Health Awareness Report
2023 Health Base [19]
May 2023
37 News Items
| wdt_ID | NIH REF | KEY | HEADLINE | SUMMARY | SOURCE | JOURNAL | CONTENT | ITEM # |
|---|---|---|---|---|---|---|---|---|
| 81 | 2319-001 | H04 | Enhancing Coffee's Flavor | Researchers have developed a mathematical model to examine the role of uneven coffee extraction. By splitting the coffee into two regions, they discovered that uneven flow can indeed result in weaker espresso. The model system showed that more tightly packed coffee caused an initial disparity in flow resistance, which decreased further during extraction. Understanding how to prevent uneven extraction can lead to better brews and substantial financial savings through more efficient use of coffee. | American Institute of Physics | Physics of Fluids | Espresso coffee is brewed by first grinding roasted coffee beans into grains. Hot water then forces its way through a bed of coffee grains at high pressure, and the soluble content of the coffee grains dissolves into the water (extraction) to produce espresso. -- In 2020, researchers found that more finely ground coffee beans brew a weaker espresso. This counterintuitive experimental result makes sense if, for some reason, regions exist within the coffee bed where less or even no coffee is extracted. This uneven extraction becomes more pronounced when coffee is ground more finely. -- In Physics of Fluids, from AIP Publishing, University of Huddersfield researchers explored the role of uneven coffee extraction using a simple mathematical model. They split the coffee into two regions to examine whether uneven flow does in fact make weaker espresso. -- One of the regions in the model system hosted more tightly packed coffee than the other, which caused an initial disparity in flow resistance because water flows more quickly through more tightly packed grains. The extraction of coffee decreased the flow resistance further, as coffee grains lose about 20% to 25% of their mass during the process. -- "Our model shows that flow and extraction widened the initial disparity in flow between the two regions due to a positive feedback loop, in which more flow leads to more extraction, which in turn reduces resistance and leads to more flow," said co-author William Lee. "This effect appears to always be active, and it isn't until one of the regions has all of its soluble coffee extracted that we see the experimentally observed decrease in extraction with decreasing grind size." -- The researchers were surprised to find the model always predicts uneven flow across different parts of the coffee bed. -- "This is important because the taste of the coffee depends on the level of extraction," said Lee. "Too little extraction and the taste of the coffee is what experts call 'underdeveloped,' or as I describe it: smoky water. Too much extraction and the coffee tastes very bitter. These results suggest that even if it looks like the overall extraction is at the right level, it might be due to a mixture of underdeveloped and bitter coffee." -- Understanding the origin of uneven extraction and avoiding or preventing it could enable better brews and substantial financial savings by using coffee more efficiently. -- "Our next step is to make the model more realistic to see if we can obtain more detailed insights into this confusing phenomenon," said Lee. "Once this is achieved, we can start to think about whether it is possible to make changes to the way espresso coffee is brewed to reduce the amount of uneven extraction." [] Coffee, Caffeine, Constructal theory, Turbulence, Aerodynamics, Viscosity, Extraction (dental), Psychoactive drug | 2319-001 |
| 82 | 2319-008 | H04 | Optimizing Coffee's Taste | Researchers have developed a mathematical model to examine the role of uneven coffee extraction. By splitting the coffee into two regions, they discovered that uneven flow can indeed result in weaker espresso. The model system showed that more tightly packed coffee caused an initial disparity in flow resistance, which decreased further during extraction. Understanding how to prevent uneven extraction can lead to better brews and substantial financial savings through more efficient use of coffee. | American Institute of Physics | Physics of Fluids | Espresso coffee is brewed by first grinding roasted coffee beans into grains. Hot water then forces its way through a bed of coffee grains at high pressure, and the soluble content of the coffee grains dissolves into the water (extraction) to produce espresso. -- In 2020, researchers found that more finely ground coffee beans brew a weaker espresso. This counterintuitive experimental result makes sense if, for some reason, regions exist within the coffee bed where less or even no coffee is extracted. This uneven extraction becomes more pronounced when coffee is ground more finely. -- In Physics of Fluids, from AIP Publishing, University of Huddersfield researchers explored the role of uneven coffee extraction using a simple mathematical model. They split the coffee into two regions to examine whether uneven flow does in fact make weaker espresso. -- One of the regions in the model system hosted more tightly packed coffee than the other, which caused an initial disparity in flow resistance because water flows more quickly through more tightly packed grains. The extraction of coffee decreased the flow resistance further, as coffee grains lose about 20% to 25% of their mass during the process. -- "Our model shows that flow and extraction widened the initial disparity in flow between the two regions due to a positive feedback loop, in which more flow leads to more extraction, which in turn reduces resistance and leads to more flow," said co-author William Lee. "This effect appears to always be active, and it isn't until one of the regions has all of its soluble coffee extracted that we see the experimentally observed decrease in extraction with decreasing grind size." -- The researchers were surprised to find the model always predicts uneven flow across different parts of the coffee bed. -- "This is important because the taste of the coffee depends on the level of extraction," said Lee. "Too little extraction and the taste of the coffee is what experts call 'underdeveloped,' or as I describe it: smoky water. Too much extraction and the coffee tastes very bitter. These results suggest that even if it looks like the overall extraction is at the right level, it might be due to a mixture of underdeveloped and bitter coffee." -- Understanding the origin of uneven extraction and avoiding or preventing it could enable better brews and substantial financial savings by using coffee more efficiently. -- "Our next step is to make the model more realistic to see if we can obtain more detailed insights into this confusing phenomenon," said Lee. "Once this is achieved, we can start to think about whether it is possible to make changes to the way espresso coffee is brewed to reduce the amount of uneven extraction." [] Coffee, Caffeine, Constructal theory, Turbulence, Aerodynamics, Viscosity, Extraction (dental), Psychoactive drug | 2319-008 |
| 83 | 2319-025 | H04 H06 | Guidance for Diagnosing Hoarding Disorder | Experts from Anglia Ruskin University in Cambridge, England, have developed new guidance to help doctors correctly diagnose hoarding disorder, a largely misunderstood mental health condition affecting around 2% of the population. | Anglia Ruskin University | British Journal of General Practice | Experts from Anglia Ruskin University (ARU) have published new guidance to help doctors correctly diagnose hoarding disorder. -- Hoarding disorder affects around 2% of the population but remains a largely misunderstood mental health condition. It was only added to the International Classification of Diseases in 2019, having previously been classified under Obsessive Compulsive Disorder (OCD). -- Published in the British Journal of General Practice, the new guidance was written by Dr Sharon Morein and Dr Sanjiv Ahluwalia of Anglia Ruskin University (ARU) in Cambridge, England, to help health professionals spot the signs of hoarding disorder and intervene. -- ARU experts have also organised a free conference on Wednesday, 10 May to provide the public with more information about the condition. -- Hoarding disorder involves clutter in the home environment taking over living spaces, as well as excessive acquisition and difficulty discarding possessions, and affects an individual's quality of life. -- However, it typically comes to the fore only when patients seek support for other mental health or physical conditions and can then act as a barrier to treatment due to concerns about hygiene, safety, or access to the home. -- People with hoarding disorder most commonly suffer from depression, while other comorbidities include Obsessive Compulsive Disorder (OCD), and Attention Deficit Hyperactivity Disorder (ADHD). -- Dr Morein, an Associate Professor in Psychology at Anglia Ruskin University (ARU) and leader of the ARU Possessions and Hoarding Collective said: "Labels can be very useful in the healthcare system and can be the first stage for people receiving the support they need. -- "It is really important that doctors and other frontline healthcare professionals are aware that hoarding disorder is a diagnosable medical condition and that it is usually linked to other issues so that proper support can be offered. -- "Typically, hoarding disorder is something that sneaks up on people -- it doesn't happen overnight -- and people don't necessarily recognise they have a problem. One of the major difficulties with hoarding disorder is that sufferers often don't seek help themselves, and it only presents itself to medical professionals alongside other issues. The sooner the problem is spotted, the sooner support can be provided." [] Obsessive-compulsive disorder, Obsessive-compulsive personality disorder, Bipolar disorder, Controversy about ADHD, Mental illness, Narcissistic personality disorder, Workaholic, Schizophrenia | 2319-025 |
| 84 | 2319-011 | H01 H04 | Oil and Gas Pollution's Health Damages | A recent study found that air pollution from the oil and gas sector in the United States has substantial adverse impacts on air quality, human health, and health costs. The study shows that pollutants contributed to excess deaths, asthma attacks, and new cases of childhood asthma across the US in 2016. | Boston University School of Public Health | Environmental Research: Health | These health impacts affected communities in states with high oil and gas production, as well as states with limited or no gas activity, underlining the need for comprehensive regulatory action to protect Americans from the pollutants generated by this sector. -- Despite global efforts to transition from fossil fuels to clean energy, oil and gas (O&G) production is nearing record levels in the United States, posing concern among health experts about what this O&G growth means for air quality and human health. While there is extensive research on the climate effects of O&G-produced methane -- a key contributor to air pollution -- few studies have measured the health effects of the air pollution that O&G activity generates. -- A new study led by Boston University School of Public Health (BUSPH), the University of North Carolina Institute for the Environment (UNC-IE), PSE Healthy Energy, and Environmental Defense Fund fills this gap. -- Published in the journal Environmental Research: Health, the study found that air pollution from the oil and gas sector in the United States has substantial adverse impacts on air quality, human health, and health costs. -- The findings show that the pollutants nitrogen oxide (NO2), fine particulate matter (PM2.5) and ozone (O3) from U.S. oil and gas production contributed to 7,500 excess deaths, 410,000 asthma attacks, and 2,200 new cases of childhood asthma across the U.S. in 2016. Factoring in related respiratory and cardiovascular-related hospitalizations, adverse pregnancy outcomes, and other health challenges, oil and gas production was responsible for $77 billion in annual health costs. Comparatively, this total is three times the estimated climate impact costs of methane emissions from oil and gas operations. -- These impacts were largely concentrated in areas with significant oil and gas production, such as southwest Pennsylvania, Texas, and Eastern Colorado. But the health effects also extended into densely populated cities with little or no gas activity, such as Chicago, New York City, Baltimore, Washington DC, and Orlando. -- The study results suggest that O&G emissions reduction policies, such as the forthcoming EPA methane regulations, may produce immediate and significant air quality benefits to human health along with significant climate benefits. The researchers urge policymakers to consider these "co-benefits" in future emissions reduction strategies. They also stress that strategies that focus on end-of-pipe pollution controls during combustion -- such as in power plants, vehicles, buildings, and industry -- are only addressing part of the problem. -- "These substantial impacts from oil and gas production show that there are serious consequences across the full life cycle of oil and gas, from 'well to wheels,' 'well to power plant,' and 'well to furnace,'" says study corresponding author Jonathan Buonocore, assistant professor of environmental health at BUSPH. "The health impacts are not just from the combustion of oil and gas. In order for energy, air quality, and decarbonization policies to successfully protect health, they need to incorporate health impacts across this full life cycle." -- The five states with the highest impacts from O&G pollution were Texas, Pennsylvania, Ohio, Oklahoma, and Louisiana were those with significant oil and gas activity. However, Illinois and New York -- states that produce very little O&G -- still landed in the 6th and 8th spots. -- "The fact that air pollution and health impacts cross state boundaries indicates a strong need for regional to nationwide coordination," says study senior author Saravanan Arunachalam, research professor at UNC-IE. "States that have the highest emissions are not necessarily always the ones with the highest health risk due to these emissions, although Texas ranks first in both." [] Air pollution, Pollution, Indoor air quality, Automobile emissions control, Environmental impact assessment, Smog, Asthma, Fracking | 2319-011 |
| 85 | 2319-009 | H01 H02 H04 | Viruses and Carbon Cycle | With global warming, the roles microbes play in ecosystems are changing. However, scientists know little about how viral infections could change the way microbes react to warming. The study suggests that viruses could alter carbon balance, causing some ecosystems to switch from net carbon sources to net carbon sinks. | DOE/US Department of Energy | FEMS Microbiology Ecology | Microbes play important roles in ecosystems, and these roles are changing with global warming. Scientists also now know that most types of microbes are infected by viruses, but they know relatively little about how these viral infections could change how microbes react to warming. In this study, scientists describe many different ways that increasing temperatures could affect viruses and their microbial hosts. These changes could ultimately affect the responses of whole ecosystems to warming. The work exposes several important gaps in researchers' current knowledge about the connections between viruses, warming, and ecosystem functioning. Filling these gaps is crucial for understanding and predicting the effects of climate change on ecosystems. -- This study creates a roadmap for understanding the many different ways that viruses could modify the effects of warming on communities of microbes. Viruses likely have strong effects on processes with microbes and the ways ecosystems function. Incorporating these previously ignored effects into ecosystem models will help scientists improve their predictions of how ecosystems could respond to climate change. -- Microorganisms play integral roles in ecosystems by controlling the flow of energy and matter through processes like photosynthesis (carbon uptake), respiration (carbon release), and decomposition (carbon recycling). Climate change is currently altering how ecosystems function by changing how organisms operate within microbial food webs. Scientists know that viruses can have strong impacts on microbial processes, but they have less knowledge of how these impacts will change with future warming. -- In this study, scientists from Duke University, the University of Tennessee Knoxville, the Netherlands Institute of Ecology, and Oak Ridge National Laboratory reviewed the potential impacts of warming on viruses and how these might alter scientific understanding of ecosystem responses to climate change. Warming likely affects several different stages of the viral infection cycle, as well as virus-host dynamics. However, there are still many gaps in our understanding about these effects. Because viruses are ubiquitous across all habitats and have strong effects on microbial functioning, filling these gaps is critical to understanding how warming will affect the flow of energy and matter within ecosystems. The researchers' preliminary models show that viruses could potentially tip the scales on natural carbon balances, causing some ecosystems to switch from being net carbon sources (releasing more carbon than they store) to being net carbon sinks (absorbing carbon). This study shows how incorporating viruses into predictive models can lead to new and unexpected effects on ecosystems in response to climate change. -- This work was supported by the Department of Energy Office of Science, Biological and Environmental Research program. [] Carbon dioxide sink, Microorganism, Climate change mitigation, Forest, Global warming, Fossil fuel, Climate engineering, Consensus of scientists regarding global warming | 2319-009 |
