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Hong Kong residents aged 18 to 49 who have chronic illnesses can receive a subsidised flu jab later this year under health authorities’ plan to expand the city’s vaccination programme, the Post has learned.

The new move would help to identify the city’s hidden population with chronic illnesses and provide them with stronger community healthcare support services, according to a government source on Friday.

“Apart from encouraging more people to get vaccinated against the flu, the expansion will also help authorities to identify more residents with chronic illnesses when they make declarations [of their condition], so that they can be better supported with electronic health information and district health centres,” the source said.

Details of the plan are expected to be announced later.

Currently, the government provides free or subsidised seasonal influenza vaccination to residents aged 6 months to 18 years, and those aged 50 or older. Those aged 18 to 49 are only eligible if they are disabled or if they are social security recipients with chronic illnesses.

High-risk groups, such as residents of care homes, healthcare workers and those who work in the poultry and animal slaughter industries, are also eligible.

Over the past two centuries, vaccines have been critical for preventing infectious diseases. The World Health Organization estimates that vaccination prevents between 3 million and 5 million deaths annually from diseases like diphtheria, tetanus, influenza, measles and, more recently, COVID-19.

While there has long been broad scientific consensus that vaccines prevent or mitigate the spread of infections, there is new research suggesting that the therapeutic impact might go beyond the benefit of preventing infectious diseases.

An April 2025 study published in the prominent journal Nature found tantalizing evidence that the herpes zoster – or shingles – vaccine could lower the risk of dementia in the general population by as much as 20%.

Related: Huge Study Reveals 2 Vaccines That Appear to Reduce Dementia Risk

We are a team of physician scientists with expertise in the clinical and basic science of neurodegenerative disorders and dementia.

We believe that this study potentially opens the door to other breakthroughs in understanding and treating dementia and other degenerative disorders of the brain.

A role for vaccines in reducing dementia risk?

One of the major challenges researchers face when trying to study the effects of vaccines is finding an unvaccinated “control group” for comparison – a group that is similar to the vaccine group in all respects, save for the fact that they haven’t received the active vaccine.

That’s because it’s unethical to assign some patients to the control group and deprive them of vaccine protection against a disease such as shingles.

The Nature study took advantage of a policy change in Wales that went into effect in 2013, stating that people born on or after September 2, 1933, were eligible for the herpes zoster vaccination for at least a year, while those born before that cutoff date were not.

The vaccine was administered to prevent shingles, a painful condition caused by the same virus that causes chickenpox, which can lie dormant in the body and be reactivated later in life.

The researchers used the policy change as a natural laboratory of sorts to study the effect of shingles vaccination on long-term health outcomes. In a statistically sophisticated analysis of health records, the team found that the vaccine reduced the probability of getting dementia by one-fifth over a seven-year period.

This means that people who received the shingles vaccine were less likely to develop clinical dementia over the seven-year follow-up period, and women benefited more than men.

The study design allowed researchers to compare two groups without actively depriving any one group of access to vaccination. The two groups were also of comparable age and had similar medical comorbidities – meaning similar rates of other medical conditions such as diabetes or high blood pressure.

Results from this and other related studies raise the possibility that vaccines may have a broader role in experimental therapeutics outside the realm of infectious diseases.

These studies also raise provocative questions about how vaccines work and how our immune system can potentially prevent dementia.

How vaccines might be protective

One scientific explanation for the reduction of dementia by the herpes zoster vaccine could be the direct protection against the shingles virus, which may play a role in exacerbating dementia.

However, there is also the possibility that the vaccine may have conferred protection by activating the immune system and providing “trained immunity,” in which the immune system is strengthened by repeated exposure to vaccines or viruses.

The study did not differentiate between different types of dementia, such as dementia due to Alzheimer’s disease or dementia due to stroke. Additionally, researchers cannot draw any definitive conclusions about possible mechanisms for how the vaccines could be protective from an analysis of health records alone.

The next step would be a prospective, randomized, double-blind, placebo-controlled study – the “gold standard” for clinical trials in medicine – to directly examine how the herpes zoster vaccine compares with a placebo in their ability to reduce the risk of dementia over time.

Such studies are necessary before any vaccines, as well as other potential therapies, can be recommended for routine clinical use in the prevention of dementia.

