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Biomedical subjects

M Doré

Publications and source records attributed to M Doré.

At least 37 records · Page 2Linked to original sources
PubMed1996

Chemoattractant-induced changes in surface expression and redistribution of a functional ligand for P-selectin on neutrophils.

Adhesion between platelets and neutrophils is mediated through the interaction of P-selectin on activated platelets with a carbohydrate-containing structure on neutrophils, and occurs under both static and shear conditions. Recent studies using flow chambers have shown that neutrophils become activated after binding to surface-adherent platelets expressing P-selectin. The objective of the present study was to investigate the effect of such activation on the interactions of platelet P-selectin with its ligand on neutrophils. Flow cytometric analyses using P-selectin chimeras revealed that activation induced a rapid and marked reduction in chimera binding, with levels of binding decreased by 71% after 15 minutes of stimulation with the chemotactic agent, FMLP. Using a visual assay of platelet-neutrophil rosetting, we showed that the P-selectin ligand was translocated and clustered at the uropod of neutrophils following the shape changes and polarization induced by chemotactic stimulation. Activated neutrophils bound to surface-adherent platelets also displayed the clustering of P-selectin ligand at the uropod, and these neutrophils detached from the platelets when a shear stress (2 dynes/cm2) was applied through the adhesion chamber. These results indicate that chemotactic stimulation of neutrophils induces changes in the surface expression and distribution of a biologically relevant ligand for P-selectin, and that these changes might influence the adhesive interactions occurring between neutrophils and activated platelets.

Adult↗
PubMed1996

Regulation of P-selectin expression by inflammatory mediators in canine jugular endothelial cells.

Canine endothelial cells express the adhesion molecule P-selectin to mediate the initial attachment of leukocytes to the vessel wall. Although it is known that agents like histamine and thrombin stimulate the surface expression of P-selectin, the effect of inflammatory mediators and cytokines such as lipopolysaccharides (LPS), tumor necrosis factor-alpha (TNF-alpha), and interleukin-1 beta (IL-1 beta) on canine P-selectin expression has not been investigated. Therefore, the objective of this study was to analyze the regulation of P-selectin messenger RNA (mRNA) and protein by these cytokines in canine endothelial cells isolated from jugular veins. Analyses of cytoplasmic RNA by Northern blotting showed that stimulation of culture endothelial cells with either LPS (100 ng/ml) or recombinant human TNF-alpha (30 U/ml) for 3 or 6 hours significantly increased (P < 0.05) steady-state levels of mRNA for P-selectin (3.8- +/- 1.0- and 3.0- +/- 0.4-fold increase for LPS at 3 and 6 hours, respectively, and 2.5- +/- 0.8- and 2.7- +/- 0.9-fold increase for TNF-alpha at 3 and 6 hours, respectively). P-selectin mRNA had decreased by 48 hours to levels found in unstimulated cells. In contrast, human IL-1 beta had no effect on P-selectin mRNA. Increased levels of mRNA with LPS stimulation were associated with the synthesis of new protein, as demonstrated by the positive staining in LPS-stimulated cells using immunocytochemistry with a monoclonal antibody against canine P-selectin (MD3). These results reveal that important inflammatory mediators and cytokines such as LPS and TNF-alpha induce the synthesis of new P-selectin and suggest that this process could represent a means of sustaining local leukocyte recruitment for several hours during an acute inflammatory reaction.

Analysis of Variance↗
PubMed1996

Acute inflammatory reaction after myocardial ischemic injury and reperfusion. Development and use of a neutrophil-specific antibody.

Reperfusion of the infarcted canine myocardium after 1 hour of ischemia is associated with an acute inflammatory infiltrate at the border of the infarct. In this paper, we demonstrate that early margination and emigration of neutrophils originate in thin-walled (approximately 5 micrometers) venous cisterns that average 200 micrometers in length and vary from 10 to 70 micrometers in width and show strong constitutive expression of both ICAM-1 and P-selectin; this class of vessels (venous cisterns) appears to be a unique feature in heart. A monoclonal antibody (SG8H6) with specificity for canine neutrophils was developed that allowed much more sensitive immunohistochemical detection of neutrophils in tissue and allowed us to follow tissue infiltration with time. Samples from 1 hour of reperfusion revealed dense margination and substantial emigration of neutrophils associated with the venous cisterns and collecting venules. By 2 hours, there was intense local emigration to the extravascular space between cardiac myocytes. By 3 hours, the infiltrate extended deeper into the infarct, and there was a continuous border zone of neutrophil infiltration that overlapped a region where intact cardiac myocytes strongly expressed ICAM-1 mRNA and extended into the necrotic tissue. At later times, neutrophil migration into infarcted tissue continued to progress. Neutrophil transmigration into reperfused myocardium is more extensive than previously described, and its extravascular distribution during early reperfusion is primarily in the viable border zone of the myocardium where myocyte ICAM-1 mRNA is found. These data are compatible with the hypothesis that extravascular neutrophils may participate in reperfusion injury.

