Publisher Health

Many fungus strains have been used and selected by the food industry for their capacities to ferment, produce flavors or produce heterologous molecules. According to a new study, 2 fungi used to produce food products have potential probiotic effects on gut inflammation. The study, published in mSystems, a journal of the American Society for Microbiology, demonstrates a possible new way to develop new probiotics.
“There is much to learn by studying the role of the fungal strains in the microbiota and host health and also that species simply used in food processes can be the source of new probiotics,”?said lead study author Mathias L. Richard, Ph.D., Research Director at INRAE in the Micalis Institute in Jouy-en-Josas, France.
To date, very little is known about the diversity of foodborne yeasts and their potential effect on gut microbiota and gut health. Yeasts are microscopic fungi?consisting of solitary cells that reproduce by budding. Some have been used for hundreds of years, like Saccharomyces cerevisiae for wine and bread production, or many others for cheese crust production or ripening, like Debaryomyces hansenii.
The researchers conducted the new study because they are working to further knowledge of the potential effect of the fungal microbiota on human health. In this particular study, the idea was to target specifically the fungi that are used by food companies to produce food products (cheeses, charcuterie). “Since our interest is more focused on the role of fungi in gut health and on the development of Inflammatory Bowel Diseases (Crohn’s disease and ulcerative colitis), we monitored the effect of these fungi on adapted in vitro and in vivo models,” Richard said.
The researchers first selected yeasts that were intensively used in food production and represented a wide range of different yeasts species and then tested them either in simple interaction tests with cultured human cells or in a specific animal model mimicking ulcerative colitis.
They found that in the collection of strains used for food production, some strains can have a beneficial effect on the gut and the host in inflammatory context. They identified 2 strains of yeasts, Cyberlindnera jadinii and Kluyveromyces lactis, that had potential beneficial effects on inflammatory settings in a mouse model of ulcerative colitis. Several additional experiments were performed in an attempt to decipher the mechanism behind these effects. In the case of C. jadinii, the protection seemed to be driven by the modification of the bacterial microbiota after the administration of C. jadinii to the mice, which in turn modified the sensitivity to gut inflammation through a still unknown mechanism.
“These 2 strains have never been specifically described with such beneficial effect, so even if it needs to be studied further, and particularly to see how they are efficient in humans, it is a promising discovery,” Richard said.
C. jadinii and K. lactis strains have potential as probiotic yeast strains to fight against inflammation in the gut, but further studies are needed to understand the mechanisms by which these strains act on gut health.

Curbing carbon emissions and eating healthier may both start at the dinner table.
According to a new study co-authored by a Tulane University researcher and published in the journal Nature Food, making simple substitutions like switching from beef to chicken or drinking plant-based milk instead of cow’s milk could reduce the average American’s carbon footprint from food by 35%, while also boosting diet quality by between 4-10%, according to the study.
These findings highlight the potential of a “small changes” approach that researchers believe could encourage more consumers to adopt climate-friendly eating habits. Food production accounts for 25-33% of the nation’s greenhouse gas emissions with beef production being a primary contributor.
“This study shows that cutting dietary carbon emissions is accessible and doesn’t have to be a whole lifestyle change,” said Diego Rose, senior author and nutrition program director at Tulane University School of Public Health and Tropical Medicine. “It can be as simple as ordering a chicken burrito instead of a beef burrito when you go out to eat. When you’re at the grocery store, move your hand one foot over to grab soy or almond milk instead of cow’s milk. That one small change can have a significant impact.”
The study, which analyzed diet data from over 7,700 Americans, identified commonly eaten foods with the highest climate impact and simulated replacing them with nutritionally similar, lower-emission options.
“For us, substitutes included swapping a beef burger for a turkey burger, not replacing your steak with a tofu hotdog,” said Anna Grummon, lead author and assistant professor of pediatrics and health policy at Stanford University. “We looked for substitutes that were as similar as possible.”
The largest projected reductions in emissions were seen in mixed dishes: burritos, pastas and similar popular dishes where it’s easy to substitute a lower-impact protein instead of beef.

