scholarly journals The volume of changes in the cells of the brain under the influence of carbon monoxide poisoning

2020 ◽  
Vol VII (4) ◽  
pp. 198-242
Author(s):  
I. Spirtov
Keyword(s):  
Mental Illness ◽  
Carbon Monoxide ◽  
Nervous System ◽  
Mental Disorders ◽  
Carbon Monoxide Poisoning ◽  
Sense Organ ◽  
Healthy People ◽  
Extensive Literature ◽  
Post Mortem ◽  
The Brain

The effect of carbon monoxide on the nervous system, obvious and in everyday, not particularly severe cases of poisoning with this gas, is illustrated by the extensive literature, growing from year to year, of cases where, after poisoning with carbon monoxide, severe pathological phenomena from the nervous system developed; At the same time, in one number of cases, such phenomena constituted a direct continuation of the poisoning, in other cases they developed after the first aftermath of poisoning passed and proceeded more or less prolonged, so to speak, a light difference, during which the subjects were poisoned, who were not healthy people in all relations. These post-mortem pathological phenomena capture both the intellectual sphere, as well as the motor and sensitive areas, namely, they were observed: ammesia, aphasia, stupor, dementia, further: general agitation, mental illness, similar to primary mental disorders and contractions, weakening of the sensitivity of one or another sense organ.

scholarly journals About blood circulation in the brain during acute poisoning with carbon monoxide

2020 ◽  
Vol VIII (3) ◽  
pp. 102-121
Author(s):  
I. Spirtov
Keyword(s):  
Carbon Monoxide ◽  
Nervous System ◽  
Mental Disorders ◽  
Blood Circulation ◽  
Medical Literature ◽  
Acute Poisoning ◽  
Chronic Poisoning ◽  
The Brain

In view of the observed cases of various diseases of the nervous system, which are associated with single poisoning with carbon monoxide, the number of which in the medical literature is increasing every year, as well as in the form of nervous and mental disorders in chronic poisoning with the same gas, Maureau, Е. Вескеr, E. V. Hardin and me, it seemed very interesting to trace the course of blood circulation in the brain during the process of poisoning itself, all the while I gratefully accepted the proposal and permission of the highly respected prof. V. M. Bekhterev to carry out research in his laboratory on this issue.

RAS in the Central Nervous System: Potential Role in Neuropsychiatric Disorders

2018 ◽  
Vol 25 (28) ◽  
pp. 3333-3352 ◽  
Author(s):  
Natalia Pessoa Rocha ◽  
Ana Cristina Simoes e Silva ◽  
Thiago Ruiz Rodrigues Prestes ◽  
Victor Feracin ◽  
Caroline Amaral Machado ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Central Nervous System ◽  
Nervous System ◽  
Therapeutic Potential ◽  
Neuropsychiatric Disorders ◽  
Extensive Literature ◽  
Ang Ii ◽  
Mas Receptor ◽  
The Central Nervous System ◽  
The Brain

Background: The Renin-Angiotensin System (RAS) is a key regulator of cardiovascular and renal homeostasis, but also plays important roles in mediating physiological functions in the central nervous system (CNS). The effects of the RAS were classically described as mediated by angiotensin (Ang) II via angiotensin type 1 (AT1) receptors. However, another arm of the RAS formed by the angiotensin converting enzyme 2 (ACE2), Ang-(1-7) and the Mas receptor has been a matter of investigation due to its important physiological roles, usually counterbalancing the classical effects exerted by Ang II. Objective: We aim to provide an overview of effects elicited by the RAS, especially Ang-(1-7), in the brain. We also aim to discuss the therapeutic potential for neuropsychiatric disorders for the modulation of RAS. Method: We carried out an extensive literature search in PubMed central. Results: Within the brain, Ang-(1-7) contributes to the regulation of blood pressure by acting at regions that control cardiovascular functions. In contrast with Ang II, Ang-(1-7) improves baroreflex sensitivity and plays an inhibitory role in hypothalamic noradrenergic neurotransmission. Ang-(1-7) not only exerts effects related to blood pressure regulation, but also acts as a neuroprotective component of the RAS, for instance, by reducing cerebral infarct size, inflammation, oxidative stress and neuronal apoptosis. Conclusion: Pre-clinical evidence supports a relevant role for ACE2/Ang-(1-7)/Mas receptor axis in several neuropsychiatric conditions, including stress-related and mood disorders, cerebrovascular ischemic and hemorrhagic lesions and neurodegenerative diseases. However, very few data are available regarding the ACE2/Ang-(1-7)/Mas receptor axis in human CNS.

