India has warned Pakistan about the “high probability” of flooding in the river Sutlej, with incessant rainfall in the northern states forcing the release of excess water from major dams, sources said on Tuesday.
The alerts were routed to Islamabad through the Ministry of External Affairs on “humanitarian grounds”, they said. Three alerts were issued by India last week for possible flooding in the river Tawi.
The warning issued on Tuesday was for probable floods on Wednesday in the Sutlej, the sources said. In Punjab, the Sutlej, Beas and Ravi rivers and seasonal rivulets are in spate because of heavy rainfall in their catchment areas.
India suspended the routine exchange of hydrological data with Pakistan under the Indus Waters Treaty after the Pahalgam terror attack in which 26 people, mostly tourists, were killed in Jammu and Kashmir on April 22.
Despite the suspension, the fresh flood warnings were communicated purely on humanitarian grounds to Pakistan to prevent loss of lives and property, the sources said. Signed in 1960 and brokered by the World Bank, the Indus Waters Treaty has long governed the sharing of river waters between India and Pakistan.
Scientists from Trinity College Dublin have discovered that electrically stimulating “macrophages” – one of the immune systems key players – can “reprogram” them in such a way to reduce inflammation and encourage faster, more effective healing in disease and injury.
This breakthrough uncovers a potentially powerful new therapeutic option, with further work ongoing to delineate the specifics.
Macrophages are a type of white blood cell with several high-profile roles in our immune system. They patrol around the body, surveying for bugs and viruses, as well as disposing of dead and damaged cells, and stimulating other immune cells – kicking them into gear when and where they are needed.
However, their actions can also drive local inflammation in the body, which can sometimes get out of control and become problematic, causing more damage to the body than repair. This is present in lots of different diseases, highlighting the need to regulate macrophages for improved patient outcomes.
In the new study, just published in the international journal Cell Reports Physical Science, the Trinity team worked with human macrophages isolated from heathy donor blood samples provided via the Irish Blood Transfusion Board, St James’s Hospital. They stimulated these cells using a custom bioreactor to apply electrical currents and measured what happened.
The scientists discovered that this stimulation caused a shift of macrophages into an anti-inflammatory state that supports faster tissue repair; a decrease in inflammatory marker (signalling) activity; an increase in expression of genes that promote the formation of new blood vessels (associated with tissue repair as new tissues form); and an increase in stem cell recruitment into wounds (also associated with tissue repair).
We have known for a very long time that the immune system is vital for repairing damage in our body and that macrophages play a central role in fighting infection and guiding tissue repair.”
Dr. Sinead O’Rourke, Research Fellow in Trinity’s School of Biochemistry and Immunology, and first author of the research article
“As a result, many scientists are exploring ways to ‘reprogram’ macrophages to encourage faster, more effective healing in disease and to limit the unwanted side-effects that come with overly aggressive inflammation. And while there is growing evidence that electrical stimulation may help control how different cells behave during wound healing, very little was known about how it affects human macrophages prior to this work.”
“We are really excited by the findings. Not only does this study show for the first time that electrical stimulation can shift human macrophages to suppress inflammation, we have also demonstrated increased ability of macrophages to repair tissue, supporting electrical stimulation as an exciting new therapy to boost the body’s own repair processes in a huge range of different injury and disease situations.”
The findings from the interdisciplinary team led by Trinity investigators, Professor Aisling Dunne (School of Biochemistry and Immunology) and Professor Michael Monaghan (School of Engineering) is especially significant given that this work was performed with human blood cells (showing its effectiveness for real patients), electrical stimulation is relatively safe and easy in the scheme of therapeutic options, and the outcomes should be applicable to a wide range of scenarios.
Corresponding author Prof. Monaghan added: “Among the future steps are to explore more advanced regimes of electrical stimulation to generate more precise and prolonged effects on inflammatory cells and to explore new materials and modalities of delivering electric fields. This concept has yielded compelling effects in vitro and has huge potential in a wide range of inflammatory diseases.”
