Lay Down Your Cross

If the strong Black woman is to ever gain visibility, then we need to be strong enough to allow ourselves the opportunity to rest. The implications that we are insurmountable beings have meant that Black women are routinely denied considerations by society. A host of Black feminist thinkers have indicated the unique spaces of oppression which the Black woman has occupied and continues to struggle within because of this institutional neglect. Black women have been the bridge which, not only supports the change that we wish to see, but also maintains the disparaging stereotypes which obstructs our efforts towards self-definition. The frustrations weigh heavily upon Black women, as they are forced to surrender need and charity in order to protect the utility of our families and communities. It is my belief that Black women need to lay down this burden of being everything to everyone, if we have any hope of experiencing the kind of freedom which have been liberally extended to others. Cast-off the shame that has silenced the strong Black woman; there is power to be gained when we stop allowing others to determine our worth

How Much Does It Cost to Operate Tiny Home Villages for People Experiencing Homelessness

Los Angeles is in a homelessness crisis. Millions of dollars are poured into preventing its causes and curtailing the increased medical costs and crime rates that stem from it. The solutions vary, but one new solution in the form of tiny home villages hopes to provide a cheap and effective way to get people experiencing homelessness off the streets. In 2021, Los Angeles began opening tiny home villages, also referred to as cabin communities, for unhoused people during the COVID-19 pandemic. There are currently 11 tiny home villages in Los Angeles, operated in a joint effort between the government and non-profits, who provide wraparound support to those experiencing homelessness through shelter, mental health support, food, and various other services. Yet, three years after these tiny home villages began operating in Los Angeles, little is known to the general public about their operations and efficacy regarding funding, functionality, and success. This report seeks to fill these knowledge gaps and provide recommendations for maximizing the use of tiny home villages for the unhoused community in Los Angeles for years to come

Our Voices

In declaration, we come together, calling for all who experience the intersection of oppressions to have the opportunity to claim and use their own Voices

L-plastin is essential for alveolar macrophage production and control of pulmonary pneumococcal infection

We report that mice deficient for the hematopoietic-specific, actin-bundling protein L-plastin (LPL) succumb rapidly to intratracheal pneumococcal infection. The increased susceptibility of LPL(−/−) mice to pulmonary pneumococcal challenge correlated with reduced numbers of alveolar macrophages, consistent with a critical role for this cell type in the immediate response to pneumococcal infection. LPL(−/−) mice demonstrated a very early clearance defect, with an almost 10-fold-higher bacterial burden in the bronchoalveolar lavage fluid 3 h following infection. Clearance of pneumococci from the alveolar space in LPL(−/−) mice was defective compared to that in Rag1(−/−) mice, which lack all B and T lymphocytes, indicating that innate immunity is defective in LPL(−/−) mice. We did not identify defects in neutrophil or monocyte recruitment or in the production of inflammatory cytokines or chemokines that would explain the early clearance defect. However, efficient alveolar macrophage regeneration following irradiation required LPL. We thus identify LPL as being key to alveolar macrophage development and essential to an effective antipneumococcal response. Further analysis of LPL(−/−) mice will illuminate critical regulators of the generation of alveolar macrophages and, thus, effective pulmonary innate immunity

NASA Near Earth Network (NEN) and Space Network (SN) CubeSat Communications

There has been a recent trend to increase capability and drive down the Size, Weight and Power (SWAP) of satellites. NASA scientists and engineers across many of NASA's Mission Directorates and Centers are developing exciting CubeSat concepts and welcome potential partnerships for CubeSat endeavors. From a "Telemetry, Tracking and Command (TT&C) Systems and Flight Operations for Small Satellites" point of view, small satellites including CubeSats are a challenge to coordinate because of existing small spacecraft constraints, such as limited SWAP and attitude control, and the potential for high numbers of operational spacecraft. The NASA Space Communications and Navigation (SCaN) Program's Near Earth Network (NEN) and Space Network (SN) are customer driven organizations that provide comprehensive communications services for space assets including data transport between a mission's orbiting satellite and its Mission Operations Center (MOC). This paper presents how well the SCaN networks, SN and NEN, are currently positioned to support the emerging small small satellite and CubeSat market as well as planned enhancements for future support

The PSEN1, p.E318G Variant Increases the Risk of Alzheimer's Disease in APOE-ε4 Carriers

