Publications by authors named "Gorog P"

In recent years a significant demand to develop computer-assisted diagnostic tools to assess prostate cancer using whole slide images has been observed. In this study we develop and validate a machine learning system for cancer assessment, inclusive of detection of perineural invasion and measurement of cancer portion to meet clinical reporting needs. The system analyses the whole slide image in three consecutive stages: tissue detection, classification, and slide level analysis.

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Congenital glioblastoma (cGBM) is a brain tumor very rarely observed in newborns and young infants, and differs in several respects from glioblastoma (GBM) of childhood and adulthood. Our aim was the presentation of a cGBM case with 14 days of postnatal survival at the Pediatric Oncology Center of the Markusovszky University Teaching Hospital in 2004. We investigated formalin-fixed, paraffin-embedded autoptic tumor samples of the newborn by immunohistochemical and molecular genetic (FISH and pyrosequencing) methods.

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The actin containing tropomyosin and troponin decorated thin filaments form one of the crucial components of the contractile apparatus in muscles. The thin filaments are organized into densely packed lattices interdigitated with myosin-based thick filaments. The crossbridge interactions between these myofilaments drive muscle contraction, and the degree of myofilament overlap is a key factor of contractile force determination.

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Axonal growth is mediated by coordinated changes of the actin and microtubule (MT) cytoskeleton. Ample evidence suggests that members of the formin protein family are involved in the coordination of these cytoskeletal rearrangements, but the molecular mechanisms of the formin-dependent actin-microtubule crosstalk remains largely elusive. Of the six formins, DAAM was shown to play a pivotal role during axonal growth in all stages of nervous system development, while FRL was implicated in axonal development in the adult brain.

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With the advent of super-resolution microscopy, we gained a powerful toolbox to bridge the gap between the cellular- and molecular-level analysis of living organisms. Although nanoscopy is broadly applicable, classical model organisms, such as fruit flies, worms and mice, remained the leading subjects because combining the strength of sophisticated genetics, biochemistry and electrophysiology with the unparalleled resolution provided by super-resolution imaging appears as one of the most efficient approaches to understanding the basic cell biological questions and the molecular complexity of life. Here, we summarize the major nanoscopic techniques and illustrate how these approaches were used in model systems to revisit a series of well-known cell biological phenomena.

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Authors present a rare manifestation of the temporal arteritis, wich caused initial diagnostic difficulties, but it responded well for corticosteroid treatment. The features of the disease, pathogenesis, possible therapy are briefly summarized beside the description of clinical course. Orv.

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Background: Increasing evidence shows that thrombogenicity and atherogenicity of lipoproteins are related to modifications involving oxidative, enzymatic, or physical alterations of these molecules. Findings on lipid peroxidation associated with cardiopulmonary bypass are conflicting, and the possible other forms of atherogenic lipid modification are unknown. The various forms of lipoprotein modifications including lipid peroxidation, desialylation, and leukocytic elastase activity after coronary artery bypass graft operations are examined.

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Migration of vascular smooth muscle cells (SMCs) leading to neointimal hyperplasia is an early and cardinal feature of atherogenesis. Migration of rat aortic SMCs from an upper chamber towards a lower one has been studied in a microchemotaxis (Boyden) chamber. Spontaneous migration of SMCs was practically prevented by the presence of endothelium in the lower chamber and was reduced if endothelial cells were substituted with endothelial cell-conditioned medium.

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Sustained presence of lipid peroxides in the circulation and their plasma carrier is a controversial issue. Particularly, there is no firm evidence for an increased plasma lipid peroxide level in patients with atherosclerosis. In this study, a strong correlation was found between plasma total lipid hydroperoxide and lipid hydroperoxide content of LDL cholesterol (r = 0.

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Outgrowth of vascular wall cells from rat aortic tissue explant was studied. In addition to fresh rat serum (3%), the complete culture medium contained either low density lipoprotein (LDL) separated from rat plasma (n-LDL, 100 microg/ml) or rat LDL modified either by activated rat polymorphonuclear leucocytes (pmn-LDL) or by exposure to UV light (uv-LDL). Compared to n-LDL, pmn-LDL significantly increased the start of cell outgrowth and the further rate of growth.

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The strong epidemiological association between elevated plasma clotting factors and coronary artery disease is generally interpreted as evidence that patients with coronary atherosclerosis are in a procoagulant (hypercoagulable) state. A dynamic global test was used to assess the overall coagulation status of 761 patients with coronary artery disease scheduled for coronary artery bypass grafting and compared to healthy matched controls (n = 100). Platelet reactivity to shear-stress was simultaneously measured from identical, non-anticoagulated blood samples.

