Biological response of the organism to the introduction of metal nanocomposites

Russian Journal of Occupational Health and Industrial Ecology ◽

10.31089/1026-9428-2019-59-9-761-762 ◽

2020 ◽

pp. 761-762

Author(s):

L. M. Sosedova ◽

V. S. Rukavishnikov ◽

E. A. Titov

Keyword(s):

Cell Death ◽

Programmed Cell Death ◽

Biological Response ◽

Brain Cell ◽

Metal Nanocomposites ◽

The Brain

The results of a study on rats toxicity of nanoparticles of metals bismuth, gadolinium and silver encapsulated in a natural biopolymer matrix arabinogalactan are presented. When intake of nanocomposite of silver revealed the readiness of the brain cell to apoptosis. The effect of bismuth and gadolinium nanocomposites did not cause an increase in the process of programmed cell death.

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Neuronal apoptosis: signal and cell diversity

Colombia Medica ◽

10.25100/cm.v40i1.634 ◽

1969 ◽

Vol 40 (1) ◽

pp. 124-133

Author(s):

Lina Vanessa Becerra ◽

Hernán José Pimienta

Keyword(s):

Cell Death ◽

Programmed Cell Death ◽

Neuronal Response ◽

Neuronal Cell ◽

Cell Types ◽

Point Of View ◽

Trophic Factors ◽

Cell Diversity ◽

Apoptotic Pathways ◽

The Brain

Programmed cell death occurs as a physiological process during development. In the brain and spinal cord this event determines the number and location of the different cell types. In adulthood, programmed cell death or apoptosis is more restricted but it may play a major role in different acute and chronic pathological entities. However, in contrast to other tissues where apoptosis has been widely documented from a morphological point of view, in the central nervous system complete anatomical evidence of apoptosis is scanty. In spite of this there is consensus about the activation of different signal systems associated to programmed cell death. In the present article we attempt to summarize the main apoptotic pathways so far identified in nervous tissue. Considering that apoptotic pathways are multiple, the neuronal cell types are highly diverse and specialized and that neuronal response to injury and survival depends upon tissue context, (i.e., preservation of connectivity, glial integrity and cell matrix, blood supply and trophic factors availability) what is relevant for the apoptotic process in a sector of the brain may not be important in another.

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Exploring the Anti-Infective Value of Inuloxin A Isolated from Inula viscosa against the Brain-Eating Amoeba (Naegleria fowleri) by Activation of Programmed Cell Death

ACS Chemical Neuroscience ◽

10.1021/acschemneuro.0c00685 ◽

2020 ◽

Vol 12 (1) ◽

pp. 195-202

Author(s):

Ikrame Zeouk ◽

Ines Sifaoui ◽

Aitor Rizo-Liendo ◽

Iñigo Arberas-Jiménez ◽

María Reyes-Batlle ◽

...

Keyword(s):

Cell Death ◽

Programmed Cell Death ◽

Naegleria Fowleri ◽

Nægleria Fowleri ◽

The Brain

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Simulation of Spread and Control of Lesions in Brain

Computational and Mathematical Methods in Medicine ◽

10.1155/2012/383546 ◽

2012 ◽

Vol 2012 ◽

pp. 1-6

Author(s):

Krishna Mohan Thamattoor Raman

Keyword(s):

Cell Death ◽

Programmed Cell Death ◽

Graph Representation ◽

Smooth Transition ◽

Network Graph ◽

Planar Network ◽

The Central Nervous System ◽

Lesion Growth ◽

And Control ◽

The Brain

A simulation model for the spread and control of lesions in the brain is constructed using a planar network (graph) representation for the central nervous system (CNS). The model is inspired by the lesion structures observed in the case of multiple sclerosis (MS), a chronic disease of the CNS. The initial lesion site is at the center of a unit square and spreads outwards based on the success rate in damaging edges (axons) of the network. The damaged edges send out alarm signals which, at appropriate intensity levels, generate programmed cell death. Depending on the extent and timing of the programmed cell death, the lesion may get controlled or aggravated akin to the control of wild fires by burning of peripheral vegetation. The parameter phase space of the model shows smooth transition from uncontrolled situation to controlled situation. The simulations show that the model is capable of generating a wide variety of lesion growth and arrest scenarios.

