We performed a search for nanoantibodies that specifically interact with the receptor-binding domain (RBD) of the SARS-CoV-2 surface protein. The specificity of single-domain antibodies from the blood sera of a llama immunized with RBD of SARS-CoV-2 surface protein S (variant B.1.1.7 (Alpha)) was analyzed by ELISA. Recombinant trimers of the SARS-CoV-2 spike protein were used as antigens. In this work, a set of single-domain antibodies was obtained that specifically bind to the RBD of the SARS-CoV-2 virus.

The late stage of the COVID-19 pandemic is marked by the appearance of mutant variants of SARS-CoV-2 that can escape the immunity against the Wuhan virus. In this work, we report on the development of a panel of antiviral agents — single-domain antibodies that recognize independent epitopes of the SARS-CoV-2 S protein. Four antibodies from this panel neutralize a wide range of virus variants, including the most common ones at present: XBB.1.5 and XBB.1.16.

A method for producing elemental boron nanoparticles with a size of less than 100 nm by ultrasonic dispersion in a liquid medium and subsequent cascade fractionation is described. The resulting boron nanoparticles were used as a target for boron neutron capture therapy (BNCT). According to the results of an experimental preclinical study of BNCT with the synthesized boron nanoparticles, neutron irradiation for 1 h of T98G human glioma cells pre-incubated in a medium with boron nanoparticles (10, 20, and 40 ppm in terms of boron-10 isotope) leads to a significant suppression of cell viability.

Specific design features and main characteristics of a compact accelerator-based epithermal neutron source for boron neutron capture therapy are described. High quality of the neutron flux generated by the accelerator-based source has been experimentally confirmed. The opportunities for medical use of the accelerator-based epithermal neutron source in oncological centers for boron neutron capture therapy are assessed.

Boron-neutron capture therapy is a unique form of adjuvant cancer therapy for various malignancies including primary malignant brain tumors, and especially glioblastoma, characterized by the fastest and most aggressive type of growth. The main advantage of boron-neutron capture therapy is the selective destruction of tumor cells without harming normal tissues. Clinical trials have shown that boron-neutron capture therapy is a promising treatment method of various malignancies.The use of nuclear reactors in therapy is unfeasible from a safety standpoint. Therefore, relatively safe accelerator- based epithermal neutron sources for boron-neutron capture therapy are in worldwide development. The accelerator-based epithermal neutron source constructed in Budker Institute of Nuclear Physics in Novosibirsk (Russia) offers a unique opportunity to test this new therapy method.Joint teams of physicists, biologists and medical doctors carry outmultiple experiments to assess the efficacy of the accelerator-based epithermal neutron source to be further used in preclinical and clinical trials, the results of which are presented in this article.To determine optimal irradiation conditions and evaluate the effect of boron-neutron capture therapy on tumor cell survival, experiments were conducted on human glioma cell line (U251MG). The cells were incubated in medium with boronophenylalanine and irradiated by epithermal neutron flux. Boron-negative cells, irradiated by neutrons, as well as those cells, which weren't irradiated by neutrons were used as controls. The colony forming assay showed that generated neutron flux doesn't affect cell viability without boron and is effective in treating tumor cells, in which boron is accumulated.Experimental studies on the influence of neutron flux and boron neutron capture therapy on animals depending on the radiation dose were conducted. The study included severe combined immunodeficiency mice pretreated with sodium borocaptate. Control group included animals without boron administration and without irradiation. Dynamic monitoring on the condition of the animals was performed. Evaluation of tissue damage was carried out using histological examinations. The result of the experiment revealed that the neutron flux in therapeutic doses doesn't affect the condition of the animals, and the dose to healthy tissues of immunodeficient mice during irradiation is tolerant.The study present a novel method of boron drug delivery to the tumor tissue by means of pegylated liposomes with a fluorescent label, which can increase the efficacy of boron-neutron capture therapy and determine the localization of the compound in tissues.

Objective : to investigate the impact of a neutron beam formed with the accelerator-based epithermal neutron source designed at the G.I. Budker Institute of Nuclear Physics (INP) on the viability of human and animal tumor cells cultured in the presence of boron-10 isotope. Material and methods. Human U251 and T98G glioma cells and Chinese hamster CHO-K1 and V-79 cells were incubated at various concentrations in the culture medium containing 10B-enriched L-boronophenylalanine. The cells were irradiated with a neuron beam using the accelerator-based epithermal neuron source. A clonogenic assay was used to evaluate the viability of the irradiated cells. The absorbed doses obtained from elastic scattering of fast neutrons by substance nuclei and the doses obtained from boron neutron capture were calculated using the NMS code. The absorbed doses of gamma-radiation were measured with a mixed radiation dosimeter. Results . The viability of boron-containing and intact human U251 and T98G cell lines and Chinese hamster CHO-K1 and V-79 cells was analyzed after neutron beam radiation. Irradiation of all four cell lines were cultured in the presence of 10B was shown to reduce their colony-forming capacity compared with the control. Elevated boron levels in the culture medium resulted in a significant decrease in the proportion of survived cells. Radiation had the most pronounced impact on the proliferative capacity of the human U251 glioma cell lines. Conclusion . The cultures of human tumor cells and mammalian cells demonstrated that the neutron beam formed with the accelerator-based epithermal neutron source designed at the INP, was effective in reducing the viability of tumor cells in the presence of 10B

