PRISM Mentors

We are studying the molecular mechanisms of neurodegeneration and axon regeneration after CNS injury and neurological diseases, using retinal ganglion cell (RGC) and optic nerve in various optic neuropathies mouse models. Regenerative and neuroprotective therapies have long been sought for CNS neurodegenerative diseases but none have been found. That there is no curative neuroprotective or restorative therapy for neurodegeneration is a central challenge for human health. My lab focuses on the mechanisms responsible for neuronal degeneration and axon regeneration after injury or diseases with the goal of building on this understanding to develop effective combined strategies to promote neuroprotection and functional recovery.

Mission:
Our mission is to understand the role of mechanosensation in the eye and how it relates to glaucoma.

Approach:
Our goal is to discover new strategies for treating glaucoma by understanding the mechanisms of mechanosensation in the eye. By combining human genetic analyses, in vitro molecular and electrophysiological approaches, and in vivo mouse models of glaucoma, we are currently studying the role of mechanosensitive ion channels in glaucoma.

Questions:
· What are the ion channels that mediate pressure sensing in the eye?
· What physiological roles do these channels play in the eye?
· Do these ion channels mediate the development of glaucoma and other ocular pathologies?

Techniques:
· in vitro electrophysiological recording  of ion channel activity
· in vitro optical imaging of ion channel activity
· in vitro mechanical stimulation of individual cells
· genetic manipulation of specific cell types
· mouse models of glaucoma

Our translational research laboratory endeavors to bring breakthroughs in stem cell biology and tissue engineering to clinical ophthalmology and reconstructive surgery. Over 6 million people worldwide are afflicted with corneal blindness, usually caused by chemical and thermal burns, ocular cicatricial pemphigoid, Stevens-Johnson syndrome, microbial infections, or chronic inflammation. These injuries often result in corneal vascularization, conjunctivalization, scarring, and opacification from limbal epithelial stem cell (LSC) deficiency (LSCD), for which there is currently no durable treatment.

The most promising cure for bilateral LSCD is finding an autologous source of limbal epithelial cells for transplantation. Utilizing recent advances in the field of induced pluripotent stem cells (iPSC), our research aims to create a reliable and renewable source of limbal epithelial cells for potential use in treating human eye diseases. These cells will be grown on resorbable biomatrices to generate stable transplantable corneal tissue. These studies will serve as the basis for human clinical trials and make regenerative medicine a reality for those with sight-threatening disease. On a broader level, this experimental approach could serve as a paradigm for the creation of other transplantable tissue for use throughout the body. Stem cell biology has the potential to influence every field of medicine and will revolutionize the way we perform surgery.

Biomaterials, medical devices, drug delivery, stem cells and 3D bioprinting for musculoskeletal tissue engineering

I am a surgeon-scientist with a clinical interest in caring for patients with hearing loss and deafness, and research interests in inner ear development and regeneration. For almost 20 years, I have been studying hair cell biology. Since 2007, my research has focused on defining the role of Wnt signaling in regulating hair cell progenitors in the developing and damaged inner ear using a combination of genetic, molecular biological, pharmacological, and imaging techniques. In particular, our work has led to the discovery of Wnt-responsive hair cell progenitors in the neonatal mouse cochlea and utricle, and more recently, functional recovery during vestibular regeneration.

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

We are interested in fundamental aspects of cell-cell recognition, migration and development with the mammalian immune and vascular systems as  models. We use molecular, genetic and single cell transcriptomic and mass cytometric approaches to study  the development and trafficking of  lymphocytes, NK cells and dendritic cells and their role in immune function in health and diseases. 
 
The vascular endothelium controls immune cell recruitment from the blood,  and thus determines the nature and magnitude of immune and inflammatory responses.     In a major new effort, we are applying single cell approaches (scRNAseq and mass cytometry), and novel computational approaches to probe endothelial cell specialization and responses in models of immune and tumor angiogenesis and inflammation.  
 
Although our focus is on fundamental problems in biology, the work is intrinsically translational and the laboratory is interested in applying its  discoveries to models of infection and immune pathology: examples include genetic studies of GPCR's and assessment of novel therapeutics in models of inflammatory bowel disease, psoriasis, cancer, aging and infection.
 
