Publisher Health

Scientists at UT Southwestern have discovered a key protein that helps the bacteria that causes Legionnaires’ disease to set up house in the cells of humans and other hosts. The findings, published in Science, could offer insights into how other bacteria are able to survive inside cells, knowledge that could lead to new treatments for a wide variety of infections.
“Many infectious bacteria, from listeria to chlamydia to salmonella, use systems that allow them to dwell within their host’s cells,” says study leader Vincent Tagliabracci, Ph.D., assistant professor of molecular biology at UTSW and member of the Harold C. Simmons Comprehensive Cancer Center. “Better understanding the tools they use to make this happen is teaching us some interesting biochemistry and could eventually lead to new targets for therapy.”
Tagliabracci’s lab studies atypical kinases, unusual forms of enzymes that transfer chemical groups called phosphates onto proteins or lipids, changing their function. Research here and elsewhere has shown that Legionella, the genus of bacteria that cause Legionnaires’ disease, is a particularly rich source of these noncanonical kinases. According to the Centers for Disease Control and Prevention, nearly 10,000 cases of Legionnaires’ disease were reported in the U.S. in 2018, though the true incidence is believed to be higher.
After identifying a new Legionella atypical kinase named MavQ, Tagliabracci and his colleagues used a live-cell imaging technique combined with a relatively new molecular tagging method to see where MavQ is found in infected human cells, a clue to its function. Rather than residing in a specific location, the researchers were surprised to see that the protein oscillated back and forth between the endoplasmic reticulum — a network of membranes important for protein and lipid synthesis — and bubble- or tube-shaped structures within the cell.
Further research suggests that MavQ, along with a partner molecule called SidP, remodels the endoplasmic reticulum so that Legionella can steal parts of the membrane to help create and sustain the vacuole, a structure that houses the parasite inside cells and protects it from immune attack.
Tagliabracci, a Michael L. Rosenberg Scholar in Medical Research and a Cancer Prevention & Research Institute of Texas (CPRIT) Scholar, says that he suspects other bacterial pathogens may use similar mechanisms to co-opt existing host cell structures to create their own protective dwellings.
This work was funded by NIH grants DP2GM137419, R01GM113079, T32GM008203-29, F30HL143859-01, Welch Foundation grants I-1911, I-1789, CPRIT grant RP170674, and Polish National Agency for Scientific Exchange scholarship PPN/BEK/2018/1/00431.
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Only one in three fertilizations leads to a successful pregnancy. Many embryos fail to progress beyond early development. Cell biologists at the Max Planck Institute (MPI) for Biophysical Chemistry in Göttingen (Germany), together with researchers at the Institute of Farm Animal Genetics in Mariensee and other international colleagues, have now developed a new model system for studying early embryonic development. With the help of this system, they discovered that errors often occur when the genetic material from each parent combines immediately after fertilization. This is due to a remarkably inefficient process.
Human somatic cells typically have 46 chromosomes, which together carry the genetic information. These chromosomes are first brought together at fertilization, 23 from the father’s sperm, and 23 from the mother’s egg. After fertilization, the parental chromosomes initially exist in two separate compartments, known as pronuclei. These pronuclei slowly move towards each other until they come into contact. The pronuclear envelopes then dissolve, and the parental chromosomes unite.
The majority of human embryos, however, end up with an incorrect number of chromosomes. These embryos are often not viable, making erroneous genome unification a leading cause of miscarriage and infertility.
“About 10 to 20 percent of embryos that have an incorrect number of chromosomes result from the egg already containing too few or too many chromosomes prior to fertilization. This we already knew,” explains Melina Schuh, director at the MPI for Biophysical Chemistry. “But how does this problem arise in so many more embryos? The time immediately after the sperm and egg unite — the so-called zygote stage — seemed to be an extremely critical phase for the embryo’s development. We wanted to find out why this is the case.”
Insights from a new model system
For their investigations, the scientists analyzed microscopy videos of human zygotes that had been recorded by a laboratory in England. They additionally set out to find a new model organism suitable for studying early embryonic development in detail. “Together with our collaboration partners at the Institute of Farm Animal Genetics, we developed methods for studying live bovine embryos, which closely resemble human embryos,” explains Tommaso Cavazza, a scientist in Schuh’s department. “The timing of the first cell divisions is comparable in human and bovine embryos. Furthermore, the frequency of chromosomes distributing incorrectly is about the same in both systems.” Another advantage of this model system is: The scientists obtained the eggs from which the bovine embryos developed from slaughterhouse waste, so no additional animals had to be sacrificed.
