Podcasts about DOI

BUFFALO, NY – August 29, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on August 29, 2025, titled “In vivo manipulation of the protein homeostasis network in rhabdomyosarcoma.” In this study led by first author Kristen Kwong and corresponding author Amit J. Sabnis from the Department of Pediatrics, Division of Oncology, University of California San Francisco, researchers discovered that disrupting the protein quality control system in cancer cells slows tumor growth in rhabdomyosarcoma (RMS), the most common pediatric soft tissue cancer. This finding points to a new strategy for treating high-risk childhood cancers that often resist current therapies. Rhabdomyosarcoma is a rare and aggressive cancer that primarily affects children and adolescents. Standard treatments like chemotherapy and radiation often have limited long-term success in high-risk cases. This study explored a different approach: targeting the cellular machinery that maintains protein quality, known as the proteostasis network. Cancer cells rely heavily on this system to survive stress caused by rapid growth and genetic instability. “To examine whether MAL3-101 or more drug-like proteostasis inhibitors represent a new therapeutic strategy for RMS, we screened proteostasis components that might recapitulate the effects of MAL3-101 in vivo.” The researchers first used a compound called MAL3-101 to disrupt protein control in RMS cells. They then identified which parts of the protein quality system were affected. Based on those findings, they searched for more drug-like compounds that could target the same pathways. They focused on a protein called p97, which plays a critical role in removing damaged or misfolded proteins. When they blocked p97 using a drug called CB-5083, the cancer cells could no longer manage internal stress and began to self-destruct. In both laboratory models and mice implanted with human RMS tumors, the treatment significantly slowed or stopped tumor growth. The drug triggered a stress response in the cells known as the unfolded protein response, which can lead to either recovery or programmed cell death. However, not all tumors responded the same way. Some resisted the treatment by activating a backup system called autophagy, which allows cells to recycle parts of themselves under stress. By comparing tumors that responded well to those that did not, the researchers found that higher autophagy activity could serve as a warning sign for resistance. This insight may help identify which patients are more likely to benefit from therapies that target protein quality control. While the results are promising, the drug's effectiveness depended on the tumor's genetic profile and how it handled stress. Combining p97 inhibition with other treatments or blocking alternative survival pathways like autophagy may improve outcomes. The researchers also noted the importance of developing safer and more targeted drugs to reduce side effects. This study opens new possibilities for personalized cancer treatment, particularly for children with aggressive or relapsed RMS. By weakening the systems that cancer cells depend on to survive, rather than only using toxic treatments to kill them, scientists aim to develop more effective and less harmful therapies for young patients. DOI - https://doi.org/10.18632/oncotarget.28764 Correspondence to - Amit J. Sabnis - amit.sabnis@ucsf.edu Video short - https://www.youtube.com/watch?v=YsdffTkXNRQ To learn more about Oncotarget, visit https://www.oncotarget.com. 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

Asthma ist im Rettungsdienst zu einem seltenen Einsatzstichwort geworden. Grund genug für uns noch einmal ganz genau draufzuschauen, damit wir up to date bleiben. Und wie du in dieser Folge erfahren wirst: Bei den Empfehlungen zur notfallmedizinischen Betreuung eines Asthmaanfalls hat sich einiges getan. Salbutamol, Ketamin, Adrenalin oder Kortikosteroide inhalativ? Mach dich fit für deinen nächsten Asthmatiker mit Rettungsdienst LUKS - Der Notfallmedizin Podcast  mit dem Thema: Asthma in der Präklinik - Da ist der Wurm drinIn dieser Folge: - Definitionen rund um den Begriff Asthma- Was hat Asthma mit Würmern zu tun? - Die Hauptprobleme des Asthmatikers und seine Symptome - ihm wachsen Kiemen? - Salbutamol oder doch lieber Adrenalin? Die richtige Therapie – evidenzbasiertHomepage des Rettungsdienst LUKSLink zur letzten Folge zum Thema Notfall: Präklinischer NIV Profi (und zu allen anderen Folgen)Aus den Rettungsdienst LUKS Nachrichten: Zusammenfassung der Leitlinie zum Hitzschlag bei foamiohttps://foamio.org/leitlinie-treatment-of-heat-stroke-der-sccm/Videos zu invasiven Massnamen bei Life in the fastlanehttps://litfl.com/airway-cricothyroidotomy-surgical/Alle Evidenzen zu dieser Folge findest du hier: Nationale Versorgungsleitlinie Asthmahttps://register.awmf.org/assets/guidelines/nvl-002l_S3_Asthma_2024-08.pdfGINA Report (Leider kostenpflichtig) https://ginasthma.org/Amboss. (n.d.). Asthma bronchiale. Abgerufen am 20. August 2025, von https://www.amboss.com/de/wissen/asthma-bronchiale/Harnisch, L., (2024). Asthma bronchiale in der Notfallmedizin.  Nofallmedizin up2date, DOI: 10.1055/a-2190-4287Lommatzsch M, Criee CP, de Jong CCM et al. S2k-Leitlinie zur fachärztlichen Diagnostik und Therapie von Asthma 2023. Herausgegeben von der Deutschen Gesellschaft für Pneumologie und Beatmungsmedizin e.V. Pneumologie 2023; 77: 461–543. DOI: 10.1055/a-2070-2135Bülow A von et al. Severe asthma trajectories in adults: findings from the NORDSTAR cohort. EurRespir J 2023; Abgerufen am 12.08.2025. doi:10.1183/13993003.02474-2022

BUFFALO, NY — August 27, 2025 — A new #research paper was #published in Volume 17, Issue 7 of Aging (Aging-US) on July 24, 2025, titled “RNA-binding protein AUF1 suppresses cellular senescence and glycolysis by targeting PDP2 and PGAM1 mRNAs.” In this study, Hyejin Mun, Chang Hoon Shin, Mercy Kim, Jeong Ho Chang, and Je-Hyun Yoon from the University of Oklahoma and Kyungpook National University investigated how changes in cellular metabolism contribute to aging. Their findings offer potential targets for therapies aimed at slowing or reducing the effects of aging. As cells age, they often lose their ability to divide and begin releasing harmful signals that damage nearby tissues. This process, called cellular senescence, is linked to many age-related diseases. A key feature of senescent cells is their altered metabolism, where they use more glucose and oxygen, even when oxygen levels are low. This leads to the production of inflammatory substances and fatty acids, which can accelerate tissue damage. The study examined how these metabolic changes are controlled at the molecular level. Researchers found that AUF1, a protein that binds to RNA, normally helps prevent aging by breaking down two enzymes involved in glucose metabolism: PGAM1 and PDP2. When AUF1 is missing or inactive, these enzymes build up. This causes the cell to produce more energy and inflammatory molecules, which are common features of senescent cells. “Our high throughput profiling of mRNAs and proteins from Human Diploid Fibroblasts (HDFs) revealed that the expression of pyruvate metabolic enzymes is inhibited by the anti-senescent RNA-binding protein (RBP) AUF1 (AU-binding Factor 1).” The team also identified another protein, MST1, which becomes active during cellular stress and aging. MST1 modifies AUF1 in a way that stops it from doing its protective job. As a result, PGAM1 and PDP2 accumulate, leading to faster aging of the cell. Experiments using human fibroblast cells and mouse models confirmed that higher levels of these enzymes are linked to stronger signs of cellular aging. These findings improve our understanding of how metabolism affects the aging process. They highlight the MST1-AUF1-PDP2/PGAM1 pathway as a key factor in the metabolic shift seen in aging cells. Since these enzymes and proteins are already known to be involved in other diseases, existing or future therapies might be used to block this pathway and reduce the effects of aging. This study offers a new direction for senotherapy—a field focused on treating or removing aging cells. By adjusting glucose metabolism through AUF1 and its targets, scientists believe it may be possible to slow aging or limit its effects on tissue function. More research is needed, but these insights could lead to new strategies for managing age-related diseases and promoting healthier aging. DOI - https://doi.org/10.18632/aging.206286 Corresponding authors - Jeong Ho Chang - jhcbio@knu.ac.kr, and Je-Hyun Yoon - jehyun-yoon@ouhsc.edu Video short - https://www.youtube.com/watch?v=Gbu6USUSkgg Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206286 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, AUF1, MST1, senescence, glycolysis To learn more about the journal, 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/ 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

Aiden Deacon from the University of Minnesota-Twin Cities, Minneapolis, discusses a research paper he co-authored that was published in Volume 16 of Oncotarget, titled “Dissecting the functional differences and clinical features of R-spondin family members in metastatic prostate cancer.” DOI - https://doi.org/10.18632/oncotarget.28758 Correspondence to - Justin Hwang - jhwang@umn.edu Video interview - https://www.youtube.com/watch?v=OXKhWWU1gnY Abstract This study investigates the R-spondin family of genes (RSPO1/2/3/4), a group of secreted proteins that act as Wnt regulators, and their subsequent role in advanced prostate cancer (PC). When evaluating transcriptomic data from primary and metastatic PC patients, we found that alterations in RSPO2 were more prevalent than in other RSPO family members or Wnt-regulating genes APC and CTNNB1. Further, we found that RSPO2 alterations in PCs were significantly associated with worse disease-free survival. Through our in silico modeling, RSPO2 exhibited strong positive associations with genes regulating epithelial-mesenchymal transition (EMT) and double-negative prostate cancer (DNPC), but had negative correlations with androgen receptor (AR) and AR-associated genes. Furthermore, 3D modeling of RSPO2 revealed structural differences between itself and other RSPOs. In cell lines, RSPO2 overexpression caused up-regulation of EMT pathways, including EMT-regulatory transcription factors ZEB1, ZEB2, and TWIST1. Conversely, this was not observed when CTNNB1 was overexpressed in the same models. These findings highlight that, in PC, RSPO2 functions as a unique member of the R-spondin family by promoting genes and signaling pathways associated with aggressive PC, and RSPO2 amplifications are associated with poor outcomes in PC patients. Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28758 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, RSPO2, prostate cancer, Wnt signaling, genomics, therapeutics 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

Motherhood takes it out of you. Physically. Mentally. Emotionally. And if you've ever felt like your energy's been zapped or your brain's running on 1%, you're not imagining it and you're definitely not alone.In this episode, Dr Renee White takes you on a deep dive into a surprising topic: creatine supplementation for women's health. That little white powder you've seen on gym shelves? It turns out, it might hold more benefits for mums than we ever realised.From brain fog and bloating to sleep, strength and recovery, Renee unpacks the latest research on how this naturally occurring compound can support women through every life stage. With her signature mix of science and soul, she breaks it down in a way that's easy to understand and incredibly relevant for busy, brilliant mums like you.You'll hear about:

BUFFALO, NY — August 26, 2025 — A new #research paper was #published in Volume 17, Issue 7 of Aging (Aging-US) on July 21, 2025, titled “Association of DNA methylation age acceleration with digital clock drawing test performance: the Framingham Heart Study.” In this study, led by first author Zexu Li from the Department of Anatomy and Neurobiology at Boston University Chobanian and Avedisian School of Medicine, and corresponding author Chunyu Liu from Boston University Chobanian and Avedisian School of Medicine and Boston University School of Public Health, researchers found that individuals with signs of faster biological aging had lower scores on a digital cognitive test taken seven years later. The findings suggest that the rate at which a person ages at the molecular level may be associated with how well their brain functions as they grow older. Using data from the Framingham Heart Study, the researchers examined the relationship between biological aging and cognitive health. They used DNA methylation (DNAm) patterns—chemical changes that occur in the DNA with aging, known as epigenetic aging—to estimate biological age acceleration, and used the digital Clock Drawing Test (dCDT) to assess cognitive performance. The dCDT is a computerized version of a traditional pen-and-paper test that evaluates memory, thinking speed, and motor control. It provides an overall score and measures performance in specific areas such as spatial reasoning and movement. Among 1,789 participants, higher levels of epigenetic age acceleration were associated with significantly lower cognitive scores, particularly those over age 65. Of all the epigenetic aging markers examined, the DunedinPACE measure showed the strongest association with reduced brain function in both younger and older adults. Other measures, such as Horvath and PhenoAge, were associated with lower scores only in older adults. Key areas affected included motor skills and spatial reasoning. The researchers also studied blood-based protein markers used in an aging measure called GrimAge. Two proteins, PAI1 and ADM, were closely associated with lower cognitive scores, especially in older individuals. These results suggest that declines in brain and motor functions may reflect broader aging-related changes throughout the body. “Digital cognitive measures displayed stronger associations with most DNAm aging metrics among older compared to younger participants, likely to reflect the cumulative and nonlinear age influences on both brain health and DNAm.” This study supports the idea that epigenetic age may be a more accurate predictor of cognitive decline than chronological age. The dCDT, which is easy to use, automated, and more precise than traditional tools, may help detect early signs of brain aging. When combined with DNAm measures, it could become a valuable part of regular health screenings. Overall, the findings provide strong evidence that faster biological aging is associated with cognitive decline. This research may lead to better ways of identifying and monitoring brain health in aging populations. DOI - https://doi.org/10.18632/aging.206285 Corresponding author - Chunyu Liu - liuc@bu.edu Video short - https://www.youtube.com/watch?v=4hyjDqnPs8w Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts To learn more about the journal, 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/ 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

Fungal infections and disease have long been overlooked in terms of healthcare burden, with poor diagnostics and limited options for treatment and management. In 2022, the WHO published its first Fungal Priority Pathogens List as an effort to establish a global prioritised framework that addresses unmet research and development needs in fungal disease and antifungal resistance, as well as guides public health action [1]. In this episode of Communicable, Angela Huttner and Josh Nosanchuk invite Hatim Sati (WHO), the project lead in creating this list, and Dimitrios Kontoyiannis (MD Anderson Cancer Center, Houston, Texas), a clinician researcher studying fungal diagnostics and antifungal discovery, for a candid discussion on the making of and relevance of such a list. Apart from reviewing the fungal pathogens, the conversation also covers limitations of the list, what to expect for the next iteration, contextualising the list in one's local region, and the impact the list has had already on research funding and public awareness.This episode was edited by Kathryn Hostettler and peer reviewed by Andrisa Xhaxha from Elbasan, Albania. ReferencesWHO fungal priority pathogens list to guide research, development and public health action. Geneva: World Health Organization; 2022. Related podcast episodesCommunicable Episode 31: Climate change and fungal spread https://share.transistor.fm/s/db58f558 Communicable Episode 08: The nightmare series, part 1 – how to deal with Candida auris https://share.transistor.fm/s/c0616c4d Further reading Seidel D, et al. Impact of climate change and natural disasters on fungal infections. Lancet Microbe 2024. DOI: 10.1016/S2666-5247(24)00039-9Fisher MC and Denning DW. The WHO fungal priority pathogens list as a gamechanger. Nat Rev Microbiol 2023. DOI: 10.1038/s41579-023-00861-xShor E, et al. Tolerance and heteroresistance to echinocandins in Candida auris: conceptual issues, clinical implications, and outstanding questions. mSphere 2025. DOI: 10.1128/msphere.00161-25Panackal AA, et al. Geoclimatic influences on invasive aspergillosis after hematopoietic stem cell transplantation. Clin Infect Dis 2010. DOI: 10.1086/652761Lázár-Molnár E, et al. The PD-1/PD-L costimulatory pathway critically affects host resistance to the pathogenic fungus Histoplasma capsulatum. PNAS 2008. DOI: 10.1073/pnas.0711918105Mashal M, “A potentially fatal fungal infections cropping up among India's Covid patients.” New York Times 2021. https://www.nytimes.com/2021/05/09/world/india-covid-mucormycosis.html Thevissen K, et al. International survey on influenza-associated pulmonary aspergillosis (IAPA) in intensive care units: responses suggest low awareness and potential underdiagnosis outside Europe. Crit Care 2020. DOI: 10.1186/s13054-020-2808-8Pappas PG, et al. Clinical mycology today: A synopsis of the mycoses study group education and research consortium (MSGERC) second biennial meeting, September 27–30, 2018, Big Sky, Montana, a proposed global research agenda. Medical Mycology 2020. DOI: 10.1093/mmy/myaa034Hostettler K, et al. Communicable Episode 31: Climate change and fungal spread. CMI Communications 2025. DOI: 10.1016/j.cmicom.2025.105126

In the last 2 episodes we covered new updates in menopausal hormone therapy. However, we did not address TESTOSTERONE use. This episode idea comes from one our podcast family members and good friend, Eric. Eric is 100% correct: Testosterone replacement, when done correctly, has come along way. When is this indicated? Is this endorsed by professional medical/endocrine groups? What's the dose? We have fun stuff to review, so listen in!1. Davis SR, Baber R, Panay N, Bitzer J, Perez SC, Islam RM, Kaunitz AM, Kingsberg SA, Lambrinoudaki I, Liu J, Parish SJ, Pinkerton J, Rymer J, Simon JA, Vignozzi L, Wierman ME. Global Consensus Position Statement on the Use of Testosterone Therapy for Women. J Clin Endocrinol Metab. 2019 Oct 1;104(10):4660-4666. doi: 10.1210/jc.2019-01603. PMID: 31498871; PMCID: PMC6821450.2. Sharon J. Parish, James A. Simon, Susan R. Davis, Annamaria Giraldi, Irwin Goldstein, Sue W. Goldstein, Noel N. Kim, Sheryl A. Kingsberg, Abraham Morgentaler, Rossella E. Nappi, Kwangsung Park, Cynthia A. Stuenkel, Abdulmaged M. Traish, Linda Vignozzi, International Society for the Study of Women's Sexual Health Clinical Practice Guideline for the Use of Systemic Testosterone for Hypoactive Sexual Desire Disorder in Women, The Journal of Sexual Medicine, Volume 18, Issue 5, May 2021, Pages 849–867, https://doi.org/10.1016/j.jsxm.2020.10.0093. Levy, Barbara MD, MSCP; Simon, James A. MD, MSCP. A Contemporary View of Menopausal Hormone Therapy. Obstetrics & Gynecology 144(1):p 12-23, July 2024. | DOI: 10.1097/AOG.00000000000055534. NAMS The 2022 hormone therapy position statement of The North American Menopause Society: chrome-extension://efaidnbmnnnibpcajpcglclefindmkaj/https://menopause.org/wp-content/uploads/professional/nams-2022-hormone-therapy-position-statement.pdf

