scholarly journals Pathoanatomical Pattern of Brain Damage of White Mice Infected with Experimental Anthrax

2020 ◽  
Vol 5 (1) ◽  
pp. 65-71
Author(s):  
D. D. Briukhova ◽  
V. I. Dubrovina ◽  
E. V. Kravets ◽  
G. B. Mukhturgin ◽  
T. A. Ivanova ◽  
...  
Keyword(s):  
Neuronal Damage ◽  
Statistical Processing ◽  
Brain Regions ◽  
The Body ◽  
Numerical Density ◽  
Quantitative Factor ◽  
Systemic Spread ◽  
Anthrax Infection ◽  
Average Size ◽  
The Brain

Background. Bacillus anthracis is a microorganism that causes anthrax. Because of irrational therapy, this particularly dangerous infectious disease leads to a systemic spread of bacteria in the body through histohematological barriers. Bacilli entering the brain subsequently lead to hemorrhagic meningitis. Despite intensive antibiotic therapy, that kind of meningitis is difficult to cure and therefore highly lethal. Studying characteristics of anthrax’s isolates of different origin and genotype is an actual area of research.The aim of the study is searching for pathomorphological and histological changes in the brain regions of experimental animals with anthrax infection, caused by B. anthracis with different plasmid spectrum.Materials and methods: The study was conducted on 200 certified white mice, three B. anthracis strains were used as research objects: B. anthracis I-323 (рХО1– /рХО2– ), B. anthracis I-275 (рХО1- /рХО2- ), and B. anthracis I-217 (рХО1+ / рХО2– ). The material for histological examination was the brain of mice, embedded in paraffin, and then sections were prepared using a microtome and stained with hematoxylin-eosin and Nissl toluidine blue. The degree of neuronal damage was assessed by calculating the semi-quantitative factor and determining the average size of the neuron nuclei, and the numerical density of cells in 1mm2 was studied. Microphotography and quantitative analysis was performed using the Motic Images Plus 2.0 application package. Statistical processing of the results was performed using the program “Statistica 6.0”.The results of the study showed that the brain of infected mice shows signs of hemorrhagic leptomeningitis, the manifestations of which are more pronounced in mice infected with weakly virulent plasmid strains of B. anthracis and fallen mice.Conclusion. Multicomponent exotoxin and specialized proteins, encoded in the pathogenicity plasmid of microorganisms, allow B. anthracis to easily overcome histohematological barriers and cause severe septic anthrax. The results obtained during the study supplement the available information on the pathogenesis of anthrax and indicate the need for further research in this direction.

scholarly journals Power Failure of Mitochondria and Oxidative Stress in Neurodegeneration and Its Computational Models

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 229
Author(s):  
JunHyuk Woo ◽  
Hyesun Cho ◽  
YunHee Seol ◽  
Soon Ho Kim ◽  
Chanhyeok Park ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Computational Models ◽  
Neuronal Damage ◽  
Living Organism ◽  
The Body ◽  
Mitochondrial Functions ◽  
A Cell ◽  
The Brain ◽  
And Oxidative Stress

The brain needs more energy than other organs in the body. Mitochondria are the generator of vital power in the living organism. Not only do mitochondria sense signals from the outside of a cell, but they also orchestrate the cascade of subcellular events by supplying adenosine-5′-triphosphate (ATP), the biochemical energy. It is known that impaired mitochondrial function and oxidative stress contribute or lead to neuronal damage and degeneration of the brain. This mini-review focuses on addressing how mitochondrial dysfunction and oxidative stress are associated with the pathogenesis of neurodegenerative disorders including Alzheimer’s disease, amyotrophic lateral sclerosis, Huntington’s disease, and Parkinson’s disease. In addition, we discuss state-of-the-art computational models of mitochondrial functions in relation to oxidative stress and neurodegeneration. Together, a better understanding of brain disease-specific mitochondrial dysfunction and oxidative stress can pave the way to developing antioxidant therapeutic strategies to ameliorate neuronal activity and prevent neurodegeneration.

