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10 projects in result set.
Whole-Cell Computational Model of Mycoplasma genitalium
- The goal of this project was to develop the first detailed, "whole-cell" computational model of the entire life cycle of living organism, <i>Mycoplasma genitalium</i>. The model describes the dynamics of every molecule over the entire life cycle and accounts for the specific function of every annotated gene product.
We anticipate that whole-cell models will be critical for synthetic biology and personalized medicine. Please see the project website <a href="http://wholecell.org">wholecell.org</a> and the Downloads page to explore the whole-cell knowledge base and simulations and obtain the model code. | |
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Registered: 2012-01-24 03:21 |
Predicting Cell Deformation from Body Level Mechanical Loads
- This project is a NIBIB/NIH funded study (1R01EB009643-01) to establish models and computational platforms to predict cellular deformations from joint level mechanical loading.
Collaborators:
Ahmet Erdemir (PI), Amit Vasanji, Jason Halloran (Cleveland Clinic)
Cees Oomens, Frank Baaijens (Eindhoven University of Technology)
Jeff Weiss (University of Utah)
Farshid Guilak (Duke University)
Summary (from grant proposal):
Cells of the musculoskeletal system are known to have a biological response to deformation. Deformations, when abnormal in magnitude, duration, and/or frequency content, can lead to cell damage and possible disruption in homeostasis of the extracellular matrix. These mechanisms can be studied in an isolated fashion but connecting mechanical cellular response to organ level mechanics and human movement requires a multiscale approach. At the organ level, physicians perform surgical procedures, investigators try to understand risk of injury, and clinicians prescribe preventive and therapeutic interventions. Many of these operations are aimed at management and prevention of cell damage, and to associate joint level mechanical markers of failure to cell level failure mechanisms. Through human movement, one explores neuromuscular control mechanisms and the influence of physical activity on musculoskeletal tissue properties. At a lower level, mechanical sensation of cell deformations regulate movement control. Physical rehabilitation and exercise regimens are prescribed to promote tissue healing and/or strengthening through cellular regeneration. The knowledge of the mechanical pathway, through which the body level loads are distributed between organs, then within the tissues and further along the extracellular matrix and the cells, is critical for the success of various interventions. However, this information is not established. The goal of this research proposal is to portray that prediction of cell deformations from loads acting on the human body, therefore a clear depiction of the mechanical pathway, is possible, if a multiscale simulation approach is used. Multiresolution models of the knee joint, representative of joint, tissue and cell structure and mechanics, will be developed for this purpose. The knee endures high rates of traumatic injury to its soft tissue structures and it is predominantly affected by osteoarthritis, chronically induced by abnormalities in mechanical loading or how it is transferred to the cartilage. Through multiscale mechanical coupling of these models, a map of cellular deformation in cartilage, ligaments and menisci under a variety of tibiofemoral joint loads will be obtained. Comprehensive mechanical testing at joint, tissue and cell levels will be conducted for parameter estimation and validation, including in vitro loading of the knee joint representative of lifelike loading scenarios. In addition, imaging modalities will capture joint and tissue anatomy, and spatial and deformation related information from cell and extracellular matrix. Advanced computational approaches will be used to obtain model properties and to facilitate multiscale simulations. The approach will combine the expertise of many investigators experienced in biomechanical modeling and experimentation at various biological scales, some with clinical expertise. In future, the research team will utilize this platform to establish the relationship between the structural and loading state of the knee and chondrocyte stresses to explore potential mechanisms of cartilage degeneration. Through documented dissemination of data and models, simulations of other pathologies and translation of the methodology to other organs can be carried out by any interested investigator. | |
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Registered: 2009-07-23 17:33 |
DeepCell: Deep convolutional neural networks for image segmentation
- The assignment of a cellular identity to individual pixels in microscopy images is a key technical challenge for many live-cell experiments. Traditional approaches to this image segmentation problem have relied on standard computer vision techniques, such as thresholding, morphological operations, and the watershed transform. While these approaches have enabled the analysis of numerous experiments, they are limited in their robustness and in applicability. Here, we show that deep convolutional neural networks, a supervised machine learning method, can robustly segment the cytoplasms of individual bacterial and mammalian cells. This approach automates the analysis of thousands of bacterial cells and leads to more accurate quantification of localization based fluorescent reporters in mammalian cells. In addition, this approach can also simultaneously segment and identify different mammalian cell types in co-cultures. Deep convolutional neural networks have had a transformative impact on the problem of image classification, and we anticipate that they will have a similar impact for live-cell imaging experiments.
