Pathological analysis of spinal cords from survivors of poliomyelitis.
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Adult↗
Biomedical subjects
N Tresser
Publications and source records attributed to N Tresser.
Spinal cord histopathology in long-term survivors of poliomyelitis.
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Adult↗
Aberrant phosphoinositide metabolism in Alzheimer's disease.
Since phosphoinositide-specific phospholipase C (PLC) is one of the key molecules in signal transduction, its involvement was assessed in Alzheimer's disease (AD). The phosphatidyl-inositol (PI)-specific PLC activity in the Alzheimer cytosolic and particulate fractions was not significantly different from that in the control fractions. The PI-specific PLC activity as a function of the free Ca2+ concentration was also similar between control and Alzheimer brains. These results suggest that the PI-specific PLC activity is not altered in AD. Immunostaining of a specific antibody against the PLC isozyme, PLC-delta, demonstrated that this enzyme was abnormally accumulated in neurofibrillary tangles (NFT), the neurites surrounding senile plaque (SP) cores, and neuropil threads in AD brains. Western blot analysis confirmed that PLC-delta was concentrated in the paired helical filament (PHF)-rich fraction of AD brains. PLC-delta marked the same neurons containing tau immunoreactivity and yet tau and PLC-delta often marked different structures within the same neuron, with tau more clearly on NFT and PLC-delta covering it superficially. The double stain with PLC-delta and basic fibroblast growth factor (bFGF) binding suggest that PLC-delta is an intracellular marker, showing little overlap with bFGF binding, an extracellular marker. All of this was consistent with the electron microscopy, with PLC-delta being NFT associated. Antibodies to other PLC isozymes did not produce positive immunostaining of these pathologic structures. Moreover, diffuse and amorphous deposits of PLC-delta were found to precede the accumulation of fibrillary deposits. These results suggest that PLC-delta accumulation plays a possible role in the formation of intraneuronal inclusions in AD.
Alzheimer Disease↗
Intracranial lipomas with teratomatous elements.
We report two cases of patients with intracranial tumors that share features with lipomas and teratomas. Although rare reports of lipomas with "hypertrophic nerves" and "teratoid tumors" have been recorded, these two cases are unusual because they contain mature neuroectoderm (choroid plexus, peripheral nerve) and mesoderm (skeletal muscle). The findings are discussed and modern classification schemes are presented. We believe that the cases are examples of a transition between lipoma and teratoma.
Adult↗
Serial MR imaging of experimental autoimmune encephalomyelitis induced by human white matter or by chimeric myelin-basic and proteolipid protein in the common marmoset.
BACKGROUND AND PURPOSE: Experimental autoimmune encephalomyelitis (EAE) in the marmoset was monitored by serial MR imaging to determine correlates to the natural-history MR studies in multiple sclerosis (MS). The relationships of MR-revealed lesions to clinical status and histopathologic findings were also explored. METHODS: We induced EAE by subcutaneous inoculation in two marmosets by human white matter (HWM) and in seven marmosets by MP4 (a chimeric recombinant fusion protein of myelin-basic and proteolipid protein) in adjuvant along with intravenous inactivated pertussis vaccine to facilitate the disease process. The HWM-inoculated animals were induced with Freund's adjuvant as the established model of marmoset EAE. The MP4-inoculated animals were induced with either Freund's incomplete adjuvant or TiterMax as part of a preclinical treatment trial. MR imaging was performed at 1.5 T at baseline, and repeated at 1- to 2-week intervals for a period of up to 16 weeks in six EAE-induced marmosets, and intermittently for up to 70 weeks in three EAE-induced and two control marmosets. Proton density- (PD-) and T2-weighted, pre- and postgadopentetate dimeglumine enhancement, T1-weighted, and magnetization transfer (MT) images were obtained. The brains were prepared for histologic evaluation of lesion distribution and counts, characterization of lesions as demyelinating or inflammatory, and histopathologic scoring. The clinical, MR, and pathologic scoring were done on grading systems, and correlated for evaluation. RESULTS: White matter (WM) changes after EAE induction were observed first at 9 days in the HWM-induced animals and at 2.5 weeks in the MP4-induced animals, with subsequent week-to-week fluctuations on PD- and T2-weighted images. Contrast-enhancing lesions were not observed in all animals. MR-revealed WM lesions correlated to histopathologic analysis of EAE lesions, measuring from 0.5 mm to 1.5 mm. The lesion count and extent of demyelination was greater in the HWM-induced animals than in the MP4-induced animals. Some MR-revealed lesions correlated directly to clinical symptoms, but the majority of lesions were clinically silent. CONCLUSION: On MR images, lesions in the EAE marmoset model were confined to the WM, and their development, resolution, distribution, and enhancing characteristics fluctuated over the duration of the study. The dynamic presentation of MR-revealed lesions confirms the parallels between EAE in the marmoset and relapsing-remitting MS. Clinical symptoms alone were not representative of ongoing pathologic brain lesions. Therefore, serial MR imaging serves as a very important adjunct to clinical and histologic surveillance of the development of new and the persistence of existing brain lesions in this animal model of MS.
Animals↗
The effect of interferon and anti-CD44 antibody on mouse glioma invasiveness in vitro.
In this study the effect of interferon and anti-CD44 antibody on the invasiveness of mouse glioma G-26 cells was evaluated. We confirmed the glial nature of G-26 glioma cells (G-26) in vitro and in vivo using immunohistochemistry: G-26 stained strongly for S-100 and stained weakly for glial fibrillary acidic protein (GFAP). Immunohistochemical evaluation for CD44 adhesion molecule showed that G-26 was positive both in vitro and in vivo. Weakly positive punctate staining for CD44 was seen in the cytoplasm of all viable glioma cells and focally strong staining was observed in a membranous pattern in the invading glioma cells. Evaluation of untreated G-26 cells using an in vitro invasion assay showed that they were able to digest a Matrigel matrix and to invade through an 8 microns microporous membrane. Treatment of the G-26 glioma cells for 3-4 days with mouse interferon alpha/beta at 8 x 10(2) or 8 x 10(3) mu/ml resulted in a significant decrease of invasiveness: 68.8% (p < 0.05) and 32.8% (p < 0.001) of cells, respectively, remained invasive when compared to control. Treatment of G-26 with antibody to the CD44 adhesion molecule significantly decreased invasiveness with 39.4% (p < 0.001) of cells remaining invasive when compared to control. We feel that both of these approaches, each of which produced significant inhibition of G-26 glioma cell invasion should be further evaluated for their usefulness in antiglioma therapy.
Animals↗