PRISM Mentors

The mission of the Water & Energy Efficiency for the Environment Lab (WE3Lab) is to reduce the cost and carbon intensity of water desalination and reuse. Ongoing research efforts include:

1) developing automated, precise, robust, intensified, modular, and electrified (A-PRIME) water desalination technologies to support a circular water economy;

2) optimizing the coordinated operation of decarbonized water and energy systems; and

3) supporting the design and enforcement of water-energy-food policies (e.g., Effluent Limitation Guidelines, the Clean Power Plan, CA Sustainable Groundwater Management Act, etc.).

I am a clinical pathologist and assistant professor in the Departments of Medicine, Pathology, and Genetics (by courtesy) at Stanford. I completed my MD-PhD training at Yale University and my residency training and a post-doctoral fellowship in the Department of Genetics at Stanford University. My experiences as a clinical pathologist and genome scientist have made me passionate about applying cutting-edge technologies to primary patient specimens in order to characterize disease pathologies at the molecular level. The core focus of my lab is to study the mechanisms by which genetic variants influence the risk of disease through effects on intermediate molecular phenotypes.

The overarching research goal of the Diehn lab is to develop and translate novel diagnostic assays and therapies to improve personalized treatment of cancer patients. We have a major focus on the development and application of liquid biopsy technologies for human cancers, with a particular emphasis on lung cancers and circulating tumor DNA (ctDNA). We also investigate mechanisms of treatment resistance to radiotherapy, immunotherapy, and targeted agents. Most of our research projects start by identifying an unmet need in the clinical management of cancer patients that we then try to solve via development or application of novel technologies. We use genomics, bioinformatics, stem cell biology, genome editing, mouse genetics, and preclinical cancer models in our work. Discoveries from our group are currently being tested in multiple clinical trials at Stanford and elsewhere in order to translate them into the clinic.

Research activities in our group focus on the computational modeling and experimental analysis of turbulent and chemically reacting flows. Applications include propulsion systems, renewable energy, carbon sequestration, and high-speed and multiphase flows. Particular emphasis is directed towards improving the fundamental understanding of underlying physical processes involving the coupling between turbulence, reaction chemistry, pollutant formation and noise emission. Our research approach combines classical theoretical analysis tools (including linear stability analysis, rapid distortion theory, and stochastic models), numerical models, and the utilization of direct numerical simulation (DNS) results for the development, analysis, and validation of computational models. Current research interests include:

• Fundamental analysis of non-equilibrium and supercritical flows
• Heat-transfer and boundary layers
• High-order numerical techniques for chemically reacting flows
• Development of models for application to kinetics-controlled combustion, including auto-ignition, low-temperature combustion, and combustion-dynamic processes
• Particle-laden flows and atmospheric entry
• Heterogeneous flows in micro-, meso-, and nano-porous flows
• CO2 capture and sequestration

Another active area of research involves the experimental analysis of ultrafast non-equilibrium processes using X-ray diffraction and spectroscopy, specfically focusing on sub-picosecond physico-chemical processes in complex fluids and chemical systems. For this, we're closely working with the SLAC National Accelerator Laboratory, the Advanced Light Source at LBNL and other facility to perform X-ray experiments.

With a creative, collaborative, biophysical mindset, we aim to understand the ability of parasites to interface with their host-cell to a point at which we can exploit the mechanisms not only for finding cures against the disease the parasites cause but also to make parasite mechanisms a tool that we can use to engineer the host’s cells. By developing approaches that allow a quantitative understanding and manipulation of molecular transport our research transforms parasites from agents of disease to tools for health.

Specifically, we are studying how the malaria parasite takes control over red blood cells. By learning the biophysical principles of transport in between the host and the parasite we can design ways to kill the parasite or exploit it to reengineer red blood cells. The transport we study is broadly encompassing everything from ions to lipids and proteins. We use variations of quantitative microscopy and electrophysiology to gain insight into the unique strategies the parasite evolved to survive.

