Biomedical subjects

C Brisson

Publications and source records attributed to C Brisson.

At least 37 records · Page 2Linked to original sources

PubMed1997

Prevalence of the sick building syndrome symptoms in office workers before and six months and three years after being exposed to a building with an improved ventilation system.

OBJECTIVE: The prevalence of symptoms associated with the sick building syndrome (SBS) has recently been shown to decrease by 40% to 50% among office workers six months after they were exposed to a building with an improved ventilation system. The objective of the present study was to find whether the decrease in the prevalence of symptoms was maintained three years later. METHODS: Workers from the same organisation occupied five buildings in 1991 and moved during that year to a single building with an improved ventilation system. All buildings had sealed windows with mechanical ventilation, air conditioning, and humidification. Workers completed a self administered questionnaire during normal working hours in February 1991 before moving, in February 1992 six months after moving, and in February 1995, three years after moving. The questionnaire encompassed symptoms of the eyes, nose and throat, respiratory system, skin, fatigue, and headache, as well as difficulty concentrating, personal, psychosocial, and workstation factors. During normal office hours of the same weeks, environmental variables were measured. RESULTS: The study population comprised 1390 workers in 1991, 1371 in 1993, and 1359 in 1995, which represents 80% of the population eligible each year. The prevalence of most symptoms decreased by 40% to 50% in 1992 compared with 1991. This was similar in 1995. These findings were significant and remained generally similar after controlling for personal, psychosocial, and work related factors. CONCLUSION: In this study, the decrease of 40% to 50% in the prevalence of most symptoms investigated six months after workers were exposed to a new building with an improved ventilation system was maintained three years later. The results of the present follow up study provide further support for a real effect of exposure to a new building with an improved ventilation system on the prevalence of symptoms associated with the SBS.

Carbon Dioxide↗

PubMed1997

Porcine and bovine steroidogenic acute regulatory protein (StAR) gene expression during gestation.

We have generated complete complementary DNA (cDNA) sequences for the porcine steroidogenic acute regulatory protein (StAR) gene, using a combination of genomic PCR amplification and reverse transcription-PCR amplification of pig ovarian cDNA. Porcine StAR cDNA consists of 855 bp and shares 90.2%, 87.3%, 84.3%, and 83.9% homologies with bovine, human, mouse, and rat StAR cDNA at the nucleotide level, and 89.1%, 88.8%, 86.7%, and 86.3% homologies with bovine, human, mouse, and rat StAR protein at the deduced amino acid level. Northern analysis of porcine StAR showed that it is expressed in adult and fetal steroidogenic tissues, including adult testes and ovaries and adult adrenal glands as well as steroidogenic tissues of pregnancy, including developing fetal testes, corpus luteum, and pregnancy, but not the fetal ovary. Major hybridizing bands of 1.8 and 1.1 kilobases were demonstrated. In contrast to human StAR, porcine StAR was not expressed in adult or fetal kidneys. Expression of porcine StAR by the pig placenta is in contrast to human StAR, which is not expressed by the human placenta. Northern analysis of bovine cotyledons using a homologous probe for bovine StAR showed that StAR is also expressed by the placenta in the bovine animal. With respect to placental expression of StAR, variations may exist among mammalian species.

Aging↗

PubMed1996

Non-receptor-mediated tissue localization of human interferon-gamma: role of heparan sulfate/heparin-like molecules.

In addition to its cellular receptor, interferon-gamma (IFN-gamma) displays a high affinity for heparan sulfate. This glycosaminoglycan found in the extracellular matrix and at the surface of some cells was studied here as a possible in vivo binding site for IFN-gamma. For this purpose, rats were injected with [125I]-labelled human IFN-gamma, which does not bind to murine IFN-gamma receptors, but binds to murine heparan sulfate. It was found, first, that [125I]-IFN-gamma does not have equal access to all tissues, accumulating mainly in the spleen, liver and kidney, but not in muscles. Furthermore, [125I]-IFN-gamma was detected by autoradiographic analysis only in restricted areas within tissues, which correlates with the known locations of heparan sulfate. Such local concentrations were detected in the liver sinusoids and in the kidney glomerulus, for example. Heparin bound to [125I]-IFN-gamma was also used to block the heparan sulfate binding site of the cytokine. In this case, blood clearance and tissue accumulation in the liver and spleen were strongly inhibited, while in the kidney the distribution, but not the accumulation, of [125I]-IFN-gamma was affected by the presence of heparin. Kinetic analysis of the binding showed that [125I]-IFN-gamma accumulated in tissues between 5 and 20 min after injection, and was then quickly cleared. Taken together, these data demonstrate that heparan sulfate molecules are involved in blood clearance and in the subsequent tissue targeting, accumulation, and localization of [125I]-IFN-gamma.

