Disease relevance of Meninges

• Since acute fat embolism may produce lesions not only in the white matter of the brain, but also in the cord, the retina, the meninges, and the skin, and since all these have been described in MS, subacute fat embolism may be the cause of MS [1].
• Although PGDS has been identified recently in rat leptomeninges, little information is available about human meninges or meningiomas [2].
• SJL IL-10(-/-) mice with high numbers of PLP(139-151)-specific precursors in the repertoire did not develop spontaneous EAE, but when they were injected with pertussis toxin, they showed atypical clinical signs of EAE with small numbers of typical mononuclear cell infiltrates predominantly in the meninges [3].
• Nonabsorptive hydrocephalus may have resulted from deposition of cystine in the meninges [4].
• BACKGROUND: We postulated a model in which cell-free CSF virions originate from two major sources, namely, systemic non-CNS and CNS tissues, the latter including brain parenchyma and meninges [5].

Psychiatry related information on Meninges

• One characteristic of Alzheimer's disease (A beta disease) is the accumulation of amyloid deposits within the extracellular space of the brain and meninges [6].

High impact information on Meninges

• In addition, susceptibility to LCM caused by docile UBC-LCMV was clearly linked to the murine major histocompatibility locus H-2D: in MHC-congeneic C57BL/10 mice, susceptibility correlated with early onset and high activity of measurable LCMV-specific cytotoxic T cells in meninges and spleens and could be mapped to H-2D [7].
• Embryonic regions expressing high levels of beta-galactosidase activity included the bulbus arteriosus, valves of the developing heart, sclerotomes, meninges, limb buds, connective tissue fascia between muscle fibers, osteoblasts in newly formed bones, fibroblasts in tendons, periosteum, dermis, and peritoneal membranes [8].
• Following injection of the virus into mid-gestation mouse embryos, clones of lacZ-positive cells were detected in skin, skull, meninges, brain, visceral yolk sac, and amnion [9].
• Histologic studies show that amyloid deposition is mainly in connective tissue structures; there is an unusual infiltration of the meninges and central nervous system [10].
• In contrast, mice receiving 4 mg/kg per week for 13 weeks showed clearance not only in meninges but also in parietal neocortical and hippocampal neurons and glia [11].

Chemical compound and disease context of Meninges

• Capsular polysaccharide and lipopolysaccharide are important microbial determinants of the ability of H. influenzae to traverse the nasopharynx and localize in the cerebrospinal fluid and meninges after bacteremia [12].
• These results show that moxalactam has good penetrability when the meninges are inflamed and that it might be considered in cases of bacterial meningitis when the susceptibility of the pathogen indicates its usefulness [13].
• Using microangiography combined with benzidine stains, we studied the development of vessels in the meninges, cortex, and white matter in 30 neonates, 16 infants and children, and eight neonates with periventricular leukomalacia [14].
• 1. The therapeutical benefit of serotonin (5-HT1) receptor agonists in the treatment of migraine headache has been attributed to their inhibitory effect on the release of pro-inflammatory neuropeptides from trigeminal afferents within the cranial meninges [15].
• Diffusion of enoxacin into the cerebrospinal fluid in dogs with healthy meninges and with experimental meningitis [16].

Biological context of Meninges

• The formation of ectopic lymphoid follicies in the meninges of patients with MS could represent a critical step in maintaining humoral autoimmunity and in disease exacerbation [17].
• Our findings point to the importance of new gene expression and cytokine expression as fundamental to the delayed response following GTN infusion, and support the hypothesis that a similar response develops in human meninges after GTN challenge [18].
• The injection of 100 units of IL-1 beta into neonatal (2-h-old) rats gave rise to an increase in permeability of vessels to serum proteins in the meninges, but no increase in vascular permeability was observed at the injection site [19].
• Both the 3.6 and 3.8kb forms of the L-myc mRNA, resulting from alternative splicing of intron I, were detected in layers of neuroectodermal origin, but not in the meninges or choroid plexus [20].
• Pharmacokinetics of trimethoprim and sulfamethoxazole in serum and cerebrospinal fluid of adult patients with normal meninges [21].

