Publisher Health

Researchers at Monash University have designed a new co-training AI algorithm for medical imaging that can effectively mimic the process of seeking a second opinion.
Published recently in Nature Machine Intelligence, the research addressed the limited availability of human annotated, or labelled, medical images by using an adversarial, or competitive, learning approach against unlabelled data.
This research, by Monash University faculties of Engineering and IT, will advance the field of medical image analysis for radiologists and other health experts.
PhD candidate Himashi Peiris of the Faculty of Engineering, said the research design had set out to create a competition between the two components of a “dual-view” AI system.
“One part of the AI system tries to mimic how radiologists read medical images by labelling them, while the other part of the system judges the quality of the AI-generated labelled scans by benchmarking them against the limited labelled scans provided by radiologists,” said Ms Peiris.
“Traditionally radiologists and other medical experts annotate, or label, medical scans by hand highlighting specific areas of interest, such as tumours or other lesions. These labels provide guidance or supervision for training AI models.
“This method relies on the subjective interpretation of individuals, is time-consuming and prone to errors and extended waiting periods for patients seeking treatments.”
The availability of large-scale annotated medical image datasets is often limited, as it requires significant effort, time and expertise to annotate many images manually.

Struggling to shave seconds off your Park Run PB — don’t worry scientists have revealed it could all be down to your genetics.
Researchers at the University of Essex discovered less than 31% of people have the unique makeup to make the most of training.
Dr Henry Chung, from School of Sport, Rehabilitation and Exercise Sciences, found the top performers had a combination of 19 key gene variants — known as single nucleotide polymorphisms (SNPs) — linked to running performance.
Following just eight weeks of endurance training they improved by an average of 11.5% and those without the genetic coding showed little or no improvement even when exposed to the exact same training.
This is the first time, in combination, that all these key markers that spark success have been listed together and examined by scientists.
Dr Chung said: “This study supports the fact that genetics play a major part in athletic performance and training responses.
“Whether you are an elite competitor or training for a fun run, your DNA can make a real difference on how much you can push your limits.

How does the brain adapt our behavior in response to an infection or injury? A multidisciplinary team of scientists from the Institut Pasteur, CNRS and Inserm have revealed the existence of a circuit involved in sensing and also in the regulation of the anti-inflammatory response orchestrated by different brain regions. This circuit detects inflammation in the blood and organizes and regulates the immune response. It embodies a two-way connection between the brain and immune system. The results were published on June 5, 2023 in the journal Neuron.
Whenever infections or injuries occur, the immune system is triggered to control the infection and repair damaged tissue. This process involves the release of pro-inflammatory mediators that inform the brain of the body’s immune status and coordinate the immune response. In response to this signal, the brain triggers a complex reaction known as “sickness behavior” whose purpose is to reassign energy to the body’s different systems. This state is associated with behavioral changes including social avoidance and lethargy, metabolic adjustments such as fever and loss of appetite, and the release of hormones such as cortisone, to increase resistance to infection while also regulating immune responses. In this study, a multidisciplinary group consisting of neurobiologists and immunologists from the Institut Pasteur, Inserm and the CNRS discovered a novel circuit used by the brain to measure inflammation levels in the blood and, in response to this, regulate inflammation. A region of the brainstem known as the vagal complex directly detects levels and types of inflammatory hormones in the bloodstream. This information is then relayed to neurons in another region of the brainstem called the parabrachial nucleus, which also receives information related to pain and certain aversive or traumatic memories. In turn, these neurons activate neurons in the hypothalamus leading to a rapid increase in cortisone, a hormone with anti-inflammatory properties, in the blood.
The scientists used state-of-the-art neuroscience approaches to identify this circuit, which enabled them to individually observe the neurons involved during inflammation. The experts observed how the activity of specific neurons in the parabrachial nucleus could regulate the production of white blood cells involved in the immune response. “This research demonstrates that neural activity in the brain alone can have a powerful effect on the development of immune responses during infection or injury. It therefore provides a clear example of the powerful two-way connection between the body and brain. It also fuels our ambition to discover the impact of our brain on the way we interact with microbes, fight off pathogens and heal wounds,” explains Gérard Eberl, Head of the Institut Pasteur’s Microenvironment and Immunity Unit.
The discovery of this circuit opens up new opportunities for research that will jointly contribute to the fields of neurobiology and immunology: “This study gives us additional tools to better understand the impact of systemic inflammation on our brain, mood and on certain neurodegenerative processes,” adds Gabriel Lepousez, a neurobiologist in the Perception and Memory Unit (Institut Pasteur/CNRS).
Given the established role of the parabrachial nucleus in aversive memory processes, potential infectious threats could be averted if this circuit is reactivated by the memory of past inflammatory or aversive experiences. Drawing on this neuro-immune communication, the immune system could therefore benefit from the brain’s ability to predict and anticipate threats in our environment.
This research was funded by the organizations cited above and also by AG2R-LA MONDIALE and MTRL.

