Biomedical subjects

P Esser

Publications and source records attributed to P Esser.

At least 55 records · Page 3Linked to original sources

PubMed1996

[Disorder of the blood-aqueous barrier after eye muscle operation in children].

UNLABELLED: We wanted to study the effect of squint surgery on the blood-aqueous barrier in children. Our interest was to ascertain whether or not there is a breakdown of the blood-aqueous barrier after routine squint surgery, and whether this would need antiinflammatory treatment with steroids. PATIENTS AND METHODS: Forty-seven eyes of 18 girls and 7 boys (age range 4-14 years) were examined. The children were generally healthy and had not undergone any previous eye surgery. The mean age of patients (n = 25) was 7.8 +/- 3.1 years. Using the laser flare meter Kowa FM-500, the flare (photocounts/ms) in the anterior chamber was measured before and on the 2nd day after squint surgery (n = 32). Fifteen eyes served as controls and were not operated on. Following surgery, the operated eyes were treated with aminoglycoside eye drops (three times daily). No steroids or non-steroidal antiinflammatory drugs were applied before or after surgery. RESULTS: The flare values were 4.10 +/- 1.29 photocounts/ms before and 3.89 +/- 1.27 photocounts/ms after squint surgery. There was no significant increase (P = 0.58) of flare on the 2nd postoperative day. CONCLUSION: Our data confirm that there is no clinically significant disruption of the blood-aqueous barrier following squint surgery. We therefore conclude that there is no need for postoperative therapy with steroids.

Adolescent↗

PubMed1996

[Risks and therapy options in dural arteriovenous fistulas between branches of the external carotid artery and the cavernous sinus. A case report and review of the literature].

INTRODUCTION: Dural arteriovenous fistula of the Arteria carotis externa and the sinus cavernosus are rare vascular malformations. In the literature the prognosis and necessity of treatment is described very variable. PATIENTS AND METHODS: A 90 year old female presents in our outpatient clinic with acute exophthalmus, dilated episcleral veins, cerebral bruits and beginning orbital apex syndrome. After normal computerized axial tomography (CAT) without and with contrast medium, we were able to diagnose a dural AV-fistula by angiography. Shortly after dismission the patient had a spontaneous subarachnoidal haemorrhage with severe neurological symptoms. CONCLUSIONS: The suspect of an intracranial AV-malformation implies a detailed diagnostic search with precise localisation of the process. In any patient with intracerebral and intracranial fistula there has to be an individual check of possible and necessary treatment. It is impossible to classify dural AV-fistula as a benign disease with harmless clinical course.

Aged↗

PubMed1996

CD 95 expression in traumatic proliferative vitreoretinopathy: a target for the induction of apoptosis.

Apoptotic cell death is a central mechanism underlying growth regulation in normal and pathologic neoplastic and nonneoplastic tissue formation. Apoptosis has also been detected in traction membranes of patients with proliferative vitreoretinopathy (PVR). Herein we report that CD 95 (Fas/APO-1), the cell-surface receptor for a potent proapoptotic cytokine, the CD 95 ligand, is expressed in traction membranes of patients with traumatic PVR. Retinal pigment epithelial (RPE) cells, which are thought to contribute to traction membrane formation, express CD 95 in vitro. However, these cells are resistant to CD 95 antibody-induced apoptosis, presumably because they synthesize cytoprotective proteins, which interfere with the CD 95-dependent killing cascade. Coexposure to inhibitors of RNA or protein synthesis sensitizes human RPE cells for CD 95-mediated apoptosis. In contrast, these agents have little effect on the resistance of these cells to tumor necrosis factor-alpha(TNF-alpha). Pre-exposure to TNF-alpha augments CD 95-mediated killing but not its own toxicity in the presence of inhibitors of RNA and protein synthesis. Preexposure to cycloheximide does not abrogate CD 95-mediated apoptosis, suggesting that labile, short-lived proteins do not mediate the cytotoxic effects of CD 95 antibodies. Taken together, our data indicate that immune-mediated CD 95-dependent killing of proliferating cells in vitreoretinal traction membranes might occur in vivo and could possibly be enhanced using novel approaches of immunopharmacotherapy.

