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Author Correction: Forecasting risk gene discovery in autism with machine learning and genome-scale data

Scientific reports 2020年第1期10卷 20994页

作者： Leo Brueggeman Tanner Koomar Jacob J Michaelson Department of Psychiatry University of Iowa Iowa City IA USA. Interdisciplinary Genetics Program University of Iowa Iowa City IA USA. Medical Scientist Training Program University of Iowa Iowa City IA USA. Department of Psychiatry University of Iowa Iowa City IA USA. jacob-michaelson@uiowa.edu. Interdisciplinary Genetics Program University of Iowa Iowa City IA USA. jacob-michaelson@uiowa.edu.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

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Short-term safety and effectiveness of a second-generation motion-guided total knee system

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Arthroplasty Today 2018年第2期4卷 240-243页

作者： Harris, Adam I. Luo, Tianyi David Lang, Jason E. Kopjar, Branko San Antonio Orthopaedic Specialists San Antonio TX United States Physician Scientist Training Program Wake Forest Baptist Medical Center Department of Orthopaedic Surgery Winston-Salem NC United States Blue Ridge Bone and Joint Arden NC United States Department of Health Services University of Washington Seattle WA United States

Background: Modern knee prostheses are designed to more closely replicate normal knee kinematics. The JOURNEY II Bi-Cruciate Stabilized Total Knee System (Smith & Nephew Inc., Memphis, TN) is a second-generation motion-guided knee system that demonstrates axial rotation patterns during flexion, which resemble those of the normal knee. The aim of this study was to assess the short-term safety and effectiveness of this system in standard clinical practice. Methods: A total of 186 subjects (209 primary total knee arthroplasties [TKAs]) were enrolled at 12 U.S. sites. Subjects were operated on between December 2011 and October 2013 and followed for 24 months. Radiographic, clinical, and patient-reported outcome data were collected at 6-, 12-, and 24-month postoperatively. Results: At 24-month follow-up, the average objective Knee Society Score was 96.20 (standard deviation [SD] = 6.63), the average satisfaction score was 35.22 (SD = 6.63), the average expectation score was 10.91 (SD = 3.16), and the average functional activities score was 81.49 (SD = 14.65). On a 0-10 scale, pain level for walking was 0.79 (SD = 1.51) and 1.50 (SD = 1.97) for climbing stairs or inclines. The cumulative incidence of reoperation at 2-year follow-up was 1.48% (95% confidence interval [CI] 0.48%-4.52%). Ten TKAs in 7 patients were treated with closed manipulations for stiffness. Iliotibial band syndrome was reported in 2 TKAs. Two deep infections occurred, 1 requiring reoperation. No dislocations occurred in the study cohort. Conclusions: In short-term follow-up, the JOURNEY II Bi-Cruciate Stabilized Guided Motion Total Knee System appears to be a safe and effective device for TKA. © 2017 The Authors

关键词： Guided motion Patient satisfaction TKA Total knee arthroplasty

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1683. Empathy Scale Validation Among Expectant Seroconcordant Couples Enrolled in HIV Care and Treatment in Zambézia Province, Mozambique

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Open Forum Infectious Diseases 2019年第SUPPLEMENT_2期6卷 S616–S616页

作者： Sack, Daniel DeSchacht, Caroline Erin, Graves Aaron, Kipp Barreto, Ezequiel Van Rompaey, Sara Audet, Carolyn Vanderbilt Medical Scientist Training Program Nashville Tennessee Friends in Global Health Maputo Maputo Mozambique Vanderbilt University Nashville Tennessee

