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Human health and development depend on dynamic networks of physical, and functional, interactions between proteins. However, the details of these networks – how they are formed and how they function – are largely unknown.

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New Publication from the Kotton Lab on the generation of human alveolar epithelial type I cells from pluripotent stem cells

Kotton and colleagues generate human alveolar epithelial type I cells (AT1s) from induced pluripotent stem cells (iPSCs). The resulting cells can be grown as 3D organoids or in 2D air-liquid interface cultures, displaying many of the molecular, morphologic, and functional phenotypes of primary AT1s.

Click here to see the article

CReM Researchers Awarded $14 Million to Understand and Treat Genetic Lung Diseases

A team of researchers led by Darrell N. Kotton, MD, the David C. Seldin Professor of Medicine, has been awarded a five-year, $14 million grant from the NIH’s National Heart, Lung, and Blood Institute (NHLBI) for their research, “Developing Pluripotent Stem Cells to Model and Treat Lung Disease.” The new award will fund an integrated, multi-investigator program project grant where four interacting labs headed by four physician-scientists, all located in the Center for Regenerative Medicine (CReM) of Boston University and Boston Medical Center, will develop next generation stem cell-based therapies for currently incurable genetic lung diseases affecting children and adults, including childhood and adult interstitial lung diseases, an inherited form of emphysema, cystic fibrosis and primary ciliary dyskinesia.

The Kotton Lab publishes new paper on iPSC modeling of childhood interstitial lung disease caused by ABCA3 mutations

Mutations in ATP-binding cassette A3 (ABCA3), a phospholipid transporter critical for surfactant homeostasis in pulmonary alveolar type II epithelial cells (AEC2s), are the most common genetic causes of childhood interstitial lung disease (chILD). Treatments for patients with pathological variants of ABCA3 mutations are limited, in part due to a lack of understanding of disease pathogenesis resulting from an inability to access primary AEC2s from affected children. Here, we report the generation of AEC2s from affected patient induced pluripotent stem cells (iPSCs) carrying homozygous versions of multiple ABCA3 mutations. We generated syngeneic CRISPR/Cas9 gene-corrected and uncorrected iPSCs and ABCA3-mutant knockin ABCA3:GFP fusion reporter lines for in vitro disease modeling. We observed an expected decreased capacity for surfactant secretion in ABCA3-mutant iPSC-derived AEC2s (iAEC2s), but we also found an unexpected epithelial-intrinsic aberrant phenotype in mutant iAEC2s, presenting as diminished progenitor potential, increased NFκB signaling, and the production of pro-inflammatory cytokines. The ABCA3:GFP fusion reporter permitted mutant-specific, quantifiable characterization of lamellar body size and ABCA3 protein trafficking, functional features that are perturbed depending on ABCA3 mutation type. Our disease model provides a platform for understanding ABCA3 mutation–mediated mechanisms of alveolar epithelial cell dysfunction that may trigger chILD pathogenesis.

Click here to read the article

Latest publication from the Murphy Lab featured on the cover of Blood Advances: De Novo Hematopoiesis from the Fetal Lung!

Hemogenic endothelial cells (HECs) are specialized cells that undergo endothelial-to-hematopoietic transition (EHT) to give rise to the earliest precursors of hematopoietic progenitors that will eventually sustain hematopoiesis throughout the lifetime of an organism. Although HECs are thought to be primarily limited to the aorta-gonad-mesonephros (AGM) during early development, EHT has been described in various other hematopoietic organs and embryonic vessels. Though not defined as a hematopoietic organ, the lung houses many resident hematopoietic cells, aids in platelet biogenesis, and is a reservoir for hematopoietic stem and progenitor cells (HSPCs). However, lung HECs have never been described. Here, we demonstrate that the fetal lung is a potential source of HECs that have the functional capacity to undergo EHT to produce de novo HSPCs and their resultant progeny. Explant cultures of murine and human fetal lungs display adherent endothelial cells transitioning into floating hematopoietic cells, accompanied by the gradual loss of an endothelial signature. Flow cytometric and functional assessment of fetal-lung explants showed the production of multipotent HSPCs that expressed the EHT and pre-HSPC markers EPCR, CD41, CD43, and CD44. scRNA-seq and small molecule modulation demonstrated that fetal lung HECs rely on canonical signaling pathways to undergo EHT, including TGFβ/BMP, Notch, and YAP. Collectively, these data support the possibility that post-AGM development, functional HECs are present in the fetal lung, establishing this location as a potential extramedullary site of de novo hematopoiesis.

