L'information différentielle : une solution à la surabondance des normes ?

La présente étude empirique questionne l'efficacité du principe de l'information différentielle adoptée au Canada. Une analyse de contenu des états financiers d'un échantillon aléatoire de 240 PME québécoises, permet notamment de constater la fréquence d'utilisation de ce principe, à la lumière de certaines caractéristiques des entreprises.comptabilité; états financiers; normes; PME; harmonisation

A collaborative model to implement flexible, accessible and efficient oncogenetic services for hereditary breast and ovarian cancer : the C-MOnGene study

Medical genetic services are facing an unprecedented demand for counseling and testing for hereditary breast and ovarian cancer (HBOC) in a context of limited resources. To help resolve this issue, a collaborative oncogenetic model was recently developed and implemented at the CHU de Québec-Université Laval; Quebec; Canada. Here, we present the protocol of the C-MOnGene (Collaborative Model in OncoGenetics) study, funded to examine the context in which the model was implemented and document the lessons that can be learned to optimize the delivery of oncogenetic services. Within three years of implementation, the model allowed researchers to double the annual number of patients seen in genetic counseling. The average number of days between genetic counseling and disclosure of test results significantly decreased. Group counseling sessions improved participants' understanding of breast cancer risk and increased knowledge of breast cancer and genetics and a large majority of them reported to be overwhelmingly satisfied with the process. These quality and performance indicators suggest this oncogenetic model offers a flexible, patient-centered and efficient genetic counseling and testing for HBOC. By identifying the critical facilitating factors and barriers, our study will provide an evidence base for organizations interested in transitioning to an oncogenetic model integrated into oncology care; including teams that are not specialized but are trained in genetics

Jocelyne Alloucherie

In a catalogue documenting Alloucherie's production since the 1970s, Gosselin links the relationship between the artist's installations and nature to a unifying principle harmonizing body, matter, and memory. Albertazzi evokes Heidegger's essay on art and space to get at the essence of notions of belonging and place, while Gould proposes an approach based on familiarity/foreignness as subject. Artist's statement. Biographical notes. 24 bibl. ref

Both Cerebral and Hematopoietic Deficiencies in CCR2 Result in Uncontrolled Herpes Simplex Virus Infection of the Central Nervous System in Mice

<div><p>CCR2 is a chemokine receptor expressed on the surface of blood leukocytes, particularly «Ly6C^hi» inflammatory monocytes and microglia. Signaling through this receptor is thought to influence the immune activity of microglia as well as monocytes egress from the bone marrow (BM) and their trafficking into the central nervous system (CNS) in several neurological diseases. During experimental herpes simplex virus 1 (HSV-1) encephalitis (HSE), CCR2 deficiency has been reported to exacerbate the outcome of the disease. However, the precise contribution of CCR2 expressed in cells of the CNS or peripheral monocytes in the protection against HSE remains unclear. To dissect the differential role of CCR2 during HSE, chimeric mice with receptor deficiency in the brain or blood cells were generated by transplanting wild-type (WT) C57BL/6 or CCR2^-/- BM-derived cells in CCR2^-/- (WT→CCR2^-/-) and WT (CCR2^-/-→WT) mice, respectively. Our results indicate that following intranasal infection with 1.2x10⁶ plaque forming units of HSV-1, CCR2 deficiency in hematopoietic cells and, to a lesser extent, in CNS exacerbates the outcome of HSE. Mortality rates of CCR2^-/- (71.4%) and CCR2^-/-→WT (57.1%) mice were significantly higher than that of WT (15.3%; <i>P</i><0.01 and <i>P</i><0.05, respectively) but the difference did not reach statistical significance for WT→CCR2^-/- animals (42.8%; <i>P</i> = 0.16). Both peripheral and CNS deficiencies in CCR2 resulted in increased infectious viral titers and wider dissemination of HSV antigens in the brain as well as an overproduction of inflammatory cytokines and chemokines including IL-1β, IL-6, CCL2, CCL3 and CCL5. Furthermore, CCR2 deficiency in the hematopoietic system altered monocytes egress from the BM and their recruitment to the CNS, which may contribute to the failure in HSV-1 containment. Collectively, these data suggest that CCR2 expressed on cells of CNS and especially on peripheral monocytes is important for the control of HSV-1 replication and inflammatory environment during experimental HSE.</p></div

Impact of CCR2 deficiency in resident cells of the CNS or in the hematopoietic system on cytokines and chemokines production during HSE.

