Category: Medicine

Technion-developed technology allows patients to detect dangerous sleep disorders from home using a simple wearable device and artificial intelligence, eliminating need for costly lab tests.

Nearly 40% of the global population suffers from sleep-related disorders, according to the World Health Organization. Among the most serious, and often undiagnosed, conditions is sleep apnea, a disorder estimated to affect nearly one billion people worldwide.

Diagnosing sleep apnea traditionally requires an overnight stay in a specialised sleep laboratory, such as the facility at Ichilov Hospital in Tel Aviv. 

Patients are connected to multiple sensors that monitor brain activity, breathing patterns, heart rate, and oxygen levels throughout the night. The process is complex, expensive, and often inaccessible, with costs ranging from $1,170 to $11,700 depending on the clinic.

An Israeli startup, Sleep AI, aims to change that. Developed by researchers at the Technion, the technology uses a lightweight oximeter linked to a mobile app and powered by artificial intelligence. Patients can complete the test from home by simply wearing the device overnight while data is uploaded to the company’s cloud platform for analysis.

Within minutes, physicians receive a detailed medical report that not only evaluates sleep quality, but also maps sleep architecture, identifies signs of sleep apnea, and assesses cardiovascular risks linked to nighttime oxygen deprivation.

Unlike consumer smartwatches, Sleep AI is designed as a medical-grade diagnostic tool. In clinical testing conducted in sleep centres, the system demonstrated an overall accuracy rate of 89% for detecting sleep apnea, rising to 99% for moderate and severe cases.

The company is now pursuing international regulatory approvals with the goal of making sleep apnea diagnosis faster, cheaper, and more widely available — potentially even covered by health insurance in the future.

By moving diagnosis from the sleep lab to the home, Sleep AI hopes to make sleep health screening a routine part of modern medical care.

Researchers at the Technion have discovered how changes in genetic regulatory sequences can lead to alterations in the form and structure of animals – even when genetic regulatory systems are stable and resistant to change. The study, published in Science Advances, was led by Dr. Ella Preger-Ben Noon and Ph.D. candidate Areej Said-Ahmad from the Ruth and Bruce Rappaport Faculty of Medicine.

Photo Credit: Rami Shelush

The loss of morphological traits is a common phenomenon in evolution. Well-known examples include the loss of legs in snakes and the loss of eyes in cavefish. In many cases, such changes do not result from the loss of the genes responsible for these traits, but rather from changes in how those genes are regulated during development. However, many developmental genes are controlled by multiple regulatory sequences with overlapping activity, forming a stable and robust regulatory system.

This study addresses a fundamental question in biology: how do organisms change form over the course of evolution despite the presence of stable genetic regulatory systems? These systems rely on DNA sequences known as enhancers, which activate genes at precise times, levels, and locations during development. Enhancers often act redundantly, so that if one is impaired, others can compensate and maintain proper gene expression. This redundancy confers stability and resistance to change, but also raises a paradox: how do changes in gene expression still occur, leading to alterations in the shape and structure of organs?

To address this question, the researchers focused on Drosophila flies, particularly the species Drosophila sechellia, in which tiny hair-like structures (trichomes) have disappeared from the larval body during evolution. This trait is controlled by the shavenbaby gene, whose expression is regulated by multiple enhancers. Contrary to expectations that such a system would protect gene expression from change, the researchers found that four different enhancers of shavenbaby lost their activity over the course of evolution, each through a distinct mechanism.

Through detailed DNA sequence analysis and functional experiments, the researchers found that the loss of enhancer activity occurred via different molecular mechanisms, including deletion of essential sequences, loss of binding sites for activators and gain of repressor binding sites, acquisition of a silencer, and even the unmasking of pre-existing repression. In other words, the same evolutionary outcome – the loss of gene expression – was achieved through different molecular pathways within the same genomic region.

