Culture

The avian influenza virus subtype H16N3 is currently detectable in many countries. To examine the potential threat to humans of H16N3, researchers recently performed an extensive avian influenza surveillance in major wild bird gatherings across China from 2017-2019. The findings are published in Transboundary and Emerging Diseases.

The investigators isolated two H16N3 subtype influenza viruses that can bind to both human and avian-type cell receptors. They also found evidence that genetic material from other species has been introduced into the H16N3 avian influenza virus, which suggests that it may infect other species and could therefore pose a threat to animal and human health in the future.

"Consequently, it is necessary to increase monitoring of the emergence and spread of avian influenza subtype H16N3 in wild birds," the authors wrote.

Leafhoppers are tiny insects. They are only about 3 millimeters long, smaller than a grain of rice. But they can cause big damage to crops, including beans.

In temperate areas, leafhoppers can cause bean crop losses of up to 20 percent. They are even more damaging in tropical areas. There, leafhopper infestations can lead to crop losses of more than 75 percent.

To combat the leafhopper threat, researchers are continuously trying to develop resistant varieties of crops.

In a new study, Tim Porch and his team describe a new pinto bean, called TARS-LH1. Porch is a researcher at the USDA-ARS Tropical Agriculture Research Station in Mayagüez, Puerto Rico.

This new pinto bean has increased resistance to leafhoppers. It also has other desirable traits, such as high yields and drought tolerance.

"Continuous improvement of common beans is necessary," says Porch. "That's because pathogens, pests, the environment and the market are continuously changing and evolving."

Even in changing markets, pinto beans - a common target of leafhoppers - are a vital crop. They account for more than a third of all edible dry beans produced in the United States.

Pinto beans are targeted by two different species of leafhoppers. One species - Empoasca fabea - predominates in temperate areas. Another species - Empoasca kraemeri - is the main pest in tropical areas.

TARS-LH1 is resistant to both kinds of leafhoppers.

Field testing of TARS-LH1 for leafhopper resistance and other traits was carried out in multiple locations. Temperate test sites were located at the Michigan State University Crop and Soil Science Research Farm in East Lansing, Michigan. Tropical tests were completed in Haiti and Puerto Rico.

"Since this pinto bean was tested over several years in different locations, we confirmed that it has resistance to both species of leafhoppers," says Porch. "It also has broad adaptation to different climates."

A key challenge during field tests was accurately collecting data to measure leafhopper damage. Measuring damage is key to verifying whether specific varieties of beans are resistant to these pests.

Leafhoppers feed on plant sap. Their feeding causes damage, called hopperburn. Hopperburn can include leaf burn: leaves turn yellow, particularly at the tip and around the edges. It can also include leaf curl: entire leaves curl down.

Researchers carefully counted the numbers of leafhoppers and flightless leafhopper nymphs on common bean leaves. They also evaluated leaf burn and leaf curl symptoms.

"By combining the careful and laborious counting of pests with a rapid evaluation of leaf damage, we were able to estimate leafhoppers per plant for a large number of plots and trials," says Porch.

As a result, the researchers were able to show that the TARS-LH1 pinto bean is resistant to leafhopper attacks. But that's not all! TARS-LH1 is also drought tolerant. Droughts often occur simultaneously with leafhopper infestations.

"Since TARS-LH1 combines drought tolerance with the leafhopper resistance, it provides a key combination of traits," says Porch.

Finding ways to conserve water use in agriculture is becoming increasingly important. There's also a drive to use less pesticide to control insects.

"TARS-LH1 could contribute to reducing these major inputs in common bean farming," says Porch. "It could also increase the production of organic beans."

Porch and colleagues are still working on breeding newer, better varieties of beans. "We want to include additional traits, such as heat tolerance and resistance to pathogens like rust and common bacterial blight, along with the leafhopper resistance," says Porch.

Bean varieties that are resistant to pests and have other desirable traits, such as TARS-LH1, can benefit breeders, farmers and consumers alike.

"Ultimately, our goal is to generate broadly resilient and productive common beans," he says.

Engineers at the University of California San Diego have developed a new method that doesn't require any special equipment and works in just minutes to create soft, flexible, 3D-printed robots.

The innovation comes from rethinking the way soft robots are built: instead of figuring out how to add soft materials to a rigid robot body, the UC San Diego researchers started with a soft body and added rigid features to key components. The structures were inspired by insect exoskeletons, which have both soft and rigid parts--the researchers called their creations "flexoskeletons."

The new method allows for the construction of soft components for robots in a small fraction of the time previously needed and for a small fraction of the cost.

"We hope that these flexoskeletons will lead to the creation of a new class of soft, bioinspired robots," said Nick Gravish, a mechanical engineering professor at the Jacobs School of Engineering at UC San Diego and the paper's senior author. "We want to make soft robots easier to build for researchers all over the world."

The new method makes it possible to build large groups of flexoskeleton robots with little manual assembly as well as assemble a library of Lego-like components so that robot parts can be easily swapped.

The flexoskeletons are made from 3D printing a rigid material on a thin sheet that acts as a flexible base. They are printed with various features that increase rigidity in specific areas--again inspired by insect exoskeletons, which combine softness and rigidity for movement and support.

Researchers detail their work in the April 7 issue of the journal Soft Robotics.The team plans to make their designs available to researchers at other institutions as well as high schools.

