Year: 2025

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Scientists Discover How Aspirin Could Prevent Metastasis in Some Cancers

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Credit: Pixabay CC0

Scientists have uncovered the mechanism behind how aspirin could reduce the metastasis of some cancers by stimulating the immune system.

In the study published in Nature, the scientists say that discovering the mechanism will support ongoing clinical trials, and could lead to the targeted use of aspirin to prevent the spread of susceptible types of cancer and the development of more effective drugs to prevent cancer metastasis.

The scientists caution that aspirin can have serious side effects and that trials are underway to establish safety and efficacy.

A reduction in the spread of some cancers

Studies of people with cancer have previously observed that those taking daily low-dose aspirin have a reduction in the spread of some cancers, such as breast, bowel, and prostate cancers, leading to ongoing clinical trials. However, until now it wasn’t known exactly how aspirin could prevent metastases.

In this study, led by researchers at the University of Cambridge, the scientists say their discovery of how aspirin reduces cancer metastasis was serendipitous.

They were investigating the process of metastasis, because, while cancer starts out in one location, 90% of cancer deaths occur when cancer spreads to other parts of the body.

Lung cancer metastasis. Credit: National Cancer Institute

The scientists wanted to better understand how the immune system responds to metastasis. This is because when individual cancer cells break away from their originating tumour and spread to another part of the body, they are particularly vulnerable to immune attack.

An effect on cancer metastasis

The immune system can recognise and kill these lone cancer cells more effectively than cancer cells within larger originating tumours, which have often developed an environment that suppresses the immune system.

The researchers previously screened 810 genes in mice and found 15 that had an effect on cancer metastasis. In particular, they found that mice lacking a gene that produces a protein called ARHGEF1 had less metastasis of various primary cancers to the lungs and liver.

The researchers determined that ARHGEF1 suppresses T cells, which can recognise and kill metastatic cancer cells.

To find a suitable drug, the scientists traced signals in the cell to determine that ARHGEF1 is switched on when T cells are exposed to a clotting factor called thromboxane A2 (TXA2).

This was an unexpected revelation for the scientists, because TXA2 is already well-known and linked to how aspirin works.

Reduces the production of TXA2

TXA2 is produced by platelets; aspirin reduces the production of TXA2, leading to the anti-clotting effects, which underlies its ability to prevent heart attacks and strokes.

This new research found that aspirin prevents cancers from spreading by decreasing TXA2 and releasing T cells from suppression. They used a mouse model of melanoma to show that in mice given aspirin, the frequency of metastases was reduced compared to control mice, and this was dependent on releasing T cells from suppression by TXA2.

Professor Rahul Roychoudhuri, from the University of Cambridge, who led the study, said:

Despite advances in cancer treatment, many patients with early stage cancers receive treatments, such as surgical removal of the tumour, which have the potential to be curative, but later relapse due to the eventual growth of micrometastases – cancer cells that have seeded other parts of the body but remain in a latent state.

Most immunotherapies are developed to treat patients with established metastatic cancer, but when cancer first spreads there’s a unique therapeutic window of opportunity when cancer cells are particularly vulnerable to immune attack.

We hope that therapies that target this window of vulnerability will have tremendous scope in preventing recurrence in patients with early cancer at risk of recurrence.

More accessible globally

Dr Jie Yang, who carried out the research, at the University of Cambridge, said:

It was a Eureka moment when we found TXA2 was the molecular signal that activates this suppressive effect on T cells.

Before this, we had not been aware of the implication of our findings in understanding the anti-metastatic activity of aspirin. It was an entirely unexpected finding which sent us down quite a different path of enquiry than we had anticipated.

Aspirin, or other drugs that could target this pathway, have the potential to be less expensive than antibody-based therapies, and therefore more accessible globally.

In the future, the researchers plan to help the translation of their work into potential clinical practice by collaborating with Professor Ruth Langley, of the MRC Clinical Trials Unit at University College London, who is leading the Add-Aspirin clinical trial, to find out if aspirin can stop or delay early stage cancers from coming back.

Caution on aspirin use

Professor Langley, who was not involved in this study, commented:

This is an important discovery. It will enable us to interpret the results of ongoing clinical trials and work out who is most likely to benefit from aspirin after a cancer diagnosis.

In a small proportion of people, aspirin can cause serious side-effects, including bleeding or stomach ulcers. Therefore, it is important to understand which people with cancer are likely to benefit and always talk to your doctor before starting aspirin.

Source: UK Research and Innovation

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Our HIV Response Will Collapse Without US Funding – Unless We Act Urgently

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Reassurances that state clinics will pick up the lost services are empty

Sign outside a Wits RHI clinic in Johannesburg. Photo: Ihsaan Haffejee

By Francois Venter

South Africa faces its worst health crisis in 20 years. Worse than COVID, and one that will overshadow diabetes as a major killer, while pouring petrol on a dwindling TB fire. But it is preventable if our government steps up urgently.

Nearly eight-million people have HIV in South Africa; they need life-long antiretroviral medicines to stay healthy.

