Thekra Rawashdeh’s Post

This study implicates activated glial measures, and GFAP in particular, as a CSF biomarker of nonrelapsing progressive MS biology and demonstrates commonalities of relapsing and nonrelapsing progressive disease mechanisms across the MS clinical spectrum. https://ja.ma/3PQgUAU

A host–microbiota interactome reveals extensive transkingdom connectivity The myriad microorganisms that live in close association with humans have diverse effects on physiology, yet the molecular bases for these impacts remain mostly unknown. Classical pathogens often invade host tissues and modulate immune responses through interactions with human extracellular and secreted proteins (the ‘exoproteome’). Commensal microorganisms may also facilitate niche colonization and shape host biology by engaging host exoproteins; however, direct exoproteome–microbiota interactions remain largely unexplored. https://lnkd.in/dmyK_KNs

Our new review in European Journal of Clinical Sciences is out! 🥳 In this paper we collected the available evidence on the role of bioenergetics dysregulation and redox imbalance in the primary mitochondrial diseases and how these processes are intertwined with neuroinflammatiry processes underlying disease pathophysiology. https://lnkd.in/dHWQExDw

Key protein in the inflammatory pathway driving fatty liver disease The liver has its own native population of immune cells that stick to the endothelial cells surrounding the liver capillaries. Together, they act as the gatekeepers of immunity, filtering or scavenging harmful microorganisms, dead debris and lipids (fats) from incoming blood. However, when there are too many lipids, the environment turns toxic, killing the native immune cells and stressing the endothelial cells to trigger inflammatory response. The scientists found how this summons non-native monocytes to the liver, and how Notch signalling transforms them into inflammatory macrophages. Probing deeper, the scientists discovered as well that removing Rbpj, a seminal protein in the Notch pathway, not only blocks those non-native monocytes from turning into inflammatory macrophages, but also allows them to transform into protective monocytes instead. These protective monocytes possess more lipid-scavenging receptors and can take up more lipids, thereby helping to protect the endothelial cells and quell inflammation. This distinctive, dual function of Rbpj makes it a key therapeutic target in inventing new reparative strategies for MASH. Applying a simple treatment of nanoparticles carrying Rbpj inhibitors was able to successfully retard inflammation and lower the grade of the MASH, proving to be an extremely effective and targeted solution with no side-effects. #ScienceMission #sciencenewshighlights https://lnkd.in/g3mNgAmP

Rethinking Macrophage Activation: Mitochondrial Function in Immune Responses. Scientists used to think that this shift in what the mitochondria are doing was crucial for the macrophages to function in this aggressive, infection-fighting mode. But recent research, like the one described, is showing that this might not be exactly true. The research found that even without changing how mitochondria work, macrophages can still go into this pro-inflammatory state and fight infections effectively. They also noticed that certain chemicals inside the cells, which are important for sending signals during the immune response, can build up even if the mitochondria keep working normally. This suggests that the old idea—that mitochondria need to stop their usual energy production for macrophages to fight effectively—might not be completely accurate. Title: Pro-Inflammatory Macrophage Activation Does Not Require Inhibition - Of Mitochondrial Respiration Reviewer: Christopher Lawson Rating: ⭐⭐⭐⭐ Authors: Linsey Stiles, Ajit Divakaruni, Cristiane Benincá PhD, Zena Marie Del Mundo, Brandon Desousa, Amy Rios. 𝐋𝐢𝐧𝐤: https://lnkd.in/eqrk_Jey

Discover the most comprehensive review on #ferroptosis to date, crafted by the Germany-wide research consortium (DFG Priority Program SPP2306) and leading external experts! This thorough examination delves into ferroptosis, its mechanisms, research tools and methods, and its potential as a therapeutic target. The review provides both seasoned scientists and newcomers with a detailed overview and inspires further research into the molecular pathways that modulate ferroptosis. Vivek Venkataramani and I are proud to be part of this impactful review. 🔗 Read the full article: https://lnkd.in/gcXjtP7h #CellDeath #DiseaseResearch #RedoxBiology #ScientificDiscovery #DFG #SPP2306

I'm happy to share my review paper which was recently published in Frontiers in Bioscience-Landmark. In this comprehensive and state-of-art work, we introduced the emerging role of ROS in modulating the epigenetic landscape and the entire genome, and its contribution to the pathophysiology of cardiovascular diseases. We also addressed the clinical implications and therapeutic interventions including antioxidant therapies and epigenetic drugs, which hold the potential to enhance the outcomes in patients. If you are passionate about epigenetics and cardiovascular research, don't miss out this read! #epigenetics #cardiovasculardiseases #cardiovascularresearch #noveltherapies #epigeneticdrugs #antioxidanttherapies

Did you know that it's been a bit of a mystery why we experience itch? That is - until now. Scientists at Harvard Medical School recently discovered that Staphylococcus aureus is responsible for a common kind of itch by activating nerve cells in the skin, and it can do this whether or not you're experiencing inflammation. Learn more about how they uncovered the molecular mechanisms underlying this phenomenon and how we might use this knowledge to treat diseases associated with itch in the future:https://bit.ly/4cdGUzG #FoodAllergies #FoodAllergy

Identifying phages that specifically target bacterial physiology is challenging due to traditional plaque morphology's limitations in distinguishing distinct phages, requiring extensive isolation and analysis. Presenting Phage Discovery by Co-culture (Phage DisCo), a technique involving the co-cultivation of isogenic bacterial strains tagged with fluorescence and a single perturbation impacting phage infection. Variations in fluorescent signals indicate the perturbation's role in hindering phage infection. This validation of Phage DisCo demonstrates its capability to predict plaque morphology and facilitate the discovery of phage-associated elements like receptors and defense systems. #PhageResearch #MicrobiologyInnovation