Tech

Perfumes that use the most popular scents do not always obtain the highest number of ratings, according to an analysis of online perfume reviews.

A study of 10,000 perfumes and their online ratings reveals which odours are likely to bring success, with some surprising combinations providing a boost to ratings.

Perfumes are described in terms of 'notes', which can be single odour ingredients, such as vanilla, musk or jasmine, as well as more generic smells like 'floral notes'. Perfume smell is then described in terms of a combination of these notes. Combinations of several notes that are commonly used in perfumes are called 'accords'.

Now, Vaiva Vasiliauskaite and Dr Tim Evans from the Department of Physics at Imperial College London have used complex network analysis to determine the most popular notes and accords. They studied 1,000 notes in over 10,000 perfumes and their success in online shops. Their study is published today in the open-access journal PLOS ONE.

They found that some notes and accords are 'over-represented' in the dataset, meaning they appear more often than by chance, but that these are not necessarily the ones that are present in perfumes with the highest number of ratings.

While some common accords, like lavender and geranium, are often present in 'successful' perfumes, some less-common notes and accords have an even stronger link with perfume popularity, for example jasmine plus mint, or musk plus vetiver and vanilla.

The researchers say this could be a new avenue for perfumers to discover scent combinations that are likely to be successful but are not yet widespread.

Vaiva said: "Our work provides insights into factors that play a role in the success of perfumes. It also sets up a framework for a statistical analysis of fragrances based on simple properties and customer reviews. It could be a beneficial tool for systematic ingredient selection and act as an artificial 'Nose' - a traditional craft-master of perfumery."

The team acknowledge that brand influences perfume popularity but found no correlation between perfume price or time since release and success. The smell itself did have a large relation to perfume success.

Their mathematical analysis also allowed them to determine which notes had particularly high 'enhancement' effects - those that played a significant role in improving the rating of the accord they were added to. The best enhancers tended to be generic notes, such as `floral notes', or were well represented in the database, such as musk or vanilla.

The Global Precipitation Measurement mission or GPM core satellite passed over the storm and measured the rate in which rain was falling throughout it.

The GPM core satellite passed over Hurricane Barbara at 3:21 a.m. EDT (0721 UTC) on July 3, 2019. GPM found the heaviest rainfall rates were occurring around the eye. There, rain was falling at a rate of more than 50 mm (2 inches) per hour. GPM is a joint mission between NASA and the Japan Aerospace Exploration Agency, JAXA.

NOAA's National Hurricane Center noted at 4 a.m. EDT (0900 UTC), the eye of Hurricane Barbara was located near latitude 13.5 degrees North and longitude 125.6 degrees West.  Barbara is moving toward the west-northwest near 14 mph (22 kph).

Barbara is about 1,995 miles (3,210 km) east of Hilo, Hawaii. A motion toward the west-northwest or northwest, but at a slightly slower forward speed, is expected Wednesday through Friday.

Maximum sustained winds remain near 155 mph (250 kph) with higher gusts.  Barbara is a category 4 hurricane on the Saffir-Simpson Hurricane Wind Scale.  Gradual weakening is expected on Wednesday, followed by faster weakening on Thursday and Friday. Barbara is forecast to weaken to a tropical storm some time on Friday.

Hurricane-force winds extend outward up to 45 miles (75 km) from the center, and tropical-storm-force winds extend outward up to 185 miles (295 km). The estimated minimum central pressure is 933 mb (27.55 inches).

A joint Australian-Indian 18-year study made possible by the recruitment, diagnosis, and the DNA screening of thousands of people in India has identified a new clue in the quest for causes of schizophrenia, and for potential treatments.

A collaboration between The University of Queensland (UQ) and a team of Indian researchers led by Professor Rangaswamy Thara, co- founder and director of the Schizophrenia Research Foundation in Chennai, searched the genomes of more than 3000 individuals and found those with schizophrenia were more likely to have a particular genetic variation.

Professor Bryan Mowry from UQ's Queensland Brain Institute (QBI) said such studies had predominantly been done in populations with European ancestry, with more than 100 schizophrenia-associated variants identified previously.

“Looking at other populations can highlight different parts of the genome with a more robust association with the disease,” Professor Mowry said.

“This study identified a gene called NAPRT1 that encodes an enzyme involved in vitamin B3 metabolism—we were also able to find this gene in a large genomic dataset of schizophrenia patients with European ancestry.

“When we knocked out the NAPRT1 gene in zebrafish, brain development of the fish was impaired—we are now working to understand more deeply how this gene functions in the brain.”

"The zebrafish brain failed to divide symmetrically which is significant, because MRI studies in people with schizophrenia have shown defects in the corpus callosum - the bridge between the left and right sides of the brain."

Professor Mowry said that much of the variation in schizophrenia, which occurred in about one per cent of the population, was due to genetic factors.

