Publisher Health

Breast cancer is one of the most common forms of cancer, according to the World Health Organization (WHO). Each year, around 2.3 million people worldwide contract the disease. If doctors detect breast cancer early enough, patients usually respond well to treatment. However, things become much more difficult if the cancer has already metastasised. Metastasis occurs when circulating cancer cells break away from the original tumour, travel through the body via blood vessels and form new tumours in other organs.
To date, cancer research has not paid much attention to the question of when tumours shed metastatic cells. Researchers previously assumed that tumours release such cells continuously. However, a new study by researchers at ETH Zurich, the University Hospital Basel and the University of Basel has now come to a surprising conclusion: circulating cancer cells that later form metastases mainly arise during the sleep phase of the affected individuals. The results of the study have just been published in the journal Nature.
Circadian rhythm-regulated hormones control metastasis
“When the affected person is asleep, the tumour awakens,” summarises study leader Nicola Aceto, Professor of Molecular Oncology at ETH Zurich. During their study, which included 30 female cancer patients and mouse models, the researchers found that the tumour generates more circulating cells when the organism is asleep. Cells that leave the tumour at night also divide more quickly and therefore have a higher potential to form metastases, compared to circulating cells that leave the tumour during the day.
“Our research shows that the escape of circulating cancer cells from the original tumour is controlled by hormones such as melatonin, which determine our rhythms of day and night,” says Zoi Diamantopoulou, the study’s lead author and a postdoctoral researcher at ETH Zurich.
Adjusting therapies to the tumour
In addition, the study indicates that the time in which tumour or blood samples are taken for diagnosis may influence the findings of oncologists. It was an accidental finding along these lines that first put the researchers on the right track, “Some of my colleagues work early in the morning or late in the evening; sometimes they’ll also analyse blood at unusual hours,” Aceto says with a smile. The scientists were surprised to find that samples taken at different times of the day had very different levels of circulating cancer cells.
Another clue was the surprisingly high number of cancer cells found per unit of blood in mice compared to humans. The reason was that as nocturnal animals, mice sleep during the day, which is when scientists collect most of their samples.
“In our view, these findings may indicate the need for healthcare professionals to systematically record the time at which they perform biopsies,” Aceto says. “It may help to make the data truly comparable.”
The researchers’ next step will be to figure out how these findings can be incorporated into existing cancer treatments to optimise therapies. As part of further studies with patients, ETH Professor Nicola Aceto wants to investigate whether different types of cancer behave similarly to breast cancer and whether existing therapies can be made more successful if patients are treated at different times.
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Materials provided by ETH Zurich. Original written by Vanessa Bleich. Note: Content may be edited for style and length.

Major depressive disorder (MDD), or depression, is a severe mental disorder often associated with increased suicide rates. There are about 250 million people with depression globally but our understanding of the neural underpinnings of how sad information is processed in people with depression and how it differs from that in healthy persons is still yet to be known.
Located near the bottom of the skull, the pons is one of the lowermost structures of the brain and a part of the brainstem. Recent clinical and research evidence has suggested that the pons is relevant to emotional reactivity and processing affective information. However, current literature on human affective processing focuses primarily on changes to the cortico-limbic network. The pons is a neglected area, which greatly limits our understanding of depression pathology.
A research team led by Professor Tatia Lee, Director of the State Key Laboratory of Brain and Cognitive Sciences of The University of Hong Kong (HKU), in collaboration with Professor Lin Chen of Chinese Academy of Sciences, conducted studies to explain the neural mechanisms of the pons-corticolimbic network in perpetuating sad mood in depression. The study findings were published in Communications Biology.
The team first conducted a high-resolution 7 Tesla functional Magnetic Resonance Imaging (MRI) study with 41 healthy individuals aged 19 to 31 years to confirm the pons and other neural correlates were involved in affective processing. They then applied the data to a second functional MRI study on 49 clinical participants with MDD and 39 healthy controls to examine the connectivity differences between the two groups.
A key finding is that the amygdala-pons connectivity in the pons-corticolimbic network was significantly stronger in patients with major depressive disorder than in the healthy control group. Furthermore, the connectivity strength was positively associated with the severity of psychological symptoms of depression.
The significant overlapping of the neural networks in processing sad and fearful information may explain the high occurrence of individuals having both depression and anxiety disorders at the same time.
