Culture

A study published in Nature shows that a segment of DNA that causes their carriers to have an up to three times higher risk of developing severe COVID-19 is inherited from Neandertals. The study was conducted by researchers at Karolinska Institutet and Max Planck Institute for Evolutionary Anthropology.

COVID-19 affects some people much more severely than others. Some reasons for this - such as old age - are already known, but other as yet unknown factors also play a role. This summer, a large international study linked a gene cluster on chromosome 3 to a higher risk of hospitalisation and respiratory failure upon infection with the SARS-CoV-2 virus.

Hugo Zeberg and Svante Pääbo at Karolinska Institutet in Sweden and Max Planck Institute for Evolutionary Anthropology in Germany now report that the version of the gene cluster associated with a higher risk of severe COVID-19 is very similar to the corresponding DNA sequences of a roughly 50,000-year-old Neandertal from Croatia, and indeed comes from Neandertals.

"It turns out that this gene variant was inherited by modern humans from the Neandertals when they interbred some 60,000 years ago," says Hugo Zeberg. "Today, the people who inherited this gene variant are three times more likely to need artificial ventilation if they are infected by the novel coronavirus SARS-CoV-2."

The study also reveals considerable differences in how common this genetic risk variant is in different parts of the world. It is particularly common among people in South Asia where about half of the population carry the Neandertal risk variant. In Europe, one in six people carry the risk variant, while in Africa and East Asia it is almost non-existent.

The study provides no explanation as to why this genetic variant confers a higher risk.

"It is striking that the genetic heritage from the Neandertals has such tragic consequences during the current pandemic. Why this is must now be investigated as quickly as possible," says Svante Pääbo, director at the Max Planck Institute for Evolutionary Anthropology.

Homeless New Yorkers who menstruate face numerous challenges due to inadequate access to toilets, bathing spaces, and laundering services, as well as pervasive menstrual stigma. The study by researchers at Columbia University Mailman School of Public Health and the CUNY School of Public Health and Health Policy highlights the need for improved quality, supply, and accessibility of bathrooms for sheltered and street-dwelling homeless, and ease of access to bathing and laundering, particularly as the number of women in the city's shelter system is near record highs.

In partnership with the Coalition for the Homeless, the researchers conducted in-depth interviews with 22 individuals ages 18 and older living on the street and in shelters in New York City in 2019. They also interviewed 15 staff at government agencies, shelters, and service provider organizations and conducted field audits of public toilets.

Results, which include interview excerpts, are published in the journal Health and Place.

"Homelessness, and a lack of adequate access to bathing and laundering, particularly for those living on the street, intensifies the difficulties around the pressure 'to pass,' as someone who is not homeless in order to enable increased access to toilets, which you need even more when managing monthly menstruation," says first author Marni Sommer, DrPH, associate professor of sociomedical sciences at Columbia Mailman School. "A constant threat of feeling unclean, combined with pervasive menstrual stigma, takes a toll on these individuals' self-esteem, their confidence, their sense that they can be respected in the world around them, and even their ability to seek out services, training and work."

Among the study's findings:

Respondents report that shelter bathrooms are often dirty or flooded, making them unpleasant, unsafe, and sometimes, impossible to use. Gaining access to a private sector restroom is predicated on their ability to "pass" as someone who is not homeless.

Showering facilities across the city, made available by various service providers, are few in number for those living on the street, with limited hours and days of operation, and often seen as unclean and unsafe.

Few shelters offer laundry services, and for those that do, many require payment. Numerous study participants said they dispose of items that are bloodstained or heavily soiled given the laundering challenges.

Access to menstrual products is complicated by the embarrassment and shame of having to disclose one's menstruating status to shelter or service provider staff in order to meet one's basic needs.

"The subject of the menstruation management needs of individuals experiencing homelessness has received very little attention from researchers or policymakers in the U.S.," says Sommer. "Our research clearly demonstrates the injustice of this neglect, and the need to improve bathroom quality, supply and accessibility, as well as improve ease of access to bathing and laundering resources. Such actions are essential given the high numbers of those experiencing homelessness in New York City, and in the time of COVID, a clarion call for clean and accessible public toilets is especially timely."

The researchers disclose several limitations, including that they were unable to include individuals experiencing homelessness who struggle with mental health conditions, who are also less likely able to "pass" and access public or commercial restrooms. And, although the recruitment sought to be inclusive, ultimately everyone who was available for and interested in participating in an interview identified as a woman; thus, the researchers were unable to capture the experience of transmasculine and gender non-binary individuals, for whom adequate menstrual management can be a serious safety issue.

Background on Homelessness in New York City

In 2019, New York City homeless shelters held an average of 62,391 people per night, with the shelter system serving 133,284 separate individuals in 2018, a 59 percent increase over the prior decade, according to Coalition for the Homeless. A point-in-time count in 2019 by the Department of Homeless Services estimated 3,588 more individuals sleeping on the street, a number that may be a significant underestimate due to the difficulties associated with locating this population.

Outer ear infections, which affect millions of people each year, are typically caused by the bacteria Pseudomonas aeruginosa or Staphylococcus aureus. Repeatedly administering antibiotic drops, the standard treatment, can be a problem for some people, and the only single-use suspension currently available needs to be kept and handled cold. Now, researchers reporting in ACS Biomaterials Science & Engineering have developed a single-use treatment that doesn't require refrigeration.

Treatment for ear infections usually involves a patient or caregiver administering antibiotic drops for 7-14 days, multiple times each day. However, this regimen can be difficult for some, especially for people with hand or head tremors, nursing home residents, those in the military and people lacking access to regular health care. Incorrect or missed applications can mean the infection lasts longer than it should, or keeps coming back. In addition, the microbes could develop resistance to the drug. The U.S. Food and Drug Administration recently approved a treatment for ear infections that can be administered in a single dose by healthcare workers, but the medication requires refrigeration and several preparation steps prior to application. This would limit its use, particularly in remote areas. Monica Serban and colleagues wanted to develop a simple, safe, single-dose drug delivery system for ear infections that wouldn't need to be kept cold.

