Culture

New research being presented at the European Congress on Obesity (ECO) held online this year, suggests that among girls a low body mass index (BMI) during childhood indicates a higher risk of developing anorexia nervosa as young adults, whereas a high BMI or overweight in childhood indicates a higher risk of bulimia nervosa.

"By examining the records of thousands of girls over their lifetime in national health registers, we have discovered early warning profiles that could signal girls at risk for anorexia nervosa and bulimia nervosa", says lead author Dr Britt Wang Jensen from Bispebjerg and Frederiksberg Hospital, Copenhagen, Denmark. "The difference in childhood BMI of girls who later developed eating disorders started to emerge at an early age. These results highlight the importance of regularly monitoring weight and height during childhood to identify these patterns as early as possible."

In the UK, the annual number of new cases of anorexia nervosa among 8 to 12-year-olds doubled from 1.5/100,000 in 2006 to 2019 to 3.2/100,000 [1]. Whether premorbid (pre-illness) BMI is associated with anorexia nervosa and bulimia nervosa is unclear. So far, studies have reported conflicting findings, with some suggesting that a high BMI precedes both diseases, whereas others suggest that a low BMI precedes anorexia nervosa and a high BMI precedes bulimia nervosa.

To explore this further in a population-based cohort, Danish researchers analysed data for 66,576 girls from the Copenhagen School Health Records Register born between 1960 and 1996 who had information on height and weight measured at annual school health examinations from ages 7 to 13 years. Cases of anorexia nervosa and bulimia nervosa were identified by linking with the Danish National Patient Register and the Danish Psychiatric Central Research Register. The girls were followed from ages 10 to 50 years.

During the study, 514 women were diagnosed with anorexia nervosa at an average age of 20 years, and 315 women were diagnosed with bulimia nervosa at an average age of 23 years.

The analyses suggest significant "inverse associations" between childhood BMI and the risk of anorexia nervosa in later life, which means that the risk of anorexia nervosa fell as BMI increased. For example, when comparing two 7-year-old girls with an average height and one z-score difference in BMI (equivalent to 2.4 kg), the girl with the higher BMI had a 14% lower risk of developing anorexia nervosa than the girl with the lower BMI; at age 13 years the risk was 28% lower.

In contrast, significant and positive associations were observed between childhood BMI and the risk of bulimia nervosa. For example, when comparing two 7-year-old girls with an average height and one z-score difference in BMI (equivalent to 2.4 kg), the heaviest girl had a 50% higher risk of bulimia nervosa than the leaner child in later life; at age 13 years the risk was 33% higher.

In addition, compared to girls with normal weight at age 7 years, girls with overweight had twice the risk of developing bulimia nervosa in later life; at age 13 years the risk remained but was lower. The associations did not vary by age at diagnosis.

The authors say that further studies are needed to uncover the mechanisms underlying these associations. They acknowledge that the findings are associations only, and point to several limitations, including that diagnoses in this study may be more severe cases as they are based on hospital admissions and contacts, which may limit the generalisability of these findings to less severe forms of these eating disorders. Moreover, the analyses were restricted to girls as there were too few cases to analyse among boys.

The first global review of complementary medicines (herbal and dietary supplements) for weight loss in 16 years--combining 121 randomised placebo-controlled trials including nearly 10,000 adults--suggests that their use cannot be justified based on the current evidence.

The findings of two studies, being presented at The European Congress on Obesity (ECO) held online this year, suggest that although some herbal and dietary supplements show statistically greater weight loss than placebo, it is not enough to benefit health, and the authors call for more research into their long-term safety.

"Over-the-counter herbal and dietary supplements promoted for weight loss are increasingly popular, but unlike pharmaceutical drugs, clinical evidence for their safety and effectiveness is not required before they hit the market", says lead author Erica Bessell from the University of Sydney in Australia. "Our rigorous assessment of the best available evidence finds that there is insufficient evidence to recommend these supplements for weight loss. Even though most supplements appear safe for short term consumption, they are not going to provide weight loss that is clinically meaningful."

The authors report on herbal supplements, containing a whole plant or combinations of plants as the active ingredient, and dietary supplements containing naturally occurring isolated compounds from plants and animal products, such as fibres, fats, proteins, and antioxidants. They can be purchased as pills, powders, and liquids.

Between 1996 and 2006, 1,000 dietary supplements for weight loss included on the Australian Register of Therapeutic Goods weren't evaluated for efficacy. Supplements can be sold and marketed to the public with sponsors (who import, export or manufacture goods) required to have, but not necessarily provide, evidence backing their claims. Just 20% of new listings are audited annually to make sure they meet the requirement. In some countries, the only requirement is that supplements contain acceptable levels of non-medicinal products.

Estimates suggest that 15% of Americans trying to lose weight have tried a weight loss supplement, a USD$41 billion global industry in 2020 [1]. Despite their increasing popularity, it has been 16 years since the last review of the scientific literature on all available herbal and dietary supplements.

Herbal medicines not effective for weight loss

To provide more evidence, Australian researchers did a systematic review of all randomised trials comparing the effect of herbal supplements to placebo on weight loss, up to August 2018 [2]. Data were analysed for 54 studies involving 4,331 healthy overweight or obese adults aged 16 years or older. Weight loss of at least 2.5kg (5.5lbs) was considered clinically meaningful. They also evaluated study design, reporting, and clinical value.

Herbal supplements included in the analysis were: green tea; Garcinia cambogia and mangosteen (tropical fruits); white kidney bean; ephedra (a stimulant that increases metabolism); African mango; yerba mate (herbal tea made from the leaves and twigs of the Ilex paraguariensis plant); veld grape (commonly used in Indian traditional medicine); licorice root; and East Indian Globe Thistle (used in Ayurvedic medicine).

The analysis found that only one single agent, white kidney bean, resulted in a statistically, but not clinically, greater weight loss than placebo (-1.61kg; 3.5Ibs).

In addition, some combination preparations containing African Mango, veld grape, East Indian Globe Thistle and mangosteen showed promising results, but were investigated in three or fewer trials, often with poor research methodology or reporting, and the findings should be interpretated with caution, researchers say.

Dietary supplements don't work for weight loss

A new systematic review up to December 2019, also identified 67 randomised trials comparing the effect of dietary supplements containing naturally occurring isolated compounds to placebo for weight loss in 5,194 healthy overweight or obese adults (aged 16 years or older) [3].

