March 18, 202513 min readNew Treatments Are Rewriting Our Understanding of SchizophreniaAs a complex picture of schizophrenia emerges, so do new ways to treat the disorderBy Diana Kwon edited by Madhusree Mukerjee Galen DaraCharlene Sunkel was 19 when she started hearing voices and strange thoughts began filling her head. People wanted to infiltrate her mind, to poison her, to rat her out to the police. She stopped making eye contact, convinced that it would enable others to steal her thoughts. Once sociable and outgoing, Sunkel withdrew from friends and family, worried that they were conspiring against her. On her way to work, she had visions of men in hoods from the corner of her eye. As the illness progressed, she lost the ability to understand what people were saying, and when she spoke, the words would not come out right. About a year after her symptoms started, Sunkel was diagnosed with schizophrenia.Delusions, hallucinations and disordered thinking are collectively known as psychosis. These positive symptoms are among the most widely recognized aspects of schizophrenia. For about two thirds of patients with schizophreniawhich affects approximately 23 million people around the worldtraditional antipsychotic drugs are often highly effective at treating psychosis. But these drugs frequently come with problematic side effects. And they do little to help with the so-called negative symptoms of schizophrenia, such as emotional flatness and social withdrawal, or with other issues involving thinking and memory referred to as cognitive problems.Until quite recently, all antipsychotics worked in essentially the same way. They blocked the activity of dopamine, a chemical messenger in the brain involved in motivation, learning, habit formation, and other processes.On supporting science journalismIf you're enjoying this article, consider supporting our award-winning journalism by subscribing. By purchasing a subscription you are helping to ensure the future of impactful stories about the discoveries and ideas shaping our world today.But the arrival last September of a new drug, KarXT, supports an emerging awareness among clinicians that schizophrenia is more complex than most of them had realized. KarXT is the first antipsychotic to target a molecule other than dopamine. It may be a key aspect of the disorder in some people, but dopamine is just one of many different neurotransmitters involved in the illness. That complexity may provide fresh avenues for treatment.There is no schizophrenia. There are schizophrenias. Romina Mizrahi, professor of psychiatryTo Thomas Kabir, a senior researcher at the University of Oxford with a lived experience of psychosis, KarXTs potential to not only reduce symptoms of psychosis but also improve thinking is especially exciting. People typically dont have hallucinations and delusions for years on end, he says. It is the cognitive issues that really affect peoples day-to-day lives.Perhaps most significant, a growing body of evidence suggests that schizophrenia, which can involve alterations not only in the brain but also in the bodyparticularly in the immune systemdoes not look the same in everyone who has the condition. There is no schizophrenia. There are schizophrenias, says Romina Mizrahi, a professor of psychiatry at McGill University. What clinicians need now, she adds, is a way to categorize individuals based on the underlying biology of their illness so that treatments can be better tailored to their needs.Scientists have been trying to understand the neurobiological underpinnings of schizophrenia for more than a century. German psychiatrist Emil Kraepelin, who in 1893 penned one of the earliest official descriptions of schizophrenia, called it dementia praecox, meaning premature dementia. Because the condition tends to show up in adolescents or young adults, Kraepelin held that schizophrenia was a neurodegenerative disease, similar to those that often afflict the elderly.In contrast, Swiss psychiatrist Eugen Bleuler, whose long hours with patients at the Rheinau psychiatric hospital in Zurich led to more than a decades worth of meticulous notes about their behavior, held that the disorder did not always involve progressive deterioration or begin solely in adolescence. In 1908 he coined the term schizophrenia, meaning split mind, to characterize the fragmentation of mental functions that he saw as central to the condition.Bleuler was prescient in other ways. He referred to the group of schizophrenias, reflecting his view that it was a collection of disorders with a range of severity, a spectrum of symptoms and variable outcomes. And he postulated that the ailments have both a biological and a psychological basis. The tendency for schizophrenia to run in families has since been documentedthe disorder is about 80 percent heritable. But specific genes have been difficult to pin down, and researchers suspect hundreds of them might be involved. Many studies also point to the importance of the environment. Adverse experiences in childhood, being exposed to infections in the womb, growing up in cities and heavy cannabis use all contribute to increased risk.Despite growing evidence of schizophrenia being rooted in changes occurring during childhood, Kraepelins idea that schizophrenia is neurodegenerative persistsalthough it is hotly debated. In some patients, symptoms worsen over time, and this progression is often accompanied by tissue loss in the brain. Several researchers have argued that this deterioration can instead be attributed to factors secondary to the illness, such as poverty and stress.When antipsychotic drugs first emerged, they seemed to drastically simplify the picture. In the 1950s a pair of psychiatrists in France discovered serendipitously that chlorpromazine, a compound designed to be an anesthetic for surgery, helped to address hallucinations and delusions. Chlorpromazine and the other antipsychotics that followed brought an end to an era of crude and often dangerous treatments for schizophrenia, such as