The team tested two delivery systems by mixing activated tetraethyl orthosilicate with large molecular weight polymers. The materials are liquids when squeezed through a syringe, but they rapidly form gels upon entering the ear, where they can release an antibiotic by diffusion. The hydrogels are stable through a range of temperatures, from 39.2 F to 104 F. The antibiotic ciprofloxacin doesn't require refrigeration, and when added to the gels, the materials killed P. aeruginosa or S .aureus in cultures at a 100-times lower antibiotic dose than that used in most ear drops. Also, the gels didn't harm or irritate model human skin. When placed in mouse ears, the materials were eliminated within 10 days, and they didn't impact the mice's hearing more than traditional ear drops. 

The authors acknowledge funding from the National Institutes of Health.

The abstract that accompanies this paper can be viewed here.

A recent publication in the Journal of Neuroscience by a group of researchers at the University of Kentucky looks at Encoding the Odor of Cigarette Smoke. Tim McClintock, a physiology professor at UK, says their work lays a foundation for two things.

"One is basic knowledge of how we tell one smell from another. We call this odor discrimination. The other is blocking the detection of unwanted odors. Cigarette smoke is an unwanted odor due to its general - though relatively mild - offensiveness, and for its clinical significance. The odor of cigarette smoke triggers the desire to smoke in both smokers and reformed smokers. Now that we know the receptors that respond to this odor, we can start to work on blocking them."

McClintock says they expect blockers to improve smoking cessation, which has very low success rates and has sometimes involved approaches such as vaping that he says are also detrimental to one's health.

In addition to opening the door to developing blockers of odors, McClintock says this work will help researchers understand why formulating fragrances and flavors with specific properties is so difficult. "Ergo, the oft-used phrase 'the art of perfumery'. Eventually we will turn this art into science."

The study was made possible thanks to recent technological advances in this field, "It has only been six years since we announced the invention of a new technology that allows us to identify the receptors responding to odors. We've been gradually working up from single odors towards more complex mixtures ever since," said McClintock.

The sense of smell uses hundreds of receptors as the detectors for odor molecules. "They work like a gymnasium scoreboard where patterns of lights form numbers and words; or like a computer screen where the pixels are the units forming patterns. Every odor produces its own unique pattern on the scoreboard. We can now read the pattern even for complex odors like cigarette smoke," explained McClintock. Cigarette smoke is a complex odor with more than 400 types of odor molecules.

The study used the new technology for preclinical experiments with mice to identify responsive receptors. They also used human perception studies to evaluate which odor molecules in cigarette smoke matter most. The human studies also asked volunteers to judge several things about artificial mimics of cigarette smoke odor. The data from the volunteers then allowed researchers to identify one odor molecule that is very important for the perception of cigarette smoke. The receptors for this molecule are the most important ones to block in order to improve smoking cessation.

UNIVERSITY OF CENTRAL FLORIDA

AI Can Detect COVID-19 in the Lungs Like a Virtual Physician, New Study Shows

The new UCF co-developed algorithm can accurately identify COVID-19 cases, as well as distinguish them from influenza.

ORLANDO, Sept. 30, 2020 - A University of Central Florida researcher is part of a new study showing that artificial intelligence can be nearly as accurate as a physician in diagnosing COVID-19 in the lungs.

The study, recently published in Nature Communications, shows the new technique can also overcome some of the challenges of current testing.

Researchers demonstrated that an AI algorithm could be trained to classify COVID-19 pneumonia in computed tomography (CT) scans with up to 90 percent accuracy, as well as correctly identify positive cases 84 percent of the time and negative cases 93 percent of the time.

CT scans offer a deeper insight into COVID-19 diagnosis and progression as compared to the often-used reverse transcription-polymerase chain reaction, or RT-PCR, tests. These tests have high false negative rates, delays in processing and other challenges.

Another benefit to CT scans is that they can detect COVID-19 in people without symptoms, in those who have early symptoms, during the height of the disease and after symptoms resolve.

However, CT is not always recommended as a diagnostic tool for COVID-19 because the disease often looks similar to influenza-associated pneumonias on the scans.

The new UCF co-developed algorithm can overcome this problem by accurately identifying COVID-19 cases, as well as distinguishing them from influenza, thus serving as a great potential aid for physicians, says Ulas Bagci, an assistant professor in UCF's Department of Computer Science.

Bagci was a co-author of the study and helped lead the research.

"We demonstrated that a deep learning-based AI approach can serve as a standardized and objective tool to assist healthcare systems as well as patients," Bagci says. "It can be used as a complementary test tool in very specific limited populations, and it can be used rapidly and at large scale in the unfortunate event of a recurrent outbreak."

Bagci is an expert in developing AI to assist physicians, including using it to detect pancreatic and lung cancers in CT scans.

He also has two large, National Institutes of Health grants exploring these topics, including $2.5 million for using deep learning to examine pancreatic cystic tumors and more than $2 million to study the use of artificial intelligence for lung cancer screening and diagnosis.

To perform the study, the researchers trained a computer algorithm to recognize COVID-19 in lung CT scans of 1,280 multinational patients from China, Japan and Italy.

Then they tested the algorithm on CT scans of 1,337 patients with lung diseases ranging from COVID-19 to cancer and non-COVID pneumonia.

When they compared the computer's diagnoses with ones confirmed by physicians, they found that the algorithm was extremely proficient in accurately diagnosing COVID-19 pneumonia in the lungs and distinguishing it from other diseases, especially when examining CT scans in the early stages of disease progression.

"We showed that robust AI models can achieve up to 90 percent accuracy in independent test populations, maintain high specificity in non-COVID-19 related pneumonias, and demonstrate sufficient generalizability to unseen patient populations and centers," Bagci says.

The UCF researcher is a longtime collaborator with study co-authors Baris Turkbey and Bradford J. Wood. Turkbey is an associate research physician at the NIH's National Cancer Institute Molecular Imaging Branch, and Wood is the director of NIH's Center for Interventional Oncology and chief of interventional radiology with NIH's Clinical Center.

This research was supported with funds from the NIH Center for Interventional Oncology and the Intramural Research Program of the National Institutes of Health, intramural NIH grants, the NIH Intramural Targeted Anti-COVID-19 program, the National Cancer Institute and NIH.