The near-total removal of US government funding last week, a programme called PEPFAR, will see every important measure of the HIV programme worsen, including hospitalisations, new infections in adults and children, and death. Unless government meaningfully steps in to continue funding the network of highly efficient organisations that currently fill key gaps in national care, an epidemic that was tantalisingly close to coming under control will again be out of our reach. Millions of people in South Africa will become infected with HIV and hundreds of thousands more will die in the next ten years. 2025 will end much more like 2004, when we started our HIV treatment programme.

Many fail to recognize the danger. Commentators, public health officials, and government spokespeople have downplayed the US financial contributions to the HIV response, suggesting services can be absorbed within current services. The funding cuts amount to approximately 17% of the entire budget for HIV and largely go to salaries for health staff. On the face of it, this indeed seems replaceable. So why are the consequences so deadly?

To understand the impact, one must recognize how US funding has supported HIV care. The money is largely allocated to a network of non-government organisations through a competitive, focused, and rigorously monitored program in four key areas:

  1. Active case finding: The best way to prevent new cases of HIV is find everyone with the disease early on, and get them on treatment. These organisations deploy people in high-risk areas, to test for HIV and screen for TB, and shepherd people who test positive to treatment programmes. People are almost always healthy when they start treatment, and remain healthy, with greatly reduced time to transmit the virus, and much less chance of ever “burdening” the health sector with an opportunistic infection. They are hugely cost-effective.
  2. Tracing people who disappear from care: Patients on antiretrovirals fall out of care for many reasons, ranging from changing their address, to life chaos such as losing their job or mental illness. Or they are simply mixed up in the filing dysfunction within clinics. The US supported programmes helped finding people ‘lost from care’, maintaining systems able to track who has not come back, and how to contact them, often spending considerable time cleaning redundant records as people move between facilities.
  3. Vulnerable population programmes: Services include those for sex workers, LGBTQ+ people, adolescents, people who use drugs, and victims of gender violence. These programs are for people who need tailored services beyond the straightforward HIV care offered in state clinics. They are often discriminated against in routine services and also at significant risk of contracting HIV.
  4. Supporting parts of the health system: This includes technical positions supporting medicine supply lines, laboratories and large information systems, as well as organisations doing advocacy or monitoring the quality of services. All of this keeps the health system ticking over.

In central Johannesburg, where I work, HIV testing services have collapsed. The people who fell out of programmes are not coming back. HIV prevention and TB screening have largely stopped.

Reassurances that state clinics will pick up testing are empty – the staff do not exist, and testing has not resumed. State clinics do not trace people who fall out of care for any illness, let alone for HIV. The data systems maintained by PEPFAR-supported organisations are now gone.

What happens now? The first hard sign that things are failing will be a large drop in the number of people starting treatment, versus what happened in the same month one year ago. The next metric to watch will be hospitalisations for tuberculosis and other infections associated with untreated HIV infection. This will happen towards the end of the year, as immune systems fail. Not long after, death rates will rise. We will see that in death certificates among younger people – the parents and younger adults.

Unfortunately, much of this information will not be available to the health department for at least a year or two, because among the staff laid off in this crisis are the data collectors for the programmes that tracked vital metrics.

The above should come as no surprise, especially to the public health commentators and health department, which is why it is so surprising to hear how certain they are that the PEPFAR programme can easily be absorbed into the state services. The timing of this crisis could not be worse, with huge budget holes in provincial health departments.

Why should this be a priority? After starting the HIV programme in 2004, we spent the next few years muddling through how to deliver antiretrovirals to millions of people in primary care, before we realised we also needed to diagnose them earlier. In 2004, the average CD4 count (a measure of immune strength) at initiation of treatment was about 80 cells/ul, devastatingly low – normal is > 500 cells/ul. A quarter were ill with TB.

This CD4 count average took years to go up, but only by pushing testing into clinic queues, communities, and special services for key populations, not waiting till they were sick. Recently, the average initiation CD4 count was about 400 cells/ul, stopping years of transmission, with most people healthy, and only a small number with TB.

There are many reasons to criticise the relationship between PEPFAR and the health department. It suited both parties to have a symbiotic relationship that meant each got on with their job and ticked their respective output boxes, but neither had to tussle with the messiness of trying to move the PEPFAR deliverables into the health department. As we move forward, learning from these fragilities to plan for the future of the HIV care programme, and for other diseases, will be critical.

Since the suspension of funding, many people have said, “We don’t hear much about HIV anymore”. That is because when the system works well, you don’t hear about it. Some things are far better compared to 2004:

  • We have a government not in denial about HIV being a problem nor encouraging pseudoscience or crackpots.
  • Our frontline health workers, in over 3000 clinics, have vast experience initiating and maintaining antiretrovirals.
  • Antiretrovirals are cheaper, more potent, more durable, and safer.
  • Treatment protocols are simpler.
  • New infection rates are way down.
  • Government delivery systems have improved.
  • Data systems suggest that the majority of ‘lost’ patients are in care, often simply in another clinic.

