Culture

A scientist from RUDN University analysed the effect of visual impairment on a person's perception of unfamiliar sounds when learning a foreign language. The experiment showed that lack of access to visual cues makes learning difficult.Results of workpublished in the journal Medical Hypotheses.

In the traditional sense, speech perception is primarily associated with hearing. However, the visual channel is just as important - when a person sees the interlocutor, they analyze their posture, gestures, facial expression. In addition, visual information helps people perceive long and conceptually complex messages, and allows people with hearing impairments to communicate and understand each other in noisy environments. According to some studies, if only the auditory canal is available during a conversation - for example, as in people with visual impairments or when talking on the phone - the accuracy of information perception decreases. Other scholars believe that visual cues are not required for speech perception, and people with visual impairments can understand information even better by developing hearing. This can be explained by the fact that they have been using this channel for a long time as the main source of information, and therefore can analyze it more closely. For example, assess the intonation of the interlocutor, pay attention to the intermittent speech, the frequency of breathing. Young scientist from RUDN Georgios Georgiou found out whether visual impairment can affect the perception of speech when learning a foreign language.

Until now, scientists have concentrated on how a person perceives familiar sounds (that is, those that occur in his native language), while the sounds found in foreign speech can be more difficult to perceive due to the influence of the first language. Georgiou conducted an experiment to study the perception of unfamiliar sounds by people learning a second language. The subjects passed tests to distinguish and recognize sounds recorded by native speakers of a language they did not know, and were assigned to groups according to the similarity with the sounds they knew. The scientist also compared the pronunciation of students with the pronunciation of native speakers. An example of a sound that is difficult for Russians to perceive is the preposition "the" from the English language. Its pronunciation is often explained through articulation - the position of the tongue and lips in relation to the teeth, the width of the mouth opening, and so on.

According to the results of the experiment Georgiou made a conclusion, that certain types of sounds in foreign language are more difficult for visually impaired people than for students with normal vision. This is most noticeable for two or more non-native sounds that are similar in sound to each other. He argues that it will be difficult for people with visual impairments to develop stable mental representations for non-native speech sounds, or to maintain the flexibility to perceive non-standard speech solely through auditory and kinesthetic feedback. At the same time, sighted people will have more opportunities to do this because they have access to visual cues.

"People who are visually impaired are likely to have worse speech perception, especially in contexts where flexibility is required - for example, noisy environments, accented speech, and so on. This is because speech perception will function in a monomodal manner, preventing the extraction of most of the acoustic invariants found in actual movements of the vocal tract. While there is evidence against this hypothesis, much of the earlier work did not take into account several factors that may affect speech perception, while research on second language perception in people with visual impairments is limited.", -explains Georgios Georgiou, Researcher, Department of General and Russian Linguistics, Faculty of Philology, RUDN.

This hypothesis is consistent with earlier evidence that blind speakers of French in Canada reproduce native vowels with reduced acoustic contrast, and phonetic differences in speech appeared later in children with visual impairments than in children with normal vision.

Alkylation reactions are used in the petrochemical industry to obtain high-octane number components for gasolines. A chemist from RUDN University found a way to speed this process up to 24 times. To do so, he developed a catalyst based on silica and niobium. The results of his work were published in the Molecular Catalysis journal.

In the course of alkylation, an atom of hydrogen in an organic compound is replaced with other substances, the so-called alkylating agents. Alkylation is used in the chemical and petrochemical industries, for example, to obtain high-octane number components in gasolines. For the process to go on quickly and efficiently, it needs catalysts including mineral acids and zeolites--minerals that are capable of selectively releasing substances and then adsorbing them back. However, mineral (e.g. sulphuric or phosphoric) acids can be expensive and dangerous: in order to extract them from the reaction mix, one needs additional reagents that can be hard to handle. Unlike mineral acids, zeolites are safe and cheap to produce. The only problem lies in their microporous structure that limits the size of the molecules they can react with. A chemist from RUDN University created a catalyst that is free from these disadvantages and able to speed up the alkylation reaction up to 24 times. To do so, his team used niobium and SBA-15, a mesoporous ordered form of silica.

"SBA-15 materials are relevant as catalytic support due to their high surface area and pore volume in the mesopore range that convert it in an outstanding catalyst support. We aimed to evaluate the acidity of several Al-SBA-15 supported niobium oxide catalysts prepared by a mechanochemical protocol with different metal loadings," said Rafael Luque PhD, the head of the Molecular Design and Synthesis of Innovative Compounds for Medicine Science Center at RUDN University.

The team paid attention to the reductive-oxidative and acidic properties of niobium-based compounds that are important for a catalyst and decided to test niobium in an alkylation reaction. To do so, they put niobium oxide nanoparticles (that had been mechanochemically ground down to several nanometers in size) on the support. The metal content in the new material varied from 0.5% to 1% and the size of the particles was controlled with a transmission electron microscope. The team used energy-dispersive X-ray spectroscopy to secure even distribution of particles across the surface of the support.

To analyze the catalytic properties of the new material, the chemists carried out the reaction of toluene alkylation with benzyl alcohol and benzyl chloride that acted as alkylating agents. As a result of the experiment, the team confirmed a positive effect of niobium particles on the reaction: its time of reaction reduced from 4 hours to 10 minutes. The catalyst with lower niobium content (0.5%) turned out to be more effective due to better dispersion. The team believes that when the catalyst was synthesized, niobium oxide deposited on the support, and the more niobium, the bigger the catalyst particles turned out to be. This reduced the effective contact area of the particles and therefore had a negative impact on the material's catalytic activity.

