The role of subcutaneous adipose tissue in psoriasis.

It is widely accepted that obesity is a systemic comorbidity factor in psoriasis. At the same time, there is rapidly growing evidence that the adipose tissue is not only systemically but also locally involved in the pathophysiology of psoriasis and in response to successful anti-psoriatic treatment.

Description of radiation- and ultrasound-induced cell death by a stochastic process.

Cell survival is a stochastic process with the stochastic component being strongly dependent on the irradiation conditions. This process is described by a stochastic model which allows differentiation between the deterministic and stochastic components of survival. The proposed model is tested for four irradiation experiments (2 with ionizing radiation and 2 with ultrasound) and very good agreement with experimental results is demonstrated. It identifies the higher stochasticity of the cell survival for the temporally varying radiation fields and provides the possibility to compare the stochasticity of survival in different radiation fields.

Hits to bone cell nuclei from nonuniform radioactive labels.

The stochastic aspects of alpha-particle traversals through nuclei of bone-lining cells from nonuniform radioactive labels are worked out. Both the residence time of the target and the hit rate are considered random variables. It is shown that with any type of bone remodeling the fraction of cells not hit increases with increasing nonuniformity of the label concentration. Thus, a completely uniform concentration represents the most dangerous situation. A possible negative correlation between residence times and hit rates, observed in some experiments, tends to decrease the probability of alpha-particle hits. As a practical application, the theory is applied to the International Commission on Radiological Protection model of the distribution of 239Pu in the human body. In the case of 50 years of chronic ingestion of 1 annual limit of intake (ALI) per year for class W and chronic inhalation of 1 ALI/year for class Y compounds, more than 19.4 and 8.5% of the nuclei of bone-lining cells are traversed by at least one alpha-particle, respectively.

Stochastic resonance as a possible mechanism of amplification of weak electric signals in living cells.

The most important but still unresolved problem in bioelectromagnetics is the interaction of weak electromagnetic fields (EMFs) with living cells. Thermal and other types of noise pose restrictions in cell detection of weak signals. As a consequence, some extant experimental results that indicate low-intensity field effects cannot be accounted for, and this renders the results themselves questionable. One way out of this dead end is to search for possible mechanisms of signal amplification. In this paper, we discuss a general mechanism in which a weak signal is amplified by system noise itself. This mechanism was discovered several years ago in physics and is known, in its simplest form, as a stochastic resonance. It was shown that signal amplification may exceed a factor of 1000, which renders existing estimations of EMF thresholds highly speculative. The applicability of the stochastic resonance concept to cells is discussed particularly with respect to the possible role of the cell membrane in the amplification process.

Statistics of hits to bone cell nuclei.

The statistics of hits to the nuclei of bone cells irradiated from alpha sources labeling bone tissue is described. It is shown that the law of remodeling of a bone structural unit (BSU), which describes the distribution of quiescence periods of this unit, affects the statistics of hits. It the irradiation of bone cells occurs during the whole cell cycle, the mean number of hits is independent of the law of remodeling. In this case the variance of hits has the minimum value for constant quiescence periods of BSUs (deterministic remodeling) and the maximum value for exponentially distributed quiescence periods (random remodeling). For the first generation of bone cells, i.e. for the cells which existed at the moment of the uptake of the nuclide, the mean number of hits depends on the law of remodeling. For random remodeling the mean number is equal to the mean value for the complete remodeling cycle. For deterministic remodeling the mean is only half this value. For the first generation of bone cells, changing the law of remodeling from random to deterministic increases the probability of no hits to the nuclei of bone cells. For the same mean value of hits, the difference does not exceed 13.3% of the total number of cells. For the subsequent generations of bone cells, such a change of the law of remodeling decreases the probability of no hits by 20.4%.

Hit rates and radiation doses to nuclei of bone lining cells from alpha-particle-emitting radionuclides.

Factors relating the local concentration of a bone-seeking alpha-particle emitter to the mean hit rate have been determined for nuclei of bone lining cells using a Monte Carlo procedure. Cell nuclei were approximated by oblate spheroids with dimensions and location taken from a previous histomorphometric study. The Monte Carlo simulation is applicable for planar and diffuse labels at plane or cylindrical bone surfaces. Additionally, the mean nuclear dose per hit, the dose mean per hit, the mean track segment length and its second moment, the percentage of stoppers, and the frequency distribution of the dose have been determined. Some basic features of the hit statistics for bone lining cells have been outlined, and the consequences of existing standards of radiation protection with regard to the hit frequency to cell nuclei are discussed.

