scholarly journals Problem issues of the pathogenesis of inflammatory reaction and the course of coronavirus infection

2021 ◽  
pp. 76-86
Author(s):  
L.D. Todoriko
Keyword(s):  
Inflammatory Reaction ◽  
The Body ◽  
Systematic Evaluation ◽  
Regulatory Processes ◽  
Coronavirus Infection ◽  
Almost All ◽  
Molecular Pathophysiology ◽  
Disease Analysis ◽  
Cluster 2

Objective — to analysis and systematization of literature data about pathogenesis of the inflammatory reaction and the clinical course of coronavirus infection caused by SARS-CoV-2. Materials and methods. Access to various full-text and abstract databases was used for the search query «coronavirus», «COVID-19», «SARS-CoV-2» and their systematic evaluation was carried out. The most complete database of available literature sources (about 70) was obtainedon the molecular pathophysiology of COVID-19. Results and discussion. The results of the analysis of the molecular pathophysiology of COVID-19 showed that the biomedical terms associated with COVID-19/SARS-CoV-2 form several clusters: cluster 1 is inflammation and the formation of a cytokine storm; cluster 2 — pathophysiological justification of the treatment of coronavirus infection, cluster 3 — comorbid conditions. Analytics of cluster 1 showed one of the most interesting working hypotheses today is model of bradykinin storm. This hypothesis can explain the multisymptomatic nature of COVID-19, including some of its strangest manifestations. The essence of the theory of bradykinin is that, when the virus begins to affect the regulation of renin-angiotensin-aldosterone system (RAAS) through the activation of angio­tensin-converting enzyme type II, it causes the mechanisms that regulate bradykinin levels to fail. Bradykinin’s receptors repeatedly are sensitized and the body also ceases to efficiently break down bradykinin. ACE break down bradykinin, but when the virus suppresses its activity, it cannot work with the same efficiency. The end result of such an imbalance is the release of excessive amounts of bradykinin, due to its mass unrestrained accumulation with the formation of a phenomenon — bradykinin storm. According to the bradykinin hypothesis, this particular variant of the storm is ultimately responsible for the polymorbidity of the clinical picture and the fatal effects cause d by COVID-19. Conclusions. The bradykinin hypothesis of the development of a systemic inflammatory response in SARS-CoV-2 virus is a model that contributes to a better understanding of the pathogenesis and course of COVID-19 and adds novelty to data that are already known. It predicts almost all known symptoms today and offers quality treatments for the disease. Analysis of the processed data from the literature of cluster 2, devoted to the pathophysiological rationale treatment of coronavirus infection led to the role of vitamin D — as a nutrient involved in regulatory processes with participation of RAAS.

scholarly journals THE BIOLOGICAL SIGNIFICANCE OF SELENIUM AND ITS PLACE IN RNA VIRAL DISEASES

2020 ◽  
Vol 21 (4) ◽  
pp. 21-31
Author(s):  
T.M. Guseynov ◽  
◽  
R.T. Guliyeva ◽  
F.R. Yakhyayeva ◽  
◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Immune Response ◽  
Viral Infections ◽  
Biological Significance ◽  
The Body ◽  
Viral Diseases ◽  
Essential Trace Element ◽  
Regulatory Processes ◽  
P Protein ◽  
Almost All

ABSTRACT. Selenium as an essential trace element takes part in the regulation of many vital processes. This is realized with the help of over 25 selenoproteins that affect oxidative stress, immune response, hormonal metabolism, cognitive function, etc. Recently (in the next 30 - 40 years), there have been reports of the effect on viral infections, which have now become widespread. It turned out that almost all RNA viruses are selenium-dependent objects, that is, their genome contains the codes of the most important selenium containing proteins, including such as glutathione peroxidase, thioredoxinreductase, selenium-P protein, etc. Their synthesis during the development of a viral infection at the expense of the host leads to a weakening of the synthesis of the body's own intracellular selenium proteins, which contributes to the development of oxidative stress and a failure of the immune response. And this leads to the devastation of the selenium depot of the body, intended for the synthesis of its selenium proteins, which participate in vital regulatory processes. This circumstance determines, to replenish the body's resources with selenium, the expediency of using selenium-containing pharmacopoeia preparations as adjuvant in the treatment of RNA viral infections.