A sensible emergency plan would do this:

  • Fund existing programmes for a limited time, understanding that the level of reach and expertise is impossible for the health department to replicate at short notice.
  • Couple this with a plan to make posts more sustainable over the next year or two.
  • Learn from the PEPFAR programme that rigorously held organisations accountable, so that provinces can similarly be answerable for their HIV metrics.
  • Ask hard questions why single patient identifiers, and government information systems, that could easily be linked to laboratory, pharmacy and radiology databases, are still not integrated within the public systems, as they are throughout the private health system.
  • Accept that certain key functions and clinics may best be sited outside of the health department.

This will not save the large and valuable research programmes, which need other help. Much of the rest of Africa needs a Marshall Plan to rescue their entire HIV service, as they are almost totally dependent on US government funding.

But ideas like the above will preserve the current South African HIV response and allow us to imagine interventions that could end the disease as a threat for future generations.

No one disputes we need a move away from donor-assisted health programmes. But the scale and immense urgency of this oncoming emergency needs to be understood. We need a plan and a budget, and fast. Or we will have an overwhelmed hospital system and busy funeral services again.

Professor Francois Venter works for Ezintsha, a policy and research unit at Wits. He has been involved in the HIV programme since 2001, and ran several large PEPFAR programmes till 2012. Venter and his unit do not receive funding from PEPFAR, USAID or CDC. Thank you to several experts for supplying analysis and ideas for the initial draft of the article.

Published by GroundUp and Spotlight

Republished from GroundUp under a Creative Commons Attribution-NoDerivatives 4.0 International License.

Read the original article.

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Scientists Crack the Puzzle of How Retinoic Acid Works Against Neuroblastoma

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Photo by Anna Shvets

Neuroblastoma is a solid tumour that occurs in children. When high-risk, the disease has a poor prognosis. Decades ago, adding the drug retinoic acid to neuroblastoma treatment increased survival by 10–15%. However, this effect was only evident in post-chemotherapy consolidation after bulky primary tumours had largely been eliminated. Why retinoic acid is effective in this setting but not against primary tumours, has been speculated about for nearly 50 years. 

St. Jude Children’s Research Hospital scientists resolved the mystery in a new study, showing retinoic acid uses a novel mechanism to kill metastasised neuroblastoma. The drug “hijacks” a normal developmental pathway to trigger cancer cell death. The findings, which have implications for future combination therapy approaches, appears in Nature Communications. 

“We’ve come up with an explanation for a decades-long contradiction about why retinoic acid works in post-chemotherapy consolidation but has little impact on primary neuroblastoma tumours,” said senior co-corresponding author Paul Geeleher, PhD. “Retinoic acid’s activity heavily depends on the cellular microenvironment.” 

The cellular microenvironment is the soup of chemicals, proteins and other signals that surround a cell, and which is unique to that part of the body. For example, the bone marrow microenvironment contains signals to grow blood cells and restructure bone. Metastasised neuroblastoma cells often migrate to bone marrow, where the bone morphogenetic protein (BMP) pathway signalling is highly active. The researchers showed that BMP signaling makes neuroblastoma cells much more vulnerable to retinoic acid. 

“Unexpectedly, we found that cells expressing genes from the BMP signaling pathway were very sensitive to retinoic acid,” said co-first and co-corresponding author Min Pan, PhD, St. Jude Department of Computational Biology. “However, since the bone marrow microenvironment causes neuroblastoma cells there to have higher BMP activity, it neatly explained why retinoic acid is very effective at treating those cells during consolidation therapy, but not the primary tumours during up-front treatment.” 

Hijacking development to drive metastatic neuroblastoma cell death 

Using gene editing technology, the scientists uncovered the relationship between BMP signaling and retinoic acid. They assembled a group of neuroblastoma cell lines susceptible to retinoic acid, then cut out genes to find which were responsible for the drug’s activity. Genes in the BMP pathway had the largest effect while providing a plausible explanation for retinoic acid’s varying outcomes in patients.

“We found that, in neuroblastoma, BMP signaling works with retinoic acid signaling in the same way as during development,” said co-first author Yinwen Zhang, PhD, who characterised how transcription factors, the proteins that bind DNA to regulate gene expression, led to different results in highly retinoic acid-sensitive or insensitive neuroblastoma cells. “If there are a lot of BMP-signaling pathway transcription factors already on DNA, then retinoic acid signaling combines with it to promote downstream cell death–related gene expression. This occurs both in normal embryonic development and neuroblastoma cells in certain microenvironments.” 

“We are the first to uncover such an example of ‘hijacking’ a normal embryonic developmental process preserved in cancer that we can exploit therapeutically,” Geeleher said. “Now, we can look for similar processes in other diseases to design less toxic and more effective treatment strategies.” 

Source: St. Jude Children’s Research Hospital

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Gut Microbes also Feed on Sugar to Produce Crucial Short-chain Fatty Acids

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Gut microbes that were thought to feed exclusively on dietary fibre also get fed sugar from our guts, from which they produce short-chain fatty acids that are crucial to many body functions. The Kobe University discovery of this symbiotic relationship also points the way to developing novel therapeutics.

