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References in periodicals archive ?
Results of immuno-histochemical staining for neurofilament and NSE were positive and similar to the labeling pattern of the neuroectodermal component of the original mass.
While it turned out that the rate of change in neurofilament concentration was closely linked to brain degradation, correlation with the deposition of toxic amyloid proteins was far less pronounced.
However, normal brain MRI is also commonly seen.[4],[5] Other changes include cerebral and/or cerebellar and/or brainstem atrophy.[3] The brain MRI of reported patient with homozygous c.1634G>A mutations showed Arnold-Chiari I malformation rather than white matter changes.[1] The presence of giant axon with accumulation of neurofilaments and axonal spheroids is the hallmarks in nerve biopsy.[3] Our patient presented typical progressive sensorimotor neuropathy and cerebellar ataxia.
CSF neurofilament heavy-chain (NfH) values were found to correlate with EDSS in a 17-year follow-up period, to reflect chronic axonal destruction (65), and also to estimate the amount of brain and spinal cord atrophy on MRI (66).
Caption: Figure 2: (a) Histologic sections showing a cellular proliferation of pleomorphic cells, some of which are multinucleated (H&E stain, 100x original magnification); lymphocytic infiltration is also seen (b); (c) neoplastic cells show eosinophilic cytoplasm and intracytoplasmic vacuoles, with mitotic figures identified (H&E stain, 400x original magnification); immunohistochemistry shows diffuse reactivity for S-100 (d), GFAP (e), and neurofilament (f); the Ki-67 proliferative index is moderately elevated (g).
NSE and neurofilament protein immunohistochemical markers showed strong cytoplasmic staining in the majority of the tumor cells.
Furthermore, PNET-like areas show lower GFAP expression but positive staining for S-100, synaptophysin, NeuN, and neurofilament protein (NFP) [10-12].
The primary antibodies included mouse anti-C-terminal-binding protein-2 (CtBP2) (612044; BD Biosciences, USA) at 1: 500 dilution; mouse anti-glutamate receptor 2, extracellular, clone 6C4 (GluA2) (MAB397; Millipore, Germany) at 1: 2000 dilution; rabbit anti-NMDAR1 (GluN1) (AB9864R; Millipore, Germany) at 1: 1000 dilution; chicken anti-200 kD neurofilament heavy chain (NF) (cat.
Glial fibrillary acid protein (GFAP), ubiquitin c-terminal hydrolase LI (UCH-L1), as well as other proteins, including microtubule-associated protein tau, amyloid beta peptide (A[beta]342), and neurofilament light (NfL), have been proposed as promising diagnostic and prognostic biomarkers in TBI.
The expression of S-100 and neurofilament was observed in small intestinal conduit group but was less organised than in the autologous nerve graft group.
Three of the neuronal antibodies (NF protein, clone 2F10, DakoCytomation, Glostrup, Denmark; nonphosphorylated neurofilament SMI32, Covance, Princeton, New Jersey; MAP2, clone AP20, Merck Millipore, Darmstadt, Germany) used did not label the neuronal cell bodies (Table).