Anatomical context of Meninges

• By 6 months of age, MRL/Mp-lpr/lpr mice developed prominent mononuclear cell infiltrates restricted to the choroid plexus and meninges, whereas congeneric MRL/Mp- +/+ mice (which lack the lpr gene) showed delayed but widespread inflammatory infiltrates involving cerebral vessels and meninges, with sparing of the choroid plexus [22].
• Some MBP-CFA-challenged resistant rats showed minimal inflammation in the central nervous system, which was, however, confined to the meninges of the lower spinal cord [23].
• MRI showed a marked enhancement throughout her meninges and ependyma, and TTR amyloid deposition was confirmed by meningeal biopsy [24].
• The IL-1 beta-induced increases in vessel permeability in the meninges, parenchyma, and choroid plexus were polymorphonuclear neutrophil dependent, since leukocyte depletion by irradiation or polymorphonuclear neutrophil anti-serum pre-treatment eliminated the response in the juvenile animals and in the adults [19].
• Prior studies have documented these concentrations of cefamandole in cerebrospinal fluid in the presence of inflamed meninges [25].

Associations of Meninges with chemical compounds

• To assess the differential diagnostic value of this finding, gadolinium diethylenetriaminepentaacetic acid-enhanced MR studies of a control group of other extraaxial lesions as well as superficial intraaxial tumors that abut the meninges were reviewed [26].
• Aztreonam was administered as a single, 2-g intravenous dose to 25 patients with noninflamed meninges and to 9 patients with inflamed meninges [27].
• N-Formimidoyl thienamycin penetrated uninflamed meninges, and peak concentrations were significantly augmented by coadministration of MK791 [28].
• We assume that the histamine content of whole brain with meninges in Ws/Ws rats is < 60% of that in +/+ rats [29].
• These preliminary data indicate that pefloxacin diffuses well into the CSF of patients with inflamed meninges [30].

Gene context of Meninges

• Finally, the administration of neutralizing mAb specific for TNF-alpha and GM-CSF increased mortality in C. neoformans-infected mice, and induced the rapid progression of disease with involvement of the brain and meninges [31].
• Finally, histological examination in hydrocephalic mice undergoing HGF treatment revealed reduction of collagen fibers in the meninges and normalization of their structures [32].
• Finally, pattern formation requires the integrity of the external limiting membrane, defects of which lead to overmigration of neurons in meninges and to human type 2 lissencephaly [33].
• A recent study on the relative disappearance of MAG versus MBP in primary and recurrent lesions of Theiler's infection had shown that numerous mononuclear cells in meninges and perivascular spaces specifically bound anti-MAG antibody [34].
• During embryonic brain development, Hlf expression was restricted to the anterior pituitary and meninges [35].

Analytical, diagnostic and therapeutic context of Meninges

• Immunohistochemistry revealed strong cytoplasmic staining for VEGF in a metastatic lesion from breast cancer infiltrating the meninges [36].
• In situ hybridization of fetal (E15) rat sections localized laminin gamma 1 chain mRNA primarily to meninges of the brain, auditory and peripheral nerve fibers, gastrointestinal system, and developing lung airway epithelium [37].
• Intranasal administration of S. pneumoniae with hyaluronidase induced meningitis in 50% of inoculated mice, as defined by a positive cerebrospinal fluid (CSF) culture and an inflammatory infiltrate in the meninges [38].
• After a 1 h intravenous injection of 12.5 and 25 mg/kg enoxacin in dogs with healthy meninges, the concentrations in cerebrospinal fluid observed between 90 and 240 min averaged 2.6 (1.8-3.3) mg/l and 6.5 (4.7-8.4) mg/l respectively [16].
• CYP1A1 and CYP1A2 levels were determined in subcellular fractions of multiple brain regions, as well as tissue homogenates of circumventricular organs, and the meninges by Western blotting and catalytic activity in control male rats and rats treated with the inducer beta-naphthoflavone (BNF) [39].

References