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Breakthrough study finds genetic link to Parkinson's and ADHD

<p>A major scientific study has found a surprising link between the genes that control brain size and the risk of brain-related conditions. </p> <p>A Queensland Institute of Medical Research Associate Professor Miguel Renteria led an international team of experts who scanned DNA data and MRI scans from 76,000 participants.</p> <p>“Genetic variants associated with larger brain volumes in key brain regions also increase the risk of Parkinson’s disease, while variants linked to smaller brain volumes in key regions are associated with an increased risk of ADHD,” Renteria said. </p> <p>“It brings us closer to answering key questions about how genetics influence brain structure, and how we can potentially treat these conditions in future.”</p> <p>Parkinson’s Australia CEO Olivia Nassaris has celebrated the results of the study, saying the surprising results open the door to future treatment options for Parkinson’s, which currently has no cure or cause.</p> <p>“The more answers we have the closer we are to understanding this condition,” she said.</p> <p>Michael Wiseman, who has been living with Parkinson’s for eight years, said he is pleased more research is being done about the neurodegenerative condition.</p> <p>“I know it’s not going to benefit me in any way, as far as a cure or anything … I just hope they keep going, kicking some goals and finding results because it’s an insidious sort of thing, it’s a passenger I’ll have until I go to the grave.”</p> <p><em>Image credits: Shutterstock </em></p>

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Trying to lose weight? Here’s why your genetics could be just as important as your exercise regime

<p><em><a href="https://theconversation.com/profiles/henry-chung-1279176">Henry Chung</a>, <a href="https://theconversation.com/institutions/university-of-essex-1291">University of Essex</a>; <a href="https://theconversation.com/profiles/chris-mcmanus-2226445">Chris McManus</a>, <a href="https://theconversation.com/institutions/university-of-essex-1291">University of Essex</a>, and <a href="https://theconversation.com/profiles/sally-waterworth-2226444">Sally Waterworth</a>, <a href="https://theconversation.com/institutions/university-of-essex-1291">University of Essex</a></em></p> <p>Weight loss is a complicated process. There are so many factors involved including your diet, how much sleep you get each night and the kind of exercise you do. Our recent study shows that your <a href="https://www.tandfonline.com/doi/full/10.1080/02701367.2024.2404981">specific genetic profile</a> may also have a dominant effect on how well you lose weight through exercise. This might explain why two people who do an identical workout will see very different results.</p> <p>We identified 14 genes that appeared to significantly contribute to how much weight a person lost through running. This suggests that some of us have a natural talent when it comes to burning fat and losing weight through exercise.</p> <p>To conduct our study, we recruited 38 men and women born in the UK aged between 20 and 40. None of the participants regularly exercised at the start of the study. The group was randomly divided, with one half following a strict eight-week endurance programme that consisted of three weekly runs of 20-30 minutes.</p> <p>The other group acted as a <a href="https://www.britannica.com/science/control-group">control</a>. They were instructed to refrain from exercise and continue their daily routines as normal over this study period, including diet and lifestyle habits.</p> <p>All participants conducted a running test to see how far they could run in 12 minutes, and were weighed before and after the study period. This was to gauge their initial fitness level and see how much they changed over the duration of the study. <a href="https://www.nhs.uk/conditions/obesity/">Body mass index</a> (BMI) was also calculated.</p> <p>Additionally, a saliva sample was collected from each person with a <a href="https://muhdo.com/?gclid=Cj0KCQjwiIOmBhDjARIsAP6YhSUB3WI81JP4Q_snYLhh-SBVNeCJNy2m63C8bKJFvO-nJ5UsHuCCdqMaAhTeEALw_wcB">DNA test kit</a> at the end of the study to assess their unique genetic profile.</p> <p>It’s important to note that everyone who participated in the study had a similar body weight, BMI and aerobic fitness level at the start of the study. This is beneficial for <a href="https://casp-uk.net/news/homogeneity-in-research/">multiple reasons</a>. It meant everyone was at the same starting point, and some <a href="https://www.sciencedirect.com/topics/nursing-and-health-professions/confounding-variable">confounding variables</a> were already controlled for such as <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10128125/">fitness level</a>. This ultimately improves accuracy in interpreting the results.</p> <h2>Exercise genes</h2> <p>Everyone in the exercise group managed to lose weight – around 2kg on average. The control group, on the other hand, put on a little bit of weight.</p> <p>While a 2kg weight loss may not sound like a lot, it’s significant considering the exercise regime only lasted eight weeks and participants made no <a href="https://www.intechopen.com/chapters/87186">changes to their diet</a>.</p> <p>More significant, however, was the large variation in results among those that exercised – with an up to 10kg difference in weight loss between some of the participants. In fact, everyone within the exercise group improved at different rates.</p> <p>Since we controlled for factors such as the <a href="https://pubmed.ncbi.nlm.nih.gov/3529283/">intensity, duration and frequency</a> of the exercises and used participants who’d had a similar body weight and fitness level at the start of the study, this suggests that some people naturally benefited more than others from endurance training.</p> <p>When we looked at the genetic profiles of our participants, we found that differences in each person’s response to the exercise was strongly associated with their specific genetics.</p> <p>We showed there was a strong linear correlation between the amount of weight participants lost and 14 genes that have previously been shown to be associated with body weight, metabolism or <a href="https://www.nature.com/articles/s41380-018-0017-5">psychological conditions</a> that affect BMI. The greater number of these genes a participant had, the more weight they lost. Our results also revealed that around 63% of the variance in weight lost among participants were explained by the genes identified.</p> <p>For example, research has shown the <a href="https://www.ncbi.nlm.nih.gov/gene/10891">PPARGC1A gene</a> plays a role in metabolism and the <a href="https://link.springer.com/article/10.1007/S11033-020-05801-Z">use of fats for energy</a> while exercising. Our study found that all participants who lost more than 1.5kg from exercise had this gene. Those who lost less than this did not have this gene.</p> <p>Our findings align with what <a href="https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0249501&amp;s2=P875440273_1683331208925004155">previous studies</a> have shown. But while previous papers have only looked at the link between individual genes and weight loss, ours is the first to show that 14 different genes appear to work in combination to affect whether a person loses weight from endurance exercise.</p> <h2>Piece of the puzzle</h2> <p>Our study also suggests that while some people possess genes that make it easier for them to get fit and lose weight, people with these favourable genetics can only flourish if they actually exercise. In fact, our control group also had a number of these listed genes, but without exercise these genes could not activate, and so the participants did not lose any weight.</p> <p>While our study provides compelling findings, it’s not without limitations. Since we only looked at endurance-based exercise, it will be important for future studies to investigate whether there are similar links between weight loss, genetics and combinations of different types of training (such as a mixture of endurance and strength sessions into a training plan).</p> <p>It’s also worth mentioning that exercise is only <a href="https://www.who.int/activities/controlling-the-global-obesity-epidemic">one piece of the puzzle</a> when it comes to weight loss. So even if you have all 14 of these genes, you won’t lose any weight or get fit if you don’t exercise and maintain a healthy diet and sleep pattern.</p> <p>On the flip side, someone that only has a few of these favourable genes can still benefit if they exercise and are mindful of other aspects of their lifestyle.<img style="border: none !important; box-shadow: none !important; margin: 0 !important; max-height: 1px !important; max-width: 1px !important; min-height: 1px !important; min-width: 1px !important; opacity: 0 !important; outline: none !important; padding: 0 !important;" src="https://counter.theconversation.com/content/240506/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1" /></p> <p><em><a href="https://theconversation.com/profiles/henry-chung-1279176">Henry Chung</a>, Lecturer in Sport and Exercise Science, <a href="https://theconversation.com/institutions/university-of-essex-1291">University of Essex</a>; <a href="https://theconversation.com/profiles/chris-mcmanus-2226445">Chris McManus</a>, Lecturer, School of Sport, Rehabilitation and Exercise Sciences, <a href="https://theconversation.com/institutions/university-of-essex-1291">University of Essex</a>, and <a href="https://theconversation.com/profiles/sally-waterworth-2226444">Sally Waterworth</a>, Lecturer, School of Sport, Rehabilitation and Exercise Sciences, <a href="https://theconversation.com/institutions/university-of-essex-1291">University of Essex</a></em></p> <p><em>Image credits: Shutterstock </em></p> <p><em>This article is republished from <a href="https://theconversation.com">The Conversation</a> under a Creative Commons license. Read the <a href="https://theconversation.com/trying-to-lose-weight-heres-why-your-genetics-could-be-just-as-important-as-your-exercise-regime-240506">original article</a>.</em></p>

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How to write a memoir

<p><strong>How to start a memoir</strong></p> <p><em>My Story </em>by Russell Durling is my 85-year-old father’s account of the highlights of his life. He is writing and editing it, by hand, in several notepads I gave him as a Christmas gift to encourage the memoir project he had talked about for years.</p> <p>In it, my dad shares stories of summer jobs when he was a teenager, breaking up log jams on the Saint John River near his hometown of Meductic, New Brunswick. He’d move from log to floating log to reach shore again safely – and he loved every minute of this adventure, even when he’d land in the water.</p> <p>Reading an early draft, I learned new details of his history, like how when they were children, his cousin Clara had a pet crow. He also wrote about lessons learned from his Royal Canadian Mounted Police career, which was spent mostly in Nova Scotia, and shared insights about how to retire well. Pro tip from my father: to add a decade to your life, ditch the city (if you can).</p> <p>This memoir will be a treasure for our family, and I’m glad my father was finally able to start writing it, after spending a long time talking about wanting to. And I get it. Writing your life story can feel like a daunting project. But it’s worth it, both to the writer and their potential readers. If you’re having a hard time putting pen to paper, here’s advice on how to start a memoir.</p> <p><strong>First, ask yourself why you're writing a memoir </strong></p> <p>Esmeralda Cabral is a writer who works with people who wouldn’t normally consider themselves writers through her workshop, <em>Writing Your Life</em>. Often, she helps people create written treasures for their families, and sometimes they’re writing just for themselves. To her, and those she teaches, memoir writing can be a way of remembering and reflecting on experiences both positive and negative.</p> <p>“There is a clarity that comes when you put something down on paper,” says Cabral. “Remembering and writing helps us make sense of things. If you don’t write it down or tell it, it’s lost. And that’s a shame.”</p> <p>Begin by jotting down your reasons for writing your story. You could summarise those reasons on a Post-It and stick it on your fridge as an encouraging reminder to stay motivated. After all, there are many good reasons to write: to remember and reflect on your past, to capture your adventures, to share life lessons with family and friends, or maybe even to be published. Consider sharing your plan with a friend or family member who can check in and cheer your progress.</p> <p><strong>Where to start</strong></p> <p>You don’t have to start a memoir with day one. In fact, as much as your future readers love you, they may find that approach less than gripping.</p> <p>In her workshops, Cabral helps people to start a memoir by using a photo that is meaningful to them. She asks them to imagine sitting down with a good friend and telling them the story behind it. Or begin your writing with an event or story you are particularly interested in sharing. What grabs you as a big moment? Select a vivid memory and start there.</p> <p>“Plug your nose and jump in and write down all your memories as truthfully as you can,” summarises New York Times bestselling author Anne Lamott in <em>Bird by Bird: Some Instructions on Writing and Life</em>. Maybe start with a birthday party you remember, or your first-grade classroom. Try writing at the same time every day, so you can build a routine that will keep you putting words on the page.</p> <p><strong>Write what you want </strong></p> <p>In every life, there is light and shadow, joy and grief. If you are hesitant to write your memoir because you have difficult stories that might hurt others, there is a solution. First, “You don’t have to write about everything,” says Cabral. “It’s okay to have secrets that go with you to the grave.”</p> <p>Simply knowing you have the freedom to not go to the darkest of places in your writing can lift you over those psychological hurdles of hesitation. However, writing often takes on a life of its own. If you find yourself standing outside a door you had marked as “Do Not Enter,” consider Cabral’s advice: “Write about the hard things as if the person you are writing about is reading it. Be as kind as you can. Leave them with dignity.”</p> <p><strong>Who is your audience?</strong></p> <p>If you’re writing for your eyes only, as a kind of personal therapy, then you may be purposely opening doors and exploring what’s on the other side. That’s okay, too. You are creating a treasure for yourself, and that can be very healthy. </p> <p>Besides, whether the writing is for you or for others, you can always hit the delete button or visit the paper shredder later, if you wish. For now, just get it down.</p> <p><strong>Stop yourself from sticking to rules</strong></p> <p>Avoid letting worries over style or structure stop you from writing. If you care enough about grammar, you can ask someone you trust to read it over later on, or even hire a freelance editor if you’re really fretting over verb tenses. Remember, perfection in writing is not your goal.</p> <p><strong>Readers are interested</strong></p> <p>Writers also might hesitate to share stories because they fear they are boring. “I hear a lot of people say, ‘Oh no, that wouldn’t be interesting to anyone but me,’” says Cabral. But our life stories are of interest to others, whether they feel ordinary to us or if they really are extraordinary. They remind us we are all in this together.</p> <p>Writer Pauline Dakin, author of the award-winning 2017 memoir <em>Run, Hide, Repeat: A Memoir of a Fugitive Childhood</em>, was surprised how much the unusual story of her childhood on the run connected with readers. She’s since heard from hundreds of people. “They often begin by saying, ‘My family wasn’t nearly as crazy as yours, but…,’” she says. “They are relieved to hear my story. It makes them feel they are not alone.”</p> <p>We are all far more interesting than we know, she adds. It’s just a matter of believing we have a story to tell.</p> <p><em>Image credits: Getty Images</em></p> <p><em>This article originally appeared on <a href="https://www.readersdigest.co.nz/uncategorized/how-to-write-a-memoir" target="_blank" rel="noopener">Reader's Digest</a>. </em></p>