BUFFALO, NY — August 21, 2025 — A new #research paper was #published in Volume 17, Issue 7 of Aging (Aging-US) on July 17, 2025, titled “The influence of cancer on a forensic age estimation tool.” In this study by Charlotte Sutter, Daniel Helbling, Cordula Haas and Jacqueline Neubauer from the Zurich Institute of Forensic Medicine, University of Zurich and Onkozentrum Zurich, the researchers investigated how cancer might affect the accuracy of forensic tools used to estimate a person's age from blood samples. DNA methylation is a natural chemical modification of DNA that changes with age. Forensic scientists can use these changes to predict someone's age from biological traces, such as blood found at a crime scene. However, medical conditions like cancer can alter these patterns and potentially reduce the accuracy of such predictions. This study investigated whether various cancer types influence the DNA markers used in age estimation. “Our study is among the first to show whether it might be necessary to account for the influence of cancer on forensic age estimation tools in order to enhance estimation accuracy as much as possible.” The researchers applied the VISAGE enhanced age estimation tool, a widely used DNA methylation-based method, to blood samples from 100 cancer patients and 102 healthy individuals. Age predictions in the control group were generally accurate, with small average errors. Patients with solid tumors, including breast and lung cancers, showed only slightly less accurate results. In contrast, individuals with blood cancers, particularly chronic lymphocytic leukemia (CLL) and acute myeloid leukemia (AML), sometimes had large errors, with ages overestimated by as much as 50 years. Despite these few extreme cases, the study found that cancer does not typically have a strong impact on the accuracy of this forensic tool. Most cancer patients, even those undergoing treatment, had DNA methylation patterns similar to those of healthy individuals. The researchers found no consistent differences based on cancer type, stage, or treatment, except in isolated cases involving aggressive forms of cancer. The findings support the continued use of current forensic age estimation methods. While aggressive cancers may occasionally affect prediction accuracy, such cases are rare. The researchers suggest noting these conditions as a possible factor in unusually large errors, without requiring changes to standard practice. This study provides valuable information about how health conditions, such as cancer, may influence DNA-based age estimation. It strengthens confidence in the reliability of forensic age prediction tools, even when applied to individuals with a medical history of cancer. DOI - https://doi.org/10.18632/aging.206281 Corresponding author - Cordula Haas - cordula.haas@irm.uzh.ch Video short - https://www.youtube.com/watch?v=lcpwE50O4ss Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206281 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, forensic age, estimation age prediction, cancer, DNA methylation, age acceleration To learn more about the journal, 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/ 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 – August 19, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on August 19, 2025, titled “The SCD1 inhibitor aramchol interacts with regorafenib to kill GI tumor cells in vitro and in vivo.” In this study, led by first authors Laurence Booth and Michael R. Booth, along with corresponding author Paul Dent from Virginia Commonwealth University, researchers investigated how aramchol, a drug originally developed for liver disease, works with the cancer drug regorafenib in gastrointestinal (GI) tumor cells. They found that the combination is effective, especially in tumor cells with a specific genetic variant. The combined approach offers a potential new strategy for treating liver and colon cancers. Gastrointestinal cancers, such as liver and colon cancer, are serious global health challenges. Regorafenib, already approved for cancer treatment, can have limited impact and frequently causes side effects. Aramchol, a drug developed to treat fatty liver disease, affects how cancer cells process fats and energy. In this study, researchers tested whether combining these two drugs could improve GI cancer treatment, both in cells and mouse models. The results showed that the drug combination killed liver and colorectal cancer cells more effectively than either drug alone. In animal models, mice with human liver tumors had slower tumor growth, without showing signs of weight loss or other toxicity. The researchers also found that aramchol and regorafenib work together to block important survival pathways inside cancer cells. This combination was especially effective in cells with a genetic variant called ATG16L1 T300, which is more common in people of African ancestry. The treatment triggered stress responses in the cancer cells and disrupted key proteins required for survival. It also activated autophagy, a natural recycling process that clears out damaged parts, eventually leading to cancer cell death. “Aramchol interacted with the multi-kinase inhibitors sorafenib, regorafenib or lenvatinib, to kill GI tumor cells, with regorafenib exhibiting the greatest effect.” Aramchol is currently in clinical trials for fatty liver disease and has a well-established safety profile, while regorafenib is already FDA-approved for cancer treatment. Together, their combination could advance fast into clinical testing for patients with GI cancers. However, researchers note that additional studies are needed to support the launch of early-phase clinical trials. Altogether, this study may offer a more effective and less toxic alternative to current treatments for GI cancers. It also highlights the role of genetic variants in shaping treatment response, suggesting that future therapies could be more precisely tailored to each patient's unique genetic profile. DOI - https://doi.org/10.18632/oncotarget.28762 Correspondence to - Paul Dent - paul.dent@vcuhealth.org Video short - https://www.youtube.com/watch?v=5saAqsqxi-Q Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28762 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, macroautophagy, flux; ER stress, aramchol, regorafenib 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 — August 19, 2025 — A new #research paper was #published in Volume 17, Issue 7 of Aging (Aging-US) on July 7, 2025, titled “Epigenetic age and accelerated aging phenotypes: a tumor biomarker for predicting colorectal cancer.” In this study led by Su Yon Jung from the University of California, Los Angeles, researchers found a strong association between accelerated epigenetic aging and an increased risk of colorectal cancer in postmenopausal women. The study also indicated that lifestyle factors influence this risk. Colorectal cancer is one of the leading causes of cancer-related deaths worldwide, particularly in people over the age of 50. However, individuals do not all age at the same biological rate. Two people of the same chronological age can differ in their biological aging, which reflects the condition of their cells and tissues. This study focused on a specific measure of biological aging known as epigenetic aging, which is based on chemical changes to DNA. The researchers used data from the Women's Health Initiative Database for Genotypes and Phenotypes (WHI-dbGaP), which includes genetic and health information from postmenopausal white women aged 50 to 79. They applied three established “epigenetic clocks” to estimate epigenetic age from blood samples collected up to 17 years before a colorectal cancer diagnosis. These clocks measure how quickly a person is aging at the molecular level by tracking DNA methylation. Women with a higher epigenetic age than expected were significantly more likely to develop colorectal cancer “[…]we examined biological aging status in PBLs via three well-established epigenetic clocks—Horvath's, Hannum's and Levine's […].” The study also explored the role of lifestyle in modifying this risk. Women who consumed more fruits and vegetables showed no increased risk, even if they were epigenetically older. In contrast, women with both lower fruit and vegetable intake and signs of accelerated aging were up to 20 times more likely to develop colorectal cancer. This suggests that a healthy diet may help reduce cancer risk associated with biological aging. Another key finding involved women who had both ovaries removed before natural menopause. These women had a higher epigenetic age and, when combined with accelerated aging, a greater likelihood of developing colorectal cancer. This highlights the potential influence of hormonal and reproductive factors on aging and disease risk. The researchers validated their findings across several independent datasets, supporting the potential of blood-based epigenetic aging markers as early indicators of colorectal cancer risk. These markers could help guide early detection and prevention strategies in aging populations. However, the authors emphasize the need for independent large-scale replication studies. Overall, this study contributes to a better understanding of the association between epigenetic aging and cancer. It also supports the idea that modifiable lifestyle factors may reduce disease risk, even among those aging more rapidly at the cellular level. DOI - https://doi.org/10.18632/aging.206276 Corresponding author - Su Yon Jung - sjung@sonnet.ucla.edu Video short - https://www.youtube.com/watch?v=cq1MphQKmSk Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts To learn more about the journal, 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/ 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

Estevanico was a translator and guide, and was probably the first person of any race from outside the Americas to enter what’s now Arizona and New Mexico – which happened in 1539. Research: Birzer, Dedra McDonald and J.M.H. Clark. “Esteban Dorantes.” Peoples of the Historical Slave Trade. Journal of Slavery and Data Preservation. https://enslaved.org/fullStory/16-23-92882/ Birzer, Dedra McDonald. "Esteban." Oxford African American Studies Center. May 31, 2013. Oxford University Press. Date of access 30 Jul. 2025, https://oxfordaasc.com/view/10.1093/acref/9780195301731.001.0001/acref-9780195301731-e-34375 Chipman, Donald E. and Robert S. Wedd. “How Historical Myths Are Born...... And Why They Seldom Die.” The Southwestern Historical Quarterly , January, 2013. https://www.jstor.org/stable/24388345 Clark, J.M.H. "Esteban the African ‘Estebanico’." Oxford African American Studies Center. May 31, 2017. Oxford University Press. Date of access 30 Jul. 2025, https://oxfordaasc.com/view/10.1093/acref/9780195301731.001.0001/acref-9780195301731-e-73900 Docter, Mary. “Enriched by Otherness: The Transformational Journey of Cabeza de Vaca.” Christianity and Literature , Autumn 2008, Vol. 58, No. 1. Via JSTOR. https://www.jstor.org/stable/44313875 "Estevanico (1500-1539)." Encyclopedia of World Biography, Gale, 1998. Gale Academic OneFile, link.gale.com/apps/doc/A148426031/GPS?u=mlin_n_melpub&sid=bookmark-GPS&xid=41f83344. Accessed 28 July 2025. Flint, Richard. “Dorantes, Esteban de.” New Mexico Office of the State Historian. Via archive.org. https://web.archive.org/web/20110728080635/http://www.newmexicohistory.org/filedetails.php?fileID=464 Gordon, Richard A. “Following Estevanico: The Influential Presence of an African Slave in Sixteenth-century New World Historiography.” Colonial Latin American Review Vol. 15, No. 2, December 2006. Gordon-Reed, Annette. “Estebanico’ s America.” The Atlantic. June 2021. Herrick, Dennis. “Esteban.” University of New Mexico Press. 2018. Project MUSE. https://muse.jhu.edu/book/60233. Ilahiane, Hsain. “Estevan de Dorantes, Estevanico: The First Moroccan and African Explorer of the American Southwest.” Southwest Center. Via YouTube. 2/21/2024. https://www.youtube.com/watch?v=RLm0BsFDfvk Ilahiane, Hsain. “Estevan De Dorantes, the Moor or the Slave? The other Moroccan explorer of New Spain.” The Journal of North African Studies, 5:3, 1-14, DOI: 10.1080/13629380008718401 Ladd, Edmund J. “Zuni on the Day the Men in Metal Arrived.” From The Coronado Expedition to Tierra Nueva. Shirley Cushing Flint and Richard Flint, eds. University Press of Colorado. 2004. https://muse.jhu.edu/book/3827 Logan, Rayford. “Estevanico, Negro Discoverer of the Southwest: A Critical Reexamination.” Phylon (1940-1956), Vol. 1, No. 4 (4th Qtr., 1940). Via JSTOR. https://www.jstor.org/stable/272298 Sando, Joe S. “Pueblo nations: eight centuries of Pueblo Indian history.” Santa Fe, N.M. : Clear Light. 1992. Shields, E. Thomson. "Esteban." Oxford African American Studies Center. December 01, 2006. Oxford University Press. Date of access 30 Jul. 2025, https://oxfordaasc-com.proxy.bostonathenaeum.org/view/10.1093/acref/9780195301731.001.0001/acref-9780195301731-e-17021 Simour, Lhoussain. “(De)slaving history: Mostafa al-Azemmouri, the sixteenth-century Moroccan captive in the tale of conquest.” European Review of History—Revue europe´enne d’histoire, 2013 Vol. 20, No. 3. http://dx.doi.org/10.1080/13507486.2012.745830 Smith, Cassander L. “Beyond the Mediation: Esteban, Cabeza de Vaca's ‘Relación’ , and a Narrative Negotiation.” Early American Literature , 2012, Vol. 47, No. 2. Via JSTOR. https://www.jstor.org/stable/41705661 See omnystudio.com/listener for privacy information.

In this episode, Joe Moore is joined by Kat Murti, Executive Director of Students for Sensible Drug Policy (SSDP), the largest youth-led network working to end the war on drugs. SSDP organizes at the campus, local, state, federal, and international levels, with more than 100 chapters across the U.S. and sister organizations worldwide. Kat shares her personal journey into drug policy reform, from witnessing DEA raids on AIDS patients in the 1990s to fighting for civil liberties as a student at UC Berkeley. She explains how SSDP empowers young people to challenge outdated laws and promote policies rooted in compassion, scientific evidence, and human rights. Topics Discussed The War on Drugs as a War on Us: Kat's early realizations about the drug war's racism, injustice, and destruction of civil liberties. Her Path to SSDP: From working on California's Prop 19 cannabis campaign to serving on SSDP's board and eventually becoming Executive Director. Meta Censorship Campaign: Why Meta's restrictions on drug education and harm reduction content harm communities, and how SSDP is organizing public pressure to protect freedom of information online. Forced Institutionalization & Executive Orders: Kat critiques recent federal moves to expand forced treatment, cuts to naloxone training programs, and the misguided use of tariffs as “solutions” to the overdose crisis. The Fight Against DEA Scheduling of DOI & DOC: Why these research chemicals are vital to neuroscience and medicine, how SSDP challenged the DEA in court, and what's at stake for future research. Illogical Drug Policy & Careerism: How prohibition persists due to political incentives, propaganda, and entrenched bureaucratic interests. Building a Better Future: Realigning incentive structures, embracing harm reduction, and supporting community-based solutions to drug use. Key Takeaways The war on drugs is deeply racist, anti-science, and erodes civil liberties. Meta's censorship of harm reduction information actively endangers lives. Forced treatment doesn't work—addressing social conditions and providing safe housing does. DOI and DOC, rarely if ever used recreationally, are critical to medical research, and scheduling them would halt decades of progress. Real reform means both ending prohibition and creating environments where people feel supported, connected, and empowered. Links & Resources Students for Sensible Drug Policy (SSDP): ssdp.org Kat Murti on Twitter/X: @KatMurti Kat Murti on Instagram: @KittyRevolution SSDP Petition against Meta Censorship: ssdp.org

Credits: 0.25 AMA PRA Category 1 Credit™   CME/CE Information and Claim Credit: https://www.pri-med.com/online-education/podcast/frankly-speaking-cme-446 Overview: Overwhelmed by in-basket tasks? Discover a practical scheduling intervention that gives you time during the clinic day to manage portal messages. Learn how “portal practice slots” can reduce burnout, improve workflow, and empower you to advocate for changes that support sustainable, high-quality primary care. Episode resource links: J Gen Intern Med. DOI: 10.1007/s11606-025-09582-8 Guest: Robert A. Baldor MD, FAAFP Music Credit: Matthew Bugos Thoughts? Suggestions? Email us at FranklySpeaking@pri-med.com  

Credits: 0.25 AMA PRA Category 1 Credit™   CME/CE Information and Claim Credit: https://www.pri-med.com/online-education/podcast/frankly-speaking-cme-446 Overview: Overwhelmed by in-basket tasks? Discover a practical scheduling intervention that gives you time during the clinic day to manage portal messages. Learn how “portal practice slots” can reduce burnout, improve workflow, and empower you to advocate for changes that support sustainable, high-quality primary care. Episode resource links: J Gen Intern Med. DOI: 10.1007/s11606-025-09582-8 Guest: Robert A. Baldor MD, FAAFP Music Credit: Matthew Bugos Thoughts? Suggestions? Email us at FranklySpeaking@pri-med.com  

Fast fat loss in menopause is not really the goal. Let's be realistic and say this right out of the gate. Fast fat loss is a myth.  You may, however, drop inflammation fairly quickly with the right type of exercise.    Part 1: The Fat Burning Fundamentals Let's start with the basics. When we talk about fat burning during exercise, we need to understand two key concepts:  Percentage of Fat Used for Fuel  Total Calories Burned Here's something surprising: At rest, we burn about 85% fat for fuel. Your body is already a fat-burning machine when you're sitting on the couch!  Here's where it gets interesting.. During low-intensity exercise like walking, you burn a higher percentage of fat for fuel, but you're burning calories at a slower rate overall. During high-intensity exercise like running, you burn a lower percentage of fat for fuel, but you're torching calories much faster. Part 2: The EPOC Effect - Your Metabolic Afterburn EPOC or Excess Post-Exercise Oxygen Consumption, but I like to call it your metabolic afterburn. This is the energy your body continues to burn AFTER your workout is over. High-intensity exercise creates a significant EPOC effect. Your body keeps burning calories for hours after you finish your workout as it works to restore oxygen levels, repair tissues, and return to its normal state. It's like your metabolism stays revved up long after you've stopped moving. Low-intensity exercise produces minimal EPOC. Once you stop walking, your metabolism pretty quickly returns to baseline. You burned calories during the activity, but the party's over when you stop. This is where high-intensity exercise starts to look really appealing for fat loss. You're not just burning calories during the workout - you're creating a metabolic boost that lasts for hours. Know the Best Strategy for Fast Fat Loss in Menopause May Surprise You Part 3: Sprints vs Steady-State Running - The Game Changer When we compare running at a slow to moderate pace versus doing sprint intervals, the sprint work wins hands down for fat loss.  Sprint intervals create a massive EPOC effect. Your body works harder to recover from intense bursts, burning calories long after you're done. Sprint intervals are incredibly effective at burning both total body fat AND visceral belly fat. The beauty of sprints is that you can get incredible results in much less time. A 15-20 minute sprint session can be more effective for fat loss than an hour of steady jogging. For busy women in menopause, this efficiency factor is huge. Part 4: The Cortisol Connection - Why This Matters in Menopause Now we need to talk about cortisol, because this is where things get really important for women in menopause. High-intensity exercise creates a greater rise in cortisol compared to low-intensity exercise. This isn't necessarily bad! This cortisol response is actually normal and necessary. It's how your body releases blood sugar to be used as fuel and creates energy for exercise. Low-intensity exercise like walking creates little rise in cortisol. Comfortable walking, dancing, yoga, or tai chi often actually REDUCE cortisol levels. The problem isn't the acute cortisol rise from exercise itself. The problem is chronic elevated cortisol combined with high-intensity exercise when your system is already overloaded. If your stress bucket is already overflowing from work, relationships, poor sleep, and hormonal changes, adding high-intensity exercise makes it spill over. When cortisol is chronically elevated, it can sabotage your adrenal function and ultimately affect your thyroid. This is particularly relevant during menopause when our hormone systems are already in flux.  Choosing the Right Cardio for Fast Fat Loss in Menopause The Hot Not Bothered is open for enrollment as this episode goes live. If you need support getting a start, restart or reset, now is the time! Learn More Here   Part 5: The Real Running vs Walking Debate Here's where I want to challenge the traditional running versus walking debate. Maybe it's less about the percentage of fat burned for fuel and more about not burning yourself out. Let me give you a practical example from my own experience: Walking at a 5.0 pace on the treadmill is NOT comfortable for me. It's an effort - I'm breathing hard, I'm sweating, I'm working. But jogging at 5.8? That's actually quite slow for running. It's likely harder on my knees while not really providing enough impact to benefit my bone density. Here's a crucial point: Every time you run - meaning both feet leave the ground - you add four times your body weight in impact to your knee joints. Yet ironically, this repetitive impact isn't the kind of stimulus that optimally benefits bone density once you do it regularly. While jumping and purposeful impact exercises do provide bone density benefits, repetitive exercise loads like jogging don't create additional stress - they just create more of the same stress. So sometimes, a challenging walk might actually give you better results than an easy jog, with less wear and tear on your joints. The sad myth about running vs walking is that it will result in fast fat loss in menopause - or any time for that matter. Smarter Workouts for Fast Fat Loss in Menopause — Without Burnout Part 6: When Your Body Is Telling You to Slow Down Chronic cortisol elevation is often linked to inadequate recovery - particularly nutrition - than to workout intensity itself. If you're on a chronically low-carbohydrate or low-calorie diet, you may experience prolonged cortisol elevations regardless of your exercise. When your body lacks fuel, it compensates by releasing more cortisol to break down fat, muscle, and even bone tissue for energy. Chronic cortisol is more likely under these conditions: Too much too soon (occasional overreaching isn't a problem, but repeated overreaching is) Undereating before, during, or after exercise Lack of rest time between workouts for repair Inadequate sleep Planned diet or fasting state Lower intensity workouts may work better because you're not eating enough, not sleeping enough, or not managing your overall stress load. The biggest problem? Not eating enough. Going too low carb. Making statements like "my body loves this" when it's giving you signs you're exhausted, holding onto weight, or failing to gain muscle. No, it doesn't love it. Part 7: Making the Right Choice for YOU How do you decide between running and walking, or between steady-state and sprint work? Assess your current stress load: How's your sleep? Are you eating enough, especially carbohydrates? How are your energy levels throughout the day? Are you seeing the results you want? If you're well-rested, well-fed, and managing stress effectively, higher intensity work including sprints is incredibly effective for fat loss. If you're stressed, under-fueled, or sleep-deprived, walking or other lower-intensity activities is better right now.  That's not settling for less - that's being smart about working WITH your body instead of against it. The best exercise program is what you can do consistently while feeling energized and strong, not depleted and exhausted. Fast Fat Loss in Menopause Differs for Every Body in Every Stage Part 8: Practical Applications For sprint work: Start with just 1-2 sprint sessions per week. These could be 15-30 second all-out efforts followed by as much time needed for recovery, repeated 4-6 times. This gives you maximum fat-burning benefit with minimal time investment. For steady-state work: If you choose to run steadily, make sure it's at an intensity that's appropriately challenging. If you choose to walk, don't be afraid to make it challenging - hills, speed, or resistance can all increase the demand. For recovery: Always prioritize adequate nutrition and sleep. Your results happen during recovery, not just during the workout. Listen to your body's feedback. If you're consistently tired, holding onto weight despite "doing everything right," or feeling burnt out, it might be time to dial down the intensity and focus on recovery. Conclusion The bottom line? Both running and walking can be effective for fat loss, but the devil is in the details.  Sprint work offers incredible efficiency and targets visceral fat effectively. Steady-state cardio has its place, especially when recovery demands are high. The key is matching your exercise intensity to your body's current capacity for stress and recovery. During menopause, this becomes even more critical as our hormone systems are already adapting to change. Your exercise program should energize you, not exhaust you. It should work with your lifestyle, not against it. And it should leave you feeling strong and capable, not depleted and overwhelmed.   Remember, there's no real magic trick for fast fat loss in menopause. However, you can get there faster - sometimes by slowing down and sometimes by sprinting. But always by weight lifting.    References for Fast Fat Loss in Menopause:  Psychoneuroendocrinology. 2022, PMID: 35777076. Front Public Health, 2019, PMID: 31921741. Experimental Physiology, 2020, PMID: 32613697. Journal of Exercise Science & Fitness, 2023, PMID: 37927356. Diabetes & Metabolism, 2016, DOI: 10.1016/j.diabet.2016.07.031.   Other Episodes You Might Like: Previous Episode - Take Up Space: A Perimenopause BodyBuilder on Her Strength Journey Next Episode - The New Menopause Therapy: Confessions of a Femme Fatale More Like This What's Better Running or Walking for Midlife Fat Loss (and why) 8 Ways to Make Walking in Menopause MORE Beneficial   Resources:  Join the Hot, Not Bothered! Challenge to learn why timing matters and why what works for others is not working for you. Use Flipping 50 Scorecard & Guide to measure what matters with easy at-home self-assessment test you can do in minutes. Don't know where to start? Book your Discovery Call with Debra.

