Category: 8. Health

The study encourages a “whole-body” view of physiology, instead of focusing on isolated measurements such as heart or breathing rate |Image used for representational purpose only
| Photo Credit: Getty Images/iStockphoto

The skull is so effective at protecting the brain that it has impeded the progress of neuroscience.

In particular: A nice, thick skull poses challenges for imaging the brain in natural environments or while a person is moving.

Meanwhile, with the recent advent of ultrafast ultrasound, the possibility of studying and monitoring real-time microvascular brain activity poses a novel opportunity for neuroscientists, from better understanding dementia to increased accuracy during neurosurgery to revolutionizing treatment for comatose patients.

Now, a team of Dutch researchers has shown that a mobile ultrafast ultrasound scanner — functional ultrasound imaging (fUSi) — affixed inside a three-dimensional printed helmet can image brain activity in a patient pushing a cart while walking and performing everyday tasks in an everyday environment (it was not wireless — they used a 100-m-long extension cord).

“We’ve basically shown that functional ultrasound imaging is a technique that can be a high-resolution mobile brain scanner for the research side, and if you’re looking from a medical side, I would say that now the brain is not a black box anymore,” said Sadaf Soloukey, MD, PhD, neurosurgical resident at Erasmus MC in Rotterdam, the Netherlands, and lead author of the paper published recently in Science Advances. “We now with ultrasound have the possibility to see directly in real time inside the brain.”

How They Made It Work

The study involved two patients with artificial skull implants and included sensory, motor, and multitasking experiments generating reproducible data over 21 months. One of the patients died partway through the study due to tumor regrowth, despite being tumor progression-free for multiple years. Both patients had PEEK implants; the second patient’s implant was placed following a high-velocity trauma.

The skull implants are key for the acoustic requirements of ultrasound. That’s less limiting than one may think because these are the patients researchers want to study anyway, said Charles Liu, MD, PhD, a professor of neurological surgery and director of the University of Southern California Neurorestoration Center in Los Angeles.

“They’re a natural patient population,” said Liu, who wasn’t involved in the study but published a 2024 paper in Science Translational Medicine that also used fUSi to visualize brain activity during video game and guitar playing by an individual with a skull implant.

Liu recalled that when the researcher Mickael Tanter, PhD, and his team in France first published on the topic of ultrafast ultrasound, people were skeptical.

The potential for fUSi is apparent “when another group publishes something that essentially corroborates what you said in relatively short order in another big journal,” Liu said.

Why Ultrafast Ultrasound Is so Promising

One reason: Ultrafast ultrasound can record 10,000 frames per second.

“That allows you to separate the tiny blood flow in the brain from the motion of the brain,” explained Pieter Kruizinga, PhD, an imaging physicist and co-author of the Science Advances paper. “The tiny blood flow in the small vessels is responsible for neurovascular coupling, so you really need this ultrasound on steroids. It’s the workhorse in our lab to look at brain perfusion, basically. And the frequencies we use, they don’t penetrate through the skull. Why you see a child in a womb so nicely is because you have this water, and then it hits the skull, and you get all these nice signals from it. But to penetrate through the skull is very difficult.”

Liu noted that there is some early research examining ways to overcome the skull challenge, such as some coming out of the French lab led by Tanter using nanobubbles as a contrast agent. New fUSi technology would also be ideal for working with people who have implanted neuromodulation devices such as deep brain stimulators, Liu said. His own upcoming research involves imaging the spinal cord during the filling and emptying of the human bladder.

Brain surgery applications of fUSi are also on the horizon. Presurgical functional MRI (fMRI) is usually used as a map by neurosurgeons heading into surgery, and once underway, they move to relying on cortical stimulation to make decisions.

During surgery, the fMRI map is often “no longer relevant because things shift; the brain can swell out or drop in, and even as your surgery is progressing, things can move. Sometimes when I’m taking out a tumor, different parts might collapse,” said Richard G. Everson, MD, an assistant professor of neurosurgery at UCLA. “Having a portable, repeatable system that we can operate in a handheld manner like an ultrasound would be a really great instrument to have. I think the writing is on the wall that this will and can work, but it’s certainly not at any sort of level of being clinically ready.”

