This research will address climate change and its impact on migration to the US, specifically how it impacts Central America. Migration from this region is at an all-time high. Climate change, especially droughts and the decrease in precipitation, as well as extreme weather events, have agitated migration patterns in Central America and will compound in the near future with the increase of climate refugees from the region, putting additional stress on the already failing US immigration system. Before this problem gets out of hand, research needs to be conducted to understand the severity of the situation and steps towards a solution. This paper aims to uncover hidden data that often goes unseen that demonstrates the hardships and impossible situations that inhabitants of Central America are faced with. These hardships, compounded with new and emerging climate crises, are forcing many to migrate to more hospitable environments, namely, the United States. This study will first begin with an overview of the current situation and explain the problem at hand. It will then delve into the personal experiences of the participants of this study, those that are immigrants themselves, and those that have various and unique perspectives on this climate migration. This research will study how they have been impacted by climate-related issues such as extreme weather events, variability of precipitation, crop failure, etc. Finally, it will discuss the future of this issue and propose solutions and methods of adaptation for the coming decades.

In the retina, loss of neurons results in blindness, because the mammalian retina cannot regenerate. Although mammals cannot regenerate neurons, species such as fish and amphibians can make fully functional neurons after injury and restore their vision. Muller Glia (MG) cells in fish and amphibians are the source of this regeneration. These cells respond to injury by dedifferentiating into progenitor cells that then become neurons, replacing the dead neurons and in turn restoring sight. At the Reh Lab, we have found a way to stimulate functional regeneration in mammals through these MG cells by expressing a gene called Ascl1. This technique has limitations however, as it only causes 25% of MG to undergo neurogenesis. One of the variables potentially limiting regeneration is inflammation, as inflammation has been known to be detrimental to neurogenesis. Monocytes invade the retina after injury and potentially cause inflammation that limits retinal regeneration. To determine monocyte impact on retinal regeneration we employed a transgenic technique to ablate monocytes. I then performed our retinal regeneration paradigm and determined whether regeneration is enhanced in the absence of monocyte invasion. Using immunohistochemistry and confocal microscopy I found more regenerated neurons in retinas that lacked monocytes. These data further confirm that inflammation limits the regeneration capacity of the retina, and provides future topics to improve neural repair through modifying the immune response.

Blindness caused by retinal degeneration is untreatable, and is a condition currently suffered by millions. The field of retinal reprogramming aims to establish a way to treat this type of vision loss, by finding a way for the eye to essentially produce new retinal neurons after they have been lost to degeneration. Often, this is done through directing cell fate by expressing or repressing various transcription factors such as Ascl1, a potent pro-neural transcription factor involved in retinal reprogramming. Ascl1 expression in mouse Muller glia, a support cell in the retina, can stimulate the regeneration of certain subtypes of retinal neurons, but the variety of retinal cells produced through this strategy is still limited. The class of transcription factors known as ‘Krüppel-like factors,’ or KLFs, regulates important cell processes, such as cell proliferation and development, with several KLFs functioning in the development of neurons. Due to the inhibitory function of KLFs during neuron development, we propose that the loss of inhibitory KLF genes in Muller glia may allow for activation of neurogenesis. Therefore, coupling the knockout of KLF genes with Ascl1 expression in Muller glia may be a key to enhancing reprogramming capabilities of Ascl1. For this project, I knocked out KLF genes in young mouse Muller glia in culture using the CRISPR/Cas9 system, and induced Ascl1 expression to stimulate reprogramming of the Muller glia. We used scRNA sequencing to determine if the knockout reprogrammed cells were molecularly similar to various retinal cell types that are typically lost with degenerative blindness. Preliminary sequencing results revealed that knockout of one candidate, KLF15, appears to promote neurogenesis. Findings from this experiment will allow us to increase our understanding of the role of KLF genes in retinal cell development as we work towards a future treatment for degenerative vision loss.

