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Health, Featurable
To minimize inhalation of air pollution while walking and cycling and still reaping the benefits of exercising, UBC researches say cyclist should be riding at speeds between 12 to 20 km/h, while pedestrians should be walking at two to six km/h. “The faster you move, the harder you breathe and the more pollution you could potentially inhale, but you also are exposed to traffic for a shorter period of time. This analysis shows where the sweet spot is,” said Alex Bigazzi, a UBC transportation expert in the department of civil engineering and school of community and regional planning who conducted this analysis.



Using a US Census-based computer model of 10,000 people, Bigazzi calculated ideal travel speeds, called the minimum-dose speeds (MDS) for different age and sex groups. The ideal speed linked to the least pollution risk for female and male cyclists under 20, on a flat road was calculated to be at 12.5 and 13.3  kilometres per hour, respectively. For pedestrian in the same age group, a walking speed around 3 kilometres per hour was determined to be associated with least pollution risk. Their older counterparts on the other hand should aim at reaching at least four kilometres per hour in order to breath in the least amount of pollution over a distance. Ideal travel speeds for other road grades were also computed by Bigazzi. “If you move at much faster speeds than the MDS—say, cycling around 10 kilometres faster than the optimal range—your inhalation of air pollution is significantly higher,” said Bigazzi. “The good news is, the MDS numbers align pretty closely with how fast most people actually travel.” A recently published paper in the International Journal of Sustainable Transportation describes the findings from Bigazzi’s research on the amount of toxic chemicals absorbed by cyclist on busy street. More research is needed to further assess the minimum-dose speed estimates with on-road data.

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Technology
The next generation of batteries could function on a molecule that transports oxygen in blood and could also work in an environmentally friendly way. These batteries have recently emerged and are called Lithium-oxygen  (Li-O2) batteries. They could be a possible successor to lithium-ion batteries -the industry standard for consumer electronics- as they can function for a longer time period. Once these batteries substitute the lithium-ion batteries electronic devices can run for weeks. For example electric cars could function four to five times longer than the current rate. However, before this transition is made possible, scientists should find ways to make the Li-O2 batteries efficient for commercial use and stop the formation of lithium peroxide, a solid precipitate that coats the surface of the batteries’ oxygen electrodes. In order to make this possible a catalyst should be found which could efficiently aid a process known as oxygen evolution reaction, in which lithium oxide products decompose back into lithium ions and oxygen gas. The Yale lab of Andre Taylor, associate producer of chemical and environmental engineering, has recognized the heme molecule as a better catalyst. The heme molecule was shown to improve the Li-O2 cell function by reducing the amount of energy needed to better the battery’s charge/discharge cycle times. “When you breathe in air, the heme molecule absorbs oxygen from the air to your lungs and when you exhale, it transports carbon dioxide back out,” Taylor said. “So it has a good binding with oxygen, and we saw this as a way to enhance these promising lithium-air batteries.” The lead author of the research Won-Hee Ryu a former postdoctoral researcher in Taylor’s lab said the the heme molecule makes up one of the two parts of hemoglobin, which is a carrier of blood in animal blood. Ryu also said in an Li-O2 battery, the molecule would lower the energy needed by the battery for the electrochemical reaction to take place. The researchers said their discovery could help in the reduction  amount of animal waste disposal. “We’re using a biomolecule that traditionally is just wasted,” said Taylor. “In the animal products industry, they have to figure out some way to dispose of the blood. Here, we can take the heme molecules from these waste products and use it for renewable energy storage.”
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Health
Sydney Friedman and his wife Constance donated $3.3-million to fund scholarships for students studying  in the broad area of health. This donation comes after the recent sale of the late couple’s home. They both dedicated their professional lives to UBC and their legacy of generosity will live on with this huge donation. The Friedmans were the first appointment to UBC’s new Faculty of Medicine in 1950, teaching the first graduating class of 1954. They founded the department of anatomy, where Sydney Friedman lead from 1950-1981. Constance researched and taught at UBC until retiring in 1985. She and her husband published over 200 papers together. Sydney Friedman passed away in February 2015 while Constance passed away in June 2011. “The Friedmans were instrumental in making the UBC Faculty of Medicine the exceptional medical school that it is today,” said UBC President Prof. Santa Ono. “The university is grateful for everything they did and the endowment that allows that good work to continue.” The Constance Livingstone Friedman and Sydney Friedman Foundation fund scholarships, following the sale of the couple’s former home this summer. The donation funds two awards — the Friedman Scholars in Health Award and the Friedman Travel Award. The objective of the Friedman Travel Award is to provide the recipient with the chance to experience different cultures in order to enrich their global viewpoint with patients. In 2016, four Friedman Scholars in Health (graduate students in the broad field of health) were granted $25,000 to $50,000 each to further their work through studying outside of Canada. In addition, two MD program graduates were awarded with $5,000 each to travel in the course of their first year out of school. More than 60 years later, the Friedman house and its gardens stand as an example of the mid century modern artistic taste. Many feared the house would be knocked down, but following media coverage a buyer was found who was happy to preserve the property. “Everyone at the foundation was relieved the home would be preserved. It’s what Sydney and Constance wanted. They would be thrilled to know that the medical school they helped to build and the students they so cherished will be able to benefit,” said Dr. Al Boggie, co-president of the Friedman Foundation.
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Health
New study finds the mechanism for insulin resistance leading to type 2 diabetes. Earlier work by  Joshua Knowles, MD, PhD, an assistant professor of cardiovascular medicine at Stanford, and his team showed the connection of a human gene, NAT2, variant with insulin resistance in humans. The fact that type 2 diabetes was caused by insulin resistance was known to researchers for decades. However, the cause for this phenomenon was a mystery. Insulin, a hormone secreted by the pancreas, helps fat and muscle cells take up glucose from the blood. Insulin resistance is caused when human cells don’t respond to insulin, resulting in the build up of glucose in the blood and subsequently leading to the production of even more insulin. “We’ve identified a mechanism for insulin resistance that involves a gene that ties insulin resistance to mitochondrial function, “ said Knowles. Scientists at the Stanford University School of Medicine and the University of Wisconsin have begun to find the connections between a gene, mitochondria, insulin resistance, and how well the body’s metabolism functions in causing diabetes. Suppressing a similar gene in mice called Nat1, causes metabolic dysfunction, such as lower insulin sensitivity and higher levels of blood sugar, insulin and triglycerides. In addition, mice without the Nat1 gene gained more weight and showed a decreased ability to use fat for energy. This new study reveals that suppressing the expression of the Nat1 gene in mice hinders the function of mitochondria. These cell structures make ATP, the energy of cells, without which the cells cannot survive. Individuals with Insulin resistance don’t necessarily develop type 2 diabetes. However, the condition will result in decreased uptake of sugar by muscle and fat cells leading to cardiovascular disease, inflammation, polycystic ovary syndrome, fatty liver diseases and other health conditions. Severe Insulin resistance leading to damaged body tissues is common. A study in 2015 estimated that close to 35 percent of US adults are insulin-resistant to a degree to be at a higher risk for diabetes and cardiovascular disease. Knowles said, the reasons for this skyrocketing increase in the US are poor diet and  sedentary habits.
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