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Biomedical subjects

P Jolicoeur

Publications and source records attributed to P Jolicoeur.

At least 19 recordsLinked to original sources
PubMed1992

Mental rotation, physical rotation, and surface media.

Subjects made mirror-normal discriminations on alphanumeric characters shown in different orientations in the picture plane. Either the characters or the background rotated during stimulus presentation in Experiments 1-3. Character rotation in the direction of mental rotation facilitated mental rotation, whereas rotation in the opposite direction inhibited it. In Experiment 4, characters were presented in different surface media so as to stimulate only one representation at a time. Mental rotation performance was similar whether the stimuli were defined by luminance, color, texture, relative motion, or binocular disparity, suggesting that mental rotation occurs at a level beyond that of the independent analyses of these different media. These results support those of Experiments 1-3 in excluding the participation of low-level motion analysis centers in the mental rotation processes.

Adult↗
PubMed1992

Reference frame and effects of orientation on finding the tops of rotated objects.

Effects of stimulus orientation across trial blocks and the spatial reference frame were investigated with a task in which Ss, with their head upright or tilted, judged a dot to be near the top or the bottom of rotated line drawings of objects. Objects used in this task were also named. Response times from the first block of trials increased linearly for objects rotated from 0 degrees to 120 degrees from the upright. Across blocks, orientation effects diminished for naming but remained the same for top-bottom discriminations. Practice with top-bottom discriminations diminished orientation effects when the same objects were subsequently named. The spatial reference frame for top-bottom discriminations was midway between retinal and environmental coordinates. Specifying the location of object features is of greater importance for top-bottom discriminations than for naming and underlies orientation effects in these tasks.

Adult↗
PubMed1992

Orientation congruency effects in visual search.

Subjects searched for the letter E in a background of Ls and Fs in displays that had 1, 2, 4, 8, or 12 letters. The letters could be shown at one of six orientations (upright or rotated clockwise in 60 degrees increments). The displays were either congruent for orientation (all letters had the same orientation) or incongruent (letters in haphazard orientations except for the target on E-present trials). Search time increased linearly with the number of letters in the display, and more so for E-absent trials than for E-present trials. Letter orientation, in general, increased search time and produced an M-shaped function. Furthermore, orientation effects were attenuated in congruent displays relative to those produced by incongruent displays. The results demonstrated systematic orientation effects on the time to search for a simple pattern embedded in simple backgrounds, and provided converging evidence for the orientation-congruency effect found by Jolicoeur (1990b, Journal of Experimental Psychology: Human Perception and Performance, 16, 351-364).

Adult↗
PubMed1992

U3 long terminal repeat-mediated induction of intracellular immunity by a murine retrovirus: a novel model of latency for retroviruses.

BL/VL3 radiation leukemia virus (RadLV) is a thymotropic, highly leukemogenic murine leukemia virus (MuLV) which is unable to replicate in vitro in mouse fibroblasts. We have previously reported that the U3 long terminal repeat region of its genome is responsible for this block (E. Rassart, Y. Paquette, and P. Jolicoeur, J. Virol. 62:3840-3848, 1988). By using hybrids of permissive and resistant cells infected with BL/VL3 RadLV or fibrotropic MuLV, we found that the resistant phenotype was dominant. Investigation to determine at which step of the virus cycle the block operates revealed that integration, transcription, and translation of the BL/VL3 viral genome occurred at normal levels in nonpermissive cells. The BL/VL3 RadLV Pr65gag proteins made in nonpermissive cells were also myristylated and located at the membrane, and the levels of their cleaved products were similar to those of fibrotropic MuLV. However, processing of BL/VL3 RadLV Pr85env was impaired in nonpermissive cells. Virions were not released into the culture medium of nonpermissive cells, as measured by reverse transcriptase activity and by content in p30 or gp70 protein and as documented by lower levels of budding particles seen by electron microscopy. These results indicate that BL/VL3 RadLV replication is blocked at a late stage of the virus cycle, i.e., at virion assembly. Interestingly, these BL/VL3 RadLV-infected nonpermissive fibroblasts were resistant to superinfection by fibrotropic Moloney MuLV, and this resistance also occurred at a late step of the Moloney virus cycle. Since this block is dominant, it appears that the U3 long terminal repeat region of the BL/VL3 viral genome has the ability to induce a cellular suppressor factor(s), thus bringing intracellular immunity against itself and against other ecotropic MuLVs.