Dietary supplements included in the analysis were: chitosan (a complex sugar from the hard outer layers of lobsters, crabs, and shrimp that claims to block absorption of fat or carbohydrates); glucomannan (a soluble fibre found in the roots of the elephant yam, or konjac, that promotes a feeling of fullness); fructans (a carbohydrate composed of chains of fructose) and conjugated linoleic acid (that claims to change the body composition by decreasing fat).

The analysis found that chitosan (-1.84 kg), glucomannan (-1.27 kg), and conjugated linoleic acid (-1.08 kg) resulted in statistically, but not clinically, significant weight loss compared to placebo.

Some dietary supplements, including modified cellulose (plant fibre that expands in the stomach to induce a feeling of fullness) and blood orange juice extract, showed promising results but were only investigated in one trial and need more evidence before recommending them for weight loss, researchers say.

"Herbal and dietary supplements might seem like a quick-fix solution to weight problems, but people need to be aware of how little we actually know about them", says Bessell. "Very few high-quality studies have been done on some supplements with little data on long-term effectiveness. What's more, many trials are small and poorly designed, and some don't report on the composition of the supplements being investigated. The tremendous growth in the industry and popularity of these products underscores the urgency for conducting larger more rigorous studies to have reasonable assurance of their safety and effectiveness for weight loss."

Vegetarians appear to have a healthier biomarker profile than meat-eaters, and this applies to adults of any age and weight, and is also unaffected by smoking and alcohol consumption, according to a new study in over 166,000 UK adults, being presented at this week's European Congress on Obesity (ECO), held online this year.

Biomarkers can have bad and good health effects, promoting or preventing cancer, cardiovascular and age-related diseases, and other chronic conditions, and have been widely used to assess the effect of diets on health. However, evidence of the metabolic benefits associated with being vegetarian is unclear.

To understand whether dietary choice can make a difference to the levels of disease markers in blood and urine, researchers from the University of Glasgow did a cross-sectional study analysing data from 177,723 healthy participants (aged 37-73 years) in the UK Biobank study, who reported no major changes in diet over the last five years.

Participants were categorised as either vegetarian (do not eat red meat, poultry or fish; 4,111 participants) or meat-eaters (166,516 participants) according to their self-reported diet. The researchers examined the association with 19 blood and urine biomarkers related to diabetes, cardiovascular diseases, cancer, liver, bone and joint health, and kidney function.

Even after accounting for potentially influential factors including age, sex, education, ethnicity, obesity, smoking, and alcohol intake, the analysis found that compared to meat-eaters, vegetarians had significantly lower levels of 13 biomarkers, including: total cholesterol; low-density lipoprotein (LDL) cholesterol--the so-called 'bad cholesterol; apolipoprotein A (linked to cardiovascular disease), apolipoprotein B (linked to cardiovascular disease); gamma-glutamyl transferase (GGT) and alanine aminotransferase (AST)--liver function markers indicating inflammation or damage to cells; insulin-like growth factor (IGF-1; a hormone that encourages the growth and proliferation of cancer cells); urate; total protein; and creatinine (marker of worsening kidney function).

However, vegetarians also had lower levels of beneficial biomarkers including high-density lipoprotein 'good' (HDL) cholesterol, and vitamin D and calcium (linked to bone and joint health). In addition, they had significantly higher level of fats (triglycerides) in the blood and cystatin-C (suggesting a poorer kidney condition).

No link was found for blood sugar levels (HbA1c), systolic blood pressure, aspartate aminotransferase (AST; a marker of damage to liver cells) or C-reactive protein (CRP; inflammatory marker).

"Our findings offer real food for thought", says Dr Carlos Celis-Morales from the University of Glasgow, UK, who led the research. "As well as not eating red and processed meat which have been linked to heart diseases and some cancers, people who follow a vegetarian diet tend to consume more vegetables, fruits, and nuts which contain more nutrients, fibre, and other potentially beneficial compounds. These nutritional differences may help explain why vegetarians appear to have lower levels of disease biomarkers that can lead to cell damage and chronic disease."

The authors point out that although their study was large, it was observational, so no conclusions can be drawn about direct cause and effect. They also note several limitations including that they only tested biomarker samples once for each participant, and it is possible that biomarkers might fluctuate depending on factors unrelated to diet, such as existing diseases and unmeasured lifestyle factors. They also note that were reliant on participants to report their dietary intake using food frequency questionnaires, which is not always reliable.

Mild Covid-19 infection is very unlikely to cause lasting damage to the structure or function of the heart, according to a study led by UCL (University College London) researchers and funded by the British Heart Foundation (BHF) and Barts Charity.

The researchers say the results, published in JACC Cardiovascular Imaging, should reassure the public, as they relate to the vast majority of people who had Covid-19 infections with mild or no symptoms.

This study of 149 healthcare workers recruited from Barts Health and Royal Free London NHS Trusts is the largest and most detailed study to date into mild Covid-19 infection and its longer-term impact on the heart. It follows concerns that because severe hospitalised Covid-19 infections are associated with blood clots, inflammation of the heart and heart damage, mild infections may cause similar complications. However, up until now, there has been little information specifically looking at this group of people and the effects on the heart further down the line after infection.

Researchers identified participants with mild Covid-19 from the COVIDsortium, a study in three London hospitals where healthcare workers had undergone weekly samples of blood, saliva and nasal swabs for 16 weeks. Six months after mild infection, they looked at the heart structure and function by analysing heart MRI scans of 74 healthcare workers with prior mild Covid-19 and compared them to the scans of 75 healthy age, sex and ethnicity matched controls who had not previously been infected.

They found no difference in the size or amount of muscle of the left ventricle - the main chamber of the heart responsible for pumping blood around the body - or its ability to pump blood out of the heart. The amount of inflammation and scarring in the heart, and the elasticity of the aorta - which is important for blood to easily flow out of the heart - remained the same between the two groups.

When the researchers analysed blood samples, they found no differences in the two markers of heart muscle damage - troponin and NT-proBNP - six months after mild Covid-19 infection.

Now, the team of researchers and cardiologists suggest that there is little benefit from screening the hearts of people who've had mild infection, and research should focus on those who've suffered severe Covid-19, high risk groups or those with ongoing symptoms.

Dr Thomas Treibel (UCL Institute of Cardiovascular Science and Barts Health NHS Trust), said: "Disentangling the impact Covid-19 has on the heart has been a challenge. But we're now at the stage of the pandemic where we can really start to get a grip on the longer-term implications Covid-19 has on the health of our heart and blood vessels.