“Mindfulness Makes You a Way Better Lover”

2017 ◽  
Author(s):  
Jeff Wilson
Keyword(s):  
The Body ◽  
Buddhist Meditation ◽  
Self Help ◽  
Key Concepts ◽  
Almost All ◽  
New Applications ◽  
Ted Talks

American self-help authors, coaches, and sexologists selectively adopt and apply Buddhist meditation techniques to meet their goals and sell products. This chapter draws upon books, articles, podcasts, TED talks, and other sources to demonstrate how these new applications of mindfulness are touted to enhance the sex act, delivering greater pleasure or effectively managing dysfunction. Key concepts include analysis of the economics involved in the appropriation of Buddhist practices, the role of gender in the “secular” use of meditation (almost all books recommend mindful sex for women, but few focus on men), the mixed Asian and Western frameworks for understanding the body and the meaning of sex, and the alternate uses to which elements of Buddhism may be put in different cultural settings. A specific genre of the use of meditation serves as a means to explore secular developments that draw upon Buddhist sources in a sometimes uneasy relationship.

scholarly journals Normal red blood cells’ shape stabilized by membrane’s in-plane ordering

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
L. Mesarec ◽  
W. Góźdź ◽  
A. Iglič ◽  
V. Kralj-Iglič ◽  
E. G. Virga ◽  
...  
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Extrinsic Curvature ◽  
The Body ◽  
Main Function ◽  
Disorder Phase Transition ◽  
Body Tissues ◽  
Almost All ◽  
Membrane Shape

AbstractRed blood cells (RBCs) are present in almost all vertebrates and their main function is to transport oxygen to the body tissues. RBCs’ shape plays a significant role in their functionality. In almost all mammals in normal conditions, RBCs adopt a disk-like (discocyte) shape, which optimizes their flow properties in vessels and capillaries. Experimentally measured values of the reduced volume (v) of stable discocyte shapes range in a relatively broad window between v ~ 0.58 and 0.8. However, these observations are not supported by existing theoretical membrane-shape models, which predict that discocytic RBC shape is stable only in a very narrow interval of v values, ranging between v ~ 0.59 and 0.65. In this study, we demonstrate that this interval is broadened if a membrane’s in-plane ordering is taken into account. We model RBC structures by using a hybrid Helfrich-Landau mesoscopic approach. We show that an extrinsic (deviatoric) curvature free energy term stabilizes the RBC discocyte shapes. In particular, we show on symmetry grounds that the role of extrinsic curvature is anomalously increased just below the nematic in-plane order-disorder phase transition temperature.

scholarly journals The role of the lymphatic system in the homeostasis of the interstitial fluid in the lung and pleural liquid

2019 ◽  
Vol 18 (1) ◽  
pp. 104-112 ◽  
Author(s):  
G. I. Lobov
Keyword(s):  
Endothelial Cells ◽  
Respiratory System ◽  
Interstitial Fluid ◽  
Lymphatic System ◽  
Lymphatic Vessels ◽  
Current Data ◽  
The Body ◽  
Almost All ◽  
Preclinical And Clinical Studies

Accomplishments in the identifcation of lymphatic endothelial cells and the ability to differentiate them from the endothelial cells of blood vessels have contributed to progress in recent decades in studying the role of the lymphatic system in the body. Preclinical and clinical studies of the last decade have shown that changes in the lymphatic vascular network are observed in almost all lung diseases. At the same time, it remains unclear whether the lymphatic vessels and lung nodes are being part of the overall process of lung remodeling or they make a defnite contribution to the pathogenesis of diseases of the respiratory system. This review presents current data on the morphology and physiology of lymphatic vessels and nodes, their role in the regulation of interstitial fluid homeostasis, lipid transportation and immune responses as well as describes the mechanisms of regulation of the transport function of lymphatic vessels. Data on the role of the lymphatic system of the lungs in the exchange of fluid in the interstitial space of the lungs are presented in the review. The results of studies of the last two decades on the formation and reabsorption of pleural fluid and the role of various lymphatic networks in regulating its volume are described. Finally, modern ideas on the mechanisms of pulmonary edema are outlined and important questions of the lymphatic biology of the respiratory system are identifed, still remaining unanswered today.

scholarly journals The role of plasma serine leukocyte proteinase inhibitor in the body's defense against COVID-19

2021 ◽  
Vol 98 (5) ◽  
pp. 567-578
Author(s):  
A. L. Kravtsov ◽  
S. A. Bugorkova
Keyword(s):  
Blood Plasma ◽  
Proteinase Inhibitor ◽  
Global Economy ◽  
Neutrophil Extracellular Traps ◽  
The Body ◽  
Human Blood Plasma ◽  
Leukocyte Elastase ◽  
Extracellular Traps ◽  
Coronavirus Infection

