This is a summary list of all laboratories at eagle-i Network Shared Resource Repository . The list includes links to more detailed information, which may also be found using the eagle-i search app.
The main focus of the Becker lab has been on the mechanisms and consequences of post-ischemic myocardial inflammation.
We have found that the acute inflammation accompanying myocardial infarction begins shortly after reperfusion and enlarges the area of irreversible injury. Limiting inflammation by various means, such as with antibodies or drugs, can reduce infarct size and improve left ventricular function. Inflammation begins with conversion of endothelial cells in the ischemic myocardium to a pro-inflammatory phenotype, with increased expression of leukocyte adhesion proteins, such as intercellular adhesion molecule-1 (ICAM-1), and microvascular trapping of neutrophils with accumulation in the myocardium.
ICAM-1 gene upregulation in the post-ischemic myocardium is mediated by tumor necrosis factor alpha (TNFalpha) through the NFkB pathway, but also by activation (phosphorylation) of the transcription factor Stat3, bound to the transcriptional activator Sp1. Stat3 is phosphorylated in turn by interaction with Rac1, an essential subunit of the endothelial NADPH oxidase, through a novel multiprotein complex involving Stat3, Rac1, and protein kinase C (PKC).
Left ventricular hypertrophy (LVH) is one of the most potent risk factors for cardiovascular disease (CVD), including ischemic heart disease, chronic heart failure and CVD death. Common risk factors include hypertension and diabetes while a significant portion of the risk is also determined by genes. On a cellular level, studying cardiomyocytes (CMs) has yielded important insights into disease mechanism. There is now growing evidence suggesting that changes in the composition of the cardiac matrix particularly in diabetes contributes to the disease process in CMs. We propose to examine the role and impact of a 'diabetic' cardiac matrix, its interaction with cardiomyocytes and the role of genetic factors by using human induced pluripotent stem cell derived cardiomyocytes (hiPSC-CMs) as a `patient in a dish' model. Our proposal builds on extensive data which is available as part of the NHLBI HyperGen-LVH study. This includes GWAS and Whole Exome Sequence data. In addition, we have already developed hiPSC-CMs lines from 250 HyperGen participants. In Aim 1, we propose to culture hiPSC-CMs from these individuals on a matrix obtained from decellularized hearts of the db/db mouse to investigate cellular and molecular changes. In Aim 2 we perform expression analysis to determine global expression changes associated with the diabetic matrix followed by a pathway analysis to determine functional networks. Finally, in Aim 3, we perform eQTL analysis to determine single nucleotide polymorphisms (SNPs) associated with the response. Utilizing WES data, we will also perform a combined sequence and expression analysis to identify potential rare variants. Our proposal utilizes existing resources, including genetic and phenotypic data in addition to previously established hiPSC-CMs. Our experiments will provide novel insights into the molecular mechanisms underlying the cardiomyocyte-cardiac matrix interaction, its pathways and genetic factors modulating the response. A better understanding of the role of these interactions and networks can build the basis to develop novel treatment options as well as markers for the identification of individuals at increased risk. This becomes particularly important with an aging population and the increase in prevalence of diabetes.
We are interdisciplinary researchers with diverse backgrounds based in the Department of Computer Science at the University of Victoria. Our offices are located in the Engineering/Computer Science building.
Our research interests include:
- cognitive support and technology diffusion
- human computer interaction
- human and social implications of technology use
- interface design
- knowledge engineering
- software engineering
- technology and pedagogy
Our primary objective is to develop tools that support people in performing complex cognitive tasks. Our projects benefit from the collaborative approach taken within our group and with other researchers. As a group, we operate by thinking creatively, exploiting our synergies, and applying innovative research techniques.
Located in the Leichtag Biomedical Research Building on UCSD’s main campus, the Frazer Laboratory’s research focuses on the genetics and functional genomics of cardiovascular diseases and cancer. Our research mission is to identify common and rare genetic variants that are associated with human disease in order to functionally assess their role in disease pathogenesis, progression, and prognosis. With our discoveries we hope to accelerate the translation of genomic research into clinical therapies and applications.
