Brain organoids: a promising model to assess oxidative stress‐induced Central Nervous System damage

2021 ◽  
Author(s):  
Foluwasomi A. Oyefeso ◽  
Alysson R. Muotri ◽  
Christopher G. Wilson ◽  
Michael J. Pecaut
Keyword(s):  
Oxidative Stress ◽  
Central Nervous System ◽  
Nervous System ◽  
Central Nervous System Damage

scholarly journals Troublesome Heterotopic Ossification after Central Nervous System Damage: A Survey of 570 Surgeries

PLoS ONE ◽  
2011 ◽  
Vol 6 (1) ◽  
pp. e16632 ◽  
Author(s):  
François Genêt ◽  
Claire Jourdan ◽  
Alexis Schnitzler ◽  
Christine Lautridou ◽  
Didier Guillemot ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Heterotopic Ossification ◽  
Central Nervous System Damage

Abstract 103: ACE2 Overexpression Prevents DOCA-Salt Hypertension by Modulating Oxidative Stress and Nitric Oxide in the Central Nervous System

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Srinivas Sriramula ◽  
Huijing Xia ◽  
Eric Lazartigues
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Central Nervous System ◽  
Nervous System ◽  
Nadph Oxidase ◽  
Salt Treatment ◽  
Salt Hypertension ◽  
The Central Nervous System ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Elevated reactive oxygen species (ROS) in the central nervous system (CNS) through NADPH oxidase and diminished Nitric oxide (NO) levels are involved in the pathogenesis of hypertension. We previously reported that central Angiotensin Converting Enzyme 2 (ACE2) overexpression prevents the development of hypertension induced by DOCA-salt in a transgenic mouse model (syn-hACE2; SA) with human ACE2 targeted selectively to neurons in the CNS. While baseline blood pressure (BP; telemetry) was not different among genotypes, DOCA-salt treatment (1mg/g body wt DOCA, 1% saline in drinking water for 3 weeks) resulted in significantly lower BP level in SA mice (122 ±3 mmHg, n=12) compared to non-transgenic (NT) littermates (138 ±3 mmHg, n=8). To elucidate the mechanisms involved in this response, we investigated the paraventricular nucleus (PVN) expression of Nox-2 (catalytic subunit of NADPH oxidase), 3-nitrotyrosine, and endothelial nitric oxide synthase (eNOS) and anti-oxidant enzymes superoxide dismutase (SOD) and catalase in the hypothalamus. DOCA-salt treatment resulted in decreased catalase (95.2 ±5.6 vs. 113.8 ±17.6 mmol/min/ml, p<0.05) and SOD (4.1 ±0.4 vs. 5.9 ±0.2 U/ml, p<0.01) activities in hypothalamic homogenates of NT mice, which was prevented by ACE2 overexpression (141.8 ±9.9 vs. 142.1 ±9.2 mmol/min/ml and 5.9 ±0.3 vs. 7.9 ±0.2 U/ml, respectively). NT mice treated with DOCA-salt showed increased oxidative stress as indicated by increased expression of Nox-2 (61 ±5 % increase, n=9, p<0.001 vs. NT) and 3-nitrotyrosine (89 ±32 % increase, n=9, p<0.01 vs. NT) in the PVN which was attenuated in SA mice. Furthermore, DOCA-salt hypertension resulted in decreased phosphorylation of eNOS-ser1177 in the PVN (33 ±5 % decrease, n=9, p<0.05 vs NT) and this decrease was prevented by ACE2 overexpression. Taken together, these data provide evidence that brain ACE2 regulates the balance between NO and ROS levels, thereby preventing the development of DOCA-salt hypertension.