One flexoskeleton component takes 10 minutes to print and costs less than $1. Flexoskeleton printing can be done on most low-cost commercially available printers. Printing and assembling a whole robot takes under 2 hours.

Researchers surveyed a range of materials until they found the right flexible surface to print the flexoskeletons on--that turned out to be a sheet of polycarbonate. Careful observation of insect behavior led them to add features to increase rigidity.

The ultimate goal is to create an assembly line that prints whole flexoskeleton robots without any need for hand assembly. A swarm of these small robots could do as much work as one massive robot on its own--or more.

In 1989, iRobot cofounder Rodney Brooks, then at the MIT Artificial Intelligence Lab, advocated for space missions that would consist of "large numbers of mass produced simple autonomous robots that are small by today's standards." He and coauthor Anita Flynn titled the paper "Fast, cheap and out of control: a robot invasion of the solar system." The paper was seminal for Gravish, who hopes this study is one step further in that direction--but for the entire field of robotics, not just space.

Social media should be used to chart the economic impact and recovery of businesses in countries affected by the COVID-19 pandemic, according to new research published in Nature Communications. University of Bristol scientists describe a 'real time' method accurately trialled across three global natural disasters which could be used to reliably forecast the financial impact of the current global health crisis.

Traditional economic recovery estimates, such as surveys and interviews, are usually costly, time-consuming and do not scale-up well. However, researchers from Bristol's School of Engineering Maths and Department of Civil Engineering show they were able to accurately estimate the downtime and recovery of small businesses in countries affected by three different natural hazards using aggregated social media data.

The method relies on the assumption that businesses tend to publish more social media posts when they are open and fewer when they are closed, hence analysing the aggregated posting activity of a group of businesses over time it is possible to infer when they are open or closed.

Using data from the public Facebook posts of local businesses collected before, during and after three natural disasters comprising the 2015 Gorkha earthquake in Nepal, the 2017 Chiapas earthquake in Mexico, and the 2017 hurricane Maria in Puerto Rico, the team charted the number of smaller urban businesses who were closed and then were able to measure their recovery post-event. The team validated their analysis using field surveys, official reports, Facebook surveys, Facebook posts text analysis and other studies available in literature.

Importantly, the framework works in 'real time' without the need for text analysis which can be largely dependent on language, culture or semantic analysis and can be applied to any size area or type of natural disaster, in developed and developing countries, allowing local governments to better target the distribution of resources.

Dr Simini, Senior Lecturer and the study's lead author explains: "The challenge of nowcasting the effect of natural hazards such as earthquakes, floods, hurricanes, and pandemics on assets, people and society has never been more timely than ever for assessing the ability of countries to recover from extreme events.

"Often, small to medium-sized businesses slip through the net of traditional monitoring process of recovery. We noticed in areas struck by natural hazard events that not all areas and populations react in the same way."

Dr Flavia De Luca, lead author and Senior Lecturer in Bristol's Department of Civil Engineering, added: "We had the idea of supporting post-emergency deployment of resources after a natural hazard event using public Facebook posts of businesses to measure how a specific region is recovering after the event. It was amazing to find out that the approach was providing information on the recovery in 'real time'.

"We would like to test the method to measure the economic impact of the COVID-19 pandemic."

Researchers at the University of Iowa and the University of Georgia have developed a vaccine that fully protects mice against a lethal dose of MERS, a close cousin of the SARS-CoV2 coronavirus that causes COVID-19.

The vaccine uses a harmless virus to deliver a MERS coronavirus protein into cells to generate an immune response, and may hold promise for developing vaccines against other coronaviruses diseases, including COVID-19.

The team led by Paul McCray, MD, at the UI Carver College of Medicine, and Biao He, PhD, at the University of Georgia College of Veterinary Medicine, tested a MERS vaccine candidate in mice engineered to be susceptible to the MERS coronavirus. The vaccine is an innocuous parainfluenza virus (PIV5) carrying the "spike" protein that MERS uses to infect cells. All the vaccinated mice survived a lethal dose of the MERS coronavirus. The results of the study were published April 7 in the journal mBio.

"Our new study indicates that PIV5 may be a useful vaccine platform for emerging coronavirus diseases, including SARS-CoV-2, the virus causing the ongoing COVID-19 pandemic," says McCray, UI professor of pediatrics. "Using the same strategy, vaccine candidates based on PIV5 expressing the spike protein of SARS-CoV-2 have been generated. We are planning more studies in animals to test the ability of PIV5-based vaccines in preventing disease caused by SARS-CoV-2."

MERS (Middle East Respiratory Syndrome) and COVID-19 are both caused by coronaviruses. MERS is deadlier and is fatal in about one third of known cases, but there have been only 2,494 cases since 2012, when the virus first emerged. In contrast, there have been over 1.25 million confirmed cases of COVID-19 worldwide since it first emerged in late 2019 in Wuhan, China, and almost 70,000 people have died from the disease.

The study found that just one, relatively low dose of the vaccine given to the mice intranasally (inhaled through the nose) was sufficient to fully protect all the treated mice from a lethal dose of MERS coronavirus.

When the researchers analyzed the immune responses generated by the vaccine, they found that both antibodies and protective T cells were produced. However, the antibody response was quite weak and it seems most likely that the vaccine's protective effect is due to the T cell response in the mouse lungs.

