Hello Nature readers, would you like to get this Briefing in your inbox free every day? Sign up here.
Dairy cattle seem to survive infection with the H5N1 strain of influenza virus, which has killed millions of wild birds.Credit: Ben Brewer/Reuters
As the first-known outbreak of H5N1 avian influenza in cows continues in the United States, scientists are increasingly concerned that the animals will become a permanent reservoir for the virus, giving it more chances to mutate and jump to humans. Cows usually survive infection, which could make them a good place for viruses to acquire mutations by swapping genetic material — and there are a lot of cows. One dairy worker in Texas has definitely already been infected with H5N1 (with only mild symptoms) but there could be far more unidentified cases because testing of people is limited.
A new version of DeepMind’s AlphaFold tool gives scientists the ability to predict protein structures during interactions with other molecules. The tool could be transformative for drug discovery because it can predict the shape of proteins that contain function-altering modifications, or their structure alongside those of DNA, RNA and other cellular players that are crucial to a protein’s duties. “This is just revolutionary,” says biochemist Frank Uhlmann. “It’s going to democratize structural-biology research.” Access to the AlphaFold3 server, however, is limited — partly to protect the advantage of DeepMind’s own drug-discovery spin-off company.
The United States has introduced a new policy that provides stricter oversight of biological experiments that could be misused or spark a pandemic. It took more than four years of deliberations to develop a system that evaluates the risks and benefits of pathogen research without paralysing fundamental science. The policy, which comes into effect next year, sets a standard that might inspire other countries to re-evaluate their current approaches, says biosecurity researcher Filippa Lentzos.
Mexico has two scientist-candidates for president in its elections next month. Leading in the polls is environmental engineer Claudia Sheinbaum Pardo, who has vowed to “make Mexico a scientific and innovation power”. Sheinbaum Pardo would be the first woman and first environmental engineer to lead Mexico. Her rivals include computer engineer Xóchitl Gálvez Ruiz, who criticises Sheinbaum Pardo for not challenging current president Andrés Manuel López Obrador’s policies, including support for Mexico’s oil industry, a controversial science law and cuts to science spending. Some academics echo those concerns: “Is she going to continue López Obrador’s attacks on science or will she … radically change?” asks mathematician Raúl Rojas González.
Rejuvenating the immune system seems to revitalise many organs in an animal’s body — at least in mice. This raises the tantalising prospect of treating immune ageing to control age-related diseases. But interfering with the highly complex immune system can be perilous. Pioneers are setting their sights on low-risk but important goals, such as strengthening older people’s responses to vaccinations and boosting the efficiency of cancer immunotherapies.
In The Light Eaters, journalist Zoë Schlanger takes a deep dive into plant intelligence and consciousness — topics that were long considered pseudoscience. Some cautious studies have popped up, for example of a vine that changes the shape of its leaves to mimic those of neighbouring plants. “As a plant scientist, I am fascinated by what draws us to wanting to define plants as sentient or conscious — or not — through the lens of our limited human understanding of those terms,” writes reviewer Beronda Montgomery.
Do you have a work dilemma you’d like some help with? E-mail [email protected]
QUOTE OF THE DAY
In 2009, neuroscientist Larry Young wrote in Nature about his influential research into how the hormone oxytocin influences complex social behaviours such as the parent-infant bond and romantic love. Young has died, aged 56. (Nature | 5 min read)
Today, I want to share news of the Nature Awards Microbiome Accelerator for researchers with aspirations to translate their microbiome research to transform health outcomes. Four applicants will each receive US$10,000 and entry to an immersive residential programme. Learn more and apply here — the deadline is 24 June.
With contributions by Katrina Krämer, Smriti Mallapaty and Sarah Tomlin
Want more? Sign up to our other free Nature Briefing newsletters:
• Nature Briefing: Microbiology — the most abundant living entities on our planet — microorganisms — and the role they play in health, the environment and food systems.
Stem-cell researcher Carolina Florian didn’t trust what she was seeing. Her elderly laboratory mice were starting to look younger. They were more sprightly and their coats were sleeker. Yet all she had done was to briefly treat them — many weeks earlier — with a drug that corrected the organization of proteins inside a type of stem cell.
When technicians who were replicating her experiment in two other labs found the same thing, she started to feel more confident that the treatment was somehow rejuvenating the animals. In two papers, in 2020 and 2022, her team described how the approach extends the lifespan of mice and keeps them fit into old age1,2.
The target of Florian’s elixir is the immune system. The stem cells she treated are called haematopoietic, or blood, stem cells (HS cells), which give rise to all immune cells. As blood circulates, the mix of cells pervades every organ, affecting all bodily functions.
But the molecular composition of the HS cells changes with age, and this distorts the balance of immune cells that they produce. “Fixing the drift in them that occurs with time seems to fix a lot of the problems of ageing — not only in the immune system but also in the rest of the body,” says Florian, who is now at the Bellvitge Biomedical Research Institute in Barcelona, Spain.
