Podcasts about DOI

BUFFALO, NY – June 20, 2025 – A new #review was #published in Volume 16 of Oncotarget on June 10, 2025, titled “Beyond DNA damage response: Immunomodulatory attributes of CHEK2 in solid tumors.” In this paper, led by first author Helen Qian and corresponding author Crismita Dmello from Northwestern University Feinberg School of Medicine, researchers compiled growing evidence that the CHEK2 gene, long known for its role in repairing DNA damage, may also influence how tumors respond to immunotherapy. Their analysis suggests that problems in CHEK2 function might make cancer cells more vulnerable to immune system attacks, highlighting a new opportunity to improve treatment outcomes in solid tumors. Immune checkpoint inhibitors (ICIs) have transformed cancer treatment; however, they are effective in only a subset of patients. This review suggests that tumors with reduced CHEK2 activity may accumulate more mutations that produce signals the immune system can recognize. These signals, known as neoantigens, help immune cells identify and destroy cancer cells more effectively. The review connects this process not only to CHEK2's established role in the DNA damage response but also to a newly proposed function in shaping the immune environment of tumors. CHEK2 normally helps maintain genomic stability by enabling precise DNA repair. When this function is lost, cells rely on more error-prone repair methods, leading to additional mutations. These mutations can increase tumor mutational burden, which has been linked to better outcomes with immunotherapy. Beyond DNA repair, the review highlights a second mechanism: activation of the cGAS-STING pathway. This pathway detects fragments of damaged DNA and triggers inflammation that attracts immune cells to the tumor. The authors highlight studies where CHEK2-deficient tumors responded better to PD-1 inhibitors, a common type of immune checkpoint inhibitor. In both lab models and early-stage clinical settings, CHEK2 loss was associated with increased infiltration of CD8+ T cells—immune cells essential for attacking cancer cells. In cancers such as glioblastoma and renal cell carcinoma, which are typically resistant to immunotherapy, reduced CHEK2 expression was linked with more favorable immune activity and higher expression of interferon-related genes. The compiled evidence points to CHEK2 as a potential biomarker for identifying patients likely to respond to immunotherapy. In addition, combining CHEK2 inhibitors with existing immunotherapies may enhance anti-tumor effects, particularly in cancers with limited treatment options. The review notes that some clinical trials using the CHEK1/2 inhibitor prexasertib alongside immune checkpoint therapies have already shown promising early results. “The initial results from this Phase I clinical trial support the immunomodulatory role of CHEK2 expression and even suggest CHEK2 potentiates immunosuppression.” Although more research is needed to confirm these mechanisms and improve treatment approaches, this review underscores the expanding role of DNA repair genes like CHEK2—not only in maintaining genome integrity but also in helping the immune system fight cancer. DOI - https://doi.org/10.18632/oncotarget.28740 Correspondence to - Crismita Dmello - stellacpak@outlook.com Video short - https://www.youtube.com/watch?v=C26pEBc0itk 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

Dr. Josh Mitteldorf summarizes his #research perspective #published in Volume 17, Issue 5 of Aging (Aging-US), titled “Methylation clocks for evaluation of anti-aging interventions.” DOI - https://doi.org/10.18632/aging.206245 Corresponding author - Josh Mitteldorf - aging.advice@gmail.com Author interview - https://www.youtube.com/watch?v=efgNvr5ezTk Video short - https://www.youtube.com/watch?v=YjUvpqMzCGc Abstract Methylation clocks have found their way into the community of aging research as a way to test anti-aging interventions without having to wait for mortality statistics. But methylation is a primary means of epigenetic control, and presumably has evolved under strong selection. Hence, if methylation patterns change consistently at late ages it must mean one of two things. Either (1) the body is evolved to destroy itself (with inflammation, autoimmunity, etc.), and the observed methylation changes are a means to this end; or (2) the body detects accumulated damage, and is ramping up repair mechanisms in a campaign to rescue itself. My thesis herein is that both Type 1 and Type 2 changes are occurring, but that only Type 1 changes are useful in constructing methylation clocks to evaluate anti-aging interventions. This is because a therapy that sets back Type 1 changes to an earlier age state has stopped the body from destroying itself; but a therapy that sets back Type 2 changes has stopped the body from repairing itself. Thus, a major challenge before the community of epigenetic clock developers is to distinguish Type 2 from Type 1. The existence of Type 1 epigenetic changes is in conflict with conventional Darwinian thinking, and this has prompted some researchers to explore the possibility that Type 1 changes might be a form of stochastic epigenetic drift. I argue herein that what seems like directed epigenetic change really is directed epigenetic change. Of five recent articles on “stochastic methylation clocks,” only one (from the Conboy lab) is based on truly stochastic changes. Using the Conboy methodology and a methylation database, I construct a measure of true methylation drift, and show that its correlation with age is too low to be useful. Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206245 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, methylation, stochastic, entropy, programmed aging, aging clock, epigenetic clock 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 episode of Strength In Knowledge, we dive into the fascinating world of ergonomics and product design through the lens of groundbreaking research on backpack development. Join us as we unpack the study by Mohamed Z. Ramadan and Sultan N. Al-Tayyar, who explored how to engineer a backpack that reduces strain, improves posture, and enhances comfort for users across different age groups and physical demands.From design theory to real-world testing, we explore how their ergonomic innovations aim to minimize the musculoskeletal risks associated with traditional backpacks—especially relevant for students, commuters, and healthcare professionals alike. Whether you're a physical therapist, strength coach, or simply someone tired of shoulder pain, this is one episode you won't want to miss.

BUFFALO, NY — June 18, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 5, on May 12, 2025, titled “Frailty transitions in electronic health records: who first? what first?” The study, led by Fabienne Hershkowitz Sikron from Meuhedet HMO, analyzed how frailty develops over time in older adults using electronic health record data from nearly 120,000 individuals aged 65 and above. Researchers found that frailty worsened in over 13% of participants within a year, particularly among women, adults aged 85 or older, and people with chronic illnesses, while nearly 3% showed signs of improvement. The findings highlight early indicators of decline that could help guide preventive care and improve outcomes for aging populations. Frailty is a condition marked by increased vulnerability to health complications and tends to change gradually. The study used the Meuhedet Electronic Frailty Index (MEFI) to track yearly transitions in frailty among older adults in Israel. While many people remained in the same frailty category, a significant proportion experienced deterioration in just one year, and a smaller group improved. “Worsening frailty is defined as a higher frailty level one year later in 2024 compared to 2023. A new frailty deficit is defined as a deficit appearing in 2024 that was not present in 2023.” Those most at risk of worsening included adults over 85, women, individuals from lower socio-economic backgrounds, and members of the Arab sector. Additional predictors of decline included recent hospitalizations, multiple chronic diseases, and signs of cognitive or mobility issues. Importantly, the first signs of worsening were often not new chronic conditions but more manageable health deficits such as sleep disturbances, muscle weakness, hearing loss, and memory decline. Those who improved were more likely to be younger, male, from higher socio-economic backgrounds, and have fewer chronic conditions and hospitalizations. The study also found that common chronic illnesses like diabetes and hypertension were often already present and did not usually signal the beginning of frailty progression. Instead, declines in overall function and quality of life were more frequently the first new issues to appear. This suggests that early intervention on modifiable health deficits could delay or prevent further decline. This work is one of the first large-scale, real-world studies to identify both who is most likely to worsen first and what health problems typically appear first. The authors emphasize the importance of using routinely collected electronic medical data to monitor frailty and tailor care. By doing so, health providers can implement timely strategies to reduce disease burden and support aging individuals in maintaining independence. These findings support the creation of proactive health programs focused on maintaining physical strength, cognitive function, and sensory abilities. Preventing frailty progression can reduce hospitalizations, ease disease burden, and help older adults maintain independence and a higher quality of life. DOI - https://doi.org/10.18632/aging.206247 Corresponding author - Fabienne Hershkowitz Sikron - fabian_hershkowitz@meuhedet.co.il Video short - https://www.youtube.com/watch?v=4xa11ApI4ho 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

Send us a textIn this episode, Dr. Elfrieda “Freddy” Hiebert talks to us about language, learning to read, and authentic interactions with interesting texts. Freddy is known for her work addressing how fluency, vocabulary, and knowledge can be fostered through appropriate texts. Through documents such as Becoming a Nation of Readers, published by the Center for the Study of Reading in 1985 and Every Child a Reader, published by the Center for the Improvement of Early Reading Achievement in 1999, she has contributed to making research accessible to educators. Her work has also appeared in journals such as The Reading Teacher, Reading and Writing, Reading Research Quarterly, Reading Psychology, Education Sciences, Literacy Research: Theory, Method, and Practice, Journal of Literacy Research, Educational Researcher, and Educational Leadership. She has also authored many books and book chapters. Her work has been recognized by a number of organizations, including the Oscar Causey Award for Outstanding Contributions to Reading Research from the Literacy Research Association in 2015. Freddy has had a long career as a literacy educator, first as a teacher's aide and teacher of primary-level students in California and, subsequently, as a teacher educator and researcher at the universities of Kentucky, Colorado-Boulder, Michigan, and California-Berkeley. Since 2011, she has served as President and CEO of TextProject, Inc, a non-profit corporation that prioritizes creating products and prototypes for student reading programs, primarily based on the TExT model of text complexity, providing teacher support resources and classroom reading activities, and supporting and disseminating related research.To cite this episode: Persohn, L. (Host). (2025, June 17). A conversation with Elfrieda “Freddy” Hiebert. (Season 5, No. 11) [Audio podcast episode]. In Classroom Caffeine Podcast series. https://www.classroomcaffeine.com/guests. DOI: 10.5240/4631-DA23-14D0-79DB-B764-KResources mentioned in this episode:Connect with Classroom Caffeine at www.classroomcaffeine.com or on Instagram, Facebook, Twitter, and LinkedIn.

BUFFALO, NY - June 17, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on June 10, 2025, titled “Exceptional responders to immunotherapy in pancreatic cancer: A multi-institutional case series of a rare occurrence.” The study, led by first author Kavin Sugumar and corresponding author Jordan M. Winter, from University Hospitals Seidman Cancer Center, reports on a rare group of pancreatic cancer (PC) patients who responded remarkably well to immunotherapy, a treatment typically considered ineffective for this cancer type. The analysis, which includes data from 14 patients across multiple U.S. institutions, identifies outcomes that could help refine treatment strategies for one of the most aggressive and deadly forms of cancer. “Between 2020–21, 471 oncologists from 91 major cancer centers in the United States were contacted.” Pancreatic cancer has among the lowest survival rates and few effective therapies. While immunotherapy has transformed the treatment landscape for several other cancers, it generally offers little benefit for pancreatic cancer. However, this study highlights a small but important group of patients who experienced significant and sustained responses to immune-based treatment without chemotherapy. Most had advanced or metastatic disease and had already progressed after standard treatments. Among the 14 patients, 82% had partial tumor shrinkage, and nearly one-third had a notable decrease in tumor markers. The median progression-free survival was 12 months, and most patients were still alive at follow-up, with survival rates of 80% at one year and 70% at two years. These outcomes contrast sharply with standard therapies, which often provide only a few months of benefit for similar patients. Interestingly, while some patients had high microsatellite instability (MSI-high)—a known marker for immunotherapy success—more than half did not, suggesting other biological mechanisms may be involved. This result highlights the need for new biomarkers to be discovered to predict treatment response in future studies. This case series is the largest focused exclusively on exceptional immunotherapy responders in pancreatic cancer. By excluding patients who received chemotherapy, the study isolates the effects of immune-based drugs, including PD-1 inhibitors such as pembrolizumab and nivolumab, CTLA-4 inhibitors like ipilimumab, and agents targeting macrophages. While the sample size is small, the findings challenge the assumption that immunotherapy is ineffective for nearly all pancreatic cancer patients. The study suggests that, under certain biological conditions, this treatment can be remarkably successful. Further research is needed to understand the underlying mechanisms. This work supports the need to reconsider how clinical trials are designed for pancreatic cancer and who is eligible for immunotherapy. Broader criteria and more personalized molecular profiling could help uncover hidden opportunities for treatment in this highly lethal cancer. DOI - https://doi.org/10.18632/oncotarget.28739 Correspondence to - Jordan M. Winter - jordan.winter@UHHospitals.org Video short - https://www.youtube.com/watch?v=VeWTcuVmqgM Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28739 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 — June 17, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 5, on May 1, 2025, titled “Oxytocin modulates insulin and GLP-1 secretion in pancreatic islets.” In this study, scientists from Fukushima Medical University School of Medicine investigated how the hormone oxytocin (Oxt) influences insulin levels by acting on specific cells in the pancreas. The team led by first author Kasumi Hattori and corresponding authors Kenju Shimomura and Yuko Maejima discovered that oxytocin may indirectly increase insulin secretion by triggering another hormone, GLP-1, from within the pancreas. This finding could lead to new strategies for improving blood sugar control in people with diabetes. Oxytocin is commonly known for its roles in childbirth and social bonding, but scientists have also been exploring its effects on metabolism. While previous studies offered mixed results about whether oxytocin raises or lowers blood sugar, this research brings new clarity. The study focused on oxytocin's impact on insulin and a hormone called GLP-1, which helps regulate insulin production. Researchers tested this by using mice with and without oxytocin receptors and found that oxytocin's ability to raise insulin levels depended on the presence of these receptors and high blood sugar conditions. Researchers found that oxytocin stimulates the release of “intra-islet GLP-1,” a form of GLP-1 produced inside the pancreas rather than the intestine. In the pancreas, insulin is produced by beta cells, while alpha cells produce glucagon, a hormone that raises blood sugar. But recent research, including this study, has shown that alpha cells can also release GLP-1, which in turn helps beta cells secrete insulin. Oxytocin appears to increase this internal GLP-1 release, especially when blood sugar levels are high, thereby leading to insulin release in a natural and targeted way. In this study researchers were also able to detect the difference between oxytocin's effect on blood sugar and its effect on insulin. They observed that right after oxytocin was given, blood sugar levels rose in all mice—even in those that lacked oxytocin receptors. However, only the mice with working oxytocin receptors showed a later increase in insulin. This suggests that oxytocin may trigger insulin production through a separate, receptor-dependent pathway involving the hormone GLP-1. "WT mice showed a significant increase in insulin levels at 15-min, while OxtR KO mice did not." This indirect action—oxytocin triggering alpha cells to release GLP-1, which then acts on beta cells—may represent a novel mechanism for controlling insulin release. It also explains why oxytocin does not increase insulin in low-glucose conditions, making it a potentially safer option for regulating blood sugar. As treatments for type 2 diabetes increasingly focus on GLP-1–based drugs, this study opens the door to using oxytocin or similar compounds to naturally enhance the body's own insulin-producing system. With further research, this mechanism could help develop new therapies that better mimic the body's natural glucose control, particularly beneficial for older adults with diabetes. DOI - https://doi.org/10.18632/aging.206244 Corresponding authors - Kenju Shimomura - shimomur@fmu.ac.jp, and Yuko Maejima - maejimay@fmu.ac.jp Video short - https://www.youtube.com/watch?v=C0K6uDX4z8U 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

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-437 Overview: This episode reviews the remarkable impact of the human papillomavirus (HPV) vaccine from 2008–2022, including significant declines in cervical precancer rates. Tune in for key data insights and updated HPV vaccination guidelines to help you close care gaps and strengthen cancer prevention efforts in your practice. Episode resource links: Gargano JW, Stefanos R, Dahl RM, et al. Trends in Cervical Precancers Identified Through Population-Based Surveillance — Human Papillomavirus Vaccine Impact Monitoring Project, Five Sites, United States, 2008–2022. MMWR Morb Mortal Wkly Rep 2025;74:96–101. DOI: http://dx.doi.org/10.15585/mmwr.mm7406a4 • HPV Vaccination Recommendations: Dosing and Schedule • Talking to parents about HPV vaccine Guest: Jill M. Terrien PhD, ANP-BC    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-437 Overview: This episode reviews the remarkable impact of the human papillomavirus (HPV) vaccine from 2008–2022, including significant declines in cervical precancer rates. Tune in for key data insights and updated HPV vaccination guidelines to help you close care gaps and strengthen cancer prevention efforts in your practice. Episode resource links: Gargano JW, Stefanos R, Dahl RM, et al. Trends in Cervical Precancers Identified Through Population-Based Surveillance — Human Papillomavirus Vaccine Impact Monitoring Project, Five Sites, United States, 2008–2022. MMWR Morb Mortal Wkly Rep 2025;74:96–101. DOI: http://dx.doi.org/10.15585/mmwr.mm7406a4 • HPV Vaccination Recommendations: Dosing and Schedule • Talking to parents about HPV vaccine Guest: Jill M. Terrien PhD, ANP-BC    Music Credit: Matthew Bugos Thoughts? Suggestions? Email us at FranklySpeaking@pri-med.com   

Dr. Bill Weiss and Alex Tebbe of the Department of Animal Sciences at The Ohio State University join Dr. Phil Cardoso of the University of Illinois to discuss their recent paper about the effects of oscillating dietary crude protein concentrations on production, nutrient digestion, plasma metabolites, and body composition in lactating dairy cows.Links to papers mentioned in this episodeTebbe and Weiss 2020, Effects of oscillating dietary crude protein concentrations on production, nutrient digestion, plasma metabolites, and body composition in lactating dairy cows.DOI: 10.3168/jds.2020-18613https://pubmed.ncbi.nlm.nih.gov/32896402/Agnew et al. 2005, Relationships between urea dilution measurements and body weight and composition of lactating dairy cows.DOI: 10.3168/jds.S0022-0302(05)72925-8https://pubmed.ncbi.nlm.nih.gov/15956310/

Dr. Stephen LeBlanc of the Ontario Veterinary College at the University of Guelph joins Dr. Phil Cardoso of the University of Illinois for a chat about metabolic disorders and fertility.Links to publications mentioned in this episodeDairy Cattle Fertility (FE20)https://hoards.com/article-27434-dairy-cattle-fertility-(fe20).htmlBook details:121 pages8.5 x 11 inchesSoftcover, perfect boundFull colorISBN 978-0-9960753-3-6Copyright 2020Jessica Gordon papers on ketosis:Gordon et al. 2017, Effects of a combination butaphosphan and cyanocobalamin product and insulin on ketosis resolution and milk production.DOI: 10.3168/jds.2016-11925https://www.journalofdairyscience.org/article/S0022-0302(17)30149-2/fulltextGordon et al. 2013, Ketosis treatment in lactating dairy cattle. DOI: 10.1016/j.cvfa.2013.03.001https://www.sciencedirect.com/science/article/abs/pii/S0749072013000285?via%3DihubPascottini and LeBlanc 2020, Metabolic markers for purulent vaginal discharge and subclinical endometritis in dairy cows.DOI: 10.1016/j.theriogenology.2020.06.005https://pubmed.ncbi.nlm.nih.gov/32622204/Stephanie's (my student) video on Metricheck toolhttps://www.youtube.com/watch?v=jIhd8buSpHU&t=160sLeBlanc 2014, Reproductive tract inflammatory disease in postpartum dairy cows. DOI: 10.1017/S1751731114000524https://www.cambridge.org/core/journals/animal/article/reproductive-tract-inflammatory-disease-in-postpartum-dairy-cows/598913738F82C7FC94A92F60C7C80524New Zealand paper:Burke et al., Relationships between endometritis and metabolic state during the transition period in pasture-grazed dairy cows.https://pubmed.ncbi.nlm.nih.gov/20965352/

Dr. Phil Cardoso and Dr. Adam Lock of Michigan State University discuss Dr. Lock's recent study on the effect of supplementing two major fatty acids, palmitic and oleic acid, in different ratios on milk production in high-, medium- and low-producing cows.Links to papers mentioned in this episodeWestern et al. 2020, Milk production responses to altering the dietary ratio of palmitic and oleic acids varies with production level in dairy cows. DOI: https://doi.org/10.3168/jds.2020-18936 https://pubmed.ncbi.nlm.nih.gov/33069410/de Souza et al. 2019, Altering the ratio of dietary C16:0 and cis-9 C18:1 interacts with production level in dairy cows: Effects on production responses and energy partitioning. DOI: 10.3168/jds.2019-16374https://pubmed.ncbi.nlm.nih.gov/31495626/Lock et al. 2006, Concepts of fat and fatty acid digestion in ruminants. https://www.researchgate.net/publication/266499830_Concepts_of_fat_and_fatty_acid_digestion_in_ruminantsBurch et al 2020, Milk production responses of dairy cows to fatty acid supplements with different ratios of palmitic and oleic acid in low- and high-fat basal diets. Abstract #175 in https://www.adsa.org/Portals/0/SiteContent/Docs/Meetings/2020ADSA/ADSA2020_Abstracts.pdf?v20200708.

