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An international team of researchers has identified a new weakness in prostate cancer cells that could lead to more effective treatments for one of the most common cancers among men.
The study, published in the Proceedings of the National Academy of Sciences (PNAS), was led by scientists from Flinders University in Australia and South China University of Technology. Their findings highlight two enzymes, PDIA1 and PDIA5, that play a key role in helping prostate cancer cells grow, survive, and resist existing treatments.
Enzymes That Protect Cancer Cells
According to the researchers, PDIA1 and PDIA5 act like molecular bodyguards for the androgen receptor (AR), a protein that drives prostate cancer growth. When these enzymes are blocked, the AR loses stability and breaks apart, causing cancer cells to die and tumors to shrink in both lab cultures and animal models.
The team also discovered that combining drugs that inhibit PDIA1 and PDIA5 with enzalutamide, a standard medication for prostate cancer, made the treatment significantly more effective.
“We’ve discovered a previously unknown mechanism that prostate cancer cells use to protect the androgen receptor, which is a key driver of the disease,” explains senior author Professor Luke Selth, Head of Prostate Cancer Research and Co-Director of the Flinders Health and Medical Research Institute’s Cancer Impact program.
“By targeting these enzymes, we can destabilize the AR and make tumors more vulnerable to existing therapies like enzalutamide.”
A Promising Combination Therapy

Lead author Professor Jianling Xie, who began the research at Flinders University, said the combination therapy worked well in both patient-derived tumor samples and mouse models, showing strong potential for clinical use.
“This is an exciting step forward,” says Dr. Xie, now based at South China University of Technology. “Our findings show that PDIA1 and PDIA5 are not just helpers of cancer growth but they’re also promising targets for new treatments that could work alongside existing drugs.”
Disrupting Cancer’s Energy Supply
The study also revealed that PDIA1 and PDIA5 do more than just protect the AR. They help cancer cells manage stress and maintain their energy production systems. When the enzymes are blocked, the mitochondria — the cell’s power generators — become damaged, leading to oxidative stress that further weakens the cancer cells.
“This dual impact of hitting both the AR and the cancer’s energy supply makes these enzymes especially attractive targets,” adds Dr. Xie. “It’s like cutting off both the fuel and the engine at the same time.”
Next Steps Toward Safer Treatments
Professor Selth notes that while current PDIA1 and PDIA5 inhibitors are promising, they still need to be refined for patient use. Some existing compounds can affect healthy cells, so future studies will focus on designing safer and more selective versions.

Prostate cancer is the second most common cancer in men worldwide. Although treatments such as hormone therapy and AR-targeting drugs have greatly improved survival rates, resistance to these therapies remains a major challenge. This new discovery may help overcome that resistance and improve treatment options for men with advanced prostate cancer.
The research received support from Cancer Council SA, Cancer Council NSW, the Flinders Foundation, the Movember Foundation, the Prostate Cancer Foundation of Australia, The Hospital Research Foundation, Cancer Australia, Masonic Charities Trust, the Australian Research Council, and several international funding organizations.

Neuroscientists from Columbia University and McGill University have identified a brain chemical that appears to drive depression and suicidal thinking in individuals who faced trauma or hardship during childhood.
The researchers found that high levels of a stress-related protein called SGK1 are closely associated with depression among people who endured early-life adversity. This discovery opens the door to a new type of antidepressant that blocks SGK1 activity and may be more effective for people who were neglected or abused as children.
Studies show that about 60% of adults in the United States diagnosed with major depression and roughly two-thirds of those who attempt suicide experienced some form of trauma or adversity during childhood.
“Current antidepressants are often less effective for people with a history of childhood adversity, who represent a large proportion of adults with depression,” says the study’s lead author, Christoph Anacker, assistant professor of clinical neurobiology in the Department of Psychiatry at Columbia University Vagelos College of Physicians and Surgeons. “What’s exciting about our study is that it raises the prospect of quickly developing new treatments, as SGK1 inhibitors are in development for other conditions, and gives us a screening tool to identify people at greatest risk.”
Why Depression After Early Trauma May Be Different
Childhood adversity (such as physical abuse or growing up in a dysfunctional family) is one of the strongest predictors of depression in adulthood.
While common antidepressants like SSRIs are helpful for many people, they are less effective for those who experienced early trauma. “This suggested to us that the biological processes that lead to depression and suicidality in general may differ from those with less stressful childhoods,” Anacker explains.