scholarly journals Efficacy and immunogenicity of MultiTEP-based DNA vaccines targeting human α-synuclein: prelude for IND enabling studies

npj Vaccines ◽  
2022 ◽  
Vol 7 (1) ◽  
Author(s):  
Changyoun Kim ◽  
Armine Hovakimyan ◽  
Karen Zagorski ◽  
Tatevik Antonyan ◽  
Irina Petrushina ◽  
...  
Keyword(s):  
Dna Vaccines ◽  
Neurodegenerative Disorder ◽  
Neuronal Damage ◽  
Lewy Bodies ◽  
Amyloid Β ◽  
The Elderly ◽  
Brain Regions ◽  
Dependent Manner ◽  
Lewy Neurites ◽  
The Brain

AbstractAccumulation of misfolded proteins such as amyloid-β (Aβ), tau, and α-synuclein (α-Syn) in the brain leads to synaptic dysfunction, neuronal damage, and the onset of relevant neurodegenerative disorder/s. Dementia with Lewy bodies (DLB) and Parkinson’s disease (PD) are characterized by the aberrant accumulation of α-Syn intracytoplasmic Lewy body inclusions and dystrophic Lewy neurites resulting in neurodegeneration associated with inflammation. Cell to cell propagation of α-Syn aggregates is implicated in the progression of PD/DLB, and high concentrations of anti-α-Syn antibodies could inhibit/reduce the spreading of this pathological molecule in the brain. To ensure sufficient therapeutic concentrations of anti-α-Syn antibodies in the periphery and CNS, we developed four α-Syn DNA vaccines based on the universal MultiTEP platform technology designed especially for the elderly with immunosenescence. Here, we are reporting on the efficacy and immunogenicity of these vaccines targeting three B-cell epitopes of hα-Syn aa85–99 (PV-1947D), aa109–126 (PV-1948D), aa126–140 (PV-1949D) separately or simultaneously (PV-1950D) in a mouse model of synucleinopathies mimicking PD/DLB. All vaccines induced high titers of antibodies specific to hα-Syn that significantly reduced PD/DLB-like pathology in hα-Syn D line mice. The most significant reduction of the total and protein kinase resistant hα-Syn, as well as neurodegeneration, were observed in various brain regions of mice vaccinated with PV-1949D and PV-1950D in a sex-dependent manner. Based on these preclinical data, we selected the PV-1950D vaccine for future IND enabling preclinical studies and clinical development.

scholarly journals Neuronal Damage after Repeated 5 Minutes of Ischemia in the Gerbil is Preceded by Prolonged Impairment of Protein Metabolism

1992 ◽  
Vol 12 (3) ◽  
pp. 425-433 ◽  
Author(s):  
R. Widmann ◽  
C. Weber ◽  
P. Bonnekoh ◽  
M. Schlenker ◽  
K.-A. Hossmann
Keyword(s):  
Protein Synthesis ◽  
Cerebral Ischemia ◽  
Neuronal Damage ◽  
Neuronal Injury ◽  
Brain Regions ◽  
Synthesis Rate ◽  
Protein Synthesis Rate ◽  
Single Episode ◽  
Inhibition Of Protein Synthesis ◽  
The Brain

The effect of single or repeated episodes of cerebral ischemia on protein biosynthesis and neuronal injury was studied in halothane-anesthetized gerbils by autoradiography of [14C]leucine incorporation into brain proteins and light microscopy. For quantification of the protein synthesis rate, the steady-state precursor pool distribution space for labeled and unlabeled free leucine was determined by clamping the specific activity of [14C]leucine in plasma, and by measuring free tissue leucine in samples taken from various parts of the brain. Control values of protein synthesis were 14.6 ± 2.2, 5.8 ± 2.3, 14.2 ± 3.1, and 10.0 ± 3.8 nmol g−1 min−1 (means ± SD) in the frontal cortex, striatum, CA1 sector, and thalamus, respectively. Following a single episode of 5 or 15 min of ischemia, protein synthesis recovered to normal in all brain regions except the CA1 sector, where it returned to only 50% of control after 6 h and to less than 20% after 3 days of recirculation. After three episodes of 5 min of ischemia spaced at 1 h intervals, protein synthesis remained severely suppressed in all brain regions after both 6 h and 3 days of recirculation. Inhibition of protein synthesis after 6 h predicted histological injury after 3 days of recirculation. In animals submitted to a single episode of 5 or 15 min of ischemia, histological damage was restricted to the CA1 sector but injury occurred throughout the brain after three episodes of 5 min of ischemia. These observations demonstrate that persisting inhibition of protein synthesis following cerebral ischemia is an early manifestation of neuronal injury. Prevention of neuronal injury requires restoration of a normal protein synthesis rate.