The researchers note several factors that make PIV5 expressing a coronavirus spike protein an appealing platform for vaccine development against emerging coronaviruses. First, PIV5 can infect many different mammals, including humans, without causing disease. PIV5 is also being investigated as a vaccine for other respiratory diseases including respiratory syncytial virus (RSV) and influenza. Second, the fact that a low dose of the vaccine was sufficient to protect the mice might be beneficial for creating enough vaccine for mass immunization. And finally, the vaccine in the current study was the most effective MERS vaccine to date in animal models of the disease.

Washington, DC - April 7, 2020 - No vaccines exist that protect people against infections by coronaviruses, including SARS-CoV-2, which causes COVID-19, or the ones that cause SARS and MERS. As COVID-19 continues to wreak havoc, many labs around the world have developed a laser-like focus on understanding the virus and finding the best strategy for stopping it.

This week in mBio, a journal of the American Society of Microbiology, a team of interdisciplinary researchers describes a promising vaccine candidate against the MERS virus. Since the MERS (Middle East Respiratory Syndrome) outbreak began in 2012, more than 850 people have died, and studies suggest the virus has a case fatality rate of more than 30%.

In the new paper, the researchers suggest that the approach they took for a MERS virus vaccine may also work against SARS-CoV-2. The vaccine's delivery method is an RNA virus called parainfluenza virus 5 (PIV5), which is believed to cause a condition known as kennel cough in dogs but appears harmless to people. The researchers added an extra gene to the virus so that infected cells would produce the S, or spike, glycoprotein known to be involved in MERS infections.

"We know people have been exposed to PIV5, but it seems to be an innocuous virus in humans," said pediatric pulmonologist and coronavirus expert Paul McCray, M.D., at the University of Iowa, in Iowa City, who co-led the new study with virologist Biao He, Ph.D., at the University of Georgia, in Athens. "PIV5 doesn't seem to cause a cytopathic effect." The MERS virus cannot replicate in mice, so to test the vaccine McCray developed a mouse model that mimics human infections. The mice had been genetically engineered to express DPP4, the protein used by the MERS virus as an entry point for human cells.

Lab tests showed that a single dose of the vaccine, given intranasally, effectively caused infected cells to produce the S protein, which in turn triggered immune responses against the protein in the animal host.

Four weeks after the mice received the vaccine, they were exposed to a strain of the MERS virus, adapted to the mice to cause a lethal infection. The MERS virus was also given to groups of mice that had received a different PIV5 vaccine--one without the genes for the S protein--or an intramuscular vaccine with inactivated MERS virus.

All the mice immunized with the modified PIV5 virus survived MERS virus infection. In contrast, all the mice immunized with the PIV5 without S died from the infection. The intramuscular vaccine of inactivated MERS virus only protected 25% of the mice from a lethal infection. The mice that received inactivated MERS virus showed above-average levels of eosinophils, white blood cells that indicate infection or inflammation. This connection raises a safety concern for inactivated MERS virus as a potential vaccine, said He. The study demonstrates that an intranasal, PIV5-based vaccine is effective against MERS in mice, said He, and should be investigated for its potential against other dangerous coronaviruses, including SARS-CoV-2.

"We're quite interested in using viruses as gene delivery vehicles," said McCray, who has also investigated similar strategies as a way to treat cystic fibrosis. Now, like colleagues around the world, McCray and He have both focused their research efforts on SARS-CoV-2, taking a similar tack to working with mouse models of infection and testing vaccines.

Finding an effective vaccine against the coronavirus that causes COVID-19 is a race against time, McCray said. "One hundred percent of the population is not going to be exposed to the virus the first time around, which means there will be more people to infect when it comes again," he said. "We don't know yet if people get lasting immunity from the SARS-CoV-2 infection, so it's important to think about ways to protect the population."

New understandings of how lipids function within tears could lead to better drugs for treating dry eye disease.

A new approach has given Hokkaido University researchers insight into the synthesis and functions of lipids found in tears. Their findings, published in the journal eLife, could help the search for new treatments for dry eye disease.

The film of tears covering the eye's surface is vital for eliminating foreign objects, providing oxygen and nutrients to the eye's outer tissues, and reducing friction with the eyelid. The film is formed of an outer lipid layer and an inner liquid layer. The outer lipid layer, which is itself formed of two sublayers, prevents water evaporation from the liquid layer. Dry eye disease develops when the glands that produce these lipids dysfunction. However, it has remained unclear how those generally incompatible layers -- water and lipid -- can form and maintain tear films.

Hokkaido University biochemist Akio Kihara and colleagues wanted to understand the functions of a subclass of lipids called OAHFAs (O-Acyl)-ω-hydroxy fatty acids) that are present in the inner lipid sublayer (amphiphilic lipid sublayer) just above the liquid layer of the tear film. OAHFAs are known to have both polar and non-polar ends in its molecule, giving them affinity for both water and lipid.

To do this, they turned off a gene called Cyp4f39 in mice that is known for its involvement in ω-hydroxy fatty acid synthesis. Previous attempts at studying the gene's functions in this way had led to neonatal death in mice, as it impaired the skin's protective role. The team used a way to turn the gene off, except in the skin.