"We've been able to capitalise on our incredible frontline staff who've been exposed to the virus this past year and we're pleased to show that the majority of people who've had Covid-19 seem to not be at increased risk of developing future heart complications. We now need to focus our attention on the long term impact the virus has in those who've been hit hardest by the disease."

Dr Sonya Babu-Narayan, Associate Medical Director at the British Heart Foundation and consultant cardiologist, said: "These findings one year on from the start of the pandemic are welcome reassurance to the hundreds of thousands of people who have experienced Covid-19 with mild or no symptoms.

"Throughout the pandemic, BHF researchers have made progress investigating the short and long-term effects of Covid-19 on the heart and circulatory system. There's still a lot more work to be done, but for now it seems the good news is that mild Covid-19 illness does not appear to be linked to lasting heart damage."

There were small abnormalities identified by MRI but these were not found more often in people who had mild Covid-19 than those that have never had it. The changes could have been caused by something other than coronavirus and they may not make any noticeable difference to the health of that person.

The use of non-steroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen, does not lead to higher rates of death or severe disease in patients who are hospitalised with COVID-19, according to a new observational study of more than 72,000 people in the UK published in The Lancet Rheumatology journal.

NSAIDs are common treatments for acute pain and rheumatological diseases such as rheumatoid arthritis and osteoarthrosis. Early in the pandemic, there was debate on whether the use of such drugs increased the severity of COVID-19, which led to urgent calls for investigations between NSAIDs and COVID-19.

The ISARIC CCP-UK (International Severe Acute Respiratory and emerging Infection Consortium Clinical Characterisation Protocol United Kingdom) study, which is the largest of its kind, provides clear evidence that the continued use of NSAIDs in patients with COVID-19 is safe.

In the study, around a third of patients (30.4%. 1,279 out of 4,211) who had taken NSAIDs prior to hospital admission for COVID-19 died, a rate which was similar (31.3%. 21,256 out of 67,968) in patients who had not taken NSAIDs. In patients with rheumatological disease, the use of NSAIDs did not increase mortality.

Prof Ewen Harrison, of the University of Edinburgh and lead author of the study, said: "NSAIDs are commonly used to treat people all over the world for a range of conditions, from minor aches and pains to chronic conditions such as arthritis and cardiovascular disease. Many people rely on them to be able to carry out their day-to-day activities. When the pandemic began over a year ago, we needed to be sure that these common medications would not lead to worse outcomes in people with COVID-19. We now have clear evidence that NSAIDs are safe to use in patients with COVID-19, which should provide reassurance to both clinicians and patients that they can continue to be used in the same way as before the pandemic began." [1]

The study collected data on the medication patients had been prescribed, were currently taking, or had taken within 14 days prior to being admitted to hospital, as well as demographic information, and medical history. The study cohort included patients with confirmed or highly suspected COVID-19 infection admitted to 255 healthcare facilities in England, Scotland, and Wales, between January and August 2020. Of the 72,179 patients eligible for the study, 5.8% (4,211) had taken NSAIDs prior to admission

Modelling analyses were used to estimate the effects of NSAIDs taken prior to hospitalisation on mortality rates in hospital, disease severity, admission to critical care, requirement for invasive or non-invasive ventilation, use of supplemental oxygen, or development of acute kidney injury, which were then compared to patients who had not taken NSAIDs. Those who took NSAIDs were no more likely to be admitted to critical care, need invasive or non-invasive ventilation, or require oxygen.

The authors noted some limitations to the study. Despite being the largest ongoing prospective study of patients admitted to hospital, it only represents 60% of hospitalised patients in the UK over the time of the study and it did not include patients with severe COVID-19 who were not hospitalised. However, it would be expected that most patients who had severe COVID-19 would have been admitted to hospital and therefore included in the study, the authors said. The study did not determine whether patients continued to be given NSAIDs while they were in hospital, so the authors cannot make any recommendations on this.

Additionally, the study could not capture how long patients were taking NSAIDs prior to hospital admission and whether they were being taken for long-term conditions or short-term symptom relief. In the UK, ibuprofen is the most commonly used NSAID, so it is unclear whether the results of this study are generalisable to other countries where other NSAIDs are more frequently used. Further analyses performed suggested other non-ibuprofen NSAIDs had a similar safety profile to ibuprofen. Further research and clinical trials may help definitively establish whether NSAIDs are safe in different populations and whether their anti-inflammatory effects have any impact on patients with COVID-19.

With the COVID-19 vaccines on many people's minds, some may be surprised to learn that we do not yet have vaccines for many common infectious diseases.

Take salmonella, for example, which can infect people through contaminated food, water and animals. According to the World Health Organization, non-typhoidal salmonella infection affects more than 95 million people globally each year, leading to an estimated 2 million deaths annually. There is no approved vaccine for salmonella in humans, and some strains are antibiotic-resistant.

But just as scientists spent decades doing the basic research that made the eventual development of the COVID-19 vaccines possible, University of Florida researchers led by Mariola Edelmann in the department of microbiology and cell science, UF/IFAS College of Agricultural and Life Sciences, are laying the groundwork for an effective vaccine for salmonella and other hard-to-treat bacterial infections. In their study supported by the National Institutes of Health and published in PLOS Pathogens, the UF/IFAS scientists demonstrate a novel approach to triggering immunity against salmonella.

This approach takes advantage of how cells communicate with each other, said Winnie Hui, first author of the study, which was conducted while she was a doctoral candidate in microbiology and cell science.

"Cells communicate with each other through particles called extracellular vesicles or EVs. Think of these like molecular telephones that let cells talk to each other. We wanted to know if some of those messages included information related to immune response," said Hui, who graduated from the UF/IFAS College of Agricultural and Life Sciences in 2019 and is now a postdoctoral researcher in the UF College of Medicine, division of rheumatology and clinical immunology.

"Host EVs have not been previously studied in the context of fighting enteric bacterial infections, so that is part of what makes our approach new and adds to the field," said Edelmann, senior author on the study, Hui's dissertation director and an assistant professor of microbiology and cell science.

Edelmann hypothesized that a specific type of EVs called exosomes were part of the immune response against salmonella and may one day hold the key to developing a vaccine.

To test their idea, the research team took exosomes from white blood cells infected with salmonella. Inside those exosomes, which measure just a few dozen nanometers across, they found salmonella antigens, which are bits of salmonella protein known to trigger an immune response.

