Aging is a degenerative process characterized by a progressive deterioration of cellular components and organelles resulting in mortality. The nematode Caenorhabditis elegans has been used extensively to study the biology of aging, and several determinants of C. elegans longevity are conserved in higher order organisms. The specific mechanisms of longevity in C. elegans have not been completely identified and many pathways are still poorly understood. Dietary restriction (DR) is one promising pro-longevity intervention, though its mechanism is poorly defined. DR, a reduction in caloric intake in the absence of malnutrition, extends lifespan in C. elegans and in a wide range of other species, including yeast, flies, mice, and primates. However this extension is highly dependent on genetic background. To investigate this, we are performing a genome-wide screen of the Vidal RNA interference (RNAi) Library, which has a catalog of 11,511 clones. By knocking down specific genes within the C. elegans genome through RNAi, we are able to observe an extension or reduction in longevity in response to DR. We have screened over 1500 genes; 61 of which are short-lived and 67 of which are long-lived. We are currently following up on our collected data by measuring the full lifespans using the RNAi clones that significantly shortened or extended lifespans in our screen. By screening such a large number of genes, the widespread effect, and hopefully mechanism, of DR will be elucidated. We hope to see genes significantly affected by DR cluster into groups with common functionality, or along the same pathway, and then follow up on those specific pathways to clarify the mechanisms underlying DR. If these pathways are conserved, research findings relating to C. elegans may be applicable to other organisms. We hope to confirm these results and further investigate the interaction between DR and other potential longevity pathways.

Humans are exposed to environmental toxins which can contribute to acute or chronic diseases, such as Parkinson's disease. Different people, however, have variable susceptibility to these toxins due to genetic variability within the population. In this project, we will utilize the model organism Saccharomyces cerevisiae(yeast) to investigate the molecular mechanisms of differential responses to environmental toxins that target the mitochondria. Many yeast single-gene deletion mutants will be exposed to mitochondrial toxins using a high-throughput Biosreen C instrument(combined shaker, incubator and plate reader, allowing for growth rate determination of yeast cells) and subsequently, bioinformatic methods will be exploited to identify genes involved in the response to mitochondrial stress and mechanisms of toxicity. We explored optimum concentration of different toxins for mutant yeast, expecting that different mutations will response genotype-dependently to different compounds. Identifying genotype-dependent responses to the environmental mitochondrial toxins may illuminate how mitochondria toxins contribute to disease and identify genetic factors invovled in susceptibility.

The hypoxia-inducible factor (HIF-1) is an oxygen-dependent transcription factor that plays a crucial role in an animal’s response to changing oxygen availability. When oxygen is plentiful, HIF-1 is ubiquitinated and targeted for degradation by the von Hippel Lindau protein (VHL-1), which inactivates HIF-1. Recent studies have shown that HIF-1 stabilization through mutation of vhl-1 increases longevity in the model organism Caenorhabditis elegans. This is contrary to humans, where VHL-1 mutations cause a disease characterized by angiomas, renal carcinomas and various other tumors as a direct result of aberrant HIF-1 activation. Since nematodes are post-mitotic organisms in adulthood, constitutive activation of HIF-1 does not cause tumor formation and is able to increase lifespan. In order to better understand how HIF-1 increases longevity and to relate these findings to mammals, our project aims to find the specific genes and tissues downstream of HIF-1 that benefit worm longevity without the consequences of VHL disease. To identify these genes, we conducted an RNAi screen for genes that are necessary for HIF-1-mediated longevity. Using the results of this screen, we are creating transgenic worms that overexpress these genes under specific nematode promoters. To test for the tissue specificity of HIF-1-mediated longevity, we are stabilizing HIF-1 in different tissues using tissue specific promoters. Our initial data are promising; we have found two genes downstream of HIF-1 that when overexpressed increase nematode longevity. At least one of these genes, flavin-monooxygenase-2, is a well-conserved protein known to be involved in xenobiotic metabolism. Additionally, we have found that expressing stabilized HIF-1 in neurons is sufficient to increase nematode lifespan. Our continuing studies will identify additional target genes and tissues important for HIF-1 mediated longevity and will attempt to elucidate the mechanism by which they increase lifespan.