Acute Disease↗
PubMed1995

P-selectin- and CD18-mediated recruitment of canine neutrophils under conditions of shear stress.

Neutrophil mobilization at sites of inflammation or thrombosis involves the participation of several adhesion molecules expressed on neutrophils and vascular endothelial cells. Local vascular damage with disruption of the endothelium results in adhesion of platelets to the exposed subendothelium, and these platelets could also participate in neutrophil recruitment. This initial phase of mobilization could be followed by heterotypic aggregation to recruit more leukocytes in the area. The present study first examined the interactions of adherent canine platelets and flowing canine neutrophils using an in vitro system that simulates vascular flow conditions. Results showed that collagen-adherent platelets express the adhesion molecule P-selectin on their surface and can support neutrophil arrest (612 +/- 43 neutrophils/mm2) at shear stresses of approximately 2.5 dynes/cm2. Both transient adhesion (manifested by a rolling-type behavior) and complete arrest were observed. These interactions could be totally inhibited by a monoclonal antibody directed against platelet P-selectin (24 +/- 18 neutrophils/mm2) but not by a monoclonal antibody against neutrophil CD18 (625 +/- 46 neutrophils/mm2). Additionally, under shear mixing conditions (700 RPM), canine blood leukocytes exhibited aggregation (> 80% singlets recruited into aggregates after 5 minutes), and this process does not involve P-selectin but is dependent on the neutrophil integrin CD18. However, stimulation of the blood with platelet-activating factor (5-20 ng/ml) induced a rapid aggregation with a significantly greater number of aggregates when compared with stirring alone (68.3% +/- 3.2% versus 35.2% +/- 6.3% at 1 minute, P < 0.05), and this aggregation was both P-selectin and CD18 dependent. Overall, these two mechanisms of leukocyte recruitment (neutrophil arrest on adherent platelets and aggregation) could act sequentially and in a cooperative manner to bring into close contact platelets and neutrophils at sites of inflammation and thrombosis in pathologic conditions in the dog.

Animals↗
PubMed1994

P-selectin and ICAM-1-dependent adherence reactions: role in the genesis of postischemic no-reflow.

The aim of this study was to determine whether immunoneutralization of P-selectin or intercellular adhesion molecule-1 (ICAM-1) (endothelial cell adhesion molecules involved in leukocyte rolling and firm adhesion, respectively) would attenuate the development of postischemic capillary no-reflow. Microvascular patency was assessed in vascularly isolated canine gracilis muscles by perfusion with contrast media (India ink) at the end of the experimental protocol. Computerized video imaging was used to quantitate the number of ink-containing microvessels (< 10 microns diam) per muscle fiber in histological samples obtained from isolated canine gracilis muscles subjected to 4.5 h of continuous perfusion (nonischemic control), 4 h of ischemia and 30 min of reperfusion (I-R), I-R + P-selectin monoclonal antibodies (MAbs) (MD6 or PB1.3), and I-R + ICAM-1 MAbs (CL18/6C7 or R6.5). The efficacy of a P-selectin MAb (MD3) that binds to a nonfunctional epitope was also evaluated. I-R was associated with a marked reduction in the number of patent capillaries per fiber (3.1 +/- 0.2 vs. 1.1 +/- 0.2 patent capillaries/fiber for control and I-R, respectively). Immunoneutralization with MAbs directed against functional epitopes on P-selectin (MD6 or PB1.3) significantly improved capillary perfusion (2.3 +/- 0.3 and 3.6 +/- 0.6 patent capillaries/fiber, respectively). On the other hand, MAb MD3, which binds to nonfunctional epitopes on P-selectin, failed to limit the development of postischemic no-reflow (1.0 +/- 0.2 patent capillaries/fiber). Immunoneutralization of ICAM-1 with CL18/6C7 and R6.5 increased the number of patent capillaries per fiber to 1.8 +/- 0.1 and 2.5 +/- 0.3, respectively. These data indicate that P-selectin and ICAM-1-dependent adherence reactions play an important role in the development of the no-reflow phenomenon in postischemic skeletal muscle.