scholarly journals Influencia del estrés en la Enfermedad de Alzheimer. // Stress influence in Alzheimer’s disease

Ciencia Unemi ◽  
2018 ◽  
Vol 10 (25) ◽  
pp. 123
Author(s):  
Maria Alejandra Vallejo-Johnson ◽  
Patricia Marcial-Velastegui
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neuronal Damage ◽  
The Body ◽  
Daily Routine ◽  
Stressful Situation ◽  
The Individual ◽  
Stress Influences ◽  
The Brain

Existen diversos estudios que proponen las causas de la Enfermedad de Alzheimer (EA), las cuales pueden ser: biológicas, genéticas, cronológicas y ambientales, dentro de ésta última se encuentra el estrés como una influencia para el inicio de dicha patología. Según las distintas teorías del estrés, el sujeto, al encontrarse frente a una situación estresante, sufre diversos cambios en su cuerpo para sobrellevar dicho acontecimiento. El cerebro es el encargado de poner al cuerpo en alerta y en marcha para actuar frente a dicho cambio. El estrés prolongado conlleva a alteraciones en las vías cerebrales, específicamente un daño neuronal del hipocampo, el cual es el encargado de los recuerdos y memoria. Éste al verse afectado, repercute en la memoria del sujeto y por lo tanto empieza a fallar; el sujeto se ve en la incapacidad para recordar y realizar distintas actividades rutinarias. Mediante la investigación documental y encuestas a profesionales de la salud, se obtuvo información tanto del estrés como de la Enfermedad de Alzheimer para luego concluir en la influencia del mismo en el origen de la enfermedad. Se concluye que el estrés perenne repercute en la muerte de neuronas del hipocampo lo que conlleva a la EA. AbstractThere are different studies that propose that the causes of Alzheimer might be biological, genetic, chronological and environmental. Within the environmental aspects, the stress influences the beginning of this pathology. There are several studies that propose the causes of Alzheimer's disease (AD), which can be: biological, genetic, chronological and environmental, within the latter is the stress that influences the beginning of this pathology. According to different theories of stress, the individual, while facing a stressful situation, experiences many changes in the body in order to deal with this situation. The brain is in charge of alerting the body to protect itself against that change. The long-term stress alters the brain pathways, producing specifically a neuronal damage in the hippocampus that is responsible for memories and memory. This affects memory and therefore individual begins to fail, and then, the person cannot remember how to do the daily routine. Through bibliographical research and surveys applied to healthcare professionals, information was obtained on both stress and Alzheimer's disease to establish the influence of that condition on the disease. The study concludes that long-term stress affects the death of neurons in the hippocampus, which leads to AD.

Combination of Scutellaria baicalensis and Metformin Ameliorates Diet-Induced Metabolic Dysregulation in Mice via the Gut–Liver–Brain Axis

2020 ◽  
Vol 48 (06) ◽  
pp. 1409-1433
Author(s):  
AbuZar Ansari ◽  
Shambhunath Bose ◽  
Soo-Kyoung Lim ◽  
Jing-Hua Wang ◽  
Young-Hee Choi ◽  
...  
Keyword(s):  
Microbial Population ◽  
Metabolic Diseases ◽  
Neuronal Damage ◽  
The Body ◽  
Scutellaria Baicalensis ◽  
Metabolic Markers ◽  
Metabolic Dysregulation ◽  
High Fructose ◽  
The Brain

Scutellaria baicalensis (SB), a herbal medicine, is commonly used to treat metabolic diseases, while Metformin (MF) is a widely used drug for type 2 diabetes. The purpose of this study was to investigate whether co-treatment of SB with MF could produce a potential therapeutic effect on high-fat and high-fructose diet (HFFD)-induced metabolic dysregulation. First, we optimized the dose of SB (100, 200, 400, and 800[Formula: see text]mg/kg) with MF (200[Formula: see text]mg/kg) in HFFD-induced C57BL6J mice. Next, the optimized dose of SB (400[Formula: see text]mg/kg) was co-administered with MF (50, 100, and 200[Formula: see text]mg/kg) in a similar animal model to find the effective combinations of SB and MF. Metabolic markers were determined in serum and tissues using different assays, histology, gene expression, and gut microbial population. The SB and MF co-treatment significantly decreased the body, liver, and VAT weights. The outcome of OGTT was improved, and the fasting insulin, HbA1c, TG, TC, LDL-c, AST, and ALT were decreased, while HDL-c was significantly increased. Histological analyses revealed maintained the integrity of liver, adipose tissue, and intestine prevented lipid accumulation in the liver and intestine and combated neuronal damage in the brain. Importantly, controlled the expression of PPAR[Formula: see text], and IL-6 genes in the liver, and expression of BDNF, Glut1, Glut3, and Glut4 genes in the brain. Treatment-specific gut microbial segregation was observed in the PCA chart. Our findings indicate that SB and MF co-treatment is an effective therapeutic approach for HFFD-induced metabolic dysregulation which is operated through the gut–liver–brain axis.

