Insane in the Chromatophores

During experiments on the axons of the Woods Hole squid (loligo pealei), we tested our cockroach leg stimulus protocol on the squid’s chromatophores. The results were both interesting and beautiful. The video is a view through an 8x microscope zoomed in on the dorsal side of the caudal fin of the squid. We used a suction electrode to stimulate the fin nerve. Chromatophores are pigmeted cells that come in 3 colors: Brown, Red, and Yellow. Each chromatophore is lined with up to 16 muscles that contract to reveal their color.

The video shows a closeup of Chromatophores, cells that are used to change the color of the squid. They open an close based on an electric signal from the brain (called a “spike”). By connecting an iPod to the nerve, we can cause those spikes through the current that should normally go to the magnets in the earbuds. It takes low frequency currents to make spikes fire, which is why it seems to only respond to the bass track (“the beat”).

via Insane in the Chromatophores – YouTube.

Best viewed with the sound off.

Robot learns to recognise itself in mirror

A robot named Nico could soon pass a landmark test – recognising itself in a mirror.

Such self-awareness would represent a step towards the ultimate goal of thinking robots.

Nico, developed by computer scientists at Yale University, will take the test in the coming months.

The ultimate aim is for Nico to use a mirror to interpret objects around it, in the same way as humans use a rear-view mirror to look for cars.

“It is a spatial reasoning task for the robot to understand that its arm is on it not on the other side of the mirror,” Justin Hart, the PhD student leading the research told BBC News.

So far the robot has been programmed to recognise a reflection of its arm, but ultimately Mr Hart wants it to pass the “full mirror test”.

The so-called mirror test was originally developed in 1970 and has become the classic test of self-awareness.

More usually performed on animals, the creature is given time to get used to the mirror and is then anesthetized and marked on the face with odourless, non-tactile dye.

The animal’s reaction to their reflection is used as a gauge of their self-awareness, based on whether they inspect the mark on their own body, or react as if it does not appear on themselves.

To date, only a few non-human species pass these tests, including some primates, elephants and dolphins. Human babies are unable to pass the test until they are 18 months old.

Increasingly scientists have used similar tests to analyse self-awareness in robots but none have yet programmed a robot to fully recognise itself from appearance alone.

via BBC News – Robot learns to recognise itself in mirror.

Breakthrough to help paralyzed regain speech

Paralysis sufferers could soon learn to talk again after scientists discovered how the brain allows humans to pronounce vowels, a new study has claimed. Scientists are investigating the use of brain waves to create a new form of communication which could return the power of speech to paralysis sufferers like Physicist Stepehen Hawking.

Diagnosed with Lou Gehrig’s disease at 21, Hawking, now 70, relies on a computerised device to speak. The new research could pave way for prosthetic devices in the brain returning the power of speech to those paralysed by injury or disease.

Researchers followed 11 epilepsy patients who had electrodes implanted in their brains to pinpoint the origin of their seizures, with neuron activity as they uttered one of five vowels or syllables containing the vowels recorded . They found two areas , the superior temporal gyrus and a region in the medial frontal lobe, housing neurons related to speech and attuned to vowels.

Neurons in the superior temporal gyrus, responsible for processing sounds responded to all the vowels, whereas those that fired exclusively for only one or two vowels were found in the medial frontal region involved in memory.

“We know that brain cells fire in a predictable way before we move our bodies,” Dr Itzhak Fried, of University of California, said. “We hypothesized that neurons would also react differently when we pronounce specific sounds. If so, we may one day be able to decode these unique patterns of activity in the brain and translate them into speech,” Fried said.

“Once we understand the neuronal code underlying speech, we can work backwards from brain-cell activity to decipher speech. This suggests an exciting possibility for people who are physically unable to speak,” said Fried.

via Breakthrough to help paralyzed regain speech – The Times of India.

Arctic sea ice likely to hit record low next week

Sea ice in the Arctic Ocean is likely to shrink to a record small size sometime next week, and then keep on melting, a scientist at the U.S. National Snow and Ice Data Center said on Monday.