lobotomies.At first, no one knew why chlorpromazine and its derivatives worked. Later studies in mice revealed that these medications blocked receptors for dopamine. (Receptors are molecules that serve as code-locked doors, allowing only certain molecules, in this case dopamine, to enter a cell.) These findings, along with observations that high doses of amphetaminesdrugs known to release dopaminecan cause short-term psychosis in healthy people, paved the way for the so-called dopamine hypothesis of schizophrenia. It posits that the symptoms of schizophrenia are caused by an excess of dopamine in the brain.Though effective at treating psychosis, dopamine blockers are no panacea for schizophrenia. They come with a host of side effects, such as tremors resembling those in Parkinsons patients (who suffer from a paucity of dopamine), sedation, and significant weight gain that can subsequently lead to an increased risk of diabetes and heart problems. In fact, cardiovascular disease is one of the most common causes of death in people with schizophrenia who have a long history of using dopamine blockers.Ni-ka Ford; Source: Schizophrenia: From Neurochemistry to Circuits, Symptoms and Treatments, by Oliver D. Howes et al., in Nature Reviews Neurology, Vol. 20; December 2023 (reference)In the years after her diagnosis, Sunkel was hospitalized multiple times and prescribed many different medications that came with debilitating side effects, including intense restlessness, tremors and sedation. One drug led to spasms so severe that she was unable to move or speak. Though deemed treatment-resistant, a label given to people whose symptoms do not improve after two or more drugs, Sunkel ultimately found clozapine, a dopamine-blocking antipsychotic.Despite its side effects, the medication has significantly helped to improve her quality of life, says Sunkel, who is now in her 50s and working as chief executive officer of the Global Mental Health Peer Network in South Africa. But in up to 60 percent of people with treatment-resistant schizophrenia, clozapine, too, can be ineffective.For decades the only available antipsychotic drugs were dopamine blockers. From the 1990s onward, however, researchers began employing techniques such as positron-emission tomography (PET), an imaging method that enables them to view the activity of specific molecules inside the living brain. That work suggested a more complicated story.Neuroscientists used PET imaging and other means to identify neurochemical alterations in the brain that are associated with schizophrenia. They found dopamine activity to be increased in a specific region of the striatum, a structure located deep in the brain that is largely involved in helping us forge mental links between disparate events or things. This anomaly may increase the chances of someone with schizophrenia making false associations or having misperceptions. In addition, scientists discovered that dopamine levels are lowered in the prefrontal cortex, thereby interfering with executive functions such as problem-solving and emotion regulation, which can be impaired in people with the condition.These studies also shed light on why antipsychotics dont always work. In 2012 Oliver Howes, a professor of molecular psychiatry at Kings College London, and his team reported that people who do not respond to traditional antipsychotics have different patterns of dopamine activity in the brain than those who do respond.Such investigations established that dopamine is not the only neurotransmitter involved in schizophrenia. Others include glutamate, a key molecule involved in activating neurons. A group led by psychiatrist John Krystal of the Yale School of Medicine, as well as others, has demonstrated that ketaminea drug that blocks the activity of glutamatecan produce symptoms of psychosis in healthy people. Large-scale searches for genetic variants associated with schizophrenia have also revealed that alterations in genes involved in glutamate signaling are among the key risk factors for developing the disorder. In recent decades many glutamate-targeting drugs have been developed, but none have yet made it through clinical trials.Another key neurotransmitter, called acetylcholine, acts on muscarinic receptors found throughout both the body and the brain that are involved in such processes as movement, memory and learning. The new schizophrenia drug, KarXT, which is marketed and sold as Cobenfy by Bristol Myers Squibb (BMS), selectively activates muscarinic receptors in the brain. In clinical trials, the drug was found to be effective in treating psychosis and seemed to improve cognitive function, without the side effects that make traditional antipsychotics difficult for patients to remain on for long periods. The drug did have gastrointestinal effects, most of which were mild.KarXT is the first antipsychotic to target a molecule other than dopamine.Although more data are needed on the long-term effects of KarXT, the drug has enthused researchers in the schizophrenia fieldThere is indeed another, startlingly different way in which schizophrenia can arise. April Burrell was a healthy, vibrant 21-year-old until a traumatic event changed everything. She developed psychosis and hallucinations and eventually went into a completely catatonic state, unable to move or communicate. She was diagnosed with a severe form of schizophrenia and admitted to the Pilgrim Psychiatric Center in Brentwood, N.Y., where she would spend nearly 20 years.It was only when Sander Markx, a psychiatrist at Pilgrim, gathered a multidisciplinary team and ordered a full medical workup that Burrells doctors discovered her blood contained autoantibodiesantibodies that were attacking her own body, damaging cells in her brain. She received a new diagnosis of neuropsychiatric lupus, an autoimmune disease. After six months of an intensive immunosuppressive treatment regimen, Burrell made an almost full recovery in 2020. You wouldve thought she was a brand-new person, her brother, Guy Burrell, told