Charles on… anything that comes along

Over at the ZDNet blogs, David Berlind has written a long article about how Apple has - get this - something approaching a monopoly in music downloads (gasp!) and that even so the US is telling other countries not to treat it as an issue meriting antitrust treatment.

Quoth Berlind:

For the Feds to bust up a monopoly, they must first prove it exists and proving it exists starts with (1) defining a market and (2) demonstrating how one company dominates that market. When US Department of Justice first started going after Microsoft for being a monopolist, it defined the market Microsoft was dominating as “Intel-based desktop operating systems.”

And he’s surprised. And Paul Thurrott, whose rehabilitation had been going so well, chimes in:

If Microsoft[’s antitrust trial experience] can serve as a lesson, and they should, Apple should be stopped before the abuses get too great and harm too many consumers.

I’m surprised either is surprised. In case they hadn’t been watching or listening through the Microsoft antitrust trials, and the 1995 DoJ settlement that preceded it (and whose violation led to the big antitrust bustup), it is not illegal in the US to have a monopoly of a market. Got that? Absolutely nothing wrong with having 80%, 90%, 100% of any given market. No sir. That’s the American way.

What is illegal, and led to the late-90s trial, is to use a monopoly in one market to push out rivals in another. Such as having a monopoly of desktop operating systems, and using it to push out people in, oh, say, browsers. That’s what Microsoft was found guilty of having done.

Now, Apple has a lock on the music downloads market. Riiight… and where is it using that to push into other areas? Digital music players, you say? But it dominated that before the iTunes Music Store came along. And there’s a format which all music players can play - MP3 - and you can buy CDs which you can rip into that format. Apple isn’t getting into, say, the CD business (if it were to change the format on CDs from AIFF to AAC wrapped in its Fairplay DRM, now that would be an antitrust issue).

In all: this is not an issue, because it’s not an abuse of monopoly, which is what you need to get an antitrust case going in the US. Berlind and Thurrott have, strangely, revealed themselves as having taken no notice of the whole background to the US case. (See the Wikipedia entry on the Sherman Antitrust Act, which is the relevant one here.)

OK, other territories look at these things differently; France and Sweden are thinking about whether DRM is good or bad (not very clearly). But honestly..

Another Berlind quote, just to show that he’s not with the legal program:

When I first saw the DOJ come up with that definition, that I realized how a clever lawyer can make any company seem like a monopolist. All you have to do is define a market in such a way that the company you’re chasing after conveniently dominates it.

Yes, but that’s not illegal.

Looking back on Microsoft’s history of entanglement with US trustbusters, I still think it was right of the government to interfere.

Yes, because Microsoft used one monopoly to get another.
And why didn’t I put this at the end of the article? Because you have to do that stupid registration crap, which is just a method of grabbing all your details so they can email you junk forever. No thanks, even if I could be bothered to do it to point out the errors of people who don’t know their stuff. (Thurrott just doesn’t have comments nor trackbacks on his blog, which lends it a certain pre-Reformation feel.)

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This time a year ago, we had just begun to descend into the hell that is fitting a profoundly deaf infant with hearing aids. This entailed fortnightly visits to the hospital to get ear moulds made - which then always turned out to be an insufficiently good fit, for two reasons: first, he was growing fast (as they do at that age), and second the amplification necessary to stimulate his benighted cochlea was so great that it inevitably led to the whistle of feedback as reflected, amplified sound escaped from the poorly-fitting ear moulds. Plus he didn’t find them that great, and would from time to time reach up and calmly take them off and hand them to whichever parents was about, with a half-apologetic look on face; the other half of the expression seemed like mild surprise that we thought these things worth bothering with.

That’s behind us now. But the other day we had one of the last stings in the tail of this strange 18 months: the genetics appointment.

We knew - well, everyone told us, and everything confirmed it - that child3’s deafness must be due to (deep breath) autosomal recessive genes, because there are no records of hearing problems going back generations in either family; certainly nobody deaf. Which implied that child3 just got unlucky. The genes did their dance, he got the ones which stepped on each others’ feet.

But precisely which genes? Apparently it takes more than six months for the NHS to do a bit of gene sequencing. But now we had been called to the gene counsellor. We were tense.