"We managed to create a catalyst that reduces the time of alkylation reactions from several hours to just 10 minutes, is free from the chemical limitations of zeolites, and poses no danger unlike mineral acids," added Rafael Luque.

Man-made global heating has long been presented as a relatively simple chain of cause and effect: humans disrupt the carbon cycle by burning fossil fuels, thereby increase the concentration of CO2 in the atmosphere, which in turn leads to higher temperatures around the globe. "However, it becomes increasingly clear that this is not the end of the story. Forest fires become more frequent all over the world, release additional CO2 into the atmosphere, and further reinforce the global warming that enhanced forest fire risk in the first place. This is a textbook example of what climate scientists call a positive feedback mechanism," stresses David De Vleeschouwer, a postdoctoral researcher at MARUM - Center for Marine Environmental Sciences at the University of Bremen.

To reveal these kind of climate-carbon cycle feedback mechanisms under natural circumstances, David De Vleeschouwer and colleagues exploited isotopic data from deep-ocean sediment cores. "Some of these cores contain sediments of up to 35 million years old. Despite their respectable age, these sediments carry a clear imprint of so-called Milankovi? cycles. Milankovi? cycles relate to rhythmic changes in the shape of the Earth's orbit (eccentricity), as well as to the tilt (obliquity) and orientation (precession) of the Earth's rotational axis. Like an astronomical clockwork, Milankovi? cycles generate changes in the distribution of solar insolation over the planet, and thus provoke cadenced climate change", explains David De Vleeschouwer. "We looked at the carbon and oxygen isotope composition of microfossils within the sediment and first used the eccentricity, obliquity and precession cadences as geological chronometers. Then, we applied a statistical method to determine whether changes in one isotope system lead or lag variability in the other isotope."

His colleague Maximilian Vahlenkamp adds: "When a common pattern in both isotope systems occurs just a little earlier in the carbon system compared to the oxygen isotope system, we call this a carbon-isotope lead. We then infer that the carbon cycle exerted control over the climate system at the time of sediment deposition." Paleoclimatologists and paleoceanographers often use carbon isotopes as an indicator of carbon-cycle perturbations, and oxygen isotopes as a proxy for changes in global climate state. Changes in the isotopic composition of these deep-sea microfossils may indicate, for example, an increase in the continental carbon storage by land plants and soils, or global cooling with a growth of ice caps.

"The systematic and time-continuous analysis of leads and lags between carbon cycle and climate constitutes the innovative character of this study. Our approach allows to sequence Earth's history at high resolution over the past 35 million years", says Prof Heiko Pälike. "We show that the past 35 million years can be subdivided in three intervals, each with its specific climate-carbon cycle modus operandi." On average, the authors found oxygen isotopes to lead carbon isotope variations. This means that, under natural conditions, climate variations are largely regulating global carbon cycle dynamics. However, the research team focused on times when the opposite was the case. Indeed, De Vleeschouwer and colleagues found a few examples of ancient periods during which the carbon cycle drove climate change on approximately 100,000-year timescales, just as it is the case now on much shorter timescales - "but then of course without human intervention," states Pälike.

During the oldest interval, between 35 and 26 million years ago, the carbon cycle took the lead over climate change mostly during periods of climate stability. "Periods of climate stability in the geologic record often have an astronomical cause. When the Earth's orbit around the sun is close to a perfect circle, seasonal insolation extremes are truncated and more equable climates are enforced," explains David De Vleeschouwer. "Between 35 and 26 million years ago, such astronomical configuration would have been favourable for a temporal expansion of the Antarctic ice sheet. We propose that under such a scenario, the intensity of glacial erosion and subsequent rock weathering increased. This is important, because the weathering of silicate rocks removes CO2 from the atmosphere, and thus ultimately controls the greenhouse effect."

But around 26 million years ago, the modus operandi radically changed. The carbon cycle took control over climate at times of climate volatility, not stability. "We believe this change traces back to the uplift of the Himalayan mountains and a monsoon-dominated climate state. When seasonal insolation extremes are amplified through an eccentric Earth orbit, monsoons can become truly intense. Stronger monsoons permit more chemical weathering, the removal of CO2 from the atmosphere and thus a carbon-cycle control over climate."

The mechanisms proposed by the authors not only explain the observed patterns in carbon and oxygen isotopes, they also provide new ideas as to how the climate system and the carbon cycle interacted through time. "Some hypotheses need further testing with numerical climate and carbon cycle models, but the process-level understanding presented in this work is important because it provides a glimpse at the machinery of our planet under boundary conditions that are fundamentally different from today's," says De Vleeschouwer. Moreover, this work also provides scenarios that can be used to evaluate the ability of climate-carbon cycle models when they are pushed to the extreme scenarios of the geologic past.

Immune cells that can recognise residual HIV-infected cells in people living with HIV (PLWH) who take antiretroviral therapy (ART) remain active for years, says a new study published today in eLife.

The findings also suggest the majority of these immune cells, called CD8+ T cells, should have the capacity to detect the HIV-infected cells that drive HIV-1 rebound following interruptions to treatment. This insight could contribute to the development of new curative strategies against HIV infection.

ART has transformed HIV-1 from a fatal disease to a chronic condition in PLWH. However, it must be taken by those with the infection for the rest of their lives, as interrupting treatment often allows the virus to rebound within weeks. This rebound results from cells harbouring HIV-1 DNA that is integrated into the human genome.