| 86 | 2319-006 | H01 H03 H04 | Omega-3s and Brain Development | Scientists have discovered a lipid transporter crucial to regulating the cells responsible for creating myelin, which protects nerves. | Duke-NUS Medical School | Journal of Clinical Investigation | Scientists from Singapore have demonstrated the critical role played by a special transporter protein in regulating the brain cells that ensure nerves are protected by coverings called myelin sheaths. The findings, reported by researchers at Duke-NUS Medical School and the National University of Singapore in the Journal of Clinical Investigation, could help to reduce the damaging impacts of ageing on the brain. -- An insulating membrane encasing nerves, myelin sheaths facilitate the quick and effective conduction of electrical signals throughout the body's nervous system. When the myelin sheath gets damaged, nerves may lose their ability to function and cause neurological disorders. With ageing, myelin sheaths may naturally start to degenerate, which is often why the elderly lose their physical and mental abilities. -- "Loss of myelin sheaths occurs during the normal ageing process and in neurological diseases, such as multiple sclerosis and Alzheimer's disease," said Dr Sengottuvel Vetrivel, Senior Research Fellow with Duke-NUS' Cardiovascular & Metabolic Disorders (CVMD) Programme and lead investigator of the study. "Developing therapies to improve myelination -- the formation of the myelin sheath -- in ageing and disease is of great importance to ease any difficulties caused by declining myelination." -- To pave the way for developing such therapies, the researchers sought to understand the role of Mfsd2a, a protein that transports lysophosphatidylcholine (LPC) -- a lipid that contains an omega-3 fatty acid -- into the brain as part of the myelination process. From what is known, genetic defects in the Mfsd2a gene leads to significantly reduced myelination and a birth defect called microcephaly, which causes the baby's head to be much smaller than it should be. -- In preclinical models, the team showed that removing Mfsd2a from precursor cells that mature into myelin-producing cells -- known as oligodendrocytes -- in the brain led to deficient myelination after birth. Further investigations, including single-cell RNA sequencing, demonstrated that Mfsd2a's absence caused the pool of fatty acid molecules -- particularly omega-3 fats -- to be reduced in the precursor cells, preventing these cells from maturing into oligodendrocytes that produce myelin. -- "Our study indicates that LPC omega-3 lipids act as factors within the brain to direct oligodendrocyte development, a process that is critical for brain myelination," explained Professor David Silver, the senior author of the study and Deputy Director of the CVMD Programme. "This opens up potential avenues to develop therapies and dietary supplements based on LPC omega-3 lipids that might help retain myelin in the ageing brain -- and possibly to treat patients with neurological disorders stemming from reduced myelination." -- Previously, Prof Silver and his lab discovered Mfsd2a and worked closely with other teams to determine the function of LPC lipids in the brain and other organs. The current research provides further insights into the importance of lipid transport for oligodendrocyte precursor cell development. -- "We're now aiming to conduct preclinical studies to determine if dietary LPC omega-3 can help to re-myelinate damaged axons in the brain," added Prof Silver. "Our hope is that supplements containing these fats can help to maintain -- or even improve -- brain myelination and cognitive function during ageing." -- "Prof Silver has been relentless in investigating the far-reaching role of Msdf2a ever since he discovered this important lipid transport protein, alluding to the many possible ways of treating not only the ageing brain but also other organs in which the protein plays a role," said Professor Patrick Casey, Senior-Vice Dean for Research. "It's exciting to watch Prof Silver and his team shape our understanding of the roles that these specialised lipids play through their many discoveries." [] Myelin, Multiple sclerosis, Axon, Carpal tunnel, Brain tumor, Optic nerve, Sciatic nerve, Pernicious anemia | 2319-006 |
| 87 | 2319-012 | H01 H02 H04 | Detailed Image of Human Retina | Researchers are creating a high-resolution atlas that depicts the development of the human retina. The atlas helps scientists better understand diseases. | ETH Zurich | Nature Biotechnology | What cell types are found in which human tissue, and where? Which genes are active in the individual cells, and which proteins are found there? Answers to these questions and more are to be provided by a specialised atlas -- in particular how the different tissues form during embryonic development and what causes diseases. In creating this atlas, researchers aim to map not only tissue directly isolated from humans, but also structures called organoids. These are three-dimensional clumps of tissue that are cultivated in the laboratory and develop in a way similar to human organs, but on a small scale. -- "The advantage of organoids is that we can intervene in their development and test active substances on them, which allows us to learn more about healthy tissue as well as diseases," explains Barbara Treutlein, Professor of Quantitative Developmental Biology at the Department of Biosystems Science and Engineering at ETH Zurich in Basel. -- To help produce such an atlas, Treutlein, together with researchers from the Universities of Zurich and Basel, has now developed an approach to gather and compile a great deal of information about organoids and their development. The research team applied this approach to the organoids of the human retina, which they derived from stem cells. -- Many proteins visible simultaneously -- At the heart of the methods the scientists used for their approach was the 4i technology: iterative indirect immunofluorescence imaging. This new imaging technique can visualise several dozen proteins in a thin tissue section at high resolution using fluorescence microscopy. The 4i technology was developed a few years ago by Lucas Pelkmans, a professor at the University of Zurich and coauthor of the study that has just been published in the scientific journal Nature Biotechnology. It is in this study that the researchers applied this method to organoids for the first time. -- Typically, researchers use fluorescence microscopy to highlight three proteins in a tissue, each with a different fluorescent dye. For technical reasons, it is not possible to stain more than five proteins at a time. In 4i technology, three dyes are used, but these are washed from the tissue sample after measurements have been taken, and three new proteins are stained. This step was performed 18 times, by a robot, and the process took a total of 18 days. Lastly, a computer merges the individual images into a single microscopy image on which 53 different proteins are visible. They provide information on the function of the individual cell types that make up the retina; for example, rods, cones, and ganglion cells. -- The researchers have supplemented this visual information of retinal proteins with information on which genes are read in the individual cells. -- High spatial and temporal resolution -- The scientists performed all these analyses on organoids that were of different ages and thus at different stages of development. In this way, they were able to create a time series of images and genetic information that describes the entire 39-week development of retinal organoids. "We can use this time series to show how the organoid tissue slowly builds up, where which cell types proliferate and when, and where the synapses are located. The processes are comparable to those of retinal formation during embryonic development," says Gray Camp, a professor at the University of Basel and a senior author of this study. -- The researchers published their image information and more findings on retinal development on a publicly accessible website: EyeSee4is. [] Confocal laser scanning microscopy, Retina, Medical ultrasonography, Stem cell treatments, Conflict resolution, Psychology, HPV vaccine, DNA microarray | 2319-012 |
| 88 | 2319-010 | H01 H02 H03 H06 | Belonging Exercise Boosts Academic Persistence | A new study shows that incoming college students who participated in an online belonging exercise completed their first year at a higher rate than their peers, but only when their institution had strong strategies and resources in place to support diverse students' belonging. | Indiana University | Science | A new study led by Indiana University researchers finds that incoming students who participated in an online belonging exercise completed their first year as full-time college students at a higher rate than their peers, but only when their institution had strong strategies and resources in place to support diverse students' belonging. -- Led by the College Transition Collaborative and the IU Equity Accelerator, the research team offered a brief online reading and writing exercise to nearly 27,000 students from 22 diverse colleges and universities across the United States in fall 2015 and 2016, including IU. These results, the country's largest multi-site randomized controlled trial of this belonging intervention, were published May 5 in Science. -- "There are hundreds of thousands of students being left behind and not supported by institutions in the way they need to be supported," said IU Equity Accelerator founder Mary Murphy, professor of psychological and brain sciences and Class of 1948 Herman B Wells Endowed Professor in the IU Bloomington College of Arts and Sciences. "The Equity Accelerator is helping institutions understand what they can do to help students feel like they belong, that they are supported academically. -- "It is important that students never feel alone, and that the institution offers tangible affordances that are recognized and used by students to help them feel a sense of belonging and to be academically successful in college." -- The researchers found significant effects on students' persistence, course taking and sense of belonging after engaging with the reading and writing exercise. The intervention increased the rate at which students completed their first year of college as full-time students, especially among students in groups that had historically progressed at lower rates. However, across the 22 institutions, the impacts were much greater when the institutions had strategies and resources in place to help students feel like they belong. -- The researchers have calculated that their results can be generalized to more than 1 million students annually at 749 four-year colleges and universities in the United States, where the 12-month drop-out rate for first-time undergraduate freshmen is 24.1 percent, according to the Education Data Initiative. If all schools in the generalizability sample implemented the online social-belonging intervention, 12,136 more full-time students would complete the first year of college each year. The benefits are greatest among historically lower-performing groups -- students whose combined race/ethnicity and generation status is historically lower performing at a particular institution -- which helps to reduce inequality on campuses. -- The social-belonging intervention was delivered through an online module in the summer before students began college, typically as part of a pre-semester checklist of necessary forms and requirements. It included survey results from older students showing that everyday worries about belonging are normal in the transition to college and can improve over time; carefully curated stories from older students describing these worries and how they improved from them; and an opportunity to reflect on these stories in writing. -- Results varied across the 22 institutions, since each offers different strategies, resources and programs to support the particular groups of students who historically struggle with first-year college completion. The researchers say institutional transformation and increasing support for students on campus -- as well as students' knowledge of, attitudes about and usage of these resources -- are critical to improving student success. -- "This work is globally reimagining the role of institutions on student outcomes, not just from an academic perspective but also students' life outcomes," said Sara Woodruff, chief strategy officer at the IU Equity Accelerator. "This is a call to action for the ways in which institutions take their power and use it to really move students. Through the Equity Accelerator, we're helping institutions reexamine the contract they are creating with students, helping them call out inequities that exist and telling them in real, granular terms what they can do to change." -- The IU Equity Accelerator, formed in July 2022, is a focused research organization whose mission is to use and apply social and behavioral science to provide more equitable learning and working environments where everyone can meet their full potential. Institutions nationwide that are working to improve students' belonging can work with the Equity Accelerator to identify, from their own students' perspectives, what resources and strategies are needed to facilitate student belonging on campus. [] Special education, Intellectual giftedness, Political corruption, Economic growth, Suicide, Macroeconomics, Microeconomics, Dementia | 2319-010 |
| 89 | 2319-023 | H06 | Merging Finances for Happier Marriages | New research suggests that married couples who manage their finances together may love each other longer. | Indiana University | Journal of Consumer Research | The Beatles famously sang, "Money can't buy me love," but married couples who manage their finances together may love each other longer, according to research from the Indiana University Kelley School of Business. -- Prior research suggests a correlation that couples who merge finances tend to be happier than those who do not. But this is the first research to show a causal relationship -- that married couples who have joint bank accounts not only have better relationships, but they fight less over money and feel better about how household finances are handled. -- "When we surveyed people of varying relationship lengths, those who had merged accounts reported higher levels of communality within their marriage compared to people with separate accounts, or even those who partially merged their finances," said Jenny Olson, assistant professor of marketing at Kelley. "They frequently told us they felt more like they were 'in this together.' -- "This is the best evidence that we have to date for a question that shapes couples' futures; and the fact that we observe these meaningful shifts over two years, I think it's a pretty powerful testament to the benefits of merging. On average, merging should warrant a conversation with your partner, given the effects that we're seeing here." -- The findings appear in the article "Common Cents: Bank Account Structure and Couples' Relationship Dynamics," which will appear in the Journal of Consumer Research. -- Olson and her co-authors recruited 230 couples, who were either engaged or newly married at the time, and followed them over two years as they began their married lives together. Everyone began the study with separate accounts and consented to potentially changing their financial arrangements. This was the first marriage for everyone involved in the study. -- Some couples were then randomly assigned to keep their separate bank accounts, and others were told to open a joint bank account instead. A third group was allowed to make the decision on their own. -- Couples who were told to open joint bank accounts reported substantially higher relationship quality two years later than those who maintained separate accounts, Olson said, adding that merging promotes greater financial goal alignment and transparency, and a communal understanding of marriage. -- "A communal relationship is one where partners respond to each other's needs because there's a need. 'I want to help you because you need it. I'm not keeping track,'" she said. "There's a 'we' perspective, which we theorized would be related to a joint bank account." -- Olson said that couples with separate accounts viewed financial decision-making as more of an exchange. [] Love, Platonic love, Narcissism, Happiness, Emotion, Maternal bond, Neurology, Double blind | 2319-023 |