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"Ended for good": Prince William launches project inspired by Lady Di

<p>Prince William has launched his most ambitious project to date, announcing his plan to end homelessness in the UK within five short years. </p> <p>The Prince of Wales set out to visit six areas in the UK that experience different types of homelessness with a distinct set of challenges, outlining a detailed plan to see homelessness eradicated. </p> <p>On his two-day tour, the 41-year-old royal shared that his late mother, Princess Diana, was a big inspiration behind the project, after she helped open William's eyes to the nation-wide problem. </p> <p>In the south London borough of Lambeth, Prince William described how he was inspired by "heart-breaking" visits to shelters he made with his mother as a child. </p> <p>"My first visit to a homelessness shelter was when I was 11 with my mother," he told the Mosaic Clubhouse, which supports people with mental health problems.</p> <p>"The visits we made, left a deep and lasting impression."</p> <p>"I met so many extraordinary people and listened to so many heart-breaking personal stories. Too many people have found themselves without a stable and permanent place to call home."</p> <p>"Through these visits, I have seen first-hand the breadth and complexities of homelessness."</p> <p>William said he hoped the Homewards program would "inspire belief throughout the UK and beyond that homelessness can be ended for good".</p> <p>Prince William's Homewards program focuses on preventing homelessness before it begins, bringing together all organisations working in the sector to create solutions that target local challenges.</p> <p>The launch of the project, which was two years in the making, comes days before what would have been Diana's 62nd birthday on July 1st. </p> <p>A major focus of Homewards will be on providing homes to those who need them.</p> <p>"I am pleased to stand here today at the start of our path to ending homelessness," he said.</p> <p>"Over the next five years, I believe that we have a unique opportunity to develop innovative new solutions and scale tangible impact. This will inspire belief throughout the UK – and beyond – that homelessness can be ended for good."</p> <p><em>Image credits: Getty Images</em></p>

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Robert Irwin gets candid about health issue affecting his family

<p dir="ltr">Robert Irwin has opened up about how dementia has affected his family.</p> <p dir="ltr">The 19-year-old appeared on <em>The Project</em> as a co-host when they began discussing dementia - a disorder that can affect thinking, memory and behaviour.</p> <p dir="ltr">The son of the late Steve Irwin said that he doesn’t think there’s anyone living who hasn’t encountered a person with dementia.</p> <p dir="ltr">“I think there’s no-one living who hasn’t encountered someone or has a loved one who has experienced this,” he said.</p> <p dir="ltr">“I know my grandfather on my mum’s side had a form of dementia and a lot of family friends have had that as well and it’s just, it’s devastating.</p> <p dir="ltr">“Someone you love, someone you’re close to you see going through that and just not being able to relive and enjoy the moments they had it’s heartbreaking.</p> <p dir="ltr">“But I guess it just reminds you you’ve got to spend every second with the people you love and really surround yourself with love and light and hopefully this is light at the end of the tunnel for a safe way for people to stop this.”</p> <blockquote class="twitter-tweet"> <p dir="ltr" lang="en">Alzheimer’s is the merciless brain condition that slowly erodes the cognitive function and precious memories of thousands of Australians. But, a revolutionary new treatment could turn the tide in the fight against the disease. <a href="https://twitter.com/hashtag/TheProjectTV?src=hash&amp;ref_src=twsrc%5Etfw">#TheProjectTV</a> <a href="https://t.co/IVuMloeUN5">pic.twitter.com/IVuMloeUN5</a></p> <p>— The Project (@theprojecttv) <a href="https://twitter.com/theprojecttv/status/1599316365369901058?ref_src=twsrc%5Etfw">December 4, 2022</a></p></blockquote> <p dir="ltr">Robert went on to say that he will continuing his father’s legacy and how proud he is to be a part of it, speaking about a recent performance with the Wiggles.</p> <p dir="ltr">“The Wiggles are just legendary, my dad actually did a really fun collaboration project with them at Australia Zoo way back in the day 20 years ago,” he said.</p> <p dir="ltr">“So we’ve worked with them for a long time so the fact all of the original Wiggles came back to support our charity Wildlife Warriors means the world.</p> <p dir="ltr">“Dad set this up as a way to support wildlife conservation here in Australia and on the global stage and a night like that just makes us realise his legacy is alive and thriving and it’s the honour of a lifetime to keep that going.”</p> <p dir="ltr">Robert recently celebrated his <a href="https://oversixty.com.au/lifestyle/family-pets/robert-irwin-turns-19-in-style" target="_blank" rel="noopener">19th birthday</a> at Australia Zoo with his mother and rumoured girlfriend, Scarlett Buckley, who is the niece of the late Heath Ledger.</p> <p dir="ltr"><em>Image: The Project</em></p>

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Family told to make way for highway project hours after moving in to new home

<p dir="ltr">Hours after picking up the keys to his newly-built family home, Anil Konda was informed that his whole property would be used in upgrades to Queensland’s Bruce Highway.</p> <p dir="ltr">After putting down an initial deposit on the land in Griffin, in Brisbane’s north, Mr Konda relocated his young family of four to Queensland, and they found a rental to stay in, a new school for the kids, and endured 11 months of building delays before stepping into their new home.</p> <p dir="ltr">But their good news was short-lived, with the state government’s Department of Transport and Main Roads (TMR) sending an email requesting Mr Konda to call them for more information on the “future land requirement” before calling him that afternoon.</p> <p dir="ltr">"When I asked specific details like, 'How is it impacted? Am I going to lose a certain amount of land?', they told me like it's going to be the entire thing," he told the <em><a href="https://www.abc.net.au/news/2022-10-19/qld-home-owners-angry-bruce-highway-update-land-resumption/101549992" target="_blank" rel="noopener">ABC</a></em>.</p> <p dir="ltr">"The entire house has to be taken out."</p> <p dir="ltr">Mr Konda said the family wanted to see the construction of their new home in person since it was their first house, and that even if they can live in their home for the next few years, they know it will be taken away.</p> <p dir="ltr">“They just took away the joy of our new home,” he said.</p> <p dir="ltr">"We don't have the belongingness (sic)."</p> <p dir="ltr">But Mr Konda’s family isn’t alone.</p> <p dir="ltr">Their home is part of the relatively new Aspire development, where there are still vacant lots, houses in the midst of construction, and residents who have mostly moved in within the past few months.</p> <p dir="ltr">A TMR spokesperson confirmed that the owners of 24 residential lots have been contacted about the plans.</p> <p dir="ltr">Charmaine and James Jackson are owners of another of the affected blocks of land, which they purchased and built their dream home on in 2021, the same year they had their second child.</p> <p dir="ltr">"It was eight days after he was born we went to the office to pick out our tile colours, our paint and everything like that," Mrs Jackson said.</p> <p dir="ltr">With their youngest just turning one, they had hopes of staying in the home until both boys had left school.</p> <p dir="ltr">"I just need an explanation," Mr Jackson said.</p> <p dir="ltr">"How could this have happened where you've allowed people so freshly to have built new houses only to tell them that they're going to be torn down in the middle of a housing crisis."</p> <p dir="ltr">After receiving the email, Mr Jackson contacted TMR to ask why the title was allowed to be registered.</p> <p dir="ltr">"They said when Aspire put in the planning application we didn't have planning up-to-date at that time to confirm any impacts," he said.</p> <p dir="ltr">Transport and Main Roads Minister Mark Bailey said the highway project was still in its very early planning stages, and that more specific numbers of residents who will be impacted will be determined as planning progresses.</p> <p dir="ltr">"If we do require someone's property, we get independent evaluations and market rates, so that we make sure that people who are impacted in the end, that they are looked after and that they get fair value and compensation,” he said.</p> <p dir="ltr">"It's never a good process and of course these are relatively recent approvals by the local governments involved, so I can appreciate why they would feel aggrieved by the process."</p> <p><span id="docs-internal-guid-66db1177-7fff-63f2-89c4-11e610be4b34"></span></p> <p dir="ltr"><em>Image: ABC News (Facebook)</em></p>

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How a new art project in Bathurst is embracing the many identities of the town