Around ten years ago, Anacker’s team discovered unusually high levels of SGK1 — a stress-responsive protein — in the blood of unmedicated patients with depression.
Evidence of SGK1’s Role in Depression and Suicide
In the latest research, the scientists examined the brains of adults who had died by suicide and found elevated SGK1 levels. Those who had suffered childhood trauma showed the highest concentrations, up to twice as much as others who had also died by suicide.
The researchers also studied children exposed to early adversity and discovered that those carrying genetic variants that increase SGK1 production were more likely to experience depression as teenagers. These findings point to SGK1 as a biological driver of depression and suicidal behavior, particularly among people affected by trauma early in life.
Developing a New Kind of Antidepressant
Based on these results, Anacker and his colleagues suggest that drugs designed to block SGK1 might help prevent or treat depression in individuals with a history of trauma. In experiments with mice, SGK1 inhibitors delivered into the bloodstream prevented the animals from developing depressive-like behaviors during chronic stress.

SGK1 inhibitors are already being evaluated for use in other conditions, including atrial fibrillation. Anacker’s team now hopes to begin clinical trials in people who have depression and a background of early life adversity. The researchers also propose that genetic screening could identify individuals most likely to benefit from an SGK1-targeted antidepressant.
“There’s an urgent need to identify and treat people with the greatest risk of depression and suicide after exposure to early life adversity and SGK1 is a promising avenue to explore,” Anacker says.
The research, titled “Hippocampal SGK1 promotes vulnerability to depression: the role of early life adversity, stress, and genetic risk,” was published in Molecular Psychiatry.
Authors include Amira Millette (Columbia), Milena T. van Dijk (Columbia), Irina Pokhvisneva (McGill), Yifei Li (Columbia), Rory Thompson (Columbia), Sachin Patel (McGill), Rosemary C. Bagot (McGill), Aniko Naray-Fejes-Toth (Dartmouth), Geja Fejes-Toth (Dartmouth), Patricia Palufo-Silveira (McGill), Gustavo Turecki (McGill), Juan Pablo Lopez (Karolinksa Institute), and Christoph Anacker (Columbia).
The study was funded by a NARSAD Young Investigator award from the Brain & Behavior Research Foundation and the Columbia University Department of Psychiatry.

An extensive review of existing studies, published in The BMJ on November 10, finds no clear evidence that using acetaminophen (Tylenol) during pregnancy increases the risk of autism or ADHD in children. The new analysis was conducted in response to growing public debate about the safety of acetaminophen use while pregnant.
Researchers reported that the reliability of earlier studies and reviews on this topic is rated as low to critically low. They noted that any apparent associations observed in past studies may be influenced by factors shared within families, such as genetics and environmental conditions, rather than by the medication itself.
Safety Guidance for Pregnant Women and Health Professionals
The study authors emphasize that regulators, healthcare providers, pregnant women, parents, and those affected by autism and ADHD should be aware of the poor quality of prior evidence. They recommend that acetaminophen continue to be used when needed to relieve pain or reduce fever during pregnancy, consistent with current medical advice.
Acetaminophen (called paracetamol outside the USA and Japan) remains the standard and recommended treatment for pain and fever in pregnancy and is considered safe by regulatory agencies around the world.
Previous systematic reviews exploring potential risks have been inconsistent in quality. Many did not properly adjust for key factors shared by family members, such as parental health or lifestyle, making it difficult to determine whether acetaminophen itself has any true impact on a baby’s brain development.
To clarify this uncertainty, the researchers conducted an “umbrella review” (a comprehensive summary of systematic reviews) to evaluate how strong and reliable the existing evidence is, and to examine whether there is a measurable association between acetaminophen use in pregnancy and the risk of autism or ADHD in children.