Source:
Journal reference:
O’Rourke, S. A., et al. (2025). Electromodulation of human monocyte-derived macrophages drives a regenerative phenotype and impedes inflammation. Cell Reports Physical Science. doi.org/10.1016/j.xcrp.2025.102795
Gmail is a hugely popular email service, with over 2.5 billion users. So when rumors start to swirl about Gmail problems, people pay attention. On Monday, Google made an unusual statement, formally denying that it had issued a broad warning about a major Gmail security issue.
“Gmail’s protections are strong and effective, and claims of a major Gmail security warning are false,” the post read. “While it’s always the case that phishers are looking for ways to infiltrate inboxes, our protections continue to block more than 99.9% of phishing and malware attempts from reaching users.”
It’s a bit odd that Google had to deny sending a warning. As a Gmail user, I didn’t see any major security warning, even though news outlets reported on it.
Salesforce data was affected in June
Perhaps Gmail users were confusing the nonexistent warning with another one.
Back in June, Google posted a blog entry about how its Threat Intelligence group is tracking hackers who are impersonating IT support personnel over the phone. The hackers’ goal is to trick employees into sharing their credentials so they can steal a company’s Salesforce data. (Salesforce is a cloud-based platform that helps businesses manage their customer interactions.)
On Aug. 5, the post was updated to note that one of Google’s own corporate Salesforce instances was affected by this kind of activity.
“Analysis revealed that data was retrieved by the threat actor during a small window of time before the access was cut off,” the post read. “The data retrieved by the threat actor was confined to basic and largely publicly available business information, such as business names and contact details.”
Emails were sent to those affected by this incident on Aug. 8, so if you didn’t receive one, your data wasn’t affected.
In late July, Google also posted a warning about the acceleration of phishing attacks and offered some tips on how to protect yourself.
Tighten up your security
While Google didn’t send out the massive warning last week that was reported, the Salesforce social-engineering hack is a good reminder that even if your Gmail account seems fine, there are ways to improve your email security.
“Each data breach is a reminder of the importance of good security habits,” said Adam Benjamin, CNET managing editor of software and services. “Services like password managers help you set a strong, unique password for each login and minimize the fallout if your information does wind up in the hands of someone else.”
A password manager can help you keep your accounts secure without having to memorize dozens of passwords and remember which is for each account. A recent CNET survey revealed that 49% of US adults have risky password habits. CNET has a list of the best password managers and the pros and cons of each.
Gout could be treated by an ancient gene that humans lost millions of years ago, suggests new research.
A form of arthritis caused by crystals that build up in joints and cause swelling and pain, gout is one of humanity’s oldest diseases.
Once regarded as an illness of the wealthy and believed to have been suffered by Henry VIII, the painful condition is the most common form of arthritis in men and affects around one in 40 adults.
Gout has seen a resurgence in recent years with an almost 1,000% rise in cases in just four years in some parts of England.
Symptoms include sudden, severe pain in a joint, often the big toe, as well as hot, swollen, red skin over the affected joint.
Now, scientists at Georgia State University in the United States may have found an ancient solution to treat it.
They used CRISPR gene editing to bring back a gene that humans lost millions of years ago – and in the process, lowered uric acid levels that cause gout and other conditions, including fatty liver disease.
The research team say that the missing piece is uricase, an enzyme most animals still have.
They explained that uricase breaks down uric acid, the waste product that builds up in blood.
When levels climb too high, uric acid forms crystals in the joints and kidneys, leading to painful gout, kidney disease and other health problems.
But humans and other apes lost the uricase gene around 20 to 29 million years ago.
Jan Romero
By Talker
Some scientists suggest that wasn’t entirely bad at the time.
Researchers, including Dr. Richard Johnson at the University of Colorado, have proposed that higher uric acid levels helped early primates turn fruit sugar into fat, a survival advantage during food shortages.
But what once helped our ancestors survive now contributes to modern diseases, and that’s what Georgia State Professor Eric Gaucher and his team set out to challenge.
Study co-author Prof. Gaucher said: “Without uricase, humans are left vulnerable.
“We wanted to see what would happen if we reactivated the broken gene.”