scholarly journals Pilot study on the evaluation of the effectiveness of psychocorrection methods that include EEG-training and VR headset in athletes involved in extreme kinds of sports

2021 ◽  
Vol 11 (2) ◽  
pp. 67-75
Author(s):  
V. I. Pustovoit ◽  
S. E. Nazaryan ◽  
E. Ya. Adoeva ◽  
M. S. Klyuchnikov ◽  
N. A. Kirichenco ◽  
...  
Keyword(s):  
Statistical Processing ◽  
Optimal Level ◽  
The Body ◽  
Control Group ◽  
Quantitative Criterion ◽  
Male Athletes ◽  
Intensity Index ◽  
The Third ◽  
Psychoemotional State ◽  
The Brain

Objective: to evaluate the effectiveness of psychocorrection based on the methods of self­regulation in athletes.Materials and methods: the effectiveness was evaluated on 104 male athletes who had an optimal level of psychoemotional state of the body during a background examination by electroencephalography (EEG). The subjects were randomly assigned to three groups of psychocorrection: control, EEGtraining, and VR­therapy. Mathematical and statistical processing was carried out in Statistica 7.Results: the average values of the wave intensity index (WII) after psychological correction using the following methods: EEG­training and VRtherapy showed positive EEG dynamics in athletes of the second group (EEG­training) 65,6 % (21) and the third group (Vr­therapy) 73,8 % (31) of the subjects, respectively. Whereas in the control group, self­healing was recorded in 9 (30 %) athletes without psychocorrection procedures.Conclusion: the quantitative criterion of WII is a universal informative indicator of the functional activity of the brain for evaluating the effectiveness of psychocorrection aimed at optimizing the psychoemotional state. Psychocorrection of athletes using EEG­training and VR­therapy provides efficiency in 73.8 and 65.6 % of cases, which significantly softens pre­start tension as a result of reducing anxiety and restoring the psychoemotional state of the body to an optimal level by involving the psychological reserve.

The impact of physical exercise on hippocampus, in physiological condition and ageing-related decline: current evidence from animal and human studies

2021 ◽  
Vol 22 ◽  
Author(s):  
Giovanni Lauretta ◽  
Silvia Ravalli ◽  
Grazia Maugeri ◽  
Velia D’Agata ◽  
Michelino Di Rosa ◽  
...  
Keyword(s):  
Physical Exercise ◽  
Well Being ◽  
Brain Regions ◽  
The Body ◽  
Current Evidence ◽  
Psychological Benefits ◽  
Functional Changes ◽  
Human Lifespan ◽  
The Impact ◽  
The Brain

: Physical exercise (PE), notoriously, promotes a state of general well-being, throughout the entire human lifespan. Moreover, maintaining an adequate and regular PE habit results to be a powerful preventive factor towards many diseases and may also help in managing existing pathological conditions. PE induces structural and functional changes in various districts of the body, determining biological and psychological benefits. Additionally, in elderly, PE might represent a remarkable tool reducing cognitive impairments related to the normal aging processes and it has also been found to have an impact in neurodegenerative diseases such as Alzheimer’s disease. The present review aims to provide an overview about PE effects on hippocampus, since it is one of the brain regions most susceptible to aging and, therefore, involved in diseases characterized by cognitive impairment.

scholarly journals Calcium channel blockade with nimodipine reverses MRI evidence of cerebral oedema following acute hypoxia

2017 ◽  
Vol 39 (2) ◽  
pp. 285-301 ◽  
Author(s):  
Matthew J Rowland ◽  
Martyn Ezra ◽  
Anderson Winkler ◽  
Payashi Garry ◽  
Catherine Lamb ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Neuronal Damage ◽  
Acute Hypoxia ◽  
Low Frequency ◽  
Brain Regions ◽  
Calcium Flux ◽  
Cell Swelling ◽  
Grey Matter Volume ◽  
Brain Response ◽  
The Brain

