Present day partisanship and the legacy of structural inequality has helped fuel the spread of COVID-19 in Native nations

The pandemic has had a disproportionate impact on Native nations in the US with COVID-19 rates 350 percent higher among Native Americans compared to whites. In new research Raymond Foxworth, Laura E. Evans, Gabriel R. Sanchez, Cheryl Ellenwood, and Carmela M. Roybal contextualize the history of colonization and policy neglect by federal and state governments to explain the unequal impact of the pandemic. They find that this disparity is related to a lack of basic infrastructure like safe running water, a shortage of health information available in Native languages, and the high rate of non-tribal members visiting tribal lands during the pandemic. State-level partisanship also plays an important role; Republican dominated states were less likely to implement pandemic mitigation policies such as mask mandates, which in turn has put Native American lives in danger

Science Engagement Through Hands-On Activities that Promote Scientific Thinking and Generate Excitement and Awareness of NASA Assets, Missions, and Science

The public with hands-on activities that infuse content related to NASA assets, missions, and science and reflect authentic scientific practices promotes understanding and generates excitement about NASA science, research, and exploration. These types of activities expose our next generation of explorers to science they may be inspired to pursue as a future STEM career and expose people of all ages to unique, exciting, and authentic aspects of NASA exploration. The activities discussed here (Blue Marble Matches, Lunar Geologist Practice, Let's Discover New Frontiers, Target Asteroid, and Meteorite Bingo) have been developed by Astromaterials Research and Exploration Science (ARES) Science Engagement Specialists in conjunction with ARES Scientists at the NASA Johnson Space Center. Activities are designed to be usable across a variety of educational environments (formal and informal) and reflect authentic scientific content and practices

Generating Excitement and Increasing Awaressness of NASA Planetary Science and Astromaterials Assets

Students, educators, the public, and the scientific community are so often inspired by NASA science and exploration. Millions have joined NASA during live mission event broadcasts and also follow NASA on social media. Exploration of worlds in our solar system enable the scientific community to obtain and analyze data that provide clues to better understand the history and evolution of our solar system. Missions that collect and return samples to Earth from a target solar system body provide scientists with samples they can research and analyze in their laboratories. For those who are not planetary scientists, they may not understand the significance of these samples and/or the importance of sample return missions. The Astromaterials Research and Exploration Science (ARES) Science Engagement team, through work supported by NASAs Science Mission Directorate (SMD) Science Education Cooperative Agreement Notice NNH15ZDA004C, provides access to samples from NASAs Astromaterials Collections through NASA sponsored exhibits at educator and scientific conferences, NASA relevant public outreach events, and collaborations with other Science Activation Teams supported by the SMD Cooperative Agreement Notice. The goal of this work is to generate excitement while enhancing knowledge and awareness of NASAs unique assets, thus highlighting NASA planetary science and exploration

Complement peptide C3a receptor 1 promotes optic nerve degeneration in DBA/2J mice.

BACKGROUND: The risk of glaucoma increases significantly with age and exposure to elevated intraocular pressure, two factors linked with neuroinflammation. The complement cascade is a complex immune process with many bioactive end-products, including mediators of inflammation. Complement cascade activation has been shown in glaucoma patients and models of glaucoma. However, the function of complement-mediated inflammation in glaucoma is largely untested. Here, the complement peptide C3a receptor 1 was genetically disrupted in DBA/2J mice, an ocular hypertensive model of glaucoma, to test its contribution to neurodegeneration. METHODS: A null allele of C3ar1 was backcrossed into DBA/2J mice. Development of iris disease, ocular hypertension, optic nerve degeneration, retinal ganglion cell activity, loss of RGCs, and myeloid cell infiltration in C3ar1-deficient and sufficient DBA/2J mice were compared across multiple ages. RNA sequencing was performed on microglia from primary culture to determine global effects of C3ar1 on microglia gene expression. RESULTS: Deficiency in C3ar1 lowered the risk of degeneration in ocular hypertensive mice without affecting intraocular pressure elevation at 10.5 months of age. Differences were found in the percentage of mice affected, but not in individual characteristics of disease progression. The protective effect of C3ar1 deficiency was then overcome by additional aging and ocular hypertensive injury. Microglia and other myeloid-derived cells were the primary cells identified that express C3ar1. In the absence of C3ar1, microglial expression of genes associated with neuroinflammation and other immune functions were differentially expressed compared to WT. A network analysis of these data suggested that the IL10 signaling pathway is a major interaction partner of C3AR1 signaling in microglia. CONCLUSIONS: C3AR1 was identified as a damaging neuroinflammatory factor. These data help suggest complement activation causes glaucomatous neurodegeneration through multiple mechanisms, including inflammation. Microglia and infiltrating myeloid cells expressed high levels of C3ar1 and are the primary candidates to mediate its effects. C3AR1 appeared to be a major regulator of microglia reactivity and neuroinflammatory function due to its interaction with IL10 signaling and other immune related pathways. Targeting myeloid-derived cells and C3AR1 signaling with therapies is expected to add to or improve neuroprotective therapeutic strategies

Inhibition of monocyte-like cell extravasation protects from neurodegeneration in DBA/2J glaucoma.