These findings demonstrate that the same evolutionary outcome can arise through multiple routes. The presence of multiple enhancers, while they contribute to stable gene expression, also creates points of vulnerability where mutations can reduce their activity. The study shows that stability does not necessarily act as a barrier to evolution, as there are diverse molecular ways to circumvent it. These insights are relevant to a wide range of biological systems and deepen our understanding of how variation in form and structure arises in nature.

In addition to fatigue and increased hunger, living with constant sleep deprivation and stress has other effects, some long-term. Experts explain the risks – and how to limit the damage, or at least some of it

By now, this has become a daily challenge: how many hours of sleep can one get in a night riddled with air-raid alerts, racing to shelter and attempts at shuteye before being woken up again. And not just how many hours in total, but also how long one can sleep uninterrupted. All this comes before the real challenge – staying awake during the day, functioning as normally as possible and perhaps even forgetting – until the next siren – that this is an open-ended state of emergency. 

This reality has direct and indirect health implications, some immediate and clearly felt in the ability to function and in planning and concentration. In the longer run, this stressful reality, marked by constant alertness and sleep deprivation, could have a cumulative effect on other bodily systems, including the immune and cardiovascular systems, as well as mental health. 

“The professional term for what has been happening now is ‘sleep deprivation’ due to air-raid alerts,” says Prof. Yaron Dagan. “This deprivation harms two main things: one is cognitive – that is to say, everything related to thinking, perception, problem-solving, concentration and memory; the other is emotional – people are gloomier, less patient, and generally in a worse mood, which sometimes results in reckless decision-making.”

Dagan, director of the Institute for Sleep Medicine at Assuta Medical Centers, explains that healthy sleep is crucial for waking life, particularly for our cognitive system, “which reboots brain memory in order to clear it for the next 24 hours. This activity takes place in several areas in the brain, and without uninterrupted or adequate sleep – the processes served by sleep are impaired.” One stage of sleep, he emphasises, is crucial for emotional processing, learning and memory formation. “This stage occurs in 90-minute cycles, and with sleep deprivation it’s disrupted, affecting our thinking and behaviour when awake.”

Is there anything that can be done, considering that it is entirely unclear how long this routine will continue? Perhaps a nap here and there? “In principle, sleep is not a bank – you cannot not sleep for a week and then fill the deficit by sleeping for a week,” says Dagan. “What we recommend is what’s called a ‘combat nap’ – a planned 30-45-minute nap to replenish your batteries. Even if someone can’t doze off, simply lying down, closing one’s eyes and relaxing is enough. This is the best way to deal with this sleep deprivation. It cannot fully replace nighttime sleep, but it certainly helps you feel refreshed.” 

Proper or healthy sleep is not just a matter of quantity; uninterrupted sleep is just as important as getting enough hours. “Sleep that is too short or interrupted – both have the same effects and cause the same harm as sleep deprivation,” explains Prof. Giora Pillar, head of the sleep clinic in Clalit Health Services’ Haifa District and sleep researcher at the Technion’s Faculty of Medicine. “There have been studies on this. In one, students were allowed to sleep for eight hours, but their sleep was interrupted. The damage was found to be the same.” 

A vicious cycle

The immediate effects are not limited to fatigue and exhaustion. Along with sleep deprivation, unending stress is not only mental but also physiological, affecting many bodily systems. When a person remains alert for an extended period, high levels of stress hormones such as cortisol and adrenaline are secreted. Chronic exposure to these hormones can harm the immune system, increase inflammation and blood pressure and impair cardiovascular function. In addition, stress has been linked to sleep disorders (creating a vicious cycle) and to the worsening of chronic diseases such as asthma and diabetes, as well as to an increased risk of heart disease. Over time, this condition may erode physiological systems and cause an overall deterioration in health. 

Over the past two and a half years, with one operation following another and one air-raid siren after another, stress has become a familiar term. In general, it refers to a physical and emotional reaction to threatening or dangerous situations – not just wartime or physical danger, but also everyday pressures such as work overload, mental overload or difficulties in other aspects of life. In today’s reality, however, it’s almost impossible to isolate stress from sleep deprivation. “Stress is a mediating factor,” says Prof. Pillar. “It causes sleeplessness in itself, as well as many other complications.” 