Acute cerebral hypoxia causes rapid calcium shifts leading to neuronal damage and death. Calcium channel antagonists improve outcomes in some clinical conditions, but mechanisms remain unclear. In 18 healthy participants we: (i) quantified with multiparametric MRI the effect of hypoxia on the thalamus, a region particularly sensitive to hypoxia, and on the whole brain in general; (ii) investigated how calcium channel antagonism with the drug nimodipine affects the brain response to hypoxia. Hypoxia resulted in a significant decrease in apparent diffusion coefficient (ADC), a measure particularly sensitive to cell swelling, in a widespread network of regions across the brain, and the thalamus in particular. In hypoxia, nimodipine significantly increased ADC in the same brain regions, normalizing ADC towards normoxia baseline. There was positive correlation between blood nimodipine levels and ADC change. In the thalamus, there was a significant decrease in the amplitude of low frequency fluctuations (ALFF) in resting state functional MRI and an apparent increase of grey matter volume in hypoxia, with the ALFF partially normalized towards normoxia baseline with nimodipine. This study provides further evidence that the brain response to acute hypoxia is mediated by calcium, and importantly that manipulation of intracellular calcium flux following hypoxia may reduce cerebral cytotoxic oedema

scholarly journals An Embodied Account of Argument Structure Development

2010 ◽  
Vol 36 (1) ◽  
pp. 261
Author(s):  
Josita Maouene ◽  
Nitya Sethuraman ◽  
Mounir Maoene ◽  
Linda B. Smith
Keyword(s):  
Cognitive Neuroscience ◽  
Argument Structure ◽  
Body Part ◽  
Brain Regions ◽  
The Body ◽  
Body Parts ◽  
Structure Development ◽  
Body Experiences ◽  
Verb Meaning ◽  
The Brain

In lieu of an abstract, here is a brief excerpt:All information enters the cognitive system through the body. Thus, it is possible that the body—and its morphology—may play a role in structurng knowledge and acquisition. This idea is particularly cogent in the case of verbs, since early learned verbs are about bodily actions and since recent advanc-es in cognitive neuroscience (Pulvermueller, 2005; James and Maouene, 2009) indicate that the neural processing of common verbs activates the brain regions responsible for the specific body parts that perform those actions. Here we provide initial evidence these body-part verb relations may also be related to the argument structures associated with specific verbs. We will conclude that in the same way that verb meaning and argument structure develop out of correlations in linguistic experiences, they may also develop out of correlations in body experiences. 

scholarly journals Species-Specific Features of Neuron-Glial Populations in the Brain of Tailless Amphibians

2019 ◽  
pp. 445-459
Author(s):  
Liubov’ N. Afanaskina ◽  
Nadezhda N. Medvedeva
Keyword(s):  
Brain Regions ◽  
Bufo Bufo ◽  
Cellular Level ◽  
The Body ◽  
Rana Arvalis ◽  
Species Specific ◽  
The Relationship ◽  
The Brain ◽  
Tailless Amphibians

The midbrain roof and cerebellum cortex are the main integrative centers in amphibians. They serve to analyze and process nerve impulses, form the organism’s response, regulate and coordinate movements, connect amphibians with their environments. The present study addresses the relationship between the species of the tailless amphibians inhabiting the southern part of the Krasnoyarsk region (Bufo bufo Linnaeus, Rana arvalis Nilsson, Pelophylax ridibundus Pallas, and Rana amurensis Boulenger) and the morphological parameters of the populations of neurons and glia in layer VI of the midbrain roof and layers of the cerebellum cortex. The species-specific structure of amphibians’ brain regions has been found to be evident not only at the organ level (size and shape), but also at the level of the organization of neuron and glial cell populations. Distinctive species-specific differences can be found in the parameters of cell area (the area of the body, the area of the nucleus and the area of the cytoplasm) and the distribution density of neurons and gliocytes. The development of specific morphological features at the cellular level of the arrangement of the midbrain and cerebellum layers in different species of tailless amphibians is associated with long-term phylogenetic transformations of their nervous system and adaptation of amphibians to the terrestrial-aquatic habitat

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