Schuh’s team fertilized the bovine eggs in vitro and then used live-cell microscopy to track how the parental genetic material unites. They found that the parental chromosomes cluster at the interface between the two pronuclei. In some zygotes, however, the researchers noticed that individual chromosomes failed to do so. As a result, these chromosomes were ‘lost’ when the parental genomes united, leaving the resulting nuclei with too few chromosomes. These zygotes soon showed developmental defects.
“The clustering of chromosomes at the pronuclear interface seems to be an extremely important step,” Cavazza explains. “If clustering fails, the zygotes often make errors that are incompatible with healthy embryo development.”
Dependent on an inefficient process
But why do parental chromosomes often fail to cluster correctly? The Max Planck researchers were able to uncover that as well, as Cavazza reports: “Components of the cytoskeleton and the nuclear envelope control chromosome movement within the pronuclei. Intriguingly, these elements also steer the two pronuclei towards each other. So we are dealing with two closely linked processes that are essential, but often go wrong. Thus, whether an embryo will develop healthily or not depends on a remarkably inefficient process.”
The scientists’ findings are also relevant for in vitro fertilization in humans. It has been discussed for some time whether the accumulation of the so-called nucleoli at the pronuclear interface in human zygotes could be used as an indicator for the chance of successful fertilization. Zygotes in which these pronuclear components all cluster at the interface have a better chance of developing successfully, and could therefore be preferentially used for fertility treatment. “Our observation that chromosomes need to cluster at the interface to guarantee healthy embryo development supports this selection criterion,” Schuh says.
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An analysis of historical medical records found that men who were prenatally exposed during early gestation to the Dutch famine of 1944-1945 were 30 percent more likely to be overweight with a Body Mass Index of 25 or over at age 19, compared to a similar group not exposed to the famine. Professor L. H. Lumey at Columbia University Mailman School of Public Health led the study, which is published in the International Journal of Obesity. The study confirms evidence on the health risks of prenatal famine exposure, which also includes diabetes and schizophrenia.
The mechanism by which famine exposure raises the risk for later excess weight is still unknown. The researchers speculate that famine exposure could lead to changes in DNA methylation that stimulate being overweight. Or that surviving babies might have genetic profiles enabling them to thrive on fewer calories. “If so, it is tragic and ironic that surviving the famine would increase one’s risk for obesity,” says first author L. H. “Bertie” Lumey, MD, PhD, professor of epidemiology at Columbia Mailman School. “A slower metabolism that would have helped them survive the pandemic, in times of plenty could also contribute to weight problems and related health issues.”
The researchers studied heights and weights of 371,100 men in the Netherlands born between 1943 and 1947 and examined for military service at age 19, including men with and without prenatal exposure to the Dutch famine. They found that a heightened overweight risk was present in men with famine exposure starting at the very beginning of gestation, not with exposure starting in the middle or at the end of gestation — a finding they say points to the start of pregnancy as a sensitive period of fetal development.
The study shows that the heightened overweight risk was limited to sons of manual workers born in the large cities of Western Netherlands, consistent with historical evidence on the socioeconomic and geographic populations known to be most affected by the famine.
Not surprisingly, excess weight presented its own risks. Those who were overweight at age 19 had a 30 percent greater mortality risk through age 63 relative to those with a BMI in the normal range. This was independent of famine exposure.
Further development of a 1976 Paper
The new paper extends and refines a 1976 study by Columbia researchers using current definitions of overweight. Contrary to the earlier paper, current analytic approaches show no weight changes in sons of non-manual workers exposed in early gestation in the famine cities. The researchers note that the military examinations did not include waist or hip circumference or other measures of body mass distribution which could be even better indicators of chronic disease risk.
The new study also looked at whether or not a decline in birthrates among manual workers during the famine explained the relationship between prenatal famine exposure and risk for excess weight. It didn’t.
“Our study builds on the rigorous science behind the original research in the 1970s led by Columbia epidemiologists Mervyn Susser and Zena Stein,” says Lumey.