Next, the researchers wanted to know if these exosomes might function as a vaccine, helping the body build up its defenses against salmonella, said Lisa Emerson, one of the study's co-authors and a doctoral student in Edelmann's laboratory.

"We put the exosomes in 'nanobubbles' that the mice inhaled. Later, we ran tests to see how their immune systems responded," said Emerson, who is in the UF/IFAS College of Agricultural and Life Sciences.

The researchers found that after they introduced the exosomes containing salmonella antigens, the exosomes localized to tissues that produce mucous, activating specific cells at these sites. Weeks later, mice developed antibodies against salmonella and specific cellular immune responses, which typically target this bacterium for elimination. For the researchers, this is a promising result.

"There are two types of immune responses generated when our bodies encounter a pathogen. The first one is called innate immunity, which is an immediate response to an infection, but it is also less specific. The other response is called adaptive immunity, and this protective response is specifically tailored to a given pathogen, but it also takes longer to develop. Exosomes generated by infected white blood cells stimulated both of these responses in animals," said Hui.

While these results show promise, more research will be needed before we have a salmonella vaccine that works in humans, Hui said.

"Our study has identified a novel role of exosomes in the protective responses against salmonella, but we also think that exosomes can find broader applications for other intestinal infections and beyond," Edelmann said.

"Exosomes have this unique capability to encapsulate precious cargo while enabling its targeted delivery to tissue of interest. For many conditions and infections, this precise delivery of therapeutic payload is what makes a difference, and we are currently also evaluating exosomes in delivering cargo to other tissues of choice," said Edelmannn whose work is supported by several federal funds focused on the roles of extracellular vesicles in bacterial infections and disease and host-directed therapies against intestinal infections.

For some people, social gatherings can be a time to imbibe. And for some, that can turn into a time to overindulge. But how do your neighborhood and your social network affect binge drinking?

Along with colleagues at the RAND corporation in Santa Monica, Indiana University researcher Hank Green examined how neighborhood and social network characteristics were related to adult binge drinking. He and his co-authors found that both factors play a role in how much someone drinks, information that can help us better understand binge drinking among adults.

The study was published in the journal Health and Place, indexed in Science Direct and PubMed.

"Adults living in cohesive neighborhoods where people get along, help and look out for one another had a lower likelihood of any binge drinking at all compared to those living in less cohesive neighborhoods," the co-authors point out.

"Living in a highly cohesive neighborhood may impact social norms and constrain behavior in such a way that binge drinking is very unlikely, even if the opportunity to drink arises," Green said.

The researchers also found that, for those who live in neighborhoods they consider safe and orderly, and who have a more interconnected social network, the likelihood of social drinking increases, and drinking heavily might occur in those social drinking situations, regardless of how cohesive they find their neighborhood to be. However, the study also found that those neighborhood and network factors also restrict how often someone binge-drinks, probably through social control processes such as friends and neighbors looking out for each other or commenting on someone's drinking, etc.

"We also found that binge drinking was more likely among adults who lived in orderly neighborhoods and who had denser social networks, but reported lower neighborhood cohesion," said Green, associate professor at the IU School of Public Health-Bloomington.

In neighborhoods ranked by study participants as disordered, unsafe, and lacking cohesion, neighborhood factors lose their overall impact. Social networks tend to take over the role of social control, according to the study. In these types of neighborhoods, it's people with more interconnected social networks who binge less often.

Researchers utilized online surveys from adults ages 30-80 drawn randomly from the RAND American Life Panel. The main predictor variables were neighborhood cohesion (do neighbors help neighbors, do neighbors get along); neighborhood order (my neighborhood is clean, safe); and social network density. Associations of these measures with past month binge drinking (any, number of days) were examined, controlling for demographic characteristics.

Green said the study could help inform intervention practices such as cognitive behavioral therapy because those approaches already focus on identifying people and places that trigger binge drinking and addressing those triggers with behavioral changes. Indirectly, Green said, the study suggests that those interventions could also focus on people and places that discourage binge drinking or facilitate less frequent binge drinking and better drinking choices. Those interventions could also consider a broader definition of "place" that moves beyond a specific location to consider how larger areas like neighborhoods might impact drinking.

"Because neighborhood and social network factors work in tandem to affect the likelihood of binge drinking and the frequency of binge drinking, interventions for problem drinking should incorporate both of these aspects to make them more effective," Green said.

The protein, known as NusG, pauses the transcription machinery at specific DNA sequences to facilitate what is called "intrinsic termination" and prevent unwanted transcription that could disrupt cellular function.

A new study, led by Penn State researchers, shows that NusG and the related protein, NusA, together facilitate termination at about 88% of the intrinsic terminators in the bacteria Bacillus subtilis. Understanding this process expands our basic knowledge of this key cellular function and could eventually aid in the development of antibiotics that target and disrupt gene regulation in bacteria. A paper describing the research appears online in the journal eLife.

"For a cell to access the genetic information stored in DNA, it first must be transcribed into RNA by an enzyme called RNA polymerase," said Zachary F. Mandell, a graduate student at Penn State and first author of the paper. "This process is highly coordinated to ensure that the right genes are expressed at the right times and at appropriate levels for the cell to function properly. We are interested in understanding the mechanisms that allow the cell to stop transcription at precise locations along the genome."

Proper regulation of gene expression occurs in three basic stages. First, transcription is initiated by RNA polymerase that binds to the DNA at the beginning of the sequence that is being transcribed. NusA and NusG then bind to RNA polymerase during the elongation process to make an RNA copy of the DNA sequence. Finally, the transcription must be terminated at the appropriate spots in the genome.

"Termination of transcription is especially important in bacteria because the genes are packed tightly together along the genome, such that failure to terminate transcription at the right locations could lead to inappropriate gene expression," said Paul Babitzke, professor of biochemistry and molecular biology at Penn State and the leader of the research team.

The mechanisms for termination in bacteria traditionally have been classified as either "factor-dependent," which relies on a protein called Rho, or intrinsic termination, which was thought to be "factor-independent." Intrinsic termination relies on an RNA hairpin structure that forms in the RNA molecule being produced, which causes the RNA to be released from the transcription machinery.

NusG and NusA are both proteins classified as transcription factor that help regulate gene expression and are part of the complex of proteins that read and transcribe DNA during elongation. NusA interacts with the RNA molecule being produced and NusG can bind to the DNA to pause elongation. Based on previous research, NusA is thought to play a role in intrinsic termination by aiding in the formation of the RNA hairpin, but the role of NusG in termination had not been established.

