Category: Journalism

What’s she building in there?

The problem
NORTHERN MAP TURTLES (that’s Glyptemys geographica for those of you who like Latin) are found in northern states and southern Ontario and Quebec. They hibernate through the coldest parts of the year in communal groups on the floor of lakes and rivers. They don’t come up to breathe for the entire hibernation. Since they spend a lot of time in the sun during the summer, Map Turtles like areas that have fallen trees or other objects to bask on near large bodies of water. Basking sets their body temperature, but the more important question is just how energetically vital is sun-basking to these northern turtles?

The researcher
University of Ottawa professor Gabriel Blouin-Demers studies the physiological ecology of reptiles. He integrates laboratory experiments with field observations to better understand how phenotypes or biological traits—especially behavioural—are set by reptiles’ physiologies.
Blouin-Demers hopes that the research coming out of his laboratory can contribute to reptile conservation. Reptiles are in fact the most threatened vertebrates in Canada.

The project
The northern Map Turtles that Blouin-Demers studied were from Lake Opinicon (100 km south of Ottawa). He implanted thermometers into the abdomen of juvenile turtles to continuously monitor their body temperature for two years. Using their body temperature, Blouin-Demers can calculate the turtles’ metabolic rates to estimate how important thermoregulation is to the energy available for growth and reproduction.

The key
Blouin-Demers determined that basking has a huge impact on the energy budgets of northern Map Turtles. The turtles spend three-quarters of their day basking in the sun.
More importantly, he found that if northern Map Turtles don’t bask, their metabolic rate slows by as much as a third. This amounts to a huge loss in available energy for growth, reproduction, and everyday turtlely business. Despite the clear importance of basking, Blouin-Demers discovered that the turtles bask a little less than the theoretically expected optimal amount. Blouin-Demers speculates that this is because basking is a mutually exclusive behaviour: Turtles can’t multi-task while basking. They bask on land but do all their other important activities (like foraging and mating) in the water, so they must compromise.

What’s she building in there?

The problem
OIL IS EVIL. Humanity go green now. Solar panels suck. Apocalypse therefore inevitable.

The researcher
Karin Hinzer is the Canada Research Chair in Photonic Nanostructures and Integrated Devices. In 2007, Hinzer founded SunLab at the University of Ottawa, and since then has collaborated with many industrial partners. Just this year, a collaborative effort earned SunLab the 2010 Canadian Innovation Award.

The project
One such joint project is the Advancing Photovoltaics for Economical Concentrator Systems (APECS). APECS is a project that demonstrates the use of innovative technology in a practical setting. In January, Hinzer will install experimental solar panels on the roof of the Sports Complex parkade here at the University of Ottawa and at a sister site in northern California.

The key
Hinzer will use efficient gallium/arsenide(Ga/As) based multi-junction solar cells in the APECS project. Traditional silicon solar cells only absorb a small range of photons efficiently, while multi-junction cells absorb over a broader spectrum and so increase the efficiency. However, these solar cells are not cheap. APECS seeks to bring the cost down in a couple of ways.
First, Ga/As cells are usually grown on expensive germanium sheets, but Hinzer is testing Ga/As cells grown on much cheaper silicon sheets. Secondly, Hinzer is reducing the cost by getting more light to a smaller area. The way Hinzer does this is analogous to a kid using a magnifying glass to turn a normal sunbeam into a highly focused death ray for burning ants. But instead of using normal lenses, Hinzer uses waveguides that have been tested in SunLab under an artificial sun. Since the waveguides are much lighter than traditional lens systems, it won’t need the same kind of heavy-duty foundation that other big solar panels require. Therefore, it can be set on rooftops.
But having an efficient solar cell is only half the battle. If there’s only a little light shining on the solar panels, they won’t produce much electricity, no matter how efficient they are. To get around this, the modules will automatically track the motion of the sun to maximize their efficiency throughout the day. Solar panels work best when the sun’s rays are perpendicular to their surface. This is why APECS will have one station here in Ontario and a second one in California. Each panel will have an associated weather station, which Hinzer will use to compare any differences in efficiency to differences in latitude and weather.