The challenges of untangling dementia

Dementia is a major noncommunicable disease that is a leading cause of death around the world.

A January 2025 study provided updated figures on lifetime dementia risk across different subsets of the US population. The researchers estimate that the lifetime risk of dementia after age 55 is 42% – more than double earlier estimates.

The dementia risk was 4% by age 75, and 20% by age 85, with the majority of risk occurring after 85. The researchers projected that the number of new cases of dementia in the US would double over the next four decades from approximately 514,000 cases in 2020 to 1 million in 2060.

Once considered a disease largely confined to the developed world, the deleterious effects of dementia are now apparent throughout the globe, as life expectancy increases in many formerly developing countries.

While there are different forms of dementia with varying clinical manifestations and underlying neurobiology, Alzheimer’s disease is the most common.

Prospective studies that specifically test how giving a vaccine changes the risk for future dementia may benefit from studying patient populations with specific types of dementia because each version of dementia might require distinct treatments.

Unfortunately, for the past two to three decades, the amyloid hypothesis of Alzheimer’s disease – which posits that accumulation of a protein called amyloid in the brain contributes to the disorder – dominated the scientific conversation. As a result, most of the efforts in the experimental therapeutics of Alzheimer’s disease have focused on drugs that lower the levels of amyloid in the brain.

However, results to date have been modest and disappointing. The two recently approved amyloid-lowering therapies have only a minimal impact on slowing the decline, are expensive and have potentially serious side effects. And no drug currently approved by the Food and Drug Administration for clinical use reverses the cognitive decline.

Studies based on health records suggest that past exposure to viruses increase the risk of dementia, while routine vaccines, including those against tetanus, diphtheria, pertussis, pneumonia, shingles and others, reduce the risk.

Innovation and an open mind

There is sometimes a tendency among scientists to cling to older, familiar models of disease and a reluctance to move in more unconventional directions.

Yet the process of doing science has a way of teaching researchers like us humility, opening our minds to new information, learning from our mistakes and going where that data takes us in our quest for effective, life-saving therapies.

Vaccines may be one of those paths less traveled. It is an exciting possibility that may open the door to other breakthroughs in understanding and treating degenerative disorders of the brain.

Anand Kumar, Professor and Department Head of Psychiatry, University of Illinois Chicago and Jalees Rehman, Department Chair and Professor of Biochemistry and Molecular Genetics, University of Illinois Chicago

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Early withdrawal of a treatment for patients with a rare kidney disease is possible without relapse, safer for patients and saves the NHS millions of pounds, new research has revealed.

Atypical Haemolytic Uraemic Syndrome (aHUS) is a life-threatening condition caused by an uncommon defect in the immune system which, in the past, led to kidney failure.

Newcastle University worked with Newcastle Hospitals to carry out clinical trials into the pioneering drug, eculizumab, which led to the NHS approving the treatment from 2015, positively transforming the outlook for patients with the disease.

Now a new study by Newcastle University, UK, funded by the National Institute for Health and Care Research (NIHR) and published today in The Lancet Regional Health Europe, found most patients can stop eculizumab after six months and their disease will not relapse.

Careful monitoring by medical experts allows the drug to be stopped, with the potential to restart the treatment if the disease returns.

The withdrawal of eculizumab is not only of huge benefit to patients’ health and wellbeing but also represents considerable savings to the NHS of £4.2 million per patient over their lifetime.

‘Free from treatment burden’

Neil Sheerin, Professor of Nephrology at Newcastle University and Consultant Nephrologist at The Newcastle Upon Tyne Hospitals NHS Foundation Trust, led the study.

Our findings are exciting as they have the potential to significantly change the way we manage aHUS and this may be life-changing for some patients.

Initially, when a patient started treatment for aHUS they faced a lifetime of eculizumab and the dangers associated with it.

Now we have shown that many people can stop the treatment, freeing them from the burden of regular intravenous injections and removing risk of serious infection associated with the drug.

In addition, significant efficiency savings for the NHS of £110.4 million over five years could be realized in this patient population through more targeted use of this high-cost treatment.”

Neil Sheerin, Professor of Nephrology at Newcastle University

When first approved by the National Institute for Health and Care Excellence, it was recommended that patients stay on eculizumab for the rest of their lives unless there was a medical reason to stop.

