资源环境科技发展态势分析平台

Education is a key dimension of well-being and a crucial indicator of development(1-4). The Sustainable Development Goals (SDGs) prioritize progress in education, with a new focus on inequality(5-7). Here we model the within-country distribution of years of schooling, and use this model to explore educational inequality since 1970 and to forecast progress towards the education-related 2030 SDG targets. We show that although the world is largely on track to achieve near-universal primary education by 2030, substantial challenges remain in the completion rates for secondary and tertiary education. Globally, the gender gap in schooling had nearly closed by 2018 but gender disparities remained acute in parts of sub-Saharan Africa, and North Africa and the Middle East. It is predicted that, by 2030, females will have achieved significantly higher educational attainment than males in 18 countries. Inequality in education reached a peak globally in 2017 and is projected to decrease steadily up to 2030. The distributions and inequality metrics presented here represent a framework that can be used to track the progress of each country towards the SDG targets and the level of inequality over time. Reducing educational inequality is one way to promote a fairer distribution of human capital and the development of more equitable human societies.

Activation of the non-canonical NF-kappa B signalling pathway by AZD5582 results in the induction of HIV and SIV RNA expression in the blood and tissues of antiretroviral-therapy-treated humanized mice and rhesus macaques.

Long-lasting, latently infected resting CD4(+) T cells are the greatest obstacle to obtaining a cure for HIV infection, as these cells can persist despite decades of treatment with antiretroviral therapy (ART). Estimates indicate that more than 70 years of continuous, fully suppressive ART are needed to eliminate the HIV reservoir(1). Alternatively, induction of HIV from its latent state could accelerate the decrease in the reservoir, thus reducing the time to eradication. Previous attempts to reactivate latent HIV in preclinical animal models and in clinical trials have measured HIV induction in the peripheral blood with minimal focus on tissue reservoirs and have had limited effect(2-9). Here we show that activation of the non-canonical NF-kappa B signalling pathway by AZD5582 results in the induction of HIV and SIV RNA expression in the blood and tissues of ART-suppressed bone-marrow-liver-thymus (BLT) humanized mice and rhesus macaques infected with HIV and SIV, respectively. Analysis of resting CD4(+) T cells from tissues after AZD5582 treatment revealed increased SIV RNA expression in the lymph nodes of macaques and robust induction of HIV in almost all tissues analysed in humanized mice, including the lymph nodes, thymus, bone marrow, liver and lung. This promising approach to latency reversal-in combination with appropriate tools for systemic clearance of persistent HIV infection-greatly increases opportunities for HIV eradication.