For the first time in a human trial, SGLT2 inhibitors have been shown to reduce circulating inflammatory cells linked to cardiovascular disease, in addition to their established effects on glycaemia and body weight. The findings were published in Circulation.
“There had been some suggestive studies in animals with these medications indicating they might be modulating the immune system – affecting inflammation – but that hadn’t really been shown in humans,” said Dr Mona Mashayekhi (Division of Diabetes, Endocrinology and Metabolism, Vanderbilt Health). “This study provides the first direct evidence of SGLT2 inhibitors altering human immune cells which may potentially reduce cardiovascular risk.
“This finding is significant because it’s the first time this medication has been shown to have an immune effect at the cellular level with some specificity. If we understand how these medicines are reducing obesity-associated inflammation and heart disease and kidney disease, then we can identify the best patient for this treatment or discover other drug targets in that pathway that could really be beneficial.”
The research team enrolled 16 women with obesity and prediabetes and treated them with empagliflozin. Baseline assessments were performed, followed by three months of treatment. Immune changes were also reviewed in a comparator cohort of women who followed a low-calorie diet for three months. Measurements were taken at two weeks and at three months.
Using genetic sequencing and cellular imaging, investigators found that monocyte–platelet aggregates (MPAs) were significantly decreased. Individuals receiving empagliflozin showed a significant reduction in MPAs within two weeks, with a further decrease by week 12. Only the medication group exhibited reduced MPAs, indicating effects beyond weight loss.
Investigators also documented metabolic reprogramming of circulating monocytes, which shifted from a hyper-inflammatory state toward a more stable phenotype oriented toward normal cellular energy metabolism.
Mashayekhi and colleagues have begun a randomised placebo-controlled trial (planned n = 74) of participants with obesity and metabolic syndrome, currently recruiting at Vanderbilt Health. Immune measures will be assessed over three months as in the pilot; adipose tissue will also be sampled and analysed.
Glucagon-like peptide-1 (GLP-1) receptor agonists are effective treatments for obesity, but discontinuation is common due to cost, insurance coverage limitations, side effects, patient preference, and other factors – commonly leading to rapid weight regain. Results from a pilot randomised trial, which are published in Obesity Science & Practice, suggest that structured support may attenuate early weight gain after GLP-1 cessation.
In the trial, 39 adults with prior GLP-1-induced weight loss were randomised to usual care, a digital wellness application, or medically tailored meals at the time of GLP-1 cessation, continuing for 4 months.
Surveys showed that diet quality, perceived health, adherence, and satisfaction did not differ significantly by group, though some estimates suggested possible trends favouring the wellness application. Relative to the control group, the other groups experienced less weight gain. Over 4 months, participants in the control group gained an estimated 10.75% body weight, compared with 3.60% in the wellness application group and 3.58% in the medically tailored meals group.
“People invest significant time and effort in improving their health and achieving weight loss,” said corresponding author Kelseanna Hollis-Hansen, PhD, MPH, of Tufts University Food is Medicine Institute. “We need evidence-based strategies to support them if and when they discontinue GLP-1 medication, so they can maintain those gains and continue building long-term health, vitality, and well-being.”
In January 2026, Tim Andrews, who had received a genetically edited pig kidney in January 2025, became the recipient of a human kidney. A new Mass General Brigham paper, published in The Lancet, details Andrews’ experience and how xenotransplantation could bridge the gap between end-stage kidney failure and a human transplant, allowing a patient to forgo dialysis in the meantime.
Authors report that Andrews, 66 at the time of xenotransplantation, successfully lived with the genetically edited kidney for 271 days – during which he did not need dialysis – before receiving a human kidney from a donor. His case represents the longest dialysis-free survival following porcine kidney xenotransplantation in a living human and the first transition to human kidney transplantation.
A record-setting bridge transplant
“The organ shortage is the greatest crisis we have right now in transplantation,” said lead author Leonardo Riella, MD, PhD, of the Center for Transplantation Sciences and the Division of Nephrology at Mass General Brigham.
“We know that the best treatment option for patients with end-stage kidney disease who have developed renal failure is transplantation, but we simply don’t have enough human organs to transplant in a timely manner. Our vision is that xenotransplantation could help address this gap – initially as a bridge to get patients off dialysis while they wait for a human donor kidney, and potentially, as we establish long-term safety and durability, as a destination therapy in its own right.”
