Publisher Health

Published in Molecular Psychiatry, a team of scientists from the University of Minnesota Medical School, University of Texas Health San Antonio, and the Biomedical Research Institute (BRI) of the Foundation for Research and Technology Hellas (FORTH) in Greece found that the disruption of a circadian clock gene may be involved in the development of autism spectrum disorder.
Autism spectrum disorder, or ASD, refers to a neurodevelopmental disorder characterized by a wide range of behavioral conditions including challenges with social skills, repetitive behaviors, speech and nonverbal communication. According to the Centers for Disease Control and Prevention, ASD affects one in 44 children in the U.S.
About 50-80% of children with ASD have sleep problems, compared to less than 30% in the general population. The causes of sleep problems in ASD are not entirely clear, but a malfunctioning body clock could be the culprit.
“It has long been recognized that the function of the body clock is frequently disrupted in autism patients and these patients often exhibit various sleep problems,” said Ruifeng Cao, MD, PhD, an assistant professor of neuroscience at the U of M Medical School, Duluth Campus and co-author of the study. “But, it is not known whether clock gene disruption can directly cause autism.”
The study found that the disruption of an essential clock gene in preclinical models can lead to autistic-like phenotypes. Specifically, the global or cerebellar deletion of the Bmal1 gene can cause severe impairments in sociability, social communication and excessive repetitive behaviors.
The models also illustrated damages to their cerebellum — or cerebellar ataxia. The research team further studied the pathological changes in the cerebellum and found a number of cellular and molecular changes that indicate neurodevelopmental deficits.
“Clock gene disruption could be a mechanism underlying several forms of autism and potentially other neurodevelopmental conditions, and this finding paves the way for further exciting research,” said Christos Gkogkas, PhD, a lab principal investigator in neurobiology at BRI of FORTH.
The research team plans to continue to study other clock genes that are found mutated in ASD. More importantly, they recommend development of novel therapeutic strategies based on their findings.
The study is supported by grants from the National Institute of Health and the Winston and Maxine Wallin Neuroscience Discovery Fund.
The research team consists of Drs. Harry Orr, Alfonso Araque, Paulo Kofuji, and Jonathan Gewirtz (now at Arizona State University) from the U of M Medical School; Dr. Victor Jin from UT Health San Antonio; and Dr. Christos Gkogkas from BRI-FORTH in Greece.
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Materials provided by University of Minnesota Medical School. Original written by Kat Dodge. Note: Content may be edited for style and length.

New research from the University of Pennsylvania published in Nature Physics details the relationship between a disordered material’s individual particle arrangement and how it reacts to external stressors. The study also found that these materials have “memory” that can be used to predict how and when they will flow. The study was led by Larry Galloway, a Ph.D. student in the lab of Paulo Arratia, and Xiaoguang Ma, a former postdoc in the lab of Arjun Yodh, in collaboration with the labs of Douglas Jerolmack and Celia Reina.
A disordered material is randomly arranged at the particle-scale, e.g. atoms or grains, instead of being systematically distributed — think of a pile of sand instead of a neatly stacked brick wall. Researchers in the Arratia lab are studying this class of materials as part of Penn’s Materials Research Science & Engineering Center, where one of the program’s focuses is on understanding the organization and proliferation of particle-scale rearrangements in disordered, amorphous materials.
The key question in this study was whether one could observe the structure of a disordered material and have some indication as to how stable it is or when it might begin to break apart. This is known as the yield point, or when the material “flows” and begins to move in response to external forces. “For example, if you look at the grains of a sand castle and how they are arranged, can I tell you whether the wind can blow it over or if it has to be hit hard to fall over?” says Arratia. “We want to know, just by looking at the way the particles are arranged, if we can say anything about the way they’re going to flow or if they are going to flow at all.”
While it has been known that individual particle distribution influences yield point, or flow, in disordered materials, it has been challenging to study this phenomenon since the field lacks ways to “quantify” disorder in such materials. To address this challenge, the researchers collaborated with colleagues from across campus to combine expertise across the fields of experimentation, theory, and simulations.
For the experiments, the researchers track individual particles on top of a liquid-air interface akin to what coffee grounds floating on top of water look like, the researchers say. Then, they use a magnetic needle that moves back and forth to apply a shearing force. With this system, the researchers are able to systematically apply forces to 50,000 particles, track their detailed movement, and use complex image analysis to see if, for example, two neighboring particles remain next to one another after a shearing force is applied.