BACKGROUND: Glaucoma is characterized by the progressive dysfunction and loss of retinal ganglion cells. Recent work in animal models suggests that a critical neuroinflammatory event damages retinal ganglion cell axons in the optic nerve head during ocular hypertensive injury. We previously demonstrated that monocyte-like cells enter the optic nerve head in an ocular hypertensive mouse model of glaucoma (DBA/2 J), but their roles, if any, in mediating axon damage remain unclear. METHODS: To understand the function of these infiltrating monocyte-like cells, we used RNA-sequencing to profile their transcriptomes. Based on their pro-inflammatory molecular signatures, we hypothesized and confirmed that monocyte-platelet interactions occur in glaucomatous tissue. Furthermore, to test monocyte function we used two approaches to inhibit their entry into the optic nerve head: (1) treatment with DS-SILY, a peptidoglycan that acts as a barrier to platelet adhesion to the vessel wall and to monocytes, and (2) genetic targeting of Itgam (CD11b, an immune cell receptor that enables immune cell extravasation). RESULTS: Monocyte specific RNA-sequencing identified novel neuroinflammatory pathways early in glaucoma pathogenesis. Targeting these processes pharmacologically (DS-SILY) or genetically (Itgam / CD11b knockout) reduced monocyte entry and provided neuroprotection in DBA/2 J eyes. CONCLUSIONS: These data demonstrate a key role of monocyte-like cell extravasation in glaucoma and demonstrate that modulating neuroinflammatory processes can significantly lessen optic nerve injury

Expression of liver fatty acid binding protein alters growth and differentiation of embryonic stem cells

Although expression of liver fatty acid binding protein (L-FABP) modulates cell growth, it is not known if L-FABP also alters cell morphology and differentiation. Therefore, pluripotent embryonic stem cells were transfected with cDNA encoding L-FABP and a series of clones expressing increasing levels of L-FABP were isolated. Untransfected ES cells, as well as ES cells transfected only with empty vector, spontaneously differentiated from rounded adipocyte-like to fibroblast-like morphology, concomitant with marked reduction in expression of stage-specific embryonic antigen (SSEA-1). These changes in morphology and expression of SSEA-1 were greatest in ES cell clones expressing L-FABP above a threshold level. Immunofluorescence confocal microscopy revealed that L-FABP was primarily localized in a diffuse-cytosolic pattern along with a lesser degree of punctate L-FABP expression in the nucleus. Nuclear localization of L-FABP was preferentially increased in clones expressing higher levels of L-FABP. In summary, L-FABP expression altered ES cell morphology and expression of SSEA-1. Taken together with the fact that L-FABP was detected in the nucleus, these data suggested that L-FABP may play a more direct, heretofore unknown, role in regulating ES cell differentiation by acting in the nucleus as well as cytoplasm

Fucosyltransferase gene expression in goat endometrium during the estrous cycle and early pregnancy

Regulation of the expression of the alpha(1,2)fucosyltransferase (FUT)genes and their enzymatic products, including the H-type 1 antigen (HT1), on the luminal surface of the uterus is believed to be critical for establishment of pregnancy in mammals. The FUT1 gene is a marker for conception rates in dairy cows and HT1 is a marker for uterine receptivity in rodents. To determine the spatiotemporal expression patterns of FUT1 and FUT2 genes in goats, endometrial tissues were obtained on six days spanning the estrous cycle (Days 5, 11, 13, 15, 17 and 19)and seven days spanning early pregnancy (Days 5, 11, 13, 15, 17, 19 and 25). In all data, we found no effect of status (cyclic or pregnant; P \u3e 0.1)and pooled data where appropriate. We cloned FUT1 cDNA from goat endometrium and made probes from it for Northern and slot blot analyses. The analyses indicated that FUT1 gene expression was high until Day 13, and then declined. In situ hybridization revealed a change in the cell-specificity of FUT1 gene expression over the estrous cycle and early pregnancy. In situ hybridization signal intensity scores indicated that FUT1 expression by uterine epithelium was high on Day 5, moderate on Day 11, and minimal on subsequent days. In situ hybridization signals in uterine glandular epithelial cells remained high from Day 5 to Day 13, with weaker signals thereafter. Quantitative reverse transcription-PCR (RT-qPCR)assays were used for quantitation of FUT1 and FUT2 mRNAs. Quantitative RT-qPCR data were generated from endometrium collected from cyclic and pregnant animals on Days 5, 11 and 17. Relative levels of FUT1 mRNA were high on Days 5 and 11, but then fell 5-fold by Day 17 (P \u3c 0.01). FUT2 mRNA concentrations were below the accurate detectable limit of the assay. High levels of HT1 were observed on the apical surface of uterine luminal epithelia on Days 5, 15, 17 and 19, with much lower levels on Days 11 and 13. Thus, data suggests that FUT1 is the primary enzyme responsible for the high levels of HT1 antigen present on the uterine luminal epithelium between Days 5 and 11 of the estrous cycle and early pregnancy. But changes in the expression of the FUT1 gene does not directly correlate to HT1 staining, which increased from Day 13–15. Future studies are required to understand the regulation of the HT1 antigen on the luminal surface of endometrium