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 Найдено в других БД:Каталог книг и продолжающихся изданий (37)Нанотехнологии (1)Труды Института высокотемпературной электрохимии УрО РАН (66)Труды сотрудников Института органического синтеза УрО РАН (76)Труды сотрудников Института теплофизики УрО РАН (66)Труды сотрудников Института химии твердого тела УрО РАН (62)Расплавы (13)Публикации Чарушина В.Н. (9)Каталог библиотеки ИЭРиЖ УрО РАН (1)Электронная энциклопедия «Дискурсология» (1)
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1.
Инвентарный номер: нет.
   
   S 54


    Shmagel, K. V.
    Molecular bases of immune complex pathology [Electronic resource] / K. V. Shmagel, V. A. Chereshnev // Biochemistry. - 2009. - Vol. 74, № 5. - P469-479. - Bibliogr. : p. 477-479 (126 ref.)
ББК 57
Рубрики: БИОЛОГИЧЕСКИЕ НАУКИ
Кл.слова (ненормированные):
IMMUNE COMPLEXES -- COMPLEMENT -- CR1 RECEPTORS
Аннотация: The binding of antigens with antibodies forms immune complexes in the body. Usually these complexes are eliminated by the system of mononuclear phagocytes without development of pathological changes. This review highlights principal mechanisms responsible for safe removal of immune complexes in primates and humans. Special attention is given to diseases known as "immune complex diseases", when antigen-antibody complexes induce inflammatory reactions. The review considers key experimental works that significantly contributed to current knowledge of etiology and pathogenesis of type III hypersensitivity. Some factors of the development of immune complex syndrome such as level of humoral immune response to antigen, isotype and affinity of forming antibodies, the amount of immune complexes, and the consequences of their interaction with the complement system and Fc-receptors are analyzed based on the molecular mechanisms involved. The review contains a retrospective analysis of the most significant scientific achievements in immune complex pathology investigation within the last 100 years

\\\\expert2\\NBO\\Biochemistry\\2009, v.74, p. 469-479.pdf
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2.
Инвентарный номер: нет.
   
   H 91


   
    Human immunodeficiency virus infection: From biological observations to mechanistic mathematical modelling / G. Bocharov, V. A. Chereshnev, I. C. Gainova [et al.] // Mathematical modelling of natural phenomena. - 2012. - Vol. 7, № 5. - P78-104. - Bibliogr. : p. 93-104 (275 ref.)
ББК 61
Рубрики: ЗДРАВООХРАНЕНИЕ. МЕДИЦИНСКИЕ НАУКИ
Кл.слова (ненормированные):
HOST-PATHOGEN INTERACTION -- IMMUNE SYSTEM -- HUMAN IMMUNODEFICIENCY
Аннотация: HIV infection is multi-faceted and a multi-step process. The virus-induced pathogenic mechanisms are manifold and mediated through a range of positive and negative feedback regulations of immune and physiological processes engaged in virus-host interactions. The fundamental questions towards understanding the pathogenesis of HIV infection are now shifting to 'dynamic' categories: (i) why is the HIV-immune response equilibrium finally disrupted? (ii) can one modify the dynamic equilibrium for host benefit? (iii) can one predict the outcome of a system perturbation via antiviral drugs or drugs modulating the host immune response dynamics? Answering these questions requires a major interdisciplinary effort, and in particular, the development of novel mathematical approaches for a coherent quantitative description and prediction of intra-patient HIV evolution, the immunological responses to HIV infection, and the systems level homeostatic regulation of specific effector and regulatory lymphocyte populations in correlation with disease status. Here we summarized fundamental biological features of HIV infection and current mathematical modelling attempts to understand HIV pathogenesis

\\\\expert2\\NBO\\Mathematical Modelling and Natural Phenomena\\2012. V. 7, N 5. P. 78-104.pdf
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3.
Инвентарный номер: нет.
   
   C 51


    Chereshnev, V. A.
    Beta-endorphin as the endogenous regulator of immune processes / V. A. Chereshnev, S. V. Gein // Rossiǐskii fiziologicheskiǐ zhurnal imeni I.M. Sechenova. - 2009. - Vol. 95, № 12. - P1279-1290
ББК 61
Рубрики: ЗДРАВООХРАНЕНИЕ. МЕДИЦИНСКИЕ НАУКИ
Кл.слова (ненормированные):
BETA ENDORPHIN -- OPIATE RECEPTOR -- ADAPTIVE IMMUNITY
Аннотация: Endogenous opioid peptides represent the group of bioregulatory factors possessing a wide range of biologically active effects. One of most essential functions of endogenous opioids appears to be the realization of cellular interaction between nervous and immune systems. Beta-endorphin is a peptide hormone that is the most active and multi-functional representative of the opioid peptide family. This review summarizes current observations on the nature ofbeta-endorphin, its production by the immune system cells, opiate receptor structure and expression, as well as the peptide effect on the processes of cellular activation, proliferation, and differentiation in innate and adaptive immunity

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4.
Инвентарный номер: нет.
   


