I just finished re-watching this episode, and every time I watch it, the bar is named “Sharrie’s”, not “Sherrie’s”.

The bartender was Mr. ToughDude, who wouldn’t want a girly name like “Sherrie’s”. lol…. more seriously: All of the clues from House’s subconscious have been very indirect. Sherry wine is too close to Sherrie’s bar. Throw in another vowel change (like renaming William James SIDIS to James SIDAS in “Ignorance Is Bliss”). … whatever the reason, it’s “Sharrie’s”. Thanks.

House, being House, realised she had taken Amantadine but didn’t think anything of it, till the bus hit and his amazing brain thought “that could kill her if the garbage truck that just hit her gives her internal injuries!”

You’d all like the show a little better if you used your imagination a bit more, instead of taking everything happens literally and not filling in any gaps with simple explanations! ;p

btw, love the blog, I would just accept most of the medicine if it wasn’t for this! Thanks!!

Could someone please explain further the genetics of Huntington’s disease to me? (I’m a layman with no medical training) When I googled it, it said something about the it being a dominant gene on only one of a pair of chromosomes (the 4th pair). Does this mean that

A: if two HD-positive parents mate, the child has a 75% chance of having the gene, but if he does get it, will definitely have one HD gene and one non-HD gene?

or

B: If two HD-positive parents mate, the child has a 25% chance of not getting it, 50% chance of getting one HD gene and one non-HD gene, and 25% chance of getting two HD genes (meaning that his child will have 100% chance of having HD)?

or is it more complicated than that?”

Human genetics paper to the rescue! First, you seem to be confused about the nature of “dominant” in the end there. You only need one gene gone wrong to cause Huntington’s (basically the definition of dominant), so the offspring with one non-HD gene will still be affected.

The basic punnet-square genetics for an autosomal dominant trait and two affected parents (clearly you’re thinking of parents with one normal and one affected gene each – let’s call it Hh) will have 25% hh (or unaffected), 50% Hh and 25% HH (or affected, a total of 75% and not all with one normal gene).

Of course, Huntington’s is a little more complicated than that. It comes down to the number of repeats of a certain trinucleotide within the coding region of the gene. Less than 28 repeats is both normal and stable, and the person will be unaffected. More than that is unstable, and the number of repeats will tend to increase during meiosis. For about 28-35 repeats, you won’t be affected but the number will increase in successive generations. 36-39 repeats sometimes results in Huntington’s, and sometimes doesn’t, and anything over 39 is the full mutation and generally results in Huntington’s. The higher the number is, the more severe it gets, with earlier onset and faster progression.

The reason it is dominant is that when there’s too many repeats, the resultant protein tends to aggregate (form clumps) in the brain cells, eventually leading to cell death. Therefore, only one bad allele is required for the disorder to manifest.

I hope that helped, and wasn’t too confusing.

Two things. His “deep brain stimulation” ‘thing’ has been done at least without the “deep” part in research. I believe “deep brain” has been done as well but am not sure. But i also believe that “deep brain” part was done on animals.

There are indeed “brain reading machines” that can , indeed, show the images in your thoughts. They use FMRI and special software that basically just reads neurons. It is extremely cool and extremely scary stuff.

Wilson would very likely donate one of his.

Isn’t that a possibility, aside from the exchange transfusion?