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Focused Ultrasound-Enhanced Delivery of Intranasally Administered Anti-Programmed Cell Death-Ligand 1 Antibody to an Intracranial Murine Glioma Model

Pharmaceutics ◽

10.3390/pharmaceutics13020190 ◽

2021 ◽

Vol 13 (2) ◽

pp. 190

Author(s):

Dezhuang Ye ◽

Jinyun Yuan ◽

Yimei Yue ◽

Joshua B. Rubin ◽

Hong Chen

Keyword(s):

Cell Death ◽

Programmed Cell Death ◽

Immune Checkpoint ◽

Immune Checkpoint Inhibitors ◽

Near Infrared ◽

Focused Ultrasound ◽

Checkpoint Inhibitors ◽

Brain Parenchyma ◽

Perivascular Spaces ◽

The Brain

Immune checkpoint inhibitors have great potential for the treatment of gliomas; however, their therapeutic efficacy has been partially limited by their inability to efficiently cross the blood–brain barrier (BBB). The objective of this study was to evaluate the capability of focused-ultrasound-mediated intranasal brain drug delivery (FUSIN) in achieving the locally enhanced delivery of anti-programmed cell death-ligand 1 antibody (aPD-L1) to the brain. Both non-tumor mice and mice transcranially implanted with GL261 glioma cells at the brainstem were used in this study. aPD-L1 was labeled with a near-infrared fluorescence dye (IRDye 800CW) and administered to mice through the nasal route to the brain, followed by focused ultrasound sonication in the presence of systemically injected microbubbles. FUSIN enhanced the accumulation of aPD-L1 at the FUS-targeted brainstem by an average of 4.03- and 3.74-fold compared with intranasal (IN) administration alone in the non-tumor mice and glioma mice, respectively. Immunohistochemistry staining found that aPD-L1 was mainly located within the perivascular spaces after IN delivery, while FUSIN further enhanced the penetration depth and delivery efficiency of aPD-L1 to the brain parenchyma. The delivered aPD-L1 was found to be colocalized with the tumor cells after FUSIN delivery to the brainstem glioma. These findings suggest that FUSIN is a promising technique to enhance the delivery of immune checkpoint inhibitors to gliomas.

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Inflammation but not programmed cell death is activated in methamphetamine-dependent patients: Relevance to the brain function

International Journal of Psychophysiology ◽

10.1016/j.ijpsycho.2020.09.004 ◽

2020 ◽

Vol 157 ◽

pp. 42-50

Author(s):

Nooshin Ghavidel ◽

Fariba Khodagholi ◽

Abolhassan Ahmadiani ◽

Reza Khosrowabadi ◽

Sareh Asadi ◽

...

Keyword(s):

Cell Death ◽

Programmed Cell Death ◽

Brain Function ◽

The Brain

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Remodeling the Adolescent Brain

Coming of Age ◽

10.1093/oso/9780195314373.003.0003 ◽

2019 ◽

pp. 22-40

Author(s):

Cheryl L. Sisk ◽

Russell D. Romeo

Keyword(s):

Cell Death ◽

Nervous System ◽

Programmed Cell Death ◽

Synapse Formation ◽

Neural Mechanisms ◽

Axon Outgrowth ◽

Synapse Elimination ◽

Loss Of Function ◽

The Brain

Chapter 3 covers the basic neural mechanisms by which the brain undergoes an extreme makeover during adolescence. It starts with the proposition that the nervous system has only so many tools in the toolbox to accomplish this makeover and these tools can be categorized as either progressive or regressive. Progressive tools include neurogenesis, migration, axon outgrowth, and synapse formation. Regressive tools include programmed cell death and experience-dependent synapse elimination. Two analogies are used to help readers understand this process: house remodeling and gardening. These analogies are woven into the concepts of progressive and regressive developmental events, and they can be imagined as mechanisms that result in either gain or loss of function (e.g., a house addition might equal new neurons or new projections) or maximize efficiency and success (pruning of seedlings might equal programmed cell death). Research on increased myelination during adolescence is also discussed.

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