Publisher Health

What It’s Like to Be Vaccinated in a Subway StationJoseph Goldstein📍Reporting from New York CityAt the Jamaica-179th Street Station in Queens, the nurses administering the vaccines began wrapping up at 1 p.m.“I got two extra Covid shots,” Dolfina Arloro, a pharmacist, called out to a trickle of people coming through the turnstiles. “Anyone want a Covid vaccine?”There were no takers, but already 300 people had been vaccinated at that station that day. The program is continuing through Saturday.

For coffee drinkers, a common scenario might involve drinking an extra cup only to end up with a racing heart and a subtle reminder to themselves to cut down the caffeine. But for those who have a different thinking pattern, one that includes heart-focused anxiety, the racing heart might conclude with the fear of a heart attack and a trip to the emergency room.
It turns out young Latinx adults who experience heart-focused anxiety could be at greater risk for mental health disorders.
“We have empirical evidence that individual differences in heart-focused anxiety are related to more severe co-occurring anxiety and depressive symptomatology among a particularly at-risk segment of the Latinx population,” reports Michael Zvolensky, Hugh Roy and Lillie Cranz Cullen Distinguished University Professor of psychology at the University of Houston, in the Journal of Racial and Ethnic Health Disparities. The population segment to which Zvolensky refers is Latinx young adults with previous trauma who were born in the United States. Their trauma might include racism related and transgenerational stress.
This is only the second study on heart-related anxiety in the Latinx community, both conducted by Zvolensky.
“In our first study, we assessed middle aged adults, presumably more concerned about their health. This study is unique, however, because even among a group generally too young to experience mounting health concerns, we are seeing a similar pattern, which tells us it’s probably relevant to the whole Latinx population,” said Zvolensky.
According to previous research, the Latinx population can somaticize mental health problems, meaning they don’t view them as mental health issues, but rather turn them into physical symptoms and report them as such. As examples, anxiety might be reported as a headache or a problem with breathing.

Biologist Sasha Mendjan at the Austrian Academy of Sciences in Vienna and his team have used human pluripotent stem cells to grow sesame-seed-sized heart models, called cardioids, that spontaneously self-organize to develop a hollow chamber without the need of experimental scaffolds. This advance, which allows for the creation of some of the most realistic heart organoids to date, appears on May 20th in the journal Cell.
Previously, scientists have built 3D cardiac organoids via tissue engineering, an approach that generally involves assembling cells and scaffolds like building a house out of brick and mortar. But these engineered organoids do not have the same physiological responses to damages as human hearts and thus often fail to serve as good disease models.
“Tissue engineering is very useful for many things like, for example, if you want to do measurements on contraction,” says Mendjan. But in nature, the organs aren’t built this way. In the embryo, organs develop spontaneously through a process called self-organization. During development, the cellular building blocks interact with each other, moving around and changing shape as an organ’s structure emerges and grows.
“Self-organization is how nature makes snowflake crystals or birds behave in a flock. This is difficult to engineer because there seems to be no plan, but still something very ordered and robust comes out,” he says. “The self-organization of organs is much more dynamic, and a lot is going on that we do not understand. We think that this ‘hidden magic’ of development, the stuff we do not yet know about, is the reason why currently diseases are not modeled very well.”
Mendjan and his team wanted to mimic development by self-organization in a dish. They coaxed stem cells to self-organize by activating all six known signaling pathways involved in embryonic heart development in a specific order. As the cells differentiated, they started to form separate layers, similar to the structure of the heart wall. After one week of development, these organoids self-organized into a 3D structure that had an enclosed cavity, a similar spontaneous growth trajectory as human hearts. In addition, the team found the cardioids’ wall-like tissue contracted rhythmically to squeeze liquid around the inside the cavity.
“It’s not that we are using something different than other researchers, but we are just using all of the signals known,” Mendjan says. He adds that not all pathways are needed to direct stem cells to become heart cells. “So they thought, ‘Okay, they’re not really necessary in vitro.’ But it turns out all these pathways are necessary. They are important to make the cells self-organize into an organ.”
The team also tested how the cardioids respond to tissue damages. They used a cold steel rod to freeze parts of the mini-hearts and killed many cells at the site. Cell death is commonly observed after injuries such as a heart attack. Immediately, the team saw cardiac fibroblasts — a type of cell responsible for wound healing — start to migrate toward the injury sites and produce proteins to repair the damage.
“We want to come up with human heart models that develop more naturally and are therefore predictive of disease,” Mendjan says. “This way, companies will be more open to bringing more drugs into the clinical trials because they are much more certain of the outcome of the trial.”
The team has plans to grow cardiac organoids with multiple chambers like what’s seen in a real human heart. Many congenital heart diseases happen when other chambers start to form, so the multi-chamber model would help doctors better understand how defects develop in fetuses.
This work was funded by the Austrian Academy of Sciences (OEAW) and the Research Promotion Agency (FFG).
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Materials provided by Cell Press. Note: Content may be edited for style and length.