We are actively recruiting fellows with experience in biocomputation and coding who can take advantage of the datasets we are generating;   or experience in vascular biology, immunology,  imaging and cytometry.

One of the key ways that the gut microbiome impacts human health is through the production of bioactive metabolites. By understanding how microbes produce these molecules, we aim to develop new approaches to promote human health and treat disease. Our laboratory employs bacterial genetics, metabolomics, and gnotobiotic mouse colonization to uncover the chemistry that underlies host-microbe interactions in the gut.

Our lab is broadly interested in how intestinal microbes shape our immune system to promote both health and disease. Recently we discovered that a type of intestinal epithelial cell, called tuft cells, act as sentinels stationed along the lining of the gut. Tuft cells respond to microbes, including parasites, to initiate type 2 immunity, remodel the epithelium, and alter gut physiology. Surprisingly, these changes to the intestine rely on the same chemosensory pathway found in oral taste cells. Currently, we aim to 1) elucidate the role of specific tuft cell receptors in microbial detection. 2) To understand how protozoa and bacteria within the microbiota impact host immunity. 3) Discover how tuft cells modulate surrounding cells and tissue.

Our laboratory uses chemical and genetic approaches to study the signaling pathways that control mammalian energy homeostasis. We focus on blood-borne metabolic hormones and other hormone-like molecules. Ultimately, we seek to translate our discoveries into therapeutic opportunities that matter for obesity and other age-associated metabolic diseases.

Research in the Pollack lab centers on translational genomics, with a current focus on diseases of the prostate. The lab employs next-generation sequencing, single-cell genomics, genome editing, and cell/tissue-based modeling to uncover disease mechanisms, biomarkers and therapeutic targets. Current areas of emphasis include: (1) Defining molecular features of prostate cancer that distinguish indolent from aggressive disease; (2) Determining disease mechanisms and new therapeutic targets in benign prostatic hyperplasia (BPH); and (3) Defining disease drivers in rare neoplasms (e.g., ameloblastoma).

The Svensson Laboratory is dedicated to the discovery of new fundamental pathways that regulates cellular and organismal metabolism. The main focus is to identify novel functions for new molecules controlling the regulation of glucose and lipid homeostasis using a combination of genomic, proteomic and physiology approaches.

Chromatin regulators are highly altered in diseases. Of interest, these proteins are easily targetable by drugs. Furthermore, the plasticity of epigenetic events makes them a powerful target for new therapeutic strategies and reversion of disease phenotype. Histone and DNA modifications influence many processes including transcription, replication, genomic stability and cell division, which are altered in diseases. Therefore, understanding the molecular basis of chromatin modifiers in both normal and pathological cells could help us frame new potential biomarkers and targeted therapies. My long-term interest lies in understanding the impact chromatin modifiers have on disease development and progression so that more optimal therapeutic opportunities can be achieved. My laboratory explores the direct molecular impact of chromatin-modifying enzymes during cell cycle progression, and characterizes the unappreciated and unconventional roles that these chromatin factors have on cytoplasmic function such as protein synthesis. By gaining molecular understanding into the mechanism of action of chromatin modifiers in normal and pathological cells, we will improve our basic knowledge and provide needed insights into new potential targeted therapies in diseases.

Department URL:
https://www.google.com/search?client=safari&rls=en&q=stanford+department+of+pathology&ie=UTF-8&oe=UTF-8

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.

Our lab has several major focuses:
1. Using iPSC-derived cardiomyocytes to develop a better understanding of hypertrophic cardiomyopathy and congenital heart disease.
2. The role of alterations in mitochondrial structure and function in normal physiology (such as exercise) and in disease such as dilated and hypertrophic cardiomyopathy.
3. Single cell analysis of mitochondrial function reveals significant heterogeneity.
4. Differences between right and left ventricular responses to stress and in their modes of failure, including gene expression and miR regulation.
5. Use of iPSC-CMs in pharmacogenomics, specifically determining the role of gene variants in doxorubicin cardiotoxicity.