<p>For many, Bathurst’s Mount Panorama is exclusively a car racing venue. For Indigenous Australians it is a place called Wahluu, where First Nations women once offered their sons for tribal initiation.</p> <p>It is a cherished Wiradyuri territory that hosts dreaming and creation stories. Earlier this year, further development on the site <a href="https://www.sbs.com.au/nitv/article/2021/05/03/wahluu-womens-site-be-protected-says-federal-environment-minister">was blocked</a>, with the federal government acknowledging the cultural significance of the location for the Wiradyuri people.</p> <p>In some respects, the conflicting identity of Bathurst’s mountain can be reconciled through the forms of masculinity it represents: the male-centric sport of car racing – so central to the town’s present-day image – and the rite of passage of young Aboriginal men into adulthood.</p> <p>Now, a new art project, <a href="https://kateofthesmiths.com.au/fast-cars-dirty-beats/">Fast Cars &amp; Dirty Beats</a> is navigating these cultural differences by fostering a sense of community.</p> <p>Created by artistic director Kate Smith, Fast Cars &amp; Dirty Beats embraces Mount Panorama’s/Wahluu’s dual identity that, for some, is representative of a cultural divide between black and white Australia. Smith’s vision is not culturally constrained, but rather expressive of a location that is complex and multicultural.</p> <p>Liaising with Bathurst Wiradyuri Elders, Smith and her artistic collaborators have developed a series of community-focused projects revolving around the cultural significance of Wahluu/Mount Panorama.</p> <p>One of these initiatives, Mountain Tales, was launched on the first of July as part of Bathurst’s Winter Festival. Mountain Tales is the culmination of a year-long community engagement connecting local schoolchildren, teachers and parents with skilled craftspeople and musicians, fashioning decorative lanterns and the cultivation of a drumming community.</p> <p><strong>A lantern procession</strong></p> <p>Although it was raining for the July launch, more than 300 locals formed a dramatic lantern procession on the cold winter’s night.</p> <p>I was swept up in the pageantry unravelling across the CBD, eventually settling at Bathurst’s historical <a href="https://tremainsmill.com/">Tremain’s Mill</a>. Here the community proudly displayed their beacons of light, paying homage to the Chinese presence in Bathurst since the 1800s.</p> <p>Supporting the procession, Rob Shannon’s drummers created a collective heartbeat, fostering a sense of joy and belonging.</p> <p>After this ceremony of light and sound, members of the community told stories about the significance of Mount Panorama/Wahluu. Yarns were shared concerning the mountain being a place where locals experienced a first kiss or participated in some youthful skylarking.</p> <figure class="align-center zoomable"><a href="https://images.theconversation.com/files/473106/original/file-20220707-22-kkwl50.jpg?ixlib=rb-1.1.0&amp;q=45&amp;auto=format&amp;w=1000&amp;fit=clip"><img src="https://images.theconversation.com/files/473106/original/file-20220707-22-kkwl50.jpg?ixlib=rb-1.1.0&amp;q=45&amp;auto=format&amp;w=754&amp;fit=clip" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px" srcset="https://images.theconversation.com/files/473106/original/file-20220707-22-kkwl50.jpg?ixlib=rb-1.1.0&amp;q=45&amp;auto=format&amp;w=600&amp;h=800&amp;fit=crop&amp;dpr=1 600w, https://images.theconversation.com/files/473106/original/file-20220707-22-kkwl50.jpg?ixlib=rb-1.1.0&amp;q=30&amp;auto=format&amp;w=600&amp;h=800&amp;fit=crop&amp;dpr=2 1200w, https://images.theconversation.com/files/473106/original/file-20220707-22-kkwl50.jpg?ixlib=rb-1.1.0&amp;q=15&amp;auto=format&amp;w=600&amp;h=800&amp;fit=crop&amp;dpr=3 1800w, https://images.theconversation.com/files/473106/original/file-20220707-22-kkwl50.jpg?ixlib=rb-1.1.0&amp;q=45&amp;auto=format&amp;w=754&amp;h=1005&amp;fit=crop&amp;dpr=1 754w, https://images.theconversation.com/files/473106/original/file-20220707-22-kkwl50.jpg?ixlib=rb-1.1.0&amp;q=30&amp;auto=format&amp;w=754&amp;h=1005&amp;fit=crop&amp;dpr=2 1508w, https://images.theconversation.com/files/473106/original/file-20220707-22-kkwl50.jpg?ixlib=rb-1.1.0&amp;q=15&amp;auto=format&amp;w=754&amp;h=1005&amp;fit=crop&amp;dpr=3 2262w" alt="A paper lantern in the shape of a car." /></a><figcaption><span class="caption">Cars are central to Australia’s image of Bathurst – but they’re not the whole story.</span> <span class="attribution">Kate Smith</span></figcaption></figure> <p>Wiradyuri Elder Wirribee Aunty Leanna Carr-Smith explained to the group how the area plays host to both women’s and men’s business. But such stories are only for the ears of Indigenous women and men.</p> <p>There is a secrecy about Wahluu. Some stories are off limits to white Australians.</p> <p><strong>Wiradyuri Ngayirr Ngurambang – Sacred Country</strong></p> <p>The most breathtaking project launched at the Mountain Tales event is Aunty Leanna/Wirribee and Nicole Welch’s collaboration with Smith, <a href="https://www.dropbox.com/s/4hanss4771t8aim/SacredCountryV6_withAudio.mp4?dl=0">Wiradyuri Ngayirr Ngurambang – Sacred Country</a>, a film emblazoned across Tremain’s Mill.</p> <p>The old mill precinct is a reminder of colonisation and its violence. For this occasion it operated as a backdrop through which Indigenous and non-Indigenous Australians connected. Beaming the film’s panoramic landscapes across this built environment juxtaposed the two cultures.</p> <p>Considering the urgency of global warming, the film brings together drone footage of Wahluu/Mount Panorama and aerial photography of other Indigenous landscapes in the region. It is an ethereal perspective. The soundscape is as rich and textured as the landscape, conveying an extraordinary, yet fragile, beauty.</p> <figure class="align-center zoomable"><a href="https://images.theconversation.com/files/473108/original/file-20220707-12-yw20iu.jpg?ixlib=rb-1.1.0&amp;q=45&amp;auto=format&amp;w=1000&amp;fit=clip"><img src="https://images.theconversation.com/files/473108/original/file-20220707-12-yw20iu.jpg?ixlib=rb-1.1.0&amp;q=45&amp;auto=format&amp;w=754&amp;fit=clip" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px" srcset="https://images.theconversation.com/files/473108/original/file-20220707-12-yw20iu.jpg?ixlib=rb-1.1.0&amp;q=45&amp;auto=format&amp;w=600&amp;h=516&amp;fit=crop&amp;dpr=1 600w, https://images.theconversation.com/files/473108/original/file-20220707-12-yw20iu.jpg?ixlib=rb-1.1.0&amp;q=30&amp;auto=format&amp;w=600&amp;h=516&amp;fit=crop&amp;dpr=2 1200w, https://images.theconversation.com/files/473108/original/file-20220707-12-yw20iu.jpg?ixlib=rb-1.1.0&amp;q=15&amp;auto=format&amp;w=600&amp;h=516&amp;fit=crop&amp;dpr=3 1800w, https://images.theconversation.com/files/473108/original/file-20220707-12-yw20iu.jpg?ixlib=rb-1.1.0&amp;q=45&amp;auto=format&amp;w=754&amp;h=649&amp;fit=crop&amp;dpr=1 754w, https://images.theconversation.com/files/473108/original/file-20220707-12-yw20iu.jpg?ixlib=rb-1.1.0&amp;q=30&amp;auto=format&amp;w=754&amp;h=649&amp;fit=crop&amp;dpr=2 1508w, https://images.theconversation.com/files/473108/original/file-20220707-12-yw20iu.jpg?ixlib=rb-1.1.0&amp;q=15&amp;auto=format&amp;w=754&amp;h=649&amp;fit=crop&amp;dpr=3 2262w" alt="Film still." /></a><figcaption><span class="caption">Projected onto the wall of Tremain’s Mill, Wiradyuri Ngayirr Ngurambang – Sacred Country is a meeting of Indigenous landscapes with colonial Australian history.</span> <span class="attribution">Kate Smith</span></figcaption></figure> <p>Wiradyuri Ngayirr Ngurambang – Sacred Country also explores shared understandings between First Nations and non-First Nations women. Their interracial connection is enacted through a seamless editing style that bridges the Tarana landscape to the Wahluu/Macquarie River, and then eventually to Wahluu/Mount Panorama.</p> <p>The film’s boundless landscapes evoke an all-embracing hospitality that traverses cultural differences. Sometimes the imagery creates vaginal shapes that feminises the country. The land and its creatures come across as alive and vibrant.</p> <p>Sky and earth are mirrored, inspiring our contemplation of eternity and the Indigenous custodianship of Country.</p> <p>Departing later that night, I pondered eternity. One lifetime is nothing compared to 65,000 years of Indigenous connection to Country. This awareness was both profound and comforting. But the night of collective celebration and storytelling also encouraged me, and no doubt others, to delight in life’s briefest moments.</p> <p><em>Wiradyuri Ngayirr Ngurambang – Sacred Country is playing at Tremain’s Mill, Bathurst, until July 17.</em> <img style="border: none !important; box-shadow: none !important; margin: 0 !important; max-height: 1px !important; max-width: 1px !important; min-height: 1px !important; min-width: 1px !important; opacity: 0 !important; outline: none !important; padding: 0 !important;" src="https://counter.theconversation.com/content/185860/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1" /></p> <p><em><a href="https://theconversation.com/profiles/suzie-gibson-111690" target="_blank" rel="noopener">Suzie Gibson</a>, Senior Lecturer in English Literature, <a href="https://theconversation.com/institutions/charles-sturt-university-849" target="_blank" rel="noopener">Charles Sturt University</a></em></p> <p><em>This article is republished from <a href="https://theconversation.com" target="_blank" rel="noopener">The Conversation</a> under a Creative Commons license. Read the <a href="https://theconversation.com/how-a-new-art-project-in-bathurst-is-embracing-the-many-identities-of-the-town-185860" target="_blank" rel="noopener">original article</a>.</em></p> <p><em>Image: Kate Smith</em></p>

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Genetic mutations slowly accumulated over a lifetime change blood production after 70 years of age

<p class="spai-bg-prepared">Ageing is likely caused by the gradual accumulation of molecular damage, or genetic mutations, in the cells of our bodies that occurs over a lifetime. But how this translates into the rapid deterioration in organ function that’s seen after the age of 70 has so far not been clear.</p> <p class="spai-bg-prepared">Now, scientists have discovered that the accumulation of genetic mutations in blood stem cells are likely responsible for the abrupt change in how <a class="spai-bg-prepared" href="https://cosmosmagazine.com/science/biology/why-do-we-have-blood/" target="_blank" rel="noreferrer noopener">blood</a> is produced in the body after 70 years of age.</p> <p class="spai-bg-prepared">The <a class="spai-bg-prepared" href="https://www.nature.com/articles/s41586-022-04786-y" target="_blank" rel="noreferrer noopener">new study</a>, published in <em class="spai-bg-prepared">Nature</em>, points to a change in the diversity of stem cells that produce blood cells as the reason why the prevalence of reduced cell regeneration capacity, <a class="spai-bg-prepared" href="https://www.frontiersin.org/articles/10.3389/fonc.2020.579075/full" target="_blank" rel="noreferrer noopener">cytopenia</a> (one or more blood cell types is lower than it should be), immune disfunction, and risk of blood cancer dramatically rises after 70.</p> <p class="spai-bg-prepared">“We’ve shown, for the first time, how steadily accumulating mutations throughout life lead to a catastrophic and inevitable change in blood cell populations after the age of 70,” says joint-senior author Dr Peter Campbell, head of the Cancer, Ageing and Somatic Mutation Program at the Wellcome Sanger Institute, UK.</p> <p class="spai-bg-prepared">“What is super exciting about this model is that it may well apply in other organ systems too.”</p> <p><strong>Blood cells are made in a process called haematopoiesis</strong></p> <p class="spai-bg-prepared">All of the cells in our blood – including red cells, white cells and platelets – develop in a process called haematopoiesis from haematopoietic stem cells in our bone marrow. These stem cells are what’s known as multipotent progenitor cells, which simply means that they can develop into more than one cell type.</p> <p class="spai-bg-prepared">Researchers were interested in better understanding how this process changes as we age, so they sequenced the entire genomes of 3,579 haematopoietic stem cells from a total of 10 people – ranging in age from newborn to 81 years.</p> <div class="newsletter-box spai-bg-prepared"> <div id="wpcf7-f6-p193434-o1" class="wpcf7 spai-bg-prepared" dir="ltr" lang="en-US" role="form"> </div> </div> <p class="spai-bg-prepared">Using this information, they were able to construct something similar to a family tree (<a class="spai-bg-prepared" href="https://www.nature.com/scitable/topicpage/reading-a-phylogenetic-tree-the-meaning-of-41956/#:~:text=A%20phylogenetic%20tree%2C%20also%20known,genes%20from%20a%20common%20ancestor." target="_blank" rel="noreferrer noopener">a phylogenetic tree</a>) for each stem cell, showing how the relationships between blood cells changes over the human lifespan.</p> <p class="spai-bg-prepared">They found that in adults under 65, blood cells were produced from between 20,000 and 200,000 different stem cells – each contributing roughly equal amounts to production.</p> <p class="spai-bg-prepared">But after 70 years of age they observed a dramatic decrease in the diversity of stem cells responsible for haematopoiesis in the bone marrow. In fact, only 12-18 independent expanded sets of stem cell clones accounted for 30-60% of cell production.</p> <p class="spai-bg-prepared">These highly active stem cells had outcompeted others and progressively expanded in numbers (clones) across that person’s life, and this expansion (called <a class="spai-bg-prepared" href="https://www.nature.com/articles/s41586-022-04785-z" target="_blank" rel="noreferrer noopener">clonal haematopoiesis</a>) was caused by a rare subset of mutations known as driver mutations that had occurred decades earlier.</p> <p class="spai-bg-prepared">“Our findings show that the diversity of blood stem cells is lost in older age due to positive selection of faster-growing clones with driver mutations. These clones ‘outcompete’ the slower growing ones,” explains lead researcher Dr Emily Mitchell, a haematology registrar at Addenbrooke’s Hospital,UK, and PhD student at the Wellcome Sanger Institute, US.</p> <p class="spai-bg-prepared">“In many cases this increased fitness at the stem cell level likely comes at a cost – their ability to produce functional mature blood cells is impaired, so explaining the observed age-related loss of function in the blood system.”</p> <p class="spai-bg-prepared">Which clones became the dominant stem cells varied between individuals, which explains why variation is seen in disease risk and other characteristics in older adults.</p> <p class="spai-bg-prepared">“Factors such as chronic inflammation, smoking, infection and chemotherapy cause earlier growth of clones with cancer-driving mutations. We predict that these factors also bring forward the decline in blood stem cell diversity associated with ageing,” says joint-senior author Dr Elisa Laurenti, assistant professor at the Wellcome-MRC Cambridge Stem Cell Institute, UK.</p> <p class="spai-bg-prepared">“It is possible that there are factors that might slow this process down, too,” she adds. “We now have the exciting task of figuring out how these newly discovered mutations affect blood function in the elderly, so we can learn how to minimise disease risk and promote healthy ageing.”</p> <p><img id="cosmos-post-tracker" class="spai-bg-prepared" style="opacity: 0; height: 1px!important; width: 1px!important; border: 0!important; position: absolute!important; z-index: -1!important;" src="https://syndication.cosmosmagazine.com/?id=193434&amp;title=Genetic+mutations+slowly+accumulated+over+a+lifetime+change+blood+production+after+70+years+of+age" width="1" height="1" /></p> <div id="contributors"> <p><em><a href="https://cosmosmagazine.com/science/mutations-change-blood-production/" target="_blank" rel="noopener">This article</a> was originally published on <a href="https://cosmosmagazine.com" target="_blank" rel="noopener">Cosmos Magazine</a> and was written by <a href="https://cosmosmagazine.com/contributor/imma-perfetto" target="_blank" rel="noopener">Imma Perfetto</a>. Imma Perfetto is a science writer at Cosmos. She has a Bachelor of Science with Honours in Science Communication from the University of Adelaide.</em></p> <p><em>Image: Getty Images</em></p> </div>