"While more than 95% of proviral DNA is unable to replicate and reactivate HIV-1, the remaining fraction that we define in our study as the 'HIV-1 reservoir' maintains its ability to produce infectious virus particles and cause viral rebound," explains lead author Joanna Warren, Postdoctoral Investigator at the Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, US. "The largest and most well-characterised HIV-1 reservoir resides in 'resting' CD4+ T cells, which circulate in the blood and are long-lived."

There are a couple of strategies to allow people with HIV-1 to stop ART without viral rebound. Both approaches may harness HIV-1-specific CD8+ T cells to achieve the reduction or elimination of the HIV-1 reservoir. However, variations (or mutations) in viral particles that exist in the HIV-1 reservoir may limit the capacity of these T cells to recognise and clear virus-infected cells, meaning the cells can escape detection and go on to cause viral rebound. "In our study, we wanted to determine the frequency and patterns of T-cell escape mutations in the HIV-1 reservoir of people who are on ART," Warren says.

To do this, the team measured HIV-1-specific T-cell responses and isolated reservoir virus in 25 PLWH who are on ART. Of these participants, four started on ART during acute HIV-1 infection, which means virus levels were controlled early, while the other 21 started on ART during chronic HIV-1 infection, which means considerable virus mutation occurred before virus levels were controlled.

In the HIV-1 proteome (the entire set of proteins expressed by the virus) for each participant, the team identified T-cell epitopes (regions of proteins that trigger an immune response). They sequenced HIV-1 'outgrowth' viruses from resting CD4+ T cells and tested mutations in T-cell epitopes for their effect on the size of the T-cell response. These strategies revealed that the majority (68%) of T-cell epitopes did not harbour any detectable escape mutations, meaning they could be recognised by circulating T cells.

"Our findings show that the majority of HIV-1-specific T cells in people on ART can detect HIV viruses that have the capacity to rebound following treatment interruption," concludes senior author Nilu Goonetilleke, a faculty member at the Department of Microbiology and Immunology, University of North Carolina at Chapel Hill. "This suggests that T cells likely help to control viral rebound and could be leveraged in future treatment strategies against HIV."

Only about one in every 170 children take them. But "orphan drugs" accounted for 1 in every 15 private insurance dollars spent on children's health care in the United States in 2018, according to a new study. That's up 65% from just five years before.

Even though insurance companies pay much of the cost of high-priced orphan drugs that treat rare childhood diseases, families' share of the cost has risen rapidly.

In fact, the study shows that out-of-pocket costs for these families were higher than those faced by adults who also take orphan drugs.

Some families spend thousands of dollars each year to buy orphan drugs, which are drugs that have received a special designation from the U.S. Food and Drug Administration. About 1 in 8 families paid more than $2,000 a year in 2018 - double the percentage who spent that much in 2013.

The study, published in the October issue of the journal Health Affairs by researchers from the University of Michigan and Boston University, looks at private insurer payments and out-of-pocket spending on 526 orphan drugs. It used a database that every year included data about the drug costs of 4.4 to 5.8 million children age 17 and under.

The special FDA "orphan" designation is designed to incentivize drug companies to develop treatments for rare conditions. A company that receives the designation for its product has a greater amount of time when it has the exclusive rights to market the product and fend off competitors.

Certain drugs drove most of the increase

The researchers report that the prices for small-molecule drugs drove much of the increase in orphan drug spending, with a 162% rise in five years, compared with 16% for biologic drugs, which are derived from living organisms.

Just three drugs approved for the same condition account for more than 23% of all spending on orphan drugs for privately insured children in 2018, the analysis shows. All three - sold as Norditropin, Humatrope and Genotropin - were originally developed to boost the height of children with growth hormone deficiency.

But other research has shown that many children who don't have this rare condition also receive these three drugs through off-label prescribing aimed at boosting their height.

There are no clear guidelines for determining which children should receive the drugs, and insurance companies vary widely in their decisions about covering the cost of the drugs for such uses.

In some patients who died with severe COVID-19 and respiratory failure, a jelly was formed in the lungs. Researchers have now established what the active agent in the jelly is and thanks to that, this new discovery can now be the key to new effective therapies. This according to a new study at Umeå University, Sweden.

"There are already therapies that either slow down the body's production of this jelly or breaks down the jelly through an enzyme. Our findings can also explain why cortisone seems to have an effect on COVID-19," says Urban Hellman, researcher at Umeå University.

When performing lung scans on critically ill patients with COVID-19 infection, medical professionals have been able to see white patches. Additionally, the autopsies of some deceased COVID-19 patients have shown that the lungs were filled with a clear liquid jelly, much resembling the lungs of someone who has drowned. It was previously unknown where this jelly originated from.

Now though, a group of researchers at the Translational Research Centre at Umeå University have shown that the jelly consists of the substance hyaluronan, which is a polysaccharide in the glycosaminoglycan group.

The presence of hyaluronan is normal in the human body, with various functions in different tissues, but it generally acts as a useful characteristic in the connective tissue. Not least, hyaluronan is involved in the early stages of wound healing. Hyaluronan is also produced synthetically in the beauty industry for lip augmentation and anti-wrinkle treatments.

Since hyaluronan can bind large amounts of water in its web of long molecules, it forms a jelly-like substance. And it is this process that runs riot in the alveoli of COVID-19 patients' lungs resulting in the patient needing ventilator care and, in worst case, dies from respiratory failure.