In 2022-2023, an outbreak of monkeypox, now known as mpox (caused by the monkeypox virus or MPXV) led to 87,000 human cases in 170 countries[1]. Most cases were reported outside the usual areas in which the virus circulates. Since the outbreak began, surveillance of the virus has been stepped up in Europe, with nearly 5,000 cases being reported in France[2]. Scientists and clinicians from the Institut Pasteur, the CNRS, Inserm, the VRI and the Paris Public Hospital Network (AP-HP) studied 470 sera from vaccinated or MPXV-infected individuals to elucidate the mechanisms involved and determine correlates of protection against infection or disease severity[3]. They determined the sensitivity of the virus to neutralizing antibodies and analyzed the immune response of these vaccinated or MPXV-infected individuals. The study revealed the role of complement4, a component of the innate immune system, in this response. The findings were published in the journal Cell Host & Microbe on May 4, 2023.
In 2022-2023, an unprecedented epidemic of 87,000 cases of mpox occurred in non-endemic areas, affecting people with no direct link to travel in Central or West Africa, where the virus has historically been present. MPXV is mainly transmitted to humans by rodents, with human-to-human transmission occurring via respiratory droplets or close contact. Symptoms are less severe than those of smallpox, and the case-fatality rate is lower. According to Santé publique France, approximately 5,000 cases of MPXV infection have been reported in France since May 2022.2 MPXV is still circulating at very low levels in non-endemic areas, which is why it is important to improve characterization and analyze the immune response of people infected with the virus or vaccinated with IMVANEX, the third-generation vaccine currently available, initially developed for smallpox.
The research teams worked in collaboration with clinicians, vaccinologists and virologists from three French hospitals (Henri Mondor Hospital in Créteil, La Pitié-Salpêtrière Hospital and Orléans Hospital) to carry out this multidisciplinary research. The large number of sera analyzed provided good statistical power, meaning that the analysis could be narrowed to subgroups of patients based on various criteria such as age.
In this study, published in Cell Host & Microbe, the leading journal on interactions between microbes and the immune system, the scientists studied the sensitivity of MPXV to neutralizing antibodies (NAbs) generated after infection with the virus and/or vaccination with IMVANEX. The IMVANEX vaccine has been used as pre- and post-exposure prophylaxis in high-risk populations, but its effectiveness is not yet well characterized. To analyze the sensitivity of the virus, the team of scientists developed two cellular tests to quantify neutralizing antibodies, using either the attenuated virus as a vaccine (MVA) or an MPXV strain isolated in a recently infected individual.
The study demonstrated the role of complement,[4] already known for other poxviruses, and the neutralizing activity of the antibodies generated by infection or vaccination. Robust levels of anti-MVA antibodies were detected after infection, vaccination with the historic smallpox vaccine, or administration of IMVANEX or another MVA-based vaccine candidate. MPXV was minimally sensitive to neutralization in the absence of complement. The addition of complement from sera enhanced detection of individuals with antibodies and increased their level of anti-MPXV antibodies. Four weeks after infection, anti-MVA and -MPXV NAbs were observed in 94% and 82% of individuals, respectively. Two doses of IMVANEX generated anti-MVA and -MPXV NAbs that were detectable in 92% and 56% of vaccinees, respectively.
The highest level of antibodies was found in individuals born before 1980 (who had therefore been vaccinated for smallpox), whether after infection or after administration of IMVANEX, highlighting the impact of historic smallpox vaccination on immune responses to infection or administration of IMVANEX. This suggests that a sort of hybrid immunity was generated in infected individuals who were vaccinated in childhood.
The number of MPXV infections has been constantly on the rise since mass vaccination for smallpox was discontinued in the 1980s. “The neutralization assays developed in connection with this research may help define correlates of protection against infection or disease severity.The assays can also be used to conduct epidemiological surveys, assess the duration of protection conferred by previous infection or by authorized and candidate vaccines, and analyze the use of immunotherapeutic intervention.The assays represent useful tools to understand the mechanisms of multiplication of MPXV and its effects on public health, and to optimize patient treatment,” commented Olivier Schwartz, Head of the Institut Pasteur’s Virus and Immunity Unit and last author of the study.