How the pig kidney performed
The world’s first porcine kidney xenotransplant to a living human recipient occurred in 2024 at Massachusetts General Hospital, with the patient surviving 52 days before death from cardiac causes unrelated to the transplant. No previous studies have documented xenograft survival beyond two months, a successful “bridge” to receipt of a human organ, or the mechanisms leading to late xenograft failure in living recipients.
Andrews received the genetically engineered pig kidney under an FDA Expanded Access Investigational New Drug application. He was then monitored for kidney function, rejection, antibody development and potential pig-to-human infection. The kidney functioned immediately. An early episode of T-cell-mediated rejection resolved with treatment, no pig pathogen transmission was detected, and the patient was able to go without dialysis for 271 days.
After approximately six months, immunosuppression was reduced in the setting of infection. The xenotransplant subsequently developed microvascular injury and inflammation that progressed to organ failure. The patient then received a deceased-donor human kidney, with immediate graft function and no evidence of sensitization during follow-up.
Lessons from late graft failure
The findings illustrate both the promise and areas for improvement for xenotransplants as a bridge for patients awaiting human kidneys. Importantly, the microvascular injury to the porcine kidney has implications for the development of immunosuppressive strategies, donor genetic engineering and monitoring in future clinical transplantation studies.
“Mass General Brigham has a strong history of kidney transplantation, beginning with the first live donor kidney transplant in 1954,” said senior author Tatsuo Kawai, MD, PhD, director of the Legorreta Center for Clinical Transplantation Tolerance at Mass General Brigham. “Our findings continue that history by both furthering what we know about xenotransplants and generating knowledge that could be applied to other organ transplantation work.”
“The patients are the true pioneers here,” added Riella. “By stepping forward and being willing to participate in these early-stage studies, they are advancing the science. Without their trust and courage, we would not be able to do what we do.”
Scanning electron micrograph of a B cell. Credit: NIH
Researchers at Karolinska Institutet have mapped how so-called atypical B cells develop and change function over time. The study, published in The EMBO Journal, shows that the cells do not constitute a uniform group but instead follow several developmental pathways that converge on a common end stage. The findings may help explain why atypical B cells have previously been linked to different roles in the immune system.
B cells are an important part of the immune system and help the body recognise and fight infections. A group of B cells known as atypical B cells has attracted considerable interest among researchers in recent years. They occur in several infections, but also in connection with vaccinations and certain inflammatory diseases. Despite extensive research, it has long remained unclear how these cells arise and what function they serve.
In the new study, the researchers analysed blood samples from people who had experienced malaria as well as from healthy blood donors. By combining several advanced methods, they were able to track the development of individual B cells and examine how their properties changed over time.
Atypical B cells develop in several stages
The results show that atypical B cells are not a distinct cell type but rather exist along a continuum with early, intermediate and late developmental stages. The researchers identified three cell-surface markers, CD11c, CD24 and CD27, which made it possible to follow this progression.
“We show that atypical B cells can be understood as a continuous developmental process rather than as a fixed and clearly defined group of cells,” says Christopher Sundling, researcher at the Department of Medicine, Solna, Karolinska Institutet, and corresponding author of the study.
The study also shows that the function of the cells changes as they develop. The early stages had a greater capacity to develop into antibody-producing cells and to produce cytokines, signalling molecules that help different parts of the immune system communicate with one another.
In the later stages, the cells instead acquired characteristics suggesting that they are better able to capture and present foreign substances to other immune cells. The researchers also found that the late-stage cells had a greater capacity to associate with microbial particles.
May have different origins
Another important observation was that atypical B cells may have several different origins. The researchers found evidence that they arise from different types of memory B cells that follow parallel developmental pathways but eventually reach a similar late stage.
“Our results show that the function of these cells changes gradually during development. This may help explain why previous studies have described atypical B cells in different ways and assigned them different roles in the immune system,” says Alan-Dine Courey-Ghaouzi, doctoral student and first author of the study.
The researchers emphasise that the study was carried out in the context of malaria, but that the findings are likely to reflect general principles of how atypical B cells develop in other infections and inflammatory conditions as well.