Specific projects underway in our lab include:

1. Alterations of mitochondrial structure and function, including processes of mitofusion, mitofission, autophagy and mitophagy, in normal physiology and disease.

2. Development of high-throughput single cell imaging technologies to measure single cell mitochondrial function, and to measure single mitochondrial function to determine the role of heterogeneity in cell life-death decision-making.

3. Differences between the right and left ventricles in their responses to stresses such as increased afterload and increased preload, including gene expression and gene regulation by micro-RNAs. The use of plasma miRs as biomakers for RV failure.

4. Using patient-derived iPSC-cardiomyocytes to understand the mechanisms of cardiomyopathies common in children and to solve the genotype-phenotype conundrum in hypertrophic cardiomyopathy. The role of altered metabolism and mitochondrial function in hypertrophic cardiomyopathy.

5. Development of micro-engineered platforms for assessment of biomechanics of single iPSC-derived cardiomyocytes.

6. Developing tools to further mature hiPSC-CMs to more accurately recapitulate the mechanobiology of adult human CMS.

We also are interested in clinical heart failure and cardiac transplantation in children, specifically:

1. Understanding alterations in immune system function in patients with after implantation of a left ventricular assist device, Immune system biomarkers that predict adverse outcomes after pediatric VAD implantation.

2. Development of biomarkers for the detection and monitoring of post-transplant lymphoproliferative disorder in pediatric transplant patients.

Our team is committed to finding ways to improve maternal and infant health outcomes and equity by leading research that identifies effective leverage points for change, from upstream 'macro' social and structural factors, to downstream 'micro' clinical factors through a collaborative research approach that integrates epidemiologic approaches with community engagement and systems thinking.

Disparities are prominent in maternal and infant health, so a lot of our work is centered on equity.  Focusing on highest-risk groups will improve health for everyone.

Much of our current research focuses on severe maternal morbidity (SMM). SMM encompasses adverse conditions that put pregnant people at risk of short and long-term consequences related to labor and delivery, including death.

We also study other important perinatal outcomes, including stillbirth, preterm birth, structural congenital malformations and other maternal morbidities.  We are interested in these outcomes individually, as well as in how they are connected to each other -- from a mechanistic standpoint (ie, do they share the same causes), and a lifecourse perspective (eg, how does an adverse newborn outcome affect the mom's postpartum health, and vice versa).

Dr. Carmichael's training is in perinatal and nutritional epidemiology.  She deeply appreciates her multi-disciplinary colleagues who make this work more meaningful by bringing their own varied perspectives and lived experiences, and their expertise in clinical care, qualitative and mixed methods, community engagement, and state-of-the-art epidemiologic approaches and biostatistical methods.

The lab's current research is aimed primarily at understanding how hematopoietic stem cells interact with their microenvironment in order to subsequently modulate these interactions to ultimately improve bone marrow transplantation and unlock biological secrets that further enable regenerative medicine broadly. We are primarily focused on studying the cell surface receptors on hematopoietic stem/progenitor cells and bone marrow stromal cells, and are actively learning how manipulating these can alter cell state and cell fate.  We have also pioneered several antibody-based conditioning methods that are at various stages of clinical development to enable safer stem cell transplantation.

There are many exciting opportunities that stem from this work across a variety of disease states ranging from rare genetic diseases, autoimmune diseases, solid organ transplantation, microbiome and cancer. While we are primarily focused on blood and immune diseases, the expanded potential of this work is much broader and can be applied to other organ systems as well and we are very eager to develop collaborations across disease areas. The Czechowicz lab hopes to further add in the field of translation research.

Goals
We aim to increase our understanding of the basic science principles that govern these cells and then exploit these findings to develop improved therapies for patients
We are particularly focused on pediatric non-malignant bone marrow transplantation with a strong interest in genetic blood/immune diseases and bone marrow failure, but do complementry work on solid tumors with marrow disease, solid organ tolerance induction, autoimmune diseases and gene therapy/gene editing.

