Long-term survival after heart attack could hinge on where you live

Having a heart attack before your 50th birthday is bad enough. But new research shows if you also live in a poor neighborhood, your chances of dying within a decade of that heart attack are higher.

“This tells us that we need to focus not just on a patient’s medical problems, but on the whole person, on where they live and the resources they have that will allow them to thrive,” said the study’s lead investigator, Dr. Adam Berman, a cardiology fellow at Brigham and Women’s Hospital in Boston, a teaching affiliate of Harvard Medical School.

Berman and his team divided 2,097 people who had heart attacks before age 50 into three groups based on where they lived. They ranked home addresses using the area deprivation index, a measure of socioeconomic status that includes income, education, employment and housing quality. The study found the more disadvantaged a person’s neighborhood, the higher the chances they would die within 11 years of a first heart attack.

The research was presented recently at the American Heart Association’s virtual Scientific Sessions. It is considered preliminary until published in a peer-reviewed journal.

Prior research shows people in disadvantaged neighborhoods are less able to afford medications, are exposed to greater amounts of pollution, and have less access to healthy foods and other resources that could improve their health, Berman said. These social determinants of health have been shown to increase the risk of heart disease and stroke.

“It is likely that a variety of neighborhood and personal socioeconomic factors contribute to the underlying mechanisms that drive this association between where someone lives and their chances of dying,” he said. “We have to focus on all of those aspects in the care of our patients, particularly after they have a heart attack, and particularly in those who are young.”

Overall, the number of people in the United States having heart attacks has been declining, but for younger adults, heart attacks appear to have been increasing over the past decade. And for Black adults in their 30s and 40s, heart attacks are more common and more deadly than among young white adults, prior research shows.

The new study found those who lived in the most disadvantaged neighborhoods were more likely to be Black or Hispanic, have public or no health insurance, and experience higher rates of heart-related risk factors.

But the study included a relatively small number of women—nearly 80% of participants were men. That’s a problem, given the high rate of heart disease among Black women, said Dr. Tiffany Powell-Wiley, chief of the Social Determinants of Obesity and Cardiovascular Risk Laboratory at the National Heart, Lung, and Blood Institute. Nearly half of all adult Black women have some type of heart disease. They are more likely to die of heart disease—and at a younger age—than their white peers.

“We need to know what this looks like across genders,” said Powell-Wiley, who was not involved in the study. “I think it’s particularly important because we know that African American women have a higher risk of premature cardiovascular mortality, and so we would want to see that they are included in data that looks at this relationship.”

Overall, though, the health challenges aren’t only tied to limited resources, she said.

“There is some data showing mortality is related to the physiological stress of living in these environments. I think that’s where the science really needs to go. We need to really dig into the mechanisms by which social and environmental stressors get under the skin and lead to cardiovascular events.”

For example, Powell-Wiley said, “if you live in these neighborhoods, you’re more likely to be someone who experiences racism and discrimination, and these are layers of things that are affecting you.”

Figuring out how to alleviate those stressors is the hard part, Berman and Powell-Wiley agreed.

“Now we have to find ways to fix it empirically,” Berman said. “We have to test to see what happens if we improve healthy food access to a whole community, or if we can eliminate the cost of medications for a population. That’s the really hard part. How do we fix it in a way that’s meaningful and feasible on a medical system level?”

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Could COVID-19 immunity last decades? Here’s the science.

The body builds a protective fleet of immune cells when infected with COVID-19, and in many people, those defenses linger for more than six months after the infection clears, according to a new study.

The immune cells appear so stable, in fact, that immunity to the virus may last at least several years, the study authors said. “That amount of [immune] memory would likely prevent the vast majority of people from getting hospitalized disease, severe disease, for many years,” co-author Shane Crotty, a virologist at the La Jolla Institute of Immunology in California, told The New York Times, which first reported on the study.

That said, making predictions about how long immunity to the coronavirus lasts can be “tricky,” Nicolas Vabret, an assistant professor of medicine at the Mount Sinai Icahn School of Medicine, who was not involved in the study, told Live Science.

“It would be surprising to see the … immune cells build up in patients over six months and suddenly crash after one year,” Vabret said in an email. But “the only way to know whether SARS-CoV-2 immunity will last decades is to study the patients over the same period of time.” 

In other words, we won’t know exactly how long immunity lasts without continuing to study those who have recovered from COVID-19. However, the new study, posted Nov. 16 to the preprint database bioRxiv, does provide strong hints that the protection is long-lived — although clearly not in all people, as there have been several cases of individuals being reinfected with the coronavirus after recovering. 

The research dives into the ranks of the human immune system, assessing how different lines of defense change after a COVID-19 infection. 

These defenses include antibodies, which bind to the virus and either summon immune cells to destroy the bug or neutralize it themselves. Memory B cells, a kind of white blood cell, “remember” the virus after an infection clears and help quickly raise the body’s defenses, should the body be reexposed. Memory T cells, another kind of white blood cell, also learn to recognize the coronavirus and dispose of infected cells. Specifically, the authors looked at T cells called CD8+ and CD4+ cells.

The authors assessed all these immune cells and antibodies in 185 people who had recovered from COVID-19. A small number of participants never developed symptoms of the illness, but most experienced mild infections that did not require hospitalization. And 7% of the participants were hospitalized for severe disease. 