New publication from the Murphy Lab in Science Advances! They led a Team demonstrating that immune cells drive NET tumor progression and susceptibility to therapies

Neuroendocrine tumors (NETs) are rare cancers that most often arise in the gastrointestinal tract and pancreas. The fundamental mechanisms driving gastroenteropancreatic (GEP)–NET growth remain incompletely elucidated; however, the heterogeneous clinical behavior of GEP-NETs suggests that both cellular lineage dynamics and tumor microenvironment influence tumor pathophysiology. Here, we investigated the single-cell transcriptomes of tumor and immune cells from patients with gastroenteropancreatic NETs. Malignant GEP-NET cells expressed genes and regulons associated with normal, gastrointestinal endocrine cell differentiation, and fate determination stages. Tumor and lymphoid compartments sparsely expressed immunosuppressive targets commonly investigated in clinical trials, such as the programmed cell death protein–1/programmed death ligand–1 axis. However, infiltrating myeloid cell types within both primary and metastatic GEP-NETs were enriched for genes encoding other immune checkpoints, including VSIR (VISTA), HAVCR2 (TIM3), LGALS9 (Gal-9), and SIGLEC10. Our findings highlight the transcriptomic heterogeneity that distinguishes the cellular landscapes of GEP-NET anatomic subtypes and reveal potential avenues for future precision medicine therapeutics.

Kotton Lab featured in Boston University Article on Lung Disease Research

For more than 20 years, a team of Boston University scientists have been on a quest to not just figure out how to treat incurable lung diseases, but also how to regenerate damaged lungs so they’re as good as new.

That is the goal of pulmonologist Darrell Kotton and his lab at the Center for Regenerative Medicine (CReM), a joint effort between the University and Boston Medical Center, BU’s primary teaching hospital. By refining their work using sophisticated stem cell technology, Kotton and his team are closer to realizing that vision than ever before.

In two new studies published in Cell Stem Cell, BU researchers detail how they engineered lung stem cells and successfully transplanted them into injured lungs of mice. Two lines of cells targeted two different parts of the lung: the airways, including the trachea and bronchial tubes, and the alveoli, the delicate air sacs that deliver oxygen to the bloodstream. Their findings could eventually lead to new ways for treating lung diseases, including severe cases of COVID-19, emphysema, pulmonary fibrosis, and cystic fibrosis, a disease caused by a genetic mutation.

The Mostoslavsky Lab Publishes New Platform to Make T Cells from iPSCs

A robust method of producing mature T cells from iPSCs is needed to realize their therapeutic potential. NOTCH1 is known to be required for the production of hematopoietic progenitor cells with T cell potential in vivo. Here we identify a critical window during mesodermal differentiation when Notch activation robustly improves access to definitive hematopoietic progenitors with T/NK cell lineage potential. Low-density progenitors on either OP9-hDLL4 feeder cells or hDLL4-coated plates favored T cell maturation into TCRab+CD3+CD8+ cells that express expected T cell markers, upregulate activation markers, and proliferate in response to T cell stimulus. Single-cell RNAseq shows Notch activation yields a 6-fold increase in multi-potent hematopoietic progenitors that follow a developmental trajectory toward T cells with clear similarity to post-natal human thymocytes. We conclude that early mesodermal Notch activation during hematopoietic differentiation is a missing stimulus with broad implications for producing hematopoietic progenitors with definitive characteristics.

Click here to access the full article

New Publication for the Murphy Lab, A ‘Blueprint’ for Longevity feature in USA Today, the New York Post and 75 other Media Outlets

Age-related changes in immune cell composition and functionality are associated with multimorbidity and mortality. However, many centenarians delay the onset of aging-related disease suggesting the presence of elite immunity that remains highly functional at extreme old age.

