NYU Langone Health surgeons performed the transplant after implanting a mechanical heart pump in the severely ill patient.A severely ill 54-year-old woman earlier this month became the second person to receive a kidney transplanted from a genetically modified pig, surgeons at NYU Langone Health in New York announced on Wednesday.The patient, who had both heart failure and kidney failure, was given the organ on April 12, just eight days after receiving a mechanical heart pump. Surgical teams at NYU Langone carried out the two procedures over the course of nine days.The kidney recipient, Lisa Pisano, a native of New Jersey, was at risk of dying without the heart pump, a medical device used in patients who need a heart transplant.The kidney came from a genetically engineered pig provided by United Therapeutics Corporation, a biotech company. The pig carried a gene for producing a sugar called alpha-gal that had been “knocked out,” or blocked.NYU Langone Health studies have shown that removing the gene reduces the risk of a severe immune reaction in a patient, which can lead to the immediate rejection of an organ transplanted from an animal, a process called xenotransplantation.The NYU Langone surgeons also placed the pig’s thymus gland, which can reprogram the patient’s immune system so it doesn’t reject the pig’s organ, under the transplanted kidney in order to reduce the likelihood of rejection.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

The beginning of life is shrouded in mystery. While the intricate dynamics of mitosis is well-studied in the so-called somatic cells — the cells that have a specialized function, like skin and muscle cells — they remain elusive in the first cells of our bodies, the embryonic cells. Embryonic mitosis is notoriously difficult to study in vertebrates, as live functional analyses and -imaging of experimental embryos are technically limited, which makes it hard to track cells during embryogenesis.
However, researchers from the Cell Division Dynamics Unit at the Okinawa Institute of Science and Technology (OIST) have recently published a paper in Nature Communications, together with Professors Toshiya Nishimura from Hokkaido University (previously at Nagoya University), Minoru Tanaka from Nagoya University, Satoshi Ansai from Tohoku University (currently at Kyoto University), and Masato T. Kanemaki from the National Institute of Genetics. The study takes the first major steps towards answering questions about embryonic mitosis, thanks to a combination of novel imaging techniques, CRISPR/Cas9 genome editing technology, a modern protein-knockdown system, and medaka, or Japanese rice fish (Oryzias latipes). The timelapses that they have produced help answer fundamental questions about the intricate process of equally dividing chromosomes during embryonic mitosis, and simultaneously chart the next frontier of scientific exploration. As Professor Tomomi Kiyomitsu, senior author of the study, describes the timelapses: “they are beautiful, both on their own and because they lay a new foundation for elucidating embryonic mitosis.”
Watch Professor Kiyomitsu explain the beautiful timelapses here: https://youtu.be/HeEp1pmgWgk
Central to the mystery of embryonic mitosis is the crucial step when the chromosomes, which contain all the genetic information of the cell, are aligned and segregated equally into daughter cells. A key player in this process is the mitotic spindle, which is made of microtubules — long protein fibers used for intra-cellular structure and transport — that radiates from opposite poles of the spindle and attaches to the chromosomes in the middle. The spindle captures duplicated chromosomes properly and segregates them equally into the daughter cells during division. There are many factors determining spindle formation, and one of these is the protein Ran-GTP, which plays an essential role in cell division of female reproductive cells, which lack centrosomes — cell organelles responsible for assembling microtubules — but not in small somatic cells, which do have centrosomes. However, it has long been unclear whether Ran-GTP is required for spindle assembly in vertebrate early embryos, which contain centrosomes but have unique features, like a larger cell size.
In contrast to mammalian early embryos, embryonic cells in fish are transparent and develop synchronously in a uniform, single-cell layer sheet, which makes them significantly easier to track. The medaka turned out to be particularly well-suited for the researchers, as these fish tolerate a wide range of temperatures, produce eggs daily, and have a relatively small genome. Being temperature-tolerant means that the medaka embryonic cells could survive at room temperature, making them particularly suited for long, live timelapse photography.
The fact that medaka produce eggs frequently and have a relatively small genome size makes them good candidates for CRISPR/Cas9-mediated genome editing. With this technology, the researchers have created genetically modified, or transgenic, medaka whose embryonic cells literally highlight the dynamics of certain proteins involved in mitosis.
In studying the timelapses of the developing mitotic spindle in live, transgenic medaka embryos, the researchers discovered that large early embryos assemble unique spindles different from somatic spindles. In addition, Ran-GTP plays a decisive role in spindle formation in early embryonic divisions, but the importance diminishes in later stage embryos. This is possibly because the spindle structure is remodeled as cells get smaller during development, though the exact reason is a subject for future research.

