Pancreatic cancer is one of the deadliest malignancies, with survival rates remaining dismally low despite major advances in oncology. One of the key reasons lies in the disease's unique fibrotic microenvironment-a dense, collagen-rich tissue that acts as a physical and biochemical barrier, preventing drugs from reaching tumor cells effectively. Their study, published online on October 31, 2025, in the journal Small, highlights a new therapeutic approach to enhance drug effectiveness by dismantling fibrotic resistance mechanisms. The research was spearheaded by Ms. Mayu Ohira and Ms. Moe Kitamura, co-first authors from Okayama University, and carried out in close collaboration with Professor Atsushi Masamune of Tohoku University and Professor Mitsunobu R. Kano of Okayama University. Together, the team investigated how collagen-long considered merely a structural barrier-also acts as a signaling molecule that directly influences fibrosis and drug penetration. "Our findings reveal that collagen signaling, not just its physical density, plays a crucial role in hindering drug delivery," explained Dr. Tanaka, a co-author from Okayama University, Japan. "By inhibiting DDR1, we can interrupt this signaling cascade, loosen the fibrotic barrier, and enable better access for therapeutic agents." The study also uncovered an unexpected twist: MEK inhibitors, a class of drugs previously tested in pancreatic cancer, were found to increase collagen I expression, intensifying the fibrotic barrier and reducing treatment efficacy. This newly identified phenomenon, termed 'therapy-induced exacerbation of the fibrotic barrier,' may explain why some MEK inhibitor-based therapies have failed in clinical trials. We found that while MEK inhibitors can attack cancer cells, they also unintentionally strengthen the fibrotic barrier, making drug penetration even more difficult. Recognizing and countering this effect could fundamentally change how combination therapies are designed for pancreatic cancer." Dr. Hiroyoshi Y. Tanaka, Assistant Professor, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University The researchers emphasized the broader significance of their discovery, noting that a better mechanistic understanding of collagen signaling in fibrosis could lead to new therapeutic strategies across oncology. Looking forward, the team plans to establish combination treatments that simultaneously target tumor cells and their fibrotic surroundings. Beyond pancreatic cancer, the implications of this study extend to other fibrotic diseases where collagen accumulation limits drug access. By redefining collagen's role as both a structural and signaling component, the researchers believe their work could inform the development of more effective treatments for fibrotic conditions. As pancreatic cancer continues to pose one of the most formidable challenges in modern oncology, this collaborative study offers new hope, illuminating how rethinking fibrosis might finally help life-saving drugs reach their targets. Collagen Signaling via DDR1 Exacerbates Barriers to Macromolecular Drug Delivery in a 3D Model of Pancreatic Cancer Fibrosis. Discover how real-time cell density monitoring boosts yield, lowers media costs, and improves viability in bioprocessing. Discover how electron microscopy advances plant and microbial research with expert insights from the John Innes Centre's bioimaging facility. Discover how Abselion's Amperia™ platform delivers fast, reproducible His-tagged protein quantification with minimal prep, even from crude lysates. News-Medical.Net provides this medical information service in accordance with these terms and conditions. Please note that medical information found on this website is designed to support, not to replace the relationship between patient and physician/doctor and the medical advice they may provide. Hi, I'm Azthena, you can trust me to find commercial scientific answers from News-Medical.net. Registered members can chat with Azthena, request quotations, download pdf's, brochures and subscribe to our related newsletter content. A few things you need to know before we start. While we only use edited and approved content for Azthena answers, it may on occasions provide incorrect responses. Please confirm any data provided with the related suppliers or authors. Please do not ask questions that use sensitive or confidential information.

