Kouta Lee standing outside in front of roses. Hands are in pockets.Kouta Lee

The purpose of Kouta Lee project is to understand the correlation between diabetes and pancreatitis.  Kouta will  use  the human pancreatic tissue to induce caerulein into the acinar cells and examine the exocrine and beta-cell functions(such as BMP signaling, transcriptional repressors ID1 and ID3, and inflammatory cytokine/chemokine expression). Kouta will also induce cytokines IL-1beta and IFN gamma into the beta cells and examine the exocrine and beta-cell functions (such as the expression of chemokines in the beta cells). Immunohistochemistry will be used to examine BMP signaling effects, transcriptional repressors ID1 and ID3, and replication markers. Learning about the interaction between the exocrine and endocrine tissues will help to understand the association between diabetes, pancreatic cancer, and pancreatitis on a molecular level.

Joel Kopcow wearing lab coat Joel Kopcow

The purpose of Joel Kopcow research is the exploration of novel bioprinting platforms for tissue regeneration and revitalization.  For this project, a number of cell sources, bioinks and delivery platforms will be used to create or revitalize cartilage, bone and meniscal tissues.  A combination of various cell sources, bioinks and bioprinting devices will be explored.  Stem cells will be retrieved from cryopreserved stocks or sourced from live meniscus and knee fat pad tissue via enzymatic digestions and cultured to increase cell numbers for bioprinting.  The results of using these approaches will help to identify the most appropriate cell source, bioink formulation and delivery platform to produce viable cartilage-, bone- andmeniscal-like tissues.

Steven Decker

is studying the role of ataxin-2 in motor neuron degeneration.  Ataxin-2 (ATXN2) is a ubiquitously expressed RNA-binding protein (RBP) conserved across eukaryotic species from yeast to human.  A trinucleotide (CAG) repeat expansion mutations of the poly-glutamine (polyQ) tract of the ATXN2 gene are associated with several neurodegenerative diseases including spinocerebellar ataxia 2 (SCA2) and amyotrophic lateral sclerosis (ALS), a fatal adult-onset disorder characterized by the progressive death of motor neurons of the brain and spinal cord.  For this project, Steven will be involved in efforts to generate and characterize human iPSC lines that have been engineered to contain CAG-expanded ATXN2 mutations. This will involve training in tissue culture and stem cell handling, standard biochemical and molecular biology techniques such as western blot and RT-qPCR, as well as immunofluorescence microscopy to assess molecular and cellular phenotypes caused by the introduction of disease- associated alleles. Steven will also learn various neuronal differentiation protocols, particularly to generate spinal motor neurons from both engineered and patient-derived iPSC lines.  Steven will learn cutting-edge techniques such as designing and performing CRISPR/Cas9 genome editing in stem cells to better understand the roles of polyQ sequences in neuronal function and disease.

William Gaor

As part of a large project to  investigate the risk factor of Alzheimer’s disease, William Gaor will study the mechanism by which the presence of the allele ε4 of the APOE gene affects astrocyte-neuron interactions. He will use  Lentiviruses to force the expression of select transcription factors (TF) which can drive the differentiation of human induced pluripotent stem cells (hiPSC) into neurons and astrocytes.  Several cell lines of Alzheimer’s disease relevant genotypes with lentiviral vectors that carry specific transcription factors and select, by sub-cloning and then genotyping, the ones that have the integrated virus+TF combination. William’s role in this project is to generate human iPSC stable lines that carry the transcription factors that will drive their differentiation into neurons and astrocytes.

Paris Offor

The goal of Paris Offor project is to understand the mechanisms of gut-barrier integrity in inflammatory bowel disease (IBD).  She will use 3D organoids already developed to identify new therapeutic strategies and treatments. Her lab will focus on transitioning into 5D models of mouse models to then further understand how the epithelial cells form using tight barriers between each cell. The ultimate goal will be to transition into using human tissue models to development in better understanding inflammatory bowel disease.

Christopher Smith

Spermatogonial stem cells (SSCs) are essential for long-term spermatogenesis. There is considerable interest in human SSCs (hSSCs), as they have the potential to cure some forms of male infertility.  Christopher Smith is seeking to understand both the cellular and molecular mechanisms driving hSSC self-renewal and development in order spermatogonial stem cells (SSCs) which can lead to the development of “SSC therapy”. 

Jessica Octavio

Jessica Octavio is working on Kleefstra Syndrome (KS) one syndromic form of Autism Spectrum Disorder(ASD) that affects approximately 1 in 55 children with epigenetic dysregulation of neuronal development (Kleefstra,2012). She plans to explore the functional consequences of altered epigenetic landscapes in KS, a genetically defined form of ASD with EHMT1 LOF.  She will develop in vitro models of brain development in KS, will characterize neurodevelopmental phenotypes in cellular models of KS.  In addition she will characterize neurodevelopmental phenotypes in cellular models of KS. 

Davis Klein

As part of a large study to elucidate the evolutionary differences in brain development between humans and non-human primates, Davis Klein will develop 3D brain-like structures called brain organoids from human embryonic and induced pluripotent stem cells (iPSC) and will compare them to organoids generated from four different primate iPSC lines. Davis will be involved in the project through stem cell maintenance, brain organoid generation and maintenance, and immunohistochemical analysis.  He will also participate in MEA and growth rate data collection and analysis, literature searches, and data presentations.

Veronika Mikhaylova research is on FOXG1 syndrome, a rare and debilitating childhood neurological disorder caused by a spontaneous de novo mutation in the FOXG1 gene (which encodes for the transcription factor, forkhead box G1 protein).  The protein  plays a pivotal role in brain development and function. Children with FOXG1 syndrome develop seizures, motor disorders, stereotypies, cognitive impairment, mood and sleep disorders, as well as speech delays. The aim of the research is to characterize FOXG1 from a molecular, cellular, and electrophysiological perspective by developing brain organoids from patient-derived induced pluripotent stem cells (iPSC) based on established protocols. Veronica will attempt to identify potential therapeutic solutions for the FOXG1 syndrome. The testing of the designed therapies on the organoid model would determine the efficacy of the treatment in vitro and its potential for clinical trials.