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BUFFALO, NY — December 23, 2025 — A new #research paper was #published in Volume 17, Issue 11 of Aging-US on November 25, 2025, titled “A natural language processing–driven map of the aging research landscape.” In this study, Jose Perez-Maletzki from Universidad Europea de Valencia and Universitat de València, together with Jorge Sanz-Ros from Stanford University School of Medicine, used artificial intelligence (AI) to analyze a century of global aging research, revealing shifts in focus and highlighting underexplored areas. The team analyzed over 460,000 scientific abstracts published between 1925 and 2023 to identify key themes, trends, and research gaps in the study of aging. Their goal was to provide a comprehensive, unbiased view of how the field has evolved and where future research could have the greatest impact. The study found that aging research has moved from basic cellular studies and animal models to a growing focus on clinical topics, particularly age-related diseases such as Alzheimer's and dementia. Using natural language processing and machine learning, the researchers grouped publications into thematic clusters and tracked how interest in each topic changed over time. “By integrating Latent Dirichlet Allocation (LDA), term frequency-inverse document frequency (TF-IDF) analysis, dimensionality reduction and clustering, we delineate a comprehensive thematic landscape of aging research.” One key finding was the growing separation between basic biological studies and clinical research. While both areas have grown significantly, they often progress independently with limited overlap. Clinical studies tend to focus on geriatrics, healthcare, and neurodegenerative diseases, while basic science emphasizes cellular mechanisms such as oxidative stress, telomere shortening, mitochondrial dysfunction, and senescence. The authors note that this lack of integration limits the translation of laboratory discoveries into medical applications. The study also showed that some emerging topics, such as autophagy, RNA biology, and nutrient sensing, are expanding rapidly but remain separated from clinical applications. In contrast, long-established links, such as those between cancer and aging, remain strong. The analysis also highlighted that potentially important associations, such as those between mitochondrial dysfunction and senescence or epigenetics and autophagy, are rarely studied and may be new research opportunities. This AI-driven analysis offers a new way to guide future research by identifying how different areas of aging science are interconnected or isolated. It also highlights how research priorities may be shaped by policy or funding trends, as seen in the heavy focus on Alzheimer's disease. As the global population continues to age, understanding how biological processes relate to clinical outcomes is critical. This study not only offers a historical map of aging science but also serves as a tool to support more connected, interdisciplinary, and effective future research. DOI - https://doi.org/10.18632/aging.206340 Corresponding author - Jorge Sanz-Ros - jsanzros@stanford.edu Abstract video - https://www.youtube.com/watch?v=O4dJUGQ2ZcU Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts To learn more about the journal, visit https://www.Aging-US.com​​ and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY — December 19, 2025 — A new #research paper was #published in Volume 17, Issue 11 of Aging-US on November 18, 2025, titled “Epigenetic age predicts depressive symptoms during the COVID-19 pandemic in the Canadian Longitudinal Study on Aging: importance of biological sex.” This study, led by Cindy K. Barha of the University of Calgary and the University of British Columbia, along with Teresa Liu-Ambrose of the University of British Columbia, found that older women with a younger biological age measured years before the COVID-19 pandemic experienced a greater increase in depressive symptoms during the early lockdown period. These findings could help shape future mental health strategies, particularly for women with high emotional or caregiving demands. Epigenetic age is a biological marker that reflects how the body is aging and may differ from a person's actual age. Using long-term data from the Canadian Longitudinal Study on Aging (CLSA), the researchers investigated whether epigenetic age could predict changes in mental health during a major public health crisis. The study included over 600 adults, with an average baseline age of 63, and used two widely accepted epigenetic clocks, the DNAmAge and the Hannum Age, to estimate biological age. Depressive symptoms were tracked at four time points between 2012 and 2020, including during the height of the pandemic. “The mean participant chronological age at study entry was 63±10 years (46% female).” The analysis showed that in women, a younger biological age predicted a greater rise in depression during the early phase of the COVID-19 pandemic. This was not observed in men or in individuals with older biological ages. The study challenges the common belief that a younger biological age always signals better mental or physical resilience. The researchers suggest that women with younger biological profiles may have been more socially or professionally active before the pandemic. When lockdowns disrupted daily routines and social connections, these individuals may have experienced more emotional distress. Additional factors, such as reduced physical activity, loss of routine, and decreased social interaction, known to affect both mental health and biological aging, may have had a stronger emotional effect on this group. The findings highlight the importance of considering biological sex when studying how aging affects mental well-being during stressful events. Although the study has some limitations, including the time gap between biological age measurement and the pandemic, it gives valuable insights into how biological and social factors interact during periods of crisis. Future research could use epigenetic clocks to better identify individuals at greater risk of mental health challenges during large-scale public health emergencies. Overall, this study adds to the growing field of social epigenetics and suggests that biological age may support more targeted public health planning, especially for older adults. DOI - https://doi.org/10.18632/aging.206337 Corresponding author - Teresa Liu-Ambrose - teresa.ambrose@ubc.ca Abstract video - https://www.youtube.com/watch?v=DVm78jKsdkY Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY - December 17, 2025 – A new #research paper was #published in Oncotarget (Volume 16) on December 15, 2025, titled “Machine learning-based survival prediction in colorectal cancer combining clinical and biological features.” In this study, led by Lucas M. Vieira from the University of Brasília and the University of California San Diego, researchers used machine learning to predict survival in patients with colorectal cancer. They built a model by combining biological markers with clinical data. This approach could help improve prognosis and guide treatment strategies for one of the world's most common and deadly cancers. The team analyzed data from over 500 patients, using clinical details such as age, chemotherapy status, and cancer stage, along with molecular features like gene expression and microRNAs. Their goal was to improve how clinicians identify high-risk patients and make outcome predictions more precise. Researchers evaluated three different patient data scenarios using different machine learning techniques. The best-performing was an adaptive boosting model, which achieved 89.58% accuracy. This approach showed that integrating clinical and biological data led to significantly better predictions than using either data type alone. Among the biological markers, the gene E2F8 was consistently influential in all patient groups and is known to play a role in tumor growth. Other important markers included WDR77 and hsa-miR-495-3p, which are also associated with cancer development. Key clinical predictors included cancer stage, patient age, lymph node involvement, and whether chemotherapy was administered. “The proposed method combines biological and clinical features to predict patient survival, using as input data from patients from the United States, available in the TCGA database.” Unlike earlier models that relied on either clinical or molecular data alone, this study demonstrates the added value of combining both. Ensemble methods, which merge multiple learning algorithms, provided more stable and consistent results across all patient groups tested. These research findings could lead to new tools that help clinicians better predict how a patient's disease might progress or respond to treatment. The study also highlights the importance of collecting complete clinical information, such as lifestyle factors, which were missing from the dataset but could enhance future predictions. Overall, the study demonstrated how machine learning can support more accurate and personalized survival predictions in colorectal cancer. It also points to potential future research on markers like E2F8, which may be useful for monitoring or targeted therapy. DOI - https://doi.org/10.18632/oncotarget.28783 Correspondence to - Lucas M. Vieira - lvieira@health.ucsd.edu Abstract video - https://www.youtube.com/watch?v=cy7UL5ZUKuI Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28783 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, colorectal cancer, machine learning, feature selection, non-coding RNAs, genes To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us on social media: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY— December 17, 2025 — We are pleased to announce that we have officially joined ResearchGate, the professional network for scientists and researchers. This collaboration enhances the visibility, accessibility, and impact of research published in Aging-US among the global scientific community. By integrating ResearchGate, Aging-US offers authors and readers an additional channel to discover, share, and discuss cutting-edge findings in aging research. The journal's presence on the platform includes a dedicated profile, article listings, author profiles, and metrics that help track readership and engagement. As the field of aging research continues to grow rapidly, it is essential that high-quality studies are easy to find, access, and share. Joining ResearchGate allows Aging-US authors to connect their work with a wider network of peers, fostering collaboration, advancing understanding of the biology of aging, and helping translate discoveries into better health outcomes. ResearchGate hosts millions of researchers worldwide and provides tools for sharing publications, asking and answering research questions, and discovering new collaborators across institutions and disciplines. Aging-US's participation on the platform reinforces its commitment to open scientific dialogue and timely dissemination of rigorously reviewed aging research. Authors publishing in Aging-US can now: -Link their publications directly to their ResearchGate profiles. -Track reads, recommendations, and citations through the platform's analytics. -Engage with other scientists interested in aging, geroscience, and translational research. Readers and researchers can follow Aging-US on ResearchGate to stay updated on newly published articles, special issues, and calls for papers. To learn more about the journal, visit https://www.Aging-US.com​​ and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY — December 16, 2025 — A new #research paper was #published in Aging-US on December 10, 2025, titled “Theobromine is associated with slower epigenetic ageing.” In this study, led by Ramy Saad from King's College London and Great Ormond Street Hospital for Children NHS Foundation Trust, alongside Jordana T. Bell from King's College London, researchers found that higher levels of theobromine, a natural compound found in cocoa, are associated with slower biological aging in humans. The findings suggest that theobromine may support healthy aging. Epigenetic aging refers to biological changes that affect how genes function over time. It is measured using blood-based markers such as DNA methylation and telomere length, which together provide a more accurate picture of aging than chronological age. In this work, researchers analyzed data from two large European studies. In 509 women from the TwinsUK cohort, they found that higher blood levels of theobromine were associated with slower aging, especially based on GrimAge, an epigenetic clock that predicts the risk of age-related disease and early death. The results were confirmed in 1,160 men and women from the German KORA study. “We initially tested for the association between six metabolites found in coffee and cocoa, and epigenetic measures of ageing in blood samples from 509 healthy females from the TwinsUK cohort (median age = 59.8, IQR = 12.81, BMI = 25.35).“ Importantly, theobromine's effects were independent of related compounds such as caffeine. Even after adjusting for these other substances and different lifestyle factors, the association with slower aging remained strong. The study also associated higher theobromine levels with longer telomeres, another marker of healthy aging. While theobromine is commonly found in cocoa and chocolate, the study does not suggest increasing chocolate intake. However, it highlights the potential of everyday dietary components such as theobromine to influence aging. These findings support growing evidence that certain plant-based compounds may play a role in promoting long-term health. By identifying a connection between theobromine and slower biological aging, the study opens new directions for research into nutritional strategies for healthy aging. DOI - https://doi.org/10.18632/aging.206344 Corresponding authors - Ramy Saad - ramy.saad@kcl.ac.uk, and Jordana T. Bell - jordana.bell@kcl.ac.uk Abstract video - https://www.youtube.com/watch?v=S0P1USM8L6E Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206344 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, theobromine, epigenetic aging, DNA methylation, metabolomics, nutrition To learn more about the journal, visit https://www.Aging-US.com​​ and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY — December 12, 2025 — A new #research paper was #published in Volume 17, Issue 11 of Aging-US on November 14, 2025, titled “Methylglyoxal-induced glycation stress promotes aortic stiffening: putative mechanistic roles of oxidative stress and cellular senescence.” The study was led by first authors Parminder Singh of the Buck Institute for Research on Aging and Ravinandan Venkatasubramanian of the University of Colorado Boulder, with senior contributions from corresponding authors Pankaj Kapahi (Buck Institute for Research on Aging) and Zachary S. Clayton (University of Colorado Boulder and University of Colorado Anschutz Medical Campus). The researchers investigated how methylglyoxal (MGO), a toxic byproduct that builds up in blood vessels with age or metabolic dysfunction like diabetes, contributes to artery stiffening. Their findings are especially important to aging and diabetes-related cardiovascular risk. Aortic stiffening, which reduces the flexibility of the body's largest artery, is a key predictor of cardiovascular disease in older adults. The research team used young and aged mice to study how MGO affects vascular health. In young mice, chronic exposure to MGO increased aortic stiffness by 21%. However, when treated with Gly-Low, a supplement containing natural compounds such as nicotinamide and alpha-lipoic acid, this stiffening was completely prevented. Gly-Low also reduced the buildup of MGO and its harmful byproducts, particularly MGH-1, in both blood and tissue. “Aortic stiffness was assessed in vivo via pulse wave velocity (PWV) and ex vivo through elastic modulus.” The research showed that MGO's damage goes beyond structural changes. It also caused the endothelial cells that line blood vessels to enter senescence, a state in which cells stop dividing and begin releasing inflammatory signals. This led to lower levels of nitric oxide, a molecule essential for blood vessel relaxation. In human vascular cells in lab culture, Gly-Low reversed these aging-like changes and restored nitric oxide production. In older mice, which naturally develop stiffer arteries, Gly-Low treatment during four months significantly reduced stiffness and lowered MGO and MGH-1 levels. This suggests that Gly-Low may help slow or even reverse vascular aging by reducing glycation stress. The study also identified the glyoxalase-1 pathway as a critical mechanism. This is a natural detox system that helps clear harmful molecules like MGO. Gly-Low appeared to boost this pathway. When the pathway was chemically blocked, Gly-Low's protective effects disappeared, confirming its role in the process. Overall, the findings highlight glycation stress as a modifiable contributor to vascular aging. The results suggest that natural compound-based therapies, like Gly-Low, may offer a potential strategy to protect arteries from age- and diabetes-related damage. DOI - https://doi.org/10.18632/aging.206335 Corresponding authors: Pankaj Kapahi - pkapahi@buckinstitute.org; Zachary S. Clayton - Zachary.Clayton@cuanschutz.edu Abstract video: https://www.youtube.com/watch?v=i_rtq8eIb8c Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

