Running hard to stay in place.

Jul 16, 2016

Still here. Still going. Getting ready for HOPE XI and trying to get everything buttoned up and bolted down at work before flying to the other coast for same. That all hell appears to still be breaking loose all over the world isn't helping matters any; I'm certainly not sleeping all that well, consequently.

Rehearsal of my talk for HOPE started today. I really suck right now and need to get this one banged out before I present. At least I've finally stopped writing and rewriting the slides and settled on the text.

This appears to be the week that Windbringer's internal power cell decided to only hold an hour of charge at a time. The good news is that I've got a replacement waiting in the wings to install. The bad news is that it's going to require a full teardown; Windbringer currently has a Macbook-like chassis, meaning lots of fiddly little nonstandard screws. Tomorrow afternoon's already been blocked off.

I'm going to take some downtime for myself to get my head screwed on straight; this also means that Windbringer's going to be backing up to external storage.

Be good to each other, everyone.

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Genetic jiggery-pokery.

Jul 04, 2016

It's long been known that DNA encodes information in a four-bit pattern which can be read and processed like any other bitstream. Four different nucleotides, paired two by two, arranged in one of two configurations side by side by side in a long string of letters, many times longer than the size of the cell containing the full DNA strand. Every cell in every single lifeform contains the same DNA sequence, regardless of what the cell actually does. So how, many have asked, does a cell know if it should help produce hair, or skin, or pigments, or something else? As it turns out, there is more than one layer of information encoding at work in DNA - the way in which DNA is folded in three dimensions also encodes information used by the cell. Inside of every cell the DNA is tightly wound around a cluster of eight proteins called histones, which provide a superstructure to support the two meter long molecule. The question then becomes, how are the specific parts of the DNA molecule directly involved in what a given cell does, called nucleosomes kept accessible to the rest of the cellular machinery? Hypotheses to this effect have been going around since the 1980's but only recently has computational simulation been feasiable to put them to the test. As it turns out, the loops, twists, bends, curves, and folds that DNA undergoes around the histone octomers keep keep those functional nucleosomes exposed so that they can be acted upon. The simulations randomly pushed, pulled, prodded, and twisted virtual DNA strands to see what would happen, and they noted that nucleosomal configurations were in fact impacted. Those simulation results were then verified through laboratory observation of two species of common yeasts. It was also confirmed that point mutations can also influence the folding of DNA, which can result in changes in the frequency of synthesis of proteins due to change in accessibility of those nucleosomes. The entire (highly technical) paper (it gave me a headache on the first readthrough, okay?) is available in its entirity on PLOS ONE under a Creative Commons By Attribution v4.0 International license.

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Drug-resistent yeast, synthetic synapses on the nano scale, and memristor research.

Jul 04, 2016

For the last decade or so, bacteria that are immune to the effects of antibiotics have been a persistent and growing threat in medicine. Ultimately, the problem goes back to the antibiotic not being administered long enough to kill off the entire colony. The few survivors that managed to make it through the increasing toxicity of their environment because they either had a gene which rendered them immune (and the toxins released when the other bacteria died weren't enough to poison them) or assembled one and survived long enough to breed and pass the gene along to other bacteria. This means that the pharmaceutical industry has been scrambling to find new antibiotics that won't harm the patient any more than they absolutely have to... except that now we're seeing antibiotic resistant yeasts in the wild, also. A strain of the yeast candida auris was discovered in 2009.ev in Japan that is resistent to every commonly used drug used to treat fungal infections, including caspofungin, amphotericin B, and fluconazole. Since that time, the dangerous strain of c.auris has spread to the United States, India, South Africa, Pakistan, Kuwait, South Korea, Colombia, the UK, and Venezuela. The fungus is known to invade the body through open wounds in an opportunistic fashion and take up residence in the bloodstream, where it subsequently causes organ failure. It is also known to infect the lungs to some degree, as evidenced by having been extracted and cultured from same. The US Center for Disease Control published a bulletin on 24 June 2016 describes the outbreak in more detail, including the risk factors for contracting the infection (diabetes, recent surgery and antibiotic use (both of which impact the integrity of the body overall), and the presence of large venous catheters). Unfortunately, c.auris is difficult to differentiate from several other less-critical fungal species without extensive testing so it can be misdiagnosed until it is too late; the CDC advises the use of MALDI-TOF mass spectrometry or DNA sequencing (analyzing the D1-D2 region of the 28s rDNA) to confirm infection.