The mice were found to have damaged corneas and unstable tear films, both indicative of dry eyes. Further analyses showed that these mice were lacking OAHFAs and their derivatives in their tear films. Interestingly, the scientists also discovered that the OAHFA derivatives have polarities intermediate between OAHFAs and other lipids in the tear film. This strongly suggests that those lipids together form a polarity gradient that plays an important role in connecting the tear film's inner liquid layer and outer lipid layer, helping the film spread uniformly over the surface of the eye.

"Drugs currently used in dry eye disease target the liquid layer of the tear film, but there aren't any drugs that target its lipid layer," says Akio Kihara. "Since most cases of dry eye disease are caused by abnormalities in the lipid layer, eye drops containing OAHFAs and their derivatives could be an effective treatment."

Further studies are required to fully understand the functions and synthesis of OAHFAs.

Scientists at Sanford Burnham Prebys have found a new way to kill pancreatic cancer cells by disrupting their pH equilibrium. The study, published in Cancer Discovery, reports how depleting an ion transport protein lowers the pH to a point that compromises pancreatic cancer cell growth.

Pancreatic cancer cells--like all cancer cells--have a constant need for energy to support their growth and expansion. To meet these energy needs, they boost metabolic pathways that normal cells don't use and, as a consequence, produce excess acid that needs to be expelled. Increasingly, scientists have focused on manipulating cancer cell pH as an approach to treat cancers lacking effective therapies.

"Our study suggests that interfering with cellular pH represents a new therapeutic avenue to treat pancreatic cancer, one of the deadliest cancers for which there is currently no effective treatment," says Cosimo Commisso, Ph.D., an assistant professor in Sanford Burnham Prebys' NCI-designated Cancer Center. "We have shown that a sodium-hydrogen exchanger called NHE7 plays a significant role in pancreatic tumors, and by suppressing it, we can promote cancer cell death."

Sodium-hydrogen exchange proteins

The NHE family of sodium-hydrogen exchangers are transport proteins that regulate the internal pH of cells and their organelles such as endosomes and the Golgi apparatus. They are located in membranes and work by exchanging hydrogen ions (H+) for sodium ions (Na+) and are essential for proper cell function.

"We hypothesized that the increased acid production that occurs in tumor cells could be harnessed as a therapeutic vulnerability, so we looked for a strategy to specifically target this," says Koen Galenkamp, Ph.D., a postdoctoral fellow in Commisso's lab and the first author of the study. "By mining a number of pancreatic cancer databases, we found that NHE7 levels were higher in tumors compared to normal pancreas, and highest in the tumors of patients with the poorest prognoses."

With this information, the research team set out to understand the role of NHE7 in pancreatic cancer cells. They found that it localizes to the Golgi where it imports hydrogen ions, creating an acidic Golgi and a corresponding alkaline cytoplasm that supports cancer cell metabolism.

"This led us to test if we could make pancreatic cells vulnerable by disabling or eliminating NHE7 to undermine the alkaline cytoplasmic pH they require to stay fit," adds Galenkamp.

Through a series of experiments in pancreatic cancer cells, the research team showed that suppressing NHE7 lowers the pH of the cell's cytoplasm, triggering cell death. Importantly, in mice transplanted with human tumors, getting rid of NHE7 caused tumors to shrink or completely stop their growth.

"Pancreatic cancer is predicted to soon become the second-leading cause of cancer-related deaths in the U.S.," says Commisso. "Given that the five-year survival rate for people newly diagnosed is less than 10%, it's crystal clear that we need better therapies--and finding new cancer targets can help us tailor treatments and possibly save the lives of many more patients."

Commisso adds, "This study illustrates the potential to target pH balance as an approach to combat pancreatic cancer. Our next step is to work with the Conrad Prebys Center for Chemical Genomics--the drug discovery facility at our Institute--to find ways to disable NHE7 and limit the Golgi's ability to sequester acid. If successful, cancer cells would be unable to maintain the proper pH that they need to grow."

A new method of evaluating and prioritising treatment for patients with suspected acute stroke, which has been used by the Stockholm health authority since 2017, has led to faster health interventions and better patient care, shows a new study from Karolinska Institutet published in the journal JAMA Neurology.

Stroke can be caused by a clot in the large arteries of the brain. For every minute that an artery is blocked, two million neurons die. Without acute intervention, only 10 percent of the patients return to normal function three months after their stroke. The most effective intervention is mechanical clot removal, or endovascular thrombectomy (EVT). The earlier the blood vessel is re-opened, the greater the number of brain cells that survive. However, there is commonly some delay before treatment, as most patients are taken by ambulance to the nearest hospital for examination, and then transferred to EVT-performing university hospitals, such as the Karolinska University Hospital in Solna.

"There has been a justification for this system, as patients who don't need EVT receive the best care at the stroke unit in their local A&E hospital," says the study's lead author Michael Mazya, consultant at Karolinska University Hospital and researcher at the Department of Clinical Neuroscience, Karolinska Institutet. "The challenge for ambulance staff has been to assess which patients may benefit from direct transport to a university hospital, and which can be taken to the nearest stroke unit as usual."

To reduce the time to EVT, a new triage system has been used in the Stockholm region since October 2017. The results have now been evaluated in a new study published in the scientific journal JAMA Neurology. In patients with suspected stroke, the triage involves two steps. First the ambulance nurse tests the degree of symptom severity using the A2L2 system (where A stands for arm, and L for leg). If the patient is unable to raise his or her arm for ten seconds and the leg for five, it generally indicates a severe stroke, which often requires EVT. The second step is a telephone call to a stroke physician, to exchange additional information and decide on the optimal destination.