The majority of participants provided one blood sample, sometime between six days and eight months after the onset of their infections. Thirty-eight participants gave several blood samples between those time points, allowing the authors to track their immune response through time.

Ultimately, “one could argue that what they found is not so surprising, as the immune response dynamics they measure look like what you would expect from functioning immune systems,” Vabret said. 

The authors found that antibodies specific to the spike protein — a structure on the surface of the virus — remain stable for months and begin to wane about six to eight months after infection. At five months post-infection, nearly all the participants still carried antibodies. The volume of these antibodies differed widely between people, though, with an up to 200-fold difference between individuals. Antibody counts normally fall after an acute infection, Vabret noted, so the modest drop-off at six to eight months came as no surprise.

By comparison, memory T and B cells that recognize the virus appear extremely stable, the authors noted. “Essentially no decay of … memory B cells was observed between days 50 and 240,” or eight months later, Marc Jenkins, an immunologist at the University of Minnesota Medical School, who was not involved in the study, said in an email.

“Although some decay of memory T cells was observed, the decay was very slow and may flatten out at some point,” Jenkins added. There’s reason to believe that the number of memory T cells may stabilize sometime after infection, because T cells against a related coronavirus, SARS-CoV, have been found in recovered patients up to 17 years later, according to a study published July 15 in the journal Nature

Early in the pandemic, scientists raised concerns that immunity to the virus may wear off in about a year; this trend can be seen with the four coronaviruses that cause the common cold, Live Science previously reported. However, studies suggest that the body’s reaction to common coronaviruses may differ from that to viruses like SAR-CoV and SARS-CoV-2, which hopped from animals to humans. 

“We don’t really know why seasonal coronaviruses do not induce lasting protective immunity,” Vabret said. But the new study, along with other recent evidence, suggests that SARS-CoV-2 immunity may be more robust, said Jason Cyster, a professor of microbiology and immunology at the University of California, San Francisco, who was not involved in the study.

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That said, a few participants in the new study did not mount long-lasting immune responses to the novel virus. Their transient responses may come down to differences in how much virus they were initially exposed to, or genetics may explain the difference, Cyster said. For instance, genes known as human leukocyte antigen (HLA) genes differ widely between individuals and help alert the immune system to foreign invaders, Live Science previously reported

These inherent differences between people may help explain cases of COVID-19 reinfection, which have been relatively rare but are increasing in number, Science Magazine reported.

Again, to really understand how long COVID-19 immunity lasts, scientists need to continue to study recovered patients. “Certainly, we need to look six months down the road,” and see whether the T and B cell counts remain high, Cyster said.

Should immunity be long-term, one big question is whether that durability carries over to vaccines. But natural immunity and vaccine-generated immunity cannot be directly compared, Vabret noted. 

“The mechanisms by which vaccines induce immunity are not necessarily the same as the ones resulting from natural infection,” Vabret said. “So the immune protection resulting from a vaccine could last longer or shorter than the one resulting from natural infection.”

For example, the Pfizer and Moderna vaccines use a molecular messenger called mRNA to train the body to recognize and attack the coronavirus. No mRNA-based vaccine has ever been approved before, so “we practically know nothing about the durability of those responses,” Cyster said.

“I think [that’s] the big unknown for me, among the many,” he said.

But while some unanswered questions remain, the main takeaway from the new study is that “immune memory to SARS-CoV-2 is very stable,” Jenkins said. And — fingers crossed — perhaps those hopeful results will hold well into the future.

Originally published on Live Science. 

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Soccer players’ head injury risk could be reduced with simple adjustments to the ball

Up to 22% of soccer injuries are concussions that can result from players using their heads to direct the ball during a game.

To reduce risk of injury, a new study recommends preventing how hard a ball hits the head by inflating balls to lower pressures and subbing them out when they get wet.

The study, conducted by Purdue University engineers, found that inflating balls to pressures on the lower end of ranges enforced by soccer governing bodies such as the NCAA and FIFA could reduce forces associated with potential head injury by about 20%.

But if the ball gets too wet, it can quickly surpass the NCAA weight limit for game play and still produce a nasty impact, the researchers said.

“If the ball has too high of a pressure, gets too waterlogged, or both, it actually turns into a weapon. Heading that ball is like heading a brick,” said Eric Nauman, a Purdue professor of mechanical engineering and basic medical sciences with a courtesy appointment in biomedical engineering.

Soccer governing bodies already regulate ball pressure, size, mass and water absorption at the start of a game, but Nauman’s lab is the first to conduct a study evaluating the effects of each of these ball parameters on producing an impact associated with potential neurophysiological changes.

The results are published in the journal PLOS One.

The study also evaluated ball velocity, finding that this variable actually contributes the most to how hard a ball hits. But ball pressure and water absorption would be more realistic to control.

“You can’t control how hard a player kicks a ball. There are other ways to decrease those forces and still have a playable game,” Nauman said.

A professional soccer player heads the ball about 12 times over the course of a single game and 800 times in games over an entire season, past studies have shown.

The lower end of NCAA and FIFA pressure ranges, which the researchers discovered could help reduce the ball’s peak impact force, already aligns with pressures specified by the manufacturer on the ball. These specifications would provide an easy way to know if a pressure is low enough to reduce risk of head injury.

