Celebrating Indigenous National Cinemas and Narrative Sovereignty through the Creation of Kin Theory, an Indigenous Media Makers Database

Indigenous peoples have been misrepresented and underrepresented in media since the dawn of cinema, but they have never stopped telling their own stories and enacting agency. It is past time to recognize them on their own terms. To facilitate that, academics, activists, and industry partners can fund, hire, teach, and share more Black, Indigenous and people of color (BIPOC) led projects. The uniqueness of 2020 with COVID-19, Black Lives Matter and human rights movements, and the move online by many academics and organizations have deepened conversations about systemic inequities, such as those in media industries. To address the often-heard film industry excuse, “I don’t know anyone of color to hire,” the Nia Tero Foundation has created Kin Theory, an Indigenous media makers database, that is having a dynamic, year-long launch in 2021.Nia Tero is a global nonprofit that uplifts Indigenous peoples in their land stewardship through policy and storytelling. Kin Theory is being developed to be global in scope, celebrating the multiplicity of Indigenous national cinemas and the power of narrative sovereignty. This paper demonstrates ways in which Kin Theory is striving to Indigenize the film industry through collaborations, coalition building, and co-liberation joy. The projected outcome of this study is to highlight how Kin Theory has the potential to increase access to Indigenous media makers, strengthens relationships, makes media works more visible, and increases support for BIPOC-led projects. This paper discusses the impacts of media misrepresentations and erasure, the foundations of Kin Theory, and introduces the potential for Indigenous national cinemas and narrative sovereignty. By reporting on the launch of Kin Theory at the Big Sky Documentary Film Festival, strategies for Indigenizing the film industry are also discussed. Throughout it is argued that decolonization is not a salvage project, it is an act of creation, and diverse industry leaders are offering new systems that support this thriving revitalization

Mixed correlation function and spectral curve for the 2-matrix model

We compute the mixed correlation function in a way which involves only the orthogonal polynomials with degrees close to $n$, (in some sense like the Christoffel Darboux theorem for non-mixed correlation functions). We also derive new representations for the differential systems satisfied by the biorthogonal polynomials, and we find new formulae for the spectral curve. In particular we prove the conjecture of M. Bertola, claiming that the spectral curve is the same curve which appears in the loop equations.Comment: latex, 1 figure, 55 page

The Dn Ruijsenaars-Schneider model

The Lax pair of the Ruijsenaars-Schneider model with interaction potential of trigonometric type based on Dn Lie algebra is presented. We give a general form for the Lax pair and prove partial results for small n. Liouville integrability of the corresponding system follows a series of involutive Hamiltonians generated by the characteristic polynomial of the Lax matrix. The rational case appears as a natural degeneration and the nonrelativistic limit exactly leads to the well-known Calogero-Moser system associated with Dn Lie algebra.Comment: LaTeX2e, 14 pages; more remarks are added in the last sectio

Magnetic Domains

Recently a Nahm transform has been discovered for magnetic bags, which are conjectured to arise in the large n limit of magnetic monopoles with charge n. We interpret these ideas using string theory and present some partial proofs of this conjecture. We then extend the notion of bags and their Nahm transform to higher gauge theories and arbitrary domains. Bags in four dimensions conjecturally describe the large n limit of n self-dual strings. We show that the corresponding Basu-Harvey equation is the large n limit of an equation describing n M2-branes, and that it has a natural interpretation in loop space. We also formulate our Nahm equations using strong homotopy Lie algebras.Comment: 42 pages, minor improvements, published versio

Metabolomic Profiling Reveals a Role for Androgen in Activating Amino Acid Metabolism and Methylation in Prostate Cancer Cells

Prostate cancer is the second leading cause of cancer related death in American men. Development and progression of clinically localized prostate cancer is highly dependent on androgen signaling. Metastatic tumors are initially responsive to anti-androgen therapy, however become resistant to this regimen upon progression. Genomic and proteomic studies have implicated a role for androgen in regulating metabolic processes in prostate cancer. However, there have been no metabolomic profiling studies conducted thus far that have examined androgen-regulated biochemical processes in prostate cancer. Here, we have used unbiased metabolomic profiling coupled with enrichment-based bioprocess mapping to obtain insights into the biochemical alterations mediated by androgen in prostate cancer cell lines. Our findings indicate that androgen exposure results in elevation of amino acid metabolism and alteration of methylation potential in prostate cancer cells. Further, metabolic phenotyping studies confirm higher flux through pathways associated with amino acid metabolism in prostate cancer cells treated with androgen. These findings provide insight into the potential biochemical processes regulated by androgen signaling in prostate cancer. Clinically, if validated, these pathways could be exploited to develop therapeutic strategies that supplement current androgen ablative treatments while the observed androgen-regulated metabolic signatures could be employed as biomarkers that presage the development of castrate-resistant prostate cancer

