[Contribution of selected cellular adhesion molecules and proinflammatory cytokines in the pathogenesis of proliferative diabetic retinopathy]. / Udzial wybranych molekul adhezyjnych oraz cytokin prozapalnych w patogenezie proliferacyjnej retinopatii cukrzycowej.

UNLABELLED: Proliferative diabetic retinopathy (PDR) is caused by structural and functional disorders of the retinal vessels. Complex pathobiological mechanisms of this process have not been clearly explained so far. PURPOSE: To prove the role of immunological-inflammatory process in the development of the proliferative diabetic retinopathy. MATERIAL AND METHODS: Forty six patients, aged 63.97+/-9 were enrolled in the study, treated for diabetes type 2 for 12.56+/-6,87 years. In 19 patients (12 women and 7 men aged 64.63+/-8.38, treated for diabetes for 12.47+/-6.75 years) a parallel analysis of given parameters was performed in both serum and vitreous body samples. Vitrectomy, in course of which the vitreous body samples were obtained, was performed in these patients because of vitreous haemorrhage, causing traction retinal detachment in some patients. The control group consisted of 15 patients (9 women and 6 men), aged 63.00+/-14.58, who underwent the vitrectomy procedure because of reasons other than diabetic retinopathy. The concentration values of the soluble forms of ICAM-1, VCAM-1, IL-6 and TNF-alpha were estimated both in the serum and vitreous body samples on the basis of the ELISA method. The biochemical tests were performed routinely in the clinical laboratory. RESULTS: Mean concentrations of the investigated parameters were significantly higher in the group of patients suffering from PDR, both in the serum and in the vitreous body samples, in comparison with the values observed in the control group. In the presence of HbAlc at the level of 9.21+/-2.17% a directly proportional correlation between the TNF-alpha either in serum or in the vitreous body samples and VCAM-1 in the vitroeus body samples was found. It is worth mentioning that the increase of the TNF-alpha concentration in the vitreous body was significantly related to the rise of the VCAM-1. CONCLUSIONS: The above mention of findings prove the remarkable role of the immunological and inflammatory response in the pathogenesis of this specific vascular complication of diabetes. The research was a source of evidence which highlighted the necessity of optimal metabolic control of the disease in the prevention of vascular complications of diabetes.

[The role of transforming growth factor-beta in the pathogenesis of diabetic retinopathy]. / Rola transformujacego czynnika wzrostu-beta w patogenezie retinopatii cukrzycowej.

Diabetic retinopathy is a micro-angiopathy affecting predominantly small vessels of the retina. Proliferative diabetic retinopathy is characterised by preretinal neovascularisation and fibrosis leading to vitreous heamorrhage and tractional retinal detachment. Chronic hyperglicemia may cause growth factor alterations that are likely to participate in tissue remodeling typical for this late complication. Numerous angiogenic and mitogenic factors have been demonstrated to be present in the eye, including transforming growth factor-beta (TGF-beta), insulin-like growth factors, fibroblast growth factor, tumor necrosis factor and vascular endothelial growth factor. TGF-beta is involved in the control of endothelial cell proliferation, adhesion and deposition of extracellular matrix, thus TGF-beta may play a role in the control of endothelial cell proliferation seen in the disease. The role of TGF-beta in diabetic retinopathy enables better understanding, and thus in the future better intensive antidiabetic therapy in aspect of ophthalmic complications.

[The role of cellular adhesion molecule in the development of proliferative diabetic retinopathy]. / Rola molekul adhezyjnych w rozwoju proliferacyjnej retinopatii cukrzycowej.

Development of proliferative diabetic retinopathy's pathogenesis is still unknown. Last years publications seems to show immuno-inflammatory base of structural and functional retinal vessels endothelial cells' changes. Chronic retinal ischemia leads to development of pathological vessels and formation of fibrovascular tissue at the vitreoretinal interface. One of the important cause of the damage is leukocytes activation and adhesion to vascular endothelium, that is mediated by the specific adhesion molecules. Increase of soluble cellular adhesion molecules (CAMs) in serum, vitreous, epiretinal membranes of patients with PVR seems to confirm its role in the pathogenesis of this process. This publication attempts to estimate the CAM's role in progression of PDR.

[The role of anti-pericyte antibodies in the development of diabetic retinopathy]. / Rola przeciwcial przeciw pericytom sciany naczyniowej w rozwoju retinopatii cukrzycowej.

Diabetic retinopathy is one of the most common devastating complications of diabetes. Pericyte loss, microaneurysms and acellular capillaries are characteristic for the diabetic retina. Researches have provided evidence that hyperglycaemia is one of the main factors driving the onset and progression of diabetic retinopathy. Although it has been shown that tight metabolic control has beneficial effects on the development and progression of this complication, the increase of blood glucose concentrations does not account for all the risk for development and progression to sight threatening retinopathy. A number of reports suggest that autoimmune mechanism play a role in diabetic microangiopathy (circulating antiendothelial cells autoantibodies, antiphospholipid antibodies, presence of immunoglobulins, lymphocytes and cytokines in diabetic retinal tissue). Diabetic subjects were also found to have autoantibodies to microvascular pericytes in their circulation. These results may contribute to understanding why retinopathy progresses in some patients, despite consistent reduction of blood sugar. This publication tries to estimate the anti-pericyte autoantibodies role in progression of diabetic retinopathy.

[Selected problems of endothelial functions. I. The role of endothelium in maintaining the hematological and circulatory balance]. / Wybrane aspekty czynnosci sródblonka. I. Rola sródblonka w utrzymaniu równowagi hematologicznej i krazeniowej.

Based on literary data we carried out the analysis of the influence vascular endothelium on maintaining the haematological and circulatory balance in the organism. Particular attention was paid on its active metabolic and secretory role in this process.