To further explore the role of these two proteins in intrinsic termination, the research team produced strains of bacteria that lacked NusA, lacked NusG, and lacked both NusA and NusG. They then used a technique that they invented called "Term-Seq," in which they can preserve and identify the ends of all the RNA molecules produced in their bacterial strains. The RNA ends from the mutant strains could then be compared to RNA molecules from bacteria with normally functioning NusA and NusG.

"We found that some intrinsic termination sites were dependent on NusA, some on NusG, some on either NusA or NusG, and some required both," said Mandell. "We were somewhat surprised by how big of a role these two proteins play in intrinsic termination. A total of 88% of all intrinsic termination sites relied on NusA or NusG in some capacity. Intrinsic termination is clearly not completely 'factor-independent.'"

The researchers are still investigating the precise role that the Nus proteins play in transcription termination.

"We think that NusA helps directly in the formation of the hairpins required for intrinsic termination and that NusG is pausing elongation at termination sites to give the hairpin additional time to form," said Babitzke.

The most comprehensive study of the family tree for legumes, the plant family that includes beans, soybeans, peanuts, and many other economically important crop plants, reveals a history of whole-genome duplications. The study also helps to uncover the evolution of genes involved in nitrogen fixation--a key trait likely important in the evolutionary spread and diversification of legumes and vital for their use as "green manure" in agriculture. To reconstruct the family tree, researchers compared the DNA sequence of more than 1500 genes from 463 different legume species, including 391 newly sequenced species, that span the diversity of this large plant family.

A paper describing the study, led by Penn State Professor of Biology Hong Ma, appears in the May 2021 issue of the journal Molecular Plant.

"Legumes make up the third largest family of flowering plants and are incredibly diverse--ranging from tiny herbs to giant trees," said Ma, who is the Huck Distinguished Research Professor of Plant Molecular Biology at Penn State. "They are essential food crops for both humans and livestock, can be used as lumber, and have many other uses. Maybe most importantly, they can 'fix' nitrogen--extracting the vital nutrient from the atmosphere and storing it in nodules on their roots in a symbiotic relationship with soil bacteria--making them important as green manure to improve soil health."

There are over 19,000 species in the legume family divided into six subfamilies and then further divided into narrower and narrower groupings based on their evolutionary relationships. There are 765 genera--the grouping one level above species--of which the team sampled members of 333. To build the family tree, the team analyzed gene sequences from the transcriptomes--the portion of the genome that is expressed as genes--of most of the 463 species and a small number of shallowly sequenced whole genomes from across legume diversity.

"This is the largest study of this kind for a single plant family," said Ma. "We went to great lengths to sample as many species as we could to get a broad representation of the legume family, but it is often difficult to get well-preserved specimens that we can extract DNA or RNA from, especially for species found in remote locations. Having this broad representation of species allowed us to build the most detailed nuclear-gene family tree for legumes to date."

In addition to helping researchers understand the evolution and diversification of legumes, the new legume family tree helps to clarify the relationship between crop plants and their wild relatives. Although the close relatives of important agricultural crops are often known, studying more distant wild cousins could reveal traits that could be exploited to help plants thrive in changing environments and resist diseases or insect pests.

Across the legume family tree, the research team identified strong evidence for 28 separate whole-genome duplication events. Whole-genome duplications, evolutionary events that result in complete duplication of the entire genome, are fairly common among flowering plants and are thought to allow for functional innovation and evolutionary diversification. One of the duplication events that the team identified appears to have occurred in the ancestor of all members of the legume family.

"Because for most of the species in our study we used transcriptomes and do not have entire genome sequences, we consider these as 'proposed' genome duplication events," said Ma. "These kinds of studies are kind of like solving a mystery. If you only have one or a few witnesses it might be difficult to convince a jury of your evidence, but if you have a hundred witnesses who have different perspectives and they all point to the same thing it becomes difficult to dismiss that evidence. In our case, the different species are like our witnesses. The size of our study allowed us to identify events that we might otherwise have dismissed."

The two largest subfamilies account for over 17,000 legume species and include all of the species with the ability to fix nitrogen. Nitrogen is an important plant nutrient--most commercial fertilizers contain a mix of nitrogen, phosphorus and potassium--so the symbiotic relationship between some legumes and the microorganisms that allow them to assimilate nitrogen from the atmosphere using root nodules has spurred their success by allowing them to colonize areas with less fertile soil. The research team also identified clues to the evolution of the genes responsible for this important trait.

"Our data support the idea that nodulation and nitrogen fixation originated a single time early in the history of legumes and other related nitrogen-fixing plants and the whole-genome duplication event at the origin of legumes might have been crucial for the evolution of this process," said Ma. "In addition to this duplication event, we are also able to see gene loss in plants that do not have the ability to nodulate, and evolutionary changes in genes that contributed to their role in nodulation."

Are penalty shots a soccer player's dream or nightmare? What should be an easy shot can become a mammoth task when the hopes and fears of an entire nation rest on a player's shoulders, leading them to choke under pressure. Understanding the brain activity behind choking is the driving force behind a new study in open-access journal Frontiers in Computer Science. The study is the first to measure brain activity during penalty shots in a soccer pitch environment. It finds that people who choked activated areas of the brain involved in long-term thinking, suggesting that they were overthinking the consequences of missing the shot.

Penalty shootouts hold a special fear for many soccer fans. For instance, the English team has suffered some infamous misses over the years and their record at the penalty spot is fairly bleak. Remember Beckham's slip on the penalty spot against Portugal in the 2004 European Cup? He certainly does. Penalties can go either way, which makes them exciting to watch, but they raise some questions about performance under pressure.

"How can it be that football players with a near perfect control over the ball (they can very precisely kick a ball over more than 50 meters) fail to score a penalty kick from only 11 meters?" asks coauthor Max Slutter, an MSc student at the faculty of electrical engineering, mathematics and computer science at the University of Twente, the Netherlands. "Obviously, huge psychological pressure plays a role, but why does this pressure cause a missed penalty? We tried to answer this by measuring the brain activity of football players during the physical execution of a penalty kick."

Slutter and colleagues recruited 22 volunteers to kick penalties and measured their brain activity using a technique called functional near-infrared spectroscopy (fNIRS). fNIRS involves wearing a headset, and can measure brain activity on the move. The study is the first to investigate the neuroscience behind choking under realistic conditions outside a laboratory.