Everson’s team has already been using fUSi outside of the operating room to evaluate patients who have had surgery to remove part of the skull for a variety of reasons.

Also Needed: More Processing Speed

The next key steps for fUSi to come to the operating room are for data processing technology to allow for real-time information and benchmarking, he said, because “if it takes an hour to analyze the data, that’s no good because the surgery’s already over.”

Following brain surgery, there are limited techniques to monitor what’s happening in the brain.

“So we have, unfortunately, a lot of patients in the ICU after trauma that are waiting often to show whether or not they will wake up,” Soloukey said, and many of them have had a hemicraniectomy like the main patient in her team’s study.

In 2020, her team published a paper demonstrating the use of fUSi during awake brain surgery.

Future research could examine “If there are some functional networks that are, let’s say, a good signature of someone waking up with a coma, then it might be easier not only to monitor their progress but to predict how they might wake up,” Soloukey said. “And this is, of course, something that’s very, very difficult. It’s a sensitive topic. I know that the US and Europe also think differently about these subjects. But I think it starts with understanding what happens in a coma and trying to make good tools that can predict a patient’s outcome. Functional ultrasound is a great bedside tool for that in the ICU context — because it could be bedside.”

Story Continues

CHENNAI: Swiss-pharma major Novartis AG said early this week that its pediatric malaria treatment, Coartem Baby, received regulatory approval from Swissmedic, Switzerland’s national medicines regulatory authority. This marks a milestone in global health, as this Novartis drug is the world’s first malaria treatment specifically developed for newborns and infants weighing between 2 and 5 kilograms.

Coartem Baby is a reformulation of the existing Coartem (artemether-lumefantrine) combination therapy. The new formulation was developed through a collaboration between Novartis and the Medicines for Malaria Venture (MMV), with support from the PAMAfrica consortium.

The clinical development program was co-funded by the European & Developing Countries Clinical Trials Partnership and the Swedish International Development Cooperation Agency. The approval was based on positive data from the Phase II/III CALINA study, which demonstrated that Coartem Baby has a pharmacokinetic profile suitable for infants under 5 kilograms and exhibits good efficacy and safety.

Global Health Impact

Malaria remains one of the world’s deadliest diseases, particularly among children under five years old in Africa. In 2023, there were an estimated 36 million pregnancies in 33 African countries where malaria is widespread, with about one in three mothers infected with malaria during pregnancy, raising the risk of transmission to their newborns.

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Triple-negative breast cancer (TNBC), an aggressive and hard-to-treat form of breast cancer, has long challenged researchers due to the absence of effective targeted therapies. Now, findings from Cold Spring Harbor Laboratory in New York State have revealed a potentially significant contributor to TNBC biology: a little-studied long non-coding RNA (lncRNA) known as LINC01235.

Breast cancer is among the most common malignancies in women worldwide, and TNBC accounts for approximately 10 to 15 percent of cases. It is disproportionately diagnosed in younger women and those of African American descent. While many forms of breast cancer benefit from targeted treatments, TNBC lacks such options, making basic research crucial.

The study was led by Professor David Spector and graduate student Wenbo Xu. They discovered that LINC01235, previously associated with gastric cancer, also plays a role in TNBC by regulating a gene called NFIB, which is already linked to this cancer subtype.

Using CRISPR gene-editing and antisense knockdown techniques in tumour organoids and cancer cells, the researchers showed that lowering LINC01235 levels suppressed NFIB expression and inhibited TNBC organoid growth. Further analysis suggested that this interaction affects the NOTCH signalling pathway, known to be involved in cancer cell proliferation.

The NOTCH signalling pathway is a fundamental cell communication system that regulates how cells develop, differentiate, and interact with their environment. It is evolutionarily conserved and plays a crucial role in embryonic development, tissue homeostasis, and cell fate decisions. In TNBC aberrant NOTCH signalling can lead to uncontrolled cell proliferation, resistance to apoptosis and enhanced tumour invasiveness.

