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NIAID - National Institute of Allergy and Infectious Diseases

Project Summary HIV drug resistance represents a growing and underappreciated threat to the U.S. HIV response. Although more than 1.2 million people are living with HIV in the U.S., only about 60% achieve durable viral suppression, and resistance is a major contributor to treatment failure and regimen switching. Current resistance testing relies on centralized, PCR and sequencing-based platforms that are expensive, slow, and available only at specialty laboratories, requiring multiple clinic visits and highly trained personnel. As a result, same- day, resistance-informed treatment decisions are rarely possible, even in major U.S. cities, and are essentially inaccessible in rural areas, mobile care units, and safety-net clinics serving areas where the epidemic is increasingly concentrated. These gaps most severely affect communities already carrying the highest burden of HIV incidence and treatment failure in the U.S. Without affordable, accessible, point-of-care (POC) resistance testing, the durability of ART and the success of the national Ending the HIV Epidemic initiative are at risk. Our project aims to develop HIV-CRISP to addresses this critical gap by developing a cost-effective, same- visit “test-and-switch” POC device that integrates CRISPR-based nucleic acid detection with a bioinspired microfluidic chip (CamoChip). This fully automated platform enables simultaneous detection of HIV viral load and drug resistance to four major ART classes (NRTIs, NNRTIs, INSTIs, and PIs) during a single clinic visit. By empowering providers to make immediate, resistance-informed treatment decisions, HIV-CRISP reduces delays in therapy initiation or modification and minimizes the risk of treatment failure. The project is structured around three specific aims: Specific Aim 1: optimize a PAMmer-assisted CRISPR system for accurate detection and profiling of HIV drug resistance mutations; Specific Aim 2: enhance CamoChip readout technology for rapid, multiplex POC testing; and Specific Aim 3: integrate these components into a user-informed POC device and validate its performance against standard methods with clinical samples. Each aim not only drives independent scientific advances but also converges on the development of a transformative POC diagnostic. HIV-CRISP represents an innovation in HIV diagnostics with broad public health significance. This platform supports wide access to high-quality HIV care in under-resourced settings across the U.S. and globally, while also providing a foundation adaptable to other infectious diseases and health conditions.

National Institutes of Health

<p>The National Institute of Allergy and Infectious Diseases (NIAID) seeks to advance its mission by supporting four Clinical Trials Networks (CTNs) each comprised of a Leadership and Operations Center, Statistical and Data Management Center, and Laboratory Center (LC) working with Clinical Trials Units, to&nbsp;test&nbsp;prevention and treatment&nbsp;strategies and conduct implementation research designed to end the HIV epidemic. This NOFO will solicit applications for up to four LCs that will provide laboratory structure and technologies to one or more CTNs and conduct laboratory testing for Network trials, according to regulatory standards. The LC oversees site-affiliated clinical and specialized laboratories and ensures protocol-specified laboratory testing.&nbsp; The LC will: 1) support sample integrity from collection to final testing/storage; 2) use appropriate laboratory data capturing management and tracking systems; 3) select, determine readiness, and approve laboratories; and 4) promote state-of-the-art laboratory assays.&nbsp;The LC will increase testing capacity to meet advances in prevention and treatment of HIV and HIV-related diseases.</p><p><br>Grant authorities that allow NIAID to forecast this opportunity are as follows: Sections 301 and 405 of the Public Health Service Act as amended (42 USC 241 and 284) and under Federal Regulations 42 CFR Part 52 and 2 CFR Part 200.</p>

National Institutes of Health

The National Institute of Allergy and Infectious Diseases (NIAID) seeks to advance its mission by supporting four Clinical Trials Networks (CTNs) each comprised of a Leadership and Operations Center, Statistical and Data Management Center, and Laboratory Center (LC) working with Clinical Trials Units, to test prevention and treatment strategies and conduct implementation research designed to end the HIV epidemic. This NOFO will solicit applications for up to four LCs that will provide laboratory structure and technologies to one or more CTNs and conduct laboratory testing for Network trials, according to regulatory standards. The LC oversees site-affiliated clinical and specialized laboratories and ensures protocol-specified laboratory testing. The LC will: 1) support sample integrity from collection to final testing/storage; 2) use appropriate laboratory data capturing management and tracking systems; 3) select, determine readiness, and approve laboratories; and 4) promote state-of-the-art laboratory assays. The LC will increase testing capacity to meet advances in prevention and treatment of HIV and HIV-related diseases.Grant authorities that allow NIAID to forecast this opportunity are as follows: Sections 301 and 405 of the Public Health Service Act as amended (42 USC 241 and 284) and under Federal Regulations 42 CFR Part 52 and 2 CFR Part 200.