However, with the treatment, patients have a 500 to 1,000-fold increased risk of meningococcal sepsis and this is immediately eliminated with its withdrawal.

Professor Sheerin added: “What we now have is data to show the withdrawal of eculizumab is safe and effective after an initial six months – this is a huge step forwards in our understanding of the treatment.”

Findings of study

The study was set up to ensure patient safety and 28 participants, aged 2 to 59 from England and Scotland, who had been on eculizumab for at least six months, took part in the trial.

All patients had their treatment withdrawn. Only four participants’ kidney disease returned and the remaining 24 have remained aHus free to date.

Professor Anthony Gordon, Programme Director for the NIHR Health Technology Assessment (HTA) Programme, which funded the trial, said: “Two key priorities for the NIHR are finding the most safe and effective treatments to help people live better, healthier lives for longer, and identify how care can be delivered in the most cost-effective way. 

“The results from this trial show why embedding clinical research within the NHS is so important. Not only do they highlight that eculizumab can be safely withdrawn over time for the majority of aHUS patients, reducing the risk of adverse effects, they also show that potential savings can be made, making the NHS more efficient.”

Experts at the National Renal Complement Therapeutics Centre, a collaboration between Newcastle University and Newcastle Hospitals, will continue to monitor patients closely and adapt treatment pathways according to the evidence they generate. 

Professor Sheerin said: “This will allow us to answer important questions, such as can people withdraw again from eculizumab once they’ve relapsed, and can we predict more accurately which people will have a relapse following treatment withdrawal?”

Patient case study

Louise Percival knows first-hand the benefits of being taken off eculizumab.

The 35-year-old was diagnosed with aHus in 2017 and was on the drug until she had it withdrawn as part of the Newcastle University study.

Louise suffered a number of negative side effects from eculizumab, such as regular migraines, hair loss and breathlessness that impacted her daily life.

The pension claims handler, from York, said: “When I was diagnosed with aHUS I felt overwhelmed as it was a huge burden to live with – it was life-changing as it’s something that will never go away.

“I strongly disliked the eculizumab infusions as they had to be given religiously every two weeks, which impacted my holidays and social events.

“I’m a very active person, enjoying hiking and the gym, so the side effects and time needed for the treatment were detrimental to my quality of life.

“Not to mention I have a fear of needles, so having a cannula put in my arm every fortnight was very distressing.”

Louise has successfully stopped eculizumab with no relapses, significantly improving her quality of life.

She said: “All of the side effects disappeared and I feel like myself again.

“Initially, I was told eculizumab would be a lifelong commitment, which felt very daunting. But this amazing research has shown the treatment can successfully be withdrawn and that’s fantastic.”

The emerging role of SETD2 in regulating immune cell function is shedding light on potential therapeutic strategies for a range of immune-related diseases. As a key methyltransferase, SETD2 facilitates the trimethylation of lysine 36 on histone H3 (H3K36me3), a modification crucial for maintaining genomic stability and regulating gene transcription. Recent discoveries indicate that SETD2 not only influences tumorigenesis but also plays a pivotal role in the development, differentiation, and function of immune cells.

SETD2’s involvement in the immune system spans across both innate and adaptive immunity. It has been found to be essential in the self-renewal and differentiation of hematopoietic stem cells (HSCs), maintaining a balance critical for immune homeostasis. The loss of SETD2 in HSCs can lead to genome instability, increased differentiation towards progenitors, and HSC exhaustion. This disruption not only impairs immune function but also poses a risk of malignant transformation.

Within the innate immune response, SETD2 has a significant impact on macrophage polarization. It inhibits the M1 macrophage activation pathway by suppressing hypoxia-inducible factor 1-alpha (HIF-1α), thereby reducing inflammatory responses. Conversely, reduced levels of SETD2 are linked to increased M1 polarization and glycolytic activity, which could exacerbate conditions like acute lung injury and osteomyelitis. Furthermore, SETD2 expression in mast cells has been shown to mitigate systemic mastocytosis, where its loss can lead to advanced forms of the disease.