Study co-authors also included first author Stephanie A. Harmon with the NIH Molecular Imaging Branch, National Cancer Institute and the Clinical Research Directorate, Frederick National Laboratory for Cancer Research; Thomas H. Sanford and Dominic Labella with the State University of New York-Upstate Medical Center; Sheng Xu, Victoria Anderson, Amel Amalou, Maxime Blain, Michael Kassin, and Dilara Long with the Center for Interventional Oncology, Radiology and Imaging Sciences, NIH Clinical Center and NIH National Cancer Institute, Center for Cancer Research; Evrim B. Turkbey, Dima Hammoud, Ashkan Malayeri, Elizabeth Jones, and Ronald M. Summers with NIH Clinical Center Radiology and Imaging Sciences; Holger Roth, Ziyue Xu Dong Yang, Andriy Myronenko, Daguang Xu, and Mona Flores with the NVIDIA Corporation; Nicole Varble with the Center for Interventional Oncology, Radiology and Imaging Sciences, NIH Clinical Center and NIH National Cancer Institute, Center for Cancer Research and Philips Research North America; Stephanie M. Walker and Peter L. Choyke with the NIH Molecular Imaging Branch, National Cancer Institute; Anna Maria Ierardi, Elvira Stellato, and Guido Giovanni Plensich with the Department of Radiology Fondazione IRCCS Cà Granda, Ospedale Maggiore Policlinico Milano, in Milan; Giuseppe Franceschelli with the Diagnostic and Interventional Radiology Service, ASST Santi Paolo e Carlo, San Paolo Hospital in Milan; Cristiano Girlando and Giovanni Irmici with the Postgraduation School in Radiodiagnostics, Università Degli Studi di Milano; Kaku Tamura, Hirofumi Obinata, and Hitoshi Mori with the Self-Defense Forces Central Hospital in Tokyo; Francesca Patella and Maurizio Cariati with the Diagnostic and Interventional Radiology Service, ASST Santi Paolo e Carlo, San Paolo Hospital in Milan; Gianpaolo Carrafiello with the Department of Radiology Fondazione IRCCS Cà Granda, Ospedale Maggiore Policlinico Milano and Department of Health Sciences, University of Milano in Milan; and Peng An with the Department of Radiology, Xiangyang NO.1 People's Hospital Affiliated to Hubei University of Medicine Xiangyang in Hubei, China.

Bagci received his doctorate in computer science from the University of Nottingham in England and joined UCF's Department of Computer Science, part of the College of Engineering and Computer Science, in 2015. He is the Science Applications International Corp (SAIC) chair in UCF's Department of Computer Science and a faculty member of UCF's Center for Research in Computer Vision. SAIC is a Virginia-based government support and services company.

CONTACT: Robert H. Wells, Office of Research, robert.wells@ucf.edu

A river's only consistent attribute is change. As the Greek philosopher Heraclitus remarked, "No man ever steps in the same river twice." Although this dynamic nature is often out of sight and mind, forgetting about it has led to many a historical catastrophe.

Recently, UC Santa Barbara geomorphologist Vamsi Ganti and his collaborators published a study finding that sea level rise will cause rivers to jump course, or avulse, more often on deltas than in the past. Now his team has discovered that a perfect storm of factors -- including larger floods and finer sediment size -- will enable these destructive events to occur farther and farther inland. Their results, which appear in Geophysical Research Letters, warn of major disasters poised to hit many urban centers that historically never had to worry about these issues.

On large, relatively flat rivers, avulsions tend to occur in the backwater region, Ganti explained. "This is the zone over which the river flow feels the effect of the sea level." This region begins at the river mouth and can extend relatively far inland. For instance, the Mississippi River's backwater reach stretches 500 kilometers from the coast.

The team was looking through satellite and remote sensing data for historical avulsions and came across the unique deltas of Madagascar. The island has a host of short rivers that course down from the mountains carrying very fine sediment. This is due to the saprolitic soils -- loose, soft soils made of silt and disintegrating rock -- that dominate the country's highlands. Exacerbated by rampant deforestation on the island, the exposed soils feed the island's turbid, red rivers and make it one of the fastest eroding places on Earth, according to lead author Sam Brooke, a postdoctoral scholar in the Department of Geography.

Using multiple satellite images taken since the late 1970s, Brooke created time series animations that communicate just how fast Madagascar's river deltas are evolving. Using this data, he was able to obtain the rivers' discharge rates as well as the amount of time the channels remained full during floods.

Combining the data with the satellite imagery led to a surprising conclusion. The avulsions weren't occurring anywhere near the rivers' backwater zones. "[Instead, they were] about 20 times [farther] upstream," Brooke recalled, "way outside of where we'd expect them to be based on [...models] using simple backwater scale." The researchers realized they had to update their models of where avulsions occur on deltas.

A better model

The team's expanded theory boils down to a simple relationship. Two processes are at work in river channels -- the duration of floods, and the time it takes for the river to adjust to changes. The relative timescales of these phenomena dictate where avulsions occur.

If floods are shorter than the time the river takes to adjust, then erosion and deposition are limited to the backwater zone. However, if floods last longer than it takes the river to adjust, erosion during floods can travel far upstream of the river mouth, which makes it possible for the river to avulse much farther inland.

Large flat rivers, like the Mississippi, change slowly, but steep rivers with lots of fine sediment can adjust quite quickly. "The whole channel can be resurfaced within the backwater zone in a given flood," said Ganti, "and erosion can propagate much farther upstream." This is the case for rivers like those in Madagascar, which are relatively steep and have a lot of fine sediment.

A river floods when it's carrying enough water to overtop its banks. And for most of its length, a flooded waterway will do just that. But water level is constrained by sea level near the river's mouth up through the backwater zone. So the increased volume of water during floods begins moving faster, increasing erosion, and scouring the river bed deeper.

This wave of erosion can then spread upstream as flood conditions continue, enabling the river to avulse far upstream from the backwater zone -- much farther than anticipated.

A foreboding picture emerges

"Climate models predict that extreme floods will occur more often in a warming world," said Ganti. As a result, avulsions could begin moving even farther inland on rivers around the world.

But greenhouse gas emissions are not the only human activity affecting rivers. Sand and gravel are critical components in construction and infrastructure, and humans are now mining these resources on massive scales. Unfortunately, these make up the coarse fraction of alluvial sediment, which means that our activities are leading to finer sediment in many locations. Rivers can carry more of this fine-grained material, and the increased load reduces the amount of time it takes channels [?] to change. Once again, this enables avulsions to occur farther upstream.

