GLOBAL CHANGE BIOLOGY mini-symposium (November 14, 2024 9:00am)
Event Begins: Thursday, November 14, 2024 9:00am
Location: Dana Natural Resources Building
Organized By: Institute for Global Change Biology IGCB
Join Us for the Institute for Global Change Biology Mini-Symposium!
Explore the cutting-edge research advancing our understanding of public health, sustainability, and ecology at the Institute for Global Change Biology's upcoming mini-symposium. This event will highlight diverse and impactful projects led by our postdoctoral research fellows, showcasing insights that address pressing global challenges. Enjoy a day of science, discussion, and discovery—with snacks and lunch provided!
09:00 Coffee/Tea
09:30 Khandaker Jafor Ahmed: Exploring climate, health, and environment in
coastal vs. Lake Victoria regions of Kenya
09:45 Stephanie Schmiege: Living at the edge: Physiological controls of the
northern limits of treeline
10:00 Leo Ohyama: Macroecological dynamics of ant colony sizes
10:15 Hengxing Zou: Functional shifts of North American avian communities over
half a century
10:30 Kirby Mills: Fire and drought conditions reshape habitat suitability for large
mammals in the American West
10:45 Sarah Raubenheimer: Competition and functional traits mediate CO2
fertilization of plant growth
11:00 Coffee/Tea Snacks
11:20 Wenqi Luo: Continental-scale evaluation of soil fungal biodiversity under
future climate and land-use changes
11:35 Liting Zheng: Plant functional trait responses to long-term elevated CO2
and nitrogen enrichment, and consequences for outcomes of species
interactions
11:50 Tsun Fung Au: Tree growth responses to drought, CO2, and nitrogen
deposition
12:05 Thiago Gonçalves Souza: Increasing species turnover does not alleviate
biodiversity loss in fragmented landscapes
12:20 Kara Dobson: A global meta-analysis of passive experimental warming
effects on plant traits and community properties
12:35 Katie Rocci: Integrating microbial community data into ecosystem-scale
models in the face of climate change
12:50 Lunch
Clinical Microbiology Market worth $6.9 billion by 2029
(EMAILWIRE.COM, October 25, 2024 ) The global Clinical Microbiology Market growth in terms of revenue was estimated to be worth $5.0 billion in 2024 and is poised to reach $6.9 billion by 2029, growing at a CAGR of 6.5% from 2024 to 2029. The clinical microbiology market is driven by several key...
Synthetic Biology Market worth $31.52 billion in 2029
(EMAILWIRE.COM, November 12, 2024 ) The global Synthetic Biology Market is projected to reach USD 31.52 billion in 2029 from USD 12.33 billion in 2024, with a significant CAGR of 20.6%. Rising demand for bio-based products, growing demand for personalized therapies, especially in gene and cell therapies,...
Biology must develop its own big-data systems
Too many data-management projects fail because they ignore the changing nature of life-sciences data, argues
.From: Nature/Column: World View
The size, complexity and heterogeneity of the data generated in labs across the world can only increase, and the introduction of cloud computing will encourage the same mistakes. Just a stone's throw from where I work, at least three computer companies are already touting cloud-based data-management systems for the life sciences. We need to find ways to manage and integrate data to make discoveries in fields such as genomics, and we need to do this quickly.
At their most basic, data-management systems allow people to organize and share information. In the case of small amounts of uniform data from a single experiment, this can be done with a spreadsheet. But with multiple experiments that produce diverse data — on gene expression, metabolites and protein abundance, for example — we need something more sophisticated.
An ideal data-management system would store data, provide common and secure access methods, and allow for linking, annotation and a way to query and retrieve information. It would be able to cope with data in different locations — on remote servers, on desktops, in a database or spread across different machines — and formats, including spreadsheets, badly named files, blogs or even scanned-in notebooks.
Read the full article here.