Dr. Phil Cardoso talks with Dr. Kate Creutzinger of the University of Guelph and Dr. Katy Proudfoot of the University of Prince Edward Island about the effects of prepartum stocking density and a blind on physiological biomarkers, health, and hygiene of transition Holstein dairy cows.Links to papers mentioned in this episodeCreutzinger et al. 2020, Effects of prepartum stocking density and a blind on physiological biomarkers, health, and hygiene of transition Holstein dairy cows.DOI: 10.3168/jds.2020-18718https://www.journalofdairyscience.org/article/S0022-0302(20)30905-X/fulltextEdwards et al. 2020, Calving location preference and changes in lying and exploratory behavior of preparturient dairy cattle with access to pasture.DOI: 10.3168/jds.2019-17218https://www.journalofdairyscience.org/article/S0022-0302(20)30252-6/fulltextZobel et al. 2020, The use of hides during and after calving in New Zealand dairy cows.DOI: 10.3390/ani10122255https://www.mdpi.com/2076-2615/10/12/2255 Creutzinger et al. 2021, The effect of stocking density and a blind on the behavior of Holstein dairy cattle in group maternity pens. Part I: Calving location, locomotion, and separation behavior.DOI: 10.3168/jds.2020-19744https://www.journalofdairyscience.org/article/S0022-0302(21)00453-7/fulltextCreutzinger et al. 2021, The effect of stocking density and a blind on the behavior of Holstein dairy cows in group maternity pens. Part II: Labor length, lying behavior, and social behavior.DOI: 10.3168/jds.2020-19745https://www.journalofdairyscience.org/article/S0022-0302(21)00454-9/fulltext

Dr. Phil Cardoso talks with Dr. Peter Erickson and Tess Stahl of the University of New Hampshire about the effects of feeding diets containing supplementary sodium butyrate and monensin on growth performance, nutrient digestibility, and health in postweaned heifers. Links to papers mentioned in this episodeStahl TC, Hatungimana E, Klanderman KD, Moreland SC, Erickson PS. 2020. Sodium butyrate and monensin supplementation to postweaning heifer diets: Effects on growth performance, nutrient digestibility, and health.DOI: 10.3168/jds.2020-18584https://www.journalofdairyscience.org/article/S0022-0302(20)30720-7/fulltextRice EM, Aragona KM, Moreland SC, Erickson PS. 2019.Supplementation of sodium butyrate to postweaned heifer diets: Effects on growth performance, nutrient digestibility, and health.DOI: 10.3168/jds.2018-15525https://pubmed.ncbi.nlm.nih.gov/30738684/Górka P, Kowalski ZM, Zabielski R, Guilloteau P. 2018. Invited review: Use of butyrate to promote gastrointestinal tract development in calves.DOI: 10.3168/jds.2017-14086https://www.sciencedirect.com/science/article/pii/S0022030218302212Kononoff PJ. Snow DD, Christiansen DA. 2017. Drinking Water for Dairy Cattle. Pages 611–624 in Large Dairy Herd Management.DOI: 10.3168/ldhm.0845https://ldhm.adsa.org/Rosa F, Busato S, Avaroma FC, Linville K, Trevisi E, Osorio JS. 2018. Transcriptional changes detected in fecal RNA of neonatal dairy calves undergoing a mild diarrhea are associated with inflammatory biomarkers.DOI: 10.1371/journal.pone.0191599https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0191599Hatungimana E, Stahl TC, Erickson PS. 2020. Growth performance and apparent total tract nutrient digestibility of limit-fed diets containing wet brewer's grains to Holstein heifers.DOI: 10.1093/tas/txaa079https://academic.oup.com/tas/article/4/3/txaa079/5855081

Methane is a potent greenhouse gas that traps energy far more efficiently than carbon dioxide. Reduction of methane emissions is thus essential to slowing climate change, and livestock are a major source of these emissions. Dr. Phil Cardoso talks with Dr. Alex Hristov of Penn State University about nutritional strategies for mitigating production of methane by dairy cattle. They discuss the effectiveness of several different feed additives at reducing methane emissions and their effects on DMI and milk production.Links to papers and other sources mentioned in this episodeHristov et al. 2022. Symposium review: Effective nutritional strategies to mitigate enteric methane in dairy cattle.DOI: 10.3168/jds.2021-21398https://www.journalofdairyscience.org/article/S0022-0302(22)00392-7/fulltextInternational Methane Emissions Observatory (IMEO) https://www.unep.org/explore-topics/energy/what-we-do/imeoJoint EU-US Statement on the Global Methane Pledge https://ec.europa.eu/commission/presscorner/detail/en/statement_21_5206Hristov et al. 2015, An inhibitor persistently decreased enteric methane emission from dairy cows with no negative effect on milk production.DOI: 10.1073/pnas.1504124112https://www.pnas.org/doi/10.1073/pnas.150412411273rd Annual Meeting of EAAP. Porto, Portugal, September 5–9 2022.https://eaap2022.org/docs/Final_Programme_EAAP22.pdf#page=53Arndt et al. 2022, Full adoption of the most effective strategies to mitigate methane emissions by ruminants can help meet the 1.5 °C target by 2030 but not 2050.DOI: 10.1073/pnas.2111294119https://www.pnas.org/doi/10.1073/pnas.2111294119Duin et al. 2016, Mode of action uncovered for the specific reduction of methane emissions from ruminants by the small molecule 3-nitrooxypropanol.DOI: 10.1073/pnas.1600298113Pitta et al. 2022, The effect of 3-nitrooxypropanol, a potent methane inhibitor, on ruminal microbial gene expression profiles in dairy cows.DOI: 10.1186/s40168-022-01341-9https://microbiomejournal.biomedcentral.com/articles/10.1186/s40168-022-01341-9FAO-IPCC Expert Meeting on Climate Change, Land Use and Food Security. Rome, Italy January 23–25 2017.https://www.fao.org/3/i7068e/i7068e.pdfHristov and Melgar 2020, Short communication: Relationship of dry matter intake with enteric methane emission measured with the GreenFeed system in dairy cows receiving a diet without or with 3-nitrooxypropanol.DOI: 10.1017/S1751731120001731https://www.sciencedirect.com/science/article/pii/S1751731120001731?via%3Dihubhttps://globalresearchalliance.org/research/livestock/networks/feed-nutrition-network/Hammond et al. 2016, Review of current in vivo measurement techniques for quantifying enteric methane emission from ruminants.DOI: 10.1016/j.anifeedsci.2016.05.018https://www.sciencedirect.com/science/article/abs/pii/S0377840116302048Roque et al. 2019, Inclusion of Asparagopsis armata in lactating dairy cows' diet reduces enteric methane emission by over 50 percent.https://www.sciencedirect.com/science/article/abs/pii/S0959652619321559DOI: 10.1016/j.jclepro.2019.06.193Martins et al. 2022, Effects of feeding method and frequency on lactationalperformance and enteric methane emission in dairy cows.https://www.adsa.org/Portals/0/SiteContent/Docs/Meetings/2022ADSA/Abstracts_BOOK_2022.pdf#page=79Martins et al. 2022, Effects of botanical preparations on lactational perfor-mance and enteric methane emission in dairy cows.https://www.adsa.org/Portals/0/SiteContent/Docs/Meetings/2022ADSA/Abstracts_BOOK_2022.pdf#page=131

Dr. Phil Cardoso and Dr. Jim Drackley of the University of Illinois and Dr. Bruce Richards of Delaware Valley University discuss their recent paper comparing prepartum low-energy or high-energy diets with a 2-diet far-off and close-up strategy for multiparous and primiparous cows.Links to papers mentioned in this episodeRichards et al. 2020, Comparison of prepartum low-energy or high-energy diets with a 2-diet far-off and close-up strategy for multiparous and primiparous cows.DOI: 10.3168/jds.2020-18603https://pubmed.ncbi.nlm.nih.gov/32828502/Douglas et al. 2006, Prepartal plane of nutrition, regardless of dietary energy source, affects periparturient metabolism and dry matter intake in Holstein cows.DOI: 10.3168/jds.S0022-0302(06)72285-8https://pubmed.ncbi.nlm.nih.gov/16702281/Hawkes et al. 2020, Effects of wheat straw chop length in high-straw dry cow diets on intake, health, and performance of dairy cows across the transition period.DOI: 10.3168/jds.2019-17033https://pubmed.ncbi.nlm.nih.gov/31668439/Hawkes et al. 2020, Moisture content of high-straw dry cow diets affects intake, health, and performance of transition dairy cows.DOI: 10.3168/jds.2019-17557https://pubmed.ncbi.nlm.nih.gov/31837778/Coon et al. 2018, Effect of straw particle size on the behavior, health, and production of early-lactation dairy cows.10.3168/jds.2017-13920https://pubmed.ncbi.nlm.nih.gov/29705431/Mann et al. 2015, Dry period plane of energy: Effects on feed intake, energy balance, milk production, and composition in transition dairy cows.DOI: 10.3168/jds.2014-9024https://pubmed.ncbi.nlm.nih.gov/25771059/Drackley et al. 2014, Visceral adipose tissue mass in nonlactating dairy cows fed diets differing in energy density.DOI: 10.3168/jds.2014-8014https://pubmed.ncbi.nlm.nih.gov/24704224/IN MEMORIAM: DAVID E. BEEVERhttps://www.rabdf.co.uk/latest-news/2015/6/3/professor-david-e-beever-31st-march-1944-16th-june-2014

W dziewiątym odcinku podcastu #bezpiecznik zastanowimy się nad tym czy dom może być inteligentny? Jak i jakie technologie wpływają na jakość naszego życia. Co się dzieje z danymi, które te technologie zbierają, w czym może być to pomocne, a kiedy może nam szkodzić. Będzie trochę o tym, że przyszłość już tu jest, o prywatność trzeba dbać, i że nikt ani nic nie zastąpi podstawowej potrzeby prawa do mieszkania. Moją i Waszą gościnią jest drka Sandra Frydrysiak, która jest kulturoznawczynią, socjolożką i uznaną ekspertką ds. różnorodności, równości i integracji. Związana jest z Uniwersytetem Łódzkim oraz Uniwersytetem SWPS w Warszawie. Specjalizuje się w języku inkluzywnym i przeciwdziałaniu mikroagresji. W ramach pracy przy międzynarodowym projekcie SMARTUP (CHANSE), bada społeczny wpływ inteligentnych technologii na nasze życie.Menu wiedzy:Criado Perez, C. (2020). Niewidzialne kobiety: Jak dane tworzą świat skrojony pod mężczyzn (przeł. A. Sak). Karakter.Grühlich, J., Andrš Fárov, N., Frydrysiak, S., & Kodenko Kubala, P. (2025, July). Is digital housekeeping care? – Visions, legitimations, and negotiations of care work in the smart home. Berliner Journal für Soziologie (forthcoming).Sovacool B, Furszyfer-Del Rio DD, Martiskainen M (2021), „Can Prosuming Become Perilous? Exploring Systems of Control and Domestic Abuse in the Smart Homes of the Future.” DOI: 10.3389/fenrg.2021.765817.Strengers, Y., & Kennedy, J. (2020). The smart wife: Why Siri, Alexa, and other smart home devices need a feminist reboot. MIT Press.Zuboff, S. (2020). Wiek kapitalizmu inwigilacji: Walka o przyszłość człowieczeństwa na nowej granicy władzy. Warszawa: Społeczny Instytut Wydawniczy Znak."Wywiad udzielony w ramach projektu SMARTUP finansowanego przez Narodowe Centrum Nauki w ramach programu CHANSE [numer grantu: 2021/03/Y/HS6/00250]."

Shoplifting puts beef in locked boxes, DOI seeks new Deputy, health levy consultation, the Tynwald Day shift, pensioners' minimum wage & the search for Elvis the dog and Dusty the cat. It's Mannin Line with Andy Wint - Monday 16th June 2025

Today, Dr. Rahul Damania, Dr. Pradip Kamat, and Dr. Monica Gray, pediatric intensivists, sit down to chat about the diagnosis and management of acute myocarditis in children. They focus on a real-life case involving a one-month-old infant who presented with poor feeding, respiratory distress, and fever. Together, they break down the possible causes, key clinical signs, diagnostic approaches, and treatment options for pediatric myocarditis. Throughout the discussion, they highlight the importance of early recognition, a multidisciplinary team approach, and supportive care in improving outcomes for these critically ill infants. This episode is packed with practical insights and is designed to help pediatric intensivists tackle this challenging and potentially life-threatening condition. Tune in to hear more!Show Highlights:Definition and etiology of acute myocarditis in pediatric patientsClinical case presentation of a one-month-old infant with acute myocarditisSymptoms and clinical manifestations of acute myocarditis in childrenDiagnostic approaches for identifying acute myocarditis, including echocardiography and laboratory testsManagement strategies for acute myocarditis, including intensive care and medicationImportance of recognizing atypical presentations in infantsPrognosis and risk factors associated with acute myocarditisRole of multidisciplinary collaboration in managing acute myocarditisImpact of viral infections on the development and severity of myocarditisOutcomes and potential complications related to acute myocarditis in pediatric patientsReferences:Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter 108. Life-threatening viral diseases and their treatment. Vora S et al. Pages 1273-1278Rogers' textbook of Pediatric Intensive Care. Chapter 74: cardiomyopathy, myocarditis, and mechanical circulatory support. Harmon WG et al. Pages 1247-1255Robinson J, Hartling L, Vandermeer B, Sebastianski M, Klassen TP. Intravenous immunoglobulin for presumed viral myocarditis in children and adults. Cochrane Database Syst Rev. 2020 Aug 19;8(8): CD004370. Doi: 10.1002/14651858.CD004370.pub4. PMID: 32835416

BUFFALO, NY - June 13, 2025 – A new #review was #published in Volume 16 of Oncotarget on June 4, 2025, titled “Applying the unattainable triangle in cardio-oncology care: Balancing cost, quality, and time.” In this review, first author John Hoverson, corresponding author Stella Pak, and colleagues from the University of Texas Health Science Center at San Antonio explore how the “unattainable triangle”—a business concept describing the trade-offs between cost, quality, and time—can help improve healthcare delivery in cardio-oncology. As cancer treatments become more complex and often affect the heart, this model highlights the challenge of providing care that is fast, effective, and affordable. Cardio-oncology is an emerging field focused on preventing and managing heart problems caused by cancer therapies. The review explains that high-quality cancer care often requires advanced diagnostics and close collaboration between oncologists and cardiologists, which can drive up costs and time demands. Understanding how to balance these pressures is essential for delivering better outcomes for patients. Many cancer survivors face long-term cardiovascular complications due to their treatment. Early monitoring and intervention can reduce these risks. However, these improvements often come with financial burdens, especially when key tests are not covered by insurance. Meanwhile, both patients and clinicians must manage the burden of tight appointment schedules, long clinic visits, and increasing demands on their time. To improve care quality, the authors emphasize the need for interdisciplinary teamwork and ongoing education. Surveys show that many clinicians are still unfamiliar with cardio-oncology guidelines, which can compromise care. The review also highlights the potential for artificial intelligence and digital tools to streamline care delivery, reduce wait times, and support both patients and providers. Importantly, the authors point out that improving one area—such as quality—can come at the expense of others, like cost or time. They encourage healthcare systems to take a balanced approach, setting clear goals and using integrated care models that consider all three elements of the triangle together. “While a perfect model for managing the unattainable triangle may be simply that, ‘unattainable', investments in research, patient-centered care, data-driven decision-making, and financial alignment with payers will be crucial to the long-term success of both patient outcomes and the organization's profitability.” While achieving perfect balance may be difficult, the review suggests that using the unattainable triangle as a guiding framework can help hospitals and clinicians make smarter, more sustainable decisions. As cardio-oncology continues to expand in response to the growing number of cancer survivors with cardiovascular needs, this approach could help improve patient outcomes and strengthen healthcare systems. DOI - https://doi.org/10.18632/oncotarget.28738 Correspondence to - Stella Pak - stellacpak@outlook.com Video short - https://www.youtube.com/watch?v=65-5eUuVyyk Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28738 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, cardio-oncology, quality improvement, cardiology, oncology 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