“A new daily record … would be likely by the end of August,” said Ted Scambos, lead scientist at the data center, which monitors ice in the Arctic and elsewhere. “Chances are it will cross the previous record while we’re still in sea ice retreat.”

The amount of sea ice in the Arctic is important because this region is a potent global weather-maker, sometimes characterized as the world’s air conditioner. This year, the loss of sea ice in the Arctic has suggested a possible opening of the Northwest Passage north of Canada and Alaska and the Northern Sea Route by Europe and Siberia.

As parts of the Arctic melted, 2012 also set records for heat and drought in much of the Northern Hemisphere temperate zone, especially the continental United States.

This summer could see the ice retreat to less than 1.5 million square miles (4 million square km), an unprecedented low, Scambos said.

The previous record was set in 2007, when Arctic ice cover shrank to 1.66 million square miles (4.28 million square km), 23 percent below the earlier record set in 2005 and 39 percent below the long-term average from 1979 to 2000. …

If the sea ice record is broken this month, that would be unusually early in the season; last year’s low point came on September 9, 2011.

Typically, the melting of Arctic sea ice slows down in August as the Northern Hemisphere moves toward fall, but this year, it has speeded up, Scambos said. “I doubt there’s been another year that had as rapid an early August retreat,” he said.

Overall, the decline of Arctic sea ice has happened faster than projected by the United Nations Intergovernmental Panel on Climate Change five years ago, according to NSIDC data ( here ).

To Scambos, these are clear signs of climate change spurred by human activities, notably the emission of heat-trapping greenhouse gases including carbon dioxide.

“Everything about this points in the same direction: we’ve made the Earth warmer,” he said. …

via Arctic sea ice likely to hit record low next week | Reuters.

An Artificial Retina with the Capacity to Restore Normal Vision

Two researchers at Weill Cornell Medical College have deciphered a mouse’s retina’s neural code and coupled this information to a novel prosthetic device to restore sight to blind mice. The researchers say they have also cracked the code for a monkey retina — which is essentially identical to that of a human — and hope to quickly design and test a device that blind humans can use.

The breakthrough, reported in the Proceedings of the National Academy of Sciences (PNAS), signals a remarkable advance in longstanding efforts to restore vision. Current prosthetics provide blind users with spots and edges of light to help them navigate. This novel device provides the code to restore normal vision. The code is so accurate that it can allow facial features to be discerned and allow animals to track moving images.

The lead researcher, Dr. Sheila Nirenberg, a computational neuroscientist at Weill Cornell, envisions a day when the blind can choose to wear a visor, similar to the one used on the television show Star Trek. The visor’s camera will take in light and use a computer chip to turn it into a code that the brain can translate into an image.

“It’s an exciting time. We can make blind mouse retinas see, and we’re moving as fast as we can to do the same in humans,” says Dr. Nirenberg, a professor in the Department of Physiology and Biophysics and in the Institute for Computational Biomedicine at Weill Cornell. The study’s co-author is Dr. Chethan Pandarinath, who was a graduate student with Dr. Nirenberg and is currently a postdoctoral researcher at Stanford University.

This new approach provides hope for the 25 million people worldwide who suffer from blindness due to diseases of the retina. Because drug therapies help only a small fraction of this population, prosthetic devices are their best option for future sight.”This is the first prosthetic that has the potential to provide normal or near-normal vision because it incorporates the code,” Dr. Nirenberg explains.

Normal vision occurs when light falls on photoreceptors in the surface of the retina. The retinal circuitry then processes the signals from the photoreceptors and converts them into a code of neural impulses. These impulses are then sent up to the brain by the retina’s output cells, called ganglion cells. The brain understands this code of neural pulses and can translate it into meaningful images.

Blindness is often caused by diseases of the retina that kill the photoreceptors and destroy the associated circuitry, but typically, in these diseases, the retina’s output cells are spared.

Current prosthetics generally work by driving these surviving cells. Electrodes are implanted into a blind patient’s eye, and they stimulate the ganglion cells with current. But this only produces rough visual fields.