To identify immune-specific patterns of aging and extreme human longevity, we analyzed novel single cell profiles from the peripheral blood mononuclear cells (PBMCs) of a random sample of 7 centenarians (mean age 106) and publicly available single cell RNA-sequencing (scRNA-seq) datasets that included an additional 7 centenarians as well as 52 people at younger ages (20–89 years).

The analysis confirmed known shifts in the ratio of lymphocytes to myeloid cells, and noncytotoxic to cytotoxic cell distributions with aging, but also identified significant shifts from CD4+ T cell to B cell populations in centenarians suggesting a history of exposure to natural and environmental immunogens. We validated several of these findings using flow cytometry analysis of the same samples. Our transcriptional analysis identified cell type signatures specific to exceptional longevity that included genes with age-related changes (e.g., increased expression of STK17A, a gene known to be involved in DNA damage response) as well as genes expressed uniquely in centenarians’ PBMCs (e.g., S100A4, part of the S100 protein family studied in age-related disease and connected to longevity and metabolic regulation).

Collectively, these data suggest that centenarians harbor unique, highly functional immune systems that have successfully adapted to a history of insults allowing for the achievement of exceptional longevity.

Click here to see the article Click here to see the USA Today Article

The latest publication from the Kotton lab detailing the transcriptomic programs of iPSC-derived alveolar cells

Dysfunction of alveolar epithelial type 2 cells (AEC2s), the facultative progenitors of lung alveoli, is implicated in pulmonary disease pathogenesis, highlighting the importance of human in vitro models. However, AEC2-like cells in culture have yet to be directly compared to their in vivo counterparts at single-cell resolution. Here, we performed head-to-head comparisons among the transcriptomes of primary (1°) adult human AEC2s, their cultured progeny, and human induced pluripotent stem cell–derived AEC2s (iAEC2s). We found each population occupied a distinct transcriptomic space with cultured AEC2s (1° and iAEC2s) exhibiting similarities to and differences from freshly purified 1° cells. Across each cell type, we found an inverse relationship between proliferative and maturation states, with preculture 1° AEC2s being most quiescent/mature and iAEC2s being most proliferative/least mature. Cultures of either type of human AEC2s did not generate detectable alveolar type 1 cells in these defined conditions; however, a subset of iAEC2s cocultured with fibroblasts acquired a transitional cell state described in mice and humans to arise during fibrosis or following injury. Hence, we provide direct comparisons of the transcriptomic programs of 1° and engineered AEC2s, 2 in vitro models that can be harnessed to study human lung health and disease.

Human iPSC-hepatocyte modeling of Alpha-1-antitrypsin from the Wilson lab is out!

Individuals homozygous for the ‘‘Z’’ mutation in alpha-1 antitrypsin deficiency are known to be at increased risk for liver disease. It has also become clear that some degree of risk is similarly conferred by the heterozygous state. A lack ofmodel systems that recapitulate heterozygosity in human hepatocytes has limited the ability to study the impact of a single Z alpha-1 antitrypsin (ZAAT) allele on hepatocyte biology. Here, we describe the derivation of syngeneic induced pluripotent stem cells (iPSCs) engineered to determine the effects of ZAAT heterozygosity in iPSC-hepatocytes (iHeps). We find that heterozygous MZ iHeps exhibit an intermediate disease phenotype and share with ZZ iHeps alterations in AAT protein processing and downstream perturbations including altered endoplasmic reticulum (ER) and mitochondrial morphology, reduced mitochondrial respiration, and branch-specific activation of the unfolded protein response in cell subpopulations. Our model of MZ heterozygosity thus provides evidence that a single Z allele is sufficient to disrupt hepatocyte homeostatic function.

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The Wilson lab is focused on two major aspects of regenerative medicine:

1) Developing gene therapy approaches for the study and treatment of lung diseases: The ability to manipulate gene expression in specified lung cell populations has both experimental and therapeutic potential for lung disease. By developing viral vectors that transduce specific lung cell types in vivo, we hope to minimize potential off-target effects while maximizing our ability to target diseased cell populations. We work with lentiviral and AAV vectors to overexpress or knockdown expression of genes important to disease pathogenesis in the lung.

