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CBC
11 hours ago
- Entertainment
- CBC
How music fuelled, and was fuelled by, the No Kings protests
If you were online last week, you probably saw footage from the No Kings protests. The gigantic demonstration against U.S. President Donald Trump took place across the United States and portions of Canada — but was connected by one prevailing aspect: music. There was Les Miserables 's rousing Do You Hear the People Sing?, sung by a crowd in Auburn, Calif. There was Bella Ciao — a lesser-known piece strongly linked to the Italian anti-fascist movement of the 1940s — performed by a brass band to drown out counter-protesters in Atlanta. And there was a raft of other music, new and old, by musicians looking to tie themselves to the No Kings demonstrations. "There's a fascinating mixture of new music as well as old songs being brought back into the mix," said Benjamin Tausig, an associate professor of critical music studies at New York's Stony Brook University. It's "inspiring people in the context of protest at this moment." That's because of music's inextricable connection to — and ability to inspire — political action, he says. When used in a specific way, some songs can become almost irresistible calls to action. And the beginning of protest movements often fundamentally alter both what music we are exposed to, and what music artists choose to release, says Tausig. But when it comes to protest music, not all songs are created equal, says Noriko Manabe, chair of Indiana University's department of music theory and co-editor of the upcoming Oxford Handbook of Protest Music. And the way that we engage with that music, she says, speaks to why some of the most widespread songs used at recent protests have been older, less traditionally popular tunes. Songs like Bella Ciao, Do You Hear the People Sing? or even The Star-Spangled Banner — which had moments of its own at the protests — tend to be of a specific type, she says. They are "participatory" versus "presentational." While presentational music is meant for one skilled performer, participatory music, like other iconic protest songs such as We Shall Overcome, is not. It's "more repetitive so that people can more easily join in," she said. "Whether or not they're virtuosic is actually not the point. The point is to get as many people involved as possible." And with participation, she says, comes ideology. "The idea of moving vocal cords and muscles together, where you have to listen to other people and feel their movements — " Manabe said. "Just the act of voicing it itself makes you feel that this is part of your belief system." Co-opted music Tausig says that participatory aspect can even eclipse what the song is actually about. Historically, he says, the most popular protest songs tend to be co-opted, with no direct or apparent connection to any political movement. That's because the cultural iconography associated with them tends to hold more weight. Kendrick Lamar and Beyonce became very important in the Black Lives Matter movement, for example. "Their songs didn't even specifically have to address Black Lives Matter to still become really effective at mobilizing people," he said. Some songs are even adopted by movements they seem to be explicitly against. For example, Tausig notes, Bruce Springsteen's Born in the U.S.A., about a disillusioned Vietnam War veteran, was famously referenced in a 1984 campaign speech by U.S. President Ronald Reagan. More recently, Creedence Clearwater Revival's draft-dodging ditty Fortunate Son was played at a military parade, prompting speculation over whether it was either a form of protest or due to a common misinterpretation of the song's meaning. In both cases, he says, what the song appeared to represent was more important than what it actually said. A long history But even still, songs being used by both sides of a political debate have a long history in protest music, Manabe says. Going back to Britain in the 1600s, warring factions of Royalists and Parliamentarians would disseminate "broadsheets": large pieces of paper with often-rhyming lyrics in support of their side. But to make sure they were easy to remember, they would be set to well-known tunes. That resulted in "contrafacta": each side singing the same "song," though with completely different words supporting completely different ideals. That phenomenon continues to today. Manabe points to protests in Hong Kong in 2014, when both defenders and critics of the democracy movement used Do You Hear the People Sing? Meanwhile, rock, country, EDM and hip-hop artists seemingly jumped on the bandwagon to release or re-release their political music, creating musical touchstones and viral moments in the protests themselves. Arkansas folk musician Jesse Welles, who crafted social media fame by releasing songs tied to the news, debuted a new track No Kings which has already racked up over 150,000 views on YouTube. In Salt Lake City, EDM musician Subtronics added a "No Kings" section to his performance, gaining over two million views on TikTok. Meanwhile, the Dropkick Murphys, Soundgarden and Pavement have all made posts connecting their music, old and new, to the protests — along with Canadian Grammy-winner Allison Russell, lesser known blues, country and bluegrass musicians and even an AI hip-hop track simply titled No Kings that's amassed over 750,000 views on YouTube. "Expressing dissent or resistance to authority through nonviolence is one of the most potent weapons that we can wield," said Canadian musician Jordan Benjamin (known artistically as Grandson) who also released new music directly tied to the No Kings protests. From an artist's standpoint, the sudden swell makes sense: given the cyclical nature of pop culture, music that may have seemed old-fashioned or out of step has suddenly become more in demand. And at the beginning of such changes in direction, Tausig says, which songs will define that movement becomes an important question.