Animals↗
PubMed1993

P-selectin mediates spontaneous leukocyte rolling in vivo.

Rolling represents the initial step leading to leukocyte extravasation from blood vessels during an inflammatory reaction. In vitro studies indicate that P-selectin could be one of the ligands on endothelium involved in the rolling phenomenon, although the molecular determinants responsible for this transient attachment in vivo are still undefined. Our objectives were to develop a blocking monoclonal antibody against canine P-selectin and to use it to investigate the role of P-selectin in leukocyte rolling in vivo using the technique of intravital microscopy. P-selectin was immunoaffinity purified from canine platelets and used for the production of monoclonal antibodies. One of the hybridomas generated, MD6, was shown by enzyme-linked immunosorbent assay and by flow cytometry to bind preferentially to stimulated platelets and to completely prevent binding of stimulated platelets to neutrophils. Visualization of canine mesenteric venules by intravital microscopy showed that administration of MD6 resulted in a marked inhibition in the number of rolling leukocytes (18.96 +/- 9.92 v 156.40 +/- 19.50 leukocytes/min, P < .05; 88.3% +/- 6.0% inhibition). Control antibody MD3 (which recognizes a nonfunctional epitope of canine P-selectin) had no effect on the number of rolling leukocytes or on their rolling velocity. These results show for the first time that P-selectin plays an essential role in leukocyte rolling in vivo, and therefore may be a key participant of the inflammatory response.

Amino Acid Sequence↗
PubMed1993

Production of a monoclonal antibody against canine GMP-140 (P-selectin) and studies of its vascular distribution in canine tissues.

Rapid upregulation of the adhesion molecule GMP-140 (P-selectin) on endothelial cells is believed to play an important role in the initial binding of leukocytes to endothelium, a very early step in the inflammatory response. Activated platelets that are involved in the coagulation system and in inflammatory processes also express GMP-140 on their surfaces. The objectives of the present study were to develop a monoclonal antibody against this adhesion molecule in the dog and to use this antibody to study platelet-neutrophil interactions in whole blood and to characterize the in vivo localization of GMP-140 in canine tissues. Five Balb/c mice were immunized with thrombin-stimulated dog platelets, and clones were screened using an enzyme-linked immunosorbent assay. The clone MD3 (IgG1) showed preferential binding to activated as compared with resting platelets. Flow cytometric analysis using MD3 revealed that 27% of circulating neutrophils in unstimulated blood had platelets bound to their surfaces; stimulation with platelet activating factor increased this percentage to 85%. Immunoblot analysis of solubilized dog platelets resolved by sodium dodecyl sulfate polyacrylamide gel electrophoresis indicated that the antibody MD3 recognized an approximately 140-kd protein. Immunohistochemical study of normal dog tissues with MD3 revealed that the antigen was present in endothelial cells of arteries, capillaries, and veins, depending on the specific tissue examined. Blood vessels staining positively with MD3 were most abundant in the digestive system (liver, stomach, small and large intestines), moderate in the lungs, kidneys, spleen, lymph nodes, and endocrine glands, and minimal in the brain, myocardium, skeletal system, and skin. Based on its presence on stimulated but not resting platelets, its molecular weight, and its vascular distribution, the antigen recognized by MD3 appears to be the selectin GMP-140 of the dog. This study documents that the cellular and tissue distribution of GMP-140 in dogs is very similar to that in human beings.

Animals↗
PubMed1992

Protein kinase-C activity in phorbol myristate acetate-stimulated neutrophils from newborn and adult cattle.