In this week's replay episode from 3 years ago, we delve into the world of pediatric heart transplantation and the impact that race or insurance status may have on outcomes. What are the factors that explain worse outcomes for black children waiting for a heart transplant? How is the PHTS Racial Disparity Taskforce working to reduce inequities in this field? What role does insurance status have on these outcomes? We speak with noted heart failure and transplantation expert, Dr. Neha Bansal who is Associate Professor of Pediatrics at The Icahn School of Medicine at Mount Sinai about this recent PHTS multicenter study.DOI: 10.1016/j.healun.2022.12.002

BUFFALO, NY – August 15, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on August 13, 2025, titled “Clinical and analytical validation of MI Cancer Seek®, a companion diagnostic whole exome and whole transcriptome sequencing-based comprehensive molecular profiling assay.” In this study, first authors Valeriy Domenyuk and Kasey Benson, along with corresponding author David Spetzler from Caris Life Sciences in Irving, Texas, introduce MI Cancer Seek, an FDA-approved test designed to deliver comprehensive tumor profiling. MI Cancer Seek demonstrated strong concordance with other FDA-approved companion diagnostics and serves as a powerful tool to guide treatment decisions in both adult and pediatric cancer patients. Cancer remains one of the most complex and diverse diseases to treat. With many targeted therapies currently FDA-approved, selecting the right one for a specific patient requires detailed genetic insights. MI Cancer Seek addresses this need by analyzing both DNA and RNA from a single tumor sample. The tool identifies key biomarkers linked to FDA-approved treatments for several major cancers, including breast, lung, colon, melanoma, and endometrial cancers. One of the most significant strengths of MI Cancer Seek is its ability to deliver accurate and reliable results from minimal tissue input (50 ng). Even when analyzing formalin-fixed paraffin-embedded samples, which are widely used but often degraded, the test maintained high levels of accuracy. It successfully detected important genetic alterations such as PIK3CA, EGFR, BRAF, and KRAS/NRAS mutations and measured tumor mutational burden (TMB) and microsatellite instability (MSI), both of which are key indicators for immunotherapy response. In clinical comparisons, the test achieved over 97% agreement with other FDA-approved diagnostic tools, confirming its reliability in detecting critical biomarkers. Notably, it showed near-perfect accuracy in identifying MSI status in colorectal and endometrial cancers. The researchers also demonstrated that the test maintains precision across different lab conditions and varying DNA input levels, confirming its robustness for routine clinical use. Beyond its role as a companion diagnostic, MI Cancer Seek incorporates additional features developed under its predecessor, MI Tumor Seek Hybrid. These include detection of homologous recombination deficiency, structural variants, and cancer-related viruses. It also includes advanced tools such as the Genomic Probability Score for identifying the tissue of origin in cancers of unknown primary, as well as a gene signature to guide first-line chemotherapy in colorectal cancer. “One limitation to be considered is the low PPA for ERBB2 CNA detection.” By offering deeper genetic insights from a single, small sample, MI Cancer Seek has the potential to streamline diagnostics, reduce testing costs, and connect patients to effective therapies more quickly. As precision medicine continues to expand, this assay stands out as a comprehensive and efficient solution for meeting the evolving needs of modern oncology. DOI - https://doi.org/10.18632/oncotarget.28761 Correspondence to - David Spetzler - dspetzler@carisls.com Video short - https://www.youtube.com/watch?v=D4hd2FxCYY8 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ 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 — August 14, 2025 — A new #research paper was #published in Volume 17, Issue 7, of Aging (Aging-US) on July 3, 2025, titled “Frailty associates with respiratory exacerbations and mortality in the COPDGene cohort.” In this study, led by first author Eleanor Kate Phillips from Brigham and Women's Hospital and corresponding author Dawn L. DeMeo from Brigham and Women's Hospital and Harvard Medical School, researchers investigated how frailty impacts lung health and survival in individuals with a history of cigarette smoking. They found that frailty raises the risk of lung attacks and death, even in smokers with preserved lung function. This result shows why all current and former smokers should be checked for frailty. Frailty is a condition that makes the body more vulnerable to illness, especially in older adults. This study focused on more than 2,600 adults with a history of heavy smoking, many of whom showed no signs of lung damage on standard tests. At the second follow-up visit, participants were categorized as robust, prefrail, or frail and followed for about three years. Researchers tracked how often they experienced respiratory attacks, such as episodes of severe coughing or breathlessness, and whether they survived during that period. “COPDGene is a cohort study of individuals aged 45–80 with a minimum 10 pack-year smoking history.” The results showed that people who were frail had a three- to five-fold higher chance of developing serious or frequent respiratory attacks compared to those who were robust. These risks were not limited to people with chronic lung disease. In fact, many frail participants with normal lung function still faced a significantly higher chance of lung attacks and death. Even those in the “prefrail” stage, a milder form of frailty, were more likely to experience health complications. The research team also found that frailty was associated with an accelerated pace of biological aging, measured using a DNA-based test called DunedinPACE. This supports the idea that frailty may reflect deeper biological changes in the body that go beyond what traditional lung function tests can detect. These findings challenge the idea that standard lung tests can rule out future respiratory complications in people with a history of smoking. Altogether, the study shows that simple frailty checks could help identify early health problems, allowing for timely interventions that may prevent hospitalizations and potentially save lives. The study suggests that frailty screening may be a valuable tool in public health efforts to reduce respiratory disease and improve outcomes for aging adults. DOI - https://doi.org/10.18632/aging.206275 Corresponding author - Dawn L. DeMeo - redld@channing.harvard.edu Video short - https://www.youtube.com/watch?v=G1XQhQN6PQ8 Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206275 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, frailty, cigarette smoking, respiratory exacerbations, COPD, epigenetic aging To learn more about the journal, 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/ 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

In this 10-minute episode, Zach Baker, DPT, and Asher Roberts, DPT, unpack a 2024 study by Hashida et al. that sheds light on an often-overlooked issue: athletes may still have lingering deficits even after being cleared to return to play. Learn how a simple, feasible dual-task test can reveal residual post-concussion impairments that standard assessments might miss—and how this can impact your return-to-play decisions in the clinic.Referenced Study:Hashida et al. (2024). Feasible dual-task detects residual post-concussion deficits after return-to-play.DOI: 10.1080/02640414.2024.2447666

Send us a textHost Lindsay Persohn reflects on Season 5's journey through literacy education, where conversations explored evolving reading debates, strategies for supporting diverse learners, vocabulary development, and content-specific literacies. Lindsay also shares a recap of research presentations and publications related to podcasting by the Classroom Caffeine team.Season 6 of the show promises two compelling special series. The first examines the transformative power of graduate studies for educators, featuring candid conversations with professionals who've pursued advanced degrees and discovered new pathways for growth and impact. These discussions illuminate how continued education shapes not just career opportunities but also classroom practice and student outcomes.The second series spotlights the Spencer Foundation-supported "Stories to Live By" project, exploring how Florida teachers help students navigate climate challenges through place-based learning. As communities face hurricanes, flooding, and environmental uncertainty, these educators work at the critical intersection of climate science, political tensions, and students' lived experiences—empowering young people to think critically and act practically in response to ongoing change.Publications mentioned in this episode:Persohn, L., Burger, L., & Geren, K. V. (2025). Pod Clubs for professional community: learning, conversation, and relationships. Professional Development in Education, 1–21. https://doi.org/10.1080/19415257.2025.2514703Branson, S.M., Persohn, L., Burger, L., Geren, K.V., & Robertson Stemme, M. (2025). Collaborative Connections in ‘Pod Clubs' for Professional Learning. In C. Bohem, T. Canfer, & C. Salazar (Eds.) in Podcasting & Education: Concepts, Communities & Case Studies. Routledge.Persohn, L., & Branson, S. (2025). Scholarly Podcasting for Research Dissemination: A Scoping Review. SAGE Open, 15(1). https://doi.org/10.1177/21582440241311694 (Direct link to available publication: https://journals.sagepub.com/doi/10.1177/21582440241311694.)Persohn, L. & Branson, S.M. (2024). Broadening Legitimacy of Scholarly Podcasting as Knowledge Dissemination: Metrics, Opportunities and Considerations. Publishing Research Quarterly, 40(3). DOI: https://doi.org/10.1007/s12109-024-10005-5Connect with Classroom Caffeine at www.classroomcaffeine.com or on Instagram, Facebook, Twitter, and LinkedIn.

BUFFALO, NY - August 13, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on July 29, 2025, titled “PCAIs stimulate MAPK, PI3K/AKT pathways and ROS-Mediated apoptosis in aromatase inhibitor-resistant breast cancer cells while disrupting actin filaments and focal adhesion.” In this study, led by first author Jassy Mary S. Lazarte and corresponding author Nazarius S. Lamango from Florida A&M University College of Pharmacy and Pharmaceutical Sciences, researchers investigated a new class of compounds called polyisoprenylated cysteinyl amide inhibitors (PCAIs) as a potential treatment for aromatase inhibitor (AI) therapy resistant breast cancer. Aromatase inhibitors are a common treatment for estrogen receptor-positive (ER+) breast cancer, but many patients eventually develop resistance, leaving fewer therapeutic options. The study focused on a PCAI compound called NSL-YHJ-2-27, which was tested in long-term letrozole-treated breast cancer cells (LTLT-Ca), an experimental model of AI therapy resistance. NSL-YHJ-2-27 activated two major signaling pathways, MAPK and PI3K/AKT. Although these pathways typically support cancer cell survival, their overstimulation by PCAIs led to increased oxidative stress, damaging the cells and inducing cell death by apoptosis. The compound also reduced levels of RAC1 and CDC42, proteins involved in maintaining cell shape and movement. These alterations resulted in cytoskeletal disruption and reduced structural integrity, making the cancer cells more vulnerable and less capable of spreading. Importantly, the effects of NSL-YHJ-2-27 persisted after the compound was removed, suggesting long-term control over AI resistant cancer cells may be possible. “PCAIs inhibited cell proliferation and colony formation by 95% and 74%, respectively, increased active caspase 7 and BAX 1.5-fold and 56%, respectively. NSL-YHJ-2-27 (10 μM) induced LTLT-Ca spheroid degeneration by 61%.” As a new class of targeted molecules, PCAIs represent an innovative approach distinct from traditional endocrine therapies. Their ability to affect multiple cellular mechanisms simultaneously makes them promising candidates for future drug development. Overall, this study presents a promising new approach for treating AI therapy-resistant breast cancer. By targeting cellular pathways that support survival and mobility, PCAIs like NSL-YHJ-2-27 could provide a novel strategy to manage advanced or resistant forms of the disease. Further research, including in vivo studies and clinical trials, will be essential to confirm these findings and evaluate their therapeutic potential. DOI - https://doi.org/10.18632/oncotarget.28759 Correspondence to - Nazarius S. Lamango - nazarius.lamango@famu.edu Video short - https://www.youtube.com/watch?v=8xQEilloO9Q Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28759 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, PCAIs, ROS, MAPK, PI3K/AKT, LTLT-Ca cells 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 — August 12, 2025 — A new #research perspective was #published in Aging (Aging-US) on July 8, 2025, titled “Exercise as a geroprotector: focusing on epigenetic aging.” In this perspective, led by Takuji Kawamura from Tohoku University, researchers reviewed existing evidence from scientific studies showing that regular exercise, physical activity, and fitness may influence epigenetic aging and potentially reverse it, offering a promising way to extend healthspan and improve long-term health. Epigenetic aging refers to changes in the body's DNA that reflect how quickly a person is aging at the molecular level. It is measured using epigenetic clocks, which analyze patterns of DNA methylation, a chemical modification that can affect gene activity. Unlike chronological age, which simply counts the number of years lived, epigenetic aging presents a more accurate picture of how well the body's cells and tissues are functioning. This process is influenced by various factors, including lifestyle, and has become a powerful tool for studying aging. This perspective highlights that while general physical activity, such as walking or doing household tasks, offers health benefits, structured exercise routines that are planned, repetitive, and goal-directed appear to have stronger effects on slowing epigenetic aging. Physical fitness, especially high cardiorespiratory capacity, is also closely associated with slower epigenetic aging. The authors also discuss key findings from both human and animal studies. In mice, structured endurance and resistance training reduced age-related molecular changes in muscle tissue. In humans, multi-week exercise interventions demonstrated reductions in biological age markers in blood and skeletal muscle. One study found that sedentary middle-aged women reduced their epigenetic age by two years after just eight weeks of combined aerobic and strength training. Another study showed that older men with higher oxygen uptake levels, a key measure of cardiovascular fitness, had significantly slower epigenetic aging. “These findings suggest that maintaining physical fitness delays epigenetic aging in multiple organs and supports the notion that exercise as a geroprotector confers benefits to various organs.” The research also examines which organs benefit most from exercise. While skeletal muscle has been a central focus, new evidence shows that regular physical training may also slow aging in the heart, liver, fat tissue, and even the gut. In addition, Olympic athletes were found to have slower epigenetic aging than non-athletes, suggesting that long-term, intensive physical activity may have lasting anti-aging effects. The authors call for further research to understand why some individuals respond more strongly to exercise than others and how different types of training influence aging in various organs. They also point out the importance of developing personalized exercise programs to maximize anti-aging benefits. Overall, the findings support the growing recognition that maintaining physical fitness is not only essential for daily health but may also serve as one of the most effective tools for slowing the body's internal aging process. DOI - https://doi.org/10.18632/aging.206278 Corresponding author - Takuji Kawamura - takuji.kawamura.b8@tohoku.ac.jp Video short - https://www.youtube.com/watch?v=Wro3_wBovdE To learn more about the journal, 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/ 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 – August 11, 2025 – A new #researchpaper was #published in Volume 16 of Oncotarget on July 25, 2025, titled “Dissecting the functional differences and clinical features of R-spondin family members in metastatic prostate cancer.” In this study, researchers led by first author Aiden Deacon and corresponding author Justin Hwang from the University of Minnesota-Twin Cities investigated a group of genes known as the R-spondin family (RSPO1/2/3/4) in advanced prostate cancer (PC). The RSPO gene family regulates Wnt signaling, a pathway involved in cancer progression. Prostate cancer is the most common cancer among men in the United States and becomes especially dangerous when it spreads beyond the prostate. Most patients are treated with hormone therapies that target the androgen receptor; however, many tumors eventually become resistant. The research team analyzed thousands of tumor samples and found that RSPO2 alterations were more common than changes in other R-spondin genes or even some well-known cancer-related genes like CTNNB1 and APC. RSPO2 amplification occurred in over 20% of metastatic prostate cancer. Patients with these alterations showed signs of more aggressive disease, including higher mutation rates and greater tumor complexity. Using laboratory models, the team discovered that RSPO2 increases cancer cell growth and triggers a biological process called epithelial-mesenchymal transition (EMT). EMT is known to promote tumor spread and resistance to standard treatments. Unlike other genes in the same pathway, RSPO2 also appeared to reduce the activity of androgen receptor genes, suggesting it drives a type of prostate cancer that no longer relies on hormones for growth. “In cell lines, RSPO2 overexpression caused up-regulation of EMT pathways, including EMT-regulatory transcription factors ZEB1, ZEB2, and TWIST1.” Importantly, RSPO2 showed structural differences from other R-spondin proteins, which may allow researchers to design drugs that specifically block its activity. Current therapies targeting the Wnt pathway are limited, and there are no approved drugs that inhibit RSPO2. However, this study highlights RSPO2 as a promising therapeutic target, especially for patients who do not respond to existing hormone-based treatments. This research adds critical knowledge about how aggressive prostate cancers develop and persist despite therapy. The identification of RSPO2 as a key driver of disease progression opens new possibilities for treatment strategies aimed at improving outcomes for patients with advanced prostate cancer. DOI - https://doi.org/10.18632/oncotarget.28758 Correspondence to - Justin Hwang - jhwang@umn.edu Video short - https://www.youtube.com/watch?v=iyu5D_c1dbY Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28758 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, RSPO2, prostate cancer, Wnt signaling, genomics, therapeutics 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