2) Utilizing induced pluripotent stem cells (iPSC) to study human lung and liver diseases: The Wilson lab is interested in the application of patient-derived iPS cells for the study of lung and liver diseases, such as alpha-1 antitrypsin deficiency (AATD).

The Hawkins Lab is interested in how the human lung develops and responds to injury to better understand human lung disease. Induced pluripotent stem cells (iPSCs) offer a unique opportunity to model human lung disease and bridge the gap between research in animal models and humans.

Using this iPSC platform, we are focused on understanding the molecular mechanisms that control human lung development. We hope to apply this knowledge to advance our understanding of and develop precision medicine approaches for lung disease.

The Murphy laboratory is composed of dynamic and passionate researchers who utilize multiple stem cell-based platforms to answer basic biological questions and combat disease. Central directions of the laboratory include: developmental hematopoiesis, the modeling of blood-borne disease, and discovery and therapeutic intervention in sickle cell disease, amyloidosis, and aging.

The Murphy Lab has pioneered: The world’s largest sickle cell disease-specific iPSC library and platforms and protocols that can used to recapitulate hematopoietic ontogeny and to develop and validate novel therapeutic strategies for the disease; The successful modeling of a protein folding disorder called familial amyloidosis demonstrating the ability to model a long-term, complex, multisystem disease in a relatively short time, using lineage-specified cells (hepatic, cardiac and neuronal) derived from patient-specific stem cells; The first iPSC library created from subjects with exceptional longevity (centenarians) that serves as an unlimited resource of biomaterials to fuel the study of aging and the development of novel therapeutics for aging-related disease.

www.murphylaboratory.com

@DRGJMurphy

The Serrano Lab studies neurodevelopment and cardiovascular development in the context of rare multi-systemic disorders originated by pathogenic variants in epigenetic modifiers like KMT2D.   

We aim to identify shared molecular and cellular mechanisms driving cardiovascular and brain development with particular interest in cell differentiation, migration, and cell cycle progression.   

Our lab combines rare disease modeling in zebrafish together with cardiovascular and neurobiology techniques and human iPSC-derived brain organoids and endothelial cells.   

We believe that a patient-forward focus to our projects will help us to get better understanding of disease mechanisms through basic science research. To this end, we are active in the collaborative community among field experts and rare disease patient-advocacy groups who drive our research program to identify therapeutic targets in patient-specific iPS cells.  

The Mostoslavsky Lab is a basic science laboratory in the Section of Gastroenterology in the Department of Medicine at Boston University.

Our goal is to advance our understanding of stem cell biology with a focus on their genetic manipulation via gene transfer and their potential use for stem cell-based therapy.

The Mostoslavsky’s Lab designed and constructed the STEMCCA vector for the generation of iPS cells, a tool that has become the industry standard for nuclear reprogramming. Project areas in the lab focuses on the use of different stem cell populations, including embryonic stem cells, induced Pluripotent Stem (iPS) cells, hematopoietic stem cells and intestinal stem cells and their genetic manipulation by lentiviral vectors.

Our laboratory have already established a large library of disease-specific iPS cells with a particular interest in utilizing iPS cells to model diseases of the liver, the gastrointestinal tract, prion-mediated neurodegenerative diseases and immune-based inflammatory conditions, using iPSC-derived microglia, macrophages and T/NK cells.

The Gouon-Evans lab investigates cellular and molecular mechanisms driving liver development, regeneration and cancer. We specifically interrogate the role of progenitor/stem cells and how they share similar molecular signature and functions during these 3 processes.

Our innovative tools include: 1) directed differentiation of human pluripotent stem cells (PSC) to generate in vitro liver progenitors and their derivative hepatocytes, the main functional cell type of the liver, 2) mouse models with lineage tracing strategy to track in vivo the fate of progenitor cells, 3) PSC derivative cell transplantation into mouse models with damaged livers as cell therapy for liver diseases, 3) dissection of liver cancer specimens from patients to identify and define the impact of specific cancer stem cells in liver oncogenesis.

