Tuberculosis remains the world's leading infectious killer, claiming an estimated 1.23 million lives last year, the UN health organisation said Wednesday as it warned that recent gains made against the disease were fragile.

Deaths from TB were down three percent from 2023, while cases dropped by nearly two percent, the World Health Organization (WHO) said in its annual overview.

An estimated 10.7 million people worldwide fell ill with TB in 2024: 5.8 million men, 3.7 million women, and 1.2 million children.

A preventable and curable disease, tuberculosis is caused by bacteria that most often affect the lungs. It spreads through the air when people with TB cough, sneeze, or spit.

Now, TB cases and deaths are both declining "for the first time since the Covid-19 pandemic", which disrupted services, said Tereza Kasaeva, head of the WHO department for HIV, TB, hepatitis, and sexually transmitted infections.

"Funding cuts and persistent drivers of the epidemic threaten to undo hard-won gains, but with political commitment, sustained investment, and global solidarity, we can turn the tide and end this ancient killer once and for all," she said.

Funding for the fight against TB has stagnated since 2020.

Last year, $5.9 billion was available for prevention, diagnosis, and treatment – way off the target of $22 billion annually by 2027.

Serotonin is often described as the happiness chemical because of its well-known role in regulating mood.

However, recent research suggests this familiar molecule may play an unexpected role in cancer development. Not through its effects on the brain, but through a completely different mechanism in other parts of the body.

Despite serotonin being commonly associated with the brain, almost 95% of the body's serotonin is produced in the gut. From there, it enters the bloodstream and travels to various organs and tissues, including the liver, pancreas, muscles, bones, fat tissue, and immune cells.

Gut serotonin helps regulate blood sugar levels through its actions on the liver and pancreas, and regulates body temperature by acting on fat tissue.

It also contributes to maintaining healthy bones, stimulating appetite and gut motility, stimulating sexual health, promoting wound healing, and supporting immunity against harmful microbes. It essentially drives the functions of many cells throughout the body, and its effects extend far beyond mood regulation.

In 2019, scientists at the Icahn School of Medicine at Mount Sinai in New York discovered that serotonin can enter cells and interact directly with DNA. They found that it binds to molecular "switches" that control whether genes are active or inactive – and this binding can turn specific genes on.

Studies since then have shown that serotonin can switch on genes involved in cancer growth. This mechanism has been seen in brain, liver, and pancreatic cancers – and it may play a role in many other types of cancer.

Identifying the specific sites where serotonin binds to cancer-related genes could support the development of targeted "epigenetic" therapies – treatments that control which genes are switched on or off.

The world is undergoing rapid electronification and digital transformation, reshaping how we live. Many of us have numerous electronic devices around us at all times, from smartphones and watches to our home appliances and cars.

A sharp increase in e-waste has accompanied the surge in electronic equipment. In 2022, 62 million tons of e-waste was produced globally.

Canada's e-waste tripled between 2000 and 2019 and is expected to reach 1.2 billion kilograms by 2030. These statistics demonstrate an urgent environmental crisis that demands new ways of thinking and educating future generations.

A key part of tackling the problem is educating people about it. As educators, we need to expand school education to include resource recovery, sustainability and pro-environmental behaviors to inform students on what to do with their old gadgets.

New research from astrophysicists at Michigan State University may bring scientists closer to solving a mystery that has puzzled them for more than a century: where do galactic cosmic rays come from?

Cosmic rays are high-energy particles that travel at nearly the speed of light. They originate from locations both within the Milky Way and beyond, yet their exact sources have remained unknown since their discovery in 1912.

Shuo Zhang, an assistant professor of physics and astronomy at MSU, and her research team led two recent studies offering new insights into where these particles may have formed. The findings were presented at the 246th meeting of the American Astronomical Society in Anchorage, Alaska.

These energetic particles are believed to come from some of the universe’s most extreme environments, including black holes, supernova remnants, and regions where stars are born. Such astrophysical events also generate neutrinos, which are tiny, nearly massless particles found throughout the cosmos and even here on Earth.

“Cosmic rays are a lot more relevant to life on Earth than you might think,” Zhang said. “About 100 trillion cosmic neutrinos from far, far away sources like black holes pass through your body every second. Don’t you want to know where they came from?”

The Universe’s Ultimate Accelerators
The sources of cosmic rays are so powerful that they can accelerate protons and electrons to energy levels far exceeding what is possible with even the most advanced human-made particle accelerators. Zhang’s group focuses on these natural cosmic accelerators, known as PeVatrons, to understand where they exist, what they are made of, and how they propel particles to such extreme energies.

Gaining a deeper understanding of these mechanisms could help answer fundamental questions about galaxy evolution and the mysterious nature of dark matter.

A team of scientists at The University of Texas at Austin has created a cleaner and more efficient way to extract rare earth elements, which are vital for technologies such as electric vehicle batteries and smartphones. The technique could strengthen domestic production and lessen dependence on expensive imports.

The new process makes it possible to separate and collect rare earth elements from sources that were previously too difficult or inefficient to use, offering a potential solution to supply challenges heightened by global trade tensions.