Community Art Center

Home Port

Community Art Center

Home Port

Hong Kong Jockey Club Charities Trust

One of the world's top charity donors (500M+ USD/yr). Supports youth, elderly, sports, arts, and community programs in Hong Kong.

NIDA - National Institute on Drug Abuse

Project Summary Drug use increases HIV risk and worsens health outcomes in people living with HIV (PLWH). While antiretrovirals are effective for both prevention – using pre-exposure prophylaxis (PrEP) – and for treatment – using antiretroviral therapy (ART) – drug use further impairs medication adherence. It is thus essential to develop strategies to enable people who use drugs to achieve abstinence and prevent relapse, which is expected to reduce HIV risk, burden, and infection. Progesterone and its metabolites regulate drug craving and immune function, making them potential therapeutic targets. However, PLWH and people who use drugs often experience menstrual cycle disruptions, and the impact of PrEP or ART on hormone regulation remains unclear. Understanding these interactions could reveal strategies to reduce drug-seeking behavior and to improve HIV treatment outcomes. In our preclinical work using the EcoHIV mouse model of HIV infection, we observe disrupted estrous cyclicity, altered cytokine expression, and increased risk for cocaine relapse-related behavior. We further observe that ART restores estrous cyclicity and partially reverses altered brain cytokine expression in EcoHIV-infected mice. However, it is unknown whether ART restores cycle regularity in cocaine-exposed, EcoHIV-infected mice or whether PrEP interacts with drug exposure to affect hormonal function. The medial preoptic area (mPOA) regulates both estrous cyclicity and cocaine-related behavior, and our findings suggest EcoHIV infection increases mPOA activation in cocaine-exposed females. Progesterone and its active metabolite, allopregnanolone, act on both neurons and astrocytes. Thus, modulation of mPOA astrocytic and neuronal activity may represent a novel target for reducing drug seeking and neuroimmune dysregulation among those at risk of or living with HIV. This proposal will test the overarching hypothesis that chronic drug exposure and EcoHIV infection interact with antiretrovirals to promote estrous cycle irregularity and cocaine reinstatement via dysregulation of the mPOA. Aim 1 will assess how PrEP and ART impact estrous cyclicity, ovarian reserve, mPOA cellular activity, and neuroimmune signaling following chronic cocaine exposure. Aim 2 will use chemogenetic tools to determine the role of mPOA discrete populations of astrocytes and neurons in cocaine reinstatement after PrEP or ART+EcoHIV. Aim 3 will evaluate whether allopregnanolone administration reduces cocaine reinstatement and alters neuroimmune signaling. Together, these Aims are to expected define the mPOA as a mediator of drug seeking and immune state following treatment with antiretrovirals, and further to identify hormonal strategies to suppress relapse in individuals taking PrEP or with virally suppressed HIV infection.

Houston Endowment

Houston Endowment ($2.0B in assets) supports nonprofits in TX through grants focused on education, arts, environment, community development. Awards range from $5,000 to $400,000.

