Hyperbaric oxygen and photodynamic therapy in tumour-bearing nude mice.
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Animals↗
Biomedical subjects
J Dolezal
Publications and source records attributed to J Dolezal.
Model-based analysis of CD4+ lymphocyte dynamics in HIV-infected individuals. II. Evaluation of the model based on clinical observations.
The recently developed mathematical model of CD4+ lymphocyte depletion in HIV-infected individuals is evaluated using a comparison with available clinical data. The data used for such an evaluation are to be extrapolated from the published clinical observations as these data sets are not homogeneous covering only parts of HIV infection duration. An additional complication is due to the uncertainty of exact infection onset. Based on these considerations, several different reference data sets are generated from the available clinical data and the range of applicability of the mathematical model and its modifications is then investigated. As a result of such quantitative confrontation, it can be concluded that the appropriate setting of cell interaction parameters in the model can result in a fairly good coincidence of the simulated HIV infection dynamics with reference data sets. Perspectives and limitations of such an approach are also discussed.
CD4-Positive T-Lymphocytes↗
Influence of the cell interaction parameters on the simulated CD4+ lymphocyte depletion in HIV infection.
The previously suggested mathematical models of CD4+ lymphocyte depletion in HIV-infected individuals are analysed from the point of view of fundamental cell interaction mechanisms involved. Under the assumption of growth restriction of the HIV by cytotoxic lymphocytes, the intensity of the feedback mechanism increasing the influx of immature CD4+ lymphocytes and the intensity of the helper effect of CD4+ lymphocytes during the maturation of cytotoxic cells are evaluated and compared in a wide range of the respective model parameters. In this respect also the role of the proliferation rate of these cytotoxic lymphocytes under antigenic stimulation by HIV products is discussed. In addition, an alternative elimination mechanism of CD4+ lymphocytes is investigated, which assumes their destruction by cytotoxic lymphocytes. It is concluded that any of the considered cases of the influx amplification parameter, helper effect intensity parameter, and CD4+ lymphocyte elimination mechanism can be used for a qualitative adjustment of the model to clinical data.
CD4-Positive T-Lymphocytes↗
Model-based analysis of CD4+ lymphocyte dynamics in HIV infected individuals.
The previously suggested mathematical model of CD4+ lymphocyte depletion in HIV-infected individuals is analyzed and further developed. The model assumes that CD4+ lymphocyte depletion is caused by HIV products. Fairly good simulation of CD4+ lymphocyte dynamics is obtained, when limitation of HIV growth by specific cytotoxic T cells is included in the model. As it is probable that the substantial decrease of CD4+ lymphocytes, this type of influx control mechanism is also included in the model. It is shown that the simulated CD4+ lymphocyte dynamics agree with the observed data, analogously as in the earlier considered case of the constant influx. Moreover, the depleting effect of HIV products on mature and/or immature CD4+ lymphocytes is analyzed by the model. Also, another modification of the model assuming that CD4+ lymphocyte depletion is due to their destruction by cytotoxic T cells specific for HIV antigens, gives simulation results comparable to those obtained by the original version of the model, where the mechanism of the depletion is not specified.
CD4-Positive T-Lymphocytes↗
Environmental risk factors in Parkinson's disease.
To investigate possible risk factors for Parkinson's disease (PD) we conducted a case-control study of 150 PD patients and 150 age- and sex-matched controls. We interviewed and examined all 300 subjects. We collected demographic data including lifetime histories of places of residence, source of drinking water, and occupations such as farming. Subjects completed a detailed questionnaire regarding herbicide/pesticide exposure. Rural living and drinking well water were significantly increased in the PD patients. This was observed regardless of age at disease onset. Drinking well water was dependent on rural living. There were no significant differences between cases and controls for farming or any measure of exposure to herbicides or pesticides. These data provide further evidence that an environmental toxin could be involved in the etiology of PD.
Aged↗
Mathematical model of CD4+ lymphocyte depletion in HIV infection.
The CD4+ lymphocyte depletion in human immunodeficiency virus (HIV)-infected persons seems to be affected by HIV products. As the dynamics of the concentration of HIV products is reciprocal to that of non-replicating antigen used for induction of tolerance, the mathematical model of immunological tolerance can be used to describe the dynamics of CD4+ lymphocyte depletion. To stimulate the clinically observed dynamics, it is necessary to include the limitation of HIV growth by the corresponding cytotoxic T cells and their dependence on the helper effect of CD4+ lymphocytes. Simulation analysis suggests that qualitatively similar results are obtained if immature, mature, or both categories of CD4+ lymphocytes considered in the model are depleted by the HIV products.
Acquired Immunodeficiency Syndrome↗
Recovery from polyclonal tolerance: simulation analysis.
Mathematical model of immunological tolerance was applied to polyclonal B cell tolerance induced in mice by treatment with bacterial lipopolysaccharide (LPS) followed by the application of cyclophosphamide (CY). Satisfactory simulation results were obtained with the life-span of lymphocytes shorter than the experimentally observed one. It could be assumed that the massive decrease of lymphocyte population in polyclonal tolerance would elicit a compensatory reaction. Therefore it was postulated that some kind of feedback mechanism increased the influx of B lymphocytes. Having this factor included in the model, satisfactory agreement of the simulation results with experimental data was obtained for experimentally determined life-span of B cells.
