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Biomedical subjects

V A Gushchin

Publications and source records attributed to V A Gushchin.

At least 19 recordsLinked to original sources
PubMed1995

[Individual variability in the number of stem cells in mammalian tissues].

The distribution of animal groups (3--4 control or gamma-irradiated mice per group) were obtained when analysing published data on the mean number of the CFUs in the femoral bone marrow or stem cells of small intestinal crypt. Almost 50% of such groups have the mean number less than the geometric mean. The mean value for the group of animals deviation from the expected geometric mean for all animal population for more than 2.5 times, both for the larger values and for the smaller, was about 5% in such groups for the marrow CFUs and 20% for intestinal stem cells. The percentage of mice, that died from acute radiation sickness after acute irradiation, was related with the parameter D(0), that characterized the CFUs survivability on the exponential part of the survivability curve. The negative correlation (r = -0.83) was determined between the mean value of the small intestine crypt stem cells and the ability of intestinal stem cells to the radiation damage reparation, evaluated through the parameter D(q) of the stem enterocyte survival curve for this animal groups.

Acute Disease↗
PubMed1993

[Monotonous and wave-form changes in the myelogram of rats over a 24-hour period].

Circadian changes of the mean value of each component of rat myelogram and of the proliferative pool of bone marrow cells were obtained. These changes were imposed on a monotonous decrease in the case of subpopulations of granulocytes or on a monotonous increase in the case of subpopulations of the erythroid cells and lymphocytes (from 12.00 to 09.00 next day). This process was not influenced by the elimination of the lymphocytes from the individual myelograms. These myelogram changes appeared to be due to the circadian mature cell production rhythm and flows of the lymphocytes and of mature granulocytes between the bone marrow and the peripheral blood. These changes also suggest the antiphase monotonous correction of the erythrocytic and granulocytic precursors production during several days.

Animals↗
PubMed1991

[The mechanism of the formation of a circadian rhythm of bone marrow proliferation in rats].

Flow cytofluorimetry and statmokinetic method were used to study the circadian rhythm of bone marrow proliferation in Pliss' lymphosarcoma-bearing and intact rats. These data were compared to those obtained in the study of the mitotic activity of the bone marrow in cancer patients. It was found that, already at early stage, tumor affected the circadian rhythm of bone marrow proliferation, reducing the amplitude of oscillations. A model simulating formation of the circadian rhythm of the bone marrow was suggested basing on the possibility to arrest cells at the end of G1 phase. The rate of transition of G1 cells to S phase was determined not only by endogenous "set-points" of the rhythm which formed the basic wave of proliferation but also by conditions of animal upkeep.

Animals↗
PubMed1989

[A model of the interclonal interactions in chronic myeloleukemia].

A new model of chronic myelogenous leukemia (CML) pathogenesis based on the idea of some cellular clones dominance over the others at the stem cells level is described. The model gives good explanations to all basic clinical variants of CML as well as to all well-known cytological phenomena to be found recently in this type of leukemia. The most probable mechanisms which might be responsible for the above-mentioned phenomenon of dominance between different cellular clones are discussed.

Cell Communication↗
PubMed1989

[The rate of tumor growth and cell loss in cervical cancer].

Time of tumor volume doubling, mitotic index and share of pathologic mitoses were identified in 61 patients with squamous-cell cervical tumors and the importance of cell loss evaluated. Tumor doubling time ranged 58-1500 days (average 314 +/- 37); mitotic index--0.1-3.7% (average 1.07 +/- 0.07%); percentage of pathologic mitoses 1-89% (average 28.9 +/- 1.6%); cell loss--92.0-99.9% (average 98.2 +/- 0.2%). Cell loss was found to be significantly different in groups of patients characterized by different rates of tumor growth and was directly proportional to tumor doubling time. There were no significant differences in mitotic index or pathologic mitosis share in groups with different rates of tumor growth. It is suggested that cell loss is determined by the tumor-bearer's antitumor systems to a considerable degree.

Carcinoma, Squamous Cell↗
PubMed1985

[Calculation of the duration of mitosis for a population with an exponential growth of the cell number].

A formula was received for the mean mitotic duration of a cell population being at the phase of exponential growth of the cell number with the cell loss: tM = nM.tD.(1-phi)/ln 2, where nM is the mitotic index, tD is the doubling time of the cell number, and phi is the Steel cell loss factor. In the case when after irradiation of such a population a 100% radiation G2-block arises, the method of calculation of the tM according to the curve of the relative mitotic index decrease was shown to be independent on the value of parameter phi and to coincide with the same method to be used in the case when the cell population is at the steady state before irradiation. As the result of analysis of literary experimental data the following values were received: tM = 20 min and tM = 37-42 min for two cell subpopulations of the Ehrlich ascite tumour, resp., tM = 39 min for epithelial cells of the mouse cornea, and tM = 29 min for enterocytes of the mouse jejunum. It has been also shown that the values of the dose of cell irradiation and of the mean duration tG2" of the subphase G2" localized at the end of phase G2 and preceded by the G2-block satisfy the next formula: Ig D = -a . Ig tG2" + b.