Very little is known about NFIB’s function in this context and even less about LINC01235.

“The goal here is to understand mechanisms by which the cell functions and how disease states take over those functions, perhaps by up-regulating or down-regulating an RNA molecule,” Spector noted.

While these results are at a preliminary stage, the work points to the promise of lncRNAs as potential therapeutic targets. LINC01235 may yet prove to be a vital step towards effective treatment options for TNBC.

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For further reading please visit: 10.1158/1541-7786.MCR-24-1143 

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“All of the mice we treated showed dramatic improvement in their motor skills. The results exceeded our expectations and suggest that, after further study, this therapeutic approach could slow the progression of Parkinson’s in humans,” says Double.

But experts caution that Parkinson’s is a complex condition that will likely require multiple combined interventions. A single treatment may have limited effect, but its efficacy may be enhanced by integrating it with other therapeutic approaches.

In that context, Double’s team’s findings could be complemented by recent research from Stanford University focused on restoring communication between neurons in a subtype of Parkinson’s linked to mutations in the gene responsible for producing an enzyme called LRRK2.

In these cases, the mutation causes hyperactivity of the enzyme, altering the structure of brain cells and disrupting signaling between dopaminergic neurons and those in the striatum, a deep brain region related to movement, motivation, and decision-making.

It is estimated that about 25 percent of Parkinson’s cases are genetic in origin, and the LRRK2 mutation is one of the most frequent. The team led by Stanford neuroscientist Suzanne Pfeffer proposed that inhibiting the excessive activity of this enzyme could stabilize symptoms, especially if detected in early stages. The goal was to regenerate primary cilia, antenna-like structures that enable communication between cells.

The hypothesis was tested in mice genetically modified to exhibit LRRK2 hyperactivity and early symptoms of the disorder. For two weeks, these animals were administered with a compound called MLi-2, which binds to the enzyme and reduces its activity.

In this first test, no relevant changes were observed, which the researchers attributed to the fact that the examined neurons and glia—another type of cell in the nervous system, which support neurons—were already mature and were not in the cell division phase.

However, a review of the scientific literature revealed that, even if mature, certain neurons can regenerate their primary cilia depending on their sleep-wake cycles. “The findings that other nonproliferative cells can develop cilia made us think that the inhibitor still had therapeutic potential,” Pfeffer explains.

The team then decided to extend the treatment to three months. After this period, they found that the percentage of neurons and glial cells in the striatum with primary cilia was comparable to that of healthy mice without the genetic mutation.

This restoration of cellular structures made it possible to reactivate communication between dopaminergic neurons and the striatum. As a result, neurotransmitters affected by the LRRK2 protein induced the production of neuroprotective factors at levels similar to those of a healthy brain, something that had been diminished as a result of LRRK2 hyperactivity. In addition, density markers of dopaminergic nerve endings were doubled, suggesting a possible recovery of previously damaged neurons.

“These findings suggest that it is not only possible to stabilize the disease, but also to improve the condition of patients. This therapeutic approach has great potential to restore neuronal activity in Parkinson’s-affected circuits. There are currently several ongoing clinical trials with LRRK2 inhibitors, and we hope that these results in mice can be translated to humans,” says Pfeffer.

The authors stress that, to maximize the effectiveness of this treatment, it is essential to identify early symptoms, which can occur up to 15 years before the characteristic tremors. The hope is that people with the LRRK2 mutation will be able to start treatment early. The next step would be to assess whether other Parkinson’s variants, not associated with this genetic mutation, could also benefit from this strategy.

It is estimated that the number of Parkinson’s cases worldwide could exceed 25 million by 2050, which would represent a 112 percent increase over 2021 figures, according to projections published in the British Medical Journal. Although these estimates are not definitive, the scientific community warns that they reflect a growing challenge for public health systems. For this reason, developing therapies capable of mitigating, stabilizing, and even reversing the progression of the disease is a global priority.

This story originally appeared on WIRED en Español and has been translated from Spanish.