Animals↗
Application of mathematical model of immunological tolerance to HIV infection.
Our experimental model of immunological tolerance to non-reproducing antigens is based on the assumption that tolerance is caused by elimination or irreversible inactivation of lymphocytes reacting specifically with the tolerance inducing antigen, and that recovery from tolerance is due to the spontaneous maturation from the stem cells of new lymphocytes reacting with the tolerated antigen. The recovery starts, when the antigen is eliminated from the organism and does not induce tolerance in newly arising lymphocytes any more. Here we report the application of this model to the depletion of CD4+ lymphocytes in persons infected with HIV. This depletion seems to be effected either directly or indirectly by HIV products. Therefore, the dynamics of this depletion can be described by the equations characterizing the dynamics of lymphocytes exposed to tolerance inducing antigen, when HIV products are substituted for antigen. In contrast to non-replicating antigens, the concentration of HIV products increases, as the infection progresses. In consequence, the CD4+ lymphocyte depletion increases with time and its dynamics are reciprocal to those of tolerance to non-reproducing antigens, which decrease with time.
Acquired Immunodeficiency Syndrome↗
A contribution to mathematical modelling of immunological tolerance.
The original simple mathematical model describing the kinetics of B cell tolerance was extended by the inclusion of Th cell tolerance. It anticipates the existence of two compartments of B and Th cells reactive to the antigen--the immature cells and the mature ones. It is assumed that tolerance is induced by irreversible inactivation of the antigen-reactive cells and the escape from tolerance is due to their differentiation from the precursors. There is also considered the situation, where two categories of Th cells cooperate with the same B cells. Besides that, suppressive activity on Th cells is included in the model. The simulated values are compared with experimental data.
Animals↗
Simulation analysis of the mechanism of escape from immunoglobulin suppression.
The mathematical model of B cell tolerance was applied to idiotype and isotype suppression of short duration induced in mice by neonatal application of monoclonal antibodies specific for the respective immunoglobulin determinants. Suppressor cells play an important role in chronic idiotype or isotype suppression, but these suppressions of short duration seem to be caused by direct elimination of B cells by the injected antibodies. The recovery from suppression of short duration starts, when the injected antibody is eliminated from the organism and is caused by differentiation from stem cells of new B lymphocytes possessing the respective immunoglobulin markers. This mechanism is analogous to that assumed for immunological tolerance in the mathematical model except that the injected monoclonal antibody plays the role of tolerance-inducing antigen. However, satisfactory agreement of simulated values with the experimental ones could not be obtained, if experimentally observed elimination rate of the injected antibody was used for calculations. A better fit was obtained with elimination rate values decreasing with age which do not correspond to the actual ones of the injected antibody. At present, we do not know which mechanism is described by these "virtual" elimination rates.
Animals↗
Implications of a mathematical model for the role of lymphocytes with different lifespans in the recovery from tolerance.
An extension of the mathematical model of immunological tolerance including two categories of B and T helper cells, each having a different lifespan, is presented. The simulated recovery from tolerance is compared with experimental data on B and T helper cell tolerance to human gamma globulin (HGG) induced in adult mice. The performed simulation runs suggest the conclusion that in this case it seems impossible to incorporate a high ratio of both, long-lived B cells and/or short-lived T helper cells, if good agreement with the available experimental data should be preserved.
Animals↗
A new mathematical model of proliferation control during immune response.
A considerable proliferation of participating cells is a characteristic feature of the immune response. This proliferation may be controlled by Interleukin 2. Assumptions on the course of the immune response under such a control are formulated, and a new mathematical model of the immune response involving regulation of the proliferation of appropriate cells is constructed.
Antibody Formation↗
Compartmental model of immunological tolerance to HSA in chickens [proceedings].
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Animals↗
[Professional training of surgical assistants].
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Czechoslovakia↗
Physiological characteristics of chemostatically grown Citrobacter freundii as a function of the specific growth rate and type of nutrient limitation.
Citrobacter freundii was grown aerobically in a chemostat on a mineral medium with galactose or glucose as carbon and energy sources under limitation by carbon or nitrogen source respectively. At various specific growth rates ranging from 7 to 95% mumax the culture in steady state was analysed and growth yield, specific metabolic rate of substrate utilization, intracellular concentration of pyruvate, ATP, ADP, AMP and energy charge were determined and plotted as functions of dilution rate. In all four types of experiments the physiological state of cells remained practically independent of dilution rate up to D=0.6 mumax, and at a given specific growth rate nearly independent on mumax and type of limitation. At approximately D=0.6 mumax, which is close to the maximum output dilution rate Dm, the physiological state of the cells changed: growth yields decreased and intr cellular pyruvate and adenylates concentrations increased. Consequently, in a given medium two dilution rates exist at which growth rate dx/dt is the same but the physiology of the population is quite different.
Adenosine Diphosphate↗
[Sick call].
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Physician-Patient Relations↗
[Is every beginning difficult? Problems of young nurses].
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Nurses↗