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"I'm going rogue": Kochie gives away $3000 moments after quitting Sunrise

<p dir="ltr">When <em>Sunrise </em>host of 21 years David ‘Kochie’ Koch announced that <a href="https://www.oversixty.com.au/news/news/the-world-s-best-job-kochie-quits-sunrise">he would be parting ways with the popular breakfast TV show</a>, it should have been safe to assume that that was the only shock in store for viewers. </p> <p dir="ltr">However, Kochie had other ideas, making a bold - and generous - move, all while hinting that there was plenty more in store for his final two weeks at the helm with co-host Natalie Barr.</p> <p dir="ltr">The two were running the segment known as Bill Barrel when things took a turn, with Kochie explaining how “the rising cost of living is putting pressure on Aussies right across the country”, and how the team over at <em>Sunrise </em>wanted to offer relief and support where they could.</p> <p dir="ltr">“So,” Natalie added, “we are paying your bills.” </p> <p dir="ltr">The pair proceeded to spin the barrel, before pulling out a sheet of paper with the name of their lucky recipient - Melanie Turner from Brisbane. </p> <p dir="ltr">They were quick to get a delighted Melanie on the phone, and Kochie was all too eager to declare “congratulations, you’re this morning’s Bill Barrel winner!” </p> <p dir="ltr">Melanie, of course, thanked them for the happy surprise, before Natalie asked just what it was that she needed to pay off. </p> <p dir="ltr">“It’s my car rego,” Melanie said, “[it’s] due today, as a matter of fact.”</p> <p dir="ltr">She then revealed that her bill came to a total of $520 - an amount she was immensely grateful to be receiving. </p> <p dir="ltr">But that wasn’t the end of Melanie’s good fortune, with Natalie sharing “we’re feeling generous. Kochie’s feeling generous. He’s giving away cash today. We’re going to give you $1500 to help with that.” </p> <p dir="ltr">The $1500 should have been the most Melanie could take home to help with her bill, as the competition’s own terms and conditions list the sum as the “total maximum prize value”, but fate - or one rogue TV presenter - had more in store. </p> <p dir="ltr">Before Melanie had a chance to properly celebrate, Kochie cut in, declaring “I’ve only got two weeks to go. I’m going rogue. We’re going to do three grand.” </p> <p dir="ltr">As laughter broke out across the studio, and Melanie struggled to find the words, Kochie reiterated the prize, assuring Natalie that he was sure - even as she noted that she had “someone in my ear”. </p> <p dir="ltr">“I’m going to go rogue every day,” he continued, “for the next two weeks.”</p> <p dir="ltr"><em>Images: Sunrise / Seven</em></p>

Money & Banking

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What the “father of the cell phone” wants you to know

<p dir="ltr">The inventor of the mobile phone has shared his candid opinion about the obsession with smart devices. </p> <p dir="ltr">Martin Cooper, an American engineer dubbed the “father of the cell phone”, invented the very first mobile phone 50 years ago in 1973. </p> <p dir="ltr">Back then, the weighty block of wires and circuits were only used to make calls, a far cry from having the world at your fingertips with smartphones today. </p> <p dir="ltr">Cooper believes that despite all the good that can come from modern technology, the world has become a little obsessed with smart devices. </p> <p dir="ltr">“I am devastated when I see somebody crossing the street and looking at their cell phone. They are out of their minds,” the 94-year-old told AFP from his office in Del Mar, California.</p> <p dir="ltr">“But after a few people get run over by cars, they’ll figure it out,” he joked.</p> <p dir="ltr">Mr Cooper also indulges in the latest gadgets, as he wears an Apple Watch and uses a top-end iPhone, flicking intuitively between his email, photos, YouTube and the controls for his hearing aid.</p> <p dir="ltr">Despite keeping up with all the latest apps, updates and upgrades, he confessed that sometimes it can all seem a little overwhelming. </p> <p dir="ltr">“I will never, ever understand how to use the cell phone the way my grandchildren and great grandchildren do,” he said.</p> <p dir="ltr">“Each generation is going to be smarter … they will learn how to use the cell phone more effectively,” he said.</p> <p dir="ltr">“Humans sooner or later figure it out.”</p> <p dir="ltr"><em>Image credits: Getty Images</em></p>

Technology

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Carrie Bickmore cops a warning after going rogue on air

<p>Carrie Bickmore has reportedly copped a tense warning after making a big cash offer live on her radio show. </p> <p>The radio presenter, along with her co-host Tommy Little, were partaking in a long-running segment called The Time Game, in which listeners call in and try to guess when a stopwatch reaches exactly 5.00 seconds.</p> <p>The game, which regularly airs on their Hit Network drive show <em>Carrie and Tommy</em>, has never actually been won in the three years that the duo have been inviting listeners to play, with the cash prize rising by $100 each time the game remained unbeaten.</p> <p>During Wednesday's show, the game was commencing when Carrie decided to raise the stakes for listeners, without previously clearing her rogue idea with the radio powers that be.</p> <p>The hosts shared that the cash prize has risen to a whopping $10,000, when Bickmore decided to add another $20,000 to the prize money before listener Nick was invited to play. </p> <p>“Because our show starts at three, I’m timesing it by three: thirty grand on the line today,” Bickmore announced. “I just think it’s what people want.”</p> <p>Tommy Little seemed stunned at this sudden leap in the prize money on offer, asking his co-host, “Have you been hitting the bottle early?” and noting that their boss was “shaking her head.”</p> <p>“I’m not looking at her. If I’m not looking at her, it won’t be a problem,” Bickmore said.</p> <p>Minutes later, with the game still yet to be played, Bickmore revealed that her announcement had sent the show’s bosses into a frenzy.</p> <p>“There’s been a few meetings that’s been happening off-air in the last 10 minutes with bosses going, ‘You can’t just go saying things on-air that we can’t fulfil.’ I will fulfil it. If they can’t, I will.”</p> <p>In a spectacular twist, as Nick began to play the game, he called stop just as the stopwatch hit five seconds exactly. </p> <p>“Oh Nick, I didn’t run this past the bosses at all … I just went rogue and said $30,000 and now I’ve … oh my god, oh my god,” Bickmore said. </p> <p>“I’m so excited by this, but I’m slightly terrified, because I’m not sure if it’s my money or the company’s money that you’re about to take.”</p> <p>Thankfully for Bickmore, the Hit Network covered the $30,000 prize money, according to a statement shared to <em><a href="https://www.news.com.au/entertainment/tv/radio/tense-meetings-after-carrie-bickmore-goes-rogue-with-big-cash-offer-onair/news-story/462716cd6ad770c7dec38c912f54a2d5" target="_blank" rel="noopener">news.com.au</a></em>.</p> <p><em>Image credits: Hit Network</em></p> <div class="AV62af35d851923c62777207b4" style="box-sizing: inherit; margin: 0px auto; font-family: 'Helvetica Neue', HelveticaNeue, Helvetica, Arial, sans-serif; font-size: 18px; width: 705.202209px;"> <div id="aniBox" style="box-sizing: inherit; overflow: hidden; transition: height 1s ease 0s; opacity: 0; width: 705px; height: 1px;"> <div id="aniplayer_AV62af35d851923c62777207b4-1677109384997" style="box-sizing: inherit;"> <div id="aniplayer_AV62af35d851923c62777207b4-1677109384997gui" style="box-sizing: inherit;"> <div id="av-caption" style="box-sizing: inherit; position: relative; text-align: center; line-height: 18px; width: 705px;"> <div id="av-close-btn-overlay" class="av-pos-top-left" style="box-sizing: inherit; display: inline-block; position: relative; z-index: 9999999; vertical-align: top; padding: 30px; margin: -30px; float: left;"> <div id="av-close-btn" style="box-sizing: inherit; z-index: 9999999; position: static; top: 0px; left: 0px; width: 18px; height: 18px; background-color: rgba(0, 0, 0, 0.4); background-size: 60%; border: none; transition: all 0.15s ease-in-out 0s; background-position: center center; background-repeat: no-repeat no-repeat;"></div> </div> <p><span id="av-label" style="box-sizing: inherit; display: inline-block; text-transform: uppercase; font-size: 9px; color: #bbbbbb; z-index: 83; vertical-align: top; font-family: Helvetica, Arial, fallback, sans-serif; line-height: 10px; margin: 0px; padding: 4px;"></span></div> </div> </div> </div> </div>

