PRISM Mentors

Heilshorn's interests include biomaterials in regenerative medicine, engineered proteins with novel assembly properties, microfluidics and photolithography of proteins, and synthesis of materials to influence stem cell differentiation. Current projects include tissue engineering for spinal cord and blood vessel regeneration, designing injectable materials for use in stem cell therapies, and the design of biomaterials for culture of patient-derived biopsies and organoids. Postdoctoral candidates with expertise (or an interest in learning) preclinical animal models of injury and disease are particularly encouraged.

Department URL:
https://mse.stanford.edu

The Pop Lab is a research group led by Prof. Eric Pop in Electrical Engineering (EE) and Materials Science & Engineering (MSE) at Stanford University. We are located in the Paul Allen Center for Integrated Systems (CIS), working in the Stanford Nanofabrication Facility (SNF) and the Stanford Nano Shared Facilities (SNSF). We are affiliated with the Stanford SystemX Alliance and the Non-Volatile Memory Technology Research Initiative (NMTRI).

Our research is at the intersection of nanoelectronics and nanoscale energy conversion, exploring topics such as:

• Energy-efficient transistors, data storage (memory), and thermoelectrics
• 2D materials (graphene, h-BN, MoS2, WSe2,...) and phase-change materials (GST, VO2)
• Fundamental physical limits of current and heat flow, e.g. ballistic electrons and phonons
• Applications of nanoscale energy transport, conversion and harvesting

Our work includes nanofabrication, characterization, and multiscale simulations. On-campus collaborations include Materials Science, Physics, Chemical and Mechanical Engineering, and off-campus they range from UIUC, UC Davis, Georgia Tech, UT Dallas, Univ. of Tokyo and Singapore (NUS), to TU Wien, Univ. Bologna and Poli Milano.

To learn more about us, please visit http://poplab.stanford.edu

Prof. Wang directs the Center for Magnetic Nanotechnology and is a leading expert in biosensors, information storage and spintronics. His research and inventions span across a variety of areas including magnetic biochips, in vitro diagnostics, cancer biomarkers, magnetic nanoparticles, magnetic sensors, magnetoresistive random access memory, and magnetic integrated inductors. 

My group is interested in elucidating the mechanics of cell-matrix interactions in soft tissues. We seek to understand how the mechanical properties of the extracellular matrix regulate processes such as breast cancer progression, stem cell differentiation, and cell division. Further, we aim to determine the biophysics of cell migration and division in confining 3D microenvironments. Our approach involves the use of engineered biomaterials for 3D cell culture and instrumentation to measure forces at the microscale relevant to cells.

- Mechanical behavior of nanomaterials and nanostructured metals

- Nano and metal additive manufacturing

- Materials at extreme conditions (e.g. high pressure)

- Materials for sustainability (e.g. hydrogen economy, batteries)

Our research is concerned with the computational modeling and the experimental investigation of fluids in complex environments, including chemical reactions, phase transition, and heterogeneous flow environment. We addressing fundamental scientific questions, problems pertaining to energy-conversion and propulsion, as well as environmental issues related to wildfire predictions, carbon-capture and sequestration, and water desalination. We are developing advanced numerical algorithms, detailed physical models, and physics-informed and data-driven methods. Experimentally, our research employs X-ray absorption and scattering techniques  that involve X-ray Computed Tomography at laboratory and synchrotron sources, X-ray spectroscopy, and ultrafast X-ray techniques at the Linac Coherent Light Source to observe processes at sub-picosecond timescales.

Department URL:
https://me.stanford.edu

We are an interdisciplinary research laboratory that focuses on model-based analysis, design, and control of biological function at the molecular, cellular, and organismal levels to optimize therapeutic intervention.

Near-future research directions

• Design and implementation targeted synthetic microbe therapies
• Interorgan communication in health and disease
• Synthetic pattern formation in growing microbial populations

The Mayalu Lab is seeking bright, talented, and motivated graduate students and postdocs to fill several positions.

These are great opportunities to work on control theoretic and experimental aspects of model-based design of synthetic biological and biomedical systems. 

Postdocs with additional training in synthetic microbiology, genetic recombination technology, bioengineering or related fields are encouraged to apply to help launch the experimental research program.

Two postdoc positions in the lab of Prof. Sindy Tang are immediately available in the areas of microfluidics, nanofabrication, and spatial proteomics.

