A new study demonstrates that machine-learning strategies can be applied to routinely collected physiological data, such as heart rate and blood pressure, to provide clues about pain levels in people with sickle cell disease. Mark Panaggio of Johns Hopkins University Applied Physics Laboratory and colleagues present these findings in the open-access journal PLOS Computational Biology.
Pain is subjective, and monitoring pain can be intrusive and time-consuming. Pain medication can help, but accurate knowledge of a patient’s pain is necessary to balance relief against risk of addiction or other unwanted effects. Machine-learning strategies have shown promise in predicting pain from objective physiological measurements, such as muscle activity or facial expressions, but few studies have applied machine learning to routinely collected data.
Now, Panaggio and colleagues have developed and applied machine-learning models to data from people with sickle cell disease who were hospitalized due to debilitating pain. These statistical models classify whether a patient’s pain was low, moderate, or high at each point during their stay based on routinely collected measurements of their blood pressure, heart rate, temperature, respiratory rate, and oxygen levels.
The researchers found that these vital signs indeed gave clues into the patients’ reported pain levels. By taking physiological data into account, their models outperformed baseline models in estimating subjective pain levels, detecting changes in pain, and identifying atypical pain levels. Pain predictions were most accurate when they accounted for changes in patients’ vital signs over time.
“Studies like ours show the potential that data-driven models based on machine learning have to enhance our ability to monitor patients in less invasive ways and ultimately, be able to provide more timely and targeted treatments,” Panaggio says.
Looking ahead, the researchers hope to leverage more comprehensive data sources and real-time monitoring tools, such as fitness trackers, to build better models for inferring and forecasting pain.

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Insights into how bacterial proteins work as a network to take control of our cells could help predict infection outcomes and develop new treatments.
Much like a hacker seizes control of a company’s software to cause chaos, disease-causing bacteria, such as E. coli and Salmonella, use miniature molecular syringes to inject their own chaos-inducing agents (called effectors) into the cells that keep our guts healthy.
These effectors take control of our cells, overwhelming their defences and blocking key immune responses, allowing the infection to take hold.
Previously, studies have investigated single effectors. Now a team led by scientists at Imperial College London and The Institute of Cancer Research, London, and including researchers from the UK, Spain and Israel, has studied whole sets of effectors in different combinations.
The study, published today in Science, investigated data from experiments in mice infected with the mouse version of E. coli, called Citrobacter rodentium, which injects 31 effectors.
The results show how effectors work together as a network, allowing them to colonise their hosts even if some effectors are removed. The investigation also revealed how the host’s immune system can bypass the obstacles the effectors create, triggering complementary immune responses.

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The researchers suggest that knowing how the makeup of effector networks influences the ability of infections to take hold could help design interventions that disrupt their effects.
Study lead Professor Gad Frankel, from the Department of Life Sciences at Imperial, said: “The data represent a breakthrough in our understanding of the mechanisms of bacterial infections and host responses. Our results show that the injected effectors are not working individually, but instead as a pack.
“We found there is an inherent strength and flexibility to the network, which ensures that if one or several components don’t work, the infection can go on. Importantly, this work has also revealed that our cells have a built-in firewall, which means that we can deal with the hacker’s corruptive networks and mount effective immune responses that can clear the infection.”
Study co-lead Professor Jyoti Choudhary, from the Functional Proteomics Lab at The Institute of Cancer Research, London, said: “Our study shows that we can predict how a cell will respond when attacked by different combinations of bacterial effector proteins. The research will help us to better understand how cells, the immune system and bacteria interact, and we can apply this knowledge to diseases like cancer and inflammatory bowel disease where bacteria in the gut play an important role.
“We hope, through further study, to build on this knowledge and work out exactly how these effector proteins function, and how they work together to disrupt host cells. In future, this enhanced understanding could lead to the development of new treatments.”
During their experiments, the team were able to remove different effectors when infecting mice with the pathogen, tracking how successful each infection was. This showed that the effector network produced by the pathogen could be reduced by up to 60 percent and still produce a successful infection.