American politics can be stressful and confrontational, which can lead to anger. The combination of intense stress and negative emotions can trigger potentially fatal cardiovascular events in people who are susceptible to these health issues. But the direct link between a stressful political election and an increase in cardiac events hadn’t been established, until now. A new study in the Journal of the American Heart Association is the first to show that exposure to a stressful political election is strongly associated with an increase in potentially life-threatening cardiac events.
“This retrospective case-crossover study was conducted in North Carolina, which was a swing state in the 2016 U.S. presidential election,” said lead author Lindsey Rosman, PhD, assistant professor of medicine in the division of cardiology at the UNC School of Medicine. “People living in North Carolina were exposed to a particularly high volume of negative political commercials, advertisements and campaign events that were very intense in rhetoric. So, their stress levels may have been especially high leading up to the 2016 election.”
The study looked at data from implanted cardiac devices of 2,500 patients at three points in time: a six-week span leading up to and following the 2016 U.S. presidential election, and two control periods that consisted of a six-week span from June to July of 2016, and a six-week span from October to November of 2015. Rosman and her team found a 77% increase in the risk of arrhythmia — an abnormal heart rate or irregular heart rhythm — during the 2016 election period compared to the control periods.
“The increase in risk was significant, even after taking into account known risk factors for cardiovascular disease such as age, hypertension, health behaviors, and other medical conditions,” Rosman said.
Researchers found a significant increase in the risk of both atrial arrhythmias, like atrial fibrillation, and potentially life-threatening ventricular arrhythmias.
“We also found a higher burden of atrial fibrillation during the election, and this is important because it can increase your risk of blood clots, stroke, and other heart-related complications,” Rosman said.
The study also looked at whether registered Republicans or Democrats experienced more arrhythmias during the election period, and if political concordance — whether a person’s registered affiliation matched the election results of the county they live in — had an impact on arrhythmic events.
“We were not able to conclusively show that the election was more stressful for one party over the other because of the size of our study,” Rosman said. “Risk of heart events increased for people no matter their political affiliation, race or gender. But we did see that registered Democrats experienced nearly twice as many heart events as Republicans, which is a trend we would like to explore further.”
When it comes to political concordance, those who were politically discordant (and may have felt socially or ideologically disconnected from their community) experienced a significant increase in arrhythmic events during the 2016 election. But, there was also an increase in risk for people who aligned as politically concordant.
The consequences of increased cardiac events due to stressful elections could be significant. With U.S. presidential elections happening every four years and midterms every two, Rosman says more research on the subject is needed to study the population-level health impact. She and her team hope to perform a similar study on a nationwide scale of stress and cardiac events during the 2020 U.S. presidential election.
This study was supported by a grant from the National Heart, Lung, and Blood Institute of the National Institutes of Health to Rosman. Support for the data linkage and database management was provided by the North Carolina Translational and Clinical Sciences (NC TraCS) Institute.

Antiretroviral therapy, the common approach in the treatment of HIV, halts replication of the virus and has saved the lives of millions of people. However, for patients the drug cocktail becomes a lifetime necessity because they continue to harbor latent HIV in a small number of immune system cells. In the absence of treatment, HIV can again replicate and rebound into full blown AIDs.
A new study, however, suggests that addition of a single small molecule can rip away the cloak that shields those cells containing HIV and make them susceptible the patient’s own antibodies that otherwise are not normally of much use against HIV.
For the study, a team of researchers led by scientists at Yale and the University of Montreal Hospital Research Centre stopped antiretroviral treatment for mice carrying human plasma and blood cells infected with HIV. They then treated the mice with a drug developed at the University of Pennsylvania that mimics receptors of immune T cells called CD4. The CD4-like molecule binds to and exposes vulnerable parts of the viral envelope on infected cells.
The mice experienced either no rebound of infection or long delays before active HIV infection restarted, the researchers report May 20 in the journal Cell Host & Microbe.
Researchers hope one day the new treatment may eliminate the need for long-term antiretroviral treatments.
It’s sort of like pawn promotion in the game of chess, said Priti Kumar, associate professor of infectious diseases at Yale School of Medicine and lead author of the study
“These antibodies are like pawns,” Kumar said. “There are many of them, but they are useless against the source of virus. But with the right move, they can be promoted to a powerful position and score a decisive victory by eliminating infected cells.”
The CD-4 like molecule in the presence of antibodies acts like a “can opener” that allows antibodies to recognize the virus and trigger an immune response.
“The virus can now be recognized by patient antibodies that call the immune system’s ‘police,’ the natural killer cells, to get rid of the infected cells,” said Andrés Finzi, co-lead author of the study and professor at the Université de Montréal.
“In this way, a patient’s own antibodies and cells that are commonly present can eliminate the viral reservoir and prevent viral rebound,” Kumar said. “The hope is one day we might be able to do away with antiretroviral therapies altogether.”
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Materials provided by Yale University. Original written by Bill Hathaway. Note: Content may be edited for style and length.

