Progress on ‘Universal’ Flu Vaccine


The United States is in the grip of a tough flu season, and the current influenza vaccine is only partially effective. However, scientists say they’re getting closer to a “universal” flu shot for the leading strain of the illness — a vaccine that wouldn’t need to be redeveloped and readministered each year.

Trials in mice found that the new shot triggered lasting immunity against influenza A virus strains, which are responsible for up to 90 percent of cases this year.

“Vaccination is the most effective way to prevent deaths from influenza virus, but the virus changes very fast and you have to receive a new vaccination each year,” explained lead researcher Dr. Bao-Zhong Wang. He’s associate professor at the Institute for Biomedical Sciences at Georgia State University.

“We’re trying to develop a new vaccine approach that eliminates the need for vaccination every year,” Wang said in a university news release. “We’re developing a universal influenza vaccine. You wouldn’t need to change the vaccine type every year because it’s universal and can protect against any influenza virus.”

Currently, flu vaccines have to be changed every year to match the flu viruses predicted to be the most common in the upcoming flu season. However, the vaccines miss the mark in some flu seasons.

The experimental vaccine against influenza A targets flu viruses in a different way. As the researchers explained, the typical seasonal flu vaccine is engineered to focus on the microscopic head of the virus’s exterior surface protein. But this part of the flu virus mutates easily, so it’s a “moving target” each year.

The new vaccine goes deeper — aiming at the interior “stalk” of the virus, which is much less quick to change.

“This way you’re protected against different viruses because all influenza viruses share this stalk domain,” Wang said.

Using super-small protein “nanoparticles” to help target the stalk, Wang’s group found that the vaccine shielded mice against a wide range of influenza A viruses, including strains H1N1, H3N2, H5N1 and H7N9.

Of course, much more work needs to be done, since experiments that work in animal studies often don’t pan out in humans. The next step is to test the vaccine in ferrets, which are more similar to humans in terms of their respiratory system, Wang’s group said.

Two flu experts said such a shot is desperately needed.

“Any vaccine technology that can potentially result in a ‘universal’ vaccine is welcome news,” said Dr. Sunil Sood, chair of pediatrics at Southside Hospital in Bay Shore, N.Y.

“A layered protein nanoparticle influenza A vaccine, if ultimately tested in humans, could protect against the majority of influenza viruses that circulate yearly, because A viruses almost always predominate,” he said.

Dr. Marta Feldmesser is chief of infectious disease care at Lenox Hill Hospital in New York City. She expressed cautious optimism for the new research.

“While they demonstrate efficacy in mice, whether humans will respond similarly awaits future demonstration,” Feldmesser said.

Source:  Nature Communications.

Flip the Switch


Changes in fat metabolism may promote prostate cancer metastasis

Prostate tumors tend to be what scientists call “indolent”—so slow-growing and self-contained that many affected men die with prostate cancer, not of it. But for the percentage of men whose prostate tumors metastasize, the disease is invariably fatal.

In a set of papers published in the journals Nature Genetics and Nature Communications, researchers at Harvard Medical School and the Cancer Center at Beth Israel Deaconess Medical Center have shed new light on the genetic mechanisms that promote metastasis in a mouse model and implicated the typical Western high-fat diet as a key environmental factor driving metastasis.

“Although it is widely postulated that a Western diet can promote prostate cancer progression, direct evidence supporting a strong association between dietary lipids and prostate cancer has been lacking,” said first author Ming Chen, HMS research fellow in medicine in the laboratory of Pier Paolo Pandolfi, the HMS George C. Reisman Professor of Medicine at Beth Israel Deaconess.

Epidemiological data links dietary fats (and obesity) to many types of cancer, and rates of cancer deaths from metastatic cancers including prostate cancer are much higher in the United States than in nations where lower fat diets are more common. While prostate cancer affects about 10 percent of men in Asian nations, that rate climbs to about 40 percent when they immigrate to the U.S., mirroring the rates among the native-born U.S. population. That points to an environmental culprit that may work in concert with genetic factors to drive this aggressive, fatal disease.

