Article Database

The Mythology of the Doudou: Sexualizing Black Female Bodies, Constructing Culture in the French Caribbean

Abstract:

In lieu of an abstract, please find a brief excerpt of the chapter below:

“Since the eighteenth century, Caribbean white Creoles and travelers to Martinique and Guadeloupe have extolled the beauty of the mulatto woman, transfiguring her. into a Venus-like symbol. So much so that this figure has come to be known nowadays in French studies and mainstream culture as the doudou. In the 1890s, for an American audience and then in the 1920s for a French readership, the works of international traveler and journalist Lafcadio Hearn showcase this exotic and radicalized discourse around French Caribbean women. Yet, it is only in the interwar period that writers from these islands living in Paris–namely, Suzanne Lacascade, and Paulette and Jane Nardal–noticeably denounce such a colonial as well as masculine eroticization and exoticization of the black female body. Consequently, this introduction contrasts Hearn’s writing to that of Lacascade and the Nardal sisters, to suggest that for these French Caribbean writers during the interwar period, awareness of the gendered self went hand-in-hand with awareness of the racial self. At that time in Paris, negrophilia and primitivism were thriving: the often demeaning craze for anything black or African was inescapable. Thus, these writers had to confront European representations of their blackness, Creoleness, and femininity, that is to say of their Caribbean culture. These exoticisizing works illustrate–as Brent Hayes Edwards argues, reclaiming Etienne Balibar–that “racism always ‘presupposes’ sexism”. To understand what these women were up against, this essay first examines the polysemy inherent in the term doudou, then discusses Hearn’s radicalized and exotic discourse, before exploring the responses of Lacascade and the Nardal sisters.”

Am I My Sister’s Keeper?: The Politics of Propriety and the Fight for Equality in the Works of French Antillean Women Writers, 1920s-40s

Abstract:

In lieu of an abstract, please find a brief excerpt of the chapter below:

“While stressing French Antillean black women’s contribution to modern black humanism and internationalism in the early twentieth century, scholarly debates often challenge their feminism and political activism for being neither as radical as their European counterparts nor as sufficiently anticolonial. Such discussions may obscure the fact that the fight for European women’s rights often excluded black women. There remains a need to redefine scholarly understanding of black women’s activism and its confrontation not only with institutional power but also with patriarchy and popular culture. This essay questions these women’s politics of propriety: the ways in which class influences conceptions of respectability and how these notions in turn affect ideas of race, gender, and sexuality. Such an approach facilitates a better understanding of black women’s fight for equality.

To this end, I examine how the Guadeloupean Suzanne Lacascade and the Martinican sisters Paulette and Jane Nardal reevaluate notions of race, gender, and politics by critiquing the racist and sexist construction of blackness taking place in France from the 1920s through the 1940s. They reject the exotic embodiment of Caribbean womanhood known today as the doudou: both a sexual object and a desiring archetype. Ideas of female 129 decency are central in their struggles for equality and women’s rights. Their lofty endeavors, contrasted with “lowbrow” constructions of race and gender produced by savvy women like performer Josephine Baker and novelist Mayotte Capécia, exposed classist leanings.”

Intersecting Identities of Women in Engineering

Abstract:

Giving a voice to marginalized groups and understanding the double bind is critical, especially after the Charlotte, VA protests and the white supremacist discourse that has pervaded our country. The result of the discourse, more subtle beliefs about white superiority and institutional barriers is an overrepresentation of women of color (WOC) in the leaky STEM pipeline and thus the loss of their presence and expertise. The absence of WOC hinders knowledge production and innovation that is essential for societal advancements and scientific discovery. The “chilly climate” is often cited as an explanation for the loss of WOC from STEM. However, interactions that allow the “chilly climate” to persist have yet to be characterized. This lack of understanding can inhibit the professional engineering identity construction of WOC. Additionally, engineering education research typically focuses on a single identity dimension such as gender or socio-economic status. These studies connect an identity dimension to student outcomes and few studies clarify how the identity is situated within the social context of the engineering culture. Consequently, a need exist to examine how the engineering culture impacts multiple components of identity and intersecting identities of WOC. To address this gap, our study illuminates the intersections of identity of WOC and how they perceive the double bind of race and gender within the context of their engineering education. The data reported here are a part of a larger, sequential mixed-methods study (N=276) of undergraduate female engineering students at a large Midwestern research university. This project applies the framework of intersectionality with the following scales: Engineering Identity, Ethnic Identity, Womanist Identity, Microaggressions, and Depression. We use intersectionality to investigate the interaction between intersecting social identities and educational conditions. We introduce the Womanist Identity Attitude scale to engineering education research, which provides an efficient way to understand gender, racial, and intersecting identity development of WOC. We utilize the microaggressions scale, in order to develop quantitative measures of gender-racial discrimination in STEM and compare to previous research. We also included the Patient Health Questionnaire (PHQ-9), an instrument for measuring depression, to assess health outcomes of respondents’ experiences of gender-racial microaggressions. Our three emergent findings suggest instrument accuracy and provide insight into the identity and depression subscales. Factor analysis established a basis to refine our quantitative survey instruments, and indicated that 23 items could offer greater accuracy than the original 54 items instrument. Second, the majority of participants report a high level of identification with engineering. This result rebuffs the long-held stereotypes that females are less interested in engineering. Third, a significant portion of female respondents self-reported PHQ-9 scores in the 15-19 range, which corresponds with a “major depression, moderately severe” provisional diagnosis, the second-highest in severity in the PHQ-9 provisional diagnosis scale. These elevated levels of depression correlated significantly to frequent instances of microaggressions. These preliminary findings are providing never-before seen insight into the experiences of WOC in engineering. Our results suggest a path to accurately describe the experiences of WOC in engineering, while revealing options for improving inclusion efforts.

