Genetic predisposition without doubt is one of the risk factors of cancer initiation. It is known that single nucleotide polymorphisms (SNP) of genes that maintain the genome stability, including SNP of DNA repair, may contribute to the initiation of carcinogenesis. Single-nucleotide polymorphisms of genes that support genome stability, including SNP of DNA repair genes, can contribute to cancer initiation. Polymorphism of the excision repair gene OGG1 causes interest of leading scientific groups from various countries. It is assumed that there is relationship between the rs1052133 polymorphism in the gene and predisposition to cancer initiation. The objective of this study was to establish association between rs1052133 polymorphism of base excision repair gene OGG1 and the risk of cancer initiation in people chronically exposed to ionizing radiation. Residents (888 people) of the Techa riverside settlements, chronically exposed to low or medium radiation from the Techa River and the East-Urals Radioactive Trace were included in the study. The study allowed researchers to establish that exposed to chronic radiation people, carriers of the rs1052133*G allele have increased risk of malignant neoplasms initiation: OR=1.38; 95% CI [1.05-1.83], p=0.023. The multifactorial synergistic interactions between the dose to the red bone marrow and the rs1052133 polymorphism of the OGG1 gene was found: Testing Balanced Accuracy (TBA)=0.56; Cross Validation Consistency (CVC)=10/10; p=0.01). The study found that the rs1052133 polymorphism may be considered as genetical marker of risk of cancer initiation in people, chronically exposed to radiation with doses ranged from 0.74 to 3507.07 mGy (average 523.10+/-33.89 mGy). It was found that the presence of the rs1052133*G in combination with radiation exposure can modify the risk of solid cancers initiation, as it is indicated by the synergistic relationship between the SNP and the radiation dose.

In the previous study [1], we showed an increased risk of malignant neoplasms in carriers of the minor allele rs1052133*G of the hOGG1 gene who were affected by chronic radiation exposure at a wide range of doses (up to 3,507 mGy to the red bone marrow) at the Techa River (Southern Urals) contaminated due to the activities of the Mayak Production Association in the 1950s. The objective of the present study was to assess the contribution of radiation factor to the risk of malignant neoplasms development in persons chronically exposed at the Techa River. For this purpose, we analyzed the background level of genetically determined risk in the general population of unexposed people on the basis of meta-analysis of the world literature data on the search for the association of rs1052133 of the hOGG1 gene with the risk of malignant neoplasms development. At the final stage, the results of the meta-analysis were compared with data on exposed people. The study found that unexposed and exposed carriers of the rs1052133*G allele had a comparable increased risk of developing malignant neoplasms, odds ratio 1.20; 95% confidence interval [1.06–1.35], p=0.01 and odds ratio =1.38; 95% confidence interval [1.05–1.83], p=0.023, respectively.

The objective of this work was to study the number of different T-helper subpopulations in peripheral blood as well as the expression of TBX21, RORC, GATA3, NFKB1, MAPK8, and STAT3 genes, responsible for the regulation of T-helper differentiation in persons chronically exposed in utero. The object of the study was peripheral blood cells obtained from 156 people chronically exposed in utero and postnatally in a wide range of doses on the Techa River. The mean cumulative absorbed dose to the red bone marrow in the examined exposed individuals was 496 ± 51.2 mGy (dose range, 73.5–1298 mGy), in the comparison group 1 it was 18.7 ± 1.97 mGy (dose range, 0.78–57 mGy), and in comparison group 2 (exposed only postnatally) it was 571 ± 49.1 mGy (dose range, 86.74–1240 mGy). The subpopulation composition of T-helper cells was analyzed by flow cytometry. The relative mRNA content of TBX21, RORC, GATA3, NFKB1, MAPK8, and STAT3 genes was assessed by RT–PCR. A dose-dependent decrease in the total number of T-helper cells, effector memory T-helper cells, and central memory T-helper cells at a trend level and an increase in the relative number of naive T-helper cells in the peripheral blood of individuals exposed in utero and postnatally were found. An increase in the relative number of type 1 T-helper cells was also revealed in those exposed in utero and postnatally relative to the group of persons exposed only postnatally. These changes did not depend on the cumulative radiation doses. There were no statistically significant changes in the mRNA expression of the studied genes (GATA3, STAT3, TBX21, MAPK8, and RORc). No correlation between the mRNA expression of the studied genes and the relative number of cells in the subpopulations of T-helper types 1, 2, and 17 in the examined individuals was revealed.