"The telephone consultation allows the ambulance staff and stroke physician to discuss the preliminary diagnosis," Mazya says. "The doctor can read up on the patient's background and activate the stroke team. This really speeds up acute management and treatment decisions once the patient arrives at the hospital."

The results show that thanks to the A2L2 test and tele-consultation, 71 percent of patients in need of EVT are now taken directly to Karolinska University Hospital in Solna, as opposed to 28 percent before. The average time from stroke onset to EVT is now two hours and 15 minutes, which is 70 minutes faster than in the old system, 65 minutes faster than the Swedish national average, and a full 1 hour and 45 minutes faster than in international randomized studies of EVT.

Faster treatment delivery has resulted in 34 percent of EVT patients completely recovering their functional ability, compared with 24 percent in the old system, despite the fact that patients treated since the implementation of the new system have been older and had a higher average stroke severity.

"The results are very pleasing," says Christina Sjöstrand, senior consultant in charge of stroke care at Karolinska University Hospital and researcher at the Department of Clinical Neuroscience, Karolinska Institutet. "Much of the success is thanks to a close collaboration between key stroke professionals in all of the region's hospitals, and colleagues in pre-hospital care. We are continuing to use the new triage system throughout the Stockholm region and will be presenting more comprehensive data on patient outcomes at the World Stroke Conference in Vienna in November this year."

Joint research between Kobe University and Ushio Inc. has provided proof for the first time in the world that direct and repetitive illumination from 222nm ultraviolet radiation C (UVC), which is a powerful sterilizer, does not cause skin cancer. This suggests that 222nm UVC is also safe for human eyes and skin. This technology is expected to have a wide range of antibacterial and antiviral applications in medical facilities and daily life.

The research group consisted of members from the Division of Dermatology in the Department of Internal Related at Kobe University's Graduate School of Medicine (Professor NISHIGORI Chikako, Associate Professor KUNISADA Makoto, graduate student YAMANO Nozomi et al.) and Ushio Inc.

These research results were published online in Photochemistry & Photobiology on March 29 and Professor Nishigori is due to present this research at the 'American Society of Photobiology 2020 meeting' in Chicago on June 28.

Main Points

Provided proof for the first time in the world that 222nm ultraviolet radiation C (UVC) does not cause skin cancer.

These results indicated that UVC light is also safe for human skin and eyes.

In the animal experiments using a 222nm germicidal lamp, there were no signs of cataracts or cancer of the eyes or skin, even in mice with extreme weakness to ultraviolet radiation.

This could allow germicidal lamps to be shone directly on people's skin, enabling a wide range of antiviral and antibacterial applications in both medical fields and daily life.

Research Background

UVC emitted by the sun (with a wavelength of 280~200nm) does not reach the Earth's surface because it is absorbed by the Ozone layer. Germicide lamps that emit 254nm UVC have been developed and are utilized for sterilization because the wavelength can kill bacteria. So far these lamps are only utilized in places when people are not present because they are known to cause harmful side-effects such as skin cancer and cataracts.

The lamp used in this study has a smaller wavelength of 222nm. It is being developed in the hope that it can be utilized in the medical field. It has been shown that 222nm is comparable to 254nm, by the Division of Orthopaedic Surgery at Kobe University (Professor KURODA Ryosuke et.al.), in terms of ability to eradicate bacteria on human skin. However, if this technology is to be directly used on humans in a medical facility, it is necessary to prove that possible repeated exposure to 222nm UVC is safe and non-carcinogenic.

Research Methodology

To evaluate the safety of repeated eye and skin exposure to a 222nm germicide lamp, xeroderma pigmentosum (*2) group A model mice were used in this study. Compared to wild-type mice, these model mice have an increased sensitivity to ultraviolet radiation and an over 10,000 fold increased risk of developing skin cancer.

In the group that was exposed to UVB (280-315nm), the wavelength range equivalent to skin cancer caused by sunlight, all mice developed skin cancer and displayed adverse effects such as cataracts and cornea damage.

Conversely, mice in the 222nm germicide lamp group did not develop skin cancer at all. The effect on their eyes was investigated in cooperation with Shimane University's Department of Ophthalmology (Professor TANITO Masaki et al.). There were no abnormalities visible, even when examined under a microscope (Figure 1).

It was understood that 222nm produced no adverse effects due to the level of skin penetration. The 254nm UVC currently used in germicide lamps penetrates down to the basal cell layer, the bottommost layer of the skin, and damages the DNA of cells. On the other hand, it was shown that 222nm UVC doesn't damage the DNA of skin cells because it only travels as far as the stratum corneum, the outermost layer of the skin.

Further Research

These research results indicate that even though 222nm UVC is a powerful sterilizer, it can also be used directly on human skin. Beginning with hand sanitization in medical institutions, it is expected that this technology will have a wide range of antiviral and antibacterial applications in places that people enter, such as schools, welfare facilities, food factories, toilets and kitchens.

Washington, D.C., April 7, 2020 -- In states that have banned affirmative action, the share of underrepresented minorities among students admitted to and enrolling in public universities has steadily lost ground relative to changing demographic trends among those states' high school graduates, according to new research.

The study, by Mark Long at the University of Washington and Nicole Bateman at the Brookings Institution, was published today in Educational Evaluation and Policy Analysis, a peer-reviewed journal of the American Educational Research Association.