In 1982, The Johns Hopkins Sibling and Family Heart Study was created to study patterns of coronary heart disease in high risk families. In 2015, the GeneSTAR Center extends its research to better understanding risk factors, genomics, biological models, and cellular science to better understand the causes of heart disease and stroke.
The primary goals in the Goldstein lab are to unravel how molecular motors interact with, and control the behavior of, axonal vesicles, and to relate this understanding to the molecular basis of neuronal defects in Alzheimer's Disease (AD) and Niemann Pick type C disease.
The Laboratory for Informatics Development (LID) supports the clinical research community through a number of biomedical informatics programs and initiatives.
The Quertermous laboratory is interested in the molecular mechanisms that mediate vascular disease pathophysiology and the risk for these diseases. The approach is primarily genetic, using human cohorts and large scale genome wide studies to identify genes that associate with disease and risk, and molecular genetic studies to define the mechanisms of these associations. At the human level, we collaborate with a number of centers around the world through the CARDIoGRAM+C4D consortium to further identify coronary heart disease loci, and our group serves as the the organizing center searching for loci that associate with gold standard measures of insulin sensitivity, the GENESIS study. For loci identified through these studies, we work to identify mechanisms by which causal variation is responsible for altered gene structure or function, and employ cellular and genetic mouse models to identify how encoded factors participate in the disease process. One novel approach to understanding the link between genes and human disease is employing induced pluripotent stem cells to create disease relevant cell types in vitro that can be studied in relationship to the subjects' phenotype and genetic architecture.
Our research program seeks to identify the cellular and molecular programs regulating vascular and lung development. We then determine how these programs are perturbed by genetic abnormalities or injurious processes associated with disease. Our studies use high throughput genomic and microfluidic technologies, a variety of cell biology platforms including confocal and videomicroscopy, genetically modified mouse models of human disease, human tissue samples and induced pluripotent stem cells to answer these questions. Our major disease focus is pulmonary arterial hypertension (PAH), a condition that can be a fatal complication in children with heart defects, but also arises as a condition of unknown etiology primarily in young women. The pathological changes in the lung blood vessels that cause right-sided heart failure include loss of the distal microcirculation and obliterative proliferative changes occluding the lumen of larger arteries. Our goal is to learn how we can activate lung vascular developmental programs to regenerate lost microvessels and to reverse the obliterative changes. Over the past decade our research has led to four novel compounds in clinical trial or being positioned for clinical trial.
The Rader laboratory is focused on two major themes: 1) novel pathways regulating lipid and lipoprotein metabolism and atherosclerosis inspired by unbiased studies of human genetics; 2) factors regulating the structure and function of high density lipoproteins and the process of reverse cholesterol transport and their relationship to atherosclerosis. A variety of basic cell and molecular laboratory techniques, mouse models, and translational research approaches are used in addressing these questions.
The ability to genotype millions of polymorphisms in thousands of individuals and to sequence entire genomes affords the opportunity to understand how human diversity is associated with many diseases and longevity. It is also possible to direct the differentiation of patient-specific induced pluripotent stem cells, or iPSCs to erythroid progenitors that mature to produce hemoglobin. Both genomics and new iPSC technology can be used to study the molecular basis of phenotypic heterogeneity. This knowledge will then allow the development of predictive networks and genetic risk scores that can be used prognostically and point to functional studies of interesting variants and novel pathways that might can lead to new treatment options. We are taking this approach to the study of hemoglobin disorders focusing on sickle cell disease.
My research is on indvidualized medicine, using the genome and digital technologies to understand each person at the biologic, physiologic granular level to determine appropriate therapies and prevention. An example is the use of pharmacogenomics and our research on clopidogrel (Plavix). By determining the reasons for why such a large proportion of people do not respond to this medication, we can use alternative treatment strategies to prevent blood clots.
"This lab at UCLA does research into the relationship between brain structure and function using image data."
Moving from UCLA to USC.
Found 13 laboratories .