Autoradiography↗

PubMed1996

S-Endo 1, a pan-endothelial monoclonal antibody recognizing a novel human endothelial antigen.

A murine monoclonal antibody (mAb) S-Endo 1 has been produced to detect circulating endothelial cells detached from blood vessels in pathological conditions. We have demonstrated that the associated-antigen (S-Endo 1 Ag) was highly expressed on human vascular structure irrespective of tissue origin or vessel caliber. Its expression was not restricted to endothelium, since it was also detected at low level on smooth muscle cells, stroma cells and follicular dendritic cells. But its absence on hematopoietic cells made S-Endo 1 a helpful reagent to specifically discriminate endothelium from hematopoietic tissues. Biochemical characterization showed that S-Endo 1 recognizes a monomeric structure of approximately 118 kDa on cultured endothelial cells. S-Endo 1 was submitted to the 5th International Workshop (Boston, 1993) and did not cluster in any of the old or new endothelial clusters discussed at the conference, indicating its unique reactivity. Together with the data presented in this paper, this suggested that S-Endo 1 defines a previously undescribed endothelial molecule.

Animals↗

PubMed1996

Prevalence of the sick building syndrome symptoms in office workers before and after being exposed to a building with an improved ventilation system.

OBJECTIVE: To find if the prevalence of symptoms associated with sick building syndrome decreased among office workers after moving to a building with improved ventilation (after controlling for potential confounders). METHODS: Workers in five buildings in 1991 all moved in 1992 into a single building with improved design, operation, and maintenance of the ventilation system. All buildings had sealed windows with mechanical ventilation, air conditioning, and humidification. Workers completed a self administered questionnaire during normal working hours in February 1991 and February 1992. The questionnaire encompassed symptoms of the eyes, nose and throat, respiratory system, skin, fatigue, headache, and difficulty concentrating, personal, psychosocial, and work related factors. During normal office hours of the same week environmental variables were measured. RESULTS: The study population comprised 1390 workers in 1991 and 1371 workers in 1992 who represented more than 80% of the eligible population. The prevalence of most symptoms decreased when workers moved to the new building: skin (54%), respiratory system (53%), nose and throat (46%), fatigue (44%), headache (37%), eyes (23%). These findings were all significant and remained generally similar after controlling for personal, psychosocial, and work related factors. Furthermore, more than 60% of workers symptomatic in 1991 were asymptomatic in 1992 for all types of symptoms. In contrast, less than 15% of workers were asymptomatic in 1991 but symptomatic in 1992 for all types of symptoms. CONCLUSION: In this study, the prevalence of most symptoms usually associated with the sick building syndrome decreased by 40% to 50% after workers were transferred to a building with an improved ventilation system. The results show that it is possible to diminish the prevalence of symptoms associated with the sick building syndrome among office workers occupying a building with mechanical ventilation, air conditioning, and sealed windows.

Female↗

PubMed1996

Job strain and psychological distress in white-collar workers.