News

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Passenger killed after “rogue wave” strikes cruise ship

<p dir="ltr">An elderly woman has died and four others have been injured after a massive wave struck a cruise ship sailing towards southern Argentina at the end of its Antarctic cruise.</p> <p dir="ltr">The Viking Polaris was struck by a wave that broke cabin windows during a storm on its return to the port of Ushuaia last week, according to Argentinian authorities.</p> <p dir="ltr">While the ship suffered minimal damage, the 62-year-old US woman who was hit by broken glass died.</p> <p dir="ltr">“It is with great sadness that we confirm a guest passed away following the incident,” Viking said in a statement.</p> <p dir="ltr">“We have notified the guest’s family and shared our deepest sympathies.”</p> <p dir="ltr">The cruise operator described it as a “rogue wave incident” and confirmed that four other cruise goers suffered non-life threatening injuries and received treatment from the doctor and medical staff on board the ship.</p> <p dir="ltr">With a federal court opening a case into the incident, the cruise ship has been anchored at Ushuaia.</p> <p dir="ltr">Viking has also said it would investigate the incident and “offer our support to the relevant authorities”.</p> <p dir="ltr">“Our focus remains on the safety and wellbeing of our guests and crew, and we are working directly with them to arrange return travel,” the <a href="https://www.vikingcruises.co.uk/expeditions/my-trip/current-sailings/index.html">statement</a> from Thursday, December 1, read.</p> <p dir="ltr">The company has also cancelled its scheduled voyage to Antarctica, which was due to depart from December 5-17.</p> <p dir="ltr">The Polaris, built this year, features luxury facilities and has capacity for 378 passengers and 256 crew members.</p> <p dir="ltr">It is one of two ships Viking has for its cruises, which explore remote regions of the world.</p> <p><span id="docs-internal-guid-1e04ff18-7fff-c693-9593-a1335e57307f"></span></p> <p dir="ltr"><em>Image: Getty Images</em></p>

Cruising

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Long COVID: How lost connections between nerve cells in the brain may explain cognitive symptoms

<p>For a portion of people who get COVID, symptoms continue for <a href="https://www.ons.gov.uk/peoplepopulationandcommunity/healthandsocialcare/conditionsanddiseases/bulletins/prevalenceofongoingsymptomsfollowingcoronaviruscovid19infectionintheuk/6october2022" target="_blank" rel="noopener">months or even years</a> after the initial infection. This is commonly referred to as “long COVID”.</p> <p>Some people with long COVID complain of “<a href="https://theconversation.com/what-is-and-what-isnt-brain-fog-190537" target="_blank" rel="noopener">brain fog</a>”, which includes a wide variety of cognitive symptoms affecting memory, concentration, sleep and speech. There’s also growing concern about findings that people who have had COVID are at <a href="https://www.thelancet.com/journals/lanpsy/article/PIIS2215-0366(22)00260-7/fulltext" target="_blank" rel="noopener">increased risk</a> of developing brain disorders, such as dementia.</p> <p>Scientists are working to understand how exactly a COVID infection affects the human brain. But this is difficult to study, because we can’t experiment on living people’s brains. One way around this is to create <a href="https://www.nature.com/articles/s41578-021-00279-y" target="_blank" rel="noopener">organoids</a>, which are miniature organs grown from stem cells.</p> <p>In a <a href="https://www.nature.com/articles/s41380-022-01786-2.pdf" target="_blank" rel="noopener">recent study</a>, we created brain organoids a little bigger than a pinhead and infected them with SARS-CoV-2, the virus that causes COVID-19.</p> <p>In these organoids, we found that an excessive number of synapses (the connections between brain cells) were eliminated – more than you would expect to see in a normal brain.</p> <p>Synapses are important because they allow neurons to communicate with each other. Still, the elimination of a certain amount of inactive synapses is part of normal brain function. The brain essentially gets rid of old connections when they’re no longer needed, and makes way for new connections, allowing for more efficient functioning.</p> <p>One of the crucial functions of the brain’s immune cells, or <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5768411/" target="_blank" rel="noopener">microglia</a>, is to prune these inactive synapses.</p> <p>The exaggerated elimination of synapses we saw in the COVID-infected models could explain why some people have cognitive symptoms as part of long COVID.</p> <p><strong>Parallels with neurodegenerative disorders</strong></p> <p>Interestingly, this pruning process is believed to go awry in several disorders affecting the brain. In particular, excessive elimination of synapses has recently been linked to <a href="https://www.nature.com/articles/s41593-018-0334-7" target="_blank" rel="noopener">neurodevelopmental disorders</a> such as <a href="https://www.nature.com/articles/s41593-018-0334-7" target="_blank" rel="noopener">schizophrenia</a>, as well as <a href="https://www.frontiersin.org/articles/10.3389/fncel.2019.00063/full" target="_blank" rel="noopener">neurodegenerative disorders</a> such as Alzheimer’s and Parkinson’s disease.</p> <p>By sequencing the RNA of single cells, we could study how different cell types in the organoid responded to the virus. We found that the pattern of genes turned on and off by the microglia in our COVID-infected organoids mimicked changes seen in neurodegenerative disorders.</p> <p>This may go some way in explaining the link between COVID and the risk of developing certain neurological disorders.</p> <figure class="align-center "><img src="https://images.theconversation.com/files/491380/original/file-20221024-17-9wi5pg.png?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/491380/original/file-20221024-17-9wi5pg.png?ixlib=rb-1.1.0&amp;q=45&amp;auto=format&amp;w=600&amp;h=338&amp;fit=crop&amp;dpr=1 600w, https://images.theconversation.com/files/491380/original/file-20221024-17-9wi5pg.png?ixlib=rb-1.1.0&amp;q=30&amp;auto=format&amp;w=600&amp;h=338&amp;fit=crop&amp;dpr=2 1200w, https://images.theconversation.com/files/491380/original/file-20221024-17-9wi5pg.png?ixlib=rb-1.1.0&amp;q=15&amp;auto=format&amp;w=600&amp;h=338&amp;fit=crop&amp;dpr=3 1800w, https://images.theconversation.com/files/491380/original/file-20221024-17-9wi5pg.png?ixlib=rb-1.1.0&amp;q=45&amp;auto=format&amp;w=754&amp;h=425&amp;fit=crop&amp;dpr=1 754w, https://images.theconversation.com/files/491380/original/file-20221024-17-9wi5pg.png?ixlib=rb-1.1.0&amp;q=30&amp;auto=format&amp;w=754&amp;h=425&amp;fit=crop&amp;dpr=2 1508w, https://images.theconversation.com/files/491380/original/file-20221024-17-9wi5pg.png?ixlib=rb-1.1.0&amp;q=15&amp;auto=format&amp;w=754&amp;h=425&amp;fit=crop&amp;dpr=3 2262w" alt="" /><figcaption><span class="caption">A brain organoid used in our study. You can see the microglial cells in red.</span> <span class="attribution"><span class="source">Sellgren lab</span>, <span class="license">Author provided</span></span></figcaption></figure> <p><strong>A possible target for treatment</strong></p> <p>One limitation of our research is that our organoid models closely resemble the foetal or early brain, rather than the adult brain. So we can’t say for sure whether the changes we noted in our study will necessarily be reflected in the adult brain.</p> <p>However, some <a href="https://pubmed.ncbi.nlm.nih.gov/33248159/" target="_blank" rel="noopener">post-mortem</a> and <a href="https://pubmed.ncbi.nlm.nih.gov/35255491/" target="_blank" rel="noopener">imaging studies</a> report neuronal death and reduction in grey matter thickness in COVID patients, which hints at similar instances of synapse loss caused by an infection in adults.</p> <p>If this proves to be a fruitful line of enquiry, we believe our findings could point to a mechanism contributing to persisting cognitive symptoms after COVID and other viral infections that affect the brain.</p> <p>SARS-CoV-2 is an RNA virus and similar <a href="https://pubmed.ncbi.nlm.nih.gov/27337340/" target="_blank" rel="noopener">processes</a> have been seen in mice infected with other RNA viruses that can also cause residual cognitive symptoms, such as the <a href="https://pubmed.ncbi.nlm.nih.gov/31235930/" target="_blank" rel="noopener">West Nile virus</a>.</p> <p>From here we want to study how different drugs could inhibit the changes we saw in the infected models, hopefully paving the way towards effective treatments. In <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6410571/">other research</a>, we’ve observed that an antibiotic called minocycline can reduce the degree to which microglia prune synapses in a dish. So we want to see if this drug can help in our brain organoid models following SARS-CoV-2 infection.<!-- Below is The Conversation's page counter tag. Please DO NOT REMOVE. --><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/192702/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1" /><!-- End of code. If you don't see any code above, please get new code from the Advanced tab after you click the republish button. The page counter does not collect any personal data. More info: https://theconversation.com/republishing-guidelines --></p> <p><em>Writen by Samudyata and </em><em>Carl Sellgren</em><em>. Republished with permission from <a href="https://theconversation.com/long-covid-how-lost-connections-between-nerve-cells-in-the-brain-may-explain-cognitive-symptoms-192702" target="_blank" rel="noopener">The Conversation</a>.</em></p> <p><em>Image: Getty Images</em></p>