New research sheds light on how this visceral obesity can result in cardiac damage in different ways from general obesity measured by BMI — an important consideration for clinicians, study authors said. This observation was more pronounced in men than in women, according to the research, recently presented at the Radiological Society of North America annual meeting. Despite the high prevalence of obesity in the industrialized world, it is still unknown whether obesity has independent effects on cardiac remodeling, said Erley, a radiology resident at the University Medical Center Hamburg-Eppendorf in Hamburg, Germany. “We know from many body composition studies nowadays that visceral fat has totally different effects on other organ functions than subcutaneous fat,” Erley said. “That is why we took a look into investigating the effect of general and also visceral obesity on cardiac morphology and function in this German-based population study.” The researchers performed 3T cardiovascular MRI and excluded patients with known cardiac diseases. Based on waist-to-hip ratio, the researchers deemed 80% of patients obese (waist-to-hip ratio, ≥ 0.85 in women and ≥ 0.90 in men) compared with 20% who they considered obese according to BMI ≥ 30. Furthermore, the researchers found that with every 0.1 increase in the waist-to-hip ratio, RV end-diastolic volume decreased by 4.5 mL (P = .024) and RV stroke volume decreased by 2.9 mL (P = .033), an association weaker in women than in men. The study's results are relevant to both patients and specialists performing cardiac imaging, Erley said. “Patients should be aware that a high waist-to-hip ratio appears ‘more dangerous' than a high BMI regarding potential effects on the heart,” she said. “Medical specialists should take into account the waist-to-hip ratio and not only BMI when assessing a patient's nutritional status. Imaging specialists should be aware that concentric remodeling patterns in cardiac MRI might be attributed to visceral obesity (we currently primarily think of other diseases like hypertensive heart disease).” Kelle agreed that measuring the waist-to-hip ratio will be important going forward. Visceral obesity metrics should always be part of cardiovascular risk assessment because visceral adiposity is metabolically active and strongly linked to cardiometabolic risk, he said. “Relying solely on BMI may miss individuals at risk for concentric cardiac remodeling,” he said. “In addition, cardiac evaluation of obesity should be sex-specific. Brian Ellis is a freelance writer and editor who lives in Southwest Virginia.

A combination of missed prevention opportunities and health inequalities can result in the early deaths of people living with epilepsy and intellectual disabilities, a study has shown. However, until now there has been no national-level population-based evidence on the risks and protective factors specifically contributing to epilepsy-related deaths in people with intellectual disability. This new research aims to fill that gap, with its analysis of nearly 10,000 deaths between 2016 and 2021 constituting the largest global study examining epilepsy-related mortality in adults with intellectual disabilities and epilepsy. It found epilepsy was the primary cause of death in just over 16% of those people, and that they died at a significantly younger average age – 56 compared to 62 – than those who had issues other than epilepsy listed as the primary cause of death in their health records. The study particularly highlights significant disparities in epilepsy-related mortality based on ethnicity, with African and Asian individuals dying younger – at an average age of just 36 – than their White British counterparts. All of this, the authors say, is despite the fact targeted interventions – including annual health checks, multidisciplinary care access, and specialist psychiatric and speech and language therapy support – do exist but are rarely administered in a uniform manner. The paper showcases these interventions as being effective at increasing a person's length of life. Writing in the Journal of Neurology, Neurosurgery, and Psychiatry, the study's authors say poor quality of care, service gaps and the lack of annual health checks should be considered unacceptable in modern healthcare. As such, they have called for a systemic service redesign to try and prevent avoidable epilepsy-related deaths among people with intellectual disabilities in the future. Professor Rohit Shankar MBE, Professor of Neuropsychiatry at the University of Plymouth and Director of its Cornwall Intellectual Disability Equitable Research (CIDER) unit, said: "Among neurological conditions, epilepsy is the biggest killer apart from stroke. Our study shows that among people who also have an intellectual disability, it poses a greater threat of them dying younger with those from ethnic minorities living in the UK being even more at risk. What is arguably even more shocking is that there are strategies including psychiatric support to speech and language therapy out there to help people. It is wholly unacceptable that these are not routinely and systematically used in a proactive manner everywhere in England, particularly when we're talking about people who are extremely vulnerable and often have difficulties in communicating their needs or concerns. Professor William Henley, Professor of Medical Statistics at the University of Exeter Medical School, said: "We hope our stark and shocking findings will act as a rallying cry to make a difference for families affected by epilepsy and learning disability. The research was based on data collected through the Learning from Lives and Deaths Review Programme (LeDeR), which focuses on learning from the lives and deaths of people with learning disabilities and autistic people, using reviews to improve local services. She added: "I am pleased that the LeDeR data is still being used effectively to highlight areas of disparity in deaths of people with intellectual disability, and to indicate where policy and practice needs to be strengthened. It is of significant concern that epilepsy-related deaths are associated with a poorer quality of care and gaps in service provision when compared to non-epilepsy related deaths – issues which need addressing at individual and systemic levels." The study's authors have been working for several years with charities and other healthcare organisations who support people affected by epilepsy and learning disabilities. The Clive Treacey checklist was named in honour of a man who died aged 47 having been kept in a psychiatric unit without having his health needs fully addressed. Clive's sister, Elaine Clarke, said of the new