Neutrophils from newborn calves have been shown to be deficient in ability to generate superoxide anion (O2-) after stimulation of the respiratory burst enzyme with the phorbol ester, phorbol 12-myristate 13-acetate (PMA). This compound activates the O(2-)-generating enzyme of bovine neutrophils through a pathway involving protein kinase C (PKC). To investigate the biochemical basis underlying this functional difference between neutrophils from newborn and adult cattle, we measured and compared the activity of the enzyme PKC in nonstimulated and PMA-stimulated bovine neutrophils. Neutrophils from newborn calves (n = 5) and adult cows (n = 5) were stimulated with various concentrations of PMA (0, 10, 100, and 500 ng/ml) for 3 minutes, and PKC activity was assayed in the cytosolic and the membrane fractions. In nonstimulated cells, most PKC activity was detected in the cytosolic fraction of neutrophils from newborn and adult cattle. Activity of PKC in the cytosol was dependent on the presence of added calcium and phospholipids, whereas membrane-associated PKC in nonstimulated cells did not have such dependence. Significant differences in PKC activity were not observed between newborn and adult cattle in either the cytosolic or the membrane fractions from nonstimulated cells. Stimulation with PMA caused redistribution of PKC activity in the cell (translocation) in newborns and adults, consisting of decrease in cytosolic PKC activity and increase in membrane-associated PKC activity. Similar to that in nonstimulated cells, PKC activity in cytosolic fractions from PMA-stimulated neutrophils was dependent on the presence of cofactors (calcium and phospholipids), whereas PKC activity in the membrane did not have such requirement.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1991

Decreased respiratory burst activity in neonatal bovine neutrophils stimulated by protein kinase C agonists.

Newborn calves have a high susceptibility to bacterial infections, which may be related to the impaired neutrophil defense functions in newborns. The oxygen-dependent production of the free radical superoxide anion (O2-) represents an important part of the leukocyte respiratory burst central to neutrophil-directed defenses against bacterial infection. Because protein kinase C (PKC) activation is considered to be an important step in the signal transduction pathway for the O2- generating system, we compared O2- production by newborn and adult bovine neutrophils stimulated with 3 different PKC agonists. When the phorbol ester phorbol 12-myristate 13-acetate (PMA) was used, PKC-dependent O2- generation from newborn neutrophils was significantly reduced (P less than 0.01) for all concentrations of PMA tested (10, 100, and 500 ng/ml). In addition, newborn neutrophils had a significantly (P less than 0.01) reduced lag time for O2- generation. Similar significantly (P less than 0.01) reduced O2- generation from newborn neutrophils was observed with an additional phorbol ester (phorbol 12,13-dibutyrate); lag times were not calculated for phorbol 12,13-dibutyrate. When O2- generation was stimulated with a synthetic diacylglycerol analogue (1,2-dioctanoyl-sn-glycerol), less O2- was generated from both adult and newborn neutrophils than was obtained with the phorbol esters, and newborn neutrophils produced significantly (P less than 0.01) less O2- only at 50 microM 1,2-dioctanoyl-sn-glycerol.(ABSTRACT TRUNCATED AT 250 WORDS)

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1990

Calcium mobilization in C5a-stimulated adult and newborn bovine neutrophils.

Calcium (Ca2+) is an important second messenger central to many neutrophil (PMN) functional activities. Impaired Ca2+ mobilization in newborn PMNs following membrane perturbation could be one of the mechanisms underlying observed abnormalities in neonatal PMN function. To compare Ca2+ mobilization in bovine newborn and adult PMNs, cytosolic Ca2+ responses after stimulation with recombinant human C5a (rHC5a) were measured. PMNs from normal newborn calves (N = 6) and adult cows (N = 5) were loaded with fura-2/AM for 60 min at room temperature and the fluorescence changes monitored following stimulation with 0.1, 1, 10, or 50 nM rHC5a in Ca2(+)-containing buffer. Resting levels of Ca2+ in both newborn (54.6 +/- 1.9 nM) and adult (57.3 +/- 1.8 nM) bovine PMNs were comparable. After stimulation with rHC5a, a rapid rise of cytosolic Ca2+ was observed, which peaked within 20 sec and was followed by a sustained phase of elevated Ca2+ lasting up to 20 min. There were no significant differences (P greater than 0.05) in peak levels of cytosolic Ca2+ obtained by newborn and adult PMNs at 0.1, 10, and 50 nM rHC5a. At 1 nM rHC5a, newborn PMNs reached significantly (P less than 0.05) higher levels of cytosolic Ca2+ (217.9 +/- 21.7 nM) than did adult PMNs (158.7 +/- 7.9 nM). At 1 nM rHC5a, newborn PMNs also sustained higher levels of cytosolic Ca2+ for 3 min following the peak. At all concentrations of rHC5a tested, the time required to reach the peak and the duration of the peak were comparable in both populations. In the absence of extracellular Ca2+ (Ca2(+)-free buffer with 1 mM EGTA), resting levels of cytosolic Ca2+ were lower in both newborn (33.3 +/- 2.9 nM) and adult PMNs (27.9 +/- 2.4 nM) and the magnitude of the peak response to rHC5a was diminished at all concentrations of agonist. Additionally, in the absence of extracellular Ca2+, the return to basal cytosolic Ca2+ levels occurred rapidly and the sustained phase of increased cytosolic Ca2+ seen with rHC5a-stimulated PMNs in Ca2(+)-containing buffer was virtually eliminated. These results indicate that bovine PMNs respond well to rHC5a, that stimulated newborn bovine PMNs can mobilize Ca2+ as efficiently as adult PMNs, and that the sustained cytosolic Ca2+ response to rHC5a in both age groups requires both release of Ca2+ from intracellular stores as well as influx of extracellular Ca2+. Such data suggest that observed functional deficits in newborn bovine PMNs are probably not related to improper mobilization of Ca2+ following stimulation.