A historic study has provided first-time insights on electric scooters.
In September 2019, Virginia Tech Transportation Institute (VTTI) began the first large-scale naturalistic driving study of electric scooter, also known as e-scooter, riders. Over the span of 18 months, 50 scooters, equipped with forward-facing cameras and other research equipment, collected over 9,000 miles of data from over 200,000 rides on Virginia Tech’s Blacksburg campus. Deployment of the scooters began in August 2019. After being removed from campus during the COVID-19 pandemic, they were redeployed in August 2021 through the academic year.
“The e-scooter deployment at Virginia Tech collected the largest naturalistic e-scooter data set known to date and quantified the safety risks associated with behavioral, infrastructure, and environmental factors,” said Elizabeth White, programs and business manager for VTTI. “This was a very exciting research program to be a part of, and our collaboration with many departments on campus was invaluable to ensuring a safe deployment.
White was the lead researcher of the team that included six other Virginia Tech researchers and other industry experts. The results were recently published in published in the Journal of Safety Research.
Utilizing VTTI’s proprietary data acquisition system (DAS), researchers found that infrastructure-related factors, the behaviors of e-scooter riders and other around them, and environmental factors all created risk for e-scooter users. They found loss of control related to infrastructure was the greatest contributor, to all crash- and near-crash events, equating to 47 percent. In total, infrastructure caused 67 percent of incidents, followed by the presence of other road users at 19 percent and rider behavior at 14 percent.
Transitions from surfaces, such as moving from gravel or dirt to grass, proved to be the riskiest. Those riders were almost 60 times more likely to have a crash or near-crash experience. This was supported by data showing that riding off a designated path, or off-road, made users nearly 25 times more likely to experience such issues compared to those who rode on a shared-use path.
uring the study, there were no crashes between an e-scooter and a moving vehicle captured. Conflicts with other road users were shown to be more avoidable through evasive maneuvers when compared to infrastructure-related events. Researchers believe this is likely caused by riders misjudging the terrain or infrastructure or a lack of skill in navigating those obstacles.

