Publisher Health

Would you be more willing to get vaccinated against the COVID-19 virus if you could participate in a lottery for cash and prizes? The answer was surprisingly no, according to Boston University School of Medicine (BUSM) researchers who found that Ohio’s “Vax-a-Million” lottery-based incentive system, intended to increase COVID-19 vaccination rates, was not associated with an increase in COVD-19 vaccinations.
Prior reports in the media had suggested that the Ohio lottery increased COVID-19 vaccinations, leading other states to use COVID-19 vaccine incentive lotteries in an attempt to increase slowing vaccination rates. “However, prior evaluations of the Ohio vaccine incentive lottery did not account for other changes in COVID-19 vaccination rates in the United States, such as those that may have been due to expansion of vaccination to ages 12-15,” explained corresponding author Allan J. Walkey, MD, MSc, professor of medicine at BUSM.
Using data from the U.S. Centers of Disease Control to evaluate trends in vaccination rates among adults 18 and older, the researchers compared vaccination rates before and after the Ohio lottery versus other states in the U.S. that did not yet have vaccine incentive lottery programs. Vaccination rates in other states served as a “control” for vaccination trends measured in Ohio, allowing the researchers to account for factors besides the Ohio lottery (such expanding vaccine eligibility to adolescents) throughout the country.
“Our results suggest that state-based lotteries are of limited value in increasing vaccine uptake. Therefore, the resources devoted to vaccine lotteries may be more successfully invested in programs that target underlying reasons for vaccine hesitancy and low vaccine uptake,” said Walkey, a physician at Boston Medical Center.
The researchers believe identifying interventions that can successfully increase COVID-19 vaccination rates is a critical public health issue necessary to curb the pandemic. “It is important to rigorously evaluate strategies designed to increase vaccine uptake, rapidly deploy successful strategies, and phase out those that do not work,” Walkey said.
Although Walkey and his colleagues were sorry to see that state lottery incentives were not associated with an increase COVID-19 vaccinations, they hope their findings will lead to a shift in focus away from ineffective and expensive lotteries, and on to further study of other programs that may more successfully increase vaccine uptake.
These findings appear online in the Journal of the American Medical Association.
Allan J Walkey was funded by NIH R01HL139751, NIH R01HL151607, NIH R01HL136660, and NIH OT2HL156812-01. Anica C Law was funded by NIH K23HL 153482. Nicholas A Bosch was funded by NIH 1F32GM133061-01.
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To survive life threatening injuries, cancer cells use a technique in which they eat parts of the membrane surrounding them. This is shown for the first time in research from a team of Danish researchers.
It is the membrane of cancer cells that is at the focus of the new research now showing a completely new way in which cancer cells can repair the damage that can otherwise kill them.
In both normal cells and cancer cells, the cell membrane acts as the skin of the cells. And damage to the membrane can be life threatening. The interior of cells is fluid, and if a hole is made in the membrane, the cell simply floats out and dies — a bit like a hole in a water balloon.
Therefore, damage to the cell membrane must be repaired quickly, and now research from a team of Danish researchers shows that cancer cells use a technique called macropinocytosis. The technique, which is already a known tool for cells in other contexts, consists in the cancer cells pulling the intact cell membrane in over the damaged area and sealing the hole in a matter of minutes. Next, the damaged part of the cell membrane is separated into small spheres and transported to the cells’ ‘stomach’ — the so-called lysosomes, where they are broken down.
In the laboratory, the researchers damaged the membrane of the cancer cells using a laser that shoots small holes in the membrane and triggers macropinocytosis. Here they can see that if the process is inhibited with substances blocking the formation of the small membrane spheres, the cancer cell can no longer repair the damage and dies.
“Our research provides very basic knowledge about how cancer cells survive. In our experiments, we have also shown that cancer cells die if the process is inhibited, and this points towards macropinocytosis as a target for future treatment. It is a long-term perspective, but it is interesting,” says group leader Jesper Nylandsted from the Danish Cancer Society’s Research Center and the University of Copenhagen, who has headed the new research and who for many years has investigated how cancer cells repair their membranes.