In March3, another team showed that restoring the balance between two key types of immune cell gives old mice more youthful immune systems, improving the animals’ ability to respond to vaccines and to stave off viral infections.
How to make an old immune system young again
Other scientists have used different experimental approaches to draw the same conclusion: rejuvenating the immune system rejuvenates many organs in an animal’s body, at least in mice. And, most intriguingly, evidence suggests that immune-system ageing might actually drive the ageing of those organs.
The potential — helping people to remain healthy in their later years — is seductive. But translating this knowledge into the clinic will be challenging. Interfering with the highly complex immune system can be perilous, researchers warn. So, at first, pioneers are setting their sights on important yet low-risk goals such as improving older people’s responses to vaccinations and improving the efficiency of cancer immunotherapies.
“The prospect that reversing immune ageing may control age-related diseases is enticing,” says stem-cell scientist Vittorio Sebastiano at Stanford Medical School in California. “But we are moving forward cautiously.”
Fading immunity
The human immune system is a complex beast whose multitudinous cellular and molecular components work together to shape development, protect against infections, help wounds to heal and eliminate cells that threaten to become cancerous. But it becomes less effective as people age and the system’s composition starts to change. In older age, people become susceptible to a range of infectious and non-infectious diseases — and more resistant to the protective power of vaccines.
The immune system has two main components: a fast-acting innate system, which destroys invading pathogens indiscriminately, and a more-precise adaptive immune system, whose components learn to recognize specific foreign bacteria and viruses and generate antibodies against them.
The HS cells in the bone marrow spawn the immune cells of both arms of the system. They differentiate into two main classes — lymphoid and myeloid — which go on to differentiate further. Lymphoid cells are mostly responsible for adaptive immunity, and include: B cells, which produce antibodies; T cells, which help to attack invaders and orchestrate complex immune responses; and natural killer cells, which destroy infected cells. Myeloid cells include a raft of cell types involved mostly in innate immunity.
Proteins inside immune-cell-generating stem cells become more symmetrical with age (right).Credit: Eva Mejia-Ramirez
One of the earliest changes in the immune system as people age is the shrinking of the thymus, which begins after puberty. This organ is the crucible for T cells, but a lot of the tissue has turned to fat by the time people hit their 30s, slashing the production of new T cells and diminishing the power of the immune system. What’s more, the function of T cells alters as they age and become less specialized in their ability to recognize infectious agents.
The proportions of different types of immune cell circulating in the blood also changes. The ratio of myeloid to lymphoid cells skews markedly towards myeloid cells, which can drive inflammation. Moreover, increasing numbers of immune cells become senescent, meaning that they stop replicating but don’t die.
Any cell in the body can become senescent, typically when damaged by a mutation. Once in this state, cells start to secrete inflammatory signals, flagging themselves for destruction. This is an important anticancer and wound-healing mechanism that works well in youth. But when too much damage accumulates with ageing — and immune cells themselves also become senescent — the mechanism breaks down. Senescent immune cells, attracted by the inflammatory signals from senescent tissue, secrete their own inflammatory molecules. So not only do they fail to clean up properly, but they also add to the inflammation that damages surrounding healthy tissue. The phenomenon is known as ‘inflammaging’.
“It becomes a terrible positive feedback — a never-ending dance of destruction,” says immunologist Arne Akbar at University College London.
And evidence suggests that this feedback loop is kicked off by the immune system. In a series of experiments in mice4, Laura Niedernhofer at the University of Minnesota in Minneapolis has shown that immune-cell senescence actually drives senescence in other tissues. “These cells are extremely dangerous,” she says.
Her team used genetic methods to eliminate an important DNA-repair enzyme in the immune system of the mice. The animals remained healthy until adulthood but then, unable to correct accumulating mutations, various types of immune cell started to become senescent.
A few months later, increasing numbers of cells in organs such as the liver and kidney also fell into senescence, and the organs showed signs of damage. These effects were all reversed when the scientists gave the mice immune cells from the spleens of young, healthy mice.
All of this suggests that fixing the characteristics of immune-system ageing could help to prevent or mitigate diseases of ageing, says Niedernhofer.
Battling senescence
Many scientists are trying to do just that, from very different angles. Lots of the approaches hint that very short treatments of the immune system might have long-term effects, keeping side effects to a more manageable minimum.
One approach is to tackle senescent immune cells head on, using drugs to either remove them or block the inflammatory factors they secrete. “Senescent immune cells have long been known to be very modifiable in humans,” says Niedernhofer. “They go up if you smoke and down if you exercise.”
Are your organs ageing well? The blood holds clues
Some drugs — such as dasatinib, which is approved for the treatment of some cancers, and quercetin, which is marketed as an antioxidant dietary supplement but not approved as a drug — are known to reduce the age-related acceleration of senescence, and dozens of clinical trials are testing their impact on various age-related diseases. Niedernhofer herself is involved in a small clinical trial on older people with sepsis, a condition that becomes more deadly with age.