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11 home improvement projects you can do yourself instead of hiring a professional

<p><strong>There's no better time to DIY</strong></p> <p>There’s nothing quite as satisfying as a job well done – and these DIY projects will boost your handyman status. They are simple enough to do on your own without spending a lot of cash on tools and supplies. Fasten that tool belt and get started!</p> <p><strong>General painting</strong></p> <p>“Some DIY projects can be done by homeowners with a small investment in the right tools and a little patience. Painting is a great way to give your home a face lift, and it’s not difficult if you do some research and take your time,” says Newell Slade, general contractor. No one wants to paint a room twice, so paint like the pros and buy high quality rollers and paint and choose a paint that has a primer already in it to save time and money. “Painting can be fun and relaxing if you just let yourself take the time to do it right.”</p> <p><strong>Patch and prime</strong></p> <p>There’s plenty of thrifty painting tricks you can use, starting with prepping the wall for optimal coverage. You need a smooth surface for the walls to be blemish free. Even larger holes can easily be repaired with wall patch kits found at home improvement stores. The steps are quite simple and will give your new painted walls a beautiful, smooth finish. “Using a spackle knife, fill in each hole with lightweight putty and scrape the excess off the walls. Wait for the putty to dry and sand down the spot until it’s smooth. Then, prime and paint the repaired spots,” says J.B. Sassano, president of a home improvement franchise.</p> <p><strong>Peel-and-stick floor</strong></p> <p>Looking for an inexpensive home improvement that will make a big impact? It doesn’t get much easier than peel-and-stick flooring. “This specific tile is easier to work with and prevents adhesive from oozing through the cracks between the tiles. It can even be installed over concrete if the concrete is clean, smooth and dry,” says Monica Mangin, host of DIY series, The Weekender. If you’re feeling creative, it’s easy to create bold patterns or borders with different using a variety of patterns and colours.</p> <p><strong>Peel-and-stick panels</strong></p> <p>Panelled rooms are making a comeback. This time around, the trend is usually horizontal and installation doesn’t require a hammer and nails, even though the panels are made from wood. “Creating a wood accent wall offers a great way to add personality and texture to your space. You can customise your look by playing with thickness and pre-stained colours,” says Mangin. “Mixing and matching the colours and styles will provide an eye-catching piece that pop.”</p> <p><strong>Penny tile</strong></p> <p>A tired and worn splashback can be replaced in a day. “Penny tile is a really affordable option, especially when it comes in white, which is one of the more standard colours,” says Mangin. But you don’t necessarily have to buy more tiles to get the colours you want. Mangin says you can customise this DIY home improvement by using enamel paints to colour individual tiles and bake them in the oven to fully cure. “After the white sheets are up on the wall, decide which tiles you want to pop out and then just pop in your DIY coloured tile,” says Mangin. Plus, these tiles don’t require a tile cutter, just a utility knife to cut the mesh sheets to fit the area.</p> <p><strong>Fences</strong></p> <p>It’s been said that fences make good neighbours, but the price shock of hiring a pro seems worse than the dog next door who likes to do his business in your yard every morning. Whether you want privacy or need to replace a worn-out fence, it’s a project that Bryan Clayton, CEO of GreenPal says you can do if you remember to do two important things: get a survey done to identify the correct property lines, and mark for pipes if you have underground sprinklers. However, there are certain fences that are friendlier for a DIY home improvement. “Based on my experience the easier types of fencing to install are the black aluminium-based products made to look like wrought iron,” says Clayton. “However, for fencing styles such as chain link and solid vinyl panels, I would not recommend doing it yourself – there’s quite a bit of a learning curve associated with getting them just right.”</p> <p><strong>A lasting first impression</strong></p> <p>A faded, outdated, or squeaky door doesn’t make a good first impression and it may not provide much in the line of security or keeping out drafts. Luckily you can create a more welcoming entrance by replacing your old door with a new one. Exterior doors are available pre-hung in a weatherstripped frame so all you need are a few tools and basic carpentry tools to install it. Depending on your budget, you can choose from steel doors which require little maintenance, or fibreglass doors that require almost none. Going with steel or fibreglass can save you money over wood, and they won’t rot or warp; the more expensive ones look just like real wood.</p> <p><strong>Window screen</strong></p> <p>Using packing tape may be a quick remedy for a hole or tear in the screen, but it’s not a permanent fix. Small patch kits are sold at home improvement stores and a small hole can easily be repaired in just a few minutes with the patch and a hair dryer. Larger screen tears, like from your dog’s excitement over an online delivery, can be a DIY project too, as long as the frame is in good shape. The most popular replacement material for screens is fibreglass because of its flexibility. Since you’re replacing the screen anyway you may want to get the sun-shading fabric which blocks more sun and – bonus – is stronger than fibreglass and aluminium so it’s great for pets.</p> <p><strong>Light fixtures and plumbing fixtures</strong></p> <p>“As long as you familiarise yourself with the basics of proper safety procedures such as turning off electricity and water when working, these are DIY home improvements worth doing,” says Brian C. McHugh, owner of McHugh Construction. For lighting, the key is knowing how much space you have to house a new light fixture. For example, ceiling fans come in various blade sizes to suit the size of your room. If you’re replacing a bathroom tap, you’ll want to buy a tap that matches the existing holes in the sink. If you don’t feel confident in your DIY skills, though, it’s better to just do the choosing yourself and leave the installation to the professionals.</p> <p><strong>Caulk it up</strong></p> <p>Inspecting and repairing caulk is a project you should do yearly, according to Sassano. “Using caulk to seal cracks and gaps serves multiple purposes: It lowers heating and air conditioning bills by reducing air flow into and out of the home; it prevents moisture that can cause wood rot, mould, mildew and water damage, and it keeps insects and other pests out,” he says. The project will determine which type of caulk. For example, silicone is best for the bathtub and shower area. Start by removing the old caulk, cleaning the surface, and then apply new caulk. Caulk removal tools and solutions make the project even easier.</p> <p><strong>Landscaping</strong></p> <p>Creating a backyard oasis can be a great way to express your creativity. A raised garden bed, adding new paver stones, or creating a perennial flower garden involves more sweat equity than expertise. You can still get some help for the heavy lifting. “Ask your local landscape supply to deliver your materials instead of renting trucks or equipment,” says McHugh. “The tools for most jobs such as shovels, rakes and a wheelbarrow are things you probably already have in your garage.”</p> <p><em><span id="docs-internal-guid-44670a98-7fff-5184-42ee-20b15e18348f">Written by Lisa Marie Conklin. This article first appeared in <a href="https://www.readersdigest.co.nz/food-home-garden/diy-projects/11-home-improvement-projects-you-can-do-yourself-instead-of-hiring-a-professional" target="_blank" rel="noopener">Reader’s Digest</a>. For more of what you love from the world’s best-loved magazine, <a href="http://readersdigest.innovations.co.nz/c/readersdigestemailsubscribe?utm_source=over60&amp;utm_medium=articles&amp;utm_campaign=RDSUB&amp;keycode=WRA87V" target="_blank" rel="noopener">here’s our best subscription offer.</a></span></em></p> <p><em>Image: Getty Images</em></p>

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Genetic discovery may help scientists reverse hearing loss

<p>Neuroscience researchers have found a master gene that controls the development of special sensory cells in the ears – potentially opening the door to reversing hearing loss.</p> <p>A team led by Jaime García-Añoveros of Northwestern University, US, established that a gene called Tbx2 controls the development of ear hair cells in mice. The findings of their study are <a href="https://www.nature.com/articles/s41586-022-04668-3" target="_blank" rel="noreferrer noopener">published today in <em>Nature</em></a><em>.</em></p> <p><strong>What are hair cells?</strong></p> <p>Hair cells are the sensory cells in our ears that detect sound and then transmit a message to our brains. They are so named because they have tiny hairlike structures called stereocilia.</p> <p>“The ear is a beautiful organ,” says García-Añoveros. “There is no other organ in a mammal where the cells are so precisely positioned.”</p> <p>Hair cells are found in a structure called the organ of Corti, in the cochlea in the inner ear. The organ of Corti sits on top of the basilar membrane.</p> <p>Sound waves are funnelled through our ear canal and cause the eardrum (also known as the tympanic membrane) and ossicles (tiny bones called the malleus, incus and stapes) to vibrate. The vibrations, or waves, are transmitted through fluid in the cochlea, causing the basilar membrane to move as well.</p> <p>When the basilar membrane moves, the stereocilia tilt, causing ion channels in the hair cell membrane to open. This stimulates the hair cell to release neurotransmitter chemicals, which will transmit the sound signal to the brain via the auditory nerve.</p> <figure class="wp-block-embed is-type-video is-provider-youtube wp-block-embed-youtube wp-embed-aspect-16-9 wp-has-aspect-ratio"> <div class="wp-block-embed__wrapper"> <div class="entry-content-asset"> <div class="embed-wrapper"> <div class="inner"><iframe title="2-Minute Neuroscience: The Cochlea" src="https://www.youtube.com/embed/WeQluId1hnQ?feature=oembed" width="500" height="281" frameborder="0" allowfullscreen="allowfullscreen"></iframe></div> </div> </div> </div> </figure> <h2> </h2> <p><strong>Hair cells and hearing loss</strong></p> <p>There are actually two types of hair cells: inner and outer. We need both types to hear effectively. The outer hair cells change their shape and amplify sound for the inner hair cells, which transmit the vibrations to the brain.</p> <div class="newsletter-box"> <div id="wpcf7-f6-p190195-o1" class="wpcf7" dir="ltr" lang="en-US" role="form"> <form class="wpcf7-form mailchimp-ext-0.5.61 init" action="/science/genetic-discovery-reverse-hearing-loss/#wpcf7-f6-p190195-o1" method="post" novalidate="novalidate" data-status="init"> <p style="display: none !important;"><span class="wpcf7-form-control-wrap referer-page"><input class="wpcf7-form-control wpcf7-text referer-page" name="referer-page" type="hidden" value="https://cosmosmagazine.com/health/" data-value="https://cosmosmagazine.com/health/" aria-invalid="false" /></span></p> <p><!-- Chimpmail extension by Renzo Johnson --></form> </div> </div> <p>“It’s like a ballet,” says García-Añoveros. “The outers crouch and jump and lift the inners further into the ear.”</p> <p>Hair cells develop before we are born and do not typically divide to create new versions of themselves. As we age, our hair cells die, <a href="https://cosmosmagazine.com/health/hair-cell-loss-may-explain-hearing-loss/">leading to hearing loss</a>. Loss of outer hair cells is particularly common.</p> <p>According to the US Centers for Disease Control, about 8.5% of adults aged 55-64 in the US experience “disabling” hearing loss, with that number increasing to nearly 25% in people aged 65-74, and 50% in those 75 and older.</p> <p><strong>Could we one day reverse hearing loss?</strong></p> <p>Since hair cells don’t usually divide, we may be able to reverse hearing loss if we can reprogram stem cells or other cells in the ear to become hair cells to replace those that die.</p> <p>Scientists have already produced artificial hair cells, but until now didn’t know how to direct the cell to become an inner or an outer hair cell.</p> <p>The team at Northwestern discovered that a gene called Tbx2 controls the development of both inner and outer hair cells. If Tbx2 is “switched on” to produce the protein TBX2, the cell develops into an inner hair cell. If Tbx2 is “off”, it becomes an outer hair cell.</p> <p>“Our finding gives us the first clear cell switch to make one type versus the other,” García-Añoveros explains.</p> <p>The finding is a step towards learning how we can reprogram the cells that usually provide structural support for the hair cells to become inner or outer hair cells themselves – replacing dead hair cells and preventing or reversing hearing loss.</p> <p>“We can now figure out how to make specifically inner or outer hair cells and identify why the latter are more prone to dying,” García-Añoveros says. “We have overcome a major hurdle.”</p> <p><!-- Start of tracking content syndication. Please do not remove this section as it allows us to keep track of republished articles --></p> <p><img id="cosmos-post-tracker" style="opacity: 0; height: 1px!important; width: 1px!important; border: 0!important; position: absolute!important; z-index: -1!important;" src="https://syndication.cosmosmagazine.com/?id=190195&amp;title=Genetic+discovery+may+help+scientists+reverse+hearing+loss" width="1" height="1" data-spai-target="src" data-spai-orig="" data-spai-exclude="nocdn" /></p> <p><!-- End of tracking content syndication --></p> <div id="contributors"> <p><em><a href="https://cosmosmagazine.com/science/genetic-discovery-reverse-hearing-loss/" target="_blank" rel="noopener">This article</a> was originally published on <a href="https://cosmosmagazine.com" target="_blank" rel="noopener">Cosmos Magazine</a> and was written by <a href="https://cosmosmagazine.com/contributor/matilda-handlsey-davis" target="_blank" rel="noopener">Matilda Handsley-Davis</a>. Matilda is a science writer at Cosmos. She holds a Bachelor of Arts and a Bachelor of Science (Honours) from the University of Adelaide.</em></p> <p><em>Image: Getty Images</em></p> </div>

