Talking about T cells has become increasingly difficult even among T cell researchers as more discoveries have led to a growing number of subtypes.
To overcome this communication complication, a consortium of researchers proposed new guidelines for T cell nomenclature.
Read more.
Researchers released a consensus statement with recommendations to update T cell nomenclature and improve communication around T cell subtypes.
Investigators looked at laboratory mice with spinal cord injury and found that lesion-remote astrocytes (LRAs) play an important role in supporting nervous system repair. They saw strong evidence of the same mechanism in tissue samples from human patients with spinal cord injury.
The Lab identified one LRA subtype that sends out a protein called CCN1 to signal to immune cells called microglia.
“One function of microglia is to serve as chief garbage collectors in the central nervous system,” the senior author said. “After tissue damage, they eat up pieces of nerve fiber debris—which are very fatty and can cause them to get a kind of indigestion. Our experiments showed that astrocyte CCN1 signals the microglia to change their metabolism so they can better digest all that fat.”
The author said this efficient debris clearing might have a role in the spontaneous recovery found in many patients with spinal cord injury. In the absence of the astrocyte-derived CCN1 protein, the investigators found that recovery is drastically impaired.
“If we remove astrocyte CCN1, the microglia eat, but they don’t digest. They call in more microglia, which also eat but don’t digest,” the author said. “Big clusters of debris-filled microglia form, heightening inflammation up and down the spinal cord. And when that happens, the tissue doesn’t repair as well.”
When investigators looked at spinal cord tissue from human patients with multiple sclerosis, they found the same mechanism at work, the author said and added that these fundamental principles of tissue repair likely apply to any sort of injury of the brain or spinal cord.
One of the world’s foremost philosophers of physics, Maudlin is Professor of Philosophy at NYU and Founder and Director of the John Bell Institute for the Foundations of Physics.
He is a member of the “Foundational Questions Institute” of the Académie Internationale de Philosophie des Sciences and is the recipient of a Guggenheim Fellowship, and author of ‘The Metaphysics Within Physics’, ‘Truth and Paradox: Solving the Riddles’ and ‘Quantum Non-Locality and Relativity’
Tap the link to watch his full talk now: https://iai.tv/video/tim-maudlin-why-imaginary-numbers-are-c…um-physics
Why do imaginary numbers appear at the foundation of quantum mechanics? This question, which puzzled even great physicists like Eugene Wigner, opens up deeper issues about what it means to explain features of the mathematical formalism used in physical theory. Join philosopher of science Tim Maudlin as he explores that question through the lens of quantum dynamics, arguing that the appearance of complex numbers in Schrödinger’s equation is not arbitrary, but motivated by the need for a particular kind of wave-like structure in fundamental dynamics.
RCT results: An automated AI analysis led to reduced exam time, increased scan volume and image quality, and lower fatigue. @KagiyamaNobu
Two major trials investigating the potential of the psychedelic drug LSD for reducing anxiety are set to conclude in 2026. Scientists are feeling positive after the drug’s success in an earlier-stage trial, which could mean the treatment will be available in the US as early as 2027.
Generalised anxiety disorder is a common condition where people feel very anxious about lots of different things. It is typically treated with antidepressants and talking therapies, but around half of people don’t respond to such treatments.
Other psychedelic drugs like psilocybin and MDMA are already used to treat particularly severe cases of depression and post-traumatic stress disorder in some countries, such as Australia and Switzerland. LSD is increasingly being explored as a mental health treatment, partly because research shows it triggers profound emotional experiences in some people, and it seems to enhance the brain’s ability to rewire itself and form new thought patterns.
Image: TUMEGGY/SCIENCE PHOTO LIBRARY/GETTY IMAGES
Two later-stage trials investigating LSD for treating anxiety are due to conclude in 2026, which could lead to the drug being approved for the common mental health condition.
By Carissa Wong
In acute ischemic stroke, insulin resistance worsens outcomes by increasing blood-brain barrier permeability in the ischemic core.
Acute large‐vessel occlusion of head and neck severely affect quality of life. One of the critical pathological events associated with prognosis of acute ischemic stroke (AIS) is the disruption of the blood–brain barrier (BBB), a highly selective barrier maintaining the brain’s microenvironment.1 Ischemia causes BBB dysfunction,2 exacerbated by peripheral immune cell infiltration,3 leading to increased parenchymal injury, hemorrhage,4 and edema.4, 5 Therefore, accurately determining the evolution and severity of BBB permeability are crucial for prognostic evaluation in patients with AIS.