Aging↗
PubMed1990

A monoclonal-antibody-defined adhesion-related antigen on bovine neutrophils is required for neutrophil aggregation.

Surface adhesion molecules present on human leukocytes are known to regulate certain adhesion-related events, such as adhesion to endothelium, extravasation, and aggregation. We have used a mouse anti-human monoclonal antibody designated 60.3 (MAb 60.3) and indirect immunofluorescence technique to identify an antigen on bovine neutrophils (PMNs). MAb 60.3 bound to resting and stimulated bovine PMN in a surface-oriented pattern. Immunofluorescence flow cytometric analysis indicated that warming the PMNs from 4 degrees C to 37 degrees C slightly increased (13.9%) expression of the antigen recognized by MAb 60.3. Zymosan-activated serum (ZAS, 10%) increased antigen expression by 12.4% over those PMNs in buffer alone, and phorbol 12-myristate 13-acetate (PMA; 100 ng/ml) by 65.6%. Bacterial lipopolysaccharide (LPS; 1 micrograms/ml) from E. coli 0111:B4 did not enhance antigen expression. The functional nature of this antigen was demonstrated by use of MAb 60.3 and PMN aggregation. Preincubation of bovine PMN with MAb 60.3 for 10 min resulted in nearly complete inhibition of PMN-PMN aggregation upon subsequent stimulation with PMA (100 ng/ml); preincubation with a control antibody did not inhibit aggregation. These results indicate that bovine PMNs possess surface molecule(s) that may function in adhesion-related events, and surface expression may be enhanced by PMN stimulation.

Animals↗
PubMed1990

Endotoxin-mediated bovine alveolar macrophage procoagulant induction is dependent on protein kinase C activation.

The induction of pulmonary alveolar macrophage (PAM) tissue factor-dependent procoagulant activity is central to the deposition of inflammatory fibrin in the pulmonary alveolus. The presence of enhanced tissue factor activity is often associated with pulmonary fibrin deposition, an important pathogenetic event that can delay resolution of pulmonary inflammation and promote the induction of pulmonary fibrosis. Since tissue factor synthesis induction and activation pathways are potential therapeutic targets for modulation of alveolar macrophage tissue factor (procoagulant) activity, we examined the pathways through which endotoxin lipopolysaccharide (LPS) induces bovine PAM tissue factor-dependent procoagulant activity. PAM procoagulant activity was markedly enhanced to 10 times the levels of freshly isolated PAM after 8 h of culture in the presence of either the protein kinase C (PKC) agonist phorbol 12-myristate 13-acetate (PMA) or LPS. Both LPS-(P less than 0.002) and PMA-induced activity (P less than 0.007) was completely ablated by the PKC inhibitor 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H 7,100 microM) but was unaffected by the cyclic nucleotide-dependent protein kinase inhibitor N-(2-guanidinoethyl)-5-isoquinolinesulfonamide (HA-1004, 100 microM). The arachidonate cyclooxygenase pathway inhibitor phenylbutazone (10(-4) M) had modest effects that were not statistically significant. The unstimulated increase of procoagulant activity in 8-h cultures was unaffected by the same inhibitory modulations.(ABSTRACT TRUNCATED AT 250 WORDS)

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1990

Membrane NADPH oxidase activity and cell size in bovine neonatal and adult neutrophils.