In many respects, the symptoms of stress and sleep deprivation overlap or reinforce one another. In part, this connection is evident in eating patterns. Like stress, sleep deprivation is a risk factor. When sleep is reduced, levels of ghrelin (the hunger hormone) soar, while levels of leptin (the satiety hormone) fall. The result is increased hunger, especially for high-calorie, sugary and fatty foods. A 2004 study released by researchers from the University of Chicago demonstrated this clearly. The researchers hypothesised, based on their findings, that the body interprets sleep deprivation as a state of energy deficit – even if that’s not exactly the case.

Chronic overeating under such conditions can lead to weight gain, increased insulin resistance and a higher risk for type 2 diabetes, cardiovascular disease and other metabolic disorders. In addition, ongoing caloric excess, driven by fatigue, also hinders the body’s ability to regulate metabolism and balance energy. 

And the list of risks does not end there. According to Pillar, sleep deprivation also affects the immune system. “Sleepless patients or patients who sleep poorly, that is to say: people who suffer from chronic sleep disorders, are already suffering from irreversible complications,” he warns. “We will see higher rates of high blood pressure, more cases of metabolic syndromes, more diabetes, more obesity, more strokes and more cancer.” 

To a certain extent, these symptoms are reversible, as reality has proven. “Soldiers who sleep too little and then sleep through the weekend are not at risk in the long term,” Pillar illustrates. “Medical interns who sometimes work two 26-hour shifts a week make up for lost sleep and don’t develop long-term complications. That is to say, it’s reversible – up to a point.” 

However, given the current reality, which has already lasted more than a week and even a fortnight, the question becomes where the line lies beyond which the damage becomes irreversible, or only partly reversible. This is a crucial question. “We are already seeing patients whose diabetes is no longer balanced,” he says, “or who have high blood pressure.” 

A 2016 study published in the International Journal of Cardiology found a clear link between sleep duration and coronary heart disease. The findings indicate that people who sleep seven to eight hours per night are at low risk, with every one-hour reduction associated with an 11 percent increase in the risk of heart disease. These findings were reaffirmed last November in another study, published in BMC Cardiovascular Disorders, which indicated that people who sleep six hours or less are at almost twice the risk of dying from kidney or heart disease compared with those who sleep longer. 

An immune system out of balance

Over the past two decades, many studies have examined the link between sleep quality and immune system function. Among other findings, people who sleep less than six hours a night produce fewer antibodies after vaccination; on the morning after a sleepless night, a significant increase is seen in the production of inflammatory cytokines – proteins secreted by immune cells in response to infection or injury; and, in general, proper sleep strengthens anti-inflammatory and anti-viral reactions, while inflammatory signals from the immune system affect the structure and depth of sleep.

According to a 2019 study published in Nature Reviews Immunology, sleep deprivation increases activity in the sympathetic nervous system (responsible for the body’s response in situations of threat and danger), which in turn raises stress hormone levels and releases inflammatory cytokines. It was found that in chronic sleep disorders, the overall level of inflammation in the body increases, while antiviral responses grow weaker. 

“Sleep deprivation is documented as one of the main biological factors affecting the immune system (when not diseased),” says Prof. Cyrille Cohen, head of the laboratory of immunology and immunotherapy and dean of Bar-Ilan University’s Faculty of Life Sciences. “In principle, conditions such as stress and sleep deprivation do not weaken every component in the immune system but rather cause an imbalance in its function.” He says this may manifest in several ways. “For instance, you’re at a slightly higher risk of certain infections, mainly respiratory – and the recovery process may also be slower.” However, Cohen emphasizes that “the effect is usually mild, and varies greatly from person to person.”

Technion and top US universities unveil implantable ‘living pancreas’ that senses glucose, produces insulin and evades immune response, paving the way for self-regulating, long-term diabetes treatment without daily injections

A multinational research team led by an Israeli engineer and involving top U.S. universities has unveiled a pioneering implantable device that could someday eliminate the need for daily insulin injections for people with diabetes.