“Schizophrenia strikes at the heart of what it means to be human— it has devastating impacts on the sufferer and their ability to function.

“Our studies aim to shed more light on what makes people susceptible to schizophrenia and developing better treatments for the future,” he said.

“There are now a multitude of genetic variants linked to schizophrenia, but we don’t yet know what the hundreds of genes involved do.

“The next phase is to study their function in normal and diseased states using computational approaches and animal models, such as the zebrafish.

“We’d like to look further into populations in India, to increase our sample size to see if we can replicate this result and discover additional variants that might be involved.”

Professor Mowry and Professor Thara met in the late 1990s when they discussed studying a population in India—both are practicing psychiatrists and see first-hand the impact of schizophrenia on patients’ lives, their families and communities.

“Professor Thara is a driving force for research into schizophrenia in India, and her team in Chennai has been central in recruiting patients while QBI has been able to fund the processing of blood samples they’ve collected,” Professor Mowry said.

QBI’s Director, Professor Pankaj Sah, commended the collaborative effort of the team, which included Schizophrenia Research Foundation (SCARF) joint director Sujit John, who co-ordinated the recruitment of study participants, and QBI’s Dr Sathish Periyasamy, who analysed the data.

A study by Stanford University School of Medicine investigators has revealed that immune cells infiltrate the rare newborn nerve-cell nurseries of the aging brain. There's every reason to think those interlopers are up to no good. Experiments in a dish and in living animals indicate they're secreting a substance that chokes off new nerve cell production.

While most of the experiments in the study were carried out in mice, the central finding -- the invasion, by immune cells called killer T cells, of neurogenic niches (specialized spots in the brain where new nerve cells, or neurons, are generated) -- was corroborated in tissue excised from autopsied human brains.

The findings could accelerate progress in hunting down the molecules in the body that promote the common deterioration of brain function in older individuals and in finding treatments that might stall or even reverse that deterioration. They also signify a crack in the wall of dogma that's deemed the healthy brain impervious to invasion by the body's immune cells, whose unbridled access to the organ could cause damage.

"The textbooks say that immune cells can't easily get into the healthy brain, and that's largely true," said Anne Brunet, PhD, professor of genetics and senior author of the study. "But we've shown that not only do they get into otherwise healthy aging brains -- including human brains -- but they reach the very part of the brain where new neurons arise."

Lead authorship of the study, to be published online July 3 in Nature, is shared by medical student Ben Dulken, PhD, graduate student Matthew Buckley and postdoctoral scholar Paloma Navarro Negredo, PhD.

The cells that aid memory

Many a spot in a young mammal's brain is bursting with brand new neurons. But for the most part, those neurons have to last a lifetime. Older mammals' brains retain only a couple of neurogenic niches, consisting of several cell types whose mix is critical for supporting neural stem cells that can both differentiate into neurons and generate more of themselves. New neurons spawned in these niches are considered essential to forming new memories and to learning, as well as to odor discrimination.

In order to learn more about the composition of the neurogenic niche, the Stanford researchers catalogued, one cell at a time, the activation levels of the genes in each of nearly 15,000 cells extracted from the subventricular zone (a neurogenic niche found in mice and human brains) of healthy 3-month-old mice and healthy 28- or 29-month-old mice.

This high-resolution, single-cell analysis allowed the scientists to characterize each cell they looked at and see what activities it was engaged in. Their analysis confirmed the presence of nine familiar cell types known to compose the neurogenic niche. But when Brunet and her colleagues compared their observations in the brains of young mice (equivalent in human years to young adults) with what they saw in the brains of old mice (equivalent to people in their 80s), they identified a couple of cell types in the older mice not typically expected to be there -- and barely present in the young mice. In particular, they found immune cells known as killer T cells lurking in the older mice's subventricular zone.

The healthy brain is by no means devoid of immune cells. In fact, it boasts its own unique version of them, called microglia. But a much greater variety of immune cells abounding in the blood, spleen, gut and elsewhere in the body are ordinarily denied entry to the brain, as the blood vessels pervading the brain have tightly sealed walls. The resulting so-called blood-brain barrier renders a healthy brain safe from the intrusion of potentially harmful immune cells on an inflammatory tear as the result of a systemic illness or injury.

"We did find an extremely sparse population of killer T cells in the subventricular zone of young mice," said Brunet, who is the Michele and Timothy Barakett Endowed Professor. "But in the older mice, their numbers were expanded by 16-fold."

That dovetailed with reduced numbers of proliferation-enabled neural stem cells in the older mice's subventricular zone. Further experiments demonstrated several aspects of the killer T cells' not-so-mellow interaction with neural stem cells. For one thing, tests in laboratory dishware and in living animals indicated that killer T cells isolated from old mice's subventricular zone were far more disposed than those from the same mice's blood to pump out an inflammation-promoting substance that stopped neural stem cells from generating new nerve cells.