the Washington Post in 2023.Autoimmune encephalitis, a disease that occurs when the bodys own immune system attacks the brain, was discovered less than two decades ago. Before it was known, many of the people with this illness would havelike Burrellreceived a diagnosis of schizophrenia despite some subtle differences between the two conditions. In people with autoimmune encephalitis, for example, symptoms tend to appear more rapidly and be more severe.Some of the first cases of autoimmune encephalitis were reported in 2007. Josep Dalmau, a neurologist then at the University of Pennsylvania, and his colleagues published descriptions of patients who had autoantibodies against the NMDA receptor, the protein in the brain on which glutamateone of the key neurotransmitters that are altered in people with schizophreniaexerts its action. In the years since, researchers have documented more than two dozen autoantibodies that target the brain. A diagnosis of autoimmune encephalitis, which often requires the detection of autoantibodies in the cerebrospinal fluid (CSF), the liquid washing through the brain and spinal cord, can be life-changing. Some patients who receive immunotherapy make a full recovery.Clear-cut cases of autoimmune encephalitis are rare. According to some estimates, about 1 percent of people with psychosis have autoantibodies whose specific target in the brain has been identified. But determining the true prevalence is difficult because lumbar punctures, which are required to obtain CSF, are rarely carried out in psychiatry clinics, where most people with psychosis go for treatment.According to psychiatrist Ludger Tebartz van Elst of the University of Freiburg and its associated hospital in Germany, where lumbar punctures for people with psychosis are routine, his team has found uncharacterized neuronal autoantibodies (meaning autoantibodies that are not clearly established as causes of psychosis) in approximately 20 percent of patients with psychosis and other psychiatric conditions. Accordingly, Tebartz van Elst and others advocate using the term autoimmune psychosis to describe the ailments of these patients.Researchers are now studying whether the immune system might be at play in a greater proportion of people who receive a schizophrenia diagnosis.The question of whether these nonspecific autoantibodies might play a meaningful role in schizophrenia and other disorders of psychosis has been a matter of intense debate in recent years. Studies of their prevalence in people with psychosiswhich often examine blood because CSF is not always obtainablehave turned up inconsistent results. Researchers have also found these antibodies in healthy people, raising doubts about their clinical significance.Others believe the immune system might contribute to psychosis even in the absence of autoantibodies. Cases of psychosis triggered by infections such as influenza, syphilis and, more recently, COVID-19 are scattered throughout history. In addition, epidemiological studies have reported a greater number of mental disorders such as schizophrenia in people who are born in the winter, when infections are more prevalent, compared with those born in the summer. Assessments from countries that keep national registries of medical data, such as Denmark, have revealed that the more infections a person has, the higher their risk of developing schizophrenia.Whether infections can directly cause psychosis remains uncertain, but over the years many studies have provided evidence for the immune system being the culprit. Genomic investigations of people with schizophrenia have implicated genes linked to key proteins involved in the immune system. Further, the brains resident immune cells, the microglia, are overactive in people with schizophrenia, leading some scientists to suggest that they are involved in the disorder.Researchers are now studying whether the immune system might be at play in a greater proportion of people who receive a schizophrenia diagnosis. Some groups are conducting clinical trials to investigate whether immunotherapies could help people with schizophrenia and other psychosis-related disorders who do not meet the criteria for an autoimmune disease.At Oxford, Kabir, psychiatry professor Belinda Lennox and their colleagues are currently conducting a clinical trial to examine whether rituximab, an antibody used to treat arthritis and other autoimmune disorders, can effectively treat psychosis in people who have detectable neuronal autoantibodies in their blood. Janet Cunningham, a psychiatrist at Uppsala University in Sweden, and her team are carrying out a similar study in that country. If even a small percentage of these individuals respond to these therapies, it would be transformative, Lennox says, because you can potentially cure their lifelong illness.There is much excitement around the possibility of immunotherapies for psychosis, although experts caution against focusing solely on the immune underpinnings of the disorder. Patients can sometimes see autoimmune psychosis as a more palatable diagnosis than schizophrenia because it may provide a more promising road to recoveryand because it avoids the stigma surrounding the word schizophrenia. But immunotherapies are not without their risks. Medications such as cortisone, which are often used in cases of autoimmune psychosis, come with their own side effects, including bone fragility, slow wound healing, and psychological effects such as mood swings and confusion.Cunningham says its important to remember that existing antipsychotics do help many people with schizophrenia and other psychosis-related disorders. Weve gotten to the point where a lot of people are being helped with the medication we have, she says. Now we have to be looking at the ones we are not able to help.Kabir, the Oxford researcher who has lived experience of psychosis, first fell ill while he was a university student. His priority then was staying out of the hospital and completing his degree. The quickest way to do that was to