The study, published Jan. 28 in Science Translational Medicine, describes a living, cell‑based implant that functions as an autonomous “artificial pancreas.” Once placed in the body, the device continuously monitors blood glucose levels, produces insulin internally and releases exactly what the body needs — without external pumps, injections or patient intervention.

The breakthrough centers on a novel protective technology researchers call a “crystalline shield”, engineered to prevent the body’s immune system from rejecting the implant — a major hurdle that has stymied cell‑based therapies for decades. The shield allows the implant to operate reliably for years.

Tests in mice showed effective long‑term glucose regulation, and studies in non‑human primates confirmed that the cells inside the implant remain viable and functional, the researchers said. Those results, they added, provide strong support for future clinical testing in humans.

The work was led by Assistant Professor Shady Farah of the Technion — Israel Institute of Technology’s Faculty of Chemical Engineering, in collaboration with scientists at the Massachusetts Institute of Technology, Harvard University, Johns Hopkins University and the University of Massachusetts. The collaboration traces back to Farah’s postdoctoral work beginning in 2018 at MIT and Boston Children’s Hospital/Harvard Medical School, under tissue‑engineering pioneers including Robert Langer, a co‑founder of Moderna.

Farah’s co‑first authors on the paper are Matthew Bochenek of MIT and Joshua Doloff of Johns Hopkins. Other contributors include Technion researchers Dr. Merna Shaheen‑Mualim and former master’s students Neta Kutner and Edward Odeh, who also helped adapt the work for publication.

While the initial focus is on diabetes, the team emphasized that the platform could one day be adapted to deliver other biologic therapies continuously, offering a new approach to chronic conditions such as hemophilia and other metabolic or genetic diseases.

If successfully translated into human treatment, experts say the technology could reshape the management of chronic illness by replacing lifelong drug regimens with self‑regulated, living therapeutics working continuously inside the body.

What if a single breath — or a small wearable patch — could reveal disease long before symptoms appear? For years, Prof. Hossam Haick of the Technion – Israel Institute of Technology has been turning that revolutionary idea into a reality. By identifying invisible chemical signals emitted by the human body, Prof. Haick has helped transform how illness can be detected: faster, earlier, and without invasive tests.

Global Recognition for Transformative Innovation

His pioneering research has opened new paths for diagnosing cancer, neurological disorders, infectious diseases, and more — using breath, skin, and advanced sensing technologies rather than needles or radiation. That life-changing work has led to Prof. Haick’s election as a Fellow of the U.S. National Academy of Inventors. This prestigious distinction is widely recognized as one of the highest professional honors for academic inventors worldwide, reflecting broad international recognition of Prof. Haick’s scientific achievements, groundbreaking inventions, and far-reaching impact on health care, technology, and education.

Prof. Haick is among a select group of researchers and inventors worldwide who have completed the full innovation cycle: from basic scientific discovery, through technological development, to real-world impact that touches the lives of millions.

In an academic landscape where basic and applied science are often separate, he stands out as someone who bridges the two worlds, translating deep scientific discoveries into clinical and technological tools with global influence.

His work led to the emergence of a new scientific field — volatilomics — which studies the chemical “fingerprints” the body emits through breath and skin.

A New Vision for Early, Noninvasive Diagnosis

This groundbreaking discovery has led to fast, noninvasive tests that give accurate results in just minutes and are used in medical centers worldwide. Additionally, Prof. Haick’s team has created smart patches that can monitor health from afar, along with new imaging tools that use chemical signals instead of radiation. These tools help doctors catch diseases early and provide personalized health care.

Beyond the Laboratory

Prof. Haick has also translated innovation into real-world impact. He holds dozens of patents and has founded several startup companies that bring advanced diagnostics, wearable devices, and electronic sensing technologies into practical use. He also founded and leads seven European Union research consortia, uniting more than 70 partners across four continents to accelerate the development and clinical adoption of advanced medical technologies.