“The progression of cancer to the metastatic stage represents a pivotal event that influences patient outcomes and the therapeutic options available to patients,” said senior author Pandolfi, who is also director of the Cancer Center and the Cancer Research Institute at Beth Israel Deaconess. “Our data provide a strong genetic foundation for the mechanisms underlying metastatic progression, and we also demonstrated how environmental factors can boost these mechanisms to promote progression from primary to advanced metastatic cancer.”

The tumor suppressor gene PTEN is known to play a major role in prostate cancer; its partial loss occurs in up to 70 percent of primary prostate tumors. Its complete loss is linked to metastatic prostate disease, but animal studies suggest the loss of PTEN alone is not enough to trigger progression. Pandolfi and colleagues sought to identify an additional tumor suppressing gene or pathway that may work in concert with PTEN to drive metastasis.

Looking at recent genomic data, Pandolfi and colleagues noticed that another tumor suppressor gene, PML, tended to be present in localized (nonmetastatic) prostate tumors but was absent in about a third of metastatic prostate tumors. Moreover, about 20 percent of metastatic prostate tumors lack both PML and PTEN.

When they compared the two types of tumor—the localized ones lacking only the PTEN gene versus the metastatic tumors lacking both genes—the researchers found that the metastatic tumors produced huge amounts of lipids, or fats. In tumors that lacked both PTEN and PML tumor suppressing genes, the cells’ fat-production machinery was running amok.

“It was as though we’d found the tumors’ lipogenic, or fat production, switch,” said Pandolfi. “The implication is, if there’s a switch, maybe there’s a drug with which we can block this switch and maybe we can prevent metastasis or even cure metastatic prostate cancer,” he added.

Such a drug already exists. Discovered in 2009, a molecule named “fatostatin” is currently being investigated for the treatment of obesity. Pandolfi and colleagues tested the molecule in lab mice. “The obesity drug blocked the lipogenesis fantastically, and the tumors regressed and didn’t metastasize.”

In addition to opening the door to new treatment for metastatic prostate cancer, these findings also helped solve a long-standing scientific puzzle. For years, researchers had difficulty modeling metastatic prostate cancer in mice, making it hard to study the disease in the lab. Some speculated that mice simply weren’t a good model for this particular disease. But the lipid-production finding raised a question in Pandolfi’s mind.

“I asked, ‘What do our mice eat?’” Pandolfi recalled.

It turned out the mice ate a vegetable-based chow, essentially a low-fat vegan diet that bore little resemblance to that of the average American male. When Pandolfi and colleagues increased the levels of saturated fats, the kind found in fast food cheeseburgers and fries, in the animals’ diet, the mice developed aggressive, metastatic tumors.

The findings could result in more accurate and predictive mouse models for metastatic prostate cancer, which in turn could accelerate discovery of better therapies for the disease. Additionally, physicians could soon be able to screen their early-stage prostate cancer patients for those whose tumors lack both PTEN and PML tumor suppressing genes, putting them at increased risk for progressing to metastatic disease. These patients may be helped by starving these tumors of fat either with the fat-blocking drug or through diet.

“The data are tremendously actionable, and they surely will convince you to change your lifestyle,” Pandolfi said.

Stem Cells Of Type 1 Diabetes Patients Transformed Into Insulin-Secreting Beta Cells; Research May Lead To New Therapy


For those living with Type 1 diabetes, the condition is a part of daily life. Insulin shots, blood sugar monitoring, and carb counting become routine, and patients expect them to stay so for the rest of their lives. This form of diabetes currently has no cure, something researchers have been diligently trying to change.The most recent attempt to take down diabetes comes from researchers at Washington University School of Medicine in St. Louis and Harvard University, who have managed to change stem cells derived from diabetes patients into insulin–secreting cells.

cells

cellsStem cell-derived beta cells (blue) are capable of producing insulin (green) when they come into contact with glucose. 

Patients with Type 1 diabetes lack the ability to create their own insulin, meaning they rely on regular injections of the hormone to control blood sugar. The study hints at a possible new therapy for patients that relies on a personalized approach — using the patients’ own cells to create new ones capable of manufacturing the insulin they need. The research, published in Nature Communications, details new cells that produce insulin when they encounter sugar in both culture and mouse trials.