take medication. But later, once his symptoms had stabilized, he added in talk therapy, which he says helped both with psychosis symptoms and with other problems such as depression.Some experts say that to identify the most effective treatment for each patient, clinicians may need to determine an illnesss underlying cause. At Tebartz van Elsts clinic in Freiburg, patients who come in after experiencing psychosis get a full workup, which often involves neuroimaging, blood tests and a lumbar puncture, to rule out any secondary cause for the symptoms. Such extensive tests are not the norm, however. In many parts of the world, including the U.S., whether a person will receive these types of tests depends largely on whether they end up in the office of a psychiatrist or a neurologist.Several large, ongoing efforts are aimed at trying to better characterize people with schizophrenia. The Psychiatric Biomarker Network, led by Steven E. Hyman of the Broad Institute of M.I.T. and Harvard, was established in 2018 with the goal of finding biomarkers in cerebrospinal fluid. The Accelerating Medicines Partnership Schizophrenia, launched in 2020 by several public and private institutions in the U.S. and the European Union, has a similar aim. Researchers hope to find markers that can identify people in the prodromal phase of schizophreniathe period before symptoms appear.Being able to identify people during this phase will open up the possibility of trying to develop preventive treatments, Howes says. His team has identified prodromal signs such as neuroimaging markers and early symptoms such as the Truman sign, where people feel a nagging sense that something strange is going onakin to the way the protagonist of the 1998 movie The Truman Show felt while unknowingly living on the set of a reality TV show. If you can prevent the illness to begin with, you can prevent all the disability and the chronic course that sometimes develops.Numerous questions remain open, such as to what extent the immune system is involved in schizophrenia and how neurotransmitters might be altered in different subgroups of people with the illnesses. Researchers have also identified other potentially important mechanisms that might underlie schizophrenia, such as abnormalities in metabolism. Preliminary research suggests that eating a ketogenic diet, which is high in fat and low in carbohydrates, might ease some of the symptoms of the disorder. Talk therapy is also emerging as helpful in treating people with schizophrenia. For example, cognitive-behavioral therapy, which focuses on helping people adjust their ways of thinking and behaving, can reshape thought patterns that underlie psychosis or help patients deal with negative symptoms such as low motivation or a diminished ability to experience pleasure.Ultimately the hope is to provide better, more targeted therapies for people with schizophrenia. Some clinicians say the field of oncology has a blueprint for how to deal with such complex ailments. Cancer, which was once seen as a single disease, is now viewed as a collection of many diseases with different causes and mechanisms, all unified under a single name. In the same way that personalized therapies are becoming increasingly popular in oncology, researchers see this approach as the future for treating schizophrenia and other mental illnesses.Precision medicine is something that I think will emerge as a bigger and bigger part of the story of schizophrenia treatment, Krystal says. Eventually, he hopes, doctors will be able to tell patients, Youve got this biology, you need that treatment. That is where I think the future of understanding this biology of schizophrenia will take us.

March 15, 2025Math Puzzle: Finish the CycleBy Heinrich Hemme Eight numbers emerge in sequence according to a certain system. One number is unknown. Can you figure out what it should be?Each number is the sum of the squares of the digits of its predecessor.42 = 16 12 + 62 = 37 32 + 72 = 58 52 + 82 = 89 82 + 92 = 145 12 + 42 + 52 = 42 42 + 22 = 20 22 + 02 = 4The missing number is 20.Wed love to hear from you! E-mail us at games@sciam.com to share your experience.This puzzle originally appeared in Spektrum der Wissenschaft and was reproduced with permission.0

Lego Pokmon announced, coming 2026This is not a Drilbur.Image credit: Lego News by Tom Phillips Editor-in-Chief Published on March 18, 2025 In an announcement set to send shockwaves through wallets everywhere, Lego has announced it will launch Pokmon-themed sets in 2026.Lego's reveal today offers little other than two logos sat next to each other on a website, but already the company's accountants will rubbing their paws. Oh, and there's a Pikachu tail made of Lego too. That's nice."Electrify your imagination in 2026 and get ready to build something we've never built with Lego bricks before!" the company has teased.Pokmon has - for a long time - partnered with Mega Bloks to release various buildable sets. No longer, it appears! While Pokmon is not owned by Nintendo per se, the two companies are closely linked, and this announcement follows several successful Lego ranges based around Super Mario, The Legend of Zelda and Animal Crossing.At a guess, I'd say we're likely to see buildable models of Pokmon that you can pop on your desk or in your Ikea kallax, rather than Lego playsets featuring Pallet Town. But I'd love an Ash Ketchum minifigure, Lego, so please do consider it.Start saving up your Bottle Caps now.Elsewhere in Lego-related news, earlier this month, Nintendo announced The Lego Super Mario: Mario Kart - Mario & Standard Kart set. This particular set features a buildable Mario complete with a posable head and arms. The Nintendo mascot is sitting behind the wheel of Mario Kart's Standard Kart, described as "the most iconic Mario Kart vehicle of all".Back in the world of video games, Pokmon Legends: Z-A will launch for Nintendo Switch (and presumably there will be a Switch 2 version) late this year. It's a bit of a longer wait than we were expecting.