OBJECTIVES: In line with Karasek's job strain model, the objective of the study was to determine whether workers submitted to high job strain, a combination of high psychological demand and low decision latitude, develop more psychological distress than workers not submitted to high job strain. A second objective was to determine whether social support at work modifies the association between job strain and psychological distress. METHODS: The design was cross-sectional and included white-collar workers in the Québec city area. A self-administered 26-item questionnaire (the Job Content Questionnaire) measured psychological demand, decision latitude, and social support at work. Psychological distress was measured by the Psychiatric Symptom Index, a 14-item self-administered instrument. RESULTS: Among the 2889 participants, the prevalence of psychological distress was 27.8%. High job strain was present in 20.5% of the subjects. The crude odds ratio (OR) of high job strain with psychological distress was 3.52 [95% confidence interval (95% CI) 2.54-4.88]. The OR adjusted for age, gender, employment status, occupation, social support at work, nonwork social support, cynicism, hostility, domestic load, and stressful life events during the last 12 months was still significant (OR 2.45, 95% CI 1.66-3.62). CONCLUSIONS: Our results support the association between job strain and psychological distress. Social support at work, although significantly associated with psychological distress, did not modify the association between job strain and psychological distress.

Adolescent↗

PubMed1996

An electron microscopy study into the mechanism of gene transfer with lipopolyamines.

Cationic amphiphiles have been shown to mediate gene transfer to eukaryotic cells, although the nature and fate of the lipid-DNA complexes is still a matter of debate. Negative staining transmission electron microscopy (TEM) of the complexes in physiological medium, as well as thin-section TEM of transfected cells has been used to visualize the particles and the possible pathways leading to transgene expression. Lipopolyamines form a network of tubular micelles into which plasmid DNA is intertwined and condensed; the cationic particles contain hundreds of plasmid molecules and are heterogeneous with respect to size (0.1-0.5 microgram) and shape. Adherent cells (293M, 3T3, MRC5, primary leptomeningeal cells) take them up readily within minutes by spontaneous endocytosis. Among suspension cells, lymphocytes only incidentally show cytoplasmic inclusions and monocytes degrade the particles by phagocytosis. The marked decrease in transfection efficiency generally observed between adherent and nonadherent cells is thus due to reduce cell binding. This suggests that cationic particles bind to membrane components responsible for Ca2+-mediated cell anchoring to the extracellular matrix. Cation/anion-mediated endocytosis leads to endosomes that are entirely filled with the particles. Consequently, two escape mechanisms may operate: disruption of the lamellar envelope in close contact with tubular micelles, and endosome buffering by the lipopolyamine in response to proton entry, leading to osmotic swelling and endosome rupture. Even for moderately transfected MRC5 cells, 10(2)-10(3) particles are found either free or in cytoplasmic vacuoles 24 h after transfection, highlighting a very inefficient nuclear translocation process. Such high numbers are also the clue to the small concentration window between transfection and cytotoxicity that is often observed with nonviral vectors. Nuclear particle inclusions are sometimes seen, yet it is unclear whether plasmid uncoating (before expression) takes place by anion exchange in the cytoplasm or in the nucleus. The still lower efficiency of free plasmid translocation to the nucleus suggests an active role for the cationic lipid during this step. Although the last stages of the transfection mechanism remain unclear, the present work shows that the major barrier which hampers in vitro gene delivery with cationic vectors is nuclear translocation (and cell entry for nonadherent cells), providing precise targets for the design of improved nonviral vectors.

3T3 Cells↗

PubMed1995

Localization of mRNA coding for the three subtypes of atrial natriuretic factor (ANF) receptors in rat anterior pituitary gland cells.

Atrial Natriuretic Factor (ANF) action is mediated by highly selective and specific receptors. Three subtypes have been characterized and cloned: ANF receptor-A, -B and -C. These subtypes are all expressed in the anterior pituitary of the rat. In the present study, the mRNA for each subtype was detected by in situ hybridization. The amounts of ANFR-A and -B mRNA were found to be similar, and to be twice that of ANFR-C mRNA. At the ultrastructural level, the three types of ANFR mRNA were expressed in three anterior pituitary cell types, namely lactotrophs, corticotrophs, and gonadotrophs, identified by their hormonal content. No signal was revealed in somatotrophs or thyrotrophs. The different forms of mRNA were similar in terms of subcellular localization: in the cytoplasmic matrix and the nuclear euchromatin. These data indicate that the anterior pituitary is an important target tissue for ANF action.

Animals↗

PubMed1993

Demonstration of Rickettsia conorii-induced endothelial injury in vivo by measuring circulating endothelial cells, thrombomodulin, and von Willebrand factor in patients with Mediterranean spotted fever.