About the Dutch Famine
The Dutch famine (Hunger Winter) of 1944-45 was a period of civilian famine under German occupation at the end of World War II. Contemporary reports show that the famine was concentrated in the large cities of the Western Netherlands. It was limited to the last months of the war in the period between November 1944 and the surrender of the German forces to the Allies in May 1945. After Liberation, food supplies were rapidly distributed across the country. The food crisis provides an opportunity to study the relationship between maternal nutrition in pregnancy and offspring health.
Previous research, beginning shortly after the end of the war found a link between famine-exposed mothers and birth weight. Subsequent research established links between famine exposure and risk for obesity, diabetes, and schizophrenia, as well as the specific genomic pathways involved. Importantly, the research also ruled out a link between famine exposure and mental retardation.

Computer scientists at the University of California San Diego have developed a more accurate navigation system that will allow robots to better negotiate busy clinical environments in general and emergency departments more specifically. The researchers have also developed a dataset of open source videos to help train robotic navigation systems in the future.
The team, led by Professor Laurel Riek and Ph.D. student Angelique Taylor, detail their findings in a paper for the International Conference on Robotics and Automation taking place May 30 to June 5 in Xi’an, China.
The project stemmed from conversations with clinicians over several years. The consensus was that robots would best help physicians, nurses and staff in the emergency department by delivering supplies and materials. But this means robots have to know how to avoid situations where clinicians are busy tending to a patient in critical or serious condition.
“To perform these tasks, robots must understand the context of complex hospital environments and the people working around them,” said Riek, who holds appointments both in computer science and emergency medicine at UC San Diego.
Taylor and colleagues built the navigation system, the Safety Critical Deep Q-Network (SafeDQN), around an algorithm that takes into account how many people are clustered together in a space and how quickly and abruptly these people are moving. This is based on observations of clinicians’ behavior in the emergency department. When a patient’s condition worsens, a team immediately gathers around them to render aid. Clinicians’ movements are quick, alert and precise. The navigation system directs the robots to move around these clustered groups of people, staying out of the way.
“Our system was designed to deal with the worst case scenarios that can happen in the ED,” said Taylor, who is part of Riek’s Healthcare Robotics lab at the UC San Diego Department of Computer Science and Engineering.
The team trained the algorithm on videos from YouTube, mostly coming from documentaries and reality shows, such as “Trauma: Life in the ER” and “Boston EMS.” The set of more than 700 videos is available for other research teams to train other algorithms and robots.
Researchers tested their algorithm in a simulation environment, and compared its performance to other state-of-the-art robotic navigation systems. The SafeDQN system generated the most efficient and safest paths in all cases.
Next steps include testing the system on a physical robot in a realistic environment. Riek and colleagues plan to partner with UC San Diego Health researchers who operate the campus’ healthcare training and simulation center.
The algorithms could also be used outside of the emergency department, for example during search and rescue missions.
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The skin, which covers the surface of the human body, is its largest organ. It is the first organ to show changes stemming from organ or physiological activity. It is especially common for diabetic patients to suffer from skin diseases or infections. Recently, a POSTECH research team has succeeded in creating a 3D artificial skin that enables observation of skin diseases of diabetic patients.
A research team led by Professor Dong-Woo Cho and Minjun Ahn of POSTECH’s Department of Mechanical Engineering and Professor Byoung Soo Kim of School of Biomedical Convergence Engineering at Pusan National University has successfully produced an in vitro diseased skin model that displays the pathophysiological hallmarks of type 2 diabetes based on 3D cell printing system. These research findings were recently published in Biomaterials.
Despite continuous research to produce artificial skin with 3D cell printing technology, artificial skin displaying the pathological process present in the native skin has not been reported yet.
Inspired by the interaction between the epidermis and skin cells found in real skin, the research team hypothesized that when normal keratinocytes interact with the dermal layer made of diabetic fibroblasts, they will differentiate into diabetic epidermis. To prove this, diabetic artificial skin with skin wounds based on 3D printing technique was fabricated using each cell.
In this diabetic artificial skin, slow re-epithelialization, a typical feature of diabetic skin, was observed. In addition, when the diabetic fat tissue layer containing blood vessels was added, insulin resistance, adipocyte hypertrophy, pro-inflammatory response, and vascular dysfunction, which are commonly observed in diabetes, were confirmed.
