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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.
Kapil Sethi,Michael Bozin,Tebogo Jabane,Richard McMullin,David Cook,Rob Forsyth,Lachlan Dodds,Lydia Johns Putra 대한비뇨의학회 2017 Investigative and Clinical Urology Vol.58 No.6
Purpose: To report our outcomes with the use of a thermo-expandable metallic intraprostatic stent (Memokath) for patients with bladder outlet obstruction (BOO) secondary to prostatic obstruction, and to assess it is a feasible option for many frail and elderly men unsuitable for surgery. Materials and Methods: We reviewed patients who underwent insertion of a Memokath stent for BOO over 17 years (January 1999 to December 2015) at one regional center over a long follow-up period (median, 7 years). Patients were selected if they had obstructive urinary symptoms or urinary retention with an indwelling catheter in situ, and were ineligible for transurethral resection of the prostate (TURP) under general or spinal anesthesia. Primary outcomes assessed were the improvement in urinary symptoms and voiding parameters, as well as the ability to void spontaneously if catheterized, along with complications. Results: One hundred forty-four patients who presented with BOO or urinary retention had a Memokath stent inserted. Ninety patients (62.5%) had a successful stent insertion with a significant difference between the median preoperative (550 mL) and postoperative residual volume (80 mL, p<0.0001). Nearly two-thirds of men (64%) returned to unassisted voiding with no increased risk of complications over time. Fifty-four patients (37.5%) experienced stent failure. Main complications requiring stent removal or repositioning were migration, occlusion, refractory urinary retention and irritative voiding symptoms. Conclusions: In elderly and frail men with BOO deemed unsuitable to undergo TURP, prostatic stent is a safe and practical alternative to long-term catheterization.