Prof. Gaucher and Dr. Lais de Lima Balico used CRISPR-Cas9 – a gene-editing tool often called “molecular scissors” – to put a reconstructed ancient uricase gene into human liver cells so they could see how the enzyme worked.
The researchers found that the results were “dramatic” as uric acid dropped and fructose-driven fat build-up in liver cells was prevented.
But the team said results in isolated cells aren’t always enough, so they pushed the experiment further.
To see if the gene would behave the same way in more complex conditions, the researchers moved from simple liver cells to 3D liver spheroids. The miniature lab-grown tissues mimic how organs work in the body.
The revived uricase gene lowered uric acid there, too.
The enzyme also found its way to peroxisomes – tiny compartments inside cells where uricase normally does its job.
The researchers said that suggests the therapy could function safely in living systems, not just in isolated cells.
Prof. Gaucher said: “By reactivating uricase in human liver cells, we lowered uric acid and stopped the cells from turning excess fructose into triglycerides – the fats that build up in the liver.”
Klara Kulikova
By Talker
He said the findings, published in the journal Scientific Reports, matter far beyond gout as high uric acid, also called hyperuricemia, is tied to several modern health problems, not just painful joints.
Studies also link it to high blood pressure and cardiovascular disease, among other conditions – with risks that researchers such as Dr. Johnson have compared to high cholesterol, according to research in the journal Hypertension.
About a quarter to half of patients with high blood pressure also have elevated uric acid, and in new hypertension cases, the overlap jumps to 90%, according to the study.
Prof. Gaucher said: “Hyperuricemia is a dangerous condition.
“By lowering uric acid, we could potentially prevent multiple diseases at once.”
Current gout treatments don’t work for everyone, and some patients react badly to lab-made uricase therapies.
But the researchers say that a CRISPR-based approach could avoid those problems by restoring uricase inside liver cells.
Prof. Gaucher said: “Our genome-editing approach could allow patients to live gout-free lives and potentially prevent fatty liver disease.”
He says next come animal studies and, if results hold, human trials.
Potential delivery options range from direct injections to returning lab-modified liver cells to patients.
Prof. Gaucher says that another option is lipid nanoparticles – the same technology used in some Covid-19 vaccines.
If the approach proves safe, he said it could transform treatment for gout and related metabolic diseases.
But Prof. Gaucher added: “Genome-editing still faces substantial safety concerns.
“Once those are addressed, society will be faced with contentious ethical discussions about who should and should not have access.”
What if generative AI could design life-saving antibiotics, not just art and text? In a new Cell Biomaterialspaper, Penn researchers introduce AMP-Diffusion, a generative AI tool used to create tens of thousands of new antimicrobial peptides (AMPs) – short strings of amino acids, the building blocks of proteins – with bacteria-killing potential. In animal models, the most potent AMPs performed as well as FDA-approved drugs, without detectable adverse effects.
While past breakthroughs at Penn have shown that AI can successfully sort through mountains of data to identify promising antibiotic candidates, this study adds to a small but growing number of demonstrations that AI can invent antibiotic candidates from scratch.
“Nature’s dataset is finite; with AI, we can design antibiotics evolution never tried,” says César de la Fuente, Presidential Associate Professor in Bioengineering (BE) and in Chemical and Biomolecular Engineering in the University of Pennsylvania School of Engineering and Applied Science (Penn Engineering), in Psychiatry and Microbiology in the Perelman School of Medicine and in Chemistry in the School of Arts & Sciences, and the paper’s senior co-author.
“We’re leveraging the same AI algorithms that generate images, but augmenting them to design potent new molecules,” adds Pranam Chatterjee, Assistant Professor in BE and in Computer and Information Science within Penn Engineering, and the paper’s other senior co-author, who began work on the project while at Duke University.
Two labs, one goal
For years, de la Fuente’s lab has successfully leveraged AI to search for molecules with antimicrobial properties in unlikely places, from the proteins of woolly mammoths to those of animal venom and ancient microbes called archaea. “Unfortunately, antibiotic resistance keeps increasing faster than we can discover new antibiotic candidates,” says de la Fuente.