“Well, I can tell you today,” she said, “that…”

Don’t be Usher’s, we both thought. Just not Usher’s. In case you’re new to this one, Usher’s syndrome is the real rollercoaster version: you’re born deaf, and then in your teens you go blind. Well, in one version you do. There are three different ones, some of which start with just mild hearing loss. But you always move on to the double whammy to some extent.

“…we’ve identified it as connexin-26.”

Whew. That’s a load off. Connexin-26 - you probably won’t have met - is a gene defect which codes for proteins that are ever so subtly the wrong shape, which means that when the hair cells in the cochlea move and trigger the auditory nerve, the potassium ions that need to squeeze out and past so that they can go round again, in the manner of spear-carriers in a low-budget play trooping circularly through the scenery to give the appearance of legions, can’t.

Properly, the defect is called DFNB1 (deafen-b-one), for which “No other associated medical findings are present.”

Affter punching a fist in the air - sure, he’s deaf, but that’s all, you see? - one’s left wondering about the strangeness of this. DFNB1 - and the particular flaw in his sequence (and thus in ours, his parents) is GJB2 (for gap junction beta 2 protein), which if I’m reading the page on geneclinics (pointed to above) correctly, is a point mutation - ie, one letter of DNA wrong.

(Though even then, you scroll down the frame for DFNB1-GJB2, and you find some quite scary stuff, such as

Hystrix-like ichthyosis-deafness (HID) syndrome, an autosomal-dominantly inherited keratinizing disorder characterized by sensorineural hearing loss and hyperkeratosis of the skin. Shortly after birth, erythroderma develops, with spiky and cobblestone-like hyperkeratosis of the entire skin surface appearing by one year of age.

Thankfully, we’re not anywhere near that. And you do have my sympathies if you are.

“We’re all a junkyard of genes,” the gene counsellor said (I think that’s a correct recollection). “But most mistakes don’t make a difference.”

It’s true. And it’s fortunate - if you like - that connexin only seems to be used in the inner ear (again, if I’m understanding the description in that fantastic frame on geneclinics; read it yourself by scrolling down to the heading of “Molecular genetics”, where it describes the spear-carrier stuff; the connexins make up the scenery, but in the mutated version they leave too large a hole and all the potassium - read, spear-carriers - can’t run around fast enough. Something like that.) If this were something where the protein were used more widely, then it could be calamitous.

Of course, that’s what happens with cystic fibrosis, which is a single mutation in - I think I’m recalling this right - the gene that makes the protein used in the system which helps calcium (or is it sodium?) ions cycle in the lungs. When that goes wrong, lots more goes wrong. (I’m not online right now, else I’d look it up.)

It’s still remarkable. But we’re out of the woods. I think the genetics counsellor - who was a genetics scientist - was quite relieved to be talking to people where she didn’t have to explain genes and DNA with pictures. Some parents, she said, refuse to accept the possibility that their own genes could have caused the problems; in one case, she could see that a child needed further investigation, based on likely genetic diagnosis, but the parents wouldn’t believe it could be true. What can you say? Some people don’t realise that it’s better to find out sooner; even if the eventual diagnosis means you’re going to say goodbye, it’ll mean you have longer to say it.

But as one door closes, another opens - not always with nice stuff behind it. The diagnosis that we’re both heterozygous carriers of DFNB1 means there’s a 2/3 chance for each child of also being a carrier. Apparently the prevalence of DFNB1 in the (UK) population is 1/50; meaning that for either child, their chance of having a deaf child is 1/75, rather higher than the population’s 1/2500. (Except that other sites put the prevalence at 14/100,000 - though I don’t see how that would lead to the incidence that one sees, where DFNB1 counts for half of sensorineural hearing loss, and 1/1000 children has such loss.)

Yeah, but maths aside, what do you tell them? More to the point, why would you tell them? If we’d been able to test in the womb, would we have aborted this child? Given the happiness he’s brought us, it’s a horrible thought. And since they’re grown up with him as a sibling, they’ll know that being deaf isn’t the end of the world; it’s the start of a different one. One with messed-up genes, sure, but we’ve all got those.

(Interested parent with some genetics aptitude? More on DFNB1 at Biomed Central; there’s the Handbook of Genetic Counselling on the issue; and the truly amazing Information Hyperlinked over Proteins site, where one could wallow all day.

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