“We speculate that the pons interacts with the amygdala to perform signal exchanges following the reception of sad affective information. The hyperactive amygdala-pons connectivity may relate to the psychological symptoms commonly seen in people with depression, such as lacking interest and motivation, low self-esteem, and social withdrawal,” said Professor Lee.
It is worth noting that the hyperactive amygdala-pons connectivity is a significant indicator of depression, implying that the amygdala-pons connectivity strength could be useful for detecting vulnerability and severity of depression. Visual sad information reinforces depressed mood and stimulates the pons. This suggested that guiding one’s visual attention away from processing sad information may benefit mood regulation and lead to better overall mental health.
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The deletion of the Wt1 gene during the early stages of the embryonic reproductive organ formation leads to differences in sex development in adult mice, according to an article published in the journal PLOS Genetics and led by the lecturer Ofelia Martínez-Estrada, from the Faculty of Biology and the Biomedicine Research Institute (IRBio) of the University of Barcelona.
Among the participants in the article are the experts Francesc X. Soriano, from the Department of Cell Biology, Physiology and Immunology, and the Institute of Neurosciences of the UB (UBNeuro), and Manuel Reina, from the same Department and the Research Group Celltec UB.
A decisive gene in the biology of sex
The Wt1 gene or Wilms tumour gene is expressed during the embryonic development of mammals in many organs and tissues (urogenital system, spleen, heart, diaphragm, etc.). In scientific literature, the mutations of the Wt1 gene are related to some pathologies — syndromes such as Denys-Drash, Frasier and Meacham’s — which include genitourinary defects and differences in the sex development (such as ambiguous genitalia or abnormal development of the gonads).
These differences in the sexual development are congenital disorders in which the development of the chromosomal, gonadal or anatomic sex is atypical. Despite the efforts to understand the genetic factors that cause these alterations, the origin is unknown in many cases and it is hard to offer a precise diagnosis to the affected people.
Murine models with modifications in the expression of key genes in the sex development are shaped as decisive elements for studying this complex process in mammals. Therefore, in recent years, new genetic tools have been generated in mutant mice models to study different aspects of the biology of the WT1 gene.
As part of the study, the team presents a new genetically modified mouse model (Wt1KO) which revealed the importance of the Wt1 gene in the initial differentiation of the embryonic gonad at early stages and its impact in the formation of the reproductive system of adult mice. According to the conclusions, female and male Wt1KO mutant mice — unable to express the Wt1 gene in reproductive organs from the early formation stages- showed ambiguous genital tracts and their gonads remained at an undifferenced stage.
“In this study, we state that the Wt1 gene is necessary for activating the pathways that determine the development of the male and female sex, since embryonic mutant gonads do not express the specific genes for each genetic program,” notes lecturer Ofelia Martínez-Estrada, from the Department of Cell Biology, Physiology and Immunology of the UB.
To date, it has been hard to assess the functions of the WT1 transcription factor — coded by the mentioned gene- during the early differentiation of the gonad and its impact on adult sex development. The lack of development in gonads or in the genital tract (gonadal agenesis) and the embryonic lethality shown in Wt1KO mutant mice hindered the progress of research to elucidate the role of this gene in these development processes.
“Based on the obtained results, we propose that this murine model could contribute to improve the knowledge on the functions of the WT1 gene in some progenitor cell populations in different organs and tissues, as well as the importance of these cell populations in the formation of organs in adults,” concludes lecturer Ofelia Martínez-Estrada.
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A new study led by researchers from the Barcelona Institute for Global Health (ISGlobal), a centre supported by the “la Caixa” Foundation, has evaluated the link between air pollution and lung function of young adults who had recently attained their expected maximum lung function. The study, published in Environment International, found that participants with higher exposure to ambient and household air pollution had worse results in lung function tests.
Ambient (outdoor) air pollution comprising fine particulate matter like PM2.5 and household air pollution (HAP) caused by inefficient cooking methods using fuels like biomass, kerosene or coal, together cause up to 7 million premature deaths every year. Yet, there is limited data on the health effects of ambient air pollution from lower-middle-income countries, specifically on young adults following their lung peak growth. According to Otavio Ranzani, ISGlobal researcher and first author of the study: “There has been a lot of research on air pollution and its effects on the lung function of children. But this is one of the first studies looking at the population group of young adults in a low- and middle-income country setting.”
