Apples to apples? Hanford Site cleans 1.4 billion gallons of groundwater a year, which is about 14.5 million liters a day. I'm sure you'll object that the levels of contamination are lower (though there's a lot of nasty stuff there), and yes, it's quite possible that nothing exists exactly like what is needed at Fukushima, in large part because the other massive radioactive material cleanups were different sorts of situations. However, the quote was , "You can't filter that much. Nobody can." A statement of possibility, not of existence. Do you really believe this to be physically impossible, rather than merely unfeasible, or just very expensive?
400 tonnes of water is 400000 liters. From the link in the GP, the two treatment plants (at a Superfund site that used to process thorium into lantern mantles) process 60.5 million liters of water a year, for an average of 165000 liters a day. Building treatment plants with 400000 liter/day capacity doesn't seem like that much of a stretch.
I did mention the "for research purposes" part, but yes, I should have emphasized that means analytical chemistry methods and in vitro testing, not running your own clinical trial. Honestly, I didn't mean for the sales quote to be taken seriously- the poster I replied to speculated on the properties of this mysterious compound, and I just thought it was funny that with a little Googling, I found it not only identified, but available for sale. I can't imagine anyone actually ordered some based on my post, but yeah, this stuff is not in any way meant for human use. Up to 4% impurities, and it's likely that those impurities, like SR9009 itself, can cross the blood-brain barrier. And many carbamates are cholinesterase inhibitors, which is to say, nerve agents.
The same group did a study last year that used unmodified mice (well, largely unmodified- they had been put on a diet that promoted obesity, but they were not transgenic).
Based on the alterations in energy metabolism and gene expression we observed in normal C57BL6 and Balb/c mice, we sought to examine whether a REV-ERB alpha/beta agonist would be efficacious in a rodent model of obesity. We initiated the study with 20-week old C57BL6 mice (average weight = 41g) that had been maintained on a high fat diet for 14 weeks (20% carbohydrate 60% fat). The mice continued on the HF diet and we initiated twice per day dosing (i.p.) of SR9009. While the stress of handling and twice-daily injections caused weight loss in vehicle-treated controls, weight loss of SR9009-treated animals was 60% greater (Fig. 5a). During the treatment period, there was no significant difference in the food intake of SR9009 and vehicle treated animals, although handling itself reduced food intake explaining the weight loss observed in the controls. SR9009 treated mice exhibited a more severe reduction in adiposity (Fig. 5b). In addition to the decrease in fat mass we also observed a 12% decrease in plasma triglycerides (TGs) and a 47% decrease in plasma total cholesterol (Chol) (Fig. 5c). Plasma non-esterified fatty acids (NEFA) were also reduced (23%) along with plasma glucose (19%) in the SR9009 treated animals (Fig. 5c). There was also a trend toward a decrease in plasma insulin levels (35%).
SR9009 is available for research purposes, $150 for 25 mg. From the structure, I would say it's likely to be only slightly soluble in water; also, the only solubility data given is in DMSO. It requires storage by refrigeration or freezing, and comes packaged under inert gas, so I would say its environmental persistence would be rather low. I don't know if a molecule like this would be stable enough for oral administration, actually. In their mouse study, injections were made.
From the non-chemistry side of the etymology, it is apparently not known with certainty why a short rifle is called a carbine in the first place:
short rifle, 1580s, from French carabine (Middle French carabin), used of light horsemen and also of the weapon they carried, of uncertain origin, perhaps from Medieval Latin Calabrinus "Calabrian" (i.e., "rifle made in Calabria"). A less-likely theory (Gamillscheg, etc.) connects it to Old French escarrabin "corpse-bearer during the plague," literally (probably) "carrion beetle," said to have been an epithet for archers from Flanders.
The -yne ending is already in common use for carbon compounds with a triple bond. For example, ethyne (the IUPAC systematic name for acetylene). It's not a very good name in this case though- "carbyne" already refers to a type of reactive species of carbon with three unpaired electrons, in analogy to the more common "carbene" which has two unpaired electrons. Wikipedia suggests a better name for the carbon chain to be "linear acetylenic carbon," though I'll admit it doesn't roll off the tongue. Shorter versions of this molecular chain, which terminate with a hydrogen on each end are generally called polyacetylenes or polyynes.