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The team collected data on more than 100 different synthetic combinations of the 31 effectors, which Professor Alfonso Rodríguez-Patón and Elena Núñez-Berrueco at the Universidad Politécnica de Madrid used to build an artificial intelligence (AI) algorithm.
The AI model was able to predict the outcomes of infection with Citrobacter rodentium expressing different effector networks, which were tested with experiments in mice. As it is impossible to test in the lab all the possible networks that 31 effectors can form, employing an AI model is the only practical approach to studying biological systems of this complexity.
Co-first author Dr David Ruano-Gallego from the Department of Life Sciences at Imperial, said: “The AI allows us to focus on creating the most relevant combinations of effectors and learn from them how bacteria are counteracted by our immune system. These combinations would not be obvious from our experimental results alone, opening up the possibility of using AI to predict infection outcomes.”
Co-first author Dr Julia Sánchez-Garrido, from the Department of Life Sciences at Imperial, added: “Our results also mean that in the future, using AI and synthetic biology, we should be able to work out which cell functions are essential during infection, enabling us to find ways to fight the infection not by killing the pathogen with antibiotics, but instead by changing and improving our natural defence responses to infection.”
This project was supported by The Wellcome Trust.

An enzyme called MARK2 has been identified as a key stress-response switch in cells in a study by researchers at Johns Hopkins Bloomberg School of Public Health. Overactivation of this type of stress response is a possible cause of injury to brain cells in neurodegenerative diseases such as Alzheimer’s, Parkinson’s, and Amyotrophic Lateral Sclerosis. The discovery will make MARK2 a focus of investigation for its possible role in these diseases, and may ultimately be a target for neurodegenerative disease treatments.
In addition to its potential relevance to neurodegenerative diseases, the finding is an advance in understanding basic cell biology.
The paper describing the discovery appears online March 11 in PLoS Biology.
The study focused on the cellular response to “proteotoxic” stress — a buildup of damaged or aggregated proteins within the main part of the cell, which is a central feature of neurodegenerative diseases. It has been known that cells respond to this type of stress by reducing their production of new proteins, and that a signaling enzyme likely mediates this response. The researchers, after ruling out other signaling enzymes, were able to show that the signaling enzyme MARK2 has this role.
“Further studies of this previously unrecognized signaling pathway should expand our understanding of protein regulation in cells and the role of this process in the development of human diseases,” says Jiou Wang, PhD, a professor in the Department of Biochemistry and Molecular Biology at the Bloomberg School.
Together, Alzheimer’s, ALS, and other neurodegenerative disorders afflict well over 50 million people worldwide. To date there is no disease-slowing treatment, let alone a cure, for any of them — primarily because their causes are not well understood.

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One possible set of causes of neurodegenerative disorders relates to the proteotoxic stress and the response in brain cells. When this response is activated, reducing protein synthesis, it ideally minimizes the protein burden of the cell under proteotoxic stress, thereby allowing it to recover from the stress. But the long-term reduction of protein synthesis could end up starving the cell of needed proteins, injuring it, and potentially triggering cell death. In other cases, the failure of the proteotoxic stress response, rather than its overactivation, may be the problem, so that protein overload leads to cell injury or death.
To fully understand either scenario, scientists need to understand the signaling pathway that senses proteotoxic stress and switches on the proteotoxic stress response. Wang and colleagues in their new study set out to discover it.
Like others in this field, the research team already knew that the molecule at the end of this pathway that switches off protein production is a member of a broad class of signaling enzymes called kinases. They also knew in advance that there are several specific kinases that switch off protein production in the same way, but in response to other types of cellular stress, such as viral infection. The challenge in this study was to find the specific kinase that throws this switch in response to proteotoxic stress in the main part of the cell.
The researchers first identified the kinase MARK2 as one of several candidates for their inquiry by sifting through a large database, produced with prior research, of various kinases and the proteins they potentially act upon. Following up their leads with various cell-free and cell culture experiments, they were able to show that MARK2, and no other candidate kinase, can switch off the protein-making machinery in cells in response to proteotoxic stress, even when the other four known protein-shutdown kinases are absent.
Looking upstream in the signaling pathway, the team found that MARK2 is activated by another signaling kinase, PKCδ, which becomes available for its MARK2-activating role under conditions of proteotoxic stress, thus effectively acting as a proteotoxic stress sensor.
As a preliminary check on the clinical relevance of these findings, the researchers examined a mouse model of familial ALS and samples of spinal cord tissue from human ALS patients. They found evidence that this PKCδ-MARK2 pathway is highly active in these cases compared to non-ALS mice and humans.
“These findings are consistent with the idea that in ALS, for example, this PKCδ-MARK2 pathway is highly active and reducing protein production, which over the long term contributes to the disease process,” Wang says.
Having clarified the basics of how this pathway works, Wang and colleagues are now planning to study it in different neurodegenerative disease models to determine whether the pathway could be targeted to treat such diseases.
“I suspect that this PKCδ-MARK2 pathway will ultimately be shown to be relevant not only in neurodegenerative disorders but in many other diseases including cancers,” Wang says.