The spatial organization of proteins within biological tissues plays a critical role in the normal functioning of the tissue and disease development. The goal of this NIH-funded project is to develop a high throughput and scalable technology to perform tissue microdissection that preserves tissue spatial information and couples directly to established LC-MS/MS workflow for deep and unbiased spatial mapping of the proteome. Our approach integrates a novel tissue micro-dicing device, a nanodroplet sample preparation platform for LC-MS/MS analysis with single-cell sensitivity, and novel microfluidic device to transfer the diced tissue pixels while preserving their spatial order. This position will allow exciting opportunities to collaborate with the Pacific Northwest National Lab and the Stanford School of Medicine. 

The project is expected to accelerate MS-based spatial proteomics for deep and unbiased mapping of tissue heterogeneity down to single-cell resolution, thereby accelerating biomedical research and clinical diagnostics towards a better understanding of the role of tissue heterogeneity in pathophysiology, such as the role of the tumor microenvironment on cancer initiation and progression. The deep and unbiased proteome coverage will enable the discovery of novel protein biomarkers and molecular pathways to identify new therapeutic targets, which would be difficult using antibody-based approaches. Our ability to quantitatively map ECM and secreted proteins will facilitate the elucidation of the role of ECM, such as their remodeling, in disease progression. Finally, while this project focuses on spatial proteomics, we expect our technology and workflow to be extended to other biomolecules that LC-MS/MS can readily measure, such as lipids and metabolites, thereby opening the opportunity for spatial multi-omic measurements in future studies.

Skills useful for this project include:
• Microfluidics design and integration, and related areas
• Micro- and nanofabrication, e.g., silicon micromachining, high resolution 3D printing
(e.g., Nanoscribe)
• Experience working with biological samples (tissues)

Our lab is interested in the host pathways that determine the susceptibility of humans to viral disease. Viruses constantly evolve to exploit host machineries for their benefit whilst disarming host restriction mechanisms. Discovery of host proteins critical for viral infection illuminates basic aspects of cellular biology, reveals intricate virus host relationships, and leads to potential targets for antiviral therapeutics.

Malaria is one of the leading causes of childhood morbidity and mortality in the world. The etiologic agent of severe malaria, Plasmodium falciparum, exclusively infects red blood cells during the blood stage of its life cycle, when all of the symptoms of malaria occur. P. falciparum is an obligate intracellular parasite, suggesting that it critically depends on host factors for its biology and pathogenesis. This concept is also supported by population genetic studies, which indicate that humans have evolved certain red cell traits, such as hemoglobinopathies, to protect against malaria. The importance of these host-pathogen interactions raises the possibility that critical red cell factors could serve as targets for new, host-directed therapeutics for malaria. However, our understanding of host determinants for malaria is limited because red cells are enucleated and lack DNA, hindering genetic manipulation. In the Egan laboratory we have surmounted this hurdle by adapting advances from stem cell biology to the study of malaria host factors. Specifically, we have developed approaches to differentiate primary human CD34+ hematopoietic stem/progenitor cells down the erythroid lineage to enucleated red blood cells that can be infected by P. falciparum. This thus gives us access to the nucleated progenitor cells for genetic modification using RNAi and CRISPR-Cas9 genome editing. We are using these methods to develop forward genetic screens to identify novel host factors for malaria, as well as to perform mechanistic studies to understand the specific functions of critical host factors during the developmental cycle of malaria parasites. In addition, the lab has projects focused on understanding human adaptation to malaria using clinical samples. Our long term goal is to explore the possibility of host-directed therapeutics for malaria.

The Idoyaga Lab is focused on the function and biology of very unique cells of the immune system, Dendritic cells (DCs). DCs are specialized antigen-presenting cells that initiate and modulate our body’s immune responses to invading microbes. DCs also play a crucial role in maintaining immune unresponsiveness to our own tissues and environmental and/or innocuous substances. Considering their importance in orchestrating the quality and quantity of immune responses, DCs are an indisputable target for vaccines and therapies.

A major aim of our lab is to define metrics of immune competence in various settings, including cancer immunotherapy, organ transplantation, allergy, and chronic viral infection.  We use CyTOF mass cytometry, often in combination with other technologies, to broadly survey immune features at the cellular level, then examine links between features or groups of features and clinical outcome.  A long-term goal is to create an assay of global immune competence that could predict risk for various immune-related outcomes in both healthy individuals and in disease.