Antimicrobial resistance (AMR) is one of the most urgent public health challenges in 2025. This phenomenon occurs when microorganisms such as bacteria, viruses, fungi, and parasites evolve resistance to drugs that were once effective. According to the CDC’s 2025 report, AMR could lead to as many as 10 million deaths annually by 2050, overtaking major diseases like cancer.

AMR stems from the natural evolutionary ability of microbes to survive selective pressure from antimicrobials. This process is significantly accelerated by the overuse and misuse of these drugs in human health, veterinary medicine, and agriculture. Resistant infections often require longer treatment courses, are associated with increased disability and mortality, and lead to extended hospital stays and higher healthcare costs — placing a growing burden on health systems and global economies.

The CDC estimates at least 2.8 million resistant infections and over 35,000 related deaths annually in the US alone.

Resistance Mechanisms

AMR typically arises through two primary mechanisms: spontaneous genetic mutations and horizontal gene transfer (via conjugation, transformation, or transduction).

Recent findings outline several well-characterized resistance pathways:

• Target modification: Structural alterations in drug targets — often key proteins or cell components — can prevent effective drug binding.
• Enzyme production: Certain bacteria produce enzymes such as beta-lactamases that deactivate antibiotics like penicillins and cephalosporins. These enzymes are increasingly common in gram-negative species such as Escherichia coli and Klebsiella pneumoniae.
• Efflux pumps and permeability barriers: Some bacteria limit drug entry or actively expel antibiotics using multidrug efflux pumps. This is particularly problematic in gram-negative organisms due to their additional outer membrane.

These resistance mechanisms can coexist within a single organism, giving rise to “pan-resistant” strains that are unaffected by nearly all available antimicrobial agents.

Resistance can emerge rapidly — even during the course of treatment — turning previously susceptible infections resistant mid-therapy and narrowing treatment options dramatically.

Recent Trends and Global Data

New international data highlight the accelerating spread of AMR, with particularly concerning developments across both bacterial and fungal pathogens.

The World Health Organization (WHO)’s 2024 Bacterial Priority Pathogens List documented rising resistance rates in K pneumoniae and E coli, especially in Asia and Africa — regions where therapeutic options remain severely limited. These findings align with projections from a 2024 commentary published in The Lancet, which estimates that AMR could cause up to 10 million deaths annually by 2050, disproportionately affecting low- and middle-income countries.

In the US, the CDC reported that more than 35% of hospital-acquired urinary tract infections in 2024 were caused by multidrug-resistant (MDR) organisms. This surge is driven in large part by the horizontal transmission of resistance genes via mobile genetic elements such as plasmids and transposons.

MDR tuberculosis also continues to pose a serious global health threat. Data from Eastern Europe and parts of Asia show that over 20% of new tuberculosis cases now involve MDR strains. These cases require longer, more toxic regimens and are associated with poorer clinical outcomes, adding further strain to public health systems.

Fungal resistance is emerging as a parallel crisis. A recent review reported that more than 90% of Candida auris isolates collected from hospitals in Europe and North America were resistant to multiple antifungal agents. This poses a serious risk to patients who are immunocompromised and critically ill, particularly in ICUs where infection control remains challenging.

Despite the growing threat, treatment pipelines remain thin. While several new antimicrobial agents are under investigation, most remain in preclinical or early clinical stages. The report underscores an urgent need for sustained investment in antimicrobial drug development to replenish a shrinking therapeutic arsenal.

Adding to the concern, recent studies describe the emergence of novel resistance mechanisms in gram-positive pathogens such as methicillin-resistant Staphylococcus aureus. Some strains have developed traits that compromise the efficacy of even newly approved agents — further complicating treatment strategies and escalating costs of care.

As AMR continues to evolve across multiple fronts, these findings reinforce the need for comprehensive, coordinated strategies to monitor resistance patterns; support antimicrobial stewardship; and accelerate therapeutic innovation.

Economic Toll

The global economic impact of AMR could be staggering. The 2024 Lancet commentary projects that AMR could result in up to $100 trillion in economic losses by 2050. The burden is expected to fall disproportionately on low- and middle-income countries, where weaker health systems and limited access to effective therapies could exacerbate existing disparities in both health outcomes and economic development.