NCI - National Cancer Institute

PROJECT SUMMARY Pancreatic ductal adenocarcinoma (PDAC) will become the second leading cause of US cancer-related deaths by the year 2030. Primary PDACs are encased within a densely fibrotic, nutrient poor (“desmoplastic”) stroma enriched with extracellular matrix, fibroblasts, and immune cells. In contrast, distant metastatic PDACs grow rapidly within a nutrient replete, loosely fibrotic stroma. The project objective is to define those fundamental TME differences and the fibroinflammatory signaling networks that govern them. The hypothesis is that PDACs remodel metastatic TMEs into a loosely fibrotic, immunodeficient stroma by suppressing pathways that yield fibroinflammatory cytokines. This hypothesis will be tested by two specific aims. Aim 1: Define key differences between primary and metastatic TMEs. Primary versus metastatic TMEs will be interrogated in humans and mice by (1) scoring key histopathological TME parameters across hundreds of primary and metastatic PDAC patient tissue samples; (2) quantifying tumor: stroma cell lineage abundances and communication networks using single cell RNA-seq datasets from PDAC patients; (3) flow cytometric sorting of cell lineages that comprise primary and metastatic TMEs in gold standard PDAC mouse models. The goal of Aim 1 is to discover TME determinants of divergent clinical behaviors and biological properties between primary tumors and distant metastases. Aim 2: Evaluate mechanisms that remodel metastatic TMEs. Genetic and pharmacological gain- and loss-of-function approaches will determine if (1) suppressing inflammatory signals depletes primary tumor fibroinflammatory cytokines from metastatic secretomes; (2) (re)- introducing those cytokines back into metastatic secretomes triggers a desmoplastic stromal response that restrains distant metastatic outgrowth; (3) depleting those cytokines from primary tumor secretomes remodels the desmoplastic stroma to facilitate distant metastatic spread. The goal of Aim 2 is to identify and functionally characterize primary tumor fibroinflammatory signals that are reprogrammed to facilitate distant metastasis. These studies will positively impact cancer research by concretely demonstrating how primary and metastatic TMEs diverge from one another and illustrating precise mechanisms that drive such divergences. The findings are expected to conceptually advance our understanding of cancer progression and rationally inform therapeutic strategies against primary and metastatic tumors, even within the same individual patient(s). This research will be conducted as part of an MD-PhD dual degree fellowship training plan at the University of Miami Miller School of Medicine Medical Scientist Training Program (UMMSM MSTP). The UMMSM MSTP training environment includes access to theoretical and technical instruction, physician scientist mentors, and state-of-the-art facilities for these studies. This proposal seeks to prepare for a training goal of becoming a physician scientist in the field of oncology.

NIMH - National Institute of Mental Health

ABSTRACT The dynamics of HIV infection in the brain is poorly understood. Infected cells that transport HIV across the blood brain barrier and into the brain causes inflammation and subsequent damage to resident brain cells. This manifests as a group of symptoms collectively referred to as HIV associated neurocognitive deficits (HAND). Today, in the post ART era, HAND consists of mild to moderate symptoms. This research is significant because it uses an in vivo model to assess the unique interactions among brain cells and peripheral immune cells in vivo in an HIV infected ASRT treated model. Results from these studies will give a better understanding of the events that define neuroHIV in the ART era.

Department of Cultural Affairs and Special Events

COMMUNITY ARTS ACCESS PROGRAM

Idaho Commission on the Arts

Provides general operating support to established Idaho arts organizations for ongoing programming, operations, and capacity building, helping sustain the state's cultural infrastructure.

Idaho Commission on the Arts

The Idaho Commission on the Arts Quick Fund program provides rapid-response grants for arts programming, supporting performances, exhibitions, workshops, and cultural events that bring arts experiences to Idaho communities.

Idaho Community Foundation

Idaho Community Foundation ($200M in assets) supports nonprofits in ID through grants focused on education, community development, health, arts. Awards range from $1,000 to $50,000.

NCI - National Cancer Institute

Identification and Characterization of Mutation-Induced Alternative Splicing Events in Cancer Using Multi-Omics Data Project Summary The goal of this project is to discover mutation-induced alternative splicing events (MAS), understand their functional relevance, and identify neoantigens arising from these events to advance cancer immunotherapy. Large-scale sequencing efforts such as The Cancer Genome Atlas (TCGA) have primarily focused on identifying driver mutations in tumors, including single amino acid changes, insertions, deletions, and alterations that truncate or elongate wild-type protein sequences. However, traditional DNA mutation annotations often rely on canonical transcripts and may overlook alternative splicing events, and some mutations, such as synonymous changes, are considered silent despite their potential impact on splicing. Previously, we developed the MiSplice pipeline to detect mutation-induced splice sites and, when applied to TCGA data, identified thousands of somatic mutations that create cryptic splice sites. In this proposal, we aim to systematically investigate mutation-induced alternative splicing and its functional relevance in cancer, while also identifying the resulting neoantigens by leveraging data from the Clinical Proteomic Tumor Analysis Consortium 3 (CPTAC-3), which includes comprehensive exome sequencing, RNA-Seq, and mass spectrometry data for 774 tumors across seven cancer types, as well as 126 prospective breast cancer samples from CPTAC-2. We hypothesize that mutation-induced alternative splicing plays a significant role in cancer etiology and that the associated neoantigens can serve as novel immunogenic peptide candidates for cancer immunotherapy. We propose to test these hypotheses through two specific aims. Aim 1: Identify mutation-induced alternative splicing events and assess their functional relevance in cancer using multi-omics data (Years 1 & 2). We will use MiSplice to detect mutation-induced alternative splicing events from CPTAC data and evaluate their impact by analyzing changes in protein and phosphorylation expression, as well as pathway activation. Aim 2: Identify neoantigens arising from mutation-induced alternative splicing events with mass spectrometry support (Years 1 & 2). We will construct a tailored protein database that integrates both reference proteins and mutant proteins generated from MAS events. Using state-in-art tools such as PepQuery, we will search for corresponding peptides in the mass spectrometry data, enabling identification of mutant proteins. Neoantigen peptides derived from these expressed mutant proteins will then be prioritized as candidates for cancer immunotherapy.