Origial Source: Nature 499, 7 (04 July 2013) doi:10.1038/499007a
Conservation Biology Special Section: "Conservation in Europe as a model for emerging conservation issues globally
A Special Section: "Conservation in Europe as a model for emerging conservation issues globally" is featured in the Early View module of Conservation Biology online. The section includes:
Mapping opportunities and challenges for rewilding in Europe
Silvia Ceaușu, Max Hofmann, Laetitia M. Navarro, Steve Carver, Peter H. Verburg and Henrique M. Pereira
DOI: 10.1111/cobi.12533
Conservation in Europe as a model for emerging conservation issues globally
Luigi Boitani and William J. Sutherland
DOI: 10.1111/cobi.12530
The alignment of agricultural and nature conservation policies in the European Union
Ian Hodge, Jennifer Hauck and Aletta Bonn
DOI: 10.1111/cobi.12531
Scenarios of large mammal loss in Europe for the 21st century
Carlo Rondinini and Piero Visconti
DOI: 10.1111/cobi.12532
L. Maiorano, G. Amori, A. Montemaggiori, C. Rondinini, L. Santini, S. Saura and L. Boitani
DOI: 10.1111/cobi.12535
The role of agri-environment schemes in conservation and environmental management
Péter Batáry, Lynn V. Dicks, David Kleijn and William J. Sutherland
DOI: 10.1111/cobi.12536
Framing the relationship between people and nature in the context of European conservation
John D. C. Linnell, Petra Kaczensky, Ulrich Wotschikowsky, Nicolas Lescureux and Luigi Boitani
DOI: 10.1111/cobi.12534
The iEvoBio Meeting: intersection of biology, software, and mathematics
The iEvoBio Meeting, 2013, will take place in Snowbird, Utah between June 25-26, in conjunction with Evolution 2013. It aims to bring together biologists working in evolution, systematics and biodiversity, with software developers, and mathematicians.
The keynote speakers for iEvoBio 2013 will be Dr. Heather Piwowar and Dr. Holly Bik.
Submissions for participation in the conference are now open. There are three ways to participate:
- Lightning Talk: present for 5 min on a method, idea, or software product about bioinformatics.
- Software Bazaar: Demo your open-source software product.
- Birds of a Feather: Suggest or participate in an informal group of folks with a common interest. Suggestions will be considered both before and during the meeting.
Find out the whole Program here.
More details about registration can be found here.
International Congress for Conservation Biology 2013
The biennial International Congress for Conservation Biology is recognized as the most important global meeting for conservation professionals and students. The congress features a dynamic scientific program with more than 100 cutting edge symposia, workshops, posters, and focus groups; countless networking opportunities, fantastic field trips, and world-renowned speakers.
The 26th ICCB takes place in Baltimore, Maryland, USA, on the shores of the Chesapeake Bay in Baltimore's Inner Harbor. Chesapeake Bay is the world's most productive estuary and the region is rich in cultural and historical heritage and conservation challenges and success stories.
Event web page: ICCB 2013
ICCB : 27th International Congress for Conservation Biology 4th European Congress for Conservation Biology
IUBS 2015 Frontiers in Unified Biology
- Biological Consequences of Global Change: current challenges
- Building an Informatics Agenda that will deliver a Unified Biology
- Integrated Biology Education for Future Earth
- Integrative Climate Change Biology - Biodiversity, functional traits, and lessons from the past
- BioNomenclature: Making nomenclatural codes, concepts and tools fit for modern research
- Biology and the Societal Interfaces
- From Urban Biology to sustainable BiodiverCities
More information available on teh official conference website.
Introduction of the Capsules environment to support further growth of the SBGrid structural biology software collection
The expansive scientific software ecosystem, characterized by millions of titles across various platforms and formats, poses significant challenges in maintaining reproducibility and provenance in scientific research. The diversity of independently developed applications, evolving versions and heterogeneous components highlights the need for rigorous methodologies to navigate these complexities. In response to these challenges, the SBGrid team builds, installs and configures over 530 specialized software applications for use in the on-premises and cloud-based computing environments of SBGrid Consortium members. To address the intricacies of supporting this diverse application collection, the team has developed the Capsule Software Execution Environment, generally referred to as Capsules. Capsules rely on a collection of programmatically generated bash scripts that work together to isolate the runtime environment of one application from all other applications, thereby providing a transparent cross-platform solution without requiring specialized tools or elevated account privileges for researchers. Capsules facilitate modular, secure software distribution while maintaining a centralized, conflict-free environment. The SBGrid platform, which combines Capsules with the SBGrid collection of structural biology applications, aligns with FAIR goals by enhancing the findability, accessibility, interoperability and reusability of scientific software, ensuring seamless functionality across diverse computing environments. Its adaptability enables application beyond structural biology into other scientific fields.