“Through 3D cell printing, we can now observe skin diseases in vitro, without actually experiencing it,” remarked the researchers. “We anticipate it to be a way to replace animal models that have been conventionally used to observe skin diseases. It is significant that its applicability as a disease model for new drug development has been proven.”
This research was conducted with the support from the Creative Research Program and the Nano-New Materials Core Technology Development Program of the National Research Foundation of Korea.
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Despite the rapid and significant changes in consumption patterns witnessed during the initial months of the COVID-19 pandemic, Japanese households maintained their normal levels of greenhouse gases emissions. The “anthropause” — reduction of human activity due to the pandemic — made headlines last summer, but factory shutdowns and broken global supply chains did not translate into the adoption of eco-friendly lifestyles for the average household.
“During the early COVID-19 period, we could witness lifestyle changes happening around us fast, so we decided to explore the environmental impacts of these lifestyle changes. Some other research at that period was showing that the production-side greenhouse gases emissions decreased, but when assessing the emissions from the consumer side we noticed that they did not change so much compared to 2015 through 2019 levels,” said Project Assistant Professor Yin Long from the University of Tokyo Institute for Future Initiatives. Long is first author of the research recently published in One Earth.
Experts say that around the world, half of a nation’s carbon footprint is due to the consumption of goods and services by individual households. A carbon footprint is a measure of both the direct and indirect greenhouse gases emissions associated with growing, manufacturing and transporting the food, goods, utilities and services we use.
Researchers considered in this study approximately 500 consumption items and then tracked the carbon emissions embedded in all the associated goods and services. Eating out, groceries, clothing, electronics, entertainment, gasoline for vehicles, as well as home utilities were all included.
“The real beauty of it is the consistency of the long-term data collection in these government statistics, even during the COVID-19 period, which allows us to compare it with historical patterns” said Associate Professor Alexandros Gasparatos, an expert on ecological economics who led the study. Gasparatos holds a dual appointment with the University of Tokyo and the United Nations University in Tokyo.
The monthly carbon footprints of household consumption for the period January to May of 2020 were compared to the carbon footprints of the same months from the previous five years. In Japan, COVID-19 diagnoses began increasing in February and the first nationwide COVID-19 state of emergency was declared from mid-April to mid-May 2020.
The research team’s analyses revealed that the 2020 carbon footprint of all households, both aggregate and across different age groups, largely remained within the range of 2015 through 2019.
The carbon footprint of the emissions associated with eating out decreased during the state of emergency, but emissions from groceries increased, especially due to the purchase of more meat, eggs and dairy. Emissions associated with clothing and entertainment decreased sharply during the state of emergency, but rebounded rapidly when the emergency measure ended.
“This kind of natural experiment is telling us that the very quick and consistent change in lifestyle during the early stages of the COVID-19 pandemic did not materialize into significant and sustained changes in the carbon footprints of households,” said Gasparatos.
The nonbinding state of emergency declarations by the national and local governments in Japan requested that people limit social gatherings, dining out in groups and nonessential travel between prefectures. Compared to the legally enforced lockdowns in other countries, researchers say Japan’s minimal impositions are likely a better model of the lifestyle changes that eco-conscious households might make voluntarily.
“If we see lifestyle change as a strategy to achieve decarbonization, our results suggest that it might not automatically translate into environmental benefits. It will require a lot of effort and public education focused on the most emission-intensive household demands, such as private car use, and space and water heating,” said Gasparatos.
“We saw that factories shut down when COVID-19 happened, but consumer demand stayed the same, so factories reopened to satisfy those demands. As written in the United Nations Sustainable Development Goals, consumers and producers should share responsibility for achieving sustainable lifestyles,” said Long.

A pioneering study by UCL scientists has discovered the presence of a harmful inflammatory protein in patients with symptomatic tuberculosis (TB).
Researchers say, by targeting the IL-17 cytokine, a component produced naturally by the immune system in response to infection, excessive and damaging lung inflammation caused by TB may be significantly reduced to help speed up patient recovery.
TB is an infection caused by the bacterium Mycobacterium tuberculosis and is the leading cause of death from infections worldwide. The World Health Organisation estimates that 1.4 million people died of TB disease worldwide in 2019.
