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Biomedical subjects

T Bourcier

Publications and source records attributed to T Bourcier.

At least 55 records · Page 3Linked to original sources
PubMed2000

[Marginal corneal perforation associated with herpes simplex virus in a patient with essential cutaneous porphyria].

We report a case of herpetic perforated peripheral corneal ulcer in a patient with cutaneous porphyria and hepatitis C. The patient underwent peripheral lamellar keratoplasty. Antiherpetic antibodies were found at a significantly higher level in the aqueous humor than in the serum. Outcome was favorable with antiviral treatment. We discuss the causal role of the hepatitis C virus, porphyria and herpes simplex.

Anti-Bacterial Agents↗
PubMed2000

Regulation of human corneal epithelial cell proliferation and apoptosis by dexamethasone.

PURPOSE: To investigate whether human corneal epithelial cells express the glucocorticoid receptor (GR) and to assess the influence of dexamethasone (DEX) on these cells. METHODS: Human corneal epithelial cells were cultured in medium supplemented with various concentrations of DEX (ranging from 10(-10) to 10(-4) M). Cell proliferation was analyzed by 3-(4, 5-dimethylthiazol-2-yl)-5-(3-carboxy-methoxyphenyl)-2-(4-sulfop henyl) -2H-tetrazolium inner salt (MTS) assay at 2, 4, and 6 days of culture. Apoptosis was studied by nucleus labeling using a fluorescent dye and immunostaining by APO 2.7 at 6 days of culture. GR mRNA was detected in corneal epithelium and cultured corneal epithelial cells by means of reverse transcription-polymerase chain reaction (RT-PCR). Immunocytochemical staining of the epithelial cells was performed with a monoclonal anti-human GR. RESULTS: RT-PCR and immunocytochemistry showed the expression of GR (mRNA and protein) in corneal epithelial cells. DEX significantly increased corneal epithelial cell proliferation with concentrations ranging from 10(-10) to 10(-6) M, with a maximum effect at 10(-7) M (P < 0.005). However, DEX also induced apoptosis of cultured corneal epithelial cells at any concentration used. CONCLUSIONS: These results indicate that human corneal epithelial cells express the GR and proliferate in response to DEX stimulation which also induces corneal epithelial cell apoptosis.

Apoptosis↗
PubMed1999

Sclerochoroidal calcification associated with Gitelman syndrome.

PURPOSE: To investigate sclerochoroidal calcification in a patient with Gitelman syndrome. METHOD: Case report. Bilateral fundus abnormalities observed in a 58-year-old woman were documented with fluorescein angiography and tomodensitometry. RESULTS: Symmetric yellow-white subretinal lesions were observed in the superotemporal midperiphery of the fundus of each eye. Tomodensitometry examination was consistent with calcium deposition. The medical history included Gitelman syndrome. Sclerochoroidal calcification probably resulted from the severe hypomagnesemia. CONCLUSION: Gitelman syndrome may be a cause of sclerochoroidal calcification.

Calcinosis↗
PubMed1999

The triple procedure: in the bag placement versus ciliary sulcus placement of the intraocular lens.

AIMS: To evaluate the influence of intraocular lens (IOL) placement on triple procedure clinical results and to investigate whether it is appropriate to use phacoemulsification in patients with large lens nucleus. METHODS: 40 consecutive penetrating keratoplasties combined with cataract extraction performed in a single institution were studied. Whenever possible a capsulorhexis was performed and the IOL was placed into the capsular bag. Phacoemulsification was used when the nucleus was too large to pass through the capsulorhexis. RESULTS: Out of 25 patients with an intact capsulorhexis phacoemulsification was used in 13 (52.0%) whereas the entire nucleus passed through the capsulorhexis in the remaining 12 patients (48%). The average 12 month visual acuity was 0.46 (SD 0.21) in patients with in the bag IOL (n = 23) and 0.29 (0.08) in patients with ciliary sulcus IOL (n = 13) (p = 0.04). Elevated intraocular pressure occurred in 26.1% (6/23) of patients with in the bag IOL and 61.5% (8/13) of patients with ciliary sulcus IOL (p = 0.08). The average postoperative graft thickness at 18 months was 552 (27) microns in the former group and 650 (29) microns in the latter group (p = 0.04). No significant difference in graft survival, postoperative endothelial cell density, astigmatism, and videokeratoscopic measurements was found between both groups. CONCLUSION: In the bag placement of the intraocular lens during the triple procedure results in better outcome of transplantation than ciliary sulcus placement of the IOL. Phacoemulsification allows removal of large nuclei through a 5 mm capsulorhexis without performing relaxing incisions out towards the periphery of the capsule.

