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Over Ten Million Served
All tenured and tenure-track faculy know the trinity of promotion and tenure criteria: research, teaching, and service. While teaching and research are relatively well defined areas of institutional focus and evaluation, service work is rarely tabulated or analyzed as a key aspect of higher education's political economy. Instead, service, silent and invisible, coexists with the formal \"official\" economy of many institutions, just as women's unrecognized domestic labor props up the formal, official economies of countries the world over. Over Ten Million Served explores what academic service is and investigates why this labor is often not acknowledged as \"labor\" by administrators or even by faculty themselves, but is instead relegated to a gendered form of institutional caregiving. By analyzing the actual labor of service, particularly for women and racial, ethnic, and sexual minorities, contributors expose the hidden economy of institutional service, challenging the feminization of service labor in the academy for both female and male academic laborers.
eBook
Illumino : a history of medieval Britain in twelve illuminated manuscripts
Explores the history of medieval Britain through the biographies of twelve remarkable illuminated manuscripts and of their creators and owners. The manuscripts each serve as portals into these lives and as springboards into the era of their production. For illuminated manuscripts are among the most intricate and fascinating forms of evidence for the Middle Ages, blending the fruits of human intellect - the arts, the sciences, politics, philosophy and faith - with the materiality of their production. By undertaking the detective work needed to determine the nature of each project and the underlying human-interest stories, this book reveals their manifold social, economic and cultural contexts and charts the exchange of ideas, techniques and materials over time and space.
BOOK
A triple increase in global river basins with water scarcity due to future pollution
Water security is at stake today. While climate changes influence water availability, urbanization and agricultural activities have led to increasing water demand as well as pollution, limiting safe water use. We conducted a global assessment of future clean-water scarcity for 2050s by adding the water pollution aspect to the classical water quantity-induced scarcity assessments. This was done for >10,000 sub-basins focusing on nitrogen pollution in rivers by integrating land-system, hydrological and water quality models. We found that water pollution aggravates water scarcity in >2000 sub-basins worldwide. The number of sub-basins with water scarcity triples due to future nitrogen pollution worldwide. In 2010, 984 sub-basins are classified as water scarce when considering only quantity-induced scarcity, while 2517 sub-basins are affected by quantity & quality-induced scarcity. This number even increases to 3061 sub-basins in the worst case scenario in 2050. This aggravation means an extra 40 million km
2
of basin area and 3 billion more people that may potentially face water scarcity in 2050. Our results stress the urgent need to address water quality in future water management policies for the Sustainable Development Goals.
Here the authors find one third of global sub-basins will face severe clean water scarcity in 2050. Nitrogen pollution aggravates water scarcity in >2,000 sub-basins thus 3 billion more people will be posed with severe water scarcity in 2050.
Journal Article
Ferroptosis occurs through an osmotic mechanism and propagates independently of cell rupture
Ferroptosis is a regulated form of necrotic cell death that is caused by the accumulation of oxidized phospholipids, leading to membrane damage and cell lysis1,2. Although other types of necrotic death such as pyroptosis and necroptosis are mediated by active mechanisms of execution3–6, ferroptosis is thought to result from the accumulation of unrepaired cell damage1. Previous studies have suggested that ferroptosis has the ability to spread through cell populations in a wave-like manner, resulting in a distinct spatiotemporal pattern of cell death7,8. Here we investigate the mechanism of ferroptosis execution and discover that ferroptotic cell rupture is mediated by plasma membrane pores, similarly to cell lysis in pyroptosis and necroptosis3,4. We further find that intercellular propagation of death occurs following treatment with some ferroptosis-inducing agents, including erastin2,9 and C′ dot nanoparticles8, but not upon direct inhibition of the ferroptosis-inhibiting enzyme glutathione peroxidase 4 (GPX4)10. Propagation of a ferroptosis-inducing signal occurs upstream of cell rupture and involves the spreading of a cell swelling effect through cell populations in a lipid peroxide- and iron-dependent manner.Two complementary studies from the laboratories of Riegman et al. and Katikaneni et al., respectively, identify a key role for controlled wave-like propagation of lipid peroxide signalling during wound detection in vivo and in ferroptotic cell death.
Journal Article
A single N6-methyladenosine site regulates lncRNA HOTAIR function in breast cancer cells
N6-methyladenosine (m6A) modification of RNA regulates normal and cancer biology, but knowledge of its function on long noncoding RNAs (lncRNAs) remains limited. Here, we reveal that m6A regulates the breast cancer-associated human lncRNA HOTAIR. Mapping m6A in breast cancer cell lines, we identify multiple m6A sites on HOTAIR, with 1 single consistently methylated site (A783) that is critical for HOTAIR-driven proliferation and invasion of triple-negative breast cancer (TNBC) cells. Methylated A783 interacts with the m6A “reader” YTHDC1, promoting chromatin association of HOTAIR, proliferation and invasion of TNBC cells, and gene repression. A783U mutant HOTAIR induces a unique antitumor gene expression profile and displays loss-of-function and antimorph behaviors by impairing and, in some cases, causing opposite gene expression changes induced by wild-type (WT) HOTAIR. Our work demonstrates how modification of 1 base in an lncRNA can elicit a distinct gene regulation mechanism and drive cancer-associated phenotypes.
Journal Article