Mind

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Brain cells in a dish learnt to play Pong

<p dir="ltr">In a feat that reads like the plot of a science fiction movie, scientists have been able to get a collection of brain cells living in a dish to play a video game.</p> <p dir="ltr">The team were able to prove that their collection of 800,000 neurons, which they call DishBrain, could perform goal-directed tasks, including playing the popular tennis-like game Pong.</p> <p dir="ltr">To create DishBrain, they took brain cells from mouse embryos, along with some human brain cells created from stem cells, and grew them on top of microelectrode arrays.</p> <p dir="ltr">These arrays are capable of both reading the signals these cells produce and stimulating the cells - allowing them to play a cheeky game of Pong.</p> <p dir="ltr">Electrodes on the left and right of the array told the cells which side the ball was on, while the frequency of signals told them how far the ball was from the paddle.</p> <p dir="ltr">“The beautiful and pioneering aspect of this work rests on equipping the neurons with sensations — the feedback — and crucially the ability to act on their world,” says co-author Professor Karl Friston, a theoretical neuroscientist at UCL, London.</p> <p dir="ltr">“Remarkably, the cultures learned how to make their world more predictable by acting upon it. This is remarkable because you cannot teach this kind of self-organisation; simply because — unlike a pet — these mini brains have no sense of reward and punishment."</p> <p dir="ltr">Having published their findings in the journal <em><a href="https://doi.org/10.1016/j.neuron.2022.09.001" target="_blank" rel="noopener">Neuron</a></em>, they now plan to find out what happens when they give DishBrain medicines and alcohol.</p> <p dir="ltr">“We’re trying to create a dose response curve with ethanol – basically get them ‘drunk’ and see if they play the game more poorly, just as when people drink,” lead author Dr Brett Kagan, the Chief Scientific Officer of the biotech start-up Cortical Labs, says.</p> <p dir="ltr">Because DishBrain was built using basic structures, rather than being modelled on AI, it can be used to understand how our brains function.</p> <p dir="ltr">“In the past, models of the brain have been developed according to how computer scientists think the brain might work,” Kagan explains. </p> <p dir="ltr">“That is usually based on our current understanding of information technology, such as silicon computing.</p> <p><span id="docs-internal-guid-8d90678c-7fff-f57f-0817-60d1c6980ffc"></span></p> <p dir="ltr">“But in truth we don’t really understand how the brain works.”</p> <p dir="ltr"><img src="https://oversixtydev.blob.core.windows.net/media/2022/10/dishbrain-gif1.gif" alt="" width="1326" height="946" /></p> <p dir="ltr"><em>DishBrain viewed under a microscope, where fluorescent markers show different kinds of cells. Where multiple markers appear, the colours merge and look yellow or pink. Image: Cortical Labs</em></p> <p dir="ltr">Dr Adeel Razi, the Director of Monash University’s Computational &amp; Systems Neuroscience Laboratory, says this experiment could open the door for more discoveries.</p> <p dir="ltr">“This new capacity to teach cell cultures to perform a task in which they exhibit sentience – by controlling the paddle to return the ball via sensing – opens up new discovery possibilities which will have far-reaching consequences for technology, health, and society,” he says.</p> <p dir="ltr">“We know our brains have the evolutionary advantage of being tuned over hundreds of millions of years for survival. </p> <p dir="ltr">"Now, it seems we have in our grasp where we can harness this incredibly powerful and cheap biological intelligence.”</p> <p dir="ltr">The creation of DishBrain also creates the possibility for an alternative to animal testing for scientists investigating how new drugs work and gain insights into how conditions such as epilepsy and dementia affect our brains.</p> <p dir="ltr">“This is brand new, virgin territory. And we want more people to come on board and collaborate with this, to use the system that we’ve built to further explore this new area of science,” Dr Hon Weng Chong, Chief Executive Officer of Cortical Labs, says.</p> <p dir="ltr"><span id="docs-internal-guid-7ca96709-7fff-9046-4ac1-c1ed62769dbc"></span></p> <p dir="ltr">“As one of our collaborators said, it's not every day that you wake up and you can create a new field of science.”</p> <p dir="ltr"><em>Images: Cortical Labs / Flickr</em></p>

Mind

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Scientists have mimicked an embryo’s heart to unlock the secrets of how blood cells are born