Yahoo
2 days ago
- Science
- Yahoo
Scientists make revolutionary breakthrough that could transform energy storage: 'Truly a game-changer'
Tech Xplore recently shared how a group of scientists used AI to crack part of the code for cheaper, safer energy storage. Plus, they did it with a water-based battery that could one day cut pollution and lower energy bills. "AI is an important tool that can facilitate the advancement of science," Esther Takeuchi, chair of the Interdisciplinary Science Department at Brookhaven Lab and William and Jane Knapp Chair in Energy and the Environment at Stony Brook University, told Tech Xplore. "The research done by this team provides an example of the insights that can be gained by combining experiment and theory enhanced by the use of AI." In their study, published in PRX Energy, researchers were trying to understand why zinc-ion batteries run better when filled with a super-salty solution. To find out, they trained an AI model to simulate what happens inside the battery at an atomic level—something a standard computer would've needed years to do. "This work demonstrates the great impact artificial intelligence and machine learning can have for understanding the chemistry of materials and provides guidelines for optimizing battery electrolytes," lead researcher Deyu Lu told Tech Xplore. Turns out, the salt (zinc chloride) keeps water molecules from splitting apart into hydrogen gas, a common problem that usually wrecks performance. In this setup, the water molecules stop clinging to each other. That stabilizes the battery and keeps it running as intended. The high salt concentration also helps zinc ions move more easily between battery parts. That cuts down on energy waste and delays. Zinc-ion batteries are cheaper and less toxic to make than lithium ones. They're nonflammable, run on widely available materials, and could be a better option for storing energy from solar panels or other affordable sources, especially during outages or times of high demand. Solar installation companies such as EnergySage may soon offer such products. While this tech won't replace lithium overnight, it could soon show up in grid storage and emergency systems. This means there will be less need for pollutant sources like gas and coal, and cleaner air for the people breathing it. AI helped speed things up, but it's not all upside. Models like this require a ton of computing power. Some of them burn through electricity and water faster than you'd think. Training just one large model can produce as much pollution as five gas-powered cars do over their lifetimes. Still, used carefully, tools like this could help solve real problems. If zinc batteries become easier to make and store, clean energy becomes easier to use. That's a win worth paying attention to. "AI/ML is truly a game-changer in the study of complex materials," Lu told Tech Xplore. Should the U.S. invest more in battery innovations? Absolutely Depends on the project We're investing enough We should invest less Click your choice to see results and speak your mind. Join our free newsletter for weekly updates on the latest innovations improving our lives and shaping our future, and don't miss this cool list of easy ways to help yourself while helping the planet.