What’s he building in there?

The problem
HAS IT EVER amazed you how quickly children seem to recover from injuries? Tumbles and falls are just part of everyday play. But that’s not what it’s like for adults—or grandparents, for that matter. Falling or breaking a bone can be a dangerous event, because injuries are not easily healed.

Why is that?
The foundation of the muscles’ repair system is a particular group of stem cells called satellite cells. Unlike most cells in the body, stem cells don’t have a unique type. Instead, they have the ability to transform into any specialized cell that is required by the body. This talent allows them to regenerate injured tissue by replenishing the old and damaged cells.
But satellite cells aren’t as industrious in adults as they are in children. In fact, their activity diminishes as we age. They’re still in the body, but if modern medicine wants to harness them for directed muscle repair, the stem cells will require stimulation.

The researcher
Dr. Michael Rudnicki is the director of the Regenerative Medicine Program and the Sprott Centre for Stem Cell Research at the Ottawa Hospital Research Institute. His laboratory researches the molecular mechanisms that control stem cells during tissue regeneration.

The project
One of Rudnicki’s special interests is the function of stem cells in adult skeletal muscle—the muscle attached to bones by fibrous tendons.
Satellite cells may be the foundation of the muscles’ repair system, but they certainly don’t work alone. Ridnicki’s work stresses that myogenesis, the formation of muscle tissue, requires coordination between many different cells.

The key
A key player in myogenesis is a group of cells called fibro/adipogenic progenitors (FAPs). Rudnicki found that in healthy muscle, FAPs are dormant, but, in the event of acute muscle damage, they rapidly multiply.
That’s because FAPs are the distress beacon that signal the satellite cells. Rudnicki’s research shows that FAPs encourage the satellite cells to get active and to fuse with damaged muscle fibres or produce new fibres entirely. FAPs do this by establishing a specialized environment in the damaged muscle that facilitates the satellite cells. In myogenesis, FAPs stimulate satellite cells to regenerate muscle. In children, FAPs stimulate satellite cells and then are free to leave once myogenesis is complete; however, in elderly muscle, FAPs become firmly engrafted to the damaged site, and can no longer move on to the next injury.

What’s she building in there?

The problem
IMAGINE YOU’RE AN anaerobic bacteria. You’ve swam around eating up nutrients, but you can hear that biological clock ticking. It’s time to have your very own bouncing baby bacteria. But how do you guarantee that you and your daughter turnout exactly the same? Of course, your DNA will be unchanged, but what about everything else? What molecular interactions ensure that your daughter is exactly the same size as you—that you divide symmetrically at the midpoint?

The researcher
Natalie Goto, an associate professor at the University of Ottawa’s Chemistry Department, sees protein as the machinery of life. Proteins bind molecules together in very specific ways and their interactions act as a clock, telling cells what phase of life they are in. Goto is interested in how the shapes of proteins mediate the interactions between them.

The project
In order to divide symmetrically, rod-shaped cells must construct a new wall at their exact midpoint. In bacteria, this process is controlled by the Min family of proteins.
The protein called MinC inhibits wall formation, but only when it is binded with its sister protein, MinD. MinD likes to moor on the cell wall. MinC and MinD have an affinity for each other.—whenever MinC floats by a MinD, it cuddles up and forms a complex that stops the cell from growing a dividing wall.
But there’s one last member of the Min family: MinE. MinE continually pushes its sister proteins around. MinE shoulders its way between MinC and MinD, displacing MinC. Afterward, MinE leaves MinD, forcing it to dissociate from the wall and driving it from the middle toward the pole of the cell. With no MinC and MinD left at the centre to stop the formation of a new wall, the cell divides.

