Culture

Nearly half of individuals who contract COVID-19 experience changes in their sense of taste, a new analysis led by a University of Toledo researcher has found.

The systematic review, published in the journal Gastroenterology, could provide yet another diagnostic hint for clinicians who suspect their patients might have the disease.

"Earlier studies didn't note this symptom, and that was probably because of the severity of other symptoms like cough, fever and trouble breathing," said Dr. Muhammad Aziz, chief internal medicine resident at UToledo and the paper's lead author. "We were beginning to note that altered or lost sense of taste were also present, not just here and there, but in a significant proportion."

Aziz and his research collaborators analyzed data from five studies conducted between mid-January and the end of March. Of the 817 patients studied, 49.8% experienced changes to their sense of taste. Researchers suspect the true prevalence could be even higher because some of the studies were based on reviews of patient charts, which may not have noted every symptom.

"We propose that this symptom should be one of the screening symptoms in addition to the fever, shortness of breath and productive cough. Not just for suspected COIVD patients, but also for the general population to identify healthy carriers of the virus," Aziz said.

Prior research has found that a significant number of people who have COVID-19 don't know they've been infected and may be spreading the virus.

Aziz and his research collaborators suspect an altered sense of taste is more prevalent in patients with minor symptoms, though more studies are needed to validate that suspicion. Even so, changes in an individual's sense of taste could be a valuable way to identify carriers who are otherwise mostly asymptomatic.

Taste disorders are tied to a variety of viral illnesses. The review did not attempt to identify the reason that COVID-19 is causing changes in patients' sense of taste; however, researchers theorize it could be COVID-19's ability to bind to what's known as the ACE-2 receptor, which is expressed in epithelial cells on the tongue and mouth.

Because the novel coronavirus was unknown prior to its emergence in January, scientists have been moving rapidly to learn more about both the virus and the disease it causes.

Aziz said the drip of new information shows the need for more scientists to dig into the impacts of COVID-19.

"A lot of things are being missed, which is why I think researchers from every field should try to look into this and see if it's affecting their specialty in one way or another," he said. "Who knows what systems this virus is affecting. If we can catch it earlier in the disease course, we can prevent the spread of the virus and potentially have ways of managing it."

Having a faulty gene linked to dementia doubles the risk of developing severe COVID-19, according to a large-scale study.

Researchers at the University of Exeter Medical School and the University of Connecticut School of Medicine analysed data from the UK Biobank, and found high risk of severe COVID-19 infection among European ancestry participants who carry two faulty copies of the APOE gene (termed e4e4). One in 36 people of European ancestry have two faulty copies of this gene, and this is known to increase risks of Alzheimer's disease up to 14-fold* and also increases risks of heart disease.

Now, the research team has found that carrying these gene mutations doubles the risks of COVID-19 - even in people who had not developed these diseases.

The team has previously found that people with dementia are three times more likely to get severe COVID-19, yet they are not one of the groups advertised to shield - or shelter in place - on health grounds. Part of the increased risk effect may have been exposure to the high prevalence of the virus in care homes. However, the new study, published in the Journal of Gerontology: Medical Sciences, indicates that a genetic component may also be at play. The team found that people with the APOE e4e4 genotype were at double the risk of developing severe COVID-19, compared to those with the common e3e3 form of the APOE gene. The team used data from the UK Biobank study, which collects health and genetic data on 500,000 people.

The majority of people in the population and in the sample size have not yet been exposed to the virus. In this analysis, 2.36% (n=9,022) of participants with European ancestries (n=382,188) had the ApoE e4e4 faulty gene, but 5.13% (n=37) of those who tested positive for COVID-19 (n=721) had this gene variant, suggesting the risk is doubled compared to e3e3 (410 per 100,000 versus 179 per 100,000).

Co-author Dr. Chia-Ling Kuo, of the UConn School of Medicine, said: "This is an exciting result because we might now be able to pinpoint how this faulty gene causes vulnerability to COVID-19. This could lead to new ideas for treatments. It's also important because it shows again that increasing disease risks that appear inevitable with ageing might actually be due to specific biological differences, which could help us understand why some people stay active to age 100 and beyond, while others become disabled and die in their sixties."

Professor David Melzer, who led the team, said: "Several studies have now shown that people with dementia are at high risk of developing severe COVID-19. This study suggests that this high risk may not simply be due to the effects of dementia, advancing age or frailty, or exposure to the virus in care homes."

Melzer stresses: "The effect could be partly due to this underlying genetic change, which puts them at risk for both COVID-19 and dementia."

Shea yields are likely to benefit from a diversity of trees and shrubs in parkland habitats in West Africa, according to a new study led by scientists from Trinity College Dublin. The findings have important implications for managing a crop that is typically harvested and sold by women in rural areas, and which helps finance education for children.

Shea trees (Vitellaria paradoxa) grow in dryland savanna, forest and parkland ecosystems across an estimated 1 million km2 between western Senegal and north-western Uganda. Shea is an important agroforestry crop providing fruit near the end of the dry season; the nuts are processed into a nutritious butter that helps sustain an estimated 80 million people, as well as providing an income from local and global trade.

Shea trees benefit from bees moving pollen between their flowers to produce fruit, but the new study - just published in the Journal of Applied Ecology - found that in sites with low tree and shrub diversity, fruit production was severely limited by a lack of pollination. In higher-diversity sites, more honeybees were observed, and other bees visited flowers in greater numbers, boosting pollination services.

