Publisher Health

Australian researchers have uncovered new genetic insights into Staphylococcus aureus, revealing what makes the bacterium so dangerous when it enters the blood.
While common, Staphylococcus aureus infections — known as Golden staph — can be life-threatening if the bacteria enter the bloodstream, causing sepsis. Golden staph is notorious for its ability to become resistant to antibiotics, making it hard to treat, which can lead to adverse health outcomes for patients infected with a drug-resistant form of the bacteria.
In one of the most comprehensive studies of its kind, published in Cell Reports, researchers, led by the Peter Doherty Institute for Infection and Immunity (Doherty Institute), analysed the unique genetic profiles of more than 1,300 Golden staph strains.
By combining this data with patient and antibiotic information, the researchers found that, while patient factors are critical in determining mortality risks, specific genes are linked to antibiotic resistance, along with the bacteria’s ability to linger in the blood, evading antibiotics and the immune system.
University of Melbourne Dr Stefano Giulieri, a Clinician-Researcher at the Doherty Institute and first author of the paper, said the findings highlighted the diagnostic power of integrating clinical and genomic data.
“To the best of our knowledge, this is one of the first times that the method we used, called a genome-wide association study (GWAS), has been applied to delve into the role of bacterial genomes, host factors and antibiotics on the course of staphylococcal sepsis,” said Dr Giulieri.
“In GWAS, scientists scan the genome of a big collection of bacteria to look for tiny changes (mutations) that show up more often in strains with a certain characteristic, such as antibiotic resistance. Mutations with a strong statistical link are precious clues to figure out how bacteria acquire attributes that are important for patient outcomes.

Researchers have invented a nano-thin superbug-slaying material that could one day be integrated into wound dressings and implants to prevent or heal bacterial infections.
The innovation — which has undergone advanced pre-clinical trials — is effective against a broad range of drug-resistant bacterial cells, including ‘golden staph’, which are commonly referred to as superbugs.
Antibiotic resistance is a major global health threat, causing about 700,000 deaths annually, a figure which could rise to 10 million deaths a year by 2050 without the development of new antibacterial therapies.
The new study led by RMIT University and the University of South Australia (UniSA) tested black phosphorus-based nanotechnology as an advanced infection treatment and wound healing therapeutic.
Results published in Advanced Therapeutics show it effectively treated infections, killing over 99% of bacteria, without damaging other cells in biological models.
The treatment achieved comparable results to an antibioticin eliminating infection and accelerated healing, with wounds closing by 80% over seven days.
The superbug-killing nanotechnology developed internationally by RMIT was rigorously tested in pre-clinical trials by wound-healing experts at UniSA. RMIT has sought patent protection for the black phosphorus flakes including its use in wound healing formulations, including gels.

A major study published in JAMA led by researchers at Karolinska Institutet suggests that a possible cause of spontaneous brain haemorrhage could be transmitted via blood transfusion. At the same time, it is very unlikely that anyone should suffer a brain haemorrhage after receiving donated blood.
A common cause of spontaneous, recurring brain haemorrhages is the vascular disease cerebral amyloid angiopathy (CAA), in which proteins accumulate along the tiny blood vessels of the brain. Several studies have shown that CAA can be transferred from one individual to another through neurosurgery and probably via treatment using a certain type of growth hormone.
Few affected individuals
A new study by researchers from Karolinska Institutet, Södersjukhuset, Karolinska University Hospital in Sweden, the University of Copenhagen in Denmark, KU Leuven in Belgium and other institutions shows that patients who have received blood from donors who later suffered recurring brain haemorrhages are more than twice as likely to suffer a brain haemorrhage themselves.
The findings suggest that some factor that can give rise to spontaneous brain haemorrhages can be spread through blood transfusion. However, as only 0.1 per cent of the donors in the study subsequently suffered recurring brain haemorrhages there were consequently only a few affected patients.
“Blood transfusions are relatively common, which makes possible negative effects an important public health issue,” says the study’s last author Gustaf Edgren, researcher at the Department of Medicine, Karolinska Institutet (Solna) and specialist physician at Södersjukhuset. “However, in this case, it’s very unlikely that you’d suffer a brain haemorrhage from something transmitted through a transfusion.”
CAA could be transmissible
According to the researchers, the most important implication of the study is instead that it adds further support to the hypothesis that CAA can be transmitted between individuals, which, if true, can have consequences in several fields.