Application of Perfluorooctylbromide Nanoparticles with Ulinastatin for Early Brain Injury Caused by Carbon Monoxide Poisoning

2021 ◽  
Vol 13 (7) ◽  
pp. 1383-1390
Author(s):  
Guangcong Li ◽  
Dan Li
Keyword(s):  
Carbon Monoxide ◽  
Particle Size ◽  
Treatment Group ◽  
Cell Apoptosis ◽  
High Speed ◽  
Carbon Monoxide Poisoning ◽  
Neuronal Cell ◽  
Early Brain Injury ◽  
Group A ◽  
The Brain

ABSTRACTThis study aimed to explore the mechanism of perfluorooctylbromide (PFOB) nanoparticles (NPs) combined with ulinastatin (UTI) on early brain injury (EBI) caused by carbon monoxide poisoning (CMP). Firstly, PFOB NPs were prepared by high-speed dispersion and high-speed homogenization. The physicochemical characteristics of the particle size distribution and Zeta potential distribution of the NPs were analyzed using a laser particle size analyzer. The thermal and photoinduced phase transition characteristics of the NPs were analyzed under heating and laser irradiation conditions. Then, 50 Sprague Dawley (SD) rats were deemed as the research objects to establish the CMP rat models using hyperbaric oxygen chambers. According to different treatment methods, they were rolled into a healthy control group, a carbon monoxide (CO) model group, a PTOB treatment group, an UTI treatment group, and a PTOB + UTI treatment group. The brain tissues of each group of rats were collected 3 days after treatment. The neuronal cell apoptosis, expression of Caspase-3, messenger ribonucleic acid (mRNA) of inflammatory factors interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in rat brain tissue were detected through immunohistochemical staining, in situ cell apoptosis detection, Reverse transcription-polymerase chain reaction (RT-PCR), and Western blotting, so did the relative expression of target proteins B-cell lymphoma-2 (Bcl-2), Bcl2-Associated X (Bax) and myelin basic protein (MBP). As a result, the average particle size and the average Zeta potential of the prepared PFOB NPs was 103±31 nm and −23 ± 15 mV, respectively. When the PFOB NPs were heated to 80 °C, the particle size increased greatly and cracks appeared. The particle size of PFOB NPs also increased obviously after laser irradiation, and the PFOB inside the particles changed into gas phase. Compared to CO group, expression of Caspase-3, neuronal cell apoptosis rate, mRNA expression of IL-1β and TNF-α, and protein expression of Bax and Bcl-2 in the brain tissue of PTOB group, UTI group, and PFOB + UTI group were notably decreased (P < 0.05), while the MBP protein expression increased considerably (P < 0.05). Changes in PFOB + UTI group were more obvious than those in PTOB group and UTI group, and those indicators weren’t considerably different from the controls. In summary, PFOB NPs were successfully prepared with favorable phase transition characteristics. Moreover, PFOB NPs combined with UTI could reduce the apoptosis of brain neurons after CMP, improve the inflammatory response, and play a protective effect on EBI of CMP.

Kirlian Experimental Analysis and IoT

2021 ◽  
Vol 10 (2) ◽  
pp. 29-43
Author(s):  
Rohit Rastogi ◽  
Mamta Saxena ◽  
Devendra K. Chaturvedi ◽  
Mayank Gupta ◽  
Akshit Rajan Rastogi ◽  
...  
Keyword(s):  
Nervous System ◽  
Energy Levels ◽  
Critical Role ◽  
The Body ◽  
Extensive Literature ◽  
Entire Body ◽  
Body Parts ◽  
Sodium Potassium ◽  
Charged Ions ◽  
The Brain

Our entire body, including the brain and nervous system, works with the help of various kinds of biological stuff which includes positively charged ions of elements like sodium, potassium, and calcium. The different body parts have different energy levels, and by measuring the energy level, we can also measure the fitness of an individual. Moreover, this energy and fitness are directly related to mental health and the signals being transmitted between the brain and other parts of the body. Various activities like walking, talking, eating, and thinking are performed with the help of these transmission signals. Another critical role played by them is that it helps in examining the mechanisms of cells present at various places in the human body and signaling the nervous system and brain if they are properly functioning or not. This manuscript is divided into two parts where, in the first part, it provides the introduction, background, and extensive literature survey on Kirlian experiments to measure the human's organ energy.