This week I'm joined by Dr. Christopher Wallis, a urologist and researcher whose groundbreaking work shows something that might just change the way you think about surgery and medicine: patients are more likely to survive—and thrive—when operated on by a female surgeon and physician. We dive deep into the data, including studies across multiple countries and specialties, and unpack the consistent 5% reduction in 30-day mortality rates when the surgeon is a woman. Dr. Wallis also discusses how female anesthesiologists impact outcomes, why communication and trust matter so much in surgery, and how female physicians are often unfairly penalized for complications. This episode is more than stats—it's about challenging the system, confronting bias, and empowering both patients and physicians to make more informed, conscious choices. If you've ever wondered whether gender matters in medicine, or how we can build a better, fairer healthcare system—don't miss this one. We cover: ✔️ Why female surgeons lead to better outcomes ✔️ The role of bias and the “rigged” system women in medicine face ✔️ What patients should look for in a surgical team ✔️ Why systemic change is long overdue in healthcare Let's get into it. DOI:10.1097/SLA.0000000000006217 http://dx.doi.org/10.1136/bmj-2023-075484 https://uofturology.ca/directory/faculty/wallis-chris/ Want more honest, empowering conversations like this one?⁠⁠⁠Preorder my Next Book⁠⁠⁠ share this episode, and leave a review to help others find this important work. Let's stop leaving women out of the conversation—especially when it comes to sex, health, and healing. Listen to my Tedx Talk: ⁠⁠⁠⁠⁠⁠⁠⁠⁠Why we need adult sex ed⁠⁠⁠⁠⁠⁠⁠⁠⁠ ⁠⁠⁠⁠⁠⁠⁠⁠⁠Take my Adult Sex Ed Master Class:⁠⁠⁠⁠⁠⁠⁠⁠⁠ ⁠⁠⁠⁠⁠⁠⁠⁠⁠My Website⁠⁠⁠⁠⁠⁠⁠⁠⁠ Interested in my sexual health and hormone clinic? ⁠⁠⁠⁠⁠⁠⁠⁠⁠Waitlist is open⁠⁠⁠⁠⁠⁠⁠⁠ Thanks to our sponsor ⁠⁠⁠⁠⁠⁠⁠⁠⁠Midi Women's Health⁠⁠⁠⁠⁠⁠⁠⁠⁠. Designed by midlife experts, delivered by experienced clinicians, covered by insurance.Midi is the first virtual care clinic made exclusively for women 40+. Evidence-based treatments. Personalized midlife care.⁠⁠⁠⁠⁠⁠⁠⁠⁠https://www.joinmidi.com Learn more about your ad choices. Visit podcastchoices.com/adchoices

Welcome to "PICU Doc on Call," the podcast where real cases meet real expertise at the bedside! Join Dr. Monica Gray, Dr. Pradip Kamat, and Dr. Rahul Damania as they unravel the mysteries of pediatric critical care. In today's episode, our team dives into the compelling case of a previously healthy seven-year-old girl who arrives with seizures, right arm weakness, and sudden respiratory failure. Together, they'll break down the diagnosis and management of Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease, also known as MOGAD. This autoimmune demyelinating disorder can challenge even the most seasoned clinicians. Tune in as our experts walk you through the clinical features, essential diagnostic workup, and the critical importance of early immunosuppressive therapy. Whether you're at the bedside or on the go, this episode is packed with practical pearls and a multidisciplinary approach to recognizing and treating acute pediatric neuroimmunological emergencies in the PICU. Let's get started!Show Highlights:Presentation of a complex pediatric case involving a seven-year-old girl with new-onset seizures and acute respiratory failureDiscussion of Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD) as an autoimmune demyelinating disorderOverview of the clinical presentation and diagnostic criteria for autoimmune encephalitisImportance of a broad differential diagnosis, including infectious and autoimmune causes, in pediatric patients with seizures and neurological deficitsDiagnostic approach involving MRI, lumbar puncture, and antibody testing for MOGADManagement strategies for MOGAD, including stabilization, seizure control, and immunosuppressive therapyNeurocritical care considerations for monitoring and treating elevated intracranial pressureLong-term management challenges and the need for multidisciplinary care in pediatric patients with MOGADDiscussion of potential outcomes and the risk of relapse in children with MOGAD.Emphasis on the importance of early and comprehensive diagnostic testing to avoid misdiagnosisReferences:Fuhrman & Zimmerman - Pediatric Critical Care 6th Edition, Chapter 64Gole S, Anand A. Autoimmune Encephalitis. [Updated 2023 Jan 2]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK578203/Salama S, Khan M, Pardo S, Izbudak I, Levy M. MOG antibody-associated encephalomyelitis/encephalitis. Mult Scler. 2019 Oct;25(11):1427-1433. doi: 10.1177/1352458519837705. Epub 2019 Mar 25. PMID: 30907249; PMCID: PMC6751007Lancaster E. The Diagnosis and Treatment of Autoimmune Encephalitis. J Clin Neurol. 2016 Jan;12(1):1-13. doi: 10.3988/jcn.2016.12.1.1. PMID: 26754777; PMCID: PMC4712273.Fisher KS, Illner A, Kannan V. Pediatric neuroinflammatory diseases in the intensive care unit. Semin Pediatr Neurol. 2024 Apr;49:101118. Doi: 10.1016/j.spen.2024.101118. Epub 2024 Feb 1. PMID: 38677797.Hébert J, Muccilli A, Wennberg RA, Tang-Wai DF. Autoimmune Encephalitis and Autoantibodies: A Review of Clinical Implications. J Appl Lab Med. 2022 Jan 5;7(1):81-98. Doi: 10.1093/jalm/jfab102. PMID: 34996085.Lopez JA, Denkova M, Ramanathan S, Dale RC, Brilot F. Pathogenesis of autoimmune demyelination: from multiple sclerosis to neuromyelitis optica spectrum disorders and myelin oligodendrocyte glycoprotein antibody-associated disease. Clin Transl Immunology. 2021 Jul 26;10(7):e1316. doi: 10.1002/cti2.1316. PMID: 34336206; PMCID: PMC8312887.

Ethics in the field of infectious disease can be a delicate interplay between treating the individual patient and protecting the collective health of a society. Sometimes these two mandates go hand in hand; at other times they can appear to be in conflict. In this episode of Communicable, Dr. Angela Huttner invites Drs. Zeb Jamrozik (Melbourne, Australia) and Beenish Syed (Karachi, Pakistan), two members of ESCMID's Ethics Advisory Committee, to unpack different scenarios encountered in the field of infectious disease from an ethics standpoint: how one ethically allocates scarce resources like antimicrobials; whether there is ethical justification for coercive public-health measures like lockdowns; and whether the need to collect evidence to advance patient care could include other models besides opt-in informed consent. This episode was edited by Dr. Kathryn Hostettler and peer reviewed by Dr. Goulia Ohan of Yerevan State Medical University, Yerevan, Armenia.Further reading:Barosa M, et al. The Ethical Obligation for Research During Public Health Emergencies: Insights From the COVID-19 Pandemic. Med Health Care Philos 2024. DOI: 10.1007/s11019-023-10184-6Symons X, et al. Why should HCWs receive priority access to vaccines in a pandemic? BMC Med Ethics 2021. DOI: 10.1186/s12910-021-00650-2Thorsteinsdottir B and Madsen BE. Prioritizing health care workers and first responders for access to the COVID19 vaccine is not unethical, but both fair and effective – an ethical analysis. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine 2021. DOI: 10.1186/s13049-021-00886-2Huttner A, Leibovici L, Theuretzbacher U, Huttner B, Paul M. Closing the evidence gap in infectious disease: point-of-care randomization and informed consent. Clin Microbiol Infect 2017;23(2):73-77. DOI: 10.1016/j.cmi.2016.07.029

A version of this essay has been published by firstpost.com at https://www.firstpost.com/opinion/shadow-warrior-from-crisis-to-advantage-how-india-can-outplay-the-trump-tariff-gambit-13923031.htmlA simple summary of the recent brouhaha about President Trump's imposition of 25% tariffs on India as well as his comment on India's ‘dead economy' is the following from Shakespeare's Macbeth: “full of sound and fury, signifying nothing”. Trump further imposed punitive tariffs totalling 50% on August 6th allegedly for India funding Russia's war machine via buying oil.As any negotiator knows, a good opening gambit is intended to set the stage for further parleys, so that you could arrive at a negotiated settlement that is acceptable to both parties. The opening gambit could well be a maximalist statement, or one's ‘dream outcome', the opposite of which is ‘the walkway point' beyond which you are simply not willing to make concessions. The usual outcome is somewhere in between these two positions or postures.Trump is both a tough negotiator, and prone to making broad statements from which he has no problem retreating later. It's down-and-dirty boardroom tactics that he's bringing to international trade. Therefore I think Indians don't need to get rattled. It's not the end of the world, and there will be climbdowns and adjustments. Think hard about the long term.I was on a panel discussion on this topic on TV just hours after Trump made his initial 25% announcement, and I mentioned an interplay between geo-politics and geo-economics. Trump is annoyed that his Ukraine-Russia play is not making much headway, and also that BRICS is making progress towards de-dollarization. India is caught in this crossfire (‘collateral damage') but the geo-economic facts on the ground are not favorable to Trump.I am in general agreement with Trump on his objectives of bringing manufacturing and investment back to the US, but I am not sure that he will succeed, and anyway his strong-arm tactics may backfire. I consider below what India should be prepared to do to turn adversity into opportunity.The anti-Thucydides Trap and the baleful influence of Whitehall on Deep StateWhat is remarkable, though, is that Trump 2.0 seems to be indistinguishable from the Deep State: I wondered last month if the Deep State had ‘turned' Trump. The main reason many people supported Trump in the first place was the damage the Deep State was wreaking on the US under the Obama-Biden regime. But it appears that the resourceful Deep State has now co-opted Trump for its agenda, and I can only speculate how.The net result is that there is the anti-Thucydides Trap: here is the incumbent power, the US, actively supporting the insurgent power, China, instead of suppressing it, as Graham Allison suggested as the historical pattern. It, in all fairness, did not start with Trump, but with Nixon in China in 1971. In 1985, the US trade deficit with China was $6 million. In 1986, $1.78 billion. In 1995, $35 billion.But it ballooned after China entered the WTO in 2001. $202 billion in 2005; $386 billion in 2022.In 2025, after threatening China with 150% tariffs, Trump retreated by postponing them; besides he has caved in to Chinese demands for Nvidia chips and for exemptions from Iran oil sanctions if I am not mistaken.All this can be explained by one word: leverage. China lured the US with the siren-song of the cost-leader ‘China price', tempting CEOs and Wall Street, who sleepwalked into surrender to the heft of the Chinese supply chain.Now China has cornered Trump via its monopoly over various things, the most obvious of which is rare earths. Trump really has no option but to give in to Chinese blackmail. That must make him furious: in addition to his inability to get Putin to listen to him, Xi is also ignoring him. Therefore, he will take out his frustrations on others, such as India, the EU, Japan, etc. Never mind that he's burning bridges with them.There's a Malayalam proverb that's relevant here: “angadiyil thottathinu ammayodu”. Meaning, you were humiliated in the marketplace, so you come home and take it out on your mother. This is quite likely what Trump is doing, because he believes India et al will not retaliate. In fact Japan and the EU did not retaliate, but gave in, also promising to invest large sums in the US. India could consider a different path: not active conflict, but not giving in either, because its equations with the US are different from those of the EU or Japan.Even the normally docile Japanese are beginning to notice.Beyond that, I suggested a couple of years ago that Deep State has a plan to enter into a condominium agreement with China, so that China gets Asia, and the US gets the Americas and the Pacific/Atlantic. This is exactly like the Vatican-brokered medieval division of the world between Spain and Portugal, and it probably will be equally bad for everyone else. And incidentally it makes the Quad infructuous, and deepens distrust of American motives.The Chinese are sure that they have achieved the condominium, or rather forced the Americans into it. Here is a headline from the Financial Express about their reaction to the tariffs: they are delighted that the principal obstacle in their quest for hegemony, a US-India military and economic alliance, is being blown up by Trump, and they lose no opportunity to deride India as not quite up to the mark, whereas they and the US have achieved a G2 detente.Two birds with one stone: gloat about the breakdown in the US-India relationship, and exhibit their racist disdain for India yet again.They laugh, but I bet India can do an end-run around them. As noted above, the G2 is a lot like the division of the world into Spanish and Portuguese spheres of influence in 1494. Well, that didn't end too well for either of them. They had their empires, which they looted for gold and slaves, but it made them fat, dumb and happy. The Dutch, English, and French capitalized on more dynamic economies, flexible colonial systems, and aggressive competition, overtaking the Iberian powers in global influence by the 17th century. This is a salutary historical parallel.I have long suspected that the US Deep State is being led by the nose by the malign Whitehall (the British Deep State): I call it the ‘master-blaster' syndrome. On August 6th, there was indirect confirmation of this in ex-British PM Boris Johnson's tweet about India. Let us remember he single-handedly ruined the chances of a peaceful resolution of the Ukraine War in 2022. Whitehall's mischief and meddling all over, if you read between the lines.Did I mention the British Special Force's views? Ah, Whitehall is getting a bit sloppy in its propaganda.Wait, so is India important (according to Whitehall) or unimportant (according to Trump)?Since I am very pro-American, I have a word of warning to Trump: you trust perfidious Albion at your peril. Their country is ruined, and they will not rest until they ruin yours too.I also wonder if there are British paw-prints in a recent and sudden spate of racist attacks on Indians in Ireland. A 6-year old girl was assaulted and kicked in the private parts. A nurse was gang-raped by a bunch of teenagers. Ireland has never been so racist against Indians (yes, I do remember the sad case of Savita Halappanavar, but that was religious bigotry more than racism). And I remember sudden spikes in anti-Indian attacks in Australia and Canada, both British vassals.There is no point in Indians whining about how the EU and America itself are buying more oil, palladium, rare earths, uranium etc. from Russia than India is. I am sorry to say this, but Western nations are known for hypocrisy. For example, exactly 80 years ago they dropped atomic bombs on Hiroshima and Nagasaki in Japan, but not on Germany or Italy. Why? The answer is uncomfortable. Lovely post-facto rationalization, isn't it?Remember the late lamented British East India Company that raped and pillaged India?Applying the three winning strategies to geo-economicsAs a professor of business strategy and innovation, I emphasize to my students that there are three broad ways of gaining an advantage over others: 1. Be the cost leader, 2. Be the most customer-intimate player, 3. Innovate. The US as a nation is patently not playing the cost leader; it does have some customer intimacy, but it is shrinking; its strength is in innovation.If you look at comparative advantage, the US at one time had strengths in all three of the above. Because it had the scale of a large market (and its most obvious competitors in Europe were decimated by world wars) America did enjoy an ability to be cost-competitive, especially as the dollar is the global default reserve currency. It demonstrated this by pushing through the Plaza Accords, forcing the Japanese yen to appreciate, destroying their cost advantage.In terms of customer intimacy, the US is losing its edge. Take cars for example: Americans practically invented them, and dominated the business, but they are in headlong retreat now because they simply don't make cars that people want outside the US: Japanese, Koreans, Germans and now Chinese do. Why were Ford and GM forced to leave the India market? Their “world cars” are no good in value-conscious India and other emerging markets.Innovation, yes, has been an American strength. Iconic Americans like Thomas Edison, Henry Ford, and Steve Jobs led the way in product and process innovation. US universities have produced idea after idea, and startups have ignited Silicon Valley. In fact Big Tech and aerospace/armaments are the biggest areas where the US leads these days.The armaments and aerospace tradeThat is pertinent because of two reasons: one is Trump's peevishness at India's purchase of weapons from Russia (even though that has come down from 70+% of imports to 36% according to SIPRI); two is the fact that there are significant services and intangible imports by India from the US, of for instance Big Tech services, even some routed through third countries like Ireland.Armaments and aerospace purchases from the US by India have gone up a lot: for example the Apache helicopters that arrived recently, the GE 404 engines ordered for India's indigenous fighter aircraft, Predator drones and P8-i Poseidon maritime surveillance aircraft. I suspect Trump is intent on pushing India to buy F-35s, the $110-million dollar 5th generation fighters.Unfortunately, the F-35 has a spotty track record. There were two crashes recently, one in Albuquerque in May, and the other on July 31 in Fresno, and that's $220 million dollars gone. Besides, the spectacle of a hapless British-owned F-35B sitting, forlorn, in the rain, in Trivandrum airport for weeks, lent itself to trolls, who made it the butt of jokes. I suspect India has firmly rebuffed Trump on this front, which has led to his focus on Russian arms.There might be other pushbacks too. Personally, I think India does need more P-8i submarine hunter-killer aircraft to patrol the Bay of Bengal, but India is exerting its buyer power. There are rumors of pauses in orders for Javelin and Stryker missiles as well.On the civilian aerospace front, I am astonished that all the media stories about Air India 171 and the suspicion that Boeing and/or General Electric are at fault have disappeared without a trace. Why? There had been the big narrative push to blame the poor pilots, and now that there is more than reasonable doubt that these US MNCs are to blame, there is a media blackout?Allegations about poor manufacturing practices by Boeing in North Charleston, South Carolina by whistleblowers have been damaging for the company's brand: this is where the 787 Dreamliners are put together. It would not be surprising if there is a slew of cancellations of orders for Boeing aircraft, with customers moving to Airbus. Let us note Air India and Indigo have placed some very large, multi-billion dollar orders with Boeing that may be in jeopardy.India as a consuming economy, and the services trade is hugely in the US' favorMany observers have pointed out the obvious fact that India is not an export-oriented economy, unlike, say, Japan or China. It is more of a consuming economy with a large, growing and increasingly less frugal population, and therefore it is a target for exporters rather than a competitor for exporting countries. As such, the impact of these US tariffs on India will be somewhat muted, and there are alternative destinations for India's exports, if need be.While Trump has focused on merchandise trade and India's modest surplus there, it is likely that there is a massive services trade, which is in the US' favor. All those Big Tech firms, such as Microsoft, Meta, Google and so on run a surplus in the US' favor, which may not be immediately evident because they route their sales through third countries, e.g. Ireland.These are the figures from the US Trade Representative, and quite frankly I don't believe them: there are a lot of invisible services being sold to India, and the value of Indian data is ignored.In addition to the financial implications, there are national security concerns. Take the case of Microsoft's cloud offering, Azure, which arbitrarily turned off services to Indian oil retailer Nayara on the flimsy grounds that the latter had substantial investment from Russia's Rosneft. This is an example of jurisdictional over-reach by US companies, which has dire consequences. India has been lax about controlling Big Tech, and this has to change.India is Meta's largest customer base. Whatsapp is used for practically everything. Which means that Meta has access to enormous amounts of Indian customer data, for which India is not even enforcing local storage. This is true of all other Big Tech (see OpenAI's Sam Altman below): they are playing fast and loose with Indian data, which is not in India's interest at all.Data is the new oil, says The Economist magazine. So how much should Meta, OpenAI et al be paying for Indian data? Meta is worth trillions of dollars, OpenAI half a trillion. How much of that can be attributed to Indian data?There is at least one example of how India too can play the digital game: UPI. Despite ham-handed efforts to now handicap UPI with a fee (thank you, brilliant government bureaucrats, yes, go ahead and kill the goose that lays the golden eggs), it has become a contender in a field that has long been dominated by the American duopoly of Visa and Mastercard. In other words, India can scale up and compete.It is unfortunate that India has not built up its own Big Tech behind a firewall as has been done behind the Great Firewall of China. But it is not too late. Is it possible for India-based cloud service providers to replace US Big Tech like Amazon Web Services and Microsoft Azure? Yes, there is at least one player in that market: Zoho.Second, what are the tariffs on Big Tech exports to India these days? What if India were to decide to impose a 50% tax on revenue generated in India through advertisement or through sales of services, mirroring the US's punitive taxes on Indian goods exports? Let me hasten to add that I am not suggesting this, it is merely a hypothetical argument.There could also be non-tariff barriers as China has implemented, but not India: data locality laws, forced use of local partners, data privacy laws like the EU's GDPR, anti-monopoly laws like the EU's Digital Markets Act, strict application of IPR laws like 3(k) that absolutely prohibits the patenting of software, and so on. India too can play legalistic games. This is a reason US agri-products do not pass muster: genetically modified seeds, and milk from cows fed with cattle feed from blood, offal and ground-up body parts.Similarly, in the ‘information' industry, India is likely to become the largest English-reading country in the world. I keep getting come-hither emails from the New York Times offering me $1 a month deals on their product: they want Indian customers. There are all these American media companies present in India, untrammelled by content controls or taxes. What if India were to give a choice to Bloomberg, Reuters, NYTimes, WaPo, NPR et al: 50% tax, or exit?This attack on peddlers of fake information and manufacturing consent I do suggest, and I have been suggesting for years. It would make no difference whatsoever to India if these media outlets were ejected, and they surely could cover India (well, basically what they do is to demean India) just as well from abroad. Out with them: good riddance to bad rubbish.What India needs to doI believe India needs to play the long game. It has to use its shatrubodha to realize that the US is not its enemy: in Chanakyan terms, the US is the Far Emperor. The enemy is China, or more precisely the Chinese Empire. Han China is just a rump on their south-eastern coast, but it is their conquered (and restive) colonies such as Tibet, Xinjiang, Manchuria and Inner Mongolia, that give them their current heft.But the historical trends are against China. It has in the past had stable governments for long periods, based on strong (and brutal) imperial power. Then comes the inevitable collapse, when the center falls apart, and there is absolute chaos. It is quite possible, given various trends, including demographic changes, that this may happen to China by 2050.On the other hand, (mostly thanks, I acknowledge, to China's manufacturing growth), the center of gravity of the world economy has been steadily shifting towards Asia. The momentum might swing towards India if China stumbles, but in any case the era of Atlantic dominance is probably gone for good. That was, of course, only a historical anomaly. Asia has always dominated: see Angus Maddison's magisterial history of the world economy, referred to below as well.I am reminded of the old story of the king berating his court poet for calling him “the new moon” and the emperor “the full moon”. The poet escaped being punished by pointing out that the new moon is waxing and the full moon is waning.This is the long game India has to keep in mind. Things are coming together for India to a great extent: in particular the demographic dividend, improved infrastructure, fiscal prudence, and the increasing centrality of the Indian Ocean as the locus of trade and commerce.India can attempt to gain competitive advantage in all three ways outlined above:* Cost-leadership. With a large market (assuming companies are willing to invest at scale), a low-cost labor force, and with a proven track-record of frugal innovation, India could well aim to be a cost-leader in selected areas of manufacturing. But this requires government intervention in loosening monetary policy and in reducing barriers to ease of doing business* Customer-intimacy. What works in highly value-conscious India could well work in other developing countries. For instance, the economic environment in ASEAN is largely similar to India's, and so Indian products should appeal to their residents; similarly with East Africa. Thus the Indian Ocean Rim with its huge (and in Africa's case, rapidly growing) population should be a natural fit for Indian products* Innovation. This is the hardest part, and it requires a new mindset in education and industry, to take risks and work at the bleeding edge of technology. In general, Indians have been content to replicate others' innovations at lower cost or do jugaad (which cannot scale up). To do real, disruptive innovation, first of all the services mindset should transition to a product mindset (sorry, Raghuram Rajan). Second, the quality of human capital must be improved. Third, there should be patient risk capital. Fourth, there should be entrepreneurs willing to try risky things. All of these are difficult, but doable.And what is the end point of this game? Leverage. The ability to compel others to buy from you.China has demonstrated this through its skill at being a cost-leader in industry after industry, often hollowing out entire nations through means both fair and foul. These means include far-sighted industrial policy including the acquisition of skills, technology, and raw materials, as well as hidden subsidies that support massive scaling, which ends up driving competing firms elsewhere out of business. India can learn a few lessons from them. One possible lesson is building capabilities, as David Teece of UC Berkeley suggested in 1997, that can span multiple products, sectors and even industries: the classic example is that of Nikon, whose optics strength helps it span industries such as photography, printing, and photolithography for chip manufacturing. Here is an interesting snapshot of China's capabilities today.2025 is, in a sense, a point of inflection for India just as the crisis in 1991 was. India had been content to plod along at the Nehruvian Rate of Growth of 2-3%, believing this was all it could achieve, as a ‘wounded civilization'. From that to a 6-7% growth rate is a leap, but it is not enough, nor is it testing the boundaries of what India can accomplish.1991 was the crisis that turned into an opportunity by accident. 2025 is a crisis that can be carefully and thoughtfully turned into an opportunity.The Idi Amin syndrome and the 1000 Talents program with AIThere is a key area where an American error may well be a windfall for India. This is based on the currently fashionable H1-B bashing which is really a race-bashing of Indians, and which has been taken up with gusto by certain MAGA folks. Once again, I suspect the baleful influence of Whitehall behind it, but whatever the reason, it looks like Indians are going to have a hard time settling down in the US.There are over a million Indians on H1-Bs, a large number of them software engineers, let us assume for convenience there are 250,000 of them. Given country caps of exactly 9800 a year, they have no realistic chance of getting a Green Card in the near future, and given the increasingly fraught nature of life there for brown people, they may leave the US, and possibly return to India..I call this the Idi Amin syndrome. In 1972, the dictator of Uganda went on a rampage against Indian-origin people in his country, and forcibly expelled 80,000 of them, because they were dominating the economy. There were unintended consequences: those who were ejected mostly went to the US and UK, and they have in many cases done well. But Uganda's economy virtually collapsed.That's a salutary experience. I am by no means saying that the US economy would collapse, but am pointing to the resilience of the Indians who were expelled. If, similarly, Trump forces a large number of Indians to return to India, that might well be a case of short-term pain and long-term gain: urvashi-shapam upakaram, as in the Malayalam phrase.Their return would be akin to what happened in China and Taiwan with their successful effort to attract their diaspora back. The Chinese program was called 1000 Talents, and they scoured the globe for academics and researchers of Chinese origin, and brought them back with attractive incentives and large budgets. They had a major role in energizing the Chinese economy.Similarly, Taiwan with Hsinchu University attracted high-quality talent, among which was the founder of TSMC, the globally dominant chip giant.And here is Trump offering to India on a platter at least 100,000 software engineers, especially at a time when generativeAI is decimating low-end jobs everywhere. They can work on some very compelling projects that could revolutionize Indian education, up-skilling and so on, and I am not at liberty to discuss them. Suffice to say that these could turbo-charge the Indian software industry and get it away from mundane, routine body-shopping type jobs.ConclusionThe Trump tariff tantrum is definitely a short-term problem for India, but it can be turned around, and turned into an opportunity, if only the country plays its cards right and focuses on building long-term comparative advantages and accepting the gift of a mis-step by Trump in geo-economics.In geo-politics, India and the US need each other to contain China, and so that part, being so obvious, will be taken care of more or less by default.Thus, overall, the old SWOT analysis: strengths, weaknesses, opportunities and threats. On balance, I am of the opinion that the threats contain in them the germs of opportunities. It is up to Indians to figure out how to take advantage of them. This is your game to win or lose, India!4150 words, 9 Aug 2025 This is a public episode. If you'd like to discuss this with other subscribers or get access to bonus episodes, visit rajeevsrinivasan.substack.com/subscribe