Adolescent↗
PubMed1999

PPARgamma activation in human endothelial cells increases plasminogen activator inhibitor type-1 expression: PPARgamma as a potential mediator in vascular disease.

Plasminogen activator inhibitor type-1 (PAI-1) is a major physiological inhibitor of fibrinolysis, with its plasma levels correlating with the risk for myocardial infarction and venous thrombosis. The regulation of PAI-1 transcription by endothelial cells (ECs), a major source of PAI-1, remains incompletely understood. Adipocytes also produce PAI-1, suggesting possible common regulatory pathways between adipocytes and ECs. Peroxisomal proliferator-activated receptor-gamma (PPAR)gamma is a ligand-activated transcription factor that regulates gene expression in response to various mediators such as 15-deoxy-Delta12, 14-prostaglandin J2 (15d-PGJ2) and oxidized linoleic acid (9- and 13-HODE). The present study tested the hypotheses that human ECs express PPARgamma and that this transcriptional activator regulates PAI-1 expression in this cell type. We found that human ECs contain both PPARgamma mRNA and protein. Immunohistochemistry of human carotid arteries also revealed the presence of PPARgamma in ECs. Bovine ECs transfected with a PPAR response element (PPRE)-luciferase construct responded to stimulation by the PPARgamma agonist 15d-PGJ2 in a concentration-dependent manner, suggesting a functional PPARgamma in ECs. Treatment of human ECs with 15d-PGJ2, 9(S)-HODE, or 13(S)-HODE augmented PAI-1 mRNA and protein expression, whereas multiple PPARalpha activators did not change PAI-1 levels. Introduction of increasing amounts of a PPARgamma expression construct in human fibroblasts enhanced PAI-1 secretion from these cells in proportion to the amount of transfected DNA. Thus, ECs express functionally active PPARgamma that regulates PAI-1 expression in ECs. Our results establish a role for PPARgamma in the regulation of EC gene expression, with important implications for the clinical links between obesity and atherosclerosis.

Adipose Tissue↗
PubMed1999

Chlamydial and human heat shock protein 60s activate human vascular endothelium, smooth muscle cells, and macrophages.

Both chlamydial and human heat shock protein 60s (HSP 60), which colocalize in human atheroma, may contribute to inflammation during atherogenesis. We tested the hypothesis that chlamydial or human HSP 60 activates human endothelial cells (ECs), smooth muscle cells (SMCs), and monocyte-derived macrophages. We examined the expression of adhesion molecules such as endothelial-leukocyte adhesion molecule-1 (E-selectin), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1), and the production of the proinflammatory cytokine interleukin-6 (IL-6). We also tested whether either HSP 60 induces nuclear factor-kappaB (NF-kappaB), which contributes to the gene expression of these molecules. Either chlamydial or human HSP 60 induced E-selectin, ICAM-1, and VCAM-1 expression on ECs similar to levels induced by Escherichia coli lipopolysaccharide (LPS). Each HSP 60 also significantly induced IL-6 production by ECs, SMCs, and macrophages to an extent similar to that induced by E. coli LPS, as assessed by enzyme-linked immunosorbent assay (ELISA). In ECs, either HSP 60 triggered activation of NF-kappaB complexes containing p65 and p50 Rel proteins. Heat treatment abolished all these effects, but did not alter the ability of E. coli LPS to induce these functions. Chlamydial and human HSP 60s therefore activate human vascular cell functions relevant to atherogenesis and lesional complications. These findings help to elucidate the mechanisms by which a chronic asymptomatic chlamydial infection might contribute to the pathophysiology of atheroma.