The shea parklands are a long-established traditional food and fuel wood production system, but with growing population pressure and the introduction of the tractor, management has moved away from a shifting cultivation and pastoralist system to more intensive 'permanent' agriculture. This has resulted in a loss of fallow land and contributed to a degraded and fragmented landscape with a lower diversity of plants, which makes life hard for insect pollinators in the Sahel.

The study recommends that when areas are cleared for cultivation, shrubs and trees that are beneficial to the local pollinators should be retained. Furthermore, measures to conserve pollinators in the region should target both honeybees and other bee species.

The researchers involved in this new study - funded by a Darwin Initiative grant - came together from Trinity and INGOs, BirdLife International and the RSPB, and conducted the work with local farmers, NGOs and academics in Burkina Faso, West Africa. The findings will be used to inform local conservation.

Jane Stout, Professor in Botany at Trinity, and a senior author of the study, said:

"In the face of a global biodiversity crisis, studies like this are crucial for demonstrating the everyday importance of biodiversity. We have shown that more biodiverse parklands support more pollinators, and this makes crops more productive - benefitting local peoples' livelihoods and well-being."

Dr Aoife Delaney, lead researcher, said:

"Shea plays a special economic role in Burkina Faso. It is generally harvested and sold by women in rural areas and generates an income that is particularly linked to funding children's education, bringing wider societal benefits. The fruits ripen at a time of year when both food and money are scarcest, helping to tide families over.

"Nutritionally, shea provides essential nutrients and fats that are in short supply during the dry season, and safe-guarding the shea crop in the long-term is important for food security. Supporting pollinators and diverse plant communities in shea parklands also has secondary benefits as the majority of the trees and shrubs there benefit from pollination, including other fruit crops and species that are important for maintaining soil fertility."

Already, BirdLife International and the Burkinabe partner Naturama are working to change the way shea resources are managed within the landscape and are promoting a farmer-led approach built on simple, low cost changes in land management to enhance biodiversity on-farm. This includes natural regeneration and planting of native trees and shrubs with multiple benefits for people, livestock, insects and birds; replacing agrochemicals with locally produced mulch and compost; and introducing apiculture for pollination and food / income.

Together, the international team has produced biodiversity guidelines for Parkland Management that were adopted by the Global Shea Alliance, a 500-strong member organisation, which aims to increase sustainability across the shea value chain, both in the food and cosmetic industries. And, together with local partners, the team has been educating and increasing awareness around the important role of pollinators and undertaking training and capacity building with Burkinabe communities and in schools throughout the region.

Elaine Marshall, project manager, said:
"Our work supports the theory that when we improve plant diversity on farms we see an increase in pollinators and shea yield. We believe a landscape approach which protects these ecosystem goods and services also reduces the vulnerability of human populations across the shea belt. This work demonstrates the potential for ecosystem restoration to deliver healthier and more resilient stocks of natural capital, enhanced pollination services and improved capacity for adapting to the impacts of climate change. Restoring 'nature' should be considered as a core component of successful development aid strategy."

Professor Juliet Vickery, RSPB's Centre for Conservation Science, said:
"Retaining shrubs and trees can have multiple other benefits. It can help combat desertification in an area extremely vulnerable to the impact of climate change and provide vital habitat for many of Europe's summer migrant birds that winter or stop over in the Shea zone on their way to and from sub-Saharan Africa."

Diving as a lifestyle has evolved many times in the animal kingdom, and the ecology of all diving animals is essentially shaped by how long they can hold their breaths.

According to new research, the world's diving animals - from small insects to giant whales - are all governed by a number of similar principles.

Using the largest dataset ever compiled, an international team of scientists has examined how metabolic constraints govern the diving performance of air-breathing aquatic species, all of which have evolved to maximise the amount of time they can spend underwater.

They discovered that maximum dive duration increases predictably with body mass in all animals, but the rate at which this happens depends on metabolic mode.

Ectotherms - cold-blooded creatures such as amphibians, reptiles and insects - can remain submerged for longer at a given body mass, but the impact of an increase in body mass on dive duration in warm-blooded endotherms - including birds and mammals - is far more pronounced.

Writing in Proceedings of the Royal Society B, scientists say their findings constitute a new fundamental principle of evolutionary physiology, showing that the same 'rules' govern the evolution of diving in animals as different as water beetles and walruses.

They also say it may partly explain why many warm-blooded diving animals - including modern whales but also extinct reptiles such as ichthyosaurs and plesiosaurs - evolved relatively large body sizes, as increases in size led to greater relative increases in dive duration.

The research was completed at the University of Plymouth (UK), and led by an international team of scientists now based at Radboud University (Netherlands), Université du Québec à Rimouski (Canada) and Plymouth's School of Biological and Marine Sciences.

They compiled and analysed 1,792 records for 286 species, including 62 ectotherms and 224 endotherms, and tested whether the globally recognised oxygen store/usage hypothesis - which suggests that larger animals are able to dive for longer and deeper - applies to all diving animals, irrespective of their evolutionary origin and metabolic mode.