The key
MinE has a special site in the cell that it uses to breakup MinC and MinD and push them from the centre. Goto found that MinE folds to keep this binding site wrapped inside itself. Only when MinE opens itself up can the site disunite the other pair of proteins. Goto suspects that by keeping the binding site inaccessible, MinE can specifically focus on chasing its sister proteins from the centre. By pushing MinC and MinD duos from the centre and into the poles, MinE frees the cell to form a new wall and divide symmetrically.

What’s he building in there?

The problem
INDUSTRIAL NATIONS EMIT countless millions of tons of carbon dioxide (CO2) into the atmosphere every year. Coal combustion produces approximately a third of all that pollution and there is an immediate need to reduce emissions. One controversial idea is to bury the emissions deep in the ground before the CO2 can escape into the atmosphere and contribute to the greenhouse effect.
But you can’t just bury gas. You have to capture it first. Unfortunately, current methods of scrubbing CO2 out of a coal plant’s exhaust would require at least a quarter of all the energy produced by the power plant. It’s a prohibitively expensive procedure.

The researcher
Tom Woo is a researcher in the the Department of Chemistry and Centre for Catalysis Research and Innovation at the University of Ottawa. Woo specializes in molecular simulations and uses computer algorithms to model chemical systems at the molecular level. His simulations give fellow chemists insight into their experimental results and point them toward potential new designs for engineering materials.

The project
Compounds called metal-organic frameworks are special crystals of metal ions linked together by organic molecules. They are special because they can form very porous structures. In fact, these nanoporous materials can selectively capture CO2 molecules in their pores and hold the greenhouse gas trapped there. The rest of the combustion exhaust would float by and the CO2 would be left, filtered out of the gas.
But there’s one problem: the energy binding the CO2 to the pore is a little too weak. The material currently captures water vapour better than CO2. If the interaction trapping gas can be increased and the material made to not bind water, then nanoporous materials could be the short term solution to reducing carbon emissions.

The key
In order to design nanoporous material that better imprisons CO2, chemists must first understand the forces that hold the pollutant gas in the pore cavity. Woo’s simulations show that the forces responsible for keeping the CO2 captured are almost entirely made up of dispersion forces—a type of force that is weaker than most chemical bonds.
Woo believes that future materials can be designed to replace dispersion forces with stronger electrostatic forces. Using a stronger force ensures that the CO2 stays securely imprisoned while discouraging the seizure of water. Nanoporous materials engineered to use electrostatic interactions to selectively bind CO2 to their cavities would be an important step forward in carbon capture technology.

What’s he building in there?

The problem
HEART DISEASE IS a blanket term for any illness that causes the cardiac muscles to lack circulation (coronary heart disease) or to weaken (cardiomyopathy). Traditional medicine can only help patients cope with a weakened heart. However, techniques in cell therapy may one day allow doctors to direct special cells to regenerate tissue and repair heart damage through stem cell transplantation.
Unfortunately, stems cells are hard to come by and their use in clinics is strictly regulated. To make matters worse, cells taken from patients with cardiovascular disease are often dysfunctional. There is a desperate need for alternative cell therapies for tissue regeneration.

The researcher
Erik Suuronen is the director of the Cardiovascular Tissue Engineering Lab at the University of Ottawa Heart Institute. Suuronen wants to use stems cells and tissue engineering to treat heart disease. He hopes that one day these cell therapies will allow patients to regenerate new muscle and blood vessels rather than live their lives with chronic disease.

The project
Therapeutic cells already exist in the body, called progenitor cells. Rather than transplanting cells to the weakened muscle, Suuronen’s research aims to attract the body’s own progenitor cells to perform the repair and cause tissue regeneration. Normally, only a small number of these cells reach the damaged tissue, but if the target site could be encouraged to attract more of them then the progenitor cells would mobilize to repair and regenerate damaged tissue.

