Hey most of myspace people I talk to are pervs, but not all are pedophiles.

If your eight year old kid said she was going down the park to play with strangers, would you let her do it? Would you see her off with a smile and a wave? I’m guessing probably not.

So why, oh why, do parents let kids wander around on the internet – which is essentially a HUGE PUBLIC PARK without any guidance or warning and so on? I wouldn’t let my daughter (if I had one, which I don’t) on the web unless I was pretty sure she wouldn’t be going places that were not dangerous. I am all for respecting privacy and so forth, but when I was a kid, and I went out, my mum would ask “Where are you going, who with and what time will you be home?” She didn’t ask what I’d be doing – privacy and all that – but she was at least aware of where I’d be and when I should be back.

Just like real life, it is probable that most adults on the web have no interest in your kids. But just like real life, you can’t tell that. And yet somehow the same parent that doesn’t let their precious little Kayleigh stray more than five inches from them in real life will happily let them wander around and talk to anyone on the net. Which, to me, makes no sense and makes them pretty bad parents.

We’re not all Americans and Sun Readers.

I can’t even have a youtube file.
Retarded am I right?

ASS is responsible for the third step of the urea cycle and one of the reactions of the Citrulline-NO cycle.

Contents [hide]
1 Gene
2 Pathology
3 References
4 See also

Gene
The gene that encodes for this enzyme, ASS, is located on chromosome 9. In humans, ASS is expressed mostly in the cells of liver and kidney.

[edit] Pathology
Citrullinemia: At least 50 mutations that cause type I citrullinemia have been identified in the ASS gene. Most of these mutations substitute one amino acid for another in ASS. These mutations likely affect the structure of the enzyme and its ability to bind to citrulline, aspartate, and other molecules. A few mutations lead to the production of an abnormally short enzyme that cannot effectively play its role in the urea cycle.

Defects in ASS disrupt the third step of the urea cycle, preventing the liver from processing excess nitrogen into urea. As a result, nitrogen (in the form of ammonia) and other byproducts of the urea cycle (such as citrulline) build up in the bloodstream. Ammonia is toxic, particularly to the nervous system. An accumulation of ammonia during the first few days of life leads to poor feeding, vomiting, seizures, and the other signs and symptoms of type I citrullinemia.

Treatment for this defect includes a low-protein diet and dietary supplementation with arginine and phenylacetate. Arginine allows the urea cycle to complete itself, creating the substrates needed to originally fix ammonia. This will lower blood pH. Additionally, phenylacetate reacts with backed-up glutamine, resulting on phenylacetoglutamine, which can be excreted renally.[1]

First.