Her team is also doing experiments to assess which of the many types of immune cell is the most important in driving senescence in the body, which should help in the design of more precise therapies. Two types — T cells and natural killer cells — are emerging as key contenders, she says. She plans to screen natural products and drugs already approved for use by the US Food and Drug Administration for their ability to interact with those types of immune cell in senescence.
Akbar thinks that targeting inflammation itself might be as effective as targeting the senescent cells. He and his colleagues did a study in healthy volunteers using the investigational compound losmapimod, which blocks an enzyme involved in the production of inflammatory molecules called cytokines. They treated the volunteers with the drug for four days, and then, over the course of a week, measured their skin responses to an injection of the virus that causes chickenpox. Most people are exposed to this virus during their lives and it frequently lingers in the body. But with age, people tend to lose their immunity to it, and it can then manifest as shingles. The drug restored the immune response in the skin in older volunteers to a level similar to that seen in the younger volunteers5. In unpublished work, Akbar has found the same robust skin results up to three months later.
“Temporarily blocking inflammation in this way to allow the immune system to function might similarly boost the response of older patients to flu vaccinations,” says Akbar.
Immune boost
The value of priming the aged immune system before administering a vaccine has been demonstrated in a series of clinical trials led by researcher Joan Mannick, chief executive of Tornado Therapeutics, which is headquartered in Boston, Massachusetts. Those trials tested analogues of the drug rapamycin and other drugs with similar mechanisms, which target the immune system and are approved for prevention of organ transplant rejection and for the treatment of some cancers. The drugs block an enzyme, called mTOR, that is crucial for many physiological functions and which becomes dysregulated in old age.
For several weeks before receiving their influenza vaccinations, trial participants were treated with doses of the drugs that were low enough to avoid side effects. This treatment regimen improved their responses to the vaccine, and boosted the ability of their immune systems to resist viral infections in general.
Vaccines tend to work less efficiently in older adults, but new approaches could boost their power.Credit: Hector Vivas/Getty
But rapamycin can raise susceptibility to infection and affect metabolism, so Mannick is planning trials with similar drugs that might have a safer profile. “But there are all sorts of different ways to try to improve the immune system,” she notes.
One other way is to try to restore the function of the thymus to maintain the production of new T cells. Immunologist Jarrod Dudakov at the Fred Hutchinson Cancer Center in Seattle, Washington, is researching the basic biology of thymus cells to try to work out how they regenerate themselves after stressful assaults. “It’s all a bit early to see how this understanding will translate into the clinic,” he says. But he thinks that maintaining the ability of the thymus to generate a broad repertoire of T cells will be “foundational”.
Others are trying to combat ageing by generating thymic tissue from pluripotent stem cells for eventual transplantation. But Greg Fahy, chief scientific officer at Intervene Immune in Torrance, California, says he sees no need to wait for these long-term prospects to come to fruition, because an available drug — synthetic growth hormone — is already known to regenerate thymus tissue. He is doing a series of small studies on healthy volunteers using growth hormone as part of a cocktail of compounds. Early results indicate that the participants show increased levels of functional thymic tissue, and that their epigenetic clock — a biomarker of ageing — reverses by a couple of years6. Fahy is now extending the trial to look at whether the drug cocktail also improves physical fitness in a larger group of volunteers.
Turn back time
Another approach, not yet in the clinic, is to partially reprogram immune cells, to try to turn back the clock in cells that have become senescent. This involves transiently exposing the cells in a dish to a cocktail of transcription factors known to induce a pluripotent state in adult cells.
Reversal of biological clock restores vision in old mice
Sebastiano and his colleagues have shown in human cells that this process corrects the epigenetic changes that occur with ageing7. He has co-founded a start-up company to use the technique to try to counteract a problem in a cancer therapy known as CAR T, in which T cells are engineered outside the body to target and destroy a person’s cancer. But the T cells can turn senescent before they can be returned to the person. Rejuvenating them during the generation process would make production quicker and more robust, says Sebastiano.
Florian’s approach, too, aims to produce healthier immune cells — inside the body1,2. HS cells in the blood rack up epigenetic changes, and their environment also changes as they age. This causes proteins in the cells to arrange themselves more symmetrically — a process known as polarization — which shifts the balance of stem-cell differentiation in favour of myeloid cells over lymphoid cells. Florian’s studies used a four-day treatment with a compound, called CASIN, that inhibits one part of this process to correct the polarization, and helped the mice to live longer.
The team saw the same life-extending effects when HS cells from old mice given CASIN were transplanted into old mice that hadn’t received the treatment. “This very small step had a large impact,” says Florian.
Florian next hopes to bring her work to the clinic. As a first case study, she thinks her drug might support regeneration of the immune system after people receive chemotherapy for cancer.
How old?