Cells, Cultured↗
PubMed1999

In vitro effects of dexamethasone on human corneal keratocytes.

PURPOSE: To investigate whether cultured human keratocytes express the glucocorticoid receptor (GR) and to assess the influence of dexamethasone (DEX) on these cells. METHODS: Human keratocytes were cultured in medium supplemented with various concentrations of DEX (ranging from 10(-10) to 10(-4) M). Cell proliferation was analyzed by 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxy-methoxyphenyl)-2-(4-s ulfophenyl)-2H-tetrazolium inner salt (MTS) assay at 2, 4, and 6 days of culture. Some experiments were performed in the presence of mifepristone (RU38486), an antiglucocorticoid molecule. The early phase of apoptosis was studied by means of keratocyte staining with a fluorescein conjugate of annexin V and propidium iodide, and cells were analyzed by flow cytometry. Glucocorticoid receptor mRNA was detected in keratocytes by means of reverse transcription-polymerase chain reaction (RT-PCR). Immunocytochemical staining of the cells was performed with a monoclonal anti-human GR. RESULTS: RT-PCR and immunocytochemistry showed the expression of GR (mRNA and protein) in cultured keratocytes. Dexamethasone significantly increased keratocyte proliferation with concentrations ranging from 10(-9) to 10(-5) M, with a maximum effect at 10(-7) M (P < 0.005). Dexamethasone's proproliferative effect was inhibited by RU38486. However, DEX also induced apoptosis of cultured keratocytes at any concentration used. CONCLUSIONS: These results indicate that cultured human keratocytes express the GR and proliferate in response to DEX stimulation (10(-9)-10(-5) M), which also induces keratocyte apoptosis.

Apoptosis↗
PubMed1998

[Episcleritis and brucellosis. Apropos of a case].

A 35-year-old man presented a case of recurrent episcleritis revealing brucellosis. No concurrent diagnosis other than brucellosis could account for the episcleritis. Moreover his status was dramatically improved by specific antibiotherapy. A review of the literature showed that uveitis and optic neuropathies are the most common ocular manifestations of brucellosis. To the best of our knowledge, this is the first case of episcleritis associated with brucellosis.

Adult↗
PubMed1998

[Value of lacrymal IgE determination and conjunctival cytology in the diagnosis of chronic conjunctivitis].

PURPOSE: Chronic conjunctival inflammatory diseases may depend upon various strongly intricated mechanisms. Discriminating allergy from nonspecific inflammation has become of striking importance for diagnosis and treatment. We investigated conjunctival inflammatory response by comparing two objective biological tools, tear IgE detection and HLA DR expression by conjunctival epithelium, as indirect indicators of activation of the Th1 and Th2 subsets, respectively. METHODS: Sixty-eight patients (135 eyes) with chronic conjunctivitis underwent tear IgE dosage by an ELISA technique and quantification of HLA DR expression in impression cytology specimens. 34 had direct or indirect clinical indications of allergic mechanisms, 22 had chronic conjunctivitis without any sign of allergy, and 12 suffered from isolated nonallergic dry eyes. RESULTS: Patients clinically considered as allergic only showed positive IgE in 31 out pf 68 eyes (46 per cent), whereas 11/44 (25%) and 7/24 (29%) eyes with nonspecific conjunctivitis and dry eyes respectively were also positive. HLA DR positivity in epithelial cells was found in 18/61 (29.5%), 15/40 (37.5%) and 9/22 (41%) eyes, respectively. HLA DR expression by epithelial cells was negatively correlated with tear IgE, as most specimens positive to one criterion were negative to the other one (37 eyes DR+ IgE-, 35 eyes DR- IgE+, and 5 eyes DR+ IgE+; chi-square: p = 0.0001). CONCLUSION: As IgE synthesis and HLA DR induction may represent indirect indicators of the activation of the Th1 and Th2 subsets, association of these two simple tests could be interesting for the routine assessment of the mechanisms of inflammatory ocular surface diseases.