Second, killer T cells were seen nestled next to neural stem cells in old mice's subventricular zones and in tissue taken from the corresponding neurogenic niche in autopsied brains of old humans; where this was the case, the neural stem cells were less geared up to proliferate.

Possible brain-based antigens

A third finding was especially intriguing. Killer T cells' job is to roam through the body probing the surfaces of cells for biochemical signs of a pathogen's presence or of the possibility that a cell is becoming, or already is, cancerous. Such telltale biochemical features are called antigens. The tens of billions of killer T cells in a human body are able to recognize a gigantic range of antigens by means of receptors on their own surfaces. That's because every unexposed, or naïve, killer T cell has its own unique receptor shape.

When an initially naïve killer T cell is exposed to an unfamiliar antigen that fits its uniquely shaped receptor, it reacts by undergoing multiple successive rounds of replication, culminating in a large set of warlike cells all sharing the same receptor and all poised to destroy any cells bearing the offending antigen. This process is called clonal expansion.

The killer T cells found in old mice's brains had undergone clonal expansion, indicating likely exposure to triggering antigens. But the receptors on those killer T cells differed from the ones found in the old mice's blood, suggesting that the brain-localized killer T cells hadn't just traipsed through a disrupted blood-brain barrier via passive diffusion but were, rather, reacting to different, possibly brain-based, antigens.

Brunet's group is now trying to determine what those antigens are. "They may bear some responsibility for the disruption of new neuron production in the aging brain's neurogenic niches," she said.

CAMBRIDGE, MA -- In any conventional silicon-based solar cell, there is an absolute limit on overall efficiency, based partly on the fact that each photon of light can only knock loose a single electron, even if that photon carried twice the energy needed to do so. But now, researchers have demonstrated a method for getting high-energy photons striking silicon to kick out two electrons instead of one, opening the door for a new kind of solar cell with greater efficiency than was thought possible.

While conventional silicon cells have an absolute theoretical maximum efficiency of about 29.1 percent conversion of solar energy, the new approach, developed over the last several years by researchers at MIT and elsewhere, could bust through that limit, potentially adding several percentage points to that maximum output. The results are described today in the journal Nature, in a paper by graduate student Markus Einzinger, professor of chemistry Moungi Bawendi, professor of electrical engineering and computer science Marc Baldo, and eight others at MIT and at Princeton University.

The basic concept behind this new technology has been known for decades, and the first demonstration that the principle could work was carried out by some members of this team six years ago. But actually translating the method into a full, operational silicon solar cell took years of hard work, Baldo says.

That initial demonstration "was a good test platform" to show that the idea could work, explains Daniel Congreve PhD '15, an alumnus now at the Rowland Institute at Harvard, who was the lead author in that prior report and is a co-author of the new paper. Now, with the new results, "we've done what we set out to do" in that project, he says.

The original study demonstrated the production of two electrons from one photon, but it did so in an organic photovoltaic cell, which is less efficient than a silicon solar cell. It turned out that transferring the two electrons from a top collecting layer made of tetracene into the silicon cell "was not straightforward," Baldo says. Troy Van Voorhis, a professor of chemistry at MIT who was part of that original team, points out that the concept was first proposed back in the 1970s, and says wryly that turning that idea into a practical device "only took 40 years."

The key to splitting the energy of one photon into two electrons lies in a class of materials that possess "excited states" called excitons, Baldo says: In these excitonic materials, "these packets of energy propagate around like the electrons in a circuit," but with quite different properties than electrons. "You can use them to change energy -- you can cut them in half, you can combine them." In this case, they were going through a process called singlet exciton fission, which is how the light's energy gets split into two separate, independently moving packets of energy. The material first absorbs a photon, forming an exciton that rapidly undergoes fission into two excited states, each with half the energy of the original state.

But the tricky part was then coupling that energy over into the silicon, a material that is not excitonic. This coupling had never been accomplished before.

As an intermediate step, the team tried coupling the energy from the excitonic layer into a material called quantum dots. "They're still excitonic, but they're inorganic," Baldo says. "That worked; it worked like a charm," he says. By understanding the mechanism taking place in that material, he says, "we had no reason to think that silicon wouldn't work."

What that work showed, Van Voorhis says, is that the key to these energy transfers lies in the very surface of the material, not in its bulk. "So it was clear that the surface chemistry on silicon was going to be important. That was what was going to determine what kinds of surface states there were." That focus on the surface chemistry may have been what allowed this team to succeed where others had not, he suggests.

The key was in a thin intermediate layer. "It turns out this tiny, tiny strip of material at the interface between these two systems [the silicon solar cell and the tetracene layer with its excitonic properties] ended up defining everything. It's why other researchers couldn't get this process to work, and why we finally did." It was Einzinger "who finally cracked that nut," he says, by using a layer of a material called hafnium oxynitride.

