Wealth redistribution policies to mitigate the impact of development assistance defunding: a retrospective evaluation and forecasting analysis up to 2030.

September 7, 2026| Source: Lancet (London, England)

The ongoing decline in funding for humanitarian and development assistance stands in stark contrast to the global rise in wealth concentration and widening socioeconomic inequalities. This study aimed to assess whether the implementation of wealth redistribution policies-proposed in recent high-level international agreements to support development-could mitigate the health impact of the current official development assistance (ODA) defunding crisis. We conducted an integrated retrospective impact evaluation and forecasting analysis using longitudinal panel data from 59 low-income and lower-middle-income countries. First, we estimated the association between per-capita ODA and mortality outcomes from 2002 to 2021 using two-way fixed-effects multivariable Poisson regression models with robust standard errors, adjusting for key demographic, socioeconomic, and health-system covariates. We did extensive sensitivity and triangulation analyses to assess the robustness and plausibility of the findings. We then evaluated ten wealth redistribution policies with validated country-level microsimulation models to forecast mortality outcomes under alternative wealth redistribution scenarios versus the current defunding scenario from 2026 to 2030. In comparison with the baseline ODA category, high ODA funding was associated with a 24% reduction in age-standardised all-cause mortality (rate ratio [RR] 0·76; 95% CI 0·67-0·87) and a 33% reduction in under-5 mortality (0·67; 0·50-0·89). Forecasting analyses showed that, in comparison with the current ODA funding reductions in the 59 selected low-income and lower-middle-income countries, all ten wealth redistribution policies were associated with millions of averted deaths by 2030: overall, the lowest number of averted deaths was 6 591 984 (95% uncertainty interval 4 884 075-8 374 138) for a 3% crypto tax applied to the top 10 000 holders, while the highest number of averted deaths was 29 509 934 (20 273 842-38 603 961) for a 3% wealth tax on ultra-high-net-worth individuals; in children younger than 5 years, the corresponding numbers of averted deaths were 1 312 912 (802 926-1 785 121) for a 3% crypto tax applied to the top 10 000 holders and 3 464 607 (1 235 930-5 609 331) for a 3% wealth tax on ultra-high-net-worth individuals. The implementation of wealth redistribution policies proposed in recent high-level international agreements could mitigate the health consequences of the current ODA defunding crisis, avert millions of deaths, and support the achievement of the UN Sustainable Development Goals, particularly those related to health. Spanish Ministry of Science and Innovation.

Read the original source →

An innervated and vascularized HNSCC-on-a-chip model built on defined and tunable engineered extracellular matrices.

Understanding the tumor microenvironment requires experimental platforms that faithfully recapitulate its key components. Here, we present an innervated and vascularized head and neck squamous cell carcinoma (HNSCC)-on-a-chip platform built with fully defined and tunable engineered extracellular matrices (eECMs). In a stepwise increase of complexity, we first cocultured patient-derived HNSCC cells, cancer-associated fibroblasts, and endothelial cells within tailored eECMs, revealing extracellula

Septin binding restricts Shigella growth and triggers intracellular tolerance.

Pathogen survival relies on their ability to adapt to changing environments, yet how intracellular bacteria tolerate cell-autonomous immunity remains unclear. Septins assemble into cage-like structures around cytoplasmic Shigella targeted by autophagy, but their antibacterial activity was unknown. Using advanced microscopy and cell-free reconstitution, we show that septins polymerize into circumferentially oriented filaments that inhibit bacterial growth. RNA-sequencing reveals that septin bindi

DCAF6 reprograms TGF-β responses through TRIM33 destruction.

TGF-β signaling plays a pivotal role in regulating numerous cellular processes, primarily through the Smad-dependent pathway. Disruptions of the pathway are associated with developmental disorders and life-threatening diseases, such as cancer. It has been reported that TRIM33 inactivates Smad4 signaling and also drives its own signaling responses. However, the mechanism controlling TRIM33 activity has remained unclear. In this study, we identify DCAF6 as a previously unrecognized ubiquitin

Stimulated protein degradation to promote mitochondrial function and neuronal survival.

Targeted protein degradation is a promising modality to treat cancer or inflammation, but whether it can provide a similar benefit for disorders caused by pervasive protein dysregulation is unclear. We describe stimulated protein degradation (SPD) as a strategy that leverages agonists of stress-responsive E3 ubiquitin ligases to simultaneously eliminate multiple pathogenic factors. Specifically, we show that activators of the reductive stress response E3 CUL2 FEM1B boost degradation of multiple

Spatial coordination in the codevelopment of the human urogenital system during organogenesis.

The human urogenital system originates from a common embryonic domain, yet the mechanisms guiding its spatiotemporal coordination remain understudied. Here, we combined high-resolution spatial transcriptomics with single-cell multiomics to profile human embryos from Carnegie stages 15 to 23, capturing the codevelopmental dynamics of the urogenital system. We revealed mesonephros- and adrenal primordium-derived signals that promote gonadal specification and enable efficient in vitro generation of