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・ Glionnetia sericea
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・ Gliophorus europerplexus
・ Gliophorus graminicolor
・ Gliophorus irrigatus
・ Gliophorus laetus
・ Gliophorus lilacipes
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・ Gliosarcoma
Gliosis
・ Gliotoxin
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・ Glip
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・ Glipa albannulata
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・ Glipa annulata
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Gliosis : ウィキペディア英語版
Gliosis
Gliosis is a nonspecific reactive change of glial cells in response to damage to the central nervous system (CNS). In most cases, gliosis involves the proliferation or hypertrophy of several different types of glial cells, including astrocytes, microglia, and oligodendrocytes. In its most extreme form, the proliferation associated with gliosis leads to the formation of a glial scar.
The process of gliosis involves a series of cellular and molecular events that occur over several days.〔Fawcett, J. W., & Asher, R. A. (1999). The glial scar and central nervous system repair. Brain Res Bull, 49(6), 377-391. doi: S0361-9230(99)00072-6 ()〕 Typically, the first response to injury is the migration of macrophages and local microglia to the injury site. This process, which constitutes a form of gliosis known as microgliosis, begins within hours of the initial CNS injury.〔〔Streit, W. J., Walter, S. A., & Pennell, N. A. (1999). Reactive microgliosis. Progress in Neurobiology, 57(6), 563-581.〕 Later, after 3–5 days, oligodendrocyte precursor cells are also recruited to the site and may contribute to remyelination.〔 The final component of gliosis is astrogliosis, the proliferation of surrounding astrocytes, which are the main constituents of the glial scar.
Gliosis has historically been given a negative connotation due to its appearance in many CNS diseases and the inhibition of axonal regeneration caused by glial scar formation. However, gliosis has been shown to have both beneficial and detrimental effects, and the balance between these is due to a complex array of factors and molecular signaling mechanisms, which affect the reaction of all glial cell types.
==Astrogliosis==
(詳細はproliferation of astrocytes, a type of glial cell responsible for maintaining extracellular ion and neurotransmitter concentrations, modulating synapse function, and forming the blood–brain barrier.〔Rivera-Zengotita, M., & Yachnis, A. T. (2012). Gliosis Versus Glioma?: Don't Grade Until You Know. Advances in Anatomic Pathology, 19(4), 239-249. doi: Doi 10.1097/Pap.0b013e31825c6a04〕 Like other forms of gliosis, astrogliosis accompanies traumatic brain injury as well as many neuropathologies, ranging from Amyotrophic Lateral Sclerosis to Fatal Familial Insomnia. Although the mechanisms which lead to astrogliosis are not fully understood, neuronal injury is well understood to cause astrocyte proliferation, and astrogliosis has long been used as an index for neuronal damage.〔Zhang, D., Hu, X. M., Qian, L., O'Callaghan, J. P., & Hong, J. S. (2010). Astrogliosis in CNS Pathologies: Is There A Role for Microglia? Molecular Neurobiology, 41(2-3), 232-241. doi: DOI 10.1007/s12035-010-8098-4〕 Traditionally, astrogliosis has been defined as an increase in intermediate filaments and cellular hypertrophy as well as an increase in the proliferation of astrocytes. Although this hypertrophy and proliferation in their extreme form are most closely associated with the formation of a glial scar, astrogliosis is not an all-or-none process in which a glial scar forms. In fact, it is a spectrum of changes that occur based on the type and severity of central nervous system (CNS) injury or disease triggering the event.〔Sofroniew, M. V. (2009). Molecular dissection of reactive astrogliosis and glial scar formation. Trends Neurosci, 32(12), 638-647. doi: S0166-2236(09)00153-2 () 10.1016/j.tins.2009.08.002〕 Changes in astrocyte function or morphology which occur during astrogliosis may range from minor hypertrophy to major hypertrophy, domain overlap, and ultimately, glial scar formation.〔 The severity of astrogliosis is classically determined by the level of expression of glial fibrillary acidic protein (GFAP) and vimentin, both of which are upregulated with the proliferation of active astrocytes.〔〔Silver, J. and J.H. Miller (2004). Regeneration beyond the glial scar. Nat. Rev. Neurosci, 5(2), 146-156.〕

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