Currently, a drug called Hymecromone is used to slow down the production of hyaluronan in other diseases such as gallbladder attacks. There is also an enzyme that can effectively break down hyaluronan. As an example, this enzyme can be used in the event that an unsuccessful beauty treatment needs to be terminated abruptly.

Even cortisone reduces the production of hyaluronan. In a British study, preliminary data shows positive effects on treatments with the cortisone drug Dexamethasone in severely ill COVID-19 patients.

"It has previously been assumed that the promising preliminary results would be linked to the general anti-inflammatory properties of cortisone, but in addition to those beliefs, cortisone may also reduce the production of hyaluronan, which may reduce the amount of jelly in the lungs," says Urban Hellman.

The effects of cancer treatment on a patient's body are easy to see, whether it is a lack of hair on their head, sores on their skin or a look of fatigue on their face. And while there has been a lot of discussion around these impacts, a new study looks at just how much the stress of financial hardship caused by cancer care and treatment can affect a patient's emotional, mental and physical well-being.

"There has been increasing awareness of the potential for oncology care to result in long-term financial burdens and financial toxicity to patients and their families," said Dr. Steven Coughlin, Interim Head for the Division of Epidemiology in the Department of Population Health Sciences at the Medical College of Georgia at Augusta University. "About 28% to 48% of cancer survivors experience financial toxicity based upon monetary measures and 16% to 73% experience financial toxicity based upon subjective measures."

Coughlin, along with Dr. Jorge Cortes, director of the Georgia Cancer Center at Augusta University, Dr. Martha Tingen, associate director of the Cancer Prevention, Control and Population Health program at the Cancer Center, and Dr. Deepak Nag Ayyala, who served as the study's biostatistician, submitted a questionnaire about financial distress to 1,000 randomly selected breast cancer patients who were treated for the disease and had completed primary therapy. They interviewed the patients using a self-administered questionnaire looking for answers to whether patients were less able to provide for the financial needs of their family, had difficulty meeting their medical expenses, did not have money to cover the cost of their co-pay for medical visits and did not have money to cover the cost of their co-pay for medications. Each question was followed by three responses, "not a problem," "somewhat a problem," or "a severe problem." A total of 164 women completed the questionnaire and returned their responses. They published their findings, "Financial Distress Among Breast Cancer Survivors" in the journal Current Cancer Reports in August.

"Looking at the results, about 8.6% of the respondents reported 'being less able to provide for the financial needs of their family' was a severe problem," Coughlin said. "Nearly 14.4% said 'difficulty in meeting medical expenses' was a severe problem. Approximately 8.4% said 'no money for cost of or co-payment for medical visits' was a severe problem. And, around 8.4% answered that 'no money for cost of or co-payment for medicine(s)' was a severe problem."

"I think the concept of financial distress is an important aspect of cancer care that I do not think we've addressed enough historically," Cortes said. "We know that as the Food and Drug Administration approves newer and better drugs for breast cancer treatment, there is frequently an increasing cost with newer drugs. And with some of those therapies having to be taken over a longer period, it can increase the level and length of financial stress."

The team hopes their findings will educate oncologists across the country about the need to discuss financial distress with patients and options they have to help with the costs associated with their care. At the Georgia Cancer Center, there is a nurse navigator and a social worker patients can meet with to find foundations and organizations that can help cover some of the costs of medical visits and medications used in their treatment.

"At the Georgia Cancer Center, we have a higher population of people living in rural areas with less access to care," Cortes said. "These people may not have the financial means to cover some of the costs of their care. So, we want to work with them to share information about financial stress and entities they can reach out to for assistance."

Insulin prices are more than eight times higher in the United States than in 32 high-income comparison nations combined, according to a new RAND Corporation study.

The study compared how much different types of insulin sold in the U.S. would cost if bought at prices in other countries. The average price per unit across all types of insulin in the U.S. was $98.70. Other countries would have paid a fraction as much for the same insulins.

U.S. prices were higher than each of the 32 comparison countries individually, ranging from 3.8 times higher than those in Chile to 27.7 times those in Turkey. U.S. prices were 6.3 times higher than those in Canada, 5.9 times higher than those in Japan and 8.9 times higher than those in the United Kingdom.

The study used manufacturer prices for the analysis. The final, net prices paid for insulins are likely to be significantly lower than manufacturer prices in the U.S. because rebates and other discounts often drive down the price paid by individuals in the U.S.

But even if such rebates and discounts drive down prices by as much as 50%, the prices paid by U.S. consumer are likely to be four times the average paid in other high-income nations, according to the study.

"This analysis provides the best available evidence about how much more expensive insulin is in the U.S. than in other nations around the world," said Andrew Mulcahy, the study's lead author and a senior policy researcher at RAND, a nonprofit research organization. "Prices in the U.S. are always much higher than other nations, even if you assume steep discounts to manufacturer prices in the United States."

Insulin list prices in the United States have increased dramatically over the past decade. For example, one federal analysis found that the average U.S. wholesale-acquisition price for rapid-acting, long-acting, and short-acting insulin increased by 15% to 17% per year from 2012 to 2016.

Another study found that among adults with employer-sponsored health insurance, annual insulin spending per person doubled between 2012 and 2016, increasing from $1,432 to $2,853 even after accounting for a 50% rebate.

