- 関
- buffy coat、leptomeningeal、pia mater、pial
WordNet
- the two innermost layers of the meninges; cerebrospinal fluid circulates between these innermost layers
Wikipedia preview
出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2013/12/25 03:10:14」(JST)
[Wiki en表示]
Leptomeninges |
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Diagrammatic transverse section of the medulla spinalis and its membranes. (At border, dura mater is black line, arachnoid mater is blue line, and pia mater is red line.) |
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The medulla spinalis and its membranes. |
Latin |
Leptomeninges |
In medicine, leptomeninges (literally thin meninges) is a term used to refer to the pia mater and arachnoid mater, two of the membranes that surround the brain and the spinal cord.[1]
The morphology of the brain in meningococcal meningitis is said to be covered by exudate on the surface of, and within the leptomeninges. Because the arachnoid is connected to the pia by cob-web like strands, it is structurally continuous with the pia, hence the name pia-arachnoid or leptomeninges.
References[edit]
- ^ leptomeninges at eMedicine Dictionary
Anatomy: meninges of the brain and medulla spinalis (TA A14.1.01, GA 9.749/9.872)
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Layers |
Dura mater
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Falx cerebri · Tentorium cerebelli · Falx cerebelli · Diaphragma sellae · Trigeminal cave
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Arachnoid mater
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Arachnoid granulation · Arachnoid trabeculae
Subarachnoid cisterns: Cisterna magna · Pontine cistern · Interpeduncular cistern · Chiasmatic · Lateral cerebral fossa · Of great cerebral vein · Of lamina terminalis
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Pia mater
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Denticulate ligaments
Tela chorioidea (Tela chorioidea of third ventricle, Tela chorioidea of fourth ventricle) · Choroid plexus
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Combined
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Filum terminale · Leptomeninges
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Spaces |
Epidural space · Subdural space · Subarachnoid space (Cerebrospinal fluid)
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anat (n/s/m/p/4/e/b/d/c/a/f/l/g)/phys/devp
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noco (m/d/e/h/v/s)/cong/tumr, sysi/epon, injr
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proc, drug (N1A/2AB/C/3/4/7A/B/C/D)
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UpToDate Contents
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English Journal
- Brain gadolinium enhancement along the ventricular and leptomeningeal regions in patients with aquaporin-4 antibodies in cerebral spinal fluid.
- Long Y1, Chen M1, Zhang B1, Gao C2, Zheng Y1, Xie L1, Gao Q1, Yin J1.Author information 1Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and The Ministry of Education of China, Institute of Neuroscience and The Second Affiliated Hospital of GuangZhou Medical University, 250# Changgang East Road, GuangZhou, 510260, Guangdong Province, China; Department of Neurology, The Second Affiliated Hospital of GuangZhou Medical University, 250# Changgang East Road, GuangZhou, 510260 Guangdong Province, China.2Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and The Ministry of Education of China, Institute of Neuroscience and The Second Affiliated Hospital of GuangZhou Medical University, 250# Changgang East Road, GuangZhou, 510260, Guangdong Province, China; Department of Neurology, The Second Affiliated Hospital of GuangZhou Medical University, 250# Changgang East Road, GuangZhou, 510260 Guangdong Province, China. Electronic address: smilegaocong@126.com.AbstractBACKGROUND: Aquaporin-4 (AQP4) is densely expressed in the ependymal region and leptomeninges, and it is susceptible to pathological responses triggered by antibodies from blood and cerebral spinal fluid (CSF). Therefore, enhancement of these regions may be related to neuromyelitis optica spectrum disorder (NMOSD).
- Journal of neuroimmunology.J Neuroimmunol.2014 Apr 15;269(1-2):62-7. doi: 10.1016/j.jneuroim.2014.02.006. Epub 2014 Feb 16.
- BACKGROUND: Aquaporin-4 (AQP4) is densely expressed in the ependymal region and leptomeninges, and it is susceptible to pathological responses triggered by antibodies from blood and cerebral spinal fluid (CSF). Therefore, enhancement of these regions may be related to neuromyelitis optica spectrum d
- PMID 24582827
- Distribution of microsomal prostaglandin E synthase-1 in the mouse brain.
