Say their names: Resurgence in the collective attention toward Black victims of fatal police violence following the death of George Floyd.

The murder of George Floyd by police in May 2020 sparked international protests and brought unparalleled levels of attention to the Black Lives Matter movement. As we show, his death set record levels of activity and amplification on Twitter, prompted the saddest day in the platform's history, and caused his name to appear among the ten most frequently used phrases in a day, where he is the only individual to have ever received that level of attention who was not known to the public earlier that same week. Importantly, we find that the Black Lives Matter movement's rhetorical strategy to connect and repeat the names of past Black victims of police violence-foregrounding racial injustice as an ongoing pattern rather than a singular event-was exceptionally effective following George Floyd's death: attention given to him extended to over 185 prior Black victims, more than other past moments in the movement's history. We contextualize this rising tide of attention among 12 years of racial justice activism on Twitter, demonstrating how activists and allies have used attention and amplification as a recurring tactic to lift and memorialize the names of Black victims of police violence. Our results show how the Black Lives Matter movement uses social media to center past instances of police violence at an unprecedented scale and speed, while still advancing the racial justice movement's longstanding goal to "say their names."

A clarified typology of core-periphery structure in networks.

Core-periphery structure, the arrangement of a network into a dense core and sparse periphery, is a versatile descriptor of various social, biological, and technological networks. In practice, different core-periphery algorithms are often applied interchangeably despite the fact that they can yield inconsistent descriptions of core-periphery structure. For example, two of the most widely used algorithms, the k-cores decomposition and the classic two-block model of Borgatti and Everett, extract fundamentally different structures: The latter partitions a network into a binary hub-and-spoke layout, while the former divides it into a layered hierarchy. We introduce a core-periphery typology to clarify these differences, along with Bayesian stochastic block modeling techniques to classify networks in accordance with this typology. Empirically, we find a rich diversity of core-periphery structure among networks. Through a detailed case study, we demonstrate the importance of acknowledging this diversity and situating networks within the core-periphery typology when conducting domain-specific analyses.

Divergent discourse between protests and counter-protests: #BlackLivesMatter and #AllLivesMatter.

Since the shooting of Black teenager Michael Brown by White police officer Darren Wilson in Ferguson, Missouri, the protest hashtag #BlackLivesMatter has amplified critiques of extrajudicial killings of Black Americans. In response to #BlackLivesMatter, other Twitter users have adopted #AllLivesMatter, a counter-protest hashtag whose content argues that equal attention should be given to all lives regardless of race. Through a multi-level analysis of over 860,000 tweets, we study how these protests and counter-protests diverge by quantifying aspects of their discourse. We find that #AllLivesMatter facilitates opposition between #BlackLivesMatter and hashtags such as #PoliceLivesMatter and #BlueLivesMatter in such a way that historically echoes the tension between Black protesters and law enforcement. In addition, we show that a significant portion of #AllLivesMatter use stems from hijacking by #BlackLivesMatter advocates. Beyond simply injecting #AllLivesMatter with #BlackLivesMatter content, these hijackers use the hashtag to directly confront the counter-protest notion of "All lives matter." Our findings suggest that Black Lives Matter movement was able to grow, exhibit diverse conversations, and avoid derailment on social media by making discussion of counter-protest opinions a central topic of #AllLivesMatter, rather than the movement itself.

Rapid vascular responses to anthrax lethal toxin in mice containing a segment of chromosome 11 from the CAST/Ei strain on a C57BL/6 genetic background.