Gut microbes produce many substances that our body needs but cannot produce itself. Among them are short-chain fatty acids that are the primary energy source for the cells lining our guts but have other important roles, too, and that are thought to be produced by bacteria who feed on undigested fibre. However, in a previous study, the Kobe University endocrinologist Ogawa Wataru found that people who take the diabetes drug metformin excrete the sugar glucose to the inside of their guts. He says: “If glucose is indeed excreted into the gut, it is conceivable that this could affect the symbiotic relationship between the gut microbiome and the host.”

Ogawa and his team set out to learn more about the details of the glucose excretion and its relationship with the gut microbiota. “We had to develop unprecedented bioimaging methods and establish novel analytical techniques for the products of the gut microbial metabolism,” he says. They used their new methods to not only see where and how much glucose enters the guts, but also used mouse experiments to find out how the sugar is transformed after that. In addition, they also checked how the diabetes drug metformin influences these results both in humans and in mice.

The Kobe University team now published their results in the journal Communications Medicine. They found that, first, glucose is excreted in the jejunum and is transported from there inside the gut to the large intestine and the rectum. “It was surprising to find that even individuals not taking metformin exhibited a certain level of glucose excretion into the intestine. This finding suggests that intestinal glucose excretion is a universal physiological phenomenon in animals, with metformin acting to enhance this process,” Ogawa explains. In both humans and mice, irrespective of whether they were diabetic or not, metformin increased the excretion by a factor of almost four.

And second, on the way down, the glucose gets transformed into short-chain fatty acids. Ogawa says: “The production of short-chain fatty acids from the excreted glucose is a huge discovery. While these compounds are traditionally thought to be produced through the fermentation of indigestible dietary fibres by gut microbiota, this newly identified mechanism highlights a novel symbiotic relationship between the host and its microbiota.”

Ogawa and his team are now conducting further studies with the aim of understanding how metformin and other diabetes drugs affect glucose excretion, the gut microbiome and their metabolic products. He says: “Intestinal glucose excretion represents a previously unrecognised physiological phenomenon. Understanding the underlying molecular mechanisms and how drugs interfere with this process could lead to the development of novel therapeutics aimed at the regulation of gut microbiota and their metabolites.”

Source: Kobe University

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Brown Fat Could Help Maintain Exercise Capacity in Aging

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Photo by Barbara Olsen on Pexels

Rutgers Health researchers have made discoveries about brown fat that may open a new path to helping people stay physically fit as they age. A team from Rutgers New Jersey Medical School found that mice lacking a specific gene developed an unusually potent form of brown fat tissue that expanded lifespan and increased exercise capacity by roughly 30%. The team is working on a drug that could mimic these effects in humans.

“Exercise capacity diminishes as you get older, and to have a technique that could enhance exercise performance would be very beneficial for healthful aging,” said Stephen Vatner, university professor and director of the Cardiovascular Research Institute in the medical school’s Department of Cell Biology and Molecular Medicine and senior author of the study in Aging Cell. “This mouse model performs exercise better than their normal littermates.”

Unlike white fat, which stores energy, brown fat burns calories and helps regulate body temperature. This study revealed brown fat also plays a crucial role in exercise capacity by improving blood flow to muscles during physical activity.

The genetically modified mice produced unusually high amounts of active brown fat and showed about 30% better exercise performance than normal mice, both in speed and time to exhaustion.

The discovery emerged from broader research into healthy aging. The modified mice, which lack a protein called RGS14, live about 20% longer than normal mice, with females living longer than males – similar to the pattern seen in humans. Even at advanced ages, they maintain a healthier appearance, avoiding the typical signs of aging, such as loss of hair and graying that appear in normal elderly mice. Their brown adipose tissue also protects them from obesity, glucose intolerance, cardiovascular disorders, cancer and Alzheimer’s disease, in addition to reduced exercise tolerance.

To test whether the brown fat – rather than some other result from the missing genes –accounted for the benefits, the researchers transplanted the brown fat to normal mice. They noted that the recipients gained similar benefits within days. Transplants using regular brown fat from normal mice, by contrast, took eight weeks to produce much milder improvements.

The discovery could eventually improve human lifespans – the total time when people enjoy good mental and physical health.

“With all the medical advances, aging and longevity have increased in humans, but unfortunately, healthful aging hasn’t,” Vatner said. “There are a lot of diseases associated with aging – obesity, diabetes, myocardial ischemia, heart failure, cancer – and what we have to do is find new drugs based on models of healthful aging.”

Rather than develop a treatment that addresses aging broadly, which poses regulatory challenges, Vatner said his team plans to test for specific benefits such as improved exercise capacity and metabolism. This approach builds on their previous success in developing a drug based on a different mouse healthful longevity model.

“We’re working with some people to develop this agent, and hopefully, in another year or so, we’ll have a drug that we can test,” Vatner said.

In the meantime, techniques such as deliberate cold exposure can increase brown fat naturally. Studies have found such efforts to produce short-term benefits that range from enhanced immune system function to improved metabolic health, but Vatner said none of the studies have run long enough to find any effect on healthful aging.

He added that most people would prefer to increase brown fat levels by taking pills rather than ice baths and is optimistic about translating the newest finding into an effective medication.