One of the challenges of this study was finding a metric that could help characterize disorder; to do this, the researchers turned to a concept known as excess entropy. While this idea has been used before to study simple liquids, its application in these larger granular systems — where temperature does not influence particle motion — was conceptually very new, says Galloway. “We’re taking thermodynamics and applying some of its concepts to something that people generally don’t think thermodynamics applies to,” he says.
To help connect their experimental results to theories of excess entropy, the Arratia lab worked with colleagues from the Reina group, who have theoretical expertise in non-equilibrium thermodynamics, as well as colleagues from the Yodh lab, who have experimented with excess entropy concepts to elucidate equilibrium and non-equilibrium systems. In addition, Jerolmack’s group shared their expertise in studying particle flow to help connect the complex experimental results with simulations.
One of the most significant findings from this study is that disordered materials can “remember” the forces that were applied to them and that this memory can be measured by looking at individual particle distributions. “If you zoom in and look at where all the different particles are, you can read out what memories are stored in there,” Galloway says.
The researchers also found that disordered materials lose this memory when a threshold of stress is surpassed, which occurs at the same time the material reaches its yield point and starts to flow. “If you apply a little bit of stress, the material will remember, and it will go back to the original state,” says Arratia. “But if you start shearing with more force, it starts losing its memory. That is exactly where we find that the material gives and begins to flow, and that critical stress is related to the loss of memory.”
While the concept of memory in disordered materials had been known for some time, the strong correlation seen in their results between particle distribution, flow, and memory surprised the researchers. Moving forward, they are planning to build on this work by studying other particle sizes and types, research that could help address how universal this concept is and how their results relate to thermodynamics and excess entropy more broadly.
Arratia adds that with such a wide range of systems that act like disordered materials, from eroding hillsides at risk of causing mudslides to living organisms such as biofilms, the possible implications for fields beyond thermodynamics are numerous. “I hope that this work will become something that we can apply to different, disparate systems from skin, mudslides, biofilms, and many things that are disordered and also flow,” Arratia says.
This research was supported by Penn MRSEC (NSF-DMR-1720530), NSF-DMR-1120901 and CMMI-2047506, and U.S. Army Research Office Grant W911-NF-16-1-0290.

A study by the Barcelona Institute for Global Health (ISGlobal), a centre supported by the “la Caixa” Foundation, assessed the levels of noise generated by road traffic and examined its impact on health in 749 European cities. The findings, published in Environment International, show that nearly 60 million adults are subjected to unhealthy levels of vehicle-generated noise. Compliance with the World Health Organisation (WHO) noise-level guidelines could prevent 3,600 deaths annually from ischaemic heart disease alone.
Road traffic is the main source of environmental noise. Previous research has linked environmental noise to a range of adverse health effects: sleep disturbance, annoyance, cardiovascular and metabolic disease, adverse birth outcomes, cognitive impairment, poor mental health and well-being, and premature mortality. Long-term exposure to road traffic noise can cause a sustained stress reaction, which results in the release of stress hormones and increases in heart rate, blood pressure and vasoconstriction, eventually leading to chronic diseases such as cardiovascular disease, depression and anxiety disorders.
For this study, data on European cities were retrieved from the Urban Audit 2018 dataset. Road traffic noise exposure was estimated using noise maps produced by countries and cities under the current European legislative framework (Environmental Noise Directive) or available from local sources (e.g. city governments and research institutions). For cases in which city-level data were not available, country-specific predictive models were developed and applied to estimate exposure to road traffic noise. Data on different causes of mortality for the year 2015 were retrieved from the Eurostat database.
The results showed that more than 48% of the 123 million adults (aged 20 years or older) included in the study were exposed to noise levels exceeding the WHO-recommended threshold. Specifically, the WHO recommendation states that the average noise level recorded over a 24-hour period should not exceed 53 decibels (53 dB Lden). The percentage of the population exposed to higher-than-recommended noise levels in Europe’s capital cities ranges from 29.8% in Berlin to 86.5% in Vienna, including 43.8% in Madrid and 60.5% in Rome.
Preventable Deaths and Annoyance
Building on previous research that established associations between noise and mortality caused by ischaemic heart disease, the researchers estimated that compliance with WHO guidelines would prevent more than 3,600 deaths each year from ischaemic heart disease alone.
The study also found that more than 11 million adults were highly annoyed by road traffic noise. Annoyance was defined as the repeated disturbance of everyday activities, such as communicating, reading, working and sleeping. In this sense, annoyance goes beyond mere inconvenience, as it can increase stress and eventually give rise to various health problems.