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How r/place – a massive and chaotic collaborative art project on Reddit – showcased the best and worst of online spaces

<p>Many would be familiar with <a href="https://www.reddit.com/">Reddit</a> as one of the largest social networking sites, with a large group of forums (“subreddits”) catering to almost any interest. </p> <p>Since the beginning of April, Reddit has played host to a massive collaborative art project called <a href="https://www.reddit.com/r/place">r/place</a> that simultaneously shows us some of the best and worst attributes of cybercultures. </p> <p>Originally launched in 2017, r/place ran for 72 hours. The lifespan of the new r/place was also short – ultimately lasting for just five days. Beginning initially as a blank canvas, r/place allows users to place one coloured pixel every five minutes (or 20 minutes for unverified accounts) as they attempt to build a collective art piece. </p> <p>Traversing through r/place takes you for a journey through time, memes and cultures.</p> <p>At any one moment you might be looking at a Nine Inch Nails logo, the flags of various countries, a QR code linking you to a YouTube video titled The Most Logical Arguments AGAINST Veganism (In 10 Minutes), and a <a href="https://knowyourmeme.com/memes/people/zyzz">homage to Zyzz</a> – a popular bodybuilding figure who passed away in 2011. </p> <p>Some artworks on r/place don’t seem to represent anything at all. The sole mission of <a href="https://www.reddit.com/r/TheBlueCorner/">The Blue Corner</a> is (you guessed it) to have a blue corner depicted on the final art piece. </p> <p>The artwork constantly changes over its short lifetime. But even if the drawings of some communities may not go the distance, <a href="https://www.youtube.com/watch?v=XnRCZK3KjUY">the time lapse videos</a> depicting the ongoing mutation of the canvas has become a key part of this art piece, ensuring all contributions play a vital part in the lifecycle of r/place.</p> <h2>Collaboration – and opposition</h2> <p>r/place shows us the collaborative nature of humans in online spaces. After its emergence in 2017 it was hailed as “<a href="https://www.newsweek.com/reddit-place-internet-experiment-579049">the internet’s best experiment yet</a>” and praised for capturing “<a href="https://www.lifehacker.com.au/2017/04/place-was-the-internet-in-all-its-glory/">the internet, in all its wonderful glory</a>”. </p> <p>This collaborative online art project allows people to express their individuality as well as collective identities formed through interactions with online spaces. </p> <p>This year’s iteration of r/place, in contrast to the previous version, demonstrates the interconnectivity of communities in digital spaces. No longer is r/place solely reserved for Reddit users. Now, there is clear power in drawing on communities distributed across Twitch, Discord and Twitter. </p> <p>This influx of communities from all over the internet has not been well-received by all.</p> <p>There is a belief Twitch streamers are ruining the work <a href="https://www.reddit.com/r/place/comments/tw3fou/eu_streamer_took_over_our_small_asean_artworks/">of smaller communities</a> and are attempting to sabotage the project. </p> <p>Instead of being a democratic representation of online communities and their art, the argument goes, Twitch streamers are encouraging their fans, numbered in the hundreds of thousands, to capture hotly contested territory.</p> <p>Factions – such as those formed between <a href="https://twitter.com/Rubiu5/status/1511077247025057793">Spanish streamers and BTS fans</a> – have become the primary way to ensure power and influence over the art project. </p> <p>Smaller communities are driven out at the expense of larger influencers with more bargaining power in this pixel warfare. </p> <p>It is not just individuals taking part in this art project. Many believe “bots” are <a href="https://www.reddit.com/r/place/comments/tu2gdg/bots_by_the_username_rplace_are_attempting_to/">running rampant</a>, performing automated tasks in a way that is antithetical to the idea of this artwork as a representation of human achievement as opposed to technical prowess. </p> <p>These examples are just a fraction of the chaos over the internet in the last few days: 4chan operated <a href="https://www.reddit.com/r/place/comments/tufngh/4chan_is_trying_to_make_the_trans_community_look/">coordinated attacks</a> on the Trans flag and LGBTQ+ panels, and streamers are receiving an influx of <a href="https://clips.twitch.tv/TrappedBoringKleeCclamChamp-WJ0LwTK-Uhox6MSa">death threats</a>.</p> <h2>The best and worst of us</h2> <p>At its best, r/place is a powerful illustration of strangers coming together about their passions online and the collaborative nature of the internet. </p> <p>At its worst, it represents everything we have come to dislike about the internet: the exclusion of smaller voices at the expense of influencer cultures, factions between communities, and the toxicity of some cybercultures.</p> <p>Whatever the case, this project has been great for boosting Reddit’s publicity as the company <a href="https://fortune.com/2021/12/16/reddit-goes-public-ipo-filing/">goes public</a>.</p> <p>In its final moments earlier today, users could only place white tiles and watch the spectacle of a once vibrantly coloured collaborative art piece that caused so much chaos among online communities simply transform back into a blank canvas.</p> <p><em>Image credits: Reddit</em></p> <p><em>This article originally appeared on <a href="https://theconversation.com/how-r-place-a-massive-and-chaotic-collaborative-art-project-on-reddit-showcased-the-best-and-worst-of-online-spaces-180662" target="_blank" rel="noopener">The Conversation</a>. </em></p>

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“We really, really did it!”: Human genome finally completed

<p dir="ltr">Scientists say they have finally mapped the entire human genome, 20 years after it was first celebrated around the world.</p> <p dir="ltr">A team of international researchers have been able to fill in the gaps in the sequence that contains all of the genetic information humans need to function.</p> <p dir="ltr">The scientists worked together as part of the Telomere to Telomere (T2T) consortium and presented a gap-free sequence of the roughly three billion bases (or “letters”) in DNA.</p> <p dir="ltr">These letters, known as A, C, G and T, form pairs that are strung together to form genes and can include instructions for making proteins which are then used for everything from repairing tissue and helping our immune systems function to providing structure for our cells and allowing our bodies to move.</p> <p dir="ltr">The new research comes after the first draft of the human genome was announced in 2000, which was incomplete because technology to sequence DNA wasn’t able to read certain parts of it.</p> <p dir="ltr">These parts included really long, highly repetitive sequences of the letters which have been described as “junk DNA”.</p> <p dir="ltr">As technology evolved and the genome continued to be updated, about eight percent of the DNA in the genome was still unknown - until now.</p> <p dir="ltr">“Some of the genes that make us uniquely human were actually in this ‘dark matter of the genome’ and were totally missed,” Evan Eichler, a University of Washington researcher who was involved in the current research and the original Human Genome Project, told <em><a href="https://www.nzherald.co.nz/world/scientists-finally-finish-decoding-entire-human-genome/2YQLOXHMWP5TWJJ6HW24WH5QGA/" target="_blank" rel="noopener">NZ Herald</a></em>.</p> <p dir="ltr">“It took 20-plus years, but we finally got it done.”</p> <p dir="ltr">Many - including Eicher’s own students - thought the genome had been completed by now, making the latest achievement even more surprising.</p> <p dir="ltr">“I was teaching them, and they said, ‘Wait a minute. Isn’t this like the sixth time you guys have declared victory?’ I said, ‘No, this time we really, really did it!’”</p> <p><span id="docs-internal-guid-2005b113-7fff-3fcf-efca-0f8f8e295010"></span></p> <p dir="ltr">The research is so significant it even prompted Eichler to write his first ever tweet announcing it.</p> <blockquote class="twitter-tweet"> <p dir="ltr" lang="en">It only took a complete human genome for <a href="https://twitter.com/EichlerEE?ref_src=twsrc%5Etfw">@EichlerEE</a> actually make his first twitter post. I think this means we can expect more posts from him in the future as long as <a href="https://twitter.com/aphillippy?ref_src=twsrc%5Etfw">@aphillippy</a> <a href="https://twitter.com/sergeynurk?ref_src=twsrc%5Etfw">@sergeynurk</a> <a href="https://twitter.com/sergekoren?ref_src=twsrc%5Etfw">@sergekoren</a> <a href="https://twitter.com/ArangRhie?ref_src=twsrc%5Etfw">@ArangRhie</a> <a href="https://twitter.com/MikkoRautiaine3?ref_src=twsrc%5Etfw">@MikkoRautiaine3</a> finish some more genomes! <a href="https://t.co/aDSwBt6gW1">https://t.co/aDSwBt6gW1</a></p> <p>— Mitchell R. Vollger (@mrvollger) <a href="https://twitter.com/mrvollger/status/1509606815184547841?ref_src=twsrc%5Etfw">March 31, 2022</a></p></blockquote> <p dir="ltr">Karen Miga, another of the authors of the six studies released on Thursday, said having a complete picture of the genome would further the understanding of our evolution and pave the way for medical discoveries in areas such as ageing, cancer, and neurodegenerative conditions.</p> <p dir="ltr">“We’re just broadening our opportunities to understand human disease,” Miga said.</p> <p dir="ltr">Before now, Miga said the gaps in the map of the genome were “large and persistent” and in “pretty important regions”.</p> <p dir="ltr">The hugely collaborative work, including researchers from the University of California, the University of Washington, and the National Human Genome Research Institute, also corrects previous errors in the map.</p> <p dir="ltr">“This is a major improvement, I would say, of the Human Genome Project,” said geneticist Ting Wang, who wasn’t involved in the studies.</p> <p dir="ltr">It also turned out that these unknown stretches of DNA also contain some that play an important role in evolution and disease, and even some that are integral to making our brains larger than a chimp’s.</p> <p dir="ltr">Reading genes requires scientists to cut strands of DNA into pieces, which sequencing machines then read letter by letter. With the strands being anywhere from hundreds to thousands of letters long, scientists are then tasked with reordering the pieces so they are correct - a tough task when there are lots of repeating letters.</p> <p dir="ltr"><span id="docs-internal-guid-bcb131c9-7fff-607b-e482-d45983d9d97c"></span></p> <p dir="ltr">With technology now allowing for the genome to be complete, future research will look to map even more genomes and collect genes from both parents.</p> <p dir="ltr"><em>Image: Getty Images</em></p>