Msgr. Roger J. Landry St. Joseph's Seminary, Yonkers, New York Advent Day of Recollection “Immaculate Mary in the Life and the Mission of Priests” December 8, 2025 https://traffic.libsyn.com/secure/catholicpreaching/12.8.25_Dunwoodie_Marian_dimension_of_Priestly_Life_and_Mission_1.mp3 The post The Marian Dimension of Priestly Life and Mission, Day of Recollection for the Seminarians at St. Joseph’s Seminary (Dunwoodie), Yonkers, NY, December 8, 2025 appeared first on Catholic Preaching.

Msgr. Roger J. Landry St. Joseph's Seminary, Yonkers, New York Advent Day of Recollection “Immaculate Mary in the Life and the Mission of Priests” December 8, 2025 https://traffic.libsyn.com/secure/catholicpreaching/12.8.25_Mary_and_the_Remedy_to_Various_Challenges_in_Priestly_Life_1.mp3 The post Mary and the Remedy to Various Challenges in Priestly Life, Day of Recollection for the Seminarians at St. Joseph’s Seminary (Dunwoodie), Yonkers, NY, December 8, 2025 appeared first on Catholic Preaching.

BUFFALO, NY — December 8, 2025 — A new #research paper was #published in Volume 17, Issue 11 of Aging-US on September 12, 2025, titled “Infusion of blood from young and old mice modulates amyloid pathology.” This study was led by co-first authors Matias Pizarro from Universidad Adolfo Ibáñez and Ruben Gomez-Gutierrez from The University of Texas Health Science Center at Houston, alongside corresponding authors Claudia Duran-Aniotz from Universidad Adolfo Ibáñez and Rodrigo Morales from The University of Texas Health Science Center at Houston and Universidad Bernardo O'Higgins. The goal was to investigate how blood from young and old mice influences Alzheimer's-related changes in a transgenic mouse model. The findings indicate that age-dependent circulating factors can either worsen or mitigate brain changes associated with dementia, highlighting blood and its components as potential therapeutic targets. Alzheimer's disease is a progressive neurodegenerative disorder characterized by misfolded amyloid proteins, inflammation, and gradual cognitive decline, with aging as its main risk factor. In this work, whole blood from young adult or very old wild-type mice was repeatedly infused into Tg2576 mice, a well-established model of amyloid accumulation and memory impairment. Over several months, recipient mice received 30 weekly blood infusions, followed by behavioral testing and detailed neuropathological analyses. “Tg2576 mice express the human APP harboring the Swedish mutation.” Mice that received blood from old donors performed worse in both short- and long-term spatial memory tasks than mice infused with young blood, suggesting that aged blood contains factors that impair cognition. When the team examined brain tissue, they found more cortical amyloid deposits detected by a specific antibody in mice treated with old blood, while overall amyloid levels measured biochemically did not change, suggesting differences in plaque type or compactness rather than total amount. The expression of amyloid precursor protein in the brain was also higher after old-blood infusion, which may partly explain the shift in amyloid pathology.​ Despite these changes in plaques and memory, classical markers of astrocyte activation, a sign of brain inflammation, did not differ between groups, pointing to more subtle molecular shifts. A broad proteomic analysis of brain samples revealed dysregulation of proteins involved in synapse formation, calcium signaling, and the endocannabinoid system, pathways important for neuronal communication and plasticity. Among them, the calcium channel–related protein CACNA2D2 and the signaling protein BRAF were increased in mice that received old blood, confirming that aged blood circulation can reshape key signaling networks linked to neuronal function and degeneration. Overall, this study supports the idea that blood is not just a passive carrier but a powerful modulator of brain health during aging and disease. While young blood has been associated in previous work with improved synaptic function and reduced amyloid and tau changes, this study emphasizes the harmful impact of old blood, particularly on cortical amyloid patterns and memory. The identification of CACNA2D2 and BRAF as potential mediators of these effects suggests new avenues for targeting blood-borne factors or downstream brain pathways to slow or modify Alzheimer's-related decline. DOI - https://doi.org/10.18632/aging.206319 Corresponding authors - Claudia Duran-Aniotz - Claudia.Duran@uai.cl, and Rodrigo Morales - Rodrigo.MoralesLoyola@uth.tmc.edu Abstract video - https://www.youtube.com/watch?v=zsBDSAipH3w To learn more about the journal, visit https://www.Aging-US.com​​. MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY — December 3, 2025 — A new #essay was #published in Volume 17, Issue 11 of Aging-US on November 19, 2025, titled “On the intergenerational transfer of ideas in aging and cancer research: from the hypothalamus according to V.M. Dilman to the mTOR protein complex according to M.V. Blagosklonny.” In this work, Aleksei G. Golubev from the N.N. Petrov National Medical Research Center of Oncology reflects on the legacy of two influential Russian scientists, Vladimir M. Dilman and his son Mikhail V. Blagosklonny, who each introduced groundbreaking ideas about aging and cancer. Drawing from his own experience working in Dilman's lab, Golubev explores how their ideas remain deeply relevant to today's scientific understanding. The essay connects Dilman's “elevation theory” with Blagosklonny's “hyperfunction theory,” two frameworks that challenge the conventional view of aging as a process of decline. Instead, both propose that aging results from continued biological processes that once supported growth but eventually become harmful when left unchecked. Dilman believed that aging begins with reduced sensitivity in the hypothalamus, a brain region that regulates the body's balance. This desensitization disrupts metabolism and hormone levels, setting the stage for many chronic illnesses. Decades later, Blagosklonny expanded on this idea at the molecular level. Central to his theory is the mTOR protein complex, which regulates growth and metabolism and is now a major focus in aging research. Golubev also explores the historical and personal connections between the two scientists. Dilman, an endocrinologist trained in the Soviet Union, and Blagosklonny, a molecular biologist educated during the post-Soviet period, represent two generations shaped by a shared scientific tradition. “Dilman's scientific legacy is not as well recognized as it should be, partly due to bias in citation practices.” The essay also draws attention to a troubling trend in science: the tendency to overlook early contributions, especially from non-Western scholars. Many of Dilman's insights, such as the connection between high blood sugar, insulin resistance, and cancer, have since been validated by modern tools, yet his work is rarely cited. Golubev points out how citation practices, language barriers, and historical isolation have contributed to this lack of recognition. Finally, Golubev encourages the scientific community to look back and acknowledge the foundational work that shaped modern aging science. It also highlights the importance of cross-generational knowledge in moving science forward. By tracing the intellectual journey from hormonal regulation in the brain to molecular pathways in cells, this essay demonstrated the relevance of old ideas in a new biological era. DOI - https://doi.org/10.18632/aging.206338 Corresponding author - Aleksei G. Golubev - lxglbv@rambler.ru Abstract video - https://www.youtube.com/watch?v=LvrdghTKGws Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206338 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, gerontology, history of science, hyperfunction, mTOR, hypothalamus, cancer, metabolism, immunity To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@Aging-US LinkedIn - https://www.linkedin.com/company/aging/ Bluesky - https://bsky.app/profile/aging-us.bsky.social Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY — December 1, 2025 — A new #research paper featured on the #cover of Volume 17, Issue 11 of Aging-US was #published on October 30, 2025, titled “SAMP-Score: a morphology-based machine learning classification method for screening pro-senescence compounds in p16 positive cancer cells.” In this study led by first author Ryan Wallis along with corresponding author Cleo L. Bishop, from Queen Mary University of London, researchers developed a machine learning tool to identify compounds that induce cancer cells into senescence. The tool, called SAMP-Score, offers a new strategy for drug discovery in cancers with poor treatment options like basal-like breast cancer. Senescence is a process where damaged or aged cells stop dividing. In cancer therapy, inducing senescence is an approach to control tumor growth. However, it is difficult to detect true senescence in cancer cells that already appear aged. These cancers, often called Sen-Mark+ cancers, include basal-like breast cancer and typically lack reliable markers to confirm senescence. SAMP-Score was designed to address this problem. Instead of relying on traditional markers, the researchers built a machine learning model trained to recognize patterns based on senescent cells' shape and structure under a microscope. These visual patterns, known as senescence-associated morphological profiles (SAMPs), allowed the model to distinguish real signs of aging from other effects such as toxicity or normal variation. By analyzing thousands of cell images, the model learned to classify whether a cell had truly entered senescence. “To demonstrate the potential application of SAMP-Score in p16 positive cancer therapeutic discovery, we assessed a diversity screen of 10,000 novel chemical entities in MB-468 cells (p16 positive BLBC).” The team used SAMP-Score to screen more than 10,000 experimental compounds. One compound, QM5928, consistently triggered senescence in several cancer cell types without killing them, making it a promising candidate for further study. Importantly, it worked in cancers resistant to known drugs like palbociclib, which are often ineffective in cancers with high p16 expression like basal-like breast cancer. Further analysis revealed that QM5928 caused the p16 protein to move into the nucleus of cancer cells, a possible sign that the protein is helping stop cell division. This subtle effect was only detectable using the detailed imaging and analysis made possible by SAMP-Score, highlighting the tool's ability to distinguish true senescence from toxic responses and making it a powerful resource in cancer drug discovery. By combining machine learning with high-resolution imaging, this study introduces a new way to find and evaluate cancer therapies. SAMP-Score could accelerate efforts to develop treatments that exploit the body's natural aging processes to fight cancer, especially for patients with resistant tumors. The tool is openly available at GitHub, making it accessible for other researchers exploring senescence-based cancer therapies. DOI - https://doi.org/10.18632/aging.206333 Corresponding author - Cleo L. Bishop - c.l.bishop@qmul.ac.uk Abstract video - https://www.youtube.com/watch?v=qXI_KI3EgHE Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@Aging-US LinkedIn - https://www.linkedin.com/company/aging/ Bluesky - https://bsky.app/profile/aging-us.bsky.social Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