Possibility of recycling
One of the most dangerous properties of cancer is when the disease spreads in the body. If tumors occur in new parts of the body, the disease becomes more difficult to treat and typically requires more extensive forms of treatment. It is also when cancer cells spread through the body’s tissues that they are particularly prone to damage to their membrane.
Researchers at the Danish Cancer Society have previously shown how cancer cells can use another technique to repair the membrane, namely by tying off the damaged part, rather like when a lizard throws its tail.
However, the experiments in the laboratory could indicate that especially the aggressive cancer cells use macropinocytosis. This may be due to the fact that the cancer cell has the opportunity to reuse the damaged membrane when it is degraded in the lysosomes. This type of recycling will be useful for cancer cells because they divide frequently, requiring large amounts of energy and material for the new cells.
And although the researchers have now published the new results, their work is not over. This is explained by another member of the research team, postdoc Stine Lauritzen Sønder:
“We continue to work and investigate how cancer cells protect their membranes. In connection with macropinocytosis in particular, it is also interesting to see what happens after the membrane is closed. We believe that the first patching is a bit rough and that a more thorough repair of the membrane is needed afterwards. It can be another weak point in the cancer cells, and is something we want to examine closer,” she says.

Indiana University School of Medicine researchers are developing a new, noninvasive brain stimulation technique to treat neurological disorders, including pain, traumatic brain injury (TBI), epilepsy, Parkinson’s disease, Alzheimer’s disease and more.
“Given the increasing use of brain stimulation in human brain study and treatment of neurological diseases, this research can make a big impact on physicians and their patients,” said Xiaoming Jin, PhD, associate professor of anatomy, cell biology and physiology.
When someone experiences a brain injury, nerve injury, or neurodegeneration, such as in epilepsy and TBI, there is damage to the brain which can lead to loss and damage of nerve or neurons and development of hyperexcitability that underlies some neurological disorders such as neuropathic pain and epilepsy.
“The conventional treatment is mainly to try to directly inhibit such hyperexcitability,” Jin said, “but we found the initial damage of the brain or nerve system was caused by a loss of brain tissue, which causes the nervous system to compensate for loss of function by working harder, so we need to stimulate activity instead of inhibit it.”
The technique, described in a newly published paper in Neurotherapeutics, uses a new type of magnetoelectric nanoparticles that can be delivered to a specific part of the brain using a magnetic field. After, a magnetic wave can be emitted to stimulate neural activity in that particular part of the brain. The method is noninvasive, good for stimulating deep brain function and is more efficient than traditional methods of brain stimulation, without the need for genetic manipulation.
“This is the only new type of nanoparticle that allows us to effectively stimulate the brain without doing any invasive procedures,” Jin said. “We can inject the nanoparticle as a solution into the vein and then bring it to any part of the body. When you apply a magnet on the head, you can localize and deliver the nanoparticle to the targeted brain region.”
The team has been working on the technique for five years in collaboration with the University of Miami and hopes to begin studying the method in humans in the next couple of years. The study has received funding from the Defense Advanced Research Projects Agency (DARPA) of the United States Department of Defense, National Science Foundation, as well as the Indiana Clinical and Translational Sciences Institute (CTSI), which helped provide funding for a medical neuroscience graduate student, Tyler Nguyen, to participate in the research. Read the full published paper in Neurotherapeutics.
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Materials provided by Indiana University School of Medicine. Original written by Christina Griffiths. Note: Content may be edited for style and length.

Medical researchers led by Kyushu University have revealed a possible underlying genetic pathway behind the neurological dysfunction of Rett syndrome. The team found that deficiencies in key genes involved in the pathology triggers neural stem cells to generate less neurons by producing more astrocytes — the brain’s maintenance cells.
The researchers hope that the molecular pathology they identified, as reported in the journal Cell Reports, can lead to potential therapeutic targets for Rett syndrome in the future.