- Eskilsson A1, Tachikawa M, Hosoya KI, Blomqvist A.Author information 1Division of Cell Biology, Department of Clinical and Experimental Medicine, Faculty of Health Sciences, Linköping University Linköping, Sweden.AbstractPrevious studies in rats have demonstrated that microsomal prostaglandin E synthase-1 (mPGES-1) is induced in brain vascular cells that also express inducible cyclooxygenase-2, suggesting that such cells are the source of the increased PGE2 levels that are seen in the brain following peripheral immune stimulation, and that are associated with sickness responses such as fever, anorexia and stress hormone release. However, while most of what is known about the functional role of mPGES-1 for these centrally evoked symptoms is based on studies on genetically modified mice, the cellular localization of mPGES-1 in the mouse brain has not been thoroughly determined. Here, using a newly developed antibody that specifically recognizes mouse mPGES-1, and dual-labeling for cell-specific markers, we report that mPGES-1 is constitutively expressed in the mouse brain, being present not only in brain endothelial cells, but also in several other cell types and structures, such as capillary-associated pericytes, astroglial cells, leptomeninges and the choroid plexus. Regional differences were seen with particularly prominent labeling in autonomic relay structures such as the area postrema, the subfornical organ, the paraventricular hypothalamic nucleus, the arcuate nucleus and the median preoptic nucleus. Following immune stimulation, mPGES-1 in brain endothelial cells, but not in other mPGES-1 positive cells, was co-expressed with cyclooxygenase-2, whereas there was no co-expression between mPGES-1 and cyclooxygenase-1. These data imply a wide-spread synthesis of PGE2 or other mPGES-1 dependent product in the mouse brain that may be related to inflammation-induced sickness symptom as well as other functions, such as blood flow regulation. J. Comp. Neurol., 2014. © 2014 Wiley Periodicals, Inc.
- The Journal of comparative neurology.J Comp Neurol.2014 Mar 26. doi: 10.1002/cne.23593. [Epub ahead of print]
- Previous studies in rats have demonstrated that microsomal prostaglandin E synthase-1 (mPGES-1) is induced in brain vascular cells that also express inducible cyclooxygenase-2, suggesting that such cells are the source of the increased PGE2 levels that are seen in the brain following peripheral immu
- PMID 24668417
- Inflammation-inducible type 2 deiodinase expression in the leptomeninges, choroid plexus and at brain blood vessels in male rodents.
- Wittmann G1, Harney JW, Singru PS, Nouriel SS, Larsen PR, Lechan RM.Author information 1Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, Tupper Research Institute, Tufts Medical Center, Boston, MA 02111;AbstractThyroid hormone regulates immune functions and has anti-inflammatory effects. In promoter assays, the thyroid hormone-activating enzyme, type 2 deiodinase (D2), is highly inducible by the inflammatory transcription factor nuclear factor-kappa B (NF-κB), but it is unknown if D2 is induced in a similar fashion in vivo during inflammation. We first re-examined the effect of bacterial lipopolysaccharide (LPS) on D2 expression and NF-κB activation in the rat and mouse brain using in situ hybridization. In rats, LPS induced very robust D2 expression in normally non-D2-expressing cells in the leptomeninges, adjacent brain blood vessels, and the choroid plexus. These cells were vimentin-positive fibroblasts and expressed the NF-κB activation marker, IκBα mRNA, at 2h post-injection, prior to the increase in D2 mRNA. In mice, LPS induced intense D2 expression in the choroid plexus but not in leptomeninges, with an early expression peak at 2h. Moderate D2 expression along numerous brain blood vessels appeared later. D2 and NF-κB activation was induced in tanycytes in both species, but with a different time-course. Enzymatic assays from leptomeningeal and choroid plexus samples revealed exceptionally high D2 activity in LPS-treated rats and Syrian hamsters, and moderate but significant increases in mice. These data demonstrate the cell type-specific, highly inducible nature of D2 expression by inflammation, and NF-κB as a possible initiating factor, but also warrant attention for species differences. The results suggest that D2-mediated T3 production by fibroblasts regulate local inflammatory actions in the leptomeninges, choroid plexus and brain blood vessels, and perhaps also in other organs.
- Endocrinology.Endocrinology.2014 Mar 6:en20132154. [Epub ahead of print]
- Thyroid hormone regulates immune functions and has anti-inflammatory effects. In promoter assays, the thyroid hormone-activating enzyme, type 2 deiodinase (D2), is highly inducible by the inflammatory transcription factor nuclear factor-kappa B (NF-κB), but it is unknown if D2 is induced in a simil
- PMID 24601886
Japanese Journal
- 急性進行性感音難聴を初発症状として急速な転帰を辿った髄膜癌腫症の1例
- 急性進行性感音難聴を初発症状として急速な転帰を辿った髄膜癌腫症の1例
- 脳脊髄液adenosine deaminase(ADA)が高値を呈した星状細胞腫による髄膜膠腫症の61歳男性例
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- leptomeninges、leptomeningeal
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