Thank you to my sponsor: BlueChew BlueChew - Get your first month of BlueChew FREE Just use promo code DAVID at checkout and pay five bucks for shipping at https://bluechew.com More Red Clay Strays Tour: https://www.redclaystrays.com/tour IG: https://www.instagram.com/redclaystrays Facebook: https://www.facebook.com/RedClayStrays/ Spotify: https://open.spotify.com/artist/6IKlXZEFOvk9itrP1s0knJ YouTube: https://www.youtube.com/@RedClayStrays David Lucas Tour Dates: https://www.davidlucascomedy.com/tour Covina, CA: November 7-8 Buffalo, NY: November 28-29 Rochester, NY: December 5-6 San Diego, CA: December 19-20 0:00 Macon Georgia, Traveling, Humble beginnings 13:07 How The Red Clay Strays met, The music industry 21:38 Racial jokes, Roasting 28:03 Waffle House, Growing up with diversity, Hunting 38:21 Altitude sickness, Fishing in Alabama 44:55 Musicians and comedians, Meet and greets NEW MERCH AVAILABLE https://shopdavidlucas.com/ Connect with David Lucas Website: https://www.davidlucascomedy.com Merch: https://shopdavidlucas.com/ Instagram: https://www.instagram.com/davidlucasfunny Twitter: https://twitter.com/funnydavidlucas Youtube: ​⁠@DavidLucasComedian David Lucas was born in Macon, GA. He started acting an early age, performing in numerous stage plays at the Macon Little Theatre. He relocated to Hollywood where he was a contestant on, “MTV Yo Momma”. He has since written for several television shows and continues to perform stand up all over the country (for such comedians as Louis CK, Erik Griffin, Joe Rogan, Brendan Schaub, Tony Hinchcliffe, Bert Kreisher, DL Hughley and many more). David is a Kill Tony Hall of Famer and currently headlining his own tour! Filmed By Daniel Casas https://www.instagram.com/presentedbydaniel A 7EQUIS Network Show https://www.instagram.com/7equis https://www.7equis.com Learn more about your ad choices. Visit megaphone.fm/adchoices

Sal Vulcano takes his shoes off for the 4th time to talk with Rick about stuff. Watch on YouTube here: https://youtu.be/IVt_toaD-70

Thank you to my sponsor: Cornbread Hemp Cornbread Hemp - Right now, Fishing w/ David Lucas listeners can save 30% on their first order! Just head to https://cornbreadhemp.com/FDL and use code FDL at checkout Follow Drew Nickens IG: https://www.instagram.com/the_drewnickens/ David Lucas Tour Dates: https://www.davidlucascomedy.com/tour Chicago, IL: November 1 Covina, CA: November 7-8 Buffalo, NY: November 28-29 Rochester, NY: December 5-6 San Diego, CA: December 19-20 0:00 Drew Nickens return to Kill Tony 10:20 Drew Nickens is black, Energy drinks, Hecklers 17:19 Bert Kreischer, Conservative comedians, David's uncle 24:16 Special needs 35:42 Drew Nickens head injury 47:01 Food stamps NEW MERCH AVAILABLE https://shopdavidlucas.com/ Connect with David Lucas Website: https://www.davidlucascomedy.com Merch: https://shopdavidlucas.com/ Instagram: https://www.instagram.com/davidlucasfunny Twitter: https://twitter.com/funnydavidlucas Youtube: ​⁠@DavidLucasComedian David Lucas was born in Macon, GA. He started acting an early age, performing in numerous stage plays at the Macon Little Theatre. He relocated to Hollywood where he was a contestant on, “MTV Yo Momma”. He has since written for several television shows and continues to perform stand up all over the country (for such comedians as Louis CK, Erik Griffin, Joe Rogan, Brendan Schaub, Tony Hinchcliffe, Bert Kreisher, DL Hughley and many more). David is a Kill Tony Hall of Famer and currently headlining his own tour! Filmed By Daniel Casas https://www.instagram.com/presentedbydaniel A 7EQUIS Network Show https://www.instagram.com/7equis https://www.7equis.com Learn more about your ad choices. Visit megaphone.fm/adchoices

Kristen Bell takes her shoes off to talk Nobody Wants This Season 1 + 2 now on Netflix. Watch this episode on YouTube here: https://youtu.be/MvO2DIq59PM

Thank you to my sponsor: SKIMS SKIMS - https://www.skims.com/fdl #skimspartner More Heidi Regina Love On The Line Podcast: https://www.youtube.com/@loveonthelineshow IG: https://www.instagram.com/ginaaa.hg Kill Tony: https://www.youtube.com/@KillTony David Lucas Tour Dates: https://www.davidlucascomedy.com/tour Chicago, IL: November 1 Covina, CA: November 7-8 Buffalo, NY: November 28-29 Rochester, NY: December 5-6 San Diego, CA: December 19-20 0:00 Fishing for conversation, Heidi's new podcast, Looks and brains 6:48 Dating & career goals, Maintaining & presenting yourself 17:58 Raising children, Living in Austin 24:51 Kill Tony London 34:05 Masculine women, OF girls 43:52 Social media negativity 55:23 Roasting NEW MERCH AVAILABLE https://shopdavidlucas.com/ Connect with David Lucas Website: https://www.davidlucascomedy.com Merch: https://shopdavidlucas.com/ Instagram: https://www.instagram.com/davidlucasfunny Twitter: https://twitter.com/funnydavidlucas Youtube: ​⁠@DavidLucasComedian David Lucas was born in Macon, GA. He started acting an early age, performing in numerous stage plays at the Macon Little Theatre. He relocated to Hollywood where he was a contestant on, “MTV Yo Momma”. He has since written for several television shows and continues to perform stand up all over the country (for such comedians as Louis CK, Erik Griffin, Joe Rogan, Brendan Schaub, Tony Hinchcliffe, Bert Kreisher, DL Hughley and many more). David is a Kill Tony Hall of Famer and currently headlining his own tour! Filmed By Daniel Casas https://www.instagram.com/presentedbydaniel A 7EQUIS Network Show https://www.instagram.com/7equis https://www.7equis.com Learn more about your ad choices. Visit megaphone.fm/adchoices

A Classic RISK! episode from our early years that first ran in August of 2013, when Mather Zickel, Jen Curran, Joel Kim Booster and Julie Threlkeld told stories of times they crossed over the edge.

