Disease relevance of Arachnoid

• Prostaglandin D synthase (beta-trace) in human arachnoid and meningioma cells: roles as a cell marker or in cerebrospinal fluid absorption, tumorigenesis, and calcification process [1].
• The studies suggest that neither diatrizoate nor chymopapain causes arachnoid fibrosis [2].
• These cases support the concept that pseudotumour cerebri is a syndrome of intracranial hypertension that can be due to any disorder producing obstruction of the CSF pathways at the level of the arachnoid villi [3].
• However, thrombosis susceptibility as a result of renal disease or impaired CSF reabsorption in the arachnoid villi as a result of cystine deposition might lead to the development of IIH in cystinosis [4].
• Posterior vertebral body erosion by arachnoid diverticula in cauda equina syndrome: an unusual manifestation of ankylosing spondylitis [5].

High impact information on Arachnoid

• Gelatinolytic activity was detected earliest within the matrix of cortical blood vessels and later within neurons and pia arachnoid (> or =3 hours), particularly within piriform cortex; this activity was suppressed by injection of the metalloprotease inhibitor GM6001 or in vitro by the addition of a zinc chelator (1,10-phenanthroline) [6].
• Here, we report PGDS to be expressed consistently in 10 human arachnoid and arachnoid villi and in 21 meningiomas by immunohistochemistry, Western blot, and reverse transcription (RT)-PCR analyses [1].
• In contrast, in arachnoid villi, PGDS was seen in core arachnoid cells rather than in the cap cell cluster or arachnoid cell layer [1].
• Immunoelectron microscopy showed that E-cadherin was localized at the intermediate junctions in arachnoid villi, while it was detected diffusely at the cell surface in meningiomas [7].
• Both [3H]inulin and bleomycin were cleared from the CSF more slowly than in previous studies and more slowly than in normal dogs, which suggests that bulk CSF absorption was reduced by the drug, probably secondary to protein-induced blockage of the arachnoid granulations through which CSF is normally absorbed [8].

Chemical compound and disease context of Arachnoid

• Subdural hygroma in association with middle fossa arachnoid cyst: acetazolamide therapy [9].
• Eleven non-neoplastic masses included four vascular anomalies, three cholesterol granulomas, two arachnoid cysts, one sphenoid mucocele and one mixed sclerosing bone dystrophy with mass-like thickening of basisphenoid and basiocciput [10].
• The immunohistochemical staining of merlin showed a striking contrast between arachnoid villi and meningiomas [11].
• Progesterone receptors were found in the nuclei of cells lining the cyst, which also suggests the similarity of the cyst lining to arachnoid granulations and meningiomas as derivatives of subdural neurothelium, which also possess progesterone receptors [12].
• Radiologic examination showed slight lateral instability of the odontoid on lateral rotation, and computed tomography brain scan with Iopamidol 300 (Niopam) contrast revealed a 5-cm vermian arachnoid cyst in the posterior fossa with obstructive hydrocephalus [13].

Biological context of Arachnoid

• Expression of cell adhesion molecule E-cadherin in human arachnoid villi [14].
• RESULTS: The following intracranial pathologies were diagnosed: dysgenesis of the corpus callosum, ventriculomegaly, cerebral cysts or hemorrhage, migrational disorders, vermian dysgenesis, arachnoid cysts, macrocephaly, enlarged subarachnoid space, brain calcifications and microcephaly [15].
• The association of these two disorders suggests that in this family, a chromosome 14 gene may play a role in the development of arachnoid cysts [16].
• Expression of NF2 gene product merlin in arachnoid villi and meningiomas [11].
• C-ANP competed with alpha-125I-ANP only for binding sites on arachnoid mater, 1 microM C-ANP displacing radioligand from at least 60% of these sites [17].

Anatomical context of Arachnoid

• In arachnoid, PGDS immunoreactivity was seen in arachnoid barrier cells but was negligible in arachnoid trabecula and pia mater [1].
• However, only Cytoxan-treated animals that had relapsed exhibited central nervous system involvement originating from the arachnoid membrane [18].
• Anisotropic crystals consistent with cystine were demonstrated in biopsy samples of arachnoid and cerebral cortex [19].
• RESULTS: In uninfected and infected mouse eyes, in situ hybridization produced an autoradiographic signal for mRNA, encoding both p75 and p55 over the corneal endothelium, iris, ciliary body, choroid, and arachnoid layers of the optic nerve sheath [20].
• In the brain, the salient features were microencephaly, agyria of an unusual type, cerebellar hypoplasia and dysplasia, persistent corpus pontobulbare, obliteration of the subarachnoid space, and a midline arachnoid cyst in the posterior fossa [21].

Associations of Arachnoid with chemical compounds

• Arachnoid response to contrast media: a comparison of iophendylate and metrizamide in experimental animals [22].
• The muscarinic sites in arachnoid and pial vessels were compared by analysis of the binding of quinuclidinyl benzilate (QNB) to membrane preparations [23].
• Pia arachnoid contains substance P originating from trigeminal neurons [24].
• Brain glucose utilisation in acquired childhood aphasia associated with a sylvian arachnoid cyst: recovery after shunting as demonstrated by PET [25].
• Morphine and alfentanil permeability through the spinal dura, arachnoid, and pia mater of dogs and monkeys [26].

Gene context of Arachnoid

• Immunohistochemical studies revealed the presence of FGF and VEGF within the AD choroid plexus and an increased density of FGFr in both the choroid plexus and the arachnoid villi of AD patients [27].
• Using antigen retrieval, CT-1 immunolocalized to choroid epithelial cells in all choroid plexuses in addition to leptomeninges (arachnoid and pial-glial membranes) [28].
• Signal for mRNA encoding both TNFR subtypes was also present over the arachnoid layers surrounding trigeminal ganglia [29].
• CONCLUSIONS: the observed distribution of p55 and p75 TNFR mRNA over trigeminal sensory neurons and over the arachnoid layers surrounding trigeminal ganglia supports suggestions that TNF has a direct effect on neurons, either as a neuromodulator or neurotrophic factor, and that TNF may play a central role in blood-brain barrier regulation [29].
• In addition to these constitutive desmosomal components, representative for single-layered (simple) epithelia, the dural border cells of the arachnoid and about 60% of the meningiomas tested were positive for desmocollin 3 (Dsc3), a protein in epithelia taken as an indicator for differentiation [30].

Analytical, diagnostic and therapeutic context of Arachnoid

• These changes were reversed when a CSF leak at the site of a T12-L1 arachnoid cyst was closed following an epidural blood patch [31].
• Immunofluorescence microscopy with monoclonal antibodies demonstrated cytokeratin in the cytoplasm of primary cultures of arachnoid cells [32].
• Total cellular RNA was analyzed by Northern blotting and hybridization with a 32P-labelled human PDGF beta-receptor probe, and PDGF beta-receptor mRNA was found in both tumor and arachnoid cell cultures [33].
• METHODS: A retrospective study on the incidence of arachnoid cysts was performed in patients seen in our Epilepsy Clinic who had CT or MRI scans, interictal EEGs or ictal EEGS [34].
• All patients who underwent surgery had the same procedure: a posterior fossa craniectomy with C1 laminectomy, lysis of arachnoid adhesions, and duraplasty [35].

References