Research on immune ageing faces some fundamental challenges. One is shared with ageing studies in all organs — the inability to measure ageing precisely.
“We don’t know in a quantitative, measurable, predictive way what ageing means at the molecular level in different cell types,” says Sebastiano. “Without those benchmarks, it is very hard to show rejuvenation.” Last year, a consortium of academics got together to begin developing a consensus on biomarkers of ageing — which will be essential when scientists come to seek approval from regulatory agencies for anti-ageing therapies.
Another challenge is the difficulty in pinning down what makes one immune cell unique. Until recently, it has been hard to demonstrate which subtypes of immune cells live where, and how they change with time.
But technologies such as single-cell RNA sequencing, which quantitatively measures the genes being expressed in individual cells, have tightened up analysis. A large study of immune cells in the blood of mice and humans across a range of ages published last November, for example, revealed 55 subpopulations. Just twelve of those changed with age8.
With so many strands of research coming together, scientists are cautiously hopeful that the immune system will indeed prove to be a key lever in healthy ageing. Don’t expect an elixir of youth any time soon, says Florian — by definition, ageing research takes a long time. “But there is such great potential for translation.”
Apple TV+ took four prizes in the TV craft awards, and may win more in the broader BAFTA Television Awards. Photo: Apple TV+
The BAFTA Television Craft Awards — a branch of the BAFTAs, often thought of as the British Oscars — awarded wins to Apple TV+ hit series Slow Horses and Silo, the iPhone giant said Sunday.
The acerbic espionage drama Slow Horses won for best editing and best sound. Sci-fi series Silo landed wins for best production design and best original music.
In addition, Apple TV+ received further nominations in the upcoming BAFTA Television Awards.
Apple TV+ wins BAFTA Television Craft awards for Slow Horses, Silo and more
Apple TV+ took two awards apiece in the 2024 BAFTA Television Craft Awards for its acclaimed espionage drama Slow Horses and its sci-fi hit Silo. Slow Horses landed Best Editing: Fiction and Best Sound: Fiction, while Silo won for Best Production Design and Best Original Music.
The BAFTA Television Awards recognize the best British programs, performances and productions each year. Outside of the craft awards subset, Apple TV+ got further nominations for the upcoming awards, below.
Apple landed four BAFTA Television Craft Award wins in total, including:
Slow Horses
Editing: Fiction — Sam Williams
Sound: Fiction
Silo
Production Design — Gavin Bocquet, Amanda Bernstein
Original Music: Fiction — Atli Örvarsson
Upcoming BAFTA Television Awards nominations
Apple TV+ also got nominated for four category awards at the 2024 BAFTA Television Awards that take place Sunday, May 12:
Slow Horses
Drama Series Supporting Actor — Jack Lowden
Hannah Waddingham: Home for Christmas
Entertainment
The Enfield Poltergeist
Specialist Factual
Previous BAFTA wins for Apple TV+
Apple TV+ has previously won BAFTA Television Awards:
Best Drama Series in 2023 for acclaimed hit Bad Sisters, along with the show’s awards for Best Supporting Actress (Anne-Marie Duff) and Best Titles & Graphic Identity for Peter Anderson Studio.
Apple’s limited series The Essex Serpent landed Best Costume Design for first-time BAFTA winner Jane Petrie in 2023.
In 2022, 9/11: Inside the President’s War Room won Editing: Factual, and 1971: The Year That Music Changed Everything earned Sound: Factual.
Windows 10 has received a new optional update and it comes with some much-needed fixing to cure problems some users have been experiencing with the search function in the OS.
Microsoft tells us that: “This update makes some changes to Windows Search. It is now more reliable, and it is easier to find an app after you install it. This update also gives you a personalized app search experience.”
As Windows Latest describes, for some Windows 10 users, search has become a somewhat hit or miss affair particularly around trying to quickly fire up an app. Such as, for example, searching for the ‘Recycle Bin’ and not getting the icon for that returned, but other functions instead.
On social media, there have been a number of reports about wonky search experiences, too, such as this one on Reddit where Windows 10 refused to find a commonly-used app.
In more extreme cases, search is locking up and crashing, which is the pinnacle of irritation for this part of the UI.
Analysis: Wait a little longer
Hopefully, this kind of behavior should be a thing of the past when this update is applied. However, note that this is just an optional update at this point, so it’s officially still in testing – meaning there’s a slight chance the fix may not be fully working. Or that the KB5036979 update might cause unwelcome side-effects elsewhere in Windows 10 (it wouldn’t be the first time, certainly).
Get the hottest deals available in your inbox plus news, reviews, opinion, analysis and more from the TechRadar team.
The safest bet is to wait it out, let early adopters test this preview update, and install the finished cumulative update when it arrives in May (on Patch Tuesday, which will be May 14).
At least we know this piece of smoothing over is now incoming, so those who’ve been frustrated with iffy search results now know that – with any luck – their woes should soon be over. Or at least, they’ll face spanners in the search works with less regularity.