#masthead-section-label, #masthead-bar-one { display: none }The Coronavirus OutbreakliveLatest UpdatesMaps and CasesRisk Near YouVaccine RolloutGuidelines After VaccinationAdvertisementContinue reading the main storyCovid-19 News: A Year After W.H.O. Declared Virus Pandemic, More U.S. States Expand Access to VaccinesFor a second St. Patrick’s Day without parades, some places find other ways to celebrate.March 11, 2021, 3:23 p.m. ETMarch 11, 2021, 3:23 p.m. ETPeople waved a flag in celebration of St. Patrick’s Day last year, despite the cancellation of the parade in New York because of the pandemic. Celebrations around the country will again be cancelled this year.Credit…Spencer Platt/Getty ImagesThe pandemic in the United States, now more than a year old, is starting to hit some calendar milestones for a second time, including St. Patricks’ Day parades across the country. The sudden cancellation of the parades last year was one of the first big signs of how disruptive the pandemic would be to normal life in the U.S.Though many states and cities have been tentatively loosening various Covid restrictions lately, most places have not cleared the way for a resumption of parades, which can be among the most ruthlessly effective kinds of super-spreading events.So the St. Patrick’s Day parade in Chicago has been canceled, again; the parade in Boston canceled, again; the one in Philadelphia, canceled, again. The parade in New York City, intent on retaining its distinction as the oldest uninterrupted St. Patrick’s Day parade in the world, will once again be largely ceremonial and very low-profile, with a small group walking up Fifth Avenue at an unannounced time very early in the morning — that is, if the city and state approve doing anything at all.Some places are putting a spin on the commemorations. The 37th annual parade in St. James, on Long Island, is now going to be held by car; the one in Hilton Head, S.C., is moving to the water; and the one in Pittsburgh is moving to the fall (maybe). A drive-in Celtic rock concert is planned in Dublin, Calif.; a virtual 5K run in Naperville, Ill.; and a day of green beer in plastic cups being delivered by masked servers between plexiglass screens at McGillin’s Olde Ale House in Philadelphia.Last year, bars from Chicago to New Orleans were packed on the weekend before St. Patrick’s Day despite the cancellation of local parades, prompting stern admonitions from mayors and governors. This year, officials are pleading with people to stay at home, or at least to be vigilant when they are out.“We are not at a point where we can start having major St. Patrick’s Day celebrations,” Dr. Allison Arwady, the commissioner of the Chicago Department of Public Health, said to reporters in a recent briefing.The Coronavirus Outbreak

How do you turn “dumb” headphones into smart ones? Rutgers engineers have invented a cheap and easy way by transforming headphones into sensors that can be plugged into smartphones, identify their users, monitor their heart rates and perform other services.
Their invention, called HeadFi, is based on a small plug-in headphone adapter that turns a regular headphone into a sensing device. Unlike smart headphones, regular headphones lack sensors. HeadFi would allow users to avoid having to buy a new pair of smart headphones with embedded sensors to enjoy sensing features.
“HeadFi could turn hundreds of millions of existing, regular headphones worldwide into intelligent ones with a simple upgrade,” said Xiaoran Fan, a HeadFi primary inventor. He is a recent Rutgers doctoral graduate who completed the research during his final year at the university and now works at Samsung Artificial Intelligence Center.
A peer-reviewed Rutgers-led paper on the invention, which results in “earable intelligence,” will be formally published in October at MobiCom 2021, the top international conference on mobile computing and mobile and wireless networking.
Headphones are among the most popular wearable devices worldwide and they continue to become more intelligent as new functions appear, such as touch-based gesture control, the paper notes. Such functions usually rely on auxiliary sensors, such as accelerometers, gyroscopes and microphones that are available on many smart headphones.
HeadFi turns the two drivers already inside all headphones into a versatile sensor, and it works by connecting headphones to a pairing device, such as a smartphone. It does not require adding auxiliary sensors and avoids changes to headphone hardware or the need to customize headphones, both of which may increase their weight and bulk. By plugging into HeadFi, a converted headphone can perform sensing tasks and play music at the same time.
The engineers conducted experiments with 53 volunteers using 54 pairs of headphones with estimated prices ranging from $2.99 to $15,000. HeadFi can achieve 97.2 percent to 99.5 percent accuracy on user identification, 96.8 percent to 99.2 percent on heart rate monitoring and 97.7 percent to 99.3 percent on gesture recognition.