My research focuses on the neurobiological basis of language, reading, and cognition in children.  Functional imaging studies demonstrate that language and reading skills require the integrated activity of a network of distributed brain regions.  Diffusion magnetic resonance imaging (dMRI) documents that variations in the properties of long-range white matter pathways connecting these brain regions within the cerebrum and between the cerebrum and cerebellum are associated with variations in language and reading skills.  These white matter pathways may be disturbed in childhood illnesses, such as brain tumors. We have been collecting dMRI scans on children born preterm and full term at different ages, including infancy.  We also have been collecting clinical scans on children with brain tumors in the cerebellum and posterior fossa. We seek students who want to learn techniques for analyzing dMRI and related imaging methods in children and to link the neurobiological findings to clinical outcomes.  Selected studies include: (1) analyzing white matter pathways in preterm infants at near term age in relation to medical and environmental variables; (2) applying spherical deconvolution to scans of children age 6 to 8 years who are learning to read; (3) evaluating longitudinal change in children with mutism after resection of a posterior fossa brain tumor.

We aim to understand the genetic basis of diabetes and related metabolic conditions and to use this to leverage a better understanding of what causes diabetes and how we can improve treatment options for patients. Our work is predominantly focused on understanding what causes pancreatic islets to release insufficient insulin to control blood glucose levels after a meal in patients with type 2 diabetes, but often extends to efforts to relate this to metabolic dysfunction in other relevant tissues such as fat and liver.

We are an inter-disciplinary team of basic and clinical scientists with shared interests in using molecular genetics as a tool to uncover novel biology. We use a variety of different approaches to address important challenges in the field, which range from studies that work genome wide to those which are focused on specific genes and even precise nucleotide changes to understand their impact on pancreatic islet biology.

We have developed a series of pipelines that use primary human islets and authentic beta-cell models which allow us to generate and then integrate complex genomic, transcriptomic and cellular datasets. We use state-of-the art genome engineering approaches combined with induced pluripotent stem-cells to study the impact of T2D-associated genetic variants on islet cell development and function. We are also funded to investigate the impact of T2D risk variants on pancreatic beta-cell function in vivo.

We are a highly collaborative team and work with multiple national and international consortia involved in efforts to understand the genetic basis of type 2 diabetes (eg DIAGRAM, NIDDK Funded Accelerated Medicines Partnership) and related glycaemic traits (MAGIC). We are also part of several Innovative Medicines Initiatives (IMIs) efforts including STEMBANCC and RHAPSODY and Horizon 2020 initiatives (eg T2DSYSTEMS), which are working to develop tools and frameworks to capitalize on genetic and genomic data.

We are also part of the NIDDK funded Human Islet Research Network (HIRN) where we play a role in two of their initiatives. The Human Pancreas Atlas Program- T2 (HPAP-T2D) and the Integrated Islet Phenotype Program (IIPP). Our role is to support the genetic and genomic characterization of islets which are distributed for research and to support the genomic characterization of the pancreas’ phenotyped within the HPAP-T2D program.

Our work extends to playing a role in the interpretation of genetic variants identified in genes with known roles in monogenic forms of diabetes. We are part of the Clin Gen Expert Review Panel for Monogenic Diabetes where are expertise contributes to interpretation of coding alleles in glucokinase (GCK) and Hepatocyte Nuclear Factor 1 alpha (HNF1A). We are a number of on-going projects which are supporting efforts to better understand how to use exome-sequencing data in a diagnostic setting.

The Kay lab is interested in Gene Transfer, Genome Editing and Non-coding RNA biology.  The current research is studying: 1) rAAV vectors specifically:   developing capsid libraries, chemical modification of  vectors and screening approaches that will provide improved vectors for human application;  molecular mechanism of discordance in vector transduction between species;  molecular mechanisms involved in AAV transduction;  and chromatin formation of gene transfer vector genomes in primary tissues. 2) Approaches to achieve therapeutic levels of  non-nuclease mediated genome editing using rAAV vectors.  3)  Non coding RNAs: association between long-non coding RNAs and miRNA biogenesis in whole tissues;  tRNA derived small RNAs and their role in regulating ribosome biogenesis in cancer; and role of Line1 structural RNAs in controlling gene expression.

