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Andrew Yang: UBI Before UHI

Solving Job Loss, and the Future of Work ## Andrew Yang advocates for the implementation of Universal Basic Income (UBI) as a necessary solution to address job loss, income inequality, and societal unrest caused by technological advancements and AI-driven changes in the economy ## ## Questions to inspire discussion.

Universal Basic Income Implementation.

đŸ”č Q: What UBI amount should be set to provide an effective safety net?

A: UBI should be set at twice the poverty level, around $25,000 per person per year, providing enough for survival but not happiness to maintain work incentives while protecting against economic collapse.

đŸ”č Q: How can UBI be funded without government action initially?

A: Well-resourced tech billionaires could fund UBI directly to local communities to keep the middle class afloat during AI-driven changes, potentially catalyzing further philanthropy and government action.

Senovax takes a novel approach

Senescent “zombie” cells accumulate as we age, releasing inflammatory signals that damage surrounding tissue. Senovax takes a novel approach: train the immune system to recognize these cells and eliminate them. By exposing dendritic immune cells to lab-generated senescent cells, the body learns the markers that identify aging cells. The result: the immune system creates a “wanted poster” and begins targeting senescent cells throughout the body. Unlike drugs that must reach specific tissues, the immune system already travels everywhere — and it remembers. One treatment could potentially provide long-lasting protection.

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The Immune Cell Atlas of “Longevity Molecular Tag”: Identification of Principal Immune Cell Subsets and Their Underlying Molecular Regulatory Mechanisms

Immunosenescence represents a critical aspect of the aging process. Centenarians, serving as a nature model of “healthy aging,” demonstrate a distinctive immune “compensatory adaptation” mechanism that contributes to the maintenance of immune homeostasis. However, the specific immune cell subsets involved and the molecular mechanisms underlying these phenotypic traits remain incompletely understood. In this study, we integrated single-cell RNA sequencing data spanning the entire lifespan of East Asian populations with bulk transcriptomic data from a centenarian cohort in Guangxi. Utilizing the Scissor algorithm, we identified immune cell subpopulations positively (Scissor+) and negatively (Scissor−) associated with longevity phenotypes, thereby constructing an immune cell atlas of “Longevity Molecular Tag.” Our findings indicate that Scissor+ cells predominantly comprise natural killer (NK) cells, CD8+ T cells, and γΎ T cells, characterized by enhanced cytotoxic and immunomodulatory functions. Conversely, Scissor− cells mainly include CD4+ T cells, B cells, and dendritic cells (DCs), which are linked to inflammatory signaling pathways and Th17/Th1 differentiation. Trajectory analysis elucidated the differentiation pathways of NK, CD8+ T cells, CD4+ T cells, and B cells. Differentially expressed genes were enriched in pathways such as NF-ÎșB signaling, T cell receptor signaling, and NK cell cytotoxicity. Furthermore, co-localization analysis revealed five eQTL-colocalized events (rs3793537–GLIPR2/CD72/TLN1 and rs8019902–TRDV2/TRDC) associated with longevity. Collectively, these results suggest that centenarians achieve immune equilibrium by remodeling cytotoxic immune lineages and finely tuning inflammatory responses, thereby promoting health span and longevity. This study offers novel insights into potential strategies for modulating immunosenescence.

The Strehler-Mildvan mortality correlation arises from changes in the variability of ageing

As global human life expectancy continues to rise, accompanying increases in healthspan that prevent morbidity expansion become increasingly imperative. Population lifespan can increase in distinct ways, for instance through rectangularisation (steepening) or triangularisation (flattening) of survival curves. These two demographic changes, particularly rectangularisation, occur frequently across human and model organism populations, yet their biological determinants and effects on healthspan and morbidity are largely unknown. Notably, these modes of life-extension occur when parameters of the Gompertz mortality model (capturing exponential age-increases in mortality rate) change inversely, a widely-reported phenomenon known as the Strehler-Mildvan correlation — whose biological basis also remains unexplained. We therefore investigated longitudinal health, morbidity and lifespan in 30 Caenorhabditis elegans cohorts using multiple life-extension protocols. We report that survival curve rectangularisation results from healthspan expansion in short-lived population members, whereas triangularisation from healthspan and morbidity expansion in long-lived population members. Interestingly, rectangularisation and triangularisation respectively decrease and increase inter-individual variation in the ageing process, and the mode of life-extension that occurs depends on levels of existing variation. Notably, triangularisation was more effective at extending lifespan without morbidity expansion. Analysis of fruit fly and mouse data show that these biological determinants of the Strehler-Mildvan correlation are also largely evolutionarily conserved.

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Scientists Find Protein Inside The Body That Reverses Brain Aging

Cyclin D-binding myb-like transcription factor 1 or DMTF1a key protein in the brain can help to regenerate neural stem cells and improve aging-associated memory decline. NUS scientists found that this protein’s levels are repressed in the “aged” neural stem cells, Health & Wellness News, Health and Me

The Blood of Centenarians Reveals 37 Proteins Linked With Slower Aging

Science is one step closer to cracking the code of longevity thanks to a new study that identified dozens of proteins linked with slower aging in the blood of centenarians.

Scientists in Switzerland collected and compared blood samples from healthy younger individuals aged 30 to 60, hospitalized octogenarians aged 80 to 90, and centenarians aged 100 years and older, assessing how the expression of plasma proteins evolves and affects metabolism, immunity, and overall lifespan.

Of the more than 700 proteins measured, 37 formed a profile that was “closer to those of the youngest group than to those of octogenarians,” says Flavien Delhaes, cell physiologist at the University of Geneva and the study’s first author.

Scientists Successfully Transfer Longevity Gene, Paving the Way for Extending Human Lifespan

A gene borrowed from the naked mole rat, an animal famous for extraordinary longevity and disease resistance, helped mice live a little longer and stay healthier, pointing to a surprising biological “export” of longevity traits across species.

This isn’t just about living longer

Scientists are discovering that targeting senescent cells the “aged” cells surrounding tumors may weaken cancer itself.

Cancer often forces nearby cells into accelerated aging. Those senescent cells then release growth factors that help the tumor survive and expand.

A new therapy called Senovax aims to eliminate those surrounding cells, effectively collapsing the tumor’s support system.

Preclinical data from Immortebio shows tumor reduction in mouse models of:

Lung cancer.

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