Elsewhere with this update, Microsoft has also improved the reliability of widgets on the lock screen, with a more “customized experience” and more visuals available, so these should be better all-round, too.
The downside with KB5036979? That’s a new initiative to introduce notifications about your Microsoft Account in the Start menu and Settings app, which will doubtless consist of various prompts to sign up for an account, or to finish that process.
Jaime Guevara-Aguirre (back left) and Valter Longo (back right) pose with several of the Laron study participants.Credit: Courtesy Jaime Guevara-Aguirre & Valter Longo
A rare form of dwarfism that affects only 400–500 people worldwide has caught the interest of scientists who study ageing and metabolic diseases. This is because a series of studies have associated the condition with a number of positive health effects, including protection against diabetes, cancer1 and cognitive decline2. Mice with a similar condition live for about 40% longer than do control animals3.
Although it is unclear whether people with the condition, known as Laron syndrome or growth-hormone-receptor deficiency, live longer on average than those without it, a study published today in Med shows that they do seem to be at lower risk of developing cardiovascular disease4. They have lower blood pressure, reduced artery fat build-up and a less thick carotid artery wall than do relatives who do not have the syndrome.
“In some sense, this was the most important of all studies,” says Valter Longo, a biogerontologist at the University of Southern California in Los Angeles and a co-author of today’s paper. “It was the last piece missing in showing that they seem to be protected from all the major age-related diseases.” Studying the details of the syndrome, he adds, might inspire the development of drugs or diets with similar protective effects.
From Ecuador to the world
The study examined 24 people with Laron syndrome and 27 of their relatives, all of whom live in Ecuador, which is home to about one-third of all people with the condition, says Jaime Guevara-Aguirre, an endocrinologist at the University of San Francisco in Quito, Ecuador, and a co-author of the study. He has been following this group for more than 30 years, since he identified a cluster of cases in a few secluded villages in the Andes Mountains.
Dwarfism may stymie diseases of old age
People with Laron syndrome have a deficiency in the growth hormone receptor that prevents their bodies from properly using the hormone. These individuals have normal or high levels of growth hormone but low levels of insulin-like growth factor-1 (IGF-1), which normally helps growth hormone to promote the growth of bones and tissues.
Because having low IGF-1 levels has been associated with a higher risk of cardiovascular disease5, “everybody assumed that people with Laron probably had a lot of heart and cardiovascular problems, too”, says Longo. A previous study by the same group found that people with Laron syndrome had a normal rate of death from cardiovascular disease1. But when Guevara-Aguirre investigated some of the deaths attributed to heart attacks, he found inconsistencies. “People in those little towns sometimes attribute any death without an explanation to myocardial infarction because it’s the easiest thing,” he says.
The researchers performed a series of tests that showed that people with Laron syndrome actually had normal or improved levels of cardiovascular-disease risk compared with their relatives without the disorder.
“These are preliminary results from a very small number, but they’re interesting observations,” says Ravi Savarirayan, a clinical geneticist and researcher at Murdoch Children’s Research Institute in Melbourne, Australia. “And I think they will need to be replicated in much larger cohorts.” Savarirayan and his colleagues found similar results6 in patients with another type of dwarfism called achondroplasia. “It was just really interesting when I looked at this paper and saw a lot of similarities between the two,” he says.
Endocrinologist Manuel Aguiar-Oliveira at the Federal University of Sergipe in Brazil, who studies another rare mutation that causes short stature, also found similar cardiovascular protective effects7 in a group of people he has been following for more than 30 years in Brazil. “The data are very similar,” he says.
Researchers are intrigued by the possibility that people with Laron syndrome might live longer than average. So far, Longo, Guevara-Aguirre and their colleagues have found no sign of this, but they still hope to find a longevity signal if they compare people with the syndrome with their unaffected siblings. “I’m still trying to get the funds to do this study,” says Guevara-Aguirre.
Drug inspiration?
Haim Werner, a geneticist at Tel Aviv University in Israel who studies the protective effects of Laron syndrome against cancer, says that the current work is important in helping to characterize genes and pathways that might confer protection against cardiovascular disease. “Delineation of these genes is of crucial importance for future nutritional or pharmacological interventions,” he says.
Is a boost to height a boost to health? Dwarfism therapies spark controversy
Longo hopes that the recent results might inspire the development of new strategies to prevent cardiovascular disease in people without the condition, perhaps an oral drug to bring IGF-1 levels down by targeting the growth hormone receptor. “We just have to find out how to do it safely, so that we don’t make things worse,” he says. Aguiar-Oliveira is less enthusiastic about blocking hormones to mimic the positive effects in unaffected people. “I think this type of intervention may be risky,” he says.
