INT105921
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
We also determined the intrahepatic localization of both HSC-targeted forms of 15dPGJ2. 15dPGJ2-M6PHSA predominantly accumulated in the HSC (64%) and Kupffer cells (39%). | |||||||||||||||
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The other construct 15dPGJ2-pPBHSA predominantly co-localizes with HSC and parenchymal cells. | |||||||||||||||
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In contrast, binding of 15dPGJ2-pPBHSA to cultured HSC was not affected by polyinosinic acid, suggesting that scavenger receptors are not involved in the binding of pPBHSA to HSC. | |||||||||||||||
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Here, we demonstrate that HSC migrate to the injured kidney and are even able to migrate into damaged tubules. | |||||||||||||||
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Unexpectedly, neutralization of endogenous SDF-1 or HSC-associated CXCR4 did not result in a significantly decreased migration of exogenous HSC to the ischemic injured or contralateral kidney (Figure 1C). | |||||||||||||||
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The neutralizing capacity of anti-CXCR4 was determined by adding HSC pre-incubated with CXCR4 (20 ? | |||||||||||||||
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Moreover, gating strategies to separate the CD34+ HSC from irrelevant cell populations, as well as inclusion of CD34dim and CD34bright populations were established. | |||||||||||||||
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To localize the exogenous HSC in the injured kidney, we visualized the presence of these cells in renal tissue. | |||||||||||||||
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However, we could not observe an increased migration of the HSC towards the ischemic or contralateral kidneys locally injected with recSDF-1 compared to the control group. | |||||||||||||||
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Twenty-four hours later, there was a significant (P = 0.03) increase in HSC migrating to the ischemic injured kidney compared to the contralateral kidney as assessed by flow cytometric analysis (Figure 1). | |||||||||||||||
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Another appealing option is represented by the administration of mobilizing/proliferating agents, such as G-CSF, that is able to both enhance the HSC mobilization into the peripheral blood and facilitate the endogenous LSC activation [5]. | |||||||||||||||
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This study indicates a clinical applicable protocol for the use of HSC mobilization to ameliorate radiation-induced damage.
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Considering the localization of hOATs, it was suggested that the interactions of hOATs with NSAIDs are associated with the pharmacokinetics and the induction of adverse reactions of NSAIDs. | |||||||||||||||
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General Comments
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