What's more, sea level rise is pushing the backwater zone itself farther inland. These three factors combine to create the perfect recipe for major avulsions to occur ever farther inland on deltas, Ganti explained. This could lead to an increasing trend of homes, lives and livelihoods lost due to extreme flooding, likely in locations that never had to deal with these hazards historically.

And according to the team's previous paper these events will also become more frequent as the sea level rises.

"We should brace ourselves for avulsion as a serious flood hazard in the future," Vamsi cautioned.

River deltas have always been a critical resource for humanity, harnessed for agriculture, transportation and industry. Many of civilization's largest cities have grown along the banks of the world's great waterways. Their dynamism has always posed a challenge to society, but as rivers become less predictable and more volatile, researchers say, we will need to take more precautions to ensure our safety and wellbeing.

University of Maryland entomologists discovered that a gene critical for survival in other insects is missing in mosquitos--the gene responsible for properly arranging the insects' segmented bodies. The researchers also found that a related gene evolved to take over the missing gene's job. Although laboratory studies have shown that similar genes can be engineered to substitute for one another, this is the first time that scientists identified a gene that naturally evolved to perform the same critical function as a related gene long after the two genes diverged down different evolutionary paths.

The work emphasizes the importance of caution in genetic studies that use model animals to make conclusions across different species. It also points to a new potential avenue for research into highly targeted mosquito control strategies. The research study was published in the September 30, 2020, issue of the journal Communications Biology.

"Every single arthropod has a segmented body plan. And you would think it develops the same way in all of them. But what we found is that it doesn't," said Alys Jarvela, a postdoctoral associate in the UMD Department of Entomology and the lead author of the study. "We learn a lot in biology by studying a process in a model organism and assuming that it works essentially the same way, using the same genes, in other organisms. That is still an incredibly useful approach. But, now we know that there is also a possibility for gene substitutions to be made in nature."

Jarvela discovered the missing gene in mosquitos by accident. She was studying crickets and attempting to cross-check her genetic samples by comparing the gene sequences of crickets with those of other insects. She was specifically interested in a gene called paired, one of a handful of genes that guides the pattern of repeated parts in segmented animals like insects. Laboratory studies had shown that when paired is knocked out or silenced in fruit flies, every other segment of the insect's body fails to develop, and it doesn't survive.

"I was just trying to find the mosquito version of paired to use as a reference point, and I couldn't find, it," Jarvela said.

When she searched for paired in all publicly available databases of mosquito genomes, she discovered it was missing from every mosquito species represented.
"Once we accepted that the gene was really absent, we thought that was a pretty wild mystery and immediately changed gears to satisfy our curiosity," Jarvela said.

Jarvela's team searched the genomes of fly species closely related to mosquitos and found they all contained the paired gene. This indicated that the loss of paired is a recent evolutionary event that took place only in mosquitos. It was clear to the researchers that some other gene in mosquitos must be performing the same function as paired does in other insects.

They found clues suggesting which gene could be involved in a 1996 experiment on fruit flies. In that study, scientists knocked out paired and replaced it with a closely related gene called gooseberry, which normally has a distinct role at a later time in development. That was a highly engineered experiment, but it showed that when gooseberry was manipulated to express at the right time during development, fruit flies without the paired gene developed normal alternating segments and survived.

To find out if gooseberry had naturally evolved as a substitute for paired in mosquitos, Jarvela and her team used CRISPR to edit gooseberry out of a mosquito species called Anopheles stephensi. The mutated mosquito embryos looked like laboratory fruit fly embryos that had paired knocked out.

"This work shows that even when different species share a trait or feature, the genetic mechanisms underlying this shared trait may be different," said Leslie Pick, professor and chair of the Department of Entomology at UMD and the study's senior author. "In the case reported in this paper, segmentation still happens even though a gene we thought was essential is lost. Our next steps will be to search for additional examples of variation in gene regulatory networks in insects and try to determine how genetic rewiring occurs in nature."

Jarvela is also interested in probing other aspects of mosquito development that may be affected by the loss of the paired gene. In addition to controlling segmentation, which is critical for survival, paired influences male fertility in fruit flies.

"That means different genes probably regulate male fertility in mosquitos, and they might be unique to the mosquito, which could potentially provide a powerful avenue for controlling mosquitoes without harming other insects such as butterflies and bees," Jarvela said.

While dinosaurs ruled the land in the Mesozoic, the oceans were filled by predators such as crocodiles and giant lizards, but also entirely extinct groups such as ichthyosaurs and plesiosaurs.

Now for the first time, researchers at the University of Bristol have modelled the changing ecologies of these great sea dragons.

Mesozoic oceans were unique in hosting diverse groups of fossil reptiles, many of them over 10 metres long.

These toothy monsters fed on a variety of fishes, molluscs, and even on each other. Yet most had disappeared by the end of the Cretaceous, 66 million years ago, when the dinosaurs also died out. There are still some marine crocodiles, snakes and turtles today, but sharks, seals, and whales took over these ecological roles.

In a new study, completed when she was studying for the MSc in Palaeobiology at the University of Bristol's School of Earth Sciences, Jane Reeves, now a PhD student at the University of Manchester, used modern computational methods to explore how all these marine reptiles divided up the spoils.

Jane said: "It's difficult to work out the ecology and function of fossil animals but we decided to focus mainly on their feeding and swimming styles. I tracked down information on 371 of the best-known Mesozoic marine tetrapods, and coded each one for 35 ecological traits, including body size, diet, likely hunting style, tooth type, presence or absence of armour, limb shape and habitat."

The numerical analysis showed that all these marine reptiles could be divided into just six ecological categories linking how they moved, where they lived, and how they fed: pursuit predators that chased their prey, ambush predators that lurked and waited for the prey to swim past (two groups, one in deep water, one in shallow), a fourth group of reptiles that could still walk on land, shallow-water shell-crushers and foragers, and marine turtles with a variety of life modes.

Professor Mike Benton, who co-supervised the study, said: "A problem with studies of form and function of fossils is that we have to be careful in reconstructing the behaviour of ancient animals. But in Jane's study, she used ecological characters from the start where their function had already been established. For example, sharp pointy teeth mean fish-eating, whereas broad, flat teeth mean shell crushing."

Dr Ben Moon, another co-supervisor, said: "We knew that the different marine reptile groups came and went through the 186 million years of the Mesozoic.