Xbox Game Pass late March titles announcedAtomfall! Octopath! Blizzard Arcade Collection!Image credit: Rebellion / Xbox / Eurogamer News by Tom Phillips Editor-in-Chief Published on March 18, 2025 Microsoft has announced its next wave of Game Pass titles available in March 2025, including promising-looking new British survival game Atomfall - well, if you're a PC or Ultimate subscriber.Also included in these latest additions are Mythwrecked, which is the Hades-esque adventure game from the team behind enjoyable indie Rki, and the Blizzard Arcade Collection - which includes a selection of retro classics such as Lost Vikings and Rock & Roll Racing.Here are the list of Xbox Game Pass additions for late March 2025:Octopath Traveler 2 (Series X/S, now with Game Pass Standard) - 19th MarchTrain Sim World 5 (Console, now with Game Pass Standard) - 19th MarchMythwrecked: Ambrosia Island (Cloud, Console, and PC) - 25th MarchBlizzard Arcade Collection (Console and PC) - 20th MarchAtomfall (Cloud and Console via Game Pass Ultimate, and PC) - 27th MarchTunic, Batman: Arkham Knight and Monster Sanctury meanwhile join Xbox Game Pass Core, the lowest-tier subscription formerly branded as Xbox Live Gold.As ever, as Microsoft giveth, so it taketh away. Yet more Yakuza titles are getting the chop from the Xbox Game Pass catalogue, following the previous loss of Yakuza 5 and Yakuza 6 earlier in the month. Monster Hunter Rise is also going - presumably Capcom would prefer you now play Monster Hunter World.The full list of titles leaving Xbox Game Pass on 31st March are as follows:MLB The Show 24 (Cloud and Console)Lil Gator Game (Cloud, Console, and PC)Hot Wheels Unleashed 2 (Cloud, Console, and PC)Open Roads (Cloud, Console, and PC)Yakuza 0 (Cloud, Console, and PC)Yakuza Kiwami (Cloud, Console, and PC)Yakuza Kiwami 2 (Cloud, Console, and PC)Yakuza Like a Dragon (Cloud, Console, and PC)The Lamplighters League (Cloud, Console, and PC)Monster Hunter Rise (Cloud, Console, and PC)If you want to keep playing these games after they leave Game Pass, you'll need to purchase them. On the plus side, Game Pass subscribers get a 20 percent discount.For everything else in Microsoft's subscription service, you can check out our handy Xbox Game Pass guide listing every title available.