Explaining the experimental study, lead author Dr Gabriele Pollara (UCL Division of Infection & Immunity), said: “For most people the body’s immune response to TB is a vital defence strategy to contain the infection, but when disease develops it can worsen symptoms, cause lung damage, and promote transmission of the infection to others.
“For some time, we have thought that the body’s own immune response to TB could in fact be causing more tissue damage and promoting the spread of infection — but we did not know how this happens.
“In this study, we found that in patients with active TB, the immune system may be responding pathologically (causing harm), and that this immune response was not present in those with latent TB, who have controlled the infection.”
As part of the study, published in Science Translational Medicine, medical centres in the UK, South Africa and Peru recruited patients to take a tuberculin skin test (TST), which involves injecting a small amount of fluid (called tuberculin) into the skin on the lower part of the arm. Raised skin or swelling, detected 48 hours later, denotes a positive test.

Hospitalized COVID-19 patients with impaired first-phase ejection fraction were nearly 5 times more likely to die compared to patients with healthier measures of this early, often undetected sign of heart failure, according to new research published today in Hypertension, an American Heart Association journal. First-phase ejection fraction is a measure of the left ventricular ejection fraction until the time of maximal ventricular contraction.
Cardiovascular risk factors and/or disease have been recognized as COVID-19 risk factors that have a high negative impact on patient outcomes, since early in the SARS-CoV-2 pandemic. Researchers hypothesized that predisposition to heart failure would be associated with more severe cases of COVID-19 in hospitalized patients.
“Traditionally, heart function is measured by ejection fraction, or how much blood the left ventricle pumps out with each contraction of the heart,” said study author Phil Chowienczyk, M.B.B.S., B.Sc., professor of cardiovascular clinical pharmacology at St. Thomas’ Hospital, in London. “First-phase ejection fraction is a new measure of the heart’s function that seems to be much more sensitive of early, undetected damage to the heart than traditional ejection fraction measures.”
To determine if first-phase ejection fraction predicted adverse patient outcomes, researchers analyzed mortality rates for 129 hospitalized COVID-19 patients in Wuhan, China, and 251 hospitalized COVID-19 patients in South London, treated between February and May 2020, were analyzed. All patients had echocardiography upon hospital admission, and the average patient age was 58 years. Researchers compared echocardiography results of COVID-19 patients to adult patients with otherwise similar health profiles who had an echocardiography test before the pandemic.
First-phase ejection fraction was measured with conventional echocardiography imaging conducted at hospitalized patients’ bedsides. Researchers note that there is not a universally established ‘normal’ value for first-phase ejection fraction. Based on previous research, they estimated that the normal first-phase ejection fraction value should be above 25%. When first-phase ejection fraction was less than 25%, researchers referred to it as ‘impaired,’ suggesting relatively subtle signs of heart damage.
The authors found that COVID-19 patients with a first-phase ejection fraction of less than 25% had a nearly five-fold higher risk of death than those with an ejection fraction of 25% or higher. They also found that a similar proportion of people with similar risk factors who did not have COVID-19 had low values of first-phase ejection fraction. This suggests that the damage to the heart may be due to chronic pre-existing conditions and was not the result of COVID-19 infection.
“Patients with impaired first-phase ejection fraction could be prioritized for vaccines and, if they get COVID-19, monitored closely at the early stages of their illness to prevent deterioration,” Chowienczyk said. “The findings suggest that if we can prevent the very early chronic damage to the heart detected using first-phase ejection fraction imaging, then people will be much more likely to survive respiratory infections like COVID-19. Healthy lifestyle choices, better treatments and adherence to treatments for high blood pressure and high cholesterol are also important.”
Researchers note that this is a relatively small study, so the findings need to be confirmed in larger studies with more patients. If the results are confirmed, first-phase ejection fraction could be a new way to identify patients at elevated risk of dying from COVID-19 and possibly other types of pneumonia.