“In theory, if we could replace the damaged cells in these individuals with new pancreatic beta cells — whose primary function is to store and release insulin to control blood glucose — patients with type 1 diabetes wouldn’t need insulin shots anymore,” said Dr. Jeffery R. Millman, an assistant professor of medicine and biomedical engineering at Washington university and first author of the study, in a press release. “The cells we manufactured sense the presence of glucose and secrete insulin in response. And beta cells do a much better job controlling blood sugar than diabetic patients can.”

Millman had conducted previous studies involving the creation of beta cells derived from people who did not suffer from diabetes. In the new experiment, however, the stem cells used come from the skin of Type 1 diabetes patients.

“There had been questions about whether we could make these cells from people with type 1 diabetes,” MIllman said. “Some scientists thought that because the tissue would be coming from diabetes patients, there might be defects to prevent us from helping stem cells differentiate into beta cells. It turns out that’s not the case.”

The idea of replacing beta cells is actually more than two decades old, originating with Washington university researchers Dr. Paul E. Lacy and David W. Sharp, who began transplanting such cells into Type 1 diabetes patients. Today, there has been some success with beta cell transplants, but these cells come from pancreas tissue provided by organ donors. As with all donated types of tissues, cells, and organs, the supply falls short of the demand. The new technique would solve this problem, but Millman said scientists need to conduct more research to make sure the new cells don’t cause tumor development — a problem that has cropped up in many types of stem cell research. There has been no evidence of tumors so far in the mice, though, even up to a year after cell implantation.

Millman predicts the stem cell-derived beta cells could be ready for testing in humans in three to five years. This process would consist of implanting the cells under the skin of diabetes patients, a minimally invasive procedure that would give the cells access to a the patient’s blood supply.

“What we’re envisioning is an outpatient procedure in which some sort of device filled with the cells would be placed just beneath the skin,” he said.

Millman said that the technique could, in the future, even be used to help those with Type 2 diabetes, neonatal diabetes, and Wolfram syndrome.

Source: Millman J, Xie C, Van Dervort A, Gurtler M, Pagliuca F, Melton D. Generation of Stem Cell-derived B-cells from Patients with Type 1 Diabetes. Nature Communications. May 10, 2016.

After 100 years of debate, hitting absolute zero has been declared mathematically impossible.


The third law of thermodynamics finally gets its proof.

After more than 100 years of debate featuring the likes of Einstein himself, physicists have finally offered up mathematical proof of the third law of thermodynamics, which states that a temperature of absolute zero cannot be physically achieved because it’s impossible for the entropy (or disorder) of a system to hit zero.

While scientists have long suspected that there’s an intrinsic ‘speed limit’ on the act of cooling in our Universe that prevents us from ever achieving absolute zero (0 Kelvin, -273.15°C, or -459.67°F), this is the strongest evidence yet that our current laws of physics hold true when it comes to the lowest possible temperature.

 “We show that you can’t actually cool a system to absolute zero with a finite amount of resources and we went a step further,” one of the team, Lluis Masanes from University College London, told IFLScience.

“We then conclude that it is impossible to cool a system to absolute zero in a finite time, and we established a relation between time and the lowest possible temperature. It’s the speed of cooling.”

What Masanes is referring to here are two fundamental assumptions that the third law of thermodynamics depends on for its validity.

The first is that in order to achieve absolute zero in a physical system, the system’s entropy has to also hit zero.

The second rule is known as the unattainability principle, which states that absolute zero is physically unreachable because no system can reach zero entropy.

The first rule was proposed by German chemist Walther Nernst in 1906, and while it earned him a Nobel Prize in Chemistry, heavyweights like Albert Einstein and Max Planck weren’t convinced by his proof, and came up with their own versions of the cooling limit of the Universe.

 This prompted Nernst to double down on his thinking and propose the second rule in 1912, declaring absolute zero to be physically impossible.

Together, these rules are now acknowledged as the third law of thermodynamics, and while this law appears to hold true, its foundations have always seemed a little rocky – when it comes to the laws of thermodynamics, the third one has been a bit of a black sheep.

“[B]ecause earlier arguments focused only on specific mechanisms or were crippled by questionable assumptions, some physicists have always remained unconvinced of its validity,” Leah Crane explains for New Scientist.

