Episode Podcast 7/11/2006 Release Date

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Offline Mjhavok

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Episode Podcast 7/11/2006 Release Date
« on: 13/11/2006 04:07:02 »
Hi All,

After listening to the podcast which I think was actually recorded on Nov 5th I just wanted to mention the following regarding questions listeners had.

I did a little research on Asparagus and found via wikipedia the following "Some of the constituents of asparagus are metabolised and excreted in the urine, giving it a distinctive, mildly unpleasant odor. The smell is caused by various sulfur-containing degradation products (e.g. thiols and thioesters). Studies showed that about 40% of the test subjects displayed this characteristic smell; and a similar percentage of people are able to smell the odor once it is produced. There does not seem to be any correlation between peoples' production and detection of the smell.[1] The speed of onset of urine smell is rapid, and has been estimated to occur within 15-30 minutes from ingestion."

With regards to Huntingtons disease I actually did an essay on this in year one. Amazingly a direct correlation of CAG repeats on the gene relates to the age when a person who has the mutant gene will get huntingtons disease. I can't remember the exact figures but there is a safe zone of CAG repeats when you won't get hungtingtons disease and as you get above this number, the more CAG repeats you have the sooner you get the disease. Facinating.


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Offline chris

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Re: Episode Podcast 7/11/2006 Release Date
« Reply #1 on: 13/11/2006 15:13:35 »
Dear Steven
thanks for writing, and thanks for the added asparagus-type information!
Regarding Huntingtons, you're absolutely right: the greater the CAG expansion, the sooner the onset and the greater the pace of progression. The "safe" threshold seems to be about 30 repeats. The mutant mice created to model the disease contain 120, so they succumb quite quickly.

A more "natural" version of this experiment has gone on in South America at Lake Maracaibo, where religion and segregation has led to large numbers of people inheriting copies of the mutant gene from both parents. As you might expect, the gene dosage effect produces very pronounced disease at a much younger age.

The theory is that CAG encodes glutamine when translated, so repeated CAG encodes a long polyglutamine tract. Beyond a threshold size this does not seem to be processed correctly in the cell. This seems to be linked with intra-nuclear accumulations which eventually cause cellular dysfunction, possibly by acting as sinks for other transcription factors - in other words all of the intracellular signals get hoovered up by these piles of intracellular rubbish, leading to cell death.
A very interesting experiment done by Max Perutz before his death was to take the CAG tract from a huntingtons patient and add it to another CNS-expressed neurone-specific gene. In these mutant animals a different class of cells died, showing that it's the CAG that is toxic, rather than any product of the huntington's protein per-se.
Thanks, once again for writing, and I'm glad you liked the show.
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