I am a physician scientist with interests in cardiomyopathies, rare and undiagnosed diseases, therapeutics and genomics. I have research training in myocardial and skeletal muscle biology and genetics, genomics, and multi-scale networks. In addition to my research training, I am a physician with interest and experience treating patients with hypertrophic cardiomyopathy, neuromuscular disease associated cardiomyopathies, and inherited dilated cardiomyopathies. I have clinical training in medicine, cardiology, cardiovascular genetics, and advanced heart failure and transplant cardiology. I have extensive translational science efforts, as site PI for ongoing clinical trials for hypertrophic cardiomyopathy and dilated cardiomyopathy and for cardiomyopathy consortia including NONCOMPACT, PPCM and the Precision Medicine Study/DCM Consortium. I am Co-PI of Stanford’s NIH-funded Center for Undiagnosed Diseases, a clinical site of the Undiagnosed Diseases Network. I am also Co-PI of the NIH-funded Bioinformatics Center of the Molecular Transducers of Physical Activity Consortium. I pursue projects and collaborations at the intersection of striated muscle genetics, genomics, therapeutics and clinical investigation.

Department URL:
https://med.stanford.edu/cvmedicine.html

By studying calcineurin, the conserved Ca2+/calmodulin-regulated protein phosphatase, we aim to discover and elucidate new Ca2+-regulated signaling pathways in humans. The calcineurin phosphatase dephosphorylates proteins only when Ca2+ signaling is triggered, for example by a hormone, growth factor, neurotransmitter etc. Previous work from the Cyert lab discovered how calcineurin allows yeast cells to survive environmental stress (Goldman et al, 2014, Molecular Cell). Currently, we are studying human calcineurin which is ubiquitously expressed and plays critical roles throughout the body, but especially in the nervous, cardiac and immune systems. Calcineurin is best known for activating the adaptive immune response by dephosphorylating the NFAT transcription factors, and is the target of widely prescribed immunosuppressant drugs, FK506 (tacrolimus) and Cyclosporin A. However, these drugs cause many adverse effects due to inhibition of calcineurin in non-immune tissues, where the majority of calcineurin substrates and functions remain to be discovered. We are using a variety of experimental and computational strategies to systematically map human calcineurin signaling pathways in healthy and diseased cells. We have uncovered surprising roles for calcineurin in Notch signaling, regulation of transport though nuclear pores, and at centrosomes. See our recent paper (Wigington, Roy et al, 2020, Molecular Cell) to learn more about our studies.

The Skylar-Scott Lab specializes in cardiovascular tissue biomanufacturing, seeking to push the complexity and scale at which tissue can be designed and manufactured on demand. By integrating high-throughput culture of designer organoids with new machines and methods for advanced 3D bioprinting, our laboratory seeks to enhance the maturation and function of vascularized cardiac tissues in vitro and in vivo.

Our lab is embedded at the intersection of synthetic biology, tissue engineering, and 3D printing. We are always seeking new students and postdocs with a demonstrated passion for rethinking how we make things, with relevant expertise in bioengineering, mechanical engineering, or materials science.

I'm interested in neuroinflammation and stroke, especially the effects of inflammation on longer term outcomes after stroke. Studies involve mice and humans, and basic mechanistic studies as well as development of potential therapies for humans. Check out the websites above for more information! My lab is welcoming of people from all backgrounds, and promotes team-work and mutual support.

I am also a co-PI on the "Pathways to Neurosciences" program (https://neuroscience.stanford.edu/research/training/pathways-neurosciences), which is not a fellowship but rather a 2-year peer mentoring program to support and provide leadership training to early postdocs and late-stage graduate students who self-identify as coming from groups underrepresented in neuroscience. Please check us out and consider joining after you are on campus!

Roncarolo laboratory is exploring the basic biology and translational applications of human type 1 regulatory cells (Tr1). We are using engineered Tr1, ex vivo Tr1, and alloantigen-specific Tr1 to uncover the molecular frameworks that govern Tr1 identity, differentiation and function. We are also translating Tr1 into the clinic. First, Tr1 can be used as a supportive cell therapy to enhance stem cell engraftment and immune reconstitution after hematopoietic stem cell transplantation (HSCT). Alloantigen-specific Tr1, designed to prevent graft-vs-host disease (GvHD) after allogeneic HSCT, are already being tested in a phase I/II clinical trial (NCT03198234). Second, we are investigating the mechanisms of action and clinical potential of the engineered Tr1 called CD4(IL-10) or LV-10, generated by lentiviral transduction of CD4 T cells with IL10 gene. Besides their immunosuppressive and anti-GvHD properties, LV-10 lyse primary acute myeloid leukemia (AML) cells and delay myeloid leukemia progression in vivo. We are exploring LV-10 as a novel cell immunotherapy for AML. Finally, we are interested in curing inborn errors of immunity by stem cell transplantation or autologous stem cell gene correction. We are testing a gene editing strategy to correct pathogenic mutations in IL10 and IL10 receptor genes, which cause severe and debilitating VEO-IBD (very early onset inflammatory bowel disease) in infants and young children.