C'est l'histoire d'une maladie affreuse, doublée d'expérience sur les afro-américains et d'une dose de racisme. En gros, on fait croire à toute une catégorie de population qu'on va les traiter, mais, en fait, on veut juste les voir mourir et constater les effets de la maladie.  À noter , un film a été fait sur le sujet, Miss Ever's boys sorti en 1997. Script: Françoise Dulong et Laurent Turcot Adhérez à cette chaîne pour obtenir des avantages : https://www.youtube.com/channel/UCN4TCCaX-gqBNkrUqXdgGRA/join Pour soutenir la chaîne, au choix: 1. Cliquez sur le bouton « Adhérer » sous la vidéo. 2. Patreon: https://www.patreon.com/hndl Musique issue du site : epidemicsound.com Images provenant de https://www.storyblocks.com Abonnez-vous à la chaine: https://www.youtube.com/c/LHistoirenousledira Les vidéos sont utilisées à des fins éducatives selon l'article 107 du Copyright Act de 1976 sur le Fair-Use. Sources et pour aller plus loin: Bad Blood, The Tuskegee syphilis experiment, James H. Jones, The Free Press, 1981 Code de Nuremberg https://fr.wikipedia.org/wiki/Code_de_Nuremberg#cite_note-vialla-25 Syphilis : Symptômes et traitement, Gouvernement du Canada https://www.canada.ca/fr/sante-publique/services/maladies/syphilis.html HISTOIRE – Syphilis : le scandale des afro-américains privés de traitements, www.egora.fr Auteur : A.B. https://lesgeneralistes-csmf.fr/2014/11/14/histoire-syphilis-le-scandale-des-afro-americains-prives-de-traitements/ L'enquête Tuskegee sur la syphilis - 02/12/10. Doi : 10.1016/j.lpm.2010.03.030 , Patrick Berche, Jean-Jacques Lefrère https://www.em-consulte.com/article/274589/lenquete-tuskegee-sur-la-syphilis XVIe siècle, La syphilis, cadeau empoisonné du Nouveau Monde, Alban Dignat, 2019-12-29 https://www.herodote.net/La_syphilis_cadeau_empoisonne_du_Nouveau_Monde-synthese-310.php#:~:text=La%20terrible%20maladie%20importée%20du,vérole%2C%20surnom%20de%20la%20variole. Le diagnostic et la prise en charge de la syphilis congénitale : ne laisser passer aucune occasion, Mars 2024, Sergio Fanella MD, Ari Bitnun MD, Michelle Barton MD, Laura Sauvé MD, Société canadienne de pédiatrie https://cps.ca/fr/documents/position/syphilis-congenitale#:~:text=La%20transmission%20des%20sous%2Despèces,la%20peau%20de%20la%20mère. L'enquête Tuskegee sur la syphilis - Patrick Berche, Jean-Jacques Lefrère Vol 39 - N° 12 P. 1324-1329 - décembre 2010 La régulation éthique de la recherche aux États-Unis : histoire, état des lieux et enjeux, Par François Bonnet et Bénédicte Robert, P.87 à 108 https://shs.cairn.info/revue-geneses-2009-2-page-87?lang=fr Deux cents Noirs américains atteints de la syphilis ont été volontairement privés de tout traitement, Le Monde, Publié le 27 juillet 1972 https://www.lemonde.fr/archives/article/1972/07/27/deux-cents-noirs-americains-atteints-de-la-syphilis-ont-ete-volontairement-prives-de-tout-traitement_2375586_1819218.html 40 Years of Human Experimentation in America: The Tuskegee Study, Ada McVean, 25 Jan 2019, History https://www.mcgill.ca/oss/article/history/40-years-human-experimentation-america-tuskegee-study Éthique et syphilis : l'affaire de Tuskegee. Margaux Illy, Presses universitaires de Provence, p. 407-416 Tuskegee –un nom et toute une histoire. Ariel Fenster Vendredi 18 février 2011, Cet article provient du blogue Ariel Fenster Brandt, Allen M. No Magic Bullet: A Social History of Venereal Disease in the United States Since 1880. New York: Oxford University Press, 1987. Parascandola, John. Sex, Sin, and Science: A History of Syphilis in America. Westport, CT: Praeger Publishers, 2008. Roberts, Samuel. Infectious Fear: Politics, Disease, and the Health Effects of Segregation. Chapel Hill: University of North Carolina Press, 2009. Autres références disponibles sur demande. #histoire #documentaire #tuskegee #syphilistreatment #blacklifematters

BUFFALO, NY — June 12, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 5, on May 3, 2025, titled “APOE genotype and biological age impact inter-omic associations related to bioenergetics.” In this study, led by first author Dylan Ellis and corresponding author Noa Rappaport from the Institute for Systems Biology, researchers discovered that different versions of the APOE gene—particularly ε2 and ε4—are linked to metabolic patterns associated with aging and Alzheimer's disease risk. Both variants were linked to increased levels of diacylglycerols, a type of fat molecule connected to insulin resistance and inflammation, suggesting shared disruptions in how the body regulates energy. The research team analyzed data from over 2,200 adults without an Alzheimer's diagnosis, exploring how APOE genotypes influence biological age, a measure of health that reflects how quickly or slowly someone is aging at a cellular level. They found that the same metabolic disturbances seen in ε2 carriers were also present in people considered biologically older, revealing unexpected overlap between genetic risk and aging-related metabolic changes. To examine these connections in more detail, the researchers used a multi-omics approach, combining blood-based metabolism and protein data, gut bacteria analysis from stool samples, and clinical chemistry data. This method allowed them to map how genetic differences and biological aging affect the body's energy systems. They observed altered connections between glucose metabolism, inflammatory markers, and key molecules that play roles in energy production, indicating early disruptions that could contribute to age-related diseases. One of the study's surprising findings was that the ε2 variant, usually associated with longer life and reduced Alzheimer's risk, showed metabolic traits similar to those found in insulin-resistant individuals. This suggests that ε2 may carry metabolic disadvantages earlier in life, with its protective effects becoming more pronounced later. Conversely, ε4—linked to greater Alzheimer's risk—may exert its influence based on interactions with lifestyle factors like diet, sex, and overall health status. “‘Omics association patterns of ε2-carriers and increased biological age were also counter-intuitively similar, displaying significantly increased associations between insulin resistance markers and energy-generating pathway metabolites.” By identifying these shared biological signatures, this study offers a new framework for understanding how genes and metabolism work together to influence aging. These findings could support more personalized health strategies aimed at delaying biological aging and reducing the risk of chronic diseases. As aging populations grow worldwide, understanding these pathways is essential to improving healthspan. DOI - https://doi.org/10.18632/aging.206243 Corresponding author - Noa Rappaport - noa.rappaport@isbscience.org Video short - https://www.youtube.com/watch?v=75hZQoO5U0U Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206243 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, apolipoprotein E (APOE), biological age, metabolism, Alzheimer's disease (AD), insulin resistance 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 - June 11, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on May 29, 2025, titled “Durable complete response in leptomeningeal disease of EGFR mutated non-small cell lung cancer to amivantamab, an EGFR-MET receptor bispecific antibody, after progressing on osimertinib.” A team led by first author Jinah Kim, from the University of Vermont Medical Center, and corresponding author Young Kwang Chae, from the Feinberg School of Medicine, reports a clinical case in which a patient with advanced non-small cell lung cancer (NSCLC) carrying rare EGFR mutations responded remarkably to amivantamab after other treatments had failed. The patient experienced a complete resolution of brain and spinal fluid metastases, suggesting that amivantamab may be a viable option for patients with uncommon genetic profiles and limited therapy options. Lung cancer remains one of the leading causes of cancer-related deaths worldwide. Patients with NSCLC who have rare mutations in the EGFR gene often face limited treatment options and poor outcomes, especially when the disease spreads to the brain or spinal fluid. This case involved a 67-year-old man diagnosed with NSCLC who had two rare EGFR mutations—G719A and A289V. After disease progression on osimertinib and other therapies, the patient began amivantamab monotherapy. Within six weeks, his lung tumor shrank by over 30 percent. By six months, imaging confirmed the disappearance of brain metastases and leptomeningeal disease, a serious condition affecting the membranes of the brain and spinal cord. Blood tests showed no detectable cancer-related mutations, and the patient, previously wheelchair-bound, regained the ability to walk and perform daily activities. This response has been sustained for more than 19 months. “Treatment produced a durable response over 19 months, including a 32.2% reduction in tumor size at six weeks, and complete resolution of brain metastases and LMD by six months.” Amivantamab is a bispecific antibody that targets EGFR and MET, two key drivers of tumor growth. While it is approved in combination regimens for common EGFR mutations, its effectiveness as a single agent in rare mutations or in treating brain metastases remains largely unproven. This case challenges the assumption that large antibody drugs cannot cross the blood-brain barrier and suggests that amivantamab may have potential in managing central nervous system involvement. Further research is needed to clarify how the drug achieves these effects and to explore its broader use in patients with rare EGFR mutations and limited treatment options. This case highlights three key findings: amivantamab may be effective against rare EGFR mutations, can be used as monotherapy, and may overcome the challenges of the blood-brain barrier. Although based on a single patient, the results provide encouraging evidence to support further investigation of amivantamab in treating difficult-to-manage forms of NSCLC. DOI - https://doi.org/10.18632/oncotarget.28730 Correspondence to - Young Kwang Chae - young.chae@northwestern.edu Video short - https://www.youtube.com/watch?v=RJX3rmtH7h8 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, amivantamab, monotherapy, rare EGFR mutation, NSCLC, leptomeningeal disease 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 — June 10, 2025 — A new #research perspective was #published in Aging (Aging-US) Volume 17, Issue 5, on May 5, 2025, titled “Methylation clocks for evaluation of anti-aging interventions.” In this perspective article, Dr. Josh Mitteldorf explores how current epigenetic clocks—used to estimate biological age—might mislead scientists trying to evaluate anti-aging therapies. The paper challenges a widespread assumption: that all changes in DNA methylation with age are equally valid for measuring biological decline. Dr. Mitteldorf proposes that failing to distinguish between different types of epigenetic changes could lead to inaccurate conclusions, potentially even favoring treatments that reduce repair processes rather than extend healthy lifespan. Methylation clocks have become a popular tool in aging research. These clocks use patterns of DNA methylation, a form of gene regulation that changes over time, to predict a person's biological age. Because human aging trials are long and expensive, these clocks offer a faster way to evaluate whether a therapy slows or reverses aging. However, this article warns that not all methylation changes are equal in meaning or effect. The perspective identifies two main categories of methylation changes that occur with age. One type, called 'Type 1,' seems to support the idea that aging may be programmed, with gene activity changing in ways that could cause damage, such as more inflammation or increased cell loss. The second type, “Type 2,” involves increased gene activity aimed at repairing age-related damage. If a therapy reduces the activity of Type 2 genes, it may appear to slow aging while actually interfering with the body's repair response. “Paradoxically, an intervention that “sets back” the body's methylation clock to a younger state is shutting off vital repair mechanisms, so it is likely inimical to health and longevity.” This distinction is important because most methylation clocks, including popular models like GrimAge, do not separate these two types. As a result, they may incorrectly suggest that a treatment is reversing aging when it is only suppressing beneficial repair mechanisms. According to Dr. Mitteldorf, this could lead researchers to draw the wrong conclusions and unintentionally slow down progress in anti-aging research. The author also addresses a growing trend in the scientific community that aims to explain age-related methylation as random drift rather than directed change. In a pilot analysis using publicly available data, Dr. Mitteldorf attempted to construct a clock based purely on stochastic, or random, changes. The results showed a weak correlation with age, suggesting that random drift is an unreliable basis for assessing biological aging. Dr. Mitteldorf argues that most age-related methylation changes are likely intentional and regulated, rather than random. If so, epigenetic clocks must be refined to reflect the biological purpose behind methylation shifts. Without distinguishing between changes that indicate damage and those that indicate repair, current clocks may not only mismeasure age but also misguide intervention strategies. This article highlights the urgent need to improve how methylation data are interpreted before such clocks can reliably assess anti-aging therapies. A clearer understanding of these molecular patterns could help reshape the future of aging research and therapy evaluation. DOI - https://doi.org/10.18632/aging.206245 Corresponding author - Josh Mitteldorf - aging.advice@gmail.com To learn more about the journal, please visit our website at https://www.Aging-US.com. MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY – June 9, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on May 20, 2025, titled “Cigarette smoke and decreased DNA repair by Xeroderma Pigmentosum Group C use a double hit mechanism for epithelial cell lung carcinogenesis.” In this study, led by first author Nawar Al Nasralla and corresponding author Catherine R. Sears, from the Division of Pulmonary, Critical Care, Sleep and Occupational Medicine, Indianapolis and the Richard L. Roudebush Veterans Affairs Medical Center, researchers investigated how cigarette smoke and reduced DNA repair capacity contribute together to the development of lung cancer. They found that when a critical DNA repair protein called XPC is decreased and lung cells are exposed to cigarette smoke, the combination causes extensive damage and significantly increases cancer risk. Non-small cell lung cancer (NSCLC) develops through both genetic and environmental factors. This study focused on how cigarette smoke affects the body's natural ability to repair DNA. The researchers studied the role of XPC, a protein essential for recognizing and repairing harmful DNA changes caused by tobacco smoke. They found that low levels of XPC — commonly seen in lung cancer patients — made lung cells less capable of repairing DNA. This made the cells unstable and more likely to become cancerous. These changes were most pronounced in normal lung cells, suggesting that the earliest stages of disease occur before cancer is even detected. The findings support a “double hit” model, where both cigarette smoke and reduced DNA repair work together to drive cancer development. In laboratory experiments, normal lung cells with low XPC levels showed more damage and cell death after cigarette smoke exposure. By contrast, lung cancer cells were more resistant to smoke damage, even when XPC was low, indicating that critical changes had likely occurred earlier in the disease process. “Our study suggests that cigarette smoke exposure leads to decreased XPC mRNA expression, exacerbates total and oxidative DNA damage, hinders NER, and may contribute to lung cancer development.” The study also showed that DNA repair ability declined significantly in healthy cells after smoke exposure, but this effect was not seen in cancer cells. In addition, the researchers confirmed that XPC gene activity was lower in actual lung tumor tissue compared to nearby healthy lung tissue. This pattern was consistent across both adenocarcinoma and squamous cell carcinoma, the two main types of NSCLC. These results add to our understanding of how lung cancer begins at the molecular level. By showing how cigarette smoke and reduced DNA repair combine to create genetic instability, the research points toward new strategies for prevention. A better understanding of XPC's role could help identify high-risk individuals and inform future efforts to stop lung cancer before it begins. DOI - https://doi.org/10.18632/oncotarget.28724 Correspondence to - Catherine R. Sears - crufatto@iu.edu Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28724 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, DNA repair, DNA damage, lung adenocarcinoma, squamous cell carcinoma, Xeroderma Pigmentosum Group C (XPC) 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 we venture back in time to 2023 to review the results of the update of the Single Ventricle Reconstruction trial, specifically SVR III. How are HLHS patients are faring post Norwood at age 12? What is the overall transplant-free survival rate in this group? Are there differences in survival seen at 12 years between BTTT shunt patients and RV-PA conduit shunt patients? How do they compare in exercise capabilities? What about rates of PLE or arrhythmias seen? Are there interventions that may improve outcomes going forward? These are amongst the questions reviewed this week with the first author, Dr. Caren Goldberg who is Professor of Pediatrics at the University of Michigan. DOI: https://doi.org/10.1161/circulationaha.123.065192