The volunteers attempted to score penalties under different pressure conditions: with an open goal, against a friendly goalkeeper, and in a high-pressure situation where the goalkeeper attempted to distract them and there was a prize at stake.

"We found that players who were able to perform under pressure activated task-relevant areas of the brain," explained Dr Nattapong Thammasan, of the University of Twente. "For example, increased activation of the motor cortex was related to performing under pressure. This seems logical, as movement is one of the most important elements when taking a penalty."

For players who tended to experience more anxiety and miss penalties, another area of the brain was more active - the pre-frontal cortex. This brain region is involved in long-term thinking, suggesting that such players were thinking about the consequences of missing the shot, which impaired their performance.

Strikingly, the researchers believe that the fNIRS technology could assist players to perform better under pressure by letting them know how their brains are behaving. They hypothesize that players could train themselves to activate beneficial brain regions in high-pressure situations.

Excitingly, the technique could also be beneficial for other professions where performance under high pressure is important, such as brain surgery. It may be too late for Beckham, but next-generation brain surgeons could be on the way.

Systemic inequalities mean that low-income households in London are more likely to be exposed to higher levels of indoor air pollution, according to a report by UCL researchers.

The biggest factors are the quality of housing and the characteristics of the surrounding environment, taking location and levels of outdoor air pollution into account - factors beyond occupants' control.

Air pollution exposure is the greatest environmental health threat in the UK, with long-term exposures estimated to cause 28,000-36,000 premature deaths a year.

In the paper, published in Buildings and Cities, researchers used available data and models, assembling evidence to examine five factors explaining why lower socio-economic groups may be exposed to higher levels of indoor air pollution in their homes, focusing on London and the pollutants PM2.5, NOx and CO. These pollutants were selected as they are primarily produced by combustion processes, such as cooking or burning fuel, and are therefore found in most households.

The factors were: housing location and ambient outdoor levels of pollution; housing characteristics including ventilation properties and internal sources of pollution; occupant behaviours; time spent indoors; and underlying health conditions. London was the focus because housing there isn't typically representative of the rest of the country, with a higher proportion of renters and flats as dwellings.

The team used a systems approach highlighting interactions and links between factors to show how they lead to systemic exposure inequalities, with lower income households having limited opportunities to improve their indoor air quality.

Lead author, PhD candidate Lauren Ferguson, (UCL Energy Institute and UCL Institute for Environmental Design & Engineering) said: "This research highlights that exposure to indoor air pollution can lead to health inequalities depending on socio-economic status. Differences in housing quality and characteristics of the surrounding areas mean low-income households are likely to bear a disproportionate risk of elevated exposure to indoor air pollution.

"Poor quality housing can lead to a number of negative health effects and is therefore an area which should be targeted in order to address the growing health inequalities gap in the UK."

Air pollution exposure is associated with health problems such as respiratory and cardiovascular complications, birth defects, childhood asthma cases and sudden infant deaths. Long term exposure to particulate matter (PM) has been linked to adult depression, although this needs more research.

Low socio-economic status (SES) groups are more likely to live in higher density flats and smaller dwellings and areas of London with higher levels of air pollution.

Whilst high density dwellings often have lower ventilation levels which can prevent some outdoor air pollution from getting in, this is not sufficient to offset living in an area of high outdoor pollution. Dwellings with low levels of ventilation prevent indoor air pollution from activities including cooking and smoking from escaping, and are more vulnerable to local pollution from neighbours' cooking or smoking.

Levels of smoking are higher amongst low SES groups, with 25.5% of those in routine and manual occupations smoking regularly, compared with 15.7% in intermediate occupations and 10.2% in managerial and professional occupations. Low SES groups also report longer cooking durations, increasing exposure to pollution.

Low SES groups are more likely to spend less time outdoors, due to a variety of factors including higher levels of unemployment, fewer after-school clubs and little access to green spaces. This raises their susceptibility to developing health conditions from increased exposure to indoor air pollution.

They are at a higher risk of experiencing underlying health conditions, material deprivation and psychological stress, making them more susceptible to air pollution. Material deprivation includes lack of access to healthcare, poor diet - which is strongly linked to income class - and lack of physical activity, which is linked to spending more time indoors due to the factors mentioned above.

The paper builds on previous research in 2020 on how concentrations of indoor domestic air pollution may vary between SES groups. The researchers hope the findings will influence policy decisions regarding air pollution and housing in London, and call for action to improve housing quality, promote and support interventions to reduce exposure to outdoor air pollution and encourage behavioural change to minimise risk factors from smoking and spending large amounts of time indoors.

LUGANO, 7 May, 2021- Findings presented at today's EADV 2021 Spring Symposium suggest that an imbalance in gut microbiota (dysbiosis), could play a significant role in the progression of inflammatory skin disease, Hidradenitis Suppurativa (HS). HS is a painful, long-term skin condition, with a chronic and relapsing nature that significantly impacts patients' quality of life.

Researchers at Hacettepe University collected faecal samples from 15 patients with HS and 15 age and sex matched healthy individuals and analysed regions of the bacterial 16S rRNA gene to investigate differences in their gut microbiota. Researchers found that the relative abundance of three genera of bacteria (known collectively as Firmicutes), unclassified Clostridiales, unclassified Firmicutes and Fusicatenibacter in HS patients were significantly lower than that in controls (p = 0.005, p = 0.029, and p = 0.046, respectively). Reduced amounts of these bacteria are known to disrupt the regulatory balance within the gut and stimulate an inflammatory response.

The human gastrointestinal tract is inhabited with a wide variety of bacterial organisms, known collectively as the gut microbiome.1 Studies have increasingly demonstrated that the gut microbiome and skin are intrinsically connected, offering defence against pathogens in the environment. This relationship is known as the 'gut-skin axis' and has been linked to many inflammatory and autoimmune skin disorders, such as acne and psoriasis. This connection inspired the researchers to characterise the composition of HS patients' intestinal microbiome, hypothesising that imbalance may play a role in the high inflammatory burden of this condition. HS is a multifactorial disease caused by both genetic and environmental factors. Obesity and smoking can significantly exacerbate symptoms, and both of these have an impact on the gut microbiome.

Dr Neslihan Demirel Ogut, Usak University Training and Research Hospital explains, "Our research provides evidence the gut-skin axis is implicated in the progression of this chronic inflammatory skin disorder. While further evidence is required, our research suggests that dietary alteration and personalised probiotic supplementation might also be beneficial for HS patients, particularly since treatment options are limited for these individuals."

