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Previous Awardees

Congratulations 2026 Awardees!

The Busch Biomedical Grant program has announced 10 award recipients for 2026, totaling $599,999 across Rutgers Health, Newark, and New Brunswick campuses. On behalf of Rutgers University and its President, we want to congratulate our Awardees for their relentless pursuit of academic excellence and their vigorous biomedical research that is shaping the future biomedical community.

2026 Busch Biomedical Grant Awardees

  • Sophie Astrof

    Name: Sophie Astrof

    School: New Jersey Medical School

    Department: Cell Biology and Molecular Medicine

    Unit: Rutgers Health

    Primary Appointment Title: Professor

    Project Title: Role of Second Heart Field in Controlling Systemic Lymphatic Function

    Project Description: Congenital heart disease (CHD) is the most common birth defect, and affected children face an elevated risk of serious lymphatic complications whose causes remain poorly understood. The Astrof lab recently discovered that a shared progenitor lineage contributes to both the developing heart and the lymphovenous junction (LVJ), the gateway where lymphatic fluid drains into the bloodstream and whose proper function is fundamental to systemic lymphatic health. Using genetic engineering, 3D confocal microscopy, and single-cell RNA sequencing, this project will investigate how this lineage and Tbx1, a major CHD gene, guide LVJ formation. The work will test whether regulatory mechanisms shared between the heart and the LVJ underlie the systemic lymphatic defects observed in CHD patients and may ultimately inform new diagnostic and treatment strategies.

  • David Barker

    Name: David Barker

    School: School of Arts & Sciences

    Department: Psychology

    Unit: Rutgers-New Brunswick

    Primary Appointment Title: Associate Professor

    Project Title: Norepinephrine Control of Lateral Habenula Excitability Produces Behavioral Vulnerability to Stress

    Project Description: Traumatic stress can have lasting effects on mood, motivation, and pain, yet we still do not understand how a brief experience can leave a lasting “scar” on the brain. This project investigates the mechanisms that turn acute stress into persistent changes in behavior, focusing on an unexpected and largely unexplored role for norepinephrine in the lateral habenula. By uncovering how this stress signal reshapes the brain after trauma, the work may help explain why some stressful experiences have enduring consequences. Ultimately, these findings could point to new biological targets for preventing or treating trauma-related disorders such as PTSD.

  • Ruifeng Ray Cao

    Name: Ruifeng Ray Cao

    School: Robert Wood Johnson Medical School

    Department: Neuroscience and Cell Biology

    Unit: Rutgers Health

    Primary Appointment Title: Associate Professor

    Project Title: Transgenerational Effects of Gestational Circadian Disruption on Glucose Homeostasis

    Project Description: The increasing prevalence of type 2 diabetes (T2D) necessitates the need to identify novel risk factors and preventative strategies to combat the disease. The approximately 24-hour circadian rhythm regulates the functions of key metabolic tissues and controls glucose homeostasis, insulin sensitivity and energy expenditure. Disrupted circadian rhythm in pregnancy (e.g., due to shift work, light exposure at night, or irregular sleep patterns) can lead to dysregulation of key metabolic pathways in the mother and increased risk of gestational diabetes mellitus, which is a risk factor for T2D in the offspring. The goal of this project is to investigate mechanistic links between maternal circadian disruption and generational metabolic dysfunctions in the offspring and shed light on how chronotherapy can be integrated into diabetes intervention.

  • Marc Gartenberg with students in a lab

    Name: Marc Gartenberg

    School: Robert Wood Johnson Medical School

    Department: Biochemistry and Molecular Biology

    Unit: Rutgers Health

    Primary Appointment Title: Professor

    Project Title: An Atlas of Protein Domain Modularity from High-Throughput Gene Fusion and Fracture

    Project Description: This project investigates protein adaptability in a proteome-wide high-throughput manner by integrating yeast molecular genetics with modern methods of transposon mutagenesis, split protein complementation assays, next generation sequencing and machine learning. This work will yield an atlas of protein modularity – a set of general principles and precise rules for how protein domains can be appended and split apart.

  • Yuwei Gu

    Name: Yuwei Gu

    School: School of Arts and Sciences

    Department: Chemistry and Chemical Biology Departmenty

    Unit: Rutgers-New Brunswick

    Primary Appointment Title: Assistant Professor

    Project Title: Synthetic Sequence-Controlled Polypeptides as Programmable Models for Biomolecular Condensates

    Project Description: Biomolecular condensates formed through liquid–liquid phase separation of proteins play important roles in cellular organization and disease. However, understanding their biophysical properties has been limited by inefficient access to diverse sequence-defined polypeptides using conventional recombinant protein expression. This project will leverage the traceless cascade polymerization developed in our group to enable scalable access to libraries of sequence-defined polypeptides and systematically investigate how peptide sequence governs condensate properties, including diffusivity, viscoelasticity, and dynamic behavior. We will further leverage our unique synthetic capabilities to access polypeptides containing noncanonical amino acids and backbone architectures that are difficult to produce biologically. Together, these studies will provide fundamental insights into the molecular features governing biomolecular condensate formation and material properties. The knowledge gained will advance our understanding of disease-associated condensates, including those implicated in neurodegenerative diseases, and may ultimately inform strategies for modulating their behavior.

