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N Paquette

Publications and source records attributed to N Paquette.

12 recordsLinked to original sources
PubMed2004

[The daily public health nursing practice: the Montreal infectious diseases unit as an example].

The health of urban populations depends on multiple factors, among them access to health and social services. The Montreal Public Health Department (PHD) is part of such services, where a number of nurses are working within a multidisciplinary team. It is through the description of the work accomplished by the team for infectious diseases control and prevention, and the vignettes of real life events related to the follow-up of syphilis, tuberculosis and hepatitis A cases, as well as quarantined individual exposed to SARS that the authors want to illustrate the work of the urban public health nurses. The examples are preceded by a description of the socio-demographic characteristics of the city of Montreal, that influence health problems, and therefore nurses' work.

Demography↗
PubMed1996

PAF-induced airways hyperreactivity is modulated by mast cells in mice.

We tested the hypothesis that mast cells contribute to platelet-activating factor (PAF)-induced airways hyperreactivity and hyperpermeability in mice. Airways reactivity to acetylcholine (ACh) and lung permeability to Evans blue (EB) dye were measured before and after PAF challenge in genetically mast cell-deficient (WBB6F1 W/Wv) and normal congenic (WBB6F1 +/+) mice, as well as mast cell-reconstituted (BMT W/Wv) mice. In addition, prostaglandin D2 (PGD2), a mast cell-specific mediator, was measured in the bronchoalveolar lavage (BAL) from +/+ and W/Wv mice to determine if lung mast cell activation was a consequence of PAF challenge. Genetically PAF-sensitive AKR/J mice were also treated with the mast cell stabilizer nedocromil prior to assessment of PAF effects on ACh reactivity. Intravenous PAF (10 micrograms/kg) induced a significant (P < 0.05) increase in airways reactivity to ACh (25 micrograms/kg) in both +/+ (371 +/- 52%) and W/Wv (122 +/- 24%) mice. There was a significantly greater increase in +/+ compared with W/Wv mice. PAF-induced hyperreactivity to ACh in BMT W/Wv mice (191 +/- 44%) was significantly (P < 0.05) greater than age-matched W/Wv mice (80 +/- 16%), but not significantly different from age-matched +/+ mice (153 +/- 44%). PAF (10 micrograms/kg) also significantly (P < 0.5) increased lung permeability in +/+ and W/Wv mice, but there was no significant difference between groups. BAL PGD2 increased significantly in +/+ mice following PAF challenge (559 +/- 24 ng/ml) compared with vehicle controls (152 +/- 8 pg/ml). There was no significant increase in BAL PGD2 from W/Wv mice. Nedocromil pretreatment significantly (P < 0.05) decreased PAF-induced hyperreactivity in AKR/J mice but not in W/Wv mice (P > 0.05). We conclude that mast cells contribute significantly to PAF-induced hyperreactivity but not hyperpermeability in mice.

Acetylcholine↗
PubMed1995

Encapsulation of foscarnet in liposomes modifies drug intracellular accumulation, in vitro anti-HIV-1 activity, tissue distribution and pharmacokinetics.

OBJECTIVE: To improve the in vitro anti-HIV-1 activity, intracellular accumulation in macrophages and in vivo pharmacokinetics and tissue distribution of foscarnet (trisodium phosphonoformate; PFA) by encapsulation in liposomes. METHODS: The accumulation of free and liposome-encapsulated PFA was determined in monocyte-macrophage RAW 264.7 cells and human premonocytoid U937 cells. The antiviral activity was evaluated in U937 cells infected with HIV-1IIIB. Tissue distribution and pharmacokinetics of free and liposomal PFA were determined in female Sprague-Dawley rats following the administration of an intravenous bolus dose (10 mg PFA/kg). RESULTS: The entrapment of PFA in liposomes resulted in a higher drug accumulation in both U937 and RAW 264.7 cells. A slightly greater efficacy against HIV-1IIIB replication into U937 cells was observed upon encapsulation of PFA into liposomes. Improved pharmacokinetics was observed upon entrapment of PFA in liposomes. Much higher drug levels were found in plasma for the liposomal formulation. The systemic clearance of the liposomal drug was 77 times lower than that of free drug. The encapsulation of PFA in liposomes greatly enhanced the drug accumulation in organs of the reticuloendothelial system. CONCLUSION: The encapsulation of PFA in liposomes modified the tissue distribution and plasma pharmacokinetics of the antiviral agent, resulting in a marked improvement of drug accumulation in organs involved in HIV immunopathogenesis and in a greater PFA bioavailability. The antiviral activity of liposomal PFA was slightly greater than that of free drug in HIV-1IIIB-infected U937 cells.

Animals↗
PubMed1994

Productive infection of normal CD40-activated human B lymphocytes by HIV-1.