Insulin is a drug most commonly used to control blood sugar levels in people who have insulin-dependent diabetes. The drug is sold in many different forms, with different chemical properties and different duration of effects.

RAND researchers compiled their estimates of international insulin prices by examining industry-standard IQVIA MIDAS data on insulin sales and volume for 2018, comparing the U.S. to 32 nations that belong to the Organisation for Economic Co-operation and Development.

Although the ratio of U.S. prices to other-country prices varied depending on the comparison country and insulin category, U.S. prices were always higher and often 5 to 10 times higher than those in other countries.

The study found that U.S. prices were relatively higher for analog versus human insulins and for rapid-acting rather than short or long-acting insulins. U.S. prices were even higher when researchers compared prices pooling similar insulin products together, suggesting that the United States uses a more-expensive mix of insulin products.

The study was sponsored by the Office of the Assistant Secretary for Planning and Evaluation in the U.S. Department of Health and Human Services.

The report, "Comparing Insulin Prices in the United States to Other Countries: Results from a Price Index Analysis," is available on the website of the U.S. Department of Health and Human Services and on http://www.rand.org.

Other authors of the report are Daniel Schwam and Nate Edenfield.

RAND Health Care promotes healthier societies by improving health care systems in the United States and other countries.

Scientists have long known that the plant hormone auxin controls many aspects of plant growth, development, and responses to the environment. Only more recently have they begun to understand that there is also a link between auxin and leaf spotting diseases.

Several years ago scientists, including Barbara Kunkel, discovered an increased concentration of auxin in leaves inoculated by the bacterial pathogen, Pseudomonas syringae, that causes bacterial spot and speck diseases on many plants.

"We previously demonstrated that auxin promotes disease caused by P. syringae on Arabidopsis thaliana plants, which means that auxin is not acting as a classic plant defense hormone," Kunkel explained. "We were also one group to demonstrate that auxin also suppresses salicylic acid (SA)-mediated plant defense responses."

However, Kunkel and her colleagues knew there was more work to be done. "It was clear that there was a second role for auxin in P. syringae infection, that appeared to be independent of modulating SA-mediated defenses." In a new article published in the MPMI journal, Kunkel and colleagues at Washington University in St. Louis and the University of California San Diego present the first investigation of the role of auxin in regulating pathogen gene expression in plant tissue.

This article makes two new contributions to our understanding of the role of auxin during P. syringae infection of Arabidopsis thaliana plants. First, the research demonstrated that the canonical host auxin signaling pathway is required to suppress SA-mediated host defense and normal diseases susceptibility to P. syringae. Second, auxin plays a second role in promoting disease by regulating virulence gene expression in P. syringae.

"Our data led us to propose a working model in which auxin acts as a signal to the pathogen to switch from an early state of infection to a later stage that requires expression of a second set of virulence genes," Kunkel said. "There have been several reports that bacteria can respond to auxin and auxin has begun to be considered as a potential microbial signaling molecule. However, to the best of our knowledge, this is the first time a biologically relevant example has been demonstrated. This is an exciting breakthrough in plant-microbe interactions."

This work provides another example of how plant hormones can be used by microbes as an environmental cue, which seems to be emerging as a common strategy as scientists learn more about how pathogens and parasites sense their plant hosts. To learn more about this study, read "Dual Role of Auxin in Regulating Plant Defense and Bacterial Virulence Gene Expression During Pseudomonas syringae PtoDC3000 Pathogenesis" published in the August issue of MPMI.

Familiar stars shine, nebulae glow, and nearby galaxies tantalize in a new panorama of the northern sky assembled from 208 pictures captured by NASA's Transiting Exoplanet Survey Satellite (TESS). The planet hunter imaged about 75% of the sky in a two-year-long survey and is still going strong.

TESS has discovered 74 exoplanets, or worlds beyond our solar system. Astronomers are sifting through some 1,200 additional exoplanet candidates, where potential new worlds await confirmation. More than 600 of these candidates lie in the northern sky.

TESS locates planets by simultaneously monitoring many stars over large regions of the sky and watching for tiny changes in their brightness. When a planet passes in front of its host star from our perspective, it blocks some of the star's light, causing it to temporarily dim. This event is called a transit, and it repeats with every orbit of the planet around the star. This technique has proven to be the most successful planet-finding strategy so far, accounting for about three quarters of the nearly 4,300 exoplanets now known. The data collected also allow for the study of other phenomena such as stellar variations and supernova explosions in unprecedented detail.

The northern mosaic covers less of the sky than its southern counterpart, which was imaged during the mission's first year of operations. For about half of the northern sectors, the team decided to angle the cameras further north to minimize the impact of scattered light from Earth and the Moon. This results in a prominent gap in coverage.

The northern panorama represents only a glimpse of the data TESS has returned. The mission splits each celestial hemisphere into 13 sectors. TESS imaged each sector for nearly a month using four cameras, which carry a total of 16 sensors called charge-coupled devices (CCDs). During its primary mission, the cameras captured a full sector of the sky every 30 minutes. This means each CCD acquired nearly 30,800 full science images. Adding in other measurements, TESS has beamed back more than 40 terabytes so far - equivalent to streaming some 12,000 high-definition movies.

Remarkably, these numbers will rise sharply over the next year. TESS has now begun its extended mission, during which it will spend another year imaging the southern sky. The satellite will revisit planets discovered in its first year, find new ones, and fill in coverage gaps from its initial survey. Improvements to the satellite's data collection and processing now allow TESS to return full sector images every 10 minutes and measure the brightness of thousands of stars every 20 seconds - all while continuing its previous strategy of measuring the brightness of tens of thousands of stars every two minutes.

