Study counts half-million deaths in Iraq War
Two SFU researchers have contributed to a US-based study that placed the death toll in Iraq related to the Iraq War at approximately 500,000. The study, conducted without funding, looked at the conflict between 2003 and 2011.
Dr. Tim Takaro, health sciences professor, and doctoral student Lindsay Galway were part of a 12-person team who collaborated on the study, published in PLOS Medicine. The team included researchers from the University of Washington, the Iraqi Ministry of Health, and John’s Hopkins University.
The study aimed to estimate direct and indirect deaths attributable to the war. “Several previous Iraq mortality studies have been conducted but this is the only study to cover the entire conflict,” Galway explained. Data was collected from 2,000 randomly selected households across the country’s 18 governorates.
The methodology of the study was more sophisticated than those done in the past, due to the randomness of the sample households (a measure to avoid introducing bias to the study), and an additional set of questions given to each of the adults in the households about their siblings, which allowed the team to learn about an additional 25,000 people.
The study is also unique in that it was the first to attempt to estimate deaths among the huge portion of the Iraqi population who migrated away from the country during the conflict.
For Galway, visiting Iraq and speaking with the team’s Iraqi members was an experience she won’t soon forget. “This experience was inspiring and certainly an invaluable learning experience for me,” she said. “I left the country in awe of our Iraqi colleagues who literally risked their lives to do this work.”
Galway hopes that the study will remind people “about the health impacts of armed conflicts and the importance of studying these impacts.” She also hopes to continue working in this field, but points to the lack of funding available for the research as an obstacle.
“It is important work that needs to be done, said Galway. “Unfortunately there is very limited funding for this kind of work . . . We call on science funding agencies to invest in research to address this large public health problem.”
Cellular tails tell tales of disease
Molecular biologist, Lynne Quarmby, and doctoral student Laura Hilton, have discovered a mutation that may cause cilia (which exist on all human cells) to grow too long — the result of which can be fatal.
Quarmby and her students have found that CNK2, a regulatory protein, controls the length of cilia, which are microscopic antennae on our cells that communicate signals in our bodies. When these antennae are too long or too short, the signals they capture can be misinterpreted and cause disease or deformities. As these cells determine how we develop, their functionality is vitally important.
Quarmby first became interested in cilia while doing her PhD. “We were investigating whether a certain kind of signal transduction happened in plants, and wanted to know which of the same connections were happening in plants as were happening in animals,” Quarmby told The Peak.
The team was originally looking at trees, but it was Quarmby’s decision to use pond scum, which grows more easily in a lab, that led them to make an important discovery regarding the role that certain proteins play in regulating the cilia.
For Hilton, Quarmby’s doctoral student and lead author on the paper published in Current Biology, one of the most exciting discoveries of the project was that the rate of cilial disassembly is actively regulated. A crucial part of all cells’ lifecycle is their cilia’s assembly, the speed of which scientists have thought affects cilial length; however, Quarmby and Hilton are among the few scientists globally who have discovered important impact of the second part of the process: disassembly.
“Previous research from other labs focused largely on how regulating assembly contributed to setting the correct length for cilia. It was incredibly exciting to find that there’s a whole other side to the coin — it may really open up a whole new avenue of discovery in cilia and disease,” said Hilton.
This study not only opens new fields for investigation, but may provide treatment paths in the future for diseases caused by abnormal cilia length.
“Every time you discover a new player and how it might interact with other players in the pathway, that is a whole new opportunity for approaching therapy,” explained Quarmby. “That’s a new place where you can start to understand PKD, and the more you understand a disease, the more options you have for treatment.”