Internet pornography is a cultural and generational phenomenon. A majority of the academic studies involving pornography tend to focus on the physical and psychological responses to pornography. From a Communication perspective, Internet pornography provides an interesting area of study as both a form of media and a topic of discourse. This study analyzes textual user responses to Internet pornography via comment sections on the popular pornographic website Pornhub.com. Eight classifications of comments were developed to include comments of Praise, Self-Promotion, Self-Description, Fantasy, Advertising, Asking/ Answering, Critique, and Miscellaneous content. Publicly available user profiles were also coded in complement to their respective comments. Profiles yielded user reported Age, Sex, Sexual Orientation, Relationship Status, and more. Through classification and close textual analysis, this study attempts to understand how and why users “talk back” to their porn.

Leigh syndrome is a clinically defined collection of diseases comprised of multiple genetic defects related to mitochondrial function. This syndrome results in early death in children typically due to respiratory failure as a consequence of progressive neuropathy, and currently no viable treatment options exist. Leigh syndrome can result from mutations in several different mitochondrial genes, one of which encodes the NDUFS4 subunit of complex I in the mitochondrial electron transport chain. As the NDUFS4 knockout mice phenocopy human patients with Leigh syndrome remarkably well, this model was utilized for the purpose of this study. Dietary restriction (DR) was identified as a possible treatment for mitochondrial deficiencies through a yeast genetic screen, which found that mitochondrial gene mutants generally received a robust lifespan benefit from DR. Thus, the primary focus of our research is to determine the efficacy of rapamycin (a DR mimetic) as an intervention in the NDUFS4 -/- mitochondrial disease mouse model. Rapamycin functions as a DR mimetic through its inhibition of the mechanistic target of rapamycin (mTOR) signaling pathway, which is responsible for modulating a variety of metabolic and cellular processes. Our model suggests that the increased NADH/NAD ratio resulting from a complex I deficiency in these knockout mice is sensed as energy abundance and results in systemic metabolic derailment. We propose that inhibiting mTOR signaling addresses this defect by altering intracellular energy sensing and modifying metabolic status. In order to test the efficacy of rapamycin treatment, NDUFS4 -/- mice were treated with daily injections of rapamycin or vehicle. Lifespan data for each treatment and additional assays for health related parameters were conducted to determine the response to the treatment regime. Investigating Leigh syndrome in this context will allow us to better understand the underlying mechanisms of pathogenesis, and directly test novel interventions aimed at attenuating this disease.

Ethosuximide is a succinimide anticonvulsant used in the clinical treatment of petit mal epileptic seizures in humans. Although its exact mechanism is not fully elucidated, it is believed to inhibit T-type calcium channels. In addition to its medical use, ethosuximide has been found to increase lifespan in the model organism, the nematode C. elegans. Nematodes exhibit lifespan extension when treated with ethosuximide at concentrations below a toxic threshold. While the published experimental results on ethosuximide-treated nematodes are promising, we have discovered that ethosuximide breaks down in the presence of 254 nm ultra-violet (UV) light, forming a toxic by-product. This change in ethosuximide that results in toxicity is specifically caused by irradiation, not heat. Acute exposure of C. elegans to ethosuximide treated with UV light results in death at lower dosages compared to nematodes treated with the control, native compound. UV-treated ethosuximide toxicity is independent of chemosensation (i.e. the sensing of chemical stimuli) as evidenced by the fact that chemosensory mutants do not show enhanced resistance to the UV-treated drug. Some human patients taking ethosuximide experience a butterfly rash under the eyes following exposure to sunlight. We speculate that this rash may be indicative of a similar mechanism of UV-induced cytotoxicity occurring in these patients. Taken together, these studies will help explicate the mechanism of toxicity resulting from exposure of ethosuximide to UV light, as well as the mechanism of action of native ethosuximide.

 Aging is a degenerative process characterized by a progressive deterioration of cellular components and organelles resulting in mortality. The nematode Caenorhabditis elegans has been used extensively to study the biology of aging, and several determinants of C. elegans longevity are conserved in higher order organisms. The specific mechanisms of longevity in C. elegans have not been completely identified and many pathways are still poorly understood. Dietary restriction is one promising pro-longevity intervention, though its mechanism is poorly defined. DR, a reduction in caloric intake in the absence of malnutrition, extends lifespan in C. elegans and in a wide range of other species, including yeast, flies, mice, and primates. However, this extension is highly dependent on genetic background. To investigate this, we are performing a genome-wide screen of the Vidal RNA interference (RNAi) Library, which has a catalog of 11,511 clones. By knocking down specific genes within the C. elegans genome through RNAi, we are able to observe an extension or reduction in longevity in response to DR. We have screened over 1500 genes, 61 of which are short-lived and 67 of which are long-lived. We are currently following up on our collected data by measuring the full lifespans using the RNAi clones that significantly shortened or extended lifespans in our screen. By screening such a large number of genes, the widespread effect, and hopefully mechanism, of DR will be elucidated. We hope to see genes significantly affected by DR cluster into groups with common functionality, or along the same pathway, and then follow up on those specific pathways to clarify the mechanisms underlying DR. If these pathways are conserved, research findings relating to C. elegans may be applicable to other organisms. We hope to confirm these results and further investigate the interaction between DR and other potential longevity pathways.