The primary constituents of plaques (Aβ42/Aβ40) and neurofibrillary tangles (tau and phosphorylated forms of tau [ptau]) are the current leading diagnostic and prognostic cerebrospinal fluid (CSF) biomarkers for AD. In this study, we performed deep sequencing of APP, PSEN1, PSEN2, GRN, APOE and MAPT genes in individuals with extreme CSF Aβ42, tau, or ptau levels. One known pathogenic mutation (PSEN1 p.A426P), four high-risk variants for AD (APOE p.L46P, MAPT p.A152T, PSEN2 p.R62H and p.R71W) and nine novel variants were identified. Surprisingly, a coding variant in PSEN1, p.E318G (rs17125721-G) exhibited a significant association with high CSF tau (p = 9.2×10−4) and ptau (p = 1.8×10−3) levels. The association of the p.E318G variant with Aβ deposition was observed in APOE-ε4 allele carriers. Furthermore, we found that in a large case-control series (n = 5,161) individuals who are APOE-ε4 carriers and carry the p.E318G variant are at a risk of developing AD (OR = 10.7, 95% CI = 4.7–24.6) that is similar to APOE-ε4 homozygous (OR = 9.9, 95% CI = 7.2.9–13.6), and double the risk for APOE-ε4 carriers that do not carry p.E318G (OR = 3.9, 95% CI = 3.4–4.4). The p.E318G variant is present in 5.3% (n = 30) of the families from a large clinical series of LOAD families (n = 565) and exhibited a higher frequency in familial LOAD (MAF = 2.5%) than in sporadic LOAD (MAF = 1.6%) (p = 0.02). Additionally, we found that in the presence of at least one APOE-ε4 allele, p.E318G is associated with more Aβ plaques and faster cognitive decline. We demonstrate that the effect of PSEN1, p.E318G on AD susceptibility is largely dependent on an interaction with APOE-ε4 and mediated by an increased burden of Aβ deposition

"The Book of Negroes’ illustrated edition: circulating African-Canadian history through the Middlebrow"

This article examines the 2009 deluxe illustrated edition of Lawrence Hill’s Commonwealth Writers’ Prize– and Canada Reads–winning novel The Book of Negroes, originally published in 2007. It relates the story of Aminata, a West African girl kidnapped and sold into slavery, and her experiences on an indigo plantation in the American south, followed by further displacements to Charleston, Nova Scotia, Sierra Leone, and London. In New York, as the Revolutionary War comes to a close, Aminata becomes the scribe for the Book of Negroes, documenting the Black Loyalists, as well as the slaves and indentured servants of white Loyalists, granted passage by the British to Canada. Hill has commented that the Book of Negroes is an important document about which Canadians are largely ignorant. This desire to circulate knowledge about African-Canadian history through the novel is particularly manifest in the illustrated edition of 2009, where a photograph of the Book of Negroes features prominently, along with countless other images and captions which supplement and interrupt Hill’s narrative. This article considers the significance and implications of this “keepsake” or “souvenir” edition, particularly its circulation of knowledge about African-Canadian history through visual pleasure

The PSEN1, p.E318G variant increases the risk of Alzheimer’s disease in APOE-ԑ4 carriers

The primary constituents of plaques (Aβ42/Aβ40) and neurofibrillary tangles (tau and phosphorylated forms of tau [ptau]) are the current leading diagnostic and prognostic cerebrospinal fluid (CSF) biomarkers for AD. In this study, we performed deep sequencing of APP, PSEN1, PSEN2, GRN, APOE and MAPT genes in individuals with extreme CSF Aβ42, tau, or ptau levels. One known pathogenic mutation (PSEN1 p.A426P), four high-risk variants for AD (APOE p.L46P, MAPT p.A152T, PSEN2 p.R62H and p.R71W) and nine novel variants were identified. Surprisingly, a coding variant in PSEN1, p.E318G (rs17125721-G) exhibited a significant association with high CSF tau (p = 9.2 × 10(-4)) and ptau (p = 1.8 × 10(-3)) levels. The association of the p.E318G variant with Aβ deposition was observed in APOE-ε4 allele carriers. Furthermore, we found that in a large case-control series (n = 5,161) individuals who are APOE-ε4 carriers and carry the p.E318G variant are at a risk of developing AD (OR = 10.7, 95% CI = 4.7-24.6) that is similar to APOE-ε4 homozygous (OR = 9.9, 95% CI = 7.2.9-13.6), and double the risk for APOE-ε4 carriers that do not carry p.E318G (OR = 3.9, 95% CI = 3.4-4.4). The p.E318G variant is present in 5.3% (n = 30) of the families from a large clinical series of LOAD families (n = 565) and exhibited a higher frequency in familial LOAD (MAF = 2.5%) than in sporadic LOAD (MAF = 1.6%) (p = 0.02). Additionally, we found that in the presence of at least one APOE-ε4 allele, p.E318G is associated with more Aβ plaques and faster cognitive decline. We demonstrate that the effect of PSEN1, p.E318G on AD susceptibility is largely dependent on an interaction with APOE-ε4 and mediated by an increased burden of Aβ deposition

Erratum: Author Correction: Identification of genes required for eye development by high-throughput screening of mouse knockouts.

[This corrects the article DOI: 10.1038/s42003-018-0226-0.]