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The present work interrogates the history of Confederate memorializations by examining the relationship between these memorializations and lynching, an explicitly racist act of violence. We obtained and merged data on Confederate memorializations at the county level and lynching victims, also at the county level. We find that the number of lynching victims in a county is a positive and significant predictor of the number of Confederate memorializations in that county, even after controlling for relevant covariates. This finding provides concrete, quantitative, and historically and geographically situated evidence consistent with the position that Confederate memorializations reflect a racist history, one marred by intentions to terrorize and intimidate Black Americans in response to Black progress.

GPR44 (DP2, PTGDR2, CRTh2) is the receptor for the pro-inflammatory mediator prostaglandin D.sub.2 (PGD.sub.2) and it is enriched in human islets. In rodent islets, PGD.sub.2 is produced in response to glucose, suggesting that the PGD.sub.2 -GPR44/DP2 axis may play a role in human islet function during hyperglycemia. Consequently, the aim of this work was to elucidate the insulinotropic role of GPR44 antagonism in vitro in human beta-cells and in type 2 diabetes (T2DM) patients. We determined the drive on PGD.sub.2 secretion by glucose and IL-1beta, as well as, the impact on insulin secretion by pharmacological GPR44/DP2 antagonism (AZD1981) in human islets and beta-cells in vitro. To test if metabolic control would be improved by antagonizing a hyperglycemia-driven increased PGD.sub.2 tone, we performed a proof-of-mechanism study in 20 T2DM patients (average 54 years, HbA1c 9.4%, BMI 31.6 kg/m.sup.2). The randomized, double-blind, placebo-controlled cross-over study consisted of two three-day treatment periods (AZD1981 or placebo) separated by a three-day wash-out period. Mixed meal tolerance test (MMTT) and intravenous graded glucose infusion (GGI) was performed at start and end of each treatment period. Assessment of AZD1981 pharmacokinetics, glucose, insulin, C-peptide, glucagon, GLP-1, and PGD.sub.2 pathway biomarkers were performed. We found (1) that PGD.sub.2 is produced in human islet in response to high glucose or IL-1beta, but likely by stellate cells rather than endocrine cells; (2) that PGD.sub.2 suppresses both glucose and GLP-1 induced insulin secretion in vitro; and (3) that the GPR44/DP2 antagonist (AZD1981) in human beta-cells normalizes insulin secretion. However, AZD1981 had no impact on neither glucose nor incretin dependent insulin secretion in humans (GGI AUC .sub.C-peptide 1-2h and MMTT AUC .sub.Glucose 0-4h LS mean ratios vs placebo of 0.94 (80% CI of 0.90-0.98, p = 0.12) and 0.99 (90% CI of 0.94-1.05, p = 0.45), despite reaching the expected antagonist exposure. Pharmacological inhibition of the PGD.sub.2 -GPR44/DP2 axis has no major impact on the modulation of acute insulin secretion in T2DM patients.

This essay was adapted from a conference presentation given at the Native American and Indigenous Studies Association meeting in 2018. In it I consider the entanglements of antiblackness and settler colonialism through the incommensurabilities of Blackness and Indigeneity at the center of U.S. empire. I ask how theorizations of race and colonialism have lived consequences for how we enact solidarities across disparate histories and geographies, embody resistances at the intersections of identities, and imagine futures outside the colonial registers of possession and dispossession. Returning to the concept of arrivants, I consider further what “ground” and “normativity” actually mean in the context of antiblackness and empire, and toward that end, I hold ground as Indigenous and as relational to push against anything that might be deemed normative in gestures that highlight the processes of removal and arrival to center the refusals of subjectivity as it has been defined through enlightenment and imperialism. Finally, I argue for a reading of power that apprehends the conflicting, oppositional, and contradictory vectors of antiblackness within ongoing settler colonialism to reveal how the investments of racial capitalism pit oppressions against each other while requiring different forms of oppression to vie for ascendancy as the one truth of history.

Human mini-brains (MB) are cerebral organoids that recapitulate in part the complexity of the human brain in a unique three-dimensional in vitro model, yielding discrete brain regions reminiscent of the cerebral cortex. Specific proteins linked to neurodegenerative disorders are physiologically expressed in MBs, such as APP-derived amyloids (A[beta]), whose physiological and pathological roles and interactions with other proteins are not well established in humans. Here, we demonstrate that neuroectodermal organoids can be used to study the A[beta] accumulation implicated in Alzheimer's disease (AD). To enhance the process of protein secretion and accumulation, we adopted a chemical strategy of induction to modulate post-translational pathways of APP using an Amyloid-[beta] Forty-Two Inducer named Aftin-5. Secreted, soluble A[beta] fragment concentrations were analyzed in MB-conditioned media. An increase in the A[beta].sub.42 fragment secretion was observed as was an increased A[beta].sub.42 /A[beta].sub.40 ratio after drug treatment, which is consistent with the pathological-like phenotypes described in vivo in transgenic animal models and in vitro in induced pluripotent stem cell-derived neural cultures obtained from AD patients. Notably in this context we observe time-dependent A[beta] accumulation, which differs from protein accumulation occurring after treatment. We show that mini-brains obtained from a non-AD control cell line are responsive to chemical compound induction, producing a shift of physiological A[beta] concentrations, suggesting that this model can be used to identify environmental agents that may initiate the cascade of events ultimately leading to sporadic AD. Increases in both A[beta] oligomers and their target, the cellular prion protein (PrP.sup.C ), support the possibility of using MBs to further understand the pathophysiological role that underlies their interaction in a human model. Finally, the potential application of MBs for modeling age-associated phenotypes and the study of neurological disorders is confirmed.

Several studies have shown that epitope vaccines exhibit substantial advantages over conventional vaccines. However, epitope vaccines are associated with limited immunity, which can be overcome by conjugating antigenic epitopes with built-in adjuvants (e.g., some carrier proteins or new biomaterials) with special properties, including immunologic specificity, good biosecurity and biocompatibility, and the ability to vastly improve the immune response of epitope vaccines. When designing epitope vaccines, the following types of built-in adjuvants are typically considered: (1) pattern recognition receptor ligands (i.e., toll-like receptors); (2) virus-like particle carrier platforms; (3) bacterial toxin proteins; and (4) novel potential delivery systems (e.g., self-assembled peptide nanoparticles, lipid core peptides, and polymeric or inorganic nanoparticles). This review primarily discusses the current and prospective applications of these built-in adjuvants (i.e., biological carriers) to provide some references for the future design of epitope-based vaccines.