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Institution

University of California, Irvine

EducationIrvine, California, United States
About: University of California, Irvine is a education organization based out in Irvine, California, United States. It is known for research contribution in the topics: Population & Galaxy. The organization has 47031 authors who have published 113602 publications receiving 5521832 citations. The organization is also known as: UC Irvine & UCI.
Topics: Population, Galaxy, Poison control, Cancer, Gene


Papers
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Journal ArticleDOI
14 Sep 2012-Cell
TL;DR: Property intrinsic to early-stage neurons can overcome the inhibitory milieu of the injured adult spinal cord to mount remarkable axonal growth, resulting in formation of new relay circuits that significantly improve function.

755 citations

Journal ArticleDOI
24 Oct 2017-JAMA
TL;DR: It is suggested that robotic-assisted laparoscopic surgery, when performed by surgeons with varying experience with robotic surgery, does not confer an advantage in rectal cancer resection.
Abstract: Importance Robotic rectal cancer surgery is gaining popularity, but limited data are available regarding safety and efficacy. Objective To compare robotic-assisted vs conventional laparoscopic surgery for risk of conversion to open laparotomy among patients undergoing resection for rectal cancer. Design, Setting, and Participants Randomized clinical trial comparing robotic-assisted vs conventional laparoscopic surgery among 471 patients with rectal adenocarcinoma suitable for curative resection conducted at 29 sites across 10 countries, including 40 surgeons. Recruitment of patients was from January 7, 2011, to September 30, 2014, follow-up was conducted at 30 days and 6 months, and final follow-up was on June 16, 2015. Interventions Patients were randomized to robotic-assisted (n = 237) or conventional (n = 234) laparoscopic rectal cancer resection, performed by either high (upper rectum) or low (total rectum) anterior resection or abdominoperineal resection (rectum and perineum). Main Outcomes and Measures The primary outcome was conversion to open laparotomy. Secondary end points included intraoperative and postoperative complications, circumferential resection margin positivity (CRM+) and other pathological outcomes, quality of life (36-Item Short Form Survey and 20-item Multidimensional Fatigue Inventory), bladder and sexual dysfunction (International Prostate Symptom Score, International Index of Erectile Function, and Female Sexual Function Index), and oncological outcomes. Results Among 471 randomized patients (mean [SD] age, 64.9 [11.0] years; 320 [67.9%] men), 466 (98.9%) completed the study. The overall rate of conversion to open laparotomy was 10.1%: 19 of 236 patients (8.1%) in the robotic-assisted laparoscopic group and 28 of 230 patients (12.2%) in the conventional laparoscopic group (unadjusted risk difference = 4.1% [95% CI, −1.4% to 9.6%]; adjusted odds ratio = 0.61 [95% CI, 0.31 to 1.21];P = .16). The overall CRM+ rate was 5.7%; CRM+ occurred in 14 (6.3%) of 224 patients in the conventional laparoscopic group and 12 (5.1%) of 235 patients in the robotic-assisted laparoscopic group (unadjusted risk difference = 1.1% [95% CI, −3.1% to 5.4%]; adjusted odds ratio = 0.78 [95% CI, 0.35 to 1.76];P = .56). Of the other 8 reported prespecified secondary end points, including intraoperative complications, postoperative complications, plane of surgery, 30-day mortality, bladder dysfunction, and sexual dysfunction, none showed a statistically significant difference between groups. Conclusions and Relevance Among patients with rectal adenocarcinoma suitable for curative resection, robotic-assisted laparoscopic surgery, as compared with conventional laparoscopic surgery, did not significantly reduce the risk of conversion to open laparotomy. These findings suggest that robotic-assisted laparoscopic surgery, when performed by surgeons with varying experience with robotic surgery, does not confer an advantage in rectal cancer resection. Trial Registration isrctn.org Identifier:ISRCTN80500123