Yahoo
4 days ago
- Health
- Yahoo
How rogue jumping genes can spur Alzheimer's, ALS
Back in 2008, neurovirologist Renée Douville observed something weird in the brains of people who'd died of the movement disorder ALS: virus proteins. But these people hadn't caught any known virus. Instead, ancient genes originally from viruses, and still lurking within these patients' chromosomes, had awakened and started churning out viral proteins. Our genomes are littered with scraps of long-lost viruses, the descendants of viral infections often from millions of years ago. Most of these once-foreign DNA bits are a type called retrotransposons; they make up more than 40 percent of the human genome. Many retrotransposons seem to be harmless, most of the time. But Douville and others are pursuing the possibility that some reawakened retrotransposons may do serious damage: They can degrade nerve cells and fire up inflammation and may underlie some instances of Alzheimer's disease and ALS (amyotrophic lateral sclerosis, or Lou Gehrig's disease). The theory linking retrotransposons to neurodegenerative diseases — conditions in which nerve cells decline or die — is still developing; even its proponents, while optimistic, are cautious. 'It's not yet the consensus view,' says Josh Dubnau, a neurobiologist at the Renaissance School of Medicine at Stony Brook University in New York. And retrotransposons can't explain all cases of neurodegeneration. Yet evidence is building that they may underlie some cases. Now, after more than a decade of studying this possibility in human brain tissue, fruit flies and mice, researchers are putting their ideas to the ultimate test: clinical trials in people with ALS, Alzheimer's and related conditions. These trials, which borrow antiretroviral medications from the HIV pharmacopeia, have yielded preliminary but promising results. Meanwhile, scientists are still exploring how a viral reawakening becomes full-blown disease, a process that may be marked by what Dubnau and others call a 'retrotransposon storm.' A retrotransposon is a kind of 'jumping gene.' These pieces of DNA can (or once could) move around in the genome by either copying or removing themselves from one spot and then pasting themselves into a new spot. Retrotransposons are copy-and-pasters. Many retrotransposons are old companions: Some predate the evolution of Homo sapiens or even the split between plants and animals, Dubnau says. Their predecessors may have alternated between riding along stitched into a host chromosome and existing outside of it, he suggests. Some retrotransposons, after all that time, retain their ability to hop around human DNA. To do so, they copy themselves with the enzyme reverse transcriptase, which is also used by some viruses like HIV to copy RNA sequences into DNA. Once they're copied, the remnant viruses can pop into new locations on chromosomes. If it's terrifying to think of a genome littered with retroviral genes, some capable of bouncing around the genome, don't fret, says Douville, now at the University of Manitoba in Winnipeg. Remarkably, some retrotransposons have taken on helpful jobs, assisting the body with tasks like maintaining stem cells and development of the embryo and nervous system. And many retrotransposons are dormant or broken, and the cell has means to keep them (mostly) quiet. One technique is to stash them in DNA regions that are wound up so tight that the molecular machines needed to copy genes can't get near them. In essence, the cell shoves them into a closet and slams the door shut. But evidence is building that as people age, that closet door can creak open, letting retrotransposons spill out. Exactly what they do then isn't certain. Some scientists think it's not so much that they are jumping around and mutating DNA, but that their viralesque RNAs and proteins can screw up normal cellular activities. 'I think what's actually driving toxicity when transposons are activated is they're making all these factors that look like a virus to the cell,' says Bess Frost, a neurobiologist at Brown University in Providence, Rhode Island. The cell reacts, quite reasonably, with defensive inflammation, which is commonly associated with neurodegeneration. Retrotransposons also seem to team up with rogue proteins classically linked to neurodegeneration, damaging or killing nerve cells, and perhaps even setting off the disease in the first place. Scientists long suspected a link between viruses and ALS, which causes degeneration of the motor neurons that control movement. But the connection, when it was finally