A new study published in Gastroenterology finds that gut inflammation can change how gut bacteria break down food, possibly triggering immune reactions to foods that were previously tolerated. The findings may help explain why many people with IBD react adversely to foods such as dairy or gluten, even in remission.
About two-thirds of patients with IBD report food intolerances. Dairy, wheat and fibre are the most frequently blamed triggers, but the mechanisms have remained unclear.
The gut microbiota may hold the answer. Prior research has shown that patients with IBD often have an altered microbiota. This study identifies a novel mechanism by which that alteration drives food reactions.
“The microbiome acts as a metabolic organ, helping us digest food components, including those that can trigger gut reactions,” said Dr Alberto Caminero. “Our study shows that inflammation impairs this microbial digestive capacity, potentially contributing to adverse food reactions and opening new possibilities for microbiome-based therapies to restore this function in patients with IBD.”
Other key authors from McMaster University Medical Centre included Dr Bruna Barbosa and senior clinical collaborators Dr Neeraj Narula and Dr Premysl Bercik.
Using two mouse models of colitis, researchers found that inflammation made animals more prone to developing food sensitivities. After inflammation, exposure to dairy or gluten triggered an allergic-type immune response in the colon; reintroducing those foods later caused heightened gut sensitivity and worse colitis symptoms.
The cause traced back to the microbiota: inflammation depleted the specific bacteria that normally break down these food triggers. That shift alone was enough to increase sensitisation risk – transferring gut bacteria from inflamed mice into germ-free mice made those mice more prone to sensitisation to the same foods, while restoring the missing bacteria reduced these effects.
The pattern held in humans, too. Among patients with IBD, those who self-reported food intolerances were more likely to have both a reduced ability to break down common trigger foods and lower levels of the bacteria responsible for that job.
The researchers note that microbiota disruption is likely just one piece of a larger picture that also includes genetics, infections and stress – all of which need further research.
Together, the findings point to a possible mechanism behind food sensitivities in IBD: inflammation disrupts the gut bacteria that normally process certain foods, and this disruption – not the foods themselves – helps trigger the immune reactions patients experience.
For millions of years, parasitic worms have had to survive inside animals without being destroyed by their hosts’ immune systems. To do that, they have evolved remarkably effective ways of dampening the immune response.
Scientists are now trying to understand those tricks and work out whether they could be turned into medicines for diseases resulting from overactive immune systems.
Parasitic worms, also known as helminths, include roundworms, tapeworms, hookworms and flukes. Many live and feed in the intestines of their hosts, including humans. They still infect up to 1.5 billion people worldwide each year.
Although they can be unpleasant, these parasites deserve some grudging respect. They have evolved ways to survive inside their hosts for years and even decades. For scientists interested in autoimmune, inflammatory and allergic conditions, that’s a remarkable skill.
The human immune system walks a constant tightrope – it must be aggressive enough to fight off viruses, bacteria and parasites, but controlled enough to avoid damaging the body’s own tissues. Sometimes that balance breaks down.
There are three main ways the immune system can turn against its host. In autoimmune diseases, the immune system mistakenly attacks the body’s own cells and tissues. In inflammatory conditions, an excessive or prolonged immune response can damage healthy tissue and cause chronic symptoms. In allergic diseases, the immune system overreacts to otherwise harmless substances, treating them as dangerous threats.
Over time, scientists noticed that rates of these immune conditions were much higher in countries that had largely rid themselves of parasite infections. This led to the old friends hypothesis, which suggested that our co-evolution with the parasites inside us may have benefited our immune systems.
Scientists then wondered whether deliberately infecting patients with live parasites or their eggs could be used as a therapy. By the early 2000s, the idea had moved from an intriguing hypothesis into human clinical trials. One early example involved Trichuris suis, the pig whipworm. Patients with inflammatory bowel diseases were given 2,500 whipworm eggs to swallow, and over time, their disease symptoms improved.
Patients were given pig whipworm to swallow. Pexels/Corinna Widmer
However, deliberately infecting patients with parasites is a difficult idea to get people to accept. For this reason, researchers began to take a closer look at our “old friends” and what tricks they evolved to deceive our immune systems. It turns out that they secrete a whole array of molecules that can convince the immune system to allow them to live and feed inside their hosts. These molecules act on the immune cells to tamp down their activity.
Now, instead of giving patients live parasites, there is the intriguing possibility of using their molecules as drugs to alter or regulate the immune system.