NIAID - National Institute of Allergy and Infectious Diseases

Abstract: During HIV infection, a reservoir of infected cells is formed that persists during antiretroviral therapy (ART). Although ART is effective at controlling viral replication, people with HIV (PWH) on ART still exhibit elevated levels of inflammation and immune dysfunction, suggesting ongoing immune damage from HIV infection. The mechanisms behind continued immune dysfunction in PWH on ART remain unclear, but it is possible that chronic immune stimulation by virally encoded RNAs and proteins contributes to this process. At the same time, activation and clonal expansion of infected CD4 T cells in response to interactions with cells and cytokines of the immune system contributes to the persistence of the HIV reservoir. Our hypothesis is that bidirectional stimulation between the reservoir and the immune system creates a self-perpetuating cycle that maintains both chronic inflammation and the persistence of infected cells in PWH on ART. If this hypothesis is correct, molecular pathways that contribute to reservoir/immune crosstalk could potentially be targeted to limit reservoir persistence and reservoir-induced pathology in PWH. The goal of this proposal is to comprehensively define the relationship between the immune system of PWH and the HIV reservoir through single-cell analysis of the transcriptome and proteome of immune cells across a large (n=125) cohort of ART suppressed PWH with well characterized HIV reservoirs. Additionally, we will quantify the clonality of the HIV reservoir for each individual and define immune signatures that are associated with clonal expansion of infected cells during ART. This combined dataset will allow us, for the first time, to perform a detailed correlational analysis of transcriptomic and proteomic signatures in the immune system with key reservoir characteristics (size, transcriptional activity and clonal expansion) across a large cohort of PWH. To achieve these goals, we will leverage a unique set of PBMC and plasma samples from 125 ART-suppressed PWH through our collaboration with Dr Sulggi Lee (UCSF), as well as cutting edge multiomic methods that are already established in the Browne lab. If this project is successful, it will generate the most detailed dataset to date describing molecular connections between the HIV reservoir and the immune system, and will suggest novel ways to interrupt the dynamics that drive reservoir persistence and pathogenesis in PWH on ART.

NIMH - National Institute of Mental Health

PROJECT SUMMARY/ABSTRACT People with HIV (PWH) who experience challenges with antiretroviral therapy (ART) adherence are at increased risk for suboptimal treatment outcomes, including viral non-suppression and disengagement from care. Despite advancements in ART delivery options, personalized treatment approaches that integrate patient preferences remain underutilized, particularly among PWH facing psychosocial and documented barriers. Clinical decision support (CDS) tools offer a promising avenue to address this gap by tailoring treatment recommendations based on patient-specific needs and barriers. However, current CDS tools often fail to incorporate rich patient insights available from unstructured electronic health record (EHR) notes or systematically integrate directly reported preferences, limiting their potential to enhance adherence and outcomes. The proposed training and research plan for this K23 will enable José I. Gutierrez, Jr., PhD, FNP- BC, to acquire the expertise necessary to become an NIH-funded independent investigator who designs patient-informed CDS interventions that optimize HIV treatment delivery. Under the mentorship of an experienced multidisciplinary team, Dr. Gutierrez will use a mixed-methods approach to develop foundational components of a CDS prototype that integrates natural language processing (NLP)–derived EHR information with patient-reported preference data. Building on prior work in HIV treatment delivery and preference evaluation, he will pursue the following specific aims: (1) explore HIV treatment delivery preferences, barriers, and facilitators within EHR notes using NLP; (2) identify and quantify patient preferences, barriers, and facilitators using qualitative interviews and MaxDiff; and (3) develop the key features of a CDS prototype that generates tailored suggested actions informed by EHR and patient-preference data, and evaluate its acceptability, feasibility, usability, and intended adoption in a 9-month, cross-sectional, non-clinical user-testing study using standardized vignettes and de-identified/fictionalized cases (no live EHR). This research plan aligns with Dr. Gutierrez's career development goal to gain advanced skills in clinical informatics and NLP, qualitative and mixed-methods research, and patient-informed intervention design. Findings will provide the foundation for a subsequent NIH R01 to rigorously evaluate effectiveness in clinical settings, with the overarching goal of improving ART adherence and treatment outcomes among PWH. 1