Adolescent↗

PubMed1995

CD95 (Fas/APO-1) antibody-mediated apoptosis of human retinal pigment epithelial cells.

CD95 (Fas/APO-1) is a cytokine receptor protein that signals apoptosis. Here we report that human retinal pigment epithelial cells express CD95 but are rather resistant to agonistic CD95 antibodies. Resistance to CD95 antibodies is overcome by preexposure to the cytokines, tumor necrosis factor-alpha or interferon-gamma, or by coexposure to CD95 antibodies and inhibitors of RNA or protein synthesis. The cells are resistant to tumor necrosis factor-alpha even in the presence of cycloheximide and only moderately sensitized to tumor necrosis factor-alpha-mediated toxicity by coexposure to actinomycin D. CD95-mediated apoptosis is inhibited by dexamethasone both after cytokine sensitization and upon coexposure to CD95 antibodies and actinomycin D or cycloheximide. Induction of apoptosis via CD95 may be involved in the regulation of retinal pigment epithelial proliferation at the vitreoretinal interface.

Antigens, Surface↗

PubMed1995

[Intraocular silicone lenses and silicone oil].

BACKGROUND: Foldable silicone intraocular implants are becoming more popular in conjunction with small incision phacoemulsification. PATIENTS: We observed three patients with silicone oil droplets adherent to the posterior surface of the silicone implant, following silicone oil removal after preceding vitreoretinal surgery with the installation of silicone oil. These droplets could not be dislodged intraoperatively either with focal aspiration or irrigation. They interfered with the patients subjective visual acuity. For this reason, we performed an exchange of the silicone intraocular implant against a PMMA one-piece lens in all three cases. RESULTS: This procedure resulted in an increase of the visual acuity. The mechanism of adherence between the two silicone polymers is finally not known. CONCLUSIONS: With increased use of implantable silicone intraocular lens and silicone oil this complication may be encountered more frequently. Therefore, implantation of silicone lens in vitreoretinal high risk eyes should avoided.

Aged↗

PubMed1995

Intercellular adhesion molecule-1 levels in plasma and vitreous from patients with vitreoretinal disorders.

Intercellular adhesion molecule 1 (ICAM-1) is a member of the immunoglobulin superfamily with important functions in immune activation and inflammation. Its interaction with different cytokines [interleukin 1 (IL-1), tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma)] is important for lymphocyte migration into inflammatory sites. We used a sandwich enzyme immunoassay (EIA) for the quantitative determination of soluble ICAM-1 (cICAM-1) in vitreous and plasma from patients undergoing vitrectomy for a variety of proliferative vitreoretinal disorders. The values obtained were compared with the total vitreal protein. The respective concentrations of cICAM-1 in vitreous were as follows control samples, 3.47 +/- 1.84 ng/ml; proliferative diabetic retinopathy (PDR) of diabetes type I 27.43 +/- 14.72 ng/ml; PDR of diabetes type II, 32.46 +/- 10.31 ng/ml; idiopathic proliferative vitreoretinopathy 35.74 +/- 15.30 ng/ml; and traumatic PVR, 45.23 +/- 24.24 ng/ml. Plasma samples yielded the following concentrations: controls, 415 +/- 43.4 ng/ml; PDR of diabetes type I, 469 +/- 96.9 ng/ml; PDR of diabetes type II, 425 +/- 65.4 ng/ml; idiopathic PVR, 402 +/- 119.9 ng/ml; and traumatic PVR, 434 +/- 118.6 ng/ml. Our results demonstrate high levels of ICAM-1 in most proliferative vitreoretinal disorders. In PDR and in traumatic PVR, cICAM-1 levels were elevated significantly more than were total vitreal protein levels. In traumatic PVR, patients with a short interval between previous surgery or traumatic event demonstrated the highest levels of cICAM. Since plasma levels were not significantly altered, we suggest that local cICAM-1 production, possibly from macrophages, may be of importance in the early phase of PVR and PDR by enhancing immune activation and inflammation.

