Mass shootings are a growing public health and social policy concern in the United States. Mass shootings are defined by the Gun Violence Archive as four or more shot and/or killed in a single event, at the same general time and location, not including the shooter. Most media accounts attribute this phenomenon to lack of access to mental healthcare leading to untreated mental illness of the shooter and/or poor gun legislation leading to easy access of firearms. For this research project, I explore additional social factors which may help to determine variation in mass shooting across states. Using data from the United States Census Bureau, Uniform Crime Report, Kids Count Data Center, the Henry J Kaiser Family Foundation, and the Gun Violence Archive, I will be utilizing ordinary least squares regression to examine the role of poverty, social disorganization, gun legislation, and mental health spending to explain variation in the number of mass shootings across states during the period of 2010 to 2015. The results of these findings will provide a greater understanding of the contributors for mass shootings, further existing research, and assist policy makers in the reduction of future incidents.

Public investments in children are thought to benefit society by producing a healthy and productive workforce. However, in the race to produce competitive workers in the new international market, differing political approaches can result in variations in expenditures and disparities amongst children. In this research I analyze how overall childhood well-being differs between red states (states that voted for the Republican presidential candidate in two out of the last three elections) and blue states (states that voted for the Democratic presidential candidate in two out of the last three elections) to see if political ideologies are related to child outcomes. I also consider whether any differences between red states and blue states vary significantly for black and white youth. I look at three dimensions of childhood wellbeing: (1) health (infant mortality, percent immunized and Medicaid expenditures), (2) educational achievement (high school dropout rate and education expenditure per pupil), and (3) economic security (percent of population below the poverty line, and state expenditure on welfare programs) to determine which political orientation is associated with better conditions for youth. I expect Blue states, or Democratic leaning states, to yield better scores of adolescent wellbeing due to their advocacy for a larger social safety net. Previous research has shown that blacks typically have worse health, lower educational attainment and less economic security than do whites. Therefore, I expect blacks to fare more poorly than whites on the barometer of child well-being. I extend previous work by considering racial differences within a political orientation. Preliminary results have shown somde childhood wellbeing indicators to significantly favor whites in Blue states over Whites in Red states, however this difference was not signficant for Blacks. I have no hypothesis regarding whether the relationship between political orientation and child well-being differs significantly by race. I anticipate that my research will contribute to a more in-depth understanding of how different political outlooks influence the nation’s one of the most vulnerable populations--children. With the upcoming 2016 presidential race, this research is especially relevant.

Exposure to high levels of manganese (Mn) causes a form of Parkinsonism (PS) with clinical features similar to, but distinguishable from, Parkinson’s disease (PD). Though the clinical phenotype of Mn-induced PS is similar to PD, PD is characterized by neurodegeneration in the substantia nigra, whereas Mn-induced PS features striatal neurodegeneration. Mortalin, an important mitochondrial chaperone protein involved with the response to oxidative stress, has shown to be downregulated in PD. Moreover, in recent studies we found mortalin expression to be decreased in striatal astrocytes of Mn exposed miners and in astrocytes of the substania nigra of PD patients. Additionally, we found that in vitro, a reduction in mortalin expression impairs astrocytic protection of neurons. Importantly, Mn-induced astrocyte dysfunction is substantially reduced in cells lacking expression of α-Synuclein (α-Syn), suggesting that their interaction modulates astrocyte function, potentially affecting their neuro-protective role in PS. The interaction between α-Syn and mortalin was investigated in astrocytes isolated from brain regions associated with PD and of Mn-induced neurotoxicity. We employed an animal model of cultured astrocytes from the ventral mesencephalon, striatum, and cerebral cortex to examine this interaction. The cells were treated with 0, 10, or 100 μM Mn, then examined using western blotting and immunofluorescence microscopy. The relative levels of mortalin and α-Syn were then quantified and analyzed. We saw a decrease in the availability of functional astrocytic mortalin with increasing Mn in striatal cells compared to other regions and substantial aggregation of α-Syn, reflecting the astrocytic dysfunction. This study helps bring light to the potentially critical association between mortalin and α-Syn in motor-impaired neurodegenerative diseases and can have important implications for understanding the pathogenesis of α-Syn aggregation and ultimately, PS related neurodegeneration.
 

Exposure to manganese (Mn) causes a neurodegenerative syndrome with clinical manifestations of Parkinsonism (PS) similar to Parkinson’s disease (PD). Although both PD and Mn-induced PS feature movement dysfunction resulting from decreased striatal dopamine, pathologically, Mn-induced PS is thought to be related to striatal degeneration, while in PD, dopaminergic neuron bodies residing in the substantia nigra pars compacta are largely affected. Recent evidence has suggested that astrocytes, glial cells that play a vital role in maintaining homeostasis such as uptake and release of important molecules like precursors for neurotransmitters, may play a vital role in neuronal survival in PD and PS. In order to determine whether the regional differences in sensitivity to Mn are conferred by inherent differences in astrocytes from these brain regions I examined the role of such astrocytes in neuron survival. Contact co-cultures of two neuron-like immortalized cell lines, MES and SH-SY5Y cells, were made with astrocytes from the ventral mesencephalon (vm), striatum (str), and cortex (ctx). These were treated with 10μM and 100μM of Mn and stained for the markers MAP2, TH, and GFAP, imaged, and neurons were counted. Based on previous results, MES cells grown with str astrocytes are expected to have a lower survival rate when treated with Mn, versus those plated with vm and ctx astrocytes. If this trend is observed in the separate SH-SY5Y cell line, this would suggest other neuron-like cell lines and dopaminergic neurons respond similarly to Mn. By examining if Mn affects astrocytes, and in turn neuron survival, this could not only elucidate the pathogenesis of Mn-induced PS, but also elucidate the region specific astrocyte-neuron relationships in the brain.