Organisms have evolved specific mechanisms to respond to molecular and environmental stress. These stress-response pathways are evolutionarily conserved and can modify lifespan in model organisms, making them popular targets of aging research. Using the nematode Caenorhabditis elegans (C. elegans), we have found the loss of important genes in stress-response pathways can cause a phenomenon called age-related vulval integrity defects (Avid). Worms with Avid show a small protrusion near their vulva that can eventually lead to expulsion of the intestine and premature death. While many labs have noted this phenotype, it is unknown if Avid is a natural part of C. elegans aging or if genetic and environmental factors induce this phenotype. Because of this, there is confusion as to whether worms with Avid should be censored in aging experiments. The goal of our project is to determine the mechanism of Avid and whether it is part of normal worm aging. Our initial work has identified several conditions and genetic pathways important for Avid, including temperature, food availability, the hypoxic response pathway, the oxidative stress response pathway, and the protein assembly pathway. We have also identified that the reproductive period of the C. elegans lifecycle is influential on Avid frequency, despite the phenotype occurring post-reproductively. We are currently testing the hypothesis that Avid is caused by secretions from the bacteria worms eat that influence nematode physiology and lead to Avid. We hypothesize that the pathways that influence Avid frequency do so by altering the digestion of bacteria in the intestine or by modifying the worm’s immune response. To test our hypothesis we measured the quantity of bacteria ingested and digested by various worm strains at different temperatures and tested whether bacterial metabolites can cause Avid. We intend to combine our results and develop a more complete model of Avid.

The hypoxia-inducible factor (HIF-1) is an oxygen-dependent transcription factor that plays a crucial role in an animal’s response to changing oxygen availability. When oxygen is plentiful, HIF-1 is ubiquitinated and targeted for degradation by the von Hippel Lindau protein (VHL-1). Recent studies have shown that HIF-1 stabilization through mutation of vhl-1 increases longevity in the model organism Caenorhabditis elegans. This is contrary to humans, where VHL-1 mutations cause a disease characterized by angiomas, renal carcinomas and various other tumors as a direct result of aberrant HIF-1 activation. Since nematodes are post-mitotic organisms in adulthood, constitutive activation of HIF-1 does not cause tumor formation and is able to increase lifespan. In order to better understand the how HIF-1 increases longevity and to relate these findings to mammals, our project aims to find the specific genes and tissues downstream of HIF-1 necessary for its effect on worm longevity. Our goal is to find genes downstream of HIF-1 that benefit longevity without the consequences of VHL disease. To identify these genes, we conducted an RNAi screen for genes that are necessary for HIF-1-mediated longevity. Using the results of this screen, we are creating transgenic worms that overexpress these genes under specific nematode promoters. To test for the tissue specificity of HIF-1-mediated longevity, we are stabilizing HIF-1 in different tissues using tissue specific promoters. Our initial data are promising; we have found two genes downstream of HIF-1 that when overexpressed, increase nematode longevity. At least one of these genes, flavin-monooxygenase-2, is a well-conserved protein known to be involved in xenobiotic metabolism. Additionally, we have found that expressing stabilized HIF-1 in neurons is sufficient to increase nematode lifespan. Our continuing studies will identify additional target genes and tissues important for HIF-1 mediated longevity and will attempt to elucidate the mechanism for their action.