754 citations

Journal ArticleDOI
Jarrod Chapman1, Ewen F. Kirkness2, Oleg Simakov3, Oleg Simakov4, Steven E. Hampson5, Therese Mitros4, Thomas Weinmaier6, Thomas Rattei6, Prakash G. Balasubramanian3, Jon Borman2, Dana A. Busam2, Kathryn Disbennett2, Cynthia Pfannkoch2, Nadezhda Sumin2, Granger G. Sutton2, Lakshmi D. Viswanathan2, Brian P. Walenz2, David Goodstein1, Uffe Hellsten1, Takeshi Kawashima4, Simon E. Prochnik1, Nicholas H. Putnam1, Nicholas H. Putnam4, Nicholas H. Putnam7, Shengquiang Shu1, Bruce Blumberg5, Catherine E. Dana5, Lydia Gee5, Dennis F. Kibler5, Lee Law5, Dirk Lindgens5, Daniel E. Martínez8, Jisong Peng5, Philip A. Wigge9, Philip A. Wigge7, Bianca Bertulat3, Corina Guder3, Yukio Nakamura3, Suat Özbek3, Hiroshi Watanabe3, Konstantin Khalturin10, Georg Hemmrich10, Andre Franke10, René Augustin10, Sebastian Fraune10, Eisuke Hayakawa11, Shiho Hayakawa11, Mamiko Hirose11, Jung Shan Hwang11, Kazuho Ikeo11, Chiemi Nishimiya-Fujisawa11, Atshushi Ogura11, Atshushi Ogura7, Toshio Takahashi, Patrick R. H. Steinmetz12, Xiaoming Zhang13, Roland Aufschnaiter14, Marie Kristin Eder14, Anne Kathrin Gorny7, Anne Kathrin Gorny14, Willi Salvenmoser14, Alysha M. Heimberg15, Benjamin M. Wheeler16, Kevin J. Peterson15, Angelika Böttger17, Patrick Tischler6, Alexander Wolf17, Takashi Gojobori11, Karin A. Remington7, Karin A. Remington2, Robert L. Strausberg2, J. Craig Venter2, Ulrich Technau12, Bert Hobmayer14, Thomas C. G. Bosch10, Thomas W. Holstein3, Toshitaka Fujisawa11, Hans R. Bode5, Charles N. David17, Daniel S. Rokhsar4, Daniel S. Rokhsar1, Robert Steele5 
25 Mar 2010-Nature
TL;DR: Comparisons of the Hydra genome to the genomes of other animals shed light on the evolution of epithelia, contractile tissues, developmentally regulated transcription factors, the Spemann–Mangold organizer, pluripotency genes and the neuromuscular junction.
Abstract: The freshwater cnidarian Hydra was first described in 17021 and has been the object of study for 300 years. Experimental studies of Hydra between 1736 and 1744 culminated in the discovery of asexual reproduction of an animal by budding, the first description of regeneration in an animal, and successful transplantation of tissue between animals2. Today, Hydra is an important model for studies of axial patterning3, stem cell biology4 and regeneration5. Here we report the genome of Hydra magnipapillata and compare it to the genomes of the anthozoan Nematostella vectensis6 and other animals. The Hydra genome has been shaped by bursts of transposable element expansion, horizontal gene transfer, trans-splicing, and simplification of gene structure and gene content that parallel simplification of the Hydra life cycle. We also report the sequence of the genome of a novel bacterium stably associated with H. magnipapillata. Comparisons of the Hydra genome to the genomes of other animals shed light on the evolution of epithelia, contractile tissues, developmentally regulated transcription factors, the Spemann–Mangold organizer, pluripotency genes and the neuromuscular junction.

754 citations

Journal ArticleDOI
01 Jun 2019-Brain
TL;DR: A recently recognized brain disorder that mimics the clinical features of Alzheimer’s disease: Limbic-predominant Age-related TDP-43 Encephalopathy (LATE).
Abstract: We describe a recently recognized disease entity, limbic-predominant age-related TDP-43 encephalopathy (LATE). LATE neuropathological change (LATE-NC) is defined by a stereotypical TDP-43 proteinopathy in older adults, with or without coexisting hippocampal sclerosis pathology. LATE-NC is a common TDP-43 proteinopathy, associated with an amnestic dementia syndrome that mimicked Alzheimer's-type dementia in retrospective autopsy studies. LATE is distinguished from frontotemporal lobar degeneration with TDP-43 pathology based on its epidemiology (LATE generally affects older subjects), and relatively restricted neuroanatomical distribution of TDP-43 proteinopathy. In community-based autopsy cohorts, ∼25% of brains had sufficient burden of LATE-NC to be associated with discernible cognitive impairment. Many subjects with LATE-NC have comorbid brain pathologies, often including amyloid-β plaques and tauopathy. Given that the 'oldest-old' are at greatest risk for LATE-NC, and subjects of advanced age constitute a rapidly growing demographic group in many countries, LATE has an expanding but under-recognized impact on public health. For these reasons, a working group was convened to develop diagnostic criteria for LATE, aiming both to stimulate research and to promote awareness of this pathway to dementia. We report consensus-based recommendations including guidelines for diagnosis and staging of LATE-NC. For routine autopsy workup of LATE-NC, an anatomically-based preliminary staging scheme is proposed with TDP-43 immunohistochemistry on tissue from three brain areas, reflecting a hierarchical pattern of brain involvement: amygdala, hippocampus, and middle frontal gyrus. LATE-NC appears to affect the medial temporal lobe structures preferentially, but other areas also are impacted. Neuroimaging studies demonstrated that subjects with LATE-NC also had atrophy in the medial temporal lobes, frontal cortex, and other brain regions. Genetic studies have thus far indicated five genes with risk alleles for LATE-NC: GRN, TMEM106B, ABCC9, KCNMB2, and APOE. The discovery of these genetic risk variants indicate that LATE shares pathogenetic mechanisms with both frontotemporal lobar degeneration and Alzheimer's disease, but also suggests disease-specific underlying mechanisms. Large gaps remain in our understanding of LATE. For advances in prevention, diagnosis, and treatment, there is an urgent need for research focused on LATE, including in vitro and animal models. An obstacle to clinical progress is lack of diagnostic tools, such as biofluid or neuroimaging biomarkers, for ante-mortem detection of LATE. Development of a disease biomarker would augment observational studies seeking to further define the risk factors, natural history, and clinical features of LATE, as well as eventual subject recruitment for targeted therapies in clinical trials.

753 citations


Authors

Showing all 47751 results

NameH-indexPapersCitations
Daniel Levy212933194778
Rob Knight2011061253207
Lewis C. Cantley196748169037
Dennis W. Dickson1911243148488
Terrie E. Moffitt182594150609
Joseph Biederman1791012117440
John R. Yates1771036129029
John A. Rogers1771341127390
Avshalom Caspi170524113583
Yang Gao1682047146301
Carl W. Cotman165809105323
John H. Seinfeld165921114911
Gregg C. Fonarow1611676126516
Jerome I. Rotter1561071116296
David Cella1561258106402
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
20242
2023252
20221,224
20216,518
20206,348
20195,610