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CNS Recovery after Structural and/or Physiological/Psychological Damage

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889450404 Year: Pages: 107 DOI: 10.3389/978-2-88945-040-4 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Neurology
Added to DOAB on : 2018-02-27 16:16:44
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There is an assumption that environmental threats could cause important damages in central nervous system. As a consequence, several forms of brain structural plasticity could be affected. The environmentally mediated risks include generally physical (such as brain and spinal cord injury) and psychological / psychosocial influences (e.g. stress). In general, the response of the organism to these environmental challenges passes via adaptive responses to maintain homeostasis or functional recovery. These processes engage the immune system, the autonomic nervous system (ANS) besides the hypothalamo-hypophyseo-adrenal (HPA) axis via specific hormones, neurotransmitters, neuropeptides and other factors which participate, in several cases, in structural remodeling in particular brain areas. To what extent a brain and / or spinal cord recovery after structural and / or physiological / psychological damage could occur and by which mechanisms, this is the goal of this Research Topic. It concerns neurogenesis, growth factors and their receptors, and morphological plasticity. On the other hand, it is well known that stress experienced an obvious impact on many behavioral and physiological aspects. Thus, environmental stress affects neuroendocrine structure and function and hence such aspects may influence brain development. Knowing normal organization of neurotensin receptors’ system during postnatal development in human infant will help understanding the dysfunction of this neuropetidergic system in “sudden infant syndrome” victims. Stress could affect also other non-neuroendocrine regions and systems. GABA is one of the classical neurotransmitter sensitive to stress either when applied acutely or repetitively as well as its receptor GABAA. Furthermore, the modulation of this receptor complex notably by neurosteroids is also affected by acute stress. These steroids seem to play a role in the resilience retained by the stressed brain. Their modulatory role will be studied in the context of chronic stress in rats. Finally, one of the major impacts of stress besides changes in psychological behavior is the alteration of food intake control causing in final eating disorders. This alteration is the result of changes occurring in activity of brain regions involved in stress responses (principally HPA and ANS) and which are also involved in food intake control. The series of studies presented here, will try to explain how different stress paradigms affect this function and the eventual interactions of glucocorticoids with orexigenic (neuropetide Y: NPY/Agouti Related Peptide: AgRP) and anorexigenic peptides (Pre-opiomelanocortin peptide: POMC/Cocaine Amphetamine regulatory Transcript peptide: CART).

Cellular Mechanisms of Ototoxicity

Authors: --- --- --- --- et al.
Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889454839 Year: Pages: 292 DOI: 10.3389/978-2-88945-483-9 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Neurology
Added to DOAB on : 2019-01-23 14:53:42
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The auditory perception of sounds (environmental, vocal or music) is one of the 5 principal senses consciously monitored by our brains, and is crucial for many human endeavors as well as quality of life. Loss of optimal performance in this principal sensory system leads to loss of effective communication and intimacy, as well as increased risk of isolation, depression, cognitive decline, and greater vulnerability to predators.The vestibular system ensures that individuals remain upright and effectively monitor their posture within their spatial surroundings, move effectively, and remain focused on visual targets during motion. The loss of vestibular sensitivity results in postural instability, falls, inability to observe the environment during motion, and a debilitating incapacity to function effectively. The sensory cells for both auditory and vestibular systems are located within the inner ear of the temporal bulla.There are many causes of auditory and vestibular deficits, including congenital (or genetic) events, trauma, aging and loud sound exposures. Ototoxicity refers to damage of the auditory or vestibular structures or functions, as the result of exposure to certain pharmaceuticals, chemicals, and/or ionizing radiation exposure that damage the inner ear. Ototoxicity is a major contributor to acquired hearing loss and vestibular deficits, and is entirely preventable.In 2009, the United States Department of Defense initiated the Hearing Center of Excellence (HCE), headquartered in San Antonio, Texas, in response to the prevalence of acquired auditory and vestibular deficits in military and veteran populations. The knowledge shared in this eBook supports the HCE’s mandate to improve aural protection of military and civilian populations worldwide.The last few years have seen significant advances in understanding the cellular mechanisms underlying ototoxic drug-induced hearing loss and vestibular deficits. In this eBook, we present some of these advances and highlight gaps where further research is needed. Selected articles discuss candidate otoprotective agents that can ameliorate the effects of ototoxicity in the context of how they illustrate cellular mechanisms of ototoxicity. Our goal in illustrating these advances in mechanisms of ototoxicity is to accelerate the development of clinical therapies that prevent or reverse this debilitating disorder.