Animals↗
PubMed1992

Identification of a novel gene, Vin-1, in murine leukemia virus-induced T-cell leukemias by provirus insertional mutagenesis.

The BL/VL3 radiation leukemia virus is a nondefective retrovirus which induces clonal or oligoclonal T-cell leukemia in mice. To study the role of provirus insertional mutagenesis in the development of these neoplasias, we searched for common provirus integration sites in BL/VL3 radiation leukemia virus-induced tumors. Using cellular sequences flanking a provirus cloned from one of these thymomas, we found that the viral genome was integrated into a common region, designated Vin-1, in a low percentage (5%) of these tumors. The proviruses found in this locus were integrated in the same orientation, close to a CpG-rich island, at proximity of a transcriptional unit encoding a 6-kb RNA. Vin-1 RNA was detected in several organs of the adult mouse. Vin-1 RNA levels were high in tumors having a provirus inserted within the Vin-1 region but were also high in some other tumors whose Vin-1 region was not found to be rearranged. Vin-1 was found to be well conserved among mammalian species and was mapped to mouse chromosome 6, between raf and K-ras-2. Vin-1 appears to be a novel gene which may be involved in tumor development.

Animals↗
PubMed1992

Susceptibility of inbred strains of mice to murine AIDS (MAIDS) correlates with target cell expansion and high expression of defective MAIDS virus.

Murine AIDS (MAIDS) is readily induced by the Duplan strain of defective murine leukemia virus in susceptible C57BL/6 mice. To identify mouse strains resistant to MAIDS, and to understand the genetic factors controlling susceptibility to the disease, we screened more than 20 inbred strains of mice for their susceptibility to MAIDS. For this study, mice of the Fv-1n/n, Fv-1b/b, or Fv-1n/b genotype were inoculated with stocks of defective MAIDS virus pseudotyped with N-tropic, B-tropic, or NB-tropic helper murine leukemia virus, respectively. Strains could be classified as susceptible, resistant, or moderately resistant. None of the individual H-2 haplotypes examined appears to explain resistance to MAIDS by itself. However, a very good correlation between the susceptibility or resistance phenotype and the presence or absence of defective proviral DNA and RNA in the spleen of these animals was found. Since the presence of defective proviral DNA and RNA reflects the oligoclonal proliferation of the cells infected by the defective MAIDS virus, our results strongly suggest that this target cell expansion is genetically controlled and is necessary and perhaps even sufficient for the development of the disease.

3T3 Cells↗
PubMed1992

Efficient production of human immunodeficiency virus proteins in transgenic mice.

Transgenic mice containing the complete human immunodeficiency virus (HIV) coding sequences fused to the mouse mammary tumor virus long terminal repeat were generated. They were found to produce high levels of authentic gag and env HIV proteins in several tissues known to support mouse mammary tumor virus-driven transcription. HIV proteins were also detected in serum and in body fluids (milk and epididymal secretions) known to be natural sites of retrovirus, and specifically of HIV, production. These results indicate that primary mouse cells from different tissues have the capacity to produce HIV proteins. These mice represent a novel animal model for HIV infection.

Animals↗
PubMed1992

A viral long terminal repeat expressed in CD4+CD8+ precursors is downregulated in mature peripheral CD4-CD8+ or CD4+CD8- T cells.