Roncarolo laboratory is exploring the basic biology and translational applications of human type 1 regulatory cells (Tr1). We are using engineered Tr1, ex vivo Tr1, and alloantigen-specific Tr1 to uncover the molecular frameworks that govern Tr1 identity, differentiation and function. We are also translating Tr1 into the clinic. First, Tr1 can be used as a supportive cell therapy to enhance stem cell engraftment and immune reconstitution after hematopoietic stem cell transplantation (HSCT). Alloantigen-specific Tr1, designed to prevent graft-vs-host disease (GvHD) after allogeneic HSCT, are already being tested in a phase I/II clinical trial (NCT03198234). Second, we are investigating the mechanisms of action and clinical potential of the engineered Tr1 called CD4(IL-10) or LV-10, generated by lentiviral transduction of CD4 T cells with IL10 gene. Besides their immunosuppressive and anti-GvHD properties, LV-10 lyse primary acute myeloid leukemia (AML) cells and delay myeloid leukemia progression in vivo. We are exploring LV-10 as a novel cell immunotherapy for AML. Finally, we are interested in curing inborn errors of immunity by stem cell transplantation or autologous stem cell gene correction. We are testing a gene editing strategy to correct pathogenic mutations in IL10 and IL10 receptor genes, which cause severe and debilitating VEO-IBD (very early onset inflammatory bowel disease) in infants and young children.

We study the genetic and molecular mechanisms that regulate proliferation and differentiation in adult stem cell lineages, using the Drosophila male germ line as a model.  Our current work is focused on the switch from mitosis to meiosis and how the new gene expression program for cell type specific terminal differentiation is turned on.  One emerging surprise is the potential role of alternative processing of nascent mRNAs in setting up the dramatic change in cell state

We study the genetic and molecular mechanisms that regulate proliferation and differentiation in adult stem cell lineages, using the Drosophila male germ line as a model.  Our current work is focused on the switch from mitosis to meiosis and how the new gene expression program for cell type specific terminal differentiation is turned on.  One emerging surprise is the potential role of alternative processing of nascent mRNAs in setting up the dramatic change in cell state

The overarching goal of Brain Dyanamics Lab is to develop computational methods that could allow for anchoring psychiatric diagnosis into biological features (e.g., neural circuits, spatiotemporal neurodynamics). The lab is funded through an NIH Director’s New Innovator Award (DP2), an NIMH R01, and a faculty scholar award from Stanford’s Maternal and Child Health Research Institute. Our lab excels in developing data-driven computational methods to generate clinically and behaviorally relevant insights from high-dimensional biological data (e.g., neuroimaging) without necessarily averaging the data at the outset. The lab also actively pursue developing novel technologies for experimental design and data collection for enhancing human cognition (e.g., creativity and collaboration). Lastly, the lab also uses large-scale biophysical network modeling approaches to study effects of neuromodulation via TMS and pharmacology (e.g., psychedelics).

We are a computational neuropsychiatry lab dedicated to developing computational methods to better understand brain’s overall dynamical organization in healthy and patient populations. We employ algorithms from a wide range of fields, including Applied Mathematics, Econometrics, Machine Learning, Biophysics, and Network Science.

We have immediate multiple openings for postdoc and research engineer/scientist positions. Please contact Dr. Manish Saggar (saggar@staford.edu), Assistant Professor (Research) of Psychiatry and Behavioral Sciences (Interdisciplinary Brain Science Research), for any questions and for applications. 

See here for more details - https://braindynamicslab.github.io/misc/join/

 

Mature organs respond to the body's changing needs by moving between different 'states' of cellular flux.
The same organ exhibits different kinds of cell flux over time. This is because flux is dynamically tuned to optimize organ function. At homeostasis, cell addition balances loss, giving rise to equilibrium. Upon environmental change, transient disequilibrium promotes physiological growth or shrinkage. When disequilibrium becomes chronic, it leads to pathogenic resizing and disease. We conceptualize these differences as 'organ states' that form a phase space.

What does organ-scale cellular flux look like, and how do these dynamics arise?
We know many molecular signals that impact cellular flux. Yet, we have scarcely begun to discover how these signals alter the 'lifecycle' of individual cells or understand how cells' life cycles integrate to create diverse organ states. For most organs, even basic spatiotemporal features of these cell behaviors remain mysterious.