The key
Suuronen has developed a matrix of collagen (collagen is a common extracellular protein) and a complex sugar called sialyl LewisX. Sialyl LewisX instructs the progenitor cells to attract more therapeutic cells and regenerate the damaged tissue while the collagen acts as a “smart” scaffold that supports them during the repair.
Suuronen injected the enhanced matrix into the thigh muscles of rats with damaged blood vessels and dying muscles. The enhanced matrix recruited progenitor cells from the rats’ bone marrow into the bloodstream, leading them to the damaged site. The recruited cells then grew into new blood vessels and galvanized muscle regeneration. By successfully stimulating new muscle growth to replace lost tissue, this research suggests that heart damage could one day be repaired through cellular therapy.

What’s she building in there?

The problem
MODERN SPORTING EVENTS have grown into megaprojects. Tournaments like the FIFA World Cup or Universiade are huge investment projects that host international teams, are watched worldwide, and require vast management administrations.
With such huge costs, and equally huge potential economic benefits, the organization of such games is taken very seriously. Planning is already well underway for the 2015 Pan American Games to be hosted by Toronto.
However, with so many people involved and with so much at stake, creating an efficient framework for communication amongst the network of coordinating bodies can be a daunting task.

The researcher
Milena Parent is an expert in sports administration at the University of Ottawa’s School of Human Kinetics. She specializes in strategic management and organization theory for large-scale sporting events.

The project
By chronicling and understanding the coordination network that existed for organizing the 2010 Vancouver Olympic Games, Parent can develop broad network theories for the management of large-scale sporting events that can then be used by future organizers.
The city of Vancouver began planning for the 2010 Olympic Games nine years before the opening ceremonies. A total of 97 separate federal, provincial, and municipal departments were involved in the planning and those were just the governmental bodies.
The coordination network of stakeholders included sponsors, organizational committees, community groups, governmental departments, the media, and delegations of athletes. Each stakeholder had his or her own interests and each was needed for the sporting event to be a success.

The key
Traditional theory presents the organizational network as a wheel with the organizing committee as the hub and the stakeholders as spokes, but Parent found a strikingly different picture. She discovered centralized control of the planning process lay with the local communities or “people on the ground,” and consequently, played a more pivotal role than that assumed by officials.
In practice, there wasn’t one centralized hub, but rather groups that formed multiple hubs of organization. None of the hubs were well connected to the entire coordination network. Instead, each had strong ties to a handful of stakeholders. Stakeholders formed strong local contacts with each other, but these local networks were relatively independent with only weak links between them. According to Parent, organizers who bridged two or more of these local networks had some of the strongest positions in the planning process since they acted as the main lines of communications between the fractured groups.

What’s he building in there?

The problem
IN THE YEAR 1700, a megathrust earthquake (that’s science talk for scary-big-earthquake) occurred along the Cascadia fault in the Pacific Ocean. The fault runs along the coast from Vancouver Island down to northern California. The earthquake triggered a tsunami off the Pacific Coast, which resulted in a flood that reached inland as far as the mouth of the Fraser River, travelling all the way across the Pacific Ocean and striking the coast of Japan.

The researcher
Engineering professor Ioan Nistor is fascinated by such tsunamis. After the 2004 Southeast Asia earthquake, he and his collaborators were the first research team in the tsunami-affected areas of Thailand and Indonesia. While in the field, they inspect damage to buildings and structures. Back in his University of Ottawa lab, Nistor measures the force of surge impacts on models. He then compares what he saw in the field to laboratory and numerical models in order to gain a better understanding of the effects of tsunami bores—the fast moving walls of water that occur once tsunamis break near shore.

The project
Nistor ruminates over the various scenarios that could result from a modern-day earthquake along the Cascadia fault. By simulating earthquakes at various points along the fault and the propagation of the waves towards shore, he is able to predict the resulting tsunami’s height and speed as it crashes inland. Nistor uses these values to estimate the strength of disastrous forces to which coastal buildings would be subject.