There is reason to think that a drug like this would be broadly effective against different kinds of cancer. TR100 disrupts the actin cytoskeleton vital to all cells, and specifically disrupts its formation by targeting an isoform of the protein tropomyosin. Isoforms are different structures for the the same protein- every cell needs tropomyosin to regulate their actin filaments, but cancer cells preferentially use a certain structure of tropomyosin. Compounds with anti-actin activity have been looked at for a long time as anticancer compounds, but the known ones have been nonspecific. TR100 also has the advantage of being a relatively simple small molecule instead of a complicated biomolecule, which could make its development as a commercial drug much easier.
It is however, still (potentially) just a new chemotherapy agent, one of many out there. From what has been observed from other chemo agents, just because a compound targets a basic cellular function doesn't mean a cancer can't develop resistance. The taxanes and the Vinca alkaloids arrest mitosis (by targeting microtubules), and are excellent, widely used drugs, but are not the The Cure for Cancer. I'd imagine this compound to be along those lines- another weapon in the oncology arsenal, but not a magic bullet.
Right, but the object of the paper is to then advance what is known in that very area, in which I think it is highly successful. Varieties of thioredoxins are present in every free-living organism on earth. One of their many functions is to donate electrons to an enzyme called ribonucleotide reductase which converts ribonucleotides into deoxyribonucleotides, so in a roundabout way, working thioredoxin proteins are necessary to make DNA. Between its ubiquity and general structural similarities in modern organisms, there is reason to think that the general structure of thioredoxins was settled long ago in the history of life, before archaea and eukaryotes split off from bacteria. As other posters have noted, the timeframe of this event is generally held to have been ~3.5-3.8 billion years ago.
To be fair to the journalists, it wasn't them doing the rounding: Conservation of Protein Structure over Four Billion Years.
He was scheduled to receive the visionary award at the Academy of Science Fiction, Horror and Fantasy Films' Saturn Awards on Wednesday. The organization said the award will be presented posthumously and the 39th annual ceremony would be dedicated to Matheson. According to Robert Holguin, the academy's president:
“We are heartbroken to lose a writer of towering talent, unlimited imagination and unparalleled inspiration. Richard was a genius whose visions helped bring legitimacy and critical acclaim to science fiction and fantasy. He was also a longtime supporter of the academy, and everyone associated with the Saturn Awards feels emptier today to learn of this enormous loss.”"
Link to Original Source
From the experiments that were done to find this new layer, it seems that it is very difficult to separate from the adjoining layer (Descemet's membrane). Getting Dua's layer to separate from Descemet's membrane was a serendipitous result of simulating eye surgery (a lamellar keratoplasty, which is a partial corneal graft) involving the "big bubble technique," which uses an injection of air to separate Descemet's membrane from the corneal stroma. It turned out that it was sometimes possible to create this air bubble in specimens where Descemet's membrane had been removed, meaning there had to be another layer for air to get into. Otherwise, it wouldn't be easily detected as a separate layer.
Here's what the "big bubble technique" looks like. It's pictures of eye surgery, so don't say you weren't properly warned.
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That seems likely- data from other instruments on Cassini has suggested that aromatic hydrocarbons such as benzene and anthracene form high in Titan's atmosphere. The altitude (~1000km) is consistent with the location of the glow, and the emission line fits- a mix of polycyclic aromatic hydrocarbons has long been thought to be the source of a 3.3 micron emission line seen in interstellar dust.
OK, I did the research, by which I mean I used Google to find out what research had already been done. Honestly, these guys just about took care of it back in 2006. The answer appears to be a qualified "yes," in that many of the basic features of experimental autoimmune encephalomyelitis translate to MS, but MS is known to have more involvement from some pathways and less from others. In particular, the method of inducing EAE infection in mice led to a focus on the role of CD4+ cells (which include the TH17 cells) for years, until it was discovered that CD8+ cells also play a major role in MS. It turns out that treatments developed using EAE have had mixed results in treating human MS. For instance, there was a lot of hope in the late 1990s for a tumor necrosis factor blocker called lenercept, which was effective against EAE, but actually made MS worse. On the other hand, secukinumab, an antibody against interleukin-17 itself, has shown positive results against MS in a early proof-of-concept trial.
As the Gold, et al. paper concludes, "Autoimmune encephalomyelitis is, thus, an excellent tool for studying basic mechanisms of brain inflammation and immune-mediated CNS tissue injury, and for obtaining proof of principle, whether a certain therapeutic strategy has the potential to block these pathways. Whether they are relevant for multiple sclerosis patients in general and, if yes, for what subpopulation of patients has to be determined in respective clinical studies."