While prior research has looked at the immediate effects of affirmative action bans, this study evaluates the long-term changes, including the effects of admissions strategies that universities have implemented as alternatives. California, Texas, Washington, and Florida banned affirmative action in the late 1990s, and were followed later by Arizona, Georgia, Michigan, Nebraska, New Hampshire, and Oklahoma.

Long and Bateman analyzed trends in minority representation among applicants, admittees, and enrollees in 19 selected public universities in the states with affirmative action bans, from the time their bans went into effect through 2015. The researchers further evaluated a subset of those institutions that are considered flagship universities within their states and then those that are considered elite, based on their admissions criteria.

Averaging across the 19 universities studied, in the year prior to the affirmative action ban the share of underrepresented students (Black, Hispanic, and Native American students) among enrolled U.S. students was 15.7 percentage points below these students' share among high school graduates in the universities' states. However, this gap rose to 16.8 percentage points, on average, in the year immediately after the ban, and the gap increased in subsequent years to 17.9 percentage points.

Among the nine flagship universities in the study, the underrepresentation gap grew from 11.2 percentage points to 13.9 percentage points immediately after the ban and to 14.3 percentage points by 2015.

For the subset of 10 "elite" universities, the same pattern held, with the underrepresentation gap widening from 18.7 percentage points to 21.7 percentage points immediately following a ban and growing to 21.9 percent points by 2015.

Results from the study indicate that alternative policies--such as automatic admission for a certain top percentage of students from each high school (which leverages de facto racial and ethnic segregation of high schools), inclusion of socioeconomic factors in admission decisions, increased outreach and financial support for low-income students, and the elimination of admission preference for the children of alumni--have not been able to fully replace raced-based affirmative action.

"While the share of underrepresented minorities among enrolling undergraduate students has increased since the implementation of alternative policies, this growth is slower than the growth of underrepresented minorities in high schools," said Long, a professor of public policy and governance at the University of Washington. "When the changing demographics of state high schools are considered, the underrepresentation of Black, Hispanic, and Native American youth in the higher education system is worsening, not improving."

"Alternative policies and administrative decisions have, so far, been unable to fully replace race-based affirmative action," Long said.

The researchers note that improvement in many of the underlying conditions that generate underrepresentation in colleges--such as differences in household income, test scores, and incarceration rates--has occurred, but at a slow pace.

"The very slow rate of progress in these underlying conditions is surprising and concerning," Long said. "For example, if the past 20 years is a guide for future progress, it will take over a thousand years for the Black-White gap in median household income to close. It's clear that university leaders and state policymakers cannot rely on improvements in the underlying conditions to solve underrepresentation in higher education for many decades to come."

"University administrators need to rigorously evaluate their policies and be mindful of practices that show promise," said Long. "They should be challenged to do more and do better."

"But we should also recognize that many of the underlying conditions are outside of the control of these administrators," Long added. "If we expect flagship public universities to reflect the racial and ethnic diversity of their states, then policymakers must work harder and better to alleviate these pre-college disparities and improve college readiness for underrepresented students."

A team of international scientists has developed a suite of more than 200 new genetic techniques for using marine microbes to investigate a host of questions in biology. Published in Nature Methods, the new tools are an essential step forward in understanding the cellular instructions that underpin microbial life in the sea.

The vast resource created by the team comprises a major compilation of new techniques for performing genetic experiments on marine microbes. A persistent bottleneck in microbial oceanography is the lack of experimental model systems - well-studied organisms that can be genetically manipulated to reveal gene functions, as well as clarify how microbes contribute to ecosystem processes.

"There is an incredible diversity of microbes that we've never had the tools to truly explore, and it represents an untapped resource of knowledge and biotechnology potential," said José Antonio Fernández Robledo, a senior research scientist at Bigelow Laboratory for Ocean Sciences and one of the lead authors of the paper. "This project catalyzed development of the genetic tools that we need to interrogate these organisms, and it has opened the door for engineering them to provide new products for the biomedical and food supplement industry."

Funded by the Gordon and Betty Moore Foundation, the initiative supported development of genetic tools for a group of microbes called protists. These microscopic, single-celled organisms are among the most diverse yet least understood marine microbes. The tools created by Fernández Robledo and his coauthors set the stage for other researchers to develop protists as experimental model systems that can revealing the inner workings of the ocean and microbial life.

Fernández Robledo used advanced molecular techniques to develop a new approach to studying Crypthecodinium, a microalgae that produces a beneficial fatty acid used as food supplement. He developed a technique to insert DNA into the organism. This is the first essential step toward identifying the roles of individual Crypthecodinium genes, and ultimately being able to ask specific questions of its genome.

Fernández Robledo obtained Crypthecodinium samples from the National Center for Marine Algae and Microbiota at Bigelow Laboratory, and he was assisted by an undergraduate from Colby College as well as a master's student with this research. The protocols the team established, as well as all others described in the paper, are freely available online to help other scientists benefit from this effort.

"The process of tool development inherently includes failures as well as successes, and the challenge to secure funding for this type of work has previously restricted scientists from making progress in this area," Fernández Robledo said. "The Moore Foundation deserves a lot of credit for recognizing that the most interesting science happens at new frontiers, and that all results are valuable and sharing them helps to move the field forward."