When you are under stress, your brain may release its own cannabinoid molecules to calm you down, activating the same brain receptors as THC derived from cannabis plants.
But the brain activity patterns and neural circuits that are regulated by these brain-derived cannabinoid molecules were not well known.
A new Northwestern Medicine study in mice has discovered that a key emotional brain center, the amygdala, releases endogenous (the body’s own) cannabinoid molecules under stress, and these molecules dampen the incoming stress alarm from the hippocampus, a memory and emotion center in the brain. These results provide more support for the hypothesis that these endogenous cannabinoid molecules are a body’s natural coping response to stress.
Stress exposure heightens risk for the development or worsening of psychiatric disorders from generalized anxiety and major depression to post-traumatic stress disorder (PTSD).
“Understanding how the brain adapts to stress at the molecular, cellular and circuit level could provide critical insight into how stress is translated into mood disorders and may reveal novel therapeutic targets for the treatment of stress-related disorders,” said corresponding study author Dr. Sachi Patel, chair of psychiatry and behavioral sciences at Northwestern University Feinberg School of Medicine and a Northwestern Medicine psychiatrist.
The study could indicate that impairments in this endogenous cannabinoid signaling system in the brain could lead to a greater susceptibility to developing stress-related psychiatric disorders including depression and PTSD, although this remains to be determined in humans, Patel said.
The study will be published Sept. 12 in Cell Reports.
For the study, Northwestern scientists used a new protein sensor that can detect the presence of these cannabinoid molecules at specific brain synapses in real time to show that specific high-frequency patterns of amygdala activity can generate these molecules. The sensor also showed that these molecules were released as a result of several different types of stress in mice.

Adults aged 60 and older who spend more time engaging in sedentary behaviors like sitting while watching TV or driving may be at increased risk of developing dementia, according to a new study by USC and University of Arizona researchers.
Their study showed the risk of dementia significantly increases among adults who spend over 10 hours a day engaging in sedentary behaviors like sitting — a notable finding considering the average American is sedentary for about 9.5 hours each day.
The study, published on Tuesday, September 12 in JAMA, also revealed the way sedentary behavior is accumulated over the course of the day didn’t matter as much as the total time spent sedentary each day. Whether spent in extended periods spanning several hours or spread out intermittently throughout the day, total sedentary behavior had a similar association with dementia according to study author David Raichlen.
“Many of us are familiar with the common advice to break up long periods of sitting by getting up every 30 minutes or so to stand or walk around. We wanted to see if those types of patterns are associated with dementia risk. We found that once you take into account the total time spent sedentary, the length of individual sedentary periods didn’t really matter,” said Raichlen, professor of biological sciences and anthropology at the USC Dornsife College of Letters, Arts and Sciences.
Researchers used data from the U.K. Biobank, a large-scale biomedical database of participants across the United Kingdom, to investigate possible links between sedentary behavior and dementia risk.
As part of a U.K. Biobank sub-study, over 100,000 adults agreed to wear accelerometers, wrist-worn devices for measuring movement, for 24 hours per day for one week. The researchers focused on a sample of approximately 50,000 adults from this sub-study over the age of 60 who did not have a diagnosis of dementia at the start of the study.
The researchers then applied a machine-learning algorithm to analyze the large dataset of accelerometer readings and classify behaviors based on different intensities of physical activity. The algorithm was able to discern between different types of activity such as sedentary behavior versus sleeping. The accelerometer data, combined with advanced computing techniques, provided researchers with an objective measure of the time spent engaging in different types of sedentary behaviors.

Scientists have created a method to detect key fat-filled particles known as lipoproteins in the central nervous system, opening a new view into the workings of the brain.
Researchers found that the particles in our nervous system, molecular cousins of the well-known HDL, or “good cholesterol” particles in our bloodstream, are much more diverse than previously thought. Researchers detected more than 300 different proteins associated with the particles, far more than the 16 known previously, that fall into at least 10 different families. These particles are rich in proteins that affect wound healing, the immune response, and the creation and nurturing of brain cells called neurons that are important for cognitive function.
The most common protein on the particles is apolipoprotein E, better known as APOE. Of the three commonly studied forms of APOE, the form known as APOE4 puts people at higher risk of Alzheimer’s disease. One copy of the APOE4 gene makes a person approximately four times as likely to develop dementia; a person with two copies is about 12 times more vulnerable.
The results were published August 30 in the journal Science Advances. The leader of the study is John Melchior, a protein biochemist at the Department of Energy’s Pacific Northwest National Laboratory. Melchior is a leader in lipoprotein research — and a carrier of two copies of the APOE4 gene, adding a personal incentive to his work to understand the protein’s action in the nervous system.
“We’ve known for a long time that in the nervous system, APOE is the primary protein on these particles calling the shots. But we don’t know much more beyond that. Our technology opens the door to learning more,” said Melchior.
“What the heck is APOE4 doing? That’s the big question. Why does one form translate to less risk for dementia while a slightly different form confers significant risk? Our technology brings us one step toward more answers,” he added.
APOE: Bringing fats and proteins together
Lipoproteins are best known for their work in the circulatory system, where they transport fat and cholesterol. It’s easy for scientists to detect HDL and LDL, known to many as “good cholesterol” and “bad cholesterol,” in the bloodstream because the molecules there are plentiful.