Many groups are working to improve performance by placing more stimulators into the patient’s eye. The hope is that with more stimulators, more ganglion cells in the damaged tissue will be activated, and image quality will improve.

Other research teams are testing use of light-sensitive proteins as an alternate way to stimulate the cells. These proteins are introduced into the retina by gene therapy. Once in the eye, they can target many ganglion cells at once.

But Dr. Nirenberg points out that there’s another critical factor. “Not only is it necessary to stimulate large numbers of cells, but they also have to be stimulated with the right code — the code the retina normally uses to communicate with the brain.”

This is what the authors discovered — and what they incorporated into a novel prosthetic system.

Dr. Nirenberg reasoned that any pattern of light falling on to the retina had to be converted into a general code — a set of equations — that turns light patterns into patterns of electrical pulses. Researchers have been trying to find the code that does this for simple stimuli. “We knew it had to be generalizable, so that it could work for anything — faces, landscapes, anything that a person sees,” Dr. Nirenberg says.

In a eureka moment, while working on the code for a different reason, Dr. Nirenberg realized that what she was doing could be directly applied to a prosthetic. She and her student, Dr. Pandarinath, immediately went to work on it. They implemented the mathematical equations on a “chip” and combined it with a mini-projector. The chip, which she calls the “encoder” converts images that come into the eye into streams of electrical impulses, and the mini-projector then converts the electrical impulses into light impulses. These light pulses then drive the light-sensitive proteins, which have been put in the ganglion cells, to send the code on up to the brain.

via News | Weill Cornell Medical College | Cornell University.

Parody of the Last Supper if restored by Celia Gimenez

art-lastsupper-420×0.jpg (JPEG Image, 420 × 258 pixels).

From SMH.COM.AU

Lol.

US teen invents advanced cancer test using Google

Fifteen-year-old high school student Jack Andraka likes to kayak and watch the US television show Glee.

And when time permits, he also likes to do advanced research in one of the most respected cancer laboratories in the world.

Jack Andraka has created a pancreatic cancer test that is 168 times faster and considerably cheaper than the gold standard in the field. He has applied for a patent for his test and is now carrying out further research at Johns Hopkins University in the US city of Baltimore.

And he did it by using Google.

The Maryland native, who won $75,000 at the Intel International Science and Engineering Fair in May for his creation, cites search engines and free online science papers as the tools that allowed him to create the test. …

via BBC News – US teen invents advanced cancer test using Google.

A 15-year-old high school student from Maryland has developed a test to detect pancreatic cancer, the fourth leading cause of death in the United States.

Jack Andraka, a freshman at North County High School, was able to discover a way to diagnose pancreatic cancer before the disease spreads. The young scientist professed a love and passion for science, and these won him the grand prize at the Intel International Science and Engineering Fair for having developed a test that detects early stage pancreatic cancer.

Andraka shared: “I’m really passionate about science. It’s just my thing… I like working on medical research.”

Dr. Anirban Maitra, professor of Pathology, Oncology and Chemical and Biomolecular Engineering at Johns Hopkins School of Medicine, shared that Jack’s creation “detects an abnormal protein that you find in the blood when you have a pancreatic cancer… He conceived this idea and I think the fact that he is 15 makes this whole story more remarkable.”

The young scientist shared: “I got interested in early detection because that’s the best chance of treating the cancer… The only practical way of doing this is through routine blood tests so that’s what I developed here.” The test that he developed is 90 percent accurate, and costs less compared to other tests.

Andraka was awarded at a ceremony in Pittsburgh, and won more than $100,000 in prize money that he intends to use for college. Jane, Jack’s mom, said: “They gave him an opportunity to make his dreams come true.”

via hometestingblog.testcountry.com

2,600-Year-Old Brain Found in England, in Remarkably Fresh Condition

Archeologists working in York in the United Kingdom discovered a remarkably well-preserved human brain that was over 2,500 years old.Found by UK researchers, the brain was found in a decapitated skull aged 2,684 years. The brain is the oldest found brain in Europe or Asia, and is thought to be the best-preserved in the world.