Hundreds of studies have now investigated worm-derived molecules from dozens of parasite species. In research published in Scientific Reports and Molecular Therapy, we gathered this evidence together and showed that parasitic molecules calm the immune system in animal models of asthma, arthritis, rhinitis, colitis, sepsis and diabetes.
Animals with asthma could breathe more easily, those with arthritis had less pain and more mobility, those with sepsis did not die of septic shock, and so on across all the disease models investigated.
Multiple sclerosis shares something important with the other conditions mentioned above – it is an autoimmune disease in which the immune system mistakenly attacks nerve cells, impairing their function. But multiple sclerosis is also unique because it is the only brain disease in which molecules from parasites have been tested as potential treatments.
Could parasite molecules have beneficial effects for other brain conditions where inflammation plays a role? Inflammation is involved in many neurodegenerative diseases, such as Alzheimer’s and Parkinson’s disease, and coincidentally, incidences of these conditions have also risen since we largely banished parasites.
Are we there yet?
There is still a long road between an intriguing molecule and a medicine. A drug that works in a mouse or rat can fail in humans because our biology is more complex. But there are reasons for cautious optimism. Scientists can now isolate the molecules parasites produce, identify the processes they affect in the human body and modify them into potential drugs. AI could accelerate that search by helping scientists sift through vast numbers of molecules and predict which are most likely to work.
The hope is not that parasites themselves will become medicines, but that millions of years of evolution may have already solved some of the biological problems we are still trying to understand – and that new tools might help us borrow some of their answers.
Some of the most valuable medicines have come from unlikely places. It may be that one of nature’s least popular creatures has been carrying important lessons about controlling inflammation all along.
High-dose carbon monoxide exposure, as in acute poisoning, is neurotoxic and can cause delayed parkinsonism. It damages the basal ganglia (especially the globus pallidus) and white-matter tracts through hypoxia, mitochondrial inhibition, and oxidative stress. Cohort studies, such as Lai et al. (2015), report substantially elevated later risk of Parkinson’s disease after CO intoxication (roughly 9- to 15-fold in some analyses).
In contrast, low, chronic CO levels – comparable to those in cigarette smokers – are associated with lower Parkinson’s risk and appear neuroprotective in experimental models. Low-dose CO reduces dopaminergic neuron loss, preserves striatal dopamine, and decreases α-synuclein pathology, in part by activating haeme oxygenase-1 (HO-1) and related stress-response pathways that limit oxidative damage and promote protein clearance (Rose et al., 2024).
The most recent large human evidence comes from Bueno Lopez et al. (JAMA Neurology, 2026). In the China Kadoorie Biobank of more than 512 000 adults followed for about 12 years, regular smoking was linked to lower Parkinson’s risk (adjusted HR 0.70). Among never-smokers, higher exhaled CO showed a broadly dose-dependent inverse association with Parkinson’s risk (strongest effects around 3–11.5 ppm), without elevating risks of smoking-related diseases or other neurodegenerative conditions. These findings support CO as a plausible contributor to the long-observed smoking–Parkinson’s paradox and bolster interest in controlled low-dose CO as a research target, while underscoring that smoking itself remains harmful.
Recent investigations into R182 million in healthcare fund misallocations have called into question not only the security of the Department of Health’s tendering system but also highlighted the potential for waste and abuse under the National Health Insurance (NHI) Act. In late September, News24 broke the story of its investigation into how uncapped NHI funds were drawn from funds earmarked for critical health programmes as well as NHI were allocated to advertising campaigns.
On Friday, Minister of Health, Dr Aaron Motsoaledi, denied diverting these funds and states that the reallocation of funds was all above board, without no patients harmed.
“No money was taken from any so-called critical health project to advertise NHI; it’s the other way around. Money was taken from NHI to help departments communicate; departments that did not have a budget.”
The Department has referred the matter to the SIU, Auditor-General and Public Protector, if necessary. Parliament’s health committee led by Chairperson Faith Muthambi has said that Health Department should use the Government Communication and Information System (GCIS) – but the Minister argued that they are not up to the task.
The committee is nonetheless unrelenting in its criticism, and today [Monday] demanded documents that proved funds were reallocated correctly and that the tenders awarded were above board. Faith Muthambi stressed that health funds must stay in the public health system, saying that Minister Motsoaledi should have ordered a initial internal probe while the external investigations were ongoing.
