Search PubMed⌕ Search

Biomedical subjects

K Heimann

Publications and source records attributed to K Heimann.

At least 127 records · Page 7Linked to original sources
PubMed1993

[Proliferative vitreoretinopathy. On the significance of protein transfer through the blood-retina barrier].

In several studies, unphysiologically high concentrations of different proteins have been measured in the vitreous of patients with proliferative vitreoretinopathy (PVR). It has not yet been determined whether these high values result from the alteration of the blood-retina barrier (BRB) or whether the proteins are produced intraocularly. In the present study we measured the concentrations of IgG and complement factor C4 in vitreous aspirates and plasma samples from patients with PVR (n = 15). We calculated an IgG and C4 index analogous to the IgG index in routine cerebrospinal fluid chemistry, which is used to estimate the rate of intrathecal IgG synthesis. Comparison of the C4 index revealed no significant difference between patients and controls. Although a higher IgG index was demonstrated in pathologic vitreous, no intravitreal cells that are able to synthesize IgG have been found. These findings suggest that high levels of IgG and C4 are related to an elevated transfer at the disrupted BRB.

Blood-Retinal Barrier↗
PubMed1993

[Expulsive retinal hemorrhage. Secondary treatment by vitreoretinal surgery].

Expulsive hemorrhage is a catastrophic complication of intraocular surgery that can result in total loss of vision. Patients with massive hemorrhagic choroidal detachment were treated by vitrectomy and silicone oil or gas tamponade. A reattachment of the retina was achieved with stabilization of visual function. Properly timed drainage of the choroidal fluid components with pars plana vitrectomy and silicone or gas injection is a useful approach in these disorders and may salvage useful vision in complicated cases.

Adult↗
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

Retinal detachment in eyes with congenital glaucoma.

Five patients with congenital glaucoma were treated for complicated retinal detachment. All patients underwent a pars plana vitrectomy and fluid/gas or fluid/silicone exchange. The technical difficulties of operating on buphthalmic eyes are described. Due to subretinal reproliferation, corneal decompensation, and pressure elevation, the functional prognosis is still poor.

Adult↗
PubMed1992

Artificial iris diaphragm and silicone oil surgery.

In order to avoid contact between silicone oil and the cornea and subsequent painful corneal dystrophy in aniridial eyes, an artificial iris diaphragm was constructed. It consists of polymethylacrylat (PMMA) and simulates the situation of the iris with a central pupillary opening and inferior iridectomy. To date, these diaphragms have been implanted in 11 cases of the severest ocular trauma with accompanying aniridia and proliferative vitreoretinopathy. In the presence of sufficient residual secretion of the ciliary body (9 cases), the diaphragm assumes the function of normal iris and prevents the silicone oil from coming into contact with the corneal endothelium. The transparent diaphragm ensures a view through to the fundus. In the early postoperative period, there was, as anticipated, a fibrinous reaction in the area of the anterior segment.

Adult↗
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

Daunomycin and silicone oil for the treatment of proliferative vitreoretinopathy.

We describe the long-term results after treatment of 68 eyes showing advanced stages of proliferative vitreoretinopathy with vitrectomy, daunomycin perfusion, and silicone-oil injection. Six reoperations were performed. After 18 months, 73% of the eyes showed no signs of retinal detachment and 89% had a visual acuity of greater than 20/800. These results are better than those reported in previously published studies. Whether this improvement was due to the daunomycin treatment or to more aggressive surgical techniques such as retinotomies remains to be answered by a randomized trial.

Daunorubicin↗
PubMed1991

An immunochemical quantitative analysis of the protein pattern in physiologic and pathologic vitreous.

Biochemical changes in the vitreous in different vitreoretinal disorders have not yet been thoroughly studied. Using enzyme-linked immunosorbent analysis (ELISA), we established mean values and 95% confidence intervals for six proteins of physiologic human vitreous: albumin (293 +/- 18 mg/l), transferrin (73.7 +/- 6.6 mg/l), immunoglobulin G (IgG), (33.5 +/- 3 mg/l), alpha 1-antitrypsin (14.1 +/- 2.9 mg/l), alpha 1-acid glycoprotein (4 +/- 0.7 mg/l), and lactoferrin (less than 50 micrograms/l). These six proteins were also determined in vitreous aspirates from patients with idiopathic proliferative vitreoretinopathy (n = 10), traumatic proliferative vitreoretinopathy (n = 10), and proliferative diabetic retinopathy (n = 15). The pattern of protein levels varied widely within each of the disorders. An analysis of absolute protein levels showed significant differences in total protein and alpha 1-antitrypsin levels between controls and pathologic vitreous samples. We observed differences in transferrin between controls and proliferative diabetic retinopathy (PDR), and differences in alpha 1-acid glycoprotein between controls and both types of proliferative vitreoretinopathy (PVR). The single disorders themselves could not be differentiated by any of the proteins. When the relative contribution of single proteins to total vitreal protein was compared, albumin was lower in all three disorders than in controls. Transferrin was lower in traumatic PVR than in controls, in PDR, or in idiopathic PVR. Our results indicate that the three vitreoretinal disorders studied are characterized by a breakdown of blood-ocular barriers.

Albumins↗
PubMed1991

Vitronectin and proliferative intraocular disorders. I. A colocalisation study of the serum spreading factor, vitronectin, and fibronectin in traction membranes from patients with proliferative vitreoretinopathy.

The presence of a scaffold for cellular spreading and proliferation is a precondition for the development of traction membranes in proliferative vitreoretinopathy (PVR). This study shows the presence of the serum spreading factor, vitronectin, in the extracellular matrix of periretinal membranes removed during vitreoretinal surgery. By means of a double label immunofluorescence protocol, a partial colocalisation of vitronectin with fibronectin at the magnification of light microscopy can be detected. Fibronectin is a high-molecular glycoprotein with multiple biological functions including the mediation of cell attachment and migration. Both proteins share a special cell recognition site which could be a target for experimental pharmacological approaches to PVR. Preliminary studies of vitreous aspirates using electrophoresis and Western blotting indicate that vitronectin may play a more important role in post-traumatic PVR as compared to PVR following rhegmatogenous retinal detachment.

Blotting, Western↗
PubMed1991

Vitronectin and proliferative intraocular disorders. II. Expression of cell surface receptors for fibronectin and vitronectin in periretinal membranes.

Several cell types participate in the formation of vitreoretinal traction membranes in proliferative intraocular disorders. The communication between these cells involves hormones, growth factors, and the interaction with extracellular matrix molecules. We have previously demonstrated a partial colocalisation of two potent mediators of cell attachment, fibronectin and vitronectin, in periretinal membranes from patients with proliferative vitreoretinopathy (PVR). We found a similar pattern of vitronectin and fibronectin deposition in proliferative diabetic retinopathy (PDR) (n = 6). Now we show the expression of the corresponding cell surface receptors, integrins, for fibronectin and vitronectin by proliferating cells in 22 periretinal membranes, including traumatic (n = 8) and idiopathic (n = 8) PVR as well as PDR membranes (n = 6). Integrins are membrane receptors for extracellular matrix macromolecules which are involved in such basic biological phenomena as embryogenesis and metastasis. Future studies on the pathogenesis of vitreoretinal proliferation will have to focus on the initiation, maintenance, and regulation of this intercellular communication network involving attachment proteins and integrins.

Diabetic Retinopathy↗
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↗