Psoriasis — a chronic skin condition — is not caused or spread by spontaneous genetic mutations in the skin, new research suggests.
The team, from the Wellcome Sanger Institute and collaborators, sequenced skin samples from 111 people with psoriasis. They didn’t find any mutated genes in the psoriatic patches that weren’t also mutated in the individual’s unaffected skin tissue.
The study, published today (26 October) in Nature Genetics, suggests that unlike other inflammatory diseases, such as inflammatory bowel disease or chronic liver disease, somatic mutations were not responsible for the start or spread of psoriasis.
Confirming that psoriasis is not caused by any somatic mutations enables researchers to continue to explore other avenues.
Over time, all cells in our bodies will accumulate mutations, known as somatic mutations. These can arise from replication errors, chemicals, or environmental factors. While some of these mutations can lead to cancer, many are harmless. When a mutation gives the cell an advantage over its neighbours, it is known as a driver mutation, and this allows the mutated cells to grow and spread.
Recently, research has begun to explore the possibility of driver mutations causing non-cancerous diseases by impacting the function of the tissue or influencing the spread of disease through the body1.
In previous work by Wellcome Sanger Institute scientists, these mutations have been shown to have an impact on diseases such as inflammatory bowel disease2. In this new study, researchers from the Wellcome Sanger Institute and collaborators, explored if the same was true for psoriasis.

Published3 hours agoShareclose panelShare pageCopy linkAbout sharingBy Sophia Seth & Daisy StephensBBC SouthA 10-year-old boy with a currently incurable brain disease is feeling hopeful about a new treatment. It took three years for Olly from Andover, Hampshire, to be diagnosed with TUBB4A leukodystrophy. The condition causes disruption to the signals between nerve cells in the brain and means Olly, who was three years old when he was diagnosed in 2015, is blind and non-verbal. But Oxford-based biotech company SynaptixBio is now working on a cure. Olly’s mother, Claire, said she had a normal pregnancy, labour and birth but when her son was six months old, she noticed he could not sit up or control his head movements.After two years of tests, he was diagnosed with hypomyelination with atrophy of the basal ganglia and cerebellum (H-ABC) – a severe form of TUBB4A leukodystrophy.Image source, Family HandoutClaire, 40, said: “Finding out Olly suffered from a life-threatening illness came as a total surprise, and of course it was devastating news.”Unfortunately because it is so rare, the doctors were saying, ‘we don’t know, we don’t know about this condition, we don’t know what’s what, there’s no treatment, there’s no cure’.”SynaptixBio has teamed up with a hospital in Philadelphia and secured £13.2m in funding to try to develop a drug to help those with the condition.Scientists are working with antisense oligonucleotides (ASOs), molecules that have previously been used to treat conditions such as Duchenne muscular dystrophy.It is hoped the drug, which is currently scheduled to go to clinical trials next year, could potentially reduce the amount of mutated protein that causes H-ABC.”We hope [the drug] will alleviate the disease and potentially reverse some of the issues we are seeing in patients,” said Dr Dan Williams, chief executive of SynaptixBio.Dr Williams is also concerned about the diagnosis times for the disease.He added: “TUBB4A leukodystrophy has only recently been identified, so it’s not surprising that general knowledge isn’t widespread within the NHS.”But the concern remains that undiagnosed children may suffer more than is necessary.”Claire said she will be eagerly awaiting the results of the trial.”It does concern us when he transitions from a child into an adult,” she said.In the meantime, Olly is happy, attending a specialist school and spending time with his two brothers.Claire added: “They always include him with what they are up to. It’s lovely to see when you get a big smile from Olly.”Follow BBC South on Facebook, X, or Instagram. Send your story ideas to south.newsonline@bbc.co.uk.More on this story’There is a chance to cure our kids’Published24 August 2020Man runs 131 miles to help girl’s disease fightPublished12 April 2021Related Internet LinksSynaptixBioThe BBC is not responsible for the content of external sites.

ustralian researchers have developed cutting-edge technology known as “acoustic touch” that helps people ‘see’ using sound. The technology has the potential to transform the lives of those who are blind or have low vision.
Around 39 million people worldwide are blind, according to the World Health Organisation, and an additional 246 million people live with low vision, impacting their ability to participate in everyday life activities.
The next generation smart glasses, which translate visual information into distinct sound icons, were developed by researchers from the University of Technology Sydney and the University of Sydney, together with Sydney start-up ARIA Research.
“Smart glasses typically use computer vision and other sensory information to translate the wearer’s surrounding into computer-synthesized speech,” said Distinguished Professor Chin-Teng Lin, a global leader in brain-computer interface research from the University of Technology Sydney.
“However, acoustic touch technology sonifies objects, creating unique sound representations as they enter the device’s field of view. For example, the sound of rustling leaves might signify a plant, or a buzzing sound might represent a mobile phone,” he said.
A study into the efficacy and usability of acoustic touch technology to assist people who are blind, led by Dr Howe Zhu from the University of Technology Sydney, has just been published in the journal PLOS ONE.
The researchers tested the device with 14 participants; seven individuals with blindness or low vision and seven blindfolded sighted individuals who served as a control group.