The finding is particularly astonishing because, even when left on a counter in a chilled mortuary facility, brains tend to degrade quickly into liquid. This one, however, had the consistency of tofu, and had none of the distinctive smell so often associated with dead corpses.

Though it is difficult to ascertain cause of death after so many years, the damage to the neck vertebrae was consistent with a hanging. Sonia O’Connor and her colleagues believe that the person was hanged, and then the skull was decapitated.

Interestingly, the way that the body died worked against the preservation of the brain. The separation of the head from the rest of its body would have opened it up to immediate infection from bacteria.

But, because the brain had been preserved in a water-logged pit free of oxygen, either having been placed there or having fallen in, the brain was kept fresh. Other body parts in the same environment may not have been so well-preserved, but due to the brain’s unique properties, it was kept fresh.

Unfortunately, while the brain’s appearance has been kept fresh, the cells and tissues have long died, though that is of course expected under the circumstances.

The brain belonged to a person, probably a man, in his thirties. Though the rest of his body was not located at the site, the head of a deer was.

The skull was found in Heslington, Yorkshire, a suburban village in the northeast portion of England.

via 2,600-Year-Old Brain Found in England, in Remarkably Fresh Condition : US/World : Medical Daily.

Do those dead brain cells still have traces of their living state connections? I wonder if 500 years from now we would be able to transfer this person’s consciousness and re-activate his prehistoric experiences  and memories from the year 588 BC.

Learning 1 of cancer’s tricks

Behaving something like ravenous monsters, tumors need plentiful supplies of cellular building blocks such as amino acids and nucleotides in order to keep growing at a rapid pace and survive under harsh conditions. How such tumors meet these burgeoning demands has not been fully understood. Now chemists at the California Institute of Technology (Caltech) have shown for the first time that a specific sugar, known as GlcNAc (“glick-nack”), plays a key role in keeping the cancerous monsters “fed.” The finding suggests new potential targets for therapeutic intervention.

The new results appear in this week’s issue of the journal Science.

The research team—led by Linda Hsieh-Wilson, professor of chemistry at Caltech—found that tumor cells alter glycosylation, the addition of carbohydrates (in this case GlcNAc) to their proteins, in response to their surroundings. This ultimately helps the cancerous cells survive. When the scientists blocked the addition of GlcNAc to a particular protein in mice, tumor-cell growth was impaired.

The researchers used chemical tools and molecular modeling techniques developed in their laboratory to determine that GlcNAc inhibits a step in glycolysis (not to be confused with glycosylation), a metabolic pathway that involves 10 enzyme-driven steps. In normal cells, glycolysis is a central process that produces high-energy compounds that the cell needs to do work. But Hsieh-Wilson’s team found that when GlcNAc attaches to the enzyme phosphofructokinase 1 (PFK1), it suppresses glycolysis at an early phase and reroutes the products of previous steps into a different pathway—one that yields the nucleotides a tumor needs to grow, as well as molecules that protect tumor cells. So GlcNAc causes tumor cells to make a trade—they produce fewer high-energy compounds in order to get the products they need to grow and survive.

“We have identified a novel molecular mechanism that cancer cells have co-opted in order to produce intermediates that allow them to grow more rapidly and to help them combat oxidative stress,” says Hsieh-Wilson, who is also an investigator with the Howard Hughes Medical Institute.

This is not the first time scientists have identified a mechanism by which tumor cells might produce the intermediates they need to survive. But most other mechanisms have involved genetic alterations, or mutations—permanent changes that lead to less active forms of enzymes, for example. “What’s unique here is that the addition of GlcNAc is dynamic and reversible,” says Hsieh-Wilson. “This allows a cancer cell to more rapidly alter its metabolism depending on the environment that it encounters.”

In their studies, Hsieh-Wilson’s team found that this glycosylation—the addition of GlcNAc to PFK1—is enhanced under conditions associated with tumors, such as low oxygen levels. They also found that glycosylation of PFK1 was sensitive to the availability of nutrients. If certain nutrients were absent, glycosylation was increased, and the tumor was able to compensate for the dearth of nutrients by changing the cell’s metabolism.