Electrophoretic displays, such as the Kindle®, currently employ electrostatic effects in apolar media to create a paper-like display. In an electrophoretic display, images are comprised of black and white pixels generated by applying an electric field to reposition charged pigment particles. The optimization of this technology is limited due to the incomplete knowledge of the mechanism(s) by which particles acquire charge in these systems. My project explores the charging behavior of carbon black pigments dispersed in apolar media. Previous studies of mineral oxide particles have provided support for the theory of an acid-base charging mechanism for particles dispersed in apolar media with various charge stabilizing surfactants. My current work looks at the possible extension of the theory of an acid-base charging mechanism to carbon black pigments in apolar systems. I have investigated the charging behavior of four different carbon black pigments by measuring the electrophoretic mobility of each pigment dispersed in solutions of heptane, and a charge stabilizing surfactant at varying weight percentages. Three surfactants were used for charge stabilization: Aerosol OT, SPAN 80 and OLOA 11000. Aerosol OT is a neutral surfactant in water, whereas SPAN 80 is acidic and OLOA 11000 is basic. The surface characteristics of each carbon black pigment were studied by Inverse Gas Chromatography (IGC) and X-ray Photoelectron Spectroscopy (XPS). The preliminary findings of my investigation show the sign of the charge for the carbon black pigments to be dependent on the charge stabilizing surfactant used.

The primary cilium is a sensory organelle found on most cells. In the brain, most or all neurons contain a single primary cilium, yet its function is not entirely understood. Ciliopathies are defined as a group of disorders physiologically characterized by malformation or dysfunction of primary cilia, which in turn result in a variety of symptoms including cognitive deficits, retinal blindness, situs inversus and polydactyly. The serotonin 6 receptor (5-HT6) is the only 5-HT receptor that localizes to neuronal primary cilia, and previous research has implemented the receptor in learning, memory, and drug addiction. Our experiment will investigate the link between neuronal primary cilia and 5-HT6 in an attempt to better understand the significance of this unique localization. Using an immortalized line of rat adrenal cells (PC12), we will express the 5-HT6 receptor using viral vectors, and then pharmacologically manipulate the activity of the receptors with either an agonist (WAY 399885) or an antagonist (SB 208466). We will first stain the cells using immunohistochemistry, then image using florescence microscopy, and lastly quantify the morphological change in primary cilia length. We expect to see a shortening of primary cilium in response to the introduction of an antagonist, and an increase in length with an agonist. Since the 5-HT6 receptor has been shown to be homologous between rats and humans, a practical application of this research could eventually result in a pharmaceutical solutions to some of the cognitive symptoms associated with ciliopathies like congenital cerebellar ataxia or Joubert syndrome.

A replicative lifespan (RLS) screen in yeast (Saccharomyces cerevisiae) was recently performed in the Kaeberlein lab to determine how different mutants respond to caloric restriction (CR). The results of this screen indicated that many mutants lacking genes encoding proteins related to mitochondrial function were rescued to wild-type lifespan by CR. The beneficial effects of CR in both yeast and mammals are mediated by reduced signaling through the mechanistic target of rapamycin (mTOR) pathway and can be mimicked by the drug rapamycin, a specific inhibitor of mTOR. Based on the findings from the yeast screen, we decided to investigate the effects of rapamycin on mitochondrial disease in a mammal. Leigh syndrome is clinically defined as a collection of genetically heterogeneous human mitochondrial diseases. These diseases result from mutations in genes encoding mitochondrial proteins and are characterized by progressive neurological degeneration resulting in early childhood mortality. To test rapamycin as a therapeutic intervention for Leigh syndrome, we are using a mouse line carrying a heterozygous loss of the electron transport chain complex I subunit Ndufs4, a direct homolog of the human NDUFS4 gene whose mutation causes Leigh syndrome. Mice homozygous for loss of NDUFS4 provide a robust phenocopy of the human disease, including neurological degeneration and early life mortality. Our results so far show that rapamycin dramatically increases lifespan and rescues the Ndufs4-/- mice for several health-related parameters, such as general mobility, visual ability, and grip strength. We are working towards determining the mechanistic basis for these effects, and we hypothesize that they may result from a metabolic shift toward increase fat metabolism in the liver. Understanding how rapamycin rescues Leigh Syndrome mice has clear translational implications, as rapamycin derivatives are FDA approved and patients with Leigh syndrome and other human mitochondrial diseases currently have limited treatment options.