Lead author Dr Wilco Verberk, an Assistant Professor at Radboud University, said: "Our work provides an unprecedented analysis of the ecology of diving behaviour from a metabolic perspective, with far-reaching implications. It demonstrates that body mass and temperature affect dive duration in a similar manner in species as evolutionarily distant as insects, reptiles, birds and mammals. This shows the same general physical and physiological principles have shaped the evolution of diving in all animal groups, both ancient and modern, constituting a new fundamental principle for evolutionary physiology."

Senior author David Bilton, Professor of Aquatic Biology at the University of Plymouth and a world renowned expert on aquatic beetles, added: "Our results change our understanding of diving in animals significantly, and help us better disentangle what shapes the ecology and evolution of both extant and extinct divers. It shows that large body size and the increased oxygen storage capacity that goes with it, permit longer dives, opening many previously inaccessible aquatic ecosystems to large bodied air breathers and provides a possible explanation as to why many warm-blooded diving animals tend to be relatively large."

New research published in Experimental Physiology suggests that fire service instructors are at increased risk of cardiovascular diseases due to higher levels of inflammation in their blood, and so their exposure should be limited to nine exposures per month.

While training firefighters, fire service instructors experience core temperature increases to over 38°C when demonstrating scenarios to firefighters. Fire service instructors experience this physiological strain over ten times more frequently than firefighters. Researchers in the UK found that this causes inflammation that lasts beyond the day of their exposure. This chronic inflammation may explain the increased precedence of health problems in this group.

The researchers collected blood samples from 110 fire service personnel and compared fire service instructors to firefighters in terms of markers that indicate increased risk of heart disease. They found elevated levels in the blood of fire service instructors for all the markers they examined.

They speculated that these markers, which indicate inflammation might also be linked to other symptoms that fire service instructors report, such as mood swings, night sweats, fatigue.

Commenting on the study, lead researcher Emily Watkins said:

"By limiting exposure of fight service instructors to nine times per months, the sector will enable the instructors to do their job for as many years as they want, whilst protecting their cardiovascular health."

More than a decade before people with Huntington's disease show symptoms, they can exhibit abnormally high levels of an immune-system molecule called interleukin-6 (IL-6), which has led many researchers to suspect IL-6 of promoting the eventual neurological devastation associated with the genetic condition. A new investigation by MIT neuroscientists shows that the story likely isn't so simple. In a new study they found that Huntington's model mice bred to lack IL-6 showed exacerbated symptoms compared to HD mice that still had it.

"If one looks back in the literature of the Huntington's disease field many people have postulated that reductions to IL-6 would be therapeutic in HD," said Myriam Heiman, associate professor in MIT's Department of Brain and Cognitive Sciences and a member of The Picower Institute for Learning and Memory and the Broad Institute of MIT and Harvard. She is senior author of the paper in Molecular Neurodegeneration. Former postdoc Mary Wertz is the lead author.

To test the hypothesis that knocking out IL-6 would help HD mice, the researchers crossbred mice engineered to model HD with mice engineered to lack IL-6. They then compared the performance of offspring on a variety of standard movement tasks to that of healthy mice, mice just lacking IL-6, and mice just modeling HD but still having IL-6. The HD mice lacking IL-6 performed significantly worse than the other mouse lines, including the HD mice that still had IL-6.

The result was as surprise not only because of the record in prior studies, but also because in a paper published earlier this year, Wertz and Heiman conducted a sweeping analysis of genes that promoted neuron survival in Huntington's disease and some of the hits they turned up were ones that are associated with interleukin signaling.

Gene expression differences

Struck by the findings in the new study, the team sought to understand why they occurred. To do that, they measured gene expression in all the major cell types in the striatum, the brain region most affected in HD, by sequencing RNA in thousands of individual cells in each mouse line. When they looked at the differences in gene expression in neurons between the two HD mouse lines - the ones that had IL-6 and the ones that didn't - they saw that many genes important for synapses, the connections that link neurons into circuits, were significantly less expressed in the HD mice without IL-6.

"Perhaps this worsening of the phenotype is due to perturbation of those synaptic signaling pathways," Heiman said.

While the study shows there is definitely not a therapeutic benefit to completely knocking out IL-6, it may still be possible to find a level between overexpression and complete knockout that is therapeutic, Heiman said. It may also be possible that timing is crucial. For instance, in this study mice lacked IL-6 right from birth, but potentially intervening to modulate IL-6 levels is more beneficial at some stage of adulthood, she said. The lab plans to continue to pursue that investigation.

"What these results show us is that we really have to understand which parts of innate immune signaling are activated when and what the order of events is," she said.

Researchers at the National Institute of Standards and Technology (NIST) have developed a mathematical formula that, computer simulations suggest, could help 5G and other wireless networks select and share communications frequencies about 5,000 times more efficiently than trial-and-error methods.

The novel formula is a form of machine learning that selects a wireless frequency range, known as a channel, based on prior experience in a specific network environment. Described at a conference this week, the formula could be programmed into software on transmitters in many types of real-world networks.

The NIST formula is a way to help meet growing demand for wireless systems, including 5G, through the sharing of frequency ranges, also known as bands, that are unlicensed. Wi-Fi, for example, uses unlicensed bands -- those not assigned by the Federal Communications Commission to specific users. The NIST study focuses on a scenario in which Wi-Fi competes with cellular systems for specific frequencies, or subchannels. What makes this scenario challenging is that these cellular systems are raising their data-transmission rates by using a method called License Assisted Access (LAA), which combines both unlicensed and licensed bands.