Interrelationships between astrocyte function, oxidative stress and antioxidant status within the central nervous system

1997 ◽  
Vol 52 (4) ◽  
pp. 261-281 ◽  
Author(s):  
Stefan Peuchen ◽  
Juan P. Bolaños ◽  
Simon J.R. Heales ◽  
Angeles Almeida ◽  
Michael R. Duchen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Central Nervous System ◽  
Nervous System ◽  
Antioxidant Status ◽  
The Central Nervous System

scholarly journals Design and Implementation ofReal-time Electrical Stimulation Artifact Suppression based on STM32

2021 ◽  
Vol 12 (5) ◽  
pp. 424-427
Author(s):  
Sangsoo Park, Hojun Yeom
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Electrical Stimulation ◽  
Embedded System ◽  
Muscle Contraction ◽  
Real Time ◽  
High Performance ◽  
Floating Point ◽  
Time Signal ◽  
Central Nervous System Damage

A biosignal is used as a control signal for electrical stimulation to restore weakened muscle function due to damage to the central nervous system. In patients with central nervous system damage, sufficient muscle contraction does not occur spontaneously. In this case, applying electrical stimulation can cause normal muscle contraction. However, it is necessary to remove the electrical stimulation artifact caused by the electrical stimulation. This paper describes a system design that removes electrical stimulation artifact in real time using a Cortex-M4-based STM32F processor. The STM32F is a very advantageous MCU for such DSPs, especially because it has a built-in floating point operator. Using STM32F's various high-performance peripherals (12-bit parallel ADC and 12-bit DAC, UART, Timer), an optimized embedded system was implemented.In this paper, the simulated and real-time results were compared and evaluated with the designed fir filter. In addition, the performance of the filter was evaluated through frequency analysis. As a result, it was verified that a high-performance 32-bit STM32F with floating point calculator and various peripherals is suitable for real-time signal processing

scholarly journals Mycobacterium of tuberculosis with defective cell wall, determined in the brain of the biological model with spongional changes

2019 ◽  
Vol 23 (1) ◽  
pp. 12-19
Author(s):  
O.P. Lysenko ◽  
V.V. Vlasenko ◽  
H.K. Palii ◽  
I.H. Vlasenko ◽  
O.A. Nazarchuk
Keyword(s):  
Central Nervous System ◽  
Cell Wall ◽  
Nervous System ◽  
Mycobacterium Tuberculosis ◽  
Brain Damage ◽  
Molecular Genetic Study ◽  
Central Nervous System Damage ◽  
Infectious Dose ◽  
Microbiological Methods ◽  
The Brain

Mycobacterium tuberculosis is endowed with resistance to adverse factors and rapidly forms drug resistance. The aim is to study of the connection of tuberculosis infection and the development of brain damage with signs of spongymorphic changes. There were investigated canned 10% formalin fragments of the brain of 2 goats with signs of central nervous system damage by histological, microbiological methods. For microbiological examination, 3–5 years brain samples after were sowed on the MycСel DW nutrient medium with a growth stimulator. The molecular genetic study was performed using a polymerase chain reaction on a Molecular Imager GelDoc TM XR + (BioRad) device. The polypeptide profile was studied electrophoretically. In the goats, who died with symptoms of central nervous system damage, spongiform changes were detected in the brain. In the brain samples, DNA and mycobacterium tuberculosis with a defective cell wall have been detected, accumulation of mycobacterial antigens has been observed in the cells of the brain and in the intercellular space. Despite the fact that brain samples were in 10% formalin for 1 month, 3 years and 5 years, in all cases mycobacterium tuberculosis with a defective cell wall was isolated. Their viability was comparable to the infectiousness of prions. The isolation of mycobacterium tuberculosis with a defective cell wall from the brain did not differ in morphology and polypeptide composition from isolates from tuberculin, FLK-BLV, lymph nodes of cows, patients with tuberculosis. This indicates a high probability that mycobacterial infection, depending on the infectious dose, the characteristics of the strain and host genome, as well as the state of the immune system, can cause oncogenic action, cause active tuberculosis, brain damage, and the cardiovascular system.

scholarly journals The central nervous system is a target of acute graft versus host disease in mice

Blood ◽  
2013 ◽  
Vol 121 (10) ◽  
pp. 1906-1910 ◽  
Author(s):  
Steffen Hartrampf ◽  
Jarrod A. Dudakov ◽  
Linda K. Johnson ◽  
Odette M. Smith ◽  
Jennifer Tsai ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Central Nervous System Damage ◽  
Graft Versus Host ◽  
Alloreactive T Cells ◽  
Key Points ◽  
The Central Nervous System ◽  
Anxiety Behavior ◽  
Direct Target ◽  
Acute Graft

Key Points The central nervous system can be a direct target of alloreactive T cells during GVHD. Central nervous system damage in mouse models of GVHD lead to deficits in learning and increased anxiety behavior.

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