Projects in the Gouon-Evans lab will lead to a better understanding of the liver development, to the establishment of multi-modular approaches for improving liver regeneration with PSC derivatives, and will reveal the impact of specific cancer stem cells as a target for diagnosis and therapy in liver oncogenesis.

Medical research at Boston University is dedicated to improving lives. BU has one of the largest and fastest-growing research programs among US medical schools. Our research at the Chobanian & Avedisian School of Medicine supports all aspects of biomedical research, from exploration at the basic science level to translating fundamental discoveries into treatments that improve human health.

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Boston Children’s Hospital

Boston Children’s Hospital is home to the world’s largest and most active pediatric research enterprise and one of the largest research programs of any independent hospital. The hospital has $518 million in research funding per year and more than 1,000,000 square feet of state-of-the-art laboratory space. The research mission of Children’s Hospital encompasses basic research, clinical research, community service programs and the training of new scientists. Our more than 1,100 investigators, include 13 members of the National Academy of Sciences, 28 members of the National Academy of Medicine, 23 Fellows of the American Academy of Arts and Sciences, 13 Fellows of the American Academy for the Advancement of Sciences, 12 current members of the Howard Hughes Medical Institute (HHMI) and 13 alumni of the HHMI. Twenty-seven faculty are members of the American Association of Physicians and 47 are members of the American Society of Clinical Investigation, two organizations where members are elected based on high research and academic achievement. Over the years, four Children’s investigators have won the Nobel Prize and six have won the nearly equally prestigious Lasker Award. Children’s truly has an extraordinary research community and a level of research that rivals the very best research institutes in the world.

Boston Medical Center

Boston Medical Center is nationally recognized for clinical, health services, and policy research as it relates to low income and minority children. Areas of research include child development and early literacy, perinatal epidemiology, gene-environment interactions and low birth weight, the impact of policy, such as welfare reform, housing and nutrition on health, prenatal drug exposure on child health and development, HIV/AIDS in children, the use of information technology to improve quality, environmental health, and international and immigrant health.

Quality of Research

The quality of the research done by Children’s Hospital and Boston Medical Center faculty is especially impressive. When last compared, researchers from Children’s published more than 7 times as many papers in the top three basic science journals than any other pediatric program, and 2.4 times more than the top 20 ranked pediatric programs combined! The proportion of papers published in the top 30 basic science journals exceeded all the Boston ‘adult’ hospitals, and all medical schools (including their basic science departments), except for Stanford. Indeed, when the papers of the full-time faculty at the Whitehead Institute (17 members) and the top 17 faculty researchers at Boston Children’s Hospital are compared, the Children’s faculty published 13.9% of their papers in Cell, Science or Nature, while the Whitehead faculty proportion was only 4.6%. Similarly, in clinical research, BCRP researchers published 2.6 times more papers in the top three clinical journals (New England Journal of Medicine, JAMA and Lancet) than the next best pediatric program. Indeed, at Boston Medical Center 3.3% of pediatric papers appeared in these three journals, compared to an average of just 0.58% for the other top 20 ranked pediatric institutions. Thus, by any measure, the quality of the research at Boston Children’s Hospital and Boston Medical Center is world class.

Research is an active aspect of the residency program as well. This is reflected in the high proportion of residents with previous research experience, the enthusiasm of the residents for their journal clubs and their own research, and just by conversations in the hallways or at rounds. Many outstanding physician-scientists and general academic researchers serve as attendings and they also help focus on the interplay between science and medicine.

National Academy of Sciences, National Academy of Medicine and Howard Hughes Medical Institute Members at the BCRP. Some of the Many Distinguished Scientists at Boston Children’s Hospital (click this title to see an enlarged picture):

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May 8, 2024

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Revised clinical guidelines on mandatory reporting of substance-exposed newborns show promise

by Boston Medical Center

Researchers at Boston Medical Center (BMC) have published findings in JAMA Pediatrics that show the hospital's revised clinical guidelines for reporting substance-exposed newborns support family health.

