Adults with prediabetes randomized to 8-weeks of walking realized gut microbiome changes suggestive of more resilience, growth, and enhanced metabolic activity. DOCM
Read here ➡️ doi.org/10.2337/doc25-0067
American Diabetes Association American Diabetes Association – DiabetesPro
OBJECTIVE. To test the effect of physical activity on the gut microbiome and circulating short-chain fatty acids (SCFAs) among sedentary adults with prediabetes and overweight or obesity.
Year 2023 face_with_colon_three
Scientists have figured out a way to detonate the ‘doors’ that lead to the heart of cancerous tumors, blowing them wide open for drug treatments.
The strategy works by triggering a ‘timer bomb’ on the cells that line a tumor’s associated blood vessels.
These vessels control access to the tumor tissue, and until they are opened, engineered immune cells can’t easily gain entry to the cancer to fight it off.
Year 2025 This could essentially end disease where the diseases would be edited off and the host repaired internally.
Scientists identified 473 human genes that act as genetic “on/off switches,” shaping disease risk through tissue-specific or universal patterns regulated by DNA changes and hormones.
Study: Switch-like gene expression modulates disease risk. Image Credit: gopixa / Shutterstock.
In a recent article published in Nature Communications, researchers analyzed methylomes, transcriptomes, and genomes from 943 individuals to characterize and identify genes that exhibit distinct on-off switches and explore their epigenetic and genetic regulation.
Traumatic head injuries from collision and combat sports disrupt the blood-brain barrier and trigger inflammation for years after retirement, shows a new MRI and transcriptomic analysis of retired athletes.
Find out more in Science TranslationalMedicine.
Sci. Transl. Med. 18, eadu6037 (2026). DOI:10.1126/scitranslmed.adu6037
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Nutrient stress in DNA damage.
The dynamic interplay between nutrient stress and DNA damage governs cellular survival through coordinated regulation of genomic integrity and metabolic adaptation. Nutrient deprivation, such as glucose or amino acid limitation, engages nutrient sensors, including AMPK and mTORC1, to rewire energy homeostasis while directly influencing DNA repair via regulating PARP1, BRCA1, and other core repair machinery.
DNA damage-activated kinases (ATM/ ATR) orchestrate metabolic reprogramming to fuel repair processes, enforcing context-dependent cell fate decisions via cell cycle arrest or apoptosis regulation.
Nutrient stress exacerbates genomic instability through depleting antioxidants, such as NADPH or glutathione (GSH), promoting oxidative DNA lesions that overwhelm repair capacity, while defective DNA repair conversely drives metabolic dysregulation in tumors.
In the future, more efficacious tumor therapeutic strategies propose combining targeted nutrient stress with DNA damage repair inhibitors to exploit synthetic lethality. However, clinical translation requires resolving key challenges including tumor heterogeneity in nutrient stress-response pathways and adaptive metabolic plasticity during therapy sciencenewshighlights ScienceMission https://sciencemission.com/nutrient-stress–and-DNA-damage
Cells are constantly exposed to various stresses, including nutrient deprivation and genotoxic stress, which dynamically interact with cellular sensing pathways to influence metabolism, gene expression, and homeostasis. The integration of nutrient-sensing mechanisms and DNA damage response pathways is critical in cancer progression. While individual processes are well-characterized, their cross-regulatory mechanisms are just beginning to emerge. Deciphering the interplay between nutrient stress and DNA damage is crucial for elucidating the mechanisms underlying cellular responses to stress and developing therapeutic strategies for various diseases, including cancer. This review highlights the relationship between nutrient stress and DNA damage, especially its underlying sensing pathway and cell fate determination.
Yuan et al. report a high-quality chromosome-scale genome of the hexaploid halophyte Sesuvium portulacastrum. Comparative genomics and transcriptomics provide insights into its salt-adaptation evolution and identify the key salt-tolerant gene SpHAK3, offering genetic resources for improving crop tolerance.
The researchers also discovered a tiny antibody, called a nanobody, which mimics NPC1 at the receptor-binding site and can slip past a protective cap on Marburg’s entry protein, bind to it and block its attachment to the receptor. In lab tests, this nanobody prevented Marburg virus from entering cells. ScienceMission sciencenewshighlights.
In a new study published in Nature the researchers found that the Marburg virus (MBV), one of the world’s deadliest pathogens with an average 73% fatality rate, is unusually efficient at getting inside human cells. They also showed that the virus’s entry protein contains structural features that explain this efficiency and point to a strategy for blocking infection.
The researchers designed a tightly controlled system that enables a fair comparison of the entry proteins of Marburg and its relative Ebola. The team further found that the two viruses share the same human receptor. The authors determined structures of MBV glycoprotein (GP) in three states: unbound; bound to its endosomal receptor NPC1; and complexed with a neutralizing nanobody.
Marburg’s entry protein binds this receptor in a distinct orientation and with higher affinity, then changes shape in ways that help the virus enter cells. The authors show that the glycan cap shields the receptor-binding site from NPC1 but only partially from the nanobody, enabling limited immune evasion. After glycan cap cleavage, NPC1 binds to MBV GP in a distinct orientation compared with EBOV GP, providing an additional anchor and enhancing receptor affinity. NPC1 engagement also induces substantial conformational changes in MBV GP, probably facilitating membrane fusion. Using this approach, they showed that Marburg’s entry protein can drive viral entry into human cells up to 300 times more efficiently than Ebola’s.
A team of international researchers have developed a breakthrough way to observe what is happening inside electronic chips while they are operating—without touching them, taking them apart, or switching them off. The new technique uses terahertz waves, a safe and non-ionizing form of electromagnetic radiation, to detect tiny movements of electrical charge inside fully packaged semiconductor devices. For the first time, this allows scientists and engineers to monitor electronic components as they function in the real world.
The study, published in the IEEE Journal of Microwaves, involves researchers from Adelaide University in Australia, US technology company Virginia Diodes Inc, the Hasso Plattner Institute and the University of Potsdam, Germany.
Adelaide University Group Leader of the Terahertz Engineering Laboratory (TEL), Professor Withawat Withayachumnankul, said that semiconductors underpin almost every modern technology, from smartphones and medical devices to vehicles, power grids and defense systems.
Microscopic images of human tissue are a cornerstone of biomedical research and clinical diagnostics. Yet despite their importance, these images often remain difficult to analyze systematically and to connect with other types of biological data. A new study led by CeMM Principal Investigator André Rendeiro and published in Nature Methods introduces “LazySlide,” an open-source software tool that brings the power of foundation models and aims to democratize digital pathology analysis.
Whether it’s an inflamed artery, a tumor spreading into the lung or subtle damage in an organ, when doctors or researchers want to understand what’s happening inside a tissue, one of the most trusted tools is still the microscope. Today, they have largely gone digital: A single tissue sample can be scanned into a whole-slide image so detailed that one can zoom from a bird’s-eye view of the entire tissue down to individual cells. These images, therefore, contain enormous information about tissues from different scales.
However, these images are huge, complex, and often difficult to analyze in a modern, data-driven way. While genetics and single-cell biology have developed effective ways for sharing and comparing data, digital pathology images are hard to incorporate—stored in proprietary formats, processed with incompatible tools, and hard to connect to molecular information like RNA sequencing. Thus, the valuable resources of digitalized tissue images are largely underutilized in many research and clinical settings.