The Experts below are selected from a list of 38637 Experts worldwide ranked by ideXlab platform
Alan J Grodzinsky - One of the best experts on this subject based on the ideXlab platform.
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lose dose administration of dexamethasone is beneficial in preventing secondary tendon damage in a stress deprived joint injury explant model
Journal of Orthopaedic Research, 2020Co-Authors: Brianne K Connizzo, Alan J GrodzinskyAbstract:Secondary joint damage is the process by which a single injury can lead to detrimental changes in adjacent Tissue structures, typically through the spread of inflammatory responses. We recently developed an in vitro model of secondary joint damage using a murine rotator cuff explant system, in which injuries to muscle and bone cause massive cell death in otherwise uninjured tendon. The purpose of the present study was to test the ability cytokine-targeted and broad-spectrum therapeutics to prevent cell death and Tissue Degeneration associated with secondary joint damage. We treated injured bone-tendon-muscle explants with either interleukin-1 receptor antagonist, etanercept, or dexamethasone (DEX) for up to 7 days in culture. Only the low-dose DEX treatment was able to prevent cell death and Tissue Degeneration. We then identified a critical window between 24 and 72 h following injury for maximal benefit of DEX treatment through timed administration experiments. Finally, we performed two tendon-only explant studies to identify mechanistic effects on tendon health. Interestingly, DEX did not prevent cell death and Degeneration in a model of cytokine-induced damage, suggesting other targets of DEX activity. Future studies will aim to identify factors in joint inflammation that may be targeted by DEX treatment, as well as to investigate novel delivery strategies. Statement of clinical significance: Overall, this work demonstrates beneficial effects of DEX administration on preventing tenocyte death and extracellular matrix Degeneration in an explant model of secondary joint damage, supporting the clinical use of low-dose glucocorticoids for short-term treatment of joint inflammation. © 2019 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 38:139-149, 2020.
Kiyoshi Okuda - One of the best experts on this subject based on the ideXlab platform.
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galectin 3 contributes to luteolysis by binding to beta 1 integrin in the bovine corpus luteum
Biology of Reproduction, 2014Co-Authors: Kazuhisa Hashiba, Dariusz J Skarzynski, Masahiro Sano, Junko Niokobayashi, Takuo Hojo, Kiyoshi OkudaAbstract:ABSTRACT Luteolysis is characterized by a reduction in progesterone (P4) production and Tissue Degeneration in the corpus luteum (CL). One of major events during luteolysis is luteal cell death. Galectin-3, a ubiquitously expressed protein involved in many cellular processes, serves as an antiapoptotic and/or proapoptotic factor in various cell types. Although galectin-3 is detected in the bovine CL, its role remains unclear. The expression of galectin-3 in the bovine CL was higher at the regressed stage than at the other luteal stages. Galectin-3 was localized on luteal steroidogenic cells (LSCs). When cultured LSCs were exposed to prostaglandin F2alpha (PGF) for 48 h, the expression and secretion of galectin-3 increased. When the cultured LSCs were treated with galectin-3 for 24 h, cleaved caspase-3 expression was increased, and the cell viability was decreased, whereas P4 production did not change. Beta 1 integrin, a target protein of galectin-3, was expressed in bovine CL and possessed glycans, which ...
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roles of prostaglandin f2alpha and hydrogen peroxide in the regulation of copper zinc superoxide dismutase in bovine corpus luteum and luteal endothelial cells
Reproductive Biology and Endocrinology, 2012Co-Authors: Tomas J Acosta, Shin Yoshioka, Hironori Abe, Kiyoshi OkudaAbstract:Background Prostaglandin F2alpha (PGF) induces luteolysis in cow by inducing a rapid reduction in progesterone production (functional luteolysis) followed by Tissue Degeneration (structural luteolysis). However the mechanisms of action of PGF remain unclear. Reactive oxygen species (ROS) play important roles in regulating the luteolytic action of PGF. The local concentration of ROS is controlled by superoxide dismutase (SOD), the main enzyme involved in the control of intraluteal ROS. Thus SOD seems to be involved in luteolysis process induced by PGF in cow.
Brianne K Connizzo - One of the best experts on this subject based on the ideXlab platform.
