00:01
Cetina brevis, which is an autoimmune disease that initially presents with muscle weakness and can progress to complete impairment and muscle movement.
00:08
So the molecular mechanism by which this autoimmune disease happens is we have a neuromuscular junction, which is basically the meeting of a nerve and muscle tissue that can create a contraction of muscle tissue.
00:23
So basically, signaling molecules known as acetylcholine, bind to the acetylcholine receptors found, on muscles, which trigger an action potential and ultimately muscle contraction.
00:35
What happens in myasiniagravist patients is that antibodies are produced that block these receptors and thus prevent acetylcholine from properly binding to the receptors, which prevents muscle contractions and lead to muscle weakness and impairment of muscle movement.
00:50
So let's see which name best describes this molecular mechanism.
00:53
A states that the body produces antibodies against nerve cells, which prevents the nerve cells from releasing acetylcholine, during signal transmission.
01:01
So no.
01:02
Acetylcholine is still produced regardless.
01:04
It's just that the acetylcholine molecules can't properly bind to the receptors.
01:09
B states that the body produces antibodies against acetylcholine, which prevents acetylcholine from transmitting signals...