The layer is only a few atoms thick, or just 8 angstroms (ten-billionths of a meter), but it acted as a "nice bridge" for the excited states, Baldo says. That finally made it possible for the single high-energy photons to trigger the release of two electrons inside the silicon cell. That produces a doubling of the amount of energy produced by a given amount of sunlight in the blue and green part of the spectrum. Overall, that could produce an increase in the power produced by the solar cell -- from a theoretical maximum of 29.1 percent, up to a maximum of about 35 percent.

Actual silicon cells are not yet at their maximum, and neither is the new material, so more development needs to be done, but the crucial step of coupling the two materials efficiently has now been proven. "We still need to optimize the silicon cells for this process," Baldo says. For one thing, with the new system those cells can be thinner than current versions. Work also needs to be done on stabilizing the materials for durability. Overall, commercial applications are probably still a few years off, the team says.

Other approaches to improving the efficiency of solar cells tend to involve adding another kind of cell, such as a perovskite layer, over the silicon. Baldo says "they're building one cell on top of another. Fundamentally, we're making one cell -- we're kind of turbocharging the silicon cell. We're adding more current into the silicon, as opposed to making two cells."

The researchers have measured one special property of hafnium oxynitride that helps it transfer the excitonic energy. "We know that hafnium oxynitride generates additional charge at the interface, which reduces losses by a process called electric field passivation. If we can establish better control over this phenomenon, efficiencies may climb even higher." Einzinger says. So far, no other material they've tested can match its properties.

BOSTON - (July 3, 2019) - Researchers at Joslin Diabetes Center have shown that a protein found in the eye can protect against and potentially treat diabetic eye disease. At high enough levels, Retinol Binding Protein 3 (or RBP3) prevents the development of diabetic retinopathy. If introduced early enough in the development of the disease, RBP3 was shown to reverse the effects of the complication in rodent models of diabetes. These results are reported today in Science Translational Medicine.

"The level of RBP3 in the eye's vitreous and retina are higher in people who don't progress to diabetic eye disease than in those who do," says George King, Chief Scientific Officer at Joslin Diabetes Center and senior author on the paper. "Building on that observation, we saw that if you overexpress RBP3 by molecular methods [in animal models], you can prevent the onset of diabetic eye disease. And when we injected RBP3 itself into the vitreous of diabetic rats, we reversed some of the early changes of diabetic eye disease."

People with diabetes have a high risk of developing complications due to extended periods of elevated glucose levels. These complications could include nerve damage, kidney disease, and eye disease. But a rare subset of people who have had insulin-dependent diabetes for more than 50 years have avoided such complications. For 15 years, Joslin researchers have tracked these individuals as part of the Medalist Study. They noted that 35 percent of patients avoided retinopathy, even when they had elevated glucose levels.

Dr. King and his team deduced that these patients must have something endogenous--or created by their own body that are neutralizing the toxic effects of high glucose levels. This new study aimed to build on this observation, to determine which molecules could be responsible for the protection of the eye.

They took biosamples from the eyes of Medalists -- both from living patients during surgery and from people who had donated their eyes postmortem. They then characterized the many proteins that were present, to determine if any proteins were elevated more in the protected eyes than in eyes of people who developed retinopathy.

They recognized that RBP3, a protein only made in the retina/eye, was elevated. To determine if this was indeed the protective factor they were looking for, they constructed experiments to compare normal versus increased expression of RBP3 in mouse models. Mice with increased RBP3 expression were protected from developing diabetic retinopathy.

Next, the researchers injected pure RBP3 into the vitreous of the eyes of mice in the early stages of retinopathy. The infusion of RBP3 reversed the damages done by early eye disease. They also discovered that diabetes seems to reduce the expression of RBP3 in eye in many subjects, which could explain why its protective effects are limited to only some patients.

"If we could find out what's causing the decrease of RBP3 in the retina in the first place, we could design some kind of treatment to maintain its production, allowing all diabetic patients to have an endogenous protection against eye disease," says Dr. King.

RBP3 is found in all eyes. Normally, it is used to regenerate a certain type of vitamin A in the eye that powers sight-giving rods and cones. But when the eye is exposed to high glucose levels, RBP3 changes its role.

"It appears to decrease the toxic effects of high glucose levels that exist in diabetes by reducing the entering of glucose into several important retinal cells by inhibiting the actions of a glucose transporter, GLUT-1." says Dr. King.

Understanding these mechanisms may allow researchers to develop a targeted treatment to fight early-stage retinopathy. Currently, severe retinopathy can be addressed by the Joslin-developed treatments of either laser photocoagulation or VEGF inhibitor injections.