findings: "It's deeply shocking to see that there are so many people with a learning disability who, just like my brother Clive, continue to die avoidable deaths because they do not receive the epilepsy care and treatment that they should. If these terrible statistics belonged to almost any other part of society there would be public outrage – but the harsh reality is that people like my brother Clive, are not valued or prioritised." The findings have also been welcomed by UK-based charities, who said the research reinforces their ongoing calls for a complete overhaul of NHS care for people with epilepsy and intellectual disabilities. Today there is a stark lottery between the local NHS areas that are working with the charity to adopt the free SUDEP and Seizure Safety Checklist and areas that are still operating in ignorance that epilepsy is a cliff-edge condition that requires advocacy and risk management." Alison Fuller from Epilepsy Action said: "This research lays bare the shocking inequalities faced by people with epilepsy and a learning disability. It clearly shows that they are dying far too young and acts as a stark reminder that this group remains among the most at-risk group in our health system. Even more concerning is the finding that people from African and Asian backgrounds face an even greater risk of dying prematurely, exposing deep-rooted and persistent inequalities. With annual health checks, access to the right professionals and truly joined up person centred care plans, lives can be saved, but too often support is either inconsistent or unavailable. Kate Chate, Family Member Election Representative Co Chair for Learning Disability England, added: "It is so encouraging to see research being done into the causes of early and preventable deaths of people with learning disabilities. As a family member this kind of research that brings data to advocate for better services for people with Learning Disabilities is more than just welcome, it is very gratefully applauded." Discover how real-time cell density monitoring boosts yield, lowers media costs, and improves viability in bioprocessing. Discover how electron microscopy advances plant and microbial research with expert insights from the John Innes Centre's bioimaging facility. Discover how Abselion's Amperia™ platform delivers fast, reproducible His-tagged protein quantification with minimal prep, even from crude lysates. News-Medical.Net provides this medical information service in accordance with these terms and conditions. Please note that medical information found on this website is designed to support, not to replace the relationship between patient and physician/doctor and the medical advice they may provide. Hi, I'm Azthena, you can trust me to find commercial scientific answers from News-Medical.net. Registered members can chat with Azthena, request quotations, download pdf's, brochures and subscribe to our related newsletter content. A few things you need to know before we start. While we only use edited and approved content for Azthena answers, it may on occasions provide incorrect responses. Please confirm any data provided with the related suppliers or authors. Your questions, but not your email details will be shared with OpenAI and retained for 30 days in accordance with their privacy principles. Please do not ask questions that use sensitive or confidential information.

A project collaboratively funded by SwRI and Trinity will address both the initial lack of blood (ischemia) and the rush of blood that follows treatment (reperfusion) referred to as ischemia/reperfusion injury (IRI). "The moment oxygen comes flooding back into your cells during reperfusion, the surrounding tissue is inundated with reactive oxygen species, such as hydroxyl radicals and hydrogen peroxide. That oxidative stress can cause permanent cellular and tissue damage," said Dr. Christina Cooley, associate professor with the Department of Chemistry at Trinity University. SwRI will work with Trinity to iterate and synthesize a new borinic acid prodrug to prevent IRI using precursors developed at Trinity. "Protein misfolding during cellular stress is a key driver of tissue damage in IRI, so the new prodrug will target that," said Dr. Christopher Dorsey, a senior research scientist at SwRI who will use his pharmaceutical expertise to synthesize the new borinic formulation. That's the exciting part of this collaboration, the opportunity to give back and pass along what we learn to a team of future scientists." After the prodrug is synthesized, Cooley will work with Trinity students to conduct stability testing and other lab evaluations to gather the foundational data needed for future live studies and clinical trials. This project was funded through the inaugural Trinity-SwRI Research Collaboration Grant Program established in 2025 to encourage the advancement of medical and biomedical research through collaboration. Trinity University and SwRI contributed $250,000 toward three unique biomedical research projects this year. "Trinity University is thrilled to be collaborating with SwRI, and we look forward to exciting results from this collaboration," said Dr. David Ribble, dean of the D. R. Semmes School of Science. Dr. Joe McDonough, vice president of the Chemistry and Chemical Engineering Division, SwRI Discover how real-time cell density monitoring boosts yield, lowers media costs, and improves viability in bioprocessing. Discover how electron microscopy advances plant and microbial research with expert insights from the John Innes Centre's bioimaging facility. Discover how Abselion's Amperia™ platform delivers fast, reproducible His-tagged protein quantification with minimal prep, even from crude lysates. News-Medical.Net provides this medical information service in accordance with these terms and conditions. Please note that medical information found on this website is designed to support, not to replace the relationship between patient and physician/doctor and the medical advice they may provide. Hi, I'm Azthena, you can trust me to find commercial scientific answers from News-Medical.net. Registered members can chat with Azthena, request quotations, download pdf's, brochures and subscribe to our related newsletter content. A few things you need to know before we start. While we only use edited and approved content for Azthena answers, it may on occasions provide incorrect responses. Please confirm any data provided with the related suppliers or authors. Your questions, but not your email details will be shared with OpenAI and retained for 30 days in accordance with their privacy principles. Please do not ask questions that use sensitive or confidential information.