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How to build timber covers for wheelie bins

<p>The Sekit flat-packed system, from Bunnings (bunnings.com.au), uses ACQ treated pine and takes an hour to assemble, fitting 120 and 240 litre bins.</p> <p>A single bin cover measures 670 x 810 x 1200mm, and the double is 1340 x 810 x 1200mm.</p> <div id="firstFloatAd"> <div data-fuse="21928626849"> </div> <div data-fuse="21699960946"> </div> </div> <p>Simple latch bolts keep the doors secured and a chain joins the bin handles to the covers so both lids are raised simultaneously, making rubbish disposal much more hygienic.</p> <p>TIP – To remove the bins on collection day, unhook the lid chains before opening the doors.A chain connects the bin</p> <p>ASSEMBLE THE FRAME positioning the dividing frame against the side panels and adding the front and back supports, securing with the supplied screws. Square up the frame and secure the two diagonal back supports.</p> <div id="lastFloatAd"> <div data-fuse="21928512968"> </div> <div data-fuse="22652288252"> </div> </div> <p>INSTALL THE LIDS by aligning the holes on the lid with the holes in the frame then insert the supplied bolts, securing the outside bolts with the washer and nut and the inside bolts using a Phillips head screwdriver.</p> <p>ATTACH THE DOORS by aligning the top hinge and securing with a screw at the top, attach the base hinge, checking the door is parallel with the side then secure the second screw at the top and attach the latch bolts.</p> <p><em>Image: Bunnings</em></p>

Home Hints & Tips

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Why Daniel Johns will never perform live again

<p><span style="font-weight: 400;">He was once the frontman of one of Australia’s biggest homegrown acts. </span></p> <p><span style="font-weight: 400;">But now Silverchair lead singer Daniel Johns has said he will never perform live again. </span></p> <p><span style="font-weight: 400;">In a candid interview with </span><span style="font-weight: 400;">The Project</span><span style="font-weight: 400;">, the 42-year-old musician said he has long struggled with shutting down persistent rumours that Silverchair, who split up in 2011, would eventually reform. </span></p> <p><span style="font-weight: 400;">He said, </span><span style="font-weight: 400;">"I was like, 'This is really starting to affect my mental health'. Because I am saying 'that's it', and every time I try to tell the truth, someone told a lie."</span></p> <p><span style="font-weight: 400;">"So I was like, 'I wouldn't get Silverchair back together with a gun to my head for $1 million'. Maybe that was too harsh in hindsight."</span></p> <p><span style="font-weight: 400;">He discussed how Silverchair’s sudden rise to fame after the release of </span><em><span style="font-weight: 400;">Frogstomp</span></em><span style="font-weight: 400;"> in 1995, when Daniel was just 16, took a toll on his emotional wellbeing. </span></p> <p><span style="font-weight: 400;">Just months after the album’s release, Silverchair saw international notoriety, as they even opened for Red Hot Chili Peppers at New York’s Madison Square Garden. </span></p> <p><span style="font-weight: 400;">Daniel said that the level of fandom was “extreme”, as he was always looking over his shoulder. </span></p> <p><span style="font-weight: 400;">"And I have pretty much constantly had that since the second album, since I saw the hysteria of </span><em><span style="font-weight: 400;">Frogstomp</span></em><span style="font-weight: 400;">," he said.</span></p> <p><span style="font-weight: 400;">When discussing why he would not reform the band, he said there is too much emotional baggage from the highest points of the band’s fame to consider it. </span></p> <p><span style="font-weight: 400;">"It's not that I am not proud of the work – I am actually really proud of the work. It's just that it's emotionally triggering for me."</span></p> <p><span style="font-weight: 400;">He said he needed to walk away from the band to be "internally happy", something he has achieved since the band’s end in 2011.</span></p> <p><span style="font-weight: 400;">"But it took me years and years and years of really, really heavy, heavy therapy.</span></p> <p><span style="font-weight: 400;">"And if I didn't do that work, I don't think I'd be here."</span></p> <p><span style="font-weight: 400;">The trauma of the band’s success prompted Daniel to say he has no desire to play live again, but that doesn’t mean he won’t release new music in the future. </span></p> <p><span style="font-weight: 400;">"I don't even go to live shows because I hate that environment. So why would I want to be the focus? I honestly don't think you ever will [see me play live].”</span></p> <p><span style="font-weight: 400;">"There is so much music coming and I am really proud of it. You don't need to see it live. Just listen."</span></p> <p><span style="font-weight: 400;">You can check out the full interview with </span><span style="font-weight: 400;">The Project</span><span style="font-weight: 400;"> here:</span></p> <p><iframe width="560" height="315" src="https://www.youtube.com/embed/2N53j1Own8c" title="YouTube video player" frameborder="0" allow="accelerometer; autoplay; clipboard-write; encrypted-media; gyroscope; picture-in-picture" allowfullscreen=""></iframe></p> <p><em><span style="font-weight: 400;">Image credits: Getty Images</span></em></p>

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Physical symptoms linked to genetic risk of depression

<p><span style="font-weight: 400;">People who experience physical symptoms such as chronic pain, fatigue and migraines are also more likely to have a higher genetic risk of clinical depression, according to a new study.</span></p> <p><span style="font-weight: 400;">Researchers from the University of Queensland collaborated with the QIMR Berghofer Medical Research Institute at the Royal Brisbane and Women’s Hospital to conduct a new study published in </span><em><a rel="noopener" href="https://jamanetwork.com/journals/jamapsychiatry/article-abstract/2783096" target="_blank"><span style="font-weight: 400;">JAMA Psychiatry</span></a></em><span style="font-weight: 400;">.</span></p> <p><span style="font-weight: 400;">They analysed data from over 15,000 volunteers, who provided information about their mental health history, depression symptoms, and a DNA sample.</span></p> <p><span style="font-weight: 400;">The team found that participants who had a higher genetic risk of developing clinical depression were more likely to experience additional physical symptoms.</span></p> <p><span style="font-weight: 400;">Dr Enda Byrne, a senior research fellow in psychiatric genetics and one of the researchers involved, said the study aimed to improve understanding of the genetic risks of depression and how other symptoms can be used to aid diagnosis.</span></p> <p><img style="width: 500px; height: 281.25px;" src="https://oversixtydev.blob.core.windows.net/media/7845012/depression1.jpg" alt="" data-udi="umb://media/e08ca3fc9f134a3c8fb3556dde363b83" /></p> <p><em><span style="font-weight: 400;">Dr Enda Byrnes, the senior author of the latest study on depression and genetic risk. Image: The University of Queensland</span></em></p> <p><span style="font-weight: 400;">“A large proportion of people with clinically-diagnosed depression present initially to doctors with physical symptoms that cause distress and can severely impact on people’s quality of life,” </span><a rel="noopener" href="https://www.scimex.org/newsfeed/genetic-risk-for-clinical-depression-linked-to-physical-symptoms" target="_blank"><span style="font-weight: 400;">he said</span></a><span style="font-weight: 400;">.</span></p> <p><span style="font-weight: 400;">“Our research aimed to better understand the biological basis of depression and found that assessing a broad range of symptoms was important.</span></p> <p><span style="font-weight: 400;">“We wanted to see how genetic risk factors based on clinical definitions of depression differed - from those based on a single question to those based on a doctor’s consultation about mental health problems.”</span></p> <p><strong>Genetic risks of depression, explained</strong></p> <p><span style="font-weight: 400;">Many different factors can contribute to the onset of depression, and there is strong evidence to suggest that genetics can affect the likelihood of developing the mental illness.</span></p> <p><span style="font-weight: 400;">Individuals can be predisposed to developing depression if someone in their family has been diagnosed. If a person’s biological parent has been diagnosed with clinical depression, their genetic risk of developing the illness sits at </span><a rel="noopener" href="https://www.blackdoginstitute.org.au/wp-content/uploads/2020/04/1-causesofdepression.pdf" target="_blank"><span style="font-weight: 400;">about 40 percent</span></a><span style="font-weight: 400;">, with the other 60 percent coming from factors in their environment such as stress and age.</span></p> <p><span style="font-weight: 400;">Previous studies have also examined the role genetics plays in depression, but Dr Byrne said it can be difficult to find genetic risk factors that are specific to clinical depression.</span></p> <p><span style="font-weight: 400;">“Previous genetic studies have included participants who report having seen a doctor for worries or tension - but who may not meet the ‘official’ criteria for a diagnosis of depression,” he said.</span></p> <p><span style="font-weight: 400;">The researchers also stressed the importance of using a large number of samples in order to identify the risk factors for clinical depression but not for other definitions of depression.</span></p> <p><span style="font-weight: 400;">“It is also linked to higher rates of somatic symptoms - that is, physical symptoms that cause distress and can severely impact on people’s quality of life,” Dr Byrne said.</span></p> <p><span style="font-weight: 400;">“Our results highlight the need for larger studies investigating the broad range of symptoms experienced by people with depression.”</span></p> <p><em><span style="font-weight: 400;">Image: Getty Images</span></em></p>

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Paul Simon celebrates 80th birthday with new project

<p><span style="font-weight: 400;">On his 80th birthday, Paul Simon has announced his latest project, which comes in the form of an audiobook. </span></p> <p><a href="https://variety.com/2021/digital/news/paul-simon-new-music-audiobook-malcolm-gladwell-1235087435/"><span style="font-weight: 400;">Variety reports</span></a><span style="font-weight: 400;"> that the five-hour audiobook titled </span><em><span style="font-weight: 400;">Miracle and Wonder: Conversations With Paul Simon</span></em><span style="font-weight: 400;">, will be available on November 16th. </span></p> <p><span style="font-weight: 400;">The audiobook is named after a line in his track </span><em><span style="font-weight: 400;">The Boy in the Bubble</span></em><span style="font-weight: 400;">, and features a new song called </span><span style="font-weight: 400;"><em>Seven Psalm</em>s</span><span style="font-weight: 400;">: his first release since 2018. </span></p> <p><span style="font-weight: 400;">It also features unreleased live versions of his classic songs including </span><em><span style="font-weight: 400;">The Boxer</span></em><span style="font-weight: 400;"> and </span><em><span style="font-weight: 400;">The Sound of Silence</span></em><span style="font-weight: 400;">. </span></p> <p><span style="font-weight: 400;">Collaborating with Bruce Headlam and Malcolm Gladwell for </span><em><span style="font-weight: 400;">Miracle and Wonder</span></em><span style="font-weight: 400;">, Paul recorded over 30 hours of interviews over nine sessions for the audiobook. </span></p> <p><span style="font-weight: 400;">The autobiographical project documents Paul Simon’s upbringing in New York, the genesis of Simon and Garfunkel and the start of his solo career. </span></p> <p><span style="font-weight: 400;">The audiobook also features several cameos, including </span><span style="font-weight: 400;">Sting, Jeff Tweedy, Herbie Hancock, Rosanne Cash, and more to chat about their experiences in the music industry together. </span></p> <p><span style="font-weight: 400;">“Over my career, I must have given hundreds of interviews on various projects, but speaking and collaborating with Malcolm on this was especially enjoyable,” Simon said in a statement. </span></p> <p><span style="font-weight: 400;">Malcolm Gladwell added, “He’s the most un-rock-star rock star. Paul is surprisingly down to earth and approachable. Even if he wasn’t the most successful musician of his generation he’d be the same person.”</span></p> <p><em><span style="font-weight: 400;">Image credit: Getty Images</span></em></p>