Host allelic variation controls the response to B. anthracis and the disease course of anthrax. Mouse strains with macrophages that are responsive to anthrax lethal toxin (LT) show resistance to infection while mouse strains with LT non-responsive macrophages succumb more readily. B6.CAST.11M mice have a region of chromosome 11 from the CAST/Ei strain (a LT responsive strain) introgressed onto a LT non-responsive C57BL/6J genetic background. Previously, B6.CAST.11M mice were found to exhibit a rapid inflammatory reaction to LT termed the early response phenotype (ERP), and displayed greater resistance to B. anthracis infection compared to C57BL/6J mice. Several ERP features (e.g., bloat, hypothermia, labored breathing, dilated pinnae vessels) suggested vascular involvement. To test this, Evan's blue was used to assess vessel leakage and intravital microscopy was used to monitor microvascular blood flow. Increased vascular leakage was observed in lungs of B6.CAST.11M mice compared to C57BL/6J mice 1 hour after systemic administration of LT. Capillary blood flow was reduced in the small intestine mesentery without concomitant leukocyte emigration following systemic or topical application of LT, the latter suggesting a localized tissue mechanism in this response. Since LT activates the Nlrp1b inflammasome in B6.CAST.11M mice, the roles of inflammasome products, IL-1ß and IL-18, were examined. Topical application to the mesentery of IL-1ß but not IL-18 revealed pronounced slowing of blood flow in B6.CAST.11M mice that was not present in C57BL/6J mice. A neutralizing anti-IL-1ß antibody suppressed the slowing of blood flow induced by LT, indicating a role for IL-1ß in the response. Besides allelic differences controlling Nlrp1b inflammasome activation by LT observed previously, evidence presented here suggests that an additional genetic determinant(s) could regulate the vascular response to IL-1ß. These results demonstrate that vessel leakage and alterations to blood flow are part of the rapid response in mice resistant to B. anthracis infection.

Male CD81 knockout genotype disrupts Mendelian distribution of offspring.

CD81 is an integral membrane protein in the tetraspanin superfamily that serves as an adaptor protein. CD81 is also a maternally imprinted gene that is found in a regulated cluster of genes on mouse chromosome 7. Among offspring produced from heterozygous breeding pairs, CD81(null/null) mice grew at the same rate as CD81(+/+) and CD81(+/null) mice. Because of an inhibition in sperm-egg fusion, CD81(null/null) female mice are much less fertile than CD81(+/+) and CD81(+/null) mice. However, no published study has detailed the effect of the male CD81 genotype on the genotype and sex distribution of offspring. We set up breeding pairs of heterozygotic (C.129-Cd81(tm1) N7) female mice and male mice with CD81(+/null), CD81(+/+), or CD81(null/null) genotypes. The survival and development of CD81(+/null), CD81(+/+), and CD81(null/null) offspring were monitored and compared. Compared with those of heterozygous male breeders, CD81(null/null) pups were born at a less-than-expected ratio from CD81(null/null) males. Sex distribution did not differ among pups sired by CD81(null/null) compared with CD81(+/null) mice. The data suggest that the effect of the CD81(null/null) paternal genotype on offspring is manifested early in development or in utero.

Enhancing the ability of experimental autoimmune encephalomyelitis to serve as a more rigorous model of multiple sclerosis through refinement of the experimental design.

Advancing the understanding of the mechanisms involved in the pathogenesis of multiple sclerosis (MS) likely will lead to new and better therapeutics. Although important information about the disease process has been obtained from research on pathologic specimens, peripheral blood lymphocytes and MRI studies, the elucidation of detailed mechanisms has progressed largely through investigations using animal models of MS. In addition, animal models serve as an important tool for the testing of putative interventions. The most commonly studied model of MS is experimental autoimmune encephalomyelitis (EAE). This model can be induced in a variety of species and by various means, but there has been concern that the model may not accurately reflect the disease process, and more importantly, it may give rise to erroneous findings when it is used to test possible therapeutics. Several reasons have been given to explain the shortcomings of this model as a useful testing platform, but one idea provides a framework for improving the value of this model, and thus, it deserves careful consideration. In particular, the idea asserts that EAE studies are inadequately designed to enable appropriate evaluation of putative therapeutics. Here we discuss problem areas within EAE study designs and provide suggestions for their improvement. This paper is principally directed at investigators new to the field of EAE, although experienced investigators may find useful suggestions herein.