“The study really sheds light on the issue of how the weight and impact of the ball can change under different conditions. Sports governing bodies and manufacturers can use this research to further reduce the risk of lasting brain functional or structural injury as a result of head impacts accrued through soccer game play,” said Francis Shen, a professor of law at the University of Minnesota whose research focuses on the intersection of sports concussions and the legal system.

Nauman and Shen met through the Big Ten-Ivy League Traumatic Brain Injury Collaboration, a multi-institutional research effort to better understand the causes and effects of sport-related concussion and head injuries.

In this study, Nauman’s lab tested three soccer ball sizes—a 4, 4.5 and a 5—by kicking them against a force plate in a lab. Even though only size 5 balls are played by professional adults, the researchers also observed the smaller 4 and 4.5 sizes played by kids under the age of 12 to evaluate how much the size of a ball contributes to peak impact force.

The study included 50 trials for each ball size at four different pressures, ranging from 4 psi to 16 psi. This range includes pressures below standard manufacturing specifications and near the limit of soccer governing body regulations.

Purdue graduate student Nicolas Leiva-Molano did 200 kicks per ball size for a total of 600 kicks.

To test water absorption, the researchers submerged each ball size for 90 minutes—the duration of a game regulated by soccer governing bodies. They weighed and rotated each ball every 15 minutes.

Within the first 15 minutes, a size 5 soccer ball had already exceeded the allowable weight gain cited in NCAA soccer rules.

Based on this study’s findings, a size 4.5 soccer ball is the safest to play in terms of forces contributed by pressure, mass and water absorption. But reducing pressure and limiting water absorption made a difference for all three ball sizes.

“This was a very simple experiment. But there just hasn’t been much data out there on these issues, and that’s a huge problem,” Nauman said.

The next step would be to replicate this experiment outside of the lab, ideally in partnership with a high school or college athletic conference, which would allow the researchers to study the effects of ball hits at different parameters before and after a season.

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Physical activity could reduce heart disease deaths among American Indians

Physical activity may reduce the risk of death from cardiovascular disease among American Indians, according to new research that also studied inflammation’s role in exercise and heart health.

Past studies of people from all populations show that inflammation plays a central role in heart disease, and that exercise might reduce inflammation in the body.

For the new study, researchers focused on American Indians, “a special population that, unfortunately, is not always included in studies that show the benefit of physical activity,” said the lead researcher Dr. Ozan Unlu, chief resident of quality and patient safety at Weill Cornell Medicine in New York City.

The findings will be presented Friday at the American Heart Association’s virtual Scientific Sessions. The research is considered preliminary until published in a peer-reviewed journal.

The study looked at self-reported physical activity levels from 3,135 adults in Arizona, North Dakota, South Dakota and Oklahoma, who did not initially have cardiovascular disease and who took part in the Strong Heart Study of American Indians. Researchers also looked at their levels of fibrinogen, a blood plasma protein that is considered a marker for inflammation.

Researchers tracked the study’s participants over 26 years of follow-up, during which 378 people died from heart disease. The groups were split into four equal groups, or quartiles. After adjusting for various factors, researchers found those who were the most physically active, in the top quartile, had a 44% lower risk of dying from cardiovascular disease than those in the bottom “minimal activity” quartile. The next two quartiles had a 31% and 9% lower death risk, respectively, than those in the lowest quartile.

“This study confirms that physical activity reduces cardiovascular mortality in this unique cohort of American Indians,” Unlu said. “This is a population that doesn’t always have the resources for exercise and physical activity that are available in urban settings.”

The study’s senior researcher, Dr. Parmanand Singh, said many of the participants live on reservations in rural areas where the nearest gym or other activity-related facility could be many miles away.

“We need to dig deeper and find out what sort of facilities can be constructed on reservations that are in line with the cultural value system of the population. We have to think about other interventions, too, such as bringing health fairs or other public health initiatives to the reservations,” said Singh, assistant professor of medicine and director of nuclear cardiology at Weill Cornell Medicine.

The researchers looked at participants’ fibrinogen levels and found “physical activity was possibly reducing cardiovascular deaths by inflammatory pathways,” Unlu said.

The research was limited by its retrospective nature, Singh said. The findings need to be confirmed by future studies in which participants gradually get more physically active and researchers see if that impacts fibrinogen readings, he said.

Dr. Carl Lavie said the idea that exercise lowers fibrinogen levels and cardiovascular death rates “is nothing new, but the new thing is that in this American Indian population, the benefit of the physical activity is, at least statistically, explained by the lower fibrinogen.” He is a medical director of cardiac rehabilitation, prevention and exercise at the Ochsner Clinical School/University of Queensland School of Medicine in New Orleans.

Lavie, who was not involved in the study, said more research is needed to figure out if fibrinogen is a valid way to measure cardiovascular risk. But even now, he said, “if one happened to measure a fibrinogen level and it was high, this would even provide further support for recommending physical activity.”

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Invasive mosquito species could bring more malaria to Africa’s urban areas

A species of mosquito that can carry malaria—known as Anopheles stephensi – has invaded eastern Africa and is quickly moving across the region. Moina Spooner, from The Conversation Africa, asked Jeremy Herren and Clifford Mutero to provide insights into why this invasion is happening and what can be done to protect people from it.

