Pat Your Foot and Turn the Corner : Amiri Baraka, the Black Arts Movement, and the Poetics of a Popular Avant-Garde

My larger objective here is to engage the current cultural conversation about the nature of the Black Arts Movement and its impact on politics and culture in the United States and beyond. So while I honor the significance of Amiri Baraka\u27s work as artist, critic, and activist, my intention is to place that work within a movement in which Baraka is but one voice among many, albeit an important one. In other words, in the spirit of Baraka\u27so wn criticala nd autobiographicalw ritings, I want to emphasize, to the degree that it is possible in a short essay, the collectivity and diversity of the Black Arts Movement, and try to avoid the sort of great-man theory in which Baraka\u27s work becomes a metonymy for all Black Arts literature, drama, criticism, and so on.1 I also want to say that this is a small part of a larger work-in-progress designed to further conversation rather than shut it off with some gesture toward authority

The role of astrocytes in prion-like mechanisms of neurodegeneration

Accumulating evidence suggests that neurodegenerative diseases are not merely neuronal in nature but comprise multicellular involvement, with astrocytes emerging as key players. The pathomechanisms of several neurodegenerative diseases involve the deposition of misfolded protein aggregates in neurons that have characteristic prion-like behaviours such as template-directed seeding, intercellular propagation, distinct conformational strains and protein-mediated toxicity. The role of astrocytes in dealing with these pathological prion-like protein aggregates and whether their responses either protect from or conspire with the disease process is currently unclear. Here we review the existing literature implicating astrocytes in multiple neurodegenerative proteinopathies with a focus on prion-like behaviour in this context

Galaxy Zoo: constraining the origin of spiral arms

Since the discovery that the majority of low-redshift galaxies exhibit some level of spiral structure, a number of theories have been proposed as to why these patterns exist. A popular explanation is a process known as swing amplification, yet there is no observational evidence to prove that such a mechanism is at play. By using a number of measured properties of galaxies, and scaling relations where there are no direct measurements, we model samples of SDSS and S4G spiral galaxies in terms of their relative halo, bulge and disc mass and size. Using these models, we test predictions of swing amplification theory with respect to directly measured spiral arm numbers from Galaxy Zoo 2. We find that neither a universal cored or cuspy inner dark matter profile can correctly predict observed numbers of arms in galaxies. However, by invoking a halo contraction/expansion model, a clear bimodality in the spiral galaxy population emerges. Approximately 40 per cent of unbarred spiral galaxies at z 10^10 Msolar have spiral arms that can be modelled by swing amplification. This population display a significant correlation between predicted and observed spiral arm numbers, evidence that they are swing amplified modes. The remainder are dominated by two-arm systems for which the model predicts significantly higher arm numbers. These are likely driven by tidal interactions or other mechanisms

Distinct responses of neurons and astrocytes to TDP-43 proteinopathy in amyotrophic lateral sclerosis

Amyotrophic lateral sclerosis (ALS) is a fatal and incurable neurodegenerative disease caused by motor neuron loss, resulting in muscle wasting, paralysis and eventual death. A key pathological feature of ALS is cytoplasmically mislocalized and aggregated TDP-43 protein in >95% of cases, which is considered to have prion-like properties. Historical studies have predominantly focused on genetic forms of ALS, which represent ∼10% of cases, leaving the remaining 90% of sporadic ALS relatively understudied. Additionally, the role of astrocytes in ALS and their relationship with TDP-43 pathology is also not currently well understood. We have therefore used highly enriched human induced pluripotent stem cell (iPSC)-derived motor neurons and astrocytes to model early cell type-specific features of sporadic ALS. We first demonstrate seeded aggregation of TDP-43 by exposing human iPSC-derived motor neurons to serially passaged sporadic ALS post-mortem tissue (spALS) extracts. Next, we show that human iPSC-derived motor neurons are more vulnerable to TDP-43 aggregation and toxicity compared with their astrocyte counterparts. We demonstrate that these TDP-43 aggregates can more readily propagate from motor neurons into astrocytes in co-culture paradigms. We next found that astrocytes are neuroprotective to seeded aggregation within motor neurons by reducing (mislocalized) cytoplasmic TDP-43, TDP-43 aggregation and cell toxicity. Furthermore, we detected TDP-43 oligomers in these spALS spinal cord extracts, and as such demonstrated that highly purified recombinant TDP-43 oligomers can reproduce this observed cell-type specific toxicity, providing further support to a protein oligomer-mediated toxicity hypothesis in ALS. In summary, we have developed a human, clinically relevant, and cell-type specific modelling platform that recapitulates key aspects of sporadic ALS and uncovers both an initial neuroprotective role for astrocytes and the cell type-specific toxic effect of TDP-43 oligomers