The endothelial cell (EC) is the primary target for Rickettsia conorii (RC) in Mediterranean spotted fever (MSF). Clinical manifestations such as thrombosis and vasculitis are mediated by pathologic changes localized in blood vessels. To study the in vivo endothelial injury induced by RC, markers of endothelial damage, including circulating EC (CEC), plasmatic thrombomodulin (TM), and von Willebrand factor (vWF), were investigated in 12 patients with MSF. CEC were counted in whole blood by a new immunomagnetic separation assay using a specific anti-EC antibody, S-Endo 1. Plasmatic TM and vWF antigens were measured by enzyme-linked immunosorbent assay. High levels of CEC and cell fragments were found in patients with a severe or malignant form of MSF. Sequential studies of CEC showed a decrease from 162 +/- 454 cells/mL before treatment to 6 +/- 7 cells/mL during treatment and recovery. Mean plasma TM and vWF levels that were also elevated before therapy (TM, 106 +/- 27 ng/mL; vWF, 420% +/- 164%) decreased progressively (TM, 55 +/- 43 ng/mL; vWF, 148% +/- 26%) during treatment. The measurement of cellular and molecular markers of vascular damage such as CEC, plasmatic TM, and vWF contributes to the definition of the Rickettsia-induced endothelial injury in vivo.

Antibodies, Monoclonal↗

PubMed1993

Thrombin regulates tissue factor and thrombomodulin mRNA levels and activities in human saphenous vein endothelial cells by distinct mechanisms.

The effects of thrombin, D-phenylalanyl-L-propyl-L-arginine chloromethyl ketone (PPACK)-inhibited thrombin, and thrombin receptor agonist peptide, SFLLRNPNDKYEPF (SFLL, a portion of the receptor unmasked after thrombin cleavage), on the expression of tissue factor (TF) and thrombomodulin by human saphenous vein endothelial cells (HSVECs) in culture were studied. Unstimulated cells contained very low amounts of TF mRNA as measured by the reverse transcriptase-PCR method. Thrombin treatment increased TF mRNA to 8.0 +/- 1.9 (n = 3) times the control level. The increase was detectable within 2 h and declined to near basal level by 6 h. Induction of TF mRNA was not blocked by cycloheximide, treatment with cycloheximide alone also increased TF mRNA levels, and thrombin in combination with cycloheximide further enhanced the accumulation of TF mRNA. Thrombin caused a 14.5 +/- 1.5-fold (n = 5) increase in TF activity on the surface of HSVECs and a 20.5 +/- 1.4-fold (mean +/- S.D., n = 2) increase in the extracellular matrix. The thrombin-induced effects on TF synthesis could be fully reproduced by the thrombin receptor agonist peptide, SFLL, whereas PPACK-inhibited thrombin did not influence TF expression. Thrombin increased thrombomodulin mRNA to 190 +/- 39% (n = 5) of control levels, whereas PPACK-inhibited thrombin or SFLL did not influence thrombomodulin mRNA levels. In contrast, surface-bound thrombomodulin cofactor activity and thrombomodulin antigen in the cell lysates did not change over 24 h of incubation with thrombin. However, thrombin caused a 2-fold increase in thrombomodulin antigen released into the conditioned medium, and immunoelectron microscopy of HSVECs also demonstrated the presence of thrombomodulin vesicles close to the luminal cell surface in thrombin-treated cultures. The Western blot pattern thrombomodulin in the conditioned medium of untreated and thrombin-treated cells was found to be similar, and soluble thrombomodulin occurred mainly as fragments of the cell-associated form. We conclude that the transcriptional control by thrombin causes an increase in both TF and thrombomodulin mRNA. The increase in TF mRNA levels is also paralleled by an increase in surface expression, is dependent on the proteolytic activity of thrombin, and is mediated by the same receptor as the recently cloned thrombin receptor in platelets. Up-regulation of thrombomodulin mRNA levels by thrombin is distinct from this pathway and is associated with unchanged expression on the cell surface.

Amino Acid Chloromethyl Ketones↗

PubMed1993

Human umbilical vein endothelial cell culture on heparin-like microcarriers.