Reviewing Data From 40 Studies
The team identified nine systematic reviews that together covered 40 observational studies on acetaminophen exposure during pregnancy and later neurodevelopmental outcomes in children. Four of these reviews included meta-analyses (a statistical technique that combines data from multiple studies to produce a more precise estimate of effect).
Each review was carefully assessed for bias using recognized evaluation tools, and the researchers rated their confidence in the findings as high, moderate, low, or critically low. The amount of overlap between studies in the reviews was also recorded and found to be very high.
Although all reviews reported a possible to strong link between maternal acetaminophen use and autism or ADHD, seven of the nine reviews urged caution when interpreting those findings. Most warned that the results could be skewed by unmeasured factors, known as confounders, such as family genetics or parental health differences.
Overall, confidence in the findings was rated as low for two reviews and critically low for seven. Only one review included two studies that adequately controlled for shared genetic and environmental influences between siblings and accounted for other important factors, including parental mental health, background, and lifestyle.
Adjusted Results Show Little to No Link
In both of these well-controlled studies, any apparent connection between prenatal acetaminophen exposure and autism or ADHD risk largely disappeared or was significantly reduced after adjustments were made. The researchers suggest that these results indicate much of the previously observed risk can be explained by family-related factors rather than by the medication itself.

The authors acknowledge several limitations in the available research. The included reviews varied in scope and methodology, did not address dosage or timing of exposure, and focused only on autism and ADHD outcomes.
Even so, the new overview brings together all relevant evidence using established quality-assessment methods. It highlights what the authors describe as “the lack of robust evidence linking acetaminophen use in pregnancy and autism and ADHD in offspring.”
They conclude: “The current evidence base is insufficient to definitively link in utero exposure to acetaminophen with autism and ADHD in childhood. High quality studies that control for familial and unmeasured confounders can help improve evidence on the timing and duration of acetaminophen exposure, and for other child neurodevelopmental outcomes.”

New research suggests that drinking coffee may actually help protect against atrial fibrillation (AFib), a common heart rhythm disorder that causes the heart to beat too quickly and irregularly, sometimes leading to stroke or heart failure.
For years, doctors have advised people with AFib and other heart issues to stay away from caffeine, fearing it could worsen symptoms. But a new study from UC San Francisco and the University of Adelaide has found the opposite: participants who drank one cup of caffeinated coffee a day had a 39% lower risk of developing AFib.
Why Coffee May Help the Heart
“Coffee increases physical activity which is known to reduce atrial fibrillation,” explained Gregory M. Marcus, MD, MAS, an electrophysiologist at UCSF Health and the senior author of the study, published November 9 in JAMA. Marcus added that “caffeine is also a diuretic, which could potentially reduce blood pressure and in turn lessen AFib risk. Several other ingredients in coffee also have anti-inflammatory properties that could have positive effects.”
Rates of AFib have been climbing in recent years, largely due to aging populations and increasing obesity. More than 10 million adults in the United States have been diagnosed, and experts estimate that as many as one in three people may experience the condition at some point in their lives.
Testing Coffee’s Effect on Heart Rhythm
To explore whether coffee helps or harms, researchers designed the DECAF study (Does Eliminating Coffee Avoid Fibrillation?), the first randomized clinical trial to test the relationship between caffeinated coffee and AFib. The project was funded by the National Institutes of Health.