Episode 193: Gestational Diabetes IntroJesica Mendoza (OMSIII) describes the pathophysiology of gestational diabetes and the right timing and method of screening for it. Dr. Arreaza adds insight into the need for culturally-appropriate foods, such as vegetables in Mexican cuisine.    Written by Jesica Mendoza, OMSIII, Western University of Health Sciences, College of Osteopathic Medicine of the Pacific. Editing by Hector Arreaza, MD.You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.DefinitionGestational diabetes mellitus (GDM) is a condition that occurs to previously non-diabetic pregnant women, caused by glucose intolerance at around the 24th week of gestation. PathophysiologyGDM arises due to an underlying pancreatic beta cell dysfunction in the mother which leads to a decrease in the amount of insulin produced and thus leads to higher blood sugar levels during pregnancy. The placenta of the fetus will produce hPL (human placental lactogen) to ensure a steady supply of sugars to the fetus, creating an anti-insulin effect. However, hPL readily crosses the placental barrier causing the mothers insulin requirement to increase, when the mother's pancreas cannot increase production of insulin to that level needed to counter the effect of hPL they become diabetic, and this leads to gestational diabetes. So, basically the placenta is asking for more glucose for the baby and the mother's pancreas struggles to keep the glucose level within normal limits in the body of the mother. If left untreated, high levels of glucose in the mother can cause glucotoxicity in the mother.“Glucotoxicity” refers to the toxic effect of glucose. Glucose is the main fuel for cell functions, but when it is high in the bloodstream, it causes toxicity to organs. Prevalence of GDM.The CDC reports mean prevenance of GDM is 6.9%. In U.S. mothers the prevenance increased from 6.0% in 2016 to 8.3% in 2021. Many different factors have played a role in increasing gestational diabetes in American mothers, some of those being the ongoing obesity epidemic with excess body weight being a known risk factor for insulin resistance. Another being advanced maternal age (AMA) as more American women have children later in life their body becomes less sensitive to insulin and requires a higher insulin output on top of the insulin that is required for the fetus. The “American diet” is also something that has a big effect in diabetes development. With the increase of high-carb foods that are readily available, the diet of Americans has declined and is affecting the metabolic health of mothers as they carry and deliver their children. Despite ongoing awareness of GDM, 6% to 9% of pregnant women in the United States are diagnosed with gestational diabetes, and the prevalence continues to increase worldwide. It is estimated that in 2017 18.4 million pregnancies were affected by GDM in the world, which then continued to increase to 1 in 6 births to women with GDM in 2019. It was also found that women living in low-income communities were disproportionately affected due to limited healthcare access. Additionally, women with GDM had a 1.4-fold increase in likelihood of undergoing a c-section, with 15% increase in risk of requiring blood transfusion. Screening for GDMGestational diabetes is screened between the 24th to 28th week of gestation in all women without known pregestational diabetes. In women who have high-risk for GDM the screening occurs during the first trimester, these women usually have at least one of the following: BMI > 30, prior history of GDM, known impaired glucose metabolism, and/or a strong family history of diabetes. The screening during the first trimester is to detect “pregestational diabetes” because we have to keep a good glycemic control to improve outcomes of pregnancy. So, if it's positive, you start treatment immediately. If these women are found to have a normal glucose, they repeat the testing again as done normally, at 24-28 weeks of gestation. How do we screen?The screening itself consists of two types of approaches. The two-step approach includes a 50-gram oral glucose tolerance test (OGTT), where blood glucose is measured in an hour and if it is below 140 they are considered to not have GDM, however if the reading is greater than 140 they must then do a 3-hour, 100g oral glucose tolerance test. The 3-hour OGTT includes measuring the blood sugars at Fasting which should be less than 95, at 1 hour at less than 180, at 2 hours at less than 155, and at 3 hours at less than 140. If 2 or more of these values exceed the threshold the patient is diagnosed with gestational diabetes mellitus. The one-step approach includes 75g after an overnight fast. Blood glucose is measured while fasting which should be less than 92, at 1 hour less than 180 and at 2 hours less than 153. If any one of these values is exceeded, the patient is diagnosed with GDM.If the mother is found to be GDM positive during pregnancy she will also need continued screening post-partum to monitor for any development of overt diabetes. The testing is usually 75g 2-hour OGTT at 6-12 weeks postpartum. If this testing is normal, then they are tested using HbA1c every 3 years. If the post-partum testing shows pre-diabetes, annual testing is recommended using HbA1c measurements. Maternal complications Women with GDM are at an increased risk for future cardiovascular disease, T2DM, and chronic kidney disease. GDM is also associated with increased likelihood of developing pre-eclampsia following delivery. Pre-eclampsia is a complication seen in pregnancy characterized by high blood pressure, proteinuria, vision changes, and liver involvement (high LFTs). Pre-eclampsia can then progress to eclampsia or HELLP syndrome, both of which can include end organ damage. Additionally, she can develop polyhydramnios which leads to overstretching of the uterus and can induce pre-term labor, placental abruption, and or uterine atony, all of which additionally put the mother at increased risk for c-section. All of these maternal complications that stem from GDM lead to complications and extended hospitalization. Child's complications Although there is an increased set of risks for the mother, the neonate can also develop a variety of risks due to the increased glucose while in utero. While the fetus is growing, the placenta is the source of nutrition for the fetus. As the levels of glucose in the mother increase so does the amount of glucose filtered through the placenta and into the fetal circulation. Over time the glucose leads to oxidative stress and inflammation with activation of TGF-b which leads to fibroblast activation and fibrosis of the placenta. This fibrosis decreases the nutrient and oxygen exchange for the fetus. As the fetus attempts to grow in this restrictive environment its development is affected. The fetus can develop IUGR (intrauterine growth restriction) leading to a small for gestation age newborn which can then lead to another set of complications. The low oxygen environment can lead to increased EPO production and polycythemia at birth which can then lead to increased clotting that can travel to the newborn brain. Newborns can also be born with fetal acidosis due to the anerobic metabolism and lactic acid buildup in fetal tissues which can cause fetal encephalopathy leading to cerebral palsy and developmental delay. And the most severe of newborn complications to gestational diabetes can lead to fetal demise. Furthermore, the increase of glucose can also lead to macrosomia in the infant which can often lead to a traumatic delivery and delivery complications such as shoulder dystocia and brachial plexus injury. Brachial plexus injury sometimes resolves without sequela, but other times can lead to permanent weakness or paralysis of the affected arm. The baby can be born too small or too big.Additionally, once the fetus is born the cutting of the umbilical cord leads to a rapid deceleration in blood glucose in the fetal circulation and hypoglycemic episodes can occur, that often lead to NICU admission. The insulin that is created by the fetus in utero to accommodate the large quantities of glucose is known to affect lung maturation as well. The insulin produced inhibits surfactant production in the fetus. Upon birth some of the newborns also have to be placed on PEEP for ventilation and some children require treatment with surfactant to prevent alveolar collapse and/or progression to NRDS created by the low surfactant levels. Additionally, neonates who are macrosomic, which is usually seen in GDM mothers, are larger and stronger and when put on PEEP to help increase ventilation the newborn's stronger respiratory effort can lead to higher pulmonary pressures and barotrauma such as neonatal pneumothorax.Long term complications to the child of a mother with GDM also occur. As the child grows, they are also at an increased risk for developing early onset obesity because of the increased adipose storage triggered by the increase in insulin in response to the high glucose in utero. This then can lead to a higher chance of developing type 2 diabetes mellitus in the child. With diabetes, also comes an increase in cardiovascular risk as the child ages and becomes an adult. The effects of GDM go beyond the fetal life but continue through adulthood.What can be done?Gestational Diabetes Mellitus has many severe and lifelong consequences for both the mother and the child and prevention of GDM would help enhance the quality of life of both. Many of the ways to prevent GDM complications include patient education and dietary modifications with a diet rich in whole grains, fruits, vegetables and lean proteins. Benefits of some vegetables in the Mexican cuisine that may be beneficial: Nopales, Chayote, and Jicama. Those are good alternatives for highly processed carbs.Mothers are usually offered nutritional counseling to help them develop a tailored eating plan. This and 30 minutes of moderate exercise daily is recommended to increase insulin sensitivity and lower the post-prandial glucose levels. If within 2 weeks of implementing lifestyle changes alone the glucose measurements remain high, then medications like insulin can be put onboard to manage the GDM. If they require insulin, I think it is time to refer to a higher level of care, if available, high risk OB clinic.Conclusion: Now we conclude episode number ###, “[TITLE].” [summary here]. _____________________References:Eades CE, Burrows KA, Andreeva R, Stansfield DR, Evans JM. Prevalence of gestational diabetes in the United States and Canada: a systematic review and meta-analysis. BMC Pregnancy Childbirth. 2024 Mar 15;24(1):204. doi: 10.1186/s12884-024-06378-2. PMID: 38491497; PMCID: PMC10941381. https://pubmed.ncbi.nlm.nih.gov/38491497/QuickStats: Percentage of Mothers with Gestational Diabetes,* by Maternal Age — National Vital Statistics System, United States, 2016 and 2021. Weekly / January 6, 2023 / 72(1);16. https://www.cdc.gov/mmwr/volumes/72/wr/mm7201a4.htm?utmAkinyemi OA, Weldeslase TA, Odusanya E, Akueme NT, Omokhodion OV, Fasokun ME, Makanjuola D, Fakorede M, Ogundipe T. Profiles and Outcomes of Women with Gestational Diabetes Mellitus in the United States. Cureus. 2023 Jul 4;15(7):e41360. doi: 10.7759/cureus.41360. PMID: 37546039; PMCID: PMC10399637. https://pmc.ncbi.nlm.nih.gov/articles/PMC10399637/?utmPerlman, J. M. (2006). Summary proceedings from the neurology group on hypoxic-ischemic encephalopathy. Pediatrics, 117(3), S28–S33.DOI: 10.1542/peds.2005-0620C.Low, J. A. (1997). Intrapartum fetal asphyxia: definition, diagnosis, and classification. American Journal of Obstetrics and Gynecology, 176(5), 957–959.DOI: 10.1016/S0002-9378(97)70609-0.Hallman, M., Gluck, L., & Liggins, G. (1985). Role of insulin in delaying surfactant production in the fetal lung. Journal of Pediatrics, 106(5), 786–790.DOI: 10.1016/S0022-3476(85)80227-0.Sweet, D. G., Carnielli, V., Greisen, G., et al. (2019). European Consensus Guidelines on the Management of Respiratory Distress Syndrome – 2019 Update. Neonatology, 115(4), 432–450.DOI: 10.1159/000499361.Raju, T. N. K., et al. (1999). Respiratory distress in term infants: when to suspect surfactant deficiency. Pediatrics, 103(5), 903–909.DOI: 10.1542/peds.103.5.903.Burns, C. M., Rutherford, M. A., Boardman, J. P., & Cowan, F. M. (2008). Patterns of cerebral injury and neurodevelopmental outcomes after symptomatic neonatal hypoglycemia. Pediatrics, 122(1), 65–74.DOI: 10.1542/peds.2007-2822.Dabelea, D., et al. (2000). Long-term impact of maternal diabetes on obesity in childhood. Diabetes Care, 23(10), 1534–1540.DOI: 10.2337/diacare.23.10.1534.Dashe, J. S., et al. (2002). "Hydramnios: Etiology and outcome." Obstetrics & Gynecology, 100(5 Pt 1), 957–962.DOI: 10.1016/S0029-7844(02)02279-6.Long-term cost-effectiveness of implementing a lifestyle intervention during pregnancy to prevent gestational diabetes mellitus: a decision-analytic modelling study. Diabetologia.American College of Obstetricians and Gynecologists. (2018). Practice Bulletin No. 190: Gestational Diabetes Mellitus. Obstetrics & Gynecology, 131(2), e49–e64. https://doi.org/10.1097/AOG.0000000000002501Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/. 

Dr. Stefanie Morgan joins Dr. Robert Dudley from AgelessRx to discuss a #research paper she co-authored that was #published in Volume 17, Issue 4 of Aging, entitled “Influence of rapamycin on safety and healthspan metrics after one year: PEARL trial results.” DOI - https://doi.org/10.18632/aging.206235 Corresponding author - Stefanie L. Morgan - stefanie@agelessrx.com Author interview - https://www.youtube.com/watch?v=2qlIiVh2OJs Video short - https://www.youtube.com/watch?v=z5j2nyK2HZ8 Abstract Design: This 48-week decentralized, double-blinded, randomized, placebo-controlled trial (NCT04488601) evaluated the long-term safety of intermittent low-dose rapamycin in a healthy, normative-aging human cohort. Participants received placebo, 5 mg or 10 mg compounded rapamycin weekly. The primary outcome measure was visceral adiposity (by DXA scan), secondary outcomes were blood biomarkers, and lean tissue and bone mineral content (by DXA scan). Established surveys were utilized to evaluate health and well-being. Safety was assessed through adverse events and blood biomarker monitoring. Results: Adverse and serious adverse events were similar across all groups. Visceral adiposity did not change significantly (ηp2 = 0.001, p = 0.942), and changes in blood biomarkers remained within normal ranges. Lean tissue mass (ηp2 = 0.202, p = 0.013) and self-reported pain (ηp2 = 0.168, p = 0.015) improved significantly for women using 10 mg rapamycin. Self-reported emotional well-being (ηp2 = 0.108, p = 0.023) and general health (ηp2 = 0.166, p = 0.004) also improved for those using 5 mg rapamycin. No other significant effects were observed. Conclusions: Low-dose, intermittent rapamycin administration over 48 weeks is relatively safe in healthy, normative-aging adults, and was associated with significant improvements in lean tissue mass and pain in women. Future work will evaluate benefits of a broader range of rapamycin doses on healthspan metrics for longevity, and will aim to more comprehensively establish efficacy. Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206235 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, rapamycin, geroscience, longevity, healthspan 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

John is making a guest appearance with Jenny to continue the tradition of Research and Real talk! Join this dynamic duo as they explore a litany of topics including prebiotics, Carbs and cancer risk, genetic factors for obesity, coaching burnout, client retention, trainers and social media, and traits of a bad coach!References: 1.Yutaka Nakazawa, Masumi Kageyama, Tomohiko Matsuzawa, Ziqin Liang, Kaito Kobayashi, Hisaka Shimizu, Kazuki Maeda, Miho Masuhiro, Sei Motouchi, Saika Kumano, Nobukiyo Tanaka, Kouji Kuramochi, Hiroyuki Nakai, Hayao Taguchi, Masahiro Nakajima. Structure and function of a β-1,2-galactosidase from Bacteroides xylanisolvens, an intestinal bacterium. Communications Biology, 2025; 8 (1) DOI: 10.1038/s42003-025-07494-12. Bhupesh Kumar Thakur, Yann Malaise, Saurav Roy Choudhury, Anna Neustaeter, Williams Turpin, Catherine Streutker, Julia Copeland, Erin O. Y. Wong, William W. Navarre, David S. Guttman, Christian Jobin, Kenneth Croitoru, Alberto Martin. Dietary fibre counters the oncogenic potential of colibactin-producing Escherichia coli in colorectal cancer. Nature Microbiology, 2025; DOI: 10.1038/s41564-025-01938-43. Natalie J. Wallis, Alyce McClellan, Alexander Mörseburg, Katherine A. Kentistou, Aqfan Jamaluddin, Georgina K. C. Dowsett, Ellen Schofield, Anna Morros-Nuevo, Sadia Saeed, Brian Y. H. Lam, Natasha T. Sumanasekera, Justine Chan, Sambhavi S. Kumar, Rey M. Zhang, Jodie F. Wainwright, Marie Dittmann, Gabriella Lakatos, Kara Rainbow, David Withers, Rebecca Bounds, Marcella Ma, Alexander J. German, Jane Ladlow, David Sargan, Philippe Froguel, I. Sadaf Farooqi, Ken K. Ong, Giles S. H. Yeo, John A. Tadross, John R. B. Perry, Caroline M. Gorvin, Eleanor Raffan. Canine genome-wide association study identifies DENND1B as an obesity gene in dogs and humans. Science, 2025; DOI: 10.1126/science.ads2145

The literature shows that the incidence of heart failure with preserved ejection fraction (HFpEF) increases significantly in postmenopausal women, but how can researchers study the underlying mechanisms? In our latest episode, Dr. Jonathan Kirk (Loyola University Chicago) interviews lead author Dr. Mei Methawasin (University of Missouri, Columbia) and expert Dr. Glen Pyle (University of Guelph) about the recent study by Methawasin and co-authors investigating sex differences, menopause and HFpEF. The authors created an animal model that resembles HFpEF in women undergoing natural menopause by using 4-vinylcyclohexene dioxide (VCD) to induce “ovary-intact” menopause, combined with the 2hit regimen (HFpEF inducing regimen) to model postmenopausal HFpEF. Combining echocardiography, pressure-volume and single-cell analyses, the authors found that VCD mice, compared to ovariectomized mice and premenopausal mice, have higher testosterone levels compared to other models. By developing this robust phenotype animal model, the authors open new avenues for investigating therapeutic targets in other hormones beyond estrogen alone. Ready to explore the estrobolome, the importance of animal models of human disease, and the complex family of hormones comprising estrogen? Listen now.   Mei Methawasin, Joshua Strom, Vito A. Marino, Jochen Gohlke, Julia Muldoon, Shelby R. Herrick, Robbert van der Piji, John P. Konhilas, Henk Granzier An ovary-intact postmenopausal HFpEF mouse model; menopause is more than just estrogen deficiency Am J Physiol Heart Circ Physiol, published March 10, 2025. DOI: 10.1152/ajpheart.00575.2024

BUFFALO, NY - June 4, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on May 20, 2025, titled “Targeting PCNA/AR interaction inhibits AR-mediated signaling in castration resistant prostate cancer cells." In this study, authors Shan Lu and Zhongyun Dong from the University of Cincinnati College of Medicine investigated how interfering with a protein interaction could reduce prostate cancer growth. Their study based on prostate cancer cells shows that blocking the link between PCNA, a protein important for DNA repair, and the androgen receptor (AR), which drives prostate cancer growth, can slow down cancer cell multiplication. This discovery could lead to a new treatment for patients with advanced prostate cancer, particularly those no longer responding to hormone therapy. Prostate cancer is one of the most common cancers in men. Many patients eventually become resistant to hormone treatment. In this advanced stage, called castration-resistant prostate cancer (CRPC), tumors continue to grow by using either the full-length androgen receptor (AR-FL) or altered versions called AR variants (AR-Vs). This study shows that the interaction between AR and PCNA helps both AR-FL and AR-Vs remain active, supporting cancer cell survival and growth. The researchers identified a new region in the AR that binds to PCNA. They developed a small peptide, R9-AR-PIP, to mimic this region and block the AR-PCNA connection. They found that this peptide reduced AR's ability to bind DNA and lowered the levels of key genes involved in cancer cell growth. Importantly, the peptide was effective against both types of AR, including the variant forms that are especially challenging in CRPC. “We identified a second PIP-box (PIP-box592) in the DNA binding domain of AR and found that dihydrotestosterone enhances the binding of full-length AR (AR-FL) but not a constitutively active variant (AR-V7) to PCNA.” They also tested a small molecule, PCNA-I1S, which interferes with PCNA's ability to move to the cell nucleus and interact with AR. This molecule showed similar effects as the peptide, reducing AR activity and stopping cancer cell growth. Together, these findings suggest that targeting PCNA/AR interactions could be a promising strategy to fight CRPC, especially in patients with limited treatment options. One key result was that both the peptide and the small molecule reduced the levels of cyclin A2, a protein that helps cells divide and is often overexpressed in CRPC. Since this protein is linked to patients' poor outcomes, its reduction could be especially beneficial. This study improves our understanding of how prostate cancer continues to grow even after hormone treatments fail. By blocking a crucial helper of the androgen receptor, researchers have uncovered a new way to potentially slow or stop the disease. Further studies in animal models are needed, but this approach could lead to more effective treatments for men with advanced prostate cancer. DOI - https://doi.org/10.18632/oncotarget.28722 Correspondence to - Zhongyun Dong - dongzu@ucmail.uc.edu Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28722 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, PCNA, androgen receptor, PCNA inhibitors, AR splicing variants, CRPC 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 — June 4, 2025 — A new #editorial was #published in Aging (Aging-US) Volume 17, Issue 5, on May 29, 2025, titled “Rethinking healthcare through aging biology.” In this scientific editorial, Aging (Aging-US) Editor-in-Chief Marco Demaria from the European Research Institute for the Biology of Ageing (ERIBA), University Medical Center Groningen (UMCG) and the University of Groningen (RUG), advocates for healthcare reform that addresses the biological drivers of aging rather than individual chronic conditions. The article proposes that targeting the root causes of age-related diseases through aging biology could revolutionize preventive care, extend healthspan, and reduce long-term healthcare costs. This proactive approach aligns with a growing body of aging research focused on improving healthy longevity. Dr. Demaria explains that today's disease-focused model is inadequate for aging populations, who often suffer from multimorbidity—the presence of multiple chronic illnesses like cancer, heart disease, and type 2 diabetes. These overlapping conditions, rooted in common aging mechanisms, overwhelm healthcare systems and lead to complex treatments with limited success. The editorial suggests that identifying and intervening in the biological aging process could prevent such diseases before they emerge. In the editorial, Dr. Demaria outlines three healthcare paradigms. The first is the existing system, which reacts to disease after symptoms appear. The second involves intervening once age-related damage begins, using new tools such as senolytics, which eliminate harmful senescent cells, and rapalogs, which regulate cellular metabolism. The third and most forward-looking model focuses on preventing aging-related damage before it starts. This strategy supports lifelong biological balance and seeks to avoid early molecular decline through continuous health maintenance. Prevention is key in this model. Lifestyle choices—such as exercise, a healthy diet, quality sleep, and stress reduction—play a vital role in slowing the aging process. Dr. Demaria also points to the promise of biological age diagnostics—tools or tests that estimate a person's biological age—which allow people to track their physiological aging and adopt personalized interventions. Additionally, optimizing maternal nutrition and early-life health can contribute to lifelong disease prevention. To support this shift, the editorial calls for major changes in medical education. Physicians must be trained in geroscience, healthspan optimization, and personalized preventive care. This knowledge will prepare future clinicians not just to treat disease, but to delay or prevent it altogether. Collaboration among healthcare providers, researchers, and policymakers will be essential for building this new system. ​​“The third paradigm—preventing aging-related damage—demands a systemic shift toward predictive and preventative research, with an emphasis on multi-omic data, lifestyle interventions, and early-life interventions.” By redefining medicine around the science of aging, Dr. Demaria's editorial highlights the path toward healthier aging, longer life expectancy, and a more sustainable healthcare future. DOI - https://doi.org/10.18632/aging.206262 Corresponding author - Marco Demaria - m.demaria@umcg.nl Video short - https://www.youtube.com/watch?v=xR-16cjHnQY 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

New research suggests that tokay geckos can distinguish between different people, shedding further light on the intelligence of lizards. We delve into this study and voice warranted concerns about the intelligence of these little maniacs. Become a Patreon: https://www.patreon.com/herphighlights Merch: https://www.redbubble.com/people/herphighlights/shop Full reference list available here: http://www.herphighlights.podbean.com Main Paper References: Damas-Moreira I, Bégué L, Ringler E, Szabo B. 2025. Tokay geckos adjust their behaviour based on handler familiarity but according to context. Scientific Reports 15:11364. DOI: 10.1038/s41598-025-95936-5. Other Mentioned Papers/Studies: Correa, C., Riveros-Riffo, E., & Donoso, J. P. (2025). Lost for more than a century: the rediscovery of Alsodes vittatus (Philippi, 1902)(Anura, Alsodidae), one of the rarest and most elusive amphibians from Chile. ZooKeys, 1230, 195. Other Links/Mentions: Pensoft Publishers. 2025.Ghost Frog Found: Scientists Stumble Upon Species Missing Since 1902. Available at https://scitechdaily.com/ghost-frog-found-scientists-stumble-upon-species-missing-since-1902/ (accessed May 1, 2025). Editing and Music: Intro/outro – Treehouse by Ed Nelson Species Bi-week theme – Michael Timothy Other Music – The Passion HiFi, https://www.thepassionhifi.com

James and Dan discuss James' newly funded 'Medical Evidence Project', whose goal is to find questionable medical evidence that is contaminating treatment guidelines. Links * James' blog post (https://jamesclaims.substack.com/p/how-should-we-fund-scientific-error) from last year * The carthorse child blog post (https://medium.com/hackernoon/introducing-sprite-and-the-case-of-the-carthorse-child-58683c2bfeb) * The blog post (https://jamesclaims.substack.com/p/introducing-the-medical-evidence) announcing the project * A write up in Nature (https://www.nature.com/articles/d41586-025-01739-z?utm_source=bluesky&utm_medium=social&utm_campaign=nature&linkId=14776408) about the project Other 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, June 4). 191: Cleaning up contaminated medical treatment guidelines Everything Hertz [Audio podcast], DOI: 10.17605/OSF.IO/537BN