<p>Stem cells are the starting point for all other cells in our bodies. The <a href="https://www.eurostemcell.org/blood-stem-cells-pioneers-stem-cell-research" target="_blank" rel="noopener">first such cells to be found</a> were blood stem cells – as the name suggests, they give rise to different types of blood cells.</p> <p>But there’s much we don’t know about how these cells develop in the first place. In a study published today in <a href="https://doi.org/10.1016/j.celrep.2022.111339" target="_blank" rel="noopener">Cell Reports</a>, we have shown how a lab simulation of an embryo’s beating heart and circulation lead to the development of human blood stem cell precursors.</p> <p>The tiny device mimics embryonic blood flow, allowing us to directly observe human embryonic blood formation under the microscope. These results may help us understand how we can produce life-saving therapies for patients who need new blood stem cells.</p> <h2>Growing life-saving therapies in the lab</h2> <p>To treat aggressive blood cancers such as leukaemia, patients often need extremely high doses of chemotherapy; a <a href="https://www.cancer.nsw.gov.au/myeloma/diagnosis-and-treatment/treatment/types-of-treatment/stem-cell-transplant#:%7E:text=A%20stem%20cell%20transplant%20involves%20killing%20blood%20cells,they%20are%20collected%20beforehand%20and%20kept%20in%20storage." target="_blank" rel="noopener">blood stem cell transplant</a> then regenerates blood after the treatment. These are life-saving therapies but are restricted to patients who have a suitable tissue-matched donor of blood stem cells.</p> <p>A way around this problem would be to grow more blood stem cells in the lab. Unfortunately, past experiments have shown that harvested adult blood stem cells lose their transplantation potential if grown in the lab.</p> <p>The discovery of <a href="https://en.wikipedia.org/wiki/Induced_pluripotent_stem_cell" target="_blank" rel="noopener">induced pluripotent stem cells</a> – stem cells made out of adult cells – in 2006 led to a promising new approach. Induced pluripotent stem cells are made from the patient’s own cells, so there is no problem with tissue rejection, or the ethical issues surrounding the use of IVF embryos.</p> <p>These cell lines are similar to embryonic stem cells, so they have the potential to form any tissue or cell type – hence, they are “pluripotent”. In theory, pluripotent stem cell lines could provide an unlimited supply of cells for blood regeneration because <a href="https://en.wikipedia.org/wiki/Immortalised_cell_line" target="_blank" rel="noopener">they are immortalised</a> – they can grow in the lab indefinitely.</p> <p>But the development of processes to allow us to grow particular types of tissues, organs and cell types – such as blood – has been slow and will take decades to advance. One must mimic the complex process of embryogenesis in the dish!</p> <h2>Engineering an embryonic heart</h2> <p>Current understanding of how embryonic blood stem cells develop is based on animal models. Experiments with anaesthetised zebrafish embryos have shown that blood stem cells arise in the wall of <a href="https://pubmed.ncbi.nlm.nih.gov/20154733/" target="_blank" rel="noopener">the main blood vessel, the aorta</a>, shortly after the first heartbeat. For ethical reasons, it’s obvious this type of study is not possible in human embryos.</p> <p>This is why we wanted to engineer an embryonic heart model in the lab. To achieve this, we used <a href="https://www.elveflow.com/microfluidic-reviews/general-microfluidics/a-general-overview-of-microfluidics/" target="_blank" rel="noopener">microfluidics</a> – an approach that involves manipulating extremely small volumes of liquids.</p> <p>The first step in generating blood stem cells from pluripotent stem cells is to coax the latter to form the site where blood stem cells start growing. This is known as the AGM region (aorta-gonad-mesonephros) of the embryo.</p> <p>Our miniature heart pump and circulation (3 by 3 centimetres) mimics the mechanical environment in which blood stem cells form in the human embryo. The device pumps culture media – liquids used to grow cells – around a microfluidic circuit to copy what the embryo heart does.</p> <h2>A step closer to treatment</h2> <p>Once we got the cells to form the AGM region by stimulating cells on day two of starting our cell culture, we applied what’s known as pulsatile circulatory flow from day 10 to day 26. Blood precursors entered the artificial circulation from blood vessels lining the microfluidic channels.</p> <p>Then, we harvested the circulating cells and grew them in culture, showing that they developed into various blood components – white blood cells, red blood cells, platelets, and others. In-depth analysis of gene expression in single cells showed that circulatory flow generated aortic and blood stem precursor cells found in the AGM of human embryos.</p> <p>This means our study has shown how pulsatile circulatory flow enhances the formation of blood stem cell precursors from pluripotent stem cells. It’s knowledge we can use in the future.</p> <p>The next step in our research is to scale up the production of blood stem cell precursors, and to test their transplant potential in immune-deficient mice that can accept human transplants. We can do this by using large numbers of pluripotent stem cells grown in bioreactors that also mechanically stimulate blood stem cell formation.</p> <p>If we can easily produce blood stem cells from pluripotent stem cell lines, it would provide a plentiful supply of these cells to help treatments of cancer or genetic blood diseases.</p> <p><strong>This article originally appeared on <a href="https://theconversation.com/scientists-have-mimicked-an-embryos-heart-to-unlock-the-secrets-of-how-blood-cells-are-born-190530" target="_blank" rel="noopener">The Conversation</a>.</strong></p> <p><em>Image: UNSW</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"> <form class="wpcf7-form mailchimp-ext-0.5.61 spai-bg-prepared init" action="/science/mutations-change-blood-production/#wpcf7-f6-p193434-o1" method="post" novalidate="novalidate" data-status="init"> <p class="spai-bg-prepared" style="display: none !important;"><span class="wpcf7-form-control-wrap referer-page spai-bg-prepared"><input class="wpcf7-form-control wpcf7-text referer-page spai-bg-prepared" name="referer-page" type="hidden" value="https://www.google.com/" data-value="https://www.google.com/" aria-invalid="false" /></span></p> <p><!-- Chimpmail extension by Renzo Johnson --></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><!-- 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" 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> <p><!-- End of tracking content syndication --></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>

Body

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“Benjamin Button” mice could pave way for reverse ageing

<p>If the three blind mice from the iconic nursery rhyme were living in molecular biologist Dr David Sinclair’s lab at Harvard Medical School, they might not be blind for very long.</p> <p>Dr Sinclair and his team at Harvard Medical School have been using proteins that can turn adult cells into stem cells - a kind of cell that can be turned into any of the specialised cells our bodies need.</p> <p>These stem cells have been helping restore the sight of old mice with damaged retinas, essentially making them younger versions of themselves.</p> <p>“It’s a permanent reset, as far as we can tell, and we think it may be a universal process that could be applied across the body to reset our age,” Dr Sinclair said about his research, which was published in late 2020.</p> <p>The Australian scientist has spent the past 20 years studying ways to reverse the effects of ageing - including the diseases that can afflict us as we get older.</p> <p>“If we reverse ageing, these diseases should not happen,” he said.</p> <p>During a health and wellness talk at Life Itself, Dr Sinclair said the technology is available and it’s only a matter of when we decide to use it.</p> <p>“We have the technology today to be able to go into your hundreds without worrying about getting cancer in your 70s, heart disease in your 80s and Alzheimer’s in your 90s,” he said.</p> <p>“This is the world that is coming. It’s literally a question of when and for most of us, it’s going to happen in our lifetime.”</p> <p>Whitney Casey, an investor who has partnered with Dr Sinclair to create a DIY biological age test, said the researcher wants to “make ageing a disease”.</p> <p>“His research shows you can change ageing to make lives younger for longer,” she said.</p> <p>Dr Sinclair said that when it comes to how modern medicine addresses sickness, it doesn’t tackle the underlying cause, which is usually “ageing itself”.</p> <p>“We know that when we reverse the age of an organ like the brain in a mouse, the diseases of ageing then go away. Memory comes back, there is no more dementia,” he continued.</p> <p>“I believe that in the future, delaying and reversing ageing will be the best way to treat the diseases that plague most of us.”</p> <p>Dr Sinclair’s research comes amid a global effort by scientists working to reprogram adult cells into stem cells, started by Japanese researcher Shinya Yamanaka, who won a Nobel Prize for reprogramming adult skin cells into behaving like embryonic (or pluripotent) stem cells.</p> <p>These “induced pluripotent stem cells” became known as “Yamanaka factors”, with later research finding that exposing cells to four of the main Yamanaka factors could remove signs of ageing.</p> <p>Since their original study, where they discovered that damaged cells were able to be rejuvenated by injecting three of these factors into the eyes of mice, Dr Sinclair and his lab have reversed ageing in mouse brains and muscles, and are now working on a mouse’s whole body.</p> <p>Dr Sinclair said their discovery indicated that there is a “back-up copy” of youthful information stored in the body, which he calls the “information theory of ageing”.</p> <p>“It’s a loss of information that drives ageing cells to forget how to function, to forget what type of cell they are,” he revealed.</p> <p>“And now we can tap into a reset switch that restores the cell’s ability to read the genome correctly again, as if it was young.”</p> <p><em><span id="docs-internal-guid-5569962c-7fff-455b-2538-0661dd2d0f60">Image: Getty Images</span></em></p>