Characterizing Glioblastoma Heterogeneity via Single-Cell Receptor Quantification

Abstract:

Dysregulation of tyrosine kinase receptor (RTK) signaling pathways play important roles in glioblastoma (GBM). However, therapies targeting these signaling pathways have not been successful, partially because of drug resistance. Increasing evidence suggests that tumor heterogeneity, more specifically, GBM-associated stem and endothelial cell heterogeneity, may contribute to drug resistance. In this perspective article, we introduce a high-throughput, quantitative approach to profile plasma membrane RTKs on single cells. First, we review the roles of RTKs in cancer. Then, we discuss the sources of cell heterogeneity in GBM, providing context to the key cells directing resistance to drugs. Finally, we present our provisionally patented qFlow cytometry approach, and report results of a “proof of concept” patient-derived xenograft GBM study.

Plenty more room on the glass bottom: Surface functionalization and nanobiotechnology for cell isolation

Abstract:

Surface functionalization is a widely adopted technique for surface modification which allows researchers to customize surfaces to integrate with their research. Surface functionalization has been used recently to adapt surfaces to integrate with biological materials specifically to isolate cells or mimic biological tissues through cell patterning. Cell isolation and cell patterning both can be integrated with extant techniques or surfaces to customize the research to whatever needs to be tested. Substrates such as metals, biologically mimicking surfaces, environmental responsive surfaces, and even three-dimensional surfaces such as hydrogels have all been adapted to allow for functionalization for both patterning and isolation. In this review we have described both the advantages and disadvantages of these techniques and the related chemistries to better understand these tools and how best to apply them in the hope that we can further expand upon the research in the field.

Cell isolation via spiral microfluidics and the secondary anchor targeted cell release system

Abstract:

Mapping Tyrosine Kinase Receptor Dimerization to Receptor Expression and Ligand Affinities

Abstract:

Tyrosine kinase receptor (RTK) ligation and dimerization is a key mechanism for translating external cell stimuli into internal signaling events. This process is critical to several key cell and physiological processes, such as in angiogenesis and embryogenesis, among others. While modulating RTK activation is a promising therapeutic target, RTK signaling axes have been shown to involve complicated interactions between ligands and receptors both within and across different protein families. In angiogenesis, for example, several signaling protein families, including vascular endothelial growth factors and platelet-derived growth factors, exhibit significant cross-family interactions that can influence pathway activation. Computational approaches can provide key insight to detangle these signaling pathways but have been limited by the sparse knowledge of these cross-family interactions. Here, we present a framework for studying known and potential non-canonical interactions. We constructed generalized models of RTK ligation and dimerization for systems of two, three and four receptor types and different degrees of cross-family ligation. Across each model, we developed parameter-space maps that fully determine relative pathway activation for any set of ligand-receptor binding constants, ligand concentrations and receptor concentrations. Therefore, our generalized models serve as a powerful reference tool for predicting not only known ligand: Receptor axes but also how unknown interactions could alter signaling dimerization patterns. Accordingly, it will drive the exploration of cross-family interactions and help guide therapeutic developments across processes like cancer and cardiovascular diseases, which depend on RTK-mediated signaling.