That led to his lab teaming up with Chatterjee’s, which typically designs peptides using AI to treat diseases for which conventional methods of drug development have fallen short. “It seemed like a natural fit,” says Chatterjee. “Our lab knows how to design new molecules using AI, and the de la Fuente Lab knows how to identify strong antibiotic candidates using AI.”
Tuning out the noise
While some generative AI models, like ChatGPT, work by predicting the next word or element in a sequence, “diffusion” models start from random “noise” and iteratively refine it into a coherent output – the principle behind tools like DALL·E and Stable Diffusion.
AMP-Diffusion works the same way, only instead of “denoising” pixels, it refines sequences of amino acids. “It’s almost like adjusting the radio,” says de la Fuente. “You start with static, and then eventually the melody emerges.”
At least two other research teams have applied diffusion models to design antimicrobial peptides, but AMP-Diffusion takes a novel approach.
Instead of first training its own protein “latent space” – a kind of internal map of how proteins are structured – AMP-Diffusion builds on ESM-2, a widely used protein language model from Meta trained on hundreds of millions of natural protein sequences.
Because ESM-2 already has a rich “mental map” of how real proteins fit together, AMP-Diffusion doesn’t need to relearn basic biology. That means it can generate candidate AMPs faster, and its outputs are more likely to follow the intricate patterns that make peptides effective.
Chatterjee’s team also designed AMP-Diffusion to consult ESM-2’s built-in rules while “denoising,” essentially giving the new tool a coach that keeps it grounded in biological reality.
Instead of teaching the model the ABCs of biology, we started with a fluent speaker. That shortcut lets us focus on designing peptides with a real shot at becoming drugs.”
Pranam Chatterjee, Assistant Professor in BE and in Computer and Information Science, Penn Engineering
From 50,000 designs to two in vivo winners
Using AMP-Diffusion, the researchers generated the amino-acid sequences for about 50,000 candidates. “That’s far more candidate drugs than we could ever test,” says de la Fuente. “So we used AI to filter the results.”
Fine-tuned by hunting for antibiotic candidates everywhere from the proteins of ancient microbes to those of Neanderthals, APEX 1.1, an AI tool developed by de la Fuente’s lab, ranked the candidate AMPs according to a number of criteria. These included predicting which sequences would have strong bacteria-killing power, filtering out peptides that were too similar to known AMPs and ensuring the remaining candidates covered a diverse range of sequence types.
After synthesizing the 46 most promising candidates, the de la Fuente lab tested them in human cells and animal models. Treating skin infections in mice, two AMPs demonstrated efficacy on par with levofloxacin and polymyxin B, FDA-approved drugs used to treat antibiotic-resistant bacteria, without adverse effects. “It’s exciting to see that our AI-generated molecules actually worked,” says Chatterjee. “This shows that generative AI can help combat antibiotic resistance.”
Next steps for AI-generated antibiotics
In the future, the researchers hope to refine AMP-Diffusion, giving it the capability to denoise with a more specific goal in mind, like treating a particular type of bacterial infection, among other features. “We’ve shown the model works, and now if we can steer it to enhance beneficial drug-like properties, we can make ready-to-go therapeutics,” says Chatterjee.
For the researchers, the current study is a proof of principle: generative AI can move beyond mining what evolution has already created to actually designing new antibiotics. “Ultimately, our goal is to compress the antibiotic discovery timeline from years to days,” says de la Fuente.
Source:
University of Pennsylvania School of Engineering and Applied Science
Journal reference:
Torres, M. D. T., et al. (2025). Generative latent diffusion language modeling yields anti-infective synthetic peptides. Cell Biomaterials. doi.org/10.1016/j.celbio.2025.100183
RAWALPINDI, Sep 02 (APP):The Rawalpindi Development Authority (RDA), during its ongoing anti-dengue drive, sealed 28 buildings in Wazeer Town and Girja Road areas against violations of Dengue Standard Operating Procedures (SOPs) on Tuesday.
On the directions of Director General RDA Kinza Murtaza, the enforcement squad also removed encroachments from Sawan Bridge to Hamrahi Bus Stand at G.T. Road, Rawalpindi.