Modeling of the stochastic dynamics of radiation cell death: general approaches and some applications.

A description of the stochastic dynamics of radiation cell death based on the first-passage model is given. Both quasistochastic and stochastic methods of description are considered. Distributions of the time to cell death for stable and unstable populations are obtained. These results are used to analyze the dynamics of interphase death of thymocytes and bone marrow cells.

Description of radiation-induced cell death by a stochastic differential equation.

An attempt to describe the dose dependence of cell inactivation by a stochastic differential equation is made. For this, a stochastic variable in dose radiosensitivity is introduced. Some solutions of the stochastic equation are obtained and and analyzed. How to obtain the value of the noise intensity of radiosensitivity from the experimental data is shown. Comparison of the theory with experimental data gives good results.

Dose-effect relations for stochastic rates of injury formation in cells.

The dose dependencies of lesion formation and cell survival are obtained for the imparting energy stochastic in time. It is shown that for the second-order dependence of the number of lesions on the radiation field one obtains the linear-quadratic dose dependence in the high dose range. The appearance of the linear component is related to the fluctuations and correlations of the rate of imparted energy. Expressions are obtained for cell survival in the one-target model for pulsed and prolonged irradiations.

[Dose-effect curves in stochastic radiation intensity]. / Krivye doza--éffekt pri stokhasticheskoi intensivnosti izlucheniia.

Dose-response curves of the lesions yield and cell survival rate are obtained for radiation intensity stochastic in time. It was shown that, by analogy with the microdosimetric description, the quadratic dependence, that presents the lesions yield as a function of radiation intensity within the high dose range, is to produce a linear-quadratic dose response. The appearance of a linear component is conditioned by the correlativity of radiation. The asymptotic values are obtained for a single-hit scheme survival rate in the cases of prolonged and pulse irradiation.

[The survival rate of irradiated cells as a solution of a stochastic differential equation. A general description]. / Vyzhivaemost' obluchennykh kletok kak reshenie stokhasticheskogo differentsial'nogo uravneniia. Obshchee opisanie.

The survival rate function is described as a solution of some stochastic differential equation. Two main reasons for the formation of dispersion of irradiated cell survival were analysed: accidental changes in reactivity of individual cells during irradiation and differences in reactivity of individual cells within the exposed ensemble. It was shown that in both cases dose response of the survival dispersion was different.

[Dose-effect correlations in a stochastic function of cell reactivity]. / Sootnosheniia doza-éffekt pri stokhasticheskoi funktsii reaktivnosti kletok.

A random reactivity function involving a correlation between "refusal" probabilities in cells irradiated with various doses was estimated. The dose-effect curves were obtained for this reactivity function and their behaviour in the simplest correlation functions was analyzed.

[A model of the stochastic dynamics of interphase lymphocyte death]. / Model' stokhasticheskoi dinamiki interfaznoi gibeli limfotsitov.

Dynamics of interphase peripheral blood lymphocyte death is studied in terms of a general model based on a random damage distribution among cells and stochastic time of their death. Some particular cases of this model are analysed. Possible causes of shaping "biphase" dose-dependence curves for lymphoid cell survival after irradiation are discussed.

[One variational task of microdosimetry]. / Ob odnoi variatsionnoi zadache mikrodozimetrii.

A basic task of dosimetry, that is, the determination of the frequency distribution of specific energy as a function of radiation dose, has been formulated variationally. The optimal, by entropy, distribution has been found. The obtained ratios are used in describing the radiobiological effects with satiation.

[Accounting for recovery processes in the description of interphase cell death]. / Uchet protsessov vosstanovleniia pri opisanii interfaznoi gibeli kletok.

A phenomenological scheme is proposed to describe dose- and time-dependences of the interphase cell death in terms of a continual model of radiation injury. Different regularities of the postirradiation recovery of cells are discussed. The results obtained are in agreement with the experimental data.

[Generalization of microdosimetric correlations for the non-Poisson random process]. / Obobshchenie nekotorykh mikrodozimetricheskikh sootnoshenii na sluchai nepuassonovskogo sluchainogo protsessa.

The relationship between a radiation dose and moments of density of sensitive microvolumes distribution by the value of the absorbed specific energy was found for a random non-Poisson's distribution of the number of particle passages through a cell microvolume. A deviation from the Poisson's distribution was shown to cause a substantial modification of the microdosimetric results.