Introducing our <scp>Associate Editorial Board Chair</scp> : An interview with <scp>Justin Parreno</scp> , <scp>University of Delaware</scp> , <scp>Newark</scp> , <scp>USA</scp>
Why this work is in the frame
A frame that forgets how it found something cannot be audited. These are the routes that admitted this work.
Bibliographic record
Abstract
My lab studies a variety of different tissue types with the main focus being on how the cytoskeleton, particularly the F actin cytoskeleton, is a major regulator of cellular phenotype, both in good and in bad health. We focus on tissues that have a mechanical component such as cartilage, tendon, and the ocular lens. As of late, we are interested in understanding the multiscale transmission of mechanical loads onto the actin cytoskeleton. We aim to uncover how pathological mechanical overload in diseases or conditions such as osteoarthritis, tendinosis, or cataracts at the tissue macroscale level alters actin at the nanoscale. We believe the regulation of actin by mechanical loads is instructive to the cell leading to altered cell phenotypes. By gaining a greater insight into this, we may be able to one day develop actin-based therapeutics, hopefully against conditions such as osteoarthritis, tendinosis, or cataracts. I believe it was serendipity. As a PhD student, I was struggling with another project for a good amount of time. During this time, I started a simple side project that was basically treating cartilage cells (chondrocytes), with drugs like latrunculin and cytochalasin. I was surprised to see such profound effects on the cells and I was completely enamored by how such treatments changed cell shape. The treatments also affected cell phenotype. To the musculoskeletal field, this was old news as others, decades earlier, had similar findings. However, there was limited knowledge of the actin-based mechanisms by which these drugs exerted their effects on gene expression in chondrocytes. So, I was really interested in understanding the mechanism by which actin can regulate gene expression to control cell phenotype. It also made me curious about the regulation of actin under disease states, so here we are today, studying it many years later! Definitely my advisors and mentors. The person that got me interested in research was Dr. David Hart at the University of Calgary. In Dave's laboratory, I studied bone cells (Osteoblasts) and this is where I was first introduced to actin. From there, I moved to the University of Toronto, where I was mentored by Dr. Rita Kandel. There, we were studying articular cartilage. That is when I really became enamored with the cytoskeleton and its relationship to chondrocyte behavior. Rita has been really instrumental in my career and she instilled confidence in me that I could become an independent investigator. For my post-doc, I was mentored by Dr. Velia Fowler, at the Scripps in La Jolla, California. Partway through my post-doc Velia's lab moved to the University of Delaware, where I was eventually hired on as faculty. Under Velia's toutelage, I learned a lot about actin. In particular, she opened up my interest in Tropomyosins, which has become a major focus of my research. These mentors were really influential in not only giving me the confidence to become an independent investigator, but also guiding me along the way on this career path. I could not have done it without them. I still keep in contact with my mentors and it is always a pleasure to visit and have scientific discussions with them. In addition to my mentors, my current collaborators influence me toward embarking on new exciting research challenges. Right now, I collaborate with Drs. Dawn Elliott and Stephanie Cone, who are in the Department of Biomedical Engineering at the University of Delaware. As well, I collaborate with Drs. Charles Dhong and Xinqiao Jia in the Department of Materials Science. I also collaborate with an Orthopaedic surgeon, Dr. Alvin Su. It has been refreshing to bounce ideas off each other and have partners to venture into the unknown with. They really inspire me to do new, good science that I would have never thought about on my own. I love coming up with new, innovative ideas and approaches. My favorite pastime would be playing basketball. However, there comes a point in time where I think I might have to give it up as my knees age. I am still hanging on to this; I enjoy playing and watching basketball. Spending time with family. I have three children. That takes up a lot of my weekends and I really enjoy being a dad to them. My parents. They were very hard workers growing up. My work ethic comes from them. Without them, I do not think I could be successful. Being a first-generation Filipino; it is remarkable to think about how they came from another country to pass unto me a baton for success. I just cannot imagine all the stuff that they had to go through to set up a good life for their children. My parents are the two major influences in my life. Dr. Justin Parreno is an Assistant Professor in the Department of Biological Sciences at the University of Delaware in Newark, DE, USA. Dr. Parreno joined the faculty in May 2021, and his research program focuses on the repair and regeneration of musculoskeletal (cartilage, tendon) and ocular (lens) tissues. His lab investigates the multiscale transmission of load from the tissue scale to the nano-level cytoskeletal scale. Currently, the Parreno lab is investigating how mechanical loading transmitted onto the cellular level results in dysregulation of filamentous (F-)actin network and the contribution F-actin dysregulation plays in disease pathogenesis of Osteoarthritis, Tendinosis, and Cataracts. Dr. Parreno received his Bachelor of Science in Biology and his Master's of Medical Science with a Specialization in Bone and Joint Health from the University of Calgary, and his PhD in Laboratory Medicine and Pathobiology from the University of Toronto. He then pursued his Post-doctoral training at Scripps Research in La Jolla, California. To date, Dr. Parreno has published over 30 manuscripts, in both leading orthopedic and ocular journals, as well as leading cell biology journals. Currently, Dr. Parreno's research is funded by grant support from the NIH through the Delaware Center for Musculoskeletal Research, an American Orthopaedic Society for Sports Medicine Stephen P. Arnoczky Grant, a University of Delaware Research Foundation Grant, and a JRF Ortho grant.
Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.
Full frame distilled prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. Learned from the 10,348 direct Codex labels and 10,348 direct Gemma labels. Candidate is the union of thresholded teacher heads; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels or direct frontier model labels.
Codex and Gemma teacher scores by category
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.005 | 0.011 |
| Meta-epidemiology (narrow) | 0.002 | 0.002 |
| Meta-epidemiology (broad) | 0.003 | 0.001 |
| Bibliometrics | 0.001 | 0.001 |
| Science and technology studies | 0.002 | 0.001 |
| Scholarly communication | 0.003 | 0.004 |
| Open science | 0.003 | 0.001 |
| Research integrity | 0.002 | 0.005 |
| Insufficient payload (model declined to judge) | 0.000 | 0.001 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it