In May 2021, BMC revised its clinical guidelines to report suspected abuse after a child is born when there are tangible concerns about the parent's ability to safely care for the child, rather than automatically filing Child Protective Services (CPS) reports for all cases of prescribed use of opioids or medication for opioid use disorder. This clinical guideline shift reduced reporting to CPS by 45%, eliminating reporting in the absence of child safety concerns.

Study authors contend that automatic mandatory reporting stigmatizes evidence-based care for substance use disorders (SUDs) and contributes to unnecessary family surveillance and inefficient use of limited CPS resources.

Currently, mandatory reporting laws in Massachusetts do not differentiate between birthing patients engaged in treatment and taking medication for opioid use disorder and those who are not managing their SUD, leaving some parents to opt out of treatment. BMC advocates for all birthing patients to be treated with compassion and, for those managing addiction, to partner with their provider on care plans.

Massachusetts is currently considering legislation that would amend existing CPS reporting mandates.

"Mandatory reporting forces pediatricians to unfairly assume abuse or neglect before a baby is even born," said lead author Rohan Khazanchi, MD, MPH, a BMC resident physician in internal medicine and pediatrics and research affiliate at Harvard University's FXB Center for Health & Human Rights.

"Our study shows that BMC's clinical guidance approach is making a difference for hundreds of families who overcame tremendous barriers throughout their recovery journeys."

Researchers will continue to study the long-term outcomes of eliminating unsubstantiated neglect reporting on the health of children and their families.

In the current study, authors compared outcomes at BMC with 16 other Massachusetts-based birthing hospitals that report data to the Perinatal-Neonatal Quality Improvement Network of Massachusetts (PNQINMA). Their analysis of 3,658 parent-infant dyads from January 2017 to May 2023 focused on three short-term measures: CPS reporting prior to discharge; discharge to a biological parent's custody; and hospital length of stay. Results were promising across all measures.

"BMC continued to provide the highest levels of care and protection for newborns while also taking into consideration the potential negative side effects of mandatory reporting for recovering parents," said senior author Heather Hsu, MD, a BMC pediatric hospitalist and Assistant Professor of Pediatrics at Boston University Chobanian & Avedisian School of Medicine.

"BMC is committed to supporting families in their recovery journey and providing them with the tools they need to be successful, while removing additional stressors and stigmas. The hospital's revised guidelines help us facilitate a healthier environment for both parent and child."

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Embark on a comprehensive nursing journey with challenging coursework and hands-on practicums at the Center for Clinical Education & Research. Our team of clinical and simulation educators is committed to fostering student engagement and unlocking their full potential as they transition to professional practice. Through personalized academic and clinical support, students receive tailored assistance for success in the nursing program. Access to valuable resources empowers students to develop effective academic habits, resulting in a high rate of success.

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The purpose of the Center for Clinical Education and Research (CCER) is to support and enhance the academic and clinical education of the students in the College of Nursing and Health Sciences. The overarching goal is to contribute to the development of knowledgeable, competent, compassionate registered nurses and health science professionals who are interested in life-long learning and who will enrich their profession and thereby positively impact the health and well-being of their clients.

• Integrate simulation, experiential learning strategies, and technology throughout the lab curriculum
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The Center for Clinical Education and Research (CCER) has created a recycling program, SimCycle, to address the issue of waste by decreasing single-use plastic waste. Clear bins with the SimCycle logo are dispersed throughout the skills labs, outpatient exam rooms, and the simulation suite to collect items for repurposing. Students dispose of intravenous tubing, fluid bags, and indwelling catheter kits after practicing their skills on task trainers. Under the direction of the lab manager, a team of work-study students, graduate teaching assistants, and simulation educators developed a cleaning and repackaging process that does not sacrifice the integrity of the product for additional practice.

SimCycle enhances student awareness of single-use plastics in health care and their impact on the environment. The program has demonstrated $11,035 in financial savings since its inception in March 2021. Collaboration between students and CCER staff has created a sustainable environment that enriches the educational culture in the nursing simulation lab.

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Congratulations to Our 2024 Outstanding Student Achievement Award Winners!

Graduate Medical Sciences is pleased to award four high-achieving, graduating students with Outstanding Student Achievement Awards in the categories “Outstanding Research” and “Community Service.”