A national study from researchers at Michigan Medicine found that nearly 3% of insured U.S. adults under 65 take medications that weaken their immune systems.
The findings, published in JAMA Network Open, are based on data from over 3 million patients with private insurance. They focus on patients’ use of immunosuppressive drugs, including chemotherapy medications and steroids such as prednisone.
The analysis reveals nearly 90,000 people met the study criteria for drug-induced immunosuppression that may elevate risk for severe COVID-19 symptoms and hospitalization if they became infected. Two-thirds of them took an oral steroid at least once, and more than 40% of patients took steroids for more than 30 days in a year.
“This study gives us previously unavailable information about how many Americans are taking immunosuppressive medications,” says Beth Wallace, M.D., a rheumatologist at Michigan Medicine and lead author of the paper. “It also reinforces that many Americans continue to take oral steroids, which are associated with serious side effects and can often be avoided or substituted with alternative medications.”
When the team of researchers examined the data, a vaccine against COVID-19 was not yet available outside clinical trials. The evidence is growing, however, that taking immunosuppressive drugs may reduce the efficacy of the shot, Wallace says.
“We’re starting to realize that people taking immunosuppressive drugs may have a slower, weaker response to COVID vaccination, and, in some cases, might not respond at all,” she says. “We don’t have a full picture on how these drugs affect the vaccine’s effectiveness, so it’s difficult to formulate guidelines around vaccinating these patients.” Wallace mentions several strategies, including holding medications around the time of vaccination and giving an extra “booster” shot, that scientists are testing to look into this question.
Wallace also expresses concern over how this group of immunosuppressed patients should proceed following the CDC’s relaxation of masking and distancing guidelines for vaccinated people.
“The CDC acknowledges this cohort might not be as protected as other fully vaccinated people, but there are no set recommendations for what precautions they should take,” she says. “For now, this is going to be an individual decision people make with their doctor.”
Moving forward, Wallace says, researchers need prospectively look at vaccine response in this vulnerable population.
“Until we know more about this, we really won’t be able to say if immunosuppressed people are actually protected,” she says.
Wallace and senior author Akbar Waljee, M.D., M.Sc., as well as several co-authors, are members of the U-M Institute for Healthcare Policy and Innovation. Dr. Waljee previously led a study that quantified health risks associated with short-term steroid use in the general population. Dr. Wallace has authored several analyses of steroid use and risk among patients with autoimmune conditions.
Disclosures: Dan Clauw, M.D., reported receiving grants from Aptinyx Inc. and Lundbeck and personal fees from Tonix Pharmaceuticals, Innovative Med Concepts and Samumed outside the submitted work.
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Materials provided by Michigan Medicine – University of Michigan. Original written by Noah Fromson. Note: Content may be edited for style and length.

In spite of decades of research, cancer remains an enigma. Conventional wisdom holds that cancer is driven by random mutations that create aberrant cells that run amok in the body.
In a new paper published this week in the journal BioEssays, Arizona and Australian researchers challenge this model by proposing that cancer is a type of genetic throwback, that progresses via a series of reversions to ancestral forms of life. In contrast with the conventional model, the distinctive capabilities of cancer cells are not primarily generated by mutations, the researchers claim, but are pre-existent and latent in normal cells.
Regents’ Professor Paul Davies, director of Arizona State University’s Beyond Center for Fundamental Concepts in Science and Kimberly Bussey, cancer geneticist and bioinformatician from the Precision Medicine Program at Midwestern University, Glendale, Ariz., teamed up with Charles Lineweaver and Anneke Blackburn at the Australian National University (ANU) in Canberra to refine what they call the Serial Atavism Model (SAM) of cancer. This model suggests that cancer occurs through multiple steps that resurrect ancient cellular functions.
Such functions are retained by evolution for specific purposes such as embryo development and wound healing, and are usually turned off in the adult form of complex organisms. But they can be turned back on if something compromises the organism’s regulatory controls. It is the resulting resurrection steps, or atavistic reversions, that are mostly responsible for the ability of cancer cells to survive, proliferate, resist therapy and metastasize, the researchers said.
Davies and Bussey are also members of ASU’s Arizona Cancer Evolution Center (ACE) which seeks to understand cancer, not just in humans, but across all complex species, in the light of evolutionary processes.
“Cancer research has been transformed in recent years by comparing genetic sequences across thousands of species to determine gene ages,” Davies said. Just as geologists can date rock strata, so geneticists can date genes, a technique known as phylostratigraphy.
“The atavistic model predicts that the genes needed for cancer’s abilities are mostly ancient — in some cases little changed over billions of years,” Davies added.
Lineweaver explained, “In biology, nothing makes sense except in the light of evolution, and in the case of cancer nothing makes sense except in the light of the deep evolutionary changes that occurred as we became multicellular organisms.”
“The atavistic model of cancer has gained increasing traction around the world,” added Bussey. “In part, this is because it makes many predictions that can be tested by phylostratigraphy, unlike the conventional somatic mutation theory.”
Blackburn, a cancer biologist in ANU’s John Curtin School of Medical Research, agreed.
“Appreciation of the importance of gene ages is growing among oncologists and cancer biologists,” she said. “Now we need to use this insight to develop novel therapeutic strategies. A better understanding of cancer can lead to better therapeutic outcomes.”
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Materials provided by Arizona State University. Note: Content may be edited for style and length.