"I'm especially interested in ichthyosaurs, and we wanted to test an idea that they had migrated through ecospace during the Mesozoic. Jane's study shows definite movement through time from being semi-terrestrial at the beginning of the Triassic to a wide range of ecologies, including ambush hunting, and finally pursuit predation in the Jurassic and Cretaceous."

Dr Tom Stubbs, another co-supervisor, said: "We also wanted to test whether all these animals were competing with each other. But in fact, they seem to have avoided competition.

"For example, after a substantial extinction of marine reptiles around the end of the Triassic, the surviving ichthyosaurs and plesiosaurs showed considerable conservatism. They didn't expand their ecological roles at all, and many niches were left empty until new groups of crocodiles and turtles emerged later in the Jurassic to take over these roles."

Jane Reeves added: "It was a great experience being able to study a large variety of creatures, and to then reconstruct the ecological lifestyles of extinct animals from just their fossils.

"You do have to be very careful in doing these kinds of studies, not to make any unfounded assumptions. We know animals can be opportunistic, and don't always behave exactly how we think they should, but we're confident that the data we collected reflects the most common, day-to-day, behaviours of each animal. These results give us a great insight into what was really happening under the surface of the Mesozoic seas."

Background: Persistent poverty means that a county has had poverty rates of 20 percent or more in U.S. Census data from 1980, 1990, and 2000. These areas, representing about 10 percent of all U.S. counties, are primarily located in the rural South.

Persistent-poverty counties typically have larger populations of racial and ethnic minorities; more children under age 18; less formal education; and greater unemployment. They are also more likely to have high rates of cancer risk factors such as obesity or cigarette smoking, Moss added. She drew a distinction between counties with persistent poverty and those with current poverty, which is defined as 20 percent or more of the population living in poverty according to the 2007-2011 American Community Survey.

"Counties that have experienced persistent poverty face health risks that have accumulated for decades, and they have fewer current or past resources to protect public health," she said.

How the Study was Conducted: In this study, Moss and colleagues examined cancer mortality rates in persistently poor counties compared with other counties. The median income in the persistently poor counties was $32,156, compared with $47,154 in the counties not experiencing persistent poverty.

The researchers calculated 2007-2011 county-level, age-adjusted, overall, and type-specific cancer mortality rates.

Results: They found that the overall cancer mortality rate in persistent-poverty counties was 201.3 deaths per 100,000 people, compared with 179.3 per 100,000 people in counties not experiencing persistent poverty.

For each cancer type studied, mortality was between 11 and 50 percent higher in the counties with persistent poverty. For example, the mortality rate from lung/bronchus cancer was 16.5 percent higher; from colorectal cancer, 17.7 percent higher; from stomach cancer, 43.2 percent higher; and from liver and intrahepatic bile duct cancer, 27.6 percent higher in the persistent-poverty counties than in the counties not experiencing persistent poverty.

Author's Comments: Moss said the disparities in various cancer types reflected a number of persistent risk factors that are more common in poorer communities, such as smoking, excess weight, and higher rates of infections. These factors, in turn, are likely related to fewer systemic opportunities for accessing good health, for example, fewer job prospects, inadequate health care facilities, and less safe housing and occupational environments. However, Moss said further research should examine other potential causes of the disparities. For example, it is possible that chronic stress associated with less access to health care, more chronic unemployment, and other financial factors may lead to inflammation that gives rise to some cancers, she said.

In general, the counties experiencing current but not persistent poverty had higher cancer mortality rates than the overall U.S. population, but lower rates than the persistently poor counties. Moss said the results of this study indicate that researchers should distinguish between persistent poverty and current poverty, since persistent poverty is associated with the strongest risk of cancer mortality. She said the long-entrenched societal problems surrounding persistent poverty merit local and national interventions to improve health outcomes.

"To prevent health disparities, we need tools, people, and systems to ensure that everyone in this country has access to the tools they need to thrive, including socioeconomic opportunities, equity, and respect, as well as prevention resources and health care services," Moss said.

"We need interventions in these communities to change cancer-causing behaviors, to make cancer screening more accessible, to improve treatment, and to promote quality of life and survivorship," she continued. "Efforts to reduce the risk of cancer in these counties will require strategic coordination, collaboration, and funding, with input from community members every step of the way."

Study Limitations: The study's chief limitation is that it did not account for residential history, so the researchers could not determine whether the amount of time spent in a persistently poor county affected cancer mortality risk.

Cannabinoids, a class of prescription pills that contain synthetically-made chemicals found in marijuana, are associated with a 64 per cent increase in death among older adults with chronic obstructive pulmonary disease (COPD), according to the first published data on the impact of cannabinoids on the respiratory health of individuals with the lung disease.

The findings, published Wednesday in Thorax, have significant clinical implications as more physicians prescribe cannabinoids to patients with COPD to treat chronic muscle pain, difficulty sleeping and breathlessness.

The study, led by St. Michael's Hospital of Unity Health Toronto, found that cannabinoids can contribute to negative respiratory health events in people with COPD, including hospitalization and death. COPD is a progressive lung disease that causes difficulty breathing and chronic productive coughing, and can be associated with a variety of non-respiratory issues, like chronic muscle pain and insomnia.

"Cannabinoid drugs are being increasingly used by older adults with COPD, so it is important for patients and physicians to have a clear understanding of the side-effect profile of these drugs," says Dr. Nicholas Vozoris, lead author, a respirologist at St. Michael's and an associate scientist at the hospital's Li Ka Shing Knowledge Institute.

"Our study results do not mean that cannabinoid drugs should be never used among older adults with COPD. Rather, our findings should be incorporated by patients and physicians into prescribing decision-making. Our results also highlight the importance of favouring lower over higher cannabinoid doses, when these drugs actually do need to be used."

The study analyzed the health data of over 4,000 individuals in Ontario ages 66 years and older with COPD from 2006 to 2016. The data was equally split into two groups: older adults with COPD who were new cannabinoid users and older adults with COPD not using cannabinoids. Older adults in Ontario with COPD who were new cannabinoid users represented 1.1 per cent of the data, which was made available by ICES.

Researchers observed particularly worse health outcomes among patients with COPD who were using higher doses of cannabinoids. Compared to non-users, new higher-dose cannabinoid users had a 178 per cent relative increase in hospitalizations for COPD or pneumonia, and a 231 per cent relative increase in all-cause death.