University of Virginia School of Medicine researchers have discovered a key driver of chronic inflammation that accelerates aging. That finding could let us slow the clock to live longer, healthier lives, and may allow us to prevent age-related conditions such as deadly heart disease and devastating brain disorders that rob us of our faculties.
So what drives this harmful inflammation? The answer is improper calcium signaling in the mitochondria of certain immune cells. Mitochondria are the power generators in all cells, and they rely heavily on calcium signaling.
The UVA Health researchers, led by Bimal N. Desai, PhD, found that mitochondria in immune cells called macrophages lose their ability to take up and use calcium with age. This, the researchers show, leads to chronic inflammation responsible for many of the ailments that afflict our later years.
The researchers believe that increasing calcium uptake by the mitochondrial macrophages could prevent the harmful inflammation and its terrible effects. Because macrophages reside in all organs of our bodies, including the brain, targeting such “tissue-resident macrophages” with appropriate drugs may allow us to slow age-associated neurodegenerative diseases.
“I think we have made a key conceptual breakthrough in understanding the molecular underpinnings of age-associated inflammation,” said Desai, of UVA’s Department of Pharmacology and UVA’s Carter Immunology Center. “This discovery illuminates new therapeutic strategies to interdict the inflammatory cascades that lie at the heart of many cardiometabolic and neurodegenerative diseases.”
The Inflammation of Aging — ‘Inflammaging’
Macrophages are white blood cells that play critical roles in our immune systems and, in turn, our good health. They swallow up dead or dying cells, allowing our bodies to remove cellular debris, and patrol for pathogens and other foreign invaders. In this latter role, they act as important sentries for our immune systems, calling for help from other immune cells as needed.

Having a food allergy as a baby is linked to asthma and reduced lung function later in childhood, according to a world first study.
The research, led by Murdoch Children’s Research Institute and published in the Lancet Child & Adolescent Health, found that early life food allergy was associated with an increased risk of both asthma and reduced lung growth at six years of age.
Murdoch Children’s Associate Professor Rachel Peters said this was the first study to examine the relationship between challenge-confirmed food allergy in infancy and asthma and poorer lung health later in childhood.
The Melbourne research involved 5276 infants from the HealthNuts study, who underwent skin prick testing to common food allergens, including peanut and egg and oral food challenges to test for food allergy. At six years, children were followed up with further food allergy and lung function tests.
The study found by six years of age, 13.7 per cent reported a diagnosis of asthma. Babies with a food allergy were almost four times more likely to develop asthma at six years of age, compared to children without a food allergy. The impact was greatest in children whose food allergy persisted to age six as opposed to those who had outgrown their allergy. Children with a food allergy were also more likely to have reduced lung function.
Associate Professor Peters said food allergy in infancy, whether it resolved or not, was linked to poorer respiratory outcomes in children.
“This association is concerning given reduced lung growth in childhood is associated with health problems in adulthood including respiratory and heart conditions,” she said.

In children with suspected sinusitis, a nasal swab to test for three types of bacteria can tell whether antibiotics are likely to be effective or not, according to a new JAMA study by researchers at the University of Pittsburgh and UPMC.
“Five million kids in the U.S. get prescribed antibiotics for sinusitis each year,” said lead author Nader Shaikh, M.D., pediatrician at UPMC Children’s Hospital of Pittsburgh and professor of pediatrics and clinical and translational science at Pitt. “Our study suggests that only half of these kids see an improvement in symptoms with antibiotic use, so by identifying who they are, we could greatly reduce unnecessary antibiotic use.”
Sinusitis, which is an inflammation or swelling of the sinuses, can cause congestion, runny nose, discomfort and difficulty breathing. Doctors often prescribe antibiotics — which target only bacterial infections — to treat the condition, even though it may be caused by viruses.
“Sinusitis is one of the most common diseases we see in children, but it’s difficult to diagnose because it’s based on the duration of symptoms: If the child has a runny nose or congestion for more than 10 days, we suspect sinusitis,” said Shaikh. “For an ear infection, we can look inside the ear; for pneumonia, we listen to the lungs. But for sinusitis, we have nothing to go on from a physical exam. That was very unsatisfying to me.”
With the goal of developing a better tool to diagnose bacterial sinusitis, Shaikh and his team enrolled about 500 children with sinusitis symptoms from six centers across the U.S. and randomly assigned them to receive either a course of antibiotics or placebo. The researchers also took swabs from inside the nose — much like a COVID-19 test — from each child and tested for the three main types of bacteria involved in sinusitis.
Kids who tested positive for the bacteria had better resolution of symptoms with antibiotic treatment compared to those who did not have bacteria. These findings suggest that testing for bacteria could be a simple and effective way to detect children who are likely to benefit from antibiotics and avoid prescribing antibiotics to those who wouldn’t.
“If antibiotics aren’t necessary, then why use them?” said Shaikh. “These medications can have side effects, such as diarrhea, and alter the microbiome, which we still don’t understand the long-term implications of. Overuse of antibiotics can also encourage antibiotic resistance, which is an important public health threat.”
According to Shaikh, a common belief among parents and doctors is that yellow or green snot signals a bacterial infection. Although several small studies have suggested that nasal discharge color is not meaningful, Shaikh and his team formally tested this idea by asking parents to identify the hue of their child’s snot on a color card.