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Generation of reactive oxygen species (ROS) by platelets was detected by a cyano-tetrazolium dye (CTC) which forms fluorescent formazan on the cell surface upon reduction. Fluorescence was quantitated by a densitometric device. Resting platelets in plasma produced significant fluorescence (P < 0.

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Efflux and extravascular accumulation of intravenously administered fluorescent-labeled low-density lipoprotein (LDL) and albumin were measured in superfused mouse mesenteric preparation in anesthetized mice. Pretreatment of animals with nifedipine (1 and 3 mg/kg sc) significantly reduced both the extravascular accumulation of LDL (measured by fluorescence densitometry) and the efflux (measurement of the tracers in the superfusate) of both LDL and albumin. These effects may help to explain the possible anti-atherogenic effect of nifedipine.

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The effect of in vivo stimulation of the phagocytic system (neutrophils, monocytes and hepatic Kupffer-cells) by inducing phagocytosis of intravenously administered latex particles on lipid peroxidation and aortic intimal proliferation was tested in cholesterol-fed rabbits. Three weeks after starting the diet, aortic intimal proliferation was measured by the intimal to medial ratios and by the incorporation of [3H]thymidine, infused into the circulation for the preceding 14 days. Intimal to medial ratios were increased (0.

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Contribution of leucocytes to formation and lysis of arterial (platelet) thrombi was investigated. Secretory products of polymorphonuclear leucocytes (PMNs) during phagocytosis and cell lysates were prepared from eight volunteers. Platelet-rich thrombi were formed in flowing native human blood either by shear-stress or by collagen fibre, by haemostatometry.

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The effect of 5 days of oral nifedipine treatment (approximately 1 mg/kg per day in drinking water) on low density lipoprotein (LDL) and cholesterol accumulation in rabbit arteries was determined. Compared with control aortas, nifedipine treatment (n = 5) significantly reduced homologous 125I-tyramine cellobiose-LDL accumulation (control versus nifedipine: 45.93 +/- 4.

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The prevailing concept of an extremely rapid disappearance of 'modified' low density lipoprotein (LDL) from the circulation was reinvestigated. Rabbit LDL was 'modified' by homologous activated (phagocytosing) polymorphonuclear leucocytes (PMLN), radiolabelled with a non-degradable ligand (125I-TC-LDL) and injected into rabbits. The plasma half-lives of 'modified' and native LDL were T1/2 = 2.

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The relationship between fibrinogen and severity of disease was measured in patients with coronary arterial disease (n = 301) prior to surgical coronary revascularisation. Platelet reactivity (shear-induced haemostasis) was measured from non-anticoagulated blood, in vitro. Coagulation was assessed by the clotting time of flowing native blood (dynamic) and by the conventional (stagnant) tube tests.

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A broad-based, dynamic model of intrinsic coagulation is described. Non-anticoagulated whole blood was perfused through polyethylene tubing under standard conditions, and coagulation (cessation of flow) was monitored by pressure changes. The dynamic coagulation test (DCT) is a sequel to the shear-induced haemostasis, a platelet function test routinely performed prior to coagulation.

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The specificity of an iodometric assay for measuring lipid peroxides in lipoproteins was tested, compared with the fluorimetric thiobarbituric acid assay, and adopted for detecting lipid peroxide in plasma samples. Oxidation of low density lipoproteins in vitro by Cu2+, lipoxidase, and phagocytosing polymorphonuclear leucocytes was sensitively detected by the iodometric assay. Unlike the thiobarbituric acid assay, neither non-lipid substances commonly present in plasma, nor platelet or polymorphonuclear leucocyte by-products interfered with the iodometric assay.

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The ability of native and oxidized lipids and lipoproteins to stimulate production of reactive oxygen species (ROS; superoxide and hydrogen peroxide) by human blood monocytes has been studied in vitro. Neither native human low density lipoprotein (LDL), 'altered' LDL (oxidized either by lipoxygenase, activated human monocytes or air) nor oxidized cholesterol had any significant effect on ROS production of monocytes. However, different oxidation products of a lipid emulsion (Lipofundin; largely consisting of linoleic acid oxidized either by lipoxygenase, Fe3+ or ultraviolet irradiation) greatly enhanced ROS production of monocytes.

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