Healthy Communities in Southern Illinois

Due to industrial and lifestyle changes, rural and small town areas are losing population and suffering economic hardship. These areas also suffer from the poorest health. However, most rural or small town residents also believe in the American Dream, revitalizing their local area, and preserving the small town or rural way of life. In this paper, I look at the relationship between obesity and local infrastructure – including walkability and access to healthy food – in southern Illinois. I then make suggestions for development policies for the region in the context of local public opinion

Disaster and Gender in Southern Illinois

The unique needs of women in the context of disaster have been largely overlooked in disaster management. For this reason, women have been hard-hit by natural disasters in the United States and internationally. However, by learning from the mistakes of the past, the negative effects of disasters on women may be mitigated through disaster management that is sensitive to the different needs and experiences of women and men. Illinois is at risk for a variety of natural disasters including floods, tornadoes, earthquakes, and storms. Some areas of the state, including southern Illinois, are more vulnerable due to social characteristics such as high poverty rates, high rates of single parent households, large elderly populations, and above average rates of domestic violence and sexual assault. Men’s and women’s experiences of these social vulnerabilities within the context of disaster are different. Research on past disasters has documented the ways that gender-based social roles and social gender equality determine how hard and in what ways women are hit by disasters. More often than not women continue to shoulder the bulk of caretaking responsibilities. Further, women have different needs in regard to health, and safety from violence. The negative effects of disaster on women and the communities that they reside within can be reduced by preparedness plans that consider the needs of women. Before a disaster hits an area, local leaders should be aware of towns or counties with high rates of gender-based violence, single parent households, and poverty as those women are especially at risk in a disaster. Leaders should also be aware of areas that have a greater than average population of children, the elderly, or disabled persons. Evacuation plans should be tailored with these characteristics in mind

Geographies of Inequality: Urban Renewal and the Race, Gender, and Class of Post-Katrina New Orleans

In this paper, we address pressing questions on the perpetuation of race, gender, and class inequalities in ongoing restoration practices shaping the New New Orleans. We unpack federal and local efforts to rebuild and revitalize the city over the last ten years and map the geography of New Orleans at the neighborhood level both before and after the storm. We discuss how mismanaged resources, corrupt profit-taking, conflicts of interest for the stakeholders, and socially unconscious design conditioned a fiscally irresponsible and non-inclusive recovery. These efforts have pushed out already marginalized populations, resulted in the gentrification of historically African American neighborhoods, and ultimately maintained complex social inequalities

MOLECULAR BASIS AND MODIFICATION OF A NEURAL CREST DEFICIT IN A DOWN SYNDROME MOUSE MODEL

poster abstractTrisomy 21 occurs in 1/700 live births and leads to phenotypes associat-ed with Down syndrome (DS), including craniofacial dysmorphology and a small mandible. Ts65Dn mice are trisomic for approximately half the genes on human chromosome 21 and display DS-like craniofacial anomalies. Cells cultured from Ts65Dn and euploid 1st pharyngeal arch (PA1) and neural tube (NT) tissues were used to analyze the effects of genetic dysregulation on cell proliferation and migration. In vitro studies revealed a proliferation deficit in trisomic PA1 and migration deficits from trisomic NT originating at embryonic day 9.5 (E9.5). DYRK1A is a gene thought to be involved in DS craniofacial development and we hypothesized that dysregulation of Dyrk1a contributes to altered craniofacial development in Ts65Dn mice. We also hypothesized that Dyrk1a agonists could be used to ameliorate this phenotype. To test our hypotheses, we quantified expression of Dyrk1a using qPCR. At E9.5, Dyrk1a is upregulated in Ts65Dn as relative to euploid PA1. We also showed that cell proliferation and migration could be returned to near euploid levels with the green tea polyphenol epigallocatechin gallate (EGCG) and harmine (known Dyrk1a inhibitors) in vitro. To further test our hypothesis, pregnant Ts65Dn and euploid mothers were treated with EGCG on E7 and E8 and E9.5 trisomic and euploid embryos were assessed for embryonic volume, PA1 vol-ume, and NCC number. Preliminary evidence suggests in vivo treatment leads to an increase in embryonic volume, PA1 volume, and NCC number in both euploid and trisomic embryos. Trisomic EGCG-treated embryos had similar PA1 volumes and NCC numbers to euploid embryos treated with PBS. Gene expression analysis of EGCG-treated NCCs is currently underway to better understand the effects of EGCG in these studies. Our results provide information about the molecular basis of DS craniofacial abnormalities and may lead to evidenced-based therapeutic options

The Climate of Opinion in Illinois 2008- 2016: Roots of Gridlock

Since January 1, 2015, Illinois has been frozen in a governmental and political gridlock that has dominated the state’s political discourse, consumed the energies of all involved, and created chaos in governmental and non-profit agencies that normally deliver state services. It has also created untold hardship and suffering among those who are most dependent on state services. The conflict has especially threatened to drastically reduce the quality and missions of the institutions of public higher education in Illinois, a state system that was widely recognized as one of the best in the nation and the world