   
    Checking gene expression profile associated with IRF7 and UNC93B deficient patient peripheral blood mononuclear cells infected with pH1N1 influenza virus / K. Shinwari, G. Liu, M. A. Bolkov [et al.] // AIP Conference Proceedings. - 2022. - Vol. 2390, № 1. - Ст. 030089
Рубрики: ЗДРАВООХРАНЕНИЕ. МЕДИЦИНСКИЕ НАУКИ
Кл.слова (ненормированные):
VIRUSES -- MICROARRAYS -- GENOMICS
Аннотация: An innate immune defect is a defect in the innate immune response that reduces the response to infection, this can occurs in genes important for activation regulation and proliferation of the innate immune cells or pathways important for the function of innate immunity. The purpose of this study was to identify novel biomarkers of interferon Receptor 7 through bioinformatics analysis and elucidate the possible molecular mechanism. The GSE 66486 datasets containing microarray data from IRF7 and UNC93B patients and healthy controls were downloaded from the GEO database and analyzed by the GEO2R web tool to obtain different expressed genes (DEGs). Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, protein-protein interaction (PPI), and Biological Networks Gene Oncology tool (BiNGO) were then performed to elucidate the molecular mechanism of IRF7. A total of 490 DEGs were identified, of which 14 were hub genes, and involved in ribosome biogenesis, rRNA processing, gene expression, mRNA processing, nuclear lumen, intracellular non-membrane-bounded organelle, nucleoplasm, small-subunit processome, antigen processing and presentation pathway, and ribosome biogenesis in eukaryotes. Antigen processing and presentation pathway, and ribosome biogenesis in eukaryotes possibly form the basis of IRF7 or UNC93B disorders, while our study provides a list of genes and pathways that are disrupted in IRF7/UNC93B, which has the potential to be used in the clinic for diagnosis and targeted therapy of such disorders in future.

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5.
Инвентарный номер: нет.
   
   I-55


   
    Immune system – physiological functional system by P. K. Anokhin / V. A. Chereshnev, B. G. Yushkov, M. V. Chereshneva, T. V. Gavrilova // Interaction of the nervous and immune systevs in health and disease : VI International Symposium : abstracts. - Saint Petersburg, 2017. - P13
ББК 52
Рубрики: ПАТАЛОГИЯ, ИММУНОЛОГИЯ

\\\\Expert2\\NBO\\статьи из сборников\\Interactions of the nervous 2017 C. 13.pdf
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6.
Инвентарный номер: нет.
   


   
    Defining muscle-invasive bladder cancer immunotypes by introducing tumor mutation burden, CD8+ T cells, and molecular subtypes / Zihao Chen, Guojun Liu, Guoqing Liu [et al.]. - https://doi.org/10.1186/s41065-020-00165-7 // Hereditas. - 2021. - Vol. 158, № 1. - 12 p
Кл.слова (ненормированные):
CD8+ T CELLS -- MOLECULAR SUBTYPE -- IMMUNOTHERAPY
Аннотация: Immunotherapy, especially anti-PD-1, is becoming a pillar of modern muscle-invasive bladder cancer (MIBC) treatment. However, the objective response rates (ORR) are relatively low due to the lack of precise biomarkers to select patients. Herein, the molecular subtype, tumor mutation burden (TMB), and CD8+ T cells were calculated by the gene expression and mutation profiles of MIBC patients. MIBC immunotypes were constructed using clustering analysis based on tumor mutation burden, CD8+ T cells, and molecular subtypes. Mutated genes, enriched functional KEGG pathways and GO terms, and co-expressed network-specific hub genes have been identified. We demonstrated that ORR of immunotype A patients identified by molecular subtype, CD8+ T cells, and TMB is about 36% predictable. PIK3CA, RB1, FGFR3, KMT2C, MACF1, RYR2, and EP300 are differentially mutated among three immunotypes. Pathways such as ECM-receptor interaction, PI3K-Akt signaling pathway, and TGF-beta signaling pathway are top-ranked in enrichment analysis. Low expression of ACTA2 was associated with the MIBC survival benefit. The current study constructs a model that could identify suitable MIBC patients for immunotherapy, and it is an important step forward to the personalized treatment of bladder cancers.

\\\\Expert2\\NBO\\Электрон. библиотека (Отеч.периодика)\\Черешнев В. А\\Hereditas. - 2021. - Vol. 158, № 1.pdf
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