"We are interested in how we can treat diabetic eye disease at its earliest stages before it gets to the severe forms," says Dr. King.

One surprising finding from this study showed that RBP3, while it mainly resides in the eye, can also be detected to some degree in the bloodstream. Dr. King and team have planned follow-up studies to determine if RBP3 levels in the bloodstream correlate with severity of diabetic retinopathy. If they do, this circulating RBP3 could become a biomarker that doctors can use to screen for retinopathy during regular lab tests.

"That could be a very important screening tool for family or internal medicine doctors who are not experts at examining the eye," says Dr. King. "Right now, all people with diabetes have to be sent to ophthalmologists to really give us a sense of the status of their eyes with regard to diabetes. So, if this could be a general screen, we may be able to catch more cases of retinopathy earlier in the disease course."

Joslin and its Beetham Eye Institute have a strong history of developing treatments for retinopathy. This discovery brings them a step closer to prevention of the devastating complication.

"This has the potential to become equally as important as our previous discovery of VEGF as critical for diabetic proliferative disease or severe diabetic eye disease," King says.

Not all burning mouths are the result of a medical condition known as "burning mouth syndrome" (BMS) and physicians and researchers need better standards for an appropriate diagnosis, according to new research at the School of Dental Medicine at Case Western Reserve University.

BMS is a painful, complex condition associated with a chronic or recurring burning, scalding or tingling feeling in the mouth--sometimes accompanied by a metallic taste or dry mouth sensation.

But because other conditions have similar symptoms, diagnosing BMS can be difficult, said Milda Chmieliauskaite, a researcher and assistant professor of oral and maxillofacial medicine at the dental school.

"The issues with misdiagnosis, depend to some extent on the context, but include resources, money and patient discomfort," she said. So if a patient is misdiagnosed with burning mouth syndrome, but actually suffers from burning due to dry mouth, the patient will receive treatment for the wrong condition and the symptoms of burning will not improve.

"Often, these patients see several providers--taking up a lot of health-care resources--before they find out what's going."

That's because many dentists and clinicians aren't trained well on the topic, she said. The current method for making a diagnosis is ruling out other disorders.

So treating BMS should be approached with caution, said Chmieliauskaite, who co-authored research recently published by Oral Diseases as part of the World Workshop on Oral Medicine VII.

"A lot of the other things that cause burning in the mouth (such as diabetes, anemia and dry mouth) can be easily treated," Chmieliauskaite said.

The specific cause of BMS is uncertain, she said, but some evidence shows that it may be related to nerve dysfunction. Sometimes, chewing gum or eating certain foods lessens pain symptoms.

Best estimates are that between .1% and 4% of the population is affected by BMS, Chmieliauskaite said. The condition affects females more.

In a review of clinical trials internationally between 1994 and 2017, Chmieliauskaite and an international research team found that many of the participants may have had an underlying condition that could have explained their BMS symptoms.

Chmieliauskaite said BMS clinical trials need more rigorous standards. "We need a consensus for a single definition of BMS that includes specific inclusion and exclusion criteria," she said. "This will help us in moving the field forward in understanding of the actual disease."

"And there's still a lot more we need to study," she said.

An interdisciplinary research team at the Technical University of Munich (TUM) has built platinum nanoparticles for catalysis in fuel cells: The new size-optimized catalysts are twice as good as the best process commercially available today.

Fuel cells may well replace batteries as the power source for electric cars. They consume hydrogen, a gas which could be produced for example using surplus electricity from wind power plants. However, the platinum used in fuel cells is rare and extremely expensive, which has been a limiting factor in applications up to now.

A research team at the Technical University of Munich (TUM) led by Roland Fischer, Professor for Inorganic and Organometallic Chemistry, Aliaksandr Bandarenka, Physics of Energy Conversion and Storage and Alessio Gagliardi, Professor for Simulation of Nanosystems for Energy Conversion, has now optimized the size of the platinum particles to such a degree that the particles perform at levels twice as high as the best processes commercially available today.

Ideal: A platinum "egg" only one nanometer big

In fuel cells, hydrogen reacts with oxygen to produce water, generating electricity in the process. Sophisticated catalysts at the electrodes are required in order to optimize this conversion. Platinum plays a central role in the oxygen-reduction reaction.

Searching for an ideal solution, the team created a computer model of the complete system. The central question: How small can a cluster of platinum atoms be and still have a highly active catalytic effect? "It turns out that there are certain optimum sizes for platinum stacks," explains Fischer.

Particles measuring about one nanometer and containing approximately 40 platinum atoms are ideal. "Platinum catalysts of this order of size have a small volume but a large number of highly active spots, resulting in high mass activity," says Bandarenka.