"This work explores the use of machine learning in making decisions about which frequency channel to transmit on," NIST engineer Jason Coder said. "This could potentially make communications in the unlicensed bands much more efficient."

The NIST formula enables transmitters to rapidly select the best subchannels for successful and simultaneous operation of Wi-Fi and LAA networks in unlicensed bands. The transmitters each learn to maximize the total network data rate without communicating with each other. The scheme rapidly achieves overall performance that is close to the result based on exhaustive trial-and-error channel searches.

The NIST research differs from previous studies of machine learning in communications by taking into account multiple network "layers," the physical equipment and the channel access rules between base stations and receivers.

The formula is a "Q-learning" technique, meaning it maps environmental conditions -- such as the types of networks and numbers of transmitters and channels present -- onto actions that maximize a value, known as Q, that returns the best reward. By interacting with the environment and trying different actions, the algorithm learns which channel provides the best outcome. Each transmitter learns to select the channel that yields the best data rate under specific environmental conditions.

If both networks select channels appropriately, the ef?ciency of the combined overall network environment improves. The method boosts data rates in two ways. Speci?cally, if a transmitter selects a channel that is not occupied, then the probability of a successful transmission rises, leading to a higher data rate. And if a transmitter selects a channel such that interference is minimized, then the signal is stronger, leading to a higher received data rate.

In the computer simulations, the optimum allocation method assigns channels to transmitters by searching all possible combinations to find a way to maximize the total network data rate. The NIST formula produces results that are close to the optimum one but in a much simpler process. The study found that an exhaustive effort to identify the best solution would require about 45,600 trials, whereas the formula could select a similar solution by trying only 10 channels, just 0.02 percent of the effort.

The study addressed indoor scenarios, such as a building with multiple Wi-Fi access points and cellphone operations in unlicensed bands. Researchers now plan to model the method in larger-scale outdoor scenarios and conduct physical experiments to demonstrate the effect.

RESEARCH TRIANGLE PARK, N.C. -- As 5G hits the market, new U.S. Army-funded research has developed a radio-frequency switch that is more than 50 times more energy efficient than what is used today.

With funding from the Army Research Office, an element of the U.S. Army Combat Capabilities Development Command's Army Research Laboratory, researchers at The University of Texas at Austin and the University of Lille in France, have built a new component that will more efficiently allow access to the highest 5G frequencies, in a way that increases devices' battery life and speeds up how quickly users can do things like stream HD media.

Smartphones are loaded with switches that perform a number of duties. One major task is jumping back and forth between different networks and spectrum frequencies: 4G, WiFi, LTE, Bluetooth, etc. The current radio-frequency switches that perform this task are always running, consuming precious processing power and battery life.

"Radio-frequency switches are pervasive in military communication, connectivity and radar systems," said Dr. Pani Varanasi, division chief, materials science program at ARO. "These new switches could provide large performance advantage compared to existing components and can enable longer battery life for mobile communication, and advanced reconfigurable systems."

The journal Nature Electronics published the research team's findings.

"It has become clear that the existing switches consume significant amounts of power, and that power consumed is useless power," said Dr. Deji Akinwande, a professor in the Cockrell School of Engineering's Department of Electrical and Computer Engineering who led the research. "The switch we have developed can transmit an HDTV stream at a 100GHz frequency, and that is an achievement in broadband switch technology."

The new switches stay off, saving battery life for other processes, unless they are actively helping a device jump between networks. They have also shown the ability to transmit data well above the baseline for 5G-level speeds.

Prior researchers have found success on the low end of the 5G spectrum - where speeds are slower but data can travel longer distances. This is the first switch that can function across the spectrum from the low-end gigahertz frequencies to high-end terahertz frequencies that could someday be key to the development of 6G.

The team's switches use the nanomaterial hexagonal boron nitride, a rapidly emerging nanomaterial from the same family as graphene. The structure of the switch involves a single layer of boron and nitrogen atoms in a honeycomb pattern sandwiched between a pair of gold electrodes. Hexagonal boron nitride is the thinnest known insulator with a thickness of 0.33 nanometers.

The impact of these switches extends beyond smartphones. Satellite systems, smart radios, reconfigurable communications, and Internet of Things, are all examples of potential uses for the switches. In addition, these switches can be realized on flexible substrates making them suitable for Soldier wearable radios and communication systems that can benefit from the improved energy efficiency for longer battery life with faster data speeds as well as other defense technologies.

"This will be very useful for radio and radar technology," Akinwande said.

This research spun out of a previous project that created the thinnest memory device, also using hBN. Akinwande said sponsors encouraged the researchers to find other uses for the material, and that led them to pivot to RF switches.

PHILADELPHIA - The lens of the eye is an unusual organ. Unlike most of the body's organs, blood vessels don't reach the lens. If they did, they'd obscure our vision and we wouldn't be able to see. The lack of vasculature led scientists to believe immune cells, which travel via the bloodstream, couldn't get to this part of the body either. But a few years ago, Jefferson researchers challenged this long held assumption by demonstrating that immune cells populate the lens in response to degeneration. Now the Jefferson team finds the eye also launches an immune response in the lens after injury. The discovery adds to a growing body of evidence that is working to overturn the accepted dogma of the field.