Adult↗
PubMed1997

The nuclear factor kappa-B signaling pathway participates in dysregulation of vascular smooth muscle cells in vitro and in human atherosclerosis.

In the lesions of atherosclerosis, vascular smooth muscle cells (SMC) display many functions characteristic of cytokine activation that likely contribute importantly to ongoing inflammation during human atherogenesis. The transcription factor nuclear factor kappa-B (NFkappaB) often mediates the effects of cytokines on target cells, but the identity of Rel family members important in human SMC activation remains uncertain. In vitro, human SMC express multiple Rel family members. Of these, dimers of p65 and p50, but not a putative SMC-Rel, comprise basal and inducible NFkappaB binding activities. SMC express two inhibitor proteins IkappaBbeta and IkappaBalpha. Interleukin-1beta stimulation caused transient loss of IkappaBalpha and a sustained decrease of IkappaBbeta that correlated with increased and persistent levels of p65/p50 protein and binding activity in the nucleus. SMC cultured under serum-free conditions displayed little NFkappaB activity, but addition of serum or platelet-derived growth factor did activate NFkappaB. In situ analyses showed no evidence for basal NFkappaB activity in SMC in vivo as nonatherosclerotic arteries did not contain nuclear p65 or p50 protein. However, the nuclei of intimal SMC within human atheroma did contain both Rel proteins. We conclude that (i) dimers of p65 and p50, but not SMC-Rel, comprise NFkappaB complexes in human SMC; (ii) stimulatory components in serum activate NFkappaB and likely account for previously reported "constitutive" NFkappaB activity in cultured SMC; and (iii) exposure to inflammatory cytokines may produce prolonged NFkappaB activation in SMC because of sustained decreases in the inhibitory subunit IkappaB-beta.

Arteriosclerosis↗
PubMed1997

Functional CD40 ligand is expressed on human vascular endothelial cells, smooth muscle cells, and macrophages: implications for CD40-CD40 ligand signaling in atherosclerosis.

Increasing evidence supports involvement of inflammation and immunity in atherogenesis. We report here that CD40 ligand (CD40L), an immunoregulatory signaling molecule heretofore considered largely restricted to recently activated CD4+ T lymphocytes, is expressed by human vascular endothelial cells (EC), smooth muscle cells (SMC), and human macrophages in vitro, and is coexpressed with its receptor CD40 on all three cells types in human atherosclerotic lesions in situ. Cultured human vascular EC, SMC, and human macrophages all constitutively expressed CD40L mRNA as well as protein. Stimulation with interleukin 1beta, tumor necrosis factor alpha, or interferon gamma increased surface levels and de novo synthesis of CD40L on all three cell types. CD40L expressed on EC, SMC, and macrophages exhibited biological activity, as it induced B7.2 expression on B cells. Human vascular SMC also constitutively expressed CD40, the receptor for CD40L, and through CD40 signaling, human recombinant CD40L induced expression of proinflammatory cytokines in these cells, identifying SMC as a target for CD40L. Human atherosclerotic lesions (n = 8) showed expression of immunoreactive CD40L on EC, SMC, and macrophages, while normal arterial tissues (n = 5) contained no CD40L. In atheroma CD40L+ cells often also expressed CD40. These observations establish human vascular EC, SMC, and human macrophages as a novel source of CD40L, and point to T cell-independent CD40 signaling, and a broader function of this pathway in regulation of nonimmune cells, as illustrated here by potential autocrine and paracrine activation during atherogenesis.

Antigens, Differentiation, T-Lymphocyte↗
PubMed1997

[Cultures of corneal epithelium on hydrogel for synthetic epikeratoplasty].