Research on BBB disruption in patients with AIS primarily focuses on pathological mechanisms and imaging evaluations. Numerous studies use animal models and cell culture experiments to elucidate the physiological and molecular bases of BBB disruption.2, 5, 6, 7, 8 Additionally, imaging techniques like magnetic resonance imaging are widely used to assess evolution of BBB permeability1, 9, 10, 11, 12 and demonstrate correlations between BBB damage, cerebral edema, hemorrhagic transformation, and poor prognosis. Despite significant advances, several issues remain unresolved. First, differences between animal models and human disease limit clinical applicability. Second, while magnetic resonance imaging is widely used to provide quantitative data on BBB disruption, they still face the limitations of being time consuming and inconvenient in the clinical environment. However, BBB disruption in patients with AIS based on computed tomography perfusion (CTP) needs further study.
Insulin resistance (IR) is linked to adverse cardiovascular13, 14 and metabolic outcomes.15, 16 Therefore, identifying patients with IR aids early risk stratification and management. The triglyceride–glucose (TyG) index, which combines fasting triglyceride and glucose levels, has been proposed as a marker of IR. Currently, research on the TyG index primarily focuses on type 2 diabetes,17 obesity,18 and cardiovascular diseases.19 Recent studies have found that an elevated TyG index is associated with higher stroke recurrence,19, 20 functional deterioration,21, 22 and death.23 However, whether the underlying mechanisms involved in the association of IR with stroke outcomes have not been fully understood. IR exacerbated vascular inflammation and endothelial dysfunction,24, 25, 26 which were critical contributors to BBB disruption in AIS. Previous studies have shown that metabolic dysregulation, including hypertriglyceridemia27 and hyperglycemia,28 aggravates BBB permeability by triggering oxidative stress and inflammatory pathways.29, 30 Specifically, IR leads to the generation of reactive oxygen species and the activation of NADPH oxidase, which contribute to oxidative stress and endothelial damage.30, 31 Inflammatory cytokines such as tumor necrosis factor‐α, interleukin‐1β, and interleukin‐6 are also elevated in the insulin‐resistant state, activating nuclear factor‐κB and Janus kinase signaling pathways that further compromise endothelial tight junction proteins such as occludin, claudin‐5, and zonula occludens‐1, crucial for BBB integrity.29, 32 These mechanisms are known to increase BBB permeability, facilitating the entry of harmful substances into the brain and contributing to worsened stroke outcomes. These findings indicated that the relationship between IR and stroke outcomes may be mediated by increased BBB permeability. However, the TyG index’s relationship with BBB disruption and outcomes in patients with AIS is not well studied.
The Pooled Cohort Equations (PCE) cardiovascular risk score stratifies risk for multiple ocular diseases, according to a study published online in Ophthalmology.
Deyu Sun, Ph.D., from the David Geffen School of Medicine at the University of California Los Angeles, and colleagues conducted a historical prospective cohort study using electronic health record data from the “All of Us” Research Program to examine whether the PCE cardiovascular risk score is associated with future age-related macular degeneration (AMD), glaucoma, diabetic retinopathy (DR), retinal vein occlusion (RVO), and hypertensive retinopathy (HTR).
A total of 35,909 adults aged 40 to 79 years with complete variables for PCE calculation within a six-month period were included in the study. Individual-level PCE score was classified into four risk categories.
A new University of Toronto-led study has discovered a possible biomarker linked to multiple sclerosis (MS) disease progression that could help identify patients most likely to benefit from new drugs.
The findings were published today in Nature Immunology and validated in both mouse models and humans.
“We think we have uncovered a potential biomarker that signals a patient is experiencing so-called ‘compartmentalized inflammation’ in the central nervous system, a phenomenon which is strongly linked to MS progression,” says Jen Gommerman, a professor and chair of immunology at U of T’s Temerty Faculty of Medicine. “It’s been really hard to know who is progressing and who isn’t.”
In laboratory models, researchers at The University of Texas MD Anderson Cancer Center discovered that a mother’s circadian rhythms, or internal body clock, can influence the immune system states of her offspring, which can accurately predict the risk of bacterial infection.
These findings offer novel insights into non-genetic factors shaping immune defenses and provide a framework to study circadian rhythms as a possible reason why some patients might be more vulnerable to getting infections during disease treatment. The study, published in Science Advances, was led by Alejandro Aballay, Ph.D., professor of Genetics and dean of the UTHealth Houston Graduate School of Biomedical Sciences.
“These findings reveal a circadian mechanism that can create significant differences in infection outcomes even when genetics and environment are similar,” Aballay said. “This circadian control may help explain why patients with comparable risk profiles often experience very different responses to infection.”