Data on 1,044 participants (within the age group of 20-26 years) were collected from the Andhra Pradesh Children and Parent Study (APCAPS) cohort (2010-2012), situated in 28 villages in the peri-urban area of Hyderabad city. The researchers measured lung function with: i) FEV1 (forced expiratory volume in the first second), an indicator for resistance of airflow through the respiratory tract while forced breathing; and ii) FVC (forced vital capacity), an indicator of lung capacity. Factors like sex, health behaviours, and socioeconomic factors were identified and adjusted during the analysis.
Results showed that household air pollution (measured by use of biomass fuel) was consistently associated with decreased lung function. This effect on lung function was especially prominent in participants who lived in households that used unvented biomass stoves. The average decrease of 142 ml in lung capacity due to household air pollution was magnified to 211 ml for those who used unvented biomass stoves. The analysis also revealed a link between ambient PM2.5 with decreased lung function, but these results were less conclusive. Overall, these findings suggest that reducing levels of exposure to ambient PM2.5 and household air pollution might be effective in improving lung function in adulthood.
Some 2.6 billion people continue to use biomass for cooking and there is little research on how this affects lung function trajectories during childhood. This study provides a glimpse of the cumulative impact on respiratory health by focusing on young adults who recently attained their maximum lung function. “This cross-sectional study opens the doors for further longitudinal research on the effect of air pollution on lung development, especially in low- and middle-income country settings where individuals are commonly exposed to both high levels of ambient and household air pollution,” concludes Cathryn Tonne, ISGlobal researcher and senior author of the study.
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As scientists gradually discover evidence that people who feel younger than their chronological age are typically healthier and more psychologically resilient, the saying “you’re only as old as you feel” rings increasingly true.
Could the expression also hold true for older people recuperating from physical disabilities? Apparently so. Researchers from Bar-Ilan University in Israel have found that feeling young can increase the chances of successful rehabilitation from medical conditions, even in old age. Their study was recently published in the journal Gerontology.
The study tracked 194 adult patients aged 73-84 undergoing rehabilitation from osteoporotic fractures or stroke in several rehabilitation facilities across Israel. Fractures (mostly due to falls) and stroke are frequent health events that result in the loss of one’s functional independence, considered the greatest fear of older adults.
Patients were interviewed several times throughout their rehabilitation. They were asked about their subjective age (how young they felt), feelings and experiences. Their functional independence was assessed by nursing personnel who rated their functioning level at admission and at discharge using the Functional Independence Measurement (FIM) test.
Patients who felt younger (had a younger subjective age) at hospital admission showed better functional independence at discharge approximately one month later. The beneficial effect of feeling younger was found both for patients who rehabilitated from osteoporotic fractures (mainly due to falls) and for those who rehabilitated from a stroke. The researchers also found that those who felt younger rehabilitated better because they were more optimistic about their chances of regaining their functional abilities.
“The effect of subjective age at admission on functional independence at discharge was confirmed,” says Prof. Amit Shrira, from the Gerontology Program at the Department of Interdisciplinary Social Sciences, who led the study together with Prof. Ehud Bodner, also from the Interdisciplinary Social Sciences department. “However, the reverse effect — that of functional independence at admission on subjective age at discharge — was not confirmed. This supports the conclusion that a younger age identity is an important psychological construct that contributes to a more successful rehabilitation,” added Shrira, who conducted the research with Dr. Daphna Magda Kalir from the Gender Studies Program, among others.
Surprisingly, subjective age was the strongest predictor of rehabilitation outcomes, stronger even than patients’ chronological age and multiple chronic health conditions occurring simultaneously (physical multimorbidity) at admission. Chronological age and physical multimorbidity are generally considered by health care practitioners in determining prognosis, whereas subjective age is unknown to most practitioners. “Those who feel younger can maintain their health and functioning for longer periods, and as the current study shows, can recuperate better from disability. Therefore, by perceiving themselves to age successfully people may preserve a healthy and vigorous lifestyle,” says Shrira.
In view of the findings, the researchers suggest that clinicians consider evaluating patients’ subjective age when they design rehabilitation protocols. A younger subjective age may motivate older individuals to adhere to the rehabilitation protocol following osteoporotic fracture and stroke. Future research could assist in designing interventions geared to induce a younger subjective age in patients that might assist them in rehabilitating more successfully. Such interventions may help correct false beliefs of aging and include cognitive techniques that help change negative automatic thoughts about aging.
This study was funded by the Israeli Ministry of Science, Technology and Space.
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The pandemic has hit nursing home residents especially hard, with a disproportionately large share of COVID-19 infection and mortality rates in the United States, according to the Centers for Disease Control and Prevention (CDC).
