The Experts below are selected from a list of 324 Experts worldwide ranked by ideXlab platform
Ula V Jurkunas - One of the best experts on this subject based on the ideXlab platform.
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fuchs endothelial corneal dystrophy the vicious cycle of fuchs pathogenesis
Progress in Retinal and Eye Research, 2020Co-Authors: Stephan Ong Tone, Ula V Jurkunas, Viridiana Kocaba, Myriam Bohm, Adam Wylegala, Tomas WhiteAbstract:Fuchs endothelial corneal dystrophy (FECD) is the most common primary corneal endothelial dystrophy and the leading indication for corneal transplantation worldwide. FECD is characterized by the progressive decline of corneal endothelial cells (CECs) and the formation of extracellular matrix (ECM) excrescences in Descemet's membrane (DM), called guttae, that lead to corneal edema and loss of vision. FECD typically manifests in the fifth decades of life and has a greater incidence in women. FECD is a complex and heterogeneous genetic disease where interaction between genetic and environmental factors results in cellular apoptosis and aberrant ECM deposition. In this review, we will discuss a complex interplay of genetic, epigenetic, and exogenous factors in inciting oxidative stress, auto(mito)phagy, unfolded protein response, and mitochondrial dysfunction during CEC degeneration. Specifically, we explore the factors that influence cellular fate to undergo apoptosis, senescence, and endothelial-to-mesenchymal transition. These findings will highlight the importance of abnormal CEC-DM interactions in triggering the vicious cycle of FECD pathogenesis. We will also review clinical characteristics, diagnostic tools, and current medical and surgical management options for FECD patients. These new paradigms in FECD pathogenesis present an opportunity to develop novel therapeutics for the treatment of FECD.
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fuchs endothelial corneal dystrophy
Ocular Surface, 2010Co-Authors: Hussain Elhalis, Behrooz Azizi, Ula V JurkunasAbstract:Abstract Fuchs endothelial corneal dystrophy (FECD) is characterized by progressive loss of corneal endothelial cells, thickening of Descement's membrane and deposition of extracellular matrix in the form of guttae. When the number of endothelial cells becomes critically low, the cornea swells and causes loss of vision. The clinical course of FECD usually spans 10-20 years. Corneal transplantation is currently the only modality used to restore vision. Over the last several decades genetic studies have detected several genes, as well as areas of chromosomal loci associated with the disease. Proteomic studies have given rise to several hypotheses regarding the pathogenesis of FECD. This review expands upon the recent findings from proteomic and genetic studies and builds upon recent advances in understanding the causes of this common corneal disorder.
Lauren Cohn - One of the best experts on this subject based on the ideXlab platform.
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advances in mucous cell metaplasia a plug for mucus as a therapeutic focus in chronic airway disease
American Journal of Respiratory Cell and Molecular Biology, 2010Co-Authors: David R Curran, Lauren CohnAbstract:Mucous cell metaplasia is induced in response to harmful insults and provides front-line protection to clear the airway of toxic substances and cellular debris. In chronic airway diseases mucous metaplasia persists and results in airway obstruction and contributes significantly to morbidity and mortality. Mucus hypersecretion involves increased expression of mucin genes, and increased mucin production and release. The past decade has seen significant advances in our understanding of the molecular mechanisms by which these events occur. Inflammation stimulates epidermal growth factor receptor activation and IL-13 to induce both Clara and ciliated cells to transition into goblet cells through the coordinated actions of FoxA2, TTF-1, SPDEF, and GABAAR. Ultimately, these steps lead to up-regulation of MUC5AC expression, and increased mucin in goblet cell granules that fuse to the plasma membrane through actions of MARCKS, SNAREs, and Munc proteins. Blockade of mucus in exacerbations of asthma and chronic obst...
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advances in mucous cell metaplasia a plug for mucus as a therapeutic focus in chronic airway disease
American Journal of Respiratory Cell and Molecular Biology, 2010Co-Authors: David R Curran, Lauren CohnAbstract:Mucous cell metaplasia is induced in response to harmful insults and provides front-line protection to clear the airway of toxic substances and cellular debris. In chronic airway diseases mucous metaplasia persists and results in airway obstruction and contributes significantly to morbidity and mortality. Mucus hypersecretion involves increased expression of mucin genes, and increased mucin production and release. The past decade has seen significant advances in our understanding of the molecular mechanisms by which these events occur. Inflammation stimulates epidermal growth factor receptor activation and IL-13 to induce both Clara and ciliated cells to transition into goblet cells through the coordinated actions of FoxA2, TTF-1, SPDEF, and GABA(A)R. Ultimately, these steps lead to up-regulation of MUC5AC expression, and increased mucin in goblet cell granules that fuse to the plasma membrane through actions of MARCKS, SNAREs, and Munc proteins. Blockade of mucus in exacerbations of asthma and chronic obstructive pulmonary disease may affect morbidity. Development of new therapies to target mucus production and secretion are now possible given the advances in our understanding of molecular mechanisms of mucous metaplasia. We now have a greater incentive to focus on inhibition of mucus as a therapy for chronic airway diseases.
