Publisher Health

For humans, the early days of the COVID-19 pandemic were a stressful time, marked by fear, isolation, canceled plans and uncertainty. But for birds that inhabit developed areas of the Pacific Northwest, the reduction in noise and commotion from pandemic lockdowns may have allowed them to use a wider range of habitats in cities.
A new University of Washington study led by Olivia Sanderfoot reports that many birds were just as likely to be found in highly developed urban areas as they were in less-developed green spaces during the peak of the COVID-19 lockdowns. The paper was published Aug. 11 in the journal Scientific Reports.
“Our findings suggest that some birds may have been able to use more spaces in cities because our human footprint was a little lighter,” said Sanderfoot, who completed the study as a doctoral researcher in the UW School of Environmental and Forest Sciences and is now a postdoctoral scholar in the Department of Ecology and Evolutionary Biology at the University of California, Los Angeles.
“For about half of the species we observed, neither land use nor canopy cover had an effect on their site use. That’s very interesting, because we would expect that whether a habitat was mostly covered in concrete or vegetation would tell you something about what birds would be there,” Sanderfoot said.
In the spring of 2020, Sanderfoot and colleagues recruited more than 900 community scientists in the Pacific Northwest to participate in the study. The volunteers chose their own monitoring sites — mostly backyards and parks where they could safely comply with public health orders — and recorded the birds they observed over a 10-minute period at least once a week. This community science approach allowed the researchers to gather data despite the lockdowns and gave many volunteers a welcomed distraction from the stresses of the pandemic.
“I am loving being a part of this!” said Nadine Santo Pietro, a study volunteer, in a written comment as part of the project. “I signed up to observe once a week for 10 minutes but it has become so much more than that. … I am learning so much! And it’s given me something positive to focus on during this strange time we are in right now.”
Among the 35 species that showed the strongest changes in behavior were some of the Pacific Northwest’s most iconic, including black-capped chickadees, great blue herons, downy woodpeckers and Wilson’s warblers. The researchers focused on 46 bird species overall, which were observed by the study volunteers during more than 6,000 individual surveys.
In order to compare the volunteers’ bird observations to human activity, Sanderfoot and her colleagues used data from Google’s Community Mobility Reports, which track the relative amount that people moved around at various points during the pandemic. While most people spent spring of 2020 isolated in their homes, many began venturing out again over the course of the study period.
As people returned to public spaces and human activity increased, the study volunteers recorded an increase in sightings of several bird species. Because they were mostly monitoring in parks and backyards, which tend to be more heavily vegetated, provide more canopy cover and offer more resources for birds than other areas in cities, this could indicate that these green spaces are an important refuge for urban birds.
“The birds may have been elsewhere at the height of the lockdowns, because human activity wasn’t as much of a disturbance, but then returned to those vegetated areas as the activity increased again,” Sanderfoot said. “This could tell us how important it is to build green spaces into our cities. That’s the biggest takeaway for me.”
Other co-authors are Joel Kaufman, a professor in the UW Department of Environmental and Occupational Health Sciences, and Beth Gardner, an associate professor in the UW School of Environmental and Forest Sciences.
This research was funded by the National Science Foundation Graduate Research Fellowship Program and the McIntire-Stennis Cooperative Forestry Research Program from the USDA National Institute of Food and Agriculture.
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Materials provided by University of Washington. Original written by Will Shenton, UW College of the Environment. Note: Content may be edited for style and length.

A fundamental discovery about a driver of healthy development in embryos could rewrite our understanding of what can be inherited from our parents and how their life experiences may shape us.
The new research suggests that epigenetic information, which sits on top of DNA and is normally reset between generations, is more frequently carried from mother to offspring than previously thought.
The study, led by researchers from WEHI (Melbourne, Australia), significantly broadens our understanding of which genes have epigenetic information passed from mother to child and which proteins are important for controlling this unusual process.
Epigenetics is a rapidly growing field of science that investigates how our genes are switched on and off to allow one set of genetic instructions to create hundreds of different cell types in our body.
Epigenetic changes can be influenced by environmental variations such as our diet, but these changes do not alter DNA and are normally not passed from parent to offspring.
While a tiny group of ‘imprinted’ genes can carry epigenetic information across generations, until now, very few other genes have been shown to be influenced by the mother’s epigenetic state.