Co-authors are Haotian Gu, Ph.D.; Chiara Cirillo, M.D.; Adam A. Nabeebaccus, M.B.Ch.B., Ph.D.; Zhenxing Sun, M.D.; Lingyun Fang, M.D., Ph.D.; Yuji Xie, M.D.; Ozan Demir, M.B.B.S., M.Sc.; Nishita Desai, M.B.B.S.; Lin He, M.D., Ph.D.; Qing Lü, M.D., Ph.D.; Eleni Nakou, M.D., Ph.D.; Kevin O’Gallagher, M.B.B.S.; Christos Tountas, M.D., Ph.D.; Apostolia Marvaki, M.D., Ph.D.; Mark Monaghan, M.Sc., Ph.D.; Divaka Perera, M.D.; Ana Pericao, M.D.; Matthew Ryan, M.B.Ch.B.; Hannah Sinclair, B.M.; Vasileios Stylianidis, M.D., M.Sc.; Kelly Victor, M.Sc.; Bin Wang, M.D., Ph.D.; Jing Wang, M.D., Ph.D.; Rui Wang, M.D.; Chun Wu, M.D., Ph.D.; Yali Yang, M.D., Ph.D.; Hongliang Yuan, M.D.; Danqing Zhang, M.D.; Yongxing Zhang, M.D.; Luca Faconti, Ph.D.; Alexandros Papachristidis, M.D.; Li Zhang, M.D., Ph.D.; Gerald Carr-White, Ph.D.; Ajay M. Shah, M.D.; and Mingxing Xie, M.D., Ph.D.
The National Natural Science Foundation of China, the National Institute for Health Research and the British Heart Foundation funded this study.

Managing weight, blood pressure and cholesterol in children may help protect brain function in later life, according to new research published today in the American Heart Association’s flagship journal Circulation. This is the first study to highlight that cardiovascular risk factors accumulated from childhood through mid-life may influence poor cognitive performance at midlife.
Previous research has indicated that nearly 1 in 5 people older than 60 have at least mild loss of brain function. Cognitive deficits are known to be linked with cardiovascular risk factors, such as high blood pressure, obesity, type 2 diabetes, smoking, physical inactivity and poor diet, as well as depression and low education level.
Many diseases that cause neurological deficits, such as Alzheimer’s, have a long preclinical phase before noticeable symptoms begin, so finding links between childhood obesity and other cardiovascular risk factors is important for cognitive health. The researchers noted that there are currently no cures for major causes of dementia, so it is important to learn how early in life cardiovascular risk factors may affect the brain.
“We can use these results to turn the focus of brain health from old age and midlife to people in younger age groups,” said the study’s first author Juuso O. Hakala, M.D., a Ph.D. student at the Research Centre of Applied and Prevention Cardiovascular Medicine at the University of Turku, in Turku, Finland. “Our results show active monitoring and prevention of heart disease and stroke risk factors, beginning from early childhood, can also matter greatly when it comes to brain health. Children who have adverse cardiovascular risk factors might benefit from early intervention and lifestyle modifications.”
The Cardiovascular Risk in Young Finns Study is a national, longitudinal study on cardiovascular risk from childhood to adulthood in Finland. Researchers followed the participants’ cardiovascular risk factor profiles for 31 years from childhood to adulthood. Baseline clinical examinations were conducted in 1980 on approximately 3,600 randomly selected boys and girls, ranging in ages from 3 to 18, all of whom were white. More than 2,000 of the participants, ranging in ages from 34 to 49, underwent a computerized cognitive function test in 2011. The test measured four different cognitive domains: episodic memory and associative learning; short-term working memory; reaction and movement time; and visual processing and sustained attention.
Researchers found: Systolic blood pressure, total blood cholesterol and low-density lipoprotein (LDL) cholesterol, as well as body mass index, from childhood to midlife are associated with brain function in middle age. Consistently high systolic blood pressure or high blood total cholesterol and LDL cholesterol were linked to worse memory and learning by midlife when compared with lower measures. Obesity from childhood to adulthood was associated with lower visual information processing speed and maintaining attention. Having all three cardiovascular risk factors was linked to poorer memory and associative learning, worse visual processing, decreased attention span, and slower reaction and movement time.These results are from observational findings, so more studies are needed to learn whether there are specific ages in childhood and/or adolescence when cardiovascular risk factors are particularly important to brain health in adulthood. Study limitations include that a definite cause-and-effect link between cardiovascular risk factors and cognitive performance cannot be determined in this type of population-based study; cognition was measured at a single point in time; and because all study participants are white, the results may not be generalizable to people from other racial or ethnic groups.