Echoes of ‘Digital Vibes’
About R146 million of the funds were allotted to KMTV Media on an uncapped “R1 620 per transaction” appointment and ~R35–39 million went to Dots Design Agency. These funds were reportedly drawn from HIV/AIDS, TB, child nutrition and an NHI-related GP-contracting allocation.
Action SA has raised concerns over how such small contracts to snowball to such expenditures without the apparent knowledge of the Minister. They also emphasise that South Africans have the right to know exactly how much has been spent on NHI implementation.
Although the Minister says that no impropriety, this reflects the current situation: no total contract value, vague pricing that later bore little relation to invoices, funds redirected from core programmes, and limited apparent checks until media exposure.
For the NHI, this is a clear warning sign of a problem that has been repeatedly raised by its critics.
NHI’s Vulnerable Single Pot
Under the NHI, all healthcare funds are centralised in a single NHI Fund, pooling tax revenue (including redirection of medical scheme tax credits). This fund would as the sole purchaser of services from both public and private providers. Oversight would sit with an 11-member Board under the Minister. A Chief Executive Officer would oversee the day-to-day function of the NHI Fund and would be accountable to the Board.
All of this remains in abeyance as the NHI Act has not yet been promulgated while numerous Constitutional Court challenges are being heard.
As currently envisioned, the NHI would cost anywhere from the government’s mooted R457 billion to a more realistic (if conservative) figure in the region of R1 trillion. This would pay for, in an estimate from Genesis Analytics, increasing GP numbers by 113%, specialists by 80%, and beds by 113%. To fund this would require combining the total current public and private healthcare expenditure in South Africa and increasing that amount by 77% – and this all done with benchmark private sector efficiency. Only massive tax hikes would be able to cover this amount, which would have serious consequences for the economy.
The question has to be asked – if NHI’s spending oversight is centralised to such a degree, how can such vast public funds be reliably accounted for?
Public–Private Partnerships
Public–private partnerships (PPPs) have been suggested as an alternative model for the delivery of universal healthcare. In these, public funds are allocated via contracts for services or infrastructure. Private parties typically provide capital, management or specialised capacity in return for availability- or performance-based payments.
In KwaZulu-Natal, Inkosi Albert Luthuli Central Hospital was developed under a PPP and has been running since 2002. In the PPP, a private consortium is paid for making facilities and equipment available, with key infrastructure-related operational risks are transferred to the private party. Payments are indexed and subject to contractual penalties.
One example is the Northern Cape radiotherapy collaboration, where NC patients who would normally be transferred a great distance to Bloemfontein for their two to six week treatment are instead treated at Icon Oncology’s clinic in Kimberley. This proven model could be extended to other provinces.
Unlike the NHI, funds are not constrained to a single pot, but governance is key to ensuring that dozens or hundreds of smaller ‘pots’ just get defrauded. Nor they do not automatically deliver healthcare equity. Still, examples such as the Northern Cape radiology show that strong, interdependent relationships can develop with regular management meetings to discuss patient experience, statistics, billing and other operational matters.
But perhaps the more closely the funds are tied to the communities and the services who are investing in delivering healthcare to them, the better it will be accounted for and used.
Study opens a window to a better understanding of cellular rejuvenation processes
Fluorescence microscopy images from the Brüstle Research Group, showing the neural stem cells.
Researchers from the University Hospital of Bonn and the University of Bonn have succeeded in dramatically rejuvenating human cells in vitro. The researchers directly reprogrammed erythroid precursors into neural stem cells, resetting epigenetic clocks.
For example, blood cells from an 80-year-old were transformed into stem cells with a molecular age of less than 20 years. Since this rejuvenation occurred gradually, it is well-suited for detailed investigation of the underlying mechanisms. The results have been published in Aging Cell.
“Using this method, we have directly converted red blood cell precursors into neural stem cells,” explains Prof Oliver Brüstle (Institute of Reconstructive Neurobiology, University Hospital Bonn). In previous studies, the Bonn researchers had already shown that neurons produced in this way form connections with existing neurons after transplantation into the brains of mice.
“In our current study, however, we focused on a different phenomenon: namely, the observation that cells become significantly rejuvenated during reprogramming,” emphasises Brüstle (also TRA Life & Health, University of Bonn). To measure this, they used molecular clocks.