In order to test how robust the assumptions of the third law of thermodynamics actually are in both classical and quantum systems, Masanes and his colleague Jonathan Oppenheim decided to test if it is mathematically possible to reach absolute zero when restricted to finite time and resources.

Masanes compares this act of cooling to computation – we can watch a computer solve an algorithm and record how long it takes, and in the same way, we can actually calculate how long it takes for a system to be cooled to its theoretical limit because of the steps required to remove its heat.

You can think of cooling as effectively ‘shovelling’ out the existing heat in a system and depositing it into the surrounding environment.

How much heat the system started with will determine how many steps it will take for you to shovel it all out, and the size of the ‘reservoir’ into which that heat is being deposited will also limit your cooling ability.

Using mathematical techniques derived from quantum information theory – something that Einstein had pushed for in his own formulations of the third law of thermodynamics – Masanes and Oppenheim found that you could only reach absolute zero if you had both infinite steps and an infinite reservoir.

And that’s not exactly something any of us are going to get our hands on any time soon.

This is something that physicists have long suspected, because the second law of thermodynamics states that heat will spontaneously move from a warmer system to a cooler system, so the object you’re trying to cool down will constantly be taking in heat from its surroundings.

And when there’s any amount of heat within an object, that means there’s thermal motion inside, which ensures some degree of entropy will always remain.

This explains why, no matter where you look, every single thing in the Universe is moving ever so slightly – nothing in existence is completely still according to the third law of thermodynamics.

The researchers say they “hope the present work puts the third law on a footing more in line with those of the other laws of thermodynamics”, while at the same time presenting the fastest theoretical rate at which we can actually cool something down.

In other words, they’ve used maths to quantify the steps of cooling, allowing researchers to define set speed limit for how cold a system can get in a finite amount of time.

And that’s important, because even if we can never reach absolute zero, we can get pretty damn close, as NASA demonstrated recently with its Cold Atom Laboratory, which can hit a mere billionth of a degree above absolute zero, or 100 million times colder than the depths of space.

At these kinds of temperatures, we’ll be able to see strange atomic behaviours that have never been witnessed before. And being able to remove as much heat from a system is going to be crucial in the race to finally build a functional quantum computer.

And the best part is, while this study has taken absolute zero off the table for good, no one has even gotten close to reaching the temperatures or cooling speeds that it’s set as the physical limits – despite some impressive efforts of late.

“The work is important – the third law is one of the fundamental issues of contemporary physics,” Ronnie Kosloff at the Hebrew University of Jerusalem, Israel who was not involved in the study, told New Scientist.

“It relates thermodynamics, quantum mechanics, information theory – it’s a meeting point of many things.”

Source: Nature Communications.

Motherless babies possible as scientists create live offspring without need for female egg


A mouse embryo is fertilised
A mouse embryo is fertilised in the University of Bath experiment

Motherless babies could be on the horizon after scientists discovered a method of creating offspring without the need for a female egg.

The landmark experiment by the University of Bath rewrites 200 years of biology teaching and could pave the way for a baby to be born from the DNA of two men.

It was always thought that only a female egg could spark the changes in a sperm required to make a baby, because an egg forms from a special kind of cell division in which just half the number of chromosomes are carried over.

 Imagine that you could take skin cells and make embryos from them. This would have all kinds of utility.Dr Tony Perry, University of Bath

Sperm cells form in the same way, so that when a sperm and egg meet they form a full genetic quota, with half our DNA coming from our mother and half from our father.

But now scientists have shown embryoscould be created from cells which carry all their chromosomes which means that, in theory, any cell in the human body could be fertilised by a sperm.

Three generations of mice have already been created using the technique and are fit and healthy and now researchers are planning to test out the theory using skin cells.

Scientists now want to test whether the same result could be achieved using skin cells 
Scientists now want to test whether the same result could be achieved using skin cells 

Dr Tony Perry, a molecular embryologist and senior author of the study, said: “Some people say start the day with an egg, but what this paper says is that you don’t necessarily have to start development with one.

“It has been thought that only an egg cell was capable of reprogramming sperm to allow embryonic development to take place.