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In a small study, researchers found college athletes who contracted COVID-19 rarely had cardiac complications. Most had mild COVID symptoms that did not require treatment, and in a small percentage of those with abnormal cardiac testing, there was no evidence of heart damage on special imaging tests. All athletes returned to sports without any health concerns, according to new research published today in the American Heart Association’s flagship journal Circulation.
In spring 2020, concerns about heart damage, especially inflammation, among athletes with COVID-19 led to recommendations for cardiac screening based on symptom severity before resuming training and competition. The preferred diagnostic test for heart inflammation is an MRI of the heart, or cardiac magnetic resonance imaging. The American College of Cardiology’s Sports & Exercise Cardiology Council’s standard recommendations, issued in May 2020, do not advise cardiac MRI as an initial screening test based on COVID symptoms alone, so researchers investigated if symptom severity was associated with heart inflammation or poor recovery after COVID-19.
“Our study results support an approach to cardiac screening guided by patient symptoms and severity of COVID illness in line with current recommendations from sports-cardiology groups before resuming exercise or sports,” said senior study author Ranjit R. Philip, M.D., pediatric cardiologist at Le Bonheur Children’s Hospital and assistant professor in pediatric cardiology at the University of Tennessee Health Science Center in Memphis.
From July 9, 2020 to October 21, 2020, researchers at the University of Tennessee Health Sciences Center reviewed health records to identify 137 college athletes (average age of 20, 68% male) who were referred for cardiac screening to return to play after testing positive for COVID-19. On average, the athletes were evaluated 16 days after testing positive for the COVID-19 virus. Nearly half of the participants were African American students, nearly half were white students, and 7% were Hispanic students. Of the 11 sports represented at three universities, more than a third of the athletes were football players, followed by dance, basketball, baseball, softball, tennis, soccer, cheer, track, volleyball and golf athletes.
Most (82%) of the athletes had COVID-19 symptoms; the symptoms were mild for the majority (68%); and none required treatment or hospitalization. The most frequent symptoms were the loss of smell/taste (58%), fever (less than 2 days, 42%), headache (41%) and fatigue (40%). Less frequently reported symptoms were shortness of breath (12%) and chest pain/tightness (11%). African American and Hispanic athletes were more often symptomatic compared to white athletes (86% and 100% vs. 75%, respectively). No differences in symptoms or severity were found based on gender or sport.
All of the athletes underwent initial heart imaging tests, including ultrasound of the heart and electrocardiogram to screen for possible heart damage, and received a blood test (troponin level). Troponin is a protein that is released in the blood and found in the muscles of the heart when there is heart damage. Only participants who had abnormal test results received a cardiac MRI.
Researchers found: Less than 4% (5) of the 137 athletes showed heart abnormalities on initial screening tests. Further screening via cardiac MRI of the 5 athletes identified found no heart damage or inflammation. After COVID-19 recovery, all athletes were able to resume their full training and competition regimens without any complications.”We were encouraged to find so few abnormal tests in these athletes as well as negative cardiac MRIs in those who did have an abnormal test during the initial screening, and no athlete had any problems after returning to exercise and sport,” said Benjamin S. Hendrickson, M.D., co-author and pediatric and congenital cardiologist with Le Bonheur Children’s Hospital and assistant professor of pediatrics (cardiology) at the University of Tennessee Health Science Center.
“Our findings may offer reassurance to high school athletes, coaches and parents where resources for testing can be limited,” Philip added.
Limitations that could have affected the study’s results include the lack of a control group without COVID-19 and the use of a regular as opposed to the high-sensitivity troponin test.
The new study by Dr. Philip and colleagues also confirms recent research published April 17 in Circulation, that found no adverse cardiac events related to SARS-CoV-2 infections observed among more than 3,000 collegiate athletes during short-term clinical surveillance. Findings also suggested a safe return-to-play without cardiac testing for asymptomatic or mildly symptomatic athletes.
Other efforts to track how COVID-19 impacts college athletes includes an initiative from the American Heart Association and the American Medical Society for Sports Medicine (AMSSM) to accelerate a critical new research initiative studying cardiac conditions in athletes. The collaborative data registry, started in January 2021, aids research on COVID-19 and, long-term, it will develop a deep knowledge base on cardiac disease in athletes beyond the pandemic.