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Cellular senescence related gene signature predicts prognosis and immune features in skin cutaneous melanoma

Skin cutaneous melanoma (SKCM) is the deadliest skin cancer, with rising global incidence. Cellular senescence plays an essential role in tumorigenesis, progression, and immune modulation in cancer, however, its role in SKCM prognosis and immunotherapy response remains unclear.

We analyzed 279 senescence-related genes (SRGs) in 469 patients with SKCM from The Cancer Genome Atlas. A cellular senescence-related signature (CSRS) was constructed using univariate and LASSO Cox regression analyses. Kaplan-Meier survival curves and receiver operating characteristic (ROC) analyses were used to evaluate its predictive performance. Consensus clustering based on SRG expression stratified patients into distinct subgroups. External validation was performed using the GSE65904 dataset. We further assessed the association between CSRS, immune cell infiltration, and immunotherapy response. Additionally, immunohistochemistry validated the expression of prognosis-related SRGs and functional assays explored the role of RuvB-like AAA ATPase 2 (RUVBL2) in SKCM cells.

The CSRS effectively stratified patients with SKCM into high-and low-risk groups with significantly different survival outcomes and immune profiles. Moreover, our results suggest that higher levels of cellular senescence may enhance immunosurveillance and promote tumor suppression via a senescence-associated secretory phenotype-dependent mechanism. Based on the expression profiles of 113 SRGs, patients were classified into three distinct clusters, with Cluster 1 associated with the poorest prognosis. Among the identified SRGs, RUVBL2 was markedly upregulated in SKCM cells and its knockdown inhibited cell proliferation.

Prevention and Reversal of Hypertension‐Induced Coronary Microvascular Dysfunction by a Plant‐Based Diet

Rac1 inhibition prevents axonal cytoskeleton dysfunction in transthyretin amyloid polyneuropathy.

Magalhães et al. reveal that Rac1 hyperactivation disrupts axonal cytoskeleton and transport in a mouse model of transthyretin amyloid polyneuropathy. They show that Rac1 inhibition prevents axonal degeneration and identify a patient-associated RACGAP1 variant suggesting a neuroprotective role for Rac1 inactivation.

Godfather of AI Predicts Total Breakdown of Society

Geoffrey Hinton, one of the three so-called “godfathers” of AI, never misses an opportunity to issue foreboding proclamations about the tech he helped create.

During an hour-long public conversation with Senator Bernie Sanders at Georgetown University last week, the British computer science laid out all the alarming ways that he forecasts AI will completely upend society for the worst, seemingly leaving little room for human contrivances like optimism. One of the reasons why is that AI’s rapid deployment will be completely unlike technological revolutions in the past, which created new classes of jobs, he said.

“The people who lose their jobs won’t have other jobs to go to,” Hinton said, as quoted by Business Insider. “If AI gets as smart as people — or smarter — any job they might do can be done by AI.”

Vicarious body maps bridge vision and touch in the human brain

A central question in sensory neuroscience is how inputs from vision and touch are combined to generate cohesive representations of the external world. Here we reveal a widespread mode of brain organization in which aligned topographic maps bridge vision and somatosensation. We developed a computational model that revealed somatotopic structure in dorsolateral visual cortex. Somatotopic tuning in these regions was predictive of visual field locations more dorsally and visual body part selectivity more ventrally. These results suggest more extensive cross-modal overlap than traditionally assumed: the computational machinery classically attributed to the somatosensory system is also embedded within and aligned with that of the visual system. These aligned visual and bodily maps are a likely brain substrate for internalized somatosensory representations of visual signals, and are a candidate human homologue of findings in mice whereby somatomotor responses dominate visual cortex36.

Consistent with embodied perception theories, our model-based quantifications of somatotopic and retinotopic connectivity revealed that dorsolateral visual cortical responses to naturalistic stimuli are best explained by selectivities in both modalities, as opposed to visual selectivity alone. The necessity of incorporating body-referenced processing into models of dorsolateral visual cortex supports evidence that its role extends beyond passive visual analysis, encompassing perceptual, semantic and bodily functions optimized for behavioural interactions with the world25.

Consistent with visuospatial alignment of somatosensory tuning, we found that body part preferences in dorsolateral visual cortex predicted visual field tuning. Such alignment, previously reported at the terminus of the dorsal visual pathway around the postcentral sulcus28, therefore extends far into dorsal and lateral streams of the visual system. This alignment may be reinforced by shared developmental influences, as somatotopic and retinotopic maps are shaped trophically from birth: dorsal regions represent the upper body and visual field, and ventral regions to the lower body and visual field22, providing a roughly aligned sensory periphery optimized for efficient environmental sampling and action. The explicit interweaving of touch and retinal coordinates may subserve efficient perception of environmental affordances and a cohesive sense of spatial self-representation.

How antibody therapy clears Alzheimer’s plaques: Key immune mechanism identified

Lecanemab, sold under the name Leqembi, is a monoclonal antibody therapy for Alzheimer’s disease that clears toxic amyloid plaques and delays cognitive decline. Researchers from VIB and KU Leuven have now demonstrated the mechanism behind it for the first time.

They showed that the “Fc fragment” of this monoclonal antibody is essential for engaging microglia—the immune cells of the brain—thus initiating the cellular machinery needed for plaque removal. This is the first direct mechanistic explanation for how this class of therapies works. It clarifies uncertainties in the field and offers a blueprint for developing safer, more effective Alzheimer’s treatments. The findings are published in Nature Neuroscience.

“Our study is the first to clearly demonstrate how this anti-amyloid antibody therapy works in Alzheimer’s disease. We show that the therapy’s efficacy relies on the antibody’s Fc fragment, which activates microglia to effectively clear amyloid plaques,” says Dr. Giulia Albertini, co-first author of the study. “The Fc fragment works as an anchor that microglia latch onto when they are near plaques, as a consequence of which these cells are reprogrammed to clear plaques more efficiently.”

Signpost of cancer linked to wound-healing properties

SerpinB3 turns out to be both a healing powerhouse and a cancer accomplice—revealing new possibilities for medicine. Researchers have uncovered that SerpinB3, typically linked to severe cancers, is also a key player in natural wound healing. The protein drives skin cell movement and tissue rebuilding, especially when paired with next-generation biomaterial dressings. Its newfound role explains why cancer cells exploit it and opens the door to new wound-healing therapies.

When a routine blood test shows high levels of a protein called SerpinB3, it often alerts doctors that something is seriously wrong. Elevated SerpinB3 can be associated with difficult-to-treat cancers or severe inflammatory diseases.

SerpinB3 is known as a key protein that helps reveal when the body’s barrier tissues, such as the skin and lungs, are under intense strain from cancer or long-term illness. It has typically been viewed as a sign that these protective surfaces are in trouble.

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