The trial involved 200 patients who were regular coffee drinkers and had persistent AFib or a related condition known as atrial flutter, along with a history of AFib. All were scheduled to undergo electrical cardioversion, a procedure that uses a controlled electrical shock to restore normal heart rhythm. Participants were randomly assigned to either drink at least one cup of caffeinated coffee or an espresso shot each day, or to completely avoid coffee and other caffeinated beverages for six months.
Coffee Drinkers Had Lower Risk
At the end of the study, the group that drank coffee experienced a 39% lower risk of recurring AFib episodes. In addition to coffee’s potential anti-inflammatory effects, the researchers proposed that those who drank coffee may have naturally replaced less healthy drinks, such as sugary sodas, with coffee instead.
“The results were astounding,” said first author Christopher X. Wong, PhD, of UCSF, the University of Adelaide, and the Royal Adelaide Hospital. “Doctors have always recommended that patients with problematic AFib minimize their coffee intake, but this trial suggests that coffee is not only safe but likely to be protective.”
Authors from UCSF include Gabrielle Montenegro; Hannah H. Oo; Isabella J. Pena; Janet J. Tang, PhD; Grace Wall; Thomas A. Dewland, MD; Joshua D. Moss, MD; Edward P. Gerstenfeld, MD; Zian H. Tseng, MD; Henry H. Hsia, MD; Randall J. Lee, MD, PhD; Jeffrey E. Olgin, MD; Vasanth Vedantham, MD; Melvin M. Scheinman, MD; and Catherine Lee, PhD.
Marcus is supported by R01 HL158825-01, R01 HL167975-01, R01 DA058069-01, and R01 HL159069-01A1 grants from the National Heart, Lung and Blood Institute, as well as R01 AA022222 from the National Institute on Alcohol Abuse and Alcoholism.

A new study from Intermountain Health in Salt Lake City reports that a personalized vitamin D3 treatment plan for patients who have suffered a heart attack can greatly reduce their chances of another one.
In a large randomized clinical trial, researchers found that managing patients’ vitamin D levels through a “target-to-treat” approach — where blood levels were monitored and dosages were adjusted to reach an optimal range — cut the likelihood of a second heart attack by 50%.
The findings were presented on Nov. 9 at the 2025 American Heart Association Scientific Sessions in New Orleans.
Encouraging Early Results from Intermountain Researchers
These results are very encouraging, said Heidi May, PhD, cardiovascular epidemiologist at Intermountain Health and the study’s principal investigator. “We observed no adverse outcomes when giving patients higher doses of vitamin D3 supplementation, and to significantly reduce the risk of another heart attack, which are exciting results,” said Dr. May. “We’re excited with these results but know we have further work to do to validate these findings.”
According to researchers, the results carry global importance, as between one-half and two-thirds of people worldwide have low levels of vitamin D.
In the past, most individuals received sufficient vitamin D through sunlight exposure. Today, with lifestyle changes and medical advice aimed at reducing skin cancer risk, people spend less time in the sun and must rely more on dietary supplements such as vitamin D3 to maintain healthy levels.

From Observation to Precision Treatment
Low vitamin D levels have long been linked to poor cardiovascular outcomes in observational studies. However, earlier clinical trials that provided standard supplementation doses failed to show measurable reductions in heart disease risk. Intermountain scientists wanted to test a different idea: rather than giving everyone the same dose, what if supplementation was adjusted to reach a specific, healthy vitamin D level?
“Previous studies just gave patients supplementation without regularly checking blood levels of vitamin D to determine what supplementation achieved,” said Dr. May. “With more targeted treatment, when we checked exactly how supplementation was working and made adjustments, we found that patients had their risk of another heart attack cut in half.”
Inside the TARGET-D Clinical Trial
The Intermountain study, called the TARGET-D trial, ran from April 2017 to May 2023 and included 630 patients who had suffered a heart attack within a month of enrolling. Participants were followed until March 2025 to monitor cardiovascular outcomes.
Patients were randomly assigned to one of two groups: one received no vitamin D management, and the other underwent active, targeted vitamin D3 treatment.

The goal for the treatment group was to raise blood vitamin D levels to above 40 nanograms per milliliter (ng/mL). At the start, 85% of participants had vitamin D3 levels below that threshold (

