The Experts below are selected from a list of 150567 Experts worldwide ranked by ideXlab platform
Marko Turpeinen - One of the best experts on this subject based on the ideXlab platform.
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transepidermal water loss and absorption of hydrocortisone in widespread dermatitis
British Journal of Dermatology, 1993Co-Authors: Kristiina Aaltokorte, Marko TurpeinenAbstract:Summary Percutaneous absorption of hydrocortisone was measured in tbree children and six adults with widespread dermatitis, after the application of 1% bydrocortisone cream. Before appiication of the cream, the transepidermal water loss (TEWL) was measured on six skin areas. A highly significant correlation was found between the post-application rise in plasma cortisol level and the mean transepidermal water loss. Thus, measurement of TEWL affords a simple, non-invasive method for assessing the Systemic Effect of hydrocortisone applied to widespread dermatitis.
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transepidermal water loss and absorption of hydrocortisone in widespread dermatitis
British Journal of Dermatology, 1993Co-Authors: Kristiina Aaltokorte, Marko TurpeinenAbstract:Summary Percutaneous absorption of hydrocortisone was measured in tbree children and six adults with widespread dermatitis, after the application of 1% bydrocortisone cream. Before appiication of the cream, the transepidermal water loss (TEWL) was measured on six skin areas. A highly significant correlation was found between the post-application rise in plasma cortisol level and the mean transepidermal water loss. Thus, measurement of TEWL affords a simple, non-invasive method for assessing the Systemic Effect of hydrocortisone applied to widespread dermatitis.
Kristiina Aaltokorte - One of the best experts on this subject based on the ideXlab platform.
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transepidermal water loss and absorption of hydrocortisone in widespread dermatitis
British Journal of Dermatology, 1993Co-Authors: Kristiina Aaltokorte, Marko TurpeinenAbstract:Summary Percutaneous absorption of hydrocortisone was measured in tbree children and six adults with widespread dermatitis, after the application of 1% bydrocortisone cream. Before appiication of the cream, the transepidermal water loss (TEWL) was measured on six skin areas. A highly significant correlation was found between the post-application rise in plasma cortisol level and the mean transepidermal water loss. Thus, measurement of TEWL affords a simple, non-invasive method for assessing the Systemic Effect of hydrocortisone applied to widespread dermatitis.
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transepidermal water loss and absorption of hydrocortisone in widespread dermatitis
British Journal of Dermatology, 1993Co-Authors: Kristiina Aaltokorte, Marko TurpeinenAbstract:Summary Percutaneous absorption of hydrocortisone was measured in tbree children and six adults with widespread dermatitis, after the application of 1% bydrocortisone cream. Before appiication of the cream, the transepidermal water loss (TEWL) was measured on six skin areas. A highly significant correlation was found between the post-application rise in plasma cortisol level and the mean transepidermal water loss. Thus, measurement of TEWL affords a simple, non-invasive method for assessing the Systemic Effect of hydrocortisone applied to widespread dermatitis.
Jiangang Wang - One of the best experts on this subject based on the ideXlab platform.
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stimulation of ampk prevents degeneration of photoreceptors and the retinal pigment epithelium
Proceedings of the National Academy of Sciences of the United States of America, 2018Co-Authors: Li Kong, Jiangang Wang, John D AshAbstract:Retinal degenerative diseases are generally characterized by a permanent loss of light-sensitive retinal neurons known as photoreceptors, or their support cells, the retinal pigmented epithelium (RPE). Metabolic dysfunction has been implicated as a common mechanism of degeneration. In this study, we used the drug metformin in a gain-of-function approach to activate adenosine monophosphate-activated protein kinase (AMPK). We found that treatment protected photoreceptors and the RPE from acute injury and delayed inherited retinal degeneration. Protection was associated with decreased oxidative stress, decreased DNA damage, and increased mitochondrial energy production. To determine whether protection was a local or a Systemic Effect of metformin, we used AMPK retinal knockout mice and found that local expression of AMPK catalytic subunit α2 was required for metformin-induced protection. Our data demonstrate that increasing the activity of AMPK in retinal neurons or glia can delay or prevent degeneration of photoreceptors and the RPE from multiple types of cell-death triggers.