Rett syndrome is a progressive neurodevelopmental disorder characterized by impairments in cognition and coordination — with varying severity — and occurs in roughly one in every 10,000 to 15,000 female births. However, it is difficult to initially identify because children appear to develop normally in the first 6-18 months.
“Rett syndrome is caused by mutations in a single gene called methyl-CpG binding protein 2, or MeCP2. The gene was identified over two decades ago and much has been uncovered since, but exactly how the mutations cause the pathology remains elusive,” explains first author Hideyuki Nakashima of Kyushu University’s Faculty of Medical Sciences
In their past research, the team had identified that MeCP2 acts as a regulator for the processing of specific microRNAs to control the functions of neurons. So, they went back to investigate if that pathway was also involved in the differentiation of neural stem cells.
Compared to messenger RNA, the final template transcribed from DNA that is used by a cell to synthesize proteins, microRNAs — or miRNAs — are much smaller and act to regulate messenger RNA to make sure the cell is making the correct amount of the desired protein.
“Through our investigation, we found several microRNAs associated with MeCP2, but only one affected the differentiation of neural stem cells: a microRNA called miR-199a,” says Nakashima. “In fact, when either MeCP2 or miR-199a are disrupted, we found that it increased the production of cells called astrocytes.”
Astrocytes are like the support cells of your brain. While neurons fire off the electrical signals, astrocytes are there to help maintain everything else. During development, astrocytes and neurons are generated from the same type of stem cells, known as neural stem cells, where their production is carefully controlled. However, dysfunction in MeCP2 or miR-199a causes these stem cells to produce more astrocytes than neurons.
“Further analysis showed that miR-199a targets the protein Smad1, a transcription factor critical for proper cellular development. Smad1 functions downstream of a pathway called BMP signaling, which is known to inhibit the production of neurons and facilitate the generation of astrocytes,” states Nakashima.
To investigate the process further, the team established a brain organoid culture — a 3D culture of neural stem cells that can mimic aspects of brain development — from iPS cells derived from patients with Rett syndrome. When they inhibited BMP, short for bone morphogenetic protein, the team was able to reduce abnormal neural stem cell differentiation.
“Our findings have given us valuable insight into the role of MeCP2, miR-199a, and BMP signaling in the pathology of Rett syndrome,” concludes Kinichi Nakashima, who headed the team. “Further investigation is needed, but we hope this can lead to clinical treatments for Rett syndrome symptoms.”
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Less than half the country is fully vaccinated against Covid-19, and the contagious Delta variant is spreading. Still, the White House is putting together an “America’s Back Together” celebration for July 4.WASHINGTON — President Biden’s plan to celebrate “independence from the virus” on the Fourth of July is running into an unpleasant reality: Less than half the country is fully vaccinated against the coronavirus, and the highly contagious Delta variant is threatening new outbreaks.The president and Jill Biden, the first lady, have invited 1,000 military personnel and essential workers to an Independence Day bash on the South Lawn of the White House. Mr. Biden and his advisers, eager to claim credit for the virus’ retreat in the United States, are talking about a “summer of joy and freedom.”Mr. Biden will visit Traverse City, Mich., on Saturday as part of what the White House calls the “America’s Back Together” celebration. Dr. Biden will also take to the road, as will Vice President Kamala Harris, her husband, Doug Emhoff, and various cabinet officials who will attend festivals, parades and cookouts around the nation.But public health experts fear that scenes of cross-country celebrations — including a White House party with a liberation theme — will send the wrong message when wide swaths of the population remain vulnerable and true independence from the worst public health crisis in a century may be a long way off.