Retinal diseases such as macular degeneration and glaucoma lead to various forms of blindness as neurons in the retina die. Unlike amphibians or fish, the neurons of the mammalian retina cannot regenerate on their own and any damage is permanent. Previous research has shown that we can recover some of the lost regenerative capacity in mammalian retinas by mimicking the regeneration process in other species. This is possible by overexpressing transcription factor Ascl1 in Müller glia (MG), which are the main support cells in the retina. However, expressing Ascl1 alone can only lead to the neurogenesis of one type of neuron in the retina. This limits the therapeutic applicability of this approach because in diseases like macular degeneration or glaucoma, specific neuronal cell types are lost such as photoreceptors and ganglion cells respectively. Therefore, to regenerate these neurons we need to identify the right cocktail of transcription factors for MG reprogramming. Recent single-cell analysis from our lab has identified candidate developmental factors that could push reprogrammed cells to photoreceptors or retinal ganglion cells. This project aims to investigate the role of these factors in influencing cell fate after MG cells have been pushed to a progenitor state with Ascl1. Using lentiviral vectors, I will induce the overexpression of these candidate genes in primary cultures of young adult mouse MG that have been engineered to express Ascl1. In order to identify the nature of resulting neurons from these cultures I will perform immunocytochemistry paired with confocal microscopy, and to better understand changes in functionality of these cells I aim to perform calcium imaging. Since the electrophysiological responses of glia and neurons are distinct, cultures with reprogrammed neurons would record differently. Overall, this analysis evaluates the influence of new transcription factors on mammalian retinal regeneration.

In fish and amphibians there is a specialized zone of retinal stem-cells at the edge of the retina, called the ciliary margin zone (CMZ) which replenishes the retina with new cells if it is damaged in adult animals. However, the presence of these stem-cells has not been observed specifically in the CMZ of the developing human. Here, I investigate the developing human retina to understand if it contains stem-cells that could be harnessed for repair. I first utilized CMZ stem-cell markers found in fish and amphibians to assess in the developing human retina, including BLBP, C-myc, cyclin D3, Six3, SMAD1/5, and Zic1. Following the stainings, I observed expression of C-myc and BLBP. To maintain their long-term proliferation, stem-cells will replicate slowly. Therefore I analyzed cell cycle kinetics in the CMZ. Primary cultures of fetal human retina, called retinospheres, were made by dissecting the fetal retina into small pieces containing a portion of the CMZ and growing them in culture with retinal differentiation media. EdU, a dye that is integrated into DNA only in replicating cells, was then added to the media for different incubation intervals with EdU being 30min, 1hr, 2hrs, 4hrs, 6hrs, 8.5hrs and 25hrs, then retinospheres were fixed in PFA. Retinospheres were IHC stained with antibodies and dyes: Pax6 (a stem-cell marker), EdU (marker of cell division), Ki67 (marker of replicating cells) and DAPI. The total Ki67 positive cells in the CMZ and of EdU and Ki67 positive cells were counted so that the S-phase of mitosis could be measured to discover how fast the cells in the CMZ were dividing. I observed that cells in the CMZ were replicating slower than those further away from the CMZ, consistent with the possibility that there is a population of stem-cells in the CMZ of the developing human retina.

The Civil Rights Movement of the 1960s in the United States galvanized millions of Americans to fight for a more free and democratic society, banding together to protest racial segregation and other forms of systemic racism such as police violence against minorities. Newspapers covered these actions extensively, spreading the message of civil rights across the US. People eager for change in cities far from the centers of civil rights activism in the South, such as Seattle, responded to this national political fervor by fighting for change locally. In Seattle, activists sought an end to job and housing discrimination, de facto school segregation, and police violence through non-violent direct action. Seattle’s major print newspapers, The Seattle Times and the Seattle Post-Intelligencer covered these issues extensively, spreading news and controversial developments to their readers. In my research, I analyze newspaper coverage on activism and cases of police violence which garnered a strong public demand for justice. With the support of other sources, such as the biographies of Seattle activists, the histories of local civil rights organizations, and studies on media coverage of the police, I construct an analysis of how these newspapers shifted their coverage of civil rights activism and police violence throughout the 1960s as a response to community activism. This critical angle focuses on how the actions of Seattle’s activist community influenced newspaper media, prompting the newspapers to include more activist perspectives in their news coverage. This research, therefore, displays the power that local activists held in influencing print media coverage of their actions, and with that, the influence that activists had to shift the public perspective towards activism in the 1960s in Seattle.

