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The laboratory rat is one of the most extensively studied model organisms. Inbred laboratory rat strains originated from limited Rattus norvegicus founder populations, and the inherited genetic variation provides an excellent resource for the correlation of genotype to phenotype. Here, we report a survey of genetic variation based on almost 3 million newly identified SNPs. We obtained accurate and complete genotypes for a subset of 20,238 SNPs across 167 distinct inbred rat strains, two rat recombinant inbred panels and an F2 intercross. Using 81% of these SNPs, we constructed high-density genetic maps, creating a large dataset of fully characterized SNPs for disease gene mapping. Our data characterize the population structure and illustrate the degree of linkage disequilibrium. We provide a detailed SNP map and demonstrate its utility for mapping of quantitative trait loci. This community resource is openly available and augments the genetic tools for this workhorse of physiological studies.

Some people declare that they possess a personal visual representation of numbers: some automatically "see" the numbers they are confronted with in a precise location in a structured mental space, others "associate" specific colours with given numbers. Such visuo-spatial representations of numbers were first described by Galton in 1880 but have since received little attention from psychologists. It is the aim of this article to describe these mental representations and discuss their role in number processing. The authors first review Galton's observations, and then present their own. Finally, they discuss the relevance of these visuo-spatial representations in relation to contemporary debates on number representation and calculation.

In this study, we examine how brain damaged adults (aphasics, right-brain lesioned subjects (RBD), and demented subjects) perform a basic education skill: determining the cardinality of different sets of objects (dots). The RBD subjects encountered more difficulty with the spatial correspondence components of the task (correct pointing to the dots), while the aphasics experienced more difficulty with the verbal components (the production of the correct number-word sequence). The deficit evidenced by the demented patients was less systematic. However, qualitative analyses of patients' behavior suggested an organization that tended to minimize the impact of their cognitive deficits on the object-counting task, and an analysis of their counting indicates that the basic counting principles proposed by Gelman (1982) and Fuson (1988) may be preserved.

Immune deficiency, especially to the Epstein-Barr virus, and increased susceptibility to fatal infectious mononucleosis, acquired agammoglobulinemia, and lymphoma are the cardinal features of the X-linked lymphoproliferative syndrome. Since the establishment of the XLP Registry in September, 1978, 59 affected males in seven unrelated kindreds were comprehensively studied. A spectrum of lymphoproliferative phenotypes was observed. Thirty-four patients (57%) died from infectious mononucleosis, eight (14%) had fatal infectious mononucleosis with lymphoma (immunoblastic sarcoma), nine (15%) had depressed immunity following EBV infection, and eight (14%) developed lymphoma. Several patients with XLP lacked EBV antibodies despite infection by EBV. The results of this study suggest that EBV can be an oncogenic agent in patients who are immune deficient with XLP.

Multiple methods, pedigree analysis, clinical evaluation, and Epstein-Barr virus (EBV)-specific serology, EBV DNA hybridization of tissues to probe for viral genome, staining of touch imprints for EBV nuclear-associated antigen, establishment of spontaneous infected B-cell lines from peripheral blood or tissues, examination of peripheral blood smears, and hematopathology studies, were used to study seven patients with the X-linked lymphoproliferative syndrome and seven additional patients with life-threatening EBV-associated diseases. These studies demonstrated EBV in the tissues of all 14 patients and immunodeficient antibody responses to EBV were documented. This virus can produce various life-threatening lymphoproliferative diseases in a variety of immunodeficient patients.