"Why would we evolve a tissue that is so central to our being able to see without ways to ensure its protection, its ability to repair itself?" says, Sue Menko, PhD, Professor in the Department of Pathology, Anatomy and Cell Biology at Thomas Jefferson University, who led the research. "Immune cells are central to that protection and repair."

The lens of the eye works like a camera lens. Its main purpose is to focus images coming in through the cornea - the transparent front layer of the eye - onto the retina at the back of the eye. The images are detected by the retina and then translated in the brain as what we see. That lens must be crystal clear. As a result, scientists have always described the lens as a tissue without vasculature and therefore no source of immune cells either.

"At some point, you think about it and you wonder how that's possible," Dr. Menko says. "It doesn't really make a lot of sense."

The puzzle led Dr. Menko and her team to investigate whether immune cells are present in the eye. In a previous study, they discovered that when the lens is in a diseased state, immune cells are not only recruited there, but they also show up in the cornea, retina, and vitreous body - all parts of the eye that don't normally have immune cells. Dr. Menko's work suggested that the immune cells come from the ciliary body, a sort of muscle that helps squeeze and pull the lens, changing its shape, and helping it focus.

"The ciliary body is also a place that is vascular rich so it seemed like the most obvious place to look," Dr. Menko says.

Now, in the latest work, Dr. Menko and colleagues show that after injury to the cornea, immune cells travel from the ciliary body to the lens along fibers known as ciliary zonules. The researchers used fluorescent markers and high-powered microscopes to observe structures of mouse eyes one day after receiving a scratch on the cornea. The high-tech imaging analysis Dr. Menko's team used revealed that following injury to the cornea, the immune system launches a response to protect the lens. Immune cells are recruited to the lens via the ciliary zonules, and crawl along the surface of the lens to surveille and protect from adverse impacts of the corneal wound.

"This is really the first demonstration that surveillance by immune cells of the lens in response to injury somewhere else in the eye," Dr. Menko says.

The researchers also found that some immune cells were able to cross the lens capsule, a membranous structure that helps to keep the lens under tension. The results could point to a role for immune cells in cataract formation.

Together, the findings indicate that in response to damage or disease, the eye utilizes alternative mechanisms - rather than direct contact with the bloodstream like non-transparent tissues do - to ensure that immune cells get to sites to provide healing and protection.

"We're excited to go from thinking this doesn't make sense to proving that the body is amazing and can adapt to anything. You just have to go in and look for it," Dr. Menko says.

"We should be willing to challenge dogma because that's where discovery is," she adds. "It can enlighten what we know if we always keep our mind open to what doesn't make sense and what maybe should be challenged to understand things better."

Five years after NASA's MAVEN spacecraft entered into orbit around Mars, data from the mission has led to the creation of a map of electric current systems in the Martian atmosphere.

"These currents play a fundamental role in the atmospheric loss that transformed Mars from a world that could have supported life into an inhospitable desert," said experimental physicist Robin Ramstad of the University of Colorado, Boulder. "We are now currently working on using the currents to determine the precise amount of energy that is drawn from the solar wind and powers atmospheric escape." Ramstad is lead author of a paper on this research published May 25 in Nature Astronomy.

Earth has such current systems, too: we can even see them in the form of colorful displays of light in the night sky near the polar regions known as the aurora, or northern and southern lights. Earth's aurora are strongly linked to currents, generated by the interaction of the Earth's magnetic field with the solar wind, that flow along vertical magnetic field lines into the atmosphere, concentrating in the polar regions. Studying the flow of electricity thousands of miles above our heads, though, only tells part of the story about the situation on Mars. The difference lies in the planets' respective magnetic fields, because while Earth's magnetism comes from within, Mars' does not.

Planetary magnetic fields

Earth's magnetism comes from its core, where molten, electrically conducting iron flows beneath the crust. Its magnetic field is global, meaning it surrounds the entire planet. Since Mars is a rocky, terrestrial planet like Earth, one might assume that the same kind of magnetic paradigm functions there, too. However, Mars does not generate a magnetic field on its own, outside of relatively small patches of magnetized crust. Something different from what we observe on Earth must be happening on the Red Planet.

What's going on above Mars?

The solar wind, made up largely of electrically charged electrons and protons, blows constantly from the Sun at around a million miles per hour. It flows around and interacts with the objects in our solar system. The solar wind is also magnetized and this magnetic field cannot easily penetrate the upper atmosphere of non-magnetized planets like Mars. Instead, currents that it induces in the planet's ionosphere cause a pile-up and strengthening of the magnetic field, creating a so-called induced magnetosphere. How the solar wind powers this induced magnetosphere at Mars has not been well understood until now.

As solar wind ions and electrons smash into this stronger induced magnetic field near Mars, they are forced to flow apart due to their opposite electric charge. Some ions flow in one direction, some electrons in the other direction, forming electric currents that drape around from the dayside to the nightside of the planet. At the same time, solar x-rays and ultraviolet radiation constantly ionize some of the upper atmosphere on Mars, turning it into a combination of electrons and electrically charged ions that can conduct electricity.

"Mars' atmosphere behaves a bit like a metal sphere closing an electric circuit," Ramstad said. "The currents flow in the upper atmosphere, with the strongest current layers persisting at 120-200 kilometers (about 75-125 miles) above the planet's surface." Both MAVEN and previous missions have seen localized hints of these current layers before, but they have never before been able to map the complete circuit, from its generation in the solar wind, to where the electrical energy is deposited in the upper atmosphere.