Background Among patients enrolled in HIV care and treatment in rural Mozambique, 30% abandon treatment within a year. A cluster randomized controlled trial assessing the impact of couple-based vs. individual treatment for concordant couples on viral suppression (the HoPS+ trial) hypothesizes that harnessing family support will improve patient outcomes. Individuals with high levels of empathy will likely provide greater social support for treatment retention and adherence. This study validates a locally tailored version of the interpersonal reactivity index (IRI)—cognitive empathy (CE) and affective empathy (AE)—among expectant parents living with HIV in Zambézia province, Mozambique. Methods Using baseline data from 558 participants from the HOPS+ trial, we used a maximum likelihood exploratory factor analysis with a promax oblique rotation to assess the culturally relevant questions from the IRI. We examined discriminant and construct validity through analysis of subscale relationships by sex, age, education, and depression and intra-person reliability over time with an interclass correlation model ( n = 119). Results Our participants live in 6 districts and receive health care at 24 health facilities. The median age was 25 (IQR: 22 to 30), 50% were female, and 44% were single. Participants had a median of 5 years of formal education (IQR: 2–7). Half of them report their occupation as “farmer” and 17% screened positive for depression. On a scale of 0–4, the median baseline CE score was 2.6 (IQR: 1.9–3.2) and the median baseline AE score was 1.9 (IQR: 1–2.6). Males (2.6 vs. 2.4, P < 0.01), participants who finished primary school (2.7 vs. 2.5, P < 0.01), and older participants (2.6 vs. 2.5, P = 0.04) had higher CE scores, while depressed participants had higher AE scores (2.3 vs. 1.8, P < 0.01). We found moderate stability over time (CE ICC: 0.63, AE ICC: 0.54) in a subset of 119 study participants. Conclusion While depression is associated with 12.5% higher AE sco

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HMGA2 and protein leucine methylation drive pancreatic cancer lineage plasticity

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Nature communications 2025年第1期16卷 4866页

作者： Stephanie Dobersch Naomi Yamamoto Aidan Schutter Sarah M Cavender Tess M Robertson Nithya Kartha Annie N Samraj Ben Doron Lisa A Poole Cynthia L Wladyka Amy Zhang Gun Ho Jang Aswanth H Mahalingam Guillermo Barreto Srivatsan Raghavan Goutham Narla Faiyaz Notta Robert N Eisenman Andrew C Hsieh Sita Kugel Human Biology Division Fred Hutchinson Cancer Center Seattle WA USA. Medical Scientist Training Program University of Washington Seattle WA USA. Molecular & Cellular Biology Graduate Program University of Washington Seattle WA USA. Division of Transfusion Medicine Department of Laboratory Medicine University of Washington School of Medicine Seattle WA USA. PanCuRx Translational Research Initiative Ontario Institute for Cancer Research Toronto Ontario Canada. Department of Medical Oncology Dana-Farber Cancer Institute Boston MA USA. Université de Lorraine CNRS Laboratoire IMoPA Nancy France. Lung Cancer Epigenetic Max-Planck-Institute for Heart and Lung Research Bad Nauheim Germany. Broad Institute of MIT and Harvard Cambridge MA USA. Harvard Medical School Boston MA USA. Department of Medicine Brigham and Women's Hospital Boston MA USA. Division of Genetic Medicine Department of Internal Medicine University of Michigan Ann Arbor MI USA. Rogel Cancer Center University of Michigan Ann Arbor MI USA. Princess Margaret Cancer Centre University Health Network Toronto ON Canada. Department of Medical Biophysics University of Toronto Toronto ON Canada. Basic Sciences Division Fred Hutchinson Cancer Center Seattle WA USA. Department of Medicine University of Washington Seattle WA USA. Department of Genome Sciences University of Washington Seattle WA USA. Human Biology Division Fred Hutchinson Cancer Center Seattle WA USA. skugel@***. Department of Genome Sciences University of Washington Seattle WA USA. skugel@***.

Basal pancreatic ductal adenocarcinoma (PDAC) has the worst overall survival and is the only subtype that serves as an independent poor prognostic factor. We identify elevated levels of LIN28B and its downstream target, HMGA2, in basal PDAC. Notably, LIN28B significantly accelerates KRAS-driven PDAC progression in a mouse model. Here, we show that HMGA2 promotes basal PDAC pathogenesis by enhancing mRNA translation downstream of LIN28B. Mechanistically, HMGA2 suppresses leucine carboxyl methyltransferase 1 (LCMT1) at the chromatin level, reducing PP2A methylation and activity. This leads to increased phosphorylation of S6K and eIF4B, boosting mRNA translation. Additionally, HMGA2 downregulates B56α (PPP2R5A), disrupting functional PP2A holoenzyme assembly and further sustaining phosphorylated S6K levels. Impaired PP2A function mimics HMGA2's effects, reinforcing increased mRNA translation and basal lineage features. This work uncovers a critical link between the LIN28B/HMGA2 axis, protein synthesis, and PDAC lineage specificity via LCMT1-mediated PP2A methylation and B56α-PP2A disruption.