In addition to Fernández Robledo, several other research teams succeeded in introducing DNA into marine protists. They are now working to employ genetic techniques such as CRISPR/Cas9 to interrogate these microbial genomes, a critical step that will allow scientists to identify the functions of specific genes and potentially harness them to develop beneficial applications.

The Nature Methods paper brings together 113 coauthors from 53 institutions across 14 countries, and it offers a wealth of methods for conducting genetic research in marine protists. The project efforts were accelerated by active communication and collaboration among the researchers, who have shared their protocols in a dedicated community group called Protist Research to Optimize Tools in Genetics (PROT-G) on the protocol-hosting website protocols.io.

"This paper is a landmark achievement after several years of hard work to solve numerous technical challenges in the laboratory," said Adam Jones, program officer at the Gordon and Betty Moore Foundation. "We look forward to seeing how the protocols and guidance offered by the scientists in this newly available resource accelerate genetic tool development in marine protists."

As COVID-19 spreads across the globe, a common question is, can infectious diseases be connected to environmental change? Yes, indicates a study published today from the University of California, Davis' One Health Institute.

Exploitation of wildlife by humans through hunting, trade, habitat degradation and urbanization facilitates close contact between wildlife and humans, which increases the risk of virus spillover, found a study published in the journal Proceedings of the Royal Society B. Many of these same activities also drive wildlife population declines and the risk of extinction.

The study provides new evidence for assessing spillover risk in animal species and highlights how the processes that create wildlife population declines also enable the transmission of animal viruses to humans.

"Spillover of viruses from animals is a direct result of our actions involving wildlife and their habitat," said lead author Christine Kreuder Johnson, project director of USAID PREDICT and director of the EpiCenter for Disease Dynamics at the One Health Institute, a program of the UC Davis School of Veterinary Medicine. "The consequence is they're sharing their viruses with us. These actions simultaneously threaten species survival and increase the risk of spillover. In an unfortunate convergence of many factors, this brings about the kind of mess we're in now."

THE COMMON AND THE RARE

For the study, the scientists assembled a large dataset of the 142 known viruses that spill over from animals to humans and the species that have been implicated as potential hosts. Using the IUCN Red List of Threatened Species, they examined patterns in those species' abundance, extinction risks and underlying causes for species declines.

The data show clear trends in spillover risk that highlight how people have interacted with animals throughout history.

Among the findings:

Domesticated animals, including livestock, have shared the highest number of viruses with humans, with eight times more zoonotic viruses compared to wild mammalian species. This is likely a result of our frequent close interactions with these species for centuries.

Wild animals that have increased in abundance and adapted well to human-dominated environments also share more viruses with people. These include some rodent, bat and primate species that live among people, near our homes, and around our farms and crops, making them high-risk for ongoing transmission of viruses to people.

At the other end of the spectrum are threatened and endangered species. These are animals whose population declines were connected to hunting, wildlife trade and decreases in habitat quality. These species were predicted to host twice as many zoonotic viruses compared to threatened species that had populations decreasing for other reasons.

Threatened and endangered species also tend to be highly managed and directly monitored by humans trying to bring about their population recovery, which also puts them into greater contact with people. Bats repeatedly have been implicated as a source of "high consequence" pathogens, including SARS, Nipah virus, Marburg virus and ebolaviruses, the study notes.

"We need to be really attentive to how we interact with wildlife and the activities that bring humans and wildlife together," Johnson said. "We obviously don't want pandemics of this scale. We need to find ways to co-exist safely with wildlife, as they have no shortages of viruses to give us."

GAINESVILLE, Fla. --- The bright chirp of the coquí frog, the national symbol of Puerto Rico, has likely resounded through Caribbean forests for at least 29 million years.

A new study published in Biology Letters describes a fragmented arm bone from a frog in the genus Eleutherodactylus, also known as rain frogs or coquís. The fossil is the oldest record of frogs in the Caribbean and, fittingly, was discovered on the island where coquís are most beloved.

"It's a national treasure," said David Blackburn, Florida Museum curator of herpetology and the study's lead author. "Not only is this the oldest evidence for a frog in the Caribbean, it also happens to be one of the frogs that are the pride of Puerto Rico and related to the large family Eleutherodactylidae, which includes Florida's invasive greenhouse frogs."

Jorge Velez-Juarbe, associate curator of marine mammals at the Natural History Museum of Los Angeles County, found the fossil on a river outcrop in the municipality of San Sebastian in northwestern Puerto Rico. Velez-Juarbe and his collaborators' previous collecting efforts at the site uncovered fossil seeds, sea cows, side-necked turtles and the oldest remains of gharials and rodents in the Caribbean, dating to the early Oligocene Epoch, about 29 million years ago.

Still, "there have been many visits from which I have come out empty-handed over the last 14 years," he said. "I've always kept my expectations not too high for this series of outcrops."

On this trip in 2012, he combed the deposits for half a day without much luck when a small bone, partially exposed in the sediment, caught his eye. He examined it with his hand lens.

"At the moment, I couldn't wrap my mind as to what it was," Velez-Juarbe said. "Then once I got back home, cleaned around it with a needle to see it better and checked some references, I knew I had found the oldest frog in the Caribbean."

The ancient coquí displaces an amber frog fossil discovered in the Dominican Republic in 1987 for the title of oldest Caribbean frog. While the amber fossil was originally estimated to be 40 million years old, scientists now date Dominican amber to about 20 million to 15 million years ago, Blackburn said.