| 90 | 2319-026 | H01 H03 | Language Gene's Speech Deficits | Mutations of the Foxp2 gene disrupt the formation of synapses in the brain's striatum, which plays important roles in the control of movement. This research sheds light on how Foxp2 controls speech production. | Massachusetts Institute of Technology | Brain | Mutations of a gene called Foxp2 have been linked to a type of speech disorder called apraxia that makes it difficult to produce sequences of sound. A new study from MIT and National Yang Ming Chiao Tung University sheds light on how this gene controls the ability to produce speech. -- In a study of mice, the researchers found that mutations in Foxp2 disrupt the formation of dendrites and neuronal synapses in the brain's striatum, which plays important roles in the control of movement. Mice with these mutations also showed impairments in their ability to produce the high-frequency sounds that they use to communicate with other mice. -- Those malfunctions arise because Foxp2 mutations prevent the proper assembly of motor proteins, which move molecules within cells, the researchers found. -- "These mice have abnormal vocalizations, and in the striatum there are many cellular abnormalities," says Ann Graybiel, an MIT Institute Professor, a member of MIT's McGovern Institute for Brain Research, and an author of the paper. "This was an exciting finding. Who would have thought that a speech problem might come from little motors inside cells?" -- Fu-Chin Liu PhD '91, a professor at National Yang Ming Chiao Tung University in Taiwan, is the senior author of the study, which appears today in the journal Brain. Liu and Graybiel also worked together on a 2016 study of the potential link between Foxp2 and autism spectrum disorder. The lead authors of the new Brain paper are Hsiao-Ying Kuo and Shih-Yun Chen of National Yang Ming Chiao Tung University. -- Speech control -- Children with Foxp2-associated apraxia tend to begin speaking later than other children, and their speech is often difficult to understand. The disorder is believed to arise from impairments in brain regions, such as the striatum, that control the movements of the lips, mouth, and tongue. Foxp2 is also expressed in the brains of songbirds such as zebra finches and is critical to those birds' ability to learn songs. -- Foxp2 encodes a transcription factor, meaning that it can control the expression of many other target genes. Many species express Foxp2, but humans have a special form of Foxp2. In a 2014 study, Graybiel and colleagues found evidence that the human form of Foxp2, when expressed in mice, allowed the mice to accelerate the switch from declarative to procedural types of learning. -- In that study, the researchers showed that mice engineered to express the human version of Foxp2, which differs from the mouse version by only two DNA base pairs, were much better at learning mazes and performing other tasks that require turning repeated actions into behavioral routines. Mice with human-like Foxp2 also had longer dendrites -- the slender extensions that help neurons form synapses -- in the striatum, which is involved in habit formation as well as motor control. -- In the new study, the researchers wanted to explore how the Foxp2 mutation that has been linked with apraxia affects speech production, using ultrasonic vocalizations in mice as a proxy for speech. Many rodents and other animals such as bats produce these vocalizations to communicate with each other. [] Chemical synapse, Human brain, Alzheimer's disease, Hypothalamus, Limbic system, Brain, Parkinson's disease, Stuttering | 2319-026 |
| 91 | 2319-020 | H01 H02 H04 H06 | Marine Worms' Diet Synthesizes Phytosterols | Researchers have discovered that tiny gutless worms from the Mediterranean can synthesize phytosterols on their own, suggesting that many other animals also have the genes needed to make their own phytosterols. | Max Planck Institute for Marine Microbiology | Science | Cholesterol and phytosterol are sterols, fatty compounds essential for many biological processes such as the functioning of cell membranes. Up to now, it has been assumed that phytosterols are characteristic for plants, and cholesterol for animals, and that only plants can make phytosterols, while animals typically make cholesterol. Dolma Michellod, Nicole Dubilier and Manuel Liebeke from the Max Planck Institute for Marine Microbiology in Bremen, Germany, were therefore surprised when they discovered that a small marine worm called Olavius algarvensis, which lives in seagrass beds in the Mediterranean, has much more phytosterol than cholesterol. -- "We knew the worms couldn't be eating the seagrass because they do not have a mouth or gut," explains first author Michellod. "We next wondered if the symbiotic bacteria inside Olavius, which provide them with their nutrition, might make phytosterols, but this wasn't the case" adds Dubilier. "We were also able to exclude that the worms were taking up phytosterols through their skin. It was only then that we realized that the worms must be making the phytosterols themselves" explains Liebeke. -- The Max Planck researchers, together with colleagues from the MARUM -- Center for Marine Environmental Sciences in Bremen, the University of Münster, the University of Hamburg, North Carolina State University and Imperial College London, used a wealth of methods that included sequencing of the worm's DNA and RNA, protein and metabolite analyses and imaging of sterols to reveal that it is the worm that makes the phytosterols, and that the main phytosterol they make is sitosterol. Their study is the first to show that a metazoan animal can synthesize phytosterols and was published in the journal Science on May 5th. -- From worms to corals -- five animal phyla have the genes for making phytosterols -- Even more surprising for the researchers was their discovery that the gene needed to make sitosterol from precursors of cholesterol is widespread in the animal kingdom. "We discovered a gene that was thought to have been lost long ago in the evolution of animals," explains Liebeke. Michellod adds: "It was exhilarating to discover this gene in so many different groups of animals, from corals and earthworms to clams and mussels." "This means there is a strong selective advantage for animals in having the gene that allows them to make phytosterols. We think phytosterols might make animal membranes more permeable, but so far, that's just wild speculation," adds Dubilier. -- The Good, the Bad, and the Ugly: Understanding the role of cholesterol and phytosterols -- So far, sterol research in animals has focused on cholesterol. Known for being "The Good, the Bad, and the Ugly," some forms of cholesterol are essential for building cell membranes and producing hormones, while others are harmful and can block blood vessels, and increase the risk for cardiovascular diseases. A wealth of recent findings on the benefits of phytosterols for humans indicate that they may improve blood cholesterol levels, thereby reducing the risk of heart attacks or strokes. But the precise manner in which phytosterols provide benefits is far from understood. The researchers from the Max Planck Institute for Marine Microbiology are convinced that the tiny marine worm Olavius algarvensis is a valuable model organism for better understanding the beneficial role of plant sterols for animal health and well-being. [] Mediterranean diet, Herbivore, Dog health, Nutrition, Health science, Healthy diet, Micronutrient, Jane Goodall | 2319-020 |
| 92 | 2319-005 | H04 H06 | Art's Positive Effect on Mood | A recent study highlights the pleasure and meaning-making that can come from viewing art online. It suggests that online art viewing can boost our well-being. | Max-Planck-Gesellschaft | Computers in Human Behavior | Art can have a positive effect on our mood. But does this also work when we look at paintings on a screen? An international research team involving the University of Vienna, the Max Planck Institute for Psycholinguistics in Nijmegen and the Max Planck Institute for Empirical Aesthetics (MPIEA) in Frankfurt am Main decided to investigate this question. The study was funded by the EU Horizon ART*IS Project. The results have now been published as an open access article in the journal Computers in Human Behavior. -- 240 study participants viewed an interactive Monet Water Lily art exhibition from Google Arts and Culture. By filling out a questionnaire, they provided information about their state of mind, how much pleasure they felt when looking at the pictures, and how meaningful they considered the experience to be. The results showed significant improvements in mood and anxiety after just a few minutes of viewing. -- "Online art viewing is an untapped source of support for well-being that can be consumed as bite-sized bits of meaning-making and pleasure," says MacKenzie Trupp, first author from the University of Vienna. -- The study also found that some participants were more receptive to art than others and were able to benefit more. This advantage could be predicted using a metric called "aesthetic responsiveness." -- "Aesthetic responsiveness describes how people react to diverse aesthetic stimuli, like art and nature. The results showed that individuals with high levels of art and aesthetic responsiveness benefit more from online art viewing due to having more pleasurable and meaningful art experiences," explains Edward A. Vessel of MPIEA, developer of the Aesthetic Responsiveness Assessment (AReA). -- The findings of this study are particularly interesting for people who are unable to visit museums in person, such as those with health problems. Furthermore, the results suggest that interactive art exhibitions and similar online experiences should be designed with an awareness of individual differences in aesthetic responsiveness. The study thus expands insight into the benefits and limitations of art in digital media and points the way for increasing the wellness potential of online art. [] Collaboration, Love, Synesthesia, Cyber-bullying, Eye, Happiness, Mammal classification, Addiction | 2319-005 |
| 93 | 2319-018 | H02 | CRISPR and Genetic Variants | A new approach combines genetic association studies, gene editing, and single-cell sequencing to understand which parts of the genome drive specific traits or contribute to disease risk for genetic variants found in the 98% of the genome that does not encode proteins. | New York University | Science | A major challenge in human genetics is understanding which parts of the genome drive specific traits or contribute to disease risk. This challenge is even greater for genetic variants found in the 98% of the genome that does not encode proteins. -- A new approach developed by researchers at New York University and the New York Genome Center combines genetic association studies, gene editing, and single-cell sequencing to address these challenges and discover causal variants and genetic mechanisms for blood cell traits. -- Their approach, dubbed STING-seq and published in Science, addresses the challenge of directly connecting genetic variants to human traits and health, and can help scientists identify drug targets for diseases with a genetic basis. -- Over the past two decades, genome-wide association studies (GWAS) have become an important tool for studying the human genome. Using GWAS, scientists have identified thousands of genetic mutations or variants associated with many diseases, from schizophrenia to diabetes, as well as traits such as height. These studies are conducted by comparing the genomes of large populations to find variants that occur more often in those with a specific disease or trait. -- GWAS can reveal what regions of the genome and potential variants are implicated in diseases or traits. However, these associations are nearly always found in the 98% of the genome that does not code for proteins, which is much less well understood than the well-studied 2% of the genome that codes for proteins. A further complication is that many variants are found in close proximity to each other within the genome and travel together through generations, a concept known as linkage. This can make it difficult to tease apart which variant plays a truly causal role from other variants that are just located nearby. Even when scientists can identify which variant is causing a disease or trait, they do not always know what gene the variant impacts. -- "A major goal for the study of human diseases is to identify causal genes and variants, which can clarify biological mechanisms and inform drug targets for these diseases," said Neville Sanjana, associate professor of biology at NYU, associate professor of neuroscience and physiology at NYU Grossman School of Medicine, a core faculty member at New York Genome Center, and the study's co-senior author. -- "The huge success in GWAS has highlighted the challenge of extracting insights into disease biology from these massive data sets. Despite all of our efforts during the past 10 years, the glass was still just half full -- at best. We needed a new approach," said Tuuli Lappalainen, senior associate faculty member at the New York Genome Center, professor of genomics at the KTH Royal Institute of Technology in Sweden, and the study's co-senior author. -- A cure for sickle cell anemia -- A recent scientific breakthrough in the treatment of sickle cell anemia -- a genetic disorder marked by episodes of intense pain -- illustrates how combining GWAS with cutting-edge molecular tools like gene editing can identify causal variants and lead to innovative therapies. Using GWAS, scientists identified areas of the genome important for producing fetal hemoglobin, a target based on its promise for reversing sickle cell anemia, but they did not know which exact variant drives its production. -- The researchers turned to CRISPR -- a gene editing tool that uses "molecular scissors to cut DNA," according to Sanjana -- to edit the regions identified by GWAS. When CRISPR edits were made at a specific location in the noncoding genome near a gene called BCL11A, it resulted high levels of fetal hemoglobin. [] Gene therapy, Gene, Protein, DNA, DNA repair, Allele, Meiosis, Genetic code | 2319-018 |
| 94 | 2319-036 | H01 H03 | Genetic Changes and Dementia Risk | Scientists have identified new genetic risk factors for Lewy body dementia (LBD) and frontotemporal dementia (FTD) by analyzing thousands of DNA samples. They found several large-scale DNA changes that could be risk factors for these non-Alzheimer's dementias. | NIH/National Institute of Neurological Disorders and Stroke | Cell Genomics | Scientists at the National Institutes of Health have identified new genetic risk factors for two types of non-Alzheimer's dementia. These findings were published in Cell Genomics and detail how researchers identified large-scale DNA changes, known as structural variants, by analyzing thousands of DNA samples. The team discovered several structural variants that could be risk factors Lewy body dementia (LBD) and frontotemporal dementia (FTD). The project was a collaborative effort between scientists at the National Institute of Neurological Disorders and Stroke (NINDS) and the National Institute on Aging (NIA) at NIH. -- Structural variants have been implicated in a variety of neurological disorders. Unlike more commonly studied mutations, which often affect one or a few DNA building blocks called nucleotides, structural variants represent at least 50 but often hundreds, or even thousands, of nucleotides at once, making them more challenging to study. -- "If you imagine that our entire genetic code is a book, a structural variant would be a paragraph, page, or even an entire chapter that has been removed, duplicated, or inserted in the wrong place," said Sonja W. Scholz, M.D., Ph.D., investigator in the neurogenetics branch of NINDS and senior author of this study. -- By combining cutting-edge computer algorithms capable of mapping structural variations across the whole genome with machine learning, the research team analyzed whole-genome data from thousands of patient samples and several thousand unaffected controls. -- A previously unknown variant in the gene TCPN1 was found in samples from patients with LBD, a disease, that like Parkinson's disease, is associated with abnormal deposits of the protein alpha-synuclein in the brain. This variant, in which more than 300 nucleotides are deleted from the gene, is associated with a higher risk for developing LBD. While this finding is new for LBD, TCPN1 is a known risk factor for Alzheimer's disease, which could mean that this structural variant plays a role in the broader dementia population. -- "From a genetics standpoint, this is a very exciting finding," said Dr. Scholz. "It provides a point of reference for cell biology and animal model studies and possibly down the road, a target for intervention." -- By looking at a group of 50 genes implicated in inherited neurodegenerative diseases, the investigators were able to identify additional rare structural variants, including several that are known to cause disease. The analyses also identified two well-established risk factors for FTD changes in the C9orf72 and MAPT genes. These proof-of-concept findings bolstered the strength of the study's new findings by demonstrating that the algorithms were properly working. -- Because reference maps for currently-available structural variants are limited, the researchers generated a catalog based on the data obtained in these analyses. The analysis code and all the raw data are now available to the scientific community for use in their studies. An interactive app also allows investigators to study their genes of interest and ask which variants are present in controls vs. LBD or FTD cases. The authors assert these resources may make complex genetic data more accessible to non-bioinformatics experts, which will accelerate the pace of discovery. -- "Research to unravel the intricate genetic architecture of neurodegenerative diseases is resulting in significant advances in scientific understanding," said Bryan J. Traynor, M.D., Ph.D., senior investigator at NIA. "With each discovery, we shed light on the mechanisms behind neuronal cell death or dysfunction, paving the way for precision medicine to combat these debilitating and fatal disorders." -- Researchers expect that the dataset will continue to grow as additional data are analyzed. [] Dementia with Lewy bodies, Alzheimer's disease, Multi-infarct dementia, DNA repair, DNA, DNA microarray, RNA, Chromosome | 2319-036 |
