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Urine Leak Following Kidney Transplantation: An Evidence-based Management Plan

Published on: 2nd October, 2018

OCLC Number/Unique Identifier: 7869210591

Care of kidney transplant recipient remains complex and long-term graft survival is not seen in every transplant recipient. Due to reduced supply and increased demand of human organs, more transplants are carried out using marginal grafts on emergency lists. Transplant recipients have altered physiology due to known end-stage renal disease, recent surgery and the use of potent analgesic and immunosuppressive medications. Amongst the known surgical complications, urine leak remains the most common. It can result from poor graft preparation due to excessive peri ureteric or lower pole dissection or damage to lower polar artery resulting in ischemic necrosis. In addition, poor surgical technique, bladder outflow obstruction, iatrogenic injury to bladder or renal pelvis may contribute to urine leak. Ongoing urine leak may manifest itself as swelling, pain, high drain output, sepsis, ileus and eventual graft loss. Early identification, localisation and quantification of leak remain essential in management of these patients. In addition, sepsis should be identified and treated promptly as these patients are highly susceptible to infections. Early recognition of this complication can significantly reduce hospital stay, improve quality of life and reduce graft loss and mortality. In this article, we aim to develop an evidence-based management approach to a patient with urine leak using a clinical scenario.
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Carbonic Anhydrase I modifies SOD1-induced motor neuron toxicity in Drosophila via ER stress pathway

Published on: 1st August, 2019

OCLC Number/Unique Identifier: 8195612915

Background: Drosophila models of amyotrophic lateral sclerosis (ALS) have been widely used in understanding molecular mechanisms of ALS pathogenesis as well as discovering potential targets for therapeutic drugs. Mutations in the copper/zinc superoxide dismutase (SOD1) cause ALS by gain of toxic functions and induce toxicity in fly motor neurons. Results: In this study, we have determined that human carbonic anhydrase I (CA1) can alleviate mutant SOD1-induced motor neuron toxicity in the transgenic fly model of ALS. Interestingly, we found that motor neuron expression of CA1 could independently induce locomotion defect as well as decreasing the survival rate. In addition, CA1-induced toxicity in motor neurons is anhydrase activity-dependent. Mechanistically, we identified that both SOD1- and CA1-induced toxicity involve the activation of eIF2α in the ER stress response pathway. Downstream activation of the JNK pathway has also been implicated in the induced toxicity. Conclusion: Our results have confirmed that SOD1-induced toxicity in fly motor neuron also involves endoplasmic reticulum (ER) stress pathway. More importantly, we have discovered a new cellular role that CA1 plays by antagonizing mutant SOD1-induced toxicity in motor neurons involving the ER stress pathway. Such information can be potentially useful for further understanding disease mechanisms and developing therapeutic targets for ALS. 
Cite this ArticleCrossMarkPublonsHarvard Library HOLLISGrowKudosResearchGateBase SearchOAI PMHAcademic MicrosoftScilitSemantic ScholarUniversite de ParisUW LibrariesSJSU King LibrarySJSU King LibraryNUS LibraryMcGillDET KGL BIBLiOTEKJCU DiscoveryUniversidad De LimaWorldCatVU on WorldCat