How did Anopheles stephensi come to Africa?

This mosquito species, Anopheles stephensi, is widespread in South-East Asia and parts of the Arabian Peninsula. It is common in India, Pakistan, Iran, Iraq and Afghanistan. In the last couple of years there have been increasing reports of it in Africa. It was initially reported in Djibouti in 2013.

Recent reports indicate that it is spreading rapidly through the Horn of Africa. It was reported in Ethiopia in 2016 and in Sudan in 2017 and is likely being spread along major transportation routes. As a result, the World Health Organization has issued an alert for intensified surveillance to track the spread. We expect that it’ll eventually be found in other major African cities.

Surveillance data is needed to confirm further spread but, based on the timeline of its travel to Ethiopia and Sudan, we speculate that three years is how long it would have taken to reach Kenya and Tanzania. They are now within that risky time-frame.

Kenya and Tanzania may be at a particularly high risk due to their close proximity to the Horn of Africa. They also have large coastal cities whose weather conditions (warmer and more humid) are similar to the mosquitoes’ native range. Other cities further away, including some in West Africa, are also deemed to have a suitable environment for Anopheles stephensi.

Generally the spread of mosquitoes to new areas is facilitated by by people through ground, air and ocean transport systems. Increased international travel and human migration leads to vectors and pathogens emerging or re-emerging in regions where they’d diminished or been eradicated.

In what ways is this mosquito different from the ones that exist on the continent?

There are over 100 species of Anopheles mosquitoes in Africa, but only six species are considered “primary” vectors of malaria.

Anopheles stephensi is very effective at transmitting malaria. What’s worrying is that it also thrives in urban areas, unlike the various African Anopheles species.

Anopheles mosquitoes require water to complete their life cycle: a female mosquito lays its eggs on the surface of a water source, where they hatch and finally develop into adult mosquitoes. Female mosquitoes suck blood from people and other hosts to enable them to lay eggs. It is the blood-feeding that enables mosquitoes to transmit parasites—such as malaria—from one person to another.

Typically, the main African Anopheles vector species are found in rural landscapes—which is why the majority of Africa’s malaria cases are also in rural areas. They breed in various water habitats such as puddles, footprints and hoof prints along the edges of ponds, and irrigated farmland. These habitats do also occur in some urban areas, but they’re often polluted and less suitable for these mosquitoes. Reports do now indicate, though, that some African Anopheles are becoming more adapted to these conditions.

By contrast, while they can also survive in rural areas, Anopheles stephensi thrive in urban areas—such as plastic and cement containers that hold water. This means that this species poses a threat both in cities and in rural areas.

What new challenges does it present?

The main issue is that if the invasion becomes widely established, malaria could become more prevalent in African cities and this would put many more people at risk of infection. Consequently, malaria control efforts will be spread even thinner on the continent as malaria expands into cities.

There are already many challenges—such as a lack of resources. Currently, about half of the US$6.5 billion needed to meet the 2030 malaria targets is available. There were an estimated 219 million cases of malaria in 2017 and 92% of these occurred in the WHO African region. The funding shortfall is likely to grow if the Anopheles stephensi increases malaria cases in Africa.

Another major challenge is that both Anopheles stephensi and African malaria vectors are developing resistance to some of the insecticides used against them. These insecticides are deployed on bed-nets or used for indoor spraying.

Finally, the Anopheles stephensi presents a new challenge because it’s harder to access mosquito breeding and resting sites in urban areas and deploy control measures. In particular, it is more challenging to identify and map breeding sites in urban areas, which makes it more difficult to control larvae. In addition, indoor residual spraying is less straightforward due to the high density of dwellings and challenges accessing them all.

Has a mosquito invasion like this happened in the past? If so, what happened then?

The spread of Anopheles stephensi is reminiscent of a similar invasion by Anopheles gambiae, a mosquito species commonly found in Africa, which spread to Brazil in the 1930s and 1940s and caused devastating malaria outbreaks. For example, over a period of just eight months there were 150,000 cases of malaria and 14,000 deaths. This was recognized as one of the most serious threats to health in the Americas and an aggressive eradication campaign was initiated.

The Brazilian government reacted with an integrated control program. Insecticide spraying targeted larvae and adult insects. Cars or trucks leaving endemic areas were sprayed and there was a massive effort to improve drainage and remove the stagnant water that provided breeding sites. This concerted effort is an important example in successful vector control and resulted in the species being eradicated in South America by the 1940s.

Is there anything that can be done to stop the spread?

Action is needed immediately if there is to be a chance of curtailing the spread of Anopheles stephensi. The longer we leave it the harder it will be to contain, and unfortunately there seems to have already been significant spread with reports from across the Horn of Africa. Though mosquitoes can travel long distances and are dispersed on high altitude winds, the pattern of Anopheles stephensi spread suggests the importance of human transportation routes.

Vector surveillance is key. We need to know where Anopheles stephensi has spread and then quickly and strategically focus resources on restricting spread and locally eliminating Anopheles stephensi before it establishes a foothold. Surveillance should be carried out by National Vector and Malaria Control Programs with support from research institutions.