Todd takes his shoes off for the 3rd time.

Thank you to my sponsor: BlueChew BlueChew - Get your first month of BlueChew FREE Just use promo code DAVID at checkout and pay five bucks for shipping More Michael A. Gonzales Instagram: https://www.instagram.com/mikeagonz13/ David Lucas Tour Dates: https://www.davidlucascomedy.com/tour Nashville, TN: October 17-18 Chicago, IL: November 1 Covina, CA: November 7-8 Buffalo, NY: November 28-29 Rochester, NY: December 5-6 San Diego, CA: December 19-20 NEW MERCH AVAILABLE https://shopdavidlucas.com/ 0:00 Fishing w/ Michael Gonzales5:00 Meeting Tony Hinchcliffe10:00 We're Workaholics15:00 Never Steal My Food20:00 "I'm Tired"25:00 Roasting Scary Dude's GF30:00 Fat vs Plus Sized35:00 D1 Football Coach40:00 High Altitude Training45:00 Kill Tony Band Needs an Album Connect with David Lucas Website: https://www.davidlucascomedy.com Merch: https://shopdavidlucas.com/ Instagram: https://www.instagram.com/davidlucasfunny Twitter: https://twitter.com/funnydavidlucas Youtube: ​⁠@DavidLucasComedian David Lucas was born in Macon, GA. He started acting an early age, performing in numerous stage plays at the Macon Little Theatre. He relocated to Hollywood where he was a contestant on, “MTV Yo Momma”. He has since written for several television shows and continues to perform stand up all over the country (for such comedians as Louis CK, Erik Griffin, Joe Rogan, Brendan Schaub, Tony Hinchcliffe, Bert Kreisher, DL Hughley and many more). David is a Kill Tony Hall of Famer and currently headlining his own tour! Filmed By Daniel Casas https://www.instagram.com/presentedbydaniel A 7EQUIS Network Show https://www.instagram.com/7equis https://www.7equis.com Learn more about your ad choices. Visit megaphone.fm/adchoices

Brent Morin and Adam Ray make their 7th appearance together with Rick on TYSO.

Thank you to our sponsors: GLD & SelectQuote GLD - New customers get 50% Off AND a FREE chain with code FISHING at https://GLD.com SelectQuote - Get the right life insurance for YOU, for LESS, and save more than fifty percent at https://selectquote.com/FISHING More William Montgomery The William Montgomery Show: https://www.youtube.com/@thewilliammontgomeryshow5447 Watch William Montgomery on KT: https://www.youtube.com/@KillTony IG: https://www.instagram.com/william.f.montgomery1 David Lucas Tour Dates: https://www.davidlucascomedy.com/tour Torrance, CA: October 12 Burbank, CA: October 14 Nashville, TN: October 17-18 Chicago, IL: November 1 Covina, CA: November 7-8 Buffalo, NY: November 28-29 Rochester, NY: December 5-6 San Diego, CA: December 19-20 0:00 Fishing for carp, Kill Tony 8:42 Panic attacks, Movies, TV Shows 15:36 Ghosts, Nightmares, Food poisoning 23:49 Ninja Turtles, Scary movies, Young Dolph 34:41 Great Outdoors Comedy Festival 38:39 Riyadh Comedy Festival 41:59 Jet skis, Kayakers, Judge shows 48:22 Running for office, A big ball, University of Tennessee NEW MERCH AVAILABLE https://shopdavidlucas.com/ Connect with David Lucas Website: https://www.davidlucascomedy.com Merch: https://shopdavidlucas.com/ Instagram: https://www.instagram.com/davidlucasfunny Twitter: https://twitter.com/funnydavidlucas Youtube: ​⁠@DavidLucasComedian David Lucas was born in Macon, GA. He started acting an early age, performing in numerous stage plays at the Macon Little Theatre. He relocated to Hollywood where he was a contestant on, “MTV Yo Momma”. He has since written for several television shows and continues to perform stand up all over the country (for such comedians as Louis CK, Erik Griffin, Joe Rogan, Brendan Schaub, Tony Hinchcliffe, Bert Kreisher, DL Hughley and many more). David is a Kill Tony Hall of Famer and currently headlining his own tour! Filmed By Daniel Casas https://www.instagram.com/presentedbydaniel A 7EQUIS Network Show https://www.instagram.com/7equis https://www.7equis.com Learn more about your ad choices. Visit megaphone.fm/adchoices

Thank you to my sponsor: BlueChew BlueChew - Get your first month of BlueChew FREE Just use promo code DAVID at checkout and pay five bucks for shipping at https://bluechew.com More Jack Shaw IG: https://www.instagram.com/hijackshaw Tour Dates: https://jackshaw.komi.io David Lucas Tour Dates: https://www.davidlucascomedy.com/tour Syracuse, NY: October 3 Albany, NY: October 4th Torrance, CA: October 12 Burbank, CA: October 14 Nashville, TN: October 17-18 Chicago, IL: November 1 Covina, CA: November 7-8 Rochester, NY: December 5-6 San Diego, CA: December 19-20 0:00 Kill Tony, Roasting 10:57 Professional antagonizers, David's daughter, NoHo 15:57 Gentrification, A woman's touch in a house 23:05 Hookup stories, Low maintenance roommates, Quiet comics 28:53 Being around comedy, Crazy kids 43:37 Trial and error in comedy, Working on new jokes 50:24 No protection PSA NEW MERCH AVAILABLE https://shopdavidlucas.com/ Connect with David Lucas Website: https://www.davidlucascomedy.com Merch: https://shopdavidlucas.com/ Instagram: https://www.instagram.com/davidlucasfunny Twitter: https://twitter.com/funnydavidlucas Youtube: ​⁠@DavidLucasComedian David Lucas was born in Macon, GA. He started acting an early age, performing in numerous stage plays at the Macon Little Theatre. He relocated to Hollywood where he was a contestant on, “MTV Yo Momma”. He has since written for several television shows and continues to perform stand up all over the country (for such comedians as Louis CK, Erik Griffin, Joe Rogan, Brendan Schaub, Tony Hinchcliffe, Bert Kreisher, DL Hughley and many more). David is a Kill Tony Hall of Famer and currently headlining his own tour! A 7EQUIS Network Show https://www.instagram.com/7equis https://www.7equis.com Learn more about your ad choices. Visit megaphone.fm/adchoices

Craig takes his shoes off to talk about stuff with Rick Glassman. Watch video here: https://youtu.be/fIwvlt93zsM

Rhett & Link from (Mythical Pod and Mythical Kitchen) and their wonder holes take their shoes off.

Thank you to my sponsors: BlueChew, Skims, Cornbread Hemp BlueChew - Get your first month of BlueChew FREE Just use promo code DAVID at checkout and pay five bucks for shipping at https://bluechew.com Skims - Shop SKIMS Mens at https://www.skims.com/fdl #skimspartner Cornbread Hemp - Right now, Fishing with David Lucas listeners can save 30% on their first order! Just head to https://cornbreadhemp.com/fdl and use code FDL at checkout More Isaac Butterfield YouTube: https://www.youtube.com/@IsaacButterfield IG: https://www.instagram.com/thebuttsmarn Facebook: https://www.facebook.com/Thebuttsmarn/ Tour: https://www.isaacbutterfield.com/ 0:00 Australia vs USA 11:53 Controversial jokes 22:07 Controversial words 27:36 Race relations 43:13 Charlie Kirk 56:16 Family David Lucas Tour Dates: https://www.davidlucascomedy.com/tour Kansas City, MO: September 26-27 Albany, NY: October 4 Nashville, TN: October 17-18 Chicago, IL: November 1 Covina, CA: November 7-8 Rochester, NY: December 5-6 San Diego, CA: December 19-20 NEW MERCH AVAILABLE https://shopdavidlucas.com/ Connect with David Lucas Website: https://www.davidlucascomedy.com Merch: https://shopdavidlucas.com/ Instagram: https://www.instagram.com/davidlucasfunny Twitter: https://twitter.com/funnydavidlucas Youtube: ​⁠@DavidLucasComedian David Lucas was born in Macon, GA. He started acting an early age, performing in numerous stage plays at the Macon Little Theatre. He relocated to Hollywood where he was a contestant on, “MTV Yo Momma”. He has since written for several television shows and continues to perform stand up all over the country (for such comedians as Louis CK, Erik Griffin, Joe Rogan, Brendan Schaub, Tony Hinchcliffe, Bert Kreisher, DL Hughley and many more). David is a Kill Tony Hall of Famer and currently headlining his own tour! Filmed By Daniel Casas https://www.instagram.com/presentedbydaniel A 7EQUIS Network Show https://www.instagram.com/7equis https://www.7equis.com Learn more about your ad choices. Visit megaphone.fm/adchoices

Cristina Mariani takes her shoes off to talk with Rick. Watch on YouTube: https://youtu.be/dp7lTlHNCWY?si=qA1E4oeZ8LD0pLbB