Gut microbiota plays a critical role in human health through development of the immune response, controlled by specific pathways and the products of metabolism, known as short-chain fatty acids (SCFA). Bacteria in the gut (such as Firmicutes) produce these SCFAs that ensure a balance between immune cells that stimulate or suppress an inflammatory response is maintained. Any disruption to this balance, as demonstrated by the reduced abundance of these organisms in the gut microbiome of HS patients, may induce an unwanted inflammatory response.

Additional research is required to further understand and explain the connections between the gut microbiota and excessive inflammatory state in HS patients. "As one of the preliminary studies investigating HS, this pioneering research lays the foundation for future research into the management of this debilitating condition. It is an exciting breakthrough in a topic currently at the forefront of scientific research," says Marie-Aleth Richard, EADV Board Member and Professor at the University Hospital of La Timone, Marseille.

PHILADELPHIA-- A gene called GAS2 plays a key role in normal hearing, and its absence causes severe hearing loss, according to a study led by researchers in the Perelman School of Medicine at the University of Pennsylvania.

The researchers, whose findings are published online today in Developmental Cell, discovered that the protein encoded by GAS2 is crucial for maintaining the structural stiffness of support cells in the inner ear that normally help amplify incoming sound waves. They showed that inner ear support cells lacking functional GAS2 lose their amplifier abilities, causing severe hearing impairment in mice. The researchers also identified people who have GAS2 mutations and severe hearing loss.

"Anatomists 150 years ago took pains to draw these support cells with the details of their unique internal structures, but it's only now, with this discovery about GAS2, that we understand the importance of those structures for normal hearing," said study senior author Douglas J. Epstein, PhD, professor of genetics at Penn Medicine.

Two to three of every 1,000 children in the United States are born with hearing loss in one or both ears. About half of these cases are genetic. Although hearing aids and cochlear implants often can help, these devices seldom restore hearing to normal.

One of the main focuses of the Epstein laboratory at Penn Medicine is the study of genes that control the development and function of the inner ear--genes that are often implicated in congenital hearing loss. The inner ear contains a complex, snail-shaped structure, the cochlea, that amplifies the vibrations from sound waves, transduces them into nerve signals, and sends those signals toward the auditory cortex of the brain.

Unraveling the role of Gas2 in hearing

A few years ago, Epstein's team discovered that Gas2, the mouse version of human GAS2, is switched on in embryos by another gene known to be critical for inner ear development. To determine Gas2's role in that development, the team developed a line of mice in which the gene had been knocked out of the genome and called them Gas2-knockout mice.

Alex Rohacek, PhD, a former graduate student in the Epstein lab, was puzzled to observe that the Gas2-knockout mice had inner ears with cells and structures that seemed quite normal. However, the animals, when tested, turned out to be severely hearing-impaired, with deficits at high sound frequencies of up to 50 decibels--equivalent to a loss of 99.999 percent of the normal acoustic energy.

Tingfang Chen, PhD, a postdoctoral fellow and co-first author on the study, determined that Gas2 is normally active within inner-ear support cells called pillar cells and Deiters' cells. In these cells, the protein encoded by the gene binds to flexible, tube-like structures called microtubules in a way that bundles and stabilizes them, effectively stiffening the cells.

With help from the collaborating team of Benjamin L. Prosser, PhD, assistant professor of Physiology at Penn Medicine and an expert on microtubules, the researchers discovered that when pillar cells and Deiters' cells lack Gas2, their microtubule bundles tend to come apart, dramatically reducing the stiffness of the cells.

That turns out to have dire implications for hearing. Within the inner ear, pillar cells and Dieters' cells help form the basic structure of the cochlea and serve as physical supports for cells called outer hair cells. The outer hair cells move in response to incoming acoustical vibrations--essentially to provide a crucial amplification of that sound energy. The experiments revealed that the pillar and Deiters' cells' loss of stiffness, due to the absence of Gas2, severely degrades the sound-amplifying properties of the outer hair cells they support.

"We observed that some of Deiters' cells in the Gas2-knockout mice even buckled under the tension of the rapid movements of the outer hair cells," Epstein said.

The experiments included sophisticated imaging of propagating sound waves in the inner ears of live Gas2-knockout and normal mice, conducted by collaborator John Oghalai, MD, chair and professor of otolaryngology-head and neck surgery at the Keck School of Medicine of USC, and his team.

GAS2 also causes human hearing loss

Curiously, the researchers could find no reports of GAS2-associated congenital hearing loss in the medical literature. Even when they canvassed colleagues around the world who run hearing-loss clinics, they came up empty-handed.

Then one day, Hannie Kremer, PhD, professor and chair of molecular otogenetics at Radboud University Medical Center in the Netherlands, emailed Epstein. She and her team had been studying a Somalian family in which four of the siblings had severe hearing loss from early life. The affected family members had no mutations in known hearing-loss genes--but each carried two mutant copies of GAS2.

The study therefore establishes GAS2 as a very probable new hearing loss gene in humans--the first one known to affect the mechanical properties of inner ear support cells.

The prevalence of hearing loss in people due to GAS2 mutations remains to be determined, but Epstein noted that this type of congenital hearing loss is nevertheless an attractive target for a future gene therapy.

"In many genetic hearing loss conditions, the affected cells are permanently damaged or die, but in this one, the affected cells are intact and conceivably could be restored to normal or near-normal by restoring GAS2 function," he said.

He added that such a gene therapy might be useful not only in more obvious cases of hearing loss in early childhood, but also in cases--perhaps more numerous--in which inherited mutations lead to a slower development of hearing loss in adulthood.

Researchers from University of Southern California, Bocconi University, and Vrije Universitei Amsterdam published a new paper in the Journal of Marketing that explains the six types of judgements consumers make when determining a product's authenticity and how marketers can use this insight to deliver more authentic offerings.

The study, forthcoming in the Journal of Marketing, is titled "The Concept of Authenticity: What it Means to Consumers" and is authored by Joseph Nunes, Andrea Ordanini, and Gaia Giambastiani.

Consumers crave authenticity. Yet marketing itself is typically considered inherently inauthentic. Hence, firms must learn to understand, manage, and excel at rendering authenticity. The critical question is: how? Marketers who wish to deliver authentic consumption experiences would benefit from guidance regarding ways to enhance consumers' assessments of the authenticity of their offerings. The starting point is knowing what consumers mean when they talk about authenticity, a nebulous concept.