| 95 | 2319-024 | H01 H04 H05 | Happy Worms Mean Healthy Eggs | Selective serotonin reuptake inhibitors (SSRIs), a class of drugs used for treating depression and anxiety, have surprisingly improved the quality of aging females' egg cells in a roundworm model organism. | Northwestern University | Developmental Biology | Worms might not be depressed, per se. But that doesn't mean they can't benefit from antidepressants. -- In a new study, Northwestern University researchers exposed roundworms (a well-established model organism in biological research) to selective serotonin reuptake inhibitors (SSRIs), a class of drugs used for treating depression and anxiety. Surprisingly, this treatment improved the quality of aging females' egg cells. -- Not only did exposure to SSRIs decrease embryonic death by more than twofold, it also decreased chromosomal abnormalities in surviving offspring by more than twofold. Under the microscope, egg cells also looked younger and healthier, appearing round and plump rather than tiny and misshapen, which is common with aging. -- Astounded by the results, the researchers replicated the experiment in fruit flies -- another common model organism -- and the SSRIs demonstrated the same effect. -- Although much more work is needed, the researchers say these findings provide new opportunities to explore pharmacological interventions that might combat infertility issues in humans by improving egg quality and by delaying the onset of reproductive aging. -- The study will be published on May 8 in the journal Developmental Biology. -- "There is still a great distance between this new finding and the fertility clinic," said Northwestern's Ilya Ruvinsky, who led the study. "But the more we study the reproductive system, the better we understand it and the more opportunities we have for developing practical interventions." -- Ruvinsky is an associate research professor at Northwestern's Weinberg College of Arts and Sciences. Erin Aprison, a research associate in Ruvinsky's laboratory, is the paper's first author. Svetlana Dzitoyeva, a postdoctoral researcher in Ruvinsky's laboratory, co-authored the paper. -- Cutting out the middleman -- Previously, Ruvinsky's team discovered that male pheromones slowed the aging of females' egg cells. Published in the Proceedings of the National Academy of Sciences in May 2022, the previous study exposed female roundworms to male pheromones, which resulted in healthier offspring. [] Postpartum depression, Antiviral drug, Zebrafish, Somatic cell nuclear transfer, In vitro fertilization, Antiretroviral drug, Methamphetamine, Adult stem cell | 2319-024 |
| 96 | 2319-035 | H01 H02 H03 H04 H05 | Restoring Brain Rhythm to Counter Depression | Researchers have discovered that restoring certain signals in the brain region responsible for processing smells can counter depression in rats and mice. | NYU Langone Health / NYU Grossman School of Medicine | Neuron | Szeged in Hungary, a new study in mice and rats found that restoring certain signals in a brain region that processes smells countered depression. -- Publishing in the journal Neuron online May 9, the study results revolve around nerve cells (neurons), which "fire" -- or emit electrical signals -- to transmit information. Researchers in recent years discovered that effective communication between brain regions requires groups of neurons to synchronize their activity patterns in repetitive periods (oscillations) of joint silence followed by joint activity. One such rhythm, called "gamma," repeats about 30 times or more in a second, and is an important timing pattern for the encoding of complex information, potentially including emotions. -- Although its causes remain poorly understood, depression is reflected in gamma oscillation changes, according to past studies, as an electrophysiological marker of the disease in brain regions that manage the sense of smell, which have also been tied to emotions. These regions include the olfactory bulb adjacent to the nasal cavity, which is thought to be a source and "conductor" of brain-wide gamma oscillations. -- To test this theory, the current study authors shut down the function of the bulb using genetic and cell signaling techniques, observed a related increase of depression-like behaviors in study rodents, and then reversed these behaviors using a device that boosted gamma signals of the brain at their natural pace. -- "Our experiments revealed a mechanistic link between deficient gamma activity and behavioral decline in mice and rat models of depression, with the signal changes in the olfactory and connected limbic systems similar to those seen in depressed patients," says corresponding study author Antal Berényi, MD, PhD, adjunct assistant professor in the Department of Neuroscience and Physiology at NYU Langone Health. "This work demonstrates the power of gamma-enhancement as a potential approach for countering depression and anxiety in cases where available medications are not effective." -- Major depressive disorder is a common, severe psychiatric illness often resistant to drug therapy, the researchers say. The prevalence of the condition has dramatically increased since the start of the pandemic, with more than 53 million new cases estimated. -- Gamma Waves Linked to Emotions -- Disease-causing changes in the timing and strength of gamma signals, potentially caused by infections, trauma, or drugs, from the olfactory bulb to other brain regions of the limbic system, such as the piriform cortex and hippocampus, may alter emotions. However, the research team is not sure why. In one theory, depression arises, not within the olfactory bulb, but in changes to its outgoing gamma patterns to other brain targets. -- Removal of the bulb represents an older animal model for the study of major depression, but the process causes structural damage that may cloud researchers' view of disease mechanisms. Thus, the current research team designed a reversible method to avert damage, starting with a single, engineered strand of DNA encapsulated in a harmless virus, which when injected into neurons in the olfactory bulbs of rodents caused the cells to build certain protein receptors on their surfaces. -- This let the researchers inject the rodents with a drug, which spread system-wide, but only shut down the neurons in the bulb that had been engineered to have the designed drug-sensitive receptors. This way the investigators could selectively and reversibly switch off the communication between the bulb partner brain regions. These tests revealed that chronic suppression of olfactory bulb signals, including gamma, not only induced depressive behaviors during the intervention, but fordays afterward. [] Psychedelic drug, Mouse, Multiple sclerosis, Postpartum depression, Psycholinguistics, Thalamus, House mouse, Hypothalamus | 2319-035 |
| 97 | 2319-027 | H02 H05 | Extra Chromosome Dynamics in Fruit Flies | Researchers have revealed the dynamics of a new, very young chromosome in fruit flies that is similar to chromosomes that arise in humans and is associated with treatment-resistant cancer and infertility. The findings may one day lead to developing more targeted therapies for treating these conditions. | Stowers Institute for Medical Research | Current Biology | Most chromosomes have been around for millions of years. Now, researchers from the Stowers Institute for Medical Research have revealed the dynamics of a new, very young chromosome in fruit flies that is similar to chromosomes that arise in humans and is associated with treatment-resistant cancer and infertility. The findings may one day lead to developing more targeted therapies for treating these conditions. -- A new study published in Current Biology on May 4, 2023, reveals how this small chromosome that arose less than 20 years ago has persisted in a single, lab-reared strain of the fruit fly, Drosophila melanogaster, and is correlated with supernumerary (extra) chromosomes in humans. -- "I feel kind of like an astronomer who's watching the birth of a star," said Stowers Investigator Scott Hawley, Ph.D. "We are getting to watch the birth of a chromosome and are starting to understand both its capabilities and limitations." -- Previous research from the Hawley Lab had first identified these small, extra chromosomes, but little was known about their form, function, or dynamics during cell division. Former Hawley Lab Postdoctoral Researcher Stacey Hanlon, Ph.D., realized that this discovery could be an ideal system to investigate how new chromosomes arise, which may lead to more effective cancer treatments and methods to overcome infertility. -- Supernumerary chromosomes in humans are found in cancer cells and frequently interfere with drugs designed to target tumors, making these types of cancers, like osteosarcoma, difficult to treat. In addition, the presence of supernumerary chromosomes in men can disrupt normal chromosome segregation during sperm production, which can cause infertility. -- "Being able to understand how supernumerary chromosomes arise and what their structures are can potentially illuminate their vulnerabilities," said Hawley. "This may enable the development of potential therapeutic targets." -- Called B chromosomes -- as opposed to the standard "A" set of essential chromosomes -- these genetic elements naturally appeared in a single laboratory stock of fruit flies in Hawley's lab. Now, the researchers are witnessing chromosome birth and evolution in less than two decades. -- How does something like this new chromosome apparently arise from nothing? More important, as these newly born B chromosomes do not possess any known essential genes for fruit fly function, how do they persist in a genome? In short, by cheating. -- "I like to call these B chromosomes genetic renegades," said Hanlon. "They do not follow the rules." -- Hanlon discovered that the fruit fly B chromosomes are maintained by a mechanism called "meiotic drive" that enables the them to rebel against the usual rules of inheritance. The B chromosomes drive their way into the next generation during the formation of the egg to ensure their own persistence in more than half of the next generation. [] Human genome, Chromosomal crossover, Turner syndrome, Canine hybrids, Sex linkage, Telomere, Chromosome, Hybrid | 2319-027 |
| 98 | 2319-022 | H04 | Alternative 'Fuel' for Cell Motors | Researchers have discovered a unique two-component molecular motor that uses renewable chemical energy to pull vesicles toward membrane-bound organelles. | Technische Universität Dresden | Nature Physics | Cells have a fascinating feature to neatly organize their interior by using tiny protein machines called molecular motors that generate directed movements. Most of them use a common type of fuel, a kind of chemical energy, called ATP to operate. Now researchers from the Max Planck Institute of Molecular Cell Biology and Genetics (MPI-CBG), the Cluster of Excellence Physics of Life (PoL) and the Biotechnology Center (BIOTEC) of the TU Dresden in Dresden, Germany, and the National Centre for Biological Sciences (NCBS) in Bangalore, India, discovered a novel molecular system that uses an alternative chemical energy and employs a novel mechanism to perform mechanical work. By repeatedly contracting and expanding, this molecular motor functions similarly to a classical Stirling engine and helps to distribute cargo to membrane-bound organelles. It is the first motor using two components, two differently sized proteins, Rab5 and EEA1, and is driven by GTP instead of ATP. The results are published in the journal Nature Physics. -- Motor proteins are remarkable molecular machines within a cell that convert chemical energy, stored in a molecule called ATP, into mechanical work. The most prominent example is myosin which helps our muscles to move. In contrast, GTPases which are small proteins have not been viewed as molecular force generators. One example is a molecular motor composed of two proteins, EEA1 and Rab5. In 2016, an interdisciplinary team of cell biologists and biophysicists in the groups of MPI-CBG directors Marino Zerial and Stephan Grill and their colleagues, including PoL and BIOTEC research group leader Marcus Jahnel, discovered that the small GTPase protein Rab5 could trigger a contraction in EEA1. These string-shaped tether proteins can recognize the Rab5 protein present in a vesicle membrane and bind to it. The binding of the much smaller Rab5 sends a message along the elongated structure of EEA1, thereby increasing its flexibility, similar to how cooking softens spaghetti. Such flexibility change produces a force that pulls the vesicle towards the target membrane, where docking and fusion occur. However, the team also hypothesized that EEA1 could switch between a flexible and a rigid state, similar to a mechanical motor motion, simply by interacting with Rab5 alone. -- This is where the current research sets in, taking shape via the doctoral work of the two first authors of the study. Joan Antoni Soler from Marino Zerial's research group at MPI-CBG and Anupam Singh from the group of Shashi Thutupalli, a biophysicist at the Simons Centre for the Study of Living Machines at the NCBS in Bangalore, set out to experimentally observe this motor in action. -- With an experimental design to investigate the dynamics of the EEA1 protein in mind, Anupam Singh spent three months at the MPI-CBG in 2019. "When I met Joan, I explained to him the idea of measuring the protein dynamics of EEA1. But these experiments required specific modifications to the protein that allowed measurement of its flexibility based on its structural changes," says Anupam. Joan Antoni Soler's expertise in protein biochemistry was a perfect fit for this challenging task. "I was delighted to learn that the approach to characterize the EEA1 protein could answer whether EEA1 and Rab5 form a two-component motor, as previously suspected. I realized that the difficulties in obtaining the correct molecules could be solved by modifying the EEA1 protein to allow fluorophores to attach to specific protein regions. This modification would make it easier to characterize the protein structure and the changes that can occur when it interacts with Rab5," explains Joan Antoni. -- Armed with the suitable protein molecules and the valuable support of co-author Janelle Lauer, a senior postdoctoral researcher in Marino Zerial's research group, Joan and Anupam were able characterize the dynamics of EEA1 thoroughly using the advanced laser scanning microscopes provided by the light microscopy facilities at the MPI-CBG and the NCBS. Strikingly, they discovered that the EEA1 protein could undergo multiple flexibility transition cycles, from rigid to flexible and back again, driven solely by the chemical energy released by its interaction with the GTPase Rab5. These experiments showed that EEA1 and Rab5 form a GTP-driven two-component motor. To interpret the results, Marcus Jahnel, one of the corresponding authors and research group leader at PoL and BIOTEC, developed a new physical model to describe the coupling between chemical and mechanical steps in the motor cycle. Together with Stephan Grill and Shashi Thutupalli, the biophysicists were also able to calculate the thermodynamic efficiency of the new motor system, which is comparable to that of conventional ATP-driven motor proteins. -- "Our results show that the proteins EEA1 and Rab5 work together as a two-component molecular motor system that can transfer chemical energy into mechanical work. As a result, they can play active mechanical roles in membrane trafficking. It is possible that the force-generating molecular motor mechanism may be conserved across other molecules and used by several other cellular compartments," Marino Zerial summarizes the study. Marcus Jahnel adds: "I am delighted that we could finally test the idea of an EEA1-Rab5 motor. It's great to see it confirmed by these new experiments. Most molecular motors use a common type of cellular fuel called ATP. Small GTPases consume another type of fuel, GTP, and have been thought of mainly as signaling molecules. That they can also drive a molecular system to generate forces and move things around puts these abundant molecules in an interesting new light." Stephan Grill is equally excited: "It's a new class of molecular motors! This one doesn't move around like the kinesin motor that transports cargo along microtubules but performs work while staying in place. It's a bit like the tentacles of an octopus." -- "The model we used is inspired by that of the classical Stirling engine cycle. While the traditional Stirling engine generates mechanical work by expanding and compressing gas, the two-component motor described uses proteins as the working substrate, with protein flexibility changes resulting in force generation. As a result, this type of mechanism opens up new possibilities for the development of synthetic protein engines," adds Shashi Thutupalli. -- Overall, the authors hope that this new interdisciplinary study could open new research avenues in both molecular cell biology and biophysics. [] Chloroplast, Prokaryote, Methyl tert-butyl ether, Molecular biology, Autophagy, Hydroelectricity, Sled dog, Cell membrane | 2319-022 |