But new research from the Case Western Reserve University School of Medicine in partnership with Brown University shows that high levels of Omicron-specific immunity can be achieved in nursing home residents and their caregivers with a third dose of the COVID-19 vaccine, also known as the booster shot.
The findings were published this month in the journal eBioMedicine, part of The Lancet network.
Researchers examined blood samples from 85 nursing home residents and 48 healthcare workers in Ohio who received the COVID-19 vaccine booster to determine the level of neutralizing antibodies present. Neutralizing antibodies are protective proteins produced by the immune system in response to vaccination and can be analyzed to determine the length of time it takes for immunity to diminish.
The study found that Omicron-specific antibodies reached detectable levels in 86% of nursing home residents and 93% of healthcare workers after receiving the booster shot, compared to just 28% of nursing home residents and healthcare workers after the initial two-dose COVID-19 vaccine series. This high neutralization level occurred two weeks after the booster.
Despite nursing homes acting as an epicenter of infections and deaths throughout the pandemic, one in eight nursing home residents and one in nine staff members have not been fully vaccinated, according to the AARP.
David Canaday, lead study author and professor at the School of Medicine, said the results highlight the importance of booster vaccinations-not only for nursing home residents, but also for the general population.
“There are tens of millions of community-dwelling older adults similar to the nursing home population but are living at home,” he said. “This data shows this group of frail, older adults with similar clinical and functional limitations would benefit immensely from a booster vaccination. The data also shows that healthcare workers achieved a significant elevation in antibody levels after receiving a booster. Many of these workers are healthy, middle-aged adults similar to the general population.”
The research builds on a previous study that showed nursing home residents and healthcare workers lose more than 80% of their COVID-19 immunity six months after the initial vaccine series.Those results were presented to the CDC and published last fall.
The CDC recommends a first booster dose for people age 5 and older after completing their primary COVID-19 series. A second booster shot is recommended for people at least 50 years old and for those at least age 12 who are moderately or severely immunocompromised. Canaday’s research team has ongoing studies examining the responses to the second booster including nursing home residents.
In addition to Case Western Reserve and Brown University, the research team included collaboration with the Louis Stokes Cleveland VA Medical Center; Ragon Institute at the Massachusetts Institute of Technology; the Marcus Institute for Aging Research; and the Providence Veterans Administration Medical Center.
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The number of elderly suffering from Alzheimer’s Disease has been rapidly rising over the past decades. For a long time, scientists believed that misfolded aggregates of amyloid-beta protein accumulate and form plaques in the brain, leading to memory loss and neuronal death. However, the recent failures of the clinical trials indicate the pressing need to understand the missing link between amyloid-beta protein plaques and the disease’s symptoms, a phenomenon that has been studied for over decades.
Researchers led by Director C. Justin LEE from the Center for Cognition and Sociality within the Institute for Basic Science (IBS), South Korea, have delved extensively into this topic. Recently in 2020, the group published in the journal Nature Neuroscience that the star-shaped cells in the brain, called astrocytes, are greatly involved in Alzheimer’s Disease and its progression. Driven by this discovery, the group sought to further explore the molecular connection underlying the astrocytic response.
After studying basic cellular pathways and how they change in the star-shaped astrocytes of the brain, the IBS team now has found the missing link: the conversion of amyloid-beta to urea in the brain.
The urea cycle is widely studied and understood as a major metabolic pathway in the liver and kidneys, as a part of our digestive and excretory processes. In the liver, the urea cycle converts ammonia, a toxic product from protein digestion, into urea, which is easily excreted by our kidneys as urine. Surprisingly, previous studies have reported increased urea in the brain of Alzheimer’s Disease patients, which led the IBS team to wonder if the urea cycle played any role in the pathology of the disease. To their surprise, they found that the urea cycle is ‘switched on’ in the astrocytes of the Alzheimer’s Disease brain, in order to clean up the toxic amyloid-beta aggregates and remove them in the form of urea.
However, this isn’t as beneficial as it sounds. The group found that the switching on of the urea cycle causes the production of ornithine, another metabolite that accumulates in the cell and needs to be cleaned up. The hardworking astrocytes produce the enzyme ornithine decarboxylase 1 (ODC1) in this condition to deal with the accumulated ornithine and convert it to putrescine. This consequently increases the levels of neurotransmitter γ-aminobutyric acid (GABA), as well as toxic byproducts like hydrogen peroxide (H2O2) and ammonia in the brain.
