NSF’s Emerging Frontiers in Research and Innovation (EFRI) office funded 4 very futuristic neuroengineering grants.
Disclaimer: I was involved with the second proposal on this page.
Findings: Tapping Into What a Deer Sees, and Doesn’t
Not being a hunter, I’m not sure how much I support this, but I must admit this is at least a very interesting application of psychophysics data. Using deer as subjects in a standard battery of visual psychophysics tests, researchers have engineered a new material/pattern (”Gore Optifade”) that is superior to standard camo for evading detection by deer. Looks like deer are red-green colorblind but have higher acuity in the blue end of spectrum than humans.
Once they had assessed the deer’s visual strengths and weaknesses, Dr. Neitz and Dr. O’Neill worked out colors, textures and shapes with Guy Cramer of HyperStealth Biotechnology, a company that designs military camouflage. Mr. Cramer’s computer algorithms create fractal patterns that exploit a couple of ancient tricks used by animal predators.
The first and most obvious trick is to fade into the background, as a leopard’s spots enable it to do while it’s patiently waiting to ambush a prey. The spots aren’t shaped like leaves or branches, but they form an overall “micropattern” matching the colors and overall texture of the woodland background.
That trick, though, won’t work for a predator on the move, which is why a tiger doesn’t have spots. It has a “macropattern” of stripes that break up the shape of its body as it’s stalking or running.
There is a nice demonstration image with the article showing the same scene viewed with human vs. deer vision.
There has been a few articles recently in the NYT about the neural mechanisms used by mosquito repellents. What a wonderful idea: Do some ephys recordings to find which neurons are sensitive to DEET (the current standard for mosquito repellents, which I can attest both doesn’t work very well and eats holes in synthetic clothing) and then build targeted compounds for those receptors/neurons/pathways. I always like this type of simple and practical neuroengineering.
Right now, it appears that there’s a bit of controversy in the field. Earlier this year, in Science, a group from Rockefeller found that DEET masked sensitivity to human odors by interfering with a particular odorant receptor. This impressive result was recently question by entomologists from UC-Davis in a PNAS paper claiming that DEET acts directly on a particular olfactory receptor neuron and does not attenuate the response to the same human-emitted odorant, as found in the earlier paper. Although the results appear to be conflicting, the studies use different techniques and thus it is likely that DEET’s action might be more complex than either paper claims. Still, the idea of identifying a target for chemical intervention by looking at electrophysiological responses to DEET is smart.
In related work, earlier this year a group from Colorado State University, as described in this PNAS overview, “conducted a rigorous search of a library of N-acylpiperidines, using an artificial neural network to identify strong candidates, and then tested them in the laboratory on human volunteers.” They found a candidate molecule that has a ~4X longer repellency effect than DEET. Here’s a photo from the experiments (DEET vs. untreated hand)… ouch!
Personal genomics is just starting and this talk gives a preview of what one of the first companies is doing to bring this to market, though the field is starting to heat up with some competition.
Surprising facts from the video:
Description of the talk from Google:
The 23andMe Personal Genome Service offers customers a glimpse at their own DNA sequence, a 750-megabyte string that functions as the operating system for a human being. Common variations in this code can influence the structure and function of the associated wetware in predictable ways. Some of these variations and their effects on traits such as athletic talent, pain sensitivity and avoidance of errors will be discussed in reference to three well-documented examples.
Salon has an interesting piece condemning a recent PBS show purportedly on Alzheimer’s treatment but really more of a sketchy informercial. The program concerns a neurologist with tenuous ties to UC Irvine who advocates SPECT (single photon emission computed tomograpy, a technique which, similar to PET, uses a radiotracer) and some unfounded preventative treatments for Alzheimer’s. The neurologist Bill Amen has appeared on many big-name media outlets including CNN, the Today Show, and Fox News (and the real sign of media success — Oprah) although his approach to Alzheimer’s detection and treatment is lacking in scientific credibility:
“SPECT scans are not sufficiently sensitive or specific to be useful in the diagnosis of A.D.,” neurologist Michael Greicius , who runs the Stanford University memory clinic, and has a special interest in the use of functional brain imaging in the diagnosis of A.D., tells me. “The PBS airing of Amen’s program provides a stamp of scientific validity to work which has no scientific validity.”
Continued pontification on neuroethics issues after the jump. (more…)
If the Fish Liver Can’t Kill, Is It Really a Delicacy? [NYT, login]
Amazing. It looks like TTX (tetrodotoxin, a potent voltage-gated sodium channel blocker well-known to electrophysiologists) is not made by the pufferfish (which I had always assumed), rather it is from the bacteria/food consumed by the fish.
Decades earlier, another Japanese scientist had identified fugu’s poison as tetrodotoxin, a neurotoxin that leaves victims mentally aware while they suffer paralysis and, in the worst cases, die of heart failure or suffocation. There is no known antidote.
Researchers surmised that fugu probably got the toxin by eating other animals that carried tetrodotoxin-laden bacteria, developing immunity over time — though scientists then did not rule out the possibility that fugu produced the toxin on its own.
By this year, Mr. Noguchi had tested more than 7,000 fugu in seven prefectures in Japan that had been given only feed free of the tetrodotoxin-laden bacteria. Not one was poisonous.
“When it wasn’t known where fugu’s poison came from, the mystery made for better conversation,” Mr. Noguchi said. “So, in effect, we took the romance out of fugu.”
Aside from the interesting science, it appears there is also a small Japanese “industry” (de-ttx? detox?) seriously affected by TTX-free fugu. More after the jump (more…)
We’ve certainly come a long way. (And I never knew about Music Portal behind that thing.)
Download MP3It’s hard to judge the merits of this particular interface but I’m sure this is just the first of many such devices that we’re about to see (demo starts 2:00):
This is an Emotiv headset. More than the gaming application, I like the idea of using it for IM emoticons.
Anyone know if the consumer version will require gel for the scalp electrodes? Hmmm… if gamers are the target audience, I think I have a good idea for a cross-promotional opportunity here.
The relatively recently discovered cannabinoid receptors has me wondering how many other neuroreceptors may be left to discover. One way to estimate the number of these is to screen the genome and look for sequences that look like receptors. This paper says that people have done that for the special case of G protein-coupled receptors (GPCRs), and that the result is that, excluding receptors involved in “chemosensory responses such as taste and olfaction”, there are “367 receptors (1), of which some 200 have been shown to bind known transmitters (3). This leaves about 160 orphan GPCRs that are not activated by any known transmitters and thus are genes with unknown function.”
I didn’t notice this before, but in a study of about 4000 subjects, people who took Rimonabant (marketed as Acomplia), a selective antagonist of the cannabinoid type 1 receptor (CB1), apparently had a 3.2% incidence of depressive disorders where placebo-takers apparently had a 1.6% incidence. Also, irritability went from .6% to 1.9%, parasomnia from .2% to 1.5%, nervousness from .2% to 1.2%, sleep disorders from .4% to 1.0%, memory loss from .9% to 1.6%, hypoesthesia from .6% to 1.6%, and sciatica from .4% to 1.0%. Psychiatric adverse events were dose-dependent.