Last time we spoke about the fall of Shuri. In the unforgiving terrain of Okinawa during May 1945, American Marines confronted fierce resistance from entrenched Japanese forces. Amidst heavy rain and dwindling supplies, General Buckner's 10th Army battled uphill toward Shuri, a critical stronghold. With communication crumbling and morale wavering, the Americans pressed on, launching daring patrols. The situation reached a turning point when intelligence revealed the Japanese withdrawal plans. Buckner ordered continuous pressure, leading to the capture of significant strategic points like Shuri Castle, which was relentlessly bombarded prior to the Marine assault. On May 29, as the last remnants of Japanese forces fled south, American soldiers swept through Shuri, which lay in utter ruin, a testament to the devastating power of the campaign.  This episode is the Liberation of Mindanao Welcome to the Pacific War Podcast Week by Week, I am your dutiful host Craig Watson. But, before we start I want to also remind you this podcast is only made possible through the efforts of Kings and Generals over at Youtube. Perhaps you want to learn more about world war two? Kings and Generals have an assortment of episodes on world war two and much more  so go give them a look over on Youtube. So please subscribe to Kings and Generals over at Youtube and to continue helping us produce this content please check out www.patreon.com/kingsandgenerals. If you are still hungry for some more history related content, over on my channel, the Pacific War Channel you can find a few videos all the way from the Opium Wars of the 1800's until the end of the Pacific War in 1945.  Last week we covered the fall of Shuri and today we continue the brutal brawl for Okinawa and the liberation of Mindanao. As we last saw, the Japanese retreat from the Shuri line opened the path for General Buckner's 10th Army to move southward, with only General Fujioka's 62nd Division and a few minor rearguards standing in their way. On June 3, General Arnold's 7th Division continued its offensive to the south. Colonel Pachler's 17th Regiment successfully secured the area of Itokazu. Meanwhile, Colonel Green's 184th Regiment pushed toward the coast to completely cut off the Chinen Peninsula. Colonel Finn's 32nd Regiment was diverted into the rugged hills nearby to clean up any remaining resistance. To the west, despite persistent bad weather and challenging supply conditions, General Bradley's 96th Division also achieved success. Colonel May's 383rd Regiment secured the locations of Kamizato and Tera against relatively light resistance. At the same time, Colonel Halloran's 381st Regiment advanced to seize the entire Inasomi area. Looking northwest, General Del Valle's 1st Marine Division encountered stronger opposition. The bulk of the 5th Marines managed to push only as far as Tsukasa before being pinned down. In a strategic move, Colonel Griebel's 2nd Battalion executed a wide swing through May's rear area to capture the Gisushi region. Colonel Snedeker's 7th Marines made steady progress through the Kokuba Valley, facing small enemy blocking forces, in order to extend the line held by the 5th Marines. Meanwhile, at sea, Admiral Ugaki launched his 9th mass Kikisui attack. This operation, featuring just 50 kamikaze aircraft, faced heavy obstacles due to Typhoon Viper but still managed to damage 2 vessels. In another development, after successfully occupying Torishima Island on May 12, Colonel Clarence Wallace's 8th Marines landed on Iheyajima without encountering any opposition. In addition, preparations for the shore-to-shore assault of General Shepherd's 6th Marine Division were completed. Colonel Shapley's 4th Marines were set to land on the Nishikoku beaches before securing the Oroku Peninsula and its airfield. Consequently, during the early hours of June 4, Shepherd's Reconnaissance Company successfully assaulted Ono-Yama Island, while Shapley's assault battalions began the shore-to-shore movement to Nishikoku under the cover of artillery and naval bombardment. Despite some mechanical failures on the LVTs, the Marines successfully landed at 06:00 under sporadic machine-gun fire and then pushed onto the high ground 300 yards inland against minor resistance. After securing the initial foothold, the attack slowed against increasing resistance on the left flank. Because of this, the reserve 3rd Battalion was landed at 08:45 and subsequently advanced to the edge of the airdrome.  During the day development of the enemy's defense had revealed an inordinate number of automatic weapons, ranging in various calibers up to 40mm. Subsequently, it was disclosed that the Japanese had stripped the armament from the air defenses and damaged aircraft in the area and integrated these weapons into the ground fortifications to stiffen materially the resistance on Oroku. Besides meeting with the most extensive mine fields yet encountered during the campaign, on this day the 6th Division had its first contact with an awesome weapon: an 8-inch rocket that exploded with terrific concussion. However, there was little fragmentation and accuracy was poor. While the noise the huge projectiles made, tumbling through the air end over end, sounded "like a locomotive from hell" to the troops, the rockets were mainly a source of annoyance and caused few casualties. Rockets continued to fall in the rear areas during the night, snipers and infiltrators were active, and the entire front came under intermittent heavy mortar fire. This landing allowed Shepherd to bring in Colonel Whaling's 29th Marines by midday, which then secured the Kikibana area of Naha Bay, while the 4th Marines captured one-third of Naha's airfield. To the east, the Americans encountered less resistance than before, as the 62nd Division and other minor rearguards completed their withdrawal from the intermediate lines south of Shuri to a reserve area south of the new Kiyamu Peninsula lines. Recognizing this change, Buckner shifted the corps boundary to the west, assigning General Geiger's 3rd Amphibious Corps the task of isolating the Oroku Peninsula and occupying the Itoman-Kunishi sector, while General Hodge's 24th Corps advanced toward the Yaeju Dake-Yuza Dake escarpment.  As a result, the 7th Marines were able to move south to seize Takanyuta and isolate Admiral Ota's forces on the Oroku Peninsula. The atrocious weather had converted the already muddy roads to impassable morasses. Transport was hopelessly mired north of the Kokuba Gawa. South of the river the "trails were only negotiable by foot troops, vehicles could not have been used" even if it had been possible to bring them across the inlet. The 5th Marines managed to secure the Hill 107 area without opposition before being relieved by Colonel Mason's 1st Marines. However, the 1st Marines were unable to continue their push south toward Shindawaku Ridge due to a flooded stream. Meanwhile, Mason's 3rd Battalion attempted a wide envelopment through the 96th Division zone but was quickly halted in front of Tera. Food was scarce, but through the wholehearted cooperation of the 96th Division the Marines procured two meals of K rations per man. It was the considered opinion of at least one member of 3/1 that "this day probably was the most miserable spent on Okinawa by men of this battalion." To compound these problems and discomforts, the 3d Battalion also found itself without a supply route or communications with the regiment 11,000 yards to the rear. Further east, the 383rd Regiment advanced rapidly, engaging isolated but strong enemy delaying groups as they secured the outskirts of Iwa. Matching this progress, the 381st Regiment advanced all the way to the hills north of Aragusuku, facing steadily increasing resistance. Additionally, while the 17th Regiment established positions controlling the Minatoga-Meka road, the 184th Regiment advanced against patchy and ineffective resistance until the Minatoga area was secured. The following morning, Admiral McCain's Task Force 38 launched strikes on Okinawa and Kyushu. Unfortunately, poor situational awareness from Admiral Halsey caused the 3rd Fleet to inadvertently enter Typhoon Viper. This storm inflicted varying degrees of damage to four carriers, two escort carriers, three cruisers, one destroyer, and one tanker, while also destroying 76 planes. Additionally, kamikaze attacks succeeded in damaging the battleship Mississippi and heavy cruiser Louisville. Back on Okinawa, Shepherd's attack on the Oroku Peninsula commenced and progressed slowly but steadily against uniformly stubborn resistance. The 4th Marines secured most of the airfield and the Toma high ground, while the 29th Marines fought laboriously to advance toward Mura and Oroku, gaining up to 1,000 yards. To the east, the 7th Marines advanced to positions just north of Hanja, while the 1st Marines bypassed the inundated area in front of them by swinging east and following their 3rd Battalion toward Iwa. In fact, Mason's 3rd Battalion launched another attack aimed at Shindawaku Ridge, advancing over 3,000 yards to the area west of Iwa. Despite muddy conditions and rainy weather, Hodge's infantrymen continued to penetrate the enemy outpost zone, developing the edges of the main Japanese battle position. The outpost line of Kiyamu Peninsula was fully manned on June 4. Japanese Army headquarters estimated that the strength of its now concentrated forces totaled 30000, distributed as follows: 24th Division and attached units, 12000; 62nd Division and attached units, 7000; 44th IMB and attached units, 3000; 5th Artillery Command and attached units, 3000; and units directly under 32nd Army command, 5000. The difference in total strength between the 50000-man estimate late in May and the 30000 left in Kiyamu Peninsula was attributed to "attrition during retirement operations." Only about 20% of the remaining troops were survivors of the original crack infantry-artillery units; the rest were untrained rear echelon personnel or Boeitai. Most senior commanders at battalion level and above were still alive, however, and capable of bolstering the fighting spirit of their motley collection of men. But the 32nd Army had suffered grievous losses in weapons and equipment since L-Day. Hand grenades and explosives were almost entirely expended. 4 out of every 5 machine guns had been destroyed, and the supply of heavy infantry cannon and mortars had been reduced to the vanishing point. Despite the fact that 2 150mm guns, 16 150mm howitzers, and 10 AAA guns had been successfully withdrawn to the Kiyamu battle position, artillery ammunition levels were insufficient for more than 10 days of sustained firing. General Ushijima's 32nd Army was in desperate straits, its destruction merely a question of time, but the tradition, discipline, and indoctrination of Japanese military forces promised only a violent, last-ditch, man-to-man struggle before the battle for Okinawa was ended. By June 6, the 7th Division reached the outskirts of Gushichan, and the 96th Division advanced toward Shindawaku and Tomui. To the west, the 1st Marines finally captured Shindawaku and cleared the bypassed area behind them. Meanwhile, the 7th Marines attacked toward Hill 108, advancing 1,000 yards before encountering stiff resistance and ultimately dug in around Dakiton. Additionally, Colonel Roberts' 22nd Marines arrived to contain the Oroku Peninsula in the Hill 103 sector. Although the 29th Marines and Shapley's 1st Battalion made little progress in the Oroku-Mura area due to strong enemy resistance. Meanwhile the terrain confronting the 3rd Battalion there "consisted of a series of small temple-like hills, each of which had been converted into a fortress . . . from which mutually supporting automatic weapons could cover adjacent positions and deny the open ground between the hills." These gun positions were well dug-in and impervious to artillery fire. Because the narrow roads in the area had been made impassable by mines and shell cratering, tank support was not forthcoming, and a day of bitter fighting netted 3/29 a gain of a scant 150 yards. The remainder of the 4th Marines attacked Naha Airfield where counter fire from tanks, artillery, and support craft was immediately laid down. An urgent call for an air strike on the island was answered in less than half an hour, and "as rack after rack of bombs fell on the Nip positions, the troops stood up and cheered." The artillery piece was soon silenced, but 20mm fire was received spasmodically. Nevertheless, 3/4 pressed forward with its open flank covered by continued air strikes on Senaga Shima and completed the capture of Naha airfield before noon, whence they pushed south toward Gushi. At sea, kamikaze attacks crashed into and damaged two destroyer minesweepers, while also causing further damage to escort carrier Natoma Bay and destroyer Anthony on June 7. That day, Shepherd's Marines faced stiff resistance all along the front. The 4th Marines reduced Little Sugar Loaf where stiff resistance and bitter fighting characterized the action in the center and on the left of the 4th Marines' area. However, the attack forged ahead against machine-gun fire coming "from everywhere," while "countless caves were methodically cleaned out and sealed by the old process of direct fire, flame, and demolitions."Meanwhile the 29th Marines entered Oroku, and the 22nd Marines captured Hill 103 and the area south of Tamigusuki.  To the southeast, the 7th Marines overran Hanja and Hill 108, ultimately digging in just north of Zawa and linking up with the 1st Marines, which also advanced up to 1,200 yards as they secured Hill 75 and pushed toward Yuza. Further east, the primary offensive efforts of the 7th and 96th Divisions on June 7 and 8 were focused on probing enemy defenses and advancing assault battalions to more favorable positions for an attack. Additionally, by the afternoon of June 8, the 32nd Regiment successfully relieved the exhausted 184th in the Gushichan area. On that same day, the 1st Marines pressed forward to the high ground overlooking the Mukue River, while the 7th Marines moved through Zawa and began probing enemy positions in Itoman, encountering stiffened resistance. The first LVT's, supported by LVTa's, arrived at the newly-uncovered beaches at noon on 8 June, and shortly thereafter General Hodge sent General del Valle "congratulations for cutting the island in two." Meanwhile, on Oroku, the 29th Marines made little progress as they stalled at a key ridgeline on the left. The 4th Marines committed all three of their battalions to the attack, successfully securing the areas of Hill 39 and Gushi Ridge. The 22nd Marines continued to pivot on their right, seizing Hill 55 and making good progress along the front toward Chiwa and Tomigusuki. On June 9, although the 22nd Marines managed to secure Hill 55 and push to Hill 28, little advancement was achieved to the north. Concurrently, the 4th Marines were able to slowly push to the outskirts of Chiwa and Uibaru, with patrols clearing out Chiwa and Whaling's 3rd Battalion extending the front to the north. The action in the zone of the 4th Marines on 9 June remained unchanged from that of preceding days: “The advance was still slow and tedious against bitter resistance. Every Jap seemed to be armed with a machine gun, and there was still the same light and heavy mortar fire. Casualties continued to mount and the number of Japs killed soared over the maximum of 1500 which were supposed to be defending and there were still plenty left.” In the meantime, to the south, Del Valle sent strong patrols across the Mukue, which began to encounter significant enemy resistance. Consequently, the 7th Marines were unable to push toward Tera and Itoman. Further east, Hodge finally launched a corps attack to the south. The 96th Division focused its efforts on softening the enemy positions on the escarpment in front of them, while the 7th Division carried out the offensive. The 32nd Regiment attempted to attack the eastern end of Hill 95 but was unsuccessful; however, they managed to locate and identify the most troublesome sources of enemy fire for destruction. On a more positive note, the 17th Regiment gained a precarious foothold on the southern end of Yaeju Dake, just north of Nakaza, where they would withstand several Japanese counterattacks throughout the night. The first and greatest obstacle confronting Wallace's attack was the open ground over which both assault companies had to move. Wallace used all available support and the men camouflaged themselves with grass and rice plants, but enemy fire began almost as soon as the leading platoons moved into the open. The infantrymen crawled through the slimy rice paddies on their stomachs. Within an hour Company I was strung from the line of departure to the base of the objective which two squads had reached. About this time the Japanese opened fire with another machine gun, separating the advance squads with a band of fire. This left one squad to continue the attack; the remainder of the company was unable to move, cut off by fire or strung across the rice paddies. Those men in the squad still free to operate lifted and pulled each other to the edge of the cliff and crawled quietly forward through the high grass on top. Pfc. Ignac A. Zeleski, a BAR man, moved so stealthily that he almost touched the heels of one Japanese. Zeleski killed him, and the other men killed eight more Japanese within the first ten minutes. Another squad reached the top of the escarpment about an hour later but was caught in cross and grazing fire from three machine guns, and the entire 8-man squad was killed. Gradually, however, a few more men reached the top, and by evening there were twenty men from Company I holding a small area at the escarpment rim. Company K had a similar experience. Accurate enemy fire killed one man, wounded two others, and halted the company when it was from 200 to 300 yards from its objective. For forty-five minutes the attack dragged on until S/Sgt. Lester L. Johnson and eight men maneuvered forward through enemy fire, gained the high ground, and concentrated their fire on the enemy machine gun that was firing on the remainder of the company. This did not silence the gun but did prevent the gunner from aiming well, and Johnson waved for the rest of the company to follow. By 1330 of 9 June Company K was consolidated on the southeastern tip of the Yaeju-Dake. That evening, three small but determined counterattacks, with sustained grenade fire between each attempt, hit the small force from Company I, which held off the attackers with a light machine gun and automatic rifles. Additionally, Wallace's 1st Battalion successfully landed unopposed on Aguni Island to establish air warning and fighter director installations.  However, it's now time to leave Okinawa and shift our focus to the Philippines to cover the continuation of General Eichelberger's Mindanao Campaign. As we last saw, by May 3, General Sibert's 10th Corps had successfully invaded the island and secured the key Kabacan road junction. General Woodruff's 24th Division occupied Digos and Davao, while General Martin's 31st Division advanced up the Sayre Highway toward Kibawe. Thanks to the arrival of the 162nd Regiment from Zamboanga, the 31st Division was now able to send another regiment, the 155th, to assist in the push north against General Morozumi's 30th Division. In response to the rapid advance of the 31st Division as far as Kibawe, Morozumi was assembling his units at Malaybalay in preparation for a retreat eastward to the Agusan Valley. He dispatched the 3rd Battalion of the 74th Regiment to the south to delay the Americans in the vicinity of Maramag, at least until May 10. Meanwhile, after capturing Davao, Woodruff's goal was to mop up the sector and destroy General Harada's 100th Division in the mountainous interior. The 100th Division located the southern anchor of its defenses at Catigan, 13 miles southwest of Davao, and the northern anchor in hills some twelve miles north of Davao. The Davao River, flowing generally south-southeast into Davao Gulf at Davao, divided the defensive forces into two groupments. The Right Sector Unit, west of the river, was composed of 5 infantry battalions, 3 regular and 2 provisional. The territory east of the river was the responsibility of the Left Sector Unit--2 regular infantry battalions, 2 provisional battalions, and the Air Force's Hosono Unit of ill-armed service personnel. The Right and Left Sector Units had a little artillery attached, for General Harada kept under his direct control most of the artillery as well as many engineer and service units. As a reserve Harada had about a battalion of regular infantry. The central and strongest portion of Harada's defenses rested its right on rising ground overlooking Libby Airdrome, two miles northwest of Talomo on the coast. From this point the central defenses, along which Harada initially deployed three battalions, extended eastward across the Talomo River and some rough hills to the west bank of the Davao River. The focal point of the central defenses was Mintal, four miles up Route 1-D from Talomo. Anticipating ultimate withdrawal into the mountains via Route 1-D, the southeastern section of the so-called Kibawe-Talomo trail, Harada had prepared defenses in depth along the highway and along ancillary roads paralleling it. Much of the region west of the Davao River from Talomo northwest twelve miles to Calinan was covered with overgrown abaca, or hemp, plantations. Resembling banana plants, and growing to a height of about 20 feet, the abaca plants had originally been planted in rows 10 feet apart, with 10 feet between plants. With harvesting slack during the war, the plantations had become thick with shoots, and older plants had grown to a foot or so in diameter. Plants of various sizes were, in April 1945, scarcely a foot apart. Visibility was virtually nil, and the heat at the hemp plantations was like that of an oven. With the 162nd Regiment taking control of Digos and the area stretching from Illana Bay's shores inland to Kabacan, Woodruff was now free to utilize his entire division to engage the enemy forces in the Davao area. At the start of May, the 21st Regiment had already launched an attack to clear Libby Airdrome, Route 1-D between Mintal and Talomo, and Mintal itself. They successfully reached Mintal by May 3, effectively forcing Harada to reinforce his defenses near the Talomo River. Although the airdrome was cleared two days later, subsequent efforts up Route 1-D toward Mintal were repelled by fiercely defending Japanese forces. Due to this resistance, elements of the 34th Regiment attempted to drive north along the high ground on the east bank of the Talomo River to bypass the Japanese defenses on Route 1-D. On May 8, the 21st Regiment finally crossed to the east side at Mintal; however, in the face of Japanese artillery, mortar, and machine-gun fire, they had to withdraw back to the west bank two days later. At the same time, the 19th Regiment was expanding its hold in the Davao area, striking into the high ground controlling the coast road immediately west of the Davao River on May 10. They also cleared scattered Japanese strongpoints on hills just north of Davao and on Samal Island. Two days later, the 21st Regiment again attacked northward along the east bank of the Talomo, successfully clearing out numerous positions from which the Japanese had directed fire on Route 1-D. By May 14, the highway all the way north to Mintal was finally secured. In the meantime, the 124th Regiment started north from Kibawe on May 6. However, the recently arrived Japanese defenders at Maramag managed to delay the occupation of this town until May 12, thus accomplishing their task more than adequately. Despite this success, Eichelberger had shrewdly sensed that Morozumi would attempt to make a last stand in the hills northwest of Davao. Therefore, he decided to land the 108th Regiment behind enemy lines in the Macajalar Bay area to expedite the conquest of Mindanao and open a new supply route to the 31st Division. Accordingly, on May 10, the 108th Regiment landed unopposed along the southeastern shore of Macajalar Bay, making contact almost immediately with guerrilla units operating in the region. This regiment then drove down the Sayre Highway to meet the 31st Division advancing from the south, encountering no significant resistance until May 13, when it faced strong Japanese defenses near Dalirig. With its rear protected by the recently landed 3rd Battalion of the 164th Regiment, the 108th proceeded to attack the enemy positions with great intensity, finally forcing the Japanese to retreat to the area east of Malaybalay by May 16. Concurrently, on May 13, the 155th Regiment passed through the 124th Regiment to continue the drive northward, meeting little opposition but facing supply problems. By May 20, the Americans finally reached the outskirts of Malaybalay, where fire from remnants of the 30th Field Artillery Regiment halted their advance. Realizing that the regiment could not haul its weapons into the mountains east of Malaybalay, Morozumi had left the unit at Malaybalay to fight a rear-guard action, which was successful in keeping the 155th Infantry out of the town until late on 21 May. On 22 and 23 May the 155th continued up Sayre Highway, encountering elements of Morozumi's Northern Sector Unit that had not learned that American troops had reached Malaybalay and were still withdrawing southward to join the 30th Division's main body. Pressed by troops of the 108th Infantry, 40th Division, which had already landed at Macajalar Bay, the retreating forces gave the 155th Infantry little trouble and, about 1400 on 23 May, the 155th made contact with the 108th Infantry near Impalutao, twelve miles northwest of Malaybalay. Its share in the task of clearing Sayre Highway cost the 31st Division approximately 90 men killed and 250 wounded, while the 108th Infantry, 40th Division, lost roughly 15 men killed and 100 wounded. Together, the two units killed almost 1,000 Japanese during their operations along the highway, and captured nearly 25 more. Nevertheless, the 30th Division had managed to escape east this time to establish new positions near Silae. Back in Davao, on May 15, Woodruff directed the 21st and 34th Regiments to attack abreast to the north and northwest, targeting the Japanese center. Meanwhile, the 19th Regiment advanced north to clear the northeastern shores of Davao Gulf, link up with the guerrilla forces north of the gulf, and ultimately swing westward against the 100th Division's left flank forces. Surprised by the lack of enemy attacks against his flanks, Harada concluded that the American forces intended to neglect his flanks in favor of a frontal assault on his center. As a result, he weakened the defenses of the Left Sector Unit to reinforce the Mintal line, leaving only Admiral Doi's air-naval troops to defend his left flank. On May 17, Woodruff renewed his offensive. The 19th Regiment struck north to establish contact with the guerrilla 107th Division, while the 34th Regiment began clearing the coastal hills between the Talomo and Davao Rivers and attacked northwest toward Tugbok. The 21st Regiment also drove north toward Tugbok in the face of determined opposition. Progress in the following days was slow due to intense artillery, machine-gun, rocket, mortar, and rifle fire. However, by May 27, the 21st Regiment seized the Tugbok area, with the 34th Regiment arriving the next day to relieve them. As Harada's strongest defenses had been breached, he ordered a general withdrawal to a hastily established second line crossing Route 1-D in the vicinity of Ula. Furthermore, the 19th Regiment managed to establish contact with the guerrillas by May 24 as it secured Route 1 north of Davao. On May 29, the 19th Regiment struck westward toward Doi's Mandog defenses, closing in two days later to engage the naval troops in fierce combat. Concurrently, on May 30, the 34th Regiment attacked toward Ula, which fell easily the following day, though progress then slowed in the face of fanatic resistance. Reinforced by the recently arrived 3rd Battalion of the 163rd Regiment on June 4, the 34th began to make headway beyond Ula on the secondary road, gaining one mile by June 6 before swinging east toward Mandog. The next day, having overrun Doi's outer defenses, the 19th Regiment advanced steadily into the main positions near Mandog, which ultimately fell by June 9, just as the 34th was reaching the area. Continuing northward, the 34th was almost three miles north of Ula along both roads and found few signs of organized Japanese resistance by June 11. However, the 19th Regiment would not clear the hills north of Mandog until June 15. In the meantime, the 21st Regiment struck north from Lamogan on May 31 along secondary roads west of Route 1-D, ultimately seizing Wangan on June 16 and forcing Harada's battered forces to commence a full retreat northward in disarray. After the fall of Culanan three days later, Harada finally decided to retreat to a new line near the Bannos River. Yet Woodruff's troops continued to pursue them, rapidly crossing the Tamogan River and inflicting heavy casualties on the retreating enemy until they reached the mountain barrio of Kibangay on June 26, where the pursuit was finally halted. Looking back to the north, with Sayre Highway cleared, the 124th Regiment began probing into the mountains to the east in late May, encountering heavy resistance, rough terrain, bad weather, and supply problems. Nevertheless, by June 5, Morozumi abandoned his plan to hold the Silae area for a month and slowly began moving his best troops eastward toward Waloe in the Agusan River valley, harassed by Filipino guerrillas along the way. In the end, Silae was finally occupied on June 9, with troops of the 108th Regiment pushing further to the Bobonawan River four days later. Additionally, the 155th Regiment arrived on the Pulangi River on June 12, while elements of the 162nd Regiment struck twenty miles into the mountains east from Maramag by June 26. On June 25, the 1st Battalion of the 155th Regiment successfully landed on Butuan Bay and managed to reach Waloe before the Japanese on June 27, dispersing the 3rd Battalion of the 41st Regiment that was holding the area. However, the Japanese retreat was so slow that Morozumi was still assembling his forces about seven miles up the Agusan from Waloe by the end of the war.  Far to the northwest, units of the 31st Division had been probing southeast along the upper section of the Kibawe-Talomo trail ever since early May, and on the 11th of that month a battalion combat team of the 167th Infantry launched the reconnaissance-in-force directed by General Sibert.  Japanese along this section of the trail, about 1,000 men in all, comprised a conglomerate mass of service troops with a small leavening of infantry. Control was vested in General Tomochika, chief of staff of the 35th Army, who had set up a small headquarters groupment near barrio Pinamola, about twenty miles southeast of Kibawe. The Japanese force had a defensive potential far greater than its strength and nature would indicate, for the terrain gave the Japanese every conceivable advantage. Bounded on both sides by dense jungle and thick rain forest, the trail as far as Pinamola ran up and down steep ridges and was scarcely jeep-wide. Rains of late May soon rendered all sections of the trail completely impassable to wheeled vehicles, and supplies had to come in by airdrop, supplemented when possible by hand-carrying parties and laden Carabaos. The mud was so deep that often troops had to pull, push, or even jack the Carabaos out of gooey holes. Delayed by the Japanese, the terrain, and the weather, the 167th Infantry's battalion did not reach the Pulangi River, thirteen miles southeast of Kibawe, until 29 May.  Then, although the Japanese from the trail could no longer offer any threat to the 31st Division, the battalion continued south toward Pinamola, aided considerably by guerrillas. The remnants of the 1st Battalion, 74th Infantry, and the South Sector Unit, 30th Division, which had been driven into the mountains along Highway 3 by the swift American advance in central Mindanao had meanwhile been attached to Tomochika's forces early in June. Troops of the 167th Infantry finally reached Pinamola on 30 June as the remaining Japanese were withdrawing southward another eight miles to the crossing of the Kuluman River. Progress as far as Pinamola had cost the 167th Infantry approximately 60 men killed and 180 wounded, while the Japanese had lost almost 400 killed along the same section of the trail. Elements of the 167th Infantry held along the northwestern section of the Kibawe-Talomo trail until the end of the war, and as of 15 August the regiment was preparing to send troops across the Kuluman River to continue the advance southeastward. On that date nearly 30 miles of Japanese-improved trail, only 19 air miles--still separated the 167th Infantry from guerrilla units operating in the vicinity of Kibangay. Organized remnants of Harada's 100th Division holed up until the end of the war in rugged terrain north of this 30-mile stretch of the trail. Finally, the 24th Reconnaissance Troop successfully landed on the southeastern shore of Sarangani Bay on July 4 to establish contact with the guerrilla 116th Regiment, subsequently clearing the bay's shores against negligible resistance. On July 12, the 1st Battalion of the 21st Regiment landed on the northwest shore, just as two provisional battalions were arriving in the area from different directions. The three forces began to clear the area, successfully locating and destroying the only Japanese unit in the region by July 25. This concluded the campaign in Mindanao, during which the Americans suffered 820 men killed and 2,880 wounded. In turn, almost 10,540 Japanese were killed in eastern Mindanao by June 30, with the pursuing Filipino-American units killing another 2,325 Japanese by the war's end. Roughly 600 Japanese prisoners were captured, over 250 of whom were civilians, before August. After the war, about 22,250 Japanese troops and 11,900 civilians turned themselves in. It is also estimated that an additional 8,235 Japanese lost their lives due to starvation and disease between April and the war's end. I would like to take this time to remind you all that this podcast is only made possible through the efforts of Kings and Generals over at Youtube. Please go subscribe to Kings and Generals over at Youtube and to continue helping us produce this content please check out www.patreon.com/kingsandgenerals. If you are still hungry after that, give my personal channel a look over at The Pacific War Channel at Youtube, it would mean a lot to me. In the spring of 1945, the fierce battle for Okinawa escalated as General Buckner's troops captured crucial strongholds, pushing the Japanese forces into retreat. Meanwhile the liberation of Mindanao was kicking up. American forces launched a rapid invasion, confronting Japanese defenders who were heavily fortified in the mountainous regions. Despite the stubborn resistance, American troops relentlessly battled, ultimately culminating in significant victories and paving the way for liberation.

