United by White Supremacy

This article explores how white women in the U.S. have centered their right to citizenship on the maintenance of white supremacy. While current scholarship primarily focuses on white male supremacy and women’s historical campaigning for citizenship, little is dedicated to establishing a connection between women’s white supremacy and their organizing efforts across the generations. Through a close examination and analysis of existing literature, I argue that different groups of women in varying spaces and times assisted to create a “whites only” citizenship by emphasizing their whiteness and femininity. Since the inception of the republic, white women have repeatedly claimed their right to agency and privilege by ideologically distancing themselves from the construct of the uncivilized, masculine, and promiscuous Black woman. They assert themselves as the “civilizing” fair sex who is educated, chaste, pure, and domestic. From the fair sex advocates of the founding era to the tradwives of today’s digital world, seemingly disparate groups of women united to advocate for a “whites only” citizenship. They used every avenue possible: violence against Black women and other people of color; wrote letters and ads; held protests and rallies; participated in grassroots organizing; built far-reaching political networks; published articles; and created social media accounts. These women teach us that white supremacy is sustained by our white women friends, relatives, colleagues, and neighbors. If we start to recognize their strategic weaponization of whiteness and femininity, we can better thwart the advancement of a “whites only” citizenship. &nbsp

PERK Regulates the Proliferation and Development of Insulin-Secreting Beta-Cell Tumors in the Endocrine Pancreas of Mice

PERK eIF2alpha kinase is required for the proliferation of the insulin-secreting beta- cells as well as insulin synthesis and secretion. In addition, PERK signaling has been found to be an important factor in determining growth and angiogenesis of specific types of tumors, and was attributed to PERK-dependent regulation of the hypoxic stress response. In this report we examine the role of PERK in regulating proliferation and angiogenesis of transformed beta-cells in the development of insulinomas.The SV40 Large T-antigen (Tag) was genetically introduced into the insulin secreting beta-cells of Perk KO mice under the control of an inducible promoter. Tumor growth and the related parameters of cell proliferation were measured. In late stage insulinomas the degree of vascularity was determined.The formation and growth of insulinomas in Perk-deficient mice was dramatically ablated with much fewer tumors, which averaged 38-fold smaller than seen in wild-type control mice. Beta-cell proliferation was ablated in Perk-deficient mice associated with reduced tumor growth. In the small number of large encapsulated insulinomas that developed in Perk-deficient mice, we found a dramatic reduction in tumor vascularity compared to similar sized insulinomas in wild-type mice. Although insulinoma growth in Perk-deficient mice was largely impaired, beta-cell mass was increased sufficiently by T-antigen induction to rescue the hypoinsulinemia and diabetes in these mice.We conclude that PERK has two roles in the development of beta-cell insulinomas, first to support rapid cell proliferation during the initial transition to islet hyperplasia and later to promote angiogenesis during the progression to late-stage encapsulated tumors

Glucose dehydrogenase is required for normal sperm storage and utilization in female Drosophila melanogaster

Female sperm storage is a key factor for reproductive success in a variety of organisms, including Drosophila melanogaster. The spermathecae, one of the Drosophila sperm storage organs, has been suggested as a long-term storage organ because its secreted substances may enhance the quality of sperm storage. Glucose dehydrogenase (GLD) is widely expressed and secreted in the spermathecal ducts among species of the genus Drosophila. This highly conserved expression pattern suggests that this enzyme might have an important role in female fertility. Here, we examine the function of GLD in sperm storage and utilization using Gld-null mutant females. The absence of GLD reduced the amount of sperm stored in the spermathecae and led to a highly asymmetrical sperm distribution in the two spermathecal capsules of the mutant females. The storage defect was especially severe when the mutant females were crossed to a Gld-mutant male that had previously mated a few hours before the experimental cross. Under this mating condition, the mutant females stored in the spermathecae only one-third of the sperm amount of the wild-type control females. In addition, the mutant females used stored sperm at a slower rate over a longer period compared with wild-type females. Thus, our results indicate that GLD facilitates both sperm uptake and release through the spermathecal ducts

Writing Across the Curriculum : Problems and Possibilities for Implementation Within a Traditional High School

Curriculum and Instructio

Visualization, implementation, and application of the Walking Tree heuristics for biological string matching

Biologists need tools to see the structural relationships encoded in biological sequences (strings). The Walking Tree heuristics calculate some of these relationships. I have designed and implemented graphic presentations which allow the biologist (user) to see these relations. This thesis contains background information on the biological sequences and some background on the Walking Tree heuristics. I demonstrate my methods by showing a visual matching of mitochondrial genomes. I also show matchings based on amino acids and on hydrophobicity. I also show how the parameters of the visualization can be varied to produce more useful pictures. I implemented a parallel version of the Walking Tree heuristic and used it to produce a phylogenetic tree for picornaviruses. I also implemented several user interfaces. These programs are available on my WWW page which allows a user to produce a picture of a matching by giving the sequences in Gen Bank format and by making a few mouse clicks