OBJECTIVE: Antigen-driven B-cell proliferation and maturation occur in germinal centres present in lymphoid tissues. This process is highly dependent on functional interactions between B and T lymphocytes. In vitro activation of CD40 present on B cells mimics B cell-T interactions and allows the proliferation of normal Epstein-Barr virus (EBV)-negative B lymphocytes. In HIV-1-seropositive individuals, B cells become exposed to free viral particles and to infected T lymphocytes while migrating through germinal centres. The effect of HIV-1 viral exposure on CD40-activated B lymphocytes was therefore examined. METHODS: Freshly isolated B lymphocytes were cultured in vitro through activation of CD40. B-cell proliferation, HIV-1 infectivity and viral production were monitored following B-lymphocyte exposure to HIV-1. In addition, HIV-mediated fusion between infected B cells and uninfected CD4+ T lymphocytes was assessed in a coculture assay. RESULTS: EBV-negative, CD40-activated human B lymphocytes were directly infected by HIV-1. The infection significantly reduced their proliferation rate. Viral production was detected in B-cell culture supernatant. Numerous fusion events indicated that HIV-1 infection of B lymphocytes could spread to T lymphocytes following HIV-1-mediated fusion of these two cell types. CONCLUSION: In view of the importance of B cell-T cell interactions in the maintenance of a functional immune system, disruption of B-lymphocyte development could have direct implications on the course of AIDS progression.

Antigens, CD↗
PubMed1989

Human thymic dendritic cell-thymocyte association: ultrastructural cell phenotype analysis.

In rodent thymus, associations between dendritic cells (DC) and thymocytes have been suggested to be implicated in differentiation and/or maturation processes. In this study, we report intimate associations formed between human thymic DC and thymocytes in culture and we analyze their ultrastructural cell phenotype. Observations by phase contrast microscopy showed that DC present long and thin dendrites and bind many thymocytes. Transmission (TEM) and scanning electron microscopy (SEM) revealed that both cellular populations were in close connection and tight membrane contact could be observed. The phenotype of DC and attached thymocytes was characterized with a series of monoclonal antibodies by protein A-gold TEM and SEM immunolabelings. Quantitative evaluation of immunolabeling (number of gold granules/microns of cellular membrane) suggests the presence of two subpopulations of CD1+ thymic DC (strong and weak), whereas this discrepancy is not observed in DR+ and CD4+ DC populations. On the other hand, the majority of thymocytes bound to DC strongly express the CD1, CD4, CD8 and CD2 antigens and weakly the CD3 antigen, indicating that they represent double-positive immature thymocytes. Uniform distribution of DC and thymocytes membrane antigens was confirmed with a backscattered SEM study. This morphological and immunolabeling TEM and SEM analysis demonstrates that human thymic DC may form associations with CD4+CD8+CD3weak thymocytes and raises questions about their physiological relationship.

Antigens, CD1↗
PubMed1979

Disparity of gene conversion in frameshift mutants located in locus b2 of Ascobolus immersus.

The frequency of conversion and the disparity in the direction of conversion were studied for six frameshift mutants lying in locus b2 of Ascobolus immersus and giving more 2 wild type:6 mutant (2+6m) than 6 wild type:2 mutant (6+2m) aberrant asci (type B). The frequency of conversion decreased from left to right in the locus. The disparity steadily increased from left to right and then reached a plateau. Twenty-two frameshift mutants giving more 6+2m than 2+6m aberrant asci (type A) and closely linked to three type B mutants were also studied; they showed the same frequency of conversion and the same disparity (but in the opposite direction) as the type B mutant to which they are linked. The polar variation of both the frequency of conversion and the disparity as a function of position were expected on the basis of a previous study of 15 mutants giving postmeiotic segregations and located in locus b2. This variation is assumed to reflect the existence of a preferential region for the initiation of hybrid DNA (HDNA) during recombination and a duality in the distribution of this HDNA, with preponderant asymmetrical HDNA near the starting point and preponderant symmetrical HDNA farther from it.

Journal Article↗
PubMed1978

Intragenic suppression at the b2 locus in Ascobolus immersus. I. Identification of three distinct groups of suppression.

A reversion study of EMS- or ICR170-induced ascospore color mutants in Ascobolus immersus is reported. Twenty-three new intragenic suppressors were isolated within the b2 locus. These are localized within three distinct groups on a genetic fine-structure map containing 21 identifiable sites. The pattern of reversion is discussed according to the known specificity of EMS and ICR170 in Ascobolus immersus.

Ascomycota↗
PubMed1976

[High frequency reversion of a spontaneous mutant in Ascobolus immersus].

A spontaneous spore-colour mutation located in the gene b2 of A. immersus gives a high frequency of reversion. 8 distinct revertant phenotypes have been defined. The mutations corresponding to these revertants are located at the same site or very near the original mutation. The hypothesis that the mutation by itself is responsable for the observed reversions is advanced.

Ascomycota↗