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<jats:p> Glaucoma is a major cause of blindness and is characterized by progressive degeneration of the optic nerve and is usually associated with elevated intraocular pressure. Analyses of sequence tagged site (STS) content and haplotype sharing between families affected with chromosome 1q-linked open angle glaucoma ( <jats:italic>GLC1A</jats:italic> ) were used to prioritize candidate genes for mutation screening. A gene encoding a trabecular meshwork protein ( <jats:italic>TIGR</jats:italic> ) mapped to the narrowest disease interval by STS content and radiation hybrid mapping. Thirteen glaucoma patients were found to have one of three mutations in this gene (3.9 percent of the population studied). One of these mutations was also found in a control individual (0.2 percent). Identification of these mutations will aid in early diagnosis, which is essential for optimal application of existing therapies. </jats:p>

<jats:p>Unilateral brain damage frequently produces “extinction,” in which patients can detect brief single visual stimuli on either side but are unaware of a contralesional stimulus if presented concurrently with an ipsilesional stimulus. Explanations for extinction have invoked deficits in initial processes that operate before the focusing of visual attention or in later attentive stages of vision. Preattentive vision was preserved in a parietally damaged patient, whose extinction was less severe when bilateral stimuli formed a common surface, even if this required visual filling-in to yield illusory Kanizsa figures or completion of partially occluded figures. These results show that parietal extinction arises only after substantial processing has generated visual surfaces, supporting recent claims that visual attention is surface-based.</jats:p>

<jats:p> The <jats:italic>N</jats:italic> -methyl-D-aspartate (NMDA) receptor mediates synaptic transmission and plasticity in the central nervous system (CNS) and is regulated by tyrosine phosphorylation. In membrane patches excised from mammalian central neurons, the endogenous tyrosine kinase Src was shown to regulate the activity of NMDA channels. The action of Src required a sequence [Src(40–58)] within the noncatalytic, unique domain of Src. In addition, Src coprecipitated with NMDA receptor proteins. Finally, endogenous Src regulated the function of NMDA receptors at synapses. Thus, NMDA receptor regulation by Src may be important in development, plasticity, and pathology in the CNS. </jats:p>

<jats:p>The relation between an antigenic peptide that can stimulate a mature T cell and the natural peptide that promoted selection of this cell in the thymus is still unknown. An experimental system was devised to address this issue in vivo—mice expressing neopeptides in thymic stromal cells after adenovirus-mediated delivery of invariant chain-peptide fusion proteins. In this system, selection of T cells capable of responding to a given antigenic peptide could be promoted by the peptide itself, by closely related analogs lacking agonist and antagonist activity, or by ostensibly unrelated peptides. However, the precise repertoire of T cells selected was dictated by the particular neopeptide expressed.</jats:p>