“Rare earth elements are the backbone of advanced technologies, but their extraction and purification are energy intensive and extremely difficult to implement at the scales required,” said Manish Kumar, professor in the Cockrell School of Engineering’s Fariborz Maseeh Department of Civil, Architectural and Environmental Engineering and the McKetta Department of Chemical Engineering. “Our work aims to change that, inspired by the natural world.”​

The study, recently published in ACS Nano, describes how the team engineered artificial membrane channels, tiny pores within membranes, that imitate the highly selective transport systems of natural proteins in living organisms. In biology, such channels guide ions as they move between cells.

Each channel has unique properties that allow only ions with specific traits to pass through while blocking others. This fine-tuned selectivity is essential for many biological functions, including the way the human brain processes information.

When Nebraska woman Alex Simpson was just two months old, she was diagnosed with a rare congenital brain condition that meant she may not survive to her first birthday.

But despite medical odds, she and her family just celebrated her 20th birthday on November 4 this year.

Simpson's condition, hydranencephaly, means her cerebral hemispheres – the two large lobes that typically make up most of the human brain, responsible for cognitive function, voluntary movement, and sensory processing – are almost nonexistent. While her brainstem and some other brain parts remain, the rest of her cranial cavity is filled instead with cerebrospinal fluid.

Hydraencephaly is incurable, and is managed with intensive supportive care.

"Technically, she has about half the size of my pinky finger of her cerebellum in the back part of her brain, but that's all that's there," Alex's father, Shawn Simpson, told Omaha news station KETV earlier this month.

This means Simpson's vision and hearing are impaired, though her cerebellum maintains some awareness of her surroundings. Her family say they nevertheless have a strong relationship with her.

We don't know what causes hydranencephaly, but some research suggests it may arise when some form of vascular injury, such as a stroke or infection, blocks blood supply to the brain.

Tracking time is one of those things that seems easy, until you really start to get into the details of what time actually is. We define a second as 9,192,631,770 oscillations of a cesium atom. However, according to Einstein’s theory of general relativity, mass slows down these oscillations, making time appear to move more slowly for objects in large gravity wells. This distinction becomes critical as we start considering how to keep track of time between two separate gravity wells of varying strengths, such as on the Earth and the Moon. A new paper pre-print on arXiv by Pascale Defraigne at the Royal Observatory of Belgium and her co-authors discusses some potential frameworks for solving that problem and settles on using the new Lunar Coordinate Time (TCL) suggested by the International Astronomical Union (IAU).

So why is this a problem we should solve now? As humanity is preparing to go back to the moon, hopefully more permanently this time, we need some standardized way to navigate it. In support of their various crewed lunar missions, America, China, and the EU are working on programs that can provide Position, Navigation, and Timing (PNT) services to explorers, and importantly network infrastructure, on the Moon.

Each of these services hopes to provide meter-level accuracy for a network node’s position on the Moon, but to do so would require nanosecond-level precision in their synchronized clocks. Similarly, Earth-based satellites like GPS have to account for relativistic changes in time between the geosynchronous satellites barely in the planet’s gravity well and the users down on the surface. To help facilitate this process on the Moon, in 2024 the IAU came up with the LUnar Celestial Reference System (LCRS), and an associated coordinate time - TCL.

A weak spot in Earth's protective magnetic field is growing larger and exposing orbiting satellites and astronauts to more solar radiation, according to more than a decade of measurements by three orbiting observatories.

The observations by the European Space Agency's Swarm trio of satellites found that Earth's already weak magnetic field over the South Atlantic Ocean — a region known as the South Atlantic Anomaly (SAA) — is getting worse and that it has grown by an area half the size of continental Europe since 2014. At the same time, a region over Canada where the field is particularly strong has shrunk, while another strong field region in Siberia has grown, the measurements show.

"The region of weak magnetic field in the South Atlantic has continued to increase in size over the past 11 years since the launch of the Swarm satellite constellation," explained Chris Finlay, a geomagnetism researcher at the Danmarks Tekniske Universitet. "Although its growth was expected based on early observations, it is important to confirm this change in Earth's magnetic field is continuing." Finlay is the lead author of a new study published in the journal Physics of the Earth and Planetary Interiors that analyzes data from the Swarm satellites.

A new study has finally nailed down what links Epstein-Barr virus (EBV) – a pathogen that over 95 percent of adults worldwide have been infected with – to lupus, solving a long-standing mystery.

Lupus, also called systemic lupus erythematosus or SLE, is a chronic autoimmune disease in which the immune system attacks the body’s own tissue, and can result in a wide variety of symptoms ranging from skin rashes and fatigue to severe damage to the lungs and kidneys. Actress and singer Selena Gomez was diagnosed with lupus in her early 20s, and received a kidney transplant back in 2017 due to the effects of the disease.

She’s just one of at least 5 million people estimated to be affected by lupus, the causes of which are poorly understood. While genetics might be one possible trigger, it’s long been suspected that EBV – the same virus that causes glandular fever – is also linked to the condition.

What scientists had trouble with was figuring out exactly how the two were linked – what were the mechanisms that led one to trigger the other? 