Based on genetic data and family trees, scientists had hypothesized rain frogs lived in the Caribbean during the Oligocene, but lacked any fossil evidence. The small, lightweight bones of frogs often do not preserve well, especially when combined with the hot, humid climate of the tropics.

Matching a single bone fragment to a genus or species "is not always an easy process," Velez-Juarbe said. It can also depend on finding the right expert. His quest for help identifying the fossil turned up empty until a 2017 visit to the Florida Museum where he had once been a postdoctoral researcher.

"I got to talk with Dave about projects, and the rest is now history," he said.

Possibly first arriving in the Caribbean by rafting from South America, frogs in the genus Eleutherodactylus, which encompasses some 200 species, dominate the region today.

"This is the most diverse group by two orders of magnitude in the Caribbean," Blackburn said. "They've diversified into all these different specialists with various forms and body sizes. Several invasive species also happen to be from this genus. All this raises the question of how they got to be this way."

One partial arm bone may not tell the whole story of coquí evolution - but it's a start.

"I am thrilled that, little by little, we are learning about the wildlife that lived in Puerto Rico 29-27 million years ago," Velez-Juarbe said. "Finds like this help us unravel the origins of the animals we see in the Caribbean today."

Italy was the main origin of the individuals who first brought the novel coronavirus to Brazil, according to a study by Brazilian researchers in collaboration with colleagues in the United Kingdom, Canada and the United States.

The COVID-19 pandemic arrived in Brazil between February and early March.

"In contrast with China and other countries, where the outbreak began slowly with a small number of cases, it was started in Brazil by more than 300 people, most of whom came from Italy. The virus spread very quickly as a result," said Ester Sabino, one of the authors of the study. Sabino is a professor at the University of São Paulo's Medical School (FM-USP) and headed the university's Institute of Tropical Medicine (IMT-USP) between 2015 and 2019.

Most of these people came from Italy to São Paulo City, where the first cases of the disease in Brazil were notified, but some went to other destinations, including Rio de Janeiro, Porto Alegre, Salvador, Curitiba, Belo Horizonte, Fortaleza, Recife, Vitória and Florianópolis, contributing to the nationwide spread of the disease.

The study was supported by São Paulo Research Foundation - FAPESP under the aegis of the Brazil-UK Center for Arbovirus Discovery, Diagnosis, Genomics and Epidemiology (CADDE). The results are reported in an article published in the Journal of Travel Medicine.

The researchers estimated that 54.8% of all cases of COVID-19 imported into Brazil by March 5 derived from people infected in Italy, followed by passengers who flew in from China (9.3%) and France (8.3%).

They also estimated that 24.9% of all infected people flying to Brazil during the period traveled from Italy to São Paulo, and that Italy was the start of five of the ten main routes for infected travelers coming to Brazil (via China, France, Switzerland, South Korea and Spain).

To identify the main routes for the importation of COVID-19 to Brazil, the researchers analyzed February-March 2020 data for passengers traveling to any Brazilian airport from 29 countries with confirmed cases of the disease.

They estimated the proportion of infected travelers potentially arriving in Brazilian cities from each country and for each route based on the total number of passengers flying to any Brazilian airport during the period, country populations and the number of cases notified by these countries as of March 5, 2020.

The estimates were corroborated by the Brazilian Ministry of Health's official data on notified cases, showing that 14 of the first 29 patients diagnosed with COVID-19 in Brazil had just been to Italy. Six of them (23.1%) were notified in São Paulo.

"It was very clear that São Paulo would be the epicenter of the epidemic in Brazil because it was the final destination for the largest number of infected people coming mainly from Italy," Sabino said.

Focus on internal mobility

According to Sabino, who led the genome sequencing of the coronaviruses isolated from the first two confirmed cases of COVID-19 in Brazil, sustained community transmission of the disease now prevails and the authorities should focus on restricting internal mobility in order to contain the epidemic.

This means restricting the mobility of the inhabitants of São Paulo, where most of the confirmed cases in Brazil have been notified.

"São Paulo and to a lesser extent Rio de Janeiro will be the hubs from which the virus spreads to the rest of the country, so people should be prevented from leaving these two cities," she said.

Continuation of sequencing

The researchers led by Sabino continue to sequence SARS-CoV-2 isolated from Brazilians diagnosed with COVID-19. At one point they had to stop because some of their members were thought to have been infected.

"We had to shut down the lab, but we're back now and will analyze whether we can sequence a larger number of viral genomes," Sabino said.

The speed with which the disease spread around Brazil has disrupted the group's plans. "Transmission of the virus is proceeding so fast that the sequencing data can't help us understand how the epidemic is spreading as we planned," Sabino said.

The researchers expected to be able to sequence viruses as sporadic cases of the disease were notified in order to keep track of the transmission trajectory and contribute to the design of a containment strategy, but the number of cases arriving at the lab simultaneously turned out to be too high.

"It won't be possible to control the epidemic with sequencing alone. It's spreading very fast, and we can no longer track all the cases," Sabino said.

The number of genomes sequenced worldwide from infected patients has almost reached 800. These sequences are being made public, and can be used for research on primary resistance to help develop promising antiviral drugs against the virus, Sabino explained.

"When a candidate drug is found, a database of viral genome sequences will certainly be useful for this purpose," she said.