Diversity training in organizational environments has become commonplace in the 21st century. Most contemporary training seeks to make employees aware of implicit bias and the structural inequities that exist from systematic oppression. However, training is often not grounded in evidence-based practices and past research has shown diversity training may increase stereotyping and bias towards minorities. Additionally, high-status groups (e.g., White people, men) may perceive increased unfairness towards high-status members due to the emphasis on diversity, commonly referred as “reverse racism” or anti-White bias. This study seeks to further investigate how applicants view an organization's approach to diversity. White participants will be asked to apply for a scholarship and subsequently rejected. By investigating anti-White bias after a rejection, this study aims to examine whether Whites rationalize rejection with pro-diversity messages to protect against threat. I am also interested in perceived employability: a principle that has been shown to be linked with emotional regulation, health, and self esteem. I predict the magnitude of perceived qualification for a position moderates the degree of anti-White bias reported. Research on organizational diversity is imperative to decrease turn-over rates and increase satisfaction for minority employees.

Loss of neurons in the retina underlie many blinding diseases, such as macular degeneration, glaucoma, and diabetic retinopathy. These retinal neurons are not replaceable. The Reh Lab has developed a strategy to achieve functional regeneration of neurons in the adult mammalian retina, but not enough regeneration to restore vision loss. One of the potential limitations to restoring vision is the inflammation that occurs during retinal injury or disease. All mammalian retinas contain microglia, which are the primary immune cells of the nervous system that respond to pathogens, injury, and disease. My goal is to determine how microglia respond to damage-induced regeneration in the retina. After damaging mice retinas with an excitotoxin (NMDA), we induced neuronal regeneration with a proneural transcription factor called Ascl1. Using immunohistochemistry and confocal fluorescence microscopy, I stained various markers that represent different inflammation states of microglia. I quantified microglia and analyzed their response to neural regeneration. Data from confocal fluorescence microscopy revealed that microglia surround newly regenerated neurons and display a variety of subtypes during regeneration. Follow up single-cell sequencing experiments confirmed that these immune cells show a molecular heterogeneity of states. This study provides a better understanding about how microglia function during retinal regeneration. Results from this study can help reveal targets for manipulation to improve regeneration of the retina. Further work can be done to analyze how these microglia behaviors impact regeneration of lost retinal neurons.

In the Reh Lab, our research team focuses on neurodegenerative diseases that affect the retina by causing the death of neurons which result in irreversible blindness. In working towards treatments for retinal diseases we have engineered Muller glia to serve as a source for functional regeneration in the mammalian retina, but not enough to restore lost vision. While this is remarkable progress, limitations to this regeneration strategy still exist in regards to the amount of neurons generated. Recently, we have found that the endogenous immune cell of the retina, the microglia, responds to dead neurons by causing inflammation, which restricts the regenerative capacity of Muller glia. However, microglia are not the only immune cell present during regeneration and we currently do not have an understanding of the diversity of cell types that contribute to this regeneration restricting inflammation. My research project aimed to fill this gap by revealing which immune cells infiltrate the retina after injury and thereby revealing immunomodulation targets to improve retinal regeneration. In order to begin to understand the interaction of the peripheral immune system and the nervous system and how it impacts neurogenesis, I will present on my examination of monocyte and neutrophil invasion after retinal injury. For this study I have processed retinas using cryosectioning, immunohistochemistry, fluorescent antibody labeling, and confocal microscopy. Using this data I visualized and quantified the infiltration dynamics of monocytes and neutrophils in the damaged and regenerating retina. Data from this proposal will determine the types of immune cells and their window of infiltration for cell-type specific immunomodulation strategies to improve the regenerative capacity of the mammalian retina.This understanding of the immune component of regeneration is critical in moving forward to develop therapies for not only retinal diseases such as glaucoma but all neurodegenerative diseases such as Alzheimer’s and Parkinson’s.

The pupillary light reflex (PLR) curve is an important point-of-care biomarker for the diagnosis of traumatic brain injury (TBI). Using PLR, first responders can determine the severity of TBI in the field and direct patients to a trauma center where staff can continually assess PLR to monitor TBI severity. Manual pupillometry, the most commonly available method for first responders and most clinicians wishing to assess PLR, is qualitative and often inaccurate. The current gold-standard device for PLR measurement is digital infrared pupillometry, but such devices are fragile and expensive. Our research team has developed a smartphone-based pupillometer (PupilScreen) with the ability to assess PLR using a standard iPhone, assisted by a cloud-based neural network. To demonstrate the feasibility of using PupilScreen in a realistic clinical setting and compare the accuracy of the device to the current clinical gold-standard, we have built an annotated dataset of the PLR in n=120 patients with TBI who are hospitalized in a neurological intensive care unit. Pupillometry is performed using the mobile device and the gold-standard digital infrared pupillometer. Pupil videos are manually annotated and used in the further training of our machine learning algorithm that generates a PLR curve for each patient. We anticipate that our technology will demonstrate accuracy in assessing the PLR that exceeds that of manual pupillometry and is at least equivalent to the gold-standard digital pupillometer. This technology has the potential to alleviate the current undertreatment of many TBI patients in the United States and abroad that results from a lack of accurate and cost-effective pupillometry equipment.

Previous studies indicate that CNS administration of oxytocin (OT) reduces body weight in male high fat diet-induced obese (DIO) rodents by reducing food intake and increasing energy expenditure (EE). We recently demonstrated that hindbrain [fourth ventricular (4V)] administration of OT elicits weight loss and elevates interscapular brown adipose tissue temperature (TIBAT; surrogate marker of increased EE) in male DIO rats. What remains unclear is whether chronic CNS OT can impact body weight in female high fat diet-fed (HFD) rats and whether this involves activation of hindbrain OT receptors. We hypothesized that OT-induced stimulation of hindbrain OT receptors reduces weight gain and adiposity, in part, by reducing energy intake and increasing BAT thermogenesis in female HFD-fed rats. To test this hypothesis, we measured the effects of chronic 4V OT (≈16.1 ug/day) or vehicle infusions over 28 days on body weight, adiposity and energy intake in female HFD-fed (60% kcal from fat) rats (N=7-8/group). We found that chronic 4V OT reduced weight gain (P<0.05) and relative fat mass (P<0.05) in randomly cycling female HFD-fed rats. These effects were attributed, in part, to reduced energy intake evident during weeks 2 (P<0.05), 3 (P<0.05) and 4 (P<0.05). To assess if hindbrain OT administration also elevates BAT thermogenesis, we examined the effects of acute 4V OT (1, 5 ug) or vehicle on TIBAT in a separate group of female HFD-fed rats (N=8/group). We found that the low dose (1 ug) elevated TIBAT at 0.75, 1, 1.25, 1.5 and 2-h post-injection (P<0.05); the higher dose (5 ug) elevated TIBAT at 0.75, 1, 1.25, 1.5, 1.75 and 2-h post-injection (P<0.05). Together, these findings support the hypothesis that oxytocin action in the hindbrain reduces body weight gain and adiposity by reducing energy intake and increasing BAT thermogenesis in female HFD-fed rats.