| 99 | 2319-015 | H01 H02 H03 H04 H05 | Anti-Depressant KNT-127 Reduces Stress | Researchers have reported how KNT-127, a delta opioid receptor agonist, quickly and efficiently reduces classic parameters of depression in a mouse model. This anti-depressant agent exhibits the dual nature of being a stress reliever and an anti-depressant and could broaden the potential of existing treatments. | Tokyo University of Science | Neuropharmacology | Depression due to psychological stress affects millions of people worldwide. However, most of the existing anti-depressant drugs are slow, prone to development of resistance, and have severe side effects, demanding the need for more effective treatment options. -- Delta opioid receptors (DOPs) are known to play a key role in the development of depression and similar diseases. Previous studies have revealed that DOP agonists (substances that bind DOPs instead of the regular compound and cause the same effect) have improved efficacy and lower side effects than most existing anti-depressant drugs. Recent studies have identified KNT-127 as a potent DOP agonist with significant anti-depressant activity, quick action, and minimal side effects. However, the underlying mechanism of action is not well understood. -- To this end, Prof. Akiyoshi Saitoh, Mr. Toshinori Yoshioka, Jr. Associate Prof. Daisuke Yamada, and Prof. Eri Segi-Nishida, at the Tokyo University of Science, along with Prof.Hiroshi Nagase from the University of Tsukuba, set out to assess the therapeutic and preventive effects of KNT-127 in a mouse model with depression. The findings of this study were made available online on 30 March, 2023, and published in the journal Neuropharmacology on 4 April, 2023. -- Explaining the motivation behind their study, Prof. Saitoh explains, "We previously discovered that delta-opioid receptor (DOP) agonists may quick action and have a low risk of side effects compared to existing drugs. Thus, we have been working on their clinical development as a new treatment strategy for depression. In this study, we attempted to elucidate the mechanism of antidepressant-like effects of KNT-127, a selective DOP agonist, in a mouse model of depression." -- The hypothalamic-pituitary-adrenal axis, hippocampal neurogenesis, and neuroinflammation are regarded as the major factors in the processes leading to the development of depression. Thus, understanding the effect of KNT-127 on the above parameters was crucial towards decoding its underlying working principle. -- To this end, Prof. Saitoh and team created the depression mouse model called chronic vicarious social defeat stress (cVSDS) mice, by exposing five-week-old male mice to extreme psychological stress for 10 minutes per day, repeated for 10 days. Next, KNT-127 was given to the mice both during (10 days) and after (28 days later) the stress period, to assess its efficacy. -- They observed that prolonged administration of KNT-127 during (anti-stress effect) and after stress (anti-depressant effect) period, significantly improved social interaction and levels of serum corticosterone (a hormone secreted under stress in mice) in cVSDS mice. Moreover, KNT-127 administration during stress, suppressed stress-induced newborn neuronal death in the hippocampus, rather than increasing neurogenesis, or the formation of new neurons. In contrast, when administered after stress, KNT-127 did not affect newborn neuron survival rate at all. Furthermore, unlike conventional antidepressants, KNT-127 did not affect neurogenesis even under stress-free conditions. -- Psychological stress increases the number of microglia and activated microglia in the brains of cVSDS mice. Interestingly, under both models of delivery, KNT-127 suppressed microglial activation and hence reduced inflammation in the hippocampus. -- In a nutshell, during and post stress period, KNT-127 prevents neuronal inflammation and reduces newborn neuronal death without affecting neuron formation to exert anti-stress and anti-depressant-like effects, respectively. However, further research is warranted for better insights regarding DOP agonists and the mechanism underlying their anti-depressant effects. -- The anti-stress effect of KNT-127 may offer added benefits for patients during treatment. Prof. Saitoh elaborates, "Patients with depression often have to face situations where they cannot avoid stressful environments, even during treatment. Therefore, we believe that the additional anti-stress effect during the treatment period has important clinical significance." [] Anti-obesity drug, Antiviral drug, Postpartum depression, Substance abuse, Bipolar disorder, Clinical depression, Analgesic, Antiretroviral drug | 2319-015 |
| 100 | 2319-017 | H01 H03 H04 H06 | Toxic Metals in Mixed-Fruit Juices | A new study found that mixed-fruit juices and plant-based milks such as oat and almond were most likely to contain levels of toxic metals above federal drinking water standards. | Tulane University | Journal of Food Composition and Analysis | A new study has found that some commonly consumed beverages contained levels of toxic metals that exceed federal drinking water standards. -- Five of the 60 beverages tested contained levels of a toxic metal above federal drinking water standards, according to the study from Tulane University. Two mixed juices had levels of arsenic above the 10 microgram/liter standard. A cranberry juice, a mixed carrot and fruit juice and an oat milk each had levels of cadmium exceeding the 3 parts per billion standard. -- The sampled beverages, which included those commonly found in grocery stores -- single and mixed fruit juices, plant-based milks, sodas, and teas -- were measured for 25 different toxic metals and trace elements. Mixed-fruit juices and plant-based milks (such as oat and almond) contained elevated concentrations of toxic metals more often than other drinks, according to the findings published in the Journal of Food Composition and Analysis. -- All told, seven of the 25 elements exceeded drinking water standards in some of the drinks, including nickel, manganese, boron, cadmium, strontium, arsenic, and selenium. While lead was detected in more than 93% of the 60 samples, most contained very low levels, below 1 part per billion. The highest level (6.3 micrograms/kg ) was found in a lime sports drink, though that's below both EPA and WHO standards for drinking water. -- Tewodros Godebo, lead author and assistant professor of environmental health sciences at Tulane University School of Public Health and Tropical Medicine, said the study was important because there are few peer-reviewed studies examining the contents of American beverages. -- "It was surprising that there aren't a lot of studies out there concerning toxic and essential elements in soft drinks in the United States," Godebo said. "This creates awareness that there needs to be more study." -- These soft drinks are often consumed in smaller quantities than water, meaning the health risks for adults are most likely low. But Godebo said parents should be cautious about what drinks they offer their children. -- "People should avoid giving infants and young children mixed-fruit juices or plant-based milks at high volume," Godebo said. "Arsenic, lead, and cadmium are known carcinogens and well established to cause internal organ damage and cognitive harm in children especially during early brain development." -- Godebo said most of these elements found in beverages presumably come from contaminated soil. -- "These metals are naturally occurring so it's hard to get rid of completely," Godebo said. [] Water purification, Oat, Blackberry, Personalized medicine, Avocado, Fruit, Heavy metals, Mushroom poisoning | 2319-017 |
| 101 | 2319-029 | H01 H04 | Gene for Severe Facial Defects Identified | An international collaboration has discovered that pathogenic variants of the FOXI3 gene -- responsible for the development of the ear -- cause one form of Goldenhar syndrome, a rare congenital disease affecting early fetal development. | Université de Genève | Nature Communications | Goldenhar syndrome is a rare congenital disease, affecting early foetal development. This syndrome includes malformations of varying severity, affecting different parts of the face. Its causes and modes of transmission are still poorly understood. An international collaboration led by the University of Geneva (UNIGE) and Beihang University, in China, has discovered that pathogenic variants of the FOXI3 gene -- responsible for the development of the ear -- cause one form of this developmental disorder. The scientists were also able to identify the modes of transmission of the disease when this particular gene is involved. These results can be found in Nature Communications. -- First described in 1952 at the University of Geneva (UNIGE) by the ophthalmologist Maurice Goldenhar (1924-2001), Goldenhar syndrome or oculo-auriculo-vertebral dysplasia is a rare congenital disorder with facial asymmetry, malformations of the auditory and ocular systems, and spinal column anomalies, sometimes associated with mental retardation. It varies greatly in expression and severity depending on the individual and is thought to affect approximately one in 3,500 to 5,600 births. -- This syndrome is caused by mutations that appear during foetal development. Do these mutations occur spontaneously or is there an inherited form of the disease? The mode of transmission and the molecular mechanisms involved are still poorly understood. A recent international research effort, led by a joint team from the UNIGE and Beihang University, in China, is providing new elements for understanding the disease. The scientists have identified a gene -- FOXI3 -- whose pathogenic variants are involved in one form of the disease. -- A gene that builds the ear -- ''FOXI3 is critically involved in the development of the ear. It is an architect gene: it produces a protein that acts as a transcription factor. In other words, it controls the expression of other genes to start the construction of the ear,'' explains Stylianos Antonarakis, Emeritus Professor at the UNIGE Faculty of Medicine and co-last author of the study, which was funded by the ChildCare Foundation in Geneva. -- To determine the role of FOXI3, the scientists used the genetic profiles of a highly consanguineous Pakistani family involved in a larger research project on rare diseases. In this family, two brothers have the syndrome but not their parents, nor the other four siblings. Both patients have pathogenic mutations in both copies of the FOXI3 gene, while several other members of this family, who do not have Goldenhar syndrome, have a mutation in only one copy of the gene. -- ''This first analysis allowed us to confirm that pathogenic mutations in both copies of the FOXI3 gene, each inherited from a parent, are necessary for a form of the disease to develop,'' explains Stylianos Antonarakis. This is called autosomal recessive inheritance. -- Responsible for one form of the disease -- To find out whether pathogenic variants in FOXI3 and their autosomal recessive inheritance are systematically involved, the researchers also analysed the genetic profiles of 670 unrelated patients in Europe and China. ''Eighteen pathogenic variants in the FOXI3 gene were identified in twenty-one patients. FOXI3 is therefore only one of the genes that can cause the disease, precisely the specific form observed in our Pakistani patients,'' explains Ke Mao, researcher at Beihang University and co-first author of the study with Christelle Borel, senior research associate in the Department of Genetic Medicine and Development at the UNIGE Faculty of Medicine, and Muhammad Ansar, senior research and teaching assistant in the same department and head of the ''Eye Genetics'' research group at the Jules-Gonin eye hospital. -- Another finding that baffled the researchers was that the mode of inheritance, in many other cases, is seemingly autosomal dominant. In this case, only one of the two copies of the gene needs to carry the mutation for the disease to occur. By carefully studying the genome around the FOXI3 gene, scientists have solved this mystery. There is a functional and frequent, but specific, variant of one copy of the FOXI3 gene that, in combination with a severe mutation in the other copy of the FOXI3 gene, also causes the disorder. [] Rett syndrome, Asperger syndrome, Delirium, Chronic fatigue syndrome, Restless legs syndrome, Prion, Gene therapy, Spinal muscular atrophy | 2319-029 |
| 102 | 2319-037 | H01 H02 | Nose Shape Gene from Neanderthals | A recent study has found that humans inherited genetic material from Neanderthals that affects the shape of our noses. | University College London | Communications Biology | Humans inherited genetic material from Neanderthals that affects the shape of our noses, finds a new study led by UCL researchers. -- The new Communications Biology study finds that a particular gene, which leads to a taller nose (from top to bottom), may have been the product of natural selection as ancient humans adapted to colder climates after leaving Africa. -- Co-corresponding author Dr Kaustubh Adhikari (UCL Genetics, Evolution & Environment and The Open University) said: "In the last 15 years, since the Neanderthal genome has been sequenced, we have been able to learn that our own ancestors apparently interbred with Neanderthals, leaving us with little bits of their DNA. -- "Here, we find that some DNA inherited from Neanderthals influences the shape of our faces. This could have been helpful to our ancestors, as it has been passed down for thousands of generations." -- The study used data from more than 6,000 volunteers across Latin America, of mixed European, Native American and African ancestry, who are part of the UCL-led CANDELA study, which recruited from Brazil, Colombia, Chile, Mexico and Peru. The researchers compared genetic information from the participants to photographs of their faces -- specifically looking at distances between points on their faces, such as the tip of the nose or the edge of the lips -- to see how different facial traits were associated with the presence of different genetic markers. -- The researchers newly identified 33 genome regions associated with face shape, 26 of which they were able to replicate in comparisons with data from other ethnicities using participants in east Asia, Europe, or Africa. -- In one genome region in particular, called ATF3, the researchers found that many people in their study with Native American ancestry (as well as others with east Asian ancestry from another cohort) had genetic material in this gene that was inherited from the Neanderthals, contributing to increased nasal height. They also found that this gene region has signs of natural selection, suggesting that it conferred an advantage for those carrying the genetic material. -- First author Dr Qing Li (Fudan University) said: "It has long been speculated that the shape of our noses is determined by natural selection; as our noses can help us to regulate the temperature and humidity of the air we breathe in, different shaped noses may be better suited to different climates that our ancestors lived in. The gene we have identified here may have been inherited from Neanderthals to help humans adapt to colder climates as our ancestors moved out of Africa." -- Co-corresponding author Professor Andres Ruiz-Linares (Fudan University, UCL Genetics, Evolution & Environment, and Aix-Marseille University) added: "Most genetic studies of human diversity have investigated the genes of Europeans; our study's diverse sample of Latin American participants broadens the reach of genetic study findings, helping us to better understand the genetics of all humans." -- The finding is the second discovery of DNA from archaic humans, distinct from Homo sapiens, affecting our face shape. The same team discovered in a 2021 paper that a gene influencing lip shape was inherited from the ancient Denisovans.* [] Neandertal interaction with Cro-Magnons, Neanderthal, Mutation, Molecular biology, Virus, Human evolution, Timeline of human evolution, Bone scan | 2319-037 |