The researchers also discovered that the early embryonic cells do not have a dedicated spindle assembly checkpoint, which characterizes most somatic cells, and which serves to ensure that the chromosomes are properly aligned before segregation. As Professor Kiyomitsu surmises, “the checkpoint is not active, and yet the chromosome segregations are still very accurate. This could be explained by the fact that embryonic cells need to divide very quickly, but it is something that we want to study further.”
While genetically modifying the medaka fish and studying the early embryos have led to new key insights into embryonic mitosis, this is just the beginning for Professor Kiyomitsu and the team. In addition to questions related to the diminishing role of Ran-GTP in later stages and the missing spindle assembly checkpoint, he points to the satisfying symmetry of cell divisions in the timelapses: “The spindle formation is characterized by a high degree of symmetry, as the cells appear to be dividing in the sizes and defined directions, and the spindle is consistently in the center of the cells. How can the spindle orient itself so regularly across the cells, and how is it able to find the center every time?”
Moving beyond the timelapses, the team also hopes to further solidify this new foundation with additional medaka gene-lines to serve as models for research in embryonic cells, and at the same time optimize the genome editing process. Eventually, the team wants to test for generalizability of their findings by studying embryonic mitosis in other organisms, and at a later stage, they want to explore the evolution of spindle assembly and embryonic divisions, which would also contribute to a better understanding of human embryogenesis and to developing diagnosis and treatment of human infertility.
“With this paper, we have created a solid foundation,” summarizes Professor Kiyomitsu, “but we have also opened a new frontier. Embryonic mitosis is beautiful, mysterious, and challenging to study, and we hope that with our work, we can eventually get a little closer to understanding the intricate processes at the beginning of life.”

Better heart health was linked to less decline in mental processing speed and cognition among middle-aged Black women, although not among middle-aged white women, according to new research published today in the Journal of the American Heart Association, an open access, peer-reviewed journal of the American Heart Association.
“Take care of your heart, and it will benefit your brain,” said study lead author Imke Janssen, Ph.D., a professor of family and preventive medicine at Rush University Medical Center in Chicago. “Better cardiovascular health in women in their 40s is important to prevent later-life Alzheimer’s disease, dementia and to maintain independent living.”
Previous research has linked heart health to a lower risk of cognitive decline. This decline may begin years before the onset of dementia, Janssen explained. Questions that need to be answered include understanding when the cognitive benefits of heart health begin, whether they occur among people of different races and whether they affect different types of brain function including reasoning.
In this study, researchers compared key heart health metrics, known as the American Heart Associations’ Life’s Essential 8, among middle-aged Black and white women to cognitive testing conducted on the women every one to two years over a 20-year period.
Life’s Essential 8TM includes objectively measured weight, blood pressure, glucose, and cholesterol, as well as self-reported health behaviors such as eating healthy foods, being physically active, not smoking and getting enough sleep.
The cognitive tests assessed processing speed and working memory. Processing speed is the pace at which the brain has accurate recognition of visual and verbal information and is necessary for daily activities such as driving. In this study, cognitive processing speed was assessed as quickly and accurately recognizing sets of numbers, objects, pictures or patterns. Working memory is the ability to remember and use small pieces of information for daily tasks, including remembering names and doing math.
The study found differences in cognitive decline by race only in processing speed, not in working memory. Specifically: Black women with lower heart health, based on the Life’s Essential 8 metrics, had a 10% decrease in processing speed over 20 years. Their scores were worse for all eight risk factors for heart disease, especially blood pressure and smoking. In contrast, Black women with good heart health showed little decline in mental processing during the 20-year study. Among white women with poorer heart health, processing speed did not decline. Heart health did not affect working memory for Black or white women.”We were surprised that we did not find results like those of past studies, which showed cognitive decline in Black and white men and women, and found cardiovascular health to be more important for white adults rather than people in Black subgroups,” Janssen said. “We think these differences are due to the younger age of our participants, who began cognitive testing in their mid-40s, whereas previous studies started with adults about 10 to 20 years older. The next step is a clinical trial to confirm whether optimizing heart health in Black women at midlife may slow cognitive aging, maximize independence and reduce racial inequities in dementia risk.”
Several limitations may have affected the study’s results. The study included women from a single study site and relied on self-reported measures of heart health, which may have been inaccurate. In addition, the study did not include measures that may account for racial differences in access to health care or the potential impact of structural racism on Black participants.
Study background and details: The study included 363 Black and 402 white women from the Chicago site of the Study of Women’s Health Across the Nation (SWAN). The Chicago SWAN group started cognitive testing in 1997, when the women were between 42 and 52 years old. Cognitive testing continued every one to two years through 2017. The analytic sample consisted of 765 women who provided 5,079 cognitive processing speed and 4,933 working memory assessments over the 20-year period. Heart health based on Life’s Essential 8 was assessed at time of enrollment only.