The researchers also want to help people with Laron syndrome. Longo and Guevara-Aguirre have been advocating for pharmaceutical companies and the Ecuadorian government to provide IGF-1 to children and adolescents with the syndrome to promote growth, which some research suggests might have benefits for people with dwarfism. The researchers have also begun testing a dietary approach that they hope will improve the growth of children with the syndrome. And Guevara-Aguirre has been providing free medical care to the group. “They still call me every week with one problem here or there,” he says. “Fortunately, they don’t have many.”
If your Mac is running slow, there are a few things you can do to speed it up and better understand what’s slowing it down.
It’s not just that your Mac is old — although that is an important factor. It could be that you don’t have enough memory, especially if you like to use Google Chrome. You may have a bunch of apps running in the background. There also might be dust in the vents, keeping your Mac from running nice and cool.
This post contains affiliate links. Cult of Mac may earn a commission when you use our links to buy items.
5 reasons for a slow Mac
1. Switch from Google Chrome (and other apps) to Safari
Safari is much easier on your Mac than Google Chrome, which is a notorious power drain and memory hog. The more Chrome tabs you have open, the less memory you have available for everything else.
Safari consistently comes out on top of browser speed tests. According to Apple, Safari loads pages up to 50% faster than Chrome. So, switching to Safari from Chrome is an easy way to speed up your slow Mac. (Making the switch also gives you a security boost, especially if you max out Safari’s privacy settings.)
It’s not just Google Chrome itself, either. Apps like Slack, Discord, Spotify, Microsoft Teams and many others are made using the Chrome browser engine, too. But there’s a solution to this problem: Instead of using the official versions of those apps, you can open them and sign in from Safari, then click File > Add to Dock.
Then you’ll be able to run your web apps in their own windows, just like before, but with the energy-efficient Safari powering them instead.
2. Check what apps are running in the background on your slow Mac
Clear out the background items you don’t use. Screenshot: D. Griffin Jones/Cult of Mac
It’s good to keep an eye on what’s running in the background, especially if your Mac is running slow. It could be that you’ve installed a bunch of apps over the years, and one of them is still churning away in the background even though you never use it.
You can find this information in System Settings > General > Login Items.
On top, you’ll see apps that launch automatically when you sign in to your Mac. You can click to select one and click the − button to remove it. Below, you’ll see a list of apps allowed to run in the background. Simply uncheck them to turn them off.
Other background activities are built into macOS itself. There’s no easy way to turn them off without digging into the Terminal, but you should be aware of them:
If you sync your photo library to your Mac, it’ll download new pictures and videos in the background and scan through them to identify people and pets.
Spotlight, the universal search box that can find files, apps, messages, email and more, occasionally needs to scan your Mac to find if there’s anything new.
3. Your slow Mac is simply too old
Macs last a really, really long time — and that’s both a blessing and a curse. I used my 2015 MacBook Pro for eight years, even as its battery started swelling. Now, it’s probably a fire hazard.
Apple releases a major new version of macOS every year. And updating can make an older Mac run slowly. If you keep using an older version (while still installing Apple’s minor security updates), your Mac might run a little faster. (Or, at least, stop getting slower.) Major new releases with new features can slow down an older computer.
Toward the end of the period when Apple sold computers with Intel chips — let’s say from 2014 to 2020 — there were some pretty bad Macs. The 2014 to 2018 Mac mini is legitimately one of the worst Macs ever made. If you own one of those, I’m sorry.
Clean out your old Mac with compressed air. Photo: D. Griffin Jones/Cult of Mac
If your Mac starts getting warm, it will automatically slow down (aka “throttle”) the processor to keep it from getting too hot. Normally, your Mac will only throttle itself if you’re doing something really intense, like exporting a video. It can be frustrating if your Mac slows down in the middle of your regular work.
In an older MacBook, the vents can become blocked by dust over time and cause overheating. That’s pretty easy to fix. Carefully unscrew and remove the MacBook’s bottom case. Then use a vacuum cleaner or a can of compressed air to clear out all the visible dust.
In ordinary usage, it’s rare for a newer MacBook Air with Apple silicon to be pushed to its limits, but it can still happen. Since these laptops doesn’t come with an internal fan, you can boost their performance with a cooling pad.
This model sold on Amazon costs only $25. When you’re at your desk, you can put your MacBook on top of it. The cooling pad’s fans will keep cool air blowing underneath, where a MacBook Air gets the hottest. This particular cooling pad doubles as a USB hub, so plugging it into your Mac gives you two USB ports as well.
5. You don’t have enough memory (or storage)
Most Macs made in the last 10 years start with just 8GB of memory on the base model. Upgrading to 16GB or more is one of the most important upgrades you can make when buying a Mac, but a lot of people skip it. You can upgrade the RAM on some older Macs, but not on any recent ones running on Apple silicon.
The bad news is, if you have too many apps open at once, other apps you have open will be pushed out of memory. And that can really make your Mac run slowly if you’re trying to multitask. Short of splurging on extra memory with your next Mac, unfortunately, the only solution when this happens is to quit big apps you’re not using.