“Our results provide, for the first time, a comprehensive picture of European cities and a clearer understanding of why transport-generated noise is the second major environmental cause of adverse health outcomes in western Europe, after airborne particulate matter,” explained ISGlobal researcher Sasha Khomenko, lead author of the study. “Even so, we are convinced that the true health impact of traffic noise is much greater, as the lack of city-level data limits the health effects we can assess, thus leading to an underestimation of the impact. Moreover, the available data have only allowed us to analyse the population exposed to more than 55 dB Lden, whereas the WHO-recommended threshold is 53 dB Lden, and we suspect that adverse effects could occur even with exposure to lower noise levels.”
The team encountered methodological difficulties due to the heterogeneity and quality of the available data. The quality of each noise map was assessed, with most maps falling into the low or moderate quality categories; less than 17% of the maps were considered to be of good quality.
“The European directive on environmental noise made strategic noise mapping mandatory, but it did not set out a specific methodology or guidelines, so the results have been mixed,” commented Mark Nieuwenhuijsen, head of the Air Pollution and Urban Environment programme at ISGlobal and senior author of the study. “The EU member states have had a common methodology since January 2019, so we can expect to see much more comprehensive and accurate health impact assessments of traffic noise in the coming years.”
Consult Data for All 749 Cities
This study forms part of the European Urban Burden of Disease Project, which so far has produced rankings of mortality associated with air pollution and green space, respectively, in European cities. However, due to differences in methodologies and sources of traffic noise data, the results obtained for the various cities analysed are not considered to be comparable. As a result, a road-noise ranking was not produced, although all data have been posted on the project website, where values for all 749 cities can be consulted.

The researchers set out to see if there had been an increase in the numbers of older people who were reporting their first concerns about memory loss or cognitive decline to their doctor and what their chances of developing dementia were after consultation.
The study, published today in Clinical Epidemiology, looked at data from more than 1.3m adults aged between 65 and 99 years old, taken between 2009 and the end of 2018. The researchers identified 55,941 adults who had spoken to their GP about memory concerns and 14,869 people who had a record of cognitive decline.
For every 1,000 people that were observed for one year in 2009, there was one new case of cognitive decline being recorded. By 2018, for every 1,000 people that were observed for one year, there were three new cases of cognitive decline being recorded.
Lead author and PhD candidate Brendan Hallam (UCL Epidemiology & Health Care) said: “This is an important study which sheds new light on how prevalent memory concerns and cognitive decline are among the older generation in the UK and how likely these symptoms might progress to a dementia diagnosis.
“The study showed that while memory concern rates had remained stable, incidence of cognitive decline, a step beyond memory concern, had more than doubled between 2009 and 2018.
“There has been a drive in the past decade to encourage people to seek help earlier from their doctors if they are worried about their memory and we found that among those over 80, women and people living in more deprived areas were more likely to have a record of memory concern or cognitive decline, and their symptoms were more likely to progress to dementia diagnosis.”
The study also showed that within three years of following up a person from the date when the doctor reported a memory concern, 46% of people would go on to develop dementia. For people with cognitive decline, 52% would go on to develop dementia.
Co-author, Professor Kate Walters (UCL Epidemiology & Health Care) explained: “People who have been noted in their health records as having concerns about their memory are at just under 50% chance of developing dementia within the next three years.”
Brendan Hallam also outlined “Memory concerns and cognitive decline are not only hallmark symptoms of dementia, but they also predict a high risk of developing dementia. It is important for GPs to identify people with memory concerns as soon as possible to deliver recommendations to improve memory and allow timely diagnosis of dementia.”
The authors note one potential limitation of the present study is the potential variations in which GPs record memory concerns and memory decline. They also say more research is needed to better understand the discrepancy between rates of memory symptoms and cognitive decline in the general population and those recorded in primary care.
This work was carried out within the APPLE-Tree programme that is supported by the ESRC/NIHR [ES/S010408/1]. Brendan Hallam was funded by an ESRC studentship [ES/P000592/1].
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Materials provided by University College London. Note: Content may be edited for style and length.

Despite daily contact with Covid-19 patients early in the pandemic, some health professionals avoided falling ill. As a University of Gothenburg study shows, the explanation appears to be an antidote in the immune system: IgA antibodies to COVID-19.