"These changes promise to make TESS's extended mission even more fruitful," said Padi Boyd, the mission's project scientist at NASA's Goddard Space Flight Center in Greenbelt, Maryland. "Making high-precision measurements of stellar brightness at these frequencies makes TESS an extraordinary new resource for studying flaring and pulsating stars and other transient phenomena, as well as for exploring the science of transiting exoplanets."

TESS is a NASA Astrophysics Explorer mission led and operated by MIT in Cambridge, Massachusetts, and managed by NASA's Goddard Space Flight Center. Additional partners include Northrop Grumman, based in Falls Church, Virginia; NASA's Ames Research Center in California's Silicon Valley; the Harvard-Smithsonian Center for Astrophysics in Cambridge, Massachusetts; MIT's Lincoln Laboratory; and the Space Telescope Science Institute in Baltimore. More than a dozen universities, research institutes, and observatories worldwide are participants in the mission.

For more information on TESS, visit:

https://www.nasa.gov/tess

New York, NY--October 6, 2020--Columbia Engineering researchers report that Sofosbuvir-terminated RNA is more resistant to the proofreader of SARS-CoV-2, the virus that causes COVID-19, than Remdesivir-terminated RNA. The results of the new study, published today by the Nature Research journal Scientific Reports, support the use of the FDA-approved hepatitis C drug EPCLUSA--Sofosbuvir/Velpatasvir--in combination with other drugs in COVID-19 clinical trials.

The SARS-CoV-2 exonuclease-based proofreader maintains the accuracy of viral RNA genome replication to sustain virulence. Any effective antiviral targeting the SARS-CoV-2 polymerase must therefore display a certain level of resistance to this proofreading activity.

"We found that the RNA terminated by Sofosbuvir resists removal by the exonuclease to a substantially higher extent than RNA terminated by Remdesivir, another drug being used as a COVID-19 therapeutic," says the team's lead PI Jingyue Ju, Samuel Ruben-Peter G. Viele Professor of Engineering; professor of Chemical Engineering and Pharmacology; director, Center for Genome Technology & Biomolecular Engineering.

The new study builds upon earlier work the researchers have conducted. Last January, before COVID-19 reached pandemic status, the team posited that EPCLUSA might inhibit SARS-CoV-2, the virus responsible for COVID-19. Their reasoning was based on the analysis of the molecular structures and activities of hepatitis C viral inhibitors and a comparison of hepatitis C virus and coronavirus replication.

In a subsequent study, the researchers demonstrated that the active drug Sofosbuvir triphosphate is incorporated by SARS-CoV and SARS-CoV-2 polymerases, shutting down the polymerase reaction. Other investigators have since demonstrated the ability of Sofosbuvir to inhibit SARS-CoV-2 replication in lung and brain cells; currently, COVID-19 clinical trials with a number of hepatitis C drugs such as EPCLUSA and the combination of Sofosbuvir and Daclatasvir (which is similar to Velpatasvir) are ongoing in several countries.

Ju notes that a recent preprint from UC Berkeley indicates that a combination of Remdesivir and EPCLUSA increases Remdesivir's efficacy 25-fold in inhibiting SARS-CoV-2, the virus that causes COVID-19: "These results offer a molecular basis supporting the study of EPCLUSA in combination with Remdesivir for COVID-19 clinical trials."

In their efforts to identify the genetic basis for differences in mate choice that keep two co-existing species of butterfly separate, evolutionary biologists at Ludwig-Maximlians-Universitaet (LMU) in Munich have identified five candidate genes that are associated with divergence in visual mating preferences.

The evolution of a new species often involves a change in mating preference. This happens, for instance, when members of different populations of a given species cease to mate with each other because they no longer find potential partners sufficiently attractive.  Two closely related species of tropical butterflies, Heliconius melpomene und Heliconius cydno, provide an interesting example of this phenomenon. The two species are often seen flying together, and crosses between them can result in fertile hybrid offspring. - Nevertheless, individuals of the two species hardly ever mate with each other in the wild. How such behaviorally induced barriers to reproduction emerge is largely unknown. "When changes in behaviour are genetically hard-wired, as mate choice seems to be in our butterflies, they must involve alterations in sensation, that is, the stimuli they can detect, or changes in how these stimuli are  processed," says LMU evolutionary biologist Dr. Richard Merrill. Together with members of his group, and collaborators at the Smithsonian Tropical Research Institute in Panama and at the University of Cambridge, he has now identified five genes that are linked to the different mating preferences of H. melpomene and H. cydno. As the authors report in the open access journal Nature Communications, these genes are likely to change how visual stimuli are processed during courtship, without altering how the butterflies perceive the world in other contexts.

H. melpomene and H. cydno differ in the striking color patterns of their wings, which serve to warn off potential predators that they are distasteful. H. melpomene has black wings with red bars and thin yellow stripes, while H. cydno's wings feature white bars on a black background. Notably the males of each species show a marked attraction for females with the same 'color scheme' as themselves. In their quest for the genetic factors that underlie differences in these mating preferences, Merrill and his colleagues had previously identified three genomic regions which were associated with the different mating behaviors. One of these regions, on chromosome 18, had an especially strong effect on the degree of persistence with which the male pursues the female of his choice. Strikingly, a gene called optix, which controls the expression of the red bars on the wings of H. melpomene, lies within this same chromosomal segment. However, although this research revealed that one or more genes in this relatively short region of the chromosome must affect mate preference behaviors, the interval in question contains more than 200 genes.