Every year, more and more data demonstrate that microRNA expression levels can be changed significantly after acute radiation exposure, and microRNAs themselves play an important role in the cellular response to ionizing radiation. However, regulation of microRNA expression after chronic radiation exposure within the low and middle dose range is poorly studied. In the present study, the expression of mature miR-29a, miR-30c, and miR-150 microRNAs in whole blood from 81 individuals in the long-term period after chronic low dose-rate radiation exposure was analyzed by real-time PCR method. The mean age of the studied people was 72 years, and the accumulated radiation doses in red bone marrow (RBM), thymus, and peripheral lymphoid organs ranged from 2.13 to 1867.55 mGy and from 0.18 to 488.79 mGy, respectively. More than 70 years after the onset of radiation exposure, a statistically significant dose-dependent decrease in miR-30c microRNA expression was found in exposed individuals in RBM, thymus, and peripheral lymphoid organs.

To study the repertoire of the T-cell receptor in chronically exposed persons in the long-term period. The study involved 48 people who were divided into two groups: a group of exposed persons (31 individuals with the mean accumulated dose to red bone marrow (RBM) of 981 ± 130 mGy) and a comparison group (17 individuals, the mean accumulated dose to RBM of 25.3 ± 5.91 mGy). The study groups did not differ significantly in age, gender, and ethnicity. The repertoire of Vβ-segments of the T-cell receptor of the peripheral blood T-lymphocytes of exposed persons was analyzed by flow cytometry method. 24 Vβ-segments of the T-cell receptor were studied. Statistical processing of the obtained data was carried out using the Wilcoxon signed-rank test, and a direct description of Vβ-segment repertoire of the T-cell receptor was performed using the Lorenz curve and the Gini-TCR index. The study revealed a statistically significant increase in the number of Vβ3 and Vβ5.2 T-cell receptor segments in exposed individuals relative to the comparison group (p = 0.03 and p = 0.003, respectively). It was also shown that the distribution of the Vβ-segments of the T-cell receptor was uneven in both study groups. However, there was no significant difference between the repertoires of the T-cell receptor of the studied groups by the Gini-TCR index (p = 0.14).

The efficiency of DNA integrity repair processes after radiation exposure may depend on hereditary variations of repair genes caused by single nucleotide polymorphisms. Disturbances or even failure of repair processes trigger a chain of reactions leading to genome instability and oncogenic transformation of the cell. To investigate the association of single nucleotide polymorphism in genes of nucleotide excision repair (ERCC2 rs13 181, XPC rs2 228 001), AP site repair (APEX rs1 130 409), homologous recombination (XRCC3 rs861 539), single-strand DNA break repair (XRCC1 rs25 487), and double-strand DNA break repair (PARP rs1 136 410, XRCC4 rs2 075 685) with the risk of malignant neoplasm development of various localisations in chronically exposed persons. . The study was conducted in 861 persons who were exposed to chronic low dose rate radiation, 274 of which had malignant neoplasms (MN) of various localisations and 587 made up the comparison group (exposed persons without MN). The mean accumulated dose to red bone marrow (RBM) in the group of persons with MN was 561.65 ± 25.31 mGy, while in the comparison group it was 543.14 ± 36.06 mGy. Genotyping of polymorphic loci rs13181, rs2 228 001, rs1130409, rs861 539, rs25 487, rs1136410, and rs2075685 was performed by real-time PCR. The association of polymorphic loci with the risk of MN development was determined by the odds ratio (OR) and 95