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stimulation of ampk prevents degeneration of photoreceptors and the retinal pigment epithelium
Proceedings of the National Academy of Sciences of the United States of America, 2018Co-Authors: Lei Xu, Li Kong, Jiangang WangAbstract:Retinal degenerative diseases are generally characterized by a permanent loss of light-sensitive retinal neurons known as photoreceptors, or their support cells, the retinal pigmented epithelium (RPE). Metabolic dysfunction has been implicated as a common mechanism of degeneration. In this study, we used the drug metformin in a gain-of-function approach to activate adenosine monophosphate-activated protein kinase (AMPK). We found that treatment protected photoreceptors and the RPE from acute injury and delayed inherited retinal degeneration. Protection was associated with decreased oxidative stress, decreased DNA damage, and increased mitochondrial energy production. To determine whether protection was a local or a Systemic Effect of metformin, we used AMPK retinal knockout mice and found that local expression of AMPK catalytic subunit α2 was required for metformin-induced protection. Our data demonstrate that increasing the activity of AMPK in retinal neurons or glia can delay or prevent degeneration of photoreceptors and the RPE from multiple types of cell-death triggers.
Li Kong - One of the best experts on this subject based on the ideXlab platform.
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stimulation of ampk prevents degeneration of photoreceptors and the retinal pigment epithelium
Proceedings of the National Academy of Sciences of the United States of America, 2018Co-Authors: Li Kong, Jiangang Wang, John D AshAbstract:Retinal degenerative diseases are generally characterized by a permanent loss of light-sensitive retinal neurons known as photoreceptors, or their support cells, the retinal pigmented epithelium (RPE). Metabolic dysfunction has been implicated as a common mechanism of degeneration. In this study, we used the drug metformin in a gain-of-function approach to activate adenosine monophosphate-activated protein kinase (AMPK). We found that treatment protected photoreceptors and the RPE from acute injury and delayed inherited retinal degeneration. Protection was associated with decreased oxidative stress, decreased DNA damage, and increased mitochondrial energy production. To determine whether protection was a local or a Systemic Effect of metformin, we used AMPK retinal knockout mice and found that local expression of AMPK catalytic subunit α2 was required for metformin-induced protection. Our data demonstrate that increasing the activity of AMPK in retinal neurons or glia can delay or prevent degeneration of photoreceptors and the RPE from multiple types of cell-death triggers.
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stimulation of ampk prevents degeneration of photoreceptors and the retinal pigment epithelium
Proceedings of the National Academy of Sciences of the United States of America, 2018Co-Authors: Lei Xu, Li Kong, Jiangang WangAbstract:Retinal degenerative diseases are generally characterized by a permanent loss of light-sensitive retinal neurons known as photoreceptors, or their support cells, the retinal pigmented epithelium (RPE). Metabolic dysfunction has been implicated as a common mechanism of degeneration. In this study, we used the drug metformin in a gain-of-function approach to activate adenosine monophosphate-activated protein kinase (AMPK). We found that treatment protected photoreceptors and the RPE from acute injury and delayed inherited retinal degeneration. Protection was associated with decreased oxidative stress, decreased DNA damage, and increased mitochondrial energy production. To determine whether protection was a local or a Systemic Effect of metformin, we used AMPK retinal knockout mice and found that local expression of AMPK catalytic subunit α2 was required for metformin-induced protection. Our data demonstrate that increasing the activity of AMPK in retinal neurons or glia can delay or prevent degeneration of photoreceptors and the RPE from multiple types of cell-death triggers.
John D Ash - One of the best experts on this subject based on the ideXlab platform.
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stimulation of ampk prevents degeneration of photoreceptors and the retinal pigment epithelium
Proceedings of the National Academy of Sciences of the United States of America, 2018Co-Authors: Li Kong, Jiangang Wang, John D AshAbstract:Retinal degenerative diseases are generally characterized by a permanent loss of light-sensitive retinal neurons known as photoreceptors, or their support cells, the retinal pigmented epithelium (RPE). Metabolic dysfunction has been implicated as a common mechanism of degeneration. In this study, we used the drug metformin in a gain-of-function approach to activate adenosine monophosphate-activated protein kinase (AMPK). We found that treatment protected photoreceptors and the RPE from acute injury and delayed inherited retinal degeneration. Protection was associated with decreased oxidative stress, decreased DNA damage, and increased mitochondrial energy production. To determine whether protection was a local or a Systemic Effect of metformin, we used AMPK retinal knockout mice and found that local expression of AMPK catalytic subunit α2 was required for metformin-induced protection. Our data demonstrate that increasing the activity of AMPK in retinal neurons or glia can delay or prevent degeneration of photoreceptors and the RPE from multiple types of cell-death triggers.