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Still alive.

Jul 01, 2016

Nope. No GLaDOS references today.

As you may or may not be aware, certain parts of the world have come under fire, literally. This has hit me very hard in some very tender places, and I'm not handling it well. Dealing with it has, to a large extent, required staying offline so I don't fry my forebrain.

Work's running me pretty hard, with multiple late-nighters strung end to end.

I'm working on my slides for HOPE in my spare time. I might even get to practice them soon. After that comes more proof-of-concept code that you (yes, you!) can try at home.

Windbringer's power cell is on its way out; I just ordered a replacement, which also means that he's due for more major surgery to install it (because the Dell XPS 15 is very Macbook-like in its hardware layout).

I keep falling asleep before 2100 hours local time.

Don't think I'm sick, don't think any of my dental work is going bad. Just running hard to stay in place at the day job.

When I've got it in me to write coherent blog posts, I will do so.

Be good to each other out there. The world needs it.

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I will be presenting at The Eleventh HOPE.

May 28, 2016

UPDATE: Now that the official HOPE schedule has been published I can say that I'll be speaking in the Noether room on Sunday, 24 July 2016 at 2:00pm EST4EDT.

UPDATE: The Internet Society will be livestreaming video of the talks as they happen. Here's the page listing all of the livestreams.

I found out last weekend (yes, I've been sitting on this - timed posts are the busy blogger's friend) that the talk I submitted for The Eleventh HOPE in July of 2016 was accepted. I will be giving a presentation on Exocortex, my latest work (of mad science), entitled Constructing Exocortices with Huginn and Halo at some point that weekend. I'll be talking about both Huginn (I asked Andrew if he would present with me; he declined because he may not be able to attend HOPE this year (and Andrew, if somehow you can fit it into your busy schedule I'd really like it if you did..)) and Exocortex Halo. To be more specific, I'll be talking a little bit about how they work - what agents do and how they fit together to process information individually to carry out more complex tasks. I'll also be talking about how Halo's constructs send and receive information to and from Huginn to accomplish more sophisticated things (like generate the speech that gets played over a VoIP link or send commands to a personal search engine to index an entire site to sort through later).

This also puts me on the hook to come up with some really off-the-wall but useful stuff to show off. Thankfully I've got several hundred off-the-wall ideas already written down. Now where are my d10's...

When I know where my talk fits into the HOPE schedule I'll post with the specifics. I'd really appreciate it if everyone spread the word about my talk (and thank you in advance if you do).

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Deep learning gone wild, direct neural interface techniques, and hardware acceleration of neural networks.

Jun 05, 2016

There is a graphic novel that is near and dear to my hearts by Warren Ellis called Planetary, the tagline of which is "It's a strange world. Let's keep it that way." This first article immediately made me go back and reread that graphic novel...

The field of deep learning has been around for just a short period of time insofar as computer science is concerned. To put it in a nutshell deep learning systems are software systems which attempt to model highly complex datasets in abstract ways using multiple layers of other machine learning and nonlinear processing algorithms stacked on top of one another, the output of one feeding the input of another. People are using them for all sorts of wild stuff these days, from sifting vast databases of unstructured data for novel patterns to new and creative ways to game the stock, bond, and currency markets. Or, if you're Terence Broad of London, accidentally get DMCA takedown requests.

