News from Nowhere (1890) is the most famous work of one of the greatest British writers and thinkers, William Morris. It is a utopian picture of a future communist society, drawing on the work of Ruskin and Marx and written in response to what Morris saw as soulless and mechanical visions of socialism. In this work of his last years, Morris distilled many of his leading ideas on politics, art and society, imagining a world in which capitalism has been abolished by a workers' revolution and nature and society have become beautiful habitations for humanity. In an era that has seen the collapse of state socialism, Morris's damning critique of this conception, and his positing of a powerful alternative, have important contemporary resonances.

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A wrist guard incorporating volar padding with the pneumatic spring design principle might be more effective at preventing injuries than are currently available designs.

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Colorectal cancer (CRC) is one of the most common malignancies in both morbidity and mortality. Immune checkpoint blockade (ICB) treatments have been successful in a portion of mismatch repair-deficient (dMMR) CRC patients but have failed in mismatch repair-proficient (pMMR) CRC patients. Atypical Chemokine Receptor 4 (ACKR4) is implicated in regulating dendritic cell (DC) migration. However, the roles of ACKR4 in CRC development and anti-tumor immunoregulation are not known. By analyzing human CRC tissues, transgenic animals, and genetically modified CRC cells lines, our study revealed an important function of ACKR4 in maintaining CRC immune response. Loss of ACKR4 in CRC is associated with poor immune infiltration in the tumor microenvironment. More importantly, loss of ACKR4 in CRC tumor cells, rather than stromal cells, restrains the DC migration and antigen presentation to the tumor-draining lymph nodes (TdLNs). Moreover, tumors with ACKR4 knockdown become less sensitive to immune checkpoint blockade. Finally, we identified that microRNA miR-552 negatively regulates ACKR4 expression in human CRC. Taken together, our studies identified a novel and crucial mechanism for the maintenance of the DC-mediated T-cell priming in the TdLNs. These new findings demonstrate a novel mechanism leading to immunosuppression and ICB treatment resistance in CRC.