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Archive - Apr 19, 2015

Knuckle-Cracking Riddle Finally Solved

"Pull my finger," a phrase embraced by school-aged kids and embarrassing uncles the world over, is now being used to settle a decades-long debate about what happens when you crack your knuckles. In a new study published online on April 15, 2015 in an open-access article in PLOS ONE, an international team of researchers led by the University of Alberta (U of A) used MRI video to determine what happens inside finger joints to cause the distinctive popping sounds heard when cracking knuckles. The article is titled “Real-Time Visualization of Joint Cavitation.” For the first time, they observed that the cause is a cavity forming rapidly inside the joint, not the collapse of that cavity. In the work, the scientists present direct evidence from real-time MRI that the mechanism of joint cracking is related to cavity formation rather than cavity collapse. "We call it the 'pull my finger study'--and actually pulled on someone's finger and filmed what happens in the MRI. When you do that, you can actually see very clearly what is happening inside the joints," explained lead author Dr. Greg Kawchuk, a Professor in the Faculty of Rehabilitation Medicine. Scientists have debated the cause of joint cracking for decades, dating back to 1947 when U.K. researchers first theorized vapor bubble formation as the cause. That was put in doubt in the 1970s when another team of scientists instead fingered collapsing bubbles as the cause. The idea for the project was born when Nanaimo, British Columbia chiropractor Jerome Fryer approached Dr. Kawchuk about a new knuckle-cracking theory. They decided to skip the theories and, with University of Alberta colleagues Jacob Jaremko, Hongbo Zeng, Richard Thompson, and Australian Lindsay Rowe, decided to actually look inside the joint.

Gene Mutation Increases Artemesin Resistance of Malaria Parasite (Plasmodium falciparum) in Africa

Early indicators of the malaria parasite in Africa developing resistance to the most effective drug available have been confirmed, according to new research published in an open-access article in the May 2015 issue of Antimicrobial Agents and Chemotherapy. The article is titled “The Mu Subunit of Plasmodium falciparum Clathrin-Associated Adaptor Protein 2 Modulates in vitro Parasite Response to Artemisinin and Quinine.” Researchers at the London School of Hygiene & Tropical Medicine found Plasmodium falciparum malaria parasites with a mutation to the gene Ap2mu were less sensitive to the anti-malarial drug artemisinin. A study in 2013, also led by the School, suggested an initial link between a mutation in the ap2mu gene and low levels of malaria parasites remaining in the blood of Kenyan children after they had been treated. However, further research was needed to confirm if these genetic characteristics represented an early step towards resistance. In the new study, researchers genetically altered the malaria parasite in the laboratory to mutate ap2mu in the same way that had been observed in Kenya. They found the altered parasite was significantly less susceptible, requiring 32% more drug to be killed by artemisinin. The genetically altered parasite was also 42.4% less susceptible to the traditional antimalarial drug, quinine. Earlier this year, a different research group discovered mutations in the gene kelch13 that were linked to reduced susceptibility to artemisinin combination treatment in South East Asia. Historically, resistance to antimalarial medicines has emerged in South East Asia and then spread to Africa. But these new findings suggest a different route to drug resistance may be developing independently in Africa. Lead researcher Dr.