Het is 40.000 jaar geleden. De jonge Doi staat oog in oog met zijn verre familie, een groep dansende neanderthalers. Zullen ze hem accepteren? Wilde Eeuwen, het begin. Iedere vrijdag een nieuwe aflevering. Meer informatie: nrc.nl/wilde-eeuwenHeeft u vragen, suggesties of ideeën over onze journalistiek? Mail dan naar onze ombudsman via ombudsman@nrc.nl.Tekst en presentatie: Hendrik SpieringRedactie en regie: Mirjam van ZuidamMuziek, montage en mixage: Rufus van BaardwijkBeeld: Jeen BertingVormgeving: Yannick MortierVoor deze aflevering is onder meer gebruikt gemaakt van deze literatuur: Francesca Romagnoli e.a. (eds) 'Updating Neanderthals. Understanding Behavioural Complexity in the Late Middle Palaeolithic', Academic Press 2022 Mateja Hajdinjak e.a ‘Initial Upper Palaeolithic humans in Europe had recent Neanderthal ancestry' in Nature 8 april 2021. Rebecca Wragg Sykes. 'Kindred. Neanderthal Life, Love, Death and Art', Bloomsbury 2021 Rudolf Botha. 'Neanderthal Language. Demystifying the Linguistic Powers of our Extinct Cousins', Cambridge University Press 2020 Katerina Harvati. 'Paleoanthropology of the Balkans and Anatolia. Human Evolution and its Context', Springer Press 2016 Qiaomei Fu e.a. ‘An early modern human from Romania with a recent Neanderthal ancestor' in Nature, 13 augustus 2015. Wil Roebroeks en Paola Villa ‘Neandertal Demise: An Archaeological Analysis of the Modern Human Superiority Complex' in PLOS One, 30 april 2014. João Zilhão e.a. ‘The Peştera cu Oase People. Europe's Earliest Modern Humans' in K. Boyle e.d. (eds) Rethinking the Human Revolution, McDonald Institute for Archaeological Research, 2007.Zie het privacybeleid op https://art19.com/privacy en de privacyverklaring van Californië op https://art19.com/privacy#do-not-sell-my-info.

Dan and James chat about a a new 'pop-up journal' concept for addressing specific research questions. They also answer a listener question from a journal grammar editor and discuss a new PNAS article on paper mills Links * The pop-up journal (https://popupjournal.com) * The episode (https://everythinghertz.com/58) where Dan's wife went into labor * The PNAS paper mill paper (https://www.pnas.org/doi/10.1073/pnas.2420092122) * A blog post (https://reeserichardson.blog/2025/08/04/a-do-or-die-moment-for-the-scientific-enterprise/) from the PNAS paper lead author, Reese Richardson. * The Nature piece (https://www.nature.com/articles/d41586-025-02446-5) on the paper Social media links - Dan on Bluesky (https://bsky.app/profile/dsquintana.bsky.social) - James on Bluesky (https://bsky.app/profile/jamesheathers.bsky.social) - Everything Hertz on Bluesky (https://bsky.app/profile/hertzpodcast.bsky.social) Citation Quintana, D. S., & Heathers, J. (2025, August 7). 193: The pop-up journal, Everything Hertz [Audio podcast], DOI: 10.17605/OSF.IO/2ZMQ7

What is peer support—and why does it matter so much in high-stress jobs? In this episode, you'll learn how it works, what it's not, and why it's saving lives on the front lines.Ever wonder what peer support actually is—and why it seems like everyone's talking about it lately?Too many departments are using the term without really knowing what it means—or how to make it work. Worse, some well-meaning programs fail because they weren't clearly defined or supported.And if you're thinking of starting a team—or you already have one that feels stuck—there's a good chance the problem isn't the people. It's the lack of clarity, training, or purpose.In this episode, I break down what peer support is, what it isn't, and why it matters more than ever for first responders, medical professionals, and anyone working in a high-stress profession.BY THE TIME YOU FINISH LISTENING, YOU'LL DISCOVER:What peer support is—and why it's not the same as being a good friendThe difference between Crisis Intervention Peer Support (CISM) and Comprehensive Peer SupportThe practical steps to build or improve a peer support program that actually helpsWhether you're just getting started or trying to level up your existing team, this episode gives you a roadmap to do it right.OTHER LINKS MENTIONED IN THIS EPISODE:Share this episodeSchedule a free discovery callQPR Suicide Intervention TrainingCISM and Peer Support Training InfoCitations:Jessica N. Jeruzal, Lori L. Boland, Monica S. Frazer, Jonathan W. Kamrud, Russell N. Myers, Charles J. Lick & Andrew C. Stevens (2018): Emergency Medical Services Provider Perspectives on Pediatric Calls: A Qualitative Study, Prehospital Emergency Care, DOI: 10.1080/10903127.2018.1551450(2025, May 7). A Qualitative Study on the Design and Implementation of a First Responder Operational Stress Injury Clinic. PubMed Central. Retrieved August 2, 2025, from https://pmc.ncbi.nlm.nih.gov/articles/PMC12059418(ND). A Day Like No Other: A Case Study of the Las Vegas Mass Shooting. New Mexico Department of Homeland Security & Emergency Management. Retrieved August 2, 2025, from https://nmdhsem2024-cf.rtscustomer.com/wp-content/uploads/2024/03/Las-Vegas-Mass-Shooting-Case-Study-by-NV-Hospital-Association-2018.pdf(2025, January 15). Frank Leto—Success Stories from FDNY's Counseling Service Unit | S5 E3. First Responder Center for Excellence. Retrieved August 2, 2025, from https://www.respondertv.com/s5-e3-success-stories-from-fdnys-counseling-service-unit-witIf you're receiving value from this podcast, consider becoming a monthly supporter—your gift helps me keep producing these practical episodes. Become a supporter today. Connect with Bart LinkedIn: linkedin.com/in/bartleger Facebook Page: facebook.com/survivingyourshift Website: survivingyourshift.com Want to find out how I can help you build a peer support program in your organization or provide training? Schedule a no-obligation call or Zoom meeting with me here.

Welcome to the first episode in a five-part series on self-silencing and its profound effect on women's health. I'm Dr. Brendan McCarthy, Chief Medical Officer at Protea Medical Center, and in this episode, I break down how self-silencing — the learned suppression of one's needs, emotions, and voice — directly influences weight gain, hormone disruption, autoimmunity, cardiovascular risk, and more. This is a deeply personal and evidence-backed conversation rooted in decades of clinical experience and medical research. I discuss real patient patterns, the emotional layers behind common health complaints, and why this silent epidemic deserves more space in medicine. If you or someone you love has ever struggled with feeling unheard, unseen, or overwhelmed by caretaking roles, this is for you.   Citations: 13] Jakubowski, K. P., Barinas-Mitchell, E., Chang, Y.-F., Maki, P. M., Matthews, K. A., & Thurston, R. C. (2021). The Cardiovascular Cost of Silence: Relationships Between Self-silencing and Carotid Atherosclerosis in Midlife Women. *Annals of Behavioral Medicine, 56*(3), 282–290. DOI: 10.1093/abm/kaab046 [27] Eyal, M. (2023, October 3). Self-Silencing Is Making Women Sick. *TIME*. [5] Jack, D. C. (2010, March 29). Silencing the Self Theory. *OUPblog*.   Dr. Brendan McCarthy is the founder and Chief Medical Officer of Protea Medical Center in Arizona. With over two decades of experience, he's helped thousands of patients navigate hormonal imbalances using bioidentical HRT, nutrition, and root-cause medicine. He's also taught and mentored other physicians on integrative approaches to hormone therapy, weight loss, fertility, and more. If you're ready to take your health seriously, this podcast is a great place to start.  