Thank you to my sponsors: Thrive Market & DraftKings Thrive Market - Go to https://ThriveMarket.com/FDL to get 30% off your first order and a free $60 gift DraftKings - Your season starts now. Download the DraftKings Sportsbook app and use code FDL More Chelcie Lynn “Trailer Trash Tammy” YouTube: https://www.youtube.com/@ChelcieLynn Trailer Tales Podcast: https://www.youtube.com/@TrailerTalesPod IG: https://www.instagram.com/chelcielynn_ Facebook: https://www.facebook.com/Chelcielynnvine/ TikTok: https://www.tiktok.com/@chelcielynn Tour dates: https://www.eatmytrash.com/pages/tour-schedule David Lucas Tour Dates: https://www.davidlucascomedy.com/tour Kansas City, MO: September 26-27 Albany, NY: October 4 Nashville, TN: October 17-18 Chicago, IL: November 1 Covina, CA: November 7-8 Rochester, NY: December 5-6 San Diego, CA: December 19-20 0:00 If we won the lottery, Casting our reels, The super rich 7:59 Dave Chapelle, Childhoods Then vs Now, Raising kids 21:42 90s sitcoms, The Gen Z stare, Traveling 31:31 Fishing, Boats, Country living 40:23 Kid Rock, Comedy goals, David Lucas comedy beginning 52:07 If David weren't doing comedy, Alex Stein, Great White Sharks 58:09 Canada, London, Diverse fans Gambling problem? Call one eight hundred Gambler. In New York, call eight seven seven eight HOPENY or text HOPENY (four six seven three six nine). In Connecticut, Help is available for problem gambling. Call eight eight eight seven eight nine seven seven seven seven or visit ccpg dot org. Please play responsibly. On behalf of Boot Hill Casino & Resort (Kansas). Twenty-one plus age and eligibility varies by jurisdiction. Fees may apply in Illinois. Void in Ontario. Bonus bets expire seven days after issuance. See sportsbook dot draftkings dot com slash promos. NFL Sunday Ticket offer for new subscribers only and auto-renews until cancelled. Digital games and commercial use excluded. Restrictions apply. Additional NFL Sunday Ticket terms at youtube dot com slash go slash n f l sunday ticket slash terms. Limited time offer. NEW MERCH AVAILABLE https://shopdavidlucas.com/ Connect with David Lucas Website: https://www.davidlucascomedy.com Merch: https://shopdavidlucas.com/ Instagram: https://www.instagram.com/davidlucasfunny Twitter: https://twitter.com/funnydavidlucas Youtube: ​⁠@DavidLucasComedian David Lucas was born in Macon, GA. He started acting an early age, performing in numerous stage plays at the Macon Little Theatre. He relocated to Hollywood where he was a contestant on, “MTV Yo Momma”. He has since written for several television shows and continues to perform stand up all over the country (for such comedians as Louis CK, Erik Griffin, Joe Rogan, Brendan Schaub, Tony Hinchcliffe, Bert Kreisher, DL Hughley and many more). David is a Kill Tony Hall of Famer and currently headlining his own tour! Filmed By Daniel Casas https://www.instagram.com/presentedbydaniel A 7EQUIS Network Show https://www.instagram.com/7equis https://www.7equis.com Learn more about your ad choices. Visit megaphone.fm/adchoices

Kevin Nealon (Saturday Night Live, Happy Gilmore, The Larry Sanders Show, Weeds, Hiking with Kevin) takes his shoes off and becomes BFFs with Rick Glassman.

Thank you to my sponsors: DraftKings & BlueChew DraftKings - Your season starts now. Download the DraftKings Sportsbook app and use code FDL * BlueChew - Get your first month of BlueChew FREE just use promo code DAVID at checkout and pay five bucks for shipping at https://bluechew.com More Donnell Rawlings The Donnell Rawlings Show: https://www.youtube.com/@thedonnellrawlingsshow IG: https://www.instagram.com/donnellrawlings Facebook: https://www.facebook.com/donnellrawlingsofficial/ Tour dates: https://www.donnellrawlings.com/whereisdonnellrawlings Donnell Rawlings on KT: https://www.youtube.com/watch?v=cqXwoGrebXs Donnell Rawlings on Breakfast Club: https://www.youtube.com/watch?v=e7Q-uI0NHmM David Lucas Tour Dates: https://www.davidlucascomedy.com/tour Kansas City, MO: September 26-27 Albany, NY: October 4 Nashville, TN: October 17-18 Chicago, IL: November 1 Covina, CA: November 7-8 Rochester, NY: December 5-6 San Diego, CA: December 19-20 0:00 Eating with David Lucas, Kill Tony, Roasting 6:31 Donnell Rawlings on Breakfast Club, Crashing Out 13:02 Old school vs new school comedy, Roast Battle 26:04 Donnell Rawlings knows Korean 29:05 Corey Holcomb 37:01 Black community in comedy 39:44 Spike Lee, Tyler Perry, Kevin Hart 42:38 Wearing a dress 45:47 Dave Chappelle, Chappelle's Show, Neal Brennan 54:26 How Donnell Rawlings feels about his current career * Gambling problem? Call one eight hundred Gambler. In New York, call 8778HOPENY or text HOPENY (four six seven three six nine). In Connecticut, Help is available for problem gambling. Call eight eight eight seven eight nine seven seven seven seven or visit ccpg dot org. Please play responsibly. On behalf of Boot Hill Casino & Resort (Kansas).Fees may apply in IL. Twenty-one plus age and eligibility varies by jurisdiction. Void in Ontario. Bonus bets expire seven days after issuance. See sportsbook dot draftkings dot com slash promos. NFL Sunday Ticket offer for new subscribers only and auto-renews until cancelled. Digital games and commercial use excluded. Restrictions apply. Additional NFL Sunday Ticket terms at https://youtube.com/go/nflsundayticket/terms. Limited time offer. NEW MERCH AVAILABLE https://shopdavidlucas.com/ Connect with David Lucas Website: https://www.davidlucascomedy.com Merch: https://shopdavidlucas.com/ Instagram: https://www.instagram.com/davidlucasfunny Twitter: https://twitter.com/funnydavidlucas Youtube: ​⁠@DavidLucasComedian David Lucas was born in Macon, GA. He started acting an early age, performing in numerous stage plays at the Macon Little Theatre. He relocated to Hollywood where he was a contestant on, “MTV Yo Momma”. He has since written for several television shows and continues to perform stand up all over the country (for such comedians as Louis CK, Erik Griffin, Joe Rogan, Brendan Schaub, Tony Hinchcliffe, Bert Kreisher, DL Hughley and many more). David is a Kill Tony Hall of Famer and currently headlining his own tour! Filmed By Daniel Casas https://www.instagram.com/presentedbydaniel A 7EQUIS Network Show https://www.instagram.com/7equis https://www.7equis.com Learn more about your ad choices. Visit megaphone.fm/adchoices

The AC is broken and it's HOT. Ian Fidance and Rick Glassman take their shoes AND pants off (to put on shorts). WATCH ON YOUTUBE HERE: https://youtu.be/nUs7QYaZvpw

Blaine Anderson is a professional dating coach and match maker.

Dax Flame takes his shoes off AGAIN and talks with Rick Glassman about stuff.

Veronika Slowikowska, of Tires and the Nevermind Podcast, makes her first TYSO appearance and she and Rick meet for the first time. And let's just say they "podcast," during a sleepover, if you know what I mean. ;)

Jerrod Carmichael makes his first TYSO appearance and boy are our arms tired! Check out the follow up to Emmy Award Winning "Rothaniel," his newest stand up special, "Jerrod Carmichael: Don't Be Gay." On HBO here: https://www.hbomax.com/movies/jerrod-carmichael-dont-be-gay/797f6457-02b4-4309-8996-998dcf203d0d

Lisa takes her shoes off with Rick. Don't believe me? Hahahaha oooooookay...

Love on the Spectrum's Abbey Romeo & David Isaacman take their shoes off. With them are Abbey's mom, Christine and TYSO House Musician, George Krikes. Songs, laughs, and more on this episode of Take Your Shoes Off! Watch on YouTube here: https://youtu.be/x7xFg5bgOhQ

While sneaking into the Superman movie press junket to meet the cast, Rick pulled his hamstring. That same day, he met the new Superman himself — David Corenswet — and invited him on the pod. Later that night, Rick got a massage… while David took his shoes off for the very first time.

Paul Rudd makes good on his first appearance after needing to leave early last time. The two talk about his new movie, "Friendship", and how it's hard to make new friends as an adult. Get tickets to Rick’s stand up tour at https://www.punchup.live/rickglassman August 7-9 • Grand Rapids, MI August 14-16 • Dania Beach, FL August 23 • Los Angeles, CA September 4-6 • North Charleston, SC September 26-27 • Detroit, MI October 3 • Atlanta, GA October 4 • Raleigh, NC October 17-18 • Toronto, ON October 19 • Buffalo, NY November 1 • Brooklyn, NY December 12-13 • Las Vegas, NV Support TYSO by supporting our sponsors: • Ready to experience the magic of caffeine without the common jitters? Get 50% off Magic Mind at https://www.magicmind.com/rick • Looking for an amazing mattress with a risk-free 100 day money back guarantee? Go to https://www.helixsleep.com/tyso for 27% Off sitewide. • Ready to create your own website? Go to https://www.wix.com to start building your website today. RICK GLASSMAN https://www.instagram.com/rickglassman https://www.tiktok.com/@rickglassman https://www.patreon.com/takeyourshoesoff https://discord.gg/Z2v4HTC https://www.punchup.live/rickglassman https://www.tysocards.com https://www.rickglassman.com/store PAUL RUDD https://a24films.com/films/friendshipSupport the show: https://www.patreon.com/takeyourshoesoff