Interdisciplinary collaboration

Interdisciplinary collaboration at the Catalysis Research Center (CRC) was an important factor in the research team's results. Combining theoretical capabilities in modelling, joint discussions and physical and chemical knowledge gained from experiments ultimately resulted in a model showing how catalysts can be designed with the ideal form, size and size distribution of the components involved.

In addition, the CRC also has the expertise needed to create and experimentally test the calculated platinum nano-catalysts. "This takes a lot in terms of the art of inorganic synthesis," says Kathrin Kratzl, together with Batyr Garlyyev and Marlon Rück, one of the three lead authors of the study.

Twice as effective as the best conventional catalyst

The experiment exactly confirmed the theoretical predictions. "Our catalyst is twice as effective as the best conventional catalyst on the market," says Garlyyev, adding that this is still not adequate for commercial applications, since the current 50 percent reduction of the amount of platinum would have to increase to 80 percent.

In addition to spherical nanoparticles, the researchers hope for even higher catalytic activity from significantly more complex shapes. And the computer models established in the partnership are ideal for this kind of modelling. "Nevertheless, more complex shapes require more complex synthesis methods," says Bandarenka. This will make computational and experimental studies more and more important in the future.

Specimens kept in the collection of the Institute of Beneficial Insects at the Fujian Agriculture and Forestry University (FAFU, China) revealed the existence of two previously unknown species of endoparasitoid wasps. Originally collected in 2013, the insects are known to inhabit prairies and bushes at above 3,400 m, which is quite an unusual altitude for this group of wasps.

The new to science wasps are described and illustrated in a paper published in the open-access, peer-reviewed scholarly journal ZooKeys by the team of Dr Wangzhen Zhang (FAFU and Fuzhou Airport Inspection and Quarantine Bureau) and his colleagues at FAFU: Dr Dongbao Song and Prof Jiahua Chen.

Looking very similar to each other, the species were found to belong to one and the same genus (Microplitis), which, however, is clearly distinct from any other within the subfamily, called Microgastrinae. The latter group comprises tiny, mostly black or brown wasps that develop in the larvae of specific moths or butterflies. Interestingly, once parasitised, the host continues living and does not even terminate its own growth. It is only killed when the wasp eggs hatch and feed on its organs and body fluids before spinning cocoons.

From now on, the newly described wasps will be called by the scientific names Microplitis paizhensis and Microplitis bomiensis, where their species names refer to the localities from where they were originally collected: Paizhen town and Bomi county, respectively.

Due to their parasitism, some microgastrine wasps are considered important pest biocontrol agents. Unfortunately, the hosts of the newly described species remain unknown.

In addition, the scientists also mention a third new to science species spotted amongst the specimens they studied. However, so far they have only found its male, whereas a reliable description of a new microgastrine wasp requires the presence of a female.

Scientists at the University of Birmingham have shed fresh light on the mechanism used by certain types of bacteria to protect themselves against attack.

Gram negative bacteria can cause diseases such as pneumonia, cholera, typhoid fever and E. coli infections, as well as many hospital acquired infections. They are increasingly resistant to antibiotics - and this is partly because of the way they are built.

Gram negative bacteria are surrounded by a double membrane that forms a highly effective protective barrier and makes the cell far more resilient to antibiotics. The outer of these two membranes is composed of two types of molecule, phospholipid and lipopolysaccharide (LPS) in a unique asymmetric architecture, with LPS on the outside of the membrane and phospholipid on the inside. It is this architecture that makes gram-negative bacteria particularly resistant to antibiotics.

Understanding how these bacteria make this outer membrane could lead to the identification of new ways to combat bacterial infections, as this membrane is essential for bacterial survival.

Scientists at the University of Birmingham have recently made a step forward in understanding this process by identifying the first mechanism involved in the movement of phospholipid molecules towards this membrane. Their results are published in Nature Microbiology.

Using biophysical techniques including x-ray crystallography and nuclear magnetic resonance, the Birmingham team were able to monitor the movement of phospholipids from the inner membrane towards the outer membrane directly through a series of proteins that form a pathway known as the Mla pathway. This pathway has previously been shown to be involved in disease but its exact function was not known. These results provide the first evidence of a protein machinery involved in these transport processes and opens up the possibility of targeting it for antibiotic development.

Lead author Dr Tim Knowles says: "We've known for many years that these bacteria contain two membranes which help them survive in harsher conditions, and provide enhanced protection against attack by antimicrobial agents. Understanding more about how these membranes are formed and maintained could be a key part of research to develop new antibiotics."

A tsunami holds its wave shape over very long distances across the ocean, retaining its power and 'information' far from its source.

In communications science, retaining information in an optic fibre that spans continents is vital. Ideally, this requires the manipulation of light in silicon chips at the source and reception end of the fibre without altering the wave shape of the photonic packet of information. Doing so has eluded scientists until now.