Educating the Next Generation of Innovators

Equally significant is Prof. Haick’s role as an educator and mentor. He has published more than 500 scientific papers, authored two books, and supervised over 110 graduate and postdoctoral researchers, many of whom now lead research groups and technology companies of their own. His pioneering online course on nanotechnology and nanosensors — the first of its kind — has reached more than 1 million learners in 87 countries, extending Technion research and educational impact worldwide.

A Moment of Great Honor

Prof. Haick will be formally inducted into the NAI on June 4, 2026, at the Dolby Theatre in Los Angeles. During the ceremony he will receive a medal, certificate, lapel pin, and rosette from the NAI President and the representative of the United States Patent and Trademark Office. This extraordinary achievement reflects both Prof. Haick’s personal excellence and the Technion’s enduring mission to advance science that improves lives around the world.

Prof. Ido Kaminer and Prof. Yehonadav Bekenstein of the Technion have been awarded ERC Proof of Concept (PoC) grants by the European Research Council. The grants are expected to lead to a major leap forward in low-radiation medical imaging and in the precise mapping of biological tissues.

Two young researchers from the Technion have won the prestigious ERC PoC grants from the European Research Council (ERC). Proof of Concept grants are feasibility grants designed to promote the transition from academic research to application and commercialization, including the establishment of a startup company, and are awarded only to researchers who have previously received ERC grants. Grant amount: €150,000 each.

The two recipients are Prof. Ido Kaminer from the Andrew and Erna Viterbi Faculty of Electrical and Computer Engineering and Prof. Yehonadav Bekenstein from the Faculty of Materials Science and Engineering. Both joined the Technion faculty in the same year, 2018, and in 2025 inaugurated a joint interfaculty laboratory: the Quantum Microscopy Lab. This innovative lab is equipped with state-of-the-art microscopes capable of detecting quantum phenomena that cannot be studied by other means. The laboratory, which also includes Dr. Michael Krüger from the Faculty of Physics, was established following the Technion’s success in a call issued by the National Authority for Technological Innovation, with support from the Helen Diller Quantum Center at the Technion.

Prof. Yehonadav Bekenstein, a graduate of the Hebrew University of Jerusalem, joined the Technion faculty after a Rothschild postdoctoral fellowship at the University of California, Berkeley. He is considered a leading scientist in materials discovery, specializing in light-emitting nanomaterials and perovskites  the technology at the heart of the new sensor that earned him the grant. His scientific work has been recognized with a series of prestigious awards, including the Krill Prize for Excellence in Scientific Research and the Goldberg Prize from the Technion.

The grant Prof. Bekenstein received will be used to advance MagicLayer a sensor for a new generation of medical imaging with minimal radiation exposure. The scientifc idea of the developed technology is based on nanocrystals and ultrafast quantum light emission.

Sensors used in medical imaging are currently limited by their response speed. This relative slowness leads to the loss of valuable information and forces physicians to increase patients’ exposure to radiation. Standard crystals used in industry have reached the limits of their classical physical capabilities and struggle to deliver the field’s “holy grail,” which is a time resolution of 10 picoseconds. This is where the new sensor comes in; it is based on arrays of nanocrystals developed at the Technion. The light emitted from these arrays is correlated and responds significantly faster than existing technologies. The technology is relevant not only to medicine but also to improving electron microscopes and to real-time monitoring of radioactive gases in nuclear facilities. The research team behind the winning proposal includes Dr. Georgy Dosovitskiy, Dr. Rotem Strassberg, and Shai Levy.

Prof. Ido Kaminer, who completed all of his degrees at the Erna and Andrew Viterbi Faculty of Electrical Engineering, returned as a faculty member after a postdoctoral fellowship at MIT. He is a world-renowned scientist in photonics, electron microscopy, light–matter interactions, quantum information processing, and mathematical discoveries using artificial intelligence. His scientific work has earned him numerous honors, including the Stanisław Lem Prize, the Schmidt Science Polymath Award, the Blavatnik Award, the Krill Prize, and election to the Israeli Young Academy.