BUFFALO, NY - June 3, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on May 19, 2025, titled “PRDX1 protects ATM from arsenite-induced proteotoxicity and maintains its stability during DNA damage signaling." In this study, led by first author Reem Ali and corresponding author Dindial Ramotar from Hamad Bin Khalifa University in Qatar, researchers discovered that a protein called PRDX1 helps maintain the stability of ATM, a key protein involved in repairing damaged DNA, especially when cells are under stress from arsenite exposure. The study found that without PRDX1, cells lose their ability to repair DNA and become more sensitive to chemotherapy. This finding suggests that targeting PRDX1 could improve the success of some cancer treatments. PRDX1 is already known for its role in protecting cells from oxidative damage, but this study shows it also plays a role in the DNA repair process. ATM is an essential protein that detects breaks in DNA and starts the repair process. When PRDX1 is missing, ATM is rapidly lost, especially when cells are exposed to arsenite, a toxic substance found in the environment. Without ATM, the DNA repair system fails, leaving cells more vulnerable to damage. By using both human cell lines and clinical samples from ovarian cancer patients, the team showed that high levels of PRDX1, along with ATM and MRE11 (another DNA repair protein), were linked to tumors' aggressive features and lower patient survival rates. This pattern suggests that tumors with high PRDX1 may resist chemotherapy by increasing their DNA repair capacity. On the other hand, removing PRDX1 weakened the repair system and made cancer cells more responsive to DNA-damaging platinum drugs. The study also showed that combining low doses of arsenite with drugs that either block ATM or damage DNA caused a much higher rate of cancer cell death in cells that lacked PRDX1. These results suggest a new treatment approach: lowering PRDX1 levels to make cancer cells more sensitive to DNA-damaging platinum therapies already in use. This highlights PRDX1 not only as a protector of cell function but also as a potential weak point in cancer cells. “As such, we propose that small molecule inhibitors of PRDX1, or single nucleotide polymorphisms that compromise PRDX1 function, in combination with low doses of arsenite can be exploited to treat chemo-resistant tumours.” These findings open the door for the use of PRDX1 as a biomarker to predict treatment response and as a promising target for new combination therapies. For patients with ovarian cancer and potentially other tumors, adjusting PRDX1 levels may help overcome drug resistance and improve outcomes. DOI - https://doi.org/10.18632/oncotarget.28720 Correspondence to: Dindial Ramotar - dramotar@hbku.edu.qa Video short - https://www.youtube.com/watch?v=suOhF7mPlNQ Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28720 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, redox signaling, homologous recombination, protein interaction, cell cycle, protein modification 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 — June 3, 2025 — A new #research paper was #published in Aging (Aging-US) on May 1, 2025, as the #cover of Volume 17, Issue 5, titled “Defining the hypoxic thresholds that trigger blood-brain barrier disruption: the effect of age.” In this study, researchers Arjun Sapkota, Sebok K. Halder, and Richard Milner from San Diego Biomedical Research Institute investigated how aging affects the brain's vulnerability to low oxygen, or hypoxia. Using C57BL/6J mice ranging from 2 to 23 months of age, they identified specific oxygen levels that disrupt the blood-brain barrier (BBB)—a critical structure that protects brain tissue from harmful substances. The findings are important for understanding age-related cognitive decline and the potential risks faced by individuals with chronic oxygen-limiting conditions such as asthma, sleep apnea, emphysema, and heart disease. The BBB is essential for maintaining brain health. In this study, mild and prolonged hypoxia—called chronic mild hypoxia—was found to compromise the BBB in mice. Older mice showed significantly more BBB disruption than younger ones. Notably, barrier weakening and blood vessel changes occurred at oxygen levels of just 15% in aged mice, compared to 13% in young mice. These data suggest that the aging brain is more sensitive to oxygen deprivation, even at levels that may be considered only mildly hypoxic. The researchers also determined when this vulnerability emerged. The BBB showed increased sensitivity to low oxygen not only in aged mice but also in mice as young as 2 to 6 months, with a second spike occurring between 12 and 15 months—equivalent to middle age in mice. These findings may reflect age-dependent changes in brain vascular function and remodeling capacity. “Hypoxia-induced endothelial proliferation was relatively constant across the age range, but advanced age strongly enhanced the degree of BBB disruption (4-6-fold greater in 23 months vs. 2 months old).” Another key focus was microglial activation, a sign of brain inflammation. Aged mice exhibited higher microglial activation across all oxygen levels, including normal conditions. Chronic microglial activation is closely linked to neuroinflammation and has been implicated in diseases such as Alzheimer's. While the rate of blood vessel formation was constant across ages, the degree of BBB disruption increased sharply with age, suggesting that repair mechanisms may weaken over time. These results may help explain why older adults with chronic hypoxia-related diseases are at higher risk for neurodegeneration and cognitive decline. The study also draws attention to the risks of high-altitude exposure for aging populations, where oxygen levels naturally drop. Altogether, these findings underscore the importance of protecting brain health in older individuals by managing oxygen exposure and reducing hypoxia-related risks. The researchers emphasize the need to develop new therapies that support blood-brain barrier integrity, particularly in aging populations exposed to chronic or intermittent low-oxygen conditions. DOI - https://doi.org/10.18632/aging.206241 Corresponding author - Richard Milner - rmilner@sdbri.org Video short - https://www.youtube.com/watch?v=Nr6rTm7aJRo Keywords - aging, blood-brain barrier integrity, endothelial, proliferation, microglia, chronic mild hypoxia, hypoxic threshold To learn more about the journal, please visit our website at https://www.Aging-US.com​​ and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ 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

Jody responds to the American College of Physicians' Annals On Call Podcast episode released on May 19th, 2025.Links:Advanced Practice Clinicians Cannot Replace Primary Care Physicians. Annals On Call Podcast, 5-29-25Physician Assistant and Former PA-Turned-Physician Discuss the State of the Profession. Patients At Risk Podcast, 7-25-21 (Spotify)New Workforce Model Suggests Continued Physician Shortages In Nonprimary Care Specialties (AAMC Article)Christin Giordano McAuliffe. There Is No Substitute for Primary Care Physicians: A Response to the Association of American Medical Colleges' Workforce Model. Ann Intern Med.2025;178:590-591. [Epub 4 March 2025]. doi:10.7326/ANNALS-24-03806University of South Alabama Dual Role NP CurriculumRazavi, Moaven PhD*; O'Reilly-Jacob, Monica RN, PhD, FNP-BC†; Perloff, Jennifer PhD*; Buerhaus, Peter RN, PhD, FAAN, FAANP(h)‡. Drivers of Cost Differences Between Nurse Practitioner and Physician Attributed Medicare Beneficiaries. Medical Care 59(2):p 177-184, February 2021. | DOI: 10.1097/MLR.0000000000001477 McMenamin A, Turi E, Schlak A, Poghosyan L. A Systematic Review of Outcomes Related to Nurse Practitioner-Delivered Primary Care for Multiple Chronic Conditions. Medical Care Research and Review. 2023;80(6):563-581. doi:10.1177/10775587231186720Kippenbrock T, Emory J, Lee P, Odell E, Buron B, Morrison B. A national survey of nurse practitioners' patient satisfaction outcomes. Nurs Outlook. 2019 Nov-Dec;67(6):707-712. doi: 10.1016/j.outlook.2019.04.010. Epub 2019 May 4. PMID: 31607371.Haas, D., Pozehl, B., Alonso, W. W., & Diederich, T. (2023). Patient Satisfaction With a Nurse Practitioner–Led Heart Failure Clinic. Journal for Nurse Practitioners, 19(4), Article 104496. https://doi.org/10.1016/j.nurpra.2022.11.006https://www.techtarget.com/patientengagement/news/366584669/Nurse-Practitioners-Boost-Patient-Satisfaction-Quality-Outcomeshttps://www.aanp.org/advocacy/advocacy-resource/position-statements/quality-of-nurse-practitioner-practicehttps://www.aacnnursing.org/news-data/all-news/rounds-with-leadership-focusing-on-the-outcomes-of-np-practiceStanik-Hutt, J., Newhouse, R. P., White, K. M., Johantgen, M., Bass, E. B., Zangaro, G., Wilson, R., Fountain, L., Steinwachs, D. M., Heindel, L., & Weiner, J. P. (2013). The quality and effectiveness of care provided by nurse practitioners. Journal for Nurse Practitioners, 9(8), 492-500.e13. https://doi.org/10.1016/j.nurpra.2013.07.004Savard I, Al Hakim G, Kilpatrick K. The added value of the nurse practitioner: An evolutionary concept analysis. Nurs Open. 2023 Apr;10(4):2540-2551. doi: 10.1002/nop2.1512. Epub 2022 Dec 17. PMID: 36527435; PMCID: PMC10006655.