Chronic fatigue syndrome leaves many people completely drained of energy and struggling to think clearly, and their symptoms often worsen after mental or physical exertion — a reaction known as post-exertional malaise. Researchers studying shortness of breath in people with chronic fatigue have now found that these patients are much more likely to experience dysfunctional breathing. This irregular breathing pattern may be linked to dysautonomia, a disorder involving abnormal nerve control of blood vessels and muscles. By focusing treatment on these breathing irregularities, scientists believe it may be possible to ease some of the debilitating symptoms.
“Nearly half of our chronic fatigue subjects had some disorder of breathing — a totally unappreciated issue, probably involved in making symptoms worse,” said Dr. Benjamin Natelson of the Icahn School of Medicine, senior author of the study published in Frontiers in Medicine. “Identifying these abnormalities will lead researchers to new strategies to treat them, with the ultimate goal of reducing symptoms.”
Breathe easy
The study included 57 people diagnosed with chronic fatigue syndrome and 25 healthy individuals of similar age and activity level. All participants completed two days of cardiopulmonary exercise tests. During these sessions, the researchers monitored heart rate, blood pressure, oxygen uptake efficiency, blood oxygen saturation, and how much effort participants used to breathe. They also analyzed breathing rate and patterns to detect signs of hyperventilation and dysfunctional breathing.
Dysfunctional breathing is often seen in asthma patients, but it can develop for many different reasons. Typical features include frequent deep sighs, rapid breathing, forceful exhalation from the abdomen, or chest breathing without proper diaphragm use, which prevents the lungs from fully expanding. It can also involve a lack of coordination between chest and abdominal movements, meaning the muscles that support breathing are no longer working smoothly together.
“While we know the symptoms generated by hyperventilation, we remain unsure what symptoms may be worse with dysfunctional breathing,” said Dr. Donna Mancini of the Icahn School of Medicine, first author of the study. “But we are sure patients can have dysfunctional breathing without being aware of it. Dysfunctional breathing can occur in a resting state.”
Catching your breath
Results showed that people with chronic fatigue syndrome took in roughly the same amount of oxygen as the control group — their peak VO2 max was similar. However, 71% of the chronic fatigue group showed breathing abnormalities, such as hyperventilation, dysfunctional breathing, or both.

Almost half of the chronic fatigue participants breathed irregularly during the tests, compared to only four people in the control group. About one-third of the fatigue patients hyperventilated, while just one person in the control group did. Nine patients had both hyperventilation and dysfunctional breathing, a combination not seen in any of the controls.
Both of these breathing disorders can produce symptoms similar to those of chronic fatigue, including dizziness, difficulty concentrating, shortness of breath, and exhaustion. When both occur together, they can also cause chest pain, palpitations, fatigue, and (unsurprisingly) anxiety. The researchers believe that these breathing problems may worsen the effects of chronic fatigue or even play a direct role in post-exertional malaise.
“Possibly dysautonomia could trigger more rapid and irregular breathing,” said Mancini. “It is well known that chronic fatigue syndrome patients often have dysautonomia in the form of orthostatic intolerance, which means you feel worse when upright and not moving. This raises the heart rate and leads to hyperventilation.”
Pulmonary physiotherapy?
These findings suggest that addressing dysfunctional breathing could help relieve some symptoms of chronic fatigue. The researchers plan to continue investigating how dysfunctional breathing and hyperventilation interact. Although more studies are needed before any official treatments are recommended, they already have several promising ideas.
“Breathing exercises via yoga could potentially help, or gentle physical conditioning where breath control is important, as with swimming,” suggested Natelson. “Or biofeedback, with assessment of breathing while encouraging gentle continuous breath use. If a patient is hyperventilating, this can be seen by a device that measures exhaled CO2. If this value is low, then the patient can try to reduce the depth of breathing to raise it to more normal values.”