The objective is to conduct a pilot study on the quantity of regulatory T-cells (Treg) in the peripheral blood and to assess transcriptional activity of FOXP3 gene in chronically exposed persons. Materials and methods. The study included 77 participants who were divided into two groups: exposed people-45 individuals, with a mean cumulative dose to red bone marrow (RBM) of 641.21 ± 80.41 mGy, and a comparison group-32 individuals, with a mean cumulative RBM dose of 20.38 ± 2.51 mGy. The study on the assessment of the FOXP3 gene expression was conducted in 298 individuals: the exposed group consisted of 163 individuals with a mean cumulative dose to RBM of 702 ± 43.10 mGy; the comparison group included 135 individuals with a mean cumulative dose to RBM of 17.30 ± 1.40 mGy. The study groups did not differ significantly in age, sex, and ethnicity. Quantitative assessment of regulatory T-cells in the peripheral blood was performed using flow cytometry method by the presence of T-helper markers CD3 and CD4, high expression of marker CD25 and low expression of marker CD127. Thus, the phenotype of regulatory T-lymphocytes was described as CD3+CD4+CD25highCD127low. The relative mRNA content of the FOXP3 gene was assessed by PCR-RT. Results. More than 70 years after the onset of chronic exposure, no statistically significant changes in the pool of regulatory T-cells were detected in the exposed persons: the content of absolute and relative number of Treg did not differ statistically significantly between the studied groups (p = 0.91 and p = 0.29, respectively); no statistically significant relationship between Treg indices and the cumulative doses to RBM and thymus and peripheral lymphoid organs were found. No statistically significant differences in FOXP3 gene mRNA expression were found between exposed individuals and the comparison group. A linear positive dependence of FOXP3 gene mRNA expression on the relative number of regulatory T-cells was shown (p = 0.007).

Hematopoietic stem cell transplantation (HSCT) is a standard method for treating a number of pathologies, primarily blood diseases. Timely restoration of the immune system after HSCT is a critical factor associated with the development of complications such as relapses or secondary tumors and various infections, as well as the graft-versus-host reaction in allogeneic transplantation, which ultimately affects the survival of patients. Introduction into the recipient’s body of immune system cells that are incapable of sensitization by recipient antigens during the period of immune reconstitution can increase the rate of restoration of the immune system, as well as reduce the risk of complications. This review presents the results of studies on cell therapy with various cell subpopulations of both bone marrow and mesenchymal origin during HSCT.

Psoriatic arthritis (PsA) is a chronic immune-mediated inflammatory joint disease, often associated with psoriasis. Interactions between immune cells, mainly T lymphocytes, and cells of the osteoarticular system are central in the pathogenesis of PsA. Th1, Th17 cytokines associated with the development of PsA contribute to an increase in the production of cytokines, chemokines, matrix metalloproteinases, adhesion molecules by immune cells, chondrocytes, fibroblasts, and induction of osteoclasts. That leads to the destruction of cartilage and bone tissue. Among the cytokines potentially involved in the pathogenesis of PsA, IL-7 is of particular interest. IL-7 is a T cell survival factor. However, it can promote the production of IFNγ and TNFα by T cells. IL-7 may indirectly promote osteoclast maturation and cartilage degradation. The aim was to investigate the effect of IL-7 and blockade of the α-chain of the IL-7 receptor (IL-7R) in vitro on the production of IL-5, IL-13, IL-2, IL-6, IL-9 IL-10, IFNγ, TNFα, IL-17A, IL-17F, IL-4, and IL-22 by T cells in norm and PsA.The study included 14 patients with PsA in the acute stage of the disease and 8 healthy individuals. To determine cytokines concentration, multiplex analysis was performed using flow cytometry.It was shown that IL-7 enhances the production of Th1, Th2, Th17, Th22, and Th9 cytokines in both patients with PsA and healthy individuals. The exception was IL-2 for both groups. Under the blockade of IL-7R with monoclonal antibodies, the level of IL-6 increases and production of IFNγ, TNFα, IL-17F, IL-10, IL-5, and IL-9 by donors’ cells and production of IFNγ, TNFα, IL-22, IL-2, IL-4, IL-5, IL-13, and IL-9 by cells from patients with PsA decreases relative to production of cells stimulated with IL-7. In donors, the blockade contributed to a change in the balance of Th1/Th2 cytokines: level of IL-4, IL-13 did not change on the background of a decrease in production of IFNγ, TNFα. In patients with PsA, under blockade of IL-7R the production of IL-10 remained at an increased level and concentration of IFNγ, TNFα and IL-2, which are actively involved in the tissue damage mechanisms, decreased. The obtained data indicate the prospect of using the IL-7R as a target for the treatment of psoriatic diseases.