| 103 | 2319-028 | H02 H03 H06 | Neuropathic Pain Mechanism and Treatment | Researchers have discovered that a mechanism involving the enzyme Tiam1 in dorsal horn excitatory neurons of the spinal cord both initiates and maintains neuropathic pain and that targeting spinal Tiam1 with anti-sense oligonucleotides effectively alleviated neuropathic pain hypersensitivity. | University of Alabama at Birmingham | Neuron | Neuropathic pain -- abnormal hypersensitivity to stimuli -- is associated with impaired quality of life and is often poorly managed. Estimates suggest that 3 percent to 17 percent of adults suffer from neuropathic pain, including a quarter of people with diabetes and a third of people with HIV. -- In a paper published in the journal Neuron, researchers report that a mechanism involving the enzyme Tiam1 in dorsal horn excitatory neurons of the spinal cord both initiates and maintains neuropathic pain. Moreover, they show that targeting spinal Tiam1 with anti-sense oligonucleotides injected into the cerebrospinal fluid effectively alleviated neuropathic pain hypersensitivity. -- "Thus, our study has uncovered a pathophysiological mechanism that initiates, transitions and sustains neuropathic pain, and we have identified a promising therapeutic target for treating neuropathic pain with long-lasting consequences," said Lingyong Li, Ph.D., an associate professor at the University of Alabama at Birmingham Department of Anesthesiology and Perioperative Medicine. "Understanding the pathophysiological mechanisms underlying neuropathic pain is critical for developing new therapeutic strategies to treat chronic pain effectively." -- Li and Kimberley Tolias, Ph.D., a professor at Baylor College of Medicine in Houston, Texas, were co-leaders of the research. -- It was known that one feature of neuropathic pain is maladaptive changes in neurons of the spinal dorsal horn -- increases in the size and density of dendritic spines, the primary postsynaptic sites of excitatory synapses. However, the mechanisms driving this synaptic plasticity were unclear. Dendrites are tree-like appendages attached to the body of a neuron that receive communications from other neurons. The spinal dorsal horn is one of the three gray columns of the spinal cord. -- In related work, Li and Tolias last year found that chronic pain in a mouse model leads to an activated Tiam1 in anterior cingulate cortex pyramidal neurons of the brain, resulting in an increased number of spines on the neural dendrites. This higher spine density increased the number of connections, and the strength of those connections, between neurons, a change known as synaptic plasticity. Those increases caused hypersensitivity and were associated with chronic pain-related depression in the mouse model. -- The current neuropathic pain study by Li and Tolias used mouse models of neuropathic pain caused by nerve injury, chemotherapy or diabetes. The researchers showed that Tiam1 is activated in the spinal dorsal horn of mice subjected to neuropathic pain and that global knockout of Tiam1 in mice prevented the development of neuropathic pain. Global knockout causes no other apparent abnormalities in the mice. -- The UAB and Baylor researchers found that Tiam1 expression in the spinal dorsal horn neurons -- but not in the dorsal root ganglion neurons or excitatory forebrain neurons -- was essential for the development of neuropathic pain. Furthermore, they found that neuropathic pain development depended on Tiam1 expression in excitatory neurons -- not in inhibitory neurons. -- After showing where Tiam1 acts in neuropathic pain, Li, Tolias and colleagues showed what Tiam1 does. Tiam1 is known to modulate the activity of other proteins that help build or unbuild the cytoskeletons of cells, and the building of cytoskeleton actin filaments is part of dendritic spine creation. The researchers found that Tiam1 is necessary during the development of neuropathic pain to increase the density of dendritic spines on wide dynamic range neurons from the spinal dorsal horn and to increase synaptic NMDA receptor activity of spinal dorsal horn neurons. -- Tiam1 functions to activate the small GTPase Rac1 enzyme that promotes actin polymerization. The researchers showed that the development of Tiam1-mediated neuropathic pain was dependent on Tiam1-Rac1 signaling. They then used a small molecule inhibitor to block Rac1 activation at three different time points -- right after peripheral nerve injury, four days after nerve injury when neuropathic pain hypersensitivity gradually develops, or three weeks after nerve injury when chronic neuropathic pain is fully established. They found that neuropathic pain was prevented or reversed at each time point. Thus, Tiam1-Rac1 signaling is essential for the initiation, transition and maintenance of neuropathic pain. [] Nociceptor, Antidepressant, Sensory neuron, Gate control theory of pain, Chronic pain, Pain, Back pain, Multiple sclerosis | 2319-028 |
| 104 | 2319-021 | H01 H02 H04 H05 H06 | Traffic Controllers for Cellular Signals | Scientists have observed proteins that act like air traffic controllers, managing the flow of signals in and out of human cells, with unprecedented detail using advanced microscopy techniques. This could inform the development of better drugs for pain relief, diabetes, or heart failure. | University of Birmingham | Cell | Proteins that act like air traffic controllers, managing the flow of signals in and out of human cells, have been observed for the first time with unprecedented detail using advanced microscopy techniques. -- Described in new research published today in Cell, an international team of researchers led by Professor Davide Calebiro from the University of Birmingham has seen how beta-arrestin, a protein involved in managing a common and important group of cellular gateways, known as receptors, works. -- Beta-arrestin is involved in controlling the activity of G protein-coupled receptors (GPCRs) which are the largest group of receptors in the human body and mediate the effects of many hormones and neurotransmitters. As a result, GPCRs are major targets for drug development and between 30-40% of all current therapeutics are against these receptors. Once the receptors are activated, beta-arrestins dampen the signal in a process called desensitisation but can also mediate signals of their own. -- The new study published in Cell has unexpectedly revealed that beta-arrestins attach themselves to the outer cell membrane waiting for hormones or neurotransmitters to land on receptors. Surprisingly, the interactions between beta-arrestins and active receptors are much more dynamic than previously thought, allowing for a far better control of receptor-mediated signals. -- Davide Calebiro, Professor of Molecular Endocrinology in the Institute of Metabolism and Systems Research at the University of Birmingham and Co-Director of the Centre of Membrane Proteins and Receptors (COMPARE) of the Universities of Birmingham and Nottingham said: -- "In our study, we used innovative single-molecule microscopy and computational methods developed in our lab to observe for the first time how individual beta-arrestin molecules work in our cells with unprecedented detail. -- "We have revealed a new mechanism that explains how beta-arrestins can efficiently interact with receptors on the plasma membrane of a cell. Acting like air traffic controllers, these proteins sense when receptors are activated by a hormone or a neurotransmitter to modulate the flow of signals within our cells. By doing so, they play a key role in signal desensitisation, a fundamental biological process that allows our organism to adapt to prolonged stimulation. -- "These results are highly unexpected and could pave the way to novel therapeutic approaches for diseases such as heart failure and diabetes or the development of more effective and better tolerated analgesics." -- Pioneering research methods could lead to novel drug therapies -- This success was only possible thanks to the unique multidisciplinary collaborative environment provided by COMPARE, a world-leading research centre for the study of membrane proteins and receptors that brings together 36 research groups with complementary expertise in cell biology, receptor pharmacology, biophysics, advanced microscopy and computer science. [] Analgesic, Confocal laser scanning microscopy, Artery, Echocardiography, Psychedelic drug, Suicide, Chemotherapy, Chronic pain | 2319-021 |
| 105 | 2319-034 | H01 H03 H04 | Deep Sleep and Alzheimer's Memory Loss | Non-REM slow-wave sleep, commonly known as deep sleep, has been found to increase resilience against beta-amyloid, a protein in the brain linked to memory loss caused by dementia. This suggests that deep sleep may act as a cognitive reserve factor. | University of California - Berkeley | BMC Medicine | A deep slumber might help buffer against memory loss for older adults facing a heightened burden of Alzheimer's disease, new research from the University of California, Berkeley, suggests. -- Deep sleep, also known as non-REM slow-wave sleep, can act as a "cognitive reserve factor" that may increase resilience against a protein in the brain called beta-amyloid that is linked to memory loss caused by dementia. Disrupted sleep has previously been associated with faster accumulation of beta-amyloid protein in the brain. However, the new research from a team at UC Berkeley reveals that superior amounts of deep, slow-wave sleep can act as a protective factor against memory decline in those with existing high amounts of Alzheimer's disease pathology -- a potentially significant advance that experts say could help alleviate some of dementia's most devastating outcomes. -- "With a certain level of brain pathology, you're not destined for cognitive symptoms or memory issues," said Zsófia Zavecz, a postdoctoral researcher at UC Berkeley's Center for Human Sleep Science. "People should be aware that, despite having a certain level of pathology, there are certain lifestyle factors that will help moderate and decrease the effects. -- "One of those factors is sleep and, specifically, deep sleep." -- The research, published Wednesday in the journal BMC Medicine, is the latest in a large body of work aimed at finding a cure for Alzheimer's disease and preventing it altogether. -- As the most prevalent form of dementia, Alzheimer's disease destroys memory pathways and, in advanced forms, interferes with a person's ability to perform basic daily tasks. Roughly one in nine people over age 65 have the progressive disease -- a proportion that is expected to grow rapidly as the baby boomer generation ages. -- In recent years, scientists have probed the ways that deposits of beta-amyloid associate with Alzheimer's disease and how such deposits also affect memory more generally. In addition to sleep being a foundational part of memory retention, the team at UC Berkeley previously discovered that the declining amount of a person's deep sleep could act as a "crystal ball" to forecast a faster rate of future beta-amyloid buildup in the brain, after which dementia is more likely set in. -- Years of education, physical activity and social engagement are widely believed to shore up a person's resilience to severe brain pathology -- essentially keeping the mind sharp, despite the decreased brain health. These are called cognitive reserve factors. However, most of them, such as past years of education or the size of one's social network, cannot be easily changed or modified retroactively. -- That idea of cognitive reserve became a compelling target for sleep researchers, said Matthew Walker, a UC Berkeley professor of neuroscience and psychology and senior author of the study. -- "If we believe that sleep is so critical for memory," Walker said, "could sleep be one of those missing pieces in the explanatory puzzle that would tell us exactly why two people with the same amounts of vicious, severe amyloid pathology have very different memory?" [] Sleep, Rapid eye movement, Circadian rhythm sleep disorder, Alzheimer's disease, Sleep deprivation, Narcolepsy (sleep disorder), Obstructive sleep apnea, Sleep apnea | 2319-034 |
| 106 | 2319-013 | H01 H02 H03 H04 | Brain's Acquisition of Omega-3s | Researchers have developed a zebrafish model to better understand how the brain acquires essential omega-3 fatty acids with the potential to improve our understanding of lipid transport across the blood-brain barrier and of disruptions in this process that can lead to birth defects or neurological conditions. | University of California - Los Angeles Health Sciences | Nature Communications | Researchers at the UCLA David Geffen School of Medicine, the Howard Hughes Medical Institute at UCLA and the National Institutes of Health have developed a zebrafish model that provides new insight into how the brain acquires essential omega-3 fatty acids, including docosahexaenoic acid (DHA) and linolenic acid (ALA). Their findings, published in Nature Communications,have the potential to improve understanding of lipid transport across the blood-brain barrier and of disruptions in this process that can lead to birth defects or neurological conditions. The model may also enable researchers to design drug molecules that are capable of directly reaching the brain. -- Omega-3 fatty acids are considered essential because the body cannot make them and must obtain them through foods, such as fish, nuts and seeds. DHA levels are especially high in the brain and important for a healthy nervous system. Infants obtain DHA from breastmilk or formula, and deficiencies of this fatty acid have been linked to problems with learning and memory. To get to the brain, omega-3 fatty acids must pass through the blood-brain barrier via the lipid transporter Mfsd2a, which is essential for normal brain development. Despite its importance, scientists did not know precisely how Mfsd2a transports DHA and other omega-3 fatty acids. -- In the study, the research team provides images of the structure of zebrafish Mfsd2a, which is similar to its human counterpart. The snapshots are the first to detail precisely how fatty acids move across the cell membrane. The study team also identified three compartments in Mfsd2a that suggest distinct steps required to move and flip fatty acids through the transporter, as opposed to movement through a linear tunnel or along the surface of the protein complex. The findings provide key information on how Mfsd2a transports omega-3 fatty acids into the brain and may enable researchers to optimize drug delivery via this route. The study also provides foundational knowledge on how other members of this transporter family, called the major facilitator superfamily (MFS), regulate important cellular functions. -- The study was led by Tamir Gonen, Ph.D., of UCLA and Doreen Matthies, Ph.D., of NIH's Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD). Additional funding for the study was provided by NIH's National Institute of General Medical Sciences (NIGMS) and the Howard Hughes Medical Institute. [] Brain damage, Neurotransmitter, Deep brain stimulation, Amino acid, Peripheral nervous system, Excitotoxicity and cell damage, Multiple sclerosis, Social cognition | 2319-013 |