When the researchers analyzed human breast and lung tumor tissues, they found GlcNAc-related glycosylation was elevated two- to fourfold in the majority of tumors relative to normal tissue from the same patients. Then, working with mice injected with human lung-cancer cells, the researchers replaced the existing PFK1 enzymes with either the normal PFK1 enzyme or a mutant form that could no longer be glycosylated. The mice with the mutant form of PFK1 showed decreased tumor growth, demonstrating that blocking glycosylation impairs cancerous growth.

The work suggests at least two possible avenues for future investigations into fighting cancer. One would be to develop compounds that prevent PFK1 from becoming glycosylated, similar to the mutant PFK1 enzymes in the present study. The other would be to activate PFK1 enzymes in order to keep glycolysis operating normally and help prevent cancer cells from altering their cellular metabolism in favor of cancerous growth.

via Learning 1 of cancer’s tricks.

Neat research, but it is blind to the big picture that cancer happens for a reason. Cancer acts a protective mechanism when the body’s inflammation response fails. Cancer cells have a purpose: to keep toxins from reaching vital systems. Therefore, the above approaches will only stop cancer from protecting the person and the person will die sooner of whatever triggered the cancer response in the first place.

What you have to do is remove the substance that caused the cancer reaction. It could be many things, but start stopping now. Stop alcohol, processed sugar, artificial sweeteners (aspartame, saccharine, sucralose, acesulfame posttasium), and all foods with sodium nitrite and coal tar dyes.  It won’t be easy because our society is built to protect company profits, not people. If you think, “They wouldn’t be allowed to sell it if it wasn’t safe” you may eventually pay with your life for being naive and gullible.

 

Flat lens offers a perfect image

Applied physicists at the Harvard School of Engineering and Applied Sciences (SEAS) have created an ultrathin, flat lens that focuses light without imparting the distortions of conventional lenses.

At a mere 60 nanometers thick, the flat lens is essentially two-dimensional, yet its focusing power approaches the ultimate physical limit set by the laws of diffraction.

Operating at telecom wavelengths (i.e., the range commonly used in fiber-optic communications), the new device is completely scalable, from near-infrared to terahertz wavelengths, and simple to manufacture. The results have been published online in the journal Nano Letters.

“Our flat lens opens up a new type of technology,” says principal investigator Federico Capasso, Robert L. Wallace Professor of Applied Physics and Vinton Hayes Senior Research Fellow in Electrical Engineering at SEAS. “We’re presenting a new way of making lenses. Instead of creating phase delays as light propagates through the thickness of the material, you can create an instantaneous phase shift right at the surface of the lens. It’s extremely exciting.”

Capasso and his collaborators at SEAS create the flat lens by plating a very thin wafer of silicon with an nanometer-thin layer of gold. Next, they strip away parts of the gold layer to leave behind an array of V-shaped structures, evenly spaced in rows across the surface. When Capasso’s group shines a laser onto the flat lens, these structures act as nanoantennas that capture the incoming light and hold onto it briefly before releasing it again. Those delays, which are precisely tuned across the surface of the lens, change the direction of the light in the same way that a thick glass lens would, with an important distinction.

The flat lens eliminates optical aberrations such as the “fish-eye” effect that results from conventional wide-angle lenses. Astigmatism and coma aberrations also do not occur with the flat lens, so the resulting image or signal is completely accurate and does not require any complex corrective techniques.

The array of nanoantennas, dubbed a “metasurface,” can be tuned for specific wavelengths of light by simply changing the size, angle, and spacing of the antennas.

“In the future we can potentially replace all the bulk components in the majority of optical systems with just flat surfaces,” says lead author Francesco Aieta, a visiting graduate student from the Università Politecnica delle Marche in Italy. “It certainly captures the imagination.”

via Flat lens offers a perfect image — Harvard School of Engineering and Applied Sciences.