Esther Rickert - One of the best experts on this subject based on the ideXlab platform.
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seasonal variations in surface metabolite composition of Fucus vesiculosus and Fucus serratus from the baltic sea
PLOS ONE, 2016Co-Authors: Esther Rickert, Martin Wahl, Heike Link, Hannes Richter, Georg PohnertAbstract:Perennial macroalgae within the genus Fucus are known to exude metabolites through their outer thallus surface. Some of these metabolites have pro- and/or antifouling properties. Seasonal fluctuations of natural fouling pressure and chemical fouling control strength against micro- and macrofoulers have previously been observed in Fucus, suggesting that control strength varies with threat. To date, a study on the seasonal composition of surface associated metabolites, responsible for much of the fouling control, has not been done. We sampled individuals of the two co-occurring species F. vesiculosus and F. serratus at monthly intervals (six per species and month) during a one-year field study. We analysed the chemical composition of surface associated metabolites of both Fucus species by means of gas chromatography-mass spectrometry (GC-MS) to describe temporal patterns in chemical surface composition. Additionally, we correlated abiotic and biotic parameters recorded monthly within the sampled habitat with the variation in the chemical surface landscape of Fucus. Our study revealed that the chemical surface composition of both Fucus species exhibits substantial seasonal differences between spring/summer and autumn/winter months. Light and temperature explained most of the seasonal variability in surface metabolite composition of both Fucus species. A strong summerly up-regulation of eighteen saccharides and two hydroxy acids in F. vesiculosus as well as of four fatty acids and two saccharides in F. serratus was observed. We discuss how these up-regulated molecules may have a complex effect on associated microfoulers, both promoting or decreasing fouling depending on metabolite and bacterial identity. These seasonal shifts in the surface metabolome seem to exert a compound control of density and composition of the Fucus associated biofilm.
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Seasonally fluctuating chemical microfouling control in Fucus vesiculosus and Fucus serratus from the Baltic Sea
Marine Biology, 2016Co-Authors: Esther Rickert, M. Lenz, F. R. Barboza, S. N. Gorb, Martin WahlAbstract:Microfouling in temperate seas underlies seasonal variations. Thus, perennial macroalgae are exposed to fluctuating levels of fouling pressure. Only few studies have examined the link between fouling pressure and algal fouling control. We assessed whether microfouling control of F. vesiculosus and F. serratus against prokaryotes and pennate diatoms fluctuates with season and correlates with microfouling pressure in a 1-year field survey. Microfouler recruitment on glass (reference surface) and on Fucus , microfouling control strength of Fucus surface metabolites (tested by an in situ bioassay approach) and Fucus tissue mannitol content (used as proxy for energy availability) were determined monthly. Microfouling pressure (settled cells per unit time and area) and microfouling control of Fucus varied seasonally. Both Fucus species exhibited cuticula shedding in all seasons. We conclude that microfouling control in both Fucus species showed a lagged or synchronized relationship with mannitol or microfouling pressure.
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seasonally fluctuating fouling control of Fucus vesiculosus and Fucus serratus from the baltic sea is fouling control linked to abiotic and biotic variables
Rickert Esther (2015) Seasonally fluctuating fouling control of Fucus vesiculosus and Fucus serratus from the Baltic Sea: Is fouling control linked to, 2015Co-Authors: Esther RickertAbstract:In this doctoral project, I investigated the putative seasonal fluctuating chemical fouling control of the perennial macroalgae Fucus vesiculosus and Fucus serratus from the Baltic Sea under in situ conditions as well as potential links between the chemical fouling control and different abiotic and biotic factors. My thesis highlights the seasonal dynamics of the chemical micro- and macrofouling control of F. vesiculosus and F. serratus from the Baltic Sea tested under in situ conditions as well as the impact of environmental variables on the fouling control strength. Further, this work demonstrates that both Fucus species exhibit pro- and antifouling properties during summer when fouling pressure is highest indicating a complex regulation of biofouling control. The study thus provides new insides into the complex algae-environment-fouler interactions and their seasonal dynamics.
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seasonal fluctuations in chemical defenses against macrofouling in Fucus vesiculosus and Fucus serratus from the baltic sea
Biofouling, 2015Co-Authors: Esther Rickert, Georg Pohnert, Ulf Karsten, Martin WahlAbstract:Macroalgae, especially perennial species, are exposed to a seasonally variable fouling pressure. It was hypothesized that macroalgae regulate their antifouling defense to fouling pressure. Over one year, the macrofouling pressure and the chemical anti-macrofouling defense strength of the brown algae Fucus vesiculosus and Fucus serratus were assessed with monthly evaluation. The anti-macrofouling defense was assessed by means of surface-extracted Fucus metabolites tested at near-natural concentrations in a novel in situ bioassay. Additionally, the mannitol content of both Fucus species was determined to assess resource availability for defense production. The surface chemistry of both Fucus species exhibited seasonal variability in attractiveness to Amphibalanus improvisus and Mytilus edulis. Of this variability, 50–60% is explained by a sinusoidal model. Only F. vesiculosus extracts originating from the spring and summer significantly deterred settlement of A. improvisus. The strength of macroalgal antifouling defense did not correlate either with in situ macrofouling pressure or with measured mannitol content, which, however, were never depleted.