[Selected problems of endothelial functions. II. The role of the selectines in the damage of vascular endothelium]. / Wybrane aspekty czynnosci sródblonka. II. Udzial selektyn w uszkodzeniu sródblonka naczyniowego.

Studies in the recent years have provided numerous evidence of the inflammatory and immunological character of atherosclerosis. In the early stages of the adhesion of leucocytes and platelets to the blood vessel wall, and also in occurring intercellular interactions leading to creating the atherosclerotic lamina, the adhesive molecules from the selectine family ply the crucial role. Their expression, mainly selectines L, P and E on the endothelial surface and on the smooth muscles of the vessels, undergoes a distinct intensification under the influence of hypoxia. The begun cascade of molecular changes with the contribution of selectines leads inevitably to the development of atherosclerotic changes. The neutrophile and lymphocyte fixed to the endothelium show ability to its damage, both as a result of immediate response [release of free oxygen radicals, enzymes and cytoxic substances] and as a result of indirect action [release of cytocines which change the biological property of the endothelium--the so called endothelial activation]. In this work the role of diabetes and hypertension in the intensification of those processes has been noticed.

[Role of insulin-like growth factor I in the development of diabetic retinopathy]. / Rola insulinopodobnego czynnika wzrostu I w rozwoju retinopatii cukrzycowej.

Diabetic retinopathy is one of the main causes of blindness. This review will discuss the role of IGF-I in the pathogenesis of diabetic retinopathy. IGF-I is a growth factor with a very wide spectrum of biological activities. It especially controls cell growth and metabolic processes. Disorders of IGF-I activity, which are observed during diabetes, contribute to pathologic vascularization of the eye, particularly in the retina. Reasons for this is local hypoxia, which results from chronic hyperglycaemia; damage of blood retina barrier and disorder of the axis IGF-I--growth hormone. In the first stage of diabetic retinopathy the deficit of the systemic IGF-I can also be of importance. The role of IGF-I in diabetic retinopathy enables better understanding, and thus in the future better intensive antidiabetic therapy in aspect of ophthalmic complications.

[The Raynaud's phenomenon: still current clinical problem]. / Fenomen Raynaud--wciaz aktualny problem kliniczny.

Cardinal pathological mechanisms responsible for initiation and development of the Raynaud's phenomenon have been presented according to the current data from literature. The role of endothelin-1, cytokins and growth factor in pathophysiology of this phenomenon have been highlighted. According to own observations randomised results of investigation in these patients have shown that basic disease stimulate the development of the vasomotoric disturbances: idiopathic Raynaud's phenomenon and Raynaud's phenomenon which accompany connective tissue disease.

[Familial high myopia--challenge of modern genetics]. / Wysoka rodzinna krótkowzrocznosc--wyzwanie dla wspólczesnej genetyki.

In this paper has been accomplished an estimation of contemporary achievement in molecular researches domain's of pathology in familial high myopia. Clinical observations of monozygotic and dizygotic twins groups and also among family members with this type of myopia disclosing in following generations show, that it has inborn character. Nowadays, it has been identified three gen locci connected with heritage of this illness unit: 18p11.31, 12q21-31, 7q36. Above incontestable achievements do not interpret mechanism uprising this disease. Problem is still, to define the products planned by exchanged area of DNA, conditioning progress of high familial myopia.

[History of academic ophthalmology in Wroclaw, Poland in 1812-2002]. / Dzieje okulistyki uniwersyteckiej we Wroclawiu w latach 1812-2002.

The authors present the history of the Department of Ophthalmology in Wroclaw, since 1812. Special attention is paid to following professors of ophthalmology and directors of the University Eye Hospital: T.V.G. Benedict, A.T. Mitteldorf, R. Foerster, H.L. Cohn, H. Magnus, A. Groenouw, H. Willbrand; W. Uhthoff, Th. Axenfeld, G. Lenz, A. Huszcza, L. Baran, A. Bielschowsky, W. Dieter, A. Bednarski, M. Grzedzielski, L. Hirschfeld, W.J. Kapuscinski, S. Drozdowska, E. Ogielska, P. Hanczyc, M.H. Nizankowska

[Contribution of selected factors of inflammatory creative process in the vascular endothelial damage in the diabetes patients]. / Udzial wybranych czynników procesu zapalno-wytwórczego w uszkodzeniu sródblonka naczyniowego u chorych na cukrzyce.

Diabetes causes the development of atherosclerotic vascular changes. Leukocytes, thrombocytes and also cytokines are involved in this process via endothelial activation. Estimation of interleukin 1 beta (IL-1 beta) and fibrinogen serum level of patients suffering from diabetes in context of endothelial damage is presented. The stage of vascular endothelium damage is based on the measurement of blood endothelial cells (EC) count and concentration of the plasmatic von Willebrand factor (vWF). Endothelial destruction level was established on the base of selectin L, P and E serum concentration. Activation of inflammatory proliferative mechanisms was indicated by IL-1 beta serum level. Serum haemostasis disorders were indicated by fibrinogen concentration. Patients with diabetes t. 1 and t. 2 differentiated by age and diabetes duration time with normal blood pressure and hypertension were included into the research. We showed that in both types of diabetes endothelium damage goes with significant increase of circulated EC count and vWF concentration. Increased serum level of IL-1 beta and fibrinogen in those patients shoulds significant correlation with vascular wall destruction, visibly marked in patients with diabetes t. 2. Hiperfibrinogenaemia and increased IL-1 beta concentration associate with significant engagement of SL and SE in inflammatory proliferative process of endothelium in young people suffering from diabetes t. 1 over 6 years. Hypertension coexisting with essential disease in both types of diabetes remains important progression factor in atheromatic vascular changes.