Source: Rutgers University

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Researchers Debunk Common Beliefs About ‘Cycle Syncing’ and Muscles

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Photo by John Arano on Unsplash

New research from McMaster kinesiologists is challenging the internet belief that timing resistance training to specific phases of the menstrual cycle boosts the body’s ability to build muscle and strength.

The researchers have shown that exercising at various points in the cycle had no impact — positive or negative — on the synthesis of new muscle proteins, a process essential to building and maintaining muscle.

The results, published in the print edition of the Journal of Physiology, debunk the popularly touted practice of cycle syncing, or tailoring workouts to align with the way hormones change throughout a woman’s menstrual cycle.

“Our findings conflict with the popular notion that there is some kind of hormonal advantage to performing different exercises in each phase,” explains Lauren Colenso-Semple, lead author of the study and a former graduate student in the Department of Kinesiology, who conducted the work while at McMaster.

“We saw no differences, regardless of cycle timing.”

For the study, researchers monitored the menstrual cycles of participants — all healthy young women — for three months to confirm their cycles were normal. Contrary to popular belief, only a small percentage of women — about 12 per cent — have a consistent 28-day cycle and ovulate regularly on Day 14 or the “textbook” menstrual cycle.

Participants then ingested a tracer molecule, a benign substance designed to track and monitor muscle protein levels. They performed heavy resistance exercise during two distinct phases of their menstrual cycles: the follicular phase, when estrogen levels are at their peak; and the luteal phase, characterized by peak progesterone levels.

Researchers observed no effect of either menstrual cycle phase on the production of muscle proteins.

Cycle syncing has been made popular by internet influencers to coordinate workouts, certain diets and lifestyle behaviours with the menstrual cycle.

There are fitness apps for tracking cycles, and social media channels are rife with advice and recommendations.

Proponents routinely cite a handful of scientific studies on animals as evidence that fluctuations in ovarian hormones can affect how human muscles respond to exercise, but this study shows that not to be correct.

“Our work shows that women who want to lift weights and recondition their muscles should feel free to do so in any phase of their cycle. There is no physiological difference in response to the exercise,” says Stuart Phillips, the Canada Research Chair in Skeletal Muscle Health at McMaster who supervised the study.

“It is important to tailor your training to how you feel.”

Scientists highlight the need for further research, particularly studies that focus on women’s health. This includes investigating how training, in relation to the menstrual cycle, affects women and how both oral and non-oral contraceptives influence their responses to exercise.

This article was first published on Brighter World. Read the original article.

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Research Draws a Potential Association Between Tattoos and Cancer Risk

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Tattoo ink does not just stay under the skin – some of it makes its way into the lymph nodes. Researchers from the Department of Public Health and the Department of Clinical Research at the University of Southern Denmark (SDU), together with the University of Helsinki, have investigated whether this could have health consequences. Using data from Danish twin pairs, they found that tattooed individuals are more frequently diagnosed with skin and lymphoma cancers compared to those without tattoos.

Ink particles in the body may affect the immune system

When tattoo ink penetrates the skin, some of it is absorbed into the lymph nodes, a key part of the immune system. The researchers are particularly concerned that tattoo ink may trigger chronic inflammation in the lymph nodes, which over time could lead to abnormal cell growth and an increased risk of cancer.

“We can see that ink particles accumulate in the lymph nodes, and we suspect that the body perceives them as foreign substances,” explains Henrik Frederiksen, consultant in haematology at Odense University Hospital and clinical professor at SDU.

“This may mean that the immune system is constantly trying to respond to the ink, and we do not yet know whether this persistent strain could weaken the function of the lymph nodes or have other health consequences.”

Studying this link is challenging because cancer can take years to develop. This means that exposure in youth may not lead to illness until decades later, making it difficult to measure a direct effect.

Twin data provides a unique opportunity to study the link

The study is based on data from the Danish Twin Tattoo Cohort, where researchers have information from more than 5900 Danish twins. By analysing tattoo patterns alongside cancer diagnoses, they found a higher occurrence of both skin and lymphoma cancers in tattooed individuals.

“The unique aspect of our approach is that we can compare twin pairs where one has cancer, but they otherwise share many genetic and environmental factors,” says Jacob von Bornemann Hjelmborg, professor of biostatistics at SDU.

“This provides us with a stronger method for investigating whether tattoos themselves may influence cancer risk.”

The size of tattoos matters

The results show that the link between tattoos and cancer is most evident in those with large tattoos – defined as bigger than a palm. 

For lymphoma, the rate is nearly three times higher for the group of individuals with large tattoos compared to those without tattoos.  This rate (more specifically, ‘hazard rate’) accounts for age, the timing of the tattoo, and how long the individuals have been followed in the study. 

“This suggests that the bigger the tattoo and the longer it has been there, the more ink accumulates in the lymph nodes. The extent of the impact on the immune system should be further investigated so that we can better understand the mechanisms at play,” says Signe Bedsted Clemmensen, assistant professor of biostatistics at SDU.

Another study from the Danish Twin Tattoo Cohort shows that tattoos are becoming increasingly common. Researchers estimate that four in ten women and three in ten men will have tattoos by the age of 25.

The link to lymphoma has also been observed in an independent Swedish study from 2024.