Neutrophils (PMN) from newborn calves generate significantly less superoxide anion (O2-) than do their adult counterparts after stimulation with direct protein kinase C agonists. To better understand this observation, we compared the activity and kinetics of NADPH oxidase in membrane fractions from phorbol 12-myristate 13-acetate-stimulated adult and newborn PMN. After phorbol 12-myristate 13-acetate stimulation, PMN were sonicated and the membranes assayed for O2- production with increasing concentrations of NADPH. O2- production was calculated 1 and 2 min after the beginning of the reaction. At all concentrations of NADPH used, there was no difference (p greater than 0.05) in O2- production between adult (n = 8) and newborn (n = 9) PMN membrane preparations. Enzyme kinetics calculations revealed no differences (p greater than 0.05) between age groups in Km and Vmax or in the velocity of the reactions. Determination of the protein content in the membrane pellet, however, showed that adult PMN yielded significantly (p less than 0.01) higher amounts of protein (2.82 +/- 0.14 mg/mL) than did newborn PMN (1.78 +/- 0.07 mg/mL). This difference could be partly attributed to cell size; flow cytometric analysis showed that newborn PMN had a significantly (p less than 0.01) smaller diameter (10.94 +/- 0.07 microns) than did adult PMN (11.65 +/- 0.06 microns), and calculated cell volume and surface area were also both significantly less (p less than 0.01) in newborn PMN.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1989

Alterations in complement-induced shape change and stimulus-specific superoxide anion generation by neonatal calf neutrophils.

Increased susceptibility of neonates to infection may be related to defects in newborn neutrophil (PMN) functional activities, including altered responses to complement fragments (Cf) and defective microbicidal activity. We therefore compared the kinetics of newborn and adult bovine PMN membrane shape change responses following stimulation with zymosan-activated plasma (ZAP) as a source of Cf. Measurement of PMN membrane shape change was a rapid, sensitive, and reproducible measure of Cf stimulation within a population of PMNs; a maximum of 67-85% of the PMNs exhibited easily detectable membrane ruffling, lamellipodia formation, and polarity within 2 min. Newborn PMNs exhibited significantly increased (P less than 0.01) membrane shape change at 20, 30, 60, 120, and 300 sec after Cf stimulation. A maximum of 85.8 +/- 3.2% of newborn PMNs exhibited such Cf-induced shape changes by 120 sec. which was significantly greater (P less than 0.01) than the maximum stimulation (67.7 +/- 4.3%) attained with adult PMNs. These data indicate enhanced kinetics of induced newborn PMN membrane shape change in response to Cf stimulation. We also compared stimulus-specific superoxide anion (O2-) generation as a measure of respiratory burst activity after incubation of newborn and adult PMNs with soluble (phorbol myristate acetate, PMA) and particulate (opsonized zymosan, OZ) stimuli. When PMA was used as the stimulus, newborn PMNs generated significantly less O2- (9.3 +/- 0.5 nmol O2-/10(6) PMN, P less than 0.05) than did adult PMNs (12.4 +/- 0.3 nmol O2-/10(6) PMN). This finding was reversed when OZ was used as the stimulus; newborn PMNs generated significantly more O2- (7.7 +/- 0.4 nmol O2-/10(6) PMN, P less than 0.05) than did adult PMNs (5.5 +/- 0.5 nmol O2-/10(6) PMN). These findings collectively document biochemical and morphological differences between newborn and adult PMNs as determined by stimulus-specific O2- generation and Cf-induced membrane shape change. Such differences may be important to neonatal disease susceptibility.

Animals↗
PubMed1987

[Deinstitutionalization in Québec.].

In this article, the author raises questions about the results and consequences of deinstitutionalization in Quebec. First presented is an analysis of the phenomenon that focusses on the prevention of admissions as well as the return and the maintenance of an individual in the community. TTie analysis leads to an assesment of the phenomenon's impact on the principal actors. There are two sides to the coin; the author examines the achievements and the weaknesses that subsist In Quebec, as elsewhere, certain problems are associated to deinstitutionalization; the author offers explanations to these problems.

English Abstract↗