Overall, a combination of environmental management to eliminate larval habitats and eco-friendly biopesticides to control adult and larval stages of the mosquito is considered the most effective strategy for control of Anopheles stephensi.

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Superspreading events could help make COVID-19 endemic

The COVID-19 coronavirus is not your average virus. During the pandemic, it has become increasingly clear that averages do not apply in understanding the paths the virus takes or when or where it attacks. What some scientists and specialists in infectious diseases may say in the morning will be ridiculed before sunset. Consequently, we must be scientifically humble in predicting what is likely to happen over the next year or two.

But from the limited data that we have have, it appears that clusters of transmission from one person to a potentially large group are particularly important to maintaining the virus’s spread. In fact, these so-called superspreading events could be so significant that—without highly effective testing and contact tracing—they could cause COVID-19 to become a constant feature of our lives, even if case numbers are brought to manageable lows.

Scientists and politicians have so far relied heavily on the calculated average contagiousness of the virus to track progress in dealing with the pandemic. This is represented by the “R number”, which basically indicates how many people an infected individual will pass the virus on to. If they infect more than one, then the number of cases will grow and we have a problem. If they infect less than one, we are safer because the number of cases will decrease as people recover.

But being an average measure, R tends to obscure the real picture of a virus that typically spreads in clusters rather than from one person to one or two others. Indeed, sometimes an infected person will cause virtually no spread of the virus while another will infect almost everyone in a crowded room. When so many factors are involved outbreaks are not always predictable and this provides the basis for a future with endemic COVID-19 spread.

For example, a preprint (not yet peer reviewed) study has shown that some outbreaks in nursing homes only occurred after several new introductions of infection. This indicates that what can look like a single outbreak actually is a situation with multiple concurrent but independent introductions of COVID-19.

Another preprint study carried out in New Zealand used genetic sequencing to track how individual strains of the virus were being transmitted. It found that only one in five infections entering the country led to additional cases and most cases were linked to a single transmission cluster. Meanwhile, a single person in South Korea is thought to have infected more than 5,000 people in a large church cluster.

Such clusters of transmission appear to take place under certain conditions that enable the virus to disperse rapidly through a crowd. Crowded indoor places that are badly ventilated and where people are physically or vocally active for a relatively long period seem to create a particular risk. This may be because virus can accumulate in the air in rooms without proper ventilation and allow transmission even when social distancing is taking place.

Research from China has confirmed that ventilation is particularly important. Buses that recirculated air were found to be linked with more cases than those not using recirculation. And, in one case of a transmission cluster in a restaurant, those who sat closest to the ventilation outlet all contracted COVID-19 while none of the customers near the ventilation inlet were infected.

However, what’s puzzling is that this doesn’t explain why some potential superspreading events don’t cause an outbreak, and why there are outbreaks that do not have the known characteristics of a superspreading event. This suggests there are other unknown factors. It looks as if some clusters provide valuable information while others don’t.

Our analysis is skewed by the fact that we only have data for relatively well-defined outbreaks where everybody involved were easily identified, such as tourists on cruise ships, choirs, Zumba dance groups or church congregations. But in real life most outbreaks occur without a clear social setting or in groups where some members are difficult to track down. Further genetic surveillance of outbreaks will probably help us develop our understanding.

It’s also harder to obtain the necessary information to track clusters of infections that come from certain social or cultural groups. For example, stigma or fear of the authorities could discourage some people from reporting their illness. Those taking part in secret or illicit parties might underestimate the risk and consequences of their catching the virus.

Bad luck

Some of the worst initial outbreaks in Italy, China, Ecuador and other places may have been due to sheer bad luck: too many of the known factors occurring in the same place at the same time. It’s not a very clever or scientifically satisfying explanation, but that’s probably a feature of COVID-19 that we must live with for now.

But as Italy and Ecuador have shown, COVID-19 has the potential to turn bad luck into a disaster. This means that even if control measures such as social distancing help us to bring R below 1 and reduce ongoing community spread to relatively low levels, superspreading events can can turn comfort into chaos in a few days.

Those countries that have successfully contained epidemic for significant periods of time, such as New Zealand, have done so through very rigorous contact tracing of the person that starts a cluster of transmission combined with strategic testing. But even in these cases, new outbreaks have occurred.

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New discovery could help improve cancer vaccines

Cancer vaccines have shown promise in treating certain tumors, such as melanoma. But such vaccines have limitations. They often target normal proteins that may be more abundant in the tumor but also are present in healthy tissue, which can lead to off-target effects that cause autoimmune disorders and also reduce the effectiveness of the vaccines.

The mutated DNA of cancer cells often produces abnormal proteins, whose fragments can help distinguish the tumor from healthy tissue. Such protein fragments could be harnessed to train the immune system to attack the tumors with, in theory, few side effects. Now, a broad collaboration of scientists in academia and industry have identified the most important features of the protein fragments to help researchers design better immunotherapies against cancer.

The study, co-led by researchers at Washington University School of Medicine in St. Louis, appears Oct. 9 in the journal Cell.

These abnormal protein fragments are called neoantigens. The new study identifies five features of neoantigens that optimize the ability to trigger the body’s T cells to attack the cancer and leave healthy tissue untouched. Using the new criteria, the researchers used computer modeling to accurately predict 75% of effective neoantigens and eliminate 98% of ineffective mutant proteins in melanoma and a common type of lung cancer.