found, wasn't quite what anyone predicted. In the early 2000s, scientists reported that some people with ALS had the viral enzyme reverse transcriptase in their blood and, more rarely, spinal fluid. Some had as much reverse transcriptase as a person with an HIV infection. But at the time, says Dubnau, 'Nobody could find a virus.' Finally, Douville and colleagues discovered evidence for one of those leftover viruses, a kind of retrotransposon called HERV-K, in the brains of some people who had died of ALS. From there, scientists began to build a case linking jumping genes to ALS in people, lab animals and cells in dishes. A team reported in 2017 that numerous jumping genes had been activated in the brains of certain people with ALS. Douville's colleagues also documented damage inflicted by HERV-K: When they put a gene from the retrotransposon into mice, the animals' nerve cell projections shriveled and they exhibited ALS-like symptoms. As the scientists zeroed in on what might be waking up HERV-K, a familiar protein turned up. Called TDP-43, it had already been linked to ALS. But even before that, it was found to be involved in cells' responses to the retrovirus HIV. Scientists discovered in the 1990s that TDP-43 works in the cell's nucleus, where it hinders activation of HIV genes. It also regulates human genes there. But in the neurons of people with ALS or a related condition, frontotemporal dementia (FTD), TDP-43 departs the nucleus and goes on to form abnormal clumps in the cytoplasm. The globs have been associated with a number of neurodegenerative conditions and can spread from cell to cell. And when TDP-43 vacates the nucleus, it also creates a gap in gene regulation, throwing off the activity levels of many genes. TDP-43 gone bad is sufficient to cause neurodegeneration, but studies indicate its desertion of its nuclear role can also wake up retrotransposons. When TDP-43 leaves the nucleus, tightly coiled DNA next to certain retrotransposons starts to loosen up and unravel, a study of cells from the brains of people who died of ALS or FTD revealed. And researchers saw that in cultured cells, this loss of TDP-43 freed certain retrotransposons from their restraints. The closet door was now ajar, in other words, allowing the retrotransposons to jump out and around. Meanwhile, Dubnau and collaborators, were looking at data on TDP-43 and the genes it controls in rats, mice and people. They found that TDP-43 can naturally stick to the RNAs of a variety of jumping genes, suggesting a way that normal TPD-43 might continue to corral them, even if they've managed to get copied into RNA. That interaction was altered in people with FTD and in rodents with abnormally high or low amounts of TDP-43 — very much as if TDP-43 was unable to control the jumping genes anymore. The Dubnau group also turned to fruit flies. Both old age and the human TDP-43 gene caused retrotransposons in the fly brain to sneak out of the chromosomal closet, inducing brain cells to kill their neighbors and prompting neurodegeneration, the group reported in a series of papers from 2013 to 2023. Moreover, activation of certain retrotransposons also caused TDP-43 to clump together outside of the nucleus, creating a vicious cycle whereby TDP-43 and the retrotransposons reinforce each other's abnormal behaviors. Past a certain point, says Dubnau, 'It just takes off.' Based on the sum of all these findings, Dubnau suggests a possible way that ALS could develop: Normally, TDP-43 in the nucleus helps to repress retrotransposons. But if aging or some other disturbance causes TDP-43 to decamp, those once-silenced retrotransposons spring to life, producing virus-like RNAs and proteins. While the retrotransposons might induce disease on their own, by jumping into new DNA locations or spurring inflammation, they also act on TDP-43. They force more TDP-43 to leave the nucleus and clump in the cytoplasm, causing further neurodegeneration that spreads to neighboring cells. This isn't the cause of all kinds of ALS, which is a complex disorder with many possible triggers. But in a 2019 study of postmortem brain samples, Dubnau and colleagues found that about one in five people with ALS had high levels of retrotransposon activation and TDP-43 dysfunction. Stay in the KnowSign up for the Knowable Magazine newsletter today As that ALS story was developing, other scientists were pursuing a connection between retrotransposons and another toxic protein in neurodegeneration: the tau protein, which twists into unruly tangles in the brain cells of people with Alzheimer's disease. It affects