The key
Even though the major Canadian cities on the West Coast are located on inland waterways, simulations show that they would not be spared from devastation in the event of another Cascadia tsunami. Even though its approach is slowed in shallow waters, Nistor still expects 25-metre high surges.
Current building codes in Canada do not explicitly provide special design guidelines for structures located on tsunami-vulnerable shores. They do not account for the initial surge forces, the sweeping drag force, the increase in hydrostatic pressure, or the buoyancy force as the building floats away from its foundation. By properly quantifying these extreme loads on structures during inundation, new design guidelines for structures in tsunami-prone zones can be recommended and, in the event of a disaster, save countless lives.

What’s he building in there?

The problem

THE WORLD IS more interconnected than ever before. Social networks, the global economy, the Internet, and even delivery routes can all seem like a jumbled mess. Nowadays, it is common to see complex nets of relationships everywhere we look.
The simplest network we can imagine is life as an employee on a production line: Our neighbour to our left passes us some widget, we add our component and pass it on to the neighbour on the right. It isn’t a web at all; it’s just a chain.
Now imagine we work in a more complicated factory. Imagine we can get different widgets from multiple neighbours. In fact, even coworkers far from our workstation can toss us widgets. To make matters worse, the foreman lets us wander to and work at any part of the production line we want! What a disaster. We’d be doing a random walk on a random network while receiving random input to deal with.

The researcher
Vadim Kaimanovich, a professor in the Department of Mathematics and Statistics, creates mathematical methods that can predict the nature of complex networks. His goal is to understand when the chaotic evolution of random systems can lead to stable and predictable output.

The project
Kaimanovich uses the analogy of a production line to ask: if we start the production line at a slightly different workstation—one that is close but not exactly the same—will we get a similar widget or something completely different? If the widget doesn’t change, the production is stable. If it’s different, the production diverges.
Scientists have noted many systems that seem as complicated as our crazy production line, but seem to have stable output. However, there were no mathematically rigorous proofs for the existence of stable solutions.

The key
Using a mathematically precise measure to decipher which widgets are similar and which are different, Kaimanovich demonstrated that certain sorts of abstract “random production lines” must have groups of workstations that give stable solutions for the same kind of random input. Not surprisingly, this is the first proof of it’s kind.

What’s he building in there?

The problem
PARKINSON’S DISEASE (PD) deteriorates a patient’s central nervous system and debilitates motor skills. Doctors don’t know the cause of 90 per cent of PD cases, but better understand the source of the other 10 per cent. Heredity and genetics are the culprits in this type, called early-onset PD.
Surprisingly, the genes associated with PD are found in all kinds of life forms, including mice, yeast, and zebrafish. These genes play an important role in the special cells that control body motion and make dopamine, an indispensable chemical needed to transmit signals between neurons—these cells are called dopaminergic neurons.

The researcher
Marc Ekker, a biology professor at the U of O, works in the Center for Advanced Research in Environmental Genomics to better understand the genetics of PD. Ekker genetically alters zebrafish, whose genes are simpler than those of humans and can be associated with the disease, in order to further study the causes of PD.

The project
Since zebrafish are transparent, Ekker is able to genetically alter their neurons to fluorescent, enabling him to watch the destruction and regeneration of the dopaminergic neurons in the fishes’ brains while they are alive. He can therefore destroy individual neurons with a laser blast, poison, or alternatively, he can genetically block the gene altogether, making it inactive for the fishes’ entire life—essentially giving the zebrafish PD.

The key
Ekker looks at the genetically altered neurons in the brain and studies what they are doing to the fishes’ motion. Fish larva whose dopaminergic neurons are destroyed have very limited motor skills, and young fish without dopaminergic neurons will not respond with evasive motion when gently poked. Ekker’s zebrafish share the same symptoms as PD patients. Zebrafish, however, can regenerate the neurons. We can’t.
They can do this because of stem cells. Stem cells are different from common cells because they aren’t committed to becoming any one type such as a blood cell or a neuron. While humans have only a limited number of stem cells, zebrafish make stem cells throughout their entire life. The fish can draw on their bank of stem cells to replace the neurons.
Lucky fish.