The research team, called the Tumor Neoantigen Selection Alliance (TESLA), has made the computer model and dataset freely available to the research community to speed the development of cancer vaccines and other immunotherapies.

“For scientists working to create personalized cancer vaccines that target the unique neoantigens of an individual patient’s tumor, this is a resource that is desperately needed,” said co-senior author Robert D. Schreiber, PhD, the Andrew M. Bursky & Jane M. Bursky Distinguished Professor of Pathology and Immunology. “There has been an explosion of approaches to try and figure out which are the best mutant proteins to target in a tumor. This broad approach is more accurate and will help to design anticancer vaccines that potentially are more effective for patients.”

The features that the researchers identified as most important in selecting effective neoantigens include the abundance of a specific neoantigen in the tumor; the strength with which the neoantigen binds to vital immune proteins so the T cells can see it; the stability of the neoantigen on the immune protein complex; how much more often the immune proteins preferentially bind to the neoantigen versus the normal protein; and how foreign or distinct the neoantigen is from the normal protein.

Schreiber said that all these factors make sense in selecting the best neoantigens, but he was surprised by some of the findings on criteria that were not important for neoantigen effectiveness.

“We were able to eliminate some of the assumptions that we scientists sometimes make about what makes a good neoantigen,” said Schreiber, who also directs the Andrew M. and Jane M. Bursky Center for Human Immunology & Immunotherapy Programs at Washington University School of Medicine. “For example, there has been a general sense that the mutant proteins that make the best neoantigens are the most hydrophobic — meaning they repel water. It turns out, that characteristic didn’t show any relationship to neoantigen effectiveness.”

Schreiber also pointed out that this study is focused on neoantigens that activate what are called CD8 T cells, which he describes as the immune system’s foot soldiers, those responsible for killing the tumor cell. He said future work should focus on neoantigens that also activate a different type of cell, CD4 T cells. Schreiber calls these the generals, cells that stay behind the front lines but direct the foot soldiers in their anti-cancer mission.

“In order to get a good immune response against a tumor, you need to activate both CD4 and CD8 T cells,” Schreiber said. “In future work, we would like to conduct a similar analysis to identify the best neoantigens for triggering the CD4 T cells as well. In designing an effective vaccine, we think we need at least one good CD8 neoantigen and one good CD4 neoantigen to trigger immune rejection of a tumor.”

The TESLA initiative, led by the Parker Institute for Cancer Immunotherapy and the Cancer Research Institute, includes 33 research teams from universities, biotech companies, pharmaceutical companies and nonprofit research institutes.

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How opening a window could help you avoid COVID

While billions are being spent on the search for a COVID-19 vaccine and treatment, experts say there may be something you can do to help avoid the virus that costs nothing: open the window.

Growing evidence suggests that allowing air to circulate around enclosed spaces can help disperse the air-borne viral droplets that cause infection.

These fine clouds of particles, known as aerosols, are thought to be able to remain suspended in the air for long periods, even hours.

That’s where reaching for the window latch may help.

Epidemiologist Antoine Flahault likened dispersing the viral cloud to airing out a room when someone is smoking.

“What do you do? You open a window to let the smoke out,” he told AFP. “And it’s the same for these invisible coronavirus aerosols.”

The American Centers for Disease Control updated its advice this week to include guidance on enclosed areas.

“Avoid crowded indoor spaces and ensure indoor spaces are properly ventilated by bringing in outdoor air as much as possible,” it now says on its website.

Cheap, effective

The CDC has added aerosols to its official list of coronavirus transmission routes, although the main way the virus spreads is still through respiratory droplets emitted by infectious individuals.

Experts in other countries have argued for months for more rigorous measures to dispel the threat of aerosol transmission, which were largely absent from public health guidance at the start of the pandemic.

Germany is one country where official guidance encourages people to leave the windows open.

Chancellor Angela Merkel said last month that ventilation “could be one of the least expensive and most effective measures to stop the propagation of the pandemic.”

Bernhard Junge-Hulsing, a German doctor, advised people to keep the windows open, at home or at work, even as winter approaches.

“You can always wear a pullover,” he said.

Host of measures

But how much ventilation is enough to disperse the aerosol?

“We recommend a total recirculation of the air in a room at least six times an hour. That takes quite a lot,” said Flahault, director of the University of Geneva’s Global Health Institute.

In certain settings this can be achieved by circulation systems, which are often fitted with high-tech filters that also cleanse the air.

“Six times an hour is what you find on board a TGV (high-speed train) or aeroplane, where the air quality is very good,” said Flahault.

“But in most closed spaces we don’t have that level of ventilation.”

Although opening windows could help avoid spreading the coronavirus, experts stress that no single measure can guarantee protection.

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Could Regeneron’s antibody cocktail help President Trump?

‘If Trump recovers quickly, that will mitigate downside loss on Wall Street’: Stuart Varney

On Friday, the White House revealed that President Trump was given a dose of an antibody cocktail following his coronavirus diagnosis.

According to a statement from White House press secretary Kayleigh McEnany, Trump received an 8-gram dose of the polyclonal antibody cocktail, REGN-COV2, from pharmaceutical company Regeneron, as a “precautionary measure.”