In this Beekeeping Today Podcast Short, Dr. Dewey Caron returns with his monthly audio postcard—this time focused on August mite management and a remarkable discovery about honey bee learning. Dewey reminds beekeepers that August is a critical month to monitor and treat for varroa mites before their populations explode. He shares updates on new and emerging treatments, including Norroa (a dsRNA-based biopesticide), Mite Bee Gone (L-glutamic acid strips), and Apivar 2.0, as well as best practices for applying oxalic acid extended release strips like VarroxSan. Dewey shifts from mites to mind-blowing research on bee communication. Drawing on the work of Dr. James Nieh, he explains how the waggle dance—used by bees to communicate foraging locations—is learned through social exposure, similar to how birds and humans acquire language. This study, featured in Science, marks the first demonstration of social learning in insect spatial communication. This episode blends practical mite management insights with inspiring science, all in under 20 minutes. Stay proactive. Plan your treatments. And appreciate the depth of honey bee intelligence. Links & Resources: Overviews of mite control: Beekeeping Today Podcast Shorts on Varroa Treatments: https://www.beekeepingtodaypodcast.com/p/varroa/ University of Massachusetts Extension Flyer on Varroa: https://www.mass.gov/doc/varroa-mite-ipm-brochure-english/download NY Bee Wellness presentation of Dr David Peck of BetterBee https://www.youtube.com/watch?v=N4ALfqq3GT8 Veto Pharma (makers fo Apivar 2.0 and Apiguard and Varroa Easy Check sampling device) has 2 informative, nicely illustrated flyers: Integrated varroa mite management throughout the seasons - https://forms.newsletter.veto-pharma.com/5eff419fb85b5317165fde16/yBL1IKRLTxShk0jw3QcfXw/7eYSzqY0RyqLN5ngRfmpDw/form.html Varroa Mite Biology - https://forms.newsletter.veto-pharma.com/5eff419fb85b5317165fde16/O7Cp5mGSSpmFPTRAUADdmA/0DTVnqNkR32oXrlA35HsEA/form.html VitaBee Health products (makers of VarroxSan, VARROCheck sampling jar and Vita feed supplements) - https://www.vita-europe.com/beehealth/wp-content/uploads/vita-beekeeping-guide.pdf MiteBeeGone: https://mitebeegone.com/ Additional Resouces Thomas A. O'Shea-Wheller, Asia Hall, Kirsty Stainton, Victoria Tomkies, Giles E. Budge, Selwyn Wilkins and Ben Jones. 2025. A large-scale study of Varroa destructor treatment adherence in apiculture. Entomologia Generalis.DOI: 10.1127/entomologia/2024/2758 Reports on oxalic acid effectiveness from Canada Quebec: https://academic.oup.com/jinsectscience/article/24/3/14/7683875 and Ontario:https://www.mdpi.com/2076-0817/14/8/724 Science article on social learning in Dance Language https://labs.biology.ucsd.edu/nieh/papers/DongScience.pdf YouTube presentation at https://www.youtube.com/watch?v=elWNc_1qm60   Brought to you by Betterbee – your partners in better beekeeping. ______________ Betterbee is the presenting sponsor of Beekeeping Today Podcast. Betterbee's mission is to support every beekeeper with excellent customer service, continued education and quality equipment. From their colorful and informative catalog to their support of beekeeper educational activities, including this podcast series, Betterbee truly is Beekeepers Serving Beekeepers. See for yourself at www.betterbee.com Copyright © 2025 by Growing Planet Media, LLC

In our 17th episode of Research and Real Talk, Jenny brings back John Bauer, now of Lionel University, to discuss the newest and latest. From nutrition to gene editing and burnout to muscle memory- nothing is off the table! Join us down the rabbit hole of the ever-evolving science in fitness and wellness.References:1. TED Radio Hour https://www.npr.org/2025/04/18/g-s1-60989/how-crispr-is-changing-the-way-we-grow-our-food2. Azumi Yoshida, Hironobu Takahashi, Tatsuya Shimizu, Morphology and functionality in biomimetic cultured meat produced from various cellular origins,Biomaterials Advances, Volume 169, 2025, 214179, ISSN 2772-9508https://doi.org/10.1016/j.bioadv.2025.2141793. Juha J. Hulmi, Eeli J. Halonen, Adam P. Sharples, Thomas M. O'Connell, Lauri Kuikka, Veli‐Matti Lappi, Kari Salokas, Salla Keskitalo, Markku Varjosalo, Juha P. Ahtiainen. Human skeletal muscle possesses both reversible proteomic signatures and a retained proteomic memory after repeated resistance training. The Journal of Physiology, 2025; DOI: 10.1113/JP288104www.Lionel.edu Lionel University

Podcast Summary This episode of the Pain Exam Podcast, hosted by Dr. David Rosenblum, discusses an interesting article about Ketorolac injections for musculoskeletal conditions. The podcast covers: Ketorolac is an NSAID that provides analgesic and anti-inflammatory effects through inhibition of prostaglandin synthesis Multiple studies comparing Ketorolac injections to corticosteroids and hyaluronic acid for various conditions Research shows Ketorolac injections are equally effective as corticosteroids for subacromial conditions, adhesive capsulitis, carpal-metacarpal joint issues, and hip/knee osteoarthritis Ketorolac may be a safer alternative to steroids for certain patients, though it has its own contraindications for those with renal, gastrointestinal, or cardiovascular disease Dr. Rosenblum considers the potential of using Ketorolac injections directly at pain sites rather than intramuscularly Upcoming Courses and Conferences Ultrasound courses in New York and Costa Rica (check unwrappedpain.org) Private ultrasound sessions available Dr. Rosenblum will be speaking at Pain Week about ultrasound in pain practice and PRP Presenting at a primary care conference in London Teaching ultrasound at ISPN LAPSES conference in Chile (Dr. Rosenblum won't attend this year) Ketorolac Injections: An Effective Alternative for Musculoskeletal Pain Management Musculoskeletal conditions such as bursitis, adhesive capsulitis, and osteoarthritis affect millions and often require injectable therapies to reduce pain and inflammation. Traditionally, corticosteroid injections have been the mainstay treatment. However, concerns over side effects like tendon rupture, cartilage damage, and systemic hyperglycemia have prompted exploration of alternatives. A recent narrative review by Kiel et al. (2024) highlights ketorolac—a parenteral nonsteroidal anti-inflammatory drug (NSAID)—as a promising substitute for corticosteroids in musculoskeletal injections. Warning: OFF Label use of Ketorolac discussed. Please consult your physician. See full article  for details. Subacromial Ketorolac Injections for Shoulder Pain Subacromial bursitis and impingement syndrome are common causes of shoulder pain and disability. Several randomized controlled trials have shown that subacromial ketorolac injections provide pain relief and functional improvement comparable to corticosteroids: Goyal et al. demonstrated significant reductions in pain scores after subacromial injection of 60 mg ketorolac versus 40 mg methylprednisolone, with no difference in outcomes between groups. Taheri et al. found similar short-term pain relief at 1 and 3 months with either ketorolac or corticosteroid subacromial injections. Kim et al. reported equivalent clinical improvement in rotator cuff syndrome patients receiving ketorolac or triamcinolone injections. Min et al. noted ketorolac led to better forward flexion and patient satisfaction at 4 weeks compared to corticosteroids. These studies support ketorolac as an effective agent for subacromial injection, offering an alternative for patients where corticosteroid use is limited. Intra-articular Ketorolac Injections for Adhesive Capsulitis and Osteoarthritis Adhesive capsulitis (frozen shoulder) and osteoarthritis of the hip, knee, and carpometacarpal joint are often treated with intra-articular corticosteroids. Ketorolac injections have shown comparable efficacy in these conditions: Akhtar et al. found intra-articular ketorolac significantly reduced shoulder pain at 4 weeks in adhesive capsulitis compared to hyaluronic acid. Ahn et al. reported similar pain relief between intra-articular ketorolac and corticosteroid injections in adhesive capsulitis, with ketorolac providing superior shoulder mobility at 3 and 6 months. Koh et al. showed that adding ketorolac to hyaluronic acid injections in carpometacarpal osteoarthritis resulted in faster onset of pain relief compared to hyaluronic acid alone. Park et al. observed equivalent functional improvements with intra-articular ketorolac or corticosteroids in hip osteoarthritis. Jurgensmeier et al. demonstrated similar symptom improvement at 1 and 3 months post-injection for ketorolac and triamcinolone in hip and knee osteoarthritis. Xu et al. and Bellamy et al. confirmed ketorolac's comparable pain relief and functional benefits to corticosteroids for knee osteoarthritis, with ketorolac being more cost-effective. Lee et al. noted quicker pain reduction with intra-articular ketorolac combined with hyaluronic acid versus hyaluronic acid alone in knee osteoarthritis. aSafety and Pharmacologic Considerations Ketorolac's anti-inflammatory action stems from cyclooxygenase inhibition, reducing prostaglandin synthesis. Its half-life is approximately 5.2–5.6 hours, and it is metabolized in the liver. Unlike corticosteroids, ketorolac avoids systemic hyperglycemia and cartilage damage risks. Animal and in vitro studies suggest ketorolac may protect cartilage by inhibiting inflammatory cytokines. While gastrointestinal, renal, and cardiovascular risks associated with NSAIDs remain considerations, localized intra-articular and subacromial ketorolac injections may limit systemic exposure and adverse effects. Mild, transient post-injection pain has been reported but resolves without intervention. Conclusion Ketorolac injections, administered intra-articularly or subacromially, are a safe, effective, and economical alternative to corticosteroids for managing common musculoskeletal conditions. Their comparable efficacy in reducing pain and improving function, combined with a more favorable side effect profile, makes ketorolac an appealing option for clinicians and patients alike. Further research is warranted to fully elucidate long-term safety and optimal dosing strategies. FAQS Ketorolac Injections for Musculoskeletal Conditions: Frequently Asked Questions Musculoskeletal pain from conditions like bursitis, adhesive capsulitis, and osteoarthritis often requires injectable treatments. Ketorolac, a nonsteroidal anti-inflammatory drug (NSAID), is emerging as a promising alternative to corticosteroids. Below are common questions and answers based on a recent narrative review by Kiel et al. (2024). 1. What is ketorolac and how does it work? Ketorolac is a parenteral NSAID that reduces pain and inflammation by inhibiting cyclooxygenase enzymes, which decreases prostaglandin synthesis. It can be administered orally, intramuscularly, intravenously, or by injection directly into joints or around bursae. 2. How effective is ketorolac for musculoskeletal conditions? Studies show ketorolac injections provide significant pain relief and functional improvement comparable to corticosteroids in conditions like: Subacromial bursitis and shoulder impingement (subacromial injections) Adhesive capsulitis (frozen shoulder) (intra-articular injections) Osteoarthritis of the hip, knee, and thumb carpometacarpal joint (intra-articular injections) 3. What evidence supports subacromial ketorolac injections? Randomized controlled trials found: Goyal et al. and Taheri et al. reported similar pain reduction and functional outcomes between ketorolac and corticosteroids for subacromial injections. Kim et al. and Min et al. observed comparable or better patient satisfaction and shoulder mobility with ketorolac versus corticosteroids. 4. How does intra-articular ketorolac compare to corticosteroids for adhesive capsulitis? Akhtar et al. showed ketorolac reduced shoulder pain more than hyaluronic acid. Ahn et al. found ketorolac and corticosteroids equally effective for pain relief, with ketorolac providing better shoulder mobility at 3 and 6 months. 5. What about ketorolac for osteoarthritis? Ketorolac combined with hyaluronic acid provided faster pain relief than hyaluronic acid alone in thumb carpometacarpal joint osteoarthritis (Koh et al.). Intra-articular ketorolac had similar efficacy to corticosteroids in hip (Park et al., Jurgensmeier et al.) and knee osteoarthritis (Bellamy et al., Xu et al.). Ketorolac injections were more cost-effective compared to corticosteroids (Bellamy et al.). 6. Are ketorolac injections safe? Ketorolac's side effects are similar to other NSAIDs, mainly involving gastrointestinal, renal, and cardiovascular risks. However, localized intra-articular and subacromial injections may reduce systemic exposure. Animal studies suggest ketorolac does not harm cartilage and may protect against inflammatory damage. Mild, transient local pain post-injection is possible but usually resolves without treatment. 7. What are the limitations of ketorolac use? Ketorolac is not suitable for patients with: Renal impairment Gastrointestinal ulcers or bleeding risk Cardiovascular disease or hypertension NSAID hypersensitivity, especially in asthma or chronic urticaria patients Clinicians should assess individual risks before choosing ketorolac injections. 8. How does ketorolac's pharmacokinetics affect its use? Ketorolac has a plasma half-life of about 5.2 to 5.6 hours and is metabolized in the liver. Pharmacokinetics for subcutaneous or intra-articular administration are less defined but systemic absorption occurs. Its relatively short half-life supports repeated dosing if needed. 9. Why consider ketorolac over corticosteroids? Ketorolac avoids corticosteroid-associated risks such as tendon rupture, cartilage damage, and steroid-induced hyperglycemia. It is also more cost-effective, making it a favorable option for patients and healthcare systems. 10. What further research is needed? More large-scale, long-term studies are needed to fully understand ketorolac's intra-articular effects, optimal dosing, and safety profile compared to corticosteroids and other treatments. Summary: Ketorolac injections, whether intra-articular or subacromial, offer a safe, effective, and economical alternative to corticosteroids for managing various musculoskeletal conditions. This makes ketorolac an important option in pain management and inflammation control.     Reference: Kiel J, Applewhite AI, Bertasi TGO, Bertasi RAO, Seemann LL, Costa LMC, Helmi H, Pujalte GGA. Ketorolac Injections for Musculoskeletal Conditions: A Narrative Review. Clinical Medicine & Research. 2024;22(1):19-27. DOI: https://doi.org/10.3121/cmr.2024.1847 Disclaimer: This Podcast, website and any content from NRAP Academy (PMRexam.com) otherwise known as Qbazaar.com, LLC is  for general informational purposes only and does not constitute the practice of medicine, nursing or other professional health care services, including the giving of medical advice, and no doctor/patient relationship is formed. The use of information on this podcast or materials linked from this podcast is at the user's own risk. Professionals should conduct their own fact finding, research, and due diligence to come to their own conclusions for treating patients. The content of this podcast is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Users should not disregard or delay in obtaining medical advice for any medical condition they may have and should seek the assistance of their health care professionals for any such conditions.    

Podcast Summary This episode of the Pain Exam Podcast, hosted by Dr. David Rosenblum, discusses an interesting article about Ketorolac injections for musculoskeletal conditions. The podcast covers: Ketorolac is an NSAID that provides analgesic and anti-inflammatory effects through inhibition of prostaglandin synthesis Multiple studies comparing Ketorolac injections to corticosteroids and hyaluronic acid for various conditions Research shows Ketorolac injections are equally effective as corticosteroids for subacromial conditions, adhesive capsulitis, carpal-metacarpal joint issues, and hip/knee osteoarthritis Ketorolac may be a safer alternative to steroids for certain patients, though it has its own contraindications for those with renal, gastrointestinal, or cardiovascular disease Dr. Rosenblum considers the potential of using Ketorolac injections directly at pain sites rather than intramuscularly Upcoming Courses and Conferences Ultrasound courses in New York and Costa Rica (check unwrappedpain.org) Private ultrasound sessions available Dr. Rosenblum will be speaking at Pain Week about ultrasound in pain practice and PRP Presenting at a primary care conference in London Teaching ultrasound at ISPN LAPS  conference in Chile (Dr. Rosenblum won't attend this year) Ketorolac Injections: An Effective Alternative for Musculoskeletal Pain Management Musculoskeletal conditions such as bursitis, adhesive capsulitis, and osteoarthritis affect millions and often require injectable therapies to reduce pain and inflammation. Traditionally, corticosteroid injections have been the mainstay treatment. However, concerns over side effects like tendon rupture, cartilage damage, and systemic hyperglycemia have prompted exploration of alternatives. A recent narrative review by Kiel et al. (2024) highlights ketorolac—a parenteral nonsteroidal anti-inflammatory drug (NSAID)—as a promising substitute for corticosteroids in musculoskeletal injections. Warning: OFF Label use of Ketorolac discussed. Please consult your physician. See full article  for details. Subacromial Ketorolac Injections for Shoulder Pain Subacromial bursitis and impingement syndrome are common causes of shoulder pain and disability. Several randomized controlled trials have shown that subacromial ketorolac injections provide pain relief and functional improvement comparable to corticosteroids: Goyal et al. demonstrated significant reductions in pain scores after subacromial injection of 60 mg ketorolac versus 40 mg methylprednisolone, with no difference in outcomes between groups. Taheri et al. found similar short-term pain relief at 1 and 3 months with either ketorolac or corticosteroid subacromial injections. Kim et al. reported equivalent clinical improvement in rotator cuff syndrome patients receiving ketorolac or triamcinolone injections. Min et al. noted ketorolac led to better forward flexion and patient satisfaction at 4 weeks compared to corticosteroids. These studies support ketorolac as an effective agent for subacromial injection, offering an alternative for patients where corticosteroid use is limited. Intra-articular Ketorolac Injections for Adhesive Capsulitis and Osteoarthritis Adhesive capsulitis (frozen shoulder) and osteoarthritis of the hip, knee, and carpometacarpal joint are often treated with intra-articular corticosteroids. Ketorolac injections have shown comparable efficacy in these conditions: Akhtar et al. found intra-articular ketorolac significantly reduced shoulder pain at 4 weeks in adhesive capsulitis compared to hyaluronic acid. Ahn et al. reported similar pain relief between intra-articular ketorolac and corticosteroid injections in adhesive capsulitis, with ketorolac providing superior shoulder mobility at 3 and 6 months. Koh et al. showed that adding ketorolac to hyaluronic acid injections in carpometacarpal osteoarthritis resulted in faster onset of pain relief compared to hyaluronic acid alone. Park et al. observed equivalent functional improvements with intra-articular ketorolac or corticosteroids in hip osteoarthritis. Jurgensmeier et al. demonstrated similar symptom improvement at 1 and 3 months post-injection for ketorolac and triamcinolone in hip and knee osteoarthritis. Xu et al. and Bellamy et al. confirmed ketorolac's comparable pain relief and functional benefits to corticosteroids for knee osteoarthritis, with ketorolac being more cost-effective. Lee et al. noted quicker pain reduction with intra-articular ketorolac combined with hyaluronic acid versus hyaluronic acid alone in knee osteoarthritis. aSafety and Pharmacologic Considerations Ketorolac's anti-inflammatory action stems from cyclooxygenase inhibition, reducing prostaglandin synthesis. Its half-life is approximately 5.2–5.6 hours, and it is metabolized in the liver. Unlike corticosteroids, ketorolac avoids systemic hyperglycemia and cartilage damage risks. Animal and in vitro studies suggest ketorolac may protect cartilage by inhibiting inflammatory cytokines. While gastrointestinal, renal, and cardiovascular risks associated with NSAIDs remain considerations, localized intra-articular and subacromial ketorolac injections may limit systemic exposure and adverse effects. Mild, transient post-injection pain has been reported but resolves without intervention. Conclusion Ketorolac injections, administered intra-articularly or subacromially, are a safe, effective, and economical alternative to corticosteroids for managing common musculoskeletal conditions. Their comparable efficacy in reducing pain and improving function, combined with a more favorable side effect profile, makes ketorolac an appealing option for clinicians and patients alike. Further research is warranted to fully elucidate long-term safety and optimal dosing strategies. FAQS Ketorolac Injections for Musculoskeletal Conditions: Frequently Asked Questions Musculoskeletal pain from conditions like bursitis, adhesive capsulitis, and osteoarthritis often requires injectable treatments. Ketorolac, a nonsteroidal anti-inflammatory drug (NSAID), is emerging as a promising alternative to corticosteroids. Below are common questions and answers based on a recent narrative review by Kiel et al. (2024). 1. What is ketorolac and how does it work? Ketorolac is a parenteral NSAID that reduces pain and inflammation by inhibiting cyclooxygenase enzymes, which decreases prostaglandin synthesis. It can be administered orally, intramuscularly, intravenously, or by injection directly into joints or around bursae. 2. How effective is ketorolac for musculoskeletal conditions? Studies show ketorolac injections provide significant pain relief and functional improvement comparable to corticosteroids in conditions like: Subacromial bursitis and shoulder impingement (subacromial injections) Adhesive capsulitis (frozen shoulder) (intra-articular injections) Osteoarthritis of the hip, knee, and thumb carpometacarpal joint (intra-articular injections) 3. What evidence supports subacromial ketorolac injections? Randomized controlled trials found: Goyal et al. and Taheri et al. reported similar pain reduction and functional outcomes between ketorolac and corticosteroids for subacromial injections. Kim et al. and Min et al. observed comparable or better patient satisfaction and shoulder mobility with ketorolac versus corticosteroids. 4. How does intra-articular ketorolac compare to corticosteroids for adhesive capsulitis? Akhtar et al. showed ketorolac reduced shoulder pain more than hyaluronic acid. Ahn et al. found ketorolac and corticosteroids equally effective for pain relief, with ketorolac providing better shoulder mobility at 3 and 6 months. 5. What about ketorolac for osteoarthritis? Ketorolac combined with hyaluronic acid provided faster pain relief than hyaluronic acid alone in thumb carpometacarpal joint osteoarthritis (Koh et al.). Intra-articular ketorolac had similar efficacy to corticosteroids in hip (Park et al., Jurgensmeier et al.) and knee osteoarthritis (Bellamy et al., Xu et al.). Ketorolac injections were more cost-effective compared to corticosteroids (Bellamy et al.). 6. Are ketorolac injections safe? Ketorolac's side effects are similar to other NSAIDs, mainly involving gastrointestinal, renal, and cardiovascular risks. However, localized intra-articular and subacromial injections may reduce systemic exposure. Animal studies suggest ketorolac does not harm cartilage and may protect against inflammatory damage. Mild, transient local pain post-injection is possible but usually resolves without treatment. 7. What are the limitations of ketorolac use? Ketorolac is not suitable for patients with: Renal impairment Gastrointestinal ulcers or bleeding risk Cardiovascular disease or hypertension NSAID hypersensitivity, especially in asthma or chronic urticaria patients Clinicians should assess individual risks before choosing ketorolac injections. 8. How does ketorolac's pharmacokinetics affect its use? Ketorolac has a plasma half-life of about 5.2 to 5.6 hours and is metabolized in the liver. Pharmacokinetics for subcutaneous or intra-articular administration are less defined but systemic absorption occurs. Its relatively short half-life supports repeated dosing if needed. 9. Why consider ketorolac over corticosteroids? Ketorolac avoids corticosteroid-associated risks such as tendon rupture, cartilage damage, and steroid-induced hyperglycemia. It is also more cost-effective, making it a favorable option for patients and healthcare systems. 10. What further research is needed? More large-scale, long-term studies are needed to fully understand ketorolac's intra-articular effects, optimal dosing, and safety profile compared to corticosteroids and other treatments. Summary: Ketorolac injections, whether intra-articular or subacromial, offer a safe, effective, and economical alternative to corticosteroids for managing various musculoskeletal conditions. This makes ketorolac an important option in pain management and inflammation control.     Reference: Kiel J, Applewhite AI, Bertasi TGO, Bertasi RAO, Seemann LL, Costa LMC, Helmi H, Pujalte GGA. Ketorolac Injections for Musculoskeletal Conditions: A Narrative Review. Clinical Medicine & Research. 2024;22(1):19-27. DOI: https://doi.org/10.3121/cmr.2024.1847 Disclaimer: This Podcast, website and any content from NRAP Academy (PMRexam.com) otherwise known as Qbazaar.com, LLC is  for general informational purposes only and does not constitute the practice of medicine, nursing or other professional health care services, including the giving of medical advice, and no doctor/patient relationship is formed. The use of information on this podcast or materials linked from this podcast is at the user's own risk. Professionals should conduct their own fact finding, research, and due diligence to come to their own conclusions for treating patients. The content of this podcast is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Users should not disregard or delay in obtaining medical advice for any medical condition they may have and should seek the assistance of their health care professionals for any such conditions.  