<p>Levels of cytokines and chemokines in brain homogenates of wild-type (WT) C57BL/6, CCR2^-/-, CCR2^-/-→WT and WT→CCR2^-/- mice were evaluated prior to (day 0) and on days 6, 8 and 10 following intranasal infection with 1.2x10⁶ PFU of HSV-1. Levels of cytokines and chemokines were measured using magnetic bead-based immunoassay. Results are expressed in pg/mL of brain homogenates and represent the means ± standard deviations of 4 to 5 mice per group at each time point. Statistical analyses were performed using a one-way analysis of variance (ANOVA) with Tukey’s multiple comparison post-test. Statistically significant results obtained in CCR2^-/-, CCR2^-/-→WT and WT→CCR2^-/- compared to those of the WT group are indicated as follows: *, <i>P</i><0.05; **, <i>P</i><0.01; ***, <i>P</i><0.001.</p

Effects of CCR2 deficiency in resident cells of the CNS or in the hematopoietic system on blood leukocytes infiltration into the CNS during HSE.

<p>Leukocytes of wild-type (WT) C57BL/6, CCR2^-/-, CCR2^-/-→WT and WT→CCR2^-/- mice were analysed in brain homogenates by flow cytometry prior to (day 0) and on days 4, 6, 8 and 10 following intranasal infection with 1.2x10⁶ PFU of HSV-1. <b>(A)</b> Flow cytometry contour plots illustrating the gating strategy used for brain leukocytes differentiation in mouse sacrificed on day 6 following infection. The CD45 marker was used to discriminate microglia (i.e., CD45^low; continuous rectangle) from infiltrating leukocytes (i.e., CD45^hi; dashed rectangle). Among «CD45^hi/CD11b⁺» infiltrating myeloid cells (dashed circle), monocytes subsets were discriminated according to Ly6C expression level into «Ly6C^hi» inflammatory and «Ly6C^low» patrolling monocytes. The percentages of <b>(B)</b> infiltrating leukocytes, <b>(C)</b> inflammatory monocytes and <b>(D)</b> patrolling monocytes with respect to total brain leukocytes represent the means ± standard deviations of 4 to 5 mice per group at each time point. Statistical analyses were performed using a one-way analysis of variance (ANOVA) with Tukey’s multiple comparison post-test. Statistically significant results compared to those of WT animals are indicated as follows: *, <i>P</i><0.05; **, <i>P</i><0.01; ***, <i>P</i><0.001.</p

Impact of CCR2 deficiency in resident cells of the CNS or in the hematopoietic system on the control of viral replication during HSE.

<p>Wild-type (WT) C57BL/6, CCR2^-/-, CCR2^-/-→WT and WT→CCR2^-/- mice were sacrificed prior to (day 0) and on days 4, 6, 8 and 10 following intranasal infection with 1.2x10⁶ PFU of HSV-1. Viral titers were measured in brain homogenates by a standard plaque assay on Vero cells. Results are reported as PFU/μL of brain homogenates and represent the means ± standard deviations of 4 to 5 mice per group at each time point. Statistical analyses were performed using a one-way analysis of variance (ANOVA) with Tukey’s multiple comparison post-test. Statistically significant results compared to those for the WT group are indicated as follows: *, <i>P</i><0.05; **, <i>P</i><0.01; ***, <i>P</i><0.001. ND, not detected.</p

Impact of CCR2 deficiency in resident cells of the CNS or in the hematopoietic system on HSV-1 distribution in the brain during HSE.

<p>Representative micrographs illustrating the distribution pattern of HSV-1 proteins in the olfactory bulb, the medulla, the cerebral cortex and the striatum of wild-type (WT) C57BL/6, CCR2^-/-→WT, WT→CCR2^-/- and CCR2^-/- animals (4 to 5 mice per group) sacrificed on day 6 post-infection. Brain slices (25 μm thick) were processed for immunohistochemistry analyses with a polyclonal rabbit anti-HSV-1/2 primary antibody and an Alexa 594-conjugated chicken anti-rabbit secondary antibody (red), followed by nuclear staining with DAPI (blue). Scale bar 100 μm.</p