To understand how the immune system builds up its defenses against COVID-19, a group of researchers at the University’s Sahlgrenska Academy monitored 156 employees at five primary care health centers, belonging to the Nötkärnan group in the Gothenburg area, for six months.
Recruited during April and May 2020, none of them had been vaccinated against COVID-19, and most of them met infected patients daily.
The reason why some of the staff did not contract the disease seems to have been that IgA (immunoglobulin A) was present in their respiratory tract. These antibodies, found naturally in the secretions of mucous membranes in the airways and gastrointestinal tract, can protect the body by binding to viruses and other invading organisms.
One in ten protected
The results of the study, published in the European Journal of Immunology, show that a third of the care workers developed antibodies to COVID-19. These subjects fell into two distinct groups based on antibody patterns and COVID-19 incidence.

Epilepsy, one of the most common neurological disorders, is characterized by the spontaneous repetition of seizures caused by the hyperactivity of a group of neurons in the brain. Could we therefore reduce neuronal hyperactivity, and treat epilepsy, by reducing the amount of energy supplied to neurons and necessary for their proper functioning? This was tested by a team led by scientists from the University of Geneva (UNIGE) and the EPFL. The researchers discovered that, in mice, the seizures were actually exacerbated. They observed that a reduction in the amount of energy led to an increase in the level of calcium in neurons, making them hyperexcitable. These dysfunctions could be corrected when mice were fed a ketogenic diet, which is rich in lipids and has been used since antiquity. This work is published in the journal eLife.
Our brain, which represents only 2% of our body weight, consumes more than 20% of the sugar we ingest. This considerable need for sugar provides the energy necessary for the function of the billions of neurons responsible for the emission and propagation of nervous messages, via electrical signals. This conversion of sugar, and more precisely of glucose, into energy is carried out by the mitochondria, small intracellular organelles considered as the “energy factories” of the cell.
The key role of the cell’s “energy factories”
The laboratory of Jean-Claude Martinou, professor in the Department of Molecular and Cellular Biology at the Faculty of Science, is interested in how mitochondria work. His group had already discovered the universal carrier that allows pyruvate, a product of glucose catabolism, to enter into mitochondria. He is now investigating the role of the mitochondrial pyruvate carrier (MPC) in neuronal activity and whether a defect in the transport of pyruvate in mitochondria could be linked to certain neurological diseases, notably epilepsy.
Epileptic seizures are the manifestation of cerebral hyperactivity resulting from hyperexcitation of neurons, often in the cerebral cortex. “It seemed interesting to us to test whether suppression of the mitochondrial pyruvate carrier, and thus the decrease in the amount of energy supplied by the mitochondria, could reduce neuronal hyperexcitability occurring during epileptic seizures,” explains Jean-Claude Martinou, last author of the study.
Mice lacking the MPC are prone to epileptic seizures
The biologists administered a pro-epileptic drug, capable of inducing epileptic seizures, to normal mice and to mice whose cortical neurons lacked the MPC. In normal mice, injection of a low dose of the drug did not induce seizures. On the other hand, and contrary to the initial hypothesis, in mice lacking the MPC, very severe, even fatal, seizures occurred as soon as low doses of the pro-epileptic drug were administered.
Upon further analysis of what was happening in these neurons, the biologists found that the neurons without MPC had abnormally high levels of calcium, a crucial element for the proper transmission of nerve messages. “Pyruvate imported into mitochondria not only plays the role of a fuel for the cell, but it also allows mitochondria to sequester calcium. It turns out that it is this second function that is involved in the triggering of epileptic seizures. Since it is no longer trapped by the mitochondria, the calcium remains free in neurons and its concentration increases, which makes the neurons hyperexcitable,” explains Carmen Sandi, professor at EPFL and coauthor of the study.
The secrets of the ketogenic diet
Since ancient times, patients suffering from epilepsy have found that a ketogenic diet, rich in fats and low in carbohydrates, allows them to avoid seizures. Ketone bodies, produced during a ketogenic diet or fasting, are produced by the breakdown of lipids in the liver. They are imported into the brain for which they represent an essential energy source, especially during a fast. They can enter mitochondria without the need of carriers and are used to provide energy.
“We found that MPC-deficient mice fed on a ketogenic diet or treated with ketone bodies had much less severe seizures. With this diet, the functions of mitochondria and neurons are restored, and the calcium level is normal,” said Marine Laporte, researcher in the Department of Molecular and Cellular Biology and co-first author of the study. This work, financed by the Swiss National Science Foundation and the Kristian Gerhard Jebsen Foundation, helps to explain the epileptic seizures frequently observed in patients with mitochondrial pathologies as well as to consider a treatment based on ketone bodies, less drastic than ketogenic diets.