A collaboration between the University of Sydney Nano Institute and Singapore University of Technology and Design has for the first time manipulated a light wave, or photonic information, on a silicon chip that retains its overall 'shape'.

Such waves - whether a tsunami or a photonic packet of information - are known as 'solitons'. The Sydney-Singapore team has for the first time observed 'soliton' dynamics on an ultra-silicon-rich nitride (USRN) device fabricated in Singapore using state-of-the-art optical characterisation tools at Sydney Nano.

This foundational work, published today in Laser & Photonics Reviews, is important because most communications infrastructure still relies on silicon-based devices for propagation and reception of information. Manipulating solitons on-chip could potentially allow for the speed up of photonic communications devices and infrastructure.

Ezgi Sahin, a PhD student at SUTD conducted the experiments with Dr Andrea Blanco Redondo at the University of Sydney.

"The observation of complex soliton dynamics paves the way to a wide range of applications, beyond pulse compression, for on-chip optical signal processing," Ms Sahin said. "I'm happy to be a part of this great partnership between the two institutions with deep collaboration across theory, device fabrication and measurement."

Co-author of the study and Director of Sydney Nano, Professor Ben Eggleton, said: "This represents a major breakthrough for the field of soliton physics and is of fundamental technological importance.

"Solitons of this nature - so-called Bragg solitons - were first observed about 20 years ago in optical fibres but have not been reported on a chip because the standard silicon material upon which chips are based constrains the propagation. This demonstration, which is based on a slightly modified version of silicon that avoids these constraints, opens the field for an entirely new paradigm for manipulating light on a chip."

Professor Dawn Tan, a co-author of the paper at SUTD, said: "We were able to convincingly demonstrate Bragg soliton formation and fission because of the unique Bragg grating design and the ultra-silicon-rich nitride material platform (USRN) we used. This platform prevents loss of information which has compromised previous demonstrations."

Solitons are pulses that propagate without changing shape and can survive collisions and interactions. They were first observed in a Scottish canal 150 years ago and are familiar in the context of tsunami waves, which propagate thousands of kilometers without changing shape.

Optical soliton waves have been studied since the 1980s in optical fibres and offer enormous promise for optical communication systems because they allow data to be sent over long distances without distortion. Bragg solitons, which derive their properties from Bragg gratings (periodic structures etched in to the silicon substrate), can be studied at the scale of chip technology where they can be harnessed for advanced signal processing.

They are called Bragg solitons after Australian-born Lawrence Bragg and his father William Henry Bragg, who first discussed the concept of Bragg reflection in 1913 and went on to win the Nobel Prize in Physics. They are the only father and son pair to have won Nobel Prizes.

Bragg solitons were first observed in 1996 in Bragg gratings in optical fibres. This was demonstrated by Professor Eggleton while he was working on his PhD at Bell Labs.

The silicon-based nature of the Bragg grating device also ensures compatibility with complementary metal oxide semiconductor (CMOS) processing. The ability to reliably initiate soliton compression and fission allows ultrafast phenomena to be generated with longer pulses than previously required. The chip-scale miniaturisation also advances the speed of optical signal processes in applications necessitating compactness.

Poorer overall diet quality was linked with an increased risk of becoming frail in a study of U.S. community-dwelling older adults, published in the Journal of the American Geriatric Society. The quality of the overall diet appeared to be more important than protein intake for a lower risk of frailty.

During 4 years of follow-up, 277 of the 2154 participants--who were 70-81 years and characterized as "robust" or "pre-frail" at the start of the study--developed frailty. Poor- and medium-quality diets were associated with a 92% and 40% higher incidence of frailty compared with good-quality diets, respectively. No association for protein intake was observed.

"The role of single nutrients such as protein in the development of frailty is not fully understood and definitely needs further investigation. Nevertheless, this study contributes to the prevailing idea that the overall quality is important anyway," said lead author Linda Hengeveld, of Vrije Universiteit Amsterdam, in the Netherlands.

Researchers have conquered the monumental task of manufacturing scalable nanoprobe arrays small enough to record the inner workings of human cardiac cells and primary neurons.

The ability to read electrical activities from cells is the foundation of many biomedical procedures, such as brain activity mapping and neural prosthetics. Developing new tools for intracellular electrophysiology (the electric current running within cells) that push the limits of what is physically possible (spatiotemporal resolution) while reducing invasiveness could provide a deeper understanding of electrogenic cells and their networks in tissues, as well as new directions for human-machine interfaces.

In a paper published by Nature Nanotechnology, scientists from Surrey’s Advanced Technology Institute (ATI) and Harvard University detail how they produced an array of the ultra-small U-shaped nanowire field-effect transistor probes for intracellular recording. This incredibly small structure was used to record, with great clarity, the inner activity of primary neurons and other electrogenic cells, and the device has the capacity for multi-channel recordings.