The long terminal repeat from a thymotropic mouse mammary tumor virus variant, DMBA-LV, was used to drive the expression of two reporter genes, murine c-myc and human CD4, in transgenic mice. Expression was observed specifically in thymic immature cells. Expression of c-myc in these cells induced oligoclonal CD4+ CD8+ T-cell thymomas. Expression of human CD4 was restricted to thymic progenitor CD4- CD8- and CD4+ CD8+ T cells and was shut off in mature CD4+ CD8- and CD4- CD8+ T cells, known to be derived from the progenitor double-positive T cells. These results suggest the existence of similar and common factors in CD4+ CD8- and CD4- CD8+ T cells and support a model of differentiation of CD4+ CD8+ T cells through common signal(s) involved in turning off the expression of the CD4 or CD8 gene.

Animals↗
PubMed1992

Size effects in visual recognition memory are determined by perceived size.

Recognition memory for shapes has been shown to depend on differences between the size of shapes at the time of encoding and at the time of the memory test (Jolicoeur, 1987). Experiment 1 of the present paper replicates this effect and establishes a set of parameters used in the subsequent experiments. Experiment 2 considers the results of Experiment 1 in light of the distinction between "perceived" size, which, under normal viewing conditions, varies minimally with changes in distance between the observer and object, and "retinal" size, which varies proportionally with viewing distance as an object is moved closer to or farther from an observer. Subjects studied novel shapes and performed a recognition memory test in which the distance from the subject to the viewing screen at the time of testing was different from that at the time of encoding. The viewing distance and the size of the shapes were manipulated such that perceived and retinal sizes were dissociated. The results suggest that the size-congruency effect in memory for visual shape occurs as a result of changes in the perceived size of shapes between the encoding and the testing phases, with little or no contribution of retinal size per se.

Distance Perception↗
PubMed1992

A four-parameter generalization of the Gompertz curve suitable for somatic growth.

A four-parameter generalization of the Gompertz curve is proposed which passes through the origin with respect to total age and is often more suitable for somatic growth than the three-parameter Gompertz curve. Applied to published cross-sectional data on 44 male white rats, the new curve differs from another four-parameter curve proposed earlier by Jolicoeur and Pirlot (1988) in that it does not involve initial growth delays and it avoids an arbitrary assumption concerning the initial curvature, but it nevertheless yields approximately similar descriptions of chronological growth and complex allometry. The new four-parameter version of the Gompertz curve may be useful in cases where other growth curves do not provide a satisfactory fit.

Animals↗
PubMed1991

Retrovirus-induced spongiform myeloencephalopathy in mice: regional distribution of infected target cells and neuronal loss occurring in the absence of viral expression in neurons.

The Cas-Br-E murine leukemia virus (MuLV) induces a spongiform myeloencephalopathy resulting in a progressive hindlimb paralysis. We have used in situ hybridization with a Cas-Br-E MuLV-specific probe to study viral expression in the central nervous system. Infected cells were concentrated in regions where spongiform lesions and gliosis are detected (lumbosacral spinal cord, brainstem, deep cerebellar regions), suggesting a causative link between the level of virus expression and the degree of pathological changes in this disease. However, viral expression was not in itself sufficient to cause disease, since significant viral expression was observed in regions that did not exhibit pathological changes (cerebellar cortex, hippocampus, corpus callosum, peripheral nervous system). In both diseased and nondiseased regions, endothelial and glial cells were identified as the main target cells. Neurons in diseased regions did not show viral expression. The regional distribution of the spongiform changes appears to be laid down very early following infection, since expression could be detected at 10 days postinfection in regions that become diseased. These results indicate that nonneuronal cells have distinct properties in various regions of the central nervous system and suggest an indirect mechanism of neuronal loss consequent to viral expression in nonneuronal cells.

Animals↗
PubMed1991

The effect of anti-neoplastic drugs on murine acquired immunodeficiency syndrome.

The murine acquired immunodeficiency syndrome (MAIDS) is associated with proliferation of target cells that have been infected by a defective retrovirus. To control the growth of this primary neoplasia, virus-inoculated mice were treated with anti-neoplastic drugs. Paradoxically, cyclophosphamide, which is also immunosuppressive, was very effective in preventing the appearance and progression of the disease, in restoring a normal T cell function, and in depleting the number of infected target cells. This result suggests that the proliferating infected target cells were responsible for the immunodeficiency.