You can trust VideoGamer. Our team of gaming experts spend hours testing and reviewing the latest games, to ensure you're reading the most comprehensive guide possible. Rest assured, all imagery and advice is unique and original. Check out how we test and review games hereThe Coalitions upcoming Gears of War: E-Day returns to the series action-horror roots with a cinematic prequel focusing on Emergence Day, humanitys first interaction with the subterranean Locust.Focusing on Marcus Fenix and Dom Santiago, the upcoming prequel may not spend much time on other characters in the series. However, Lester Speight, the actor behind the series iconic Augustus Cole Train Cole has teased their return.Is Cole Train in Gears of War: E-Day?In a surprise post on Twitter yesterday, Speight simply shared an image of Gears of War: E-Day key art on their social media account.Posted without any caption, the tweet immediately saw fans clamour over what appears to be a return of the hilarious Hears character for the upcoming prequel.At this point in the Gears of War timeline, Augustus Cole is not a member of the C.O.G. military. Instead, the character is still a Thrashball player until the death of his family inspires him to take the fight to the Locust horde.The prequel likely wont include the return of Damon Baird, the final member of Delta Team, either as the character is an engineering student at the time of Emergence Day.For more on both of these characters early days, thats what Judgement was for. With this in mind, it seems that Cole Train may either appear in the form of a cameo, or as a multiplayer character. After all, Cole has appeared in some form in every game in the series including Gears POP and Gears Tactics.Not much is known about the upcoming Gears of War: E-Day title except for its premise. With the game likely releasing in late 2006, potentially coinciding with the original games 20th anniversary, itll be a while until we see the game again.For more Gears coverage, read about the scrapped Gears of War 2: Ultimate Edition remake that Xbox turned down.Subscribe to our newsletters!By subscribing, you agree to our Privacy Policy and may receive occasional deal communications; you can unsubscribe anytime.Share

You can trust VideoGamer. Our team of gaming experts spend hours testing and reviewing the latest games, to ensure you're reading the most comprehensive guide possible. Rest assured, all imagery and advice is unique and original. Check out how we test and review games here Contents hide Despite some controversy and heated discourse online, Assassins Creed Shadows is one of the most anticipated games of 2025 because of the franchise and its setting in feudal Japan. Ubisoft has shared the release time map for every region, and the newest AC is available to preload before launch. While the official launch isnt too far away, heres how to play Assassins Creed Shadows early by exploiting the New Zealand trick.When does Assassins Creed Shadows come out in New Zealand?Ubisoft has confirmed that the newest AC launches at midnight local time for consoles, which means Assassins Creed Shadows launches in New Zealand at 12AM NZDT on March 20th.Because it has a local midnight release for consoles, this means players on Xbox will be able to play Assassins Creed Shadows early from 4AM PDT/7AM EDT/11AM GMT on March 19th. Basically, players can get early access to AC before it officially unlocks in their region.Unfortunately, the NZ exploit is only possible on Xbox. Its technically doable on PS5, but its not worth the hassle as youd have to create a separate NZ account, and youd also have to pay more money just to get NZ PSN gift cards.The exploit doesnt work on PC either, but the good news is that Assassins Creed Shadows officially unlocks slightly earlier than consoles for some regions. This includes the UK where the newest AC is scheduled to unlock at 10PM GMT on March 19th for Steam and Ubisoft Connect, which is a couple hours slightly earlier than the midnight launch planned for consoles.How to play AC Shadows early via New Zealand trickAssassins Creed Shadows fans on Xbox will be able to play early from 4AM PDT/7AM EDT/11AM GMT on March 19th by exploiting the New Zealand trick. You need to pre-order and preload the game in advance, and, once the aforementioned hours have passed, simply follow the below steps:Start your XboxHead to SettingsClick SystemChoose Language and LocationChange location to New ZealandRestart your XboxYou will need to keep your Xbox console location settings as New Zealand until AC officially unlocks in your region. Once this happens, you can change your settings back to normal.In other AC news, the game is officially Steam Deck verified for launch, and Ubisoft has clarified the console specs after posting inaccuracies. The game is also available to pre-order at its cheapest price under 50.Assassins Creed ShadowsPlatform(s):PC, PlayStation 5, Xbox Series S/XGenre(s):Action AdventureRelated TopicsAssassin's Creed Shadows Subscribe to our newsletters!By subscribing, you agree to our Privacy Policy and may receive occasional deal communications; you can unsubscribe anytime.Share

While the bathroom on our cover might have very au courant vibes, it is found inside a Brooklyn town house dated to the 1840s. Actually a pair of town houses, which Tal Schori and Rustam Mehta of GRT Architects restored using rigorous European Passive House standards. Our practice loves engaging with historic architecture, says Mehta. We wanted to do right by these buildings.This is the cover story from ADs April 2025 issuePhoto: Jason SchmidtRustam Mehta and Tal Schori of GRT Architects in the Brooklyn town house project.Photo: Jason Schmidt.In Kyoto, a young couple, Sam Brustad and Yuki Shirato, turned to Pritzker Prizewinning architect Kazuyo Sejima, a cofounder of the Tokyo-based firm SANAA, to preserve their century-old machiya, a traditional Japanese residence type. Sadly, its a dying breed, says Shirato, noting that hundreds are demolished each year because many locals find the structures inconvenient, old-fashioned, or expensive to maintain.Homeowner Sam Brustad at the historic machiya in Kyoto he shares with his partner, Yuki Shirato.Photo: Yoshihiro MakinoInside the Kyoto machiya renovated by Pritzker Prizewinning architect Kazuyo Sejima of SANAA.Photo: Yoshihiro MakinoAdapted for modern life, the past, present, and future harmonize in the many extraordinary dwellings preserved on these pages.Never miss a story when you subscribe to AD.

