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Biomedical subjects

S A Trip

Publications and source records attributed to S A Trip.

5 recordsLinked to original sources
PubMed2006

Quantification of optic nerve head topography in optic neuritis: a pilot study.

AIMS: To investigate optic nerve head topography in patients with optic neuritis compared to controls using the Heidelberg retina tomograph-II (HRT-II) and to determine if detected changes are related to visual function and electrophysiology. METHODS: 25 patients with a previous single episode of unilateral optic neuritis and 15 controls were studied with HRT-II, visual evoked potentials, and pattern electroretinogram. Patients also had testing of visual acuity, visual field, and colour vision. RESULTS: In affected eyes compared to fellow eyes, there was reduction of both the mean retinal nerve fibre layer (RNFL) thickness at the disc edge (p = 0.009) and the neuroretinal rim volume (p = 0.04). In affected eyes compared to control eyes, the three dimensional optic cup shape measure was increased (p = 0.01), indicative of an abnormal cup shape. There were no other significant differences in HRT-II measures. Within patient interocular difference correlation was used to investigate the functional relevance of these changes and demonstrated associations between RNFL thickness change and changes in visual acuity, visual field, and colour vision. Colour vision change was also associated with change in neuroretinal rim volume. CONCLUSIONS: HRT detects functionally relevant changes in RNFL thickness and neuroretinal rim volume between eyes affected by optic neuritis and unaffected fellow eyes.

Adult↗
PubMed2006

In vivo diffusion tensor imaging of the human optic nerve: pilot study in normal controls.

Diffusion tensor imaging (DTI) of the optic nerve (ON) was acquired in normal controls using zonally oblique multislice (ZOOM) DTI, which excites a small field of view (FOV) using a fast sequence with a shortened EPI echo train. This combines the benefit of low sensitivity to motion (due to the single-shot acquisition used), with the additional advantage of reduced sensitivity to magnetic field susceptibility artifacts. Reducing the bright signal from the fat and cerebrospinal fluid (CSF) surrounding the nerve are key requirements for the success of the presented method. Measurements of mean diffusivity (MD) and fractional anisotropy (FA) indices were made in a coronal section of the middle portion of the optic nerve (ON) in the right (rON) and left (lON) ONs. The average values across 10 healthy volunteers were FArON = 0.64 +/- 0.09 and FAlON = 0.57 +/- 0.10, and MDrON = (1173 +/- 227) x 10(-6) mm2 s(-1) and MDlON = (1266 +/- 170) x 10(-6) mm2 s(-1). Measurements of the principal eigenvalue of the DT and its orthogonal component were also in agreement with those expected from a highly directional structural organization.

Adult↗
PubMed1999

Acetylcholinesterase activity of skeletal muscle in a non-immunogenic model for myasthenia gravis in rats.

Myasthenia gravis is caused by an autoimmune attack to acetylcholine receptors of skeletal muscle. Acetylcholine release from motor nerve terminals is upregulated in patients with myasthenia gravis and also in rat "myasthenic" models, dependent on the reduction of the number of acetylcholine receptors. This study addresses the question as to whether at "myasthenic" endplates there are changes in the activity of acetylcholinesterase. To this end we studied acetylcholinesterase activity in junctional and extrajunctional regions of dilator naris, extensor digitorum longus, and hemidiaphragm muscles from rats with alpha-bungarotoxin-induced myasthenia gravis. In all studied muscles from "myasthenic" rats there was no significant change of junctional acetylcholinesterase activity. In contrast, in dilator naris and extensor digitorum longus muscles, there was a 60% and 30% increase of extrajunctional acetylcholinesterase activity. There was no significant change in the extrajunctional activity in hemidiaphragm muscles. Velocity sedimentation analysis revealed that the increase in extrajunctional activity in extensor digitorum longus muscles could be attributed to an increase of the activity of the G4 form of acetylcholinesterase. Treatment of rats with 6.4 microgh(-1) neostigmine bromide for 29 days had no influence on junctional and extrajunctional acetylcholinesterase activity of extensor digitorum longus muscles from rats with alpha-bungarotoxin-induced myasthenia gravis.

Acetylcholinesterase↗