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To highlight tumours in the body for cancer diagnosis, doctors can use tiny optical probes (nanoprobes) that light up when they attach to tumours. These nanoprobes allow doctors to detect the location, shape and size of cancers in the body.
Most nanoprobes are fluorescent; they absorb light of a specific colour, like blue and then emit back light of a different colour, like green. However, as tissues of the human body can emit light as well, distinguishing the nanoprobe light from the background light can be tough and could lead to the wrong interpretation.
Now, researchers at Imperial College London have developed new nanoprobes, named bioharmonophores and patented at Imperial, which emit light with a new type of glowing technology known as second harmonic generation (SHG).
After testing the nanoprobes in zebrafish embryos, the researchers found that bioharmonophores, which were modified to target cancer cells, highlighted tumours more brightly and for longer periods than fluorescent nanoprobes. Their light can be easily spotted and distinguished by the tissue generally emitted light, and they also attach precisely to tumour cells and no healthy cells, making them more precise in detecting tumour edges.
Lead researcher Dr Periklis Pantazis of Imperial’s Department of Bioengineering said: “Bioharmonophores could be a more effective way to detect tumours than is currently available. They uniquely combine features that could be great for cancer diagnosis and therapy in clinical practice and could eventually improve patient outcomes following further research.”
The findings are published in ACS Nano.

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Bioharmonophores are both biocompatible and biodegradable as they are made of peptides — the same ingredients of proteins found in the body. They are metabolised naturally in the body within 48 hours and are therefore unlikely to pose long-term health risks.
To investigate precise tumour detection, the researchers first injected zebrafish embryos with malignant cancer cells, which allowed tumour cells to proliferate unchecked. Twenty-four hours later they injected bioharmonophores which were modified to target p32 peptide molecules that are specifically found in tumour cells. They then used imaging techniques at Imperial’s Facility for Imaging by Light Microscopy to study how well the modified bioharmonophores detected the tumours.
They found that bioharmonophores had outstanding detection sensitivity, meaning they attached to specific tumour cells but not to healthy ones. Fluorescence-enabled nanoprobes tend to attach less specifically, meaning they can misrepresent healthy cells as tumour cells, or vice versa.
They also found that unlike fluorescence, bioharmonophores did not ‘bleach’, meaning they did not lose their ability to emit light over time. In addition, the light emitted by bioharmonophores did not saturate as happens with fluorescent nanoprobes, meaning they got brighter when illuminated with more light. This way tumours became even clearer.
Dr Pantazis said: “It is very important that tumour nanoprobes highlight cells specifically and clearly for cancer diagnosis. Our proof-of-concept study suggests that the very bright bioharmonophores could be powerful tools in diagnosing cancer and targeting treatments in the coming years.”
The manufacture of bioharmonophores is cheap, reproducible, scalable and takes around two days at room temperature. They now need to be tested in mammals to identify how well the findings translate beyond zebrafish.
The researchers are also looking into how bioharmonophores could be used to guide surgical interventions during cancer surgery, as well as how they could generate light at different frequencies to potentially help kill tumour cells with high precision.
This work was funded by the Royal Society, Wellcome Trust, the Swiss National Science Foundation, the European Union, and the Swiss National Centre of Competence in Research.

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Materials provided by Imperial College London. Original written by Caroline Brogan. Note: Content may be edited for style and length.