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lose dose administration of dexamethasone is beneficial in preventing secondary tendon damage in a stress deprived joint injury explant model
Journal of Orthopaedic Research, 2020Co-Authors: Brianne K Connizzo, Alan J GrodzinskyAbstract:Secondary joint damage is the process by which a single injury can lead to detrimental changes in adjacent Tissue structures, typically through the spread of inflammatory responses. We recently developed an in vitro model of secondary joint damage using a murine rotator cuff explant system, in which injuries to muscle and bone cause massive cell death in otherwise uninjured tendon. The purpose of the present study was to test the ability cytokine-targeted and broad-spectrum therapeutics to prevent cell death and Tissue Degeneration associated with secondary joint damage. We treated injured bone-tendon-muscle explants with either interleukin-1 receptor antagonist, etanercept, or dexamethasone (DEX) for up to 7 days in culture. Only the low-dose DEX treatment was able to prevent cell death and Tissue Degeneration. We then identified a critical window between 24 and 72 h following injury for maximal benefit of DEX treatment through timed administration experiments. Finally, we performed two tendon-only explant studies to identify mechanistic effects on tendon health. Interestingly, DEX did not prevent cell death and Degeneration in a model of cytokine-induced damage, suggesting other targets of DEX activity. Future studies will aim to identify factors in joint inflammation that may be targeted by DEX treatment, as well as to investigate novel delivery strategies. Statement of clinical significance: Overall, this work demonstrates beneficial effects of DEX administration on preventing tenocyte death and extracellular matrix Degeneration in an explant model of secondary joint damage, supporting the clinical use of low-dose glucocorticoids for short-term treatment of joint inflammation. © 2019 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 38:139-149, 2020.
Gary A Brook - One of the best experts on this subject based on the ideXlab platform.
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acute rolipram thalidomide treatment improves Tissue sparing and locomotion after experimental spinal cord injury
Experimental Neurology, 2009Co-Authors: Guido C Koopmans, Ronald Deumens, Armin Buss, Liam Geoghegan, Aye Mu Myint, Wiel H H Honig, Nadine Kern, Elbert A Joosten, Johannes Noth, Gary A BrookAbstract:Traumatic spinal cord injury (SCI) causes severe and permanent functional deficits due to the primary mechanical insult followed by secondary Tissue Degeneration. The cascade of secondary degenerative events constitutes a range of therapeutic targets which, if successfully treated, could significantly ameliorate functional loss after traumatic SCI. During the early hours after injury, potent pro-inflammatory cytokines, including tumor necrosis factor alpha (TNF-alpha) and interleukin-1 beta (IL-1beta) are synthesized and released, playing key roles in secondary Tissue Degeneration. In the present investigation, the ability of rolipram and thalidomide (FDA approved drugs) to reduce secondary Tissue Degeneration and improve motor function was assessed in an experimental model of spinal cord contusion injury. The combined acute single intraperitoneal administration of both drugs attenuated TNF-alpha and IL-1beta production and improved white matter sparing at the lesion epicenter. This was accompanied by a significant (2.6 point) improvement in the BBB locomotor score by 6 weeks. There is, at present, no widely accepted intervention strategy that is appropriate for the early treatment of human SCI. The present data suggest that clinical trials for the acute combined application of rolipram and thalidomide may be warranted. The use of such "established drugs" could facilitate the early initiation of trials.
Soheila Karimiabdolrezaee - One of the best experts on this subject based on the ideXlab platform.
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traumatic spinal cord injury an overview of pathophysiology models and acute injury mechanisms
Frontiers in Neurology, 2019Co-Authors: Arsalan Alizadeh, Scott M Dyck, Soheila KarimiabdolrezaeeAbstract:Traumatic spinal cord injury (SCI) is a life changing neurological condition with substantial socioeconomic implications for patients and their care-givers. Recent advances in medical management of SCI has significantly improved diagnosis, stabilization, survival rate and well-being of SCI patients. However, there has been small progress on treatment options for improving the neurological outcomes of SCI patients. This incremental success mainly reflects the complexity of SCI pathophysiology and the diverse biochemical and physiological changes that occur in the injured spinal cord. Therefore, in the past few decades, considerable efforts have been made by SCI researchers to elucidate the pathophysiology of SCI and unravel the underlying cellular and molecular mechanisms of Tissue Degeneration and repair in the injured spinal cord. To this end, a number of preclinical animal and injury models have been developed to more closely recapitulate the primary and secondary injury processes of SCI. In this review, we will provide a comprehensive overview of the recent advances in our understanding of the pathophysiology of SCI. We will also discuss the neurological outcomes of human SCI and the available experimental model systems that have been employed to identify SCI mechanisms and develop therapeutic strategies for this condition.