Gut bacteria play a major role in human health, influencing everything from digestion to immunity and mood. Yet, the microbiome’s complexity is staggering. The sheer number of bacterial species and their interactions with human chemistry have made it difficult for scientists to fully understand their effects. In a groundbreaking step, researchers at the University of Tokyo applied a type of artificial intelligence known as a Bayesian neural network to study gut bacteria. Their goal was to uncover connections that traditional data analysis methods often miss.
While the human body contains roughly 30 to 40 trillion human cells, the intestines alone harbor about 100 trillion bacterial cells. In other words, we carry more bacterial cells than our own. These microbes aren’t just involved in digestion; they also produce and modify thousands of compounds called metabolites. These small molecules act as chemical messengers, circulating through the body and influencing metabolism, immunity, and even brain function. Understanding how specific bacteria produce particular metabolites could unlock new ways to support overall health.
Mapping the Microbial Puzzle
“The problem is that we’re only beginning to understand which bacteria produce which human metabolites and how these relationships change in different diseases,” explained Project Researcher Tung Dang from the Tsunoda lab in the Department of Biological Sciences. “By accurately mapping these bacteria-chemical relationships, we could potentially develop personalized treatments. Imagine being able to grow a specific bacterium to produce beneficial human metabolites or designing targeted therapies that modify these metabolites to treat diseases.”
The main challenge lies in the sheer scale of the data. With countless bacteria and metabolites interacting in complex ways, identifying meaningful patterns is extremely difficult. To tackle this, Dang and his team turned to advanced artificial intelligence (AI) methods.
Their system, called VBayesMM, uses a Bayesian approach to detect which bacterial groups significantly influence particular metabolites. It also measures uncertainty in its predictions, helping prevent overconfident but incorrect conclusions. “When tested on real data from sleep disorder, obesity and cancer studies, our approach consistently outperformed existing methods and identified specific bacterial families that align with known biological processes,” said Dang. “[This gives] confidence that it discovers real biological relationships rather than meaningless statistical patterns.”
Understanding the System’s Strengths and Limits
Because VBayesMM can recognize and communicate uncertainty, it provides researchers with more trustworthy insights than earlier tools. Although it’s optimized for large-scale data, analyzing massive microbiome datasets remains computationally demanding. Over time, however, these costs are expected to decrease as processing power improves. The system also performs best when there is extensive bacterial data compared to metabolite data; otherwise, accuracy can drop. Another limitation is that VBayesMM treats bacteria as independent actors, even though they often interact in complex, interdependent networks.
“We plan to work with more comprehensive chemical datasets that capture the complete range of bacterial products, though this creates new challenges in determining whether chemicals come from bacteria, the human body or external sources like diet,” said Dang. “We also aim to make VBayesMM more robust when analyzing diverse patient populations, incorporating bacterial ‘family tree’ relationships to make better predictions, and further reducing the computational time needed for analysis. For clinical applications, the ultimate goal is identifying specific bacterial targets for treatments or dietary interventions that could actually help patients, moving from basic research toward practical medical applications.”
By using AI to navigate the vast and intricate world of gut microbes, researchers are moving closer to unlocking the microbiome’s potential to transform personalized medicine.