“We’re still in the middle of this marathon,” said Dr. William Schaffner, an infectious disease expert at Vanderbilt University. Despite considerable progress in decreasing the number of coronavirus cases and deaths in the United States over the past few months, he said, it remains too early to “unfurl the ‘mission accomplished’ banner.”Suggesting that the country is moving past the pandemic is a delicate task for Mr. Biden and his fellow Democrats, who must balance caution with bolstering the economy and getting national morale back on track.The Democratic National Committee this week released an upbeat ad entitled “America’s Coming Back.” Its spokeswoman wrote on Twitter that the “America’s Back” mobile — a bus with the president’s image on it — would be traveling the country and offering free Jeni’s Splendid Ice Creams, a gourmet brand favored by Speaker Nancy Pelosi.The blowback was swift. “Need to rename this the ‘USS Tone Deaf McCovid Mobile,’” a Twitter user wrote.In interviews, several family members of Covid-19 victims said it was difficult to hear Mr. Biden suggest that the nation was returning to normal while they were still grieving.“There’s no return to normalcy for us,” said Sabila Khan, 42, of Jersey City, N.J., who created a Facebook support group after her father died of Covid-19. “It’s very nerve-racking when the government is encouraging you to just move beyond it. We lost our loved ones. We are never moving past this.”White House officials said Mr. Biden was hardly declaring victory or “mission accomplished,” but simply wanted to take stock of the gains the United States had made against the virus since he took office.“The Fourth of July is a moment for us to step back and celebrate our progress,” Jeffrey D. Zients, the White House coronavirus response coordinator, told reporters on Thursday. At the same time, he said, “There’s a lot more work to do. So we’re going to double down our efforts to keep pushing more and more people to get vaccinated.”The United States has made significant progress against the pandemic since Mr. Biden took office on Jan. 20 warning of a “dark winter” ahead. Daily reports of new cases are holding steady at about 12,000, the lowest since testing became widely available, according to a New York Times database — down from about 200,000 on Inauguration Day.For the first time since March 2020, the country is averaging fewer than 300 newly reported deaths a day, a decline of about 20 percent over the past two weeks. Hospitalizations are also dropping.But the advances have been uneven, with a large portion of U.S. cases emerging in a handful of hot spots, particularly where vaccination rates are low. Las Vegas, rural Utah, rural Arkansas, Cheyenne, Wyo., and the Missouri Ozarks are among the places with upticks. And because the national trend lines are flat, experts do not know precisely which way they will go.“If you looked a couple of weeks ago, most of those projections were trending downwards; it looked like we were sailing into summer,” said Lauren Ancel Meyers, an epidemiologist at the University of Texas at Austin. “Those projections now have flatlined. We’re not necessarily seeing an indication yet that things are going to surge in parts of the country, but we aren’t sure what’s going to happen.”A number of governors are planning to lift their public health emergency orders in the coming weeks; Maryland and Virginia lifted their orders on Thursday, bringing an end to mask mandates and other restrictions.But the national emergency declared by President Donald J. Trump remains in effect through late July, and the White House has told governors that Mr. Biden plans to extend it, officials said.The vaccination campaign, meanwhile, is plodding along, with about a million shots administered each day. Mr. Biden had hoped to have 70 percent of adults at least partly vaccinated by July 4, but the White House conceded last month that it would not meet that goal.The truer measure of protection, experts say, is whether people are fully vaccinated; only 46 percent of Americans fall into that category. With children under 12 still ineligible for the vaccine, it will be some time before a vast majority of the United States is fully vaccinated. Public health officials are particularly worried about outbreaks once school resumes in the fall.In an era when vaccination has become a subject of fierce political debate, White House officials are not requiring guests at the July 4 party to be vaccinated. But they will be asked to present evidence of a negative Covid-19 test taken within three days of the event, and the White House has advised those who are unvaccinated that they “should wear a mask,” Jen Psaki, the White House press secretary, said this week.Dr. Meyers, of the University of Texas, said the requirements were “very sensible” and a show of responsible behavior. “Testing, face masks, vaccinations: Those are our tickets to freedom from this threat,” she said.But the absence of a vaccination requirement for White House party guests is also evidence of the challenges ahead, said Dr. Thomas Frieden, a former director of the Centers for Disease Control and Prevention.“There is so much toxic politics around Covid that it’s constraining sensible action,” he said. “Obviously it makes sense to require proof of vaccination in various settings, but that has become a political lightning rod.”Dr. Frieden and other experts said they feared that if the Delta variant continues to circulate, it will mutate in a way that leaves even the vaccinated vulnerable. That already seems to be happening elsewhere in the world; even countries like South Korea and Israel, where the virus seemed to be in check, have new clusters of disease.