New findings from the University of Alabama at Birmingham indicate that the type of protein in the diet is not as important as the overall amount of weight loss for those with Type 2 diabetes.
Published in the journal Obesity, 106 adults with T2D were randomly assigned to either the high-protein or normal-protein diet for 52 weeks. Both diets were energy-restricted. The high-protein diet included recommendations to include lean beef in the diet, while the normal-protein diet instructed participants to refrain from eating any red meats. The team of researchers found that both a high-protein diet (40 percent of total calories from protein) and a moderate-protein diet (21 percent of total calories from protein) were effective in improving glucose control, weight loss and body composition in people with Type 2 diabetes.
Lead author James O. Hill, professor with the UAB Department of Nutrition Sciences and director of the UAB Nutrition Obesity Research Center, and co-author Drew Sayer, Ph.D., with the UAB Department of Family and Community Medicine, say that in this context of comparing two overall healthy dietary patterns that differ in the amounts of dietary protein and carbohydrate, as well as the inclusion/exclusion of lean, minimally processed beef, the results here show an individual can have some flexibility to choose a dietary pattern that most closely matches their preferences and that they are mostly like to stick with in the long term.
In the multi-site, randomized controlled trial, 71 study participants followed a higher-protein diet with four or more 4- to 6-ounce servings of lean beef per week (as the only source of red meat) or a normal-protein diet with no red meat, for 52 weeks. The high-protein diet was composed of 40 percent protein, 32 percent carbohydrate and 28 percent fat of total energy — while the normal-protein diet was composed of 21 percent protein, 53 percent carbohydrate and 26 percent fat of total energy (which is higher in protein than the average American diet, with protein intake averaging 14-16 percent of total energy).
All participants had T2D and followed the State of Slim weight management program, with both diets being reduced in calories and limited to food lists for each phase of the SOS program. In addition, participants worked up to exercising up to 70 minutes per day, six days per week.
The study was funded by the National Cattlemen’s Beef Association, a contractor to the Beef Checkoff, which was not involved in the study design, interpretation or publication.
Study Key Points Both a high-protein diet that includes red meat and a normal-protein diet without red meat are effective for weight loss and improving blood sugar control. The primary factor in managing Type 2 diabetes is weight loss itself, regardless of the specific composition of the diet. Avoiding red meat does not provide any additional benefits for weight loss or blood sugar control during a weight loss program.

Exposure to air pollution while in the womb is linked to alterations in proteins that can be detected after a baby is born, and which affect cell processes such as autophagy, the “self-eating” of damaged cells that occurs in response to stress.
Dr Olga Gorlanova, a research physician at the University Children’s Hospital, University of Basel, Switzerland, told the European Respiratory Society International Congress in Milan, Italy, that her study also showed that healthy, new-born babies had individual and different responses to their mothers’ exposure to air pollution during pregnancy. This might mean that some babies were more vulnerable to it than others. This was the case even if they were born into households in areas with relatively low levels of pollution.
Earlier work by Dr Gorlanova and her colleagues had shown that exposure to air pollution during pregnancy could affect lung function and the immune system in new-borns. In the current study, they looked at proteins involved in autophagy, ageing and cell remodelling to see how prenatal exposure to air pollution could affect them.
The researchers measured 11 proteins found in the cord blood of 449 healthy new-born babies from the Bern Basel Infant Lung Development (BILD) cohort study. The BILD study, started in 1999 in Bern, aims to recruit 1000 babies by 2025. It is investigating the effects of genetics and the environment (particularly air pollution) on lung development in babies and children.
Dr Gorlanova and colleagues measured the mothers’ exposure to nitrogen dioxide (NO2) and tiny particles called PM10,which areparticulate matter measuring 10 microns or less in diameter. Vehicle emissions, tyre and brake wear, and smoke are some of the sources of these pollutants. They found that NO2 and PM10 were both linked to changes in proteins involved in autophagy. Exposure to NO2 was linked to a decrease in the activity of the proteins SIRT1 and IL-8, and an increase in levels of the Beclin-1 protein.
“Our results indicate that NO2, a pollutant formed mainly from traffic emissions, is associated with increased levels of Beclin-1 protein, which is central to initiating autophagy. Exposure to higher NO2 was also linked to decreased levels of SIRT1, which is a protein that plays a protective role in stress resistance, inflammation and aging. IL-8 is a protein active in certain inflammatory cells,” said Dr Gorlanova.
“We grouped the babies into four distinct clusters according to the levels of air pollution they were exposed to while in the womb. The four clusters all had similar concentrations of the proteins being studied but had differences their exposure to NO2 and PM10 air pollution. One cluster had low concentrations of nine proteins, while another cluster, consisting of seven percent of all the babies, had higher levels of proteins that are involved in inflammatory and remodelling processes: IL-8 and IL-1B. Both these groups of new-borns had been exposed to lower, although differing, levels of prenatal air pollution than the other two groups. Our findings suggest that healthy new-borns have an individual response pattern to air pollution. We think that this may be an indication that some babies are more vulnerable to it than others.