The action was taken in accordance with the Punjab Development of Cities Act 1976 and the RDA Building and Zoning Regulations 2021, which the property owners had violated by constructing buildings without obtaining the necessary approvals and No Objection Certificates (NOCs).
The RDA continues its efforts to enforce health and safety standards, ensuring that all construction sites and buildings comply with regulations designed to protect public health.
The DG RDA, Kinza Murtaza, reaffirmed the Authority’s commitment, stating, “We will not compromise when it comes to the safety and well-being of Rawalpindi’s residents. Compliance with Dengue SOPs is mandatory, and strict action will be taken against violators.”
The RDA urges all property owners, builders, and residents to follow the necessary precautions and cooperate with the authority to prevent the spread of dengue in the region.
The RDA also calls on the public to cooperate in preserving encroachment-free areas and contribute to making Rawalpindi’s streets safer, more accessible, and free of unnecessary congestion, she added.
Japanese culture is synonymous with the value of respect, which makes their team a perfect fit in the game of rugby.
Particularly so at a Rugby World Cup, where the familiar sight of the Japanese players – women and men – bowing to the crowd after a game has become iconic.
The scenes have been repeated at Rugby World Cup 2025 in England, with the players having a lot of support from the neutral fans – even from the fans of the Red Roses.
After losing to New Zealand the crowd was once again acknowledged with a trademark gesture of respect. All the more poignant as the defeat means the Sakura 15 will not be able to progress to the quarter-finals regardless of their result against Spain this weekend.
“We lost both of our first two matches, but many people came into the stadium to watch, and when Japan played well the atmosphere was incredible,” said Kotomi Taniguchi.
“Even after the matches, when we went around to greet the fans, everyone stood and cheered us on, which made me feel very emotional.
“We always say to each other, ‘We are so grateful. What a wonderful country this is’ as we bow to the crowd.”
While defeat in Exeter was a disappointment, there was reason for Kanako Kobayashi to smile. The centre plies her trade there for the Chiefs, and says she was touched by the support that came from afar as well as from the locals.
“I don’t think I will ever again have such a joyful experience through rugby,” she said.
“To be able to play in the World Cup, which had been my target, and to do so at Sandy Park, makes me very happy.
“At the venue, even people I didn’t know recognised me and said things like, ‘You’re the player who was at the Chiefs, right? I remember that green head cap!’ I really felt like I was at home playing rugby.
“And when I went to greet the crowd, so many told me, ‘That was great rugby’, which moved me deeply. Many Japanese families who had supported me back then also came.
“I couldn’t meet everyone, but I received so many messages from people saying, ‘We’ll come and cheer for you,’ and I was so glad to be reunited with familiar faces.”
Kobayashi says the Japanese will put their disappointment behind them as they look forward to their final game against Spain in York on Sunday.
“It is disappointing that we cannot reach the quarter-finals, which was our target,” she said.
“But after the Ireland match we managed to implement our intent to ‘throw the first punch,’ so in this final match against Spain we want to win and show Japan’s style of rugby before heading home.”
The Please Don’t Destroy boys are being split up on “Saturday Night Live.”
Ben Marshall, who makes up one-third of the comedy trio responsible for several viral “SNL” digital shorts over the last four seasons, was one of five new additions to the featured cast announced on Tuesday. Following the news of his promotion, Variety learned that while Martin Herlihy will remain on the writing staff, John Higgins has exited the series to pursue other projects as an actor.
Marshall, Higgins and Herlihy are currently on tour together, and will continue working together on projects outside of “SNL”
On “Saturday Night Live,” Please Don’t Destroy was known for their off-beat, often self-deprecating digital shorts, following in the footsteps of the Lonely Island. They typically played themselves in the videos, which feature A-list celebrity hosts such as Taylor Swift, Timothée Chalamet, Dakota Johnson, Rami Malek and more.
The trio was formed in 2017 after Marshall, Higgins and Herlihy met and began collaborating as students at NYU. In addition to regular live performances in New York, they gained popularity for sketches they posted on social media in the early days of the COVID-19 pandemic. In 2021, they were hired to join the 47th season of “SNL” as writers.