Body

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Woman celebrates 100th birthday in jail cell

<p>Ruth Bryant celebrated her centennial birthday by crossing off a wish on her bucket list: to be arrested and sent to jail.</p> <p>The US woman was celebrating her 100<sup>th</sup> birthday on Wednesday at her assisted living community in North Carolina when deputies from the Person County Sheriff’s Office showed up and served her a warrant for “indecent exposure” at a fire department.</p> <p>Friends and family members present at Bryant’s birthday celebrations weren’t aware of the plan, <em>WRAL </em>reported.</p> <p>“I know that she is a hundred years old, but I didn’t know ... they’d be going this far,” the 100-year-old’s daughter Marian Oakley told the outlet.</p> <p><iframe src="https://www.facebook.com/plugins/video.php?href=https%3A%2F%2Fwww.facebook.com%2FKATVChannel7%2Fvideos%2F2729937517059685%2F&amp;show_text=1&amp;width=560" width="560" height="445" style="border: none; overflow: hidden;" scrolling="no" frameborder="0" allowtransparency="true" allow="encrypted-media" allowfullscreen="true"></iframe></p> <p>Police handcuffed Bryant to her walker and loaded her into the front seat of the police car before driving her to prison.</p> <p>She spent a few minutes inside a cell and was given a free phone call, a mug shot and an orange jail t-shirt.</p> <p>“I’m in the jailhouse now! I finally got here!” she said.</p> <p>She was released after paying bail in the form of a hug to the chief jailer and returned to her residence for cakes with friends.</p>

Retirement Life

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Genetic secrets of almost 2,700 cancers unveiled by landmark international project

<p>Scientists have revealed the detailed genetic makeup of thousands of cancer samples, yielding new insights into the genes that drive the many and varied forms of the disease.</p> <p>The results, <a href="https://www.nature.com/collections/pcawg/">published in a landmark collection of research papers in the journal Nature</a> interpret the complete DNA sequences, or cancer genomes, of 2,658 cancer samples. This will further our understanding of the crucial “driver” mutations that underpin cancer development and offer potential as targets for treatments such as chemotherapy.</p> <p>It is the work of some 700 scientists around the world, as part of an international project called the <a href="https://dcc.icgc.org/pcawg">Pan-Cancer Analysis of Whole Genomes</a>.</p> <p>The hallmark of a cancer cell is its unregulated growth. The mechanism that allows these cells to escape normal cellular growth regulation involves the introduction of mutations into the cancer cell’s DNA. The collection of mutations present in a particular cancer genome is thus known as that cancer’s “mutation signature”.</p> <p>Each advance in our capacity to accurately and completely sequence whole cancer genomes, and to analyse the sequence data, has enabled a more in-depth analysis of these mutation signatures. Each step forward has revealed further diversity in the mutation processes that underlie the development and progression of cancer.</p> <p><strong>Diverse mutations</strong></p> <p>It is seven years since the <a href="https://theconversation.com/cancer-signatures-offer-hope-for-treatment-and-prevention-17045">previous landmark advance in this field</a>. Back in 2013, researchers reported on the genetic makeup of 7,042 cancers of 30 different types, and identified 20 distinct mutational signatures.</p> <p>Today’s reports involve fewer cancers, but an increase in the number of cancer types to 38. But this latest advance is not really about numbers.</p> <p>The real step forward is in our understanding of the diversity of DNA mutations and mutation signatures within cancer genomes. This is primarily the result of improved methods for analysing the DNA sequence data, compared with the state of the art in 2013.</p> <p>As a result, important DNA sequence alterations that could not be detected in previous work have now been described. Each contributes important new details about each cancer genome.</p> <p>Until recently, cancer DNA mutation analyses had been focused on small alterations in “coding regions” of DNA - the roughly 1% of DNA that is responsible for making proteins. The new analyses reported today have identified non-coding driver mutations – some of them large structural mutations that can be as big as entire chromosomes.</p> <p>These new analytical capabilities have enabled the identification of 97 mutation signatures, five times more than previously known. The improved detail boosts our understanding of the diversity of cancer genomes. It also provides important new information about the order in which these mutations accumulate during cancer development.</p> <p>However, there is good evidence to suggest that more work is still required to characterise the full spectrum of cancer DNA mutations. It is anticipated that all cancers will have at least one, and perhaps as many as five, driver DNA mutations. Despite the extensive array of analytical approaches described in these new reports, the researchers were still unable to identify any driver mutations in 5% of the cancers in their study.</p> <p>The research has also shown that similar mutation signatures are present in cancers that arise in different tissues. This has implications for cancer treatment. For example, a drug successfully used to treat a breast cancer may be as effective for treating a pancreatic cancer if the two cancers share the same mutation signature.</p> <p>These data will greatly advance our ability to identify cancers with the same or similar origins via their mutation signature. It has enormous implications for diversifying the current suite of drugs available for gene-targeted cancer treatment.</p> <p>But, perhaps more significantly, it also offers the opportunity to expand our strategies for preventing cancer before it starts.</p> <p><em>Written by Melissa Southey. Republished with permission of </em><a href="https://theconversation.com/genetic-secrets-of-almost-2-700-cancers-unveiled-by-landmark-international-project-131197"><em>The Conversation.</em></a></p>

Beauty & Style

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“Rules are the rules”: Djokovic shocks tennis fans with rogue move on umpire

<p>Novak Djokovic doesn’t believe he crossed a line by touching the umpire chair during a difficult Australian Open final on Sunday Night.</p> <p>He is facing the prospect of a heavy fine for twice tapping Damien Dumusois on the foot while arguing with the official over the intense win over Dominic Thiem. </p> <p>Djokovic ended up winning the match with an intense 6-4 4-6 2-6 6-3 6-4.</p> <p>The Serbian lost his cool after being slammed with back-to-back time violations in one game for taking too long to serve.</p> <p>He walked past the umpire’s chair and tapped Dumusois on the foot, sarcastically exclaiming “You made yourself famous in this match. Great job. Especially in the second one. Great job. You made yourself famous. Well done man”, according to <em><a rel="noopener noreferrer" href="https://www.news.com.au/sport/tennis/australian-open/novak-djokovic-risks-fine-by-touching-chair-umpire-before-securing-australian-open-title/news-story/9ec211e84e91dde676bfe6c2a74c642c" target="_blank">news.com.au</a>.</em></p> <p><img style="width: 500px; height:281.25px;" src="https://oversixtydev.blob.core.windows.net/media/7834274/body-djokovic.jpg" alt="" data-udi="umb://media/3460f2b5152840ef9d118590b9433ff6" /></p> <p>Dumusois, to his credit, didn’t react. However, according to the official grand slam rule book, Djokovic could face a $30,000 fine, although penalties are discretionary.</p> <p>The rules state: “Players shall not at any time physically abuse any official, opponent, spectator or other person within the precincts of the tournament site. Violation of this Section shall subject a player to a fine up to $US20,000 for each violation.”</p> <p>Former Aussie pro Rennae Stubbs was stunned. “Wowza!!!! I cannot believe Novak just patted the umpires foot!!!!!!!!!! I mean wowza !!! The rules are the rules, you have to get that serve off before 00. I mean there is leniency sometimes because of the point prior but wtf with touching the foot!???”</p> <p>“He shouldn’t do that,” added New York Times tennis writer Ben Rothenberg.</p> <p>However, Djokovic doesn’t think that he overstepped the mark.</p> <p>“I thought it was a nice, really friendly touch. I wasn’t aggressive with him in terms of physical abuse.</p> <p>“I just couldn’t believe that I got the time violation. It kind of disturbed me. That’s all there is to it.</p> <p>“Verbally we did have some exchanges, but no insults because if I did insult him, I would get a warning.</p> <p>“Right now that you tell me that, I want to thank him for not giving me a warning for touching him. That’s all I can say.”</p> <p>Djokovic was stressed out during the match but “couldn’t believe what was happening” when he won his eighth Australian Open.</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-permalink="https://www.instagram.com/p/B8ERQDuHPcJ/?utm_source=ig_embed&amp;utm_campaign=loading" data-instgrm-version="12"> <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/p/B8ERQDuHPcJ/?utm_source=ig_embed&amp;utm_campaign=loading" target="_blank">A post shared by Novak Djokovic (@djokernole)</a> on Feb 2, 2020 at 5:47am PST</p> </div> </blockquote> <p>“Tonight it was toe-to-toe battle. I was on the brink of losing that match. I didn’t feel great on the court at all,” Djokovic said.</p> <p>“It was quite surprising, to be honest, because I felt it started off well.</p> <p>“But I played a couple of doubles, then the energy dropped and then the whole thing just started happening. I couldn’t believe what was happening.”</p>