Clinical consequences are already evident in hospitals around the world. Recent research shows that resistant healthcare-associated infections — such as bloodstream infections and ventilator-associated pneumonias — are associated with mortality rates approaching 30% higher in patients in resource-limited settings. Contributing factors include poor hospital infrastructure, limited access to diagnostics and therapeutics, and inadequate infection control measures.

Meanwhile, a 2024 review highlights the growing threat of hospital-acquired infections caused by Acinetobacter baumannii and Pseudomonas aeruginosa — both of which exhibit high levels of resistance to multiple antibiotic classes. Without effective interventions, these infections may become increasingly difficult, if not impossible, to treat, further driving up hospital mortality and straining intensive care resources.

Emerging Strategies and Solutions

Several promising strategies are being explored to slow AMR progression and strengthen the clinical response.

• Development of new antimicrobials: Recent research highlights novel compounds designed to overcome common resistance mechanisms. While early in development, these agents may offer new hope against multidrug-resistant pathogens.
• Alternative therapies: Early-phase studies suggest that bacteriophage therapy and antibacterial nanoparticles could serve as complementary approaches to combat infections that no longer respond to conventional treatments. These technologies are gaining traction but require rigorous clinical validation.
• Antimicrobial stewardship and surveillance: Effective stewardship programs remain central to the AMR response. Core components include the rational prescribing of antimicrobials, real-time infection surveillance, and access to rapid diagnostic tools for antimicrobial susceptibility testing.
• Education and global awareness: The WHO and CDC continue to emphasize the need for coordinated global education campaigns to promote the appropriate use of antimicrobials and curb self-medication — particularly in countries with weak regulatory oversight.
• National initiatives: In Spain, the 2025-2027 Plan Nacional frente a la Resistencia a los Antibióticos (National Plan against Antibiotic Resistance) stands out as a model. The plan includes enhanced epidemiologic surveillance, increased funding for antimicrobial research, ongoing training for healthcare providers, and public education campaigns. It also calls for integrated action across all levels of the health system to ensure a coordinated national response.

Conclusions

AMR is no longer a looming threat — it is a present-day global health emergency. Its continued spread is undermining the foundations of modern medicine, with far-reaching consequences for clinical care, public health, and global equity.

As resistance mechanisms become increasingly complex and widespread, the therapeutic arsenal is shrinking — particularly in hospital settings and for vulnerable populations. Meanwhile, antibiotic development continues to lag, with most new agents stalled in early-phase research.

To avoid a future where routine infections become untreatable, the global response must be ambitious and coordinated. Expanding antimicrobial stewardship, accelerating drug development through sustained investment, and enforcing rational prescribing practices are all urgent priorities. These efforts must be anchored in the One Health approach, which recognizes the interconnectedness of human, animal, and environmental health.

Education and behavior change are equally essential. Clinicians, patients, and policymakers all play a role in preserving the effectiveness of existing antimicrobials. And while emerging therapies such as phage therapy, nanomedicine, and immunomodulation offer hope, they require rigorous testing and clear regulatory pathways before they can be integrated into clinical practice.

The window for action is narrowing — but meaningful progress is still possible. With global alignment, scientific innovation, and sustained commitment, the trajectory of AMR can be reversed.

This story was translated from El Médico Interactivo.

Hi, it’s Amber in Hong Kong, where less than half of eligible women get their recommended cervical cancer screening. If only the procedure was less unpleasant …

As someone who has reported on cancer research for some years, I’ve long known that cervical cancer is one of the most preventable cancers, thanks to vaccination and early screening. Yet, I must confess I’ve never received a screening for HPV, the human papillomavirus that’s the primary cause of cervical cancer. The thought of a Pap smear makes me squirm.

An additional six million new HIV infections and four million AIDS-related deaths could occur between 2025 and 2029 if US-supported HIV treatment and prevention services collapse, according to UNAIDS.

“This is not just a funding gap. It’s a ticking time bomb,” said UNAIDS Executive Director Winnie Byanyima at the launch of the organisation’s 2025 global AIDS update on Thursday. 