This ammonia further feeds back into the urea cycle and continues this process, causing more and more accumulation of toxic byproducts. High levels of GABA released by these astrocytes play an inhibitory action on neuronal transmission, contributing to the tell-tale loss of memory in Alzheimer’s Disease.
In the above-mentioned 2020 study by the group, hydrogen peroxide was found to be the primary factor causing the severe reactivity of diseased astrocytes, causing neuronal cell death. Now, the new findings from this study precisely explain how the increased GABA, H2O2, and ammonia contribute to and exacerbate the loss of memory and neuronal cell death associated with Alzheimer’s Disease.
The first author JU Yeon Ha stated, “For years, scientists have been debating about the beneficial and detrimental role of reactive astrocytes, and with the findings of this study, our group is able to clearly demarcate the beneficial urea cycle and the detrimental conversion of ornithine to putrescine and GABA, thereby providing evidence of the dual nature of astrocytes in Alzheimer’s Disease brain.”
The group experimented further to exploit this new knowledge. They found that astrocyte-specific gene silencing of the enzyme Ornithine Decarboxylase 1 in a transgenic Alzheimer’s Disease mouse model was able to stop the excessive GABA production and neuronal inhibition in the hippocampus of the mouse brain. These animals performed better in memory-related behavioral tasks, almost completely recovering from the AD-associated loss of memory after ODC1 knockdown. Additionally, the number of amyloid-beta plaques was significantly fewer in ODC1-gene silenced mouse brains, indicating that the urea cycle was working more efficiently to clear the accumulated protein without causing the accumulation of harmful byproducts such as H2O2, GABA and ammonia.
Director C. Justin LEE, the corresponding author of the study remarked, “With the results from this study, we were able to finally delineate the pathway linking amyloid-beta plaques to astrocytic reactivity, uncovering the presence of a functional urea cycle in reactive astrocytes for the first time. We also found increased levels of enzyme ODC1 in human AD patients’ brains, raising the possibility of translating the results from our mouse study to humans and indicating that ODC1 may be a novel and powerful therapeutic target against the disease, inhibition of which could clear amyloid-beta plaques as well as improve memory.”
This research was published in Cell Metabolism, a CellPress journal with a strong impact factor of 27.28. Due to the significance and novelty of the study, the lead author Dr. JU Yeonha was invited to present the findings at the journal’s symposium Metabolites in Signalling and Disease in Lisbon, Portugal in April.

Microscopic mites that live in human pores and mate on our faces at night are becoming such simplified organisms due to their unusual lifestyles that they may soon become one with humans, new research has found.
The mites are passed on during birth and are carried by almost every human, with numbers peaking in adults as the pores grow bigger. They measure around 0.3mm long, are found in the hair follicles on the face and nipples, including the eyelashes, and eat the sebum naturally released by cells in the pores. They become active at night and move between follicles looking to mate.
The first ever genome sequencing study of the D. folliculorum mite found that their isolated existence and resulting inbreeding is causing them to shed unnecessary genes and cells and move towards a transition from external parasites to internal symbionts.
Dr Alejandra Perotti, Associate Professor in Invertebrate Biology at the University of Reading, who co-led the research, said: “We found these mites have a different arrangement of body part genes to other similar species due to them adapting to a sheltered life inside pores. These changes to their DNA have resulted in some unusual body features and behaviours.”
The in-depth study of the Demodex folliculorum DNA revealed: Due to their isolated existence, with no exposure to external threats, no competition to infest hosts and no encounters with other mites with different genes, genetic reduction has caused them to become extremely simple organisms with tiny legs powered by just 3 single cell muscles. They survive with the minimum repertoire of proteins — the lowest number ever seen in this and related species. This gene reduction is the reason for their nocturnal behaviour too. The mites lack UV protection and have lost the gene that causes animals to be awakened by daylight. They have also been left unable to produce melatonin — a compound that makes small invertebrates active at night — however, they are able to fuel their all-night mating sessions using the melatonin secreted by human skin at dusk. Their unique gene arrangement also results in the mites’ unusual mating habits. Their reproductive organs have moved anteriorly, and males have a penis that protrudes upwards from the front of their body meaning they have to position themselves underneath the female when mating, and copulate as they both cling onto the human hair. One of their genes has inverted, giving them a particular arrangement of mouth-appendages extra protruding for gathering food. This aids their survival at young age. The mites have many more cells at a young age compared to their adult stage. This counters the previous assumption that parasitic animals reduce their cell numbers early in development. The researchers argue this is the first step towards the mites becoming symbionts. The lack of exposure to potential mates that could add new genes to their offspring may have set the mites on course for an evolutionary dead end, and potential extinction. This has been observed in bacteria living inside cells before, but never in an animal. Some researchers had assumed the mites do not have an anus and therefore must accumulate all their faeces through their lifetimes before releasing it when they die, causing skin inflammation. The new study, however, confirmed they do have anuses and so have been unfairly blamed for many skin conditions.The research was led by Bangor University and the University of Reading, in collaboration with the University of Valencia, University of Vienna and National University of San Juan. It is published in the journal Molecular Biology and Evolution.