Biospecific functional polymers, i.e., polymers randomly substituted with specific chemical functional groups, were designed to interact with living systems. Interactions between polystyrene sodium sulfonate (PSSO3Na) and insulin secreting RINm5F cells have been previously described. For the sake of comparison, interactions of PSSO3Na with human umbilical vein endothelial cells (HUVEC) were studied. In this case, the interaction is indirect, i.e., mediated by a binding protein, fibronectin (Fn). This was evidenced by HUVEC culture on Fn precoated PSSO3Na microcarriers. The interactions between PSSO3Na and HUVEC result in a biologically normal proliferation of cells and synthesis and secretion of Von Willebrand Factor (VWF). These results show that different biospecific interactions may occur between cells in culture, binding proteins and polymers randomly substituted with suitable functional groups. HUVEC, when cultured on heparin-like microcarriers, behave differently from other cells like RINm5F, whose interaction with the same polymers is not mediated by binding proteins.

Adsorption↗

PubMed1993

Alpha IIb beta 3 integrin dissociation induced by EDTA results in morphological changes of the platelet surface-connected canalicular system with differential location of the two separate subunits.

Treatment of human platelets by EDTA (5 mM at 37 degrees C and pH 7.4 for 30 min) induces ultrastructural morphological changes of the surface-connected canalicular system (SCCS). The first consists in dilations of some portions of the channels, whereas the second is represented by collapse of parts of the canaliculi. The collapsed elements of the EDTA treated SCCS are made up of two parallel limiting membranes and a central striated zone. Some of the EDTA treated platelets form microaggregates, the cohesion of which is apparently due to the appearance of pentalaminar interplatelet structures. EDTA treatment is known to induce an irreversible loss of platelet aggregability which is due to irreversible dissociation of the membrane GPIIb-IIIa complexes. In the present study, we looked for involvement of GPIIb-IIIa in the formation of these pentalaminar structures, and were able to demonstrate that the morphological changes described are in fact directly dependent on the EDTA induced dissociation of GPIIb-IIIa complexes. Indeed, we observed that these changes (a) cannot be induced in type I Glanzmann's thrombasthenia, where GPIIb-IIIa complexes are absent, (b) do not appear when human platelets are preincubated with monoclonal anti-GPIIb-IIIa complex-dependent (CD41a) antibodies, which protect the complex from EDTA induced dissociation, (c) appear only at alkaline pH and at 37 degrees C, which corresponds to the range of pH and temperature where EDTA can dissociate GPIIb-IIIa complexes, (d) are accompanied by the disappearance in fluorescence flow cytometry of the heterodimer complex-dependent epitopes, when using anti-CD41a antibodies and (e) do not appear in rat platelets, where GPIIb-IIIa does not dissociate after EDTA treatment. Furthermore, using gold-labeled mAbs concomitantly with the addition of EDTA, we observed that almost only GPIIb was present in the collapsed regions of the canaliculi. Using double labeling studies with polyclonal anti-GPIIb antibodies coupled to 10 nm gold particles and polyclonal anti-GPIIIa antibodies coupled to 20 nm gold particles, we observed that while both 10 and 20 nm particles were present in the dilated portions of the canaliculi almost only the small particles, coupled to the anti-GPIIb antibodies, labeled the collapsed portions of the SCCS. On Lowicryl thin sections, polyclonal antibodies against GPIIb labeled the central striated zone while both GPIIb and GPIIIa were found in the dilated portions of the SCCS. All these observations lead us to suggest that homopolymers of GPIIb could be responsible for "zipping" of the SCCS.

Blood Platelets↗

PubMed1993

Role of cyclic AMP in promoting the thromboresistance of human endothelial cells by enhancing thrombomodulin and decreasing tissue factor activities.