A new computer process developed by chemists at ETH Zurich makes it possible to generate active pharmaceutical ingredients quickly and easily based on a protein’s three-​dimensional surface. The new process could revolutionise drug research.
“It’s a real breakthrough for drug discovery,” says Gisbert Schneider, Professor at ETH Zurich’s Department of Chemistry and Applied Biosciences. Together with his former doctoral student Kenneth Atz, he has developed an algorithm that uses artificial intelligence (AI) to design new active pharmaceutical ingredients. For any protein with a known three-dimensional shape, the algorithm generates the blueprints for potential drug molecules that increase or inhibit the activity of the protein. Chemists can then synthesise and test these molecules in the laboratory.
All the algorithm needs is a protein’s three-dimensional surface structure. Based on that, it designs molecules that bind specifically to the protein according to the lock-and-key principle so they can interact with it.
Excluding side effects from the outset
The new method builds on the decades-long efforts of chemists to elucidate the three-dimensional structure of proteins and to use computers to search for suitable potential drug molecules. Until now, this has often involved laborious manual work, and in many cases the search yielded molecules that were very difficult or impossible to synthesise. If researchers used AI in this process at all in recent years, it was primarily to improve existing molecules.
Now, without human intervention, a generative AI is able to develop drug molecules from scratch that match a protein structure. This groundbreaking new process ensures right from the start that the molecules can be chemically synthesised. In addition, the algorithm suggests only molecules that interact with the specified protein at the desired location and hardly at all with any other proteins. “This means that when designing a drug molecule, we can be sure that it has as few side effects as possible,” Atz says.
To create the algorithm, the scientists trained an AI model with information from hundreds of thousands of known interactions between chemical molecules and the corresponding three-dimensional protein structures.

Successful tests with industry
Together with researchers from the pharmaceutical company Roche and other cooperation partners, the ETH team tested the new process and demonstrated what it is capable of. The scientists searched for molecules that interact with proteins in the PPAR class — proteins that regulate sugar and fatty acid metabolism in the body. Several diabetes drugs used today increase the activity of PPARs, which causes the cells to absorb more sugar from the blood and the blood sugar level to fall.
Straightaway the AI designed new molecules that also increase the activity of PPARs, like the drugs currently available, but without a lengthy discovery process. After the ETH researchers had produced these molecules in the lab, colleagues at Roche subjected them to a variety of tests. These showed that the new substances are indeed stable and non-toxic right from the start.
The researchers aren’t now pursuing these molecules any further with a view to bringing drugs based on them to the market. Instead, the purpose of the molecules was to subject the new AI process to an initial rigorous test. Schneider says, however, that the algorithm is already being used for similar studies at ETH Zurich and in industry. One of these is a project with the Children’s Hospital Zurich for the treatment of medulloblastomas, the most common malignant brain tumours in children. Moreover, the researchers have published the algorithm and its software so that researchers worldwide can now use them for their own projects.
“Our work has made the world of proteins accessible for generative AI in drug research,” Schneider says. “The new algorithm has enormous potential.” This is especially true for all medically relevant proteins in the human body that don’t interact with any known chemical compounds.