“Our work challenges that dogma, held since early embryologists first observed mammalian eggs in around 1827 and observed fertilisation 50 years later, that only an egg cell fertilised with a sperm cell can result in a live mammalian birth.

“We’re talking about different ways of making embryos. Imagine that you could take skin cells and make embryos from them. This would have all kinds of utility.”

For the initial experiments, scientists “tricked” an egg into developing into an embryo using special chemicals which makes the egg think it has been fertilised. Crucially the cells in an embryo copy themselves completely when they divide, and so mirror closely most other cells in the body, such as skin cells.

When scientists injected the embryos with sperm, they grew into healthy mice which went on to produce their own litters.

The fertilised non-egg cell developed into an embryo in the same way as a normal egg cell 
The fertilised non-egg cell developed into an embryo in the same way as a normal egg cell 

Although the researchers began with an egg cell for the experiment, they do not believe it is required to spark the same development. In theory, the technique should work with any cell in the body as long as half the chromosomes are removed first to allow them to fuse with the sperm’s chromosomes.

Professor Robin Lovell-Badge, group leader at The Francis Crick Institute, said: “I’m not surprised that the authors are excited about this. I think it is a very interesting paper, and a technical tour de force.

“And I am sure it will tell us something important about reprogramming at these early steps of development that are relevant to fertilisation – and perhaps more broadly about reprogramming of cell fate in other situations.

“It doesn’t yet tell us how, but the paper gives a number of clear pointers.”

The technique raises the possibility that gay men, for instance, could have a child whose DNA was half of each of the couple, although a woman would still need to act as a surrogate to carry the baby.

It also raises the possibility that a man could even fertilise his own cells to produce offspring containing a mixture of genes inherited from him and his parents.

More realistically, the technique could allow women whose fertility has been wiped out by cancer drugs or radiotherapy to have their own children.

While eggs can be frozen before cancer therapy and later fertilised in an IVF clinic, currently nothing can be done once they have been lost.  It may also help women to continue having children later in life. Women are born with all their eggs and they degrade with age, which makes conception more difficult in later life. But if it was possible to fertilise a new skin cell, it could improve the chance of having a baby.

Conception using sperm and non-egg cells could also aid the preservation of endangered species, since it avoids the need to recover eggs.

In the study, 30 mouse pups were born with a success rate of 24 per cent. This compares with a 1 per cent to 2 per cent  success rate for offspring created by the Dolly the Sheep method of cloning by transferring DNA to donated eggs.

Some of the mice went on to have offspring themselves, and a number had offspring that went on to have their own pups. Fertility is generally seen as a sign of fitness and good health.

Dr Perry said that his team was planning to take the next step of attempting to produce live offspring from ordinary non-egg cells, such as skin cells.

Mouse pups were healthy and went on to produce their own offspring 
Mouse pups in the experiment were healthy and went on to produce their own offspring 

Dr Paul Colville-Nash, from the Medical Research Council, which funded the study, said: “This is an exciting piece of research which may help us to understand more about how human life begins and what controls the viability of embryos, mechanisms which may be important in fertility.

“It may one day even have implications for how we treat infertility, though that’s probably still a long way off.”

Source: Nature Communications.

Drug discovery for GPCR signalling made easy by IIT Kanpur.


 

Discovering new drugs that bind to G Protein-Coupled Receptors (GPCRs), which are central to almost every physiological process in our body such as vision, taste, immune response and cardiovascular regulation, has become easier, thanks to research by a team led by Dr. Arun K. Shukla from the Department of Biological Sciences and Bioengineering, Indian Institute of Technology (IIT) Kanpur.

Nearly 50 per cent of prescription drugs currently available in the market for the treatment of blood pressure, heart failure, diabetes, obesity, cancer and many other human diseases target GPCR receptors. All these drugs bind to their respective receptors and either activate or stop their signalling. The work by Dr. Shukla’s team has shown that the regulation of these receptors by these drugs can be simpler than generally thought — it can be mediated by engaging only the end of the receptor, which is called the tail of the receptor.

The results were published in the journal Nature Communications.

