence of the portion of proliferating cells found in different phases of the mitotic cycle from the variability in phase durations].

A mathematical model of the cell tumour kinetics has been analysed for a population being characterized with the exponential growth of the cell number, the absence of cell losses, and the proliferative pool Pc less than or equal to 1. It is shown that the values of part of proliferative cells, being in one phase of the mitotic cycle, do not depend on the kind of cell distribution function in respect to the phase duration. A graphic method is proposed for the estimation of the proliferative pool, the mean mitotic duration and the doubling time of the cell number, provided we know the mitotic, index, the index of the phase S, and the mean durations of mitotic cycle, of mitosis and of phase S.

Study of kinetics of epithelial cell populations in normal tissues of the rat's intestines and in carcinogenesis. II. Peculiarities of kinetics of enterocyte populations in experimental tumours of the colon.

Cell proliferation in adenocarcinomas induced in the rat's colon by parenteral injection of 1,2-dimethylhydrazine was compared with that in normal colonic epithelium by means of autoradiographs. The distinct zone of proliferation, typical of the intestines, was not observed in the tumours, and cells replicated nearly in all segments of neoplasms. Tumour enterocytes were found to have a longer short mitotic cycle (16 instead of 11 hrs), due, chiefly, to an extension of G1-period duration.

Study of kinetics of epithelial cell populations in normal tissues of the rat's intestines and in carcinogenesis. I. A comparison of enterocyte population kinetics in different segments of the small intestine and colon.

The peculiarities of enterocyte proliferation in the duodenum, jejunum, ileum, caecum, ascending, transverse and descending colon in the rat were studied by different methods of analysis of cell population kinetics (percentage-labelled mitosis curves, cumulative labelling curves, distribution of labelling index curves, etc.). The majority of proliferating cells in the small intestine are homogenous, as far as mitotic cycle mean duration (11-12 hrs) is concerned.

[Irreversibility of intestinal epithelium stem cell conversion into semi-stem enterocytes and the ability of the latter to reproduce themselves].

The analysis of literature experimental data on cell kinetics of the generating intestinal epithelium of rats and mice suggested the irreversibility of transformation of intestinal epithelium stem cells into non-stem proliferating enterocytes and the ability of the latter for self-reproduction. This property of half-stem enterocytes enabled us to assume that the daughter cells immediately after their appearance are always in the G1-phase of the mother cell mitotic cycle.

[Changes in the enterocyte population kinetics during the process of development of intestinal tumors in rats].

Changes in proliferation of the enterocytes from the descendent colon at different developmental stages of tumours induced with 1,2-dimethylhydrazine (DMH) were studied. As a result of carcinogen-induced disturbances in enetrocyte differentiation, the proliferative crypt zone was seen broadening, the proliferative cells appearing even in the mouths of the crypts. Further, these very superficial parts of the crypts proved to be the sites of carcinoma development in situ.

[Kinetics of populations of enterocytes of experimental tumors of the large intestine in rats].

With the aid of histoautoradiography, the proliferation of enterocytes in rat intestinal adenocarcinomas induced with subcutaneous treatment by 1,2-dimethylhydrozine has been studied. The experimental adenocarcinomas are characterized by a high proliferative activity being, however, lower than that in the proliferative zone of the normal intestinal crypt. The parameters of adenocarcinoma proliferation are very close to those of a cell population from the bottom part of crypts in the control animals.

[Splitting of phase G1 of the mitotic cycle of guinea pig large intestine crypt cells].

Changes in shape of the second wave of the labeled mitoses curve previously observed by Rowinski and Sawicki (1972) for three crypt zones of three different parts of guinea-pig ascending colon are explained by the complicated branching structure of the G1-phase. This structure is assumed to be the same for different crypt zones and for different sections of the intestine. Changes in shape of the second wave of the labeled mitoses curve are explained by the changes in distribution of proliferating cell stream between the alternative directions at the points of branching of the G1-phase, depending on the crypt zone, the intestine section, the cell state, and on the state of intestine.

[Relationship between the proliferation waves of the hepatocytes after hepatectomy and the waves of diurnal rhythm of mitotic activity. 1. Dependence of the form of the mitotic wave and the time of attaining its maximal degree on the time of operation].

The diurnal rhythm of mitotic activity (MA) of intact animal hepatocytes and the proliferative wave of hepatocytes after partial hepatactomy at time t0 are thought to appear as a result of formation of an initial proliferative wave, Pk-wave, within the G0-phase at constant moments of the day--time tk+1=tk+TMA(TMA=24hrs/K, k=1, or 2, . . .

[Inequality of numbers of cells passing daily from S phase into G2 and from G2 into mitosis for a population of young mouse hepatocytes].

The formulas are proposed which allow to verify the equality of the diurnal streams of cells from one to another phase of mitotic cycle for systems with the diurnal rythm of mitotic index. The unequality of the diurnal stream of cells from S into G2 phase and the diurnal streams from G2 into M phase for hepatocytes of 3-weeks old mice is assumed to be caused by the passage of about 75 percent of cells from G2 phase directly to the resting phase R1. Part of these cells may then return from R1 to G1 phase.

[Evaluation of the size of the proliferative pool and the length of the mitotic cycle according to the accumulation curve of labelled cells].

Abnormal increase of the accumulation curve of H3-thymidine labelled cells for the systems with proliferative pool Pc less than 1 (rat mesothelium and the basal cells of the epithelium of the hamster cheek pouch) is due to stimulation of cell transition from R1 phase to the regulatory G1r phase (the dichophase) within G1 period of the mitotic cycle. The stimulation was assumed to depend on the radiation and transmutation defects in DNA due to H3 disintegration, and to occur when the stream of labelled cells reached the G1r phase. Proliferative pool and the duration of mitotic cycle can be estimated by means of coordinates of the abnormal curve.