🥰😍WOMEN ON A MISSION TO CURE ARTHERITIS WOW! Stanford Medicine researchers led by Dr. Helen Blau and Dr. Nidhi Bhutani have identified a method to reverse cartilage loss in arthritis by targeting a protein called a "gerozyme". Their 2025 research suggests that blocking this protein can regenerate cartilage in both mouse and human tissues. Recent breakthroughs by researchers, particularly at Stanford Medicine and in studies from Australia, have shown that inhibiting specific "gerozyme" proteins can reverse cartilage loss and regenerate joint tissue in mice and human tissue. These findings, including new injectable cell therapies and "smart gels," offer potential for reversing osteoarthritis, rather than just managing symptoms, with human trials for some methods either planned or underway. https://lnkd.in/eet9PPqS
Stanford Researchers Reverse Cartilage Loss in Arthritis with Gerozyme Inhibitor
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Researchers at KAIST (Korea Advanced Institute of Science and Technology) have developed an experimental therapy that can regenerate damaged retinal nerves, something previously thought impossible in mammals. By targeting a protein called PROX1, which normally suppresses retinal cell regeneration, the therapy removes a biological “brake” and restarts the eye’s natural repair mechanisms. The treatment leverages Müller glia, specialized retinal support cells that can transform into neurons. While these cells remain largely dormant in mammals, blocking PROX1 reactivates their regenerative potential, allowing damaged retinal neurons to regrow. In laboratory mice, this approach restored vision, and the improvements persisted for more than six months marking the first long-term retinal nerve regeneration in mammals. Developed by Celliaz Inc., the therapy is expected to enter human clinical trials around 2028. If successful, it could transform treatment for degenerative eye conditions such as Retinitis Pigmentosa, offering millions of people the unprecedented possibility of restoring lost vision. Source/Credit: KAIST (Korea Advanced Institute of Science and Technology)
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Science fiction has leapt into reality as researchers have successfully grown a fully functional human kidney in the laboratory. This lab-grown kidney is capable of filtering human blood and producing urine, demonstrating a remarkable milestone in regenerative medicine and organ transplantation. The breakthrough could one day solve the global shortage of donor organs and transform how kidney disease is treated. Using advanced tissue engineering and stem cell technologies, scientists were able to replicate the intricate structure and complex functions of a natural human kidney. The lab-grown organ not only mimics normal kidney function but also shows the potential for integration into a human body, paving the way for future clinical applications. This achievement marks a historic turning point in medical science. As researchers continue refining the process, lab-grown organs may soon become a viable alternative to traditional transplants, offering hope to millions of patients with end-stage kidney disease. The era of bioengineered organs is no longer just imagination—it is rapidly becoming a life-saving reality.
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Few medical breakthroughs feel this close to changing everything. Scientists in Tokyo have reportedly grown a fully functional human kidney using a patient’s own living cells, pushing regenerative medicine closer to a future where damaged organs may be replaced without relying on donor shortages. The significance is enormous because kidneys are among the most needed organs in transplant medicine. By using the patient’s own cells, researchers may reduce the risk of immune rejection, one of the biggest problems in organ transplantation today. Instead of waiting for a donor match, doctors could eventually create personalized replacement tissue designed for the body it will enter. This approach sits at the center of stem cell research, tissue engineering, and personalized medicine. A lab grown kidney that can function like a natural organ could reshape treatment for kidney failure, chronic disease, and long transplant waiting lists. If future trials confirm long term success, this may mark the moment medicine stopped managing organ loss and started rebuilding the human body from within. #technologia #health #research #stemcells #medical
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Researchers at Stanford University School of Medicine have made an exciting discovery that could change how we treat joint pain. - WHAT is the drug called ?? They found that by blocking a specific protein related to aging, called 15-PGDH, they can actually regrow knee cartilage and prevent osteoarthritis. What makes this treatment special is that it does not use stem cells. Instead, it works by "reprogramming" the cartilage cells already in your body to act young again. This is a major breakthrough because it treats the actual cause of the disease rather than just dulling the pain. The best news is that this medicine might come in the form of a simple pill. A version of this drug has already passed early safety tests in humans for treating muscle weakness. Scientists hope that this new approach will eventually mean people no longer need to have difficult joint replacement surgeries. This could help millions of people stay active and move without pain as they get older. ANYONE got more on this …..?