Visit our webpage at http://covertlab.github.io/DeepCell | |
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Activity Percentile: 80.30 Registered: 2015-11-16 19:58 |
Live Cell NF-κB
- This project provides data and visualization tools to explore single-cell NF-κB dynamics. To view the interactive figure, please see the Downloads section. | |
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Activity Percentile: 55.30 Registered: 2013-03-05 01:40 |
Dynamic Redox Regulation of IL-4 Signaling
- Incomplete reduction of oxygen during respiration results in the formation of highly reactive molecules known as reactive oxygen species (ROS) that react indiscriminately with cellular components and adversely affect cellular function. For a long time ROS were thought solely to be undesirable byproducts of respiration. Indeed, high levels of ROS are associated with a number of diseases. Despite these facts, antioxidants, agents that neutralize ROS, have not shown any clinical benefits when used as oral supplements. This paradox is partially explained by discoveries over the last two decades demonstrating that ROS are not always detrimental and may be essential for controlling physiological processes like cell signaling. However, the mechanisms by which ROS react with biomolecules are not well understood. In this work we combined biological experiments with novel computational methods to identify the most important mechanisms of ROS-mediated regulation in the IL-4 signaling pathway of the immune system. We developed a detailed computer model of the IL-4 pathway and its regulation by ROS dependent and independent methods. Our work enhances the understanding of principles underlying regulation of cell signaling by ROS and has potential implications in advancing therapeutic methods targeting ROS and their adverse effects. | |
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Activity Percentile: 0.00 Registered: 2015-10-16 21:42 |
C++ and Python code, distributed computing and OpenMM interfaces for simulations
- please cite: "Interplay of Protein and DNA Structure Revealed in Simulations of the lac Operon" (PLOS One 2013)
for any code related to protein-DNA modeling and
"Free Energy Monte Carlo Simulations on a Distributed Network" (Lecture Notes in Computer Science Journal for PARA 2010)
http://link.springer.com/chapter/10.1007%2F978-3-642-28145-7_1
for parallel client-server code, users of additional code should cite this web site. Code is provided as-is with no warranty and examples are provided to illustrate the usage of these modeling techniques with some sample systems. Code is the intellectual property of Luke Czapla, developer and biophysicist. Examples are provided in C/C++ and Python. | |
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Activity Percentile: 0.00 Registered: 2014-02-01 22:32 |
Osmotic pressure, bacterial growth, and bacterial division.
- This project aims to test the hypothesis that bacteria exploit osmotic pressure as a physical driving force for growth and division. | |
Activity Percentile: 0.00 Registered: 2013-03-04 20:25 |
scexpress: A visual aid to examine expression patterns within single cells
- We have designed SC Express, a bioinformatics tool that produces a three-dimensional shape that is reflective of the expression patterns of a single cell. The software package accepts tab delimited text files containing the relevant gene expression data and provides a graphical user interface that enables facile comparison of any two individual cell types on the same screen. | |
Activity Percentile: 0.00 Registered: 2011-03-05 14:54 |
Acetaminophen Induced Liver Injury
- The AILI project is a type of In-Silico Liver (ISL) project, which consists of a body of Java code used and reused for exploring hypothetical liver mechanisms. For AILI, the liver mechanisms are those that cause cellular damage, specifically necrosis, because of exposure to acetaminophen. Moreover, the model, a mouse analog, is used for virtual experimentation to explore and explain AILI phenomena, analogous to wet-lab experimentation. A recent addition to this project is studying the disconnect between in vitro and in vivo wet-lab experiments by comparing and contrasting virtual Mouse and Culture Analogs. | |
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Activity Percentile: 0.00 Registered: 2015-05-07 23:25 |
Proteolytic and non-proteolytic regulation of collective cell invasion
- Cancer cells manoeuvre through extracellular matrices (ECMs) using different invasion modes, including single cell and collective cell invasion. These modes rely on MMP-driven ECM proteolysis to make space for cells to move. How cancer-associated alterations in ECM influence the mode of invasion remains unclear. Further, the sensitivity of the two invasion modes to MMP dynamics remains unexplored. In this paper, we address these open questions using a multiscale hybrid computational model combining ECM density-dependent MMP secretion, MMP diffusion, ECM degradation by MMP and active cell motility. Our results demonstrate that in randomly aligned matrices, collective cell invasion is more efficient than single cell invasion. Although increase in MMP secretion rate enhances invasiveness independent of cell–cell adhesion, sustenance of collective invasion in dense matrices requires high MMP secretion rates. However, matrix alignment can sustain both single cell and collective cell invasion even without ECM proteolysis. Similar to our in-silico observations, increase in ECM density and MMP inhibition reduced migration of MCF-7 cells embedded in sandwich gels. Together, our results indicate that apart from cell intrinsic factors (i.e., high cell–cell adhesion and MMP secretion rates), ECM density and organization represent two important extrinsic parameters that govern collective cell invasion and invasion plasticity. | |
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Activity Percentile: 0.00 Registered: 2016-03-07 06:05 |