The outbreak is centered on humans, not animals, health officials said, after a report that some monkeys were harmed in São Paulo, Brazil, out of fear of transmission, according to local authorities.Monkeys are not to blame for the monkeypox outbreak that has triggered health alerts, including a national health emergency in the United States, as the viral disease has continued to spread, the World Health Organization said this week after reports of attacks against the animals in Brazil.At least 10 monkeys were rescued last week in São José do Rio Preto in the Brazilian state of São Paulo after the authorities found signs they had been attacked or poisoned, out of fear of monkeypox transmission, according to the G1 news site in that country. Seven of the monkeys later died.The police in São Paulo are investigating those cases and said the mistreatment of animals could be punishable by three months to one year in jail.Despite the name, the risk of monkeypox transmission during this outbreak is centered on humans, not animals, Margaret Harris, a W.H.O. spokeswoman, said during a Tuesday news conference.“What people need to know very clearly is the transmission we are seeing is happening between humans to humans,” she said. “It’s close-contact transmission. The concern should be about where it’s transmitting in the human population and what humans can do to protect themselves from getting it and transmitting it. They should certainly not be attacking any animals.”The statement was prompted by a question at the news conference in Geneva about the recent monkey attacks in Brazil.The virus named after it was originally found in a group of laboratory monkeys in 1958 in Denmark, but rodents are thought to be the primary animal hosts for the virus, Ms. Harris said.Some scientists and public health officials have called for a new name for the disease, citing racist overtones and stigmatization, but no official change has been announced. They say the current name could have “potentially devastating and stigmatizing effects” or erroneously link the virus solely to the African continent, when it is now an international crisis.The W.H.O. is having ongoing conversations on what should be the right name for the virus, Ms. Harris said. She said an announcement would be coming soon.“Any stigmatization of any person infected is going to increase the transmission,” Ms. Harris said. “Because if people are afraid of identifying themselves as being infected, then they will not get care and they will not take precautions and we will see more transmission.”The monkeypox virus is primarily found in Central and West Africa, particularly in areas close to tropical rainforests — and rope squirrels, tree squirrels, Gambian pouched rats and dormice have all been identified as potential carriers.People who get sick commonly experience a fever, headache, back and muscle aches, swollen lymph nodes, and exhaustion. A rash that looks like pimples or blisters is also common. Transmission occurs with close physical contact and most commonly spreads once symptoms have appeared, about six to 13 days after exposure. A majority of cases this year have been in young men, many of whom self-identify as men who have sex with men.The United States declared a national health emergency this month over the monkeypox outbreak, with more than 10,000 confirmed cases nationwide according to the Centers for Disease Control and Prevention. The W.H.O. activated its highest level of alert for monkeypox in July, with the number of international confirmed cases rising to more than 31,000 so far.Two vaccines originally developed for smallpox can help prevent monkeypox infections, with Jynneos considered the safer choice. Supplies in the United States, however, have been limited. People can be vaccinated after exposure to the virus to prevent the development of the disease.Juliana Barbassa

Johns Hopkins Medicine researchers say that an experimental dendrimer nanoparticle treatment called OP-101 substantially reduced the risk of death and need for a ventilator in a study of 24 severely ill adults hospitalized with COVID-19.
Results of the small clinical trial, funded by Ashvattha Therapeutics, a Johns Hopkins startup company that makes the drug, specifically found that patients who received the drug had a greater than fourfold higher rate of decrease in biomarkers of inflammation and brain injury circulating in their blood compared with patients who received a placebo.
A report on the study was published July 20 in Science Translational Medicine.
“OP-101 could be a potent therapy for decreasing hyperinflammation and promoting repair in people with severe COVID, showing significant clinical benefit without the associated side effects typically seen with some other treatments,” says Sujatha Kannan, M.B.B.S., professor of anesthesiology and critical care medicine and pediatrics at the Johns Hopkins University School of Medicine.
Kannan and her husband, Kannan Rangaramanujam, Ph.D., professor of ophthalmology at the Johns Hopkins University School of Medicine and Wilmer Eye Institute, Johns Hopkins Medicine, developed OP-101 by attaching a powerful antioxidant/anti-inflammatory drug known as n-acetyl cysteine (NAC) to a nanoparticle that is 100,000 times smaller than the thickness of a sheet of paper. Each nanoparticle has a number of molecules of the drug attached to it, and can deliver the drug specifically to inflammatory cells called macrophages. The dendrimer nanoparticle delivers the drug to only those macrophages involved in inflammation at the site of injury. Currently, NAC is used in a different form to treat acetaminophen poisoning and for thinning mucus secretions in airways.
The pair of researchers are co-inventors on patents related to the drug’s discovery, and founded a biotechnology company, Ashvattha Therapeutics Inc., based in California, to develop the drug and fund clinical trials. The company licenses the technology through Johns Hopkins Technology Ventures.

