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Introduction: The National Academies of Sciences (NAS) emphasize the need for interdisciplinary team science (TS) training, but few training resources are available. COALESCE, an open-access tool developed with National Institutes of Health support and located at teamscience.net, is considered a gold standard resource but has not previously been evaluated. COALESCE launched four learning modules in 2011. The Science of TS (SciTS) module, an interactive encyclopedia, introduces foundational concepts. Three scenario-based modules simulate TS challenges in behavioral, clinical, and basic biomedical sciences. This study examined user characteristics, usage patterns, and effects of completing the four modules on TS knowledge, attitudes, and skills., Methods: Repeated measures ANOVA tested for pre-post changes in performance and compared learning by users with biomedical versus other disciplinary backgrounds., Results: From 2011 through 2017, the site attracted 16,280 new users who engaged in 6461 sessions that lasted more than 1 min. The modal registrant identified as working in a biomedical field (47%), in an academic institution (72%), and expressed greater interest in the practice than the SciTS (67%). Those completing pre- and post-tests ( n = 989) showed significant improvement in knowledge, attitudes, and skills after taking all scenario-based modules ( p < 0.005); knowledge and attitudes were unchanged after the SciTS encyclopedia. Biomedical and other health professionals improved comparably., Conclusion: Evaluation of the TS training tool at teamscience.net indicates broad dissemination and positive TS-related outcomes. Site upgrades implemented between 2018 and 2020, including adding five new modules, are expected to increase the robustness and accessibility of the COALESCE training resource., (© The Association for Clinical and Translational Science 2019.)

We have generated a human induced pluripotent stem cell (iPSC) line under feeder-free culture conditions using the urine derived cells (UCs) collected from subjects heterozygous for a novel Plasminogen Activator Inhibitor-1 (PAI-1) mutation. The Sendai Virus (SeV) vector encoding pluripotent Yamanaka transcription factors was used at a low multiplicity of infection to reprogram the PAI-1 UCs., (Copyright © 2016 The Authors. Published by Elsevier B.V. All rights reserved.)

We have generated a human induced pluripotent stem cell (iPSC) line under feeder-free culture conditions using the urine derived cells (UCs) collected from non-affected control subjects to use as a comparison group for the iPSC lines containing a Plasminogen Activator Inhibitor-1 (PAI-1 homozygous/heterozygous) mutation. The Sendai Virus (SeV) vector encoding pluripotent Yamanaka transcription factors was used at a low multiplicity of infection to reprogram the UCs., (Copyright © 2016 The Authors. Published by Elsevier B.V. All rights reserved.)

We have generated a human induced pluripotent stem cell (iPSC) line under feeder-free culture conditions using the urine derived cells (UCs) collected from subject with a novel homozygous Plasminogen Activator Inhibitor-1 (PAI-1 null) mutation. The Sendai virus (SeV) vector encoding pluripotent Yamanaka transcription factors was used at a low multiplicity of infection to reprogram the PAI-1 UCs., (Copyright © 2016 Michael Boutros, German Cancer Research Center, Heidelberg, Germany. Published by Elsevier B.V. All rights reserved.)

The average age of the US population continues to increase. Age is the most important determinant of disease and disability in humans, but the fundamental mechanisms of aging remain largely unknown. Many age-related diseases are associated with an impaired fibrinolytic system. Elevated plasminogen activator inhibitor-1 (PAI-1) levels are reported in age-associated clinical conditions including cardiovascular diseases, type 2 diabetes, obesity and inflammation. PAI-1 levels are also elevated in animal models of aging. While the association of PAI-1 with physiological aging is well documented, it is only recently that its critical role in the regulation of aging and senescence has become evident. PAI-1 is synthesized and secreted in senescent cells and contributes directly to the development of senescence by acting downstream of p53 and upstream of insulin-like growth factor binding protein-3. Pharmacologic inhibition or genetic deficiency of PAI-1 was shown to be protective against senescence and the aging-like phenotypes in kl/kl and N(ω)-nitro-l-arginine methyl ester-treated wild-type mice. Further investigation into PAI-1's role in senescence and aging will likely contribute to the prevention and treatment of aging-related pathologies., (Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.)