Before the announcement, Dr. Matt McCarthy, an infectious disease doctor, told FOX Business’s Stuart Varney that the Regeneron antibody cocktail would be the first thing he would have recommended for the president.

“If I got brought in today to the Oval Office, first thing I’d say is, has anyone reached out to Regeneron?” McCarthy said. “Has anyone talked about an antibody cocktail for him? Three days ago, the company showed that they can reduce the amount of virus in the body and that they can decrease the duration of symptoms.”

TRUMP, FIRST LADY EXPERIENCING ‘MILD SYMPTOMS’ AS WH DOC RELEASES DETAILS ABOUT TREATMENT

Regeneron declined to comment on the specifics of giving a dose of its antibody cocktail to the president.

“As a general policy, Regeneron has a compassionate use program with certain established criteria and a review committee,” the company said in a statement. “Also as a matter of policy, we don’t identify individuals without their consent who have or have not submitted a request or who are participating in our clinical trials.”

LINCOLN PROJECT WISHES TRUMP WELL, HOPES CORONAVIRUS DIAGNOSIS ‘SENDS A SIGNAL’ TO HIS SUPPORTERS

“For REGN-COV2, our first priority is to maintain a sufficient supply in order to conduct rigorous clinical trials,” the company added. “In addition to the clinical trial supply, there is limited product available for compassionate use requests that are approved under certain exceptional circumstances on a case-by-case basis.”

AFTER TRUMP COVID DIAGNOSIS, PENTAGON SAYS ALERT LEVELS REMAIN UNCHANGED

McEnany’s statement also mentioned that the president has been taking “zinc, vitamin D, famotidine, melatonin and a daily aspirin.”

“As of this afternoon, the President remained fatigued but in good spirits,” the statement said. “He’s being evaluated by a team of experts, and together we’ll be making recommendations to the President and First Lady in regards to next best steps.”

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McCarthy told Stuart Varney that regardless of statistics, the coronavirus is “unpredictable.”

“Anyone who tells you they know what’s going to happen or anyone who tells you that, oh, he’ll probably be fine, I don’t want that person making decisions for the president of the United States,” McCarthy said. “The key here is to watch how things evolve over the next few days.”

“We see patients all the time in his demographic that feel relatively well for a week and then a week later, they’re in the hospital,” he added. “That’s not to say that’s what’s going to happen here. In fact, no one knows what’s going to happen here. But the key is to keep an eye on his vital signs and, in particular, the amount of oxygen that he has. So if his oxygen saturation starts dropping, that should raise alarm bells that he needs to be headed to a more intensive monitoring system.”

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Why absence could make your heart go longer

Why absence could make your heart go longer: As Britain sees a gradual shift towards so-called remote medicine, we take a look at the inventions that are changing the face of cardiac care

  • Britain is seeing a gradual shift towards so-called remote medicine for patients
  • Complex tests now performed without patient needing to step outside house   
  • However there may be caveats if the device needs to be surgically implanted

A doctor monitoring your health without even setting eyes on you used to be the stuff of science fiction.

But thanks to modern technology, Britain is seeing a gradual shift towards so-called remote medicine, where patients are supervised round the clock by high-tech implants or devices while at home.

Complex tests and check-ups that once required bulky hospital equipment are now performed without the patient needing to step outside their front door — with the results transmitted via smartphone technology straight to their doctor’s computer.

There may be caveats if the device needs to be surgically implanted, as this carries a chance, albeit low, of triggering life-threatening infections.

A 2015 study suggested that faulty heart implants could be responsible for up to 2,000 deaths a year in the UK, although this has been strongly disputed by the British Heart Foundation. (Stock image)

Some implantable devices have also been known to go wrong. 

A 2015 study suggested that faulty heart implants — including pacemakers — could be responsible for up to 2,000 deaths a year in the UK, although this has been strongly disputed by the British Heart Foundation, which insists the devices have a good safety record.

Martin Cowie, a professor of cardiology at Imperial College London, says remote monitoring will transform patient care.

‘The pandemic has highlighted how convenient it is, and now it’s here to stay,’ he adds.

Here, we take a look at the inventions that are changing the face of cardiac care, one of the areas where this advance has been the most rapid.

NECKLACE TO DETECT A HEART ‘FLUTTER’

A high-tech pendant could make it easier to diagnose atrial fibrillation (AF), an irregular or ‘fluttering’ heartbeat, which affects around a million people in the UK.

Often triggered by high blood pressure, AF causes the heart’s electrical activity to go haywire, increasing the risk of a stroke. But patients can go days or weeks without an abnormal rhythm, making the condition hard to spot during a brief hospital visit.

The pendant, which is the brainchild of scientists at the University of Eastern Finland, is only the size of a 5p piece and can carry out pared down electrocardiograms (ECGs) — the measure of the heart’s electrical activity which is used in hospitals to diagnose AF.

Worn on a discreet silver chain, it contains an electrode, a recording device and a computer chip, which are all wirelessly connected to an app on the patient’s smartphone.

Pressed firmly against the chest for 30 seconds, it instantly transmits a read-out of the heart’s electrical activity via the app to the patient’s cardiologist. Readings should be taken several times a day.