retrotransposons because it, like TDP-43, plays a role in keeping retrotransposons quiet, says Frost. That maintenance is a downstream effect of tau's association with the cell's interior skeleton. That skeleton is physically linked to the nucleus's skeletal structure, which in turn anchors the tightly wound-up DNA that silences retrotransposons. When tau goes bad, it changes the structure of the cell's main skeleton, making it more rigid. Frost and colleagues found that this structural defect propagates all the way to the nuclear skeleton and the chromosomes, just like tightening the strands on one side of a net could change the shape of the other side. This structural effect can unlock the tightly wound bits of chromosome in fruit flies, which damages their neurons, Frost reported in 2014. By 2018, she'd shown that tau problems unleashed jumping genes in the flies. 'They were legitimately jumping,' she says, going from their original chromosomal locations to other ones in the fly's brain cells. And the jumping genes contributed to the death of nerve cells. Frost and colleagues also studied mammals — mice — and in 2022 they reported that retrotransposons were also activated in mice with dysfunctional tau. Meanwhile, Frost and others examined brain cells from people who'd died of tau-related diseases such as Alzheimer's, which also revealed activated retrotransposons. 'They were legitimately jumping.' — BESS FROST This awakening of retrotransposons appears to happen early in the disease, according to the work of another team published in 2022. In blood samples from people on their way to developing Alzheimer's disease, the copying of retrotransposon genes into RNAs spiked, creating a 'retrotransposon storm,' just before their symptoms got bad enough to be labeled Alzheimer's. This growing body of evidence suggests that reactivating once-quiet retrotransposons, whether via dysfunctional tau or TDP-43, can create havoc. A potential treatment quickly comes to mind: Since these retrotransposons are a lot like viruses, scientists reason that antiviral drugs could help. Handily, doctors already have medications that stymie retroviruses: Millions of people take antiretroviral drugs to keep HIV in check or prevent it from gaining a foothold in their cells. Indeed, multiple studies over several years have investigated drugs from the HIV treatment playbook that block the enzyme reverse transcriptase. And in cells, flies and mice the drugs have dialed down retrotransposon activity and neurodegeneration. These medications are well understood and generally safe, and are already in trials for neurodegenerative disease. For example, researchers have tested the safety of a 24-week antiretroviral course in 40 people with ALS. Not only did most people safely complete the trial, but the levels of HERV-K in their blood went down, and they seemed to have a delay in progression of their ALS symptoms, the researchers reported in 2019. Frost recently published results from a small trial in which 12 people with early Alzheimer's disease took a reverse transcriptase inhibitor for 24 weeks. Her main goal was to determine if the treatment was safe, and it was — but the researchers also observed a drop in signs of inflammation in the participants' spinal fluid. Both Dubnau and Frost serve on the scientific advisory board for Transposon Therapeutics, which tested its own reverse transcriptase inhibitor in 42 people with ALS and/or FTD. The company says the drug was tolerable and yielded signs of less neurodegeneration and inflammation, plus a delay in the inevitable worsening of symptoms. The company is planning a larger trial; it also plans to test its drug in people with ALS, Alzheimer's and a related tau-based disease, progressive supranuclear palsy. Neither Frost nor Dubnau, who together recently summarized the field for the Annual Review of Neuroscience, believes that antiretroviral drugs alone are the solution to transposon-fueled Alzheimer's or ALS. As Douville notes, the drugs were designed to act only on specific target enzymes — they won't do anything to other retrotransposon genes, RNAs or proteins, which could also spur nerve-damaging inflammation. Meanwhile, scientists are looking beyond ALS and Alzheimer's as evidence accumulates that retrotransposons may contribute to other neurodegenerative and inflammatory conditions, such as Parkinson's disease and multiple sclerosis. 'It's really picking up speed,' Frost says. This article originally appeared in Knowable Magazine, an independent journalistic endeavor from Annual Reviews. Sign up for the newsletter.
