#Exercise ↑ FOXO [#longevity’ genes and #anti-inflammatory] →ↆ #DEAF1. ↆ DEAF1 → muscle cells regain their ability to recycle damaged parts and stay healthy. Exercise helps restore homeostasis within muscle cells and keeps muscles stronger for longer. bit.ly/49PVRaU
25.01.2026 21:52 — 👍 0 🔁 0 💬 0 📌 0
Progressive #MS →hallmark of grey matter injury = compartmentalized #inflammation (CI) of the #leptomeninges. In vivo, 800x ↑ #CXCL13 + significantly ↆ BAFF assoc. w CI . Ratios → grey matter injury.bit.ly/4q0kxUZ go.nature.com/3Yk0AfL
04.01.2026 19:42 — 👍 0 🔁 0 💬 0 📌 0
Neurobehavioural links from infant screen time to anxiety
Higher infant screen time is linked to accelerated topological maturation of the visual
and cognitive control networks, leading to prolonged decision latency and increased
adolescent anxiety. Sensory ...
#Infancy particularly sensitive period for #screen exposure. Exposure <2 yrs → ↑#brain maturation, ↆ decision-making, and ↑ anxiety by #adolescence. Shared reading 3yrs ↆ the brain- alterations suggesting a protective effect. bit.ly/3MZXdZ2 [open access]
31.12.2025 22:34 — 👍 3 🔁 0 💬 0 📌 0
The neural basis of endogenous reinforcement learning.
Vividly imagining a positive interaction with someone can increase how much you like them — and alter how your brain stores information about that person. (Similar to those seen when people learn from real rewarding experiences.) bit.ly/4ac9dAe go.nature.com/48SDuS9 [open access]
11.12.2025 16:58 — 👍 5 🔁 2 💬 0 📌 0
Frontiers | Cytokines in sepsis: a critical review of the literature on systemic inflammation and multiple organ dysfunction
Sepsis constitutes a profoundly heterogeneous and dynamic clinical syndrome, precipitated by a maladaptive host response to infection in which the immune sys...
#Cytokines in #sepsis, a review. Sepsis → maladaptive host response to infection. Interplay between proinflammatory and anti-inflammatory pathways pathologically skewed. Central role of cytokine storms in activating and regulating the systemic #inflammatory cascade. bit.ly/4qR2TUD
05.11.2025 16:34 — 👍 0 🔁 0 💬 0 📌 0
Mitochondrial and lysosomal signaling orchestrates heterogeneous metabolic states of regulatory T cells
Mitochondrial and lysosomal signaling orchestrates Treg cell metabolic states and functional fitness.
A tale of two organelles: #Mitochondria and #lysosomes
Activated cell states → ↑ mitochondria vs. resting cell states. These mitochondria have more dense cristae, suggesting they are an important part of regulatory T cell activation during #inflammation. bit.ly/4qLclsH bit.ly/3LdvLWx
27.10.2025 19:27 — 👍 3 🔁 1 💬 0 📌 0
Frontiers | Editorial: The role of inflammation in organ injury
Inflammation represents one of the most fundamental and evolutionarily conserved biological responses for host defense against pathogens and tissue injury (1...
Analysis of IL-17A in multisystem #inflammatory syndrome → insights into pediatric #inflammatory responses following SARS-CoV-2 exposure. IL-17A may be not only as mechanistic player but also a valuable prognostic marker. Editorial bit.ly/4qn6rxn
22.10.2025 15:09 — 👍 1 🔁 0 💬 0 📌 0
In vivo, maternal Ig ↆ oral #rotavirus vaccine immunogenicity by ↑ vaccine clearance, thereby ↆ protection. Note: in mice, MatAb interference is mediated by milk-derived antibodies. In humans, transplacental versus breast milk antibodies likely depends on the vaccine platform. bit.ly/3L8thbU
14.10.2025 18:05 — 👍 2 🔁 0 💬 0 📌 0
The impacts of chronic infections on shaping cellular senescence - Immunity & Ageing
Cellular senescence is a fundamental biological process characterized by stable cell cycle arrest, genomic instability, and the acquisition of a proinflammatory secretory phenotype. While senescence is traditionally associated with aging, growing evidence reveals that chronic infections such as viral, bacterial, and protozoan parasites can serve as powerful inducers of senescence, contributing to premature aging and long-term tissue damage. This review explores the diverse mechanisms by which persistent pathogens trigger or sustain senescence in host cells. We highlight how these chronic infections manipulate host DNA repair, mitochondrial dynamics, telomere maintenance, oxidative stress, and immune function to promote senescence and immunosenescence. Emerging findings also reveal how pathogens hijack the host cellular machinery to induce senescence across various tissue types. In many cases, senescence not only enables pathogen persistence but also drives pathological outcomes such as fibrosis, neurodegeneration, cardiomyopathy, and immune exhaustion. Collectively, this emerging evidence highlights a unifying strategy among diverse pathogens: the exploitation of cellular senescence to support chronic infection and promote disease. Understanding how infectious agents drive senescence offers new insights into age-related pathologies and highlights potential therapeutic targets, such as senolytic and senomorphic agents, to mitigate the long-term impacts of chronic infections.