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Front Cover: Chemically Tuned Intracellular Gene Delivery by Core-Shell Nanoparticles: Effects of Proton Buffering, Acid Degradability, and Membrane Disruption (ChemMedChem 7/2022)

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ChemMedChem 2022年第7期17卷

作者： Dr. Soo Kyung Cho Rebecca T. Lee Prof. Yoon-Hwae Hwang Prof. Young Jik Kwon Crystal Bank PNU Pusan National University 2222 Nano Building Samnangjin-ro Miryang Gyeongsangnam-do 50463 Republic of Korea Department of Biomedical Engineering and Medical Scientist Training Program University of California Irvine B200 Sprague Hall Irvine CA 92697-3958 USA Department of Nano Energy Engineering Pusan National University Pusandaehak-ro 63 beon-gil 2 Jangjeon-dong Geumjung-gu Busan 46241 (Republic of Korea) Departments of Pharmaceutical Science Chemical and Biomolecular Engineering Biomedical Engineering and Molecular Biology and Biochemistry University of California Irvine 132 Sprague Hall Irvine CA 92697-3958 USA

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Exposure to Static Magnetic and Electric Fields Treats Type 2 Diabetes (vol 32, pg 561, 2020)

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CELL METABOLISM 2020年第6期32卷 1076-1076页

作者： Carter, Calvin S. Huang, Sunny C. Searby, Charles C. Cassaidy, Benjamin Miller, Michael J. Grzesik, Wojciech J. Piorczynski, Ted B. Pak, Thomas K. Walsh, Susan A. Acevedo, Michael Zhang, Qihong Mapuskar, Kranti A. Milne, Ginger L. Milne, Ginger L. Hinton, Antentor O., Jr. Guo, Deng-Fu Weiss, Robert Bradberry, Kyle Taylor, Eric B. Rauckhorst, Adam J. Dick, David W. Akurathi, Vamsidhar Falls-Hubert, Kelly C. Wagner, Brett A. Carter, Walter A. Wang, Kai Norris, Andrew W. Rahmouni, Kamal Buettner, Garry R. Hansen, Jason M. Spitz, Douglas R. Abel, E. Dale Sheffield, Val C. Department of Pediatrics and Division of Medical Genetics and Genomics University of Iowa Hospitals & Clinics Iowa City IA USA Medical Scientist Training Program Roy J. and Lucille A. Carver College of Medicine University of Iowa Iowa City IA USA Department of Physics and Astronomy University of Iowa Iowa City IA USA Fraternal Order of Eagles Diabetes Research Center Roy J. and Lucille A. Carver College of Medicine University of Iowa Iowa City IA USA Department of Physiology and Developmental Biology Brigham Young University Provo UT USA Department of Radiology Division of Nuclear Medicine University of Iowa Hospitals & Clinics Iowa City IA USA Free Radical and Radiation Biology Program Department of Radiation Oncology Holden Comprehensive Cancer Center University of Iowa Hospitals & Clinics Iowa City IA USA Department of Pharmacology Vanderbilt University Medical Center Nashville TN USA Department of Neuroscience and Pharmacology University of Iowa Hospitals & Clinics Iowa City IA USA Department of Internal Medicine Division of Cardiology University of Iowa Hospitals & Clinics Iowa City IA USA Department of Molecular Physiology and Biophysics University of Iowa Hospitals & Clinics Iowa City IA USA Department of Internal Medicine Division of Endocrinology and Metabolism University of Iowa Hospitals & Clinics Iowa City IA USA College of Public Health Department of Biostatistics University of Iowa Iowa City IA USA

Aberrant redox signaling underlies the pathophysiology of many chronic metabolic diseases, including type 2 diabetes (T2D). Methodologies aimed at rebalancing systemic redox homeostasis have had limited success. A noninvasive, sustained approach would enable the long-term control of redox signaling for the treatment of T2D. We report that static magnetic and electric fields (sBE) noninvasively modulate the systemic GSH-to-GSSG redox couple to promote a healthier systemic redox environment that is reducing. Strikingly, when applied to mouse models of T2D, sBE rapidly ameliorates insulin resistance and glucose intolerance in as few as 3 days with no observed adverse effects. Scavenging paramagnetic byproducts of oxygen metabolism with SOD2 in hepatic mitochondria fully abolishes these insulin sensitizing effects, demonstrating that mitochondrial superoxide mediates induction of these therapeutic changes. Our findings introduce a remarkable redox-modulating phenomenon that exploits endogenous electromagneto-receptive mechanisms for the noninvasive treatment of T2D, and potentially other redox-related diseases.