Bea Ramiro began to study the sea snail species Conus rolani more or less by chance. Together with two fishermen she was collecting material in the waters off the Philippine island of Cebu in 2018.
At the time, researchers knew that poison from the sea snail species Conus magus could be used as a painkiller. It can replace morphine and opioids, and some patients experience fewer side effects. Therefore, Bea Ramiro hoped she could find a new sea snail species whose poison had a similar or possibly even better effect.
In order to study sea snails, Bea Ramiro had to collect a lot of snails of the same species. And once the fishermen had reeled in the net and the snails had been divided into groups according to species, she only had enough snails of the species Conus rolani to do a proper study.
Today, Bea Ramiro is glad that this large, white and brown snail six to seven centimetres long was the only species left.
Because a new study from the University of Copenhagen to which she has contributed shows that poison from Conus rolani can function as a painkiller. The researchers have learned that a particular substance from the poison can block out pain in mice for an even longer time than morphine.
“We have discovered a so-called toxin that blocks out pain in a completely different way than well-known drugs like morphine, and hopefully this will enable us to avoid some of the most damaging effects of morphine on humans,” explains Associate Professor Helena Safavi, who has headed the study.

Intense light activates proteins shown to protect against lung damage in mice, a discovery that could have major therapeutic implications for treating diseases like acute lung injury in humans, according to a new study from researchers at the University of Colorado Anschutz Medical Campus.
“Acute lung injury has a mortality rate of 40%,” said the study’s lead author Tobias Eckle, M.D., professor of anesthesiology at the University of Colorado School of Medicine. “No specific therapy exists, and novel treatment options are needed.”
The study was published this week in the American Journal of Physiology — Lung Cellular and Molecular Physiology.
Eckle’s team, which previously demonstrated that light can protect against cardiovascular disease, housed mice under intense rather than ambient light for seven days. This prompted a strong increase in the trough and peak levels of the pulmonary circadian rhythm protein — Period 2 or PER2.
If the protein was deleted in a specific lung cell known as the alveolar type 2 cell, acute lung injury was fatal. If the protein was not deleted, 85% of the mice survived. Alveolar type 2 cells have long been recognized as playing an important role during acute lung injury but have never been linked to the light regulated protein PER2.
The study also showed that intense light therapy reduced lung inflammation or improved the function of the alveolar barrier — the blood-air barrier — in lung infections. Researchers saw the same reaction when using the flavonoid, nobiletin, found in orange peel, which also enhances the amplitude of PER2.
At the same time, the researchers found that intense light stimulated production of the BPIFB1 protein, known to be anti-bacterial and secreted within the mucus membranes of the large airways. They believe this also likely plays a role in protecting the lungs.
Discovering that intense light can protect against lung damage, Eckle said, is important due to the lack of therapies currently available to treat the condition.
“If you develop lung injury there is essentially no good therapy left,” he said. “Our study has shown that intense light elicited lung-protective mechanisms could lead to new therapies even after the onsetof acute lung injury in the future.”
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Materials provided by University of Colorado Anschutz Medical Campus. Original written by David Kelly. Note: Content may be edited for style and length.

Black and Hispanic individuals who experience a witnessed cardiac arrest at home or in public are substantially less likely than white individuals to receive cardiopulmonary resuscitation (CPR) from a bystander, according to a study being presented at the American College of Cardiology’s 71st Annual Scientific Session.
Nearly 1,000 Americans suffer from cardiac arrest (when the heart suddenly stops beating) outside of the hospital each day, with most occurring at home. People who receive CPR immediately are two to three times more likely to survive with brain functioning intact compared to those who do not receive CPR immediately. This nationwide study found that Black and Hispanic individuals were 41% less likely than white individuals to receive CPR when suffering cardiac arrest in public and 26% less likely to receive CPR when the cardiac arrest occurred at home.
“It’s critically important to understand who gets bystander CPR for a cardiac arrest and how we can improve those rates,” said Paul S. Chan, MD, professor of medicine at the University of Missouri-Kansas City School of Medicine and the Saint Luke’s Mid America Heart Institute, and the study’s senior author. “We found that bystander CPR rates are much higher in white communities compared with Black communities. In addition, there were patient-level disparities in getting bystander CPR regardless of the type of community the person was in, even though there were, in all of these cases, bystanders who could have provided aid and assistance.”