That’s where the new study, led by researchers at Stanford Medicine, came in. They developed a novel technique for identifying B cells infected by EBV and which genes within these cells were being expressed. 

B cells are white blood cells that play a key role in the body’s immune system – producing antibodies. But they have another important role too, presenting antigens – molecular "red flags" on foreign entities like viruses that trigger an immune response – to other immune cells, which scales up the response from the body’s immune system. Around 20 percent of B cells are also designed to target our own tissues, but they usually lie inactive.

The team’s technique revealed that in healthy individuals carrying EBV, fewer than 1 in 10,000 of their B cells were infected with the virus. In people with lupus, that rose to 1 in 400. 

Their findings also revealed that in these infected cells, EBV could cause them to express a “molecular switch” gene, activating a cascade of pro-inflammatory gene expression that led a B cell to transform into its antigen-presenting self. In turn, this activated other immune cells to join the response gang – including those otherwise sleepy self-attacking B cells, as well the appropriately named killer T cells that destroy the body’s own tissues.

This is what causes lupus, the researchers conclude, and they also suspect the same mechanism could be involved in other autoimmune diseases like multiple sclerosis, which has also been linked to EBV.

Researchers at the Hebrew University of Jerusalem have found that acetaminophen doesn’t only act in the brain. Their study reveals that it also blocks pain at its origin by targeting nerve endings in the body. The team discovered that its active compound, AM404, interferes with sodium channels in pain-sensing neurons, stopping pain signals before they reach the brain.

This discovery transforms scientists’ understanding of one of the world’s most widely used painkillers. By showing that acetaminophen works both in the nervous system and at the site of pain, the findings could guide the creation of next-generation pain treatments designed to be more effective and gentler on the body.

Published in the Proceedings of the National Academy of Sciences, the study was conducted by Prof. Alexander Binshtok from the Faculty of Medicine and Center for Brain Sciences (ELSC) and Prof. Avi Priel from the School of Pharmacy at Hebrew University. Together, their research uncovered a previously unknown mechanism of pain relief, challenging long-standing assumptions about how acetaminophen functions in the body.

Acetaminophen (also called paracetamol, Tylenol, or Panadol) is one of the most commonly used pain and fever medications worldwide. It is known for effectively easing mild to moderate pain and reducing fever, without the stomach irritation or anti-inflammatory effects often linked to drugs like aspirin or ibuprofen.

For decades, scientists believed that acetaminophen relieved pain by working only in the brain and spinal cord. But this new research, published in PNAS, shows that the drug also works outside the brain, in the nerves that first detect pain.

Each year, these pronghorns seek greener pastures as they follow ancient migratory paths in the longest migration in the Americas below the Arctic.

The ocean affects our daily life – through weather, shipping, even national security. 🌊

Launching tonight, Sentinel-6B will measure sea levels across 90% of Earth’s ocean to improve forecasts, keep ships safe at sea, and protect coastal communities.

Signal confirmed ✅

CopernicusEU Sentinel-6B is now in orbit and ready to begin the Launch and Early Operations phase with esaoperations.

The mission will extend long-term record of sea-surface height measurements: esa.int/Applications/O…

A groundbreaking study led by a University of Leeds scientist has unveiled new insights into how the body manages pain, offering a potential path toward treating long-term pain without relying on addictive opioids.

Professor Nikita Gamper, from the School of Biomedical Sciences at Leeds, and his research team discovered that the human body can generate its own form of natural “sleeping pills” that resemble benzodiazepines. These substances can reduce signals from specific nerves, influencing how intensely pain is felt.

The research, which builds upon earlier studies conducted by Professor Gamper and Professor Xiaona Du of Hebei Medical University in Shijiazhuang, China, could mark a turning point in pain management. With new funding secured for the coming year, the team plans to continue exploring how this biological process could lead to safer, more effective treatments for people suffering from chronic pain.

A New Path Beyond Opioids
Professor Gamper said: “We understand quite a bit about how a person ends up feeling pain, but we can’t do much about it. Despite all the amazing discoveries and textbooks written, opioids are still the gold standard.

“Nothing substantially better than opioids has been produced. If you suffer from pain, you will likely end up with either ibuprofen, which is OK for mild pain, but absolutely does nothing for very strong pain or neuropathic pain; or opioids which are very efficacious but dangerous.”

Benzodiazepines (‘benzos’) are a type of depressant medication commonly prescribed to help with sleep problems, anxiety, and seizures. In their research, Professor Nikita Gamper, Professor Xiaona Du, and Dr. Temugin Berta from the University of Cincinnati discovered that certain cells connected to human nerves, located within structures known as spinal ganglia, can release a peptide that operates in a similar way to benzos.

Because this process takes place only within the peripheral nervous system, it does not cause the entire nervous system to “go to sleep.” As a result, these naturally produced peptides could offer pain relief without the dangerous side effects or risk of addiction associated with opioid drugs.

The study’s results show that nerves are capable of “tuning out” pain signals or limiting how much pain the brain perceives, revealing a potential new mechanism for controlling discomfort at its source.