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Negative social ties as emerging risk factors for accelerated aging, inflammation, and multimorbidity

Negative social ties, or “hasslers,” are pervasive yet understudied components of social networks that may accelerate biological aging and morbidity. Using ego-centric network data and DNA methylation-based biological aging clocks (i.e., DunedinPACE and age-accelerated GrimAge2) from saliva from a state representative probability sample in Indiana, we examine how negative social ties are associated with accelerated biological aging and a broad range of health outcomes, including inflammation and multimorbidity. Negative relationships are not rare within close relationships, as nearly 30% of individuals report having at least one hassler in their network. These hasslers tend to occupy peripheral network positions and are more likely to be connected through weak, uniplex ties. Importantly, exposure to negative social ties follows patterns of social and health vulnerability, with women, daily smokers, people in poorer health, and those with adverse childhood experiences more likely to report having hasslers in their networks. Having more hasslers is associated with accelerated biological aging in both rate and cumulative burden: Each additional hassler corresponds to approximately 1.5% faster pace of aging and roughly 9 mo older biological age. Moreover, not all hasslers exert the same influence; kin and nonkin hasslers show detrimental associations, whereas spouse hasslers do not. Finally, a greater number of hasslers is associated with multiple adverse health outcomes beyond epigenetic aging. These findings together highlight the critical role of negative social ties in biological aging as chronic stressors and the need for interventions that reduce harmful social exposures to promote healthier aging trajectories.

Within primary breast tumors, a high-risk cell state may seed future metastases

Understanding which cells within a tumor will go on to form metastases remains one of the major challenges in cancer research. A study led by the Cell Plasticity in Development and Disease laboratory, headed by Ángela Nieto at the Institute for Neurosciences (IN), a joint center of the Spanish National Research Council (CSIC) and Miguel Hernández University (UMH) of Elche, offers an unexpected answer: The cells that will give rise to metastases can already be identified within the primary tumor.

The study, published in Nature Communications, combines the analysis of a mouse model of breast cancer with patient data. The results show that, at the invasive front of the tumor, there is a specific population of cells capable of both invading and either proliferating or entering a dormant state. This balance determines whether cells that escape the tumor can initiate new tumor growths in distant organs, the feared metastases.

Nieto’s team has been studying the epithelial-to-mesenchymal transition (EMT) for decades, a program that controls cell migration during embryonic development and is reactivated in tumors to enable cancer cells to spread and form metastases.

Memory T Cells in Respiratory Virus Infections: Protective Potential and Persistent Vulnerabilities

Respiratory virus infections, such as those caused by influenza viruses, respiratory syncytial virus (RSV), and coronaviruses, pose a significant global health burden. While the immune system’s adaptive components, including memory T cells, are critical for recognizing and combating these pathogens, recurrent infections and variable disease outcomes persist. Memory T cells are a key element of long-term immunity, capable of responding swiftly upon re-exposure to pathogens. They play diverse roles, including cross-reactivity to conserved viral epitopes and modulation of inflammatory responses. However, the protective efficacy of these cells is influenced by several factors, including viral evolution, host age, and immune system dynamics.

Gut microbiome is associated with recurrence-free survival in patients with resected high-risk melanoma receiving adjuvant immune checkpoint blockade

Respiratory virus infections, such as those caused by influenza viruses, respiratory syncytial virus (RSV), and coronaviruses, pose a significant global health burden. While the immune system’s adaptive components, including memory T cells, are critical for recognizing and combating these pathogens, recurrent infections and variable disease outcomes persist. Memory T cells are a key element of long-term immunity, capable of responding swiftly upon re-exposure to pathogens. They play diverse roles, including cross-reactivity to conserved viral epitopes and modulation of inflammatory responses. However, the protective efficacy of these cells is influenced by several factors, including viral evolution, host age, and immune system dynamics. This review explores the dichotomy of memory T cells in respiratory virus infections: their potential to confer robust protection and the limitations that allow for breakthrough infections. Understanding the underlying mechanisms governing the formation, maintenance, and functional deployment of memory T cells in respiratory mucosa is critical for improving immunological interventions. We highlight recent advances in vaccine strategies aimed at bolstering T cell-mediated immunity and discuss the challenges posed by viral immune evasion. Addressing these gaps in knowledge is pivotal for designing effective therapeutics and vaccines to mitigate the global burden of respiratory viruses.

Targeting biomolecular condensates: beyond dissolution

Biomolecular condensates control key cellular processes, from gene expression to signal transduction, by organizing molecules through selective compartmentalization. Increasing evidence links their dysregulation to cancer, neurodegeneration, and other diseases, positioning condensates as promising therapeutic targets. This review explores emerging strategies that go beyond dissolving pathological condensates, including approaches that induce, redirect, or reprogram their dynamics, composition, and physical state. Rather than inhibiting individual proteins, these interventions reshape the cellular organization itself. By targeting the material and functional properties of condensates, such strategies offer a new conceptual framework for therapeutic design in complex, dysregulated biological systems.

These blazing blue explosions may be born when a compact dead star slams into a Wolf-Rayet star

Luminous fast blue optical transients (LFBOTs) are among the universe’s brightest and fastest explosions but their origin is not completely understood. A new study takes a closer look at the galaxies they occur in, offering two important clues about their nature. A paper outlining these results was uploaded to the preprint server arXiv on March 24.

LFBOTs are called cow-like events, nicknamed after the first member of this class—AT2018cow—discovered in 2018. They are extremely bright explosions whose brightness peaks within a week and fades to half its peak value in the following week. Their peak brightness is typically greater than 1043 erg per second at optical wavelengths. This is comparable with that of superluminous supernovae, which take a few weeks to months to peak and are generally 10 to 100 times brighter than normal supernovae.

Moreover, LFBOTs’ light curve—a graph that shows changes in their brightness over time—cannot be explained by the decay of nickel-56, which is a common energy source for normal and core-collapse supernovae. There are several theories for their origins; however, there is a lack of consensus.

Quantum model explains how single electrons cause damage inside silicon chips

Researchers in the UC Santa Barbara Materials Department have uncovered the elusive quantum mechanism by which energetic electrons break chemical bonds inside microelectronic devices—a detrimental process that slowly degrades performance over time. The discovery, published as an Editors’ Suggestion in Physical Review B, explains decades-old experimental puzzles and moves scientists closer to engineering more reliable devices.

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