Dr Henk Braig, co-lead author from Bangor University and the National University of San Juan, said: “Mites have been blamed for a lot of things. The long association with humans might suggest that they also could have simple but important beneficial roles, for example, in keeping the pores in our face unplugged.”
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Seven out of 10 pregnant women were cured of their multidrug-resistant tuberculosis and delivered healthy babies after taking a medication that had previously been considered unsafe in pregnancy, a new Curtin and Telethon Kids Institute study has found.
Published in JAMA Network Open, the study examined the experiences of 275 pregnant women with multidrug-resistant tuberculosis living in South Africa, Peru, Brazil, Iran and Uganda.
Lead researcher Dr Kefyalew Alene, from the Curtin School of Population Health and Telethon Kids Institute, said the study had found a medication used to treat multidrug-resistant tuberculosis, Linezolid, was associated with favourable pregnancy outcomes and high treatment success.
“This is the first comprehensive review of treatment outcomes for multidrug-resistant tuberculosis in pregnant women, who remain one of the most vulnerable groups among the half a million people living with the disease globally,” Dr Alene said.
“I was surprised to find that as many as 73.2 percent of pregnant women with multidrug-resistant tuberculosis gave birth to healthy babies and that the treatment had worked for 72.5 percent of the women, meaning they were cured from the disease or had completed the treatment successfully.”
Dr Alene said the study answered a challenging global issue of when to treat pregnant patients living with multidrug-resistant tuberculosis.
“Second-line tuberculosis medicines used for the treatment of multidrug-resistant tuberculosis are thought to be toxic for the fetus and previous research has suggested waiting for the treatment to be provided until after the birth,” Dr Alene said.
“Tuberculosis can have a greater devastating impact on the mothers and the babies than the medicine’s side effects. If multidrug-resistant tuberculosis is left untreated, it could result in the risk of maternal illness and maternal and fetus death.
“This study shows we need to start the treatment as soon as possible during pregnancy. However, further research on the use of Linezolid in pregnancy is needed because long-term use can increase the risk of gastrointestinal disorders, ototoxicity, and psychiatric disorders.”
The remaining proportion of adverse pregnancy outcomes including preterm birth, pregnancy loss, low birthweight, and stillbirth was not caused by the drug, but the disease itself. Researchers concluded that if the drug was not taken, the outcome would be worse.
This study was funded by an Australian National Health and Medical Research Council Investigator Grant.
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Researchers have demonstrated how airborne diseases such as COVID-19 spread along the length of a train carriage and found that there is no ‘safest spot’ for passengers to minimise the risk of transmission.
The researchers, from the University of Cambridge and Imperial College London, developed a mathematical model to help predict the risk of disease transmission in a train carriage, and found that in the absence of effective ventilation systems, the risk is the same along the entire length of the carriage.
The model, which was validated with a controlled experiment in a real train carriage, also shows that masks are more effective than social distancing at reducing transmission, especially in trains that are not ventilated with fresh air.
The results, reported in the journal Indoor Air, demonstrate how challenging it is to for individuals to calculate absolute risk, and how important it is for train operators to improve their ventilation systems in order to help keep passengers safe.
Since COVID-19 is airborne, ventilation is vital in reducing transmission. And although COVID-19 restrictions have been lifted in the UK, the government continues to highlight the importance of good ventilation in reducing the risk of transmission of COVID-19, as well as other respiratory infections such as influenza.
“In order to improve ventilation systems, it’s important to understand how airborne diseases spread in certain scenarios, but most models are very basic and can’t make good predictions,” said first author Rick de Kreij, who completed the research while based at Cambridge’s Department of Applied Mathematics and Theoretical Physics. “Most simple models assume the air is fully mixed, but that’s not how it works in real life.