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Ray-Ban and Facebook collaborate on a controversial project

<p><span style="font-weight: 400;">Facebook and Ray-Ban have announced the launch of a “first generation” pair of sunglasses that has divided fans of the brand. </span></p> <p><span style="font-weight: 400;">The ‘smart glasses’ combine a sleek looking pair of sunnies that showcase the brand’s signature style, but with a very unique feature. </span></p> <p><span style="font-weight: 400;">The glasses boast a tony 5MP camera lens in each of the glasses that can be used to capture life’s special moments completely hands free. </span></p> <p><span style="font-weight: 400;">The glasses feature a simple touch button to start a 30-second video recording that says stored on the glasses. </span></p> <p><span style="font-weight: 400;">When the user opens the Facebook View app, the photos and videos download onto your phone and can be shared on any social media platform. </span></p> <p><span style="font-weight: 400;">Facebook's president of their Reality Labs Andrew Bosworth said the glasses are introducing a new way of connecting. </span></p> <p><span style="font-weight: 400;">"Ray-Ban Stories is designed to help people live in the moment and stay connected to the people they are with and the people they wish they were with.”</span></p> <p><span style="font-weight: 400;">He said, "We're introducing an entirely new way for people to stay connected to the world around them and truly be present in life's most important moments, and to look good while doing it."</span></p> <p><span style="font-weight: 400;">While the glasses certainly seem impressive, many potential customers have questions about privacy. </span></p> <p><span style="font-weight: 400;">Facebook predicted the hesitancy, and said the glasses were “designed with privacy in mind”.</span></p> <p><span style="font-weight: 400;">In a blog post announcing the product, they say "we have a big responsibility to help people feel comfortable and provide peace of mind, and that goes not only for device owners but the people around them, too."</span></p> <p><span style="font-weight: 400;">While Facebook assures users that the glasses are equipped with software to protect the privacy of others, it’s up to each individual customer to not abuse the new technology. </span></p> <p><span style="font-weight: 400;">Facebook's Ray-Ban Stories are now on sale from $449 in Australia, at OPSM and Sunglass Hut or Ray-Ban online.</span></p> <p><span style="font-weight: 400;">Check out the promotional video here.</span></p> <blockquote style="background: #FFF; border: 0; border-radius: 3px; box-shadow: 0 0 1px 0 rgba(0,0,0,0.5),0 1px 10px 0 rgba(0,0,0,0.15); margin: 1px; max-width: 540px; min-width: 326px; padding: 0; width: calc(100% - 2px);" class="instagram-media" data-instgrm-captioned="" data-instgrm-permalink="https://www.instagram.com/tv/CTm1mBSBE8i/?utm_source=ig_embed&amp;utm_campaign=loading" data-instgrm-version="13"> <div style="padding: 16px;"> <div style="display: flex; flex-direction: row; align-items: center;"> <div style="background-color: #f4f4f4; border-radius: 50%; flex-grow: 0; height: 40px; margin-right: 14px; width: 40px;"></div> <div style="display: flex; flex-direction: column; flex-grow: 1; justify-content: center;"> <div style="background-color: #f4f4f4; border-radius: 4px; flex-grow: 0; height: 14px; margin-bottom: 6px; width: 100px;"></div> <div style="background-color: #f4f4f4; border-radius: 4px; flex-grow: 0; height: 14px; width: 60px;"></div> </div> </div> <div style="padding: 19% 0;"></div> <div style="display: block; height: 50px; margin: 0 auto 12px; width: 50px;"></div> <div style="padding-top: 8px;"> <div style="color: #3897f0; font-family: Arial,sans-serif; font-size: 14px; font-style: normal; font-weight: 550; line-height: 18px;">View this post on Instagram</div> </div> <p style="color: #c9c8cd; font-family: Arial,sans-serif; font-size: 14px; line-height: 17px; margin-bottom: 0; margin-top: 8px; overflow: hidden; padding: 8px 0 7px; text-align: center; text-overflow: ellipsis; white-space: nowrap;"><a style="color: #c9c8cd; font-family: Arial,sans-serif; font-size: 14px; font-style: normal; font-weight: normal; line-height: 17px; text-decoration: none;" rel="noopener" href="https://www.instagram.com/tv/CTm1mBSBE8i/?utm_source=ig_embed&amp;utm_campaign=loading" target="_blank">A post shared by Ray-Ban (@rayban)</a></p> </div> </blockquote> <p><em>Image credit: <span style="font-weight: 400;">Getty Images / Instagram @rayban</span></em></p>

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Genetic link between alcoholism and Alzheimer’s risk discovered

<p><span style="font-weight: 400;">Scientists have found a genetic overlap between alcohol use disorder (AUD) and neurodegenerative disorders such as Alzheimer’s.</span></p> <p><span style="font-weight: 400;">In a </span><a rel="noopener" href="https://www.nature.com/articles/s41467-021-25392-y" target="_blank"><span style="font-weight: 400;">study</span></a><span style="font-weight: 400;"> published in </span><em><span style="font-weight: 400;">Nature Communications</span></em><span style="font-weight: 400;">, the researchers identified several genes associated with alcoholism, including two previously linked to neurodegenerative disorders.</span></p> <blockquote class="twitter-tweet"> <p dir="ltr">First of its kind study using multi-omics approach identifies large list of candidate genes associated with alcohol use disorder - study shows potential genetic link between <a href="https://twitter.com/hashtag/alcoholism?src=hash&amp;ref_src=twsrc%5Etfw">#alcoholism</a>, <a href="https://twitter.com/hashtag/Alzheimers?src=hash&amp;ref_src=twsrc%5Etfw">#Alzheimers</a> disease, &amp; other neurodegenerative disorders <a href="https://t.co/kzautcL6DN">https://t.co/kzautcL6DN</a><a href="https://twitter.com/hashtag/genetics?src=hash&amp;ref_src=twsrc%5Etfw">#genetics</a> <a href="https://t.co/nUNbvYf2L8">pic.twitter.com/nUNbvYf2L8</a></p> — Mount Sinai Genetics (@SinaiGenetics) <a href="https://twitter.com/SinaiGenetics/status/1428699409475309571?ref_src=twsrc%5Etfw">August 20, 2021</a></blockquote> <p><span style="font-weight: 400;">“Several of these genes are also associated with neurodegenerative disorders - an intriguing connection because of alcohol’s ability to prematurely age the brain,” David Goldman, a neurogenetics researcher at the National Institute on Alcohol Abuse and Alcoholism (NIAAA) told </span><span style="font-weight: 400;">The Scientist</span><span style="font-weight: 400;">.</span></p> <p><span style="font-weight: 400;">The scientists compared the genetic data of about 700,000 families involved in the NIAAA’s </span><a rel="noopener" href="https://www.niaaa.nih.gov/research/major-initiatives/collaborative-studies-genetics-alcoholism-coga-study" target="_blank"><span style="font-weight: 400;">Collaborative Studies on the Genetics of Alcoholism</span></a><span style="font-weight: 400;"> (COGA), as well as data from the </span><a rel="noopener" href="https://www.ukbiobank.ac.uk/enable-your-research/approved-research/alcohol-consumption-and-brain-health" target="_blank"><span style="font-weight: 400;">UK Biobank</span></a><span style="font-weight: 400;">, against analyses of adult and foetal brains to determine which genes were silenced or expressed.</span></p> <p><span style="font-weight: 400;">Though the study did identify many genes associated with alcohol use, the team focused on the two genes linked to neurodegenerative disorders: </span><em><span style="font-weight: 400;">SPI1</span></em><span style="font-weight: 400;"> and </span><em><span style="font-weight: 400;">MAPT</span></em><span style="font-weight: 400;">. </span></p> <p><em><span style="font-weight: 400;">SPI1</span></em><span style="font-weight: 400;"> produces a protein that controls the activity of immune cells, while </span><em><span style="font-weight: 400;">MAPT</span></em><span style="font-weight: 400;"> produces a protein found throughout the nervous system called tau.</span></p> <p><strong><em>SPI1</em> linked to Alzheimer’s</strong></p> <p><a rel="noopener" href="https://molecularneurodegeneration.biomedcentral.com/articles/10.1186/s13024-018-0277-1" target="_blank"><span style="font-weight: 400;">Previous research</span></a><span style="font-weight: 400;"> has shown that </span><em><span style="font-weight: 400;">SPI1</span></em><span style="font-weight: 400;"> influenced the likelihood of a person developing Alzheimer’s disease, with some theorising that it influences the activity of microglia, immune cells that are found in the brain.</span></p> <p><span style="font-weight: 400;">In a </span><a rel="noopener" href="https://www.nature.com/articles/s41398-019-0384-y" target="_blank"><span style="font-weight: 400;">study</span></a><span style="font-weight: 400;"> from two years ago, Manav Kapoor, a neuroscientist and geneticist at the Icahn School of Medicine at Mount Sinai and the new paper’s first author, and his team found evidence that people with AUD might have an overactive immune system - and this new paper could help explain their previous findings.</span></p> <p><span style="font-weight: 400;">The new study also found an association between the </span><em><span style="font-weight: 400;">SPI1</span></em><span style="font-weight: 400;"> gene and both heavy drinking and a diagnosis of AUD.</span></p> <p><span style="font-weight: 400;">Though alcoholism is already associated with immune dysfunction, the team found that expression of the </span><em><span style="font-weight: 400;">SPI1</span></em><span style="font-weight: 400;"> gene was higher in some foetal brains.</span></p> <p><span style="font-weight: 400;">Kapoor says this finding suggests that those genetically predisposed to AUD and heavy drinking are also predisposed to developing an overactive immune system.</span></p> <p><span style="font-weight: 400;">If this is the case, when people with particular versions of the gene drink heavily, Kapoor suggests that their immune systems could become overactivated and cause brain immune cells to alter connections between neurons.</span></p> <p><span style="font-weight: 400;">Kapoor bases this theory on a previous </span><a rel="noopener" href="https://stke.sciencemag.org/content/13/650/eaba5754" target="_blank"><span style="font-weight: 400;">study</span></a><span style="font-weight: 400;"> in mice that found that binge drinking activated brain immune cells, which selectively pruned certain synapses and caused the animals to display anxiety-like behaviours.</span></p> <p><span style="font-weight: 400;">The activation of these brain immune cells could result in the pruning of connections to neurons that produce dopamine - the chemical behind the “reward” feeling we get after drinking alcohol.</span></p> <p><span style="font-weight: 400;">As a result, people with certain versions of </span><em><span style="font-weight: 400;">SPI1</span></em><span style="font-weight: 400;"> who start drinking regularly would “have to drink more and more to get the same level of reward”, Kapoor says.</span></p> <p><span style="font-weight: 400;">“And their immune system will get more activated”, pruning more synapses.</span></p> <p><span style="font-weight: 400;">“It will become a vicious cycle,” Kapoor says.</span></p> <p><span style="font-weight: 400;">As for </span><em><span style="font-weight: 400;">MAPT</span></em><span style="font-weight: 400;">, the gene isn’t associated with AUD, but is associated with consuming more drinks per week.</span></p> <p><span style="font-weight: 400;">The tau protein it produces is thought to play a major role in neurodegenerative disorders including Alzheimer’s, Parkinson’s, frontotemporal dementia, and supranuclear palsy.</span></p> <p><span style="font-weight: 400;">However, it is still unclear how tau may factor into the consumption of alcohol.</span></p> <p><strong>Why this matters</strong></p> <p><span style="font-weight: 400;">Joel Gelernter, a geneticist and neurobiologist at Yale University School of Medicine, who was not involved in the study, says the study is “a really necessary step in unravelling the biology of alcohol intake and alcohol use disorder”.</span></p> <p><span style="font-weight: 400;">Kapoor says this work could benefit people in a few ways.</span></p> <p><span style="font-weight: 400;">First, he believes that drugs currently in development to treat neurodegenerative disorders could be repurposed to help people in reducing or stopping drinking.</span></p> <p><span style="font-weight: 400;">Second, it could be a way of reducing a person’s risk for neurodegenerative disorders.</span></p> <p><span style="font-weight: 400;">“If we can identify some group of people that are more at risk of Alzheimer’s disease, we can ask them to reduce their drinking,” he says.</span></p> <p><span style="font-weight: 400;">“That might be beneficial to them.”</span></p> <p><em><span style="font-weight: 400;">Image: Getty Images</span></em></p>