Belfast Telegraph
13-06-2025
- Belfast Telegraph
Man (60s) arrested on suspicion of murder of Annie McCarrick 24 years ago ‘was known to her'
Ms McCarrick, originally from New York, disappeared without a trace on that dayAt the site of this morning's search in Clondalkin, gardaí moved in early to place metal hoardings around the front garden of the house Robin Schiller, Conor Feehan and Denise Calnan A man who was known to US woman Annie McCarrick has been arrested in Dublin on suspicion of her murder 24 years ago. Sources said that the suspect has led 'a normal life' in the three decades since the young woman went missing on March 26, 1993. The suspect was arrested at his home yesterday morning and was questioned on suspicion of her murder. A separate home in Clondalkin previously linked to the suspect, where his parents had lived, is also being examined. The man, aged in his 60s, was detained under the provisions of Section 4 of the Criminal Justice Act 1984 at a garda station in Dublin. A spokesperson said 'elements of that house and garden' would be searched and subject to both technical and forensic examinations. They stress that the current residents of this home are not connected in any way with Annie McCarrick or her disappearance. Ms McCarrick disappeared without trace on March 26, 1993, with the last confirmed sighting of her in Sandymount in Dublin. She was 26 years old at the time of her disappearance. She was an only child and originally from New York in the US. Ms McCarrick completed her third-level studies at St Patrick's College, Drumcondra, and at St Patrick's College, Maynooth, before returning to New York in 1991, where she completed her studies at Stony Brook University. She moved to Ireland to live permanently in January 1993 and settled into rental accommodation at St Cathryn's Court in Sandymount with two other tenants. The young woman had spoken to both her flatmates before they left separately to travel home for the weekend. Ms McCarrick invited friends to her apartment for dinner the following day — Saturday, March 27. She was also making plans for her mother Nancy's visit to Ireland on March 30. On the Sunday of that weekend, friends of Annie became concerned for her welfare. She was not at home on the Saturday when they called for dinner as invited. She had not turned up for work on the Saturday or on Sunday morning. A friend called to her apartment on the evening of Sunday, March 28, and spoke to Annie's two flatmates. Groceries Annie had bought on the morning of Friday, March 26, in Quinnsworth on Sandymount Road had been left unpacked in shopping bags. A receipt in the bags confirmed the date and time of purchase as 26/03/1993 at 11.02am. This is the last confirmed activity of Annie McCarrick. Ms McCarrick was reported missing by a friend at Irishtown Garda Station on the evening of Sunday, March 28. This missing person report was confirmed by her mother Nancy when she arrived in Dublin on Tuesday, March 30. The search for Annie McCarrick has continued since. At the site of the search, on Monastery Walk in Clondalkin, gardaí moved in early to place metal hoardings around the front garden of a house and parked a mini digger in the front garden. Other equipment including a concrete saw were also brought to the house. Members of the Garda Technical Bureau arrived at the scene at 10am, and a number of detectives could be seen going into and out of the property. News Catch Up - Thursday 12th June Neighbours said they were surprised and curious to see if the search would yield anything of evidential value that could progress the case. Because Ms McCarrick disappeared more than 30 years ago, many of the current residents of Monastery Walk were not living in the estate at the time. 'I was walking the dog this morning and I could see the hoarding being put up at the house, and I thought maybe the owners were getting building work done, but then I could see a few guys in suits arriving and talking with the men putting up the hoarding, and then garda vans and vehicles started to arrive,' said one neighbour. 'We didn't know what was happening but then we started to see the news reports. I hope they find something that would bring some answers to her family,' he added.