Directly detecting these currents in space is infamously difficult. Fortunately, the currents distort the magnetic fields in the solar wind, detectable by MAVEN's sensitive magnetometer. The team used MAVEN to map out the average magnetic field structure around Mars in three dimensions and calculated the currents directly from their distortions of the magnetic field structure.

"With a single elegant operation, the strength and paths of the currents pop out of this map of the magnetic field," Ramstad said.

The Red Planet's destiny

Without a global magnetic field surrounding Mars, the currents induced in the solar wind can form a direct electrical connection to the Martian upper atmosphere. The currents transform the energy of the solar wind into magnetic and electric fields that accelerate charged atmospheric particles into space, driving atmospheric escape to space. The new results reveal several unexpected features particular to MAVEN's goal to understand atmospheric escape: the energy that drives escape appears to be drawn from a much larger volume than was often assumed.

Solar-wind-driven atmospheric loss has been active for billions of years and contributed to the transformation of Mars from a warm and wet planet that could have harbored life into a global cold desert. MAVEN is continuing to explore how this process works and how much of the planet's atmosphere has been lost.

This research was funded by the MAVEN mission. MAVEN's principal investigator is based at the University of Colorado's Laboratory for Atmospheric and Space Physics, Boulder, and NASA Goddard manages the MAVEN project. NASA is exploring our Solar System and beyond, uncovering worlds, stars, and cosmic mysteries near and far with our powerful fleet of space and ground-based missions.

Enzymes: they are the central drivers for biochemical metabolic processes in every living cell, enabling reactions to take place efficiently. It is this very ability which allows them to be used as catalysts in biotechnology, for example to create chemical products such as pharmaceutics. A topic that is currently being widely discussed is photoinduced catalysis, in which researchers harness the ability of nature to start biochemical reactions with the aid of light. What they need for this purpose is enzymes which can be activated by means of light. It is not, however, a simple matter to incorporate the few naturally occurring light-activatable enzymes into biotechnological processes, as they are highly specialised and difficult to manipulate.

Researchers at the Universities of Münster (Germany) and Pavia (Italy) have now identified an enzyme which becomes catalytically active when exposed to blue light and which immediately triggers a reaction hitherto unknown in enzymology. The reaction in question is a special monooxygenase reaction, in which an oxygen atom is transferred to the substrate. The reaction is supported by a "helper molecule" which stepwise delivers two electrons. Up to now, it had been assumed that such a light-dependent reaction cannot occur in enzymes.

"The enzyme we have identified belongs to a very large family of enzymes, and it is realistic to assume that other enzymes can be produced, by means of genetic manipulations, which can be activated by light too and which can be used in a very wide range of applications," says Dr. Steffen L. Drees, who headed the study and works at the Institute of Molecular Microbiology and Biotechnology at Münster University. One possible application, for example, is in the field of medicine, where pharmaceuticals could be activated by means of light. The study has been published in the journal "Nature Communications".

Background and method:

In their study, the researchers investigated the enzyme PqsL, which is found in the opportunistic pathogen Pseudomonas aeruginosa and, originally, is not light-dependent. The researchers stimulated the enzyme with blue light and analysed the reaction using, for example, a combination of time-resolved spectroscopic and crystallographic techniques.

The enzyme examined belongs to the family of flavoproteins and - typically for this family of proteins - uses a derivative of vitamin B2 as a so-called cofactor for catalysing the incorporation of oxygen into organic molecules. The cosubstrate NADH (reduced nicotinamide adenine dinucleotide) is needed as a "helper molecule" for the enzymatic reaction, providing the necessary electrons. The reaction mechanism the researchers observed in their study is new, however, and so far, unique. Activated by the exposure to light in the flavin-NADH complex, NADH transfers a single electron to the protein-bound flavin. In this way, a flavin radical is created - a highly reactive molecule which is characterised by an unpaired electron. Using time-resolved spectroscopy, the researchers were able to observe how the molecule formed and changed its state.

The flavin radical has a very negative redox potential, which means that it has a large capacity for transferring electrons to reaction partners. "Because of this property, we assume that the flavin radical can also enable additional reactions to take place which would expand the catalytic potential of this enzyme - as well as of other enzymes too, perhaps," says group leader Prof. Susanne Fetzner.

The enzyme identified is the only one so far which is not naturally photoactive, and carries out a light-independent reaction in the bacterial cell. "The three-dimensional structure of the enzyme shows that the outward-facing flavin co-factor might be the key to photoactivation," says Simon Ernst, first author of the study.

Photoactive enzymes enable a large number of applications - for example, multi-step catalysis in a one-vessel reaction or spatially resolved catalysis, for example to functionalise surfaces in certain patterns. They can also be useful for so-called prodrug activation in the body or on the skin - a process in which a pharmacological substance becomes active only after metabolization in the organism.

Traffic congestion is a serious problem in the United States, but a new analysis shows that interactive technology - ranging from 511 traffic information systems and roadside cameras to traffic apps like Waze and Google Maps - is helping in cities that use it.

Potentially, the researchers said, technology could limit the need to widen and expand roadways while saving commuters time and money and lessening environmental damage.