Researchers from Children’s Hospital of Philadelphia (CHOP) have determined what happens at a cellular level as the lung alveolus forms and allows newborns to breathe air. Understanding this process gives researchers a better sense of how to develop therapies and potentially regenerate this critical tissue in the event of injury. The findings were published online today by the journal Science.
The lung develops during both embryonic and postnatal stages, during which lung tissue forms and a variety of cell types perform specific roles. During the transition from embryo to newborn is when the alveolar region of the lung refines its primary function of exchanging gas, which includes the critical process of ridding the body of carbon dioxide.
Despite these critical steps involved in the formation of the lung, little is known about what happens at a cellular and genomic level. Not only is the lung alveolar critical, it can also suffer damage caused by pathogens such as influenza and the SARS-CoV2 virus that causes COVID-19. Knowing which cells are involved in the formation of healthy lung tissue at birth may provide a basis for therapies that help regenerate this critical portion of the lung.
“Extensive morphological changes properly shape the alveolar niche, but prior to this study, the research community was unsure as to the extent of cellular signaling involved to promote its proper architecture,” said first author Jarod A. Zepp, PhD, a research faculty member of the Division of Pulmonary and Sleep Medicine at CHOP and an Assistant Professor at the Perelman School of Medicine at the University of Pennsylvania. “Recent advances in technology allowed us to assess the intracellular communication that drives the generation of this critical portion of the lung.”
The study team used a multimodal approach to investigate intercellular relationships that drive the formation of the alveolus. They discovered that alveolar type 1 (AT1) epithelial cells, which form the outer layer of the alveolus tissue, represent a signaling hub that coordinates cell development, especially during the transition to air breathing. They also traced the lineage of AT1 cells and show that they align with myofibroblasts, which are a special cell type involved in tissue remodeling. Finally, the researchers also demonstrated that AT1-restricted ligands, or secreted binding molecules, are required to form these myofibroblasts and the alveolus.
“Our study reveals the complexity of the cell-types and their extensive communication with one another as they form this critical part of the lung,” Zepp said. “The recent COVID-19 pandemic has provided the research community with an increased appreciation of the intercellular communication that helps form the alveolar structure and maintain its function and provides us with vital clues on how we might be able to repair damaged tissue at a cellular level.”

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Electric stimulation may be able to help blood vessels carry white blood cells and oxygen to wounds, speeding healing, a new study suggests.
The study, published in the Royal Society of Chemistry journal Lab on a Chip, found that steady electrical stimulation generates increased permeability across blood vessels, providing new insight into the ways new blood vessels might grow.
The electrical stimulation provided a constant voltage with an accompanying electric current in the presence of fluid flow. The findings indicate that stimulation increases permeability of the blood vessel — an important characteristic that can help wound-healing substances in the blood reach injuries more efficiently.
“There was this speculation that blood vessels could grow better if you stimulated them electrically,” said Shaurya Prakash, senior author of the study and associate professor of mechanical and aerospace engineering at The Ohio State University. “And we found that the response of the cells in our blood vessel models shows significant promise towards changing the permeability of the vessels that can have positive outcomes for our ongoing work in wound healing.”
Blood vessels are crucial for wound healing: They thread throughout your body, carrying nutrients, cells and chemicals that can help control inflammation caused by an injury. Oxygen and white blood cells — which protect the body from foreign invaders — are two key components delivered by blood vessels.
But when there is an injury — for example, a cut on your finger — the architecture of the blood vessels at the wound site are disrupted. That also interrupts the vessels’ ability to help the wound heal. Blood vessels regrow on their own, almost like the branches of trees, without external sources of electricity, as part of the healing process.

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“And as the blood vessels begin to grow, they replenish the skin and cells and establish a healing barrier again,” Prakash said. “But our question was: How do you make this process better and faster, and is there any benefit to doing that?”
What they found, in laboratory tests performed using human cells, is that stimulating blood vessels with electricity showed a marked increase in blood vessel permeability, which is a physical marker suggestive of possible new vessel growth.
“These initial findings are exciting, and the next phase of the work will require us to study if and how we can actually grow new vessels,” Prakash said.
Jon Song, co-author of the paper and associate professor of mechanical and aerospace engineering at Ohio State, said the results imply that one of the primary ways blood vessels work to heal injuries is by allowing molecules and cells to move across the vessels’ walls.
“And now we have better understanding for how electric stimulation can change the permeability across the vessel walls,” Song said. “Let’s say you have a cutaneous wound, like a paper cut, and your blood vessels are severed and that’s why you have blood leaking out. What you need is a bunch of bloodborne cells to come to that place and exit out the blood vessel to initiate the wound repair.”
The study suggested that changes in blood vessel permeability could get those bloodborne cells to a wound site more quickly, though it did not explain the reasons why that happened. The study seemed to indicate that electricity affected the proteins that hold blood vessel cells together, but those results were not conclusive.
The study is an extension of work by a broader team, led by Prakash, that previously showed electric bandages could help stimulate healing in wounded dogs. That work indicated that electrical stimulation might also help manage infections at wound sites — a phenomenon the researchers also hope to research further.

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Materials provided by Ohio State University. Original written by Laura Arenschield. Note: Content may be edited for style and length.

