A big thanks to Gerald Rubin (center), vice president of Howard Hughes Medical Institute, Chevy Chase, MD, and executive director of Janelia Research Campus, Ashburn, VA, for taking part in the NIH’s Wednesday Afternoon Lecture Series (WALS). He delivered a fantastic talk titled “What the fly brain can teach us about the neural mechanisms of complex behaviors.” Afterwards, I presented him with a framed WALS certificate of appreciation. Joining us is Benjamin White (right), chief of the Section of Neural Function at NIH’s National Institute of Mental Health. The WALS lecture was held on January 30, 2019.
Credit: Brendan Lee and Zhechao Ruan, Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX
Our joints are pretty amazing marvels of engineering, but they don’t last forever. As we age, or if we suffer certain injuries, the smooth, slippery white cartilage covering the ends of our bones begins to fray and degrade. This causes osteoarthritis (OA), or ‘wear-and-tear’ arthritis. As the cartilage thins and disappears, the bones can even grow spurs that grate against each other, causing swelling and pain. It’s a major cause of disability, and there’s currently no cure—other than joint replacement, which is a pretty big deal and isn’t available for all joints. About 27 million Americans already have osteoarthritis; about 1 in 2 will suffer from some form of the disease over their lifetime. Those are lousy odds.
![Caption: [Left] The knee joint of a normal mouse that endured an ACL-type injury. The injury triggered osteoarthritis and caused the cartilage on the femur (red) and tibia (green) to degrade, allowing the bones to sandwich together. [Right] This is the knee joint of a mouse that received gene therapy after the ACL injury. The cartilage is thick and healthy, and covers the bones completely, providing a cushion.](http://directorsblog.nih.gov/wp-content/uploads/2013/03/mouse-knee-joints.jpg)