In the new study, Matteo Rossi, a PhD student working in Merrill's group, compared the sequences and activity of these genes in neural tissues - including the central brain, optic structures and the 'ommatidia' (the retinal units that form the facets of the eye) - of H. melpomene and H. cydno. They were able to identify five genes located within this interval that differed between the two species and were associated with their different visual preferences. Most importantly, three of these genes code for proteins that play key roles in neural signal transmission. "Overall, the nature of our candidate genes suggests that the different preferences for the wing coloration of potential partners are likely to be based on differences in the processing of the visual information. - It seems that the two species do not differ with respect to what they see, but they react differently to the different color patterns," says Rossi. "In this way, over the course of evolution, mating preferences can change without affecting perceptions of other aspects of the environment."

A collaboration between scientists at the U.S. Department of Energy's National Renewable Energy Laboratory (NREL), the University of Portsmouth in the United Kingdom, and other partners has yielded further insight into the workings of plastic-eating enzymes.

The research determined two synergistic enzymes--PETase and MHETase--work effectively in tandem to break down polyethylene terephthalate (PET), which is a type of plastic used to make single-use beverage bottles, clothing, and carpeting. The research follows an earlier collaboration between these partners focused on PETase.

A bacterium, Ideonella sakaiensis 201-F6, was discovered in the soil outside of a Japanese PET bottle recycling plant in 2016 and was shown to secrete both PETase and MHETase. Researchers at NREL and Portsmouth were able to engineer PETase to increase its ability to digest PET, although still not fast enough to make the process commercially viable to handle the tons of discarded bottles littering the planet.

Gregg Beckham, a senior research fellow at NREL and co-lead of a new paper outlining the latest findings, said MHETase and PETase degrade PET faster than PETase alone. "They are better together than they are separate. PETase conducts the initial breakdown of the PET polymer, and MHETase further deconstructs the soluble products of PETase to produce the building blocks of PET," he said. Genetically linking the separate enzymes makes them function even better. By itself, MHETase does not act upon PET.

The paper, "Characterization and engineering of a two-enzyme system for plastics depolymerization," appears in the journal Proceedings of the National Academy of Sciences of the United States of America. The University of Portsmouth's John McGeehan co-led the study.

Additional authors from NREL are Brandon Knott, Erika Erickson, Japheth Gado, Isabel Pardo, Ece Topuzlu, Jared Anderson, Graham Dominick, Christopher Johnson, Nicholas Rorrer, Caralyn Szostkiewicz, and Bryon Donohoe.

"The team assembled here is incredibly diverse and multidisciplinary," said Knott, a chemical engineer. That enables hypotheses generated in one area to be immediately followed up on via computational or laboratory experiments.

MHETase has not been studied to date to the same extent as PETase. The new research combined structural, computational, biochemical, and bioinformatics approaches to reveal molecular insights into its structure and how it functions.

"Now we know in molecular-level detail how the enzyme actually works on MHET," Beckham said.

Additional research discovered two other bacteria that contain enzymes like MHETase, bringing the total known enzymes that act on this synthetic substrate to three.

HOUSTON - (Oct. 6, 2020) - Fat bacteria? Skinny bacteria? From our perspective on high, they all seem to be about the same size. In fact, they are.

Precisely why has been an open question, according to Rice University chemist Anatoly Kolomeisky, who now has a theory.

A primal mechanism in bacteria that keeps them in their personal Goldilocks zones -- that is, just right -- appears to depend on two random means of regulation, growth and division, that cancel each other out. The same mechanism may give researchers a new perspective on disease, including cancer.

The "minimal model" by Kolomeisky, Rice postdoctoral researcher and lead author Hamid Teimouri and Rupsha Mukherjee, a former research assistant at Rice now at the Indian Institute of Technology Gandhinagar, appears in the American Chemical Society's Journal of Physical Chemistry Letters.

"Everywhere we see bacteria, they more or less have the same sizes and shapes," Kolomeisky said. "It's the same for the cells in our tissues. This is a signature of homeostasis, where a system tries to have physiological parameters that are almost the same, like body temperature or our blood pressure or the sugar level in our blood.

"Nature likes to have these parameters in a very narrow range so that living systems can work the most efficiently," he said. "Deviations from these parameters are a signature of disease."

Bacteria are models of homeostasis, sticking to a narrow distribution of sizes and shape. "But the explanations we have so far are not good," Kolomeisky said. "As we know, science does not like magic. But something like magic -- thresholds -- is proposed to explain it."

For bacteria, he said, there is no threshold. "Essentially, there's no need for one," he said. "There are a lot of underlying biochemical processes, but they can be roughly divided into two stochastic chemical processes: growth and division. Both are random, so our problem was to explain why these random phenomenon lead to a very deterministic outcome."

The Rice lab specializes in theoretical modeling that explains biological phenomena including genome editing, antibiotic resistance and cancer proliferation. Teimouri said the highly efficient chemical coupling between growth and division in bacteria was far easier to model.

"We assumed that, at typical proliferation conditions, the number of division and growth protein precursors are always proportional to the cell size," he said.
T

he model predicts when bacteria will divide, allowing them to optimize their function. The researchers said it agrees nicely with experimental observations and noted manipulating the formula to knock bacteria out of homeostasis proved their point. Increasing the theoretical length of post-division bacteria, they said, simply leads to faster rates of division, keeping their sizes in check.