The discovery of how to shift damaged brain cells from a diseased state into a healthy one presents a potential new path to treating Alzheimer’s and other forms of dementia, according to a new study from researchers at UC San Francisco.
The research focuses on microglia, cells that stabilize the brain by clearing out damaged neurons and the protein plaques often associated with dementia and other brain diseases.
These cells are understudied, despite the fact that changes in them are known to play a significant role Alzheimer’s and other brain diseases, said Martin Kampmann, PhD, senior author on the study, which appears Aug. 11 in Nature Neuroscience.
“Now, using a new CRISPR method we developed, we can uncover how to actually control these microglia, to get them to stop doing toxic things and go back to carrying out their vitally important cleaning jobs,” he said. “This capability presents the opportunity for an entirely new type of therapeutic approach.”
Leveraging the Brain’s Immune System
Most of the genes known to increase the risk for Alzheimer’s disease act through microglial cells. Thus, these cells have a significant impact on how such neurodegenerative diseases play out, said Kampmann.

Tohid Didar and Jeff Weitz had a solution, but they also had a problem.
Didar, an Associate Professor of Engineering at McMaster University and Weitz, a hematologist, professor of medicine and executive director of the Thrombosis & Atherosclerosis Research Institute, had collaborated to create a novel and highly promising material to improve the success of vascular grafts, but they needed a better way to test how well it worked.
Their revolutionary idea was an engineered non-stick surface combined with biological components that can repel all but a targeted group of cells — those that form the natural lining of the body’s veins and arteries.
The non-stick material prevents proteins and cells from sticking to the inner walls of blood vessels, where they can build into menacing blood clots.
That innovation may revolutionize blood vessel grafts, which are needed in transplants, bypasses and other surgeries, as a way to route blood around blocked areas, or to replace damaged or leaking blood vessels themselves.
Didar, Weitz and their collaborators had already shown their new material worked with static blood samples, but before they could test the technology in animals or humans, they needed to be as certain as possible it could work under flow conditions similar to those which occur in arteries or veins.

For decades, there’s been a persistent one-size-fits-all approach to treating obesity: Embrace a diet that’s low in calories. Yet evidence shows that this diet-focused approach simply doesn’t work for a subset of adults with obesity who are adherent in a clinical weight management program.
Now, compelling new research published in the journal eBioMedicine challenges the deeply ingrained idea that diet alone should be adequate for everyone seeking to shed pounds.
The important conclusions could significantly improve public health by guiding the advent of personalized treatment plans that will help individuals with difficult-to-treat obesity lose weight — and keep it off.
“It’s exciting and important work. These findings have clinical implications and reveal molecular mechanisms that will drive research for many years to come,” says Dr. Mary-Ellen Harper, an award-winning professor and research chair in mitochondrial bioenergetics at the uOttawa Faculty of Medicine who was the study’s senior author.
Understanding distinct obesity phenotypes is key to teasing out insights into individual variations in weight loss. And for “diet-resistant” obesity — patients in the bottom 20% for rate of weight loss following a low-calorie diet — exercise training should be prioritized, as it decreases fat mass and boosts skeletal muscle metabolism.
The research team mined clinical data from over 5,000 records. Ultimately, 228 files were reviewed and a subset of 20 women with obesity were identified to undergo a closely supervised exercise program made up of 18 progressive sessions using treadmills and weights done three times per week for six weeks.

It’s no surprise that hard physical labor wears you out, but what about hard mental labor? Sitting around thinking hard for hours makes one feel worn out, too. Now, researchers have new evidence to explain why this is, and, based on their findings, the reason you feel mentally exhausted (as opposed to drowsy) from intense thinking isn’t all in your head.
Their studies, reported in Current Biology on August 11, show that when intense cognitive work is prolonged for several hours, it causes potentially toxic byproducts to build up in the part of the brain known as the prefrontal cortex. This in turn alters your control over decisions, so you shift toward low-cost actions requiring no effort or waiting as cognitive fatigue sets in, the researchers explain.
“Influential theories suggested that fatigue is a sort of illusion cooked up by the brain to make us stop whatever we are doing and turn to a more gratifying activity,” says Mathias Pessiglione of Pitié-Salpêtrière University in Paris, France. “But our findings show that cognitive work results in a true functional alteration — accumulation of noxious substances — so fatigue would indeed be a signal that makes us stop working but for a different purpose: to preserve the integrity of brain functioning.”
Pessiglione and colleagues including first author of the study Antonius Wiehler wanted to understand what mental fatigue really is. While machines can compute continuously, the brain can’t. They wanted to find out why. They suspected the reason had to do with the need to recycle potentially toxic substances that arise from neural activity.
To look for evidence of this, they used magnetic resonance spectroscopy (MRS) to monitor brain chemistry over the course of a workday. They looked at two groups of people: those who needed to think hard and those who had relatively easier cognitive tasks.
They saw signs of fatigue, including reduced pupil dilation, only in the group doing hard work. Those in that group also showed in their choices a shift toward options proposing rewards at short delay with little effort. Critically, they also had higher levels of glutamate in synapses of the brain’s prefrontal cortex. Together with earlier evidence, the authors say it supports the notion that glutamate accumulation makes further activation of the prefrontal cortex more costly, such that cognitive control is more difficult after a mentally tough workday.
So, is there some way around this limitation of our brain’s ability to think hard?
“Not really, I’m afraid,” Pessiglione said. “I would employ good old recipes: rest and sleep! There is good evidence that glutamate is eliminated from synapses during sleep.”
There may be other practical implications. For example, the researchers say, monitoring of prefrontal metabolites could help to detect severe mental fatigue. Such an ability may help adjust work agendas to avoid burnout. He also advises people to avoid making important decisions when they’re tired.
In future studies, they hope to learn why the prefrontal cortex seems especially susceptible to glutamate accumulation and fatigue. They’re also curious to learn whether the same markers of fatigue in the brain may predict recovery from health conditions, such as depression or cancer.
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Materials provided by Cell Press. Note: Content may be edited for style and length.

