BBSRC’s Post

☑️ Cellular responses to stress --> physiological resilience == epigenetic plasticity /cf/ bivalent promoters/facultative heterochromatin ☑️ Epigenetic control throughout life (how cells control gene activity) --> at the level of both DNA (validated metabolic mechanisms of reversing biological age - the methylation clock) and Histone (as above). ☑️ Immunity, resilience and repair --> autophagic removal of bad cells, mitophagic elimination of bad mitochondria, QC processes activated in stem cell in quiescence allowing now 'unexhausted' stem cells to gently replenish senescent cells in their own time. Slowing things down through Metabolic intervention. The reversal of biological ageing has arrived! The mechanism is obvious. Metabolic Medicine all the way. Quiescence, Autophagy and Mitochondria in overdrive - all achieved through switching from glycolysis into gluconeogenesis/ketosis and exercising like one's life depends on it - exercise in fasted/fast-mimic state. Living the Persistence Hunting Evolutionary Scheme. It's what we do. What we aren't designed to do is get RSI in a darkened cubicle using a pipette which transfers liquid from one tube into another and then back again. Hmmmm.... ... a one line description of today's electroporation experiment.

PhD throwback on evolution in the lab! After exposing populations of fruit flies to a pathogen for 15 generations, I discovered that the populations exposed to the pathogen had developed resistance. Surprisingly, the resistance was primarily developed in the female flies, not the males. Unfortunately, the experiment was interrupted due to pandemic lockdowns, resulting in the loss of the evolved populations after two years! This research raises important questions about how immunity mechanisms might be distinct in males and females. How might this research benefit us? Some of my other work has revealed that males and females share some immune response mechanisms but also have distinct ones. In many cases, the same gene can have opposing effects on immunity in males and females. Understanding the physiological and genetic mechanisms of immunity in both sexes can help us rethink sex-specific disease treatments, leading to better outcomes for both genders. Melanie Boehi, thanks for the idea of getting my PhD to the public. Ashley Ruba, PhD, Daniel Dilg (photo credits) SNSF Swiss National Science Foundation for funding my research.

DID YOU KNOW: About 10% of people over 65 years old get diagnosed with Alzheimer’s disease, but research shows that for a large family in Antioquia, Colombia, the rate is much higher! Thousands of people in this family developed early-onset Alzheimer’s Disease because of a genetic variant. Those who inherited it started developing dementia at around 49 years old. A new study showed other genetic factors that might influence the age of onset in this family. Using DNA samples from 340 affected individuals, researchers compared their genetic data to other groups with different forms of Alzheimer’s Disease. They found 13 genetic variants linked to differences in when symptoms start. This research opens new paths for understanding the genetic mechanisms of Alzheimer’s & potential treatment strategies. Want to learn more about these genetic discoveries? Check out our Educational Outreach Annual Guidebook! Download now and dive into the world of Alzheimer's research (page 15): https://lnkd.in/gpMj-aNS #research #annual #guidebook #DNA

#SpeakingofScience: What's next on the horizon for #personalizedmedicine? 🔬 According to Nature Portfolio, the intricate world of #generegulation continues to offer unprecedented insights into #cellulardynamics. Led by a team of #scientists at the University of California, San Francisco, this study utilized cutting-edge #biotech to conduct parallel testing of individual cis-regulatory elements at the single-cell level. The results? A trove of #healthdata revealing the intricate orchestration of #gene expression within cells. This research sheds light on fundamental processes underlying development, #disease, and beyond. From understanding cellular differentiation to unraveling the molecular basis of complex diseases, the possibilities for #precisionmedicine are vast! 🚀 #GeneticResearch #Genealogy #MedicalResearch #HealthInnovation #ClincialResearch #Healthcare #MedTech https://lnkd.in/dYPBwUhm

#LifeSciences | 𝗔𝗱𝘃𝗮𝗻𝗰𝗶𝗻𝗴 𝘁𝗵𝗲 𝗨𝗻𝗱𝗲𝗿𝘀𝘁𝗮𝗻𝗱𝗶𝗻𝗴 𝗼𝗳 𝗖𝗲𝗹𝗹𝘂𝗹𝗮𝗿 𝗣𝗿𝗼𝗰𝗲𝘀𝘀𝗲𝘀 𝗳𝗼𝗿 𝗗𝗶𝘀𝗲𝗮𝘀𝗲 𝗧𝗿𝗲𝗮𝘁𝗺𝗲𝗻𝘁 | Researchers Alexandre Leytens, Michael Stumpe, and Jörn Dengjel from the Department of Biology at Université de Fribourg - Universität Freiburg have made a significant breakthrough in cellular biology. Their innovative method accelerates and fine-tunes the evaluation of autophagy, a fundamental cellular process, paving the way for new insights into complex diseases like cancer, Alzheimer's, and diabetes. The breakthrough technique employs advanced mass spectrometry, monitoring the activities of 40 proteins involved in autophagy, and has the amplified potential to improve understanding of various diseases. This heightened precision and speed in evaluating cellular cleaning processes can guide developments for targeted medications and enhanced disease treatments. Backed by a patent, this significant step contributes to our understanding of protein degradation and its potential for disease management. 👉 Learn more >> https://lnkd.in/gby9t-6K 👉 Original publication >> https://lnkd.in/ghgQSfw7 🇨🇭 Follow #ScienceSwitzerland for the latest news and emerging trends on Swiss science, technology, education, and innovation >> www.swissinnovation.org Follow us >> Science-Switzerland #Science | #Education | #Research | #Innovation