NCI - National Cancer Institute

PROJECT SUMMARY Oncogenic mutations in KRAS are nearly universal in pancreatic ductal adenocarcinoma (PDAC) and drive disease initiation, progression, and maintenance. Small molecules that inhibit mutant forms of KRAS (KRASi) and both mutant and wildtype RAS proteins (RASi) have recently emerged with the potential to transform the treatment landscape of PDAC. However, the mechanisms dictating efficacy and resistance to RAS inhibitors remain poorly understood. PDAC development and therapeutic response depends on co-evolution and interaction between tumor cells and the tumor immune microenvironment (TIME). This research proposal focuses on a major goal of our laboratories: to determine how remodeling of tumor-immune interactions contributes to efficacy and durability of RAS inhibition. We have developed immunocompetent mouse models that recapitulate seminal features of PDAC heterogeneity and found that while the KRASG12D inhibitor MRTX1133 and the pan-RASGTP inhibitor RMC-6236 both effectively inhibit the MAPK pathway and illicit potent tumor responses in pre-clinical studies, they result in distinct patterns of response and adaptation in tumor cells and the tumor microenvironment. We hypothesize that these differences result from poorly understood and understudied immune cell intrinsic roles of the RAS family that alter interactions between tumor and immune cells in response to RAS inhibition. Using a multidisciplinary and collaborative approach, this proposal integrates cutting-edge genetic models with innovative molecular and immunological methodology to delineate targetable immunological changes which define distinct patterns of response to KRASi and RASi in PDAC. We propose 2 aims that meet the research objectives of notice of special interest NOT-CA-24-016 (Exploratory Cancer Immunology Projects and Technologies (ExCITe)/PA-25-304, by addressing “fundamental aspects of tumor immunology and/or innovative ways to enhance anti-cancer immunity.” Aim 1 will leverage state of the art single cell technology and high dimensional spectral flow cytometry in mouse models of PDAC to comprehensively establish how TIME remodeling contributes to PDAC response and resistance following RASi/KRASi. Aim 2 will investigate immune-intrinsic roles for wild type RAS activity in the PDAC TIME through novel genetic approaches to determine how non tumor cells contribute to efficacy and resistance of RASi. Taken together, this proposal integrates expertise in PDAC pathobiology, tumor immunology, and applies novel genetic tools to unveil new mechanisms that underlie the efficacy and durability of RAS inhibition.

Illinois Arts Council Agency

Illinois Arts Council Agency provides grants to support arts and cultural programming, artist fellowships, arts education, and community-based arts projects across IL.

Illinois Arts Council Agency

Supports Illinois arts organizations, artists, and arts education programs through operational support, project grants, and touring grants.

NIGMS - National Institute of General Medical Sciences

Project Summery/Abstract Amid a public health crisis driven by antibiotic-resistant pathogenic bacteria, bacteriophages (phages), which naturally infect and kill bacteria, represent a promising alternative as antimicrobials. However, a significant challenge is posed by diverse bacterial immune mechanisms that resist phage infections. Overcoming this obstacle requires phages equipped with robust anti-immune capabilities. In this context, ΦKZ-like jumbophages (genomes > 200kb) have an exceptional ability to counter various bacterial nucleolytic immune systems throughout infection, with numerous family members targeting key Gram-negative pathogens. The jumbophage ΦKZ is a broad host range killer of the multi-antibiotic-resistant pathogen Pseudomonas aeruginosa and serves as the leading model phage for this family. Immune evasion is largely achieved through the assembly of a bacterial membrane lipid derived compartment termed the “Early Phage Infection Vesicle” (EPIV), which I co-discovered during my postdoctoral work, and a phage-encoded proteinaceous compartment called the “phage nucleus,” which shields the replicating phage genome. The long term goal of this study is to understand three unexplored aspects of jumbophage biology related to the biogenesis and functioning of the EPIV. The EPIV houses early transcription, but the phage has to solve a fundamental challenge not previously solved in bacteria–mRNA export from a lipid-bound compartment and successful docking with ribosomes, which are unusually uncoupled from transcription in this case. I hypothesize that a novel mRNA export channel, analogous to the eukaryotic nuclear pore complex, is assembled by injected ΦKZ proteins to export mRNA to ribosomes. I will uncover this complex using cryo-ET, mass spectrometry and genetics. I will additionally examine the role of EPIV assembly in enabling ‘pseudolysogeny’ in jumbophage infections. This process of phage quiescence was observed in jumbophages long ago but lacks a mechanistic understanding. I hypothesize that the EPIV has the potential to be a stable pseudolysogenic entity inside an infected bacterium that I will test herein with my multidisciplinary approach. Finally, I will attempt to elucidate the mechanism of EPIV biogenesis – it remains entirely unknown how this massive membrane-bound organelle is rapidly assembled within bacteria and how its formation is conserved across diverse jumbophage infections. To answer these questions, I will combine genetic dissection and c-ET to reveal the key participants and early assembly events of this unique phage-driven prokaryotic organelle formation. Overall, my studies stand to uncover fundamentally fascinating bacterial-phage cell biology in addition to innovative and potentially transferable mechanisms to enhance phage success in combating pathogenic bacteria. This research will be conducted at UCSF, which hosts state-of-the-art facilities and a highly intellectual and collaborative research community. It will also provide me with the training in genetics and structural biology that I need to fulfill my postdoctoral training goals and pioneer an independent research program in bacterial-phage interactions.

