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Paulo César Rodrigues Palma,Marilene Vale de Castro Monteiro,Marta Alicia Ledesma,Sebastián Altuna,Juan José Luis Sardi,Cássio Luís Zanettini Riccetto 대한배뇨장애요실금학회 2018 International Neurourology Journal Vol.22 No.3
Purpose: To evaluate the safety and efficacy of a surgical polypropylene mesh for correction of anterior vaginal prolapse, with or without apical defects, by providing simultaneous reinforcement at the anterior and apical aspects of the vagina with a single- incision approach. Methods: This was a prospective, multicenter, single-arm study involving women with baseline stage ≥2 anterior and/or apical vaginal wall prolapse according to the Pelvic Organ Prolapse Quantification (POP-Q) system. The primary endpoint was defined as achievement of POP-Q stage ≤1 status. Additionally, patient-reported outcomes were assessed using the International Consultation on Incontinence Questionnaire-Vaginal Symptoms (ICIQ-VS). The device under evaluation was Calistar A, which is fixed posteriorly to the sacrospinous ligaments with a novel tissue-anchoring system (TAS) and anteriorly to the obturator internus muscles. Postoperative follow-ups were scheduled at 7 days and at 6, 12, and 24 months. Results: Ninety-seven women were treated and assessed for the primary outcome. They were followed for up to 2 years (n=43), with a median of 12 months. Objective cure was achieved in 86 of the 97 patients (88.7%) (P<0.0005). The mean reduction in the ICIQ-VS scores was in the range of 70%–90% for every time point (P<0.05). No bleeding or surgical revision was reported. Mesh exposure occurred in 7 patients (7.2%), urinary retention in 5 (5.2%), de novo dyspareunia in 3 (3.1%), and urinary tract infections in 7 (7.2%). Conclusions: This midterm follow-up showed that apical and anterior vaginal reinforcement with a polypropylene implant fixed with a TAS provided good anatomical correction, with no major complications.
Border Control—A Membrane-Linked Interactome of <i>Arabidopsis</i>
Jones, Alexander M.,Xuan, Yuanhu,Xu, Meng,Wang, Rui-Sheng,Ho, Cheng-Hsun,Lalonde, Sylvie,You, Chang Hun,Sardi, Maria I.,Parsa, Saman A.,Smith-Valle, Erika,Su, Tianying,Frazer, Keith A.,Pilot, Guillaum American Association for the Advancement of Scienc 2014 Science Vol.344 No.6185
<P>Cellular membranes act as signaling platforms and control solute transport. Membrane receptors, transporters, and enzymes communicate with intracellular processes through protein-protein interactions. Using a split-ubiquitin yeast two-hybrid screen that covers a test-space of 6.4 x 10(6) pairs, we identified 12,102 membrane/signaling protein interactions from Arabidopsis. Besides confirmation of expected interactions such as heterotrimeric G protein subunit interactions and aquaporin oligomerization, >99% of the interactions were previously unknown. Interactions were confirmed at a rate of 32% in orthogonal in planta split-green flourescent protein interaction assays, which was statistically indistinguishable from the confirmation rate for known interactions collected from literature (38%). Regulatory associations in membrane protein trafficking, turnover, and phosphorylation include regulation of potassium channel activity through abscisic acid signaling, transporter activity by a WNK kinase, and a brassinolide receptor kinase by trafficking-related proteins. These examples underscore the utility of the membrane/signaling protein interaction network for gene discovery and hypothesis generation in plants and other organisms.</P>
Loss of glucocerebrosidase 1 activity causes lysosomal dysfunction and α-synuclein aggregation
Bae, Eun-Jin,Yang, Na Young,Lee, Cheolsoon,Lee, He-Jin,Kim, Seokjoong,Sardi, Sergio Pablo,Lee, Seung-Jae Nature Publishing Group 2015 Experimental and molecular medicine Vol.47 No.3
<P>Lysosomal dysfunction is a common pathological feature of neurodegenerative diseases. GTP-binding protein type A1 (<I>GBA1</I>) encodes β-glucocerebrosidase 1 (GCase 1), a lysosomal hydrolase. Homozygous mutations in <I>GBA1</I> cause Gaucher disease, the most common lysosomal storage disease, while heterozygous mutations are strong risk factors for Parkinson's disease. However, whether loss of GCase 1 activity is sufficient for lysosomal dysfunction has not been clearly determined. Here, we generated human neuroblastoma cell lines with nonsense mutations in the <I>GBA1</I> gene using zinc-finger nucleases. Depending on the site of mutation, GCase 1 activity was lost or maintained. The cell line with GCase 1 deficiency showed indications of lysosomal dysfunction, such as accumulation of lysosomal substrates, reduced dextran degradation and accumulation of enlarged vacuolar structures. In contrast, the cell line with C-terminal truncation of GCase 1 but with intact GCase 1 activity showed normal lysosomal function. When α-synuclein was overexpressed, accumulation and secretion of insoluble aggregates increased in cells with GCase 1 deficiency but did not change in mutant cells with normal GCase 1 activity. These results demonstrate that loss of GCase 1 activity is sufficient to cause lysosomal dysfunction and accumulation of α-synuclein aggregates.</P>