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A genetic mutation makes some people need less sleep

<p><span style="font-weight: 400;">Though most of us feel the consequences of missing out on a full night’s sleep, a lucky few don’t - thanks to a rare genetic mutation.</span></p> <p><span style="font-weight: 400;">According to a study published in </span><em><a rel="noopener" href="https://www.cell.com/neuron/fulltext/S0896-6273(19)30652-X" target="_blank"><span style="font-weight: 400;">Neuron</span></a></em><span style="font-weight: 400;">, some people who can function normally on six hours of sleep carry an altered version of a particular gene, making it the second to be associated with short sleep.</span></p> <p><span style="font-weight: 400;">In their previous research in </span><a rel="noopener" href="https://science.sciencemag.org/content/325/5942/866" target="_blank"><span style="font-weight: 400;">2009</span></a><span style="font-weight: 400;">, the team found a mother and daughter - who felt rested after about six hours of sleep at night - both had a mutation in a gene called </span><em><span style="font-weight: 400;">DEC2</span></em><span style="font-weight: 400;">.</span></p> <p><span style="font-weight: 400;">The </span><em><span style="font-weight: 400;">DEC2</span></em><span style="font-weight: 400;"> gene codes for a protein that stops other genes from expressing. One of these genes that the protein inhibits controls a hormone called orexin, which is known to regulate wakefulness.</span></p> <p><span style="font-weight: 400;">In the follow-up study, the scientists studied another family of naturally short sleepers and have identified another mutation, which they estimate about four in every 100,000 people have.</span></p> <p><span style="font-weight: 400;">The scientists engineered mice to have the same mutation and found that they slept, on average, one hour less per day than control mice without the mutation.</span></p> <p><span style="font-weight: 400;">For the family of humans with the mutation, they slept an average of two hours less per day than those without the mutation.</span></p> <p><span style="font-weight: 400;">The mutated gene, called </span><em><span style="font-weight: 400;">ADRB1</span></em><span style="font-weight: 400;">, encodes a receptor for a neural signalling molecule called noradrenaline.</span></p> <p><span style="font-weight: 400;">In mouse brains, the cells that had this receptor were active while they were awake and quiet during deep sleep, according to the researchers.</span></p> <p><span style="font-weight: 400;">They propose that the mutation makes these neurons more active, which could explain why its human carriers sleep for shorter periods of time.</span></p> <p><span style="font-weight: 400;">Though this research has been conducted on small groups, it could pave the way for the development of drugs that target these kinds of mutations or help those with sleeping disorders feel better while getting little sleep.</span></p>

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Can COVID vaccines affect my genetic code?

<p>The Pfizer and Moderna vaccines are set to become the mainstay of Australia’s COVID-19 vaccine rollout as the year progresses, according to the latest government projections <a href="https://www.abc.net.au/news/2021-06-23/gov-projects-little-need-for-astrazeneca-after-october-covid19/100239442">released this week</a>.</p> <p><a href="https://www.health.gov.au/sites/default/files/documents/2021/06/covid-19-vaccination-covid-vaccination-allocations-horizons.pdf">From September</a>, up to an average 1.3m doses of the Pfizer vaccine plus another 125,000 doses of the yet-to-be approved Moderna vaccine are expected to be available per week. These figures are set to rise from October, as use of the AstraZeneca vaccine drops.</p> <p>Both the Pfizer and Moderna vaccines are mRNA vaccines, which contain tiny fragments of the genetic material known as “messenger ribonucleic acid”. And if social media is anything to go by, <a href="https://twitter.com/AJ19803/status/1334476726022385666">some people</a> are concerned these vaccines can affect their genetic code.</p> <p>Here’s why the chances of that happening are next to zero and some pointers to how the myth came about.</p> <p><strong>Remind me, how do mRNA vaccines work?</strong></p> <p>The technology used in the Pfizer and Moderna vaccines is a way of giving your cells temporary instructions to make the <a href="https://theconversation.com/revealed-the-protein-spike-that-lets-the-2019-ncov-coronavirus-pierce-and-invade-human-cells-132183">coronavirus spike protein</a>. This protein is found on the surface of SARS-CoV-2, the virus that causes COVID-19. The vaccines teach your immune system to protect you if you ever encounter the virus.</p> <p>The mRNA in the vaccine is taken up by the cells in your body, ending up in the liquid inside each cell known as the cytoplasm. Our cells naturally make <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3941114/">thousands of our own mRNAs</a> all the time (to code for a range of other proteins). So the vaccine mRNA is just another one. Once the vaccine mRNA is in the cytoplasm it’s used to make the SARS-CoV-2 spike protein.</p> <p>The vaccine mRNA is <a href="https://theconversation.com/what-is-mrna-the-messenger-molecule-thats-been-in-every-living-cell-for-billions-of-years-is-the-key-ingredient-in-some-covid-19-vaccines-158511">short-lived</a> and is rapidly broken down after it’s done its job, as happens with all your other mRNA.</p> <p><a rel="noopener" href="https://images.theconversation.com/files/408058/original/file-20210624-13-1w14e5y.jpg?ixlib=rb-1.1.0&amp;q=45&amp;auto=format&amp;w=1000&amp;fit=clip" target="_blank"><img src="https://images.theconversation.com/files/408058/original/file-20210624-13-1w14e5y.jpg?ixlib=rb-1.1.0&amp;q=45&amp;auto=format&amp;w=754&amp;fit=clip" alt="Typical mammalian cell, showing different parts, such as nucleus and cytoplasm" /></a></p> <p><span class="caption">Vaccine mRNA is in the cytoplasm and once it’s done its job, it’s broken down.</span> </p> <p><strong>Here’s why the mRNA can’t insert into your genetic code</strong></p> <p> </p> <p>Your genetic code is made up of a different, but related, molecule to the vaccine mRNA, known as DNA, or deoxyribonucleic acid. And mRNA can’t insert itself into your DNA for two reasons.</p> <p>One, both molecules have a different chemistry. If mRNAs could routinely insert themselves into your DNA at random, this would play havoc with how you produce proteins. It would also scramble your genome, which is passed on to future cells and generations. Life forms that do this would not survive. That’s why life has evolved for this <em>not</em> to happen.</p> <p>The second reason is vaccine mRNA and DNA are in two different parts of the cell. Our DNA stays in the nucleus. But vaccine mRNA goes straight to the cytoplasm, never entering the nucleus. There are no transporter molecules we know of that carry mRNA into the nucleus.</p> <p><strong>But aren’t there some exceptions?</strong></p> <p>There are some extremely rare exceptions. One is where genetic elements, known as <a href="https://www.nature.com/scitable/topicpage/transposons-the-jumping-genes-518/">retro-transposons</a>, hijack cellular mRNA, convert it into DNA and insert that DNA back into your genetic material.</p> <p>This has occurred sporadically <a href="https://www.nature.com/articles/nrg2640">throughout evolution</a>, producing some ancient copies of mRNAs scattered throughout our genome, to form so-called <a href="https://www.nature.com/articles/s41576-019-0196-1">pseudogenes</a>.</p> <p>Some <a href="https://www.genome.gov/genetics-glossary/Retrovirus">retroviruses</a>, such as HIV, also insert their RNA into our DNA, using similar methods to retro-transposons.</p> <p>However, there is a vanishingly small chance of a naturally occurring retro-transposon becoming active in a cell that has just received a mRNA vaccine. There’s also a vanishingly small chance of being infected with HIV at precisely the same time as receiving the mRNA vaccine.</p> <p><a href="https://images.theconversation.com/files/408059/original/file-20210624-29-gcexgw.jpg?ixlib=rb-1.1.0&amp;q=45&amp;auto=format&amp;w=1000&amp;fit=clip"><img src="https://images.theconversation.com/files/408059/original/file-20210624-29-gcexgw.jpg?ixlib=rb-1.1.0&amp;q=45&amp;auto=format&amp;w=754&amp;fit=clip" alt="Blood sample labelled with HIV - Test" /></a></p> <p><span class="caption">There’s a vanishingly small chance of being infected with HIV at precisely the same time as having an mRNA vaccine.</span> </p> <p>Even if a retro-transposon were to become active or a virus such as HIV were present, the chances of it finding the COVID vaccine mRNA, among the tens of thousands of natural mRNAs, is extremely unlikely. That’s because vaccine mRNA is degraded within <a href="https://pubmed.ncbi.nlm.nih.gov/18797453/">several hours</a> of entering the body.</p> <p>Even if vaccine mRNA did become a pseudogene, it would not produce the SARS-CoV-2 virus, but just one of the viral products, the harmless spike protein.</p> <p><strong>How do we actually know this?</strong></p> <p> </p> <p>We know of no studies looking for vaccine mRNA in the DNA of people who have been vaccinated. There is no scientific basis on which to suspect this insertion has happened.</p> <p>However, if these studies were to be carried out, they should be relatively straightforward. That’s because we can now <a href="https://cellandbioscience.biomedcentral.com/articles/10.1186/s13578-019-0314-y">sequence DNA in single cells</a>.</p> <p>But in reality, it will be very hard to ever satisfy a naysayer who is convinced this genome insertion happens; they can always argue scientists need to look deeper, harder, in different people and in different cells. At some point this argument will need to be laid to rest.</p> <p><strong>So how did this myth come about?</strong></p> <p><a href="https://doi.org/10.1073/pnas.2105968118">One study</a> reported evidence for coronavirus RNA integrating into the human genome in cells grown in the lab that had been infected with SARS-CoV-2.</p> <p>However, that paper did not look at the mRNA vaccine, lacked critical controls and <a href="https://www.biorxiv.org/content/10.1101/2021.03.05.434119v1">has</a> <a rel="noopener" href="https://doi.org/10.1128/JVI.00294-21" target="_blank">since been discredited</a>.</p> <p>These types of studies also need to be seen in context of the public’s wariness of genetic technology more broadly. This includes <a rel="noopener" href="https://www.nature.com/articles/nbt1099_941d" target="_blank">the public’s concerns</a> about genetically modified organisms (GMOs), for instance, over the past 20 years or so.</p> <p>But GMOs are different to the mRNA technology used to make COVID vaccines. Unlike GMOs, which are produced by inserting DNA into the genome, vaccine mRNA will not be in our genes or passed to the next generation. It’s broken down very quickly.</p> <p>In reality, mRNA technology has <a href="https://theconversation.com/3-mrna-vaccines-researchers-are-working-on-that-arent-covid-157858">all sorts of</a> <a href="https://www.wired.co.uk/article/mrna-vaccine-revolution-katalin-kariko">applications</a>, beyond vaccines, including biosecurity and sustainable agriculture. So it would be a pity for these efforts to be held back by misinformation.</p> <p> </p> <p><span><a href="https://theconversation.com/profiles/archa-fox-1153308">Archa Fox</a>, Associate Professor and ARC Future Fellow, <em><a href="https://theconversation.com/institutions/the-university-of-western-australia-1067">The University of Western Australia</a></em>; <a href="https://theconversation.com/profiles/jen-martin-17007">Jen Martin</a>, Leader, Science Communication Teaching Program, <em><a href="https://theconversation.com/institutions/the-university-of-melbourne-722">The University of Melbourne</a></em>, and <a href="https://theconversation.com/profiles/traude-beilharz-1240711">Traude Beilharz</a>, Assoc Professor ARC Future Fellow, Biochemistry &amp; Molecular Biology, Monash Biomedicine Discovery Institute, <em><a href="https://theconversation.com/institutions/monash-university-1065">Monash University</a></em></span></p> <p>This article is republished from <a href="https://theconversation.com">The Conversation</a> under a Creative Commons license. Read the <a rel="noopener" href="https://theconversation.com/can-the-pfizer-or-moderna-mrna-vaccines-affect-my-genetic-code-162590" target="_blank">original article</a>.</p>

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