After surveying the views expressed by 41 advocacy, medical, and transplant-focused organizations on the Uniform Determination of Death Act, a brain injury expert is calling for much-needed reforms to the legal definition of death in the United States. The recently announced pause by the Uniform Law Commission, which is spearheading revisions, is disappointing, the expert notes, but should not permanently stall practical fixes to longstanding problems with the Death Act.
“This study shows that most medical organizations support revisions of the Uniform Determination of Death Act to align the legal description of the neurological criteria for death with medical standards,” said Ariane Lewis, MD, a neurocritical care specialist and professor in the Departments of Neurology and Neurosurgery at NYU Grossman School of Medicine.
Specifically, Lewis argues, the legal description for death needs to reflect medical guidelines, which do not require that loss of hormone function be considered when declaring someone brain dead. Moreover, Lewis says, the Death Act needs to be revised to include legal guidance for health care providers about what to do when a family objects to stopping mechanically assisted breathing for a relative who is already brain dead. The act, for example, needs to clarify when and for how long, if not indefinitely, a person can be kept on a ventilator after brain death if a family objects to it being removed.
Lewis says her survey results showed that 34 organizations (83%) favored revisions to the Death Act. However, she acknowledges that views about how to revise it varied. Some religious organizations and patient advocacy groups were opposed to using loss of brain function as a criteria for declaring death, favoring instead the traditional definition of death as having occurred after the heart stops beating.
Lewis, who also serves as director of neurocritical care at NYU Langone Health, has already shared her survey results and perspective with the commission, whose work to amend the Death Act was suspended in late September. Lewis has been one of 100 observers working with the commission for the past three years on revisions to the statute.
Publishing in the journal Neurocritical Care online Oct. 25, the study involved a detailed review of the comments and viewpoints submitted to the commission between January and July 2023 by 41 organizations impacted by the Death Act.
Historically, a person was considered dead when their heart stopped beating and they could no longer breathe on their own. Technological advances in mechanical ventilation changed that, allowing people, in some cases, to keep breathing after they had suffered catastrophic brain injuries leading to coma, and had lost the nerve function needed for them to breathe on their own. Such cases led in 1981 to the U.S. Uniform Determination of Death Act, which defined death as either the irreversible cessation of all brain or cardiopulmonary functions. This definition was adopted by all American states as the legal basis for declaring a person dead.

An old campaign slogan for cough syrup, “It tastes awful. And it works,” seemed to imply that any sweet content might have diminished the medicinal effect.
Sweetness, in the case of cancer, appears as a chain of sugar molecules attached to proteins by beta1,4-galactosyltransferase-3, or B4GALT3 According to the Cancer Genome Atlas, a high expression of this enzyme is associated with noticeably shortened survival rates in several types of immunotherapy cancers, such as neuroblastoma, cervical, and bladder cancer. However, the specific role of B4GALT3 in the tumor immune microenvironment — or TIME — was still unknown.
Now, a team of researchers at Kyoto University and Yokohama City University has found that B4GALT3 deficiency in mice TIME inhibits tumor growth. The study shows that a significant reduction of glycosylation — a type of protein modification — on T cell surfaces correlates with increases in CD8+ immune cells infiltrating tumors.
“In B4GALT3 knockout or KO mice, we demonstrated the potential of manipulating glycosylation of the T cell surface as a new approach to cancer immunotherapy,” says Heng Wei of Kyoto University’s Graduate School of Medicine.
By purifying membrane proteins and enzymatically cleaving them to enrich glycopeptides, the team could identify the sites and structures of glycans — complex and highly branched sugar chains — and the amount of glycoproteins. The role of glycans has attracted much attention in studies on cancer cells, which proliferate and metastasize, depending on their interaction with their microenvironment.
The team subcutaneously transplanted weakly immunogenic and strongly immunogenic tumor cells into B4GALT3 knockout and wild-type mice, to examine for tumor cell growth. Only the knockout mice suppressed the growth of strongly immunogenic tumor cells.
In addition, the increased CD8+ T cells in knockout mice secreted anti-cancer compounds Interferon-γ and Granzyme B.
“We found that the loss of B4GALT3 caused significant fluctuations in gene expression in the immune system, a discovery which has significantly changed the direction of our next phase of research,” adds coauthor Chie Naruse.
“We have gained insight into the role of glycans in cancer progression and immune response, inspiring possibilities of B4GALT3-centered cancer therapies,” says team leader Masahide Asano.