HDAC Inhibitors Act with 5-aza-2′-Deoxycytidine to Inhibit Cell Proliferation by Suppressing Removal of Incorporated Abases in Lung Cancer Cells

5-aza-2′-deoxycytidine (5-aza-CdR) is used extensively as a demethylating agent and acts in concert with histone deacetylase inhibitors (HDACI) to induce apoptosis or inhibition of cell proliferation in human cancer cells. Whether the action of 5-aza-CdR in this synergistic effect results from demethylation by this agent is not yet clear. In this study we found that inhibition of cell proliferation was not observed when cells with knockdown of DNA methyltransferase 1 (DNMT1), or double knock down of DNMT1-DNMT3A or DNMT1-DNMT3B were treated with HDACI, implying that the demethylating function of 5-aza-CdR may be not involved in this synergistic effect. Further study showed that there was a causal relationship between 5-aza-CdR induced DNA damage and the amount of [3H]-5-aza-CdR incorporated in DNA. However, incorporated [3H]-5-aza-CdR gradually decreased when cells were incubated in [3H]-5-aza-CdR free medium, indicating that 5-aza-CdR, which is an abnormal base, may be excluded by the cell repair system. It was of interest that HDACI significantly postponed the removal of the incorporated [3H]-5-aza-CdR from DNA. Moreover, HDAC inhibitor showed selective synergy with nucleoside analog-induced DNA damage to inhibit cell proliferation, but showed no such effect with other DNA damage stresses such as γ-ray and UV, etoposide or cisplatin. This study demonstrates that HDACI synergistically inhibits cell proliferation with nucleoside analogs by suppressing removal of incorporated harmful nucleotide analogs from DNA

MS-275 synergistically enhances the growth inhibitory effects of RAMBA VN/66-1 in hormone-insensitive PC-3 prostate cancer cells and tumours

Combining drugs, which target different signalling pathways, often decreases adverse side effects while increasing the efficacy of treatment. The objective of our study was to determine if the combination of our novel atypical retinoic acid metabolism-blocking agent (RAMBA) VN/66-1 and a promising histone deacetylase inhibitor N-(2-aminophenyl)4-[N-(pyridine-3-yl-methoxy-carbonyl)aminomethyl]benzamide (MS-275) would show enhanced antineoplastic activity on human PC-3 prostate cancer cells/tumours and also to decipher the molecular mechanisms of action. The combination of VN/66-1+MS-275 was found to be synergistic in inhibiting PC-3 cell growth, caused cell cytostaticity/cytotoxicity and induced marked G2/M phase arrest and apoptosis. In mice with well-established PC-3 tumours, VN/66-1 (5 and 10 mg kg−1 day−1) caused significant suppression of tumour growth compared with mice receiving vehicle alone. Furthermore, treatment with VN/66-1 (10 mg kg−1 day−1)+MS-275 (2.5 mg kg−1 day−1) for 18 days resulted in an 85% reduction in final mean tumour volume compared with control and was more effective than either agent alone. Mechanistic studies indicated that treatment of PC-3 cells/tumours with VN/66-1+MS-275 caused DNA damage (upregulation of γH2AX), hyperacetylation of histones H3 and H4, upregulation of retinoic acid receptor-β, p21WAF1/CIP1, E-cadherin, and Bad and downregulation of Bcl-2. These data suggest that the mechanism of action of the combination of agents is DNA damage-induced p21 activation, resulting in inhibition of the Cdc2/cyclin B complex and accumulation of cells in G2/M phase. In addition, the combination caused modulation and induction of apoptosis. These results suggest that VN/66-1 or its combination with MS-275 may be a novel therapy for the treatment of prostate carcinoma