"For short lengths, growth dominates, again keeping the bacteria to the right size," Kolomeisky said.

The same theory doesn't necessarily apply to larger organisms, he said. "We know that in humans, there are many other biochemical pathways that might regulate homeostasis, so the problem is more complex."

However, the work may give researchers new perspective on the proliferation of diseased cells and the mechanism that forces, for instance, cancer cells to take on different shapes and sizes.

"One of the ways to determine cancer is to see a deviation from the norm," Kolomeisky said. "Is there a mutation that leads to faster growth or faster division of cells? This mechanism that helps maintain the sizes and shapes of bacteria may help us understand what's happening there as well."

Nuclear clocks could make our time measurement even more accurate than atomic clocks. The key to this lies in thorium-229, an atomic nucleus whose lowest excited state has very low energy. A research team from the Kirchhoff Institute for Physics at the University of Heidelberg, TU Wien, Johannes Gutenberg University Mainz (JGU), the Helmholtz Institute Mainz (HIM), and GSI Helmholtzzentrum in Darmstadt has now succeeded in measuring this low energy. Using an extremely accurate detector, it was possible to detect the tiny temperature increase due to the energy released during the de-excitation of the atomic nucleus. This brings the realization of a nuclear clock a big step closer.

In radioactive decay, atomic nuclei spontaneously re-arrange, eject some part of their building blocks, and transform into a nucleus of a different atom. In this process, the new "daughter atom" usually has internally stored energy that is released in the form of gamma rays. The energies of these rays are characteristic for each type of nucleus - just like fingerprints. Researchers learn a lot about atomic nuclei by characterizing these gamma-ray fingerprints.

Back in 1976, L. A. Kroger and C. W. Reich investigated the decay of uranium-233, which is an artificial nucleus of uranium that decays to thorium-229 by emitting an alpha-particle; this is immediately followed by the emission of characteristic gamma-rays that occur in distinct and generally well-understood patterns. Kroger and Reich, however, registered an anomaly: one gamma-ray that was predicted by all nuclear theories was missing in the measured signals. The best explanation was that the internal energy stored in the lowest nuclear excitation of thorium-229 was too low to be observed by the detectors. Over the following decades, many attempts were made to observe this low-energy gamma-ray without success, constraining it to ever-lower energies.

New perspectives for constructing a nuclear clock

Nowadays, we know that the lowest excited-energy state of the thorium-229 nucleus, called an isomer state, is located at the lowest known energy among all nuclei, at an energy that is orders of magnitudes lower than usual excitation energies. Consequently, the energy of the associated gamma-ray is so low that it is placed in the ultraviolet region of the electromagnetic spectrum rather than in the typical gamma-ray region. This leads to the unique situation that the opposite process of the de-excitation by the emission of this "ultraviolet gamma-ray", namely the excitation of the lower state is possible by shining ultraviolet light onto the nucleus. It is the only nuclear system that could be excited with "table-top" laser light. This opens up exciting prospects, including the construction of a "nuclear" clock, in which time is measured by oscillations of the nucleus between these two states. The precision of such a clock is predicted to be better than that of the best current atomic clocks, which rely on oscillations between states in the electron shell, which is more susceptible to external perturbations than the 10.000 times smaller nucleus.

The key problem is, though, that the energy of the isomer state is not yet known with sufficient precision to know which ultraviolet light is needed to stimulate the oscillation. A consortium of researchers from Heidelberg, Vienna, Mainz, and Darmstadt have now repeated the iconic gamma spectroscopy measurement of Kroger and Reich, but using a highly advanced state-of-the-art gamma spectrometer, designed explicitly for registering rays of such low energy.

Cool studies give the highest precision

For this, the research team of Professor Christian Enss and Dr. Andreas Fleischmann at the Kirchhoff Institute for Physics at the University of Heidelberg developed a magnetic microcalorimeter named maXs30. This detector is cooled to minus 273 degrees Celsius and measures the minuscule temperature rise that occurs when a gamma-ray is absorbed. The temperature increase leads to a change in the detector's magnetic properties, which is then converted into an electric signal using SQUID magnetometers similar to those that are commonly used in magnetic resonance tomography. The maXs30 detector has unprecedented energy resolution and gain linearity; still, it took about 12 weeks of continuous measurement to obtain the gamma-ray spectrum with sufficient precision.

To make this challenging measurement possible, the team of Professor Christoph Düllmann in Mainz and Darmstadt produced a special sample of uranium-233. First, they chemically removed all decay daughter products that had built up over time before the sample was used. They also removed unwanted radioisotopes, the decay of which leads to an unwanted background in the measured data. Then they designed a source geometry and sample container that led to minimum interference of the weak signals on their way from the sample to the maXs30 calorimeters. These steps were required for the success of the measurement because only one in 10,000 decay processes produces a signal that is useful for the determination of the isomer energy. The measurement produced the most precise gamma-ray spectrum of uranium-233 to thorium-229 decay to date. The team of Professor Thorsten Schumm at TU Wien, together with the Heidelberg team, employed four different schemes to derive the energy of the isomer state from this data. The most precise one yielded a value of 8.10(17) electronvolts, which corresponds to light of a wavelength of 153.1(32) nanometers, with the number in parentheses indicating the uncertainty of the last digits. This measurement paves the way for a direct laser excitation of the thorium-229 isomer.