Diabetes Mellitus, Type 1↗

PubMed1994

The significance of vitronectin in proliferative diabetic retinopathy.

Vitronectin, an integrin-binding a-1-glycoprotein with potent cell-adhesion and proliferation-mediating properties, has been shown to be incorporated in surgically removed membranes from patients with proliferative vitreoretinopathy (PVR), proliferative diabetic retinopathy (PDR) and macular pucker. Therefore we developed an ELISA technique to quantify levels of vitronectin in human vitreous and plasma samples in order to be able to evaluate the significance of vitronectin in these different vitreoretinal diseases. Our results indicate a significant increase of vitronectin in all proliferative disorders except idiopathic macular pucker. Adjustment of all probes to equal total protein content yielded a significant increase only in PDR (type II diabetes). Plasma samples demonstrated a significant increase of vitronectin in patients with type II diabetes suffering from PDR. Therefore, break-down of the blood-retina barrier appears to be the most likely explanation for the increased levels of vitronectin in the vitreous. Our results indicate that vitronectin may not only be involved in the regulation of epiretinal membrane formation at significantly higher levels in patients with type II diabetes, but the increase of vitronectin in diabetic plasma may also help to explain the pathological alteration of the coagulation cascade in diabetics.

Blotting, Western↗

PubMed1994

[Protein composition of the vitreous body in proliferative diabetic retinopathy. An analysis with 2-D-electrophoresis].

Gradient SDS-polyacrylamide gel electrophoresis is a useful technique for characterization of soluble human vitreous protein. However, this technique is limited in the case of suboptimal discrimination power. In this study, we used 2-D electrophoresis to analyse the protein composition of proliferative diabetic retinopathy (PDR) intraocular fluid (n = 10), and compared it with normal vitreous (n = 10) and serum (n = 10). In normal vitreous, the protein content consisted mainly of albumin, transferrin, alpha 1-antitrypsin, IgG, and prealbumin as confirmed by the comparison with protein standards. Compared to vitreous controls, all PDR samples were shown to have lower amounts of transferrin, alpha 1-antitrypsin, and prealbumin. However, the amounts of IgG were higher than in the controls. This reflects a shift to a serum-like protein profile, indicating a blood-retinal barrier breakdown. However, we also detected in PDR vitreous three protein spots in a low-molecular-weight range (5-10 kDa) none of which could be found in native vitreous or in serum. Therefore, additional local protein synthesis appears to be present in the pathogenesis of PDR. 2-D electrophoresis permits precise characterization of the soluble vitreous proteins which may be associated with the fibrovascular proliferative vitreoretinal response.

Blood Proteins↗

PubMed1993

Macrophages in proliferative vitreoretinopathy and proliferative diabetic retinopathy: differentiation of subpopulations.

Macrophages have long been known to play a major role in the pathogenesis of proliferative vitreoretinal disorders. Using the monoclonal antibodies EBM11 (pan macrophage), 27E10 (early inflammatory stage marker), and RM3/1 (healing phase marker), different subpopulations of macrophages were differentiated in surgically removed membranes from patients with macular pucker (n = 6), proliferative vitreoretinopathy (PVR) following rhegmatogenous retinal detachment (n = 11), traumatic PVR (n = 19), and proliferative diabetic retinopathy (PDR) (n = 11). Macrophages were predominantly found in traumatic PVR and PDR. Some healing phase (RM3/1) macrophages were detected in all disease entities. Inflammatory stage macrophages (positive staining for 27E10) could not be detected in PVR following rhegmatogenous retinal detachment and idiopathic macular pucker. In traumatic PVR inflammatory stage macrophages were associated with a short history of disease whereas in PDR all types of macrophages could be detected regardless of clinical history and duration of the disease.

Antibodies, Monoclonal↗

PubMed1993

Tenascin and decorin in epiretinal membranes of proliferative vitreoretinopathy and proliferative diabetic retinopathy.