Results of a study of 145 adults, presented at a European cardiology congress in May, showed that the gadget was as good at diagnosing AF as hospital-based ECGs. Larger trials are now planned.

‘I use devices like this a lot,’ says Richard Schilling, a professor of cardiology at Barts Health NHS Trust in London. ‘This kind of patient-performed ECG has transformed the diagnosis of some conditions.’

CHECK YOUR TICKER FROM THE INSIDE

Getting a heart check usually means doctors attaching equipment to the outside of your body.

Now, an implant that does the tests from the inside — without the need for a medic even to be present — is undergoing trials at Queen Elizabeth Hospital in Birmingham and London’s Hammersmith Hospital.

The V-lap microcomputer monitors patients with heart failure, which is where the heart, weakened after a heart attack or by a condition such as untreated high blood pressure, is unable to pump sufficient blood around the body to deliver the oxygen vital organs need. 

Treatment for the 1.3 million Britons with heart failure usually starts with drugs to lower blood pressure and reduce water retention, a common symptom.

This new implant, which is inserted into the left atrium — one of the heart’s two upper chambers — during an hour-long keyhole operation, senses changes in blood pressure which are a sign of further deterioration of the organ.

Transmitted to a patient’s cardiologist twice a day, the data can give several weeks’ notice that heart function is deteriorating — enough time to increase drug dosage and stave off greater damage.

Professor Francisco Leyva-Leon, a cardiologist trialling the implant in Birmingham, says: ‘The benefits could be huge. In my hospital alone we admit more than 1,000 patients a year with heart failure.’

DAILY BLOOD STATS FROM PUFF-UP WATCH

Home blood pressure monitoring is nothing new. But devices are fairly cumbersome, involving wearing a ‘sleeve’ that wraps round the upper arm, just like the one in a GP surgery.

That could be about to change, thanks to Japanese scientists working out how to shrink the key components of the equipment into a wristwatch.

HeartGuide, which can also be used as a normal watch, has a built-in cuff under the strap that inflates around the wrist when the patient presses the watch face.

Daily readings are beamed wirelessly to a smartphone app that shares the data with doctors, who then decide if the patient’s medication needs altering — without needing a consultation.

However, at around £500, it’s not a cheap option.

‘This smart watch is an interesting idea,’ says Professor Martin Cowie. ‘But it is important to remember blood pressure goes up and down in response to activity or sleep. The patient would need to take a large number of readings.’

PACEMAKER THAT TALKS TO YOUR GP

Pacemakers have been around for more than half a century, but a new generation of miniature implants are capable of much more than just regulating the heart — they can also communicate with doctors remotely.

Alternative remedies

The aloe vera plant is often found in tropical climates

Pharmacist Gemma Fromage reveals the unexpected uses for everyday products. 

This week: Aloe vera for acid reflux.

The use of aloe vera, a plant often found in tropical climates, dates back to Ancient Egyptian times.

It is well known as a home remedy for scrapes and burns due to its anti-inflammatory properties.

The juice, derived from the inner lining of its leaves, has also been found to soothe acid reflux. A study in the Journal of Traditional Chinese Medicine showed purified aloe vera juice improved reflux symptoms as well as, and in some cases better than, traditional medications — possibly because it reduces acid production.

Pregnant women and those with diabetes are advised against taking aloe vera juice, as it may cause uterine contractions and affect blood sugar levels. 

Anyone using prescribed medicines for reflux should also consult their doctor before stopping their treatment regimen in favour of aloe vera, or adding the juice to it.

 

Pacemakers are matchbox-sized gadgets used to treat a range of conditions that affect the heart —from children born with cardiac defects to adults with AF. Implanted in the chest, they send electrical pulses to the heart to keep it beating regularly.

Older devices store readings on built-in microchips which can only be accessed by visiting a hospital up to four times a year to have them downloaded. But now doctors can gather the data without the patient needing to leave their home.

Modern pacemakers have a transmitter that ‘talks’ to a mobile-phone sized monitor. It uses an internet connection to send encrypted data straight to the doctor’s computer.

‘We already use remote monitoring for thousands of pacemaker patients,’ says Professor Francisco Leyva-Leon.

‘It means we can screen them on a regular basis and only need to call them in for a consultation if there is a potential problem.’

SKIN PATCH TO SPOT IRREGULAR RHYTHMS

A stick-on chest patch called Zio that you can even wear in the shower is increasingly being used to diagnose irregular heart rhythms without going to hospital.

The matchbox-sized patch has built-in electrodes and a recording device to pick up the heart’s electrical activity as the patient goes about their day.

Made from waterproof plastic, the patient wears it on their upper chest for up to two weeks to record their heart’s activity, before sending it back to the supplier, Surrey-based firm iRhythm.

The company uses the results to compile a report for the patient’s doctor.

A 2019 study at King’s College Hospital in London found the Zio patch was almost eight times more effective than current portable monitors at detecting heart rhythm problems.

The cost to the NHS is £800 per patch, including the analysis and the report provided for GPs.

‘Devices like the Zio skin patch are easier to wear than monitors during exercise and may even perform better,’ says Dr Sarah Clarke, a cardiologist at the Royal Papworth Hospital in Cambridge.

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