Challenges for industrial robot applications in food manufacturing

The global food industry is facing many challenges due to the impact of climate change, ever-changing demands by consumers, and increasing legislative pressures by the government, which have resulted in several drivers for changes. Current large scale rigid manufacturing systems are increasingly seen as incapable of supporting the underlining requirements for implementation of such changes. In this context, one of the key requirements is the need for improved flexibility and reconfigurability of production facilities, often provided by adoption of Industrial Robots in other manufacturing sectors. However, despite their recent technological advancements, in particular the advent of the 4th industrial revolution (Industry 4.0), and significant reduction in overall implementation cost over the last two decades, the uptake of industrial robots in food processing has been slow. This paper explores the application of industrial robots in food manufacturing, the benefits of their use and the challenges currently hindering their uptake

Galaxy Zoo: Are Bars Responsible for the Feeding of Active Galactic Nuclei at 0.2 < z < 1.0?

We present a new study investigating whether active galactic nuclei (AGN) beyond the local universe are preferentially fed via large-scale bars. Our investigation combines data from Chandra and Galaxy Zoo: Hubble (GZH) in the AEGIS, COSMOS, and GOODS-S surveys to create samples of face-on, disc galaxies at 0.2 < z < 1.0. We use a novel method to robustly compare a sample of 120 AGN host galaxies, defined to have 10^42 erg/s < L_X < 10^44 erg/s, with inactive control galaxies matched in stellar mass, rest-frame colour, size, Sersic index, and redshift. Using the GZH bar classifications of each sample, we demonstrate that AGN hosts show no statistically significant enhancement in bar fraction or average bar likelihood compared to closely-matched inactive galaxies. In detail, we find that the AGN bar fraction cannot be enhanced above the control bar fraction by more than a factor of two, at 99.7% confidence. We similarly find no significant difference in the AGN fraction among barred and non-barred galaxies. Thus we find no compelling evidence that large-scale bars directly fuel AGN at 0.2<z<1.0. This result, coupled with previous results at z=0, implies that moderate-luminosity AGN have not been preferentially fed by large-scale bars since z=1. Furthermore, given the low bar fractions at z>1, our findings suggest that large-scale bars have likely never directly been a dominant fueling mechanism for supermassive black hole growth.Comment: 13 pages, 5 figures, 2 tables, accepted by MNRA

3D Growth of Cancer Cells Elicits Sensitivity to Kinase Inhibitors but Not Lipid Metabolism Modifiers

Tumor cells exhibit altered lipid metabolism compared with normal cells. Cell signaling kinases are important for regulating lipid synthesis and energy storage. How upstream kinases regulate lipid content, versus direct targeting of lipid-metabolizing enzymes, is currently unexplored. We evaluated intracellular lipid concentrations in prostate and breast tumor spheroids, treated with drugs directly inhibiting metabolic enzymes fatty acid synthase (FASN), acetyl-CoA carboxylase (ACC), diacylglyceride acyltransferase (DGAT), and pyruvate dehydrogenase kinase (PDHK), or cell signaling kinase enzymes PI3K, AKT, and mTOR with lipidomic analysis. We assessed whether baseline lipid profiles corresponded to inhibitors' effectiveness in modulating lipid profiles in three-dimensional (3D) growth and their relationship to therapeutic activity. Inhibitors against PI3K, AKT, and mTOR significantly inhibited MDA-MB-468 and PC3 cell growth in two-dimensional (2D) and 3D spheroid growth, while moderately altering lipid content. Conversely, metabolism inhibitors against FASN and DGAT altered lipid content most effectively, while only moderately inhibiting growth compared with kinase inhibitors. The FASN and ACC inhibitors' effectiveness in MDA-MB-468, versus PC3, suggested the former depended more on synthesis, whereas the latter may salvage lipids. Although baseline lipid profiles did not predict growth effects, lipid changes on therapy matched the growth effects of FASN and DGAT inhibitors. Several phospholipids, including phosphatidylcholine, were also upregulated following treatment, possibly via the Kennedy pathway. As this promotes tumor growth, combination studies should include drugs targeting it. Two-dimensional drug screening may miss important metabolism inhibitors or underestimate their potency. Clinical studies should consider serial measurements of tumor lipids to prove target modulation. Pretherapy tumor classification by de novo lipid synthesis versus uptake may help demonstrate efficacy