Surface-mutagenesis strategies to enable structural biology crystallization platforms
A key prerequisite for the successful application of protein crystallography in drug discovery is to establish a robust crystallization system for a new drug-target protein fast enough to deliver crystal structures when the first inhibitors have been identified in the hit-finding campaign or, at the latest, in the subsequent hit-to-lead process. The first crucial step towards generating well folded proteins with a high likelihood of crystallizing is the identification of suitable truncation variants of the target protein. In some cases an optimal length variant alone is not sufficient to support crystallization and additional surface mutations need to be introduced to obtain suitable crystals. In this contribution, four case studies are presented in which rationally designed surface modifications were key to establishing crystallization conditions for the target proteins (the protein kinases Aurora-C, IRAK4 and BUB1, and the KRAS–SOS1 complex). The design process which led to well diffracting crystals is described and the crystal packing is analysed to understand retrospectively how the specific surface mutations promoted successful crystallization. The presented design approaches are routinely used in our team to support the establishment of robust crystallization systems which enable structure-guided inhibitor optimization for hit-to-lead and lead-optimization projects in pharmaceutical research.
Structural characterization of TIR-domain signalosomes through a combination of structural biology approaches
The TIR (Toll/interleukin-1 receptor) domain represents a vital structural element shared by proteins with roles in immunity signalling pathways across phyla (from humans and plants to bacteria). Decades of research have finally led to identifying the key features of the molecular basis of signalling by these domains, including the formation of open-ended (filamentous) assemblies (responsible for the signalling by cooperative assembly formation mechanism, SCAF) and enzymatic activities involving the cleavage of nucleotides. We present a historical perspective of the research that led to this understanding, highlighting the roles that different structural methods played in this process: X-ray crystallography (including serial crystallography), microED (micro-crystal electron diffraction), NMR (nuclear magnetic resonance) spectroscopy and cryo-EM (cryogenic electron microscopy) involving helical reconstruction and single-particle analysis. This perspective emphasizes the complementarity of different structural approaches.
National Academies Name Biology Teaching Fellows and Mentors
The National Academies have bestowed the title of Education Fellow in the Life Sciences to 42 educators around the country who successfully completed a summer institute aimed at fostering innovative approaches to teaching undergraduate biology.
New Report Proposes Framework to Identify Vulnerabilities Posed by Synthetic Biology
Given the possible security vulnerabilities related to developments in synthetic biology – a field that uses technologies to modify or create organisms or biological components – a new report by the National Academies of Sciences, Engineering, and Medicine proposes a framework to identify and prioritize potential areas of concern associated with the field.
If Misused, Synthetic Biology Could Expand the Possibility of Creating New Weapons - DOD Should Continue to Monitor Advances in the Field, New Report Says
Synthetic biology expands the possibilities for creating new weapons — including making existing bacteria and viruses more harmful — while decreasing the time required to engineer such organisms, concludes a new report by the National Academies of Sciences, Engineering, and Medicine.
NASA Should Expand the Search for Life in the Universe and Make Astrobiology an Integral Part of its Missions, Says New Report
To advance the search for life in the universe, NASA should support research on a broader range of biosignatures and environments, and incorporate the field of astrobiology into all stages of future exploratory missions, says a new congressionally mandated report from the National Academies of Sciences, Engineering, and Medicine.
Hannah Romeo Recognized for Excellence in Microbiology
Hannah Romeo serves as a microbiologist for the Celsis Applications Lab at Charles River Laboratories
Marquis Who's Who Honors Joseph M. Lary for Expertise in Epidemiology, Developmental Biology and Consulting
Joseph M. Lary is lauded for his work at the Centers for Disease Control and Prevention and Hood and Associates
Marquis Who's Who Selects Jaime Zsiros for Expertise in Marine Biology and Environmental Science
Ms. Jaime Zsiros is lauded as the director of business development at Mitigation Resources of North America
Marquis Who's Who Selects Sounak Ghosh Roy, PhD, for Contributions to Biology
Dr. Sounak Ghosh Roy is recognized for his research as it relates to infectious diseases and emerging viruses
Arpita Bose, PhD, Honored by Marquis Who's Who for Advancements in Microbiology
Dr. Osama O. Ibrahim Celebrated for Dedication to the Field of Microbiology
From Abyssal Depths to Astrobiology: How Dark Oxygen Is Shaping Our Understanding of Life
What can deep ocean life teach us about finding life on other worlds? This is what a recent study published in Nature Geoscience hopes to address as an int
Labroots 2024 Microbiology Virtual Event Poster Winner: Laura Alguacil Cuéllar
Labroots’ virtual events are excellent ways to connect with great people and collaborate on research within your field. These events have attendees f
Program in Biology & Undergraduate Program in Neuroscience Events 2024 - 2025 (November 13, 2024 11:00am)
Event Begins: Wednesday, November 13, 2024 11:00am
Location: Biological Sciences Building Atrium (BSB)
Organized By: Sessions @ Michigan
Events in this track are open to all current and prospective PiB and UPiN students. We hope to see you!