Animals↗
PubMed1991

The specificity of the disease induced by defective murine retroviruses containing abl, fos, or Ha-ras is usually not determined by their LTR.

The long terminal repeats (LTR) of the defective murine sarcoma viruses (MSV) containing v-abl, v-Ha-ras, or v-fos were exchanged for LTRs from other retroviruses having different tissue tropism. The new chimeric MSV were found to induce the same diseases as the parental viruses, indicating that sequences outside the LTR, most likely those of the oncogene, are responsible for the disease specificity of these defective MSV.

Animals↗
PubMed1991

Neuronal loss in a lower motor neuron disease induced by a murine retrovirus.

An animal model of neuronal loss induced by a murine retrovirus is described. The neurological disease is manifested by a lower limb paralysis and is characterized as a spongiform myeloencephalopathy. The primary determinant of neurovirulence has been mapped within the viral env sequences and a secondary determinant is present within the LTR region. A model of pathogenesis, suggesting that the disease is receptor-mediated, is proposed.

Animals↗
PubMed1991

Visual curve tracing properties.

Subjects decided whether 2 dots were on the same curve or 2 different curves, and the curvature of the curves or the proximity of other (distractor) curves to the target curve was varied. Response time increased as the arc length of the curve connecting the 2 dots increased, suggesting that the curve was traced to perform the task. Tracing rate was faster for low- than high-curvature contours and was increasingly slower as distractor contours were increasingly proximal to the traced curve. Proximity results were predicted by a model in which response time depends on the ratio of the distance between the dots and the distance between adjacent lines. Curve tracing operations used to integrate information along contours are sensitive to several properties of the contours. The implications of the sensitivity of tracing operations to these curve properties are discussed.

Adult↗
PubMed1991

Murine acquired immunodeficiency syndrome (MAIDS): an animal model to study the AIDS pathogenesis.

Murine AIDS (MAIDS) is a disease that shows many similarities with human AIDS. Several immunological parameters of the disease have been analyzed and genetic studies have mapped a gene (or genes) of resistance in the H-2 complex and shown that the genetic background of the mouse can significantly modify some features of the disease. The etiologic agent of MAIDS is a defective murine leukemia virus that seems able to induce disease in the absence of virus replication. This defective virus induces proliferation of its target cells and the cell expansion was found to be oligoclonal, thus suggesting that the immunodeficiency observed in these mice is a paraneoplastic syndrome. The excellent response of MAIDS mice to antineoplastic agents is consistent with this notion. This animal model has already been useful in stimulating the emergence of novel questions and the formulation of new hypotheses about human AIDS, namely about the role of defective HIV, the role of HIV replication in the progression of the disease, and the importance to identify the target cells of HIV in vivo. Although MAIDS and AIDS are not identical and are induced by retroviruses of different classes, the availability of such a model in an easily accessible small animal species, whose genetics is very sophisticated, may be instrumental in understanding the pathogenesis of AIDS if some of the cellular and molecular affected pathways are common in both diseases.

Animals↗
PubMed1991

The majority of cells infected with the defective murine AIDS virus belong to the B-cell lineage.

Murine AIDS (MAIDS) is caused by a defective retrovirus which encodes a gag fusion protein (Pr60gag). We previously reported that this virus induced an oligoclonal proliferation of infected cells and suggested that this cell expansion was an important event in the pathogenesis of MAIDS. To identify these target cells, we constructed novel defective viruses whose genomes could be detected with specific probes. Helper-free stocks of these viruses induced MAIDS. Using in situ hybridization and immunocytochemistry and Southern analysis, we found that most infected cells belong to the B-cell lineage. Transformation of these B cells appears to be the primary event responsible for the development of immunodeficiency. This animal model may be relevant to our understanding of AIDS, of the immunodeficiencies associated with B-cell lymphoproliferative disorders, and of the role of B-cell proliferation and transformation in the effects of superantigens, since Pr60gag appears to be a superantigen.

Animals↗