Been to the library lately?

When you are growing up, there are two institutional places that affect you most powerfully: the Church, which belongs to God and the public library, which belongs to you. The public library is a great equalizer. — Keith Richards

I grew up in the library.  I read every single book on the children’s section floor before I was out of 6th grade and had to argue with the librarian to let me upstairs.  Books were my friends and my solace.  Books gave me the huge vocabulary that let me place so high on the standardized tests.
Go read the article in the link above, it’s depressing.  One of the tech guys I follow went to a (sparsely attended) SXSW talk and tells us a little about it.
Two of my favorite people are librarians.  Neither of them get to work in libraries anymore.  My (30 year old) stepson is going to school to become a librarian.  I am having difficulty understanding his thought processes about it.  Not that I ever understand him, anyway, but library science in this day and age seems like a dead end.

Love the background slide

Kindle deletions pave way for digital book banning

Posted: 21 Jul 2009 08:40 AM PDT


If publishers can give Amazon orders, why not the courts? Why not government? The very existence of Amazon’s book-deleting system could be used to enforce libel judgments, execute injuctions, or simply to ban books at the state’s behest.

Farhad Manjoo plots out this depressing vision of 2024, at Slate.

Photo: n8agrin

Why 2024 Will Be Like Nineteen Eighty-Four [Slate]

How a virus works

How the Flu Virus Steals Your Cells, from today’s EveryLearner Knowledge News email. sends out interesting bits about the world on a regular basis.   You can try it free for a month here.


Right now, there is no bigger news than flu. So naturally, we want to know about it. Specifically, we want to know how the flu virus steals your cells, because that’s what all viruses–no matter how new–do. They nab your cells and use them for their own reproductive purposes.

They have to, because a virus is nothing more than a few strands of rogue DNA (or rogue RNA, DNA’s single-stranded cousin) wrapped in a protein coat to keep out the draft.

They are not cells, and they have none of the internal structures that cells use to go about the business of life, which is, generally, to make more life. No, viruses are just genetic material looking for a free ride–looking to hijack a cell and make its machinery do the virus’s bidding.

Rule for Viral Success #1:

Mutation, Mutation, Mutation

With so little to call their own, how have these biological pirates survived for so long? The answer lies in two traits that give viruses superb evolutionary advantages: superfast reproduction and genetic mutations.

Viruses live to reproduce. Although they must do this within host cells, once inside, viruses replicate with enough abandon to shame a rabbit. They quickly reprogram the machinery that cells use to copy their own DNA and use it to spit out copy after copy of themselves.

Genetic mutations add insult to injury. With so much reproduction going on, viruses can mutate almost as fast as they propagate. And massive mutation means that each new generation of viral invaders stands a good chance of gaining some new survival or targeting advantage.

Rule for Viral Success #2:

Pick a Likely Victim

Viruses invade all kinds of cells–plant cells, animal cells, fungi, even bacteria. Yet each virus tends to have a very specific M.O. Which cells look like likely victims to a virus depends on the unique proteins found on the virus’s protein coat and the protein receptors found on the poor target cell.

Some viruses recognize the general receptors that occur on many different kinds of cells. The virus for rabies, for example, can invade so many different kinds of cells that it can span species, infecting rodents, dogs, and humans. Flu is a pretty good species spanner, too.

Other viruses are more restricted and can invade only specific kinds of cells. The common cold virus, for example, can invade only the cells lining the human upper respiratory tract. It’s a picky thief.

Rule for Viral Success #3:

Make It an Inside Job

Viral entry mechanisms are as diverse as viruses themselves, which is why viruses often elude treatment. Some enter a target cell by binding to a specific receptor and passing through the host cell membrane to the cell interior. Others don’t need to enter the cell, but simply attach to the surface and use a needle-like structure to inject their DNA right in.

Once viral genes are inside, the virus begins its replication. It exploits the host cell’s supplies and machinery, forcing it to copy viral genes and synthesize more viral protein coats. Then, these two components come together to form copies of the virus that emerge from the host cell.

Sometimes they “bud” off the cell, like bubbles on top of a simmering stew. At other, more violent times, copies simply fill the cell until it can hold no more. It explodes, releasing its viral hoard into the surrounding area.

Either way, the viral progeny go on to infect new cells–and the cycle starts again. Disease symptoms can and do result from this cellular damage. Most often, though, the sickness you feel is the result of your immune system’s response to the foreign invader. And make no mistake, it will respond.

Rule for Viral Success #4:

Avoid the Cops

Your immune system’s first-responders act like beat cops on patrol 24/7. If they see anything amiss while walking the body’s beat, they make arrests. One kind of cellular cop, the phagocytes, will engulf strange viruses and digest them. Another kind, natural killer cells, recognizes suspect changes on the surface of infected cells and releases chemicals to disintegrate both virus and cell alike.

After spotting the infection, your body can launch a more specific and intensive attack. Proteins called antibodies surround, bind to, and neutralize viruses and other invaders in your bloodstream. Killer T cells mercilessly destroy infected cells and halt systemic infection. Both help your body remember the infection and mount a faster response to the same invader next time.

Still other players merit mention. When a cell does get infected with a virus, sometimes it manages to secrete small proteins called interferons that serve to warn neighboring cells of an imminent viral invasion. These “Paul Revere” proteins work by encouraging neighboring cells to synthesize proteins that can interfere with viral replication.

I cried …

on and off through the whole inaugural process today.  I’m simultaneously frightened and ridiculously cheered and charged up by all of it – frightened because now we’ll see what happens when the new President is really engaged – and OMFG what if he’s not as good as we hope?  Can anyone be that good, anyway?

And cheered because that hack Bush is finally gone, replaced by a man with brains and compassion and  FINALLY we can be patriotic Americans again.  I missed that.  I very much want to be proud of the person(s) in the Whitehouse.

Didn’t Barack and Michelle look fabulous?  They are classing the Whitehouse back up after its long decline into Bud Light Land.

I read this somewhere today:

Crying is a sign of hope. When we stop crying, we know we have lost. I add a swell of tears to the changing tide…

Easy Peasy

Rice Students Challenge Electronic Voting Machines
Converge (10/13/08)

As part of an advanced computer science class, Rice University professor Dan Wallach is challenging his students to rig a voting machine. Wallach split his class into teams.

During phase one, teams pretend to be unscrupulous programmers at a voting machine company by trying to make subtle changes to the machines’ software that will alter the election’s outcome without being detected by election officials. The second phase has teams playing the part of election software regulators by trying to certify the code submitted by another team during the first phase of the class.

“What we’ve found is that it’s very easy to insert subtle changes to the voting machine,” Wallach says. “If someone has access and wants to do damage, it’s very straightforward to do it.” He says the experiment shows how vulnerable certain electronic-voting systems are.

Wallach says the students often, but not always, are able to find the hacks, but that in real life it would probably be too late. “In the real world, voting machines’ software is much larger and more complex than the Hack-a-Vote machine we use in class,” Wallach says. “We have little reason to believe that the certification and testing process used on genuine voting machines would be able to catch the kind of malice that our students do in class.”


Enron founder Kenneth Lay died early Wednesday in Aspen, Colo.,
of a massive heart attack while awaiting sentencing after being
found guilty of conspiracy and fraud in the Enron trial in May.
Lay’s death came as a shock to former Enron stockholders, some
of whom lost their entire life savings in the company’s collapse,
as they were convinced Lay did not actually *have* a heart.
(Mike Ranston)

–==++ TopFive’s Five-Word Newsflash ++==–

Item: Ken Lay dead at 64.

Comment: God’s portfolio held Enron shares.

(Bill Muse)