joked in the video's caption, "Proof that our tables can pass the test of time (and the weight of our favorite pups)!" It's the cutest proof they could use to advertise the table!
In many genetic diseases, a small error in the DNA code can have devastating effects. These errors, called nonsense mutations, insert a premature stop signal in the genetic instructions that cells use to make proteins. As a result, the cell produces only a short, useless fragment of the needed protein. Without the, essential body functions break down.
This kind of error appears in a wide range of diseases, including some cancers and inherited disorders like Duchenne muscular dystrophy (DMD). Unfortunately, there are few treatments for these conditions. But new research is bringing hope by exploring how certain drugs can help cells ignore these faulty stop signs and produce complete, working proteins.Proteins are built by ribosomes, the tiny molecular machines inside cells.read the genetic instructions and assemble amino acids into proteins, like following a recipe step by step. When a nonsense mutation inserts a stop codon in the wrong place, it’s like slamming the brakes halfway through the recipe. The ribosome stops too soon, leaving the protein incomplete.
Aminoglycosides, a class of antibiotics, were the first drugs found to help ribosomes read past these incorrect stop signals. But they come with a serious catch: high doses are needed to work, and those doses often cause side effects likeand hearing loss. This makes them risky for long-term use, especially in children or those already battling chronic illness.
Now, an international team of scientists has discovered that another drug—mefloquine—could make aminoglycosides much more effective, even at lower doses. Originally used to fight malaria, mefloquine has now been shown to help ribosomes override faulty stop codons more efficiently.
The study, published inthat revealed only a pair of underwear below. Meanwhile,
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