BUFFALO, NY - December 30, 2024 – A new #editorial was #published in Oncotarget's Volume 15 on December 24, 2024, titled “Pitfalls and perils from FDA-approved germ-line cancer predisposition tests." Authored by Dr. Wafik S. El-Deiry, Editor-in-Chief of Oncotarget, and Dr. Eli Y. Adashi from Brown University, the article highlights concerns about the risks of a newly approved genetic test for cancer risk. This test, called the “Invitae Common Hereditary Cancers Panel," was approved in 2023 and examines 48 genes linked to inherited cancers, including breast, ovarian, and Lynch syndrome-related cancers. Although the test increases access to genetic information, the authors warn that using it without professional guidance may lead to confusion, stress, and potential harm. One concern is that people can order this test online without consulting healthcare professionals or genetic counselors. Without expert help, users might struggle to understand their results especially if they indicate risks that are unclear or difficult to act on. This can cause unnecessary anxiety and confusion. “The DTC option of germ-line testing for cancer susceptibility should be discouraged given the risks of anxiety, lack of adequate interpretation for variants not strongly associated with cancer, potential for minors to be tested outside the healthcare system and potential for loss of follow-up if test results are not shared with health care professionals or never make it into the medical record.” The editorial also points out ethical and medical issues when minors use these tests. If a child's test is done without medical oversight, results might not be added to their health records, making follow-up care harder to manage and potentially risking their long-term health. Cost is another issue. These tests are often not covered by insurance, which can place a financial burden on families who might need additional testing or medical advice. The researchers emphasize that genetic testing for cancer risk should always include healthcare providers and genetic counseling. This ensures users fully understand their results and receive proper guidance. The authors also call on the US Food and Drug Administration (FDA) to provide clear rules for using these tests, particularly for minors. In conclusion, while genetic testing holds great potential for improving cancer prevention and care, its benefits must not come at the cost of safety and public health. Responsible use of these tests will require collaboration between regulators, healthcare professionals, and testing companies to address the risks and ensure these tools are used effectively. DOI - https://doi.org/10.18632/oncotarget.28677 Correspondence to - Wafik S. El-Deiry - wafik@brown.edu Video short - https://www.youtube.com/watch?v=DjKpiBNDWHo Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ About Oncotarget Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science. Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science). To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY- December 19, 2024 – We are pleased to announce that Dr. Marco Demaria, a leading expert in aging and cellular senescence, will join Aging (Aging-US) as Editor-in-Chief, starting January 1, 2025. Dr. Demaria will work alongside an esteemed Editorial Board. Dr. Demaria has an impressive background in aging research. He earned his PhD in Molecular Medicine from the University of Torino, Italy. In 2010, he joined the laboratory of Aging Founding Editor, the late Dr. Judith Campisi, at the Buck Institute for Research on Aging. There he developed cellular and animal models for studying cellular aging, also known as cellular senescence, and its role in tissue repair, cancer, and aging. Currently, Dr. Demaria leads DemariaLab, whose mission is “to extend human healthspan by pioneering discoveries in molecular and cellular mechanisms that regulate the aging process.” His groundbreaking research has significantly advanced our understanding of cellular senescence and its role in aging and age-related diseases. Dr. Demaria aims to develop new therapeutic approaches to create more effective treatments that mitigate the diseases and extend the healthspan. His work specifically focuses on interfering with the mechanisms of cellular senescence using genetic, pharmacological, and nutraceutical strategies. “My research is focused on understanding the molecular basis of age-related dysfunctions and disorders, and to identify new molecular and cellular targets to improve health and longevity.” - Marco Demaria He is also a Full Professor at the European Research Institute for the Biology of Ageing (ERIBA), Director of the Mechanisms of Health, Ageing and Disease (MoHAD) at the University Medical Center Groningen (UMCG), President of the International Cell Senescence Association (ICSA), and Co-Founder of Cleara Biotech. Dr. Demaria also brings valuable editorial experience from his former positions as Editor-in-Chief of npj Aging and Editorial Board member of Aging Cell. All the above, combined with Dr. Demaria's academic contributions, commitment, and expertise, align perfectly with Aging's mission to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population. For more information about Marco Demaria, PhD, please visit www.demarialab.com and follow him on X (Twitter) @marc_dema or on Bluesky @marcdema.bsky.social. About Aging-US Please visit our website at https://www.Aging-US.com​​ and connect with us on social media at: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY- December 18, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 21 on November 22, 2024, entitled, “Anti-aging effect of extracellular vesicles from mesenchymal stromal cells on senescence-induced chondrocytes in osteoarthritis.” The study, authored by Jérémy Boulestreau, Marie Maumus, Giuliana Bertolino Minani, Christian Jorgensen, and Danièle Noël from the Institute for Regenerative Medicine and Biotherapy and Centre Hospitalier Universitaire de Montpellier, introduces a potential new therapy for osteoarthritis. This therapy uses tiny particles called extracellular vesicles (EVs), derived from fat tissue, to repair damage caused by aging cells in the joints, slowing the progression of osteoarthritis and restoring joint health. Osteoarthritis, the most common joint disorder in older adults, occurs when cartilage breaks down, leading to inflammation, stiffness, and pain. One major contributor to it is cellular senescence, a process where cells stop dividing and release harmful substances that worsen inflammation and damage joint tissues. In this study, the researchers showed that EVs from fat-derived mesenchymal stromal cells (ASC-EVs) decreased the harmful effects of senescent cells. ASC-EVs showed strong therapeutic effects in both cellular and mouse preclinical studies. They reduced inflammation and DNA damage markers in cells derived from human joints and improved cellular health. In mice with osteoarthritis, the vesicles restored joint balance, reduced cartilage damage, and preserved joint function for weeks. The findings highlight the potential of regenerative medicine, which uses the body's own mechanisms to repair damage. By targeting the aging process in joint cells, this therapy offers a breakthrough for osteoarthritis treatment. Millions of people suffering from joint pain, inflammation, and reduced mobility could benefit from this innovative approach. In the future, the researchers plan to explore ways to enhance the therapy, including whether repeated treatments could provide even longer-lasting benefits. These could lead to new options in treating osteoarthritis and other age-related conditions. “In addition to their anti-inflammatory and regenerative properties, our study confirms that ASC-EVs may be a relevant option for future clinical applications in degenerative diseases, such as OA, which are increasing with the population aging.” In conclusion, this research offers a promising regenerative therapy for osteoarthritis, with the potential to improve the quality of life for millions of older adults. DOI - https://doi.org/10.18632/aging.206158 Corresponding author - Danièle Noël - daniele.noel@inserm.fr Video short - https://www.youtube.com/watch?v=06qw2nR3ovY Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206158 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts About Aging-US The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population. The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.) Please visit our website at https://www.Aging-US.com​​ and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY- December 17, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 21 on November 29, 2024, entitled, “Thermotherapy has sexually dimorphic responses in APP/PS1 mice.” Researchers Samuel A. McFadden, Mackenzie R. Peck, Lindsey N. Sime, MaKayla F. Cox, Erol D. Ikiz, Caleigh A. Findley, Kathleen Quinn, Yimin Fang, Andrzej Bartke, Erin R. Hascup, and Kevin N. Hascup from Southern Illinois University School of Medicine, found that raising body temperature through heat therapy improved memory in male mice with Alzheimer's disease but worsened memory in females. These findings emphasize the importance of personalized treatments based on sex-specific responses to therapy. Alzheimer's disease (AD) is a progressive brain disorder characterized by memory loss and confusion. It is caused by the buildup of harmful proteins like beta-amyloid, which damages brain cells over time. In this study, genetically modified mice predisposed to develop Alzheimer disease (APP/PS1 mice) were kept in warmer environments for six months to explore the effects of heat therapy on memory and metabolism. The results revealed that male mice benefited from the therapy, with improved memory and reduced levels of beta-amyloid in their brains. Female mice, however, experienced a worsening of memory, likely due to increased inflammation triggered by the heat therapy. Inflammation, where the immune system is hyperactivated, can harm brain cells and worsen Alzheimer's disease symptoms. “Thermotherapy improved spatial navigation in male C57BL/6 and APP/PS1 mice, with the later attributed to reduced hippocampal soluble amyloid-β (Aβ)42. Female APP/PS1 mice exhibited worse spatial memory recall after chronic thermotherapy.” Heat therapy is already known to provide general health benefits, such as improving heart health and regulating blood sugar. This study suggests it could also offer a simple, non-drug approach to slowing Alzheimer's progression, particularly for men. Unlike exercise, which offers similar benefits, heat therapy is accessible for people who are weak or unable to engage in physical activity. While these findings are promising, the researchers emphasize the need for more studies to understand why men and women respond so differently to heat therapy. Future research should also investigate whether the results can be replicated in humans and how the therapy can be tailored to individual needs. In conclusion, heat therapy could present a safe and practical option for managing Alzheimer's disease, particularly in men. However, the observed gender differences highlight the importance of further research to refine its therapeutic potential and ensure it benefits everyone. DOI - https://doi.org/10.18632/aging.206156 Corresponding author - Kevin N. Hascup - khascup49@siumed.edu Video short - https://www.youtube.com/watch?v=IeMPHss4vj8 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts About Aging-US The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population. The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.) Please visit our website at https://www.Aging-US.com​​ and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