Are some ink colours worse than others?

Previous research has suggested that certain pigments in tattoo ink may be more problematic than others.

“In our study, we do not see a clear link between cancer occurrence and specific ink colours, but this does not mean that colour is irrelevant. We know from other studies that ink can contain potentially harmful substances, and for example, red ink more often causes allergic reactions. This is an area we would like to explore further,” says Signe Bedsted Clemmensen.

What are the next steps?

The researchers now plan to investigate how ink particles affect the function of lymph nodes at a molecular level and whether certain types of lymphoma are more linked to tattoos than others.

“We want to gain a better understanding of the biological mechanisms – what happens in the lymph nodes when they are exposed to ink particles over decades? This can help us assess whether there is a real health risk and what we might do to reduce it,” concludes Signe Bedsted Clemmensen.

Source: University of Southern Denmark Faculty of Health Sciences

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Six out of Ten People Globally Lack Access to Medical Oxygen

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Photo by Samuel Ramos on Unsplash

Six out of every ten people globally lack access to safe medical oxygen, resulting in hundreds of thousands of preventable deaths each year and reducing quality of life for millions more, an international report co-authored by the University of Auckland has found.

Associate Professor Stephen Howie from the University’s Faculty of Medical and Health Sciences (FMHS) was an adviser to the Lancet Global Health Commission on Medical Oxygen Security and co-author of its report Reducing global inequities in medical oxygen access released 18 February.

A key finding shows global access to medical oxygen is highly inequitable. Five billion people, mostly from low and middle-income countries don’t have access to safe, quality, affordable medical oxygen.

Associate Professor Howie, child health researcher and a specialist paediatrician says he hopes further lives will be saved because of this work, and that children and adults will not only survive but thrive.

The Auckland University team are leading the field to improve access to medical oxygen. Howie recently gave a plenary address  at the World Lung Health Conference in Bali, spelling out the challenges and opportunities to tackle the global issue.

“I have been working in the area of oxygen treatment for oxygen-starved (hypoxic) illnesses for two decades, particularly in Africa and the Pacific. My first priority was children (naturally, as a paediatrician) but we learnt soon enough that solving the problem has to involve catering for all ages.

“It is such an obvious need. I saw it at the hospitals I worked at in Africa where needless death from diseases like pneumonia happened because oxygen supplies were short, and this hit families and staff very hard. It was at that time that we made it our goal that ‘no child should die for lack of oxygen’ and this applies to adults too.” 

Fiji was particularly hard hit when the first waves of the COVID-19 pandemic arrived, at one point it had the highest rate of COVID-19 in the world. A close partnership between the Fiji Ministry of Health, the University of Auckland, Cure Kids and Fiji National University, funded by New Zealand MFAT and other donors, played an important role in supporting the pandemic response says Howie. 

I saw it at the hospitals I worked at in Africa where needless death from diseases like pneumonia happened because oxygen supplies were short, and this hit families and staff very hard. It was at that time that we made it our goal that ‘no child should die for lack of oxygen’ and this applies to adults too.

Associate Professor Stephen Howie Waipapa Taumata Rau, University of Auckland, Faculty of Medicine and Health Sciences

Dr Sainimere Boladuadua is Lancet Commission’s Western Pacific Region ambassador 

On the ground during that time was Dr Sainimere Boladuadua, a public health medicine specialist, now a doctoral student at the University of Auckland and currently undertaking a Fulbright fellowship at Johns Hopkins University in Baltimore. 

Boladuadua (Somosomo, Cakaudrove, vasu i Levuka-i-Yale, Kadavu/Fiji) also has the honour of being the Lancet Commission’s Western Pacific Region ambassador and will spearhead advocacy for improving access to medical oxygen in the region. 

“I remember those days, the adrenalin was pumping and it was scary. It was very difficult before the vaccine arrived. We had very little sleep trying to get everything set up,” she says recalling the period of the country organising itself and the national response which included setting up field hospitals. 

Boladuadua met Howie in Fiji where he helped to lead the Fiji Oxygen Project, supporting the vital work of health leaders like Dr Luke Nasedra and Dr Eric Rafai. 

“The project was just doing exactly this, trying to improve and ensure that all the health facilities had access to medical oxygen, facilities to deliver them. That no child or adult should die for lack of oxygen, and it’s such a simple medical therapy that you expect to be available but often it isn’t, says Boladuadua. 

“The reality was rural health facilities sometimes had to ration the oxygen. You have a limited supply, the cylinders that come in every month you have your quota, and if you run out then sometimes you have to prioritize who gets it, who doesn’t. Which is just so heartbreaking.” 

The Fiji Ministry of Health, supported by the project, was in the midst of covering those gaps when COVID hit, and Boladuadua says the one silver lining was that it shone a light on the gaps, putting the issue on the radar. 

“You saw the images around the world, hospitals running out of oxygen in India, family members hauling oxygen cylinders on motorcycles. I guess that made it really come up to the forefront.” 

This was the entry point for Boladudua to start work on her doctoral studies at the University with Howie as her primary academic supervisor, and unsurprisingly her PhD has a focus closely related to her previous work. 