The COVID-19 pandemic continues, causing colossal damage to the population and the global economy. As COVID-19 is studied, new data are emerging regarding the risk of severe coronavirus infection in patients with α1-antitrypsin deficiency. α1 -Antitrypsin is the main inhibitor and key endogenous regulator of the serine leukocyte proteinase activitry released from the granules of activated neutrophils to the cell surface and into the extracellular space. It has been established that the number of cases of severe course and death of COVID-19 in the territories of 68 countries of the world correlates with the frequency of the spread of mutations in the proteinase inhibitor gene among the population of these countries, at which the concentration of α1-antitrypsin in the human blood plasma is 10 times lower than normal. All this contributes to the revision of a number of provisions of the pathogenesis and therapy of a new coronavirus infection.The review presents an analysis of the literature on the role of an inhibitor of serine leukocyte proteinases in protecting the body from COVID-19. The participation of α1-antitrypsin in the inhibition of SARS-CoV-2 penetration into the respiratory tract epithelial cells, in the protection of the vascular endothelium, blood plasma proteins and elastin of the lung tissue from the damaging effect of leukocyte elastase released during neutrophil degranulation and the formation of neutrophil extracellular traps (NETs) is considered. The role of a1-antitrypsin in suppressing inflammation by limiting the secretion of proinflammatory cytokines and neutrophil extracellular traps into the blood has been shown. The individual links in the pathogenesis of the new coronavirus infection have been detailed, which will allow revising the strategy for reducing the risks of severe course of COVID-19.

scholarly journals HEMATOLOGICAL INTEGRATED INDICATORS IN ASSESSING THE CELLULAR REACTIVITY OF THE BODY IN COVID-19 CORONAVIRUS INFECTION

2021 ◽  
Vol 0 (1) ◽  
pp. 77-84
Author(s):  
Raisa M. Smolyakova ◽  
◽  
Helena А. Kozyreva ◽  
Katsiaryna M. Shpadaruk ◽  
◽  
...  
Keyword(s):  
Viral Infection ◽  
Inflammatory Reaction ◽  
The Body ◽  
Systemic Inflammatory Reaction ◽  
Acute Viral Infection ◽  
Determining Factors ◽  
Immunological Process ◽  
Coronavirus Infection ◽  
Hematological Changes ◽  
Integrated Indicators

The article analyzes the disorders in homeostasis diagnosed during the development of acute viral infection SARS-CoV-2 in patients. Hematological changes in patients with coronavirus infection were characterized by the development of disintegration of humoral mechanisms of regulation with the initiation of a systemic inflammatory reaction with an increase in the leukocyte index of intoxication, activation of necrobiotic processes, an increase in the activity of macrophage-microphage nonspecific protection with a predominance of effector links of the immunological process. The development of immunocompromise in patients with a new strain of coronavirus infection is one of the determining factors in the course of the disease.

scholarly journals Adenosine and Inflammation: Here, There and Everywhere

2021 ◽  
Vol 22 (14) ◽  
pp. 7685
Author(s):  
Silvia Pasquini ◽  
Chiara Contri ◽  
Pier Andrea Borea ◽  
Fabrizio Vincenzi ◽  
Katia Varani
Keyword(s):  
Protective Factor ◽  
Therapeutic Strategies ◽  
The Body ◽  
Main Function ◽  
Pathogenetic Mechanism ◽  
Pharmacological Profile ◽  
Endogenous Modulator ◽  
Almost All ◽  
G Protein Coupled

Adenosine is a ubiquitous endogenous modulator with the main function of maintaining cellular and tissue homeostasis in pathological and stress conditions. It exerts its effect through the interaction with four G protein-coupled receptor (GPCR) subtypes referred as A1, A2A, A2B, and A3 adenosine receptors (ARs), each of which has a unique pharmacological profile and tissue distribution. Adenosine is a potent modulator of inflammation, and for this reason the adenosinergic system represents an excellent pharmacological target for the myriad of diseases in which inflammation represents a cause, a pathogenetic mechanism, a consequence, a manifestation, or a protective factor. The omnipresence of ARs in every cell of the immune system as well as in almost all cells in the body represents both an opportunity and an obstacle to the clinical use of AR ligands. This review offers an overview of the cardinal role of adenosine in the modulation of inflammation, showing how the stimulation or blocking of its receptors or agents capable of regulating its extracellular concentration can represent promising therapeutic strategies for the treatment of chronic inflammatory pathologies, neurodegenerative diseases, and cancer.

scholarly journals The role of mesenchymal stromal cells in immune modulation of COVID-19: focus on cytokine storm

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Maria Kavianpour ◽  
Mahshid Saleh ◽  
Javad Verdi
Keyword(s):  
Stem Cells ◽  
Immune Modulation ◽  
Respiratory Illness ◽  
The Body ◽  
Cytokine Storm ◽  
Adaptive Immune ◽  
Research Findings ◽  
Coronavirus Infection ◽  
Adaptive Immune Systems