This problem can be compounded if your Mac is running low on storage, too. Usually, when your Mac is running low on memory, background apps will be offloaded into storage — but if you don’t have enough storage, that can cause more problems. Here’s what to do if you need to clear up space on your Mac.
Open Roads is an easy game to get lost in. It tells a twisting tale about generational trauma — the tension, lies and love between mother and daughter — with all the comfort and warmth of an early 2000s network drama like Gilmore Girls or Charmed. As a former suburban teen myself, this game left me feeling equally exposed and understood.
Open Roads is set in 2003, and through environment and character design alone, it captures an authentic slice of life in this post-9/11, pre-Razr era. In the early aughts, I spent my teen years bouncing between Dad’s apartment on the outskirts of the city and Mom’s house in a dusty development site surrounded by grocery stores and Blockbuster Videos, and I had big dreams of escaping both. All this is to say, I relate to Open Roads‘ main character, Tess, who’s finishing up high school and planning a future in the hot new market of webpage design. Her parents are newly divorced and she’s been living with her mom, Opal, and grandma, Helen, outside of Detroit. Helen recently passed and her home is being sold against Opal’s wishes, so she and Tess are begrudgingly clearing it out and looking for a new place to stay.
Open Roads Team
The details of Tess’ family history are slowly exposed as she explores Grandma Helen’s home, told in old newspapers, photographs, books, postcards, heirlooms, phone calls and pottery-making materials. Tess and Opal eventually discover a suitcase hidden behind a false wall in the house, and it spurs them to embark on a road trip to long-lost locations from Opal’s past. Helen was a popular advice columnist and writer similar to Dear Abby, and her leftover letters, scattered around each environment, steadily peel back the layers of secrets that have enshrouded her, her daughter’s and granddaughter’s lives.
Every character in Open Roads has something to hide. I actually clocked the big twist about halfway through the game, but there was enough drama, doubt and emotional heft to keep me invested in the narrative regardless. Do yourself a favor and don’t look up any story spoilers — just enjoy the Open Roads ride.
Open Roads Team
This is exceedingly easy to do. Open Roads has expertly written dialogue, and its characters are infused with rich histories and complex motivations. The back and forth between Tess and Opal feels genuine for a teen daughter and her mother who’ve been trapped together in a car for hours on end: They quickly spark to anger and reconciliation, and just as easily act supremely silly around each other. A foundation of tenderness underlies their interactions. The voice acting, provided by mainstream television actors Keri Russell and Kaitlyn Dever, is superb, adding to the game’s immersive pull.
Open Roads uses a mix of 3D and 2D art — the backgrounds and interactable objects are 3D, while Tess and Opal are animated in hand-drawn 2D, moving in a floaty manner that reminds me of the early Disney classics. The styles work well together, for the most part. I found the visuals jarring in one section, when Tess and Opal were having a conversation in direct sunlight and the brightness of the scene made their 2D avatars look unfinished, unblended with the setting. Generally though, Open Roads is filled with engaging environments and beautiful details, with plenty of items to investigate and small puzzles to solve. The story unfurls naturally with every action prompt, and dialogue choices alter Tess and Opal’s trajectory throughout the game.
Open Roads Team
The sound design in Open Roads is particularly spectacular. Each object that Tess interacts with has a sound specific to its texture and weight. When Tess sets a cookie tin down on a kitchen countertop, it sounds like hollow metal scraping against wood; when she picks up a discarded cigar, the audio cues are soft and papery; Tess’ footsteps sound distinct on bare floorboards, carpet and rugs, with changes in density, bass and sharpness for each new material. Picking up Tess’ flip phone to text her BFF, I can hear the groaning of thick plastic hinges and the padded creaking as she rapidly presses down on the number pad. These sounds are crucial aspects of the game, louder than the bed of acoustic guitar or light synth that make up the soundtrack, and I’m entirely here for it. Open Roads is proof that ASMR exploration games should be a thing.
The features that will stick with me after finishing Open Roads are its sound design and its authenticity. There aren’t many games focused on the everyday lives and conversations of women, let alone mothers and daughters, and Open Roads is a testament to the power of these stories. The game oozes warmth and camaraderie, and its writing displays an abundance of respect toward the characters that drive its narrative. Every person with a voice in Open Roads is a woman, and Tess, Opal, Grandma Helen and Aunt August are each dynamic, sympathetic and flawed in unique ways. Considering the developers of this game broke free from a studio whose co-founder was reportedly , this accomplishment is even more significant.
My suggestion for fully enjoying Open Roads is to set aside a lazy afternoon, grab your favorite drink and some snacks, and make sure your headphones are on nice and tight. Turn up the volume so you can hear every plunk and tap of Tess’ world, and don’t try too hard to decipher the game’s secrets. Trust in the story and take it slow. This is a game worth savoring.
Open Roads is out now on consoles and PC, and it’s part of the Xbox Game Pass library. It comes from Open Roads Team, published by Annapurna Interactive.
