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.
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.
My paper on threats to emerging financial entities went live a couple of weeks ago. It's in volume VII, issue 1 of the journal Postmodern Openings and can be read in its entirity here as a downloadable PDF file. I've taken the liberty of uploading a second copy here for archival purposes.
The paper is published under a Creative Commons By Attribution/Noncommercial/No Derivatives license.
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.