| 107 | 2319-004 | H01 H02 H04 H05 | Roots of Antibiotic Resistance | Microbiologists have studied the origins of antimicrobial resistance (AMR) in bacteria, specifically focusing on the bacterium that causes cholera, Vibrio cholerae. By studying genetic variants of a protein found in bacterial membranes, they discovered that several mutations in the cholera bacteria led to resistance to numerous antimicrobial agents, including those found in the human gut. This research can help in identifying conditions that lead to AMR and finding ways to prevent it. | University of Central Florida | PLOS Genetics | Bacteria naturally adapt to various environmental stimuli and as they mutate, these changes can make them resistant to drugs that would kill or slow their growth. -- In a recent article published in PLoS Genetics, UCF College of Medicine microbiologist Dr. Salvador Almagro-Moreno uncovers the evolutionary origins of antimicrobial resistance (AMR) in bacteria. His studies on the bacterium that causes cholera, Vibrio cholerae, provide insight into deciphering what conditions must occur for infectious agents to become resistant. -- "How AMR occurs in bacterial populations and the pathways leading to these new traits are still poorly understood," he said. "This poses a major public health threat as antimicrobial resistance is on the rise." -- Dr. Almagro-Moreno studied genetic variants of a protein found in bacterial membranes called OmpU. Using computational and molecular approaches, his team found that several OmpU mutations in the cholera bacteria led to resistance to numerous antimicrobial agents. This resistance included antimicrobial peptides that act as defenses in the human gut. The researchers found that other OmpU variants did not provide these properties, making the protein an ideal system for deciphering the specific processes that occur to make some bacteria resistant to antimicrobials. -- By comparing resistant and antibiotic sensitive variants, the researchers were able to identify specific parts of OmpU associated with the emergence of antibiotic resistance. They also discovered that the genetic material encoding these variants, along with associated traits, can be passed between bacterial cells, increasing therisk of spreading AMR in populations under antibiotic pressure. -- By understanding how mutations occur, researchers can better understand and develop therapeutics to combat resistant infections. Dr. Almagro-Moreno is also looking at environmental factors such as pollution and warming of the oceans, as possible causes of resistant bacteria. "We are studying the genetic diversity ofenvironmental populations, including coastal Florida isolates, to develop a new approach to understandinghow antimicrobial resistance evolves," he explained. -- Understanding the bacteria that causes cholera, an acute diarrheal illness linked to infected water and foods, has global implications. The disease sickens up to 4 million people worldwide and severe cases can cause death within hours. [] Cholera, Antibiotic resistance, Pathogen, Genetic recombination, Transmission (medicine), Adenoid, Plant breeding, Meningitis | 2319-004 |
| 108 | 2319-038 | H01 H02 H04 H05 | Antibiotic Resistance Roots Uncovered | Microbiologists have discovered the evolutionary origins of antimicrobial resistance (AMR) in bacteria by studying the cholera bacterium Vibrio cholerae. They found that mutations in a protein called OmpU led to resistance to numerous antimicrobial agents, including those that act as defenses in the human gut. | University of Central Florida | PLOS Genetics | Bacteria naturally adapt to various environmental stimuli and as they mutate, these changes can make them resistant to drugs that would kill or slow their growth. -- In a recent article published in PLoS Genetics, UCF College of Medicine microbiologist Dr. Salvador Almagro-Moreno uncovers the evolutionary origins of antimicrobial resistance (AMR) in bacteria. His studies on the bacterium that causes cholera, Vibrio cholerae, provide insight into deciphering what conditions must occur for infectious agents to become resistant. -- "How AMR occurs in bacterial populations and the pathways leading to these new traits are still poorly understood," he said. "This poses a major public health threat as antimicrobial resistance is on the rise." -- Dr. Almagro-Moreno studied genetic variants of a protein found in bacterial membranes called OmpU. Using computational and molecular approaches, his team found that several OmpU mutations in the cholera bacteria led to resistance to numerous antimicrobial agents. This resistance included antimicrobial peptides that act as defenses in the human gut. The researchers found that other OmpU variants did not provide these properties, making the protein an ideal system for deciphering the specific processes that occur to make some bacteria resistant to antimicrobials. -- By comparing resistant and antibiotic sensitive variants, the researchers were able to identify specific parts of OmpU associated with the emergence of antibiotic resistance. They also discovered that the genetic material encoding these variants, along with associated traits, can be passed between bacterial cells, increasing therisk of spreading AMR in populations under antibiotic pressure. -- By understanding how mutations occur, researchers can better understand and develop therapeutics to combat resistant infections. Dr. Almagro-Moreno is also looking at environmental factors such as pollution and warming of the oceans, as possible causes of resistant bacteria. "We are studying the genetic diversity ofenvironmental populations, including coastal Florida isolates, to develop a new approach to understandinghow antimicrobial resistance evolves," he explained. -- Understanding the bacteria that causes cholera, an acute diarrheal illness linked to infected water and foods, has global implications. The disease sickens up to 4 million people worldwide and severe cases can cause death within hours. [] Cholera, Antibiotic resistance, Pathogen, Genetic recombination, Transmission (medicine), Adenoid, Plant breeding, Meningitis | 2319-038 |
| 109 | 2319-030 | H02 H04 | Gamma Delta T Cells Fight Breast Cancer | Researchers have discovered a mechanism by which cancer cells escape the immune system. | University of Freiburg | Cancer Immunology Research | Triple-negative breast cancer (TNBC) is the most aggressive and deadly form of breast cancer with limited treatment options and a high probability of recurrence. Tumor growth and relapse of TNBC are driven by breast cancer stem cells, and improved therapies that can eliminate those hardy cells are urgently needed. Researchers from the University of Frieburg discovered that coordinated differentiation and changes in the metabolism of breast cancer stem cells make them invisible for the immune system. Counteracting the metabolic change with the drug zolendronate could make immunotherapy using gamma delta T cells more efficient against TNBC. The research team was led by Prof. Dr. Susana Minguet from the Cluster of Excellence CIBSS -- Centre for Integrative Biological Signalling Studies at the University of Freiburg, in collaboration with Dr. Jochen Maurer from the University Hospital RWTH Aachen, Dr. Mahima Swamy from the Universtiy of Dundee/Scotland and collaborators from the University Hospital Freiburg. The study was published in the Journal Cancer Immunology Research, a journal of the American Association for Cancer Research. -- TNBC cells hide from gamma delta T cells -- Gamma delta T cells recognize and kill cells that produce stress-induced molecules and phosphoantigens, a common characteristic of cancer cells. Because gamma delta T cells work differently to other types of T cells, they are being investigated as an alternative to existing immunotherapies. In the current study, the researchers tested the effect of gamma delta T cells on TNBC using isolated cancer cells and a recently developed mouse model that closely replicates the tumor properties found in human patients. -- While the gamma delta T cells worked well against isolated breast cancer stem cells from patients, they had a much weaker effect in the mouse model. This was due to adaptations of the cancer cells that let them stay unnoticed by the immune system, the researchers found. These adaptations included the downregulation of the so-called mevalonate pathway: a metabolic pathway that leads to the production of phosphoantigens -- one of the classes of molecules that gamma T cells recognize. This escape mechanism likely also happens in patients with TNBC: analysis of public patient databases showed that reduced expression of key molecules of the mevalonate pathway correlate with a worse prognosis. -- The immune evasion of TNBC cells is reversible -- This newly discovered escape mechanism can be counteracted by the drug zolendronate, which is FDA-approved for the treatment of osteoporosis and bone metastasis. When the researchers treated the escapist cells with zolendronate, the gamma T cells became a lot more efficient in clearing the cancer. "Our findings explain why current clinical trials using gamma delta T cells are not resulting in the expected success," Minguet summarizes. "We found a possible pharmacological-based approach to revert immune escape, which paves the way for novel combinatorial immunotherapies for triple negative breast cancer." [] Immune system, Chemotherapy, Prostate cancer, White blood cell, Monoclonal antibody therapy, Lymphoma, Necrosis, T cell | 2319-030 |
| 110 | 2319-003 | H01 | AI's Impact on Trust | With the increasing realism of AI, our trust in those we communicate with may be compromised. Researchers at the University of Gothenburg have studied the impact of advanced AI systems on our trust in individuals we interact with. | University of Gothenburg | Computer Supported Cooperative Work (CSCW) | As AI becomes increasingly realistic, our trust in those with whom we communicate may be compromised. Researchers at the University of Gothenburg have examined how advanced AI systems impact our trust in the individuals we interact with. -- In one scenario, a would-be scammer, believing he is calling an elderly man, is instead connected to a computer system that communicates through pre-recorded loops. The scammer spends considerable time attempting the fraud, patiently listening to the "man's" somewhat confusing and repetitive stories. Oskar Lindwall, a professor of communication at the University of Gothenburg, observes that it often takes a long time for people to realize they are interacting with a technical system. -- He has, in collaboration with Professor of informatics Jonas Ivarsson, written an article titled Suspicious Minds: The Problem of Trust and Conversational Agents, exploring how individuals interpret and relate to situations where one of the parties might be an AI agent. The article highlights the negative consequences of harboring suspicion toward others, such as the damage it can cause to relationships. -- Ivarsson provides an example of a romantic relationship where trust issues arise, leading to jealousy and an increased tendency to search for evidence of deception. The authors argue that being unable to fully trust a conversational partner's intentions and identity may result in excessive suspicion even when there is no reason for it. -- Their study discovered that during interactions between two humans, some behaviors were interpreted as signs that one of them was actually a robot. -- The researchers suggest that a pervasive design perspective is driving the development of AI with increasingly human-like features. While this may be appealing in some contexts, it can also be problematic, particularly when it is unclear who you are communicating with. Ivarsson questions whether AI should have such human-like voices, as they create a sense of intimacy and lead people to form impressions based on the voice alone. -- In the case of the would-be fraudster calling the "older man," the scam is only exposed after a long time, which Lindwall and Ivarsson attribute to the believability of the human voice and the assumption that the confused behavior is due to age. Once an AI has a voice, we infer attributes such as gender, age, and socio-economic background, making it harder to identify that we are interacting with a computer. -- The researchers propose creating AI with well-functioning and eloquent voices that are still clearly synthetic, increasing transparency. -- Communication with others involves not only deception but also relationship-building and joint meaning-making. The uncertainty of whether one is talking to a human or a computer affects this aspect of communication. While it might not matter in some situations, such as cognitive-behavioral therapy, other forms of therapy that require more human connection may be negatively impacted. -- Jonas Ivarsson and Oskar Lindwall analyzed data made available on YouTube. They studied three types of conversations and audience reactions and comments. In the first type, a robot calls a person to book a hair appointment, unbeknownst to the person on the other end. In the second type, a person calls another person for the same purpose. In the third type, telemarketers are transferred to a computer system with pre-recorded speech. [] Computer simulation, Virtual reality, Digital economy, Fullerene, Cognition, Earth science, Communication, Culture of fear | 2319-003 |
| 111 | 2319-014 | H01 H03 | Physical Activity for Post-Stroke Recovery | Physical activity after a stroke can be pivotal to successful recovery, as those who spend four hours a week exercising achieve better functional recovery within six months than those who do not. | University of Gothenburg | JAMA Network Open | After a stroke, physical activity can be pivotal to successful recovery. People who spend four hours a week exercising after their stroke achieve better functional recovery within six months than those who do not, a University of Gothenburg study shows. -- The study, now published in the scientific journal JAMA Network Open, is based on data concerning 1,500 stroke patients in 35 Swedish hospitals. The participants were grouped according to their poststroke patterns of physical activity. -- The results show that increased or maintained physical activity, with four hours' exercise weekly, doubled the patients' chances of recovering well by six months after a stroke. Men and people with normal cognition kept up an active life relatively more often, with better recovery as a result. -- Positive programming from exercise -- The researchers have previously succeeded in demonstrating a clear inverse association between physical activity and the severity of stroke symptoms at the actual onset of the condition. These new findings highlight the importance of maintaining a healthy, active lifestyle after a stroke. -- The first and corresponding author of the study, Dongni Buvarp, is a researcher in clinical neuroscience at Sahlgrenska Academy, University of Gothenburg. Besides her research internship, she is a resident doctor at an initial stage of specialist training at Sahlgrenska University Hospital. -- "Physical activity reprograms both the brain and the body favorably after a stroke. Exercise improves the body's recovery at the cellular level, boosts muscle strength and well-being, and reduces the risk of falls, depression, and cardiovascular disease. Regardless of how severe the stroke has been, those affected can derive benefits from exercising more," she says. -- Knowledge and support vital -- "Being physically active is hugely important, especially after a stroke. That's a message that health professionals, stroke victims and their loved ones should all know. Women and people with impaired cognition seem to become less active after stroke. The study results indicate that these groups need more support to get going with physical activity," Buvarp says. -- One weakness of the study is that, with a few exceptions, the researchers were unable to study the participants' degree of activity before the stroke. The patients included were treated in Sweden in the period from 2014 to 2019. [] Stroke, Jogging, Urinary incontinence, Functional training, Synesthesia, Multi-infarct dementia, Decade Volcanoes, Rofecoxib | 2319-014 |