News

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Hunt still on for rogue boa constrictor that could threaten kids and pets

<p>A snake catcher has issued a warning after a missing boa constrictor is on the loose in Sydney’s west. The reptile could pose a danger to a small child, cat or dog as authorities rush to locate the snake.</p> <p>The snake, which is estimated to be 2.5 metres long, was residing on a property on Torumba Circuit in Silverdale yesterday before it made its escape.</p> <p>The final clue left by the constrictor was freshly-shed snakeskin, found hanging from timber at a construction site inside Cascade Estates.</p> <p>Sean Cade, a local snake catcher working with the Department of Primary Industries (DPI) to locate the whereabouts of the serpent said the creature could be a credible danger to residents in the area.</p> <p>“This is a 2.5 metre snake, it’s the thickness of my calf muscle. It is quite a big, heavy robust snake and these guys take down prey four times their size so it’s quite easy to take a full-size cat, a small-size dog, a rabbit, guinea pig – that sort of thing,” he said.</p> <p>“It depends on what it was fed during captivity, is what it’ll be chasing.</p> <p>“If it comes across a small child, that’ll be the concern DPI and myself have. We’re just worried it’s going to get into a backyard and potentially a kid might startle it and the snake could lunge out and grab it.”</p> <p>Mr Cade said that ever since news broke out of the escaped snake, he’s been hit with multiple calls from concerned residents.</p> <p>“It’s still ongoing, obviously with this reptile on the loose some backyards are in danger of encountering this thing,” he said.</p> <p>“I had a couple of calls last night about a guy who had a couple of dachshunds, he was worried about his sausage dogs.</p> <p>“A couple of other people heard noises in their roof, so I had to crawl around their roof space last night looking for this snake.</p> <p>Boa constrictors are illegal in New South Wales outside of zoos.</p> <p>The DPI said they were a “serious threat” to wildlife and humans.</p>

Travel Trouble

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What it was like to share a prison cell with Anita Cobby's murderer

<div> <div class="replay"> <div class="reply_body body linkify"> <div class="reply_body"> <div class="body_text "> <p>A former convict has shared a chilling glimpse into the mind of one of Australia’s most notorious murderers.</p> <p>Sydney man Greg Fisher was sentenced to seven years and 10 months in jail for corporate fraud and drug-related charges, including using and dealing cocaine and crystal meth.</p> <p>When he got incarcerated in 2005 at the Lithgow Correctional Centre, he was allocated a cell with an inmate whose crimes had been described as “one of the most savage and brutal … the state has ever known”.</p> <p>Only later did Fisher find out that the man on the top bunk of his cell was John Travers, one of the five men who abducted, raped and killed Sydney nurse Anita Cobby in 1986.</p> <p>“I hadn’t put two and two together,” he told <a href="https://www.news.com.au/lifestyle/real-life/news-life/jailed-sydney-businessman-reveals-what-it-was-like-to-share-a-cell-with-notorious-killer-john-travers/news-story/1cb9241c3f0e6997c1984bbe54410c50"><em>news.com.au</em></a>. “I think I was numb anyway from the first six months I was in jail.”</p> <p>But even without knowing Travers’s true identity, Fisher said he could tell that his cellmate “simply wasn’t normal”.</p> <p>“The thing that struck me immediately was his eyes,” said Fisher. “He had eyes like I’d never seen before. Before I spoke to him, it was like I could see through them to the back of his head.</p> <p>“There was no reflection. There was no emotion. There was no soul, and I’m not a spiritual-type person at all. It was absolutely like a physical thing that I could see to the back of his head. He simply wasn’t normal.”</p> <p>He finally found out who Travers was from another inmate. </p> <p>“I immediately worried and called my lawyer and the governor,” he said. “The governor came to see me and said: ‘Look, he’s a model prisoner, and it’s up to you. I can move you if you want’.”</p> <p>However, Fisher decided against moving out due to fears that it might put him “on show”, making him a target to be beaten by other inmates.</p> <p>“It was confronting to say the least because John’s never to be released, so that’s his home,” he said. “I was given the ground rules by him straight away. I had to take the top bunk and everything had to be kept meticulously tidy. I accepted the rules, therefore we got on well.”</p> <p>Fisher said they began getting to know each other afterwards. He said Travers showed no feelings of guilt over raping, torturing and leaving 26-year-old Cobby to die at a rural farm in Prospect, NSW.</p> <p>“He kept saying he wanted to get a group of law students and a professor to take him on as a project to get him released,” said Fisher.</p> <p>When asked whether he would like to apologise to Cobby’s family, Travers said his prison sentence was enough of a punishment already. </p> <p>“He said it was all about his future now, and there was absolutely no indication of remorse,” said Fisher.</p> <p>“He was the victim now, in his eyes, because he’d been there too long.”</p> <p>In a 2015 interview with <a rel="noopener" href="https://www.abc.net.au/radionational/programs/lifematters/greg-fisher-property-developer-turned-drug-dealing-convict/6697466" target="_blank"><em>Life Matters</em></a>, Fisher said spending time behind bars with Travers made him feel conflicted. </p> <p>“John was pretty decent to me, and almost protective. But he also sickened me. So it was very mixed emotions for me.”</p> <p>Fisher was released from prison in 2012 and has since worked for charities such as Our Big Kitchen and Thread Together.</p> <p>In 1986, Travers and four other men captured Cobby near Blacktown railway station and took her to Prospect, where they beat, raped and slit her throat.</p> <p>The five men were later arrested and charged with a range of offences in what was dubbed “<a rel="noopener" href="https://www.oversixty.com.au/finance/legal/how-anita-cobby-s-murder-destroyed-her-husbands-life/" target="_blank">the trial of the century</a>”. The crimes prompted public outrage and some calls for the <a rel="noopener" href="https://www.abc.net.au/news/2019-02-22/anita-cobby-killer-michael-murphy-dead/10836460" target="_blank">death penalty</a> to be reinstated. </p> <p>In 1987, the men were sentenced to life imprisonment without the possibility of parole.</p> </div> </div> </div> </div> </div>

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Packing cells will change how you travel in 2019