"Technology has the potential to help society, and one way is to help us make better infrastructure decisions and put less pressure on roads," said Paul A. Pavlou, dean of the C.T. Bauer College of Business at the University of Houston and corresponding author for the report, published by the journal Information Systems Research.

Pavlou and colleagues Aaron Cheng of the London School of Economics and Min-Seok Pang of Temple University found that U.S. cities using Intelligent Transportation Systems (ITS) saved money, time and other resources, including:

More than $4.7 billion a year in lost work or productivity

175 million hours a year in travel time

53 million gallons a year in fossil fuel consumption and

10 billion pounds less CO2 emitted each year.

The researchers analyzed longitudinal data from ITS technologies deployed in 99 urban areas in the United States from 1994 to 2014. That included the metropolitan areas of Chicago, Los Angeles, Atlanta, New York-Newark, Houston, Dallas-Fort Worth and Washington D.C., among others.

Pavlou noted that technology has advanced - and traffic has continued to grow - since 2014, the latest year in the dataset used for the research, making it likely that today's savings would be greater.

The U.S. Department of Transportation describes ITS as "an integrated system of advanced communications technologies embedded in the transportation infrastructure and in vehicles to improve transportation safety and mobility," and has awarded grants to cities to invest in the technologies. Technologies included in the research include both those developed by DOT and commercial technologies designed to improve traffic safety and mobility.

The researchers found that the technology is most effective at reducing traffic congestion when two things happen: commuters use more online services for traffic information, including such apps as Waze, and when state governments incorporate more advanced functions into their 511 traveler information systems.

But each city is different. Pavlou noted that while Houston has not adopted the 511 system, it does collaborate with private companies to design and build intelligent transportation systems, including messaging signs, roadside cameras and solar-powered radar detection sites.

Pavlou said the study suggests alternatives to simply building more and bigger roads to keep up with population and traffic growth. Using large-scale technology systems in conjunction with real-time traffic apps at the individual level is less expensive and more effective than only spending funds to expand and maintain roadways, he said
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Houston traffic and its freeway system, for example, have grown significantly since he was a student here in the 1990s, he said. "Traffic is even worse than before since people move where the roads are built and drive more. The city is growing, but there are alternative ways that do not impose some much demand on roads with the intelligent use of technology in parallel."

May 26, 2020 - (BRONX, NY) Montefiore Health System Albert Einstein College of Medicine have begun the next stage of the Adaptive COVID-19 Treatment Trial (ACTT), to evaluate treatment options for people hospitalized with severe COVID-19 infection. The new iteration of the trial, known as ACTT 2, is sponsored by the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health.

In March, Montefiore was the first New York location to join the multicenter trial, which evaluated remdesivir, a broad-spectrum antiviral drug given intravenously. Preliminary results from the trial, announced last month and published on Friday in the New England Journal of Medicine, show that patients with COVID-19 who received remdesivir recovered in 11 days on average compared to 15 days for patients in the placebo group--a statistically significant improvement. Of the 1,063 clinical trial participants, 91 of them, nearly 10%, were from Montefiore and Einstein.

Following up on remdesivir's promising results, the trial is now studying remdesivir in combination with baricitinib or placebo in a double-blind, randomized trial. Baricitinib is marketed for reducing inflammation associated with rheumatoid arthritis. Researchers want to know if baricitinib combined with remdesivir can prevent or reduce the hyper-inflammatory "cytokine storm" that can fatally overwhelm the lungs and other parts of the body in people with COVID-19 when their immune system reacts to coronavirus infection.

"What concerns us is that in some people the immune response to coronavirus can be more deadly than the infection itself, and there is no known treatment for this yet," said Barry Zingman, M.D., professor of medicine at Einstein and clinical director, infectious diseases, at the Moses division of Montefiore Health System. "Including baricitinib in our trial may reduce COVID-19-related inflammation and combining baricitinib with remdesivir may yield an even more effective treatment option for people most severely affected by this illness." Dr. Zingman oversaw the original remdesivir study at Montefiore and is directing ACTT 2.

Patients enrolled in ACTT 2 are hospitalized with a laboratory-confirmed coronavirus infection and lung complications, including rattling sounds when breathing, a need for supplemental oxygen, abnormal chest X-rays showing pneumonia, or the need for a mechanical ventilator. All patients will receive remdesivir intravenously for up to 10 days. Half of the patients will also be given baricitinib by mouth, with the remaining half receiving an identical placebo, both for up to 14 days.

Remdesivir was developed by Gilead Sciences, Inc. Baricitinib was developed by Eli Lilly and Company.

In cells, protein is synthesized based on the genetic code. Each protein is coded by the triplet combination of chemicals called "nucleotides," and a continuous "reading" of any set of triplet codes will, after a multi-step process, result in the creation of a chain of amino acids, a protein. The genetic code is matched with the correct amino acid by a special functional RNA aptly named transfer RNA or tRNA (which, incidentally, is itself composed of its own type of "codes"). An enzyme called "aminoacyl-tRNA synthetase" or aaRS accurately assigns a specific amino acid to the correct "code" through a tRNA by recognizing unique structural components called 'identity elements' on the tRNA. In the case of the amino acid alanine, the identity element for recognition by the enzyme alanyl-tRNA synthetase (AlaRS) is an unlikely base pair "G3:U70," present in the minihelix structure (amino acid-accepting upper half region) of tRNA. Considering its importance in the recognition of the code, the base pair is popularly known as the "operational RNA code."

