Fnord.

Mouse around over the center, with your sound on. Hey, I laughed…

Great post, a long review/comparison of the Marinemaster 300 versus the Rolex anniversary Submariner. Well worth a read.

Warning: Does contain spoilers!

Having just finished the last book, I have to agree with Moosino. It’s pretty damned good.

I was thinking about this after reading this post on RMP. I have to disagree with Craig on this one. He says that

However, I’m proud to say that I’m blissfully ignorant about Harry Potter. I’ve never read one of the books, and I’ve never seen one of the movies.

Why is that?

Because it’s a children’s book series, and (this is the important part here, pay close attention) I’m not a child.

Personally, some of the other authors I like (e.g. LM Bujold) are filed in children’s or ‘young adult’ and it doesn’t bother me. In the case of Rowling, she’s a good storyteller and the plots have developed nicely across the series. I enjoyed reading them and they even re-read well.

It’s a lot lighter weight than ‘real literature’, but then again we all bottom feed sometimes.

I do have one gripe though - if Harry’s cloak is part of the Hallows, how come Mad-Eye could see through it in the earlier books?

Read what you like, and ignore the labels!

I’ve had a lot of people trying to use my wireless network of late

Sidebar: The Airport Extreme can send log messages to your Unix box via the syslog mechanism. Check out ‘Base station options’/ ‘Logging/NTP’ and ‘Send base station logging to’

I also set the LED light to blink for traffic, as I find that more useful than always-on.

See this page for syslog setup on Debian.

and I’ve been trying to close down the hatches. I’ve always used MAC filtering, so they couldn’t get on, but someone keeps trying. Given the rapid repeat, its certainly automated or just OS stupidity, but it annoys me.

Plan of attack:

So. First problem is my version 1 Squeezebox.

It’s been trouble before, but I don’t have the dosh to upgrade to the much-nicer v2 or v3. It’s WiFi is B-only. Fortunately, I had a Linksys WRT54GS spare, and had previously setup one as a bridge.

Since I wanted to put images in this post, here’s a pic of one borrowed from the Wikipedia page on it:

I found a slightly better set of instructions for bridge mode on AnandTech, and managed to get it working. I found that the newer Talisman firmware worked better than the Alchemy release.

Sidenote on firmware and Sveasoft: I am a former subscriber to Sveasoft, and have paid for a year of access. This time, subscription having expired, I downloaded the ‘Freeman’ version from this page instead, which lacks the ultra-stupid MAC-based copy protection. I am fairly certain that Sveasoft has bent or broken GPL on this, and FWIW the Freeman version is working well. Rant over.

After you do all the setup (subnet, DHCP, client-mode wireless) there’s just one real gotcha - to get it to work, you have to enable ARP proxying on the Linksys. There’s no way to do this from the web interface, and the setting is erased if you reboot the router. So you have to

echo 1 > /proc/sys/net/ipv4/conf/`route | grep default | awk '{print $NF}'`/proxy_arp

Messy, eh?

Once I had that figured out, I wanted to enable encryption. WEP is no good, so I wanted WPA or WPA2. I’m using an Airport Express which supports all of the above as my base station. Gratuitous picture:

However, the Freeman firmware pages use different terminology than the Apple admin program, so I had to google a bit. This page and this one got me going. You have to

Now, while it reboots, go to the Freeman firmware and select ‘WPA-TKIP’. Enter same key, reboot, do the SSH ARP voodoo above, and you’re good to go.

(You also have to go around to all your laptops and enter the key into their setups, but that’s much easier.)

Once I did this I hit the next problem: Slimserver is not working. I spent hours thinking it was the bridge setup, which was reasonable given the number of places you can make mistakes, but it isn’t. For some reason, the current release in debian unstable is borked, and the symptom is that the web interface never loads. You can connect to the port ok but you get no content. I erased the contents of /var/cache/slimserver/MySQL and restarted it, but got the same result.

Oddly, the web interface was working while it rebuilt the database, but somewhere in that process it Just Stopped. No error log that I can find, no errors in /var/cache/slimserver/mysql-error-log.txt either. I’m at a loss.