“Compared to many other countries, we are in a much more secure situation,” said Dr. Jennifer Nuzzo, an epidemiologist at Johns Hopkins University. But, she added, “I really do worry that as America enjoys its freedoms, we forget about the rest of the world, and that could come back to bite us.”When Mr. Biden announced his July 4 vaccination goal in early May, he said meeting it would demonstrate that the United States had taken “a serious step toward a return to normal.” For many people, that seems to be the case. The president said then that Americans would be able to gather in backyards for small Independence Day barbecues; his gathering of 1,000 guests is partly aimed at showing the country that his administration has exceeded expectations even if vaccinations have stalled.While Mr. Biden has repeatedly spoken of “independence from the virus,” Dr. Arthur L. Caplan, the director of NYU Langone Medical Center’s medical ethics division, said the president should be careful about the language he uses.“Before I went out and had my fireworks and sipped piña coladas on the White House veranda, I would say, ‘I’ve got to make clear, as president, we have major challenges unresolved,’” Dr. Caplan said. “I would say, ‘We’re doing well at halftime.’”Mitch Smith

In an article appearing in Nature Biomedical Engineering, a team of scientists from the UCLA David Geffen School of Medicine and UCLA School of Engineering report real-world results on SwabSeq, a high-throughput testing platform that uses sequencing to test thousands of samples at a time to detect COVID-19. They were able to perform more than 80,000 tests in less than two months, with the test showing extremely high sensitivity and specificity.
SwabSeq uses sample-specific molecular barcodes to simultaneously analyze thousands of samples for the presence or absence of SARS-CoV-2, the virus that causes COVID-19. SwabSeq was granted FDA Emergency Use Authorization in October and is currently deployed at UCLA in a high-complexity CLIA laboratory, which has performed over 150,000 tests since December 2020. SwabSeq is a flexible protocol and can rapidly scale up testing for novel pathogens, including COVID-19 and future emerging viruses.
“We have optimized SwabSeq to prioritize scale and low cost, key factors that are missing from current COVID-19 diagnostics,” the authors write.
“These results demonstrate the potential of SwabSeq to be used for SARS-CoV-2 testing on an unprecedented scale,” said Dr. Valerie Arboleda, Assistant Professor and lead scientist on the project. “SwabSeq offers a potential solution to the need for population-wide testing to stem the pandemic.” In the months since, the team has continued to use the test, and as of this date has performed more than 150,000 tests.
The groundbreaking technology was developed in a collaboration between scientists at the Department of Computational Medicine affiliated with both the David Geffen School of Medicine and the Samueli School of Engineering at UCLA, the Department of Human Genetics, the Department of Pathology and Laboratory Medicine, and Octant, a start-up company founded and incubated at UCLA. SwabSeq is a modification of Octant’s technology that is being applied toward drug discovery and has been made available broadly to fight the pandemic. UCLA scientists have been leading a broader coalition of academic and industrial labs around the country and the world to develop the technology to scale up COVID-19 testing.
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Over years of studying antibody responses against the flu in the Wilson lab at the University of Chicago, researchers kept coming up with a strange finding: antibodies that seemed to bind not only to the flu virus, but to every virus the lab could throw at them. Since antibodies are usually highly specific to individual pathogens, in order to maximize their targeted protective response, this pattern was extremely unusual.
Until finally, they realized: The antibodies weren’t responding to the viruses, but rather to something in the biological material in which the viruses had been grown. In every case, the virus had been propagated in chicken eggs — more specifically, in a part of the egg called the allantois. The findings were published on June 15 in mBio.
“Growing vaccines in eggs is the old school way of doing things because it’s cheap and you can grow a lot of virus in eggs,” said first author Jenna Guthmiller, PhD, a postdoctoral fellow at UChicago. “Now we’re finding that these antibodies bind to this glycan — a sugar molecule — found in eggs, which means that people who are getting vaccinated are producing an antibody response against this egg component that’s not related to the virus at all.”