The cells’ epigenetic clocks were significantly reset by the reprogramming. As a result, cells from an 80-year-old subsequently exhibited a molecular age of less than 20 years. “We also know that this epigenetic rejuvenation ensures that the cells actually behave like young cells,” says Brüstle.
It was already known that a rejuvenation effect can occur during cell reprogramming. However, it had previously only been observed when reprogramming took place in two steps: conversion of a blood cell into a pluripotent stem cell, followed by differentiation into a neural stem cell.
Rejuvenation occurs very rapidly with this two-step method. “In contrast, we converted blood cells directly into neural stem cells – that is, without first passing through the pluripotent cell stage,” said Brüstle. “In our approach, rejuvenation occurred gradually and could be tracked for over 100 days.”
This opens up a unique window into a better understanding of cellular rejuvenation processes. “Rejuvenation that extends over such a long period of time is ideal as an experimental model: Since the epigenetic clocks are slowly reset over several weeks, we can use this model to investigate which factors and active substances accelerate or slow down the rejuvenation process.”
This is particularly relevant for neuroscience, says Brüstle: “After all, age is the most important risk factor for neurodegenerative diseases such as Alzheimer’s.”
Research groups from the University Hospital of Bonn, the University of Bonn, and RWTH Aachen University participated in the study. The study was funded by the EU’s Horizon 2020 programme, the German Research Foundation (DFG), and the Federal Ministry of Research, Technology, and Space (BMFRT).
Shared family factors, such as genes and upbringing, are likely to explain a large part of the link between high screen use and mental health problems in young people. This is according to a new study from Karolinska Institutet published in Nature Human Behaviour.
“Our results suggest that the association may in some cases have been overestimated because it has not been possible to fully account for shared family factors,” says Tong Gong, research specialist at the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, and the study’s corresponding author alongside Lu Yi, senior researcher at the same department.
The researchers have followed over 21 000 Swedish twins from the age of nine, through their teenage years and into adulthood. The aim was to investigate how leisure-time screen use is linked to symptoms of depression and anxiety over time. By comparing twins within the same family, where one twin used screens more than the other, they were able to study how the association was influenced by shared genetic and environmental factors.
Clear links during adolescence
The clearest associations between screen use and mental health problems were observed during adolescence and for interactive screen activities such as gaming, chatting and surfing the internet. In contrast, significantly weaker or no links were observed for passive activities such as watching TV or videos.
Fifteen-year-olds who spent more than six hours a day on interactive screen activities had more symptoms of depression or anxiety and were more than twice as likely to be diagnosed with such a condition later in life, compared with their peers who spent no more than two hours a day using screens. However, when the researchers compared twins within the same family, most of these links weakened, particularly among identical twins.
“The correlations did not disappear entirely, but they did become significantly weaker, suggesting that both genes and upbringing play an important role,” says Tong Gong.
The researchers emphasise that the results do not mean that screen time is irrelevant to mental health. Interactive screen activities during adolescence were still linked to an increased risk of mental health problems later in life, although the uncertainty increased when shared family factors were included in the analyses.
Will examine different types of activities
The study is based on self-reported data on screen use and does not capture exactly what the young people were doing on their screens or why they were using them. Furthermore, the data was collected before social media and smartphones became as integral a part of young people’s everyday lives as they are today.
The next step is to examine different types of screen-based activities in greater detail, studying their content, the motivation behind their use, problematic use and the activities that screen time replaces. In this way, the researchers hope to gain a better understanding of how these complex relationships vary across different age groups and between girls and boys.
“Future recommendations should not focus solely on how much time children and young people spend in front of screens,” says Emma Frans, senior research specialist at the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, and co-author of the study. “To be able to give good advice, we also need to understand what they are doing on their screens, why they are doing it, and which individual and family-related factors may affect their well-being.”
The study was conducted by researchers at Karolinska Institutet in collaboration with partners from Sweden, Norway, Denmark, Germany and Australia. It was primarily funded by the Marianne and Marcus Wallenberg Foundation and the Swedish Brain Foundation. One of the co-authors, Henrik Larsson, has received research grants, honoraria, and consultancy fees from pharmaceutical companies outside the scope of this study. The other researchers declare no conflicts of interest.