Particular combinations of bacteria found in dust at day care facilities have been linked to wheezing in young children in a study presented at the European Respiratory Society International Congress in Milan, Italy. Wheezing in young children is often an early sign of asthma.
Children may spend many hours in day care each week and research suggests that conditions in day care settings can have an impact on respiratory health in early childhood. The new research offers some clues as to why attending day care can affect children’s lung health that could, in turn, point to measures for lowering the risk of asthma.
The study was presented by Dr Annabelle Bédard, a researcher at Inserm (the French National Institute of Health and Medical Research), Paris, France. She said: “We find mixtures of different bacteria and other microbes living everywhere – outside, inside our homes, on our skin and even inside our bodies. These communities of bacteria, known as microbiota, can have beneficial or harmful effects on our health.
“Young children will come into contact with the bacteria living in day care centres via their skin and mouths and by breathing them in. So, we might expect this exposure to have an impact on children’s developing lungs via the different microbiota that arise in children’s airway, gut or skin.”
The researchers used an adapted vacuum cleaner to collect samples of dust from the floor of 103 different day care settings in the Paris region. They used genetic analysis in the laboratory to identify the different types of bacteria found in each sample.
At the same time, they asked the parents of 515 children attending the day care facilities whether their children experienced any respiratory symptoms, such as wheezing. The children were around two years old on average.
Based on the types of bacteria found in the samples, researchers were able to group mixtures of microbiota from the day care centres into four broad categories. One of these categories, in which two different bacteria called Streptococcus and Lactococcus were dominant, was linked with an increase in the risk of wheezing, compared with the more common category (a mixture of Streptococcus, Neisseria and Haemophilus bacteria).

A ground-breaking study by researchers from the Cancer Science Institute of Singapore (CSI Singapore) at the National University of Singapore (NUS) has revealed crucial insights into the role of the histone methyltransferase NSD2 and its epigenetic target PKCα in causing t(4;14) translocated multiple myeloma (MM), a high-risk subtype of blood cancer, to be more aggressive and resistant to treatment.
The study was led by Professor Wee Joo Chng, Senior Principal Investigator at CSI Singapore, and Dr Phyllis Chong Shu Yun, Senior Research Fellow at CSI Singapore. The research team discovered that NSD2 triggers elevated glycolysis through the activation of PKCα, leading to the production of excessive lactate that fuels malignancy and undermines response to immunomodulatory drugs. The findings present potential targets to improve the treatment of myeloma.
Targets for therapeutic intervention
Myeloma is the second most common blood cancer, and t(4;14) myeloma comprises 15 to 20 per cent of MM cases. Compared to other types of myeloma, patients with t(4;14) myeloma have a poorer prognosis with shorter overall survival. Unfortunately, the key deregulated gene in t(4;14) myeloma is not targetable with drugs.
“Our study aims to overcome the limitations of targeting the key deregulated gene in t(4;14) myeloma. It sheds light on the metabolic reprogramming of MM in response to the oxygen- and nutrient-deprived bone marrow microenvironment. By exploring the epigenome and metabolome of NSD2, we sought alternative vulnerabilities that could revolutionise treatment strategies,” said Prof Chng, lead author of the study.
The unique connection between NSD2 and cellular metabolism, mediated by histone methylation, offers new horizons in the battle against high-risk MM subtypes. The study’s impact is multifaceted, potentially influencing the development of novel medicines and non-invasive diagnostic tests. For patients with t(4;14) myeloma, targeted metabolic interventions could bring promising therapeutic options, whether through dietary modifications or tailored pharmacological approaches. Furthermore, the discovery that lactate levels could serve as predictive biomarkers for drug response highlights the transformative potential of metabolite signatures in personalised medicine.
Striving towards tailored interventions and personalised care
This study, which was published in Cancer Research, American Association for Cancer Researchon 18 July 2023, marks a significant stride in unravelling the complexities of MM and holds promise to improving treatment outcomes for patients with high-risk subtypes.
Looking ahead, Prof Chng and his team plan to leverage the knowledge gained from this study to design therapeutic intervention for t(4;14) myeloma. The success of their metabolic characterisation of t(4;14) myeloma also paves the way for the team to extend their metabolomic framework to profile other genetically high-risk MM subtypes such as t(14;16) or with 1q21 amplifications, presenting a path towards tailored interventions and personalised care.