His new grant will be used to develop Stork – an innovative module that improves the performance of transmission electron microscopes (TEM). These instruments are widely adopted for biological applications as well as semiconductor metrology and inspection. However, their capabilities across both fields are highly limited owing to low contrast, which hinders resolution and throughput. The Stork technology makes it possible to introduce light directly onto the studied specimen, while also efficiently collecting the light emitted from it, thereby enhancing the TEM imaging capabilities dramatically. This paradigm shift in TEM technology will provide unprecedented information for imaging biological tissues and atomic-scale defects in electronic devices. The research team behind the winning proposal includes Dr. Tal Fishman, Dr. Michael Yannai, and Dr. Raphael Dahan, as well as students Marta Rozhenko and Rotem Elimelech.

Technion researchers find protein-disposal system in brain cells may actually spread toxic proteins linked to Alzheimer’s; instead of destroying them, cells sometimes expel them to neighbouring tissues, potentially accelerating disease progression in brain

In a surprising discovery, researchers at the Technion–Israel Institute of Technology have found that a cellular system tasked with disposing of toxic proteins—crucial in preventing Alzheimer’s disease—may actually be helping the disease spread across the brain.

The study, led by Professor Michael Glickman, dean of the Technion’s Faculty of Biology, and postdoctoral researcher Dr. Ajay Wagh, reveals that, instead of breaking down defective proteins inside the cell, neurons may be pushing this “trash” into surrounding brain tissue. Their findings were published recently in the journal Proceedings of the National Academy of Sciences (PNAS).

At the heart of the discovery is a mutated version of the protein ubiquitin, called UBB+1. While healthy ubiquitin helps cells identify and eliminate damaged proteins, UBB+1 disrupts this process and leads to toxic buildup, which is one of the hallmarks of Alzheimer’s disease.

Normally, a cellular protein called p62 helps neutralise this threat by packaging UBB+1 into protective vesicles, keeping it from damaging the cell. The vesicles can then take one of two paths: they’re either sent to the cell’s internal recycling centre (the lysosome), or they’re expelled into the space between cells.

It’s the second option that poses a danger. According to the Technion team, once UBB+1 is released into the brain’s extracellular fluid, fragments of the toxic protein can leak out and be absorbed by neighbouring neurons—potentially accelerating the spread of Alzheimer’s throughout the brain.

“We all want someone to take out the trash,” Glickman said. “But in this case, the cells are dumping their trash on their neighbors. Although this solves an acute problem for the individual cell, it may cause long-term damage to the entire tissue.”

The discovery could pave the way for earlier diagnoses of Alzheimer’s, possibly through testing cerebrospinal fluid for markers of UBB+1. It may also open the door to personalised treatments targeting the faulty disposal pathway.

The research was funded by the Israel Science Foundation and the European Research Council.

Study by researchers at the Technion finds that injecting cancerous serum in mice decreased cardiac fibrosis — paving the way for innovative therapies

A discovery by Prof. Ami Aronheim and his team at the Technion–Israel Institute of Technology shows that the growth of cancerous tumors may actually combat cardiac dysfunction and reduce fibrosis, the scarring process that stiffens the heart muscle.

“The failing heart can beat much better in the presence of cancer cells or a tumor,” said lead investigator Aronheim, dean of the Technion’s Ruth and Bruce Rappaport Faculty of Medicine, speaking to The Times of Israel.

“This is very surprising,” Aronheim said.

Currently, no drugs exist that can reverse fibrosis or improve the heart muscle once it has been damaged, he explained.

The new findings could open the door to the development of innovative and groundbreaking therapeutic approaches.

PhD students Lama Awwad and Laris Achlaug led the research, which was recently published in JACC: CardioOncology, a peer-reviewed journal of the American College of Cardiology.

Heart disease and cancer are the two most significant causes of death in Israel, according to the Health Ministry. While they have been considered separate diseases, researchers now confirm that they are highly connected — and they affect each other’s outcomes.

