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Morehouse School of Medicine

Articles by Morehouse School of Medicine

Seroma formation as a rare complication of lateral epicondylitis release: A case report

Published on: 27th October, 2017

OCLC Number/Unique Identifier: 7286357077

Case: A 45 year old male, >1 year status post left elbow lateral debridement for lateral epicondylitis, presented with a two week history of a progressive, tender mass on the lateral aspect of his left elbow. MRI showed evidence of a defect in the joint capsule, consistent with the formation of a seroma. The patient underwent revision of the left lateral epicondyle debridement with ECRL/EDC tendon repair and capsular reconstruction. Conclusion: Tendon repair and capsular reconstruction is an effective and successful method for the treatment of a seroma caused by leakage of joint fluid after lateral epicondylar debridement.
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Differential roles of trithorax protein MLL-1 in regulating neuronal Ion channels

Published on: 8th September, 2021

OCLC Number/Unique Identifier: 9244745887

Repressive regulation of potassium channel genes by Polycomb group (PcG) proteins contributes to PcG protein-mediated neuroprotection against neuronal ischemic injury, as seen in an ischemic stroke. Here we asked the question whether Trithorax group (TrxG) proteins, the antagonistic partners of PcG proteins (i.e, epigenetic activators targeting the same genes) may also regulate potassium channels. Results of patch-clamp studies on cultured neuronal cells showed that inhibition of TrxG protein MLL-1 led to an increase in potassium channel activity, an unexpected effect for a presumed gene activator. In contrast, decreased sodium currents were observed with MLL-1 inhibition. Increased or decreased levels of potassium channel protein Kv2.1 or sodium channel protein Nav1.2, respectively, were seen with MLL-1 inhibition, as determined by immunocytochemistry. These results, for the first time, demonstrate an involvement of TrxG protein MLL-1 in regulating neuronal ion channels, potentially repressing potassium channel genes.
Cite this ArticleCrossMarkPublonsHarvard Library HOLLISGrowKudosResearchGateBase SearchOAI PMHAcademic MicrosoftScilitSemantic ScholarUniversite de ParisUW LibrariesSJSU King LibrarySJSU King LibraryNUS LibraryMcGillDET KGL BIBLiOTEKJCU DiscoveryUniversidad De LimaWorldCatVU on WorldCat
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