3 hours agoShareSaveGraham FraserBBC ScotlandShareSaveUniversity of DundeeDoctors from Scotland and the US have completed what is thought to be a world-first stroke procedure using a robot.Prof Iris Grunwald, of the University of Dundee, performed the remote thrombectomy – the removal of blood clots after a stroke – on a human cadaver that had been donated to medical science.The professor was at Ninewells Hospital in Dundee, while the body she was operating on while using the machine was across the city at the university.Hours later, Ricardo Hanel – a neurosurgeon in Florida – used the technology to carry out the first transatlantic surgery from his Jacksonville base on a human body in Dundee over 4,000 miles (6,400km) away.University of DundeeThe team has called it a potential “game changer” if it becomes approved for use on patients. The medics believe this technology could transform stroke care, as a delay in accessing specialist treatment can have a direct impact on the chances of recovery.Prof Grunwald said: “It felt as if we were witnessing the first glimpse of the future.”Where previously this was thought to be science fiction, we demonstrated that every step of the procedure can already be done.”The University of Dundee is the global training centre of the World Federation for Interventional Stroke Treatment, and is the only place in the UK where doctors can operate on cadavers with human blood circulated in the vessels to mimic treatment on a live human.”This was the first time that we could perform the whole mechanical thrombectomy procedure in a real human body to show that all steps of the procedure are possible,” said Prof Grunwald.Juliet Bouverie, the chief executive of the Stroke Association charity, told BBC News the transatlantic procedure was “a remarkable innovation”.She added: “For too long, people living in remote and rural areas have been deprived of access to thrombectomy. “Robotics like this could rebalance the inequity which exists in stroke treatment across the UK.”University of DundeeIn the experiment, human blood was used in four different cadavers. The bodies had been donated to science, with the subjects dying in the past three years and then embalmed.Both the Dundee and Florida procedures were carried out last month using robotics from the Lithuanian firm Sentante.While there have been remote thrombectomies carried out before on a silicon model, a 3D printed replica and on an animal, this is thought to have been the first procedure on a human body.The team now hope to take part in clinical trials next year.How does the technology work?An ischaemic stroke occurs when an artery is blocked by a clot. This cuts off blood and oxygen supply to the brain, and brain cells lose function and die.The best treatment is a thrombectomy, where a specialist uses catheters and wires to remove the clot. But what happens when a patient can’t get to a specialist who can do the procedure?Prof Grunwald said the experiment demonstrated a robot could be connected to the same catheters and wires a surgeon would normally use, and a medic who is with the patient could simply attach the wires.The surgeon, in another location, could then hold and move their own wires, and the robot then carries out exactly the same movements in real time on the patient to carry out the thrombectomy.The patient would be in a hospital operating room, while the doctor could carry out the procedure using the Sentante machine from anywhere – even their own home.Prof Grunwald and Ricardo Hanel could see live X-rays of the body in the experiments, and monitor progress in real time, with the Dundee expert saying it took only took 20 minutes of training.Tech giants Nvidia and Ericsson were involved in the project to ensure the connectivity of the robot.Dr Hanel said: “To operate from the US to Scotland with a 120 millisecond lag – a blink of an eye – is truly remarkable.”SentanteSentanteThe future of stroke treatmentProf Grunwald, who has won an award from Innovate UK for her work and is also the vice president of the World Federation for Interventional Stroke Treatment, said there were two main problems with a standard thrombectomy – a global shortage of doctors who can do it, and treatment depends on your location.In Scotland, there are only three places patients can receive the procedure – Dundee, Glasgow and Edinburgh. If you don’t live there, you must travel.Prof Grunwald said: “The treatment is very time sensitive.”Every six minutes delay, you have a 1% less chance of having a good outcome.”This technology would now provide a new way where you’re not depending on where you live – saving the valuable minutes where your brain is otherwise dying.”Public Health Scotland said there were 9,625 ischaemic strokes in Scotland last year. Only 212 – or 2.2% of all patients – received a thrombectomy, while 1,045 people received medication to burst the clots. For the rest of the UK, only 3.9% of all stroke patients received a thrombectomy in the year to March 2024.”It feels amazing,” added Edvardas Satkauskas, the CEO of Sentante, speaking to BBC News from the company’s base in Lithuania.”Sometimes, the future is way closer than we think.”

3 hours agoShareSaveCash MurphySouth EastShareSaveKate DysonA woman from East Sussex who was plunged into sudden menopause after surgery to remove both ovaries is spearheading efforts to change NHS policy in this area.Kate Dyson, 44, from Hastings, underwent the surgery six months ago after having a subtotal hysterectomy just over four years ago to remove her uterus – a procedure which leaves the cervix in place.The mum-of-three says she was completely unprepared for the impact of surgical menopause, which is triggered by both ovaries being removed.”Honestly it was like falling off a hormonal cliff edge,” she told BBC Radio Sussex.”Within hours of the surgery I was home the same day. I was experiencing hot flushes, confusion, and the first night I woke up in the morning and I was absolutely dripping with sweat,” she said. Ms Dyson says she found the aftercare galling, and says this is commonplace for many women.She said: “We are discharged without hormones, without warning, and without support. In my discharge notes it simply read, ‘can try combined HRT [hormone replacement therapy] if she wishes’, as if it were suggesting a glass of wine at the weekend.”This experience prompted her to start campaign group Surge Menopause, whose aim is to push the Department of Health and Social Care (DHSC) to revolutionise its offering.Menopause ‘one-stop shop’Ms Dyson said: “We’re calling for every woman facing ovary removal to receive clear information about the impact of surgical menopause pre-surgery, supportive information about hormone therapy and automatic access to HRT where it’s safe, and proper follow-up care that responds to the severity of symptoms experienced by women in surgical menopause.”According to research by Newson Health and Dr Ceri Cashell, only 4.8% of 126 pre-menopausal women at three NHS hospitals who underwent surgery to remove both ovaries received HRT afterwards.This is despite the National Institute for Health and Care Excellence (Nice) and British Menopause Society recommending HRT until the average age of natural menopause, around the age of 51.Ms Dyson built the Surge website herself in a bid to create a “one-stop shop” for all matters around surgical menopause.Her biggest objective was to create a space where those affected could learn what life looks like “in this whole new chapter of surgical menopause”.A spokesperson from the DHSC said: “It is unacceptable women are not receiving the proper care and support following surgical menopause and the Health Secretary has been clear that we inherited a broken NHS with too many women still subject to a system that doesn’t listen to their experiences or understand their needs.”The DHSC says it is taking action to combat deficiencies in this area, including adding menopause advice to NHS health checks and bringing down gynecology waiting lists.Related storiesRelated internet links