Podcast Summary This episode of the Pain Exam Podcast, hosted by Dr. David Rosenblum, discusses an interesting article about Ketorolac injections for musculoskeletal conditions. The podcast covers: Ketorolac is an NSAID that provides analgesic and anti-inflammatory effects through inhibition of prostaglandin synthesis Multiple studies comparing Ketorolac injections to corticosteroids and hyaluronic acid for various conditions Research shows Ketorolac injections are equally effective as corticosteroids for subacromial conditions, adhesive capsulitis, carpal-metacarpal joint issues, and hip/knee osteoarthritis Ketorolac may be a safer alternative to steroids for certain patients, though it has its own contraindications for those with renal, gastrointestinal, or cardiovascular disease Dr. Rosenblum considers the potential of using Ketorolac injections directly at pain sites rather than intramuscularly Upcoming Courses and Conferences Ultrasound courses in New York and Costa Rica (check unwrappedpain.org) Private ultrasound sessions available Dr. Rosenblum will be speaking at Pain Week about ultrasound in pain practice and PRP Presenting at a primary care conference in London Teaching ultrasound at ISPN LAPSES conference in Chile (Dr. Rosenblum won't attend this year) Ketorolac Injections: An Effective Alternative for Musculoskeletal Pain Management Musculoskeletal conditions such as bursitis, adhesive capsulitis, and osteoarthritis affect millions and often require injectable therapies to reduce pain and inflammation. Traditionally, corticosteroid injections have been the mainstay treatment. However, concerns over side effects like tendon rupture, cartilage damage, and systemic hyperglycemia have prompted exploration of alternatives. A recent narrative review by Kiel et al. (2024) highlights ketorolac—a parenteral nonsteroidal anti-inflammatory drug (NSAID)—as a promising substitute for corticosteroids in musculoskeletal injections. Warning: OFF Label use of Ketorolac discussed. Please consult your physician. See full article  for details. Subacromial Ketorolac Injections for Shoulder Pain Subacromial bursitis and impingement syndrome are common causes of shoulder pain and disability. Several randomized controlled trials have shown that subacromial ketorolac injections provide pain relief and functional improvement comparable to corticosteroids: Goyal et al. demonstrated significant reductions in pain scores after subacromial injection of 60 mg ketorolac versus 40 mg methylprednisolone, with no difference in outcomes between groups. Taheri et al. found similar short-term pain relief at 1 and 3 months with either ketorolac or corticosteroid subacromial injections. Kim et al. reported equivalent clinical improvement in rotator cuff syndrome patients receiving ketorolac or triamcinolone injections. Min et al. noted ketorolac led to better forward flexion and patient satisfaction at 4 weeks compared to corticosteroids. These studies support ketorolac as an effective agent for subacromial injection, offering an alternative for patients where corticosteroid use is limited. Intra-articular Ketorolac Injections for Adhesive Capsulitis and Osteoarthritis Adhesive capsulitis (frozen shoulder) and osteoarthritis of the hip, knee, and carpometacarpal joint are often treated with intra-articular corticosteroids. Ketorolac injections have shown comparable efficacy in these conditions: Akhtar et al. found intra-articular ketorolac significantly reduced shoulder pain at 4 weeks in adhesive capsulitis compared to hyaluronic acid. Ahn et al. reported similar pain relief between intra-articular ketorolac and corticosteroid injections in adhesive capsulitis, with ketorolac providing superior shoulder mobility at 3 and 6 months. Koh et al. showed that adding ketorolac to hyaluronic acid injections in carpometacarpal osteoarthritis resulted in faster onset of pain relief compared to hyaluronic acid alone. Park et al. observed equivalent functional improvements with intra-articular ketorolac or corticosteroids in hip osteoarthritis. Jurgensmeier et al. demonstrated similar symptom improvement at 1 and 3 months post-injection for ketorolac and triamcinolone in hip and knee osteoarthritis. Xu et al. and Bellamy et al. confirmed ketorolac's comparable pain relief and functional benefits to corticosteroids for knee osteoarthritis, with ketorolac being more cost-effective. Lee et al. noted quicker pain reduction with intra-articular ketorolac combined with hyaluronic acid versus hyaluronic acid alone in knee osteoarthritis. aSafety and Pharmacologic Considerations Ketorolac's anti-inflammatory action stems from cyclooxygenase inhibition, reducing prostaglandin synthesis. Its half-life is approximately 5.2–5.6 hours, and it is metabolized in the liver. Unlike corticosteroids, ketorolac avoids systemic hyperglycemia and cartilage damage risks. Animal and in vitro studies suggest ketorolac may protect cartilage by inhibiting inflammatory cytokines. While gastrointestinal, renal, and cardiovascular risks associated with NSAIDs remain considerations, localized intra-articular and subacromial ketorolac injections may limit systemic exposure and adverse effects. Mild, transient post-injection pain has been reported but resolves without intervention. Conclusion Ketorolac injections, administered intra-articularly or subacromially, are a safe, effective, and economical alternative to corticosteroids for managing common musculoskeletal conditions. Their comparable efficacy in reducing pain and improving function, combined with a more favorable side effect profile, makes ketorolac an appealing option for clinicians and patients alike. Further research is warranted to fully elucidate long-term safety and optimal dosing strategies. FAQS Ketorolac Injections for Musculoskeletal Conditions: Frequently Asked Questions Musculoskeletal pain from conditions like bursitis, adhesive capsulitis, and osteoarthritis often requires injectable treatments. Ketorolac, a nonsteroidal anti-inflammatory drug (NSAID), is emerging as a promising alternative to corticosteroids. Below are common questions and answers based on a recent narrative review by Kiel et al. (2024). 1. What is ketorolac and how does it work? Ketorolac is a parenteral NSAID that reduces pain and inflammation by inhibiting cyclooxygenase enzymes, which decreases prostaglandin synthesis. It can be administered orally, intramuscularly, intravenously, or by injection directly into joints or around bursae. 2. How effective is ketorolac for musculoskeletal conditions? Studies show ketorolac injections provide significant pain relief and functional improvement comparable to corticosteroids in conditions like: Subacromial bursitis and shoulder impingement (subacromial injections) Adhesive capsulitis (frozen shoulder) (intra-articular injections) Osteoarthritis of the hip, knee, and thumb carpometacarpal joint (intra-articular injections) 3. What evidence supports subacromial ketorolac injections? Randomized controlled trials found: Goyal et al. and Taheri et al. reported similar pain reduction and functional outcomes between ketorolac and corticosteroids for subacromial injections. Kim et al. and Min et al. observed comparable or better patient satisfaction and shoulder mobility with ketorolac versus corticosteroids. 4. How does intra-articular ketorolac compare to corticosteroids for adhesive capsulitis? Akhtar et al. showed ketorolac reduced shoulder pain more than hyaluronic acid. Ahn et al. found ketorolac and corticosteroids equally effective for pain relief, with ketorolac providing better shoulder mobility at 3 and 6 months. 5. What about ketorolac for osteoarthritis? Ketorolac combined with hyaluronic acid provided faster pain relief than hyaluronic acid alone in thumb carpometacarpal joint osteoarthritis (Koh et al.). Intra-articular ketorolac had similar efficacy to corticosteroids in hip (Park et al., Jurgensmeier et al.) and knee osteoarthritis (Bellamy et al., Xu et al.). Ketorolac injections were more cost-effective compared to corticosteroids (Bellamy et al.). 6. Are ketorolac injections safe? Ketorolac's side effects are similar to other NSAIDs, mainly involving gastrointestinal, renal, and cardiovascular risks. However, localized intra-articular and subacromial injections may reduce systemic exposure. Animal studies suggest ketorolac does not harm cartilage and may protect against inflammatory damage. Mild, transient local pain post-injection is possible but usually resolves without treatment. 7. What are the limitations of ketorolac use? Ketorolac is not suitable for patients with: Renal impairment Gastrointestinal ulcers or bleeding risk Cardiovascular disease or hypertension NSAID hypersensitivity, especially in asthma or chronic urticaria patients Clinicians should assess individual risks before choosing ketorolac injections. 8. How does ketorolac's pharmacokinetics affect its use? Ketorolac has a plasma half-life of about 5.2 to 5.6 hours and is metabolized in the liver. Pharmacokinetics for subcutaneous or intra-articular administration are less defined but systemic absorption occurs. Its relatively short half-life supports repeated dosing if needed. 9. Why consider ketorolac over corticosteroids? Ketorolac avoids corticosteroid-associated risks such as tendon rupture, cartilage damage, and steroid-induced hyperglycemia. It is also more cost-effective, making it a favorable option for patients and healthcare systems. 10. What further research is needed? More large-scale, long-term studies are needed to fully understand ketorolac's intra-articular effects, optimal dosing, and safety profile compared to corticosteroids and other treatments. Summary: Ketorolac injections, whether intra-articular or subacromial, offer a safe, effective, and economical alternative to corticosteroids for managing various musculoskeletal conditions. This makes ketorolac an important option in pain management and inflammation control.     Reference: Kiel J, Applewhite AI, Bertasi TGO, Bertasi RAO, Seemann LL, Costa LMC, Helmi H, Pujalte GGA. Ketorolac Injections for Musculoskeletal Conditions: A Narrative Review. Clinical Medicine & Research. 2024;22(1):19-27. DOI: https://doi.org/10.3121/cmr.2024.1847 Disclaimer: This Podcast, website and any content from NRAP Academy (PMRexam.com) otherwise known as Qbazaar.com, LLC is  for general informational purposes only and does not constitute the practice of medicine, nursing or other professional health care services, including the giving of medical advice, and no doctor/patient relationship is formed. The use of information on this podcast or materials linked from this podcast is at the user's own risk. Professionals should conduct their own fact finding, research, and due diligence to come to their own conclusions for treating patients. The content of this podcast is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Users should not disregard or delay in obtaining medical advice for any medical condition they may have and should seek the assistance of their health care professionals for any such conditions.    

Michele R. Schaeffer, PhD, Andreas von Leupoldt, PhD, and Daniel Langer, PhD, join CHEST® Journal Podcast Moderator, Alice Gallo De Moraes, MD, FCCP, to discuss their research into inhaled menthol as a potential treatment for dyspnea relief during cycle exercise for patients with COPD.  DOI: 10.1016/j.chest.2025.03.002 Disclaimer: The purpose of this activity is to expand the reach of CHEST content through awareness, critique, and discussion. All articles have undergone peer review for methodologic rigor and audience relevance. Any views asserted are those of the speakers and are not endorsed by CHEST. Listeners should be aware that speakers' opinions may vary and are advised to read the full corresponding journal article(s) for complete context. This content should not be used as a basis for medical advice or treatment, nor should it substitute the judgment used by clinicians in the practice of evidence-based medicine. 

What's the episode about? In this episode, hear Kaylee Alexander discuss the digital humanities, being a research data librarian, visual culture, cemeteries, French cemetery laws, cemetery sculpture, ethically sound data visualisation and survival bias Who is Kaylee?Dr. Kaylee P. Alexander is a Research Data Librarian at the University of Utah's J. Willard Marriott Library.  She holds a Ph.D. in Art History and Visual Culture from Duke University and specializes in nineteenth-century visual culture, monuments, and funerary material culture.  Her research is embedded in transdisciplinary practices at the intersection of visual studies, cultural economics, sociology, and data science.  You can find a list of her publications on her website. She is the author of A Data-Driven Analysis of Cemeteries and Social Reform in Paris, 1804–1924 (Routledge 2024). How do I cite the episode in my research and reading lists?To cite this episode, you can use the following citation: Alexander, K. (2025) Interview on The Death Studies Podcast hosted by Michael-Fox, B. and Visser, R. Published 1 August 2025. Available at: www.thedeathstudiespodcast.com, DOI: 10.6084/m9.figshare.29763560What next?Check out more episodes or find out more about the hosts! Gota question? Get in touch.

The minds of reptiles remain largely mysterious to us, and we often wonder what kind of emotions they are capable of feeling. In this episode we dig into a new study which tries to uncover some of the mysteries of tortoise cognition, particularly whether they can experience different moods. We follow that up with a newly described species of lizard from the rocky deserts of Arabia. Main Paper References: Hoehfurtner T, Wilkinson A, Moszuti SA, Burman OHP. 2025. Evidence of mood states in reptiles. Animal Cognition 28. DOI: 10.1007/s10071-025-01973-y. Species of the Bi-Week: Šmíd J, Velenská D, Pola L, Tamar K, Busais S, Shobrak M, Almutairi M, Salim AFA, Alsubaie SD, AlGethami RHM, AlGethami AR, Alanazi ASK, Alshammari AM, Egan DM, Ramalho RO, Olson D, Smithson J, Chirio L, Burger M, Van Huyssteen R, Petford MA, Carranza S. 2025. Phylogeny and systematics of Arabian lacertids from the Mesalina guttulata species complex (Squamata, Lacertidae), with the description of a new species. BMC Zoology 10. DOI: 10.1186/s40850-025-00233-3. Other Mentioned Papers/Studies: Harding EJ, Paul ES, Mendl M. 2004. Cognitive bias and affective state. Nature 427:312–312. DOI: 10.1038/427312a. Moszuti SA, Wilkinson A, Burman OHP. 2017. Response to novelty as an indicator of reptile welfare. Applied Animal Behaviour Science 193:98–103. DOI: 10.1016/j.applanim.2017.03.018. Other Links/Mentions: Alamshah AL, Marshall BM. 2025. Big bills, small changes: with few exceptions, Jungle crows show minor variation in bill morphology across their distribution. EcoEvoRxiv. DOI: 10.32942/X2NW74. https://ecoevorxiv.org/repository/view/9694/  Editing and Music: Intro/outro – Treehouse by Ed Nelson Species Bi-week theme – Michael Timothy Other Music – The Passion HiFi, https://www.thepassionhifi.com

Jamie Hartmann-Boyce and Nicola Lindson discuss emerging evidence in e-cigarette research and interview Elias Klemperer from the University of Vermont, USA. Associate Professor Jamie Hartmann-Boyce and Associate Professor Nicola Lindson discuss the new evidence in e-cigarette research and interview Dr Elias Klemperer behavioural scientist and licenced clinical psychologist, Department of Psychiatry, University of Vermont, USA. Elias works in the field of tobacco regulatory science and tobacco control. He has a special interest in long-term users of both cigarettes and e-cigarettes, dual users, a group who take in nicotine via two methods. In the July podcast Elias Klemperer discusses his recent 2 × 2 factorial trial randomized trial of nicotine replacement therapy (patches and lozenges) in 396 young adult dual users aged 18–29 (DOI: 10.1093/ntr/ntaf119). In a randomized factorial trial participants are randomly placed into different groups to test more than one treatment at the same time. The study was funded by the National Institute of General Medical Sciences, the Food and Drug Administration, the National Institute on Drug Abuse, and the National Cancer Institute, USA. Elias Klemperer and his team carried out this study as little is known regarding nicotine replacement therapy for young adult dual users, or whether to recommend quitting versus continuing e-cigarettes during smoking cessation treatment. The participants received 12 weeks of combination NRT compared to no NRT for stopping smoking, plus text-based treatment recommendations to quit or to continue using e-cigarettes. This advice was delivered via written material, an animated video they developed in-house, and text message support during the 12-week treatment period. The study looked at abstinence from cigarettes at 12 and 24 weeks. Their study found that NRT was effective in promoting early smoking cessation among young adult dual users. Their secondary findings indicated that pairing NRT with support to quit both products could enhance the effects on prolonged cigarette abstinence. This podcast is a companion to the electronic cigarettes Cochrane living systematic review and Interventions for quitting vaping review and shares the evidence from the monthly searches. Our search for the EC for smoking cessation review carried out on 1st July 2025 found six papers linked studies included in the review (10.1101/2025.05.06.25327053; 10.1016/j.jacadv.2025.101833; 10.1016/j.drugalcdep.2025.112740; 10.1186/s13722-025-00575-w; 10.1038/s41598-025-03904-w; 10.1136/bmjopen-2024-098005). Our search for our interventions for quitting vaping review up to 1st July 2025 found one new study by Klemperer et al discussed in this podcast (10.1093/ntr/ntaf119), one new ongoing study (10.1136/bmjopen-2024-096963), and two linked papers (10.1093/heapro/daaf085; 10.1016/j.jadohealth.2025.04.012). For further details see our webpage under 'Monthly search findings': https://www.cebm.ox.ac.uk/research/electronic-cigarettes-for-smoking-cessation-cochrane-living-systematic-review-1 For more information on the full Cochrane review of E-cigarettes for smoking cessation updated in January 2025 see: https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD010216.pub9/full For more information on the full Cochrane review of Interventions for quitting vaping published in January 2025 see: https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD016058.pub2/full This podcast is supported by Cancer Research UK.