Сellular and Molecular Mechanisms of Proinflammatory Monocytes Participation in the Pathogenesis of Mental Disorders. Part 3

Psychiatry ◽  
2021 ◽  
Vol 19 (4) ◽  
pp. 125-134
Author(s):  
E. F. Vasilyeva ◽  
O. S. Brusov
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Mental Disorders ◽  
Molecular Mechanisms ◽  
Microglial Cells ◽  
Inflammatory Reactions ◽  
Mental Diseases ◽  
The Central Nervous System ◽  
The Brain

Background: at present, the important role of the monocyte-macrophage link of immunity in the pathogenesis of mental diseases has been determined. In the first and second parts of our review, the cellular and molecular mechanisms of activation of monocytes/macrophages, which secreting proinflammatory CD16 receptors, cytokines, chemokines and receptors to them, in the development of systemic immune inflammation in the pathogenesis of somatic diseases and mental disorders, including schizophrenia, bipolar affective disorder (BAD) and depression were analyzed. The association of high levels of proinflammatory activity of monocytes/macrophages in patients with mental disorders with somatic comorbidity, including immune system diseases, is shown. It is known that proinflammatory monocytes of peripheral blood, as a result of violation of the integrity of the hematoencephalic barrier can migrate to the central nervous system and activate the resident brain cells — microglia, causing its activation. Activation of microglia can lead to the development of neuroinammation and neurodegenerative processes in the brain and, as a result, to cognitive disorders. The aim of review: to analyze the results of the main scientific studies concerning the role of cellular and molecular mechanisms of peripheral blood monocytes interaction with microglial cells and platelets in the development of neuroinflammation in the pathogenesis of mental disorders, including Alzheimer’s disease (AD). Material and methods: keywords “mental disorders, AD, proinflammatory monocytes, microglia, neuroinflammation, cytokines, chemokines, cell adhesion molecules, platelets, microvesicles” were used to search for articles of domestic and foreign authors published over the past 30 years in the databases PubMed, eLibrary, Science Direct and EMBASE. Conclusion: this review analyzes the results of studies which show that monocytes/macrophages and microglia have similar gene expression profiles in schizophrenia, BAD, depression, and AD and also perform similar functions: phagocytosis and inflammatory responses. Monocytes recruited to the central nervous system stimulate the increased production of proinflammatory cytokines IL-1, IL-6, tumor necrosis factor alpha (TNF-α), chemokines, for example, MCP-1 (Monocyte chemotactic protein-1) by microglial cells. This promotes the recruitment of microglial cells to the sites of neuronal damage, and also enhances the formation of the brain protein beta-amyloid (Aβ). The results of modern studies are presented, indicating that platelets are involved in systemic inflammatory reactions, where they interact with monocytes to form monocyte-platelet aggregates (MTA), which induce the activation of monocytes with a pro inflammatory phenotype. In the last decade, it has been established that activated platelets and other cells of the immune system, including monocytes, detached microvesicles (MV) from the membrane. It has been shown that MV are involved as messengers in the transport of biologically active lipids, cytokines, complement, and other molecules that can cause exacerbation of systemic inflammatory reactions. The presented review allows us to expand our knowledge about the cellular and molecular aspects of the interaction of monocytes/macrophages with microglial cells and platelets in the development of neuroinflammation and cognitive decline in the pathogenesis of mental diseases and in AD, and also helps in the search for specific biomarkers of the clinical severity of mental disorder in patients and the prospects for their response to treatment.

Brain stem and spinal cord demyelination due to acute carbon monoxide poisoning

2021 ◽  
pp. 247-253
Author(s):  
Yan Lv ◽  
Yv Zhang ◽  
Shuyi Pam ◽  
Keyword(s):  
Spinal Cord ◽  
Carbon Monoxide ◽  
Brain Stem ◽  
Carbon Monoxide Poisoning ◽  
Recovery Period ◽  
Extended Period ◽  
Severe Case ◽  
Co Poisoning ◽  
Secondary Demyelination ◽  
The Brain

Demyelination throughout the brain stem and spinal cord caused by acute carbon monoxide (CO) poisoning has not been previously reported. Magnetic resonance imaging (MRI) has revealed that acute CO poisoning primarily affects the subcortical white matter of the bilateral cerebral hemispheres and basal ganglia. Here we report the case of a patient with delayed neuropsychological sequelae (DNS) due to acute CO poisoning. A 28-year-old man was admitted to our department following a suicide attempt by acute CO poisoning. After a six-month pseudo-recovery period, he was diagnosed with DNS, with MRI evidence of demyelinating change of the bilateral cerebral peduncles. Demyelination was identified throughout the brain stem, expanding from the bilateral cerebral peduncles to the medulla oblongata, occurring approximately six months after poisoning. One and a half years after acute CO poisoning, demyelination of the cervical and thoracic spine was observed, most notable in the lateral and posterior cords. It is evident that previously published research on this topic is extremely limited. Perhaps in severe cases of acute CO poisoning the fatality rate is higher, leading to fewer surviving cases for possible study. This may be because a more severe case of acute CO poisoning would result in the higher likelihood of secondary demyelination. This research indicates that clinicians should be aware of the risk of secondary demyelination and take increased precautions such as vitamin B supplementation and administration of low-dose corticosteroids for an extended period of time in order to reduce the extent and severity of demyelination.

Sign in / Sign up

Export Citation Format

Share Document