Satiety, nausea or anxiety can all lead to a loss of appetite. Delaying eating can be a healthy move by the body to prevent further damage and to gain time for regenerating. Researchers at the Max Planck Institute for Biological Intelligence now identified the circuit in the brain that prevents mice from eating when they feel nauseous. The decisive role is played by special nerve cells in the amygdala — a brain region involved when emotions run high. The cells are activated during nausea and elicit appetite-suppressing signals. The findings highlight the complex regulation of eating behavior, as the loss of appetite during nausea is controlled by different circuits than during satiety.
An upcoming exam, a boat trip on the high seas or the next germ at the day-care center all have one thing in common: they can really upset our stomach. Stress, motion sickness or certain infections can make us feel sick. It seems logical that we don’t eat in these circumstances and wait for the situation to improve. As a result, nausea and decreased appetite usually go hand in hand. Or have you ever felt sick and really wanted to eat at the same time?
What seems logical is a healthy defense mechanism of our body — but it has to be activated first. Clearly, the brain plays a central role in this: it is the control center for the body’s energy balance and regulates eating behavior.
So how does the brain prevent us from eating when we feel sick? Researchers in Rüdiger Klein’s department have gained new insights into this topic in mice. They focused on the amygdala, a brain region that regulates emotions, also those related to eating. It contains neurons that promote eating and those that inhibit appetite. For example, a known inhibitory cell type is activated when we are full, but how this works in the case of nausea is not well understood.
Nausea activates nerve cells
Wenyu Ding, first author of the new study, now discovered another cell group in the amygdala that has a negative influence on appetite. Unlike the previously known cell type, these cells are not activated by satiety, but when feeling nauseous. When the researchers artificially switched on the cells, even hungry mice stopped eating. Conversely, switching the cells off resulted in the mice eating, even when feeling sick.
To better understand how this cell type exerts its appetite-suppressing function, the researchers analyzed the underlying circuit: where do the cells get their information from and to which cells and brain areas do they send their projections? The following picture emerged: When a mouse feels sick, this information reaches the brain and eventually the amygdala. There, the new cell type is activated and sends its inhibitory signals to distant brain regions, including the so-called parabrachial nucleus, a brain stem region that receives a lot of information about the internal state of the body.
This stands in contrast to the circuit of the previously known cell type, which mainly interacts with neighboring cells within the amygdala. It becomes clear that the loss of appetite during satiety is not the same as the loss of appetite during nausea. In the brain, different cells and circuits are responsible for this — a complicated matter and perhaps a small consolation the next time we feel sick.
Most importantly, the new study provides important insights into how the brain and the amygdala in particular regulate eating behavior. This is the prerequisite for a better understanding of the many diseases associated with dysregulated eating behavior in humans.

New research has highlighted the profound link between dietary choices and brain health.
Published in Nature, the research showed that a healthy, balanced diet was linked to superior brain health, cognitive function and mental wellbeing. The study, involving researchers at the University of Warwick, sheds light on how our food preferences not only influence physical health but also significantly impact brain health.
The dietary choices of a large sample of 181,990 participants from the UK Biobank were analysed against and a range of physical evaluations, including cognitive function, blood metabolic biomarkers, brain imaging, and genetics — unveiling new insights into the relationship between nutrition and overall wellbeing.
The food preferences of each participant were collected via an online questionnaire, which the team catagorised into 10 groups (such as alcohol, fruits and meats). A type of AI called machine learning helped the researchers analyse the large dataset.
A balanced diet was associated with better mental health, superior cognitive functions and even higher amounts of grey matter in the brain — linked to intelligence — compared with those with a less varied diet.
The study also highlighted the need for gradual dietary modifications, particularly for individuals accustomed to highly palatable but nutritionally deficient foods. By slowly reducing sugar and fat intake over time, individuals may find themselves naturally gravitating towards healthier food choices.
Genetic factors may also contribute to the association between diet and brain health, the scientists believe, showing how a combination of genetic predispositions and lifestyle choices shape wellbeing.