Single-Cell Receptor Quantification of an In Vitro Coculture Angiogenesis Model Reveals VEGFR, NRP1, Tie2, and PDGFR Regulation and Endothelial Heterogeneity

Abstract:

Angiogenesis, the formation of new blood vessels from pre-existing ones, is essential for both normal development and numerous pathologies. Systems biology has offered a unique approach to study angiogenesis by profiling tyrosine kinase receptors (RTKs) that regulate angiogenic processes and computationally modeling RTK signaling pathways. Historically, this systems biology approach has been applied on ex vivo angiogenesis assays, however, these assays are difficult to quantify and limited in their potential of temporal analysis. In this study, we adopted a simple two-dimensional angiogenesis assay comprised of human umbilical vein endothelial cells (HUVECs) and human dermal fibroblasts (HDFs) and examined temporal dynamics of a panel of six RTKs and cell heterogeneity up to 17 days. We observed ~2700 VEGFR1 (vascular endothelial growth factor receptor 1) per cell on 24-h-old cocultured HDF plasma membranes, which do not express VEGFR when cultured alone. We observed 4000–8100 VEGFR2 per cell on cocultured HUVEC plasma membranes throughout endothelial tube formation. We showed steady increase of platelet-derived growth factor receptors (PDGFRs) on cocultured HDF plasma membranes, and more interestingly, 1900–2900 PDGFRβ per plasma membrane were found on HUVECs within the first six hours of coculturing. These quantitative findings will offer us insights into molecular regulation during angiogenesis and help assess in vitro tube formation models and their physiological relevance

Multiplexing Angiogenic Receptor Quantification via Quantum Dots

Abstract:

Clinical and biomedical research seeks single-cell quantification to better understand their roles in a complex, multicell environment. Recently, quantification of vascular endothelial growth factor receptors (VEGFRs) provided important insights into endothelial cell characteristics and response in tumor microenvironments. However, existing technologies for quantifying plasma membrane receptor tyrosine kinases (RTKs) lack multiplexing capabilities, limiting detailed characterization. Here, we use the unique spectral properties of quantum dots (Qdots) to optimize and dually quantify VEGFR1 and VEGFR2 on human umbilical vein endothelial cells (HUVECs). To enable this quantification, we reduce nonspecific binding between Qdot-conjugated antibodies and cells via buffer optimization. Second, we identify optimal labeling conditions by examining Qdot-conjugated antibody binding to five receptors: VEGFRs (VEGFR1 and VEGFR2), their coreceptor neuropilin1 (NRP1), and platelet-derived growth factor receptor (PDGFRα and PDGFRβ). We establish that 800–20 000 is the dynamic range where accurate Qdot-enabled quantification can be achieved. Through these optimizations, we demonstrate measurement of 1 100 VEGFR1 and 6 900 VEGFR2 per HUVEC. We induce ∼90% upregulation of VEGFR1 and ∼30% downregulation of VEGFR2 concentration via 24 h VEGF-A₁₆₅ treatment. We observe no change in VEGFR1 or VEGFR2 concentration with 24 h VEGF-B₁₆₇ treatment. We further apply Qdots to analyze HUVEC heterogeneity and observe that 24 h VEGF-A₁₆₅ treatment induces a ∼15% decrease in VEGFR2 heterogeneity, but little to no change in VEGFR1 heterogeneity. We observe that VEGF-B₁₆₇ induces little to no change in either VEGFR1 or VEGFR2 heterogeneity. Overall, we demonstrate experimental and analytical strategies for quantifying two or more RTKs at single-level using Qdots, which will help provide new insights into biological systems.

Sex differences in cancer mechanisms

Abstract:

We now know that cancer is many different diseases, with great variation even within a single histological subtype. With the current emphasis on developing personalized approaches to cancer treatment, it is astonishing that we have not yet systematically incorporated the biology of sex differences into our paradigms for laboratory and clinical cancer research. While some sex differences in cancer arise through the actions of circulating sex hormones, other sex differences are independent of estrogen, testosterone, or progesterone levels. Instead, these differences are the result of sexual differentiation, a process that involves genetic and epigenetic mechanisms, in addition to acute sex hormone actions. Sexual differentiation begins with fertilization and continues beyond menopause. It affects virtually every body system, resulting in marked sex differences in such areas as growth, lifespan, metabolism, and immunity, all of which can impact on cancer progression, treatment response, and survival. These organismal level differences have correlates at the cellular level, and thus, males and females can fundamentally differ in their protections and vulnerabilities to cancer, from cellular transformation through all stages of progression, spread, and response to treatment. Our goal in this review is to cover some of the robust sex differences that exist in core cancer pathways and to make the case for inclusion of sex as a biological variable in all laboratory and clinical cancer research. We finish with a discussion of lab- and clinic-based experimental design that should be used when testing whether sex matters and the appropriate statistical models to apply in data analysis for rigorous evaluations of potential sex effects. It is our goal to facilitate the evaluation of sex differences in cancer in order to improve outcomes for all patients.