Extracellular matrix (ECM) synthesis plays an important part in the pathogenesis of the intravitreal membranes and is thus characteristic of both proliferative vitreoretinopathy (PVR) and the involutive stages of proliferative diabetic retinopathy (PDR). Using a polyclonal antiserum against human decorin and a monoclonal antibody against human tenascin, we detected these molecules in membranes from patients with raumatic PVR (n = 10), idiopathic PVR (n = 8), and proliferative diabetic retinopathy (n = 8). We conclude that both tenascin and decorin play a role in the development of epiretinal PVR and PDR membranes by controlling cell adhesion and regulating ECM formation.

Antibodies, Monoclonal↗

PubMed1993

Vitreous body-derived mitogenic activity for retinal pigment epithelial cells. A further characterization.

To obtain a better insight into the possible role of vitreous body in proliferative vitreoretinopathy (PVR), we examined the influence of bovine vitreous body fractions separated by fast protein liquid chromatography (FPLC) on the growth of porcine retinal pigment epithelial (RPE) cells in vitro. Tetrazolium colorimetric assay (MTT assay) and cell counting were used for quantification. After fractionating proteins of the physiological vitreous body by FPLC gel chromatography (Superose 12/Superdex 75), we determined the mitogenic effect of the resulting fractions by either cell counting or MTT assay. With both columns we were capable of separating two fractions (20-40 kDa and 1-2 kDa) that induced RPE cell proliferation. A comparison of the mitogenesis and the protein content of the fractions indicated that we were not dealing with a nonspecific protein effect. The low-molecular fraction weighing less than 2 kDa was of particular interest to us. This was further separated by FPLC reversed-phase chromatography.

Animals↗

PubMed1992

Proliferative retinal diseases: myofibroblasts cause chronic vitreoretinal traction.

Myofibroblasts are contractile cells having features intermediate between those of the fibroblast and smooth muscle. Myofibroblasts in preretinal membranes may cause retinal traction in proliferative retinal diseases. In this study, we demonstrate the presence of a chronically contractile subpopulation of myofibroblasts in pre-retinal membranes. Apha smooth muscle actin or desmin, both markers of the myogenically differentiated and chronically contractile subpopulation could be detected in a large majority of the examined membranes. Our findings may serve to explain the cellular basis of vitreoretinal traction in proliferative vitreoretinopathy and proliferative diabetic retinopathy.

Actins↗

PubMed1992

[Idiopathic proliferative vitreoretinopathy. Activation of microglial cells as the deciding factor].

Mononuclear phagocytes are considered pacemakers in the pathogenesis of proliferative vitreoretinopathy (PVR), but their precise biological origin in preretinal PVR traction membranes has remained obscure. This study presents a combined immunohistochemical protocol for the detection of microglial cells, which was applied to 37 membranes of patients with idiopathic and traumatic PVR and with proliferative diabetic retinopathy (PDR). Microglial cells may be labeled by staining for LN-1, ricinus communis agglutinin-(RCA)-1, vimentin, HLA-DR-II, and nucleoside diphosphatase, but are negative for Leu-M1, Leu-M3, EBM-11, von Willebrand factor, CD22, cytokeratin, and glial fibrillary acidic protein (GFAP). Significant proliferation of microglial cells was found in idiopathic PVR while classical macrophages were typical of traumatic PVR. Only rarely were microglial cells detected in PDR. These findings bring into question previous concepts of the pathobiology of idiopathic PVR and support the hypothesis of idiopathic PVR as a specific disease entity.

Cicatrix↗

PubMed1992

The effects of basic fibroblast growth factor on bovine retinal pigment epithelium in vitro.

Basic fibroblast growth factor (bFGF) has been reported to initiate DNA synthesis in a variety of cells involved in the pathogenesis of proliferative vitreoretinal disorders, e.g., glial cells and fibroblasts. We analyzed the mitogenic effects of bFGF on cultured bovine retinal pigment epithelial cells in relation to time and dose response regulations and culture conditions. Maximum stimulatory effect of bFGF (+70% compared to control group) was found on day 3 following treatment of cultures with 80 ng/ml bFGF. The action of bFGF seems to depend on the serum concentration in the culture media, which means that cofactors may be present in the serum and potentiate the effects of bFGF on cell proliferation.