*Note: This is the Free Content version of my interview with Veronica French. To access the entire episode, please consider becoming a Tier 2 'Groves of Orpheus' member on Patreon, or you can purchase this episode for a one-time fee. My guest this month is Veronica French. Veronica has an MA in Religious Studies from the University of Erfurt, Germany. She specializes in the study of modern shamanism, anthropology of religion and gender studies. Her master's thesis explored how modern shamans living in Germany define a “shaman way” and their turning point or crisis, which informs their “shamanic journey.” Her undergraduate work was in medical anthropology with a focus on shamanic techniques and Chinese 5 Element, in which she explored the scholar/practitioner position. She presented previously at the 8th Biannual Conference of the European Society for the Study of Western Esotericism (ESSWE) with the paper “Performative Strategies of Creative Esotericism in 19th Century Jewish Communities” (Cork, Ireland, 2022); XXXI International Summer School on Religion Women and Religions with the paper “Modern Shamanism, Empowerment and Green Religion: Contemporary Shamanic Practice in Germany” (San Gimignano, Italy, 2024); and the International Theosophical History Conference 2024 with the paper “Modern Shamanism, Theosophy and Ecological Spirituality: Connecting Nature Spiritualities” (Ascona, Switzerland, 2024). Veronica also presented at three seminars at the University of Erfurt: “Initial Shamanic Interviews” University of Erfurt, Master's Thesis Colloquium (2023); “Green Religion and Indigeneity in Popular Media,”University of Erfurt, Green Religion? Answers to Climate Change from the Perspective of Religious Studies (2023); and “Ethnographic Work of Shamanic Practice in Eastern Germany,” University of Erfurt, Master's Writing Seminar (2023).In this discussion, Veronica shares her background and inspiration for her research into modern shamanism. We talk a bit about the terms shamanism and animism, as these are somewhat contested within academia, and Veronica shares how she is using these terms in her work. She explains what questions she was asking at the outset of her project, and also the surprising additions that arose once she started interviewing her participants. Veronica also notes the interesting data that she gathered regarding topics such as gender, identity, “lived religion,” and ecology. As Veronica has her own experience within the concept known as a the holistic milieu (referring to a broad and diverse spiritual landscape that encompasses various New Age and alternative spiritual practices; often contrasted with traditional religious institutions, as it focuses on personal spirituality, self-development, and holistic well-being rather than formal doctrines or organized worship), she found she was able to relate well to the experiences of her participants, and this aspect has led her to consider continuing her research using the method known as autoethnography. This is a qualitative research method that combines autobiographical storytelling with ethnographic analysis. It allows researchers to use their personal experiences to explore and critique cultural beliefs, practices, and social phenomena. Veronica talks about other scholars in the field who have been using this method, and how it is becoming more accepted within academia. If anyone has any questions or comments for Veronica, please post them here or contact me via email and I can pass these on to her. She welcomes further feedback and discussion! Veronica was also very kind to share some references for futher reading; please see this below. PROGRAM NOTESReferences:Olivia Cejan: "Arts and Crafts Divine" is her dissertation utilizing autoethnography and pedagogy to write about a secret society group. Talk at Copenhagen Conference:https://www.youtube.com/watch?v=4g2qvGcy5pY&t=524sCorrine Sombrun: -Her institute: https://trancescience.org/https://www.youtube.com/watch?v=4oDs10hUy6ETrailer to her movie; English subtitlesTed Talk:English subtitleshttps://www.youtube.com/watch?v=Ym0kIECFi0Uhttps://amara.org/videos/Tcvokh51yb2Y/en/1543652/?tab=revisionsAnother interview with English (Google)https://www.youtube.com/watch?v=Syy4MTHAfF4 Alice Ahern: Phd Cork Ireland, studying shamanism and pop culture:https://www.youtube.com/watch?v=OCCeV7MLtFcYoutube talk:  "The Reclamation of Feminine Wisdom in the Irish Neo-Shamanic Milieu" Traditional Religions view on Nature Religions:https://fore.yale.edu/Event-Listings/Religions-World-and-Ecology-Conference-Series/Religions-World-and-Ecology-Archivehttps://fore.yale.edu/sites/default/files/files/annual_review_environment.pdfBibliography :Eliade, Mircea. Shamanism: Archaic Techniques of Ecstasy. Princeton, N.J: Princeton University Press, 1972.Harner, Michael J. The Way of the Shaman. 10th anniversary ed. San Francisco: Harper & Row, 1990.Harvey, Graham. Animism: Respecting the Living World. Kent Town: Wakefield Press, 2005.Harvey, Graham. Shamanism: A Reader. London: Routledge, 2003.Jenkins, Willis. u.a: “Religion and Climate Change”, Annual Review of Environment and Resources 2018 (43), 85-108.Kaza, Stephanie. “The Greening of Buddhism: Promise and Perils”, in: Oxford Handbook of Religion and Ecology, Oxford 2006, 184-220.Kraft, S, T Fonneland, and J Lewis. Nordic Neoshamanisms. New York: Palgrave Macmillan, 2015. Nordic Neoshamanisms | SpringerLinkLaack, Isabel (2020) “The New Animism and Its Challenges to the Study of Religion”, Method and Theory in the Study of Religion, 1-33.Lewis, I.M., Ecstatic Religion | A Study of Shamanism and Spirit Possession | I.M.McGuire, Meredith B. Lived religion: Faith and practice in everyday life. Oxford University Press, 2008.Puca, Angela. Italian Witchcraft and Shamanism: The Tradition of Segnature, Indigenous and Trans-Cultural Shamanic Traditions in Italy. Leiden; Brill, 2024.Saler, Benson. Conceptualizing Religion: Immanent Anthropologists, Transcendent Natives, and Unbounded Categories. New York: Berghahn Books, 2000.Shelton, Dinah (2015): “Nature as a legal person”. In: Vertigo (Hors-série 22).DOI: 10.4000/vertigo.16188.Taylor, Bron Raymond. Dark Green Religion: Nature Spirituality and the Planetary Future. Berkeley: University of California Press, 2010. Dark Green Religion – Professor Bron TaylorZnamenski, Andrei A., The Beauty of the Primitive: Shamanism and Western Imagination | Oxford Academic Music and Editing: Daniel P. SheaEnd Production: Stephanie Shea 

What's the episode about?In this episode, hear Dr. Terri Daniel on toxic theology, healthy theology, complicated grief, being a non-religious chaplain, hospice and loss.Who is Terri?Dr. Terri Daniel is an inter-spiritual hospice chaplain, end-of-life educator, and grief counselor certified in death, dying and bereavement by the Association of Death Education and Counseling and in family-focused grief therapy by ThePortland Institute for Loss and Transition. She conducts workshops throughout the U.S. and is an adjunct instructor in thanatology and chaplaincy at Marian University, the University of Maryland and the Graduate Theological Union. She is also the founder of The Conference on Death, Grief andBelief, and the Ask Doctor Death podcast.Terri's academic credentials include a B.A. in Religious Studies from Marylhurst University, an M.A. in Pastoral Care from Fordham University, and a DMin from the San Francisco Theological Seminary.Over the years Terri has helped hundreds of people learn to live, die and grieve more consciously. Her work is acclaimed by hospice professionals, spiritual seekers, counselors, theologians, and academics worldwide.She is the author of four books on death, grief and beyond.​A Swan in Heaven: Conversations Between Two Worlds (2007)Embracing Death: A New Look at Grief, Gratitude andGod (2010)Turning the Corner on Grief Street: Loss and Traumaas a Journey to Awakening (2014)Grief and God: When Religion Does More Harm ThanHealing (2019) Want to complete the compassionate communities, atlas survey mentioned at the start of the episode? See below for more information! This atlas will showcase local and global efforts, connect like-minded communities, and inspire others around the world. We invite you and your members to take part in a short survey (approx. 10 minutes) about your experiences. Your inputwill help. Participation is anonymous and voluntary, and you can stop at any time. The survey can also be translated into your preferred language. For more information and toparticipate, click here. How do I cite the episode in my research and reading lists? To cite this episode, you can use thefollowing citation: Daniel, T. (2025) Interview on The Death Studies Podcast hosted by Michael-Fox, B. and Visser, R. Published 1 June 2025. Available at: www.thedeathstudiespodcast.com, DOI: 10.6084/m9.figshare.29207024 What next?Check out more episodes or find out more about the hosts! Gota question? Get in touch.

EDU Central REDUX –Building Memory with Science and Senses – Put on Your Thinking Cap (EP:42) With  Stella Collins, MSc. This month, we are revisiting a classic episode from 2021. Creating effective learning can be complicated – from our biology to our environment, there are a lot of elements that influence outcomes. And how can we get our learners curious anyway, especially in our increasingly digital spaces? Grab a hat and put it on (we mean it…. we'll wait while you go get it)  because in this episode, celebrated author and science-based learning thinker, Stella Collins, joins Stacy Craft to explore learning and the brain, memory, the powers of sensory experiences, avoiding stagnation, community, and why there is a group of people who think “Brains!” when they bite into a bar of chocolate. We also take time to unpack the LEARNS strategy for designing and providing education that people will remember. Questions? Feedback? Ideas? Contact us at edufi@mayo.edu Additional Resources: Stellar Labs Resources 6 Tricks to Making Learning Sticky!  LEARNS Teacher Centered Vs Learner Centered Nine Things Educators Need to Know About the Brain BASIC & LEARNERS Mnemonic/Acronyms Articles Benjamin C. Ingman (2019) Novelty and educational experience, The Curriculum Journal, 30:1, 69-90, DOI: 10.1080/09585176.2018.1564684 Tyng, C. M., Amin, H. U., Saad, M. N., & Malik, A. S. (2017). The influences of emotion on learning and memory. Frontiers in psychology, 8, 1454. Roumell, E. A. (2019). Priming adult learners for learning transfer: Beyond content and delivery. Adult Learning, 30(1), 15-22. Videos The Neuroscience of Learning – Bruce McCandliss Neuroscience, AI and the Future of Education | Scott Bolland | TEDxSouthBank Stellar Labs Take 5 Video Channel

Almost all pythons and some boas have heat pits on their faces. This extraordinary adaptation lets these snakes 'see' the heat signature of their unsuspecting prey. A new study has determined the evolutionary history of these amazing attributes, and worked out whether they are more prevalent in snakes with certain lifestyles. Become a Patreon: https://www.patreon.com/herphighlights Merch: https://www.redbubble.com/people/herphighlights/shop Full reference list available here: http://www.herphighlights.podbean.com Main Paper References: Biswas A, Ghosh A, Agashe M. 2025. In ‘hot' pursuit: exploring the evolutionary ecology of labial pits in boas and pythons. Proceedings of the Royal Society B: Biological Sciences 292:20250199. DOI: 10.1098/rspb.2025.0199. Species of the Bi-Week: Albuquerque NR, Martins RH, Carvalho PS, Shepard DB, Santana DJ. 2025. A new species of parrot snake, Leptophis (Serpentes: Colubridae) from the Brazilian Cerrado. PeerJ 13:e18528. DOI: 10.7717/peerj.18528. Other Mentioned Papers/Studies: Bontrager DR, Christie JT, Pierce AJ, Artchawakom T, Waengsothorn S, Jones MD. 2025. Ritualistic Male–Male Combat of the Northern King Cobra (Ophiophagus hannah) in Thailand. Ecology and Evolution 15:e71191. DOI: 10.1002/ece3.71191. 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 Steve Cook from the University of Michigan USA about the importance of correctly interpreting and assessing the available data. Associate Professor Jamie Hartmann-Boyce and Associate Professor Nicola Lindson discuss the new evidence in e-cigarette research and interview Dr Steven Cook from the Department of Epidemiology, School of Public Health University of Michigan and the Centre for Assessment of Tobacco Regulations, University of Michigan. In the May podcast Steve Cook discusses the methodological problems of cross-sectional data on the health effects of e-cigarette use a topic he addressed at the May 2025 EC Summit, Washington DC. Steve Cook underlines why all cross-sectional health effects studies should be interpreted with extreme caution unless they examine dose-response relationships and account for temporality and cigarette smoking confounding. Dr Cook emphasises the importance of other information such as smoking histories and health histories and the importance of developing a best practice to ensure that we minimize the risks associated with spurious association and maximise predictive accuracy. Steven Cook receives National Institute for Health (NIH) and Food and Drug Administration's (FDA) Center for Tobacco Products (CTP) funding. This is not deemed a conflict of interest. EC Summit, Washington DC: https://www.e-cigarette-summit.com/program-2025/ Recent paper: 10.1016/j.isci.2025.111985 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 May 2025 found 1 ongoing (NCT06922617) and 1 linked study (DOI: 10.1101/2025.02.17.25322409). Our search for our interventions for quitting vaping review up to 1st May 2025 found 1 new (DOI 10.1001/jama.2025.3810) and 4 ongoing studies (DOI 10.2196/71961, KCT0010346, NCT06909500, NCT06929520). 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.

In diese 'kumulative Vorlesung' beziehe ich Inhalte dreier Vorträge ein, da es mir aus verschiedenen Gründen, und anders als geplant, leider nicht möglich ist, die Vorlesung am Freitag nach Himmelfahrt 2025 anzubieten:Differenzlosigkeit: Mit dem Vortrag "Angst vor dem Dunkel. Sprachliche Auseinandersetzung mit Differenzlosigkeit als Quelle des Religiösen" durfte ich das 14. Kolloquium des Forschungsnetzwerks „Sprache und Wissen“ zum Thema "Sprache und Angst" in Heidelberg im Oktober 2018 mitgestalten. Im Kontext der Vorlesung "Sprache und Religion" ist vor allem der Aspekt der Differenzlosigkeit des Numinosen relevant.Unsagbarkeit: Im Vortrag „Narrative der Erweckung“ auf der zweiten Arbeitstagung Religionslinguistik „Autobiographische Transzendenzerzählungen. Konversion, Erweckung, Erwachen“ (24. und 25.05.2018, Koblenz) spreche ich über basale Vertextungsmuster, die in spezifischen religiösen Gemeinschaften elementar sind, um einen besonderen Transzendenzbezug der Einzelnen in der Gemeinschaft auszustellen. Im Mittelpunkt der Überlegungen werden deshalb (auto-)biographische Entwürfe stehen, in denen Erweckungserlebnisse narrativ verarbeitet werden. Dabei werden institutionelle Voraussetzungen von Vergemeinschaftung, rituelle und ritualisierte Kommunikationspraxen sowie langfristige Transmissions- sowie Transkriptionsprozesse in den Blick genommen, die auch den Wertewandel religiöser Gemeinschaften spiegeln. Für die Vorlesung "Sprache und Religion" ist das Thema verfestigter Sprachmuster zum Umgang mit "Unsagbarkeit" bedeutsam.Streitbarkeit: Den Vortrag "Baustelle des Frühneuhochdeutschen. Luthers Revisionen der eigenen Bibelübersetzung" habe ich im Rahmen der Ausstellung "Wie Luthers Worte fliegen lernten" der SLUB Dresden am 10. Januar 2018 gehalten. Der Übersetzer, Autor und Mensch Luther erscheint trotz aller berechtigten Kritik meist als eine übergroße Figur, die die Frühe Neuzeit und vor allem das Frühneuhochdeutsche maßgeblich prägte. Dabei wird zum einen gern übersehen, dass für seinen Erfolg spezifische Voraussetzungen notwendig waren. Zum anderen war er wohl auch nicht allein für die durchschlagende Wirkung seiner Schriften verantwortlich. Vielmehr sollte man vom Erfolg der ‚Lutherwerkstätten‘ sprechen, die medial, inhaltlich und sprachlich einzigartige Druckzeugnisse auf einer ‚Baustelle des Frühneuhochdeutschen‘ hervorbrachten – mit Sicherheit mit Luther als unruhiger Inspirationsquelle.Präsentation (*.pdf): Alexander Lasch. 2025. Sprache und Religion. Zenodo. DOI: ⁠⁠⁠⁠⁠⁠⁠⁠https://doi.org/10.5281/zenodo.15175420⁠⁠⁠⁠⁠⁠⁠⁠. Videoaufzeichnungen: ⁠⁠⁠⁠⁠⁠⁠⁠https://youtube.com/@AlexanderLasch⁠⁠⁠⁠⁠⁠⁠⁠. Informationen & Material zu allen Vorlesungen: ⁠⁠⁠⁠⁠⁠⁠⁠https://kurzelinks.de/fl7f⁠⁠⁠⁠⁠⁠⁠⁠. Worksheet zu den Vorlesungen: ⁠⁠https://kurzlinks.de/WorksheetVorlesungen⁠⁠. Intro: "Reflections" von Scott Holmes (CC BY via ⁠⁠⁠⁠⁠⁠FMA⁠⁠⁠⁠⁠⁠). #Linguistik #OER #Sprache #Sprachwissenschaft #Religion #Religionslinguistik

referencesGuerra, DJ .2022 Journal of Disease and Global Health.DOI:10.56557/jodagh/2022/v15i38023Nature Metabolism. 2019 VOL 1 | JULY 2019 | 666–67Vivaldi, A. 171? Il sei fase di uno fattimento"https://music.youtube.com/watch?v=Er1QAyuDfVI&si=naV6X9ahOU7-3941Allman, G.67/72 Melissa. from Eat a Peach lp.https://music.youtube.com/watch?v=bX72xzzoqkc&si=0KOYQdIoExKZicOi

Welcome back to part 2 of our 'Science of Prayer' series! Back in April we discussed prayer with Aiden the VVitch, with a focus on the use of prayer in a variety of spiritual and occult settings. In this episode, the hosts tackle the science behind prayer, investigating the mechanisms behind how prayer affects our brains as well as the controversial fields of faith healing and whether prayer can benefit our health. BIBLIOGRAPHY Lancet Review of religion, spirituality, and medicine which touches (heh) on faith healing: https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(98)07376-0/fulltext Intercessory prayer for...COVID?! https://www.cell.com/heliyon/fulltext/S2405-8440(23)09619-6 Some small benefits to health observed from a prayer practice: https://doi.org/10.1037/0003-066X.58.1.36 What happens to our brain during prayer? A review: DOI: 10.1097/HRP.0000000000000232 Neural mechanisms of pain modulation during prayer - the 'Mr Hansen' study: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5487465/ fMRI during Quran recitations: https://doi.org/10.1007/s11042-023-15588-3 How valid is neuroimaging during prayer, anyway? https://doi.org/10.1037/a0039124 The wild 'sutra is stored in the frontal lobe' story https://www.tandfonline.com/doi/full/10.1080/13554790903559689