Dr Yunlong Zhao from the ATI at the University of Surrey said: “If our medical professionals are to continue to understand our physical condition better and help us live longer, it is important that we continue to push the boundaries of modern science in order to give them the best possible tools to do their jobs. For this to be possible, an intersection between humans and machines is inevitable.

“Our ultra-small, flexible, nanowire probes could be a very powerful tool as they can measure intracellular signals with amplitudes comparable with those measured with patch clamp techniques; with the advantage of the device being scalable, it causes less discomfort and no fatal damage to the cell (cytosol dilation). Through this work, we found clear evidence for how both size and curvature affect device internalisation and intracellular recording signal.”

Professor Charles Lieber from the Department of Chemistry and Chemical Biology at Harvard University said: “This work represents a major step towards tackling the general problem of integrating ‘synthesised’ nanoscale building blocks into chip and wafer scale arrays, and thereby allowing us to address the long-standing challenge of scalable intracellular recording.

“The beauty of science to many, ourselves included, is having such challenges to drive hypotheses and future work. In the longer term, we see these probe developments adding to our capabilities that ultimately drive advanced high-resolution brain-machine interfaces and perhaps eventually bringing cyborgs to reality.”

Professor Ravi Silva, Director of the ATI at the University of Surrey, said: “This incredibly exciting and ambitious piece of work illustrates the value of academic collaboration. Along with the possibility of upgrading the tools we use to monitor cells, this work has laid the foundations for machine and human interfaces that could improve lives across the world.”

Dr Yunlong Zhao and his team are currently working on novel energy storage devices, electrochemical probing, bioelectronic devices, sensors and 3D soft electronic systems. Undergraduate, graduate and postdoc students with backgrounds in energy storage, electrochemistry, nanofabrication, bioelectronics, tissue engineering are very welcome to contact Dr Zhao to explore the opportunities further.

Variants in the gene ARMC5 may be associated with high blood pressure among blacks, according to a National Institutes of Health study led by researchers at the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD). The study team identified 17 variants in the ARMC5 gene that were associated with high blood pressure by analyzing genetic research databases that include those of African descent. The study is published in the July 3, 2019, issue of the Journal of the American Heart Association.

"High blood pressure increases a person's risk for heart disease and stroke," said Constantine A. Stratakis, M.D., D. Sc., NICHD Scientific Director and the study's senior author. "The condition is more common among blacks, who also tend to get it at a younger age than whites do, and we are studying the underlying causes of this health disparity."

Earlier work by the NICHD group linked some variants of ARMC5 to primary aldosteronism, a hormonal disorder that causes high blood pressure, among black patients. In the current study, the researchers analyzed datasets containing genetic information from large numbers of people, including NIH's Minority Health Genomics and Translational Research Bio-Repository Database and the Genomics, Environmental Factors and Social Determinants of Cardiovascular Disease in African-Americans Study, which are based in the United States, as well as the UK Biobank.

The researchers identified 17 variants of ARMC5 that were associated with blood pressure among blacks. One variant, called rs116201073, was "protective" and associated with lower blood pressure. It was more common than the others, and it appeared limited to people of African descent, as it is found only in Africans in the international 1000 Genomes Project.

The researchers also reconstructed the rs116201073 variant in cell lines and found that it was more active than other variants of the ARMC5 gene. However, the exact function of the ARMC5 gene is unclear, and more work is needed to understand what the gene does and how variants may protect or predispose a person to high blood pressure.

"Collectively, our research suggests that ARMC5 may play an important role in regulating blood pressure in blacks," said Mihail Zilbermint, M.D., one of the lead authors of the study. "Because the gene is linked to primary aldosteronism, ARMC5 may be involved in how the adrenal glands function and with the hormones that are important for regulating blood pressure."

Despite being one of the nation's most vital watchdogs, compliance and enforcement actions by the U.S. Food and Drug Administration (FDA) have severely declined since the Trump administration took office, according to an investigative report from Charles Piller, a contributing correspondent in the News department at Science. The FDA is the principal federal agency responsible for protecting public health through the supervision and regulation of clinical trials, food safety, product recalls, medications and medical devices, among others. The FDA issues "warning letters," which flag violations and effectively keep dangerous foods, drugs and other products off the market and away from consumers. However, according to Piller's report, agency warning letters have fallen by a third since President Donald Trump took office. There have also been significantly fewer letters during his second year than his first - indicating the overall decline does not simply reflect the slow start of a new administration, says Piller. The insights were revealed through an analysis of enforcement and compliance data from the agency's public records. While the cause of the overall decline in FDA warnings is unclear, Piller notes that agency watchers - including previous FDA insiders - find the trend alarming. A written statement by the FDA did not dispute the findings of the report, suggesting that "less discernable, but equally vital" regulatory and compliance actions are ongoing.