Annie Curtis
π€ SpeakerAppearances Over Time
Podcast Appearances
Well, me and another PI who's down in Trinity called David Hoey.
And I have to give probably credit to the postdoc who worked on this.
Her name was Jan Sue Gorgon, who's now gone back to the University of Genoa and has a position there.
So it was kind of a real combinatory effect.
So what we were wondering about is bones, right, and how bones heal when they're broken.
And this is a big issue because 10% of fractures don't heal.
And you can have two types of fractures that don't heal.
One is a non-union fracture, which never heals.
And then you have a delayed fracture, which will heal, but it takes a long time.
Yeah, constant pain and they have to like bandage it and all of that, right?
So we were wondering the role of, I'm a big fan of this immune cell called the macrophage.
So macrophage means big and eater, right?
So these macrophages, they're really important in terms of bone healing.
They come into the site and there's one type of macrophage,
You know, these are very versatile cells, like they kind of can change their function.
So one type of macrophage comes in first, it's called the M1, and it just kind of clears up the debris, right?
All the kind of mess that was left after the bone was fractured.
And then M2 is the second time which comes in later, and that kind of forms the regenerative response, right?
But obviously it's not enough because we have all these fractures that don't heal.
And what we figured out is how these macrophages do it is they send out little pockets of information.