"Older adults with COPD represent a group that would likely be more susceptible to cannabinoid-related respiratory side-effects, since older adults less efficiently break down drugs and hence, drug effects can linger in the body for longer - and since individuals with COPD have pre-existing respiratory troubles and respiratory compromise," says Dr. Vozoris, who is also a scientist at ICES.

Researchers conducted a sub-analysis to explore what impact cannabinoid drugs versus opioid drugs had on respiratory outcomes among older adults with COPD, since cannabinoid drugs are often prescribed as an alternative to opioids to treat chronic pain. The research team did not find evidence to support that cannabinoids were a safer choice over opioids for older adults with COPD in so far as respiratory health outcomes.

JUPITER, FL - Sept. 30, 2020 - Scripps Research chemist Matthew Disney, PhD, and colleagues have created drug-like compounds that, in human cell studies, bind and destroy the pandemic coronavirus' so-called "frameshifting element" to stop the virus from replicating. The frameshifter is a clutch-like device the virus needs to generate new copies of itself after infecting cells.

"Our concept was to develop lead medicines capable of breaking COVID-19's clutch," Disney says. "It doesn't allow the shifting of gears."

Viruses spread by entering cells and then using the cells' protein-building machinery to churn out new infectious copies. Their genetic material must be compact and efficient to make it into the cells.

The pandemic coronavirus stays small by having one string of genetic material encode multiple proteins needed to assemble new virus. A clutch-like frameshifting element forces the cells' protein-building engines, called ribosomes, to pause, slip to a different gear, or reading frame, and then restart protein assembly anew, thus producing different protein from the same sequence.

But making a medicine able to stop the process is far from simple. The virus that causes COVID-19 encodes its genetic sequence in RNA, chemical cousin of DNA. It has historically been very difficult to bind RNA with orally administered medicines, but Disney's group has been developing and refining tools to do so over more than a decade.

The scientists' report, titled "Targeting the SARS-CoV-2 RNA Genome with Small Molecule Binders and Ribonuclease Targeting Chimera (RIBOTAC) Degraders," appears Sept. 30 in the journal ACS Central Science.

Disney emphasizes this is a first step in a long process of refinement and research that lies ahead. Even so, the results demonstrate the feasibility of directly targeting viral RNA with small-molecule drugs, Disney says. Their study suggests other RNA viral diseases may eventually be treated through this strategy, he adds.

"This is a proof-of-concept study," Disney says. "We put the frameshifting element into cells and showed that our compound binds the element and degrades it. The next step will be to do this with the whole COVID virus, and then optimize the compound."

Disney's team collaborated with Iowa State University Assistant Professor Walter Moss, PhD, to analyze and predict the structure of molecules encoded by the viral genome, in search of its vulnerabilities.

"By coupling our predictive modeling approaches to the tools and technologies developed in the Disney lab, we can rapidly discover druggable elements in RNA," Moss says. "We're using these tools not only to accelerate progress toward treatments for COVID-19, but a host of other diseases, as well."

The scientists zeroed in on the virus' frameshifting element, in part, because it features a stable hairpin-shaped segment, one that acts like a joystick to control protein-building. Binding the joystick with a drug-like compound should disable its ability to control frameshifting, they predicted. The virus needs all of its proteins to make complete copies, so disturbing the shifter and distorting even one of the proteins should, in theory, stop the virus altogether.

Using a database of RNA-binding chemical entities developed by Disney, they found 26 candidate compounds. Further testing with different variants of the frameshifting structure revealed three candidates that bound them all well, Disney says.

Disney's team in Jupiter, Florida quickly set about testing the compounds in human cells carrying COVID-19's frameshifting element. Those tests revealed that one, C5, had the most pronounced effect, in a dose-dependent manner, and did not bind unintended RNA.

They then went further, engineering the C5 compound to carry an RNA editing signal that causes the cell to specifically destroy the viral RNA. With the addition of the RNA editor, "these compounds are designed to basically remove the virus," Disney says.

Cells need RNA to read DNA and build proteins. Cells have natural process to rid cells of RNA after they are done using them. Disney has chemically harnessed this waste-disposal system to chew up COVID-19 RNA. His system is called RIBOTAC, short for "Ribonuclease Targeting Chimera."

Adding a RIBOTAC to the C5 anti-COVID compound increases its potency by tenfold, Disney says. Much more work lies ahead for this to become a medicine that makes it to clinical trials. Because it's a totally new way of attacking a virus, there remains much to learn, he says.

"We wanted to publish it as soon as possible to show the scientific community that the COVID RNA genome is a druggable target. We have encountered many skeptics who thought one cannot target any RNA with a small molecule," Disney says. "This is another example that we hope puts RNA at the forefront of modern medicinal science as a drug target."

Venus might not be a sweltering, waterless hellscape today, if Jupiter hadn't altered its orbit around the sun, according to new UC Riverside research.

Jupiter has a mass that is two-and-a-half times that of all other planets in our solar system -- combined. Because it is comparatively gigantic, it has the ability to disturb other planets' orbits.

Early in Jupiter's formation as a planet, it moved closer to and then away from the sun due to interactions with the disc from which planets form as well as the other giant planets. This movement in turn affected Venus.

Observations of other planetary systems have shown that similar giant planet migrations soon after formation may be a relatively common occurrence. These are among the findings of a new study published in the Planetary Science Journal.

Scientists consider planets lacking liquid water to be incapable of hosting life as we know it. Though Venus may have lost some water early on for other reasons, and may have continued to do so anyway, UCR astrobiologist Stephen Kane said that Jupiter's movement likely triggered Venus onto a path toward its current, inhospitable state.

"One of the interesting things about the Venus of today is that its orbit is almost perfectly circular," said Kane, who led the study. "With this project, I wanted to explore whether the orbit has always been circular and if not, what are the implications of that?"

To answer these questions, Kane created a model that simulated the solar system, calculating the location of all the planets at any one time and how they pull one another in different directions.

Scientists measure how noncircular a planet's orbit is between 0, which is completely circular, and 1, which is not circular at all. The number between 0 and 1 is called the eccentricity of the orbit. An orbit with an eccentricity of 1 would not even complete an orbit around a star; it would simply launch into space, Kane said.