Google has unveiled Gemma, a new open-source artificial intelligence model, marking a significant step in the tech giant’s AI development efforts. This model, which is available in two variants offering either 2 billion and 7 billion parameters AI models, is designed to rival the advanced AI technologies of competitors such as Meta. For those with a keen interest in the progression of AI, it’s crucial to grasp both the strengths and weaknesses of Gemma.
Gemma is a family of lightweight, state-of-the-art open models built from the same research and technology used to create the Gemini models. Developed by Google DeepMind and other teams across Google, Gemma is inspired by Gemini, and the name reflects the Latin gemma, meaning “precious stone.” Gemma is an evolution of Google’s Gemini models, which suggests it is built on a robust technological base. Gemma AI models provide a choice between 7B parameters, for efficient deployment and development on consumer-size GPU and TPU and 2B versions for CPU and on-device applications. Both come in base and instruction-tuned variants.
However, the sheer size of the model has raised questions about its practicality for individuals who wish to operate it on personal systems. Performance benchmarks have indicated that Gemma might lag behind other models like Llama 2 in terms of speed and accuracy, especially in real-world applications. One of the commendable aspects of Gemma is its availability on platforms such as Hugging Face and Google Colab. This strategic move by Google encourages a culture of experimentation and further development within the AI community. By making Gemma accessible, a wider range of users can engage with the model, potentially accelerating its improvement and adaptation.
Google Gemma results tested
Here are some other articles you may find of interest on the subject of Google Gemma :
Despite the accessibility, Gemma has faced criticism from some quarters. Users have pointed out issues with the model’s performance, particularly regarding its speed and accuracy. Moreover, there are concerns about the extent of censorship in Google’s AI models, including Gemma. This could lead to a user experience that may not measure up to that offered by less restrictive competitors.
Gemma AI features :
Google Open Source AI:
Gemma is a new generation of open models introduced by Google, designed to assist developers and researchers in building AI responsibly.
It is a family of lightweight, state-of-the-art models developed by Google DeepMind and other Google teams, inspired by the Gemini models.
The name “Gemma” reflects the Latin “gemma,” meaning “precious stone.”
Key Features of Gemma Models:
Model Variants: Two sizes are available, Gemma 2B and Gemma 7B, each with pre-trained and instruction-tuned variants.
Responsible AI Toolkit: A toolkit providing guidance and tools for creating safer AI applications with Gemma.
Framework Compatibility: Supports inference and supervised fine-tuning across major frameworks like JAX, PyTorch, and TensorFlow through native Keras 3.0.
Accessibility: Ready-to-use Colab and Kaggle notebooks, integration with tools like Hugging Face, MaxText, NVIDIA NeMo, and TensorRT-LLM.
Deployment: Can run on laptops, workstations, or Google Cloud, with easy deployment on Vertex AI and Google Kubernetes Engine (GKE).
Optimization: Optimized for multiple AI hardware platforms, including NVIDIA GPUs and Google Cloud TPUs.
Commercial Use: Terms of use allow for responsible commercial usage and distribution by all organizations.
Performance and Safety:
State-of-the-Art Performance: Gemma models achieve top performance for their sizes and are capable of running on developer laptops or desktops.
Safety and Reliability: Gemma models are designed with Google’s AI Principles in mind, using automated techniques to filter out sensitive data and aligning models with responsible behaviors through fine-tuning and RLHF.
Evaluations: Include manual red-teaming, automated adversarial testing, and capability assessments for dangerous activities.
Responsible Generative AI Toolkit:
Safety Classification: Methodology for building robust safety classifiers with minimal examples.
Debugging Tool: Helps investigate Gemma’s behavior and address potential issues.
Guidance: Best practices for model builders based on Google’s experience in developing and deploying large language models.
Optimizations and Compatibility:
Multi-Framework Tools: Reference implementations for various frameworks, supporting a wide range of AI applications.
Cross-Device Compatibility: Runs across devices including laptops, desktops, IoT, mobile, and cloud.
Hardware Platforms: Optimized for NVIDIA GPUs and integrated with Google Cloud for leading performance and technology.
However, there is room for optimism regarding Gemma’s future. The development of quantized versions of the model could help address the concerns related to its size and speed. As Google continues to refine Gemma, it is anticipated that future iterations will overcome the current shortcomings.
Google’s Gemma AI model has made a splash in the competitive AI landscape, arriving with a mix of promise and challenges. The model’s considerable size, performance issues, and censorship concerns are areas that Google will need to tackle with determination. As the company works on these fronts, the AI community will be watching closely to see how Gemma evolves and whether it can realize its potential as a significant player in the open-source AI arena.
Filed Under: Technology News, Top News
Latest timeswonderful Deals
Disclosure: Some of our articles include affiliate links. If you buy something through one of these links, timeswonderful may earn an affiliate commission. Learn about our Disclosure Policy.