Beatrice Kenner’s inventions were focused largely on making life easier and less annoying for herself and the people around her, including period products. Mildred Smith’s invention was about family, and it grew from her disability after she developed multiple sclerosis. Research: “Deaths.” Evening Star. 11/27/1956. https://www.newspapers.com/image/869672410/ “Mildred E. Smith.” Obituary. Washington Post. 8/19/1993. https://www.washingtonpost.com/archive/local/1993/08/19/n-hugh-mcdiarmid-dies-at-86/beab0fdf-9aec-4ac1-bd0a-cfcef223f1fa/ Byram, W.F. and R.P. Phronebarger. “Current Supply System for Electric Railways.” U.S. Patent 1,134,871. 4/6/1915. Coren, Ashleigh, et al. “The Many Inventions of Beatrice Kenner.” Side Door. Smithsonian Institution. 4/6/2022. https://www.si.edu/sidedoor/many-inventions-beatrice-kenner Davidson, S.N. “Pants Presser.” U.S. Patent 1,088,329. Hambrick, Arlene. “Biographies of Black Female Scientists and Inventors: An Interdisciplinary Middle School Curriculum Guide. ‘What Shall I Tell My Children Who Are Black?’” Graduate School of the University of Massachusetts. Doctor of Education Dissertation. 1993. DOI: 10.7275/14756666 Hodal, Kate. “Cloth, cow dung, cups: how the world's women manage their periods.” The Guardian. 3/14/2019. https://www.theguardian.com/global-development/2019/apr/13/cloth-cow-dung-cups-how-the-worlds-women-manage-their-periods Jeffrey, Laura S. “Amazing American Inventors of the 20th Century.” Enslow Publishers, Inc.. 1996, 2013. Kenner, Mary Beatrice. “Busch Traffic.” Daily Press. 11/12/1984. https://www.newspapers.com/image/234268212/ Kijowska, Wiktoria. “Sanitary suspenders to Mooncups: a brief history of menstrual products.” Victoria and Albert Museum. https://www.vam.ac.uk/articles/a-brief-history-of-menstrual-products King, Helen. “From rags and pads to the sanitary apron: a brief history of period products.” The Conversation. 4/25/2023. https://theconversation.com/from-rags-and-pads-to-the-sanitary-apron-a-brief-history-of-period-products-203451 O’Sullivan, Joan. “Disease Victim Creates Game.” The Orange Leader. 10/8/1982. https://www.newspapers.com/image/1008083420/ Ravey, Julia and Dr. Ella Hubber. “Unstoppable: Mary Beatrice Davidson Kenner.” Unstoppable. BBC. 6/17/2024. https://www.bbc.co.uk/sounds/play/w3ct5rmq Sluby, Patricia Carter. “African American Brilliance.” Tar heel junior historian [2006 : fall, v.46 : no.1]. https://digital.ncdcr.gov/Documents/Detail/tar-heel-junior-historian-2006-fall-v.46-no.1/3700440?item=5369779 Smith, Mildred E. “Family Relationships Card Game.” U.S. Patent 4,230,321. 10/28/1980. https://ppubs.uspto.gov/api/pdf/downloadPdf/4230321 Tsjeng, Zing. “Forgotten Women: The Scientists.” Cassell Illustrated. 2018. Tsjeng, Zing. “The Forgotten Black Woman Inventor Who Revolutionized Menstrual Pads.” Vice. 3/8/2018. https://www.vice.com/en/article/mary-beatrice-davidson-kenner-sanitary-belt/ Washington Afro American. “Jabbo Kenner Leads Boys to Clean Life.” 11/15/1947. https://www.newspapers.com/image/1042304374/ Washington Daily News. “Mrs. Kenner Is In Clover.” 6/2/1958. https://www.newspapers.com/image/1042178951/ See omnystudio.com/listener for privacy information.

In this quick-hitting episode, Zach Baker, DPT, and Tyler Betteridge, DPT, break down a groundbreaking 2025 study that challenges the long-held "rest is best" approach to concussion care. Learn how sub-symptom threshold aerobic exercise can improve executive function in the early stages of sport-related concussion recovery—and what this means for your clinical practice. Quick, evidence-based, and directly applicable.Referenced Study:Rahimi et al. (2025). Sub-symptom threshold aerobic exercise improves executive function during the early stage of sport-related concussion recovery.PMID: 39936544 | DOI: 10.1080/02640414.2025.2453337

BUFFALO, NY - July 29, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on July 25, 2025, titled “Comprehensive genomic profiling of over 10,000 advanced solid tumors.” In this study, led by Jean-Paul De La O from Exact Sciences Corporation, researchers analyzed data from over 10,000 solid tumor samples from patients with advanced cancer and found that more than 90 percent contained genetic changes that could guide treatment. This work demonstrates the growing impact of large-scale tumor DNA and RNA testing on patient care. The researchers retrospectively analyzed OncoExTra assay information for 31 types of cancer, including breast, colorectal, prostate, lung, and ovarian cancers. Their analysis revealed that nearly a third of patients had alterations associated with approved drugs for their specific cancer, while another third had changes linked to therapies approved for other cancers. These results show that detailed genetic profiling could expand treatment choices. “Biomarkers associated with on- or off-label FDA-approved therapies were detected in 29.2% and 28.0% of samples, respectively.” Another relevant discovery was that many important mutations occurred at very low levels, which are often missed by simpler tests. By using a broad and highly sensitive approach, the scientists were able to identify these rare mutations. They also reported that 7.5 percent of samples carried gene fusions, unusual genetic events that can drive cancer growth. Such findings can be critical in selecting therapies that specifically target these abnormalities. The study also highlighted the value of RNA sequencing in detecting fusion events that traditional DNA tests might miss. Prostate cancer and certain sarcomas showed particularly high rates of these fusion alterations. This type of information can refine cancer diagnosis and improve therapy planning. In addition, the researchers identified changes in several major cancer-related pathways, including those that control cell growth, DNA repair, and immune system response. Alterations in these pathways can point to newer treatment options, such as immunotherapy or drugs designed to block specific cell signals. Overall, this study shows that comprehensive genomic profiling can guide more personalized cancer care by identifying mutations, gene fusions, and other molecular patterns. Advanced testing methods like the OncoExTra assay reveal treatment opportunities even in advanced cancers, ensuring that subtle but important genetic changes are detected. DOI - https://doi.org/10.18632/oncotarget.28757 Correspondence to - Jean-Paul De La O - jdelao@exactsciences.com Video short - https://www.youtube.com/watch?v=awiRhDfiMTE Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28757 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, solid tumors, comprehensive genomic profiling, matched therapy, gene fusions, limit of detection 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

Drs. David Andes and Isabel Spriet join Dr. Jeannette Bouchard to discuss all of the top questions our audience had on fluconazole dosing. Who needs a load? How much fluconazole is too much fluconazole? And what did one of our experts do when they were asked about dosing fluconazole in a dolphin? Listen in to find out! Listen to Breakpoints on iTunes, Overcast, Spotify, Listen Notes, Player FM, Pocket Casts, TuneIn, Blubrry, RadioPublic, or by using our RSS feed: https://sidp.pinecast.co/. Visit our website! https://breakpoints-sidp.org/ References: Fluconazole PK Variability in Critically Ill: DOI 10.3390/microorganisms9102068 DALI Antifungal Follow-up: DOI 10.1186/s13054-015-0758-3

On this episode of the Huddle, Kelly Postiglione Cook, RN, MSN, ANP-BC, CDCES, BC-ADM, and Sean Oser, MD, MPH, CDCES have a conversation about the importance of utilizing automated insulin delivery systems, like the iLet bionic pancreas, more widely in primary care. They provide insight into a study that evaluated the success of implementing use of the iLet bionic pancreas in a primary care setting, how the results illustrated that this technology can be more widely utilized in these settings, and the role diabetes care and education specialists can play in this work.This episode is sponsored by Beta Bionics. Episode References: Bionic Pancreas Research Group. Multicenter, randomized trial of a bionic pancreas in type 1 diabetes. N Engl J Med 2022;387:1161-1172 DOI: 10.1056/NEJMoa2205225 Russell SJ, Selagamsetty R, Damiano E. Real-world efficacy of the iLet bionic pancreas in adults and children during the first eighteen months of commercial availability. Presented at the American Diabetes Association 85th Scientific Sessions, June 20-23, 2025, Chicago, IL.   Oser SM, Putman MS, Russel SJ, et al. Assessing the iLet Bionic Pancreas deployed in primary care and via telehealth: a randomized clinical trial. Clin Diabetes 2025; cd240104. https://doi.org/10.2337/cd24-0104 Oser C, Parascando JA, Kostiuk M, et al. Experiences of people with type 1 diabetes using the iLet bionic pancreas in primary care: A qualitative analysis. Clin Diabetes 2024 https://doi.org/10.2337/cd24-0060.  Sulik B, Postiglione Cook K, MacLeod J. Meals no longer need to be math problems: Shifting from precise carbohydrate counting to a continuum of carbohydrate awareness as automated insulin delivery advances. Diabetes Technology and Obesity Medicine 2025;1(1):79-83. DOI: 10.1089/dtom.2025.0010.  Resources:Learn more about Beta Bionics here: https://www.betabionics.com/Explore the latest in diabetes technology on danatech: danatech l Diabetes Technology Education for Healthcare ProfessionalsLearn more about a two-part course on integrating diabetes technology into primary care, put on through the collaboration of AANP and ADCES:Part 1: Integrating Diabetes Technology into Primary Care Part 1: Overview and Clinical ScenariosPart 2: Integrating Diabetes Technology into Primary Care Part 2: Interactive Case StudiesDive deeper into how diabetes technology can be incorporated into primary care on another recent episode of The Huddle featuring Kathryn Evans Kreider DNP, FNP-BC, BC-ADM, FAANP: https://thehuddle.simplecast.com/episodes/embracing-diabetes-technology-in-primary-care Listen to more episodes of The Huddle at adces.org/perspectives/the-huddle-podcast.Learn more about ADCES and the many benefits of membership at adces.org/join.

Once Rosina Bulwer-Lytton and her husband Edward separated, his life seemed to become more and more successful while she struggled with finances. The estranged couple then spent years battling very publicly until Edward had Rosina committed. Research: “A Scene at the Hertfordshire Election.” The Tiverton Gazette. 6/29/1858. https://www.newspapers.com/image/803824054/ Blain, Virginia. “Rosina Bulwer Lytton and the Rage of the Unheard.” Huntington Library Quarterly , Summer, 1990, Vol. 53, No. 3. Via JSTOR. https://www.jstor.org/stable/3817439 Brown, Andrew. "Lytton, Edward George Earle Lytton Bulwer [formerly Edward George Earle Lytton Bulwer], first Baron Lytton (1803–1873), writer and politician." Oxford Dictionary of National Biography. September 23, 2004. Oxford University Press. Date of access 4 Jun. 2025, https://www-oxforddnb-com.proxy.bostonathenaeum.org/view/10.1093/ref:odnb/9780198614128.001.0001/odnb-9780198614128-e-17314 Bulwer-Lytton, Rosina. “Lady Bulwer Lytton's Appeal to the Justice and Charity of the English Public.” By and For the Author. 1857. Devey, Louisa, editor. “Letters of the late Edward Bulwer, lord Lytton, to his wife.” New York : G. W. Dillingham. 1889. Devey, Louisa. “Life of Rosina, Lady Lytton: With Numerous Extracts from Her Ms. Autobiography and Other Original Documents.” London, Swan Sonnschein, Lowery & Co. 1887. Flynn, Michael J. “Dickens, Rosina Bulwer Lytton, and the ‘Guilt’ of Literature and Art.” Dickens Quarterly, March 2012, Vol. 29, No. 1 (March 2012). Via JSTOR. https://www.jstor.org/stable/45292582 King, Cornelia. “Getting Even: The Mighty Pen of Lady Bulwer Lytton.” The Library Company of Philadelphia. 5/10/2022. https://librarycompany.org/2022/05/10/getting-even/ Latané, D.E. “Edward Bulwer Lytton’s committal of his wife Rosina to a private mental asylum in 1858.” Victorian Web. https://victorianweb.org/authors/bulwer/latane.html McFadden, Margaret. “Anna Doyle Wheeler (1785-1848): Philosopher, Socialist, Feminist.” Hypatia, vol. 4, no. 1, 1989, pp. 91–101. JSTOR, http://www.jstor.org/stable/3809936. Accessed 3 June 2025. Mulvey-Roberts, Marie. "Fame, notoriety and madness: Edward Bulwer-Lytton paying the price of greatness." Critical Survey, vol. 13, no. 2, May 2001, pp. 115+. Gale Literature Resource Center, link.gale.com/apps/doc/A80191856/LitRC?u=mlin_n_melpub&sid=bookmark-LitRC&xid=2669a158. Accessed 27 May 2025. Mulvey-Roberts, Marie. "Lytton, Rosina Anne Doyle Bulwer [née Rosina Anne Doyle Wheeler], Lady Lytton (1802–1882), novelist." Oxford Dictionary of National Biography. October 08, 2009. Oxford University Press. Date of access 28 May. 2025, https://www-oxforddnb-com.proxy.bostonathenaeum.org/view/10.1093/ref:odnb/9780198614128.001.0001/odnb-9780198614128-e-17316 Mulvey-Roberts, Marie. “‘The Very Worst Woman I Ever Heard of’: Rosina Bulwer Lytton and Biography as Vindication.” Women's Writing, 25:2, 253-267, DOI: 10.1080/09699082.2017.1387338 See omnystudio.com/listener for privacy information.

After a difficult childhood, Rosina Bulwer-Lytton landed in a marriage that quickly turned chaotic and stressful, and then became abusive. Part one covers the period of her life up to their separation. Research: “A Scene at the Hertfordshire Election.” The Tiverton Gazette. 6/29/1858. https://www.newspapers.com/image/803824054/ Blain, Virginia. “Rosina Bulwer Lytton and the Rage of the Unheard.” Huntington Library Quarterly , Summer, 1990, Vol. 53, No. 3. Via JSTOR. https://www.jstor.org/stable/3817439 Brown, Andrew. "Lytton, Edward George Earle Lytton Bulwer [formerly Edward George Earle Lytton Bulwer], first Baron Lytton (1803–1873), writer and politician." Oxford Dictionary of National Biography. September 23, 2004. Oxford University Press. Date of access 4 Jun. 2025, https://www-oxforddnb-com.proxy.bostonathenaeum.org/view/10.1093/ref:odnb/9780198614128.001.0001/odnb-9780198614128-e-17314 Bulwer-Lytton, Rosina. “Lady Bulwer Lytton's Appeal to the Justice and Charity of the English Public.” By and For the Author. 1857. Devey, Louisa, editor. “Letters of the late Edward Bulwer, lord Lytton, to his wife.” New York : G. W. Dillingham. 1889. Devey, Louisa. “Life of Rosina, Lady Lytton: With Numerous Extracts from Her Ms. Autobiography and Other Original Documents.” London, Swan Sonnschein, Lowery & Co. 1887. Flynn, Michael J. “Dickens, Rosina Bulwer Lytton, and the ‘Guilt’ of Literature and Art.” Dickens Quarterly, March 2012, Vol. 29, No. 1 (March 2012). Via JSTOR. https://www.jstor.org/stable/45292582 King, Cornelia. “Getting Even: The Mighty Pen of Lady Bulwer Lytton.” The Library Company of Philadelphia. 5/10/2022. https://librarycompany.org/2022/05/10/getting-even/ Latané, D.E. “Edward Bulwer Lytton’s committal of his wife Rosina to a private mental asylum in 1858.” Victorian Web. https://victorianweb.org/authors/bulwer/latane.html McFadden, Margaret. “Anna Doyle Wheeler (1785-1848): Philosopher, Socialist, Feminist.” Hypatia, vol. 4, no. 1, 1989, pp. 91–101. JSTOR, http://www.jstor.org/stable/3809936. Accessed 3 June 2025. Mulvey-Roberts, Marie. "Fame, notoriety and madness: Edward Bulwer-Lytton paying the price of greatness." Critical Survey, vol. 13, no. 2, May 2001, pp. 115+. Gale Literature Resource Center, link.gale.com/apps/doc/A80191856/LitRC?u=mlin_n_melpub&sid=bookmark-LitRC&xid=2669a158. Accessed 27 May 2025. Mulvey-Roberts, Marie. "Lytton, Rosina Anne Doyle Bulwer [née Rosina Anne Doyle Wheeler], Lady Lytton (1802–1882), novelist." Oxford Dictionary of National Biography. October 08, 2009. Oxford University Press. Date of access 28 May. 2025, https://www-oxforddnb-com.proxy.bostonathenaeum.org/view/10.1093/ref:odnb/9780198614128.001.0001/odnb-9780198614128-e-17316 Mulvey-Roberts, Marie. “‘The Very Worst Woman I Ever Heard of’: Rosina Bulwer Lytton and Biography as Vindication.” Women's Writing, 25:2, 253-267, DOI: 10.1080/09699082.2017.1387338 See omnystudio.com/listener for privacy information.