Metapelites containing muscovite, cordierite, staurolite and biotite (Ms+Crd+St+Bt) are relatively rare but have been reported from a number of low‐pressure (andalusite–sillimanite) regional metamorphic terranes. Paradoxically, they do not occur in contact aureoles formed at the same low pressures, raising the question as to whether they represent a stable association. A stable Ms+Crd+St+Bt assemblage implies a stable Ms+Bt+Qtz+Crd+St+Al2SiO5+Chl+H2O invariant point (IP1), the latter which has precluded construction of a petrogenetic grid for metapelites that reconciles natural phase relations at high and low pressure. Petrogenetic grids calculated from internally consistent thermodynamic databases do not provide a reliable means to evaluate the problem because the grid topology is sensitive to small changes in the thermodynamic data. Topological analysis of invariant point IP1 places strict limits on possible phase equilibria and mineral compositions for metamorphic field gradients at higher and lower pressure than the invariant point. These constraints are then compared with natural data from contact aureoles and reported Ms+Crd+St+Bt occurrences. We find that there are numerous topological, textural and compositional incongruities in reported natural assemblages that lead us to argue that Ms+Crd+St+Bt is either not a stable association or is restricted to such low pressures and Fe‐rich compositions that it is rarely if ever developed in natural rocks. Instead, we argue that reported Ms+Crd+St+Bt assemblages are products of polymetamorphism, and, from their textures, are useful indicators of P–T paths and tectonothermal processes at low pressure. A number of well‐known Ms+Crd+St+Bt occurrences are discussed within this framework, including south‐central Maine, the Pyrenees and especially SW Nova Scotia.
Achromatic (luminance) vision is used by animals to perceive motion, pattern, space and texture. Luminance contrast sensitivity thresholds are often poorly characterised for individual species and are applied across a diverse range of perceptual contexts using over-simplified assumptions of an animal’s visual system. Such thresholds are often estimated using the Receptor Noise Limited model (RNL) using quantum catch values and estimated noise levels of photoreceptors. However, the suitability of the RNL model to describe luminance contrast perception remains poorly tested.Here, we investigated context-dependent luminance discrimination using triggerfish (Rhinecanthus aculeatus) presented with large achromatic stimuli (spots) against uniform achromatic backgrounds of varying absolute and relative contrasts. ‘Dark’ and ‘bright’ spots were presented against relatively dark and bright backgrounds. We found significant differences in luminance discrimination thresholds across treatments. When measured using Michelson contrast, thresholds for bright spots on a bright background were significantly higher than for other scenarios, and the lowest threshold was found when dark spots were presented on dark backgrounds. Thresholds expressed in Weber contrast revealed increased contrast sensitivity for stimuli darker than their backgrounds, which is consistent with the literature. The RNL model was unable to estimate threshold scaling across scenarios as predicted by the Weber-Fechner law, highlighting limitations in the current use of the RNL model to quantify luminance contrast perception. Our study confirms that luminance contrast discrimination thresholds are context-dependent and should therefore be interpreted with caution.
Infection of macaques with neurovirulent strains of simian immunodeficiency virus (SIVmac) is an experimental model for the neurological manifestations of AIDS. Loss of neurons has been reported in the cerebral cortex following immunodeficiency viral infection, but thalamic structures which may contribute to electrophysiological changes and neurological deficits have not been examined. In this study, the lateral geniculate nucleus (LGN) of macaques inoculated with macrophage-tropic, neurovirulent virus SIVmac239 (R71 and 17E) was examined for neuron loss using the optical fractionator method. Estimates of the number of neurons in the P layers of the lateral geniculate nucleus of age-matched control macaques ranged from 1.0 to 1.3 x 10(6), while the number of neurons in SIV infected macaques ranged from 0.8 to 1.1 x 10(6), reflecting neuron loss of up to 28%. Neuron loss was not observed in the magnocellular layer. The total number of glia and glial density were unchanged. Loss of neurons in the lateral geniculate nucleus was correlated with the pattern of neuropathological changes. Neuron loss was most severe in animals with encephalitis concentrated in the brain stem and subcortical white matter and was less apparent in animals with diffuse encephalitis. Neuron loss in the lateral geniculate nucleus did not explain changes observed in the visual evoked potential, which was severely affected in two animals which showed a loss of 24 and 26%, while it was normal in a third animal which showed neuron loss of 28%.
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