Our goal is to explain—and ultimately even predict—how large populations of individual cells act to create diverse organ states in response to external change. We believe that the cell dynamics of adult organs can be understood in the granular way that we currently understand embryonic gastrulation. Toward this vision, we build new experimental approaches and conceptual models to decipher how cell life cycles and molecular signaling together create the organ phase space.

The fly gut is our testing ground for probing cell dynamics at the organ-scale…
The adult Drosophila midgut, or fly gut, is a stem-cell based digestive organ. Its relative simplicity (~10,000 cells), extreme genetic tractability, and ease of handling make it ideal for exploring how single-cell behaviors scale to produce whole-organ phenotypes. Because the organ phase space and the cellular life cycle are general features of adult organs, the lessons we learn from the fly gut will provide a general template for organs in other animals, including humans.

…and is a powerful model to study how dynamic cell flux maintains healthy organ form.
The fly gut is also an archetypical example of an epithelial tube, which is both the most primitive organ form and the form of most organs in our own bodies. As our ability to grow human organs in a dish becomes closer to reality, understanding how general principles of epithelial organization operate with the particular dynamics of adult organs becomes crucial for designing better, safer organ therapies. We leverage these well-understood principles of epithelial organization in order to study how the dynamics of cellular flux in the fly gut both reinforce and respond to organ shape.

How do cells in our nervous system develop highly specialized functions after birth, and how do they degenerate as we age? An emerging molecular mechanism is 3D genome architecture—the folding of 6 billion base pairs of DNA (~2 meters) into a tiny cell nucleus (~10 microns). This folding can strategically position genes and their regulatory elements in 3D to orchestrate dynamic gene expression, and has been implicated in many developmental and degenerative diseases (e.g., autism, schizophrenia, Alzheimer’s). However, traditional technologies and algorithms struggle to capture the full complexity of genome architecture of a single cell, and the enormous heterogeneity between cells. In addition, most studies interrogate genome architecture in vitro, taking cells out of their physiological context. The Tan Laboratory of 3D Genomics at Stanford Neurobiology studies the single-cell 3D genome architectural basis of neurodevelopment and aging by developing the next generation of in vivo multi-omic assays and algorithms, and applying them to the human and mouse cerebellum and beyond (e.g., cancer, immunology).

The human brain contains about 100 billion neurons, each making thousands of synaptic connections. While individual neurons can themselves perform sophisticated information processing, it is the assembly of neurons into circuits via specific patterns of synaptic connections that endows our brain with the computational capacity to sense, act, think, and remember.

How are neurons organized into specialized circuits to perform specific functions? How are these circuits assembled during development? We are investigating these questions in the brains of the fruit fly (~100 thousand neurons) and mouse (~100 million neurons). We have developed molecular-genetic and viral tools, and are combining them with transcriptomic, proteomic, physiological, and behavioral approaches to study these problems.

We work on technology development for genome engineering, discovery-focused synthetic biology, and epigenetic gene therapy. We aim to develop new technologies for studying the mammalian genome and treating complex diseases.

For technology development, we are interested in novel technologies that reprogram the mammalian genome and epigenome. We developed the first nuclease-dead dCas9 from the natural CRISPR-Cas9 nuclease. We developed a series of CRISPR tools that greatly enriched the CRISPR toolbox and expanded genome engineering beyond editing. These tools include CRISPR interference (CRISPRi) and CRISPR activation (CRISPRa) for targeted gene activation and repression, LiveFISH for live imaging of DNA and RNA, CRISPR-GO for manipulating the 3D genome organization, and miniature Cas (CasMINI) and hyper-efficient Cas12a (hyperCas12a) for in vivo applications. We harness natural molecules for molecular engineering and evolve novel functions. These tools are broadly used by the community for research and and translational applications.

For discovery-focused synthetic biology, we apply synthetic biology to design and engineer molecules and molecular circuits in mammalian cells. We use synthetic systems to study how cells can be rationally designed as an 'engineering' entity and be harnesses for disease treatment. For example, we engineer T cells to detect new antigens to kill cancer cells or stem cells to integrate environment cues to determine cell fate. By engineering at the scale from molecular to cellular to organismal level, we hope to make synthetic biology a better discovery tool.