Background: The use of chitosan-based gels is still limited due to their restricted solubility in acid solutions, where the molecules have a positive charge. The functionalization of chitosan makes it possible to significantly expand the possibilities of using both the polymer itself and hydrogels based on its derivatives. Objective: To evaluate the effect of the conditions for the production of cryo- and hydrogels based on carboxyethylchitosan (CEC) crosslinked with glutaraldehyde on gel swelling and its resistance to degradation depending on pH and cytotoxic effects and to test the hypothesis that the amount of crosslinking agent during synthesis may affect the cytotoxicity of the gel. Methods: Gels’ swelling values and degradation resistance were determined using the gravimetric method. The cytotoxic effect was evaluated during the co-cultivation of gels in the presence of human fibroblasts using light optical microscopy and flow cytometry. Results: All CEC-based cryogels had a higher equilibrium swelling value and degradation time than the CEC hydrogel in the pH range from 4.6 to 8.0. This demonstrates the superiority of cryogels relative to CEC-based hydrogels in terms of swelling potential and degradation resistance, while an increase in the number of crosslinks with glutaraldehyde contributes to longer swelling of the cryogel. The positive control (intact fibroblasts) and all gel samples were statistically identical in the number of viable cells. On the third day, the viability of the fibroblast cells was consistently high (above 95%) and did not differ between all tested CEC-based gels. And in general, the cell morphology analysis results corresponded with the results obtained in the flow cytometry-based cytotoxicity test. We also did not find proof in our experiment to support our hypothesis that the amount of crosslinking agent during synthesis may affect the cytotoxicity of the material.

BACKGROUND: The period of intrauterine development is highly susceptible to the effects of ionizing radiation. While the consequences of radiation exposure during pregnancy are not yet fully understood, it is believed that individuals exposed to ionizing radiation in utero are at a greater risk of long-term health consequences. AIM: To analyze the expression of mRNA of cell cycle genes (TP53, MDM2, CDKN1A, ATM) in individuals exposed during intrauterine development to chronic radiation exposure after the Techa River accident. MATERIAL AND METHODS: The study was conducted over 60–70 years after the onset of chronic radiation exposure in a group of 170 individuals. Among them, 54 individuals were exposed to radiation during both prenatal and postnatal periods of development, while 80 individuals were exposed to chronic radiation after birth. The comparison group consisted of 36 individuals living in similar socio-economic conditions, with a lifetime cumulative dose of red bone marrow radiation not exceeding 70 mGy. RESULTS: Individuals residing in coastal villages along the Techa River, who were exposed to radiation during both the prenatal and postnatal stages of development, experience a reduction in the relative mRNA content of the MDM2 and CDKN1A genes compared to the control group and individuals who were exposed to chronic radiation after birth. The results of the correlation analysis indicate that there is no association between changes in mRNA expression of the studied genes and the accumulated absorbed dose of intrauterine and postnatal exposure of red bone marrow. CONCLUSION: The reduced transcriptional activity of the MDM2 and CDKN1A genes in individuals exposed to chronic radiation in utero may play a role in the development of long-term effects of radiation exposure in humans.

We studied the apoptotic death of peripheral blood lymphocytes in individuals chronically exposed to radiation with a history of obligate forms of precancerous conditions. The study included 242 subjects chronically exposed to low-intensity radiation in the range of low and medium doses (mean dose of irradiation of the red bone marrow 555±39 mGy). Of these, 121 subjects had obligate forms of precancerous conditions. In irradiated individuals with obligate forms of precancers, a statistically significant increase in the frequency of apoptosis of peripheral blood lymphocytes at an early and late stages was revealed. Correlation analysis revealed no dependence of the apoptotic death of peripheral blood lymphocytes on the dose of red bone marrow irradiation.