The other problem that I have is probably my error - I can’t load the Linksys web interface unless I’m cabled into it. I enabled the remote admin, but it may be subnet-related or such.

I really wish that the ARP proxy setup was a) permanent and b) web-interface-settable. Yeesh.

I also am a bit peeved at Slimserver. It’s the program single most likely to break on a Debian dist-upgrade.

Ahh well, maybe with G-only and WPA it’ll cut down on the neighbors trying to associate with my base station…

Update 8/19/07: Squeezebox got updated and appears to stay up now, so I’m reopening this one. Fixed the missing anandtech URL, sorry. I should also note that the WPA+G change did remove the slowdowns and associations — hooray! Now tackling the ARP proxy and such. Post to follow!

(Picture from this Flickr page.)

So what’s life like if you’re stuck on the low side of the bell curve?

According to Wray Herbert and this post, it’s different:

As reported in the July issue of the journal Psychological Science, the dull-witted report drifiting not when they are bored, but rather when their minds are overtaxed by some unusually challenging task. It’s like they don’t have the mental resources to stay on task, so they stop striving. Their minds are escaping more than wandering.

Read it. It’s fascinating. The blog is chock full or more tidbits too, so check it out.

Via DadTalk, a nice essay on the psychology of a bubble.

The author is also a Piggington fan, and posits that San Diego is smack dab in such a cycle:

I’ve always been fascinated by the psychology of groups, and of course we’re renters, so both posts are fascinating to me. I find myself

Piggington has very solid data on a bubble:

so I guess we’ll just have to see what happens. The essays (DadTalk and Irvine Housing Blog) are both excellent and worth a read.

Via the fascinating weblog of Telstar Logistics, a Flickr set on modern military ruins in San Francisco:

In 1990, the San Francisco Bay Area was home to several large U.S. military facilities.

By 2000, they were all gone.

These are scenes from the Bay Area’s recently-abandoned, Cold War-era bases: Hunter’s Point Naval Shipyard (San Francisco), Treasure Island Naval Station (San Francisco), Alameda Naval Air Station (Alameda), the SF-88 Nike Missile Site (Marin Headlands), Hamilton Field Air Force Base (Novato), Mare Island Naval Shipyard (Vallejo), Naval Security Group Activity base (Skaggs Island), and portions of Moffett Field Federal Airfield (Mountain View).

Very cool indeed. If you like this sort of thing, be sure and check out Subtopia as well.

I like this one for its brevity and thought:

234.
Why should the whole lake have the same name?

and this one too:

383.
A screwdriver is for screws. When you pry
open a paint can with it, you have committed
metaphor, which is the second use of things,
their will gone. As for us, since we don’t know
what our purpose is, all we do is metaphori-
cal.

and one more as a bonus. I remember this one whenever I hear the old city-vs-country argument.

431.
What’s the difference between provincialism,
which unthinkingly takes its situation for ev-
eryone’s, and cosmopolitanism, which is con-
fident it has the right to?

…all from James Richardson’s ‘Aphorisms’.

Enjoy!

Via this Salon article, news of paper on PLoS by Lisa Gross with the imposing title of “The Toxic Origins of Disease.”

(Sidebar:

What if scientific and medical literature were considered a public resource, available to use any way you chose at no cost; all you would have to do is give credit to the author and source as described in the Creative Commons Attribution License?

That’s from this page, which phrases it better than I can. PLoS, the Public Library of Science, solves many of the super-expensive-journal problems I had in school and the ability to google-read-cite is magnificent. I’m a big fan.)

Anyway. The paper hypothesizes that Bisphenol A, a very common polymer used to make polycarbonates and epoxy resins, causes obesity. There’s a lot of it around, and it is known to act like an estrogen receptor agonist. That’s bad:

Recent studies have confirmed that bisphenol A exposure during development has carcinogenic effects and produce precursors of breast cancer.[6] Bisphenol A has been shown to have developmental toxicity, carcinogenic effects, and possible neurotoxicity.