Acute ablation of PERK results in ER dysfunctions followed by reduced insulin secretion and cell proliferation

<p>Abstract</p> <p>Background</p> <p>A deficiency in <it>Perk </it>(EIF2AK3) causes multiple neonatal defects in humans known as the Wolcott Rallison syndrome. <it>Perk KO </it>mice exhibit the same array of defects including permanent neonatal diabetes (PND). PND in mice was previously shown by us to be due to a decrease in beta cell proliferation and insulin secretion. The aim of this study was to determine if acute ablation of PERK in the 832/13 beta cells recapitulates these defects and to identify the primary molecular basis for beta cell dysfunction.</p> <p>Results</p> <p>The INS1 832/13 transformed rat beta cell line was transduced with a dominant-negative <it>Perk </it>transgene via an adenoviral vector. <it>AdDNPerk</it>-832/13 beta cells exhibited reduced expression of <it>insulin </it>and <it>MafA </it>mRNAs, reduced insulin secretion, and reduced cell proliferation. Although proinsulin content was reduced in <it>AdDNPerk</it>-832/13 beta cells, proinsulin was abnormally retained in the endoplasmic reticulum. A temporal study of the acute ablation of <it>Perk </it>revealed that the earliest defect seen was induced expression of two ER chaperone proteins, GRP78/BiP and ERp72. The oxidized states of ERp72 and ERp57 were also increased suggesting an imbalance in the redox state of the ER.</p> <p>Conclusion</p> <p>Acute ablation of Perk in INS 832/13 beta cells exhibited all of the major defects seen in <it>Perk KO </it>mice and revealed abnormal expression and redox state of key ER chaperone proteins. Dysregulation of ER chaperone/folding enzymes ERp72 and GRP78/BiP occurred early after ablation of PERK function suggesting that changes in ER secretory functions may give rise to the other defects including reduced insulin gene expression, secretion, and cell proliferation.</p

PERK EIF2AK3 control of pancreatic β cell differentiation and proliferation is required for postnatal glucose homeostasis

SummaryMutations in PERK (EIF2AK3) result in permanent neonatal diabetes as well as several other anomalies that underlie the human Wolcott-Rallison syndrome, and these anomalies are mirrored in Perk knockout mice. To identify the cause of diabetes in PERK-deficient mice, we generated a series of tissue- and cell-specific knockouts of the Perk gene and performed a developmental analysis of the progression to overt diabetes. We discovered that PERK is specifically required in the insulin-secreting β cells during the fetal and early neonatal period as a prerequisite for postnatal glucose homeostasis. However, PERK expression in β cells is not required at the adult stage to maintain β cell functions and glucose homeostasis. We show that PERK-deficient mice exhibit severe defects in fetal/neonatal β cell proliferation and differentiation, resulting in low β cell mass, defects in proinsulin trafficking, and abrogation of insulin secretion that culminate in permanent neonatal diabetes

PERK eIF2 alpha kinase is required to regulate the viability of the exocrine pancreas in mice

<p>Abstract</p> <p>Background</p> <p>Deficiency of the PERK eIF2α kinase in humans and mice results in postnatal exocrine pancreatic atrophy as well as severe growth and metabolic anomalies in other organs and tissues. To determine if the exocrine pancreatic atrophy is due to a cell-autonomous defect, the <it>Perk </it>gene was specifically ablated in acinar cells of the exocrine pancreas in mice.</p> <p>Results</p> <p>We show that expression of PERK in the acinar cells is required to maintain their viability but is not required for normal protein synthesis and secretion. Exocrine pancreatic atrophy in PERK-deficient mice was previously attributed to uncontrolled ER-stress followed by apoptotic cell death based on studies in cultured fibroblasts. However, we have found no evidence for perturbations in the endoplasmic reticulum or ER-stress and show that acinar cells succumb to a non-apoptotic form of cell death, oncosis, which is associated with a pronounced inflammatory response and induction of the pancreatitis stress response genes. We also show that mice carrying a knockout mutation of PERK's downstream target, ATF4, exhibit pancreatic deficiency caused by developmental defects and that mice ablated for ATF4's transcriptional target CHOP have a normal exocrine pancreas.</p> <p>Conclusion</p> <p>We conclude that PERK modulates secretory capacity of the exocrine pancreas by regulating cell viability of acinar cells.</p