New research from the University of St Andrews has revealed that human readiness for intergroup violence is not a single or unified mindset. Published in the Proceedings of the National Academy of Sciences, the new study, spanning 58 countries and involving more than 100 researchers from various institutions around the world, demonstrates that violent extremist intentions are driven by two fundamentally different psychological motivations.

These are defensive extremism, which aims to protect a group from perceived threats, and offensive extremism, which seeks to establish group dominance and expand influence.

This preregistered study analyzed data from 18,128 participants globally. The findings indicate that defensive extremist intentions are consistently more prevalent, showing higher levels of endorsement than offensive intentions in 56 out of the 58 surveyed nations. This suggests a widespread tendency to find protective violence more morally acceptable than violence aimed at conquest.

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Spotlight: Hiba Baaziz and Daniela Cimini (Virginia Tech) discuss recent work from Zych et al. (https://hubs.la/Q0485YJy0), showing that low RCC1 levels impair protein export in micronuclei, causing overgrowth and rupture. https://hubs.la/Q0485R1g0

Micronuclei (MN), a hallmark of chromosome instability, frequently rupture, leading to protumorigenic consequences. MN rupture requires nuclear lamina defects, yet their underlying causes remain unclear. Here, we demonstrate that MN lamina gaps are linked to excessive MN growth resulting from impaired protein export. This export defect arises from reduced levels of the transport protein RCC1 in MN. Overexpressing RCC1 increases protein export and protects MN from rupture. Differences in RCC1 levels linked to chromatin state also explain why high euchromatin content increases the stability of small MN. Additional RCC1 loss in euchromatic MN results in impaired protein import. For these MN, increasing RCC1, directly or through increasing histone methylation, accelerates rupture. Our findings define a new model of MN rupture, where defects in protein export drives continuous MN growth causing nuclear lamina gaps that predispose MN to membrane rupture and where chromatin-specific features can alter rupture of small MN by further impairing nuclear transport.

Zych et al. demonstrate that reduced RCC1 levels in micronuclei impair protein export, causing persistent micronuclear growth, nuclear lamina gap expansion

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A Chinese worker in Israel posted this video on Douyin. In the comment section, people were shocked: \.

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