Publications by authors named "S Louis Bridges"

335 Publications

3-Dimensional simulations and student learning in orthodontic education.

Eur J Dent Educ 2021 Sep 16. Epub 2021 Sep 16.

Division of Pediatric Dentistry and Orthodontics, Faculty of Dentistry, The University of Hong Kong, Hong Kong, China.

Introduction: The electronic dental model (e-model) is an example of a digital 3-Dimensional technology to support inquiry-based learning in undergraduate dental education. As student perceptions of and engagement with e-models vary, it is uncertain whether these perceptions have implications for their learning processes and outcomes.

Methods: Third-year dental students (N=40) completed a questionnaire to identify their perceptions of and preferences for model modalities. They were divided into three groups based on their preference: Preferring plaster models(Group 1); Preferring e-models(Group 2); No preference(Group 3). Students from three groups (N=9) attended a hands-on digital occlusion evaluation workshop, and then completed a case-based diagnostic evaluation test using digital occlusion evaluation software. Camtasia Studio™ recorded real-time and on-screen data of the number of mouse-clicks and time spent.

Results: Students reported positive feedbacks on the use of e-models, and 72.5% of the students preferred combination use of e-models and plaster models. After attending the hands-on digital dental occlusion evaluation workshop, Group 2 scored higher on the diagnostic evaluation test (p<0.05) and registered more mouse-clicks than Group 1 when evaluating the arch symmetry (p<0.05). Group 2 registered fewer mouse-clicks than Group 3during tooth size measurement (p<0.05). There was no significant difference regarding the time used to answer the knowledge questions among the three groups.

Conclusion: Undergraduate dental students indicated a generally high acceptance of e-models for their learning in orthodontics, and more prefer a blended approach. Students preferring e-models presented higher performance outcomes, which supports cognitive load theory regarding prior exposure to simulation-based environments.
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http://dx.doi.org/10.1111/eje.12718DOI Listing
September 2021

Comparison of Experiences in Two Birth Cohorts Comprising Young Families with Children under Four Years during the Initial COVID-19 Lockdown in Australia and the UK: A Qualitative Study.

Int J Environ Res Public Health 2021 08 29;18(17). Epub 2021 Aug 29.

Telethon Kids Institute, 15 Hospital Avenue, Nedlands, WA 6009, Australia.

This study aims to understand the experience and impact of the initial COVID-19 lockdown in young families with children aged below 4 years. Free text questions were administered to participants in the ORIGINS (Australia) and Born in Bradford (UK) cohort studies to collect qualitative information on worries, concerns and enjoyable experiences during the pandemic. A total of 903 (400 for ORIGINS and 503 for BiB) participants completed the two surveys during April 2020. Despite varying in geography, levels of socio-economic disadvantage and their situational context during the pandemic, respondents from both cohorts reported similar worries and challenges during the lockdown period, including: employment/finances, health anxiety, mental health and social isolation, caring for children and child development. Families across the globe experienced both positive and negative immediate impacts of COVID-19. Population-based data can be used to inform the development of support services, public health campaigns and universal interventions to assist families in future health crises.
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http://dx.doi.org/10.3390/ijerph18179119DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8431681PMC
August 2021

Cell type-selective targeted delivery of a recombinant lysosomal enzyme for enzyme therapies.

Mol Ther 2021 Aug 14. Epub 2021 Aug 14.

Regeneron Pharmaceuticals, Tarrytown, NY 10591, USA. Electronic address:

Lysosomal diseases are a class of genetic disorders predominantly caused by loss of lysosomal hydrolases, leading to lysosomal and cellular dysfunction. Enzyme replacement therapy (ERT), where recombinant enzyme is given intravenously, internalized by cells, and trafficked to the lysosome, has been applied to treat several lysosomal diseases. However, current ERT regimens do not correct disease phenotypes in all affected organs because the biodistribution of enzyme uptake does not match that of the affected cells that require the enzyme. We present here targeted ERT, an approach that utilizes antibody-enzyme fusion proteins to target the enzyme to specific cell types. The antibody moiety recognizes transmembrane proteins involved in lysosomal trafficking and that are also preferentially expressed in those cells most affected in disease. Using Pompe disease (PD) as an example, we show that targeted ERT is superior to ERT in treating the skeletal muscle phenotypes of PD mice both as a protein replacement therapeutic and as a gene therapy.
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http://dx.doi.org/10.1016/j.ymthe.2021.08.020DOI Listing
August 2021

Higher Serum Urate Levels Are Associated With an Increased Risk for Sudden Cardiac Death.

J Rheumatol 2021 Jun 15. Epub 2021 Jun 15.

This research project is supported by cooperative agreement U01 NS041588 co-funded by the National Institute of Neurological Disorders and Stroke (NINDS) and the National Institute on Aging (NIA), National Institutes of Health, Department of Health and Human Service. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NINDS or the NIA. Representatives of the NINDS were involved in the review of the manuscript but were not directly involved in the collection, management, analysis or interpretation of the data. Additional funding was provided by grants R01 HL080477 and K24 HL111154 from the National Heart, Lung, and Blood Institute (NHLBI) and grant P50AR060772 from the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS). Representatives from the NHLBI or the NIAMS did not have any role in the design and conduct of the study, the collection, management, analysis, and interpretation of the data, or the preparation or approval of the manuscript. L.D. Colantonio, MD, PhD, N.S. Chaudhary, MBBS, MPH, N.D. Armstrong, PhD, P. Muntner, PhD, M.R. Irvin, PhD, Department of Epidemiology, University of Alabama at Birmingham, Birmingham, Alabama, USA; R.J. Reynolds, PhD, K.G. Saag, MD, MSc, Department of Medicine, Division of Clinical Immunology and Rheumatology, University of Alabama at Birmingham, Birmingham, Alabama, USA; T.R. Merriman, PhD, Department of Medicine, Division of Clinical Immunology and Rheumatology, University of Alabama at Birmingham, Birmingham, Alabama, USA, and Department of Biochemistry, University of Otago, Dunedin, New Zealand; A. Gaffo, MD, MSPH, Department of Medicine, Division of Clinical Immunology and Rheumatology, University of Alabama at Birmingham, and Birmingham Veterans Affairs Medical Center, Birmingham, Alabama, USA; J.A. Singh, MD, MPH, Department of Epidemiology, University of Alabama at Birmingham, Department of Medicine, Division of Clinical Immunology and Rheumatology, University of Alabama at Birmingham, and Birmingham Veterans Affairs Medical Center, Birmingham, Alabama, USA; T.B. Plante, MD, MHS, Department of Medicine, Larner College of Medicine at the University of Vermont, Burlington, Vermont, USA; E.Z. Soliman, MD, MSc, MS, Epidemiological Cardiology Research Center (EPICARE), Wake Forest School of Medicine, Winston-Salem, North Carolina, USA; J.R. Curtis, MD, MS, MPH, Department of Epidemiology, University of Alabama at Birmingham, and Department of Medicine, Division of Clinical Immunology and Rheumatology, University of Alabama at Birmingham, Birmingham, Alabama, USA; S.L. Bridges Jr., MD, PhD, Department of Medicine, Division of Rheumatology, Hospital for Special Surgery, and Joan and Sanford I. Weill Department of Medicine, Division of Rheumatology, Weill Cornell Medicine, New York, New York, USA; L. Lang, PhD, Department of Medicine, University of Colorado Denver, Denver, Colorado, USA; G. Howard, DrPH, Department of Biostatistics, University of Alabama at Birmingham, Birmingham, Alabama, USA; M.M. Safford, MD, Department of Medicine, Weill Cornell Medical College, New York, New York, USA. LDC receives research support from Amgen. AG receives research support from Amgen and honoraria from UpToDate. JAS receives consultant fees from Crealta/Horizon, Medisys, Fidia, UBM LLC, Medscape, WebMD, Clinical Care Options, Clearview Healthcare Partners, Putnam Associates, Spherix, Trio Health, Focus Forward, Navigant Consulting, Practice Point Communications, Simply Speaking, the National Institutes of Health, and the American College of Rheumatology; is a member of the Executive Committee of Outcome Measures in Rheumatology (OMERACT), and is a stockholder of Amarin Pharmaceuticals and Viking Therapeutics. MMS receives research support from Amgen. PM receives research support from Amgen and serves as a consultant for Amgen. KGS receives research support from Horizon, Takeda, Sobi, and Shanton; and serves as a consultant/advisor for Arthrosi, Atom Bioscience, LG Pharma, Mallinkrodt, Sobi, Horizon, and Takeda. The remaining authors have no conflicts of interest relevant to this article. Address correspondence to Dr. L.D. Colantonio, 1720 2nd Ave South, RPHB 527C, Birmingham, AL 35294-0013, USA. Email: Accepted for publication June 2, 2021.