DNA damage caused by factors such as ultraviolet radiation affect nearly three-quarters of all stem cell lines derived from human skin cells, say Cambridge researchers, who argue that whole genome sequencing is essential for confirming if cell lines are usable.
Stem cells are a special type of cell that can be programmed to become almost any type of cell within the body. They are currently used for studies on the development of organs and even the early stages of the embryo.
Increasingly, researchers are turning to stem cells as ways of developing new treatments, known as cell-based therapies. Other potential applications include programming stem cells to grow into nerve cells to replace those lost to neurodegeneration in diseases such as Parkinson’s.
Originally, stem cells were derived from embryos, but it is now possible to derive stem cells from adult skin cells. These so-called induced pluripotent stem cells (iPSCs) have now been generated from a range of tissues, including blood, which is increasing in popularity due to its ease of derivation.
However, researchers at the University of Cambridge and Wellcome Sanger Institute have discovered a problem with stem cell lines derived from both skin cells and blood. When they examined the genomes of the stem cell lines in detail, they found that nearly three quarters carried substantial damage to their DNA that could compromise their use both in research and, crucially, in cell-based therapies. Their findings represent the largest genetic study to date of iPSCs and are published today in Nature Genetics.
DNA is made up of three billions pairs of nucleotides, molecules represented by the letters A, C, G and T. Over time, damage to our DNA, for example from ultraviolet radiation, can lead to mutations — a letter C might change to a letter T, for example. ‘Fingerprints’ left on our DNA can reveal what is responsible for this damage. As these mutations accumulate, they can have a profound effect on the function of cells and in some cases lead to tumours.

Researchers and entrepreneurs have developed an implant made of collagen protein from pig’s skin, which resembles the human cornea. In a pilot study, the implant restored vision to 20 people with diseased corneas, most of whom were blind prior to receiving the implant. The study jointly led by researchers at Linköping University (LiU) and LinkoCare Life Sciences AB has been published in Nature Biotechnology. The promising results bring hope to those suffering from corneal blindness and low vision by providing a bioengineered implant as an alternative to the transplantation of donated human corneas, which are scarce in countries where the need for them is greatest.
“The results show that it is possible to develop a biomaterial that meets all the criteria for being used as human implants, which can be mass-produced and stored up to two years and thereby reach even more people with vision problems. This gets us around the problem of shortage of donated corneal tissue and access to other treatments for eye diseases,” says Neil Lagali, professor at the Department of Biomedical and Clinical Sciences at LiU, one of the researchers behind the study.
An estimated 12.7 million people around the world are blind due to their corneas, which is the outermost transparent layer of the eye, being damaged or diseased. Their only way of regaining vision is to receive a transplanted cornea from a human donor. But just one in 70 patients receives a cornea transplant. Furthermore, most of those who need cornea transplants live in low and middle-income countries in which access to treatments is very limited.
“Safety and effectiveness of the bioengineered implants have been the core of our work, says Mehrdad Rafat, the researcher and entrepreneur behind the design and development of the implants. He is an adjunct associate professor (senior lecturer) at LiU’s Department of Biomedical Engineering and founder and CEO of the company LinkoCare Life Sciences AB, which manufactures the bioengineered corneas used in the study.
“We’ve made significant efforts to ensure that our invention will be widely available and affordable by all and not just by the wealthy. That’s why this technology can be used in all parts of the world,” he says.
The cornea consists mainly of the protein collagen. To create an alternative to human cornea, the researchers used collagen molecules derived from pig skin that were highly purified and produced under strict conditions for human use. The pig skin used is a byproduct of the food industry, making it easy to access and economically advantageous. In the process of constructing the implant, the researchers stabilized the loose collagen molecules forming a robust and transparent material that could withstand handling and implantation in the eye. While donated corneas must be used within two weeks, the bioengineered corneas can be stored for up to two years before use.