1. The effects of forskolin, prostaglandin E1 (PGE1), dibutyryl cyclic AMP (db cyclic AMP), dibutyryl cyclic GMP (db cyclic GMP) and 3-isobutyl-l-methyl-xanthine (IBMX) were investigated on the expression of tissue factor and thrombomodulin activities on the surface of human saphenous vein endothelial cells (HSVEC) in culture. 2. Forskolin (10(-6) to 10(-4) M), PGE1 (10(-7) to 10(-5) M) and db cyclic AMP (10(-4) to 10(-3) M) caused a concentration-dependent decrease of cytokine-induced tissue factor activity. 3. Similar concentrations of forskolin, PGE1 and db cyclic AMP enhanced significantly constitutive thrombomodulin activity and reversed the decrease of this activity caused by interleukin-1 (IL-1). 4. IBMX (10(-4) M) decreased tissue factor activity and enhanced the effect of forskolin on tissue factor and thrombomodulin activities. 5. Forskolin (10(-4) M) decreased the IL-1-induced tissue factor mRNA and increased the thrombomodulin mRNA level. IL-1 did not change the thrombomodulin mRNA level after 2 h of incubation with HSVEC in culture. 6. Dibutyryl cyclic GMP (10(-4) M to 10(-3) M) did not influence tissue factor or thrombomodulin activity. 7. Our data suggest that elevation of intracellular cyclic AMP levels may participate in the regulation of tissue factor and thrombomodulin expression, thus contributing to promote or restore antithrombotic properties of the endothelium.

1-Methyl-3-isobutylxanthine↗

PubMed1992

Antibodies to thrombomodulin induce receptor-mediated endocytosis in human saphenous vein endothelial cells.

The membrane glycoprotein thrombomodulin (TM) is an essential endothelial cell (EC) cofactor, which forms a 1:1 stoichiometric complex with thrombin. Binding of thrombin to the high affinity TM receptor transforms its procoagulant activity into an anticoagulant potential, by activating protein C. The fate of TM in the presence of thrombin is still unclear: some authors claim that the thrombin-TM complex is internalized in EC, while others find this complex to be stable for at least 2 h at 37 degrees C on the EC surface. In the present study, we investigated the interactions of thrombin and Fab-fragments of anti-TM antibodies, coupled to 5 or 15 nm gold particles with saphenous vein endothelial cells. Our results demonstrate that TM can be observed both on the plasma membrane and in coated structures only in the presence of anti-TM antibodies. Addition of thrombin decreased the extent of this labeling, while in double labeling experiments, where cells were incubated with 5 nm gold coupled thrombin and 15 nm gold coupled Fab fragments of anti-TM antibodies, thrombin was cointernalized only when anti-TM antibodies were present. These results show that thrombin-TM complex is not significantly internalized in EC. The internalization of this complex induced by anti-TM antibodies could play an important role in the thrombotic complications induced by anti-EC autoantibodies.

Amino Acid Sequence↗

PubMed1992

Rapid isolation of human endothelial cells from whole blood using S-Endo1 monoclonal antibody coupled to immuno-magnetic beads: demonstration of endothelial injury after angioplasty.

The presence in whole blood of circulating endothelial cells (EC) has been a subject of debate for many years. It could represent a good marker of vessel injury. We demonstrate here that human endothelial cells can be directly isolated and identified in circulating blood by means of an endothelial cell specific monoclonal antibody, S-Endo1, coupled to micromagnetic beads. The specificity and efficacy of the assay were established using normal blood samples with cultured EC added. Specific rosettes formed between EC and beads could subsequently be isolated with a magnet. The rosetted cells were recovered with a yield greater than 80%. Their endothelial origin was confirmed by the positive labelling of von Willebrand factor and thrombomodulin, as well as the presence of Weibel-Palade bodies. We applied this method to demonstrate significantly increased levels of EC in venous and arterial human blood samples in patients undergoing heart catheterization. This new whole blood immuno-separation method may be useful in determining endothelial cell injury in vascular disorders.

Antibodies, Monoclonal↗

PubMed1992

Alpha IIB beta 3 integrin dissociation induced by EDTA results in formation of Birbeck granule-like structures in human blood platelets.