Animals↗

PubMed1992

[Proliferative vitreoretinopathy. Activation of the complement system].

The complement system is a principal constituent of humoral immune reactions. Because of the multitude of biological effects related to complement activation, we analyzed its potential pathophysiological importance in the development of proliferative vitreoretinopathy (PVR). Vitreous aspirates from patients with idiopathic PVR (n = 7) and traumatic PVR (n = 11) were examined for total vitreal protein, complement components C3, C3d, and C1q-fixed immunoglobulins using enzyme-linked immunosorbent assay (ELISA), SDS-Page and Western blotting. Total vitreal protein and C3 components were significantly elevated both in traumatic and idiopathic PVR. Elevated levels of C3d titers in both PVR forms reflect an activation of the complement system. C1q-fixed IgG suggests complement activation via the classic pathway as a result of a humoral antibody-dependent immune reaction.

Autoimmune Diseases↗

PubMed1992

[Contractile elements in proliferative retinal diseases].

Contraction of epiretinal membranes remains the leading cause of failure in retinal surgery. The mechanism of contraction of cellular units is as yet unknown. We have used immunohistochemical methods to demonstrate the intracellular localization of the proteins actin, myosin, tropomyosin and vinculin, which are thought to be responsible for cellular contraction, in 26 surgically obtained epiretinal traction membranes from patients with traumatic (n = 12) and idiopathic (n = 7) proliferative vitreoretinopathy, and proliferative diabetic retinopathy (n = 7). The use of cell marker proteins for glial cells (GFAP) and retinal pigment epithelium (cytokeratin) demonstrates that the prevalence of contractile components is independent of cellular construction. We suggest that an intracellular mechanism is responsible for the contraction of epiretinal membranes in proliferative vitreoretinal disorders.

Contractile Proteins↗

PubMed1991

Retinal microglia: a new cell in idiopathic proliferative vitreoretinopathy?

Despite numerous studies of the role of mononuclear phagocytes in proliferative vitreoretinopathy, the origin of these cells has remained obscure. Notably, retinal microglial cells have consistently been neglected. Applying double label immunohistology with a set of new cell markers to 37 preretinal traction membranes, we have identified a distinct population of proliferating cells presumably of microglial origin. The identification of microglia relies on positive labels for LN-1, Ricinus communis agglutinin-1, vimentin, HLA-DR, and nucleoside diphosphatase, and negative labels for Leu-M1, Leu-M3, EBM-11, von Willebrand factor, CD22, cytokeratin, and glial fibrillary acidic protein. Microglia are much more prevalent in idiopathic than in traumatic proliferative vitreoretinopathy and insignificant in proliferative diabetic retinopathy. HLA-DR expression was not restricted to pigment epithelium as previously reported but also observed in microglia, macrophages, endothelial and glial cells. The detection of retinal microglial cell proliferation suggests a pathogenetic role of these cells and questions current concepts of the cellular biology of proliferative vitreoretinopathy.

Antigens↗

PubMed1991

[Thrombospondin and its importance in proliferative retinal diseases].

Thrombospondin (TSP), a platelet-derived protein of the integrin-binding family with adhesive and mitogenic properties was localized in surgically obtained epiretinal traction membranes from patients with traumatic (7/8) and idiopathic (8/8) proliferative vitreoretinopathy (PVR) and proliferative diabetic retinopathy (PDR) (6/8). Using double-label immunofluorescence techniques, we demonstrated co-localization of TSP with the endothelial cell marker, von Willebrand factor, in PDR; however, only a minority of labeled macrophages showed simultaneous staining for TSP. Therefore, macrophages are probably not a major source of TSP in PVR. We demonstrated co-distribution of blood coagulation factor XIII and two of its cross-linking substrates, fibronectin and TSP, in epiretinal membranes, as well as the detection of plasmin and presumably plasmin-induced TSP breakdown products in physiologic and pathologic vitreous. These results suggest that the coagulation system has a functional role in proliferative retinal disorders and imply that the application of inhibitors of the coagulation cascade like heparin may be a potential therapeutic approach.

Antibodies, Monoclonal↗