Cellular #senescence→ genomic instability, #inflammatory phenotype and #pathogen persistence→ disease (e.g. fibrosis, neurodegeneration, cardiomyopathy, and immune exhaustion). Review: bit.ly/4q7b0vN
12.10.2025 20:06 — 👍 3 🔁 0 💬 0 📌 0
Targeting immunosenesence promotes clearance of senescent cells - Immunity & Ageing
Known as immunosenescence, the major dysregulation of the immune system with age is associated with poor vaccination efficacy, and increased susceptibility to infections, age-related pathologies, and neoplasms, with incidences exacerbated with age. Cellular senescence is a crucial process that puts cells in an irreversible cell-cycle arrest which prevents damaged or stressed cells from uncontrolled propagation and eventually potential malignancy. Paradoxically, senescence also contributes to the occurrence of cancer and increases the risk of metastasis through different secretory mediators. Altogether, the recent use of senotherapy to eliminate senescent cells has been shown to delay tumorigenesis, attenuate age-related deterioration of organs, and promote healthy aging. Interestingly, immune cells have been shown to specifically interact with, and kill senescent cells, thus opening new opportunities for the development of specific therapeutic strategies similar to immunotherapy in cancer. Through its detrimental impact on the immune system, immunosenescence is also leading to the accumulation of senescent cells with age thus further contributing to the occurrence and worsening of multiple age-related pathologies such as cancer. Understanding the molecular and cellular events occurring during the aging process, and triggering immunosenescence as well as the mechanisms by which senescent cells escape immune surveillance would help to improve immune responses to senescent cells and their clearance. In this review, we highlight how senescent cells interact with immune cells, and how immunosenescence-associated phenotypical and functional deregulation hinder the ability of immune cells to clear senescent cells. We further characterize strategies aimed at promoting the clearance of senescent cells by the immune system.
Chronic #SASP production→ ↑ #inflammation. Accumulation of #senescent cells→ ↑ cancer and other age-associated pathologies. Targeting and clearance of senescent cells ↆ pathologies. bit.ly/46Sbu1r
08.10.2025 19:20 — 👍 2 🔁 0 💬 0 📌 0
Drug Discovery / Aging / Fitness
Convincing myself that aging is simply loss of regulation/repair and could be quantified and reversed!
I wrote a book! BIOLOGICAL YOUTH http://amazon.com/dp/1535584459
Official journals of the Sleep Research Society and the Australasian Sleep Association.
🩺 Family Physician
🌱 Lifestyle Medicine Expert
💪 Empowering you to take control of your health naturally
Sharing evidence-based strategies to help you:
• Optimize your wellness journey
• Prevent chronic disease
• Feel your best!
Medical journalist with @gohealio.bsky.social. 🩺
Website - SkinDoctor.ai - Enhancing the beautiful you, Naturally
Contact: hopp.bio/drlazukcosme...
My personal share on all things about health and wellbeing.
#dermatologist #health #skincare #beauty #cosmetics #aesthetics #skindoctor #medsky
Assistant Professor at U Michigan
Innate immunity, cell death, virology
she/her
https://medresearch.umich.edu/labs-departments/labs/Barnett-Lab
University of Cincinnati MD/PhD student, M4 | PhD in Immunology
Studying newborn immunity to viral pneumonia | Future Pediatrician-Scientist
immunologist + climber enjoying life in and out of lab in sunny san diego ☀️
Postdoctoral fellow at BC Children's Hospital, University of British Columbia. Goblet cell, mucus, and gut microbes.
Scientist @ Krembil Brain Institute
Assistant Professor @ University of Toronto
I study how the immune system contributes to neuroinflammation and neurodegeneration
I am an Immunology and Hematology researcher at Western University in London Ontario
Diabetes researcher/immunologist at the University of Alberta
Scientific Director - CIHR Institute of Aging, Scientist - Robarts Research Institute, Distinguished University Professor - Western University #WomanInSTEM 🇨🇦
Principal Investigator at The University of British Columbia studying tuberculosis, macrophages, drug discovery. www.thesunlab.ca
Infection immunologist w/ interest in #MAIT cells. Associate Professor, #Tsinghua SIGS, Shenzhen CN, ex-Karolinska Institutet SE, Duke-NUS SG, Monash AU.
Immunologist working in vaccine research in the Sander Lab @Charité - University Medical Center, Berlin. Interested in T cells, B cells, dendritic cells and all things vaccine related. Special interest in MAIT cells.
Senior Scientist, Princess Margaret Cancer Center, University Health Network
Professor, Department of Immunology, University of Toronto
Canada
DVM, MSc
PhD student | Immunology | Asthma 🫁
University of Manitoba 🇨🇦
Dr. Wael Elhenawy
Assistant Professor @UAlberta, MMI
CRC-Tier II in Microbiome. Crohn's disease-associated bacteria/Microbial evolution/ Biofilms/Genomics. Opinions are my own.
https://www.elhenawylab.com
Professor of Translational Immunology • Infection & Immunity • Public Involvement and Engagement • Scientist and migrant • Superbugs