That’s from Wikipedia’s entry on the chemical, which is fairly conservative. OK, so we know its bad news, and maybe you should lose the Nalgene bottle for something in stainless steel. (For their part, Nalgene has their position here.) I don’t think it passed, but California was going to ban B-A from kid’s products. (Update: it died in committee.)

The Gross paper is fascinating. As you’d probably expect, the companies involved have a bit of an agenda:

By the end of 2004, they had identified 115 published studies on low doses of bisphenol A. They also found a troubling trend. Ninety percent of government studies found significant effects of bisphenol A at doses below the EPA’s lowest adverse effect level, but not a single industry study found any effect. Many of the industry studies, they pointed out, either used a rat strain with very low sensitivity to estrogen or misinterpreted failure to find effects with positive controls. Vom Saal and Hughes urged the EPA to conduct a new risk assessment on bisphenol A.

The news gets even worse:

Soto exposed pregnant rodents to “minuscule doses of bisphenol A, the same doses that humans are exposed to, according to the CDC.” In rats, this treatment produced overweight female offspring; in mice, adding the estrogenic chemical produced female offspring that behaved like males. Both rats and mice also had altered ovarian cycles. In a second round of experiments in mice, in utero bisphenol A exposures induced changes in mammary gland development that began in fetal life and persisted.
…
The changes in the breast and genital tract were expected, Soto says, but some of the behavioral effects and obesity came as a complete surprise. “We were looking at an estrogen thinking it was going to affect the reproductive system and mammary gland only, but then these two other things emerged without us ever imagining that.”

Bisphenol A might induce epigenetic changes by altering patterns of DNA methylation, a chemical modification that controls gene expression, or by activating or silencing genes at the moment of exposure during a critical period of development. Soto is pursuing these possibilities. “A single exposure during a point of vulnerability may suffice,” Soto says. “You know the thalidomide story. You can have thalidomide every day of your life and you will be fine. But [take it] at certain times during pregnancy, your child will end up with no arms.”

OK, that last bit is rather alarmist in tone. The link to obesity, however, seems to be more solid:

In the thrifty phenotype hypothesis, undernutrition in the womb programs metabolic systems to expect a postnatal world of undernutrition. From an evolutionary perspective, genes that promote insulin resistance (thereby limiting glucose uptake) and fat storage would prove advantageous in times of famine. But in a world of fast foods, empty calories, and supersized meals, the same genes would promote obesity, insulin resistance, and type 2 diabetes. Interestingly, a class of drugs used to treat type 2 diabetes (called thiazolidinediones) activates PPAR to reverse insulin resistance in muscle and liver, but in doing so increases fat mass by facilitating triglyceride uptake in adipocytes.

When vom Saal generates growth-restricted mouse pups by exposing mothers to bisphenol A, the babies go through a “ballistic postnatal growth period.” A second group of mice starts out “really heavy” and stays that way. Vom Saal’s two types of obese mice have 430 genes with different activity in their fat cells, exhibit substantial differences in glucose tolerance and leptin levels (leptin regulates appetite and energy expenditure), and lose weight at different rates.

Though understanding the underlying causes of these differences will take “multiple lifetimes of work,” vom Saal says, it’s clear that both animals end up heavy in entirely different ways, with entirely different physiological, fat metabolism, and regulatory systems. “We think that environmental chemicals like bisphenol A are likely to target subpopulations of individuals that are rendered very sensitive to these chemicals by virtue of their genes, genetic background, maternal–fetal interactions . . . and the amount of hormones they’re exposed to.”

I had previously posted about sugar, and it’s probably also true that we have a lot more obese people now that we used to. The idea that, as Leonard put it, “Does plastic make us fat?” was an important question.

One of the Gross papers’ points that struck me was that

What’s more, production of these chemicals closely tracks the rise of obesity.

Along with the explosions in autism and asthma, the sudden change in the morphology of Americans since the 70s demands answers. Why did we start to get fat (and ill) all of a sudden? What changed? The sugar/corn syrup change is probably part of it, but the correlation with bisphenol-A production is also a possibility. Correlation is not causation, of course, but I rather hope that we can overcome the vested interests and figure out what the hell happened. Papers like this are an excellent start.