On CinemAddicts Episode 271, we review movies that are coming out December 13, 2024. New films covered include "The Man in the White Van," "Young Werther," "Nickel Boys," and "Endless Summer Syndrome." Cinema-Attic inhabitant Bruce Purkey also delivers a couple of recommends with "Beetlejuice Beetlejuice," "Smile 2," and "Adult Swim Yule Log 2: Branching Out." (0:00) - Intro (15:45) - The Man in the White Van arrives in theaters December 13. Photo/poster: Relativity Media.  (22:18) - Young Werther hits Theaters, Digital, and On Demand 12/13. Photo/poster: Lionsgate.  (32:12) - Nickel Boys hits NY December 13 and Los Angeles December 20th. More cities in subsequent weeks. Photos/poster courtesy of Orion Pictures (42:44) - Bruce Purkey is stuck in the Cinem-Attic!! (44:12) - Endless Summer Syndrome - in theaters and VOD 12/13. Photo/poster: Altered Innocence. (53:28) - The Man in the White Van (61:54) - Smile 2 (68:03) - Beetlejuice Beetlejuice (72:12) - Adult Swim Yule Log 2: Branching Out ***Support CinemAddicts by purchasing/renting movies using our Amazon affiliate links or our SiteStripe.  ***CinemAddicts Movie Picks (worth Renting/Purchasing) include: Seven Cemeteries Dominique The Unlikely Pilgrimage of Harold Fry Red Rooms Take Cover For Ad-Free CinemAddicts episodes, subscribe to our CinemAddicts YouTube Channel. Like Our CinemAddicts Facebook Page Join our CinemAddicts Facebook Group for daily movie recommendations. Questions/comments on CinemAddicts email Greg Srisavasdi at info@findyourfilms.com. Our website is Find Your Film. Shop our CinemAddicts Merch store (shirts, hoodies, mugs). Interested in what book Eric Holmes is adapting into a screenplay? Check out Patera. CinemAddicts hosts: Bruce Purkey, Eric Holmes, Greg Srisavasdi Thanks to our Patreon Community 1. Ryan Smith 2. Stephen Schrock 3. Susan 4. Charles Peterson 5. Nelson B. McClintock 6. Diana Van De Kamp 7. Pete Abeyta 8. Tyler Andula 9. Stephen Mand 10. Edmund Mendez 11. Abbie Schmidt 12. Jeff Tait 13. Superfan Giovanni 14. Robert Prakash 15. Kristen 16. Chris M 17. Jeremy Chappell 18. Lewis Longshadow 19. Iver 20. Alex Clayton 21. Daniel Hulbert 22. Andrew Martin 23. Angela Clark 24. Myron Freeman 25. Kayn Kalmbach 26. Aaron Fordham 27. Tracy Peters 28. Grant Boston 29. Ken Cunningham

BUFFALO, NY - December 11, 2024 – A #news feature on the #research paper “Next-generation cell-penetrating antibodies for tumor targeting and RAD51 inhibition” by Rackear et al. was #published in Oncotarget's Volume 15 on November 22, 2024, titled “Advancements in cell-penetrating monoclonal antibody treatment." This new publication by Sai Pallavi Pradeep and Raman Bahal from the Department of Pharmaceutical Sciences at the University of Connecticut highlights significant advancements in monoclonal antibody (mAb) therapies. The focus is on the 3E10 antibody, originally derived from autoimmune mouse studies in systemic lupus erythematosus. Unlike traditional mAbs, which struggle to reach intracellular targets, this cell-penetrating antibody targets cancer cells by addressing a major limitation of current therapies. By targeting RAD51, a key intracellular protein involved in DNA repair, the 3E10 antibody shows great promise for cancer treatment, particularly in cancers with defective DNA repair pathways. mAbs have already changed the landscape of cancer therapy, offering treatments that are more targeted and have fewer side effects compared to chemotherapy. However, current therapies are limited since mAbs only target proteins on the surface of cancer cells. This research pushes the boundaries by demonstrating how 3E10 antibodies can penetrate cells and access their internal molecules. This unique capability expands the potential of mAb therapies and targeted cancer treatments. Different humanized versions of the 3E10 antibody were created and carefully tested. Some versions were particularly effective at blocking RAD51, while others showed promise for carrying other therapeutic molecules like genetic material into the cancer cells. This flexibility means that 3E10 could be used to treat different cancer types and deliver various therapeutic molecules directly into tumor cells. This progress offers exciting new possibilities for treating cancer tumors that are resistant to conventional therapies. In conclusion, the 3E10 antibody's dual function—targeting DNA repair pathways and delivering therapeutic molecules—positions it as a transformative tool in cancer research and targeted cancer treatments. DOI - https://doi.org/10.18632/oncotarget.28674 Correspondence to - Raman Bahal - raman.bahal@uconn.edu Video short - https://www.youtube.com/watch?v=3uMdPvThFHA Sign up for free Altmetric alerts about this article: https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28674 Subscribe for free publication alerts from Oncotarget: https://www.oncotarget.com/subscribe/ Keywords - cancer, monoclonal anti-bodies, cell penetration, nucleic acid delivery, 3E10 About Oncotarget Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science. Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science). To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh Media Contact MEDIA@IMPACTJOURNALS.COM 18009220957