Sunday World
12-06-2025
- Sunday World
Man (60s) arrested on suspicion of murdering Annie McCarrick ‘was known to her'
At the site of this morning's search in Clondalkin, gardaí moved in early to place metal hoardings around the front garden of the house A man who was known to missing US woman Annie McCarrick is currently being held on suspicion of her murder. Sources said that the suspect has led 'a normal life' in the three decades since the young woman went missing on March 26, 1993. The suspect was arrested at his home this morning and is currently being quizzed on suspicion of her murder. A separate home in Clondalkin previously linked to the suspect, where his parents had lived, is also being examined. Gardaí arrested a man in relation to the murder of Annie McCarrick, who went missing on March 26, 1993. The man, aged in his 60s, is detained under the provisions of Section 4 of the Criminal Justice Act 1984 at a garda station in Dublin. A spokesperson said 'elements of that house and garden' would be searched and subject to both technical and forensic examinations. They stress that the current residents of this home are not connected in any way with Annie McCarrick or her disappearance. Ms McCarrick disappeared without trace on March 26, 1993, with the last confirmed sighting of her in Sandymount in Dublin. She was 26 years old at the time of her disappearance. She was an only child and originally from New York in the US. Ms McCarrick completed her third-level studies at St Patrick's College, Drumcondra, and at St Patrick's College, Maynooth, before returning to New York in 1991, where she completed her studies at Stony Brook University. She moved to Ireland to live permanently in January 1993 and settled into rental accommodation at St Cathryn's Court in Sandymount with two other tenants. Annie McCarrick The young woman had spoken to both her flatmates before they left separately to travel home for the weekend. Ms McCarrick invited friends to her apartment for dinner the following day – Saturday, March 27. She was also making plans for her mother Nancy's visit to Ireland on March 30. On the Sunday of that weekend, friends of Annie became concerned for her welfare. She was not at home on the Saturday when they called for dinner as invited. She had not turned up for work on the Saturday or on Sunday morning. A friend called to her apartment on the evening of Sunday, March 28, and spoke to Annie's two flatmates. Groceries Annie had bought on the morning of Friday, March 26, in Quinnsworth on Sandymount Road had been left unpacked in shopping bags. A receipt in the bags confirmed the date and time of purchase as 26/03/1993 at 11.02am. This is the last confirmed activity of Annie McCarrick. Ms McCarrick was reported missing by a friend at Irishtown Garda Station on the evening of Sunday, March 28. The last confirmed sighting of Annie McCarrick in 1993 This missing person report was confirmed by her mother Nancy when she arrived in Dublin on Tuesday, March 30. The search for Annie McCarrick has continued since. At the site of the search in an estate in Clondalkin, gardaí moved in early to place metal hoardings around the front garden of a house and parked a mini digger in the front garden. Other equipment including a concrete saw were also brought to the house. The current occupiers of the house are not in any way the subject of the investigation. Members of the Garda Technical Bureau arrived at the scene at 10am, and a number of detectives could be seen going into and out of the property. It is understood the house has been heavily renovated and extended in recent years, and its current footprint extends beyond the footprint of the original house when it was built. The property has a long narrow garden to the rear. The location in Clondalkin is a mature estate of detached and semi-detached houses. Neighbours said they were surprised and curious to see if the search would yield anything of evidential value that could progress the case. Because Annie McCarrick disappeared more than 30 years ago, many of the current residents of the estate were not living in the estate at the time. 'I was walking the dog this morning and I could see the hoarding being put up at the house, and I thought maybe the owners were getting building work done, but then I could see a few guys in suits arriving and talking with the men putting up the hoarding, and then garda vans and vehicles started to arrive,' said one neighbour. 'We didn't know what was happening but then we started to see the news reports. I hope they find something that would bring some answers to her family,' he added. At around 12.30pm a garda van was reversed into the garden and a number of boxes were brought into the house. It left half an hour later, and work continued behind the metal fences. The van returned shortly after 2pm and then left again. Numerous garda vehicles remained at the scene throughout the afternoon as teams of gardai worked behind the metal screens. This morning's arrest and search operation is being led by an investigation team from the DMR South Central Division, the Serious Crime Unit based at Irishtown Garda Station under the direction of a Senior Investigating Officer and with the assistance of the Serious Crime Review Team and the Garda National Bureau of Criminal Investigation. The search is being carried out by the DMR South Central divisional search team supported by the Garda National Technical Bureau. The search operation has the support of other State and external expertise if required. An Garda Síochána said it would continue to keep the family of Annie McCarrick fully updated in relation to this investigation. They have been fully appraised of today's developments. An Garda Síochána appeal to anyone with information, no matter how small or insignificant that they might believe it to be, to contact the investigation team. Gardaí also appeal to anyone that may have previously come forward – but who felt that they could not provide gardaí with all of the relevant information they had in relation to this matter – to please make contact with An Garda Síochána again. Any information will be welcomed by the investigation team and will be treated in the strictest confidence. The investigation team can be contacted at Irishtown Garda Station on 01 666 9600 or anyone who wishes to provide information confidentially should contact the Garda Confidential Line on 1800 666 111.