These students have made exceptional contributions to their departments and communities that have set them apart from their peers during their time at GMS. Meet each awardee below:

Katharine Babcock, PhD, ’24

Phd in anatomy & neurobiology.

Katharine Babcock is a January 2024 graduate of the PhD program in Anatomy & Neurobiology. She has been at Boston University for almost 10 years. From September 2014 to September 2016, Katharine worked as a research assistant at the BU Chronic Traumatic Encephalopathy (CTE) Center Brain Bank, before pursuing her master’s in the same lab until 2018.

From 2018 to 2023, Katharine pursued her PhD, graduating in January 2024. She is now a postdoctoral fellow at the CTE Center, working to publish two of her thesis chapters.

Katharine’s community service project, “BUtiful Brains,” won her the Outstanding Student Achievement Award in the PhD Community Service category.

Read Katharine’s full story here!

Anna Smith ’24

Phd in molecular & translational medicine, program in biomedical sciences.

Anna Smith is a PhD candidate in the Graduate Program in Molecular and Translational Medicine (MTM). She has been at Boston University for almost five years, having matriculated into the PhD Program in Biomedical Sciences in Fall 2019.

Anna is completing her dissertation research in the lab of Associate Professor of Medicine Valerie Gouon-Evans, PhD, PharmD. Dr. Gouon-Evans directs the Boston University Liver Biologists (BULB) Program and is the associate director of the MTM program. Anna’s research focuses on finding alternatives to liver transplantation that transplant healthy liver cells instead of an entire organ. She defended her dissertation, “Human Primary and iPSC-Derived Hepatocyte Cell Therapies to Treat Liver Disease,” in March 2024 and will graduate in May 2024.

Anna’s dissertation research won her this year’s Outstanding Student Achievement Award in the PhD Research Category.

Read more about Anna’s work here!

Gwendolyn Strickland ’24

Master of science in genetic counseling / master of public health dual degree.

Gwendolyn Strickland is a master’s candidate in the Master of Science in Genetic Counseling Program. She matriculated into Boston University in Fall 2022 to pursue a dual MS/Master of Public Health degree at GMS and the School of Public Health (SPH).

Gwendolyn worked with the Boston Medical Center (BMC) Refugee Women’s Health Clinic to implement a group care model focused on case management services for recently arrived pregnant patients from Haiti. The project began as her SPH practicum. Gwendolyn hopes to take what she’s learned from this community service project and apply it to the field of genetic counseling by increasing awareness and access to genetic services for people who hold marginalized identities.

Gwendolyn’s project won her the Outstanding Student Achievement Award in the Master’s Community Service category.

Read Gwendolyn’s full story here!

Melanie Delgado ’24

Master of science in medical science (mams) program.

Melanie Delgado is a May 2024 master’s candidate in the Master of Science in Medical Science (MAMS) program. She matriculated into the MAMS program in Fall 2022.

Melanie works for Michael Levy, MD, PhD, the director of the Neuroimmunology Clinic and Research Laboratory at Massachusetts General Hospital. There, she oversees a clinical trial investigating a new drug in the treatment of anti-NMDAR encephalitis. As part of her master’s thesis, Melanie also developed a cross-sectional study to better understand the use, dosing and adverse effects of medical marijuana in the symptom management of rare neuroimmune diseases.

Melanie will soon present her data at the 2024 European Committee for Treatment and Research of Multiple Sclerosis (ECTRIMS) Conference in Copenhagen, Denmark. Her research also won her the Outstanding Student Achievement Award in the Master’s Research Category.

Read more about Melanie’s research here!

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BMC’s Yawkey building doors are now closed as an entrance as part of our ongoing efforts to enhance our campus and provide you with the best clinical care.

All patients and visitors on our main campus must enter our hospital via Shapiro, Menino, or Moakley buildings, where they will be greeted by team members at a new centralized check-in desk before continuing to the hospital. We are excited to welcome you and appreciate your patience as we improve our facilities.

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Self-Assessments – Check Yourself Before You Wreck Yourself, Research Professional's Network workshop, 3-4:30 pm

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Signup link CRRO Research Professionals Network, May 2024