关键词： redox type 2 diabetes insulin resistance electromagnetic fields ROS superoxide glutathione radical pair mechanism mitochondria liver

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Correction to: USP20 positively regulates tumorigenesis and chemoresistance through β-catenin stabilization

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Cell death and differentiation 2023年第3期30卷 857-858页

作者： Chenming Wu Kuntian Luo Fei Zhao Ping Yin Ying Song Min Deng Jinzhou Huang Yuping Chen Lei Li SeungBaek Lee JungJin Kim Qin Zhou Xinyi Tu Somaira Nowsheen Qifeng Luo Xiumei Gao Zhenkun Lou Zhongmin Liu Jian Yuan Research Center for Translational Medicine East Hospital Tongji University School of Medicine Shanghai 200120 China. Key Laboratory of Arrhythmias of the Ministry of Education of China East Hospital Tongji University School of Medicine Shanghai 200120 China. Department of Oncology Mayo Clinic Rochester MN 55905 USA. Department of Pathology East Hospital Shanghai 200120 China. Mayo Clinic Medical Scientist Training Program Mayo Clinic School of Medicine and Mayo Clinic Graduate School of Biomedical Sciences Mayo Clinic Rochester MN 55905 USA. Department of Molecular Pharmacology and Experimental Therapeutics Mayo Clinic Rochester MN 55905 USA. Department of Gastrointestinal Surgery Shanghai East Hospital School of Medicine Tongji University Shanghai 200120 Shanghai P. R. China. Tianjin State Key Laboratory of Modern Chinese Medicine Tianjin University of Traditional Chinese Medicine 300193 Tianjin China. Department of Oncology Mayo Clinic Rochester MN 55905 USA. Lou.zhenkun@mayo.edu. Research Center for Translational Medicine East Hospital Tongji University School of Medicine Shanghai 200120 China. Zhongmin_Liu@***. Key Laboratory of Arrhythmias of the Ministry of Education of China East Hospital Tongji University School of Medicine Shanghai 200120 China. Zhongmin_Liu@***. Research Center for Translational Medicine East Hospital Tongji University School of Medicine Shanghai 200120 China. Yuanjian229@***. Key Laboratory of Arrhythmias of the Ministry of Education of China East Hospital Tongji University School of Medicine Shanghai 200120 China. Yuanjian229@***. Department of Oncology Mayo Clinic Rochester MN 55905 USA. Yuanjian229@***. Department of Molecular Pharmacology and Experimental Therapeutics Mayo Clinic Rochester MN 55905 USA. Yuanjian229@***.

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Bilateral pseudo-internuclear ophthalmoplegia in a patient with myasthenia gravis

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American Journal of Ophthalmology Case Reports 2018年 12卷 76-78页

作者： McClard, Cynthia K. Lyons, Lance J. Yalamanchili, Sushma School of Medicine Baylor College of Medicine Houston TX United States School of Medicine Baylor College of Medicine Medical Scientist Training Program Houston TX United States Department of Ophthalmology UTMB Galveston TX United States Department of Ophthalmology Methodist Eye Associates Blanton Eye Institute Houston Methodist Hospital Houston TX United States

Purpose: To report a case of myasthenia gravis presenting with a false localizing sign, a bilateral pseudo internuclear ophthalmoplegia. Observations: A 61 year-old male presented with a five-week history of painless binocular oblique diplopia that was associated with fatigue, vocal hoarseness and bilateral ptosis, the latter two of which worsened through the course of the day. Exam was remarkable for an apparent bilateral internuclear ophthalmoplegia (INO). MRI of the brain with and without contrast and MRA of the head and neck were within normal limits. Lab work was positive for anti-AChR binding, blocking, and modulating antibodies, as well as anti-striated muscle and anti-titin antibodies. The patient was initiated on therapy for myasthenia gravis. Conclusion and importance: Although myasthenia gravis often presents with ptosis or diplopia, rarely patients may develop pseudo-INO secondary to extraocular muscle weakness. True INO occurs with damage to the medial longitudinal fasciculus, a myelinated tract of fibers that controls yoked horizontal eye movements. Clinicians should be suspicious of the false localizing sign of a pseudo-INO associated with myasthenia gravis when more common causes of INO have been excluded. © 2018

关键词： False localizing signs Myasthenia gravis Ocular myasthenia gravis Pseudo internuclear ophthalmoplegia

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Correction: Multi-modal proteomic characterization of lysosomal function and proteostasis in progranulin-deficient neurons

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Molecular neurodegeneration 2023年第1期18卷 96页