For millions suffering from long COVID, their persistent breathlessness, brain fog and fatigue remain a maddening mystery, but a group of leading microbiologists think they may have cracked the case. The culprit for some long COVID cases, they suggest, might be other infections that accompany SARS-CoV-2. A review published in eLife by 17 experts, including those from Rutgers Health, argues that co-infections acquired before or during COVID could cause symptoms to persist indefinitely for many people. "This is an aspect of long COVID that is not talked about a lot," said Maria Laura Gennaro, a microbiologist at the Rutgers New Jersey Medical School who chaired the Microbiology Task Force for the National Institutes of Health's Researching COVID to Enhance Recovery initiative, a large-scale study of long COVID. Long COVID symptoms, which have affected up to 400 million people worldwide, range from mild impairment to severe disability, striking the brain, heart, lungs and digestive system. Yet no proven treatments exist because the underlying causes remain unknown. The new review synthesizes existing research and expert judgment to make a case that has received little attention: Infections beyond the coronavirus may be critical players. About 95% of adults carry latent EBV, typically without symptoms until an immune disruption such as COVID awakens the dormant virus. Later research linked EBV reactivation to long COVID hallmarks such as fatigue and cognitive problems. About one-quarter of the world's population carries latent TB. Evidence suggests COVID can deplete the immune cells that normally keep TB in check, potentially triggering reactivation. The relationship runs both ways: TB infection also may worsen COVID outcomes. Infections before COVID could leave the immune system compromised. The authors noted that 44 nations have experienced tenfold increases in at least 13 infectious diseases compared with pre-pandemic levels. One explanation they cite, called "immunity theft," describes heightened vulnerability to other infections following acute COVID. If co-infections contribute to long COVID, existing drugs might help. Antibiotics and antivirals could potentially be repurposed to target underlying infections. Clinical trials could test whether treating specific co-infections relieves symptoms. The associations they discuss are biologically plausible but remain speculative. No one has established a causal link between any co-infection and long COVID. She said proving the hypothesis would require large epidemiological studies and animal experiments, which is complicated by the absence of good animal models for long COVID. The researchers hope their work will open new lines of investigation. For the millions living with long COVID, the review offers no immediate answers, but its authors suggest that effective treatment may require looking beyond COVID itself. Discover how real-time cell density monitoring boosts yield, lowers media costs, and improves viability in bioprocessing. Discover how electron microscopy advances plant and microbial research with expert insights from the John Innes Centre's bioimaging facility. Discover how Abselion's Amperia™ platform delivers fast, reproducible His-tagged protein quantification with minimal prep, even from crude lysates. News-Medical.Net provides this medical information service in accordance with these terms and conditions. Please note that medical information found on this website is designed to support, not to replace the relationship between patient and physician/doctor and the medical advice they may provide. Hi, I'm Azthena, you can trust me to find commercial scientific answers from News-Medical.net. Registered members can chat with Azthena, request quotations, download pdf's, brochures and subscribe to our related newsletter content. A few things you need to know before we start. While we only use edited and approved content for Azthena answers, it may on occasions provide incorrect responses. Please confirm any data provided with the related suppliers or authors. Your questions, but not your email details will be shared with OpenAI and retained for 30 days in accordance with their privacy principles. Please do not ask questions that use sensitive or confidential information.