Objective : to investigate the impact of a neutron beam formed with the accelerator-based epithermal neutron source designed at the G.I. Budker Institute of Nuclear Physics (INP) on the viability of human and animal tumor cells cultured in the presence of boron-10 isotope. Material and methods. Human U251 and T98G glioma cells and Chinese hamster CHO-K1 and V-79 cells were incubated at various concentrations in the culture medium containing 10B-enriched L-boronophenylalanine. The cells were irradiated with a neuron beam using the accelerator-based epithermal neuron source. A clonogenic assay was used to evaluate the viability of the irradiated cells. The absorbed doses obtained from elastic scattering of fast neutrons by substance nuclei and the doses obtained from boron neutron capture were calculated using the NMS code. The absorbed doses of gamma-radiation were measured with a mixed radiation dosimeter. Results . The viability of boron-containing and intact human U251 and T98G cell lines and Chinese hamster CHO-K1 and V-79 cells was analyzed after neutron beam radiation. Irradiation of all four cell lines were cultured in the presence of 10B was shown to reduce their colony-forming capacity compared with the control. Elevated boron levels in the culture medium resulted in a significant decrease in the proportion of survived cells. Radiation had the most pronounced impact on the proliferative capacity of the human U251 glioma cell lines. Conclusion . The cultures of human tumor cells and mammalian cells demonstrated that the neutron beam formed with the accelerator-based epithermal neutron source designed at the INP, was effective in reducing the viability of tumor cells in the presence of 10B

The expression levels of the FCRL1 gene, which encodes a human B-cell surface receptor, were compared in healthy individuals and patients with autoimmune diseases. The expression levels were evaluated using DNA dot hybridization on membranes with spotted cDNA samples derived from blood-cell sub-populations of patients with autoimmune diseases. Quantification of the hybridization signals showed that FCRL1 expression in peripheral blood B-lymphocytes of patients with multiple sclerosis, lupus anticoagulants, Takayasu’s arteritis, and von Willebrand disease was significantly higher than in healthy individuals. Monoclonal and polyclonal FCRL1-specific antibodies that enable FCRL1 detection in Western blotting, immunohistochemistry, and flow-cytometry assays were generated. It was found that FCRL1 is expressed on the surfaces of mature CD19+ B-cells. In the tonsils, FCRL1-positive cells were located in the crypt area, i.e., in the mantle zone of secondary lymphoid follicles and among the cells of lymphoid epithelium. FCRL1-positive cells were also found in B-cell follicles of the spleen.

Application of main histocompatibility complex tetrames (MHC-tetramers) for antigen specific T-cells detection and analysis coupled with flow cytometry opened new opportunities for T-cell response analysis. MHC-multimers allow the detection of T-cells against viral, cancer and vaccine antigens with exceptional sensitivity and specificity. This approach has become the gold standard for quantative analysis of T-cell immune response. Certain aspects of analysis using MHC-tetramer are examined, and importance of this approach in T-cell response efficacy evaluation in anti-HIV vaccine trials as well as in HIV positive patients are discussed.

The IFGP gene family has recently been found in human and mouse cells and is structurally related to the leukocytic Fc receptor genes. Expression of six human and four mouse IFGP genes was studied. Apart from mouse IFGP2, the genes of the family are expressed predominantly in hematopoietic cells. Expression of human IFGP1-IFGP5 and mouse IFGP3 is restricted to B cells. Mouse IFGP1 is expressed in B cells and, possibly, in nonlymphoid cells. IFGP6 is specifically expressed in CD8+ T cells and natural killers. Alternative splicing was demonstrated for the first time for the human IFGP1 and IFGP6 mRNAs. The alternative transcripts code for an IGFP1 isoform devoid of the transmembrane domain and an IFGP6 isoform with a changed cytoplasmic tail. It was assumed that the receptors of the family play a role in controlling differentiation and/or function of effector lymphocytes of the three main types: B cells, CD8+ T cells, and natural killers.

The results of a quantitative study of the expression of mink C gamma-allotypes (H3, H4, H6, and H8) in sera are presented. H6 and H8 were found to be stably expressed, and the individual concentrations of the allotypes varied within one order of magnitude. Gene dosage effects were observed for H6 and H8: average sera allotype concentrations in homozygotes were twice those in heterozygotes. In contrast, the serum concentrations of H3 and H4 varied by three orders of magnitude, ranging from minor (2-200 micrograms/ml) to high (1-10 mg/ml). No gene dosage effects were observed for the expression of H3 and H4. Histograms for the population of H3 concentrations showed three peaks, sharply differing from those of H4, H6, and H8. There was no association between the minor expression of H3 and H4. The data obtained indicate that the expression of mink C gamma-allotypes is regulated by different allotype-specific mechanisms.