Proteomic profiling reveals diagnostic signatures and pathogenic insights in multisystem inflammatory syndrome in children | Communications Biology - Nature.com
Novel FFPE proteomics method suggests prolactin induced protein as hormone induced cytoskeleton remodeling spatial biomarker | Communications Biology - Nature.com
EXCRETE workflow enables deep proteomics of the microbial extracellular environment | Communications Biology - Nature.com
Automated single-cell proteomics providing sufficient proteome depth to study complex biology beyond cell type classifications - Nature.com
The Biology Of Sex
Many of us were taught biological sex is a question of female or male, XX or XY ... but it's far more complicated. This hour, TED speakers explore what determines our sex. Guests on the show include artist Emily Quinn, journalist Molly Webster, neuroscientist Lisa Mosconi, and structural biologist Karissa Sanbonmatsu.
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Listen Again: The Biology Of Sex
Original broadcast date: May 8, 2020. Many of us were taught biological sex is a question of female or male, XX or XY ... but it's far more complicated. This hour, TED speakers explore what determines our sex. Guests on the show include artist Emily Quinn, journalist Molly Webster, neuroscientist Lisa Mosconi, and structural biologist Karissa Sanbonmatsu.
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NPR Privacy Policy
Listen Again: The Biology Of Sex
Original broadcast date: May 8, 2020. Many of us were taught biological sex is a question of female or male, XX or XY ... but it's far more complicated. This hour, TED speakers explore what determines our sex. Guests on the show include artist Emily Quinn, journalist Molly Webster, neuroscientist Lisa Mosconi, and structural biologist Karissa Sanbonmatsu.
Learn more about sponsor message choices: podcastchoices.com/adchoices
NPR Privacy Policy
Listen Again: The Biology Of Sex
Original broadcast date: May 8, 2020. Many of us were taught biological sex is a question of female or male, XX or XY... but it's far more complicated. This hour, TED speakers explore what determines our sex. Guests on the show include artist Emily Quinn, journalist Molly Webster, neuroscientist Lisa Mosconi, and structural biologist Karissa Sanbonmatsu.
Learn more about sponsor message choices: podcastchoices.com/adchoices
NPR Privacy Policy
University of Toronto physicists discover new laws governing the “developmental biology of materials”
Toronto, ON – When one atom first meets another, the precise nature of that interaction can determine much about what kinds of physical properties and behaviours will emerge. In a paper published today in Nature Physics, a team led by U of T physicist Joseph Thywissen reported their discovery of a new set of rules […]
Proteomics in systems biology : methods and protocols
Regenerative Medicine - from Protocol to Patient 1. Biology of Tissue Regeneration
Research in Computational Molecular Biology 20th Annual Conference, RECOMB 2016, Santa Monica, CA, USA, April 17-21, 2016, Proceedings
Synthetic Biology Analysed Tools for Discussion and Evaluation
Hydrocarbon and Lipid Microbiology Protocols Single-Cell and Single-Molecule Methods
Hydrocarbon and Lipid Microbiology Protocols Ultrastructure and Imaging
The Biology Of Why Coronavirus Is So Deadly
The Biology Of Why Coronavirus Is So Deadly
COVID-19 is caused by a coronavirus called SARS-CoV-2. Coronaviruses belong to a group of viruses that infect animals, from peacocks to whales. They’re named for the bulb-tipped spikes that project from the virus’s surface and give the appearance of a corona surrounding it.
A coronavirus infection usually plays out one of two ways: as an infection in the lungs that includes some cases of what people would call the common cold, or as an infection in the gut that causes diarrhea. COVID-19 starts out in the lungs like the common cold coronaviruses, but then causes havoc with the immune system that can lead to long-term lung damage or death.