A groundbreaking Blood Pressure Treatment Efficacy Calculator, developed using data from nearly 500 randomized clinical trials involving more than 100,000 participants, now enables doctors to estimate how much different medications can lower a patient’s blood pressure.
Recently published in The Lancet, the research behind this tool could transform how high blood pressure is managed. It allows doctors to tailor therapy to each patient’s needs based on how much they need to reduce their blood pressure.
“This is really important because every 1mmHg reduction in systolic blood pressure lowers your risk of heart attack or stroke by two percent,” said Nelson Wang, cardiologist and Research Fellow at The George Institute for Global Health.
“But with dozens of drugs, multiple doses per drug, and most patients needing two or more drugs, there are literally thousands of possible options, and no easy way to work out how effective they are,” he said.
Turning Data Into Smarter Treatment Choices
The new calculator addresses this complexity by analyzing average treatment effects across hundreds of studies. It also classifies therapies as low, moderate, or high intensity, depending on how much they reduce blood pressure (BP) — an approach already used in cholesterol management.
A single blood pressure medication, which is still the standard way most treatments begin, typically lowers systolic BP by only 8-9 mmHg. Many patients, however, need drops of 15-30 mmHg to reach healthy targets.

Dr. Wang explained that although doctors have traditionally adjusted therapy by monitoring each patient’s blood pressure readings, those measurements are too variable to depend on alone.
The Problem With “Noisy” Blood Pressure Readings
“Blood pressure changes from moment to moment, day to day and by season — these random fluctuations can easily be as big or larger than the changes brought about by treatment,” he said.
“Also, measurement practices are often not perfect, bringing in an additional source of uncertainty — this means it’s very hard to reliably assess how well a medicine is working just by taking repeated measurements.”
Anthony Rodgers, Senior Professorial Fellow at The George Institute for Global Health, noted that while high blood pressure is the most common reason people visit their doctor, there has never been a single, comprehensive source showing how effective different drugs are, particularly when combined or used at different doses.
A New Approach to Managing Hypertension
“Using the calculator challenges the traditional ‘start low, go slow, measure and judge’ approach to treatment, which comes with the high probability of being misled by BP readings, inertia setting in or the burden on patients being too much,” he said.

“With this new method you specify how much you need to lower blood pressure, choose an ideal treatment plan to achieve that based on the evidence, and get the patient started on that ideally sooner rather than later.”
The next step will be to test this approach in a clinical trial, where treatments are prescribed according to how much a patient needs to lower their blood pressure, using the calculator as a guide.
A Global Health Challenge
High blood pressure remains one of the world’s most serious health threats, affecting an estimated 1.3 billion people and contributing to about ten million deaths every year.1
Often referred to as a “silent killer” because it produces no obvious symptoms, hypertension can go unnoticed until it leads to heart attack, stroke, or kidney disease. Fewer than one in five people with the condition have it adequately controlled.2
“Given the enormous scale of this challenge, even modest improvements will have a large public health impact — increasing the percentage of people whose hypertension is under control globally to just 50% could save many millions of lives,” Professor Rodgers said.
The Blood Pressure Treatment Efficacy Calculator is freely available at www.bpmodel.org.
Notes Global report on hypertension: the race against a silent killer. Geneva: World Health Organization; 2023. Licence: CC BY-NC-SA 3.0 IGO World Heart Federation. Hypertension. https://world-heart-federation.org/what-we-do/hypertension/