In the context of additional radiation exposure, single nucleotide polymorphisms in the genes encoding the antioxidant system enzymes can contribute to the oxidative stress enhancement, damage to DNA, and therefore lead to the increase in the risk of malignant neoplasm (MN) development. The study was aimed to determine the association of the СYBA (rs4673), GPX1 (rs1050450), MPO (rs2333227), CAT (rs7943316), SOD2 (rs4880) polymorphic loci with the risk of MN development in individuals affected by low dose rate chronic radiation exposure considering intergenic interactions and the radiation dose. Two groups of individuals were included in the study: exposed individuals with no MNs — 384 people with the mean accumulated dose to the red bone marrow (RBM) of 796.95 ± 35.97 mGy; exposed individuals with the history of MNs — 227 people with the mean accumulated dose to RBM of 520.06 ± 38.72 mGy. Amplification of the rs4880, rs2333227, rs7943316, rs4673, rs1050450 polymorphic loci was performed with real time PCR. Compliance with the Hardy–Weinberg equilibrium was reported for all gene polymorphisms. It has been found that the rs4880*С (SOD2) and rs1050450*Т (GPX1) alleles are associated with the risk of MN development in accordance with the dominant (OR = 1.49 (1.02–2.18), р = 0.04) and recessive (OR = 2.00 (1.11–3.62), р = 0.02) inheritance modes, respectively. An interfactor interaction model with the 100% reproducibility and 66% accuracy (р = 0.001) has been obtained that includes the SOD2 (rs4880), СYBA (rs4673) polymorphisms and the factor of accumulated dose to RBM. Thus, polymorphic loci of the genes regulating the oxidative status of the cells are associated with the increased risk of MN development in individuals, who have experienced chronic radiation exposure with predominant exposure of RBM.

The objective of this work was to study the expression of the TBX21, RORC, GATA3, NFKB1, MAPK8, and STAT3 genes responsible for the regulation of the differentiation of various T-helper subpopulations in individuals chronically exposed to radiation. The object of the study was peripheral blood cells obtained from 120 persons chronically exposed to radiation in a wide range of doses on the Techa River. The mean cumulative absorbed dose to red bone marrow in the examined exposed individuals was 742.7 ± 78.6 mGy (dose range, 73.5-3516.1 mGy); in the comparison group, 17.4 ± 2.2 mGy (dose range, 0.0-55.5 mGy). The subpopulation composition of T-helpers (Th1, Th2, and Th17) was analyzed by flow cytofluorometry. The relative mRNA content of the TBX21, RORC, GATA3, NFKB1, MAPK8, and STAT3 genes was estimated by real-time PCR. The study made it possible to note a decrease in the relative number of T-helpers 2 in the populations of T-helpers of the central memory in the group of chronically exposed persons compared to the comparison group. In the population of T-helpers of the central memory, a statistically significant increase in the relative number of T-helpers 1 was shown, depending on the accumulated absorbed dose to red bone marrow. No changes in mRNA expression of the studied genes were observed. The analysis of the correlation between the expression of GATA3, MAPK8, STAT3, RORC, and TBX21 mRNA and the relative number of cells in subpopulations of T-helper types 1, 2, and 17 in the examined people did not reveal statistically significant patterns.

The gut is inhabited by a trillion bacteria that produce up to 60% of the host’s metabolites. The gut microbiome plays an important role in regulating host immune function. A lot of research concerned the effect of probiotic on the pathologies associated not only with dysbiosis and metabolic disorders, but there is breakthrough in the treatment of inflammation, oncology and neurodegenerative disorders. Animals with mutation of the genes leading to pathology used to assay probiotic effect. To understand direct action of probiotics, cells derived from control mice or cell culture of tumor genesis in vitro studies are used. However, there is little research of the probiotic effect on cells derived from mice with pathology. In this study, we assessed the phenotypes of dendric cells derived from Muc2 -/- mice with chronic inflammation and assessed the effect of L. johnsonii on the dendric cells. It is known that the key features of IBD models are thinning of mucin layer and changes in the intestinal microbiome. We compared the efficiency of maturation and activation of dendric cells derived from the bone marrow of Muc2 -/- mice and dendric cells obtained from healthy C57BL/6 mice free from specific species pathogens. We evaluated the expression of co-stimulatory molecules, the proliferative index, and the ability to trigger the T regulatory response of dendric cells, which were stimulated with the probiotic L. johnsonii . Markers of dendritic and T cells were assessed by flow cytometry using antibodies to extra- and intracellular proteins. The proliferative activity of splenocytes was assessed using the WST test. It was shown that dendric cells derived from the Muc2 -/- had an immature phenotype. Dendric cells of Muc2 -/- mice could not effectively stimulate the proliferation of allogeneic and syngeneic T cells. L. johnsonii was able not only to stimulate the maturation of dendric cells derived from Muc2 -/- mice, but also to increase the expression of FoxP3 on CD25 + T cell that were co-cultured with DCs. Thus, we believe that this probiotic bacterium can reduce signs of inflammation and reduce pathological processes in animals of an experimental model of IBD in vivo .