 Receptors found on the cell surface receive signals and transmit them to inside the cells. A part of the receptor is embedded in the cell membrane and the other part protrudes outside the membrane and inside of the cell. The part of the receptor that protrudes outside the membrane changes its shape whenever a stimulus in the body binds to itm. In response to this change in the outside part of the receptor, a corresponding change happens in the shape of the receptor that is positioned inside the cell. This change in the shape of the receptor positioned inside the cell allows it bind to other proteins called effectors. These effectors cause specific effects in the cell, referred to as cell signalling, which leads to physiological changes in our body.

For example, a hormone in the blood called angiotensin binds to its receptor and activates the effector protein inside the cell causing an increase in blood pressure.

The mechanism

In people with normal blood pressure, a specific type of proteins called arrestins, which are effector proteins of GPCRs, bind to the receptor and pull it inside the cell (a process called receptor endocytosis). This prevents the angiotensin from binding to the receptor, thereby help in controlling the blood pressure.

In the case of people with high blood pressure, the prescribed drug binds to the receptor. So even if angiotensin is present on the surface of the cell, it cannot bind to the receptor and start the signalling process that increases blood pressure.

New approach

“We were interested in understanding how different receptors interact with effectors and how the receptors recognise the stimuli,” says Dr. Shukla. “We looked at the interaction of a receptor, which is a target for heart failure drugs, with its specific effectors, namely arrestins. When arrestins bind to the receptor, they arrest or disrupt the receptor signalling.”

“The text book understanding is that arrestins have to simultaneously bind at two sites — the tail of the receptor and the core of the receptor — for the drug to become effective in pulling the receptor inside the cell [to prevent the stimuli from binding to the receptor and start signalling],” says Dr. Shukla.

“Through specific engineering of the receptor we basically disrupted one of the two binding sites, namely the core of receptor. We found that even without the second site, the arrestin was able to pull the receptor inside the cell by binding just to the tail of the receptor [which is the other binding site],” he says.

There is a key region in the core which the team genetically deleted thereby making the core of the receptor ineffective.

“Whenever researchers are designing a drug to stop GPCR signalling, they look for a drug that simultaneously triggers the binding of arrestins to both the sites in the receptor. Our work changes the way people will look at drug discovery for GPCR signalling,” he says. “The drug has to trigger binding of arrestin to just at the tail of the receptor to arrest the signalling. Researchers can now design simple drugs to accomplish this.”

Study maps brain’s ageing connections


brain
Human Brain Project

Brain connections that play a key role in complex thinking skills show the poorest health with advancing age, new research suggests.

 Connections supporting functions such as movement and hearing are relatively well preserved in later life, the findings show.

Scientists carrying out the most comprehensive study to date on ageing and the brain’s connections charted subtle ways in which the brain’s connections weaken with age.

Knowing how and where connections between brain cells – so-called white matter – decline as we age is important in understanding why some people’s brains and thinking skills age better than others.

Worsening as we age contribute to a decline in , such as reasoning, memory and speed of thinking.

Researchers from the University of Edinburgh analysed brain scans from more than 3,500 people aged between 45 and 75 taking part in the UK Biobank study.

Researchers say the data will provide more valuable insights into healthy brain and mental ageing, as well as making contributions to understanding a range of diseases and conditions.

The study was published in Nature Communications journal.

Dr Simon Cox, of the University of Edinburgh’s Centre for Cognitive Ageing and Cognitive Epidemiology (CCACE), who led the study, said: “By precisely mapping which connections of the brain are most sensitive to age, and comparing different ways of measuring them, we hope to provide a reference point for future brain research in health and disease.

“This is only one of the first of many exciting brain imaging results still to come from this important national health resource.”

Professor Ian Deary, Director of CCACE, said: “Until recently, studies of with this number of people were not possible. Day by day the UK Biobank sample grows, and this will make it possible to look carefully at the environmental and genetic factors that are associated with more or less healthy brains in older age.”

Professor Paul Matthews of Imperial College London, Chair of the UK Biobank Expert Working Group, who was not involved in the study, said: “This report provides an early example of the impact that early opening of the growing UK Biobank Imaging Enhancement database for access by researchers world-wide will have.

“The large numbers of subjects in the database has enabled the group to rapidly characterise the ways in which the changes with age – and to do so with the confidence that large numbers of observations allow.