Most of our recent scientific efforts are centered on the role of liver-specific microRNA miR-122 in the hepatitis C virus (HCV) life cycle. Specifically, we discovered that the HCV RNA genome binds two molecules of miR-122 at its 5’ end. This oligomeric complex forms in all HCV genotypes and its main role is to protect the viral RNA from degradation by riboexonucleases. Excitingly, sequestration of miR-122 by modified antisense oligonucleotides results in loss of HCV RNA abundance in cultured cells and infected chimpanzees. Encouraged by these results, Santaris Inc. and Regulus Inc. have performed phase I, and phase II clinical trial in HCV-infected patients. It was found that virus load diminished by several logs in all treated patients. In addition, HCV RNA was non-detectable in a few patients. Thus, treatment of patients with anti-miR-122 oligonucleotides is being explored as an additional option to combat HCV. In addition, we have made the surprising discovery that the HCV genome is fragmented to yield small circular RNAs in infected cells. We are investigating the functional consequences of this finding by hypothesizing that the circular RNAs modulate viral gene expression and innate immune responses in infected and in uninfected bystander cells.

The goals of the Sonnenburg Lab research program are to (i) elucidate the basic mechanisms that underlie dynamics within the gut microbiota and (ii) devise and implement strategies to prevent and treat disease in humans via the gut microbiota. We investigate the principles that govern gut microbial community function and interaction with the host using experimental systems ranging from gnotobiotic mice to humans. We pursue molecular mechanisms of host-microbial interaction using an array of technologies including gnotobiotic and conventional mouse models, quantitative imaging, molecular genetics and synthetic biology, and a metabolomics pipeline focused on defining microbiota-dependent metabolites. The synergy of these diverse techniques provides insight into the dynamics of a microbial ecosystem in response to cues ranging from nutrition to pathogen-induced inflammation. Studies of microbiomes diverse human cohorts, ranging from indigenous populations in Africa, Asia, and South America to dietary intervention trials in cohorts of US residents, have provided great insight into microbiome dynamics and fuel a pipeline of reverse translational studies.

The Yeh Lab studies the apicoplast, a unique plastid organelle in Plasmodium falciparum parasites that cause malaria. We are particularly focused on unbiased chemical and genetic screens to discover new cell biology and therapeutic targets for this important global health disease. Our work highlights the untapped opportunities in exploring divergent biology in non-model organisms, a theme we plan to expand in the lab by studying ocean algae (malaria's cousins!) and their role in the global ecosystem.

The @wormsenseLab at Stanford University seeks postdoctoral scholars with an interest in the genetics, biophysics, and cell biology of sensation. Experience with in vivo and in vitro live imaging as well as gene-editing techniques in a genetic model organism such as C. elegans is preferred, but not essential. In appointing postdocs, we look for curiosity, excellence in the practice of reproducible research, and the ability to lead and work in teams — learning from and teaching others. You may launch research into the molecular and physical events responsible for touch and its degradation by persistent mechanical stress and chemotherapeutics. The latter project involves a collaboration with Katie Wilkinson (Prof. Biology, SJSU), an expert in rodent proprioception. You may also propose to join NeuroPlant, an interdisciplinary, team-based discovery platform for discovering novel ligand-receptor pairs that modulate nervous system function and for deciphering the neural codes responsible for chemical attraction and repulsion. As a NeuroPlant postdoc, you will be encouraged to select a co-advisor from the project faculty team. The @wormsenseLab believes that interdisciplinary scientists are needed in diverse careers and have helped to launch former postdocs into tenure-track academic positions, research and business development in industry, start-ups, and venture capital firms.

The @wormsenseLab at Stanford University seeks postdoctoral scholars with an interest in the genetics, biophysics, and cell biology of sensation.  In appointing postdocs, we look for curiosity, excellence in the practice of reproducible research, and the ability to lead and work in teams — learning from and teaching others. You may launch research into the molecular and physical events responsible for touch and its degradation by persistent mechanical stress and chemotherapeutics.  You may also propose to join NeuroPlant, an interdisciplinary, team-based discovery platform for discovering novel ligand-receptor pairs that modulate nervous system function and for deciphering the neural codes responsible for chemical attraction and repulsion. As a NeuroPlant postdoc, you will be encouraged to select a co-advisor from the project faculty team. The @wormsenseLab believes that interdisciplinary scientists are needed in diverse careers and have helped to launch former postdocs into tenure-track academic positions, research and business development in industry, start-ups, and venture capital firms. You can learn more about our researchers from this 2019 Life in a Lab profile.