Mount St. Helens shook local communities and spewed volcanic ash into the sky for two months before it finally had its major eruption. In those two months newspapers eagerly tracked the activity, crafted a story, and relayed it to their audiences. When the mountain erupted on May 18, 1980, the world caught a glimpse of nature’s power and found a dramatic climax to their two-month story. In the immediate aftermath, accounts of what had happened took various forms, ranging from personal hymns to films, with each of them showing a different response to the eruption. These responses showcase a population reconsidering what it means to live alongside nature. Today, forty years later, Mount St. Helens’ story is still being told through a wide array of sources. In my research, I analyze works approaching the eruption, reacting in the immediate aftermath, and those which have come out in memory. I note the content of these sources as well as their framing to construct an analysis of how changing treatment of the Mount St. Helens story reveals society’s approach to nature before the eruption and how that approach changed in response to the events of May 18. I specifically focus on sources consumed and produced by the broader public, such as films and songs, using private correspondence or scientific conferences only as a source of what does not make widespread narratives. This approach encapsulates how people of various communities make sense of living alongside the natural world, and especially how they conceptualize sudden change events like volcanic eruptions. My research uncovers both flaws in the population’s conceptual relationship to nature as well as their tendencies to remember natural events, specifically Mount St. Helens, in a way that maintains or minimally changes the way the see themselves in the world.

In neonates, hypoxic-ischemic encephalopathy (HIE) increases the risk of impaired neurodevelopmental outcomes and death. In high resource settings, HIE occurs in 1-4 per 1,000 live births, and in low resource settings, 12 per 1,000 live births. Where available, therapeutic hypothermia (TH) is the standard of care for neuroprotection in HIE. However, the protection provided by TH is incomplete, motivating the search for adjunctive therapies. To assist in testing new therapies, researchers have attempted to predict injury severity in animals before ex vivo quantification, but the association between early injury and long-term outcomes has not been studied in the Vannucci model of hypoxic-ischemic brain injury - the most widely used HIE model in rats. This study sought to determine the association of early injury identified by in vivo magnetic resonance imaging (MRI) with weight gain and behavioral testing data. Using the Vannucci model, postnatal day (P) 10 rats underwent ligation of the left carotid artery followed by 3 hours of hypoxia and then 5 hours of normothermia in room air. Animals were then randomized, with half receiving an additional 3 hours of TH while the other half were returned to their cage. On P12, MRIs were performed, and injury quantification was determined using imaging software FSLeyes. Animals were weighed daily for one week following the HIE injury and then every 2-3 days until P43. Behavioral testing was conducted on P42 and P43 and included open field, novel object recognition, and CatWalk. We hypothesize that greater injury on the early MRI will be associated with reduced weight gain after injury and worse performance on behavioral testing.

Hypoxia ischemia (HI) is one of the leading injuries in term neonates and can lead to death or long-term disability. The current standard of care is therapeutic hypothermia (TH). Our lab has developed a model for HI injury in rats which is used to test the efficacy of potential treatments. At postnatal day (P) 10, which is the equivalent of a full-term human neonate, rats undergo unilateral carotid artery ligation followed by hypoxia. The animals are given a 30-minute rest period before rectal temperatures are gauged to determine the post-surgical (time 0) temperatures. Animals are then placed in warm water baths for a period of normothermia (NT). Every 15-30 minutes rectal temperatures are recorded, and water baths are adjusted in order for the rats to maintain the goal temperature of 36.5°C (± 0.5°C). After 6 hours of NT, a randomized subset of animals undergo 3 hours of TH to reach 32°C (± 0.5°C). On P43 the rats are euthanized and perfused transcardially for brain removal and formalin fixation. The brains are assigned an injury severity score between 0 and 4, and % injury by volume is detected by MRI. The correlation between time 0 temperature and injury score will be calculated, as well as the correlation between the coefficient of variation of the temperatures for each animal throughout NT and the injury score. Further statistical analysis will be conducted throughout this experiment as the project is currently ongoing, including analysis by treatment group (NT vs TH). This project aims to determine if time 0 temperatures and variation of temperature are indicative of injury severity. Based on a similar study observing the relationship between the time 0 temperatures of ferrets and HI injury severity score, we expect to see that rats with lower time 0 temperature and greater temperature variation will have more severe brain injuries.