For epigenetic gene therapy, we combine epigenome engineering, synthetic biology, and disease models to develop novel therapy to treat cancer, neurodegeneration, and complex genetic diseases. We aim to reveal the importance of noncoding elements including enhancers in the regulation of genome and disease. We harness safe and powerful tools to precisely rewrite the epigenome marks to reverse or cure diseases. We developed PAC-MAN as a treatment to influenza and broad variants of SARS-CoV-2. We aim to greatly expand genome and epigenome engineering towards neurodegenerative diseases and complex diseases.

Dr. Cong's group is developing novel technology for genome editing and single-cell genomics, leveraging scalable methods inspired by data science and machine learning and artificial intelligence.

His group has a focus on using these gene-editing tools to study immunological and neurological diseases. His work has led to one of the first FDA-approved clinical trials using CRISPR/Cas9 gene-editing for in vivo gene therapy. More recently, his group invented tools for cleavage-free large gene insertion via mining microbial recombination protein (Wang et al. 2022), and developed single-cell perturbating - tracking approach for studying cancer immunology and neuro-immunology (Hughes et al. 2022). We have also strong interest in using deep learning for predicting and designing gene-editing system and protein function (Hughes et al. 2022 and Yuan et al. 2023). Dr. Cong is a recipient of the NIH/NHGRI Genomic Innovator Award, a Baxter Foundation Faculty Scholar, and has been selected by Clarivate Web of Science as a Highly Cited Researcher.

We study how genetic and environmental factors contribute to biological diversity and adaptation. We are particularly interested in understanding (1) how behavior evolves through changes in brain function and (2) how animal physiology evolves through repurposing existing cellular components.
Our mission is to perform rigorous, ethical, and ecologically relevant science across many areas of organismal biology. We aspire to maintain an environment that fosters creativity, diversity, and inclusion as well as engagement with communities in the areas where we work.
We stand in solidarity with the BlackLivesMatter Movement. Scientists and the institutions we work in are complicit in centuries of racism and we will hold ourselves and our institutions accountable by using lab meetings to reflect on our own privileges and by demanding action from Stanford University. We will continue supporting the careers of our Black colleagues by inviting them to seminars, reading their papers, and promoting their work through collaboration and our social media spaces. We are committed to including classrooms in predominantly Black neighborhoods to our Froggers School Program.

The primary goal of this laboratory is to promote the health and well being of children and adolescents with chronic pain and their families. In line with this goal, research projects focus on biological, neurological, cognitive, affective, and social risk and resiliency factors of the pain experience. Projects include brain imaging, longitudinal clinical cohort, and treatment intervention studies.

The gene encoding the p53 transcription factor is the most commonly mutated gene in human cancer, yet we lack a complete understanding of how its loss promotes cancer and how to target this pathway therapeutically. My lab studies p53 in the context of two very deadly and common cancer, pancreatic cancer and lung cancer, to understand how p53 loss promotes tumor initiation and progression. We are investigating not only how p53 mutation changes tumor cells themselves but also how these changes in tumor cells alter the cells of the tumor microenvironment to promote cancer development. We strive to understand p53 function using varied approaches, including mass spectrometry, CRISPR screening, ATAC-sequencing, spatial transcriptomics and in vivo mouse analyses. Using these combined approaches, we are gaining key new insights into the fundamental functions of p53 in vivo, which will ultimately inform us on how to target this critical pathway therapeutically.

The Steinmetz group develops experimental approaches to read, edit and write entire genomes across scales. By applying these technologies, members of the lab aim at understanding the genetic basis of complex phenotypes, the mechanisms of transcription, and the molecular systems underpinning disease. One of the most daunting obstacles in biomedicine is the complex nature of most phenotypes (including cancer, diabetes, heart disease and several rare diseases) due to epistatic interactions between multiple genetic variants and environmental influences. Our aim is to transform the way we approach biomedical research, eventually by assigning a function to every nucleotide in the human genome. Along the way, we continually innovate and improve novel genomics technologies, enabling us to achieve our goals faster and more efficiently. For example, we will develop novel tools for precision genome editing, increase the scale and complexity of functional genomics screens, learn how to write genomes with unique traits from scratch, and apply long-read sequencing methods to understand disease mechanisms. Ultimately, we are working towards an era in which we can predict phenotypic traits from genetic and environmental information. Achieving this ambitious goal would have far-reaching implications, from facilitating precision medicine for everyone, and to predicting how natural populations will respond to changing environments.