Currently, the orbit of Venus is measured at 0.006, which is the most circular of any planet in our solar system. However, Kane's model shows that when Jupiter was likely closer to the sun about a billion years ago, Venus likely had an eccentricity of 0.3, and there is a much higher probability that it was habitable then.

"As Jupiter migrated, Venus would have gone through dramatic changes in climate, heating up then cooling off and increasingly losing its water into the atmosphere," Kane said.

Recently, scientists generated much excitement by discovering a gas in the clouds above Venus that may indicate the presence of life. The gas, phosphine, is typically produced by microbes, and Kane says it is possible that the gas represents "the last surviving species on a planet that went through a dramatic change in its environment."

For that to be the case, however, Kane notes the microbes would have had to sustain their presence in the sulfuric acid clouds above Venus for roughly a billion years since Venus last had surface liquid water -- a difficult to imagine though not impossible scenario.

"There are probably a lot of other processes that could produce the gas that haven't yet been explored," Kane said.

Ultimately, Kane says it is important to understand what happened to Venus, a planet that was once likely habitable and now has surface temperatures of up to 800 degrees Fahrenheit.

"I focus on the differences between Venus and Earth, and what went wrong for Venus, so we can gain insight into how the Earth is habitable, and what we can do to shepherd this planet as best we can," Kane said.

COLUMBUS, Ohio - When people have the option to click "like" on a media article they encounter online, they spend less time actually reading the text, a new study suggests.

In a lab experiment, researchers found that people spent about 7 percent less time reading articles on controversial topics when they had the opportunity to upvote or downvote them than if there was no interactive element.

The finding was strongest when an article agreed with the reader's point of view.

The results suggest that the ability to interact with online content may change how we consume it, said Daniel Sude, who led the work while earning a doctoral degree in communication at The Ohio State University.

"When people are voting whether they like or dislike an article, they're expressing themselves. They are focused on their own thoughts and less on the content in the article," Sude said.

"It is like the old phrase, 'If you're talking, you're not listening.' People were talking back to the articles without listening to what they had to say."

In another finding, people's existing views on controversial topics like gun control or abortion became stronger after voting on articles that agreed with their views, even when they spent less time reading them.

"Just having the ability to like an article you agreed with was enough to amplify your attitude," said study co-author Silvia Knobloch-Westerwick, professor of communication at Ohio State.

"You didn't need to read the article carefully, you didn't have to learn anything new, but you are more committed to what you already believed."

The study, also co-authored by former Ohio State doctoral student George Pearson, was published online recently in the journal Computers in Human Behavior and will appear in the January 2021 print edition.

The study involved 235 college students. Before the study, the researchers measured their views on four controversial topics used in the experiment: abortion, welfare benefits, gun control and affirmative action.

Participants were then showed four versions of an online news website created for the study, each on one of the controversial topics. Each webpage showed headlines and first paragraphs for four articles, two with a conservative slant and two with a liberal slant. Participants could click on the headlines to read the full stories.

Two versions of the websites had a banner that said, "Voting currently enabled for this topic," and each article had an up arrow or down arrow that participants could click on to express their opinion.

The other two websites had a banner that said, "Voting currently disabled for this topic."

Participants were given three minutes to browse each website as they wished, although they were not told about the time limit. The researchers measured the time participants spent on each story and whether they voted if they had the opportunity.

As expected, for each website, participants spent more time reading articles that agreed with their views (about 1.5 minutes) than opposing views (less than a minute).

But they spent about 12 seconds less time reading the articles they agreed with if they could vote.

In addition, people voted on about 12 percent of articles that they didn't select to read, the study showed.

"Rather than increasing engagement with website content, having the ability to interact may actually distract from it," Sude said.

The researchers measured the participants' views on the four topics again after they read the websites to see if their attitudes had changed at all.

Results showed that when participants were not able to vote, time spent reading articles that agreed with their original views strengthened these views. The more time they spent reading, the stronger their views became.

When participants were able to vote, their voting behavior was as influential as their reading time. Even if they stopped reading and upvoted an article, their attitudes still became stronger.

"It is important that people's views still became stronger by just having the opportunity to vote, Knobloch-Westerwick said.

"When they had the opportunity to vote on the articles, their attitudes were getting more extreme with limited or no input from the articles themselves. They were in an echo chamber of one."

Sude said there is a better way to interact with online news.

"Don't just click the like button. Read the article and leave thoughtful comments that are more than just a positive or negative rating," he said.

"Say why you liked or disliked the article. The way we express ourselves is important and can influence the way we think about an issue."

Small watery droplets on the edges of blueberry bush leaves are loaded with nutrients for many insects, including bees, wasps and flies, according to a Rutgers-led study, the first of its kind.

The study, published in the journal Proceedings of the Royal Society B: Biological Sciences, suggests that these droplets are an important but underexplored feature in plants, with profound implications for insects in agricultural and natural ecosystems.

"Our study shows for the first time that plant 'guttation' - fluid from sap secreted at the edges and tips of leaves - is a nutrient-rich source of food for insects," said senior author Cesar Rodriguez-Saona, a professor and extension specialist in the Department of Entomology in the School of Environmental and Biological Sciences at Rutgers University-New Brunswick.

Many insects such as bees, wasps and flies drink the small droplets, which arise on nights with high levels of moisture in soil, and biologists considered them only as a source of water for insects. But the droplets are rich in carbohydrates and contain proteins that are essential for many insect species, according to Rodriguez-Saona.

In an experiment in Rutgers blueberry fields, insects with three different feeding lifestyles (an herbivore, a parasitic wasp and a predator) increased their ability to survive and reproduce when they fed on plant guttation droplets during their entire adult lives.

The droplets were also present in blueberry fields through the entire season and their presence doubled the abundance of beneficial insects - parasitic wasps and predators - that protect plants from pests. As a result, droplets might reduce the many problems caused by pests in crops, including invasive pests. And the researchers suggest that might occur in numerous crops where the droplet phenomenon is common, such as rice, wheat, barley, rye, oats, sorghum, corn, tobacco, tomatoes, strawberries and cucumbers, among others.

"These findings are important for the conservation of beneficial insects because they can find and feed on droplets when pollen, nectar, hosts or prey are scarce," Rodriguez-Saona said.

Overall, the results demonstrate that the droplet phenomenon is highly reliable, compared with other plant-derived food sources such as nectar, and it increases the communities and fitness of insects, the study says.