<p>Packing cells – people either love them or think they are a huge waste of money. We’ve detailed the pros and cons of packing cells so that you can make your own mind up.</p> <p><strong>1. What are they?</strong></p> <p>Packing cells are little cubes or zippered bags of various sizes that act as removable compartments for your suitcase or backpack.</p> <p><strong>2. How do you use them?</strong></p> <p>Packing cells allow you to organise your suitcase. You sort the items you need into individual bags. Put your dirty clothes in one, underpants in another. Put your socks in one, camera gear in another. You get the point. If you’re sharing a suitcase with a travelling companion, you can put your clothes into individual packing cells – that way your clothes won’t get all mixed up.</p> <p><strong>3. What do fans say about them?</strong></p> <p>A Facebook thread on packing cells went viral this week due to the number of people commenting. Comments such as: “Best things ever – saves so much room and keeps things tidy and organised” were common. Here’s a few more comments: “They have really changed our packing. Highly recommend. No more digging through the whole bag trying to find a pair of undies.” – Alicia thoman “We use them all the time now. Each person has their own pack and then you just take it out of the case – so much easier.” – Clare Ditchburn “They are the best, love mine, make so much more room in your suitcase.” – Kathy Stringfellow</p> <p><strong>4. What do the critics say?</strong></p> <p>Critics say that packing bags are a waste of money. Some argue that the bags are just more stuff you don’t need. Why pay the money when it doesn’t really take that long to find something in your bag. Is the 20 seconds really worth the cash?</p> <p><strong>5. Tips for using them</strong></p> <p>Generally, most people we found who have used the packing bags say they love them. So how do you use them effectively?</p> <ul> <li>Use a different colour per traveller</li> <li>Make sure you buy enough of them</li> <li>Get packing bags that have a clear window or mesh to allow you to see what is in the bag. Otherwise you’re going to spend just as much time hunting for the stuff you need.</li> <li>You can make your own packing bags from laundry bags, old airline amenities bags or plastic zip-lock bags.</li> <li>Buy a selection of different sizes</li> <li>Use them for small and necessary items.</li> <li>Use one for medications</li> <li>Keep one for chargers and phones</li> <li>Have a waterproof one for wet clothes</li> <li>Have one for dirty clothes</li> <li>Where do you buy them?</li> </ul> <p>You don’t need to pay much for packing bags. They are available in loads of places from Kathmandu to Big W, ALDI, Bags to Go, eBay. A simple web search will bring up dozens of different types.</p> <p><em>Written by Alison Godfrey. Republished with permission of </em><a href="https://www.mydiscoveries.com.au/stories/packing-cells-hack/"><em>MyDiscoveries</em></a><em>.</em></p>

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The radical idea offering hope for millions of Aussies suffering from autoimmune disease

<p><strong>Professor Chris Goodnow, Deputy Director of the Garvan Institute of Medical Research, talks about the radical idea that’s offering hope for millions of Australians currently suffering from autoimmune disease.</strong></p> <p>Autoimmune diseases are on the rise in Australia, and fast becoming a problem for our already-stretched healthcare system. One in 8 people will be affected by an autoimmune disease like arthritis, multiple sclerosis, Type 1 diabetes and coeliac disease at some point in their life. These conditions can have a devastating effect, not just on patients, but on their family members and friends as well.</p> <p>While much about autoimmune disease remains a mystery, early findings from research at the Garvan Institute offers hope, with many believing it it may lead to a cure.</p> <p><strong>What we know about autoimmune disease</strong></p> <p>Most of our understanding of autoimmune disease is restricted to what’s going on in the body. We know autoimmune disease occurs when the body attacks and damages its own tissue, we know the symptoms, we have methods to manage these diseases as best we can, and we know what to expect when someone’s diagnosed. What’s less clear, and what the Garvan Institute’s Hope Research project is trying to answer, is why the immune system is doing this, and whether this is curable.</p> <p><img width="499" height="555" src="https://oversixtydev.blob.core.windows.net/media/7268400/artwork-2_499x555.jpg" alt="Artwork 2" style="display: block; margin-left: auto; margin-right: auto;"/></p> <p><strong>How close are we to understanding causes?</strong></p> <p>The encouraging news is we’re closer to an understanding than we’ve ever been, which could one day lead to a cure. The Garvan Institute has been leading the way in autoimmune disease research, thanks largely to work spearheaded by a radical hypothesis from the organisation’s Deputy Director, Professor Chris Goodnow.</p> <p>Over a decade ago, Professor Goodnow theorised that there was a common cause for all autoimmune diseases – disruptions in the immune system’s clever “checkpoint” process causing “rogue clone” cells to spread and replicate.</p> <p>The technology to put this theory to the test didn’t exist previously. But recent advances have given Professor Goodnow and his team the ability to isolate individual disease-causing cells from the blood of patients and target the “rogue clones”. And this has far-reaching implications of the management and treatment of these diseases.</p> <p>“For the last 10 years, we’ve had a pretty good idea as to what might cause autoimmune disease, and we’ve figured out many of the mechanisms that normally stop it. But we haven’t had the tools and the technology to be able to test those ideas,” Professor Goodnow explains.</p> <p>“In the last three years, we’ve acquired the tools and technology here at the Garvan Institute. We are now bringing them together with a fantastic team of medical experts at the major hospitals around Sydney to really focus those tools and know-how on cracking this problem.”</p> <p><strong>Why it’s important to understand the causes of autoimmune disease</strong></p> <p>While many autoimmune diseases can be managed, there’s yet no cure. But the revolutionary research from Professor Goodnow and the team at the Garvan Institute suggests this is about to change. If researchers can pin down the “rogue cells” and what prompted them to go rogue, they could theoretically use existing immunotherapies and drugs to eradicate them from the body, targeting the disease at the source.</p> <p>The Garvan Institute has already made exciting strides through the work of Dr Joanne Reed, who put Professor Goodnow’s theory to the test in a pilot study for Sjögren’s syndrome. The results she recorded were nothing short of spectacular.</p> <p>“Excitingly, our pilot study has already identified disease causing rogue clones in Sjögren’s syndrome,” Dr Reed says.</p> <p>“We’ll now apply this discovery to 36 clinically diverse autoimmune diseases.”</p> <p><img width="500" height="334" src="https://oversixtydev.blob.core.windows.net/media/7268452/rsz_joanne_reed_with_etienne_masle-farquhar2_500x334.jpg" alt="Rsz _joanne _reed _with _etienne _masle -farquhar2" style="display: block; margin-left: auto; margin-right: auto;"/></p> <p><strong>The challenges of this revolutionary research?</strong></p> <p>As is often the case, progress in the world of science doesn’t come cheap. The costs associated with the Hope Research project’s revolutionary work are substantial.</p> <p>“To identify the rogue cells in one person costs thousands of dollars; to identify the mutations in those rogue cells costs $5,000-$20,000. It will get cheaper the more we do it, and the more the technology continues to mature,” Professor Goodnow says.</p> <p>“You could say we should just wait 10 years, until the technology has gotten cheaper, but we can’t wait. We want to know the root cause of autoimmune disease <em>now</em>. We’ve got the technology. We know what we need to do. We just need the resources to do it.”</p> <p><strong>How you can help</strong></p> <p>Contributing funds to the Garvan Institute is a good way to start, and you’ll be surprised how far your dollar goes to tackling autoimmune disease.</p> <p>As Professor Goodnow says, “For every dollar you give, we will leverage that many, many times over, in terms of being able to reach a cure for these diseases.”</p> <p><a href="https://www.garvan.org.au/foundation/give-hope/?utm_source=fairfax&amp;utm_medium=sponsoredcontent&amp;utm_campaign=give_hope" target="_blank"><span style="text-decoration: underline;"><strong>You can contribute</strong></span></a> to Garvan’s fight against autoimmune disease. Visit <span style="text-decoration: underline;"><strong><a href="https://www.garvan.org.au/foundation/give-hope/?utm_source=fairfax&amp;utm_medium=sponsoredcontent&amp;utm_campaign=give_hope" target="_blank">garvan.org.au/give-hope</a></strong></span><a href="#_msocom_1"></a></p> <div>THIS IS SPONSORED CONTENT BROUGHT TO YOU IN CONJUNCTION WITH THE GARVAN INSTITUTE.</div>