Animals↗
PubMed1984

[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. The kinetics of cell line HL-60 (the experimental data of Foa et al., 1982) can be described at the first approximation, by a model of the exponential growth state with the cell death at the G0-phase, with Pc = 0.80, phi = 0.24, m = 1.61, delta = 0.39, and the life time of the non-proliferating cells tQ = 24 hours.

Cell Count↗
PubMed1984

[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. a. (1978) was shown. A more satisfactory explanation of these data has been offered.

Cell Count↗
PubMed1984

[Calculation of Steel's cell loss factor and of the cellular kinetic parameters for a population with an exponential growth of the cell number and an equal probability of cell death in all phases of the life cycle].

A method of calculation of parameter m (equal to a doubled probability of birth of cells which did not pass into phase G0 from the mitotic cycle) and of the proliferative pool was shown to be the same for the exponential growth phase of cell population with the equal probability of cell death (lambda = const) at all phases of the life cycle (the Steel model of type E), and for the case "lambda = 0" (the Steel model of type B). The method is proposed for the calculation of parameter lambda and of the Steel cell lose factor phi = lambda/[lambda + [ln 2)/tD)]. It is noted that the value of parameter phi for the type E model can be estimated by the Steel formula: phi congruent to 1-tDpot/tD--where tD is the doubling time of the cell number, and tDpot = tcln 2/ln m. Here tc is the mean mitotic cycle duration.

Cell Count↗
PubMed1984

[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. For cell populations with the daily rhythm of the mitotic index the calculation of the length of mitosis was made more exactly using the colchicine method.

Adaptation, Physiological↗
PubMed1982

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. The reduced cell loss in the epithelium and resultant disturbances of its steady state led to the accumulation of great numbers of atypical cells in the superficial layers of the crypts and formation of carcinomas in situ in the descending colon. The microscopically unaltered sections of the mucosa, prior to development of overt neoplastic changes carcinomas in situ, superficial cancers and small-size adenocarcinomas revealed a simplified structure of enterocyte population, as compared with normal epithelium. As tumours progressed, the heterogeneity of its component cell subpopulations increased, and several subpopulations, differing in mean duration of the mitotic cycle, were formed. Pathologic mitoses made up a greater portion (50-60 per cent) of the dividing cells of the descending colon, as compared with ordinary 4 per cent at all stages of experimental tumour induction.

1,2-Dimethylhydrazine↗
PubMed1982

[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 + 0.5 M)-phase) are known from experimental data. The approximate values of phi, Pc, tDpot and tM were calculated for six solid transplanted tumors. It is noticed that using this mathematical model the cell kinetics was described satisfactory for not all the tumours examined.

Animals↗
PubMed1981

[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.

Cell Count↗
PubMed1980

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. All proliferating cells in all the zones of the colonic crypts and the bottom of the small intestine crypts are divided into subpopulations, having different mean durations of the mitotic cycle. It is suggested that, in the crypt bottom in all intestines as well as the crypt's maximum proliferation zones in most of the colonic segments, a considerable fraction of cells has a very long mitotic cycle or enters resting phase R1. The average value of the mean durations of the mitotic cycle of all colonic enterocyte subpopulations is 18-22 hours. On the basis of the authors' findings and literature data, a model for the enterocyte life cycle is proposed, according to which the cell flux is branched during the mitotic cycle and the crypt develops from a stem enterocyte population located at its bottom.

Animals↗
PubMed1980

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. They were also characterized by a more pronounced heterogeneity as far as the values of ts and tG2 are concerned, and, probably, by the formation of an R2-population. Both the index of S-phase (29%) and labelled cell fraction (87%) after 6 injections of 3H-thymidine spaced at six-hour intervals, were lower in adenocarcinomas than in the zone of maximum proliferation in the descending colon (45 and 100%, respectively) and yet higher than the same parameters calculated for the whole population of the intestinal epithelium (17 and 60%, respectively). As far as proliferation parameters go, adenocarcinoma cells highly resemble those of the crypt bottom population in control animals, which was found to consist of several subpopulations with a varying mean duration of the mitotic cycle, and where stem enterocytes are likely to occur. When enterocytes become malignant, disturbances in their differentiation decrease cell shedding into the intestinal lumen and, thus, cause tumours to arise and develop.

Adenocarcinoma↗
PubMed1979

[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.

Animals↗