Protein kinases are enzymes that take phosphate groups from adenosine triphosphate (ATP) molecules, the energy in your body, and add them to other specific molecules inside the cell. This transfer of the phosphate group can activate or deactivate the target molecule, thus regulating cellular activities such as growth, replication, and respiration. The kinases studied here are hemopoietic cell kinases (Hck kinases) under the class of Scr kinases. Hck kinases are present in bone marrow and are often associated with myeloid leukemias and myeloproliferative disorders. Studies have shown that in the active conformation, the Hck kinase detaches two of its domains, SH2 and SH3, resulting in a more extended conformation. Using a Waters Synapt G2 HDMS, ion mobility mass spectrometry (IM-MS) techniques were used to probe the size of inactive and active Hck kinases by measuring drift times of their gas-phase ions traveling through a neutral background gas under the presence of a weak electric field. Drift times were then converted into collision cross section (CCS) values, which depend on the size and shape of the ion of interest. Eight different small molecules (< 500 Da) were used to inhibit Hck kinases, and changes in conformation were investigated using IM-MS. Preliminary data shows no significant changes in global conformation or size, conflicting with the previous studies. To investigate more subtle changes in conformation, collision induced unfolding (CIU) methods are used. By selecting an ion of interest using a quadrupole mass filter, protein unfolding is monitored using ion mobility as a function of ion activation prior to ion mobility analysis. This process allows an investigation of the subtle conformational changes in the Hck kinase upon the binding of small inhibitor molecules.

Electrospray ionization (ESI) is a powerful tool for transferring intact protein complexes from solution to the gas phase. ESI creates multiply charged ions with a net positive (cation) or negative (anion) charge. Although the structures of gas-phase protein cations have been investigated extensively, relatively little research addressing the structures of negatively charged protein ions exists in the literature. In my research, I use ion mobility (IM) to measure drift times, or the time an ion takes to traverse a gas-filled drift tube in the presence of a weak electric field. The drift times for ions depend on their charge and collision cross section (CCS), which to a first approximation, is the orientationally averaged projected cross section of its structure. Therefore, the drift times of ions depend on their structure. Preliminary CCS values that I have measured for protein complex anions are slightly smaller than values in the literature for the analogous protein complex cations, which suggests that the anions are more compact than the cations. One challenge in interpreting those results is the anions had a lower absolute number of charges than the analogous cations, so the results may not be directly comparable. The focus of my research is to make more direct comparisons between the structures of protein complex cations and anions. To this end, I am developing methods to reduce the number of charges on protein complex cations to values equal to those observed previously for the anions. CCS values determined for these charge-reduced cations will be directly comparable to those measured for the anions, and should reveal any structural differences between protein complex cations and anions. These results will also be useful for calibrating other IM experiments and determining how best to use IM to characterize the native structures of protein complexes.

Aging is a process characterized by the degeneration of bodily components and functions. Scientists are limited in their ability to study this process in humans, in part because a human lifespan is too long to conveniently study. Instead, model organisms are studied extensively in the hope that discoveries made will be applicable to another organism of interest. Model organisms are usually short-lived, easy to manipulate, and easy to handle. One of the best examples of a model organism is the budding yeast Saccharomyces cerevisiae. S. cerevisiae lifespans are easy to measure and reproduce, and since they have a short lifespan we can study a large amount at one time. Aging in Saccharomyces can be measured in two different ways. A yeast cell can be kept in a non-dividing, nutrient limited environment and tested to see if it can successfully re-enter the cell cycle, when it cannot, its lifespan has ended. This method is used to measure the chronological lifespan, and the model can be applied to human cells that are no longer replicating (post-mitotic cells). There is another model we can use to understand a different aging process, called the replicative lifespan. The replicative lifespan refers to the number of times a mother cell can divide to produce daughter cells, and is a much better representation of cells that are still dividing (mitotically active cells) in other organisms. As undergraduates, we help study this process by physcially separating daughter cells from the mothers using fiberoptic needles (dissecting) and counting them at regular intervals. When the mother cell no longer produces daughter cells, the replicative lifespan has ended. The data collected can be compared to past and expected results in order to help us gauge how well the cells are dividing. By manipulating the environment that each cell line is grown in, we can gain insight towards specific drugs and conditions that mother cells divide best in, and apply this to other mitotically active cells in other organisms. Both measurements of lifespan can be manipulated in similar ways, and many labs have started to establish a bank of genes and environmental factors that can be manipulated in order to change the outcomes.