The researchers analyzed over 110,000 cardiac arrests that occurred in the U.S. between 2013-2019. All events included in the analysis occurred outside of a hospital setting but were witnessed by a bystander. Researchers found that when the cardiac arrest occurred in public, 46% of Black and Hispanic people received CPR compared with 60% of white people. At home, 39% of Black and Hispanic people received CPR compared with 47% of white people. The patterns were the same regardless of the racial makeup or income level in the neighborhood where the cardiac arrest occurred.
“This disparity wasn’t only present in majority white communities, but also in majority Black and Hispanic communities,” Chan said. “A white person going into cardiac arrest in a community that was more than 50% Black and Hispanic was still more likely to get bystander CPR than a Black or Hispanic person in that community.”
Although the study did not examine specific factors behind CPR rates, the researchers said access to CPR training likely plays a role, since people are more likely to attempt CPR if they have been trained in it. The cost of CPR training, as well as when and where it is offered, may pose barriers for some communities.
“We need to think creatively about how to offer CPR instruction to vulnerable populations that have historically not received training and focus on conducting more trainings in the communities where the disparities are greatest,” Chan said. “For example, we could make CPR training available at little to no cost and do it at times and locations that are more convenient, such as Black churches or Hispanic community centers, or allow many people to be trained at once, for example as part of a Juneteenth or Martin Luther King Jr. Day event.”
In addition, researchers said potential variability in whether 911 dispatchers instruct bystanders on giving CPR while waiting for an ambulance and rates of dispatcher-assisted CPR could also be affected by language barriers. Implicit or explicit bias could also factor into bystanders’ willingness to assist people of color, Chan said, adding that it is important for images and manikins used in CPR training to reflect a diversity of racial groups.
Researchers said that overall rates of CPR were relatively low across all racial groups in the study. Even though bystanders were present in all cases, data showed CPR was attempted less than half the time.
“We still have a long way to go in getting the message out that people need to start CPR and not just call 911,” Chan said.
In the past decade, recommendations have shifted to focus on hands-only CPR, in which a bystander administers chest compressions at a rate of 100-120 compressions a minute but does not pause to give mouth-to-mouth, while waiting for paramedics to arrive. CPR is recommended for anyone who suddenly collapses and is unresponsive; checking for a pulse is no longer considered necessary before starting CPR.
Researchers plan to examine racial disparities in CPR rates in public settings to find out whether the type of location (for example, a gym versus a workplace) impacts the likelihood of receiving CPR.

Shaving critical minutes off the time it takes to diagnose a heart attack and begin treatment could be as simple as the push of a button. Using a programmable button to page a phlebotomist for a blood draw reduced the time it took to identify patients suffering a heart attack by more than 11 minutes on average, in a study presented at the American College of Cardiology’s 71st Annual Scientific Session.
According to researchers, the study represents the first time programmable button technology — designed to help consumers easily order products online — has been applied in a medical setting.
“Often in medicine you need a rapid response, but there are many processes that require numerous laborious steps that take time, and in the setting of a potential heart attack, time is muscle. The longer the wait, the more damage there is to the heart muscle and less chances for recovery,” said Milind R. Dhond, MD, medical director of cardiovascular medicine at NorthBay Healthcare in Fairfield, California, and the study’s lead author. “This approach potentially can cut out many steps. It’s using innovative technology in an innovative way by bringing together the technology and the application to improve the process.”
To diagnose a heart attack, doctors look at the level of troponin in the blood as an indicator of damage to the heart muscle. Drawing blood and sending it to the lab for analysis is integral to the process used to determine whether a heart attack is occurring before clinicians intervene to open the blocked artery.
Researchers adapted the Internet of Things (IoT) button developed by Amazon Web Services to page an on-call phlebotomist for a blood draw whenever a patient arrived in the hospital’s emergency department with chest pain. The device is a physical, handheld button that communicates wirelessly, triggering a pre-programmed process when pressed — a process similar to the “Buy now with 1-click” option Amazon developed for its web-based product ordering system. Having the button handy allowed triage nurses to rapidly summon a phlebotomist for patients with chest pain while continuing the rest of the patient intake process.
For the study, researchers compared the records of 2,098 patients who presented to the NorthBay emergency department with chest pain between January 2020 and April 2021, when the IoT button was in use, with records from 1,614 patients who presented to the same emergency department with chest pain in 2019 prior to the implementation of the button. The demographics and cardiovascular risk factors of the two groups were similar.