網膜損傷

WordNet

any physical damage to the body caused by violence or accident or fracture etc. (同)hurt, harm, trauma
an act that causes someone or something to receive physical damage
wrongdoing that violates anothers rights and is unjustly inflicted
an accident that results in physical damage or hurt (同)accidental injury
in or relating to the retina of the eye; "retinal cells"
the innermost light-sensitive membrane covering the back wall of the eyeball; it is continuous with the optic nerve

PrepTutorEJDIC

『負傷』,『損害』,損傷 / (名誉などを)傷つけること,侮辱《+『to』+『名』》
(目の)網膜

UpToDate Contents

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1. 救急外来における眼部損傷の概要 overview of eye injuries in the emergency department
2. 網膜剥離 retinal detachment
3. 救急外来における眼部損傷に対するアプローチ approach to eye injuries in the emergency department
4. 児童虐待：小児への虐待による頭部外傷（AHT）の眼の所見 child abuse eye findings in children with abusive head trauma aht
5. 幹細胞の概要 overview of stem cells

English Journal

Neuropathological changes in a lamb model of non-accidental head injury (the shaken baby syndrome).

Finnie JW, Blumbergs PC, Manavis J, Turner RJ, Helps S, Vink R, Byard RW, Chidlow G, Sandoz B, Dutschke J, Anderson RW.SourceHanson Institute Centre for Neurological Diseases, SA Pathology, P.O. Box 14 Rundle Mall, Adelaide, South Australia 5000, Australia; School of Medical Sciences, University of Adelaide, Adelaide, South Australia, Australia; School of Veterinary Science, University of Adelaide, Adelaide, South Australia, Australia.
Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia.J Clin Neurosci.2012 Aug;19(8):1159-64. Epub 2012 Jun 15.
Non-accidental head injury (NAHI), also termed the "shaken baby syndrome", is a major cause of death and severe neurological dysfunction in children under three years of age, but it is debated whether shaking alone is sufficient to produce brain injury and mortality or whether an additional head imp
PMID 22705132

Retinal pigment epithelium response to oxidant injury in the pathogenesis of early age-related macular degeneration.

Mettu PS, Wielgus AR, Ong SS, Cousins SW.AbstractAge-related macular degeneration (AMD) represents the leading cause of vision loss in the elderly. Accumulation of lipid- and protein-rich deposits under the retinal pigment epithelium (RPE) heralds the onset of early AMD, but the pathogenesis of subretinal deposit formation is poorly understood. Numerous hypothetical models of deposit formation have been proposed, including hypotheses for a genetic basis, choroidal hypoperfusion, abnormal barrier formation, and lysosomal failure. This review explore the RPE injury hypothesis, characterized by three distinct stages (1) Initial RPE oxidant injury, caused by any number of endogenous or exogenous oxidants, results in extrusion of cell membrane "blebs," together with decreased activity of matrix metalloproteinases (MMPs), promoting bleb accumulation under the RPE as basal laminar deposits (BLD). (2) RPE cells are subsequently stimulated to increase synthesis of MMPs and other molecules responsible for extracellular matrix turnover (i.e., producing decreased collagen), affecting both RPE basement membrane and Bruchs membrane (BrM). This process leads to progression of BLD into basal linear deposits (BLinD) and drusen by admixture of blebs into BrM, followed by the formation of new basement membrane under the RPE to trap these deposits within BrM. We postulate that various hormones and other plasma-derived molecules related to systemic health cofactors are implicated in this second stage. (3) Finally, macrophages are recruited to sites of RPE injury and deposit formation. The recruitment of nonactivated or scavenging macrophages may remove deposits without further injury, while the recruitment of activated or reparative macrophages, through the release of inflammatory mediators, growth factors, or other substances, may promote complications and progression to the late forms of the disease.
Molecular aspects of medicine.Mol Aspects Med.2012 Aug;33(4):376-98. Epub 2012 May 3.
Age-related macular degeneration (AMD) represents the leading cause of vision loss in the elderly. Accumulation of lipid- and protein-rich deposits under the retinal pigment epithelium (RPE) heralds the onset of early AMD, but the pathogenesis of subretinal deposit formation is poorly understood. Nu
PMID 22575354

Japanese Journal

LABORATORY INVESTIGATION : Possible implications of acid-sensing ion channels in ischemia-induced retinal injury in rats

Miyake Takatomo,Nishiwaki Akiko,Yasukawa Tsutomu [他]
Japanese journal of ophthalmology : the official English-language journal of the Japanese Ophthalmological Society 57(1), 120-125, 2013-01-00
NAID 40019546548

Protective action of nipradilol mediated through S-nitrosylation of Keap1 and HO-1 induction in retinal ganglion cells

Koriyama Yoshiki,Kamiya Marie,Takadera Tsuneo,Arai Kunizo,Sugitani Kayo,Ogai Kazuhiro,Kato Satoru
Neurochemistry International 61(7), 1242-1253, 2012-12-00
… Nip has been described as having neuroprotective effects through cGMP-dependent pathway in retinal ganglion cells (RGCs). … Furthermore, RGC death and levels of 4-hydroxy-2-nonenal (4HNE) were increased after optic nerve injury in vivo. … Pretreatment with Nip significantly suppressed RGC death and accumulation of 4HNE after injury through an HO-1 activity-dependent mechanism. …
NAID 120004966623

A distinct effect of transient and sustained upregulation of cellular factor XIII in the goldfish retina and optic nerve on optic nerve regeneration

Sugitani Kayo,Ogai Kazuhiro,Hitomi Kiyotaka,Nakamura-Yonehara Kayo,Shintani Takafumi,Noda Masaharu,Koriyama Yoshiki,Tanii Hideji,Matsukawa Toru,Kato Satoru
Neurochemistry International 61(3), 423-432, 2012-08-00
… Unlike in mammals, fish retinal ganglion cells (RGCs) have a capacity to repair their axons even after optic nerve transection. … The levels of retinal TG (TG R) mRNA increased in RGCs 1-6 weeks after nerve injury to promote optic nerve regeneration both in vitro and in vivo. … This screening showed that the activity of only cellular coagulation factor XIII (cFXIII) was increased in goldfish optic nerves just after nerve injury. …
NAID 120004754689