EDTA (5 mM at 37 degrees C and pH 7.4 for 30 min) induces morphologic changes in the platelet surface-connected canalicular system (SCCS), in particular the collapse of some portions of the canaliculi. These collapsed elements are made up of two parallel limiting membranes and a central irregular striated zone, a pentalaminar organization that clearly resembles that of Langerhans cell Birbeck granules (BG). Such BG-like structures are also seen between adjacent platelets in EDTA-treated platelet microaggregates. EDTA is known to induce an irreversible dissociation of the platelet membrane glycoprotein(GP)IIb-IIIa, the alpha IIb beta 3 platelet-specific intergrin, a calcium-dependent heterodimer that serves as an inducible receptor for fibrinogen and is essential for platelet aggregation. Hence, we looked for involvement of the GPIIb-IIIa in the formation of these BG-like modifications. We observed that these changes i) cannot be induced in type I Glanzmann's thrombasthenia, where the GPIIb-IIIa complexes are absent; ii) did not appear when human platelets were pre-incubated with MoAb anti-GPIIb-IIIa complex, which protected GPIIb-IIIa from EDTA-induced dissociation; iii) appeared only at alkaline pH and 37 degrees C, which corresponds to the range of pH and temperature where EDTA can dissociate the GPIIb-IIIa complexes; iv) are accompanied by the dissappearance on fluorescence flow cytometry analysis of the heterodimer specific epitopes; and v) do not appear in rat platelets at pH 7.4 where GPIIb-IIIa does not dissociate after EDTA treatment. Thus, the appearance of BG-like structures in the platelet SCCS is directly dependent on the EDTA-induced dissociation of the GPIIb-IIIa complexes. Furthermore, using gold-labeled MoAb concomitantly with the addition of EDTA, we observed that only GPIIb is present in the collapsed portions of the canaliculi. On Lowicryl thin sections essentially polyclonal antibodies to GPIIb labeled the central striated zone. All these observations lead us to suggest that homopolymers of GPIIb could be responsible for "zipping" of the SCCS and raise the question of the participation of a Langerhans cell integrin in the formation of Langerhans cell BG.

Blood Platelets↗

PubMed1992

Health problems of women employed in jobs involving psychological and ergonomic stressors: the case of garment workers in Québec.

Health problems of women whose jobs involved intense time pressure were evaluated in a study of 800 sewing-machine operators employed in Québec between 1976 and 1985. Information on workers' occupational characteristics were obtained from public records. Symptoms of anxiety and depression, use of medication and disability status were determined by interview. Garment workers had an increased prevalence of slight, moderate and severe disability and higher levels of symptoms of anxiety and depression when compared to workers in other occupations. Garment workers paid piecework rates took medication for stomach problems in greater proportion than workers paid an hourly wage. Furthermore, workers who spend 5-9, 10-14, 15-19 and 20 or more years in piecework had an increased prevalence of severe disability compared to the baseline category 0-4 years, with adjusted risk ratios of 2.2 (95% CI = 1.14-4.6), 3.3 (95% CI = 1.5-6.9), 3.6 (95% CI = 1.5-8.4 and 2.3 (95% CI = 0.8-6.6) respectively, independent of age, smoking habits, education, type of task and total length of employment. These findings suggest that short-term, non-disabling conditions associated with time pressure by previous authors may have more important long-term sequelae then had been previously documented.

Aged↗

PubMed1992

Quantitative image analysis of angiogenesis in rats implanted with a fibrin gel chamber.

Angiogenesis, a fundamental process in various physiological and pathological events, is generally studied using in vivo models, such as the chick chorioallantoic membrane or the rabbit cornea, which are difficult to quantitate. We developed the quantitation of angiogenesis in an in vivo model previously described by Dvorak et al [6]. Perforated plexiglass chambers filled with human or rat fibrin were implanted into the dorsal subcutaneous space of a Wistar rat. After four days of implantation, a sequentially organized invasion of the fibrin gel by various blood cell types occurred through the holes and neovascularized granulation tissue buds appeared. These buds presented mature neovessels and a new collagen matrix. Three dimensional computer image analysis of the chambers was performed using macroscopic and microscopic parameters: total vascularized area, bud height and equivalent diameter, number of vessels per bud and percentage of central vessels. The time course of the angiogenic response to rat or human fibrin gel was studied and 14 days was found to be the optimum period of implantation. The bud height and number of neovessels were not found to be significantly different when rat or human fibrin gels were used. This quantitative study was a prerequisite for further investigations of the effects of biological and pharmacological agents on angiogenesis.

Animals↗