BUFFALO, NY- December 11, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 21 on November 14, 2024, entitled, “Adolescents and young adults with sickle cell disease exhibit accelerated aging with elevated T-cell p16INK4a expression.” Researchers Samuel R. Wilson, Natalia Mitin, Vanessa L. Ayer Miller, Andrew B. Smitherman, and Marcus A. Carden, from the University of North Carolina at Chapel Hill, Sapere Bio, Campbell University, and Cogent Biosciences have discovered that young people with sickle cell disease (SCD) exhibit signs of accelerated biological aging compared to those without the disease. By measuring levels of p16INK4a, a key marker of cellular aging, the team found significantly higher levels in individuals with SCD. Remarkably, some participants showed biological aging equivalent to an additional 43 years. These findings suggest that SCD may drive faster aging in the body, offering new insights into the disease's long-term impact. Sickle cell disease (SCD) is a genetic condition primarily affecting individuals of African or Mediterranean descent. While treatments have advanced, people with SCD often face significant health challenges, including complications that mimic the effects of aging. Cellular aging, or senescence, occurs when cells stop dividing yet continue to send harmful signals that damage surrounding tissues. Researchers believe this process happens at an accelerated rate in people with SCD, underscoring the importance of finding ways to slow it down and mitigate its impact. The study compared p16INK4a levels in 18 adolescents and young adults with SCD to 27 healthy people of the same age. The results showed that even the youngest participant with SCD had higher levels of this aging marker than anyone in the non-SCD group. “Our youngest participant, a 15-year-old with SCD, had a higher p16 expression than all the comparators, underscoring the early rise of p16 expression in this population.” The researchers believe this faster aging could be caused by the chronic inflammation, lack of oxygen, and stress on the body associated with SCD. Along with managing the symptoms of the disease, SCD patients also face a higher risk of aging-related problems like organ damage and physical decline much earlier in life. The findings suggest that measuring p16INK4a levels could help clinicians identify patients at risk for these problems earlier and offer targeted care. The study also opens the door to new treatments, such as drugs that aim to remove old, damaged cells. These therapies could potentially slow down the aging process. Further research is essential to confirm these findings and to gain a deeper understanding of how to support SCD patients effectively. Larger, long-term studies could investigate whether therapies targeting cell aging can help prevent complications and improve the quality of life for individuals with SCD. In conclusion, this study marks an important step in understanding how SCD accelerates aging and offers new ways to improve the lives of those living with the condition. DOI - https://doi.org/10.18632/aging.206152 Corresponding author - Samuel R. Wilson - samuel.wilson@med.unc.edu Video short - https://www.youtube.com/watch?v=QXVdxBikaqg About Aging-US The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population. The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.) Please visit our website at https://www.Aging-US.com​​. MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY- December 10, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 21 on November 18, 2024, entitled, “Prostaglandin E2 regulates senescence and post-senescence neoplastic escape in primary human keratinocytes.” Researchers Elise Srour, Nathalie Martin, Claire Drullion, Clémentine De Schutter, Joëlle Giroud, Adrien Pioger, Julie Deslé, Laure Saas, Joe Nassour, Julien Théry, Gauthier Decanter, Nicolas Penel, Chantal Vercamer, Clara Salazar-Cardozo, Corinne Abbadie, and Olivier Pluquet from CNRS, University of Lille, the Oscar Lambret Center, and the University of Colorado School of Medicine have revealed how a molecule called Prostaglandin E2 (PGE2) influences skin aging and cancer risk. Their study shows that PGE2 not only drives skin cells to age but also enables some of these aging cells to bypass natural limits and develop into pre-cancerous cells. This process provides insights into why older skin is more susceptible to cancer. The study focused on keratinocytes, the primary cells in the outer layer of the skin. As these cells age, they enter a state called senescence, where they stop dividing to prevent damaged cells from turning cancerous. While this process typically serves as a protective mechanism, the researchers found that, in certain cases, some senescent cells can escape this state, re-enter the cell cycle, and acquire characteristics of early cancer. By examining keratinocytes from donors of different ethnicities and ages, the researchers identified the PTGS2/PGE2/EP4 pathway as a key driver of this escape process. The researchers show that blocking PGE2 or its associated pathway reduced the chances of aged cells becoming precancerous. This suggests that drugs targeting this pathway, including some anti-inflammatory medications already in use, might be repurposed to slow skin aging and prevent early-stage skin cancers. Additionally, the study also found that PGE2 levels increase in the skin as it ages, further supporting its role in skin health and disease. "These results indicate that the PTGS2/PGE2/EP4 pathway is required to induce and maintain the senescent phenotype of NHEKs, and that PGE2 level is a potential determinant of the initial steps of the age-related oncogenic process." The team also highlighted the broader implications of their work. The PTGS2/PGE2/EP4 pathway is not only linked to skin health but also to age-related inflammation, a condition that contributes to several diseases. By addressing this pathway, researchers hope to address not only skin aging but other health challenges linked to aging and chronic inflammation. In conclusion, this study reveals important molecular drivers of skin aging and early cancer, leading the way for new approaches that can promote healthier skin. DOI - https://doi.org/10.18632/aging.206149 Corresponding author - Olivier Pluquet - olivier.pluquet@ibl.cnrs.fr Video short - https://www.youtube.com/watch?v=4aNf3X2RJSw About Aging-US The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population. The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.) Please visit our website at https://www.Aging-US.com​​ and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY - December 9, 2024 – A new #research paper was #published in Oncotarget's Volume 15 on November 22, 2024, entitled “Computed tomography-based radiomics and body composition model for predicting hepatic decompensation." Mayo Clinic researchers Yashbir Singh, John E. Eaton, Sudhakar K. Venkatesh, and Bradley J. Erickson have developed an innovative AI tool to predict hepatic decompensation in individuals with primary sclerosing cholangitis (PSC). PSC is a chronic disease that damages the bile ducts and can lead to liver failure. Hepatic decompensation marks a critical stage of advanced liver disease, and clinicians have long faced challenges in predicting who is at risk. The Mayo Clinic's new AI tool addresses this gap by combining body fat and muscle composition data with insights extracted from computed tomography (CT) scans using computational radiomics. By analyzing these tissues, the AI model identifies patterns linked to an increased risk of liver failure. The study involved 80 PSC patients, including 30 with hepatic decompensation, 30 without, and 20 patients in an external validation set. The AI model achieved impressive results, correctly identifying at-risk patients with 97% accuracy. By recognizing these risks early, clinicians may be able to intervene sooner and improve patient outcomes. While the study focused on PSC, the team emphasized the broader implications of their work. “It may hold promise for the detection of other PSC-related complications, such as cholangiocarcinoma, as well as applications in more prevalent chronic liver diseases like non-alcoholic fatty liver disease (NAFLD).” This non-invasive, data-driven approach offers a powerful way to assess health risks and provide more tailored treatments. Despite the promising findings, the researchers acknowledge the limitations of the study, which include a limited sample size and a single-center design. “However, further research is necessary to validate our findings on a large-scale, independent dataset, ensuring the robustness and generalizability of the model.” In conclusion, this study shows how detailed information from CT scans can help clinicians predict severe liver problems in patients with PSC. By identifying hidden patterns in the images, they can better understand risks and create personalized treatment plans. This approach could improve care for PSC and other long-term liver diseases. DOI - https://doi.org/10.18632/oncotarget.28673 Correspondence to - Bradley J. Erickson - bje@mayo.edu Video short - https://www.youtube.com/watch?v=QCekNtYni4w Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28673 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, radiomics, body composition, machine learning, primary sclerosing cholangitis, computer tomography About Oncotarget Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science. Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science). To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY - December 4, 2024 – A new #editorial was #published in Oncotarget's Volume 15 on November 22, 2024, entitled “B7-H4: A potential therapeutic target in adenoid cystic carcinoma." Researchers Luana Guimaraes de Sousa and Renata Ferrarotto from The University of Texas MD Anderson Cancer Center made an important discovery about adenoid cystic carcinoma (ACC), a rare and aggressive cancer of the secretory glands. The study found that B7-H4, an inhibitory immune checkpoint, helps ACC tumors avoid attacks from the immune system. This discovery could lead to new treatments for ACC, which currently has very limited options for patients, especially when the cancer spreads to other organs. ACC is known for behaving in two distinct ways. The aggressive form, called ACC-I, spreads quickly to organs like the liver and lungs and leads to a short survival time of approximately three years. The less aggressive form, ACC-II, grows more slowly and often allows patients to live much longer, sometimes over 20 years. However, treatment options for both forms are limited, and once the cancer spreads, it becomes difficult to treat. The study showed that the protein B7-H4 is found at high levels in the aggressive ACC-I tumors. This protein blocks immune cells from entering the tumor, allowing the cancer to grow without being attacked by the immune system. Patients with high levels of B7-H4 in their tumors were found to have worse survival outcomes. To explore possible treatments, the researchers tested a new drug called AZD8205, designed to specifically target and block B7-H4. In preclinical tests on mice, the drug showed remarkable success. Tumors derived from patients shrank in every case, and in many cases of aggressive ACC, the tumors disappeared completely. Importantly, the drug had little effect on less aggressive ACC-II tumors, which have lower levels of B7-H4. This shows that the treatment is highly specific to tumors with high B7-H4 levels. These results have already led to clinical trials that are testing similar drugs in patients with ACC. “These trials represent attractive, rationale therapeutic opportunities for patients facing this rare, aggressive, and chemo-refractory disease, for which no systemic therapy is currently available.” In conclusion, this discovery represents a significant breakthrough in ACC research, identifying B7-H4 as a crucial factor in cancer growth and immune evasion. By leading the way for personalized treatments, it offers promising new therapeutic options and the potential for improved outcomes for ACC patients. DOI - https://doi.org/10.18632/oncotarget.28661 Correspondence to - Renata Ferrarotto - rferrarotto@mdanderson.org Sign up for free Altmetric alerts about this article: https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28661 Subscribe for free publication alerts from Oncotarget: https://www.oncotarget.com/subscribe/ About Oncotarget Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science. Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science). To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY- December 4, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 21 on November 22, 2024, entitled, “The effects of young and aged, male and female megakaryocyte conditioned media on angiogenic properties of endothelial cells.” Researchers Murad K. Nazzal, Hanisha L. Battina, Nikhil P. Tewari, Sarah L. Mostardo, Rohit U. Nagaraj, Donghui Zhou, Olatundun D. Awosanya, Saveda K. Majety, Sue Samson, Rachel J. Blosser, Ushashi C. Dadwal, Patrick L. Mulcrone, and Melissa A. Kacenaat from Indiana University School of Medicine and Richard L. Roudebush Veterans' Administration Medical Center, have uncovered how certain bone marrow cells, called megakaryocytes (MKs), promote the growth of new blood vessels (angiogenesis) to aid in bone healing. Their findings help explain why healing slows with age and offer insights into potential treatments to accelerate fracture recovery in older adults. Broken bones are common in older adults, and slower healing can lead to complications and longer hospital stays. Accelerating the healing process could significantly improve the quality of life for millions. In this study, researchers investigated the effects of substances secreted by MKs, collected from young and older male and female mice. These substances, known as conditioned media (CM), were tested for their ability to stimulate the growth and function of endothelial cells (EC), which form the building blocks of blood vessels. Blood vessels play a critical role in healing by delivering oxygen and nutrients to damaged areas, making angiogenesis a vital part of the recovery process. The results showed that CM from younger MKs mice was more effective at helping blood vessels grow. Interestingly, MKs from female mice performed better than those from males, regardless of age. For example, substances from female MKs mice boosted blood vessel growth by over 115% and significantly improved the movement of cells needed for healing. The researchers also studied changes in genes related to blood vessel growth, and found that aging affects how these genes work. These changes may explain why older people heal more slowly after breaking a bone. “An understanding of which factors regulate which mechanisms of EC functionality may allow for isolation of one or a few factors that influence EC migration changes with aging, resulting in the development of targeted therapy to improve EC migration, subsequent angiogenesis, and fracture healing.” In conclusion, this research paves the way for developing new therapies to help older individuals recover from fractures more quickly, reducing pain and improving mobility. One potential approach could involve creating treatments that replicate the effects of MKs from younger individuals or isolating the specific substances that promote blood vessel growth. This represents an important step toward addressing the growing challenge of delayed healing in an aging population. DOI - https://doi.org/10.18632/aging.206077 Corresponding authors - Patrick L. Mulcrone - pamulcro@iu.edu, and Melissa A. Kacena - mkacena@iupui.edu About Aging-US The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population. The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.) Please visit our website at https://www.Aging-US.com​​. MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY - December 3, 2024 – A new #review was #published in Oncotarget's Volume 15 on November 22, 2024, entitled “Mesenchymal stem cells - the secret agents of cancer immunotherapy: Promises, challenges, and surprising twists." Authored by Theia Minev, Shani Balbuena, Jaya Mini Gill, Francesco M. Marincola, Santosh Kesari, and Feng Lin from CureScience Institute, Sonata Therapeutics, and Pacific Neuroscience Institute and Providence Saint John's Health Center, this review explores the potential role of mesenchymal stem cells (MSCs) in cancer treatment. These stem cells can naturally target tumors and deliver therapeutic agents directly to cancer cells, potentially improving treatment outcomes while reducing side effects commonly associated with traditional therapies like chemotherapy. However, the authors also note significant challenges, pointing out that under certain conditions, MSCs may unintentionally promote tumor growth, highlighting the need for careful therapeutic design. MSCs are cells that can develop in different types of tissues, such as bone, fat, or cartilage, and act as natural repair agents. What makes them particularly special is their ability to respond to biological signals, like inflammation, which is often present in cancer. This enables them to locate tumors, and once there, they can deliver cancer treatments directly to the affected area. Clinical trials are already investigating MSC-based treatments for cancers such as brain tumors, melanoma, and ovarian cancer. Some results are promising, showing that MSCs can effectively deliver treatments and boost the immune system's fight against cancer. However, other trials have also revealed the complexities of MSC behavior, including variability in their effects and the potential to create conditions that support tumor growth. “This variability may be due to the tumor immune microenvironment's effects, where immune cells are inhibited by various factors, creating a conducive environment for tumor growth.” The authors also suggest that “Developing personalized MSC therapies tailored to the specific characteristics of a patient's tumor and immune system could enhance the efficacy and safety of MSC-based treatments.” Achieving this requires a deeper understanding of how MSCs interact with cancer cells and their surrounding environment. In conclusion, this review highlights both the potential and challenges of (MSCs in cancer therapy. With ongoing research and technological advancements, MSCs could become a key component of personalized cancer treatments, offering new hope for patients worldwide. DOI - https://doi.org/10.18632/oncotarget.28672 Correspondence to - Feng Lin - flin@curescience.org Video short - https://www.youtube.com/watch?v=Wwc3zDDitlc Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ About Oncotarget Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science. Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science). To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh MEDIA@IMPACTJOURNALS.COM