Aging in the budding yeast Saccharomyces cerevisiae can be measured by its replicative life span, which is defined by the finite number of mitotic divisions of mother cells. The Kaeberlein lab measures the replicative life span of S. cerevisiae through the microdissection of dividing mother cells. This laborious process separates daughter cells from their mothers, which quantifies the replicative life span. We are assessing how various environmental factors affect the replicative life span of the cells. Our research project involves paraquat, a commonly used pesticide that produces reactive oxygen species within cells. This substance is normally considered to be toxic, and as expected, we have observed that the replicative lifespan of yeast is decreased in the presence of high concentrations of paraquat. However, we have also found that low concentrations of paraquat increased the replicative life span of the yeast. This observation is an example of hormesis- a phenomenon where beneficial effects are obtained at low doses of an agent that is otherwise toxic when given at higher doses. These findings are significant because a similar effect has been published with the nematode worm, Caenorhabditis elegans. C. elegans and S. cerevisiae are evolutionarily separated by approximately one billion years, suggesting that there is a conserved mechanism of life span extension influenced by paraquat. We are currently characterizing the effect of paraquat and other environmental conditions that will help us to find conserved pathways that modulate longevity.

Manganism, a movement disorder characterized by neuronal death in the basal ganglia and symptomatology similar to Parkinson’s disease, has been shown to involve manganese-mediated increase of toxic reactive oxygen species (ROS) production in mitochondria. The protein alpha-synuclein, a product of the SNCA gene, has been implicated in glial and neuronal degeneration in Parkinson’s disease, and preliminary data from our laboratory suggests that removal of alpha-synuclein from astrocytes confers some protection against ROS toxicity. Astrocytic hydrogen peroxide metabolism has been shown to produce ROS capable of damaging a variety of cellular macromolecules. The present study seeks to compare the effectiveness of toxicant attenuation in SNCA knock-out and wild type astrocytes in response to hydrogen peroxide after gradated 24-hour manganese pre-treatments. Calcium imaging with fluo-4 dye will be performed to measure astrocytic calcium by quantifying the amplitudes and durations of induced calcium waves, known to form an important mechanism of astrocytic communication, after addition of hydrogen peroxide. Based on previous studies, we predict that increased manganese dosages will correlate with elevated calcium wave amplitudes in both SNCA knock-out and control cultures. We further predict significantly lower calcium wave amplitudes in wild type cultures after each manganese treatment.

The nematode Caenorhabditis elegans is a powerful model for the analysis of the conserved mechanisms that modulate healthy aging, from organismal to molecular levels. As animals age, tissues deteriorate at different rates. It has been shown previously in the Kaeberlein lab that deletion of the hypoxia-inducible factor, HIF-1, extended lifespan of worms at high temperature (25°C), but did not do so at low temperature (15°C). Accordingly, it was speculated that at low temperature, worms were not as healthy. At low temperature, we noticed an abnormal vulva phenotype and called it age-related vulva integrity defect (Avid). As worms age, their vulvae protrude and rupture, causing internal organs such as the intestine to erupt out of their bodies. Through investigation, we realized that animals lacking oocytes tend to show more Avid phenotype, compared with the animals that produce enough oocyte. It has been shown before that at 15°C worms produce around 300 fertilized and unfertilized oocytes, while at 25°C this number increases to 400. My preliminary results suggest that germline is involved in the progress of Avid. I studied animals with germline defects and observed 100% Avid phenotype in germless mutants. Avid is a sign of healthspan as animals age, and decline in germline fecundity due to aging can induce Avid. Healthspan is defined as the period of life spent in relatively good health, and maintenance of healthspan is an important component of aging. Our data indicate that Avid can be used as a measurement tool of the age-related healthspan of worms.

This action-research project describes a particular student-lead model created to foster community and awareness of global health across campus. We, the student leaders, who form the Global Health Undergraduate Leadership Committee (GHULC), have shaped this model to best respond to an ongoing challenge of engaging all undergraduates in awareness and community building around global health issues. The model for this approach involves bimonthly meetings with the committee and two advisors in addition to attending events planned by the GHULC and the Department of Global Health. Methods we have taken to increase undergraduate involvement in the minor include regular information sessions about the minor, monthly student-planned Community Connections events on critical issues, a joint student- and faculty-run journal club, peer advising, walking tours of Global Health organizations in Seattle, and a GHULC blog. Preliminary quantitative data suggests that there has already been an increase in the number of students enrolled in the minor this year as well as an increase in the academic diversity of participating students. Our next step will be to develop a qualitative assessment of the GHULC’s impact by administering a feedback form to all Global Health minor students regarding their perception of and involvement in the minor. We intend to gather this information on a yearly basis in order to improve the minor as well as the GHULC’s role with the goal of continuing to increase diversity, engagement, and mentorship.