Stephan Ong Tone - One of the best experts on this subject based on the ideXlab platform.
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fuchs endothelial corneal dystrophy the vicious cycle of fuchs pathogenesis
Progress in Retinal and Eye Research, 2020Co-Authors: Stephan Ong Tone, Viridiana Kocaba, Myriam Bohm, Adam Wylegala, Tomas L WhiteAbstract:Abstract Fuchs endothelial corneal dystrophy (FECD) is the most common primary corneal endothelial dystrophy and the leading indication for corneal transplantation worldwide. FECD is characterized by the progressive decline of corneal endothelial cells (CECs) and the formation of extracellular matrix (ECM) excrescences in the Descemet's membrane (DM), called guttae, that lead to corneal edema and loss of vision. FECD typically manifests in the fifth decades of life and has a greater incidence in women. FECD is a complex and heterogeneous genetic disease where interaction between genetic and environmental factors results in cellular apoptosis and aberrant ECM deposition. In this review, we will discuss a complex interplay of genetic, epigenetic, and exogenous factors in inciting oxidative stress, auto (mito)phagy, unfolded protein response, and mitochondrial dysfunction during CEC degeneration. Specifically, we explore the factors that influence cellular fate to undergo apoptosis, senescence, and endothelial-to-mesenchymal transition. These findings will highlight the importance of abnormal CEC-DM interactions in triggering the vicious cycle of FECD pathogenesis. We will also review clinical characteristics, diagnostic tools, and current medical and surgical management options for FECD patients. These new paradigms in FECD pathogenesis present an opportunity to develop novel therapeutics for the treatment of FECD.
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fuchs endothelial corneal dystrophy the vicious cycle of fuchs pathogenesis
Progress in Retinal and Eye Research, 2020Co-Authors: Stephan Ong Tone, Ula V Jurkunas, Viridiana Kocaba, Myriam Bohm, Adam Wylegala, Tomas WhiteAbstract:Fuchs endothelial corneal dystrophy (FECD) is the most common primary corneal endothelial dystrophy and the leading indication for corneal transplantation worldwide. FECD is characterized by the progressive decline of corneal endothelial cells (CECs) and the formation of extracellular matrix (ECM) excrescences in Descemet's membrane (DM), called guttae, that lead to corneal edema and loss of vision. FECD typically manifests in the fifth decades of life and has a greater incidence in women. FECD is a complex and heterogeneous genetic disease where interaction between genetic and environmental factors results in cellular apoptosis and aberrant ECM deposition. In this review, we will discuss a complex interplay of genetic, epigenetic, and exogenous factors in inciting oxidative stress, auto(mito)phagy, unfolded protein response, and mitochondrial dysfunction during CEC degeneration. Specifically, we explore the factors that influence cellular fate to undergo apoptosis, senescence, and endothelial-to-mesenchymal transition. These findings will highlight the importance of abnormal CEC-DM interactions in triggering the vicious cycle of FECD pathogenesis. We will also review clinical characteristics, diagnostic tools, and current medical and surgical management options for FECD patients. These new paradigms in FECD pathogenesis present an opportunity to develop novel therapeutics for the treatment of FECD.
Tomas L White - One of the best experts on this subject based on the ideXlab platform.
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fuchs endothelial corneal dystrophy the vicious cycle of fuchs pathogenesis
Progress in Retinal and Eye Research, 2020Co-Authors: Stephan Ong Tone, Viridiana Kocaba, Myriam Bohm, Adam Wylegala, Tomas L WhiteAbstract:Abstract Fuchs endothelial corneal dystrophy (FECD) is the most common primary corneal endothelial dystrophy and the leading indication for corneal transplantation worldwide. FECD is characterized by the progressive decline of corneal endothelial cells (CECs) and the formation of extracellular matrix (ECM) excrescences in the Descemet's membrane (DM), called guttae, that lead to corneal edema and loss of vision. FECD typically manifests in the fifth decades of life and has a greater incidence in women. FECD is a complex and heterogeneous genetic disease where interaction between genetic and environmental factors results in cellular apoptosis and aberrant ECM deposition. In this review, we will discuss a complex interplay of genetic, epigenetic, and exogenous factors in inciting oxidative stress, auto (mito)phagy, unfolded protein response, and mitochondrial dysfunction during CEC degeneration. Specifically, we explore the factors that influence cellular fate to undergo apoptosis, senescence, and endothelial-to-mesenchymal transition. These findings will highlight the importance of abnormal CEC-DM interactions in triggering the vicious cycle of FECD pathogenesis. We will also review clinical characteristics, diagnostic tools, and current medical and surgical management options for FECD patients. These new paradigms in FECD pathogenesis present an opportunity to develop novel therapeutics for the treatment of FECD.