“My research question is how to improve access to care for children with acute respiratory infections in Fiji and obviously links to the supply of oxygen as well.” 

She says respiratory conditions are rising and pneumonia is still one of the leading causes of death and disease particularly in under five year-olds across the Pacific and even in New Zealand. 

“Within New Zealand, our Pacific children experience a larger acute respiratory burden than children of any other ethnic group.” 

Boladuadua says she’s grateful to Professor Cameron Grant, Head of Paediatrics, Child & Youth Health at FMHS who encouraged her to apply for the Fulbright Scholarship. As well as support from her friends, doctoral candidates Alehandrea Manuel (who has since completed her PhD) and Ashlea Gillon. 

“Professor Grant was a Fulbright scholar 30 years ago and he said it would be life changing, and it has been in so many ways,” she says of working closely with the team at Johns Hopkins and the opportunities presented such as the lecture she’s been asked to present next month at the School of Public Health: ‘Decolonising Global Health – a Pacific perspective’.

“What appealed to me was they had a Centre for Indigenous Health that worked very closely with Native American communities. And although Johns Hopkins is in Baltimore, their work is very much within the communities themselves, in the tribal lands of the Navajo and White Mountain Apache peoples in the Southwest of the US. 

“They’ve got sites in all these communities and the staff – data collectors, researchers, the research nurses and everyone in those teams, the majority are Native American. So it’s about responding to their health needs and also building local capacity.” 

Learning how the Indian Health System has accommodated traditional medicine has inspired Boladuadua and she’s brimming with ideas that she’s eager to bring back to Aotearoa later this year when she returns. 

“I wanted to see how you can use traditional knowledge and practices with western knowledge, I wanted to learn how that happened. They’re just doing it so beautifully here. I am learning so much and it has been life changing with all the different perspectives, exposure and the incredible people I’m able to work with.”  

Source: University of Auckland

Categories : Cancer Surgeries & ProceduresTags : Leave a comment

‘Ultra-rapid’ Testing for Cancer Genes in the Operating Theatre

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A novel tool for rapidly identifying the genetic “fingerprints” of cancer cells may enable future surgeons to more accurately remove brain tumours while a patient is in the operating room, new research reveals. Many cancer types can be identified by certain mutations, changes in the instructions encoded in the DNA of the abnormal cells.

Led by a research team from NYU Langone Health, the new study describes the development of Ultra-Rapid droplet digital PCR, or UR-ddPCR, which the team found can measure the level of tumour cells in a tissue sample in only 15 minutes while also being able to detect small numbers of cancer cells (as few as five cells/mm2).

The researchers say their tool is fast and accurate enough, at least in initial tests on brain tissue samples, to become the first practical tool of its kind for detecting cancer cells directly using mutations in real time during brain surgery.

The researchers showed that UR-ddPCR had markedly faster processing speed than standard droplet digital polymerase chain reaction (ddPCR). Standard ddPCR can accurately quantify tumor cells, but it typically takes several hours to produce a result, making it impractical as a surgical guide.

“For many cancers, such as tumors in the brain, the success of cancer surgery and preventing the cancer’s return is predicated on removing as much of the tumor and surrounding cancer cells as is safely possible,” said study co-senior study investigator and neurosurgeon Daniel A. Orringer, MD.

“With Ultra-Rapid droplet digital PCR, surgeons may now be able to determine what cells are cancerous and how many of these cancer cells are present in any particular tissue region at a level of accuracy that has never before been possible,” said Dr Orringer.

Published in the journal Med, the study showed that UR-ddPCR produced the same results as standard ddPCR and genetic sequencing in more than 75 tissue samples from 22 patients at NYU Langone undergoing surgery to remove glioma tumours. Results from UR-ddPCR were also checked against known samples with cancer cells and samples without any cancer.

“Our study shows that Ultra-Rapid droplet digital PCR could be a fast and efficient tool for making a molecular diagnosis during surgery for brain cancer, and it has potential to also be used for cancers outside the brain,” said senior study investigator Gilad Evrony, MD, PhD.

To develop UR-ddPCR, researchers looked for efficiencies in each of the steps involved in standard ddPCR. The team shortened the time needed to extract DNA from tumour samples from 30 minutes to less than 5 minutes in a manner that is still compatible with subsequent ddPCR. The researchers also found efficiencies by increasing the concentrations of the chemicals used in testing, reducing the overall time needed for some steps from two hours to less than three minutes. Time savings were also achieved by using reaction vessels prewarmed to each of the two temperatures required by the PCR rather than repeatedly cycling the temperature of a single reaction vessel between two temperatures.

For the study, researchers used UR-ddPCR to measure the levels of two genetic mutations, IDH1 R132H and BRAF V600E, which are prevalent in brain cancers. They combined UR-ddPCR with another technique the researchers developed earlier, called stimulated Raman histology, to calculate both the fraction and the density of tumour cells within each tissue sample.

Researchers caution that widespread use of the tool awaits further refinements and clinical trials. They say their next step is to automate UR-ddPCR to make it faster and simpler to use in the operating room. Subsequent clinical trials will be necessary to compare patient outcomes using their tool compared to current diagnostic technologies. They also plan to develop the technology to identify other common genetic mutations for other cancer types.