“This study highlights the feasibility of defining what is typical, to inform the development of quantitative MRI measures for decision making in the clinic.”

Scientists Harness Crystals to Create Clean Energy Solution


Hematite, once regarded as a powerful tool by ancient shamans, and then disregarded as anything other than a shiny (and often magnetic) rock for many, many years, has once again been realized for its value in cultivating energy by modern scientists. For many years, scientists have struggled to find an efficient method to split water to mine electron-rich hydrogen for clean energy. It had always been found that Hematite could work, but its low performance stopped it from being a solution to clean energy… until now. By re-growing the minerals surface, a smoother version of hematite doubled the electrical yield, which then opened the door to harvesting energy using artificial photosynthesis. This was all published only in the last week in the journal Nature Communications. hemetiteformula

By simply smoothing the surface characteristics of hematite, this close cousin of rust can be improved to couple with silicon, which is derived from sand, to achieve complete water splitting for solar hydrogen generation,’ said Wang, whose research focuses on discovering new methods to generate clean energy. ‘This unassisted water splitting, which is very rare, does not require expensive or scarce resources.’

 

‘Upon running the tests, they immediately saw a dramatic improvement in voltage, as well as an increase of photovoltage from .24 volts to .80 volts, which was a dramatic increase in the amount of power generated than ever before seen!
The team described that with some more modifications, this hematite-silicon method of splitting water would be easily amenable to large scale utilization!Ematite508Not to mention, the re-growth technique might also be usable on other materials. Hematite may not be the only crystal that can do this, and if so, there are a lot of possibilities for this technology in the future.

‘This offers new hope that efficient and inexpensive solar fuel production by readily available natural resources is within reach,’ said Wang. ‘Getting there will contribute to a sustainable future powered by renewable energy.’

 

This Fake Skin Allows Prosthetic Hands To Feel Heat, Humidity, And Pressure


Prosthetic hand

In a new study, researchers used a flexible material made of nanoribbons to create fake skin, which is able to decipher between hot and cold, wet and dry, and levels of pressure. 

Amputees may soon be able to feel and touch things again even without their limb: scientists have developed artificial skin that is able to detect pressure, temperature, and humidity, making prosthetic limbs far more realistic than in the past.

Currently, certain prosthetic limbs are able to be controlled by an amputee’s thoughts, which is quite remarkable in itself. But the artificial skin may be the next step in making a prosthetic truly an extension of the body. The stretchy material the researchers created, which acts as the “skin,” even has a built-in heater to make it feel like real flesh. Ultimately, the researchers hope, the fake skin will be able to interlock with the patient’s nerves so they can feel what it touches.

“The prosthetic hand and laminated electronic skin could encounter many complex operations such as hand shaking, keyboard tapping, ball grasping, holding a cup of hot or cold drink, touching dry or wet surfaces and human to human contact,” the authors wrote in theirstudy, which was published in Nature Communications.

The artificial skin was developed using a silicone material that is stretchy and transparent. It’s called polydimethylsilozane (PDMS), and it contains silicon nanoribbons that are able to generate electricity when they’re touched or stretched — and are able to detect whether something is warm or cold. In order to test the humidity sensors in the skin, which were able to distinguish between wet and dry, the researchers had the prosthetic hand touch a variety of wet and dry diapers. It was able to successfully sense whether they were wet or dry — something that might prove useful in the future for busy parents.

The researchers were smart in the way they designed the skin and how it wraps around the prosthetic hand. For smaller areas that should be highly sensitive, such as the fingertips, they packed the nanoribbons tightly to increase the amount of sensitivity to touch. Around the wrist, which requires more flexibility in movement, the researchers allowed the nanoribbons to loop around and give room for expansion.

Recreating sense of touch for amputees is, in essence, a notion that involves cheating the brain. Dustin Tyler, a bioengineer at Case Western Reserve University and the author of a previous study that examined creating fake touch through prosthetics, led a study that was able to create sensations artificially. “If we get it correct, the brain interprets it that it’s coming from the hand in the first place,” Tyler said. “The brain doesn’t know we cheated it.”