Caring

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Police chase rogue wallaby across Sydney Harbour Bridge

<p>In scenes that would seem to confirm every tourist’s stereotype about Australia, police have apprehended a wallaby that was found bouncing along Sydney Harbour Bridge this morning, after shocking motorists on their morning commute.</p> <p><iframe src="https://www.facebook.com/plugins/video.php?href=https%3A%2F%2Fwww.facebook.com%2Fnswpoliceforce%2Fvideos%2F10155559323521185%2F&amp;show_text=0&amp;width=560" width="560" height="315" style="border: none; overflow: hidden;" scrolling="no" frameborder="0" allowtransparency="true" allowfullscreen="true"></iframe></p> <p>Traffic controllers monitored the marsupial as it hopped across the bridge, before taking the Cahill Expressway exit to Macquarie Street where it was eventually stopped by police.</p> <p>Drivers who couldn’t believe their eyes called into <a href="https://www.2gb.com/" target="_blank"><span style="text-decoration: underline;"><em><strong>2GB</strong> </em></span></a>to report the sighting.</p> <p>'I was driving along the Harbour Bridge, I'm slowing down to 40 when I see a wallaby just sitting there, it was pretty small, might have been a wallaby,' a listener named Jesse said.</p> <p>Another listener named Ray added: “There was a little rock wallaby in the middle of the road just minding its own business with a police car there with flashing lights.”</p> <blockquote class="twitter-tweet"> <p dir="ltr">'It doesn't get more Australian than that!': Police rescue wallaby making its way into Sydney after crossing over the Harbour Bridge <a href="https://t.co/eyWALbDzFw">https://t.co/eyWALbDzFw</a> <a href="https://twitter.com/hashtag/7News?src=hash&amp;ref_src=twsrc%5Etfw">#7News</a> <a href="https://t.co/w9C6eHUDvt">pic.twitter.com/w9C6eHUDvt</a></p> — 7News Yahoo7 (@Y7News) <a href="https://twitter.com/Y7News/status/953006374828630019?ref_src=twsrc%5Etfw">January 15, 2018</a></blockquote> <p>After the wallaby was pinned down, animal welfare officers took the out-of-place marsupial to Targona Zoo for veterinary assessment. Police believe it made its way to the bridge from a golf course in Cammeray.</p> <p>What are your thoughts? Have you ever seen anything more Australian than this?</p> <p><em>Hero image credit: Facebook / NSW Police </em></p>

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Exercise slows ageing of cells

<p>The secret to keeping your body youthful may be found in the way you move.</p> <p>A new study has found that high-intensity interval training (HIIT) can essentially stop cellular ageing in its tracks and, in some cases, rejuvenate the cells that repair damage in the body.</p> <p>For the study, researchers from the Mayo Clinic took 36 men and 36 women split into younger (aged between 18 and 30) and older (aged between 65 and 80) age groups.<br /> <br /> The participants were then assigned a three-month programme of HIIT, strength training or a combination of the two.</p> <p>They already knew that both <a href="http://www.smh.com.au/lifestyle/diet-and-fitness/time-to-get-fit-a-guide-to-hiit-20160518-goxmgm.html">HIIT</a> and <a href="http://www.smh.com.au/lifestyle/health-and-wellbeing/fitness/the-science-of-strength-seven-ways-muscle-makes-us-healthier-20170312-guwcpv.html">strength training</a> provided enormous health benefits to our bodies, they just didn't know exactly how or why, or which was better.</p> <p>So, to understand the way exercise affects us at a molecular level, the researchers then took biopsies from the participants' thigh muscles and compared them with samples from sedentary volunteers.</p> <p>The strength-training group predictably saw the greatest improvements in muscle mass, but the findings that have been described as "<a href="https://www.psychologytoday.com/blog/the-athletes-way/201703/mayo-clinic-study-identifies-how-exercise-staves-old-age">earth shattering</a>" were at a cellular level in the HIIT group. </p> <p>Mitochondria are the "<a href="https://www.umdf.org/what-is-mitochondrial-disease/">powerhouses" of our cells</a>, responsible for creating more than 90 per cent of the energy needed by the body to sustain life and support organ function. Their function typically declines with age.  </p> <p>However, in the HIIT group, the mitochondrial functioning improved by 69 per cent among the older participants, and by 49 per cent among the younger group. </p> <p>As well as improving their insulin levels, heart and lung health, some in the high-intensity biking group also saw a reversal of the age-related decline in mitochondrial function and proteins needed for building muscle.</p> <p>The research provided an explanation for the many health benefits of exercise said the lead senior author, Sreekumaran Nair.</p> <p>"Based on everything we know, there's no substitute for these exercise programmes when it comes to delaying the ageing process," says Nair, of the study published in the journal <a href="http://www.cell.com/cell-metabolism/abstract/S1550-4131(17)30099-2?_returnURL=http%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS1550413117300992%3Fshowall%3Dtrue">Cell</a>. "These things we are seeing cannot be done by any medicine."</p> <p>He adds: "If people have to pick one exercise, I would recommend high-intensity interval training, but I think it would be more beneficial if they could do three to four days of interval training and then a couple days of strength training."  </p> <p>Emmanuel Stamatakis of the Charles Perkins Centre at the University of Sydney says it is a "fascinating piece of research".</p> <p>"This not only sheds light on how high-intensity interval exercise works at the cellular level, but [also] on the potential of vigorous exertion in general," says Stamatakis, who was not involved with the research. </p> <p>It also shows what is happening beneath the sweat that makes HIIT more beneficial to our bodies than other forms of exercise. Which aspect of HIIT is responsible for such dramatic changes, however, is still an unknown.</p> <p>"Assuming that the key attribute of HIIT is the vigorous intensity that challenges the human physiology to make rapid adaptations, this research supports well what we saw recently <a href="http://jamanetwork.com/journals/jamainternalmedicine/article-abstract/2596007">in a large epidemiologic study</a> where even one to two sessions per week of  predominantly sport/ exercise of vigorous intensity were associated with substantial all-cause, CVD and cancer mortality benefits," Stamatakis explains.</p> <p>"These benefits were comparable with meeting the physical activity recommendations by doing regular physical activity of mostly moderate intensity."</p> <p>Now the question is whether HIIT is right for everyone. Given how few of us manage to meet the recommendations, Stamatakis remains unsure.</p> <p>"There <a href="https://ijbnpa.biomedcentral.com/articles/10.1186/s12966-015-0254-9">is a big debate</a> as to whether HIIT is the way to go for better population health, but it is certain that it has a time and a place," he says. "Although not every physically inactive person would be willing or able to join a HITT program, this new piece of research highlights that in addition to  public health messages like 'move as often as possible, a little is better than nothing', we need to also add 'aim to huff and puff sometimes'."</p> <p>This might be as simple as taking the stairs whenever you can – both a form of incidental and HIIT exercise. </p> <p>"For many people, stair climbing will involve bouts of high-intensity activity lasting one or more minutes, and if this is repeated regularly enough in everyday life it could potentially improve fitness and other aspects of cardiovascular and metabolic health quite rapidly," Stamatakis says.   </p> <p>And of course, it will keep us young.</p> <p>"There are substantial basic science data to support the idea that exercise is critically important to prevent or delay ageing," says Nair, who plans to look at the effect of exercise on other tissues in the body. "There's no substitute for that."</p> <p><em>Written by Sarah Berry. Appeared on <span style="text-decoration: underline;"><strong><a href="http://www.stuff.co.nz/" target="_blank">Stuff.co.nz.</a><br /></strong></span></em></p>

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