The fact that vaccines grown in eggs can lead to this off-target antibody response is unexpected, but the implications aren’t yet known. It could mean that the immune system diverts resources away from developing protective antiviral antibodies to produce these egg sugar antibodies instead, which could have implications for vaccine effectiveness.
It’s important to note that these antibodies do not bind to known egg allergens, indicating that they likely are not the culprits behind egg allergies, Guthmiller said. “It doesn’t seem to be harmful, but it may not be beneficial, and it may be affecting immunity, and that’s the important next step.”
It took the team years to determine that the antibodies were linked, not to the viruses they were studying, but rather to the eggs in which they were grown. “No joke, we spent years thinking about this,” said Guthmiller. “But once we figured it out, it was straightforward. And we found that it’s very specific to the flu vaccine grown in this one compartment, in the allantois. This isn’t seen with vaccines grown in other chicken cells.”
The antibodies target a sugar molecule, known as a glycan, called N-acetyllactosamine (LacNAc), with a sulfur modification. LacNAcs are a common glycan in humans, but the specific sulfur modification of LacNAc found in eggs is not known to be expressed in humans. Because of this, humans can produce antibodies against this sulfur-modified glycan.
When the researchers dug into past studies on flu antibody responses, they found that this antibody response against LacNAc appears to be fairly common following flu vaccination. However, some people do not seem to develop the anti-egg antibodies, and it doesn’t appear that producing the anti-egg antibodies reduces the immune system’s ability to produce anti-flu antibodies — though it’s not clear whether or not there is an impact on vaccine effectiveness.
“There’s a little bit of evidence so far that suggests vaccines prepared by other methods are more effective than those grown in eggs, but the precise reasons aren’t known,” said Guthmiller. “This could be a potential mechanism, but we weren’t able to address that in this study.”
So far, there is no evidence that the presence of these antibodies has any negative impact on an individual’s health. “We just really don’t know what function these antibodies have,” said Guthmiller. “So many people get the flu vaccine every year, and adverse events are extremely uncommon, so there’s no reason to suspect that this might cause any problems.”
More research is needed to determine what, if anything, these anti-egg antibodies mean for the effectiveness of the flu vaccine. “We don’t know how these antibodies impact our flu-specific response. There may be competition between B cells against the flu and these egg glycans, which could be impacting immunity. And if there is an association between egg antibodies and reduced immunity, we need to look at alternative methods for flu vaccine production. Anything that can improve vaccine production is something that we should be considering seriously.”
The study, “An Egg-Derived Sulfated N-Acetyllactosamine Glycan Is an Antigenic Decoy of Influenza Virus Vaccines,” was supported by the National Institute of Allergy and Infectious Diseases (U19AI082724, U19AI109946, U19AI057266, P01 AI097092, R01AI145870-01, HHSN272201400005C, HHSN272201400008C, and 75N93019C00051) and the National Center for Functional Glycomics (R24 GM137763). Additional authors include Henry A. Utset, Carole Henry, Lei Li, Nai-Ying Zheng, Marcos Costa Vieira, Min Huang, Sarah Cobey, and Patrick Wilson of UChicago; Weina Sun and Peter Palese of Icahn School of Medicine at Mount Sinai; and Seth Zost and Scott E. Hensley of Perelman School of Medicine, University of Pennsylvania.

Researchers at the Francis Crick Institute and University of Dundee have screened thousands of drug and chemical molecules and identified a range of potential antivirals that could be developed into new treatments for COVID-19 or in preparation for future coronavirus outbreaks.
While COVID-19 vaccines are being rolled out, there are still few drug options that can be used to treat patients with the virus, to reduce symptoms and speed up recovery time. These treatments are especially important for groups where the vaccines are less effective, such as some patients with blood cancers.
In a series of seven papers, published today (2 July) in the Biochemical Journal (see https://portlandpress.com/collection/11714/Tackling-SARS-CoV-2-Biochemistry), the scientists identified 15 molecules which inhibit the growth of SARS-CoV-2 by blocking different enzymes involved in its replication.