Episode SummaryErin and Rachel travel 700 years into the future to discuss WALL-E (2008), Pixar's robot romance with an unintentionally anti-capitalist message. Fatphobia and misogyny make this dystopian tale unwatchable despite its endearing protagonist, striking animation, and moments of nostalgia. Episode BibliographyThe 81st Academy Awards | 2009. (2009, February 22). Oscars.org. https://www.oscars.org/oscars/ceremonies/2009Akers, D. (2008, June 9). Wall-E: A Movie With a Full Heart, or A Tribute to Justin. Spectrum. https://spectrummagazine.org/news/wall-e-movie-full-heart-or-tribute-justin/Allen, C. (2008, July 13). Wall-E doesn't say anything. Los Angeles Times. https://www.latimes.com/la-op-allen13-2008jul13-story.htmlAnderson, C.T. (2012). Post-apocalyptic nostalgia: WALL-E, garbage, and American ambivalence toward manufactured goods. Literature Interpretation Theory, 23(3), 267-282, DOI: 10.1080/10436928.2012.703598Ball, S. (2009, January 23). Mr. Oscar, Tear Down This Wall! Andrew Stanton on How Animated Films are Pigeonholed -- and How Wall-E is Every Man. Newsweek. https://web.archive.org/web/20090204034311/http://blog.newsweek.com/blogs/popvox/archive/2009/01/23/breaking-out-of-the-box-wall-e-director-andrew-stanton-on-the-oscars-the-blurring-of-the-line-between-animation-and-film-and-writing-strong-female-characterBandyk, M. (2009, January 22). Academy Awards Controversy: Wall-E Gets Snubbed For Best Picture Oscar. USNews. https://web.archive.org/web/20110717180938/http://money.usnews.com/money/blogs/risky-business/2009/01/22/academy-awards-controversy-wall-e-gets-snubbed-for-best-picture-oscarBarbagallo, R. (2009). Design With a Purpose, an interview with Ralph Eggleston. Animation Art Conservation. https://www.animationartconservation.com/design-with-a-purpose%2c-an-interview-with-ralph-eggleston.htmlBeck, B. (2009). Don't make me laugh: People are funny in WALL-E and Tropic Thunder.  Multicultural Perspectives, 11(2), 90-93. DOI: 10.1080/15210960903028768Bold, K. (2008, July 23). ‘WALL-E' and the professor. Today@UCI. https://web.archive.org/web/20080726230400/http://today.uci.edu/Features/profile_detail.asp?key=369Bose, M. (2017). Immaterial thoughts: Brand value, environmental sustainability, and WALL-E. Criticism, 59(2), 247-277. DOI: 10.13110/criticism.59.2.0247Caraway, K., & Caraway, B.R. (2020). Representing ecological crises in children's media: An analysis of The Lorax and Wall-E. Environmental Communication, 14(5), 686-697, DOI: 10.1080/17524032.2019.1710226Coconut Press. (2022, July 1). The Making of WALL-E: The Imperfect Lens (Disney Pixar video). YouTube. https://www.youtube.com/watch?v=G8tlVs4r7zgDesowitz, B. (2009). Hello, WALL•E!: Pixar Reaches for the Stars. Animation World Magazine. https://web.archive.org/web/20090720073659/http://mag.awn.com/article_view.php?id=3682&page=allDisney Enterprises, Inc./Pixar. (2008, June 12). WALL-E Press Kit. Disney. https://web.archive.org/web/20110711103245/http://adisney.go.com/disneyvideos/animatedfilms/wall-e/media/downloads/WALLEProductionNotes.pdfEbert, R. (2008, June 26). Droid Story. Roger Ebert. https://www.rogerebert.com/reviews/wall-e-2008Film Review: WALL-E. (2008, October 1). BBC. http://news.bbc.co.uk/cbbcnews/hi/newsid_7500000/newsid_7504500/7504559.stmFlaig, P. (2016). Slapstick after Fordism: WALL-E, automatism and Pixar's fun factory. Animation: An Interdisciplinary Journal, 11(1), 59-74. DOI: 10.1177/1746847715625017Frick, A. (2008, July 1). Right-Wing Apoplectic Over Pixar's WALL-E: ‘Malthusian Fear Mongering,' ‘Fascistic Elements'. Think Progress. https://archive.thinkprogress.org/right-wing-apoplectic-over-pixars-wall-e-malthusian-fear-mongering-fascistic-elements-92e1523a8a6e/Gaffey, A.J. (2018). Flip the switch: Virtue, programming, and the prospect of automatic agency in Wall-E. Southern Communication Journal, 83(1), 41-56. DOI: 10.1080/1041794X.2017.1399434Glint, J.M.S., & Bhuvaneswari, G. (2025). Memory, Social Identity and Technology at Odds: The Implication on Physical Well‑Being in Wall‑E. Human Arenas. DOI: 10.1007/s42087-024-00471-wHill, J. (2008, June 17). When it comes to the retail world, Speed Racer whomps WALL-E. Jim Hill Media. https://jimhillmedia.com/when-it-comes-to-the-retail-world-speed-racer-whomps-wall-e/Hobbes, M., & Gordon, A. [Hosts]. (2022, May 31). MP Watch Part: Wall-E and Spy [Audio podcast episode]. In Maintenance Phase. https://www.maintenancephase.com/Horn, S., & Moro, E. (2008, April 7). Wall•E Preview. IGN. https://web.archive.org/web/20080411234805/http://movies.ign.com/articles/865/865021p4.htmlHuxley, T. (2008, November 13). Q&A With WALL•E's Ben Burtt. Pixar Planet. https://pixarplanet.com/blog/qa-with-walles-ben-burtt/Justin Wright. (n.d.). Wikipedia. Retrieved April 13, 2025, from https://en.wikipedia.org/wiki/Justin_WrightKorfiatis, K., Photiou, M., & Petrou, S. (2020). Effects of ecoanimations on nine and twelve year old children's environmental conceptions: How WALL-E changed young spectators' views of earth and environmental protection. The Journal of Environmental Education, 51(5), 381-394. DOI: 10.1080/00958964.2020.1747965 Lloyd, A. (2023, December 1). Counteracting Bone and Muscle Loss in Microgravity. NASA. https://www.nasa.gov/humans-in-space/counteracting-bone-and-muscle-loss-in-microgravity/Mattie, S. (2014). WALL-E on the problem of technology. Perspectives on Political Science, 43(1), 12-20. DOI: 10.1080/10457097.2013.784576Murray, R.L., & Heumann, J.K. (2011). That's all folks? Ecocritical readings of American animated features. University of Nebraska Press. Ness, M. (2017, September 28). Robots in Love: WALL-E. Reactor. https://reactormag.com/robots-in-love-wall-e/Pixar. (2016a, October 16). Robo-Everything | WALL•E | Disney•Pixar. YouTube. https://www.youtube.com/watch?v=gqquKFkH-iI&list=PLLhVNqe2jAb8X9ocSkynckJmcP5y0B4Vc&index=9Pixar. (2016b, October 19). Captain's Log | WALL•E | Disney•Pixar. YouTube. https://www.youtube.com/watch?v=PRUoIOkp9AU&list=PLLhVNqe2jAb8X9ocSkynckJmcP5y0B4Vc&index=5Pixar. (2016c, October 19). Live Action | WALL•E | Disney•Pixar. YouTube. https://www.youtube.com/watch?v=FQh4z-j0ScI&list=PLLhVNqe2jAb8X9ocSkynckJmcP5y0B4Vc&index=15Pixar. (2016d, October 19). Trash Planet | WALL•E | Disney•Pixar. YouTube. https://www.youtube.com/watch?v=UmnSYmqpIEY&list=PLLhVNqe2jAb8X9ocSkynckJmcP5y0B4Vc&index=14Pixar. (2016e, October 19). WALL•E and EVE | WALL•E | Disney•Pixar. YouTube. https://www.youtube.com/watch?v=m-AYOhIYZlQ&list=PLLhVNqe2jAb8X9ocSkynckJmcP5y0B4Vc&index=12Potokar, S. (2017, March 8). Wall-E Animation Foley and Sound Design. YouTube. https://www.youtube.com/watch?v=0IPxIvbc_csPrice, D. A. (2009). The Pixar Touch: The Making of a Company. Knopf Doubleday Publishing Group.Recording Academy. (2025). 51st Annual GRAMMY Awards. GRAMMY.com. https://www.grammy.com/awards/51st-annual-grammy-awardsRoberts, S. (2008). Andrew Stanton Interview, Wall-E. Movies Online. https://web.archive.org/web/20080626061223/http://www.moviesonline.ca/movienews_14899.htmlRobinson, T. (2008, June 26). Andrew Stanton. A.V. Club. https://web.archive.org/web/20080908045321/http://www.avclub.com/content/interview/andrew_stantonStanton, A. (Director). (2008). WALL-E [Film]. Pixar Animation Studios.Suellentrop, C. (2008, June 30). Another Brick in the ‘WALL-E'. The New York Times. https://archive.nytimes.com/opinionator.blogs.nytimes.com/2008/06/30/another-brick-in-the-wall-e/Tranter, P., & Sharpe, S. (2012). Disney-Pixar to the rescue: Harnessing positive affect for enhancing children's active mobility. Journal of Transport Geography, 20, 34-40. DOI: 10.1016/j.jtrangeo.2011.04.006van Oosterwijk, I., & McCarthy, W. (2023). Once upon a dystopian time: The portrayal and perception of environmentalism in Pixar's Finding Nemo and WALL-E. Quarterly Review of Film and Video, 40(7), 848-873. DOI: 10.1080/10509208.2022.2049181 WALL-E. (n.d.). Wikipedia. https://en.wikipedia.org/wiki/WALL-EWALL-E. (n.d.). Box Office Mojo. https://www.boxofficemojo.com/release/rl3615065601/Willman, C. (2008, July 14). 'WALL-E': How he found 'Hello, Dolly!' Entertainment Weekly. https://ew.com/article/2008/07/14/wall-e-how-he-found-hello-dolly/Yates, M. (2015). Labor as “nature,” nature as labor. Interdisciplinary Studies in Literature and Environment, 22(3), 525-543.

This week we move into the arena of preventive cardiology when we review a recent report from the team at Northwestern and Princeton on the impact of early childhood food insecurity on cardiovascular health of people in young adulthood. How does food insecurity in young childhood impact the cardiac health of adults? Why is most of the impact seen on BMI but not other measures of cardiovascular health. How can food programs that support improved food and nutrition security work to improve long term cardiovascular health of children and adults? Do the benefits of such programs outweight their costs? Dr. Nilay Shah of Northwestern University shares his deep insights into his work and these questions this week.DOI: 10.1001/jamacardio.2025.1062

Tetanus has probably been around for most of human history, or even longer. But it’s preventable today thanks to vaccines. Research: "Emil von Behring." Notable Scientists from 1900 to the Present, edited by Brigham Narins, Gale, 2008. Gale In Context: Science, link.gale.com/apps/doc/K1619001490/GPS?u=mlin_n_melpub&sid=bookmark-GPS&xid=464250e5. Accessed 17 Apr. 2025. Breasted, J.H., translator. “OIP 3. The Edwin Smith Surgical Papyrus, Volume 1: Hieroglyphic Transliteration, Translation, and Commentary.” Oxford University Press. 1930. Chalian, William. “An Essay on the History of Lockjaw.” Bulletin of the History of Medicine, FEBRUARY, 1940, Vol. 8, No. 2. Via JSTOR. https://www.jstor.org/stable/44446242 Emil von Behring: The founder of serum therapy. NobelPrize.org. Nobel Prize Outreach 2025. Thu. 17 Apr 2025. https://www.nobelprize.org/prizes/medicine/1901/behring/article/ Galassi, Francesco Maria et al. “Tetanus: historical and palaeopathological aspects considering its current health impact.” Journal of preventive medicine and hygiene vol. 65,4 E580-E585. 31 Jan. 2025, doi:10.15167/2421-4248/jpmh2024.65.4.3376 George, Elizabeth K. “Tetanus (Clostridium tetani Infection).” StatPearls. January 2025. https://www.ncbi.nlm.nih.gov/books/NBK482484/ Hippocrates. “VI. Diseases, Internal Affections.” Harvard University Press. 1988. Jean-Marc Cavaillon, Historical links between toxinology and immunology, Pathogens and Disease, Volume 76, Issue 3, April 2018, fty019, https://doi.org/10.1093/femspd/fty019 Jones CE, Yusuf N, Ahmed B, Kassogue M, Wasley A, Kanu FA. Progress Toward Achieving and Sustaining Maternal and Neonatal Tetanus Elimination — Worldwide, 2000–2022. MMWR Morb Mortal Wkly Rep 2024;73:614–621. DOI: http://dx.doi.org/10.15585/mmwr.mm7328a1 Kaufmann, Stefan H E. “Remembering Emil von Behring: from Tetanus Treatment to Antibody Cooperation with Phagocytes.” mBio vol. 8,1 e00117-17. 28 Feb. 2017, doi:10.1128/mBio.00117-17 Kreston, Rebecca. “Tetanus, the Grinning Death.” Discover. 9/29/2015. https://www.discovermagazine.com/health/tetanus-the-grinning-death Milto, Lori De, and Leslie Mertz, PhD. "Tetanus." The Gale Encyclopedia of Public Health, edited by Brigham Narins, 2nd ed., vol. 2, Gale, 2020, pp. 1074-1076. Gale In Context: Environmental Studies, link.gale.com/apps/doc/CX7947900274/GPS?u=mlin_n_melpub&sid=bookmark-GPS&xid=a44bc544. Accessed 14 Apr. 2025. Milto, Lori De, and Leslie Mertz, PhD. "Tetanus." The Gale Encyclopedia of Public Health, edited by Brigham Narins, 2nd ed., vol. 2, Gale, 2020, pp. 1074-1076. Gale In Context: Environmental Studies, link.gale.com/apps/doc/CX7947900274/GPS?u=mlin_n_melpub&sid=bookmark-GPS&xid=a44bc544. Accessed 15 Apr. 2025. National Institutes of Health. “Tetanus.” https://history.nih.gov/display/history/Tetanus Ni, Maoshing. “The Yellow Emperor's Classic of Medicine: A New Translation of the Neijing Suwen with Commentary.” Shambhala. 1995. Smithsonian. “The Antibody Initiative: Battling Tetanus.” https://www.si.edu/spotlight/antibody-initiative/battling-tetanus Sundwall, John. “Man and Microbes.” Illustrated lecture given under the auspices of the Kansas Academy of Science, Topeka, January 12, 1917. https://archive.org/details/jstor-3624335/ The Nobel Prize in Physiology or Medicine 1901. NobelPrize.org. Nobel Prize Outreach 2025. Thu. 17 Apr 2025. https://www.nobelprize.org/prizes/medicine/1901/summary/ Tiwari, Tejpratap S.P. et al. “Chapter 21: Tetanus.” CDC Pink Book. https://www.cdc.gov/pinkbook/hcp/table-of-contents/chapter-21-tetanus.html Von Behring, Emil and Kitasato Shibasaburo. “The Mechanism of Immunity in Animals to Diphtheria and Tetanus.” Immunology. 1890. http://raolab.org/upfile/file/20200612164743_201234_56288.pdf War Office Committee for the Study of Tetanus. “Memorandum on Tetanus.” Fourth Edition. 1919. https://archive.org/details/b32171201/ World Health Organization. “Tetanus.” 7/12/2024. https://www.who.int/news-room/fact-sheets/detail/tetanus See omnystudio.com/listener for privacy information.

Thomas J. Dorsey liberated himself from enslavement and became one of the most sought-after caterers in Philadelphia. His son William Henry Dorsey was born a free Black man before the Civil War, and became an artist, collector and scrapbooker. Research: "Thomas J. Dorsey." Contemporary Black Biography, vol. 90, Gale, 2011. Gale In Context: U.S. History, link.gale.com/apps/doc/K1606005269/GPS?u=mlin_n_melpub&sid=bookmark-GPS&xid=0c6af117. Accessed 2 Apr. 2025. 1838 Black Metropolis. “What Resistance looked like in 1838.” https://www.1838blackmetropolis.com/post/what-resistance-looked-like-in-1838 Aston Gonzalez (2019) William Dorsey and the construction of an African American history archive, Social Dynamics, 45:1, 138-155, DOI: 10.1080/02533952.2019.1589323 Berlin, Ira. "UNIVERSITY PRESSES; Scrapbooks of a Black Heritage." The New York Times Book Review, 22 Sept. 1991. Gale General OneFile, link.gale.com/apps/doc/A175323797/GPS?u=mlin_n_melpub&sid=bookmark-GPS&xid=cdf57532. Accessed 2 Apr. 2025. Cashin, Sheryll. “The Agitator's Daughter: A Memoir of Four Generations of One Extraordinary African-American Family.” Public Affairs. 2008. Conrad, Sharron Wilkins. “Nineteenth-Century Philadelphia Caterer Thomas J. Dorsey.” American Visions. August/September 2000. Cromwell, J.W.C. “An Art Gallery and Museum, Not In the Guide Book.” New National Era, Washington D.C. 10/1/1874. https://www.loc.gov/resource/sn84026753/1874-10-01/ed-1/?sp=2&st=text&r=0.437,-0.008,0.25,0.231,0 Du Bois, W. E. B. “The Philadelphia Negro; A Social Study.” Philadelphia, Published for the University. 1899. https://archive.org/details/philadelphianegr00dubo/ Franqui, Leah. “Cultural Histories: Philadelphia’s Black Culinary Trailblazers and the Birth of Catering.” Solo Real Estate. https://www.solorealty.com/blog/cultural-histories-philadelphias-black-culinary-trailblazers-and-the-birth-of-catering/ Greenlee, Cynthia. “A Priceless Archive of Ordinary Life.” The Atlantic. 2/9/2021. https://www.theatlantic.com/culture/archive/2021/02/race-save-black-history-archives/617932/ Howard, Sherry. “Connecting with a 19th-century Black history & art collector.” Auction Finds. https://myauctionfinds.com/2021/04/01/connecting-with-a-19th-century-black-history-art-collector/ Lane, Roger. “Willam Dorsey’s Philadelphia and Ours.” Oxford University Press. 1991. “Seen and Heard in Many Places.” The Philadelphia Times. 10/19/1896. “Seen And Heard in Many Places.” The Philadelphia Times. 10/17/1896. Morehouse College. “Honoring a Forgotten Past: An Author’s Journey.” 2/15/2021. https://news.morehouse.edu/morehouse-faculty/honoring-a-forgotten-past-an-authors-journey Solomon, Tessa. “How Two African American Collectors Celebrated Black Artistry Amid the Civil War.” ArtNews. 4/7/2021. https://www.artnews.com/feature/who-are-william-henry-dorsey-edward-thomas-19th-century-collectors-1234587386/ Still, William. “The underground rail road. A record of facts, authentic narratives, letters, &c., narrating the hardships, hair-breadth escapes, and death struggles of the slaves in their efforts for freedom, as related by themselves and others, or witnessed by the author; together with sketches of some of the largest stockholders, and most liberal aiders and advisers, of the road.” Philadelphia, Porter & Coates. 1872. https://archive.org/details/undergroundrailr00stil Strimer, Steve. "Dorsey, Basil." Oxford African American Studies Center. May 31, 2013. Oxford University Press. Date of access 2 Apr. 2025, https://oxfordaasc-com.proxy.bostonathenaeum.org/view/10.1093/acref/9780195301731.001.0001/acref-9780195301731-e-38488 TerBush, James and Barbara Dreyfuss. “A Cape May Connection.” Cape May Magazine. Mid-summer 2021. https://www.capemaymag.com/feature/a-cape-may-connection/ The Evening Telegraph. “Caterers and Restaurateurs.” 3/30/1867. https://www.newspapers.com/image/78649823/ The Manuscript Society. “William Henry Dorsey: Preserving Black History.” 2/16/2021. https://manuscript.org/2021/02/william-henry-dorsey-preserviing-19th-century-life/ The Philadelphia Inquirer. 2/23/1875. Page 5. https://www.newspapers.com/image/168293006/ The Philadelphia Times. “William H. Dorsey’s African Museum.” 10/25/1896. https://www.newspapers.com/image/52857231/ See omnystudio.com/listener for privacy information.