Nunes says "When consumers talk about authentic consumption experiences, they really are referencing six types of judgements they make involving: accuracy, connectedness, integrity, legitimacy, originality, and proficiency." Accuracy refers to the seller being transparent and reliable in what is conveyed to consumers. Connectedness describes consumers' feelings of engagement and at times a sense of transformation. Integrity means the source is seen as intrinsically motivated, while acting autonomously and consistently. Legitimacy refers to conformity in terms of adhering to norms, standards, rules, or traditions. Originality refers to a product or service standing out from the mainstream. Finally, proficiency refers to the display of skills, craftsmanship, and/or expertise in the offering.

Knowing that judgments of accuracy, connectedness, integrity, legitimacy, originality, and proficiency are what comprise assessments of authenticity, managers can more efficiently and effectively deduce actionable strategies in terms of positioning. Ordanini continues, "From this research, practitioners can also tell which of these six judgments to emphasize and when in their customer marketing and communications. For example, companies selling hedonic products should see relatively large returns perception-wise from emphasizing proficiency because it matters more for hedonic products than for utilitarian products." The mattress company Tuft & Needle (what is more hedonic than sleep?) illustrates this by focusing on their belief in "quality craftsmanship without the gimmicks" on their website.

Anesthestic drugs act on the brain but most anesthesiologists rely on heart rate, respiratory rate, and movement to infer whether surgery patients remain unconscious to the desired degree. In a new study, a research team based at MIT and Massachusetts General Hospital shows that a straightforward artificial intelligence approach, attuned to the kind of anesthetic being used, can yield algorithms that assess unconsciousness in patients based on brain activity with high accuracy and reliability.

"One of the things that is foremost in the minds of anesthesiologists is 'Do I have somebody who is lying in front of me who may be conscious and I don't realize it?' Being able to reliably maintain unconsciousness in a patient during surgery is fundamental to what we do," said senior author Emery N. Brown, Edward Hood Taplin Professor in The Picower Institute for Learning and Memory and the Institute for Medical Engineering and Science at MIT, and an anesthesiologist at MGH. "This is an important step forward."

More than providing a good readout of unconsciousness, Brown added, the new algorithms offer the potential to allow anesthesiologists to maintain it at the desired level while using less drug than they might administer when depending on less direct, accurate and reliable indicators. That can improve patient's post-operative outcomes, such as delirium.

"We may always have to be a little bit 'overboard'," said Brown, who is also a professor at Harvard Medical School. "But can we do it with sufficient accuracy so that we are not dosing people more than is needed?"

Used to drive an infusion pump, for instance, algorithms could help anesthesiologists precisely throttle drug delivery to optimize a patient's state and the doses they are receiving.

Artificial intelligence, real-world testing

To develop the technology to do so, postdocs John Abel and Marcus Badgeley led the study, published in PLOS ONE [LINK TBD], in which they trained machine learning algorithms on a remarkable data set the lab gathered back in 2013. In that study, 10 healthy volunteers in their 20s underwent anesthesia with the commonly used drug propofol. As the dose was methodically raised using computer controlled delivery, the volunteers were asked to respond to a simple request until they couldn't anymore. Then when they were brought back to consciousness as the dose was later lessened, they became able to respond again. All the while, neural rhythms reflecting their brain activity were recorded with electroencephalogram (EEG) electrodes, providing a direct, real-time link between measured brain activity and exhibited unconsciousness.

In the new work, Abel, Badgeley and the team trained versions of their AI algorithms, based on different underlying statistical methods, on more than 33,000 two-second-long snippets of EEG recordings from seven of the volunteers. This way the algorithms could "learn" the difference between EEG readings predictive of consciousness and unconsciousness under propofol. Then the researchers tested the algorithms in three ways.

First, they checked whether their three most promising algorithms accurately predicted unconsciousness when applied to EEG activity recorded from the other three volunteers of the 2013 study. They did.

Then they used the algorithms to analyze EEG recorded from 27 real surgery patients who received propofol for general anesthesia. Even though the algorithms were now being applied to data gathered from a "noisier" real-world surgical setting where the rhythms were also being measured with different equipment, the algorithms still distinguished unconsciousness with higher accuracy than other studies have shown. The authors even highlight one case in which the algorithms were able to detect a patient's decreasing level of unconsciousness several minutes before the actual attending anesthesiologist did, meaning that if it had been in use during the surgery itself, it could have provided an accurate and helpful early warning.

As a third test, the team applied the algorithms to EEG recordings from 17 surgery patients who were anesthetized with sevoflurane. Though sevoflurane is different from propofol and is inhaled rather than infused, it works in a similar manner, by binding to the same GABA-A receptors on the same key types of brain cells. The team's algorithms again performed with high, though somewhat reduced accuracy, suggesting that their ability to classify unconsciousness carried over reliably to another anesthetic drug that works in a similar way.

The ability to predict unconsciousness across different drugs with the same mechanism of action is key, the authors said. One of the main flaws with current EEG-based systems for monitoring consciousness, they said, is that they don't distinguish among drug classes, even though different categories of anesthesia drugs work in very different ways, producing distinct EEG patterns. They also don't adequately account for known age differences in brain response to anesthesia. These limitations on their accuracy have also limited their clinical use.

In the new study, while the algorithms trained on 20-somethings applied well to cohorts of surgery patients whose average age skewed significantly older and varied more widely, the authors acknowledge that they want to train algorithms distinctly for use with children or seniors. They can also train new algorithms to apply specifically for other kinds of drugs with different mechanisms of action. All together a suite of well trained and attuned algorithms could provide high accuracy that accounts for patient age and the drug in use.

Abel said the team's approach of framing the problem as a matter of predicting consciousness via EEG for a specific class of drugs made the machine learning approach very simple to implement and extend.

"This is a proof of concept showing that now we can go and say let's look at an older population or let's look at a different kind of drug," he said. "Doing this is simple if you set it up the right way."

The resulting algorithms aren't even computationally demanding. The authors noted that for a given 2 seconds of EEG data, the algorithms could make an accurate prediction of consciousness in less than a tenth of a second running on just a standard MacBook Pro computer.

The lab is already building on the findings to refine the algorithms further, Brown said. He said he also wants to expand testing to hundreds more cases to further confirm their performance, and also to determine whether wider distinctions may begin to emerge among the different underlying statistical models the team employed.