Lead Author Professor Jianfeng Feng, University of Warwick, emphasised the importance of establishing healthy food preferences early in life. He said: “Developing a healthy balanced diet from an early age is crucial for healthy growth. To foster the development of a healthy balanced diet, both families and schools should offer a diverse range of nutritious meals and cultivate an environment that supports their physical and mental health.”
Addressing the broader implications of the research, Prof Feng emphasized the role of public policy in promoting accessible and affordable healthy eating options. “Since dietary choices can be influenced by socioeconomic status, it’s crucial to ensure that this does not hinder individuals from adopting a healthy balanced dietary profile,” he stated. “Implementing affordable nutritious food policies is essential for governments to empower the general public to make informed and healthier dietary choices, thereby promoting overall public health.”
Co-Auhtor Wei Cheng, Fudan University, added: “Our findings underscore the associations between dietary patterns and brain health, urging for concerted efforts in promoting nutritional awareness and fostering healthier eating habits across diverse populations.”
Dr Richard Pemberton, Certified Lifestyle Physician and GP, Hexagon Health, who was not involved in the stud, commented: “This exciting research further demonstrates that a poor diet detrimentally impacts not only our physical health but also our mental and brain health. This study supports the need for urgent government action to optimise health in our children, protecting future generations. We also hope this provides further evidence to motivate us all to make better lifestyle choices, to improve our health and reduce the risk of developing chronic disease.”

Researchers at the Centre for Genomic Regulation in Barcelona and the University of Cologne in Germany have developed a new experimental strategy to tackle scarring and fibrosis. Experiments with patient-derived human cells and animal models showed the strategy was effective, non-toxic and its effects reversible. The findings are published today in the journal Nature Communications.
Scarring occurs from the secretion and accumulation of various components — primarily proteins known as collagens — into the space between individual cells, usually occurring as a response to injury or damage. Excessive collagen secretion can also cause the buildup of fibrotic tissue, a more serious condition where excess connective tissue is formed to the extent that it compromises the function of tissues and sometimes entire organs. Around 45% of deaths in the industrialised world are attributed to some form of tissue fibrosis.
Treatment options for both scarring and fibrosis are usually limited to surgery. Outside the body, scar tissue is often beneath the outer layer of the skin. Since most topical creams are not able to penetrate deeply enough to reach the affected areas effectively, their ability to remodel or heal the tissue is limited. Inside the body, scarring and fibrosis can affect many different tissues and organs, each with its unique environment and challenges and with no one-size-fits-all treatment option.
“Existing treatment options are usually ineffective because they try and fail to mop the excessive collagen up. In this work, we tried a completely different idea: to block the floodgates at the cellular level. The strategy works at the cellular level, releasing enough collagen so that tissues don’t fall apart while protecting them from excessive amounts that impairs their function,” explains ICREA Research Professor Vivek Malhotra, co-corresponding author of the study and researcher at the Centre for Genomic Regulation (CRG) in Barcelona, Spain.
The researchers’ new strategy involves using molecules known as peptides to block the export of collagen from inside cells. The peptides disrupt an interaction between two proteins called TANGO1 and cTAGE5. Both proteins bind to each other and are essential for the export of collagens from their site of synthesis inside the cell to the exterior. The two proteins “sit” at the endoplasmic reticulum exit site, a place in the cell where materials like proteins are packaged and transported out the cell.
“Targeting the endoplasmic reticulum exit site has been historically considered impossible because a third of all human proteins go through it, so inhibiting its activity would likely have many off-target, toxic effects. In other words, it’s been ‘undruggable’. Only recently have there been indications that there is some specificity for the secretory materials. In this study we aimed to achieve this specificity by inhibiting the interface between TANGO1 and cTAGE5 with targeted precision,” explains Dr. Ishier Raote, first author of the study who carried out the work at the Centre for Genomic Regulation.
Proteins are like puzzle pieces. To know how two pieces fit together, you need to see their shapes clearly. Both TANGO1 and cTAGE5 are large, complex proteins which constantly shapeshift. To date, their exact structure remains unknown, which in turn means we don’t understand how they connect at the molecular level, hindering efforts to design drugs that can block the interaction.