Source: NYU Langone Health / NYU Grossman School of Medicine

Categories : Neurodegenerative Diseases NeurologyTags : Leave a comment

More Evidence Shows that 40Hz Gamma Stimulation is Beneficial for Brain Health

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A decade of studies from labs around the world provide a growing evidence base that increasing the power of the brain’s gamma rhythms could help fight Alzheimer’s, and perhaps other, neurological diseases.

Source: Pixabay

A decade after scientists in The Picower Institute for Learning and Memory at MIT first began testing whether sensory stimulation of the brain’s 40Hz “gamma” frequency rhythms could treat Alzheimer’s disease in mice, a growing evidence base supporting the idea that it can improve brain health – in humans as well as animals – has emerged from the work of labs all over the world. A new review article in PLOS Biology describes the state of research so far and presents some of the fundamental and clinical questions at the forefront of the non-invasive gamma stimulation now.

“As we’ve made all our observations, many other people in the field have published results that are very consistent,” said Li-Huei Tsai, Picower Professor at MIT, director of MIT’s Aging Brain Initiative, and senior author of the new review with postdoc Jung Park. “People have used many different ways to induce gamma including sensory stimulation, transcranial alternating current stimulation or transcranial magnetic stimulation, but the key is delivering stimulation at 40 Hz. They all see beneficial effects.”

A decade of discovery at MIT

Starting with a paper in Nature in 2016, a collaboration led by Tsai has produced a series of studies showing that 40Hz stimulation via light, sound, a combination of the two, or tactile vibration reduces hallmarks of Alzheimer’s pathology such as amyloid and tau proteins, prevents neuron death, decreases synapse loss, and sustains memory and cognition in various Alzheimer’s mouse models. The collaboration’s investigations of the underlying mechanisms that produce these benefits has so far identified specific cellular and molecular responses in many brain cell types including neurons, microglia, astrocytes, oligodendrocytes and the brain’s blood vessels. Last year, for instance, the lab reported in Nature that 40Hz audio and visual stimulation induced interneurons in mice to increase release of the peptide VIP, prompting increased clearance of amyloid from brain tissue via the brain’s glymphatic “plumbing” system.

Meanwhile, at MIT and at the MIT spinoff company Cognito Therapeutics, phase II clinical studies have shown that people with Alzheimer’s exposed to 40Hz light and sound experienced a significant slowing of brain atrophy and improvements on some cognitive measures compared to untreated controls. Cognito, which has also measured significant preservation of white matter in volunteers, has been conducting a pivotal, nationwide phase III clinical trial of sensory gamma stimulation for more than a year.

“Neuroscientists often lament that it is a great time to have AD if you are a mouse,” Park and Tsai wrote in the review. “Our ultimate goal, therefore, is to translate GENUS discoveries into a safe, accessible, and non-invasive therapy for AD patients.” The MIT team often refers to 40Hz stimulation as “GENUS” for Gamma Entrainment Using Sensory Stimulation.

A growing field

As Tsai’s collaboration, which includes MIT colleagues Edward Boyden and Emery N. Brown, has published its results, many other labs have produced studies adding to the evidence that various methods of non-invasive gamma sensory stimulation can combat Alzheimer’s pathology. Among many examples cited in the new review, in 2024 a research team in China independently corroborated that 40Hz sensory stimulation increases glymphatic fluid flows in mice. In another example, a Harvard Medical School-based team in 2022 showed that 40Hz gamma stimulation using Transcranial Alternating Current Stimulation significantly reduced the burden of tau in three out of four human volunteers. And in another study involving more than 100 people, researchers in Scotland in 2023 used audio and visual gamma stimulation (at 37.5Hz) to improve memory recall.

Open questions

Amid the growing number of publications describing preclinical studies with mice and clinical trials with people, open questions remain, Tsai and Park acknowledge. The MIT team and others are still exploring the cellular and molecular mechanisms that underlie GENUS’s effects. Tsai said her lab is looking at other neuropeptide and neuromodulatory systems to better understand the cascade of events linking sensory stimulation to the observed cellular responses. Meanwhile the nature of how some cells, such as microglia, respond to gamma stimulation and how that affects pathology remains unclear, Tsai added.

Even with a national Phase III clinical trial underway, it is still important to investigate these fundamental mechanisms, Tsai said, because new insights into how non-invasive gamma stimulation affects the brain could improve and expand its therapeutic potential.

“The more we understand the mechanisms, the more we will have good ideas about how to further optimize the treatment,” Tsai said. “And the more we understand its action and the circuits it affects, the more we will know beyond Alzheimer’s disease what other neurological disorders will benefit from this.”

Indeed the review points to studies at MIT and other institutions providing at least some evidence that GENUS might be able to help with Parkinson’s disease, stroke, anxiety, epilepsy, and the cognitive side effects of chemotherapy and conditions that reduce myelin such as multiple sclerosis. Tsai’s lab has been studying whether it can help with Down syndrome as well.

The open questions may help define the next decade of GENUS research.

Source: Picower Institute at MIT