Though researchers like Tyler have developed “feeling” hands in the past, this is the first time using the stretchy material. “Recent efforts to develop smart prosthetics, which exploit rigid and/or semi-flexible pressure, strain and temperature sensors, provide promising routes for sensor-laden bionic systems, but with limited stretchability, detection range and spatio-temporal resolution,” the authors write in the Abstract. “Here we demonstrate smart prosthetic skin instrumented with ultrathin, single crystalline silicon nanoribbon strain, pressure and temperature sensory arrays as well as associated humidity sensors, electroresistive heaters and stretchable multi-electrode arrays for nerve stimulation.”

It will be some time before the researchers are able to create a connection between the prosthetic skin and the brain in order to let amputees themselves feel its sensations. But it provides hope for those who previously could only have a robotic extension as a prosthetic, rather than a sensitive, feeling, and touching one. “This collection of stretchable sensors and actuators facilitate highly localized mechanical and thermal skin-like perception in response to external stimuli, thus providing unique opportunities for emerging classes of prostheses and peripheral nervous system interface technologies,” the authors write.

Source: Kim J, Lee M, Shim H, Ghaffari R, Cho Hye, Son D. “Stretchable silicon nanoribbon electronics for skin prosthesis.” Nature Communications, 2014.

New hologram technology created with tiny nanoantennas.


Researchers have created tiny holograms using a “metasurface” capable of the ultra-efficient control of light, representing a potential new technology for advanced sensors, high-resolution displays and information processing.

The metasurface, thousands of V-shaped nanoantennas formed into an ultrathin gold foil, could make possible “planar photonics” devices and optical switches small enough to be integrated into computer chips for information processing, sensing and telecommunications, said Alexander Kildishev, associate research professor of electrical and computer engineering at Purdue University.

Laser light shines through the nanoantennas, creating the hologram 10 microns above the metasurface. To demonstrate the technology, researchers created a hologram of the word PURDUE smaller than 100 microns wide, or roughly the width of a human hair.

“If we can shape characters, we can shape different types of light beams for sensing or recording, or, for example, pixels for 3-D displays. Another potential application is the transmission and processing of data inside chips for information technology,” Kildishev said. “The smallest features – the strokes of the letters – displayed in our experiment are only 1 micron wide. This is a quite remarkable spatial resolution.”

holograms with laser lights
Laser light shines through the metasurface from below, creating a hologram 10 microns above the structure. (Xingjie Ni, Birck Nanotechnology Center)

Findings are detailed in a research paper appearing on Friday (Nov. 15) in the journal Nature Communications.

Metasurfaces could make it possible to use single photons – the particles that make up light – for switching and routing in future computers. While using photons would dramatically speed up computers and telecommunications, conventional photonic devices cannot be miniaturized because the wavelength of light is too large to fit in tiny components needed for integrated circuits.

Nanostructured metamaterials, however, are making it possible to reduce the wavelength of light, allowing the creation of new types of nanophotonic devices, said Vladimir M. Shalaev, scientific director of nanophotonics at Purdue’s Birck Nanotechnology Center and a distinguished professor of electrical and computer engineering.

“The most important thing is that we can do this with a very thin layer, only 30 nanometers, and this is unprecedented,” Shalaev said. “This means you can start to embed it in electronics, to marry it with electronics.”

The layer is about 1/23rd the width of the wavelength of light used to create the holograms.

The Nature Communications article was co-authored by former Purdue doctoral student Xingjie Ni, who is now a postdoctoral researcher at the University of California, Berkeley; Kildishev; and Shalaev.

Under development for about 15 years, metamaterials owe their unusual potential to precision design on the scale of nanometers. Optical nanophotonic circuits might harness clouds of electrons called “surface plasmons” to manipulate and control the routing of light in devices too tiny for conventional lasers.

The researchers have shown how to control the intensity and phase, or timing, of laser light as it passes through the nanoantennas. Each antenna has its own “phase delay” – how much light is slowed as it passes through the structure. Controlling the intensity and phase is essential for creating working devices and can be achieved by altering the V-shaped antennas.

The work is partially supported by U.S. Air Force Office of Scientific Research, Army research Office, and the National Science Foundation. Purdue has filed a provisional patent application on the concept.

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