The apartments large living area leads to the bedroom, while the service spaces have been distributed in a functional way: a walk-in closet, bathroom, small storage room, and a niche that contains the kitchen of dark-stained ribbed oak. A pair of custom full-height twin doors in natural oak conceals a service space on one side and access to the bedroom on the other, ensuring privacy. The bathroom, on the other hand, is accessed directly from the bedroom through a concealed door made of iron and glass. The feeling is that of passing through fluid spaces that lead from one to the next and where filtered light falls on the different surfaces.A detail of the bedroom with red headboard and a painting by Georgina Pantazopoulou.The whole project is driven by a desire to create a spatial continuity with more expansive views, multiple perspectives, and sight lines that are partially concealed without being closed off completely. Thus, the kitchen, although its open to the living room, is not visible from the entrance, while the bed is concealed behind the volume of the walk-in closet, creating a refined visual game.Close attention was paid to every detail, starting with the selection of materials, such as the ribbed oak wood in the kitchen, which was reused from a previous installation. The floor, on the other hand, is completely new. We used a resin film that allows you to see the grain underneath it. It gives the home an unusual allure and a decidedly contemporary feel.Custom wood washstand cabinet with Mipa terrazzo top. Stone finish made to design by Bianco67; Marset wall sconce (Roc).The bathroom is a bright space, characterized by the use of large terrazzo tiles for both the floor and the shower and a custom wooden bathroom cabinet with washbasin, also made entirely of terrazzo.The owners favorite part of the apartment? The kitchen and living room, says Marco Paris without hesitation. I love the decision to place it in an alcove. When I cook and host friends, they can be on the sofa, sitting at the table, or on the terrace, and I can still be part of the conversation. Its a place where all the activity in the home comes together, a center point for the energy of the house. The connection with cooking, preparing meals, and hospitality is something I always experienced in my parents home, and now, in a small way, I can relive it in my new space too.

Exit email Trump plan to fund Musks Starlink over fiber called betrayal of rural US Director of $42 billion broadband fund pushed out, says program is being ruined. Jon Brodkin Mar 17, 2025 2:19 pm | 87 Credit: Getty Images | Yuichiro Chino Credit: Getty Images | Yuichiro Chino Story textSizeSmallStandardLargeWidth *StandardWideLinksStandardOrange* Subscribers only Learn moreA federal broadband official departed the US government with a warning that a Trump administration plan will strand rural Americans with worse Internet access in order to help Elon Musk secure public money for Starlink."Stranding all or part of rural America with worse Internet so that we can make the world's richest man even richer is yet another in a long line of betrayals by Washington," wrote Evan Feinman, who had been a Commerce Department official and director of the $42.45 billion Broadband Equity, Access, and Deployment (BEAD) program since 2022.As Politico reported, Feinman made the statement in "a blistering email to his former colleagues on his way out the door Sunday warning that the Trump administration is poised to unduly enrich Elon Musk's satellite Internet company with money for rural broadband."Feinman left the department on Friday. His departure came less than two weeks after Secretary of Commerce Howard Lutnick announced that BEAD was reversing the Biden administration's decision to prioritize fiber Internet networks when distributing grants from the $42.45 billion fund.ProPublica's Craig Silverman reported that "Feinman's term ended and he was not reappointed." Silverman also posted the full email sent by Feinman to colleagues.Warning of deeply negative outcomesFeinman wrote that he is "disappointed not to be able to see this project through" and that "the new administration seems to want to make changes that ignore the clear direction laid out by Congress, reduce the number of American homes and businesses that get fiber connections, and increase the number that get satellite connections."The degree of the shift away from fiber "remains unknown, but regardless of size, it will be a disservice to rural and small-town America," he wrote. Feinman said some versions of the proposal are "benign," but he warned of "significant risk that the changes being proposed will be ill-considered and create deeply negative outcomes."Feinman urged people to contact their representatives in Congress and the Trump administration and urge them to avoid "the worst version" of the planned changes. "They should fix BEAD by removing the requirements that have nothing to do with building infrastructure, NOT change it to benefit technology that delivers slower speeds at higher costs to the household paying the bill... There is still time to help the administration make the right call here. Reach out to your congressional delegation and reach out to the Trump Administration and tell them to strip out the needless requirements, but not to strip away from states the flexibility to get the best connections for their people," he wrote.The 2021 law that created the BEAD program said the government must prioritize technology that "can easily scale speeds over time to meet the evolving connectivity needs of households and businesses; and support the deployment of 5G, successor wireless technologies, and other advanced services."During the Biden administration, the Commerce Department's National Telecommunications and Information Administration (NTIA) decided that fiber architecture is the only technology that achieves the BEAD law's goal of building future-proof