| 112 | 2319-016 | H04 H05 | Smart Surgical Implants for Early Warning | Newly developed 'smart' coatings for surgical orthopedic implants can monitor strain on the devices to provide early warning of implant failures while killing infection-causing bacteria, researchers report. The coatings integrate sensors with a nanostructured antibacterial surface inspired by the wings of dragonflies and cicadas. | University of Illinois at Urbana-Champaign, News Bureau | Science Advances | Newly developed "smart" coatings for surgical orthopedic implants can monitor strain on the devices to provide early warning of implant failures while killing infection-causing bacteria, University of Illinois Urbana-Champaign researchers report. The coatings integrate flexible sensors with a nanostructured antibacterial surface inspired by the wings of dragonflies and cicadas. -- In a new study in the journal Science Advances, a multidisciplinary team of researchers found the coatings prevented infection in live mice and mapped strain in commercial implants applied to sheep spines to warn of various implant or healing failures. -- "This is a combination of bio-inspired nanomaterial design with flexible electronics to battle a complicated, long-term biomedical problem," said study leader Qing Cao, a U. of I. professor of materials science and engineering. -- Both infection and device failure are major problems with orthopedic implants, each affecting up to 10% of patients, Cao said. Several approaches to fighting infection have been attempted, but all have severe limitations, he said: Biofilms can still form on water-repelling surfaces, and coatings laden with antibiotic chemicals or drugs run out in a span of months and have toxic effects on the surrounding tissue with little efficacy against drug-resistant strains of bacterial pathogens. -- Taking inspiration from the naturally antibacterial wings of cicadas and dragonflies, the Illinois team created a thin foil patterned with nanoscale pillars like those found on the insects' wings. When a bacterial cell attempts to bind to the foil, the pillars puncture the cell wall, killing it. -- "Using a mechanical approach to killing bacteria allowed us to bypass a lot of the problems with chemical approaches, while still giving us the flexibility needed to apply the coating to implant surfaces," said pathobiology professor Gee Lau, a coauthor of the study. -- On the back side of the nanostructured foil, where it contacts the implant device, the researchers integrated arrays of highly sensitive, flexible electronic sensors to monitor strain. This could help physicians watch the healing progress of individual patients, guide their rehabilitation to shorten the recovery time and minimize risks, and repair or replace devices before they hit the point of failure, the researchers said. -- The engineering group then teamed up with veterinary clinical medicine professor Annette McCoy to test their prototype devices. They implanted the foils in live mice and monitored them for any sign of infection, even when bacteria were introduced. They also applied the coatings to commercially available spinal implants and monitored strain to the implants in sheep spines under normal load for device failure diagnosis. The coatings performed both functions well. -- The prototype electronics required wires, but the researchers next plan to develop wireless power and data communications interfaces for their coatings, a crucial step for clinical application, Cao said. They also are working to develop large-scale production of the nanopillar-textured bacteria-killing foil. -- "These types of antibacterial coatings have a lot of potential applications, and since ours uses a mechanical mechanism, it has potential for places where chemicals or heavy metal ions -- as are used in commercial antimicrobial coatings now -- would be detrimental," Cao said. [] Salmonella infection, Bacteria, Earthquake, Malignant melanoma, Natural killer cell, Robotic surgery, Tapeworm, Global spread of H5N1 in 2006 | 2319-016 |
| 113 | 2319-032 | H01 H04 H06 | Improved Mental Well-Being in Older People | Depressive symptoms have decreased among older people and they are more satisfied with their lives so far than people at the same age three decades ago. | University of Jyväskylä - Jyväskylän yliopisto | Journal of Aging and Health | This was observed in a study conducted at the Gerontology Research Center at the Faculty of Sport and Health Sciences, University of Jyväskylä (Finland). The study examined differences in depressive symptoms and life satisfaction between current 75- and 80-year-olds and the same-aged people who lived in the 1990s. -- The results showed that 75- and 80-year-old men and women today experience fewer depressive symptoms than those who were 75 and 80 years old in the 1990s. The differences were partly explained by the better perceived health and higher education of those born later. -- "In our previous comparisons, we found that older people today have significantly better physical and cognitive functioning at the same age compared to those born earlier," says Professor Taina Rantanen from the Faculty of Sport and Health Sciences. "These new results complement these positive findings in terms of mental well-being." -- Today, 75- and 80-year-olds are more satisfied with their lives to date. However, there was no similar difference in satisfaction with their current lives. In fact, 80-year-old men who lived in the 1990s were even more satisfied with their current lives than 80-year-old are men today. -- "These men born in 1910 had lived through difficult times, which may explain their satisfaction with their current lives in the 1990s when many things were better than before," says postdoctoral researcher Tiia Kekäläinen. -- "Individuals adapt to their situation and living conditions. Both in the 1990s and today, the majority of older adults reported being satisfied with their current lives." -- The study was conducted at the Faculty of Sport and Health Sciences and Gerontology Research Center at University of Jyväskylä, Finland. The first cohort consisted of 617 individuals born in 1910 and 1914 who participated in the Evergreen study in 1989-1990. The second cohort consisted of 794 individuals born in 1938-1939 and 1942-1943 who participated in the AGNES study in 2017-2018. In both cohorts, the participants were assessed at the age of 75 or 80 years. The study was funded by the Academy of Finland and the European Research Council. [] Occupational therapy, Hair, Candidiasis, Alzheimer's disease, Measles, Seasonal affective disorder, Panic attack, Hypoallergenic | 2319-032 |
| 114 | 2319-019 | H01 H04 | AI's Potential for Microbial Experiments | An artificial intelligence system enables robots to conduct autonomous scientific experiments potentially driving a drastic leap forward in the pace of discovery in areas from medicine to agriculture to environmental science. | University of Michigan | Nature Microbiology | An artificial intelligence system enables robots to conduct autonomous scientific experiments -- as many as 10,000 per day -- potentially driving a drastic leap forward in the pace of discovery in areas from medicine to agriculture to environmental science. -- Reported today in Nature Microbiology, the team was led by a professor now at the University of Michigan. -- That artificial intelligence platform, dubbed BacterAI, mapped the metabolism of two microbes associated with oral health -- with no baseline information to start with. Bacteria consume some combination of the 20 amino acids needed to support life, but each species requires specific nutrients to grow. The U-M team wanted to know what amino acids are needed by the beneficial microbes in our mouths so they can promote their growth. -- "We know almost nothing about most of the bacteria that influence our health. Understanding how bacteria grow is the first step toward reengineering our microbiome," said Paul Jensen, U-M assistant professor of biomedical engineering who was at the University of Illinois when the project started. -- Figuring out the combination of amino acids that bacteria like is tricky, however. Those 20 amino acids yield more than a million possible combinations, just based on whether each amino acid is present or not. Yet BacterAI was able to discover the amino acid requirements for the growth of both Streptococcus gordonii and Streptococcus sanguinis. -- To find the right formula for each species, BacterAI tested hundreds of combinations of amino acids per day, honing its focus and changing combinations each morning based on the previous day's results. Within nine days, it was producing accurate predictions 90% of the time. -- Unlike conventional approaches that feed labeled data sets into a machine-learning model, BacterAI creates its own data set through a series of experiments. By analyzing the results of previous trials, it comes up with predictions of what new experiments might give it the most information. As a result, it figured out most of the rules for feeding bacteria with fewer than 4,000 experiments. -- "When a child learns to walk, they don't just watch adults walk and then say 'Ok, I got it,' stand up, and start walking. They fumble around and do some trial and error first," Jensen said. -- "We wanted our AI agent to take steps and fall down, to come up with its own ideas and make mistakes. Every day, it gets a little better, a little smarter." -- Little to no research has been conducted on roughly 90% of bacteria, and the amount of time and resources needed to learn even basic scientific information about them using conventional methods is daunting. Automated experimentation can drastically speed up these discoveries. The team ran up to 10,000 experiments in a single day. [] Protein biosynthesis, Computer vision, Dog health, Amino acid, The evolution of human intelligence, Glutamic acid, Protein, Industrial robot | 2319-019 |
| 115 | 2319-033 | H01 H02 H04 | Understanding Self-Directed Ageism | Age-related changes in cognitive function may increase the risk of older people viewing themselves through a negative and ageist lens, research suggests. | University of Queensland | Trends in Cognitive Sciences | The study led by Professor Julie Henry from UQ's School of Psychology looked at why self-directed ageism is common. -- "Older people are regularly exposed to ageism such as negative assumptions about their worth, capacity or level of understanding, as well as jokes about older age," Professor Henry said. -- "At the same time, as we grow older, we rely more strongly on prior knowledge and cues from our environment to guide how we feel, think and behave. -- "In a world that devalues ageing, these cognitive changes make it more difficult for older people to challenge internalised ageist beliefs, known as self-directed ageism." -- Self-directed ageism can present as self-doubt -- 'I'm too old to learn this new technology' or 'I'm too old to make new friends' -- and negative perceptions of one's own aging, such as 'I'm so much worse at this than I used to be'. -- Self-directed ageism can also present as concern over being judged according to age-based stereotypes, such as 'If I forget to do this, they're going to think it's because I'm old'. -- Professor Henry said when ageism is internalised and becomes self-directed, it has been linked to a shorter lifespan, poorer physical and mental health, slower recovery from disability and cognitive decline. -- "It can also be harmful when older adults allow their negative beliefs about ageing to undermine their confidence to take on new or challenging experiences and opportunities," Professor Henry said. -- "Interventions, such as creating more opportunities for positive social interactions between younger and older people, are needed to prevent negative views of ageing from developing in the first place. -- "Our research also suggests that older adults will benefit directly from a reduction in cues to ageism in our wider social environment. [] Hair, COX-2 inhibitor, Cataract, Cancer, List of cognitive biases, Seasonal affective disorder, Urinary incontinence, Poison ivy | 2319-033 |
| 116 | 2319-007 | H01 H03 H04 | Crab Populations and Sense of Smell | A new study from U of T Scarborough has found that climate change is causing a commercially significant marine crab to lose its sense of smell, which could contribute to the thinning of their populations. | University of Toronto | Global Change Biology | A new U of T Scarborough study finds that climate change is causing a commercially significant marine crab to lose its sense of smell, which could partially explain why their populations are thinning. -- The research was done on Dungeness crabs and found that ocean acidification causes them to physically sniff less, impacts their ability to detect food odours and even decreases activity in the sensory nerves responsible for smell. -- "This is the first study to look at the physiological effects of ocean acidification on the sense of smell in crabs," says Cosima Porteus, an assistant professor in the department of biological sciences at U of T Scarborough and co-author of the study along with postdoc Andrea Durant. -- Ocean acidification is the result of the Earth's oceans becoming more acidic due to absorbing increasing amounts of carbon dioxide in the atmosphere. It's a direct consequence of burning fossil fuels and carbon pollution, and several studies have shown it's having an impact on the behaviour of marine wildlife. -- Dungeness crabs are an economically important species found along the Pacific coast, stretching from California to Alaska. They are one of the most popular crabs to eat and their fishery was valued at more than $250 million in 2019. -- Like most crabs, they have poor vision, so their sense of smell is crucial in finding food, mates, suitable habitats and avoiding predators, explains Porteus. They sniff through a process known as flicking, where they flick their antennules (small antenna) through the water to detect odours. Tiny neurons responsible for smell are located inside these antennules, which send electrical signals to the brain. -- The researchers discovered two things when the crabs were exposed to ocean acidification: they were flicking less and their sensory neurons were 50 per cent less responsive to odours. -- "Crabs increase their flicking rate when they detect an odour they are interested in, but in crabs that were exposed to ocean acidification, the odour had to be 10 times more concentrated before we saw an increase in flicking," says Porteus. -- There are a few potential reasons why ocean acidification seems to be impacting sense of smell in crabs. Porteus points to other research done at the University of Hull that showed ocean acidification disrupts odour molecules, which can impact how they bind to smell receptors in marine animals such as crabs. -- For this study, published in the journal Global Change Biology, Porteus and Durant were able to test the electrical activity in the crabs' sensory neurons to determine they were less responsive to odours. They also discovered that they had fewer receptors and their sensory neurons were physically shrinking by as much as 25 per cent in volume. [] Crab louse, Olfaction, Plastic surgery, Developmental psychology, Menopause, Aspirin, Epidemiology, Baldness | 2319-007 |
| 117 | 2319-031 | H01 H04 | Chimpanzees Combine Calls for Communication | UZH researchers suggest that the ability of chimpanzees to combine vocalizations into larger communicatively meaningful structures might be evolutionarily more ancient than previously thought. | University of Zurich | Nature Communications | Similar to humans, chimpanzees combine vocalizations into larger communicatively meaningful structures. UZH researchers suggest that this ability might be evolutionarily more ancient than previously thought. -- A key feature of human language is our ability to combine words into larger compositional phrases i.e. where the meaning of the whole is related to the meaning of the parts. Where this ability came from or how it evolved, however, is less clear. -- Chimpanzees, our closest-living relative, are known to produce a number of different vocalizations to manage their social and ecological lives and, under some circumstances, combine these calls into larger sequences. By conducting careful, controlled experiments with wild chimpanzees in Uganda, researchers from the University of Zurich (UZH) showed that these combinations are understood by chimpanzees. -- Chimpanzees react most strongly to call combinations -- "Chimpanzees produce 'alarm-huus' when surprised and 'waa-barks' when potentially recruiting conspecifics during aggression or hunting," says Maël Leroux, a postdoctoral student at the Department of Comparative Language Science of UZH, who led the study. "Our behavioral observations suggest that chimpanzees combine these calls when exposed to a threat where recruiting group members is advantageous, such as when encountering a snake, but until now experimental verification has been missing." -- The researchers presented chimpanzees with model snakes and were able to elicit the call combination. Critically, chimpanzees responded strongest to playbacks of the combination than when hearing either the "alarm-huu" or "waa-bark" alone. "This makes sense because a threat that needs recruitment is an urgent event and suggests listening chimpanzees really are combining the meaning of the individual calls," adds study last author and UZH professor Simon Townsend. -- Primate roots of compositionality -- An important implication of the new findings is the potential light they can shed on the evolutionary roots of language's compositional nature. "Humans and chimpanzees last shared a common ancestor approximately 6 million years ago. Our data therefore indicate that the capacity to combine meaningful vocalizations is potentially at least 6 million years old, if not older," says Townsend. "These data provide an intriguing glimpse into the evolutionary emergence of language" added Leroux. In a nutshell, it points towards compositionality originating prior to the appearance of language itself, though follow-up observational and experimental work, ideally in other great ape species, will be central to confirming this. [] Jane Goodall, Bonobo, Great Ape language, Convergent evolution, Psycholinguistics, Hominidae, Puma, Adult stem cell | 2319-031 |
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