SARS-CoV-2 is genetically very similar to other human respiratory coronaviruses, including SARS-CoV and MERS-CoV. However, the subtle genetic differences translate to significant differences in how readily a coronavirus infects people and how it makes them sick.
SARS-CoV-2 has all the same genetic equipment as the original SARS-CoV, which caused a global outbreak in 2003, but with around 6,000 mutations sprinkled around in the usual places where coronaviruses change. Think whole milk versus skim milk.
Compared to other human coronaviruses like MERS-CoV, which emerged in the Middle East in 2012, the new virus has customized versions of the same general equipment for invading cells and copying itself. However, SARS-CoV-2 has a totally different set of genes called accessories, which give this new virus a little advantage in specific situations. For example, MERS has a particular protein that shuts down a cell’s ability to sound the alarm about a viral intruder. SARS-CoV-2 has an unrelated gene with an as-yet unknown function in that position in its genome. Think cow milk versus almond milk.
How the virus infects
Every coronavirus infection starts with a virus particle, a spherical shell that protects a single long string of genetic material and inserts it into a human cell. The genetic material instructs the cell to make around 30 different parts of the virus, allowing the virus to reproduce. The cells that SARS-CoV-2 prefers to infect have a protein called ACE2 on the outside that is important for regulating blood pressure.
The infection begins when the long spike proteins that protrude from the virus particle latch on to the cell’s ACE2 protein. From that point, the spike transforms, unfolding and refolding itself using coiled spring-like parts that start out buried at the core of the spike. The reconfigured spike hooks into the cell and crashes the virus particle and cell together. This forms a channel where the string of viral genetic material can snake its way into the unsuspecting cell.
An illustration of the SARS-CoV-2 spike protein shown from the side (left) and top. The protein latches onto human lung cells. 5-HT2AR/Wikimedia
SARS-CoV-2 spreads from person to person by close contact. The Shincheonji Church outbreak in South Korea in February provides a good demonstration of how and how quickly SARS-CoV-2 spreads. It seems one or two people with the virus sat face to face very close to uninfected people for several minutes at a time in a crowded room. Within two weeks, several thousand people in the country were infected, and more than half of the infections at that point were attributable to the church. The outbreak got to a fast start because public health authorities were unaware of the potential outbreak and were not testing widely at that stage. Since then, authorities have worked hard and the number of new cases in South Korea has been falling steadily.
How the virus makes people sick
SARS-CoV-2 grows in type II lung cells, which secrete a soap-like substance that helps air slip deep into the lungs, and in cells lining the throat. As with SARS, most of the damage in COVID-19, the illness caused by the new coronavirus, is caused by the immune system carrying out a scorched earth defense to stop the virus from spreading. Millions of cells from the immune system invade the infected lung tissue and cause massive amounts of damage in the process of cleaning out the virus and any infected cells.
Each COVID-19 lesion ranges from the size of a grape to the size of a grapefruit. The challenge for health care workers treating patients is to support the body and keep the blood oxygenated while the lung is repairing itself.
How SARS-CoV-2 infects, sickens and kills people
SARS-CoV-2 has a sliding scale of severity. Patients under age 10 seem to clear the virus easily, most people under 40 seem to bounce back quickly, but older people suffer from increasingly severe COVID-19. The ACE2 protein that SARS-CoV-2 uses as a door to enter cells is also important for regulating blood pressure, and it does not do its job when the virus gets there first. This is one reason COVID-19 is more severe in people with high blood pressure.
SARS-CoV-2 is more severe than seasonal influenza in part because it has many more ways to stop cells from calling out to the immune system for help. For example, one way that cells try to respond to infection is by making interferon, the alarm signaling protein. SARS-CoV-2 blocks this by a combination of camouflage, snipping off protein markers from the cell that serve as distress beacons and finally shredding any anti-viral instructions that the cell makes before they can be used. As a result, COVID-19 can fester for a month, causing a little damage each day, while most people get over a case of the flu in less than a week.
At present, the transmission rate of SARS-CoV-2 is a little higher than that of the pandemic 2009 H1N1 influenza virus, but SARS-CoV-2 is at least 10 times as deadly. From the data that is available now, COVID-19 seems a lot like severe acute respiratory syndrome (SARS), though it’s less likely than SARS to be severe.