Exciting Advancements in ALS Research 🧠, and it's a Canadian study 🇨🇦 Recent studies have brought promising news for those affected by Amyotrophic Lateral Sclerosis (ALS). A groundbreaking discovery has identified a protein interaction that could halt or reverse the progression of ALS. Researchers at Western University found that targeting the interaction between TDP-43 and RGNEF proteins significantly reduces nerve cell damage and improves motor functions in animal models. This breakthrough is a potential game-changer in ALS treatment: "In virtually all ALS patients, a protein called TDP-43 is responsible for forming abnormal clumps within cells, which causes cell death. In recent years, Strong's team discovered a second protein, called RGNEF, with functions that are opposite to TDP-43. The team's latest breakthrough identifies a specific fragment of that RGNEF protein, named NF242, that can mitigate the toxic effects of the ALS-causing protein. The researchers discovered that when the two proteins interact with each other, the toxicity of the ALS-causing protein is removed, significantly reducing damage to the nerve cell and preventing its death." Original article: https://lnkd.in/ekGqMxVN

𝐒𝐈𝐍𝐆𝐋𝐄-𝐂𝐄𝐋𝐋 𝐌𝐔𝐋𝐓𝐈𝐌𝐎𝐃𝐀𝐋 𝐎𝐌𝐈𝐂𝐒 𝐔𝐍𝐕𝐄𝐈𝐋𝐄𝐃 𝐓𝐇𝐄 𝐌𝐘𝐒𝐓𝐄𝐑𝐘 𝐒𝐔𝐑𝐑𝐎𝐔𝐍𝐃𝐈𝐍𝐆 𝐓𝐇𝐄 𝐑𝐄𝐆𝐄𝐍𝐄𝐑𝐀𝐓𝐈𝐕𝐄 𝐂𝐀𝐏𝐀𝐂𝐈𝐓𝐘 𝐎𝐅 𝐂𝐄𝐋𝐋𝐒 𝐈𝐍 𝐊𝐈𝐃𝐍𝐄𝐘 A friend of mine wondered, "Damian, what's the reason behind your excitement about these single-cell technologies? You mentioned we each have more than 30 trillion cells! Who on earth would be interested in analyzing all of these? That's crazy, sorry!" he said. I didn't perceive this as an insult. Actually—most genomics scientists I know are "insanely unconventional"—so are their ideas. He was right. That idea is quite INSANE! However, we don't have to analyze every individual cell within the organism to draw fascinating conclusions that could pave the way for future scientific breakthroughs. Let me illustrate this with an example from a recent paper published in the journal 'Science.' Scientists knew that acute kidney injury—arising from various causes—can be transient with tissue recovery or lead to long-term damage, fibrosis, & eventual progression to chronic kidney disease. While they understand what determines the outcome of this complex process—previous studies implicated a transcription factor named SOX9 as a potential contributor. Trusting their instincts, these scientists used mouse models of acute kidney injury to scrutinize this transcription factor more closely. The team led by Shikhar Aggarwal identified a SOX9 switch—revealing that regenerating kidney cells transiently activate SOX9. However, some cells subsequently deactivate it, while others do not! This subsequent deactivation—or lack thereof—with resulting fibroproliferative effects through the WNT signaling pathway—distinguishes cells undergoing healthy recovery from those experiencing fibrosis & long-term injury. This study would not have been possible without single-cell technologies! It—along with other modern functional genomics technologies—has contributed to these exciting findings. This has the potential to change what was previously feasible in "the regenerative capacity" of this organ. Does this imply that we are closer to regenerating organs like the kidney? Or perhaps now we will identify the best targets to selectively silence pro-fibrotic cells? ~~~ We're 𝐄𝐩𝐢𝐠𝐞𝐧𝐨𝐦𝐲𝐬𝐭𝐢𝐪, & talk about: #precisionmedicine #epigenomics #genetherapy #epigenetics #genomics #singlecell #genetics #science Transcend the Border of your 𝐃𝐍𝐀-𝐁𝐥𝐮𝐞𝐩𝐫𝐢𝐧𝐭. Let 𝐄𝐩𝐢𝐠𝐞𝐧𝐨𝐦𝐲𝐬𝐭𝐢𝐪 be your Guide. 𝐄𝐧𝐥𝐢𝐠𝐡𝐭𝐞𝐧 𝐭𝐡𝐞 𝐃𝐚𝐫𝐤—𝐰𝐡𝐞𝐫𝐞 𝐌𝐲𝐬𝐭𝐢𝐪𝐮𝐞 𝐚𝐛𝐢𝐝𝐞𝐬...