Our research lab focuses on studying the molecular mechanisms of ion channels and transporters. We use a combination of biophysical methods to probe membrane protein structure and dynamics, together with functional assays and electrophysiological analysis. Ongoing projects in our lab include:
• Examining the molecular mechanisms of chloride/proton transporters
• Developing new small-molecule probes to studying mammalian chloride channels
• Exploring the biophysics and physiology of the mammalian chloride channels
• Using electrophysiology techniques to study the molecular effects of ultrasound neuromodulation on ion channels in brain tissue

Department URL:

https://med.stanford.edu/mcp.html

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.

Our laboratory studies the mechanisms by which highly complex behaviors are mediated at the neuronal level, mainly focusing on the example of dynamic social interactions and the neural circuits that drive them. From dyadic interactions to group dynamics and collective decision making, the lab seeks a mechanistic understanding for the fundamental building blocks of societies, such as cooperation, empathy, fairness and reciprocity. The computations underlying social interactions are highly distributed across many brain areas. Our lab is interested in which specific areas are involved in a particular function, why such an architecture arises and how activity in multiple networks is coordinated. Our goal is to develop a roadmap of the social brain and use it for guiding restorative treatments for conditions in which social behavior is impaired, such as Autism Spectrum Disorders and Schizophrenia.

The goal of our research is to understand the algorithms the brain uses to learn. A fundamental feature of our neural circuits is their plasticity, or ability to change. How does the brain use this plasticity to tune its own performance? What are the learning rules that determine whether a neural circuit changes in response to a given experience, and which specific neurons or synapses are altered?  Our research integrates molecular, cellular, systems and computational neuroscience approaches in mice to uncover the logic of how the cerebellum implements learning.

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).

My work focuses on neuroimmunology and how the central and peripheral immune system responds to brain injury, and in particular, stroke. We study how microglia and astrocytes respond with an emphasis on both the basic biology and clinically-relevant outcomes. We are also interested in how stroke can provoke long-lasting adaptive immune responses that lead to post-stroke dementia, a serious and currently untreatable consequence of stroke. The basic science lab performs primarily studies in mice and on human samples, while the Stanford Stroke Recovery Program (https://med.stanford.edu/neurology/divisions/stroke/recovery.html) enrolls stroke survivors and collects clinical data and human samples to ask whether findings in mice are applicable to humans. My lab values diversity of all types and there are projects available for postdoctoral scholars either in mouse or human studies.

Epilepsy affects ~1% of all children and is defined by recurrent, unprovoked seizures, impaired cognitive abilities, and diminished quality of life. The predisposition for seizures is thought to result from abnormal plasticity and excessive synchrony in affected neural networks. Myelin plasticity is a newly recognized mode of activity-dependent neural network adaptation. The potential for dysregulated myelin plasticity in disease states such as epilepsy is unexplored. Myelination of axons increases conduction velocity and promotes coordinated network function including oscillatory synchrony. During and after age-dependent developmental myelination, increases in myelin occur when humans and rodents acquire new skills. While adaptive myelin plasticity modulates networks to support function in the healthy state, it is unknown whether this process also contributes to network dysfunction in neurological disease.

The Knowles lab conducts basic, translational and clinical research to study how seizures shape white matter, and how changes in white matter shape the course of epilepsy and its comorbidities. We discovered that generalized (absence) seizures induce aberrant myelination that promotes seizure progression. Thus, maladaptive myelination may be a novel pathogenic mechanism in epilepsy and other neurological diseases.  Using innovative imaging, electrophysiological, histological and molecular biology techniques, we are studying multiple questions.

How does white matter structure change throughout the brain over the course of epilepsy?
How does white matter structure impact network synchronization, seizures and cognition?
What signaling pathways underlie aberrant white matter plasticity in different forms of epilepsy?
What can we learn from white matter changes found with various imaging modalities in humans with epilepsy?