“We have seen services vanish overnight. Health workers have been sent home. And people – especially children and key populations – are being pushed out of care.” 

“Key populations” refer to people most vulnerable to HIV infection, including sex workers, men to have sex with men, people who inject drugs and young women.

Some of the immediate effects of the US withdrawal of funds since Donald Trump assumed the presidency in January include the closure of health facilities, healthworker job losses, and disrupted treatment, testing and prevention services.

The US President’s Emergency Plan for AIDS Relief (PEPFAR) had committed $4.3 billion in bilateral support in 2025 and “those services were stopped overnight when the US government shifted its foreign assistance strategies,” notes the UNAIDS report. 

PEPFAR had supported HIV testing for 84.1 million people and HIV treatment for 20.6 million people.

“Disruptions are being felt across the HIV response and pose a huge risk of increased mortality, a surge of new HIV infections, and the development of resistance to the most commonly used treatment regimens.”

In Mozambique, for example, over 30,000 health personnel have lost their jobs.

UNAIDS itself faces huge job losses, and is reducing its Geneva head office staff from 127 to a mere 19 employees, according to a report this week by Geneva Solutions.

The UN agency’s restructuring plan will cut staff by 54% globally, leaving 280 staff worldwide. 

HIV prevention programmes hit hard

External funding financed almost 80% of HIV prevention in sub-Saharan Africa, 66% in the Caribbean and 60% in the Middle East and North Africa, according to UNAIDS.

PEPFAR alone reached 2.3 million adolescent girls and young women with comprehensive HIV prevention services in 2024 and enabled 2.5 million people to use pre-exposure prophylaxis (PrEP). Many of these programmes have now stopped completely, according to UNAIDS. 

PrEP involves taking medication to prevent HIV infection and is usually taken by people at high risk of infection, and PEPFAR funded over 90% of PrEP initiations globally in 2024.

“Countries are reporting limited availability of PrEP and reduced activities to prevent new HIV acquisitions, including among adolescent girls and young women,” said UNAIDS.

In Nigeria, budget cuts have reduced PrEP initiation from 40,000 to 6000 people per month.

At the end of 2024, just before a sudden collapse in funding, new HIV infections had been reduced by 40% and AIDS-related deaths by 56% since 2010, Byanyima notes in the report. Countries had also reduced the annual number of children acquiring HIV from their mothers by 62% to 120,000 since 2010.

However, prevention efforts were already flatlining before the withdrawal of US aid. In 2024, there were 1.3 million new infections, which was almost the same as the year before.

“Over 210,000 girls and young women aged 15 to 24 acquired HIV in 2024 – an average of 570 new infections every day,” according to the UNAIDS report.

In 2024, 630,000 people died from AIDS-related causes, 61% of them in sub-Saharan Africa. “Community-led services, which are vital to reaching marginalised populations, are being defunded at alarming rates,” said UNAIDS.

“In early 2025, over 60% of women-led HIV organisations surveyed had lost funding or were forced to suspend services.”

Domestic budgets inadequate

Only 25 of the 60 low- and middle-income countries included in the report have increased their domestic budgets for HIV in 2026. The average increase amounts to 8%, approximately $180 million in additional domestic resources. 

“This is promising, but not sufficient to replace the scale of international funding in countries that are heavily reliant,” UNAIDS notes.

“It is important for donors to recognize that the option of increasing domestic HIV funding is not immediately or equally available to all countries,” UNAIDS notes.

“Combinations of debt distress, slow economic growth and underperforming tax systems leave many countries, notably in sub-Saharan Africa, with limited fiscal space to increase their domestic funding for HIV. “

It cites the recent International Conference on Financing for Development in Seville in Spain, as offering a way forward with “calls for debt relief, international tax cooperation and reform of international financial institutions”.

These measure would provide “the first steps towards a new economic settlement that can give countries the fiscal space needed to invest in the global HIV response”, UNAIDS notes.

“Urgent action and revived solidarity are needed to sustain the progress made and prevent a resurgence of HIV.”

Image Credits: UNAIDS.