The researchers developed and ran tests for around 5,000 molecules provided by the Crick’s High Throughput Screening team to see if any of these effectively blocked the functioning of any of seven SARS-CoV-2 enzymes. The tests were based on fluorescent changes with a special imaging tool detecting if enzymes had been affected.
They then validated and tested the potential inhibitors against SARS-CoV-2 in the lab, to determine if they effectively slowed viral growth. The team found at least one inhibitor for all seven enzymes.
Three of the molecules identified are existing drugs, used to treat other diseases. Lomeguatrib is used in melanoma and has few side-effects, suramin is a treatment for African sleeping sickness and river blindness and trifluperidol is used in cases of mania and schizophrenia. As there is existing safety data on these drugs, it may be possible to more quickly develop these into SARS-CoV-2 antivirals.
John Diffley, lead author of the papers and associate research director and head of the Chromosome Replication Laboratory at the Crick, said: “We’ve developed a chemical toolbox of information about potential new COVID-19 drugs. We hope this attracts attention from scientists with the drug development and clinical expertise needed to test these further, and ultimately see if any could become safe and effective treatments for COVID-19 patients.”
The 15 molecules were also tested in combination with remdesivir, an antiviral being used to treat patients with COVID-19. Four of these, all which target the SARS-CoV-2 enzyme Nsp14 mRNA Cap methyltransferase, were found to improve the effectiveness of this antiviral in lab tests.
The scientists now plan to run tests to see if any pairing of the 15 molecules they identified decrease the virus’ growth more than if they are used alone. Targeting enzymes involved in virus replication could also help prepare for future viral pandemics.
“Proteins on the outside of viruses evolve rapidly but within different classes of viruses are well conserved proteins that change very little with time,” adds John.
“If we can develop drugs that inhibit these proteins, in the situation of a future pandemic, they could provide a valuable first line of defence, before vaccines become available.”
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Materials provided by The Francis Crick Institute. Note: Content may be edited for style and length.

As smart watches are increasingly able to monitor the vital signs of health, including what’s going on when we sleep, a problem has emerged: those wearable, wireless devices are often disconnected from our body overnight, being charged at the bedside.
“Quality of sleep and its patterns contain a lot of important information about patients’ health conditions,” says Sunghoon Ivan Lee, assistant professor in the University of Massachusetts Amherst College of Information and Computer Sciences and director of the Advanced Human Health Analytics Laboratory.
But that information can’t be tracked on smartwatches if the wearable devices are being charged as users sleep, which prior research has shown is frequently the case. Lee adds, “The main reason users discontinue the long-term use of wearable devices is because they have to frequently charge the on-device battery.”
Pondering this problem, Lee brainstormed with UMass Amherst wearable computing engineer Jeremy Gummeson to find a solution to continuously recharge these devices on the body so they can monitor the user’s health 24/7.
The scientists’ aha moment came when they realized “human skin is a conductible material,” Lee recalls. “Why can’t we instrument daily objects, such as the office desk, chair and car steering wheel, so they can seamlessly transfer power through human skin to charge up a watch or any wearable sensor while the users interact with them? Like, using human skin as a wire.
“Then we can motivate people to do things like sleep tracking because they never have to take their watch off to charge it,” he adds.

The government has been accused of creating a ‘two tier welfare system’ for people who have terminal illnesses by two charities.A review of rules which fast-track access to benefits for people who only have six months or less to live was launched two years ago in England and Wales but has not been published. Scotland and Northern Ireland have taken steps to scrap the rule.Marie Curie and the MND Association say the difference between their regions leads to “a two-tier system”.A spokesperson from the Department of Work and Pensions told BBC News: “We are committed to supporting people nearing the end of their lives. Our priority is dealing with people’s claims quickly and compassionately, which we’ve continued to do throughout the pandemic.”But the BBC has heard from terminally ill people who had their payments reduced when their disability allowance was moved to Personal Independence Payments.