PURPOSE: To improve the LLH480 hydrogel cytocompatibility and to assess the interactions between corneal epithelium and biomaterials. METHODS: Rabbit corneal epithelium organotypic cultures were carried out on hydrogel samples coated with fibronectin, laminin, type IV collagen, or heparan sulfate proteoglycan. The control group consisted of epithelial cultures carried out on hydrogel with no coating. Cellular migration was quantified, and statistically analyzed. 8-day cultures were processed for transmission electron microscopy. RESULTS: Epithelial migration on hydrogel was significantly increased (p < 0.001) in the heparan sulfate proteoglycan group, significantly decreased (p < 0.05 and p < 0.001) with laminin or type IV collagen coating, and showed no significant modifications in the fibronectin group. Transmission electronic microscopy showed a monolayer of epithelial cells adherant to the surface of the hydrogel. Deposit of extracellular matrix and sketch of adhesion focal points were also noted. CONCLUSION: LLH480 cytocompatibility can be improved by heparan sulfate proteoglycan coating.

Animals↗
PubMed1995

Synergistic interaction of interleukin-1 beta and growth factors in primary cultures of rat aortic smooth muscle cells.

Activated macrophages release cytokines and growth factors that may contribute to the growth of vascular smooth muscle cells in injured blood vessels. In the present study, we investigated the interactions between interleukin-1 beta (IL-1 beta) and basic fibroblast growth factor (FGF-2) in primary rat aortic smooth muscle cells, relative to their effects on DNA synthesis and cell proliferation. We report that femtomolar levels of IL-1 beta, which alone were non-mitogenic or weakly mitogenic, synergistically increased FGF-2-induced [3H]thymidine incorporation and cell proliferation. The potentiating effect of IL-1 beta extended to PDGF-AB and EGF, but not to IGF-1-induced thymidine incorporation. An antagonist of the IL-1 receptor, IL-1ra, blocked the co-mitogenic effect of IL-1 beta. Stimulation of cells with FGF-2 and IL-1 beta increased both DNA content and proliferation, an observation that was consistent with the thymidine incorporation experiments. An inhibitor of NO synthase, N5-iminoethyl L-ornithine (L-NIO), did not block the co-mitogenic effect of IL-1 beta, despite effective inhibition of NO synthase activity, suggesting that the synergistic interaction between IL-1 beta and FGF-2 was independent of the NO/cGMP pathway. The mechanism of co-mitogenesis appeared to be independent of the intermediacy of PDGF-AA, IL-6, and prostanoids, and was not associated with increased levels of c-fos mRNA, FGF receptor-1 protein, or FGF-2-induced early and delayed tyrosine phosphorylation events. We conclude that IL-1 beta interacts with FGF-2 to amplify the proliferation of primary rat aortic smooth muscle cells, an effect that may be important in vascular smooth muscle cell proliferation following vascular injury.

Animals↗
PubMed1995

Acidic fibroblast growth factor (FGF) but not basic FGF induces sleep and fever in rabbits.

Acidic fibroblast growth factor (FGF) and basic FGF belong to a growth factor family. Interleukin-1, another member of that family, is involved in sleep regulation. FGFs and interleukin-1 share structural and functional features. We therefore determined whether acidic FGF and basic FGF were somnogenic. Male New Zealand White rabbits were provided with electroencephalographic (EEG) electrodes, a brain thermistor, and a lateral intracerebroventricular (icv) cannula. The animals were injected icv with isotonic NaCl (control) and on separate days with one of three doses of acidic or basic FGF (0.01, 0.1, or 1.0 micrograms) or with heat-treated acidic FGF (1.0 micrograms). The EEG, brain temperature, and motor activity were recorded for 23 h. The biological activity of basic FGF was determined in vitro by its ability to induce DNA synthesis in rat aortic smooth muscle cells. Acidic FGF induced prolonged dose-related increases in non-rapid eye movement sleep beginning in the 1st postinjection h and continuing for 12-23 h after the treatment. Acidic FGF also induced fevers of approximately 1 degree C after the 1.0 micrograms dose. Both activities of acidic FGF were lost after heat treatment. In contrast, basic FGF lacked somnogenic and pyrogenic activity, although it did induce DNA synthesis. Current results suggest that acidic FGF is part of the complex cytokine network in brain involved in sleep regulation.

Animals↗