Objective: To determine the association of serum urate (SU) levels with sudden cardiac death and incident coronary heart disease (CHD), separately, among adults without a history of CHD.

Methods: We conducted a case-cohort analysis of Black and White participants aged ≥ 45 years enrolled in the REason for Geographic And Racial Differences in Stroke (REGARDS) study without a history of CHD at baseline between 2003 and 2007. Participants were followed for sudden cardiac death or incident CHD (i.e., myocardial infarction [MI] or death from CHD excluding sudden cardiac death) through December 31, 2013. Baseline SU was measured in a random sample of participants (n = 840) and among participants who experienced sudden cardiac death (n = 235) or incident CHD (n = 851) during follow-up.

Results: Participants with higher SU levels were older and more likely to be male or Black. The crude HR (95% CI) per 1 mg/dL higher SU level was 1.26 (1.14-1.40) for sudden cardiac death and 1.17 (1.09-1.26) for incident CHD. After adjustment for age, sex, race, and cardiovascular risk factors, the HR (95% CI) per 1 mg/dL higher SU level was 1.19 (1.03-1.37) for sudden cardiac death and 1.05 (0.96-1.15) for incident CHD. HRs for sudden cardiac death were numerically higher among participants aged 45-64 vs ≥ 65 years, without vs with diabetes, and among those of White vs Black race, although values for effect modification were all ≥ 0.05.

Conclusion: Higher SU levels were associated with an increased risk for sudden cardiac death but not with incident CHD.
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http://dx.doi.org/10.3899/jrheum.210139DOI Listing
June 2021

Fine-mapping, trans-ancestral and genomic analyses identify causal variants, cells, genes and drug targets for type 1 diabetes.

Nat Genet 2021 07 14;53(7):962-971. Epub 2021 Jun 14.

Department of Pathology, Immunology, and Laboratory Medicine, University of Florida, Gainesville, FL, USA.

We report the largest and most diverse genetic study of type 1 diabetes (T1D) to date (61,427 participants), yielding 78 genome-wide-significant (P < 5 × 10) regions, including 36 that are new. We define credible sets of T1D-associated variants and show that they are enriched in immune-cell accessible chromatin, particularly CD4 effector T cells. Using chromatin-accessibility profiling of CD4 T cells from 115 individuals, we map chromatin-accessibility quantitative trait loci and identify five regions where T1D risk variants co-localize with chromatin-accessibility quantitative trait loci. We highlight rs72928038 in BACH2 as a candidate causal T1D variant leading to decreased enhancer accessibility and BACH2 expression in T cells. Finally, we prioritize potential drug targets by integrating genetic evidence, functional genomic maps and immune protein-protein interactions, identifying 12 genes implicated in T1D that have been targeted in clinical trials for autoimmune diseases. These findings provide an expanded genomic landscape for T1D.
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http://dx.doi.org/10.1038/s41588-021-00880-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8273124PMC
July 2021
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