We are seeking an individual for a postdoctoral fellowship in perinatal / neonatal health who has training and experience in epidemiology or a related field (e.g. PhD or MD with relevant research training). The primary mentor is Dr. Henry C. Lee, Associate Professor of Pediatrics (Neonatology), and Chief Medical Officer of the California Perinatal Quality Care Collaborative (CPQCC) . The CPQCC and its sister organization, the California Maternal Quality Care Collaborative (CMQCC) have their data centers and leadership based at the division of neonatology at Stanford, and have active research programs in perinatal health. The ability to link maternal, neonatal, and long-term follow-up data allow for opportunities to conduct large population-based epidemiologic studies, health services research, and work in reducing disparities. The emphasis of this fellowship will be on the population of extremely preterm birth, including prediction / modeling of outcomes for periviable infants, and development of tools for counseling families affected by extremely preterm birth. The postdoctoral fellow will collaborate with epidemiologists, biostatisticians, and clinician-scientists, with opportunities for mentorship and collaborative research on related topics.

The laboratory of Dr. Marlene Rabinovitch, Professor of Pediatrics (Cardiology) is seeking a highly-motivated and accomplished postdoctoral scholar to join their team of investigators  in conjunction with the Basic Science and Engineering (BASE) Initiative  of the Children’s Heart Center at Stanford University.

A successful applicant will be immersed in cutting-edge molecular, sequencing, imaging and high throughput ‘omics’  technologies applied to human vascular and immune cells  and in their application  to mouse and rat models of  human vascular disease with a focus on pulmonary arterial hypertension.  Our research interests relate to the impact of metabolic reprogramming on gene regulation and RNA translation, the impact of changes in shear stress and DNA damage on the epigenome, bioengineering blood vessels, immune and vascular cell interactions .  We incorporate transgenic models of disease, iPSC generated vascular and immune cells, gene editing, high-throughput drug testing, single cell RNA Sequencing and high dimensional single cell mapping of tissues.  Please consult our website for more details.

All our projects offer opportunities for co-mentoring in Basic, Engineering and Cardiovascular Science.

My research focuses on studying normal and aberrant blood cell development. We are interested in understanding the pathogenesis of acute leukemia and bone marrow failure syndromes. We also work with medicinal chemists and computational biologists to develop novel therapies to treat these diseases.

Mission: Our mission is to both use neuroscience as a tool for improving education, and use education as a tool for furthering our understanding of the brain. On the one hand, advances in non-invasive, quantitative brain imaging technologies are opening a new window into the mechanisms that underlie learning. For children with learning disabilities such as dyslexia, we hope to develop personalized intervention programs that are tailored to a child’s unique pattern of brain maturation. On the other hand, interventions provide a powerful tool for understanding how environmental factors shape brain development. Combining neuroimaging with educational interventions we hope to further our understanding of plasticity in the human brain.
The Lab: The Brain Development & Education Lab is located in the Graduate School of Education at Stanford University and represents a collaboration between the Division of Developmental and Behavioral Pediatrics within the School of Medicine, the Graduate School of Education and the Wu Tsai Neuroscience Institute (we recently moved from The University of Washington’s Institute for Learning & Brain Sciences). The focus of the lab is understanding the interplay between brain maturation and cognitive development.  The lab is interdisciplinary, drawing on the fields of neuroscience, psychology, education, pediatrics and engineering to answer basic scientific and applied questions.  Current projects focus on understanding how the brain’s reading circuitry develops in response to education and how targeted behavioral interventions prompt changes in the brain’s of children with dyslexia. A major component of this work is the development of software to measure properties of human brain tissue, localize differences and quantify changes over development.

Together with Tom Shutt, Dan works on the LUX and LZ dark matter experiments to search for dark matter in the form of Weakly Interacting Massive Particles, or WIMPs. The detectors use liquid xenon as a target medium in a time projection chamber, or TPC. The Large Underground Xenon (LUX) experiment is currently operating a 250-kg target in the former Homestake gold mine in the Black Hills of South Dakota. Preparations are underway at SLAC to design and build the 7-ton successor, known as LUX-ZEPLIN (LZ). The group is involved in many aspects of data analysis, detector design, xenon purification, control andreadout systems, and detector performance studies.