In October 1962, China and India waged a war to contest the demarcation of their shared border, a culmination of years of escalating hostilities between the two governments. One month later, after overwhelming the Indian military, the Chinese declared a unilateral ceasefire. By contrast, seven years earlier at the 1955 Asian-African Conference in Bandung, Indonesia, leaders from each country signed pledges for peace and mutual non-aggression. Speeches by Indonesian host and president Sukarno, Indian prime minister Jawaharlal Nehru, and Chinese foreign minister Zhou Enlai imparted on attendees, most of whom represented newly decolonized countries, a sense of cautious optimism for their collective advancement. However, the "Bandung spirit" dissipated by 1965, as evidenced by the cancellation of the Second Asian-African Conference in Algeria. While most scholars focus on the Sino-Soviet Split and 1965 Algerian coup to explain the Bandung spirit's rupture, I study the 1962 border war and failed mediation efforts by neutralist governments, like Indonesia, as evidence of the Asian-African alliance's early fracturing. Drawing from primary sources such as English and Indonesian language newspapers, Indian, Chinese, and Indonesian government documents, and the writings of Indian and Indonesian politicians, I argue that Indonesians advocated for a stricter definition, relative to Nehru, of anti-imperialism tinged with Asian nationalism. Indonesian leaders’ reluctance to defend Nehru, their partner at Bandung, demonstrate that the Sino-Indian War exposed ideological differences between India and Indonesia, thus facilitating the Bandung Spirit’s demise. By framing the war with the Bandung Conference, I explore how governments fall short of their lofty visions of anti-imperialism and perpetuate the nationalistic hierarchies they originally eschew.

This research project involves analyzing planetesimal accretion through the use of an N-body simulation. A terrestrial planet passes through many stages of growth including: dust grains, pebbles, planetesimals, embryos, to planets. This study focuses on the formation process between planetesimals and embryos. Current simulations demonstrating terrestrial formation use parameters similar to those of our own solar system. This investigation attempts to envision this process at a more “bunched” up scale, such as in the case of the Trappist-1 system. Our inner solar system, a radial distance from the Sun to Mars, is about 25 times larger than the entire Trappist-1 system, meaning that its planets were formed much closer to its star. Through the use of N-body simulations, we can begin to understand the unknown formation of this system as well as others with similar characteristics. These N-body simulations are processed through the University of Washington’s supercomputer Hyak, approximating the motion of the particles that represent the planetesimals and detect if any are in a collision course. Two short period simulations were run using a number of sophisticated collision models that differ in how the particles interact and formation efficiency. The previous collision model used parameters calculated in 2005. The second newer model uses parameters from 2021, which I have programmed into the model's initial condition files. The study’s purpose is to compare the outputs of the collision models through a variety of quantitative and qualitative factors, concentrating on particle growth and runaway growth. More specifically, the data is measured through plots that depict the semi major axis vs. eccentricity, max mass over mean mass as a function of time, and the ratio of collisions that result in a merger. This will later lead to the investigation of which models can accurately replicate terrestrial formations such as the Trappist-1 system.

Computing solutions to partial differential equations using the fast Fourier transform can lead to unwanted oscillatory behavior. Because of the periodic nature of the Fourier transform, waves that leave the interval on one side reappear on the other. However, the fast Fourier transform is a very efficient numerical tool, so it is important to find a way to damp these oscillations so that this transform can still be used. Our goal is to accurately model nonlinear partial differential equations on an infinite domain by considering a finite interval and implementing various damping techniques outside of the interval. We consider the Korteweg-de Vries equation with an initial condition that produces leftward traveling oscillations and a rightward traveling soliton. To damp the wrap-around oscillations, we have used the Strang-splitting method to solve the heat equation with a non-zero diffusion coefficient on the left side of the interval. To stop the soliton from wrapping around, we judiciously multiply the solution values by a decaying exponential on the right side of the interval. We have found that this damping process produces much more accurate solutions at larger times than the undamped solution when modeling solutions on an infinite interval. This method also applies to the nonlinear Schrodinger equation with some additional modifications.