The diseases also share similar risk factors, including smoking, obesity, diabetes, environmental factors and aging.

“These are two diseases that are all around us, and that people we know suffer from,” Awwad, 28, told The Times of Israel in a recent Zoom interview together with Achlaug.

Moreover, Awwad said, the two conditions share similar mechanisms, which involve inflammation, growth signals, and survival.

Heart disease is a cancer-spreader

In research conducted by Aronheim’s lab five years ago, the scientific team found that a stressed heart can actually accelerate the growth and spread of cancer.

“When we first looked at how heart failure affects cancer, we showed that a damaged heart can make the cancer more aggressive and more metastatic,” Aronheim said.

This can happen because cytokines, chemical messengers that immune cells use to communicate with one another, are released by the heart. These cytokines promote the growth and spread of cancer cells.

However, while doing these experiments, the researchers noticed an unexpected — and inverse — result. In tumor-bearing mice, heart failure was “much less pronounced.”

“This led us to start to think about studying the other direction, how cancer affects heart failure,” Aronheim said.

The scientists implanted cancer cells in mice with heart failure.

“We were surprised to find an improvement not only in the ability of the mice’s hearts to pump blood but also an improvement in the muscular system,” said Achlaug, 31. “It was very motivating.”

Moreover, the extent of fibrotic, or scarred, tissue was significantly decreased in a short period of time.

“This was a breakthrough for us,” Aronheim said. “Of course, it was clear to us that it’s not a possible treatment to use another disease for the sake of repairing heart dysfunction. So we had to study the mechanism.”

The researchers hypothesized that exposing immune cells to cancer cells can yield a process called “immunomodulation,” which enables the immune system to regenerate and begin fighting inflammation.

To test their hypothesis, the scientists injected serum extracted from the blood of the tumor-bearing mice into heart-diseased mice. These mice exhibited rapid improvements in cardiac function and reduced fibrosis.

The researchers analyzed the molecules in the serum and found that the cytokines were released from natural killer cells, also known as NK cells. These are a type of immune cell that attacks foreign cells when activated.

The cytokines activated macrophages, a type of white blood cell that plays a crucial role in consuming pathogens. The cytokines helped reprogram the macrophages into anti-inflammatory, healing-focused cells.

The work of Aronheim’s lab has shed light on the common biological pathways between cancer and heart disease, said Izhak Kehat, head of the department of physiology, biophysics, and systems biology, in the Technion’s Faculty of Medicine, who was not involved in the project.

“Tumors can release signals that affect the whole body’s repair and immune response,” Kehat said. “And some of these signals can be harnessed to improve heart disease.”

Awwad said the research team has a patent on the serum with “a cocktail of positive factors.”

“We have to test its toxicity and prove that it’s safe to use,” Achlaug explained.

Breaking down social — and scientific — barriers

Awwad, who lives in Tamra, an Arab town in the Galilee, and Achlaug, who lives in Kfar Kama, a Circassian town 60 kilometers (37 miles) away, spoke about their challenges as researchers and as mothers of small children.

They credited their husbands, who are both engineers (Awwad’s husband works at Google and Achlaug’s husband works at Apple), and “who can sometimes work from home during the week,” Achlaug said.

“And also when we take our work home on weekends,” Awwad added.

She noted that approximately 50 percent of the Technion’s graduate students are women, and about 50% of those are Arabs. However, she said there are few female researchers because of the “long hours we spend in the lab.”

In the Circassian community, which numbers 5,000 in Israel, Achlaug said there are only two other women who have PhDs.

When they attend scientific conferences abroad, Awwad said that people are less curious about them as women and more interested in their lives as Arabs in Israel.

“People ask me a lot of questions about ‘what’s really happening,’” Awwad said. “It’s good because I like to calm them down.”

Achlaug said they never encountered hostility at conferences, but she was “a little nervous” when presenting her paper to a group of scientists from Beirut.

“But there’s a sense of honor among researchers to focus on science,” she said.

“Then, afterwards,” Awwad said, “they can have their opinions.”