Lanthanum chloride induces autophagy in rat hippocampus through ROS-mediated JNK and AKT/mTOR signaling pathways

Metallomics ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 439-453 ◽  
Author(s):  
Xiang Gao ◽  
Jinghua Yang ◽  
Yingqi Li ◽  
Miao Yu ◽  
Shiyu Liu ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Signaling Pathways ◽  
Learning And Memory ◽  
Memory Impairment ◽  
Mtor Signaling ◽  
Lanthanum Chloride ◽  
Rat Hippocampus ◽  
Central Nervous System Damage

Lanthanum (La) can cause central nervous system damage in rats and lead to learning and memory impairment, but the relevant mechanisms have not been fully elucidated.

Targeting the PI3K/AKT/mTOR Signaling Pathway in Primary Central Nervous System Lymphoma: Current Status and Future Prospects

2020 ◽  
Vol 19 (3) ◽  
pp. 165-173
Author(s):  
Xiaowei Zhang ◽  
Yuanbo Liu
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
B Cell ◽  
Signaling Pathway ◽  
Central Nervous System Lymphoma ◽  
B Cell Lymphoma ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Antitumor Effects ◽  
Term Survival

Primary Central Nervous System Lymphoma (PCNSL) is a rare invasive extranodal non- Hodgkin lymphoma, a vast majority of which is Diffuse Large B-Cell Lymphoma (DLBCL). Although high-dose methotrexate-based immunochemotherapy achieves a high remission rate, the risk of relapse and related death remains a crucial obstruction to long-term survival. Novel agents for the treatment of lymphatic malignancies have significantly broadened the horizons of therapeutic options for PCNSL. The PI3K/AKT/mTOR signaling pathway is one of the most important pathways for Bcell malignancy growth and survival. Novel therapies that target key components of this pathway have shown antitumor effects in many B-cell malignancies, including DLBCL. This review will discuss the aberrant status of the PI3K/AKT/mTOR signaling pathways in PCNSL and the application prospects of inhibitors in hopes of providing alternative clinical therapeutic strategies and improving prognosis.

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

Crosstalk Between Insulin and Toll-like Receptor Signaling Pathways in the Central Nervous system

2014 ◽  
Vol 50 (3) ◽  
pp. 797-810 ◽  
Author(s):  
Fatemeh Hemmati ◽  
Rasoul Ghasemi ◽  
Norlinah Mohamed Ibrahim ◽  
Leila Dargahi ◽  
Zahurin Mohamed ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Signaling Pathways ◽  
Receptor Signaling ◽  
Toll Like Receptor ◽  
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 mTORC1 is necessary but mTORC2 and GSK3β are inhibitory for AKT3-induced axon regeneration in the central nervous system

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Linqing Miao ◽  
Liu Yang ◽  
Haoliang Huang ◽  
Feisi Liang ◽  
Chen Ling ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Axon Regeneration ◽  
Nodal Point ◽  
Mtor Signaling ◽  
Negative Regulator ◽  
Molecular Dissection ◽  
Parallel Pathways ◽  
Downstream Effectors ◽  
The Central Nervous System

Injured mature CNS axons do not regenerate in mammals. Deletion of PTEN, the negative regulator of PI3K, induces CNS axon regeneration through the activation of PI3K-mTOR signaling. We have conducted an extensive molecular dissection of the cross-regulating mechanisms in axon regeneration that involve the downstream effectors of PI3K, AKT and the two mTOR complexes (mTORC1 and mTORC2). We found that the predominant AKT isoform in CNS, AKT3, induces much more robust axon regeneration than AKT1 and that activation of mTORC1 and inhibition of GSK3β are two critical parallel pathways for AKT-induced axon regeneration. Surprisingly, phosphorylation of T308 and S473 of AKT play opposite roles in GSK3β phosphorylation and inhibition, by which mTORC2 and pAKT-S473 negatively regulate axon regeneration. Thus, our study revealed a complex neuron-intrinsic balancing mechanism involving AKT as the nodal point of PI3K, mTORC1/2 and GSK3β that coordinates both positive and negative cues to regulate adult CNS axon regeneration.

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.

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