Next steps include investigating the nutritional quality of droplets from other plant species and their fitness benefits for insects, as well as testing whether insecticides remain in droplets after being applied and affect beneficial insects.

It's called senescence, when stressed cells can no longer divide to make new cells, and it's considered a factor in aging and in some diseases. Now scientists have some of the first evidence that at a younger age at least, senescent cells show up quickly after a major injury and are protective.

Their model is hemorrhagic shock, a significant loss of blood and the essential oxygen and nutrients it delivers that accounts for about 30-40% of trauma-related deaths from things like car accidents and shootings; and their focus the liver, one of the many major organs that can fail in response.

Medical College of Georgia scientists report in the journal Aging Cell that shortly after hemorrhagic shock occurs, a population of liver cells quickly become senescent.

“If the cells switch immediately to a senescent state, they may help prevent organ failure,” says Dr. Raghavan Pillai Raju, biomedical researcher in the MCG Department of Pharmacology and Toxicology and the study’s corresponding author.

To find out if the rapid movement to senescence they saw for some liver cells was good or bad, they gave some of the rats in their studies senolytics, a relatively new class of drugs that target senescent cells for elimination. Laboratory studies of these drugs have shown they can prevent or improve age-related problems like frailty, cataracts and vascular and heart dysfunction. Early trials in humans have also reported success in reducing the progression of problems like diabetes and kidney related damage.

But when younger rats in hemorrhagic shock were given the drugs as part of the fluids used for resuscitation shortly after blood loss, they all quickly died.

“We wondered if it was the drugs themselves that were lethal to the rats,” said Dr. Xiaogang Chu, MCG research associate and the study’s first author. Animals and humans may not respond the same to a drug. However when they gave senolytics to healthy rats, they were fine.

“The results suggest that the induction of acute senescence may be a necessary process in hemorrhagic shock,” they write. Death of the senescent cells appears to exacerbate the tissue injury resulting from blood loss, and the drugs that target those cells also have off-target effects that are problematic with an injury as opposed to age-related senescence, they write.

They also wanted to know if giving a drug cocktail to improve organ function by strengthening cell powerhouses called mitochondria, which are weakened by the blood and oxygen deficit, would alter emergence of the senescent cells in the liver. They found the cell population that quickly emerged was essentially the same as those without the organ-specific support.

Raju and his colleagues suspect the rapid transition to senescence that occurred in a population of liver cells was an attempt to stabilize after the trauma, and likely transient.

This is the first evidence that cellular senescence can develop within a few hours after tissue injury, that hemorrhagic injury can make that happen and that the senescent cells that emerge are not detrimental in this scenario.

Cell senescence is known to be triggered by cell stress, like DNA damage, activation of oncogenes, dysfunction of the mitochondria and oxidative stress, an unhealthy buildup of reactive oxygen species that contributes to a number of maladies like heart disease, and a factor in normal aging. In fact, there are parallels between significant injury and aging, particularly the fact that mitochondrial function -- energy production by the cell -- decreases in both, Raju says.

"As we age, our cells slowly stop dividing, they express certain markers, they secrete certain proteins like cytokines and this state of cellular arrest of proliferation under stress, this is senescence," says Raju. Senescence is an important function throughout life that starts as soon as development, when endless decisions are being made about which cells to keep and eliminate, or at least quieten, and continues throughout life as part of your daily cell activity.

While not a given, senescence can be a death sentence for cells, which start to secrete factors called SASPs, which get the attention of the immune system so the cell may be tagged for elimination by immune cells called macrophages, which find and consume them.

But it may also make cells far less vulnerable to programmed cell death, or apoptosis, which cells can initiate when they have irreparable damage, like what may result from dramatic loss of blood and oxygen, Raju says. "Apoptosis is suicide versus homicide," he says. And senescence appears to enable cells to opt for a lower-functioning state instead of death.

This "hunkered down" state, which rapidly followed hemorrhagic shock, may enable the liver cells to survive until the blood, oxygen and nutrient deficit passes, he says, but what fraction of cells switch to this hunkered mode and whether, as speculated, they can reverse the state remain unknowns he wants to pursue. Raju's team has documented apoptosis by some liver cells in response to hemorrhagic shock.

"I want to see if these senescent cells are persisting or dying," Raju says. He also wants to know the impact of using the senescent cell suppressing drugs before injury, to further assess the drugs' impact and see if the rapid emergence of senescent cells is impacted.

They also found increased levels of the SASPs, or senescence-associated secretory phenotype markers, things like growth factors and enzymes that break down proteins and peptides, secreted at high levels by senescent cells, again much like in the livers of aged rats. SASPs can be good and bad, causing problems like insulin resistance and inflammation, but also aiding wound healing and tissue regeneration. The SASP complement can vary depending on what sent a cell into senescence and the cell type. There were also upticks in proteins, for example, that can arrest the cell cycle and mediators of DNA damage known to be critical to cell senescence, along with others.

While many of our cells routinely are not actively dividing, they have that potential, Raju says. Cell division is important to replace high turnover cells in areas like the gut and skin, and also to enable wound healing, but even that rate slows with age.

Other than the fact that senescence can prevent cells from becoming rapidly dividing cancer cells, it is widely considered a detriment to health in aging. The MCG scientists suspected the liver cells showing signs of senescence would be bad too, and that killing them might help patients, as it appears to do in aging, Raju says. But instead they found senescence is not bad and may actually be good in the aftermath of injury. In fact, the cells can even heal in this hunkered-down state.

Raju got interested in senescence because of his interest in injury, which can happen across a lifetime. But there are definite trends that recovery rates decrease with age, says Raju, who would like to help change that.

"Survival rates decrease significantly as we pass middle age," he says. Middle age starts about age 40 and just under 50% of Americans fall into that category, according to a 2019 Brookings Institution study of U.S. Census Bureau data.

The liver, which has unique abilities to regenerate in the face of injury or disease, peaked his interest because there was some thought that you could both induce and reverse senescence in this resilient organ.

While he says you can't generalize that what happens in one tissue, like the liver, will happen in another organ, Raju expects something similar happens in other organs in the face of serious injury. Whether the apparent positive effect of senescence in response to injury holds at an older age, when injury recovery declines, is another question they want to answer.