Mercury and Methylmercury Toxicology and Risk Assessment

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ISBN: 9783038979708 / 9783038979715 Year: Pages: 142 DOI: 10.3390/books978-3-03897-971-5 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Technology (General) --- Chemical Engineering
Added to DOAB on : 2019-06-26 08:44:06
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Mercury is a global pollutant that affects the health of both humans and ecosystems. This Special Issue collects three review papers and six research articles that report on the latest findings on the mechanisms of mercury toxicology and its impacts on environmental health. This collection of papers provides useful, new information on the mechanisms of mercury toxicity and methods of improving the risk assessment of mercury exposure.

mTOR in Human Diseases

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ISBN: 9783039210602 / 9783039210619 Year: Pages: 480 DOI: 10.3390/books978-3-03921-061-9 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Medicine (General)
Added to DOAB on : 2019-06-26 08:44:06
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The mechanistic target of rapamycin (mTOR) is a major signaling intermediary that coordinates favorable environmental conditions with cell growth. Indeed, as part of two functionally distinct protein complexes, named mTORC1 and mTORC2, mTOR regulates a variety of cellular processes, including protein, lipid, and nucleotide synthesis, as well as autophagy. Over the last two decades, major molecular advances have been made in mTOR signaling and have revealed the complexity of the events implicated in mTOR function and regulation. In parallel, the role of mTOR in diverse pathological conditions has also been identified, including in cancer, hamartoma, neurological, and metabolic diseases. Through a series of articles, this book focuses on the role played by mTOR in cellular processes, metabolism in particular, and highlights a panel of human diseases for which mTOR inhibition provides or might provide benefits. It also addresses future studies needed to further characterize the role of mTOR in selected disorders, which will help design novel therapeutic approaches. It is therefore intended for everyone who has an interest in mTOR biology and its application in human pathologies.

Keywords

acute myeloid leukemia --- metabolism --- mTOR --- PI3K --- phosphorylation --- epithelial to mesenchymal transition --- mTOR inhibitor --- pulmonary fibrosis --- transcriptomics --- miRNome --- everolimus --- mTOR --- thyroid cancer --- sodium iodide symporter (NIS)/SLC5A5 --- dopamine receptor --- autophagy --- AKT --- mTOR --- AMPK --- mTOR --- Medulloblastoma --- MBSCs --- mTOR --- T-cell acute lymphoblastic leukemia --- targeted therapy --- combination therapy --- mTOR --- metabolic diseases --- glucose and lipid metabolism --- anesthesia --- neurotoxicity --- synapse --- mTOR --- neurodevelopment --- mTOR --- rapamycin --- autophagy --- protein aggregation --- methamphetamine --- schizophrenia --- tumour cachexia --- mTOR --- signalling --- metabolism --- proteolysis --- lipolysis --- mTOR --- mTORC1 --- mTORC2 --- rapamycin --- rapalogues --- rapalogs --- mTOR inhibitors --- senescence --- ageing --- aging --- cancer --- neurodegeneration --- immunosenescence --- senolytics --- biomarkers --- leukemia --- cell signaling --- metabolism --- apoptosis --- miRNA --- mTOR inhibitors --- mTOR --- tumor microenvironment --- angiogenesis --- immunotherapy --- fluid shear stress --- melatonin --- chloral hydrate --- nocodazole --- MC3T3-E1 cells --- primary cilia --- mTOR complex --- metabolic reprogramming --- cancer --- microenvironment --- nutrient sensor --- oral cavity squamous cell carcinoma (OSCC) --- NVP-BEZ235 --- mTOR --- p70S6K --- mTOR --- advanced biliary tract cancers --- mTOR --- NGS --- illumina --- IonTorrent --- eIFs --- mTOR --- autophagy --- Parkinson’s disease --- mTOR --- PI3K --- cancer --- inhibitor --- therapy --- mTOR --- laminopathies --- lamin A/C --- Emery-Dreifuss muscular dystrophy (EDMD) --- Hutchinson-Gilford progeria syndrome (HGPS) --- autophagy --- cellular signaling --- metabolism --- bone remodeling --- ageing --- mTOR --- fructose --- glucose --- liver --- lipid metabolism --- gluconeogenesis --- Alzheimer’s disease --- autophagy --- mTOR signal pathway --- physical activity --- microRNA --- mTOR --- spermatogenesis --- male fertility --- Sertoli cells --- n/a

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