  • Edmarie Guzmán-Vélez

    Name: Edmarie Guzmán-Vélez

    School: IFH Center for Healthy Aging Research

    Department: Neurology

    Unit: Rutgers-New Brunswick

    Primary Appointment Title: Assistant Professor

    Project Title: Social Exposome and Risk for Dementia in Young to Middle Adulthood

    Project Description: This pilot study investigates how the social exposome, cumulative social, structural, and environmental exposures across the lifespan, shapes biological brain aging and cognitive health, a mechanism that remains poorly understood despite the growing global burden of Alzheimer's disease and related dementias. Using data from 150 racially, ethnically, and socioeconomically diverse adults aged 21 to 65 in the New Jersey Health Cohort, researchers will examine joint social exposome components spanning socioeconomic adversity, discrimination, healthcare access, and neighborhood deprivation. These scores will be linked to validated neuropsychological assessments and to three established epigenetic clocks derived from blood-based DNA methylation that capture accelerated biological aging. The study will examine associations between social exposome and cognitive performance and test whether disadvantage is associated with accelerated epigenetic aging. By focusing on adults across the lifespan rather than only older populations, this work aims to elucidate how social disadvantage becomes biologically embedded well before dementia symptoms emerge.

  • Yang Lyu

    Name: Yang Lyu

    School: School of Arts and Sciences

    Department: Molecular Biology and Biochemistry

    Unit: Rutgers-New Brunswick

    Primary Appointment Title: Assistant Professor

    Project Title: Sweet Sensory Signaling as a Modulator of Metabolic Vulnerability in Alzheimer’s Disease

    Project Description: Alzheimer’s disease is a growing public health challenge, yet we still do not fully understand how everyday dietary experiences influence brain vulnerability. While diet-related disease risk is usually attributed to the nutrients we ingest, increasing evidence suggests that the perception of sweet taste itself may influence aging, metabolism, and disease risk independently of sugar consumption. Using the fruit fly Drosophila, this project will test whether sweet taste increases brain vulnerability by manipulating sweet taste neurons without changing food intake and examining effects on AD-related behavior, brain pathology, and metabolism. We will also test whether serotonin signaling, a potential pathway linking taste and metabolism, can be targeted to reduce these effects.

  • Geoffrey Markowitz

    Name: Geoffrey Markowitz

    School: Cancer Institute of New Jersey

    Department: Medical Immunology

    Unit: Rutgers Health

    Primary Appointment Title: Instructor

    Project Title: T Cell Metabolic Engineering Driven by Functional Avidity

    Project Description: CD8+ T cells are critical determinants of the anti-tumor immune response, with immunogenic tumors frequently elicit a polyclonal T cell response containing a spectrum of T cell receptor (TCR) functional avidities and heterogeneity in functionality. T cell states are associated with and enforced by different metabolisms, however, the metabolic machinery induced by distinct TCR signal strengths, underlying mechanisms, and impact on T cell phenotype and anti-tumor efficacy are not well understood. This project will utilize genetic and pharmacologic approaches to modulate differential metabolisms induced by distinct TCR signal strength and evaluate effects on immunologic and metabolic phenotypes in both mouse model systems for mechanistic insights and human clinically-validated therapeutic T cell products for translational impact.

  • Benjamin Samuels

    Name: Benjamin Samuels

    School: School of Arts and Sciences

    Department: Psychology

    Unit: Rutgers-New Brunswick

    Primary Appointment Title: Associate Professor

    Project Title: Sex-specific Lateral Hypothalamus CRF Circuits in Stress-induced Eating Pathology

    Project Description: Stress alters eating, but not in the same way for everyone. Stress can suppress appetite in some people and drive overeating in others, with the direction varying by sex and by the food available. Using a chronic social stress paradigm effective in both sexes, we found that stress reduces normal chow intake only in male mice while increasing palatable food intake only in females. In addition, directly activating a small population of corticotropin-releasing factor (CRF) neurons reproduces both effects without any stress exposure. We plan to test whether these neurons are necessary for each sex-specific phenotype and whether their separate projections from lateral hypothalamus to the ventral tegmental area and parabrachial nucleus explain the divergence.

  • Robin Stephens

    Name: Robin Stephens

    School: Rutgers New Jersey Medical School Center for Immunity and Inflammation

    Department: Pharmacology, Physiology and Neuroscience

    Unit: Rutgers Health

    Primary Appointment Title: Associate Professor

    Project Title: Protection by Memory T cells in Malaria is limited by Mitochondrial Damage

    Project Description: Malaria kills over 600,000 children annually partially due to a defect in immunity. Increasing evidence points instead to dysfunctional memory T cells (Tmem) as a mechanism for incomplete protection. Our preliminary data show signs of memory T cell death on re-infection and point to problems with T cell mitochondria, the powerhouse of the cell, which can cause cell death. Here, we will define structural and functional mitochondrial defects in Plasmodium-specific memory T cells and then test whether blocking cell death or promoting removal of damaged mitochondria, to enhance effectiveness of the remaining ones, can rescue memory T cell survival during reinfection. These studies are likely to define a new mechanism for poor immunity to malaria and reveal new targets to strengthen naturally acquired immunity to malaria by linking defective T cell recall to mitochondrial quality control.