Broad is working on his master's degree in Creative Computing, and as part of that work developed a deep learning system which he trained on lots of video footage to see if it became a more effective encoder by letting it teach itself how to watch video, in essence. It's not an obvious thing but representing video as data ("encoding") is a wild, hairy, scary field... there are dozens of algorithms for doing so and even more container formats for combining audio, video, and other kinds of data into a single file suitable for storage and playback. Broad built his deep learning construct to figure out more efficient ways of representing the same data in files all by itself, without human signal processing experts intervening. He then ran the movie Bladerunner through his construct, dumped its memory and uploaded it to video sharing site Vimeo. What happened shortly thereafter was that one of Warner Brothers' copyright infringement detection bots mistook the video output by Broad's deep learning construct by dumping its memory for a direct rip of the movie because the output of his deep learning system was so accurate and sent an automatic takedown request to the site because it couldn't tell the difference from the original. One of the videos in the article is a short side-by-side comparison of the original footage to the construct's memory. There are differences, to be sure - some of the sequences are flickering, rippling blotches of color that are recognizable if you look back at the original every few seconds, but other sequences are as a good a replica as I've ever seen. Some of the details are gone, some of the movement's gone, but a surprising amount of detail remains. If you grew up watching nth-generation bootlegs of the Fox edit of Bladerunner where the color's all messed up, you know what I'm talking about.

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It wasn't going to end easily, was it?

Jun 14, 2016

You know that problem child molar I just had worked on for the nth time? The one that required heroic measures and possibly divine intervention a couple of weeks ago? I went in yesterday to get the permanent crown installed.

It seemed like a pretty standard routine: Sit down, get the topical gel, and then out came the local anesthetic. My dentist went in for the first jab.

And hit the nerve.

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Gene therapy for the win, CRISPr with RNA, and growing telomeres without gene hacking.

Jun 05, 2016

The past couple of weeks have brought with them some pretty interesting advances in the field of genetic engineering. So, let's get into it.

The first is, as far as anybody can tell, a working genetic therapy regimen for SCID, or severe combined immunodeficiency syndrome. SCID has long been colloquially referred to as "bubble boy syndrome" after David Vetter was born in 1971.ev with the condition and a movie was released about his life in 1976.ev, due to the fact that children born with the condition utterly lack a functional immune system; the slightest illness is likely to kill them in short order. Of the hundreds of immune disorders that humans can be born with, SCID is interesting in that there are no less than thirteen genetic mutations which can cause simultaneous B- and T-lymphocyte dysfunction. While there have been a number of treatments developed over the years which have met varying degrees of success none of them has been called anything like a cure, let alone a commercially viable one. Pharmaceutical megacorporation GalaxoSmithKline has unveiled Strimvelis, a practical implementation of a gene therapy technique developed at the San Raffaele Telethon Institute for Gene Therapy in Milan that, as far as anybody can tell completely cures SCID. It involves extracting bone marrow from the patient, separating the stem cells from the marrow, and applying a retrovirus that deletes the defective gene and replaces it with a corrected sequence of base pairs. The modified stem cells are then re-inserted into the patient where they pick up production of B- and T-lymphocytes that function normally. Eighteen children over the last fifteen years have undergone treatment with Strimvelis and every one of them no longer show signs of being afflicted with SCID, a helpful sign if I ever saw one but, as with many things, guardian optimism is the way to go. Advisors in the EU formally recommended that Strimvelis go on the market in April, and there are reportedly plans on the desktop for seeking US approval in 2017.ev. Suffice it to say that this is going to kick over a lot of anthills when it hits the market; for a very serious disease this completely breaks the "treat it continually" model of commercial medicine, especially for a rare disease which perhaps one hundred people are born with every year.

It remains anybody's guess how GSK is going to make their projected 14% return on investment on Strimvelis. I'm kind of afraid to see what the price tag is going to be.

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Well, that was a hair raising experience.

Jun 02, 2016

Last Thursday morning I went in to have a certain problematic molar taken care of at the dentist's office before it got much worse. To recap briefly, there is a particular molar on the bottom-left side of my mouth that has been through hell: It's broken several times (once particularly memorable time while eating a German soft pretzel, of all things), it's been filled several times, and I've honestly lost track of the number of root canals performed done on it (somewhere between three and six in the last fifteen years). While getting the abscessed #19 tooth taken care of, it was observed that it was looking a little dodgy. To be somewhat more specific, the crown on it was loose and wiggling, and I started to notice a black line on the gum just below it.

The rest is going under a cut because I'd like to save people who don't specifically want the down-low the writeup. For those of you with relatively delicate constitutions suffice it to say that I hope I never experience that again in my life.

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