What isn’t known
There are still many mysteries about this virus and coronaviruses in general – the nuances of how they cause disease, the way they interact with proteins inside the cell, the structure of the proteins that form new viruses and how some of the basic virus-copying machinery works.
Another unknown is how COVID-19 will respond to changes in the seasons. The flu tends to follow cold weather, both in the northern and southern hemispheres. Some other human coronaviruses spread at a low level year-round, but then seem to peak in the spring. But nobody really knows for sure why these viruses vary with the seasons.
What is amazing so far in this outbreak is all the good science that has come out so quickly. The research community learned about structures of the virus spike protein and the ACE2 protein with part of the spike protein attached just a little over a month after the genetic sequence became available. I spent my first 20 or so years working on coronaviruses without the benefit of either. This bodes well for better understanding, preventing and treating COVID-19.
By Benjamin Neuman, Professor of Biology, Texas A&M University-Texarkana. This article is republished from The Conversation under a Creative Commons license. Read the original article.
Algae here, alien life out there — Cal State L.A.-JPL partnership connects engineers to astrobiology
JPL hires Cal State Los Angeles civil engineering students with NASA grant. The interns can do research for NASA and learn about connections between astrobiology and science here on Earth.
Transforming 3D biology using AI: Tomocube’s HT-X1™ Plus accelerates cellular and organoids label-free analysis
This new system raises the bar in high-resolution, high-throughput 3D imaging for cells and organoids, providing researchers with faster, more detailed, and more accurate insights into biological processes.
Sapient Partners with Rancho BioSciences to Accelerate the Next Generation of its Human Biology Database
Infrastructure expansion will enable rapid ingestion, homogenization of new multi-omics and real-world data for accelerated delivery of multidimensional insights to inform drug development
Jacques Fresco, 'a major figure in the birth of modern molecular biology,' dies at 93
Jacques R. Fresco, the emeritus Damon B. Pfeiffer Professor in the Life Sciences and an emeritus professor of molecular biology, died on Dec. 5. He served on Princeton's faculty for 53 years before retiring in July 2013.
Austin Newton, 'pioneer in molecular biology,' dies at 85
Austin Newton, a founding member of the Department of Molecular Biology, established a new experimental system and mentored generations of undergraduates, graduate students and postdoctoral fellows. He died May 13 in Princeton at age 85.
The endosomal trafficking regulator LITAF controls the cardiac Nav1.5 channel via the ubiquitin ligase NEDD4-2 [Computational Biology]
The QT interval is a recording of cardiac electrical activity. Previous genome-wide association studies identified genetic variants that modify the QT interval upstream of LITAF (lipopolysaccharide-induced tumor necrosis factor-α factor), a protein encoding a regulator of endosomal trafficking. However, it was not clear how LITAF might impact cardiac excitation. We investigated the effect of LITAF on the voltage-gated sodium channel Nav1.5, which is critical for cardiac depolarization. We show that overexpressed LITAF resulted in a significant increase in the density of Nav1.5-generated voltage-gated sodium current INa and Nav1.5 surface protein levels in rabbit cardiomyocytes and in HEK cells stably expressing Nav1.5. Proximity ligation assays showed co-localization of endogenous LITAF and Nav1.5 in cardiomyocytes, whereas co-immunoprecipitations confirmed they are in the same complex when overexpressed in HEK cells. In vitro data suggest that LITAF interacts with the ubiquitin ligase NEDD4-2, a regulator of Nav1.5. LITAF overexpression down-regulated NEDD4-2 in cardiomyocytes and HEK cells. In HEK cells, LITAF increased ubiquitination and proteasomal degradation of co-expressed NEDD4-2 and significantly blunted the negative effect of NEDD4-2 on INa. We conclude that LITAF controls cardiac excitability by promoting degradation of NEDD4-2, which is essential for removal of surface Nav1.5. LITAF-knockout zebrafish showed increased variation in and a nonsignificant 15% prolongation of action potential duration. Computer simulations using a rabbit-cardiomyocyte model demonstrated that changes in Ca2+ and Na+ homeostasis are responsible for the surprisingly modest action potential duration shortening. These computational data thus corroborate findings from several genome-wide association studies that associated LITAF with QT interval variation.