Psoriatic arthritis (PsA) is a chronic immune-mediated inflammatory disease of the joints, spine, and entheses that can occur in patients with psoriasis. The prevalence of psoriatic arthritis is high in Russia, in recent years there has been an increase in its incidence rates. The pathogenesis of PsA is based on the activation of Th1, Th17 cells. Pro-inflammatory cytokines produced by the cells are involved in the cascade of reactions leading to the joint deformity and bone destruction. For some autoimmune diseases associated with the Th1/Th17 response, IL-7 has been found to be involved in pathogenetic mechanisms. At the same time, IL-7 is assumed to support autoreactive T lymphocytes. Effect of the cytokine on cells is provided by the binding to a specific receptor thus causing a signal transmission into the cell and inducing the processes of differentiation, proliferation, and production of cytokines. In animal models of autoimmune diseases, usage of blocking antibodies to α-chain of the IL-7 receptor (IL-7R) was shown to cause reduced inflammation in target tissues and decreased number of infiltrating T lymphocytes. Therefore, the aim of this work was to investigate the in vitro effects of IL-7 and blockade of the α-chain of the IL-7 receptor on the contents of Th1, Th17 lymphocytes and expression of IL-7 receptor subunits on these cells in normal subjects and in psoriatic arthritis. The study included nine patients with PsA in the stage of exacerbation of the underlying disease (mean age 44±6.5 years) and 6 healthy individuals (mean age 45±2.7 years). The in vitro effects of IL-7 and specific blocking monoclonal antibodies (aCD127) was evaluated in cultures of mononuclear cells from peripheral blood. Flow cytometry was used to determine the expression of IL-7 receptor subunits (CD127, CD132) and to assess cell phenotypes in peripheral blood and cultured cells. We have shown for the first time that patients with PsA have an increased number of CD127+CD132- and CD127+CD132+ cells among Th17 lymphocytes, as well as CD127+CD132-, CD127+CD132+ and CD127-CD132+ cells among Th1 lymphocytes, which suggests participation of IL-7 in maintaining these cell populations. Upon the in vitro supplement of IL-7, an increase in the Th1 cell contents and a decreased number of Th17 cells were observed, both in donors and PsA patients, and the opposite effect was observed under the conditions of IL-7R of blockade. Under the influence of IL-7, as well as with blocking antibodies, there was a significant decrease in CD127 expression on Th1, Th17 lymphocytes. However, a decrease in the number of CD127-132+ among Th1, Th17 lymphocytes occurred only following blockade with antibodies. That is, despite redistribution of Th1 and Th17 lymphocytes in culture, the cells of these populations were not activated under the IL-7 receptor blockade. The obtained data may serve as a basis for choosing the IL-7 receptor as a target in the development of targeted drugs for the treatment of PsA.

The oral delivery of bacteria in the human intestine is of great interest because of its potential to correct the gut microbiota and treat inflammatory bowel diseases. The aim of this study was to evaluate sodium N-(2-sulfonatoethyl)chitosan gel cross-linked with glutaraldehyde as a delivery carrier for probiotic bacteria to the gut using in vitro and in vivo experiments. The bacterial test strain was B. subtilis 20. The cytotoxicity of the gel was evaluated via cell culture using flow cytometry and light microscopy. The gel as a delivery system was assessed by the dye release in medium with different pH levels in vitro, and by bacterial titer monitoring in mouse feces using the microbiology method in vivo. Results of an in vitro experiment showed that tested gel has no cytotoxicity. The use of gel as a carrier for bacterial delivery into the intestine was more effective than oral gavage of bacterial suspension. Therefore, gel delivery of bacteria decreased the titer level by up to two times. However, a gavage of bacterial suspension decreased the titer level by over 200 times. Tested gel has the potential to be a carrier for the safe delivery of bacteria to the intestine through the stomach, reducing the rate of the elimination of probiotic bacteria from the intestine.