Abstract The outbreak of coronavirus disease 2019 (COVID-19) pandemic is quickly spreading all over the world. This virus, which is called SARS-CoV-2, has infected tens of thousands of people. Based on symptoms, the pathogenesis of acute respiratory illness is responsible for highly homogenous coronaviruses as well as other pathogens. Evidence suggests that high inflammation rates, oxidation, and overwhelming immune response probably contribute to pathology of COVID-19. COVID-19 causes cytokine storm, which subsequently leads to acute respiratory distress syndrome (ARDS), often ending up in the death of patients. Mesenchymal stem cells (MSCs) are multipotential stem cells that are recognized via self-renewal capacity, generation of clonal populations, and multilineage differentiation. MSCs are present in nearly all tissues of the body, playing an essential role in repair and generation of tissues. Furthermore, MSCs have broad immunoregulatory properties through the interaction of immune cells in both innate and adaptive immune systems, leading to immunosuppression of many effector activities. MSCs can reduce the cytokine storm produced by coronavirus infection. In a number of studies, the administration of these cells has been beneficial for COVID-19 patients. Also, MSCs may be able to improve pulmonary fibrosis and lung function. In this review, we will review the newest research findings regarding MSC-based immunomodulation in patients with COVID-19.

scholarly journals Role of Intestinal Microbiota in Metabolism of Gastrodin In Vitro and In Vivo

Metabolites ◽  
2019 ◽  
Vol 9 (4) ◽  
pp. 69
Author(s):  
Mahesh Raj Nepal ◽  
Ki Sun Jeong ◽  
Geon Ho Kim ◽  
Dong Ho Cha ◽  
Mi Jeong Kang ◽  
...  
Keyword(s):  
Intestinal Microbiota ◽  
The Body ◽  
Pharmacokinetic Parameters ◽  
Gastrodia Elata ◽  
Intestinal Contents ◽  
Almost All ◽  
Hydroxybenzyl Alcohol

Alteration in the number and composition of intestinal microbiota affects the metabolism of several xenobiotics. Gastrodin, isolated from Gastrodia elata, is prone to be hydrolyzed by intestinal microbiota. In the present study, the role of intestinal microbiota in gastrodin metabolism was investigated in vitro and in vivo. Gastrodin was incubated in an anaerobic condition with intestinal contents prepared from vehicle- and antibiotics-treated rats and the disappearance of gastrodin and formation of 4-hydroxybenzyl alcohol (4-HBA) was measured by liquid chromatography coupled to mass spectroscopy (LC-MS/MS). The results showed that almost all gastrodin incubated with control intestinal contents was metabolized to its aglycone in time- and concentration-dependent manners. In contrast, much less formation of 4-HBA was detected in intestinal contents from antibiotics-treated rats. Subsequently, in vivo pharmacokinetic study revealed that the antibiotic pretreatment of rats significantly affected the metabolism of gastrodin to 4-HBA. When administered orally, gastrodin was rapidly absorbed rapidly into plasma, metabolized to 4-HBA, and disappeared from the body within six hours. Interestingly, the pharmacokinetic parameters of 4-HBA were changed remarkably in antibiotics-treated rats, compared to control rats. The results clearly indicated that the antibiotics treatment of rats suppressed the ability of intestinal microbiota to metabolize gastrodin to 4-HBA and that, thereby, the pharmacodynamic action was significantly modulated.

scholarly journals The Role of Inflammatory Cytokines, the RANKL/OPG Axis, and the Immunoskeletal Interface in Physiological Bone Turnover and Osteoporosis

Scientifica ◽  
2013 ◽  
Vol 2013 ◽  
pp. 1-29 ◽  
Author(s):  
M. Neale Weitzmann
Keyword(s):  
Bone Turnover ◽  
Inflammatory Cytokines ◽  
Osteoclast Formation ◽  
The Body ◽  
Immune Functions ◽  
Regulatory Processes ◽  
Downstream Effector ◽  
Receptor Activator ◽  
Skeletal Integrity

Although it has long been recognized that inflammation, a consequence of immune-driven processes, significantly impacts bone turnover, the degree of centralization of skeletal and immune functions has begun to be dissected only recently. It is now recognized that formation of osteoclasts, the bone resorbing cells of the body, is centered on the key osteoclastogenic cytokine, receptor activator of NF-κB ligand (RANKL). Although numerous inflammatory cytokines are now recognized to promote osteoclast formation and skeletal degradation, with just a few exceptions, RANKL is now considered to be the final downstream effector cytokine that drives osteoclastogenesis and regulates osteoclastic bone resorption. The biological activity of RANKL is moderated by its physiological decoy receptor, osteoprotegerin (OPG). New discoveries concerning the sources and regulation of RANKL and OPG in physiological bone turnover as well as under pathological (osteoporotic) conditions continue to be made, opening a window to the complex regulatory processes that control skeletal integrity and the depth of integration of the skeleton within the immune response. This paper will examine the interconnection between bone turnover and the immune system and the implications thereof for physiological and pathological bone turnover.

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