World-wide obesity has nearly tripled since 1975, according to the World Health Organization. Numerous causes of obesity have been hypothesized including increased dietary fat, carbohydrate or ultra-processed food (UPF) consumption, inactivity, hyperlipidemia and hyperinsulinemia. Based on these hypotheses, solutions have been sought that involved decreasing consumption of suspected agents. Well-controlled studies have shown that increased consumption of UPF is associated with increased food consumption and weight gain while decreasing UPF consumption in the same subjects was associated with weight loss. However, these studies do not identify a specific cause of obesity since the diets include multiple variables.
In a new perspective, Barbara E. Corkey, PhD, professor emeritus of medicine and biochemistry at Boston University Chobanian & Avedisian School of Medicine, presents an alternative testable and actionable hypothesis/model about the cause of obesity. If validated, it could indicate clear steps to reverse obesity.
Humans vary in the efficiency with which they burn and store nutrients in response to overeating. Some people waste more energy when they overeat and store less. Those individuals tend not to gain weight easily. Humans also vary in their reaction to food deprivation. Some conserve energy better than others and when they diet, they don’t lose weight easily. “These are normal variations and we are each a bit different, due to genetics, but we respond to the same signals,” said Corkey.
Her hypothesis postulates that obesogens (certain chemical compounds that are hypothesized to disrupt normal development and the balance of lipid metabolism) which have entered the environment in the last 50 years, generate misinformation in our bodies, such as inappropriate insulin secretion or hunger, that lead to obesity. Obesogens, she believes, can generate changes in redox state (a normal signal of either excess or the need for energy) that are unrelated to energy needs but falsely stimulate hunger or fuel storage when not needed
“The increasing incidence of obesity correlates with heightened consumption of UPF along with thousands of potential environmental toxins including some derived from fertilizers, insecticides, plastics and air pollutants. Identifying these agents would allow us to remove them or inhibit their ability to generate misinformation,” said Corkey.
Corkey’s model, if validated, could impact many if not all obesity-related diseases. Her paper examines readily available ways to test her model. She believes the best outcome from this work would be identification of obesogens and their removal. The second best outcome would be treatments that block their effect on the body’s normal regulatory mechanisms for insulin secretions.

Where did it come from? More than three years into the pandemic and untold millions of people dead, that question about the Covid-19 coronavirus remains controversial and fraught, with facts sparkling amid a tangle of analyses and hypotheticals like Christmas lights strung on a dark, thorny tree. One school of thought holds that the virus, known to science as SARS-CoV-2, spilled into humans from a nonhuman animal, probably in the Huanan Seafood Wholesale Market, a messy emporium in Wuhan, China, brimming with fish, meats and wildlife on sale as food. Another school argues that the virus was laboratory-engineered to infect humans and cause them harm — a bioweapon — and was possibly devised in a “shadow project” sponsored by the People’s Liberation Army of China. A third school, more moderate than the second but also implicating laboratory work, suggests that the virus got into its first human victim by way of an accident at the Wuhan Institute of Virology (W.I.V.), a research complex on the eastern side of the city, maybe after well-meaning but reckless genetic manipulation that made it more dangerous to people. Listen to This ArticleFor more audio journalism and storytelling,