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The accumulation of lipofuscin, a fatty material, on the macula — the small part of the retina needed for sharp, central vision is directly linked to retinal pigment epithelium cell death, causing progressive, irreversible vision loss. Technologies developed by two Weill Cornell Medicine innovators could improve the quality of life for patients with retinal diseases by restoring their vision. Dr. Marcelo Mario Nociari, assistant professor of immunology in ophthalmology at Weill Cornell Medicine, collaborated with Dr. Daniel Pelaez from University of Miami to identify small molecules that could protect against cell death caused by lipofuscin toxicity as a potential therapy for Stargardt disease, a rare genetic eye disease with no FDA-approved treatment, and age-related degeneration of the retina. Dr. Sheila Nirenberg, the Nanette Laitman Professor in Neurology and Neuroscience and a professor of systems and computational biomedicine at Weill Cornell Medicine, has created an award-winning prosthetic retina to enable patients with low vision to see. Her system pairs gene therapy that makes surviving retinal cells light-sensitive with a tiny camera-equipped chip in visor-like glasses that translates visual input into the retina’s code. This technology is currently in development by Weill Cornell startup Bionic Sight for a variety of retinal diseases. #LowVisionAwarenessMonth #RareDiseaseDay
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🔬 The Nucleate Artery: New Ways to Restore Function in Tissues and Nerves 📰 In our latest issue of The Nucleate Artery, we explore how researchers are uncovering the hidden drivers of tissue damage and degeneration, as well as the molecular mechanism that could open doors to new treatments: 💧 Cancer treatment can beat the tumour but leave behind lasting damage. National University of Singapore researchers found that cholesterol buildup in lymphatic tissue may be quietly driving lymphoedema, pointing to a new potential therapeutic target. ⚡ What if the key to slowing ALS lies not in the nerve cells themselves, but in their ability to generate energy? A*STAR Institute of Molecular and Cell Biology (A*STAR IMCB) scientists identified a single protein disrupting the cellular power supply of motor neurons and demonstrated how switching it off could extend survival and restore movement in preclinical models. 🔓 Why the most aggressive pancreatic cancers actively lock their cells into an immature state, and how Duke-NUS Medical School researchers found a molecular key that could reverse this process, making tumours more vulnerable to chemotherapy. Plus, stay updated on the latest biotech news, seminars, networking events and more. Read the full issue here! 👉 https://lnkd.in/gJ_kmek6 Newsletter team: Senuri De Silva, Devika Menon, Jiaqi Liang Nucleate Team: Ying Tong Yeo, Jessie Wong Ling Ai, PhD, John Joson Ng, Aakash Kumar, Hana Maldivita Tambrin, PhD, Dillon Chew, Diya Srivastava, Dijin Zhang, Faith Cheong, Shuxuan Lao, Vasilina Gedzun, Shamieraah J., Chermaine Tan, Arnab Ray, Jose M. Guijarro Nuez, Mei Jia T., Alefiya Dohadwala, Chi Dam, Chelsia Goh 呉翊湞 #NucleateSingapore #NucleateArtery
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Neutrophils Don't Always Die after NETosis! That assumption may be incomplete. During my PhD in Biomedical Engineering at the University of Illinois Chicago, I studied anuclear neutrophils (PMN cytoplasts) generated during vital NETosis in acute lung injury. What we found challenges conventional dogma: · These cytoplasts (PMNcyto) presist in vivo. · They retain antimicrobial and migratory capacity · Mitochondrial transfer could revitalize and enhance the duration of their host defense functions. In other words: Anucleation is not necessarily the end of neutrophil function. It may represent a metabolically suppressed but recoverable immune state. These PMNcyto are potential cell therapeutics with capacity to tackle multi-drug resistant (MDR) infections. This work bridges: 🧬 Innate Immunology 🔋 Immuneometabolism 🫁 Lung Injury Biology 🧪 Translational Cell Engineering Link to preprint: https://lnkd.in/gH3t_qPV Innate Immune Function of Neutrophil Cytoplasts Generated Post-Vital NETosis Nithish Raj Prasad, Balaji Ganesh, Steven Dudek, Chinnaswamy Tiruppathi, Asrar Malik #Neutrophils #InnateImmunity #Mitochondria #Immunometabolism #ARDS #TranslationalResearch #Preprint #PhDResearch
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Recent research has identified a mechanism that could enable full skin regeneration without scarring by targeting nerve signaling pathways. In mouse models, blocking excessive nerve growth at wound sites—using approaches such as botulinum toxin A—restored the skin’s ability to regenerate diverse cell types, similar to embryonic healing. This discovery suggests that adult skin retains an inherent regenerative potential that is typically suppressed after birth. These findings open new avenues for developing therapies aimed at improving wound healing and minimizing scarring in human patients.
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📢 Publication Update I’m pleased to share our latest research published in the Journal of Nanoparticle Research: “DoE-driven development, characterisation, in-silico ADME, and evaluation of surface functionalized SPIONs for enhanced blood–brain barrier permeability and targeted delivery of S-adenosylmethionine.” 🔗 https://lnkd.in/ebbbFUBG As Co-Principal Investigator, it was a privilege to contribute to this collaborative work focused on advancing nanotechnology-based strategies for brain-targeted drug delivery in Alzheimer’s disease. 🔬 What we explored: Design of Experiments (DoE)–guided optimisation of superparamagnetic iron oxide nanoparticles (SPIONs) Surface functionalisation with citric acid and transferrin to enable receptor-mediated targeting across the blood–brain barrier (BBB) In-silico ADME evaluation supporting the translational potential of S-adenosylmethionine (SAMe) Comprehensive physicochemical, structural, and magnetic characterisation 📊 Key findings: • Optimised nanoparticles with controlled size and stability • High drug loading (~72%) and strong colloidal stability • Confirmed superparamagnetic behaviour (Ms ≈ 52 emu/g) • Transferrin receptor–mediated uptake, enabling targeted brain delivery • Significant cognitive improvement in zebrafish Alzheimer’s models compared with existing formulations.
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