Visualising the topography of the acoustic radiation in clinical diffusion tensor imaging scans.

PURPOSE: It has long been thought that the acoustic radiation (AR) white matter fibre tract from the medial geniculate body of the thalamus to the Heschl's gyrus cannot be reconstructed via single-fibre analysis of clinical diffusion tensor imaging (DTI) scans. A recently developed single-fibre probabilistic method suggests otherwise. The method uses dynamic programming (DP) to compute the most probable paths between two regions of interest. This study aims to observe the ability of single-fibre probabilistic analysis via DP to visualise the AR in clinical DTI scans from legacy pilot cohorts of subjects with normal hearing (NH) and profound hearing loss (HL). METHODS: Single-fibre probabilistic analysis via DP was applied to reconstruct 3D models of the AR in the two cohorts. DTI and T1 data at 1.5 T for subjects with NH (n = 11) and HL (n = 5), as well as 3 T for NH (n = 1) and HL (n = 1), were used. RESULTS: The topographical features of AR previously observed in post-mortem and multi-fibre analyses can be visualised in DTI scans of 16 subjects and 2 atlases with a success rate of 100%. Relative to MNI coordinates, there was no significant difference in the varifold distances between the topography of the tracts in the 1.5 T cohort. CONCLUSION: The AR can be visualised in clinical 1.5 T and 3 T DTI scans using single-fibre probabilistic analysis via DP, hence, the potential for DP to visualise the AR in medical and pre-surgical applications in pathologies such as vestibular schwannoma, multiple sclerosis, thalamic tumours and stroke as well as hearing loss.

Dietary antioxidant supplementation reduces lipid peroxidation but impairs vascular function in small mesenteric arteries of the streptozotocin-diabetic rat.

Impaired endothelium-dependent relaxation could underlie many of the vascular complications associated with insulin-dependent diabetes mellitus, and may be mediated by increased oxidative stress. The effect of antioxidants on vascular endothelial function and oxidative stress of streptozotocin-diabetic rats was assessed by dietary supplementation with vitamins E and C. Diabetic (i.v. streptozotocin, 45 mg/kg) male Sprague-Dawley rats were fed one of six supplemented diets containing 75.9, 250, or 500 mg vitamin E/kg chow, 250 mg vitamin C/kg H2O, 250 mg vitamin E/kg chow plus 250 mg vitamin C/kg H2O, or chow deficient in vitamin E, and then compared to standard-fed control rats. After 4 weeks, small mesenteric arteries were dissected and mounted on a small vessel myograph, concentration response curves were then constructed to noradrenaline, acetylcholine and sodium nitroprusside. Acetylcholine-mediated relaxation was impaired in arteries from diabetic rats (pEC50 6.701+/-SEM 0.120, n = 8) compared to controls (7.386+/-0.078, n = 6; p < 0.05). The 500 mg/kg vitamin E diet further impaired maximum relaxation to acetylcholine (58.2+/-10.5 vitamin E, n = 7 vs 84.4+/-5.3 % standard, p < 0.05), and the combined vitamin E plus C diet impaired maximum relaxation to sodium nitroprusside (48.5+/-4.1 in vitamin E + C, n = 8 vs 75.6+/-3.9 % standard; p < 0.01). However, plasma 8-epi-prostaglandin (PG)F2alpha (measured as an estimate of oxidative stress) was dose-dependently decreased in rats on vitamin E supplemented diets. Dietary antioxidant supplementation did not reverse impaired endothelial function in this model of uncontrolled diabetes despite a concomitant decrease in oxidative stress.

Endothelial dysfunction in streptozotocin-diabetic rats is not reversed by dietary probucol or simvastatin supplementation.

Oxidative stress and dyslipidaemia are key features of diabetes mellitus and may be involved in mediating the vascular endothelial dysfunction associated with this disease. The aim of this study was to examine the effect of dietary lipid-lowering and antioxidant agents on vascular endothelial function and oxidative stress. Diabetic male Sprague-Dawley rats (i.v. streptozotocin, 45 mg/kg) were fed for 4 weeks on a standard diet or on a diet supplemented with either the lipid-lowering antioxidant probucol (1% w/w in diet) or the 3-hydroxy 3-methylglutaryl coenzyme-A (HMG-CoA) reductase inhibitor simvastatin (0.01% w/w in diet). Responses to noradrenaline, acetylcholine, and sodium nitroprusside were assessed in small mesenteric arteries (mean internal diameter 300+/-5 microm, n = 80) mounted on a small vessel myograph. Plasma concentrations of total cholesterol and triglycerides were significantly raised in standard-fed diabetic rats and significantly reduced in probucol and simvastatin-fed diabetic rats 8-epi-prostaglandin (PG)F2alpha, an indicator of oxidative stress, was raised in liver and aorta from diabetic rats compared to controls. Probucol supplementation reduced 8-epi-PGF2alpha in aorta and liver of diabetic rats but increased 8-epi-PGF2alpha content in plasma and aorta from control animals. The abnormal relaxation to acetylcholine in arteries from the diabetic rats (pEC550 diabetic 6.763+/-0.172 vs control 7.541+/-0.175; p < 0.05) was not improved by probucol or simvastatin. These data, therefore, do not support a role for oxidative stress or dyslipidaemia in mediating the impaired ACh-induced endothelium-dependent relaxation of small mesenteric arteries from the streptozotocin-diabetic rat.