“Pretty” parrots are more likely to be snatched up for Indonesia’s illegal wildlife trade, a new study reveals.
The findings not only expose the key drivers behind the country’s illegal trade in these birds, but offer lessons for the potential emergence and spread of infectious diseases that jump from animals to humans — like COVID-19 and avian flu.
The study, involving researchers from The Australian National University (ANU), analysed two decades worth of data on the illegal trade of parrots in Southeast Asia.
The researchers found some key reasons parrots were at risk of being poached — with a bird’s attractiveness and the ability to sell it on legal markets being two main motivations.
“High demand for parrots as pets, and their removal from the wild for the trade have significantly contributed to their severe decline worldwide,” co-author Professor Rob Heinsohn from ANU said.
“One-third of the nearly 400 parrot species are threatened by extinction today.

Researchers have discovered a new coronavirus, found in a child with pneumonia in Malaysia in 2018, that appears to have jumped from dog to human.
If confirmed as a pathogen, the novel canine-like coronavirus could represent the eighth unique coronavirus known to cause disease in humans. The discovery also suggests coronaviruses are being transmitted from animals to humans more commonly than was previously thought.
“How common this virus is, and whether it can be transmitted efficiently from dogs to humans or between humans, nobody knows,” said Gregory Gray, M.D., a professor of medicine, global health and environmental health at the Duke University.
“What’s more important is that these coronaviruses are likely spilling over to humans from animals much more frequently than we know,” said Gray, who led the research that appears in the journal Clinical Infectious Diseases. “We are missing them because most hospital diagnostic tests only pick up known human coronaviruses.”
Working with visiting scholar Leshan Xiu, a Ph.D. student, Gray was on a team that in 2020 developed a molecular diagnostic tool to detect most coronaviruses from the Coronaviridae family that includes SARS-CoV-2, which causes COVID-19.
The team used that tool to examine 301 archived pneumonia cases and picked up signals for canine coronaviruses from eight people hospitalized with pneumonia in Sarawak, a state in East Malaysia.

Two experimental drug approaches that target vulnerabilities in cancer cell metabolism may extend survival and enhance the effectiveness of standard chemotherapies for a highly aggressive type of pediatric brain cancer.
The findings were reported by Johns Hopkins Kimmel Cancer Center researchers in two published studies.
Medulloblastoma is the most common malignant pediatric brain tumor. A subset of patients with tumors known as Group 3 MYC-amplified medulloblastoma have an overall survival rate of less than 25%. In these patients, the cancer-promoting MYC oncogene drives cancer cell growth by altering cancer cell metabolism. Cancer cells use energy in ways that are different from normal cells, so they are potentially vulnerable to therapies that target the abnormal metabolic pathways downstream of MYC.
In the first study, published March 22 in the Journal of Neuropathology and Experimental Neurology, pediatric oncologist and senior author Eric Raabe, M.D., Ph.D., associate professor of oncology at the Johns Hopkins University School of Medicine, focused on the metabolism altering drug DON (6-diazo-5-oxo-L-norleucine). DON is a naturally occurring compound studied in adult and pediatric cancer clinical trials since the 1980s, but it was never systematically tested against MYC-driven brain tumors.
Although DON was safe in children in early cancer clinical trials, it is not currently clinically available.
The research team, led by Barbara Slusher, Ph.D., M.A.S., director of Johns Hopkins Drug Discovery and professor of neurology at the Johns Hopkins University School of Medicine, modified DON to increase its ability to cross the blood-brain barrier, creating a DON prodrug, JHU395. In a prodrug, the chemistry is changed so that the drug is activated only in cancer cells.