Millions of people die prematurely every year from diseases and cancer caused by air pollution. The first line of defence against this carnage is ambient air quality standards. Yet, according to researchers from McGill University, over half of the world’s population lives without the protection of adequate air quality standards.
Air pollution varies greatly in different parts of the world. But what about the primary weapons against it? To find answers, researchers from McGill University set out to investigate global air quality standards in a study published in the Bulletin of the World Health Organization.
The researchers focused on air pollution called PM2.5 — responsible for an estimated 4.2 million premature deaths every year globally. This includes over a million deaths in China, over half a million in India, almost 200,000 in Europe, and over 50,000 in the United States.
“In Canada, about 5,900 people die every year from air pollution, according to estimates from Health Canada. Air pollution kills almost as many Canadians every three years as COVID-19 killed to date,” says co-author Parisa Ariya, a Professor in the Department of Chemistry at McGill University.
Small but deadly
Among the different types of air pollution, PM2.5 kills the most people worldwide. It consists of particles smaller than approximately 2.5 microns — so small that billions of them can fit inside a red blood cell.
“We adopted unprecedented measures to protect people from COVID-19, yet we don’t do enough to avoid the millions of preventable deaths caused by air pollution every year,” says Yevgen Nazarenko, a Research Associate at McGill University who conducted the study with Devendra Pal under the supervision of Professor Ariya.
The researchers found that where there is protection, standards are often much worse than what the World Health Organization considers safe. Many regions with the most air pollution don’t even measure PM2.5 air pollution, like the Middle East. They also found that the weakest air quality standards are often violated, particularly in countries like China and India. In contrast, the strictest standards are often met, in places like Canada and Australia.
Surprisingly, the researchers discovered that high population density is not necessarily a barrier to fighting air pollution successfully. Several jurisdictions with densely populated areas were successful in setting and enforcing strict standards. These included Japan, Taiwan, Singapore, El Salvador, Trinidad and Tobago, and the Dominican Republic.
“Our findings show that more than half of the world urgently needs protection in the form of adequate PM2.5 ambient air quality standards. Putting these standards in place everywhere will save countless lives. And where standards are already in place, they should be harmonized globally,” says Nazarenko.
“Even in developed countries, we must work harder to clean up our air to save hundreds of thousands of lives every year,” he says.

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Ten days after receiving a second dose of a messenger RNA, or mRNA, vaccine for COVID-19, patients without COVID-19 symptoms are far less likely to test positive and unknowingly spread COVID-19, compared to patients who have not been vaccinated for COVID-19. The Pfizer-BioNTech and Moderna messenger RNA vaccines for COVID-19 are authorized for emergency use in the U.S.
With two doses of a messenger RNA COVID-19 vaccine, people with no symptoms showed an 80% lower adjusted risk of testing positive for COVID-19 after their last dose. Those are the findings of a Mayo Clinic study of vaccinated patients. These finding appear in the journal Clinical Infectious Diseases.
The authors say these findings underscore the efficacy of messenger RNA vaccines for COVID-19 to significantly limit the spread of COVID-19 by people with no symptoms who may unknowingly spread the infection to others.
The researchers retrospectively looked at a cohort of 39,000 patients who underwent pre-procedural molecular screening tests for COVID-19. More than 48,000 screening tests were performed, including 3,000 screening tests on patients who had received at least one dose of a messenger RNA COVID-19 vaccine. These screening tests were part of routine COVID-19 testing prior to treatments not related to COVID-19, such as surgeries and other procedures. Patients in the vaccinated group had received at least one dose of a messenger RNA COVID-19 vaccine.
“We found that those patients without symptoms receiving at least one dose of the first authorized mRNA COVID-19 vaccine, Pfizer-BioNTech, 10 days or more prior to screening were 72% less likely to test positive,” says Aaron Tande, M.D., a Mayo Clinic infectious diseases specialist and co-first author of the paper. “Those receiving two doses were 73% less likely, compared to the unvaccinated group.”
After adjusting for a range of factors, researchers found an 80% risk reduction of testing positive for COVID-19 among those with two doses of a messenger RNA COVID-19 vaccine.
The study was based on patients receiving screening tests between Dec. 17, 2020, and Feb. 8 at Mayo Clinic in Minnesota and Arizona and at Mayo Clinic Health System in Minnesota and Wisconsin.
Additional authors are Benjamin Pollock, Ph.D., co-first author; Nilay Shah, Ph.D.; Gianrico Farrugia, M.D.; Abinash Virk, M.D.; Melanie Swift, M.D.; Laura Breeher, M.D.; Matthew Binnicker, Ph.D.; and Elie Berbari, M.D. ? all of Mayo Clinic. Funding for the study was provided by Mayo Clinic.

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Materials provided by Mayo Clinic. Original written by Robert Nellis. Note: Content may be edited for style and length.