TREATMENT OF CRANIOFACIAL DEFICITS ASSOCIATED WITH DOWN SYN-DROME IN A MOUSE MODEL

poster abstractTrisomy 21 is the genetic source of the group of phenotypes commonly known as Down syndrome (DS). These phenotypes include cognitive im-pairment, heart defects and craniofacial abnormalities, including a small mandible. The Ts65Dn mouse model contains three copies of approximately half the genes found on human chromosome 21 and exhibits similar pheno-types to individuals with DS including a small, dysmorphic mandible. Our lab has traced this deficit to a smaller first branchial arch (BA1) consisting of fewer neural crest cells (NCCs) at embryonic day 9.5 (E9.5). At E9.5, Dyrk1a, a gene known to affect craniofacial development, is upregulated in the BA1, likely contributing to its cell deficit. Using epigallocatechin gallate (EGCG), an extract from green tea and a known inhibitor of Dyrk1a, we are attempting to rescue this deficit. We hypothesize the consumption of EGCG by pregnant mothers at E7 and E8 will rescue the mandibular deficit in de-veloping embryos by reducing the expression or activity of Dyrk1a. From our data we conclude the treatment of pregnant mothers with EGCG results in increased embryo size of trisomic embryos. Further analysis will be done to determine embryo volume, the volume of the BA1, and number of NCCs within the BA1 to determine the effects of EGCG in vivo. This research will better our understanding of craniofacial development and could lead to po-tential genetic-based therapies in the future

Correction of Craniofacial Deficits using Epigallocatechin-3’-gallate Treatment in a Down Syndrome Mouse Model

poster abstractDown syndrome (DS) is caused by trisomy of human chromosome (HSA21). Individuals with DS display distinct craniofacial abnormalities including an undersized, dismorphic mandible which leads to difficulty with eating, breathing, and swallowing. Using the Ts65Dn DS mouse model (three copies of ~50% HSA21 homologs), we have traced the mandibular deficit to a neural crest cell (NCC) deficiency and reduction in first pharyngeal arch (PA1 or mandibular precursor) at embryonic day 9.5. Previous studies have shown that this deficit is caused when NCC fail to migrate from the neural tube to populate the PA1 and fail to proliferate in the PA1. At E9.5, Dyrk1A, a triplicated DS candidate gene, is overexpressed in the PA1 and may cause the NCC and PA1 deficits. We hypothesize that treatment of pregnant Ts65Dn mothers with Epigallocatechin-3’-gallate (EGCG), a known Dyrk1A inhibitor, will correct NCC deficits and rescue the undersized PA1 in trisomic E9.5 embryos. To test our hypothesis, we treated pregnant Ts65Dn mothers with EGCG, where embryos received treatment from either E7-E8 or E0-E9.5. Our preliminary study found variable increases in PA1 volume and NCC number between treatment regimens, with several treatment groups indicating EGCG treatment has the potential to rescue the NCC deficit in the mandibular precursor. We found an increase in NCC number and PA1 volume with E7-E8 EGCG treatment in 21-24 somite embryos from trisomic mothers and in euploid embryos from euploid mothers treated from E0-E9.5. With EGCG treatment, we also observed a decrease in the average somite number of embryos from trisomic mothers, but an increase in those mothers’ average litter size. This study is important because it helps define the specific dosage and timing of ECGC and how it may affect specific DS phenotypes. These findings provide preclinical testing for a potential therapy for craniofacial disorders linked to DS

Mandibular and Neural Crest Cell Deficits Seen in TsDn65 Down Syndrome Mouse Model Rescued By Green Tea Polyphenol, EGCG

poster abstractDown Syndrome (DS) is caused by trisomy of the human chromosome 21 (Hsa21) and occurs in ~1 of every 700 births. DS is distinguished by over 80 phenotypic abnormalities including skeletal deficits and craniofacial phenotypes characterized by a flattened skull, slanted eyes, and a smaller mandible. To study these abnormalities, we utilize the Ts65Dn DS mouse model containing a triplication of approximately half of the gene homologues found on Hsa21 and mirrors the skeletal and mandibular phenotypes observed in DS. In Ts65Dn mice, the origin of the mandibular deficits were traced to a reduction in size of the 1st branchial arch (BA1), the developmental precursor to the mandible, occurring at embryonic day 9.5 (E9.5). At E9.5, we observe a lack of proliferation and migration of neural crest cells (NCC) from the neural tube (NT) into the BA1, causing a reduced BA1. We hypothesize that an overexpression of Dyrk1a, a Hsa21 homologue, contributes to the mandibular deficit seen in E9.5 Ts65Dn embryos. We propose that EGCG, a green tea polyphenol, will inhibit DYRK1a activity, rescuing the BA1 deficit. To test our hypothesis, Ts65Dn mothers were treated with EGCG from E0-E9.5 and sacrificed to retrieve the E9.5 embryos. Our results from unbiased stereological assessments show that E0-E9.5 EGCG in vivo treatment has the potential to increase NCC number, BA1 volume, and embryo volume of trisomic embryos. This data provide preclinical testing for a potential therapy of DS craniofacial disorders, which may extend to treating bone deficits in DS and osteoporosis