Africatown-Central District Preservation & Development Association

The Imagine Africatown Fall and Winter Activation project will create a temporary art based neighborhood destination at Midtown located at 2301 East Union Street. The project will celebrate the African American/African Diaspora legacy and culture in the Central District with art, pop up events, and other programming. This project will be completed by March 28, 2019.

NIGMS - National Institute of General Medical Sciences

PROJECT ABSTRACT: The mechanism and regulation of protein synthesis determines the diversity and capacity of the cellular proteome. At the center of this regulation is the ribosome - a megadalton RNA-protein complex composed of two-subunits – which integrates a wide variety of cellular signals. The ribosome’s exquisite sensitivity to regulatory cues is underscored by the fact that the majority of clinically used antibiotics exert their effect by either dysregulating or blocking specific aspects of the protein synthesis mechanism. Understanding the kinetic and structural basis of protein synthesis promises to elucidate core paradigms of gene expression control and to inform strategies for addressing the global threat posed by drug-resistant and emerging pathogens. Moreover, given that loss of translational control is a hallmark of cancer, a mechanistic understanding of ribosome function holds significant promise for developing novel small-molecule therapies, which are currently lacking in the treatment of human disease. Historically, investigations into structure-function relationships governing the protein synthesis mechanism have focused on bacterial systems approaches. Comparable studies in human systems have been hindered by the demand for large amounts of homogeneous protein synthesis machinery. As a result, the molecular distinctions between bacterial and mammalian protein synthesis - which underpin antibiotic specificity and potential therapeutic windows – remain obscure. Current evidence suggests that the elongation phase of protein synthesis, during which messenger RNA (mRNA) is decoded into protein, is the most time consuming, physiologically regulated and small-molecule sensitive. We and others hypothesize that elongation is particularly susceptible to regulation because it involves transient, repetitive interactions of the ribosome with auxiliary factors, coordinated through finely tuned conformational transitions that are acutely sensitive to perturbation. Small effects on many individual steps compound to exert large impacts on protein production. The proposed research seeks to rigorously and robustly define and quantify the elemental reactions underpinning the elongation phase of protein synthesis in bacteria and human. Our objectives are to: 1) elucidate the conserved mechanistic principles and divergent features of protein synthesis across evolution to define paradigms for selective control; 2] identify novel strategies for more effective antibiotic interventions for the treatment of infectious disease; and 3] evaluate the therapeutic potential of targeting dysregulated translation in cancer. To achieve these goals, we will deploy a suite of advanced biophysical methodologies - including single- molecule fluorescence imaging and state-of-the-art cryo-electron microscopy - to establish comprehensive and integrated kinetic and structural frameworks defining the elemental steps of elongation in bacteria and humans. The insights gained will advance our understanding of translation control, reveal atomic-resolution descriptions of drug actions on bacterial and human ribosomes, and inform new strategies for improving the efficacy of clinical treatments for both microbial and human disease.

Imminent Mode

Vermillion is organizing a one-day art show event called: IMMINENT MODE: FAST FORWARD. The event will take place on August 8, 2019, it will be located at 1508 11th Ave. It will take place during the Capitol Hill Artwalk. The event will bring local artists together and is free and open to all.