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- 저자 : Strong Amy L. (검색결과 2 건)
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Yoon, Jaeseung,Ben-Ami, Hagit Cohen,Hong, Young Seok,Park, Soyeon,Strong, Lydia L.R.,Bowman, John,Geng, Chaoxian,Baek, Kwanghee,Minke, Baruch,Pak, William L. 경희대학교 생명자원과학연구원 2000 硏究論文集 Vol.21 No.-
The Drosophila trp gene encodes a light-activated Ca^(2+) channel subunit, which is a prototypical member of a novel class of channel proteins. Previously identified trp mutants are all recessive, loss-of-function mutants characterized by a transient receptor potential and the total or near-total loss of functional TRP protein. Although retinal degeneration does occur in these mutants, it is relatively mild and slow in onset. We report herein a new mutant, Trp^(p365), that does not display the transient receptor potential phenotype and is characterized by a substantial level of the TAP protein and rapid, semi-dominant degeneration of photoreceptors. We show that, in spite of its unusual phenotypes, Trp^(p365) is a trp allele because a Trp^(p365) transgene induces the mutant phenotype in a wild-type back-ground, and a wild-type trp transgene in a Trp^(p365) background suppresses the mutant phenotype. Moreover, amino acid alterations that could cause the Trp^(p365) phenotype are found in the transmembrane segment region of the mutant channel protein. Whole-cell recordings clarified the mechanism underlying the retinal degeneration by showing that the TRP channels of Trp^(p365) are constitutively active. Although several genes, when mutated, have been shown to cause retinal degeneration in Drosophila, the underlying mechanism has not been identified for any of them. The present studies provide evidence for a specific mechanism for massive degeneration of photoreceptors in Drosophila. Insofar as some human homologs of TRP are highly expressed in the brain, a similar mechanism could be a major contributor to degenerative disorders of the brain.
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Flexor Tendon Rupture Secondary to Gout
Lynn Jeremy V.,Strong Amy L.,Chung Kevin C. 대한성형외과학회 2023 Archives of Plastic Surgery Vol.50 No.5
Extra-articular deposition of monosodium urate crystals is a widely recognized manifestation of gout. However, gouty infiltration of flexor tendons in the hand resulting in tendon rupture is exceedingly rare. This case report highlights a patient with gouty infiltration of flexor tendons in the right middle finger resulting in rupture of both the flexor digitorum profundus and flexor digitorum superficialis. Given the extent of gouty infiltration and need for pulley reconstruction, the patient was treated with two-stage flexor tendon reconstruction. Febuxostat was prescribed preoperatively to limit further deposition of monosodium urate crystals and continued postoperatively to maximize the potential for long-lasting results. Prednisone was prescribed between the first- and second-stage operations to prevent a gout flare while the silicone rod was in place. In summary, tendon rupture secondary to gouty infiltration is the most likely diagnosis in patients with a history of gout presenting with tendon insufficiency.
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