The evolution of this complex tRNA-aaRS system is a fascinating enigma, as the existing evolutionary evidence suggests that the upper half of the tRNA containing this operational code appeared earlier in evolutionary history than the lower half part that binds to the triplet code of mRNA. Interestingly, in a primitive microorganism, Nanoarchaeum equitans, the genes coding for each AlaRS subunit α and β are split, with the two genes being separated by half the length of the chromosome.

This interesting fact inspired a team of scientists at Tokyo University of Science, led by Prof. Koji Tamura, to hypothesize that these split forms of AlaRS in N. equitans might be connected with the evolutionary history of aaRS enzyme activity.

Prof. Tamura emphasizes the significance of their study, published in Journal of Molecular Evolution, in the evolutionary context, "AlaRS-α shows the G3:U70-independent addition of alanine to RNA minihelix regions. Our data indicate the existence of a simplified process of alanine addition to tRNA by AlaRS early in the evolutionary process, before the appearance of the G3:U70 base pair."

The aforementioned minihelix parts of tRNAs were previously known to function as the region of occurrence of addition of amino acids by many aaRSs. To understand the interaction process of the minihelix (minihelixAla) of alanine-specific tRNA (tRNAAla) and AlaRS subunits, the researchers cloned the coding sequences of α and β subunits of N. equitans and then purified the synthesized proteins.

The researchers noticed that, at a relatively high concentration, AlaRS-α alone was capable of adding alanine to both tRNAAla and minihelixAla. Then also observed that AlaRS-α alone interacts with the end of the alanine-accepting region of tRNAAla, but not with the G3:U70 base pair. This was in stark contrast to prior knowledge regarding tRNAAla and AlaRS system. In brief, when both AlaRS-α and AlaRS-β were present, AlaRS behaved in a G3:U70-dependent manner, but working alone, AlaRS-α could add alanine to tRNAAla and minihelixAla in a G3:U70-independent manner. The researchers deduced that "the G3:U70 may be a late-arriving 'operational RNA code,' relevant to later alanylation systems incorporating further specificity through the evolution of the AlaRS-β subunit."

So, what makes the findings of this study so important? Prof. Tamura explains the significance of the striking results of their research, "our findings reveal for the first time that a G3:U70-independent mechanism of alanine addition exists. Furthermore, using 'RNA minihelix' molecules, which are considered to be the primitive form of tRNA, we could also illuminate the 'morphology' of tRNA before the evolutionary appearance of the G3:U70 base pair.''

While discussing the broader implication of their study, Prof. Tamura comments thoughtfully "The breakthroughs in science almost always came from the curiosity-driven research, and the results of our study approach the mystery of the origin of life. It has the potential to transform many areas". His team is now focusing on an extensive structural analysis using the mutants of N. equitans AlaRS-α, but their current findings, published in August issue in printing and selected as the cover of the August issue, are enough to give cause to rethink chapters scientists that have believed to be fundamental in evolutionary history!

The evolutionary processes underlying metastasis-the development of secondary malignant growths away from the primary tumor site-in human patients are still incompletely understood.

Metastases can form in locoregional lymph nodes draining the primary tumor-a form of progression that portends a worse prognosis but can still be curable-or they can develop in distant organs. The latter case defines stage IV disease and treatments for it are typically considered palliative.

It is unknown whether lymph node and distant metastases are only distinguished by their different prognostic implications, or whether the biology underlying their formation is also distinct.

In a new study, published in Nature Genetics, Kamila Naxerova, PhD, of the Center for Systems Biology at Massachusetts General Hospital, Johannes Reiter, PhD, of the Canary Center for Cancer Early Detection at Stanford and colleagues now show that lymph node and distant metastases develop through different evolutionary mechanisms.

Reconstructing the evolutionary histories of dozens of primary colorectal cancers and their metastases, the team showed that lymph node metastases are a genetically highly diverse group. Their pronounced heterogeneity indicates that they can be seeded by many different primary tumor sub-lineages.

In contrast, distant metastases are homogeneous. They typically resemble each other and have a recent common ancestor, suggesting that fewer primary tumor cells possess the ability to form lesions in distant organs. Moreover, the genetic diversity within individual lymph node metastases is also higher than the genetic diversity within individual distant lesions.

These results show that the selective pressures shaping metastasis development in different anatomical sites differ substantially. Lymph node metastasis formation is comparatively "easy" and can be achieved by many cells. Dissemination to and outgrowth in distant organs, on the other hand, appears to be much more challenging and represents a major bottleneck in tumor progression. A significantly smaller fraction of genetic lineages within a primary tumor appears to be capable of this feat. Perhaps these differences can explain why diagnosis of lymph node metastases generally is a less ominous sign than the presence of distant metastases.

In future studies, it will be important to study the molecular and cell biological mechanisms underlying differential selection in lymph nodes and distant sites.

For example, it is possible that distant metastasis is more difficult to achieve because target organs like the liver are located further away from the primary tumor than locoregional lymph nodes, requiring cells to travel farther distances.

Or perhaps, the microenvironment of the lymph node is for some reason a more hospitable milieu for disseminating tumor cells than the parenchyma of distant organs. Understanding the molecular factors that are rate-limiting for metastasis formation in different sites could lead to novel preventative treatments.