In recent studies it was demonstrated that temperature-dependent optical spectroscopy is a valuable tool for revealing the differences in the geometries of flexible molecules like oligothiophenes (OTs) in the ground (S(0)) and first excited (S(1)) electronic states, by examining the symmetry relations between the absorption and emission spectra: while at low temperature the spectra show mirror symmetry, pointing to planar geometries in S(0) and S(1), the symmetry relation breaks down at ambient temperature due to thermal population of torsional modes. In the present joint spectroscopic and theoretical study, we demonstrate that this behavior is also observed for di- and tetramethyl-substituted OTs, suggesting an essentially planar equilibrium geometry not only in S(1) but also in S(0), despite the increasing sterical hindrance which is imposed by the substituents. This rather surprising result is rationalized by the softness of the carbon-sulfur bond, which is able to adapt to the geometrical constraints.
The nomenclature most commonly applied to the motor-related nuclei of the human thalamus differs substantially from that applied to the thalamus of other primates, from which most knowledge of input-output connections is derived. Knowledge of these connections in the human is a prerequisite for stereotactic neurosurgical approaches designed to alleviate movement disorders by the placement of lesions in specific nuclei. Transfer to humans of connectional information derived from experimental studies in nonhuman primates requires agreement about the equivalence of nuclei in the different species, and dialogue between experimentalists and neurosurgeons would be facilitated by the use of a common nomenclature. In this review, the authors compare the different nomenclatures and review the cyto- and chemoarchitecture of the nuclei in the anterolateral aspect of the ventral nuclear mass in humans and monkeys, suggest which nuclei are equivalent, and propose a common terminology. On this basis, it is possible to identify the nuclei of the human motor thalamus that transfer information from the substantia nigra, globus pallidus, cerebellum, and proprioceptive components of the medial lemniscus to prefrontal, premotor, motor, and somatosensory areas of the cerebral cortex. It also becomes possible to suggest the principal functional systems involved in stereotactically guided thalamotomies and the functional basis of the symptoms observed following ischemic lesions in different parts of the human thalamus.
The olfactory p a r t of the telencephalon or rhinencephalon is a complex of pallial and subpallial centers which a r e more or less closely related functionally to the sense of smell and wliich a r e more or less clearly separated morphologically from the nonolfactory centers throughout the phyletic series. I n macrosmatic mammals there is marked development of the cerebral olfactory centers due to the special importance of the sense of smell for somatic as well as for vegetative life. In these forms, we can subdivide the rhinencephalon in accordance with classical terminology into primary, secondary, and tertiary olfactory centers.The olfactory and the accessory olfactory bulbs represent the primary olfactory centers evolved for the reception and the elaboration of impulses coming directly from neuroscrisory olfactory cells. The secondary olfactory centers, which receive the axons of mitral cells through the olfactory tracts, include nucleus olfactorius anterior, the prepiriform cortex (gyrus olfactorius lateralis), gyms olfactorius medialis together with the rostra1 tip of the hippocampal cortex (cortex hippocampi cruralis of Herrick, '24), the nucleus of the lateral olfactory tract, and the medial septa1 nucleus. The tertiary olfactory centers comprise the posterior pirif orm cortex of the piriform lobe (Brodmann, '09, field 25; Ram6n y Cajal, ' 11, 6corce teniporale suphieure ; Gray, '24 ; M.
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We present a new, large, Italian family affected by Gerstmann-Sträussler-Scheinker syndrome (GSS) associated with the Pro to Leu point mutation at codon 102 of the prion protein gene (PRNP). The affected members of this family show a remarkable phenotypic variability of the disease: three of them had a clinical picture characterized by dementia and a brief illness duration (less than 1 year), while the other five members presented an ataxic, slowly evolving syndrome (a clinical duration of 3 to 4 years) with no evidence of cognitive impairment. Despite these remarkable clinical differences among affected members, we found no correlation between the clinical presentation and the codon 129 or codon 219 genotypes. These data suggest that factors as yet unidentified may influence the clinical expression of the disease.
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