Honoring the enslaved African American foremothers of modern women's health: Meditations on 40 years of Black feminist praxis.

This article analyzes 40 years of Black feminist scholarship, art, and grassroots activism dedicated to the lives and legacies of the "foremothers of American gynecology." Infamously, in Montgomery, Alabama, between 1845 and 1849, up to 16 enslaved women were exploited at a backyard hospital, some subjected to surgical experimentation by Dr James Marion Sims. He was a famous and world-renowned surgeon who died in 1883, with a reputation as "the father of modern gynecology." Sims achieved the medical knowledge that catapulted him into American and European fame, using skills gained from the exploitation of the enslaved women in his early career. Famously, three of these women are referenced by their first names: Anarcha, Lucy, and Betsey. This research asks: how have these important figures been remembered in 20th and 21st-century Black feminist scholarship, art, and grassroots community activism? Further, what are the broader impacts of this pathbreaking truth, reckoning, and reconciliation work?

Do "knowledge attributions" involve metarepresentation just like belief attributions do?

The authors distinguish knowledge and belief attributions, emphasizing the role of the former in mental-state attribution. This does not, however, warrant diminishing interest in the latter. Knowledge attributions may not entail mental-state attributions or metarepresentations. Even if they do, the proposed features are insufficient to distinguish them from belief attributions, demanding that we first understand each underlying representation.

CUX1 transcription factor is required for optimal ATM/ATR-mediated responses to DNA damage.

The p110 Cut homeobox 1 (CUX1) transcription factor regulates genes involved in DNA replication and chromosome segregation. Using a genome-wide-approach, we now demonstrate that CUX1 also modulates the constitutive expression of DNA damage response genes, including ones encoding ATM and ATR, as well as proteins involved in DNA damage-induced activation of, and signaling through, these kinases. Consistently, RNAi knockdown or genetic inactivation of CUX1 reduced ATM/ATR expression and negatively impacted hallmark protective responses mediated by ATM and ATR following exposure to ionizing radiation (IR) and UV, respectively. Specifically, abrogation of CUX1 strongly reduced ATM autophosphorylation after IR, in turn causing substantial decreases in (i) levels of phospho-Chk2 and p53, (ii) γ-H2AX and Rad51 DNA damage foci and (iii) the efficiency of DNA strand break repair. Similarly remarkable reductions in ATR-dependent responses, including phosphorylation of Chk1 and H2AX, were observed post-UV. Finally, multiple cell cycle checkpoints and clonogenic survival were compromised in CUX1 knockdown cells. Our results indicate that CUX1 regulates a transcriptional program that is necessary to mount an efficient response to mutagenic insult. Thus, CUX1 ensures not only the proper duplication and segregation of the genetic material, but also the preservation of its integrity.