The researchers overcame this challenge by using AlphaFold2, an artificial-intelligence program that can guess the shapes of the two proteins without needing structural data about their 3D shape. The predictions made by AI allowed the authors of the study to design peptides which can pass through a cell membrane and disrupt the interaction between TANGO1 and cTAGE5.
The researchers tested the peptides using normal human fibroblasts, the most common type of cell found in connective tissue. The peptides successfully inhibited collagen export, causing it to accumulate inside the cells. The effect was also reversible, with collagen levels increasing again after the peptides were removed within a 48-hour period.
The researchers observed similar effects in experiments with fibroblasts from patients with scleroderma, a complex autoimmune disease characterized by fibrosis of the skin and internal organs. The peptides were then tested using zebrafish, a common animal model to study tissue development and wound healing. The strategy visibly reduced collagen deposition in wound areas.
The researchers next plan to evaluate the efficacy of the peptides in pig skin because it closely resembles human skin. They will also finetune the properties of the peptides to increase their potency.
“We believe this represents a new strategy to control the effects of collagen hypersecretion. This could range from alleviating the cosmetic effects of skin scarring to the treatment of autoimmune diseases like scleroderma, as well as to manipulate post-surgery related events associated with wound healing to prevent fibrosis,” concludes Dr. Malhotra.
The study was coordinated by researchers at the Centre for Genomic Regulation in Spain and the University of Cologne in Germany. It also includes collaborators from the Institut Jacques Monod in France, EMBL Barcelona, the Institute for Stem Cell Science and Regenerative Medicine (inStem) in India, ICFO-Institut de Ciencies Fotoniques in Spain, and the Max Planck Institute for Biology of Aging in Germany.

Researchers at Texas Children’s Cancer Center and the Center for Cell and Gene Therapy at Baylor College of Medicine, Texas Children’s Hospital and Houston Methodist published results of a phase I clinical trial of a novel immunotherapy for high-risk sarcomas in the journal Nature Cancer.
The therapy uses chimeric antigen receptor (CAR) T cells engineered to target the HER2 protein, which is overexpressed on the surface of sarcoma cells. The HEROS 2.0 trial showed that this therapeutic approach is safe and is associated with clinical benefit. “CAR T cell therapy has been a highly successful strategy for recurrent or high-risk leukemias or lymphomas, but challenges remain in using this therapy for solid tumors,” said first and corresponding author Dr. Meenakshi Hegde, associate professor of pediatrics — hematology and oncology at Baylor and pediatric oncologist at Texas Children’s Cancer Center. “The results of this trial show that we are moving the dial in harnessing the power of CAR T cells as an effective anticancer therapy for sarcomas.”
In a previous clinical trial, the HEROS study, researchers found that CAR T cells directed at HER2+ tumor cells had a favorable safety profile, but clinical benefit was limited by poor CAR T expansion and persistence. In HEROS 2.0, researchers added successive HER2-CAR T cell infusions following lymphodepletion, which uses chemotherapy to deplete the patient’s own T cells, to make room for the infused therapeutic HER2-CAR T cells to expand.
“We also increased the number of allowable HER2-CAR T infusions to sustain the exposure time of CAR T cells, with the goal of increasing the antitumor effect,” Hegde said. “This study showed that CAR T expansion and persistence was improved with lymphodepletion and repeat cycles of treatment.”
Thirteen patients were enrolled in the HEROS 2.0 trial at Texas Children’s Cancer Center and Houston Methodist Hospital, and seven patients received multiple CAR T infusions. HER2-CAR T expansion occurred following 19 of 21 total infusions, and clinical benefit was seen in 50% of treated patients. An exceptional response in a patient with metastatic rhabdomyosarcoma was detailed in a publication in Nature Communications in 2020. The patient remains healthy and cancer free, more than five years after treatment. Nine patients in the first two cohorts developed low-grade cytokine release syndrome (CRS), an acute inflammatory response seen as a side effect of CAR T treatment. Two patients in the third cohort experienced dose-limiting CRS, which necessitated ending the dose-escalation.
“We are now studying the tumors and the way we engineer the CAR T cells to better facilitate the safe delivery of higher doses, thereby enhancing antitumor activity by increasing the magnitude of CAR T cell expansion and persistence,” Hegde said. “HEROS 2.0, the second edition of the HEROS trials, exemplifies how the crosstalk between the bench and the bedside results in refinement of first-in-child studies and more durable clinical benefit,” said senior author Dr. Nabil Ahmed, professor of pediatrics — hematology and oncology at Baylor and pediatric oncologist at Texas Children’s Cancer Center.
The researchers currently are recruiting for the HEROS 3.0 trial, which will evaluate the safety of giving HER2-CAR T cells in combination with chemotherapy and an immune checkpoint inhibitor drug.