作者： Saadia Hasan Michael S Fernandopulle Stewart W Humble Ashley M Frankenfield Haorong Li Ryan Prestil Kory R Johnson Brent J Ryan Richard Wade-Martins Michael E Ward Ling Hao National Institute of Neurological Disorders and Stroke (NINDS) National Institutes of Health (NIH) Bethesda MD USA. Department of Neurodegenerative Disease UK Dementia Research Institute Institute of Neurology University College London London UK. Augusta University University of Georgia Medical Partnership Athens GA USA. Cambridge Institute for Medical Research University of Cambridge Cambridge UK. Medical Scientist Training Program Feinberg School of Medicine Northwestern University Chicago IL USA. Department of Physiology Anatomy and Genetics Oxford Parkinson's Disease Centre Kavli Institute for Nanoscience Discovery University of Oxford Dorothy Crowfoot Hodgkin Building South Parks Road OX1 3QU Oxford UK. Department of Chemistry George Washington University Washington DC USA. National Institute of Neurological Disorders and Stroke (NINDS) National Institutes of Health (NIH) Bethesda MD USA. wardme@nih.gov. Department of Chemistry George Washington University Washington DC USA. linghao@gwu.edu.

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Poorer dexterity is associated with underlying Alzheimer’s disease brain pathology

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Alzheimer's & Dementia 2022年第S6期18卷

作者： Lily Eliza Gupta Akshay Kohli Jennifer M. Oh Kao Lee Yang Tobey J Betthauser Nathaniel A. Chin Veena A. Nair Vivek Prabhakaran Ozioma C. Okonkwo Shi-Jiang Li Barbara B. Bendlin Alzheimer's Disease Research Center University of Wisconsin-Madison School of Medicine and Public Health Madison WI USA Wisconsin Alzheimer's Disease Research Center University of Wisconsin School of Medicine and Public Health Madison WI USA Department of Medicine University of Wisconsin-Madison School of Medicine and Public Health Madison WI USA Neuroscience Training Program University of Wisconsin School of Medicine and Public Health Madison WI USA University of Wisconsin School of Medicine and Public Health Madison WI USA Neuroscience and Public Policy Program University of Wisconsin Madison WI USA Wisconsin Alzheimer’s Institute University of Wisconsin-Madison School of Medicine and Public Health Madison WI USA Geriatric Research Education and Clinical Center William S. Middleton Veterans Hospital Madison WI USA Department of Radiology University of Wisconsin School of Medicine and Public Health Madison WI USA Medical College of Wisconsin Milwaukee WI USA Department of Medicine University of Wisconsin School of Medicine and Public Health Madison WI USA

Background There has been increasing recognition for the decline of motor function in Alzheimer’s disease (AD) progression and its substantial role in disease morbidity. However, less is known about regional pathology burden—including amyloid-β and tau protein deposition and cortical trophy—and its relationship to motor performance. Here investigate this relationship using standardized motor function assessment tools. Method Participants along a control-to-impaired continuum were enrolled in the Alzheimer’s Disease Connectome Project and underwent T1-weighted MRI (N=206), with a subset undergoing [C-11]PiB (N=61) and [F-18 ]Flortaucipir PET (N=58) (Table 1) imaging for amyloid and tau pathology, respectively. T1-weighted scans were processed using Freesurfer to estimate regional cortical thickness. [C-11]PiB distribution volume ratios (DVR; cerebellar GM reference region) and [F-18] Flortaucipir standardized uptake value ratios (SUVr; inferior cerebellar GM reference region) were assessed. Regions of interest (ROI) for analysis included the parahippocampal, entorhinal, motor, and frontal regions. Motor function was assessed utilizing NIH toolbox tests including the 2-minute walking, 9-hole pegboard dexterity, and dynamometer grip strength assessments. Motor performance was analyzed using participants uncorrected standardized scores. Scores were collected from participant-reported dominant hand assessments. Multiple linear regression models tested relationships between AD biomarker burden and motor performance while controlling for age and sex of participants. Result Increased amyloid-β (β-0.42, p-value: <0.05) and tau (β: -0.53, p-value: <0.05) burden in primary motor cortices were associated with worse dexterity scores independent of age and sex. Grip strength did not show a significant correlation to cortical amyloid-β (β: -0.14, p-value 0.33) or tau burden (β: 0.23, p-value: 0.36). Higher cortical thickness in primary motor regions were associated with higher dex

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