To date, few publications describe CEC's properties and possible applications-thus, further evaluation of these properties is a point of interest. The present in vitro model study aimed to evaluate a carboxyethylchitosan (CEC) gel with a degree of substitution of 1, cross-linked with glutaraldehyde at a polymer:aldehyde molar ratio of 10:1, as a potential carrier for delivering bacteriophages to various pH-fixed media (acidic, alkaline), and including gastrointestinal tract (GIT) variable medium. A quantitative analysis of bacteriophages released from the gel was performed using photon correlation spectrophotometry, and phage activity after emission into medium was evaluated using the spot test. The results showed that the CEC gel's maximum swelling ratios were at a nearly neutral alkaline pH. Increasing temperature enhances the swelling ratio of the gel independent from pH, up to 1127% at 37 °C and alkaline pH. The UV and photon correlation spectrophotometry showed equal gel release kinetics in both fixed media with acidic (pH = 2.2) and alkaline (pH = 7.4) pH environments at 37 °C, with the maximum release within two hours. However, phage lytic activity in the spot test during this simulation was absent. At the same time, we obtained an opaque phage lytic activity in the alkaline pH-fixed medium for at least three hours. Phages released from the tested CEC gel in different pHs suggest that this gel could be used for applications that require fast release at the treatment site both in acidic and alkaline pH. Such treatment sites could be a wound or even soil with mild acidic or alkaline pH. However, such CEC gel is not suitable as a delivery system to the GIT because of possible transported acid-sensitive agent (such as phages) release and destruction already in the stomach.

An estimate of relative expression of mature microRNAs assessed in peripheral blood cells in persons chronically exposed to low-dose radiation in the long-term period was performed. The study included people exposed in the 1950s on the Techa River (Southern Urals, Russia). The cumulative red bone marrow doses (RBM) of the persons in the main study group (33 persons) ranged from 77.7 to 2869.8 mGy (mean value of 698.5 mGy). The comparison group consisted of 30 people with RBM dose not exceeding 70 mGy over their lifetime. Reverse transcription of RNA samples was performed using specific stem-loop primers (“stem-loop”). Changes in the relative content of microRNAs were assessed by real-time PCR on the CFX96 detection system (BioRad, United States). Statistical analysis of the results was performed using the Mann–Whitney U criterion. A significant increase in hsa-miR-125b, hsa-miR-181a, and hsa-miR-16-5p content was detected in exposed people after 60 years, and their expression was found to depend on the RBM dose.

Arthropathy is one of the most prevalent diseases, which are based on the destruction and remodeling of cartilage and bone tissue. The inflammation that precedes destruction can be caused by mechanical stress on the joints, or by autoimmune reactions. Recently, IL-7 is considered as one of the key cytokines that promote the production of matrix metalloproteinases, catabolic enzymes, T cell-mediated activation of monocytes, and maturation of osteoclasts. The soluble form of the IL-7 receptor can help prolong the lifespan of IL-7 and thereby it ensures the bioavailability of the cytokine and mediates effect of IL-7 on cells. The aim of this study was to determine the soluble form of the IL-7 receptor (sIL-7R) in the blood plasma of patients with rheumatoid arthritis (RA), osteoarthritis (OA), psoriatic arthritis (PsA) and psoriasis vulgaris (PS), as well as healthy individuals. The RA patients included in the study had moderate to high disease activity according to the DAS28 index. Patients with PsA predominantly had moderate and low disease activity (DAS28) and were characterized by mild to moderate disease severity (PASI). In accordance with the PASI index, patients with PS with mild and severe severity of the disease were included in the study. All patients with OA had a metabolic phenotype that is accompanied by an elevated body mass index.sIL-7R was determined in blood plasma by enzyme-linked immunosorbent assay. It was found that in patients with arthropathy, the level of soluble form of IL-7 was increased relative to healthy individuals, with the exception of the group of patients with PsA. Also, a high concentration of sIL-7R was observed in patients with PS. Analyzing the clinical characteristics of the patients, we found that sIL-7R levels were elevated in RA and PsA patients with high disease activity by DAS28. In addition, positive correlations were found between the concentration of sIL-7R and DAS28 in RA and PsA. In patients with PsA with moderate severity of the disease (PASI), the concentration of sIL-7R was also increased relative to donor's values. On the contrary, in patients with PS, a high level of sIL-7R was noted regardless of the severity of the disease. In patients with OA, no relationship was found between sIL-7R levels and clinical parameters.Thus, an elevated level of sIL-7R in patients with arthropathy may indicate the involvement of IL-7 and its receptor system in the pathogenesis of joint diseases. The IL-7 receptor may become a promising target both in the treatment of joint diseases and other autoimmune diseases, including psoriasis.