networks. Fiber brings high-speed broadband to homes and businesses and is essential for providing backhaul to support advanced wireless services, the Biden NTIA said.Feinman's email said that "even though the law pretty clearly requires that fiber builds be the program's 'priority projects,' the administration wants to increase the usage of low-earth satellites and diminish the usage of fiber." Additionally, fixed wireless providers that use earth-based networks instead of satellites will effectively be "shut out of the BEAD program," he wrote.Some states are on the 1-yard lineRepublicans criticized the Biden administration for not yet distributing grant money, but the NTIA said in November that it had approved initial funding plans submitted by every state and territory. Feinman said the change in direction will delay grant distribution."Some states are on the 1-yard line. A bunch are on the 5-yard line. More will be getting there every week," he wrote. "These more-sweeping changes will only cause delays. The administration could fix the problems with the program via waiver and avoid slowdowns."The program is on pause, even if the new government leaders don't admit it, according to Feinman. "The administration wants to make changes, but doesn't want to be seen slowing things down. They can't have both. States will have to be advised that they should either slow down or stop doing subgrantee selection," he wrote.Delaware, Louisiana, and Nevada had their final proposals approved by the NTIA in January, a few days before Trump's inauguration. "Shovels could already be in the ground in three states, and they could be in the ground in half the country by the summer without the proposed changes to project selection," Feinman wrote.The three states with approved final proposals are now "in limbo," he wrote. "This makes no sensethese states are ready to go, and they got the job done on time, on budget, and have plans that achieve universal coverage," his email said. "If the administration cares about getting shovels in the ground, states with approved Final Proposals should move forward, ASAP."Other states that were nearing the final stage are also in limbo, Feinman wrote. "No decision has been made about how much of the existing progress the 30 states who are already performing subgrantee selection should be allowed to keep," he wrote. "The administration simply cannot say whether the time, taxpayer funds, and private capital that were spent on those processes will be wasted and how much states will have to re-do."Size of spending limit could be crucialFeinman said some changes being floated aren't that big a deal. This includes scrapping requirements that Republicans have described as "woke" priorities."This will include all provisions related to labor and wage, climate resiliency, middle-class affordability, etc. I do not regard the inclusion or removal of these provisions as significant; they were inserted by the prior administration for messaging/political purposes, and were never central to the mission of the program, nor were they significant in the actual conduct of the program," Feinman wrote.Feinman also expects a new per-location spending limit. "This could be fine," he wrote. "There weren't any cases of a state planning to spend hundreds of thousands to connect one location anyway. However, if it's heavy-handed or imposed in a manner that ignores the needs of rural communities, it could be very bad."Feinman said the specific amount of the spending limit would be important because giving grants to Musk's Starlink or Amazon's Kuiper satellite service would cost much less than funding fiber projects. "More people will get Starlink/Kuiper, and fewer people will get fiber connection," he wrote. "This could be dramatic, or it could be measured, depending on where the admin sets the threshold limit, and whether states are permitted to award projects above the new threshold on the basis of value dollar, or if they're forced to take the cheapest proposal, even if it provides poorer service."We contacted the Commerce Department about Feinman's departure and email, and will update this article if we get a response.Jon BrodkinSenior IT ReporterJon BrodkinSenior IT Reporter Jon is a Senior IT Reporter for Ars Technica. He covers the telecom industry, Federal Communications Commission rulemakings, broadband consumer affairs, court cases, and government regulation of the tech industry. 87 Comments

Nous, Yahoo, faisons partie de la famille de marques Yahoo. Lorsque vous utilisez nos sites et applications, nous utilisons des cookies pour:vous fournir nos sites et applications;authentifier les utilisateurs, appliquer des mesures de scurit, empcher les spams et les abus; etmesurer votre utilisation de nos sites et applications. Si vous cliquez sur Accepter tout, nos partenaires, dont 238 font partie du Cadre de transparence de consentement de lIAB Europe, et nous-mme stockerons et/ou utiliserons galement des informations sur un appareil (en dautres termes, utiliserons des cookies), et nous servirons des donnes de golocalisation prcise et dautres donnes personnelles telles que ladresseIP et les donnes de navigation et de recherche, pour fournir des publicits et des contenus personnaliss, mesurer les publicits et les contenus, tudier les audiences et dvelopper des services. Si vous ne souhaitez pas que nos partenaires et nousmmes utilisions des cookies et vos donnes personnelles pour ces motifs supplmentaires, cliquez sur Refuser tout. Si vous souhaitez personnaliser vos choix, cliquez sur Grer les paramtres de confidentialit. Vous pouvez rvoquer votre consentement ou modifier vos choix tout moment en cliquant sur les liens Paramtres de confidentialit et des cookies ou Tableau de bord sur la confidentialit prsents sur nos sites et dans nos applications. Dcouvrez comment nous utilisons vos donnes personnelles dans notre Politique de confidentialit et notre Politique concernant les cookies.