Older people who have higher levels of triglycerides, a type of fat, may have a lower risk of dementia and a slower cognitive decline over time compared to people who have lower levels, according to new research published in the October 25, 2023, online issue of Neurology®, the medical journal of the American Academy of Neurology. While the study found a link, it does not prove that higher levels of triglycerides prevent dementia.
Triglycerides are fatty acids and are the most common type of fat in the blood. Triglycerides contribute up to 95% of dietary fats, which are the main energy source of the brain.
“Higher triglyceride levels may be reflective of better overall health and lifestyle behaviors that would protect against dementia,” said study author Zhen Zhou, PhD, of Monash University in Melbourne, Australia. “Our findings suggest that triglyceride levels may serve as a useful predictor for dementia risk and cognitive decline in older populations.”
Researchers used health care data to identify 18,294 people in one cohort with an average age of 75 who did not have a prior diagnosis of Alzheimer’s disease or dementia.
Participants were followed for an average of six years. During that time, 823 people developed dementia.
Researchers looked at participants’ measurements of total cholesterol, triglycerides, low-density lipoprotein cholesterol (LDL) and high-density lipoprotein cholesterol (HDL) each year of the study.
Then researchers divided participants into four groups based on fasting triglyceride levels. Of the total group, average triglycerides were 106 milligrams per deciliter (mg/dL). For adults, a normal or healthy triglyceride level is below 150 mg/dL.

Zika virus infection in pregnant rhesus macaques slows fetal growth and affects how infants and mothers interact in the first month of life, according to a new study from researchers at the California National Primate Research Center at the University of California, Davis. The work, published Oct. 25 in Science Translational Medicine, has implications for both humans exposed to Zika virus and for other viruses that can cross the placenta, including SARS-CoV2, responsible for the COVID-19 pandemic.
“Initially I thought this was a story about Zika, but as I looked at the results I think this is also a story about how fetal infections in general affect developmental trajectories,” said Eliza Bliss-Moreau, professor of psychology at UC Davis and senior author on the paper.
In most people, Zika virus infection causes mild or no symptoms and leaves long-lasting immunity. But during pregnancy, the virus can cross the placenta and cause damage to the nervous system of the fetus. In extreme cases, it can cause microcephaly in humans.
While no local transmission of the virus has been reported in the U.S. since 2018, the mosquitoes that carry Zika virus continue to expand their range throughout Africa, the Americas, Asia and the Pacific.
UC Davis researchers previously showed that Zika virus could enter the fetal brain in pregnant macaques. The new study, led by Bliss-Moreau with Associate Specialist Gilda Moadab, Project Scientist Florent Pittet and colleagues at the CNPRC and UC Davis Department of Psychology, looked at the effects of Zika infection during the second trimester of pregnancy on infants up to a month after birth.
Infection in second trimester
Pregnant animals did not become visibly ill with the virus, but ultrasounds showed fetal growth slowed after infection, Pittet said. At birth, Zika-exposed infants were “at the low end” of the range for head size in rhesus macaques.

A study spearheaded by Oregon State University has shown why certain polyunsaturated fatty acids work to combat a dangerous liver condition, opening a new avenue of drug research for a disease that currently has no FDA-approved medications.
Scientists led by Oregon State’s Natalia Shulzhenko, Andrey Morgun and Donald Jump used a technique known as multi-omic network analysis to identify the mechanism through which dietary omega 3 supplements alleviated nonalcoholic steatohepatitis, usually abbreviated to NASH.
The mechanism involves betacellulin, a protein growth factor that plays multiple positive roles in the body but also contributes to liver fibrosis, or scarring, and the progression to cirrhosis and liver cancer.
“We only succeeded in finding these surprising results because we implemented an entirely unbiased approach that incorporated a diverse type of big data analysis ranging from lipids and metabolites to whole tissue and single-cell RNA sequences,” said Morgun, a researcher in the OSU College of Pharmacy.
Findings were published in EMBO Molecular Medicine.
NASH is associated with a disorder known as metabolic syndrome. It develops when fat in the liver becomes toxic, killing liver cells, inflaming the organ and promoting fibrosis. The disease can lead to permanent scarring (cirrhosis), liver failure and possibly death.
People are considered to have metabolic syndrome if they have at least two of the following conditions: abdominal obesity, high blood pressure, high blood sugar, low blood levels of “good” cholesterol and high levels of bad cholesterol and triglycerides.