The emergence in the Neolithic of patrilineal1 social systems, in which children are affiliated with their father’s lineage, may explain a spectacular decline in the genetic diversity of the Y chromosome2 observed worldwide between 3,000 and 5,000 years ago. In a study to be published on 24 April in Nature Communications, a team of scientists from the CNRS, MNHN and Université Paris Cité3 suggest that these patrilineal organisations had a greater impact on the Y chromosome than mortality during conflict.

This conclusion was reached after analysing twenty years of anthropological field data — from contemporary non-warlike patrilineal groups, particularly from the scientists’ own fieldwork carried out in Asia — and modelling various socio-demographic scenarios. The team compared warrior and non-warrior scenarios and showed that two processes play a major role in genetic diversity: the splitting of clans into several sub-clans and differences in social status that lead to the expansion of certain lineages to the detriment of others.
This study calls into question the previously proposed theory that violent clashes, supposedly due to competition between different clans, in which many men died, were at the origin of the loss of genetic diversity of the Y chromosome. The results of this study also provide new hypotheses on human social organisation in the Neolithic and Bronze Age.
Notes : In these systems, children are affiliated with their father’s lineage. Women marry men from different groups andmove to live with their husbands. The chromosome responsible for male sexual characteristics. From the laboratoire d’Eco-anthropologie (CNRS/Muséum national d’Histoire naturelle/Université Paris Cité).

Researchers from Aston University have found that people following healthy eating accounts on social media for as little as two weeks ate more fruit and vegetables and less junk food.
Previous research has shown that positive social norms about fruit and vegetables increases individuals’ consumption. The research team sought to investigate whether positive representation of healthier food on social media would have the same effect. The research was led by Dr Lily Hawkins, whose PhD study it was, supervised by Dr Jason Thomas and Professor Claire Farrow in the School of Psychology.
The researchers recruited 52 volunteers, all social media users, with a mean age of 22, and split them into two groups. Volunteers in the first group, known as the intervention group, were asked to follow healthy eating Instagram accounts in addition to their usual accounts. Volunteers in the second group, known as the control group, were asked to follow interior design accounts. The experiment lasted two weeks, and the volunteers recorded what they ate and drank during the time period.
Overall, participants following the healthy eating accounts ate an extra 1.4 portions of fruit and vegetables per day and 0.8 fewer energy dense items, such as high-calorie snacks and sugar-sweetened drinks, per day. This is a substantial improvement compared to previous educational and social media-based interventions attempting to improve diets.
Dr Thomas and the team believe affiliation is a key component of the change in eating behaviour. For example, the effect was more pronounced amongst participants who felt affiliated with other Instagram users.
The 2018 NHS Health Survey for England study showed that only 28% of the UK population consumed the recommended five portions of fruit and vegetables per day. Low consumption of such food is linked to heart disease, cancer and stroke, so identifying ways to encourage higher consumption is vital. Exposing people to positive social norms, using posters in canteens encouraging vegetable consumption, or in bars to discourage dangerous levels of drinking, have been shown to work. Social media is so prevalent now that the researchers believe it could be an ideal way to spread positive social norms around high fruit and vegetable consumption, particularly amongst younger people.
Dr Thomas said:
“This is only a pilot intervention study at the moment, but it’s quite an exciting suite of findings, as it suggests that even some minor tweaks to our social media accounts might lead to substantial improvements in diet, at zero cost! Our future work will examine whether such interventions actually do change our perceptions of what others are consuming, and also, whether these interventions produce effects that are sustained over time.”
Dr Hawkins, who is now at the University of Exeter, said:
“Our previous research has demonstrated that social norms on social media may nudge food consumption, but this pilot demonstrates that this translates to the real world. Of course, we would like to now understand whether this can be replicated in a larger, community sample.”