SETD2 also plays a critical role in the adaptive immune system, particularly within T cell development and function. The absence of SETD2 impairs T cell receptor (TCR) recombination, leading to developmental arrest and T cell lymphopenia. Additionally, SETD2 influences the balance between Treg and Th17 cell differentiation, where it promotes Treg stability while suppressing pro-inflammatory Th17 responses. Such regulatory effects are crucial for controlling autoimmune reactions and maintaining immune tolerance.

In B cell biology, SETD2 is indispensable for immunoglobulin gene rearrangement, crucial for antibody diversity and adaptive immunity. Loss of SETD2 leads to defective V(D)J recombination, hampering B cell development and predisposing cells to lymphomagenesis. Moreover, germinal center B cells with reduced SETD2 function exhibit impaired DNA damage sensing, promoting B-cell lymphoma progression.

As research advances, understanding the mechanistic pathways regulated by SETD2 will unlock new possibilities for therapeutic intervention. Targeting SETD2 could potentially modulate immune cell functions, offering novel treatments for autoimmune diseases, inflammatory conditions, and hematological malignancies.

A six-year-old girl has died of the flu at Northern Beaches hospital after being twice sent home from the Sydney Children’s hospital, and the New South Wales health minister has said her parents “deserve answers”.

The girl presented to the emergency department at the Sydney Children’s hospital in Randwick on Monday and was discharged after a clinical assessment.

A spokesperson for the Sydney Children’s Hospitals Network (SCHN) said she presented again “shortly after” and was diagnosed with influenza.

She was then discharged with at-home guidance, the spokesperson said.

The girl was later admitted to the Northern Beaches hospital where she died on Tuesday, police confirmed.

The SCHN spokesperson said upon learning of the girl’s death, “they expressed their deepest condolences to the family for the loss of their child”.

The hospital network will be conducting an initial review into the patient’s care while at the Randwick hospital, and will work with the Northern Sydney Local Health District as part of the joint independent clinical governance process.

The NSW health minister, Ryan Park, said: “I’m heartbroken to learn of the death of a child following presentation to Sydney Children’s Hospital in Randwick and Northern Beaches Hospital.

“I wish to express my deepest condolences to the family for their devastating loss,” Park said.

“I want to understand how and why this tragedy has occurred and the parents deserve answers,” Park said.

The matter has been referred to the coroner and is also the subject of a joint Serious Adverse Event Review, he said.

Park said he was “mindful how distressing these events are for staff, and I know they’ll be impacted by this tragedy”.

The St Luke’s Grammar School principal, Geoff Lancaster, told the ABC that the young girl was “bright, vivacious, kind and free-spirited”.

Most vaccines are designed to provide immunity against just one pathogen. Vaccines for chicken pox (caused by varicella-zoster virus) were only developed to fight that one disease, for example.

But in the wake of the COVID-19 pandemic, immune system researchers around the world are working to go beyond traditional single-pathogen vaccines.

Our pipeline is challenging that approach.”

Alba Grifoni, Ph.D., Research Assistant Professor at La Jolla Institute for Immunology (LJI)

As they report in Cell, Grifoni and her colleagues have developed a research pipeline to fuel the development of “universal vaccines.” These vaccines would address broad viral families and mutated viral variants. If successful, this approach could lead to vaccines with the power to neutralize emerging SARS-CoV-2 variants and many other viruses with pandemic potential.

The science of universal vaccines

Many viruses belong to large viral families, and they share a family resemblance. The virus that causes COVID-19, called SARS-CoV-2, is a type of coronavirus (CoV is short for coronavirus). This means SARS-CoV-2 is closely related to common cold coronaviruses, as well as MERS coronavirus (MERS-CoV) and SARS coronavirus (SARS-CoV).

All of these coronaviruses share certain “conserved” protein sequences that have stayed the same as the viruses have evolved. These closely related viruses share many of the same features and are recognized by some of the same T cells. T cells are white blood cells that can recognize and kill virus-infected cells to stop an infection from spreading.

In previous studies, LJI researchers discovered that some cross-reactive T cells can detect these conserved sites, called epitopes, to target both SARS-CoV-2 and common cold coronaviruses.

Grifoni’s laboratory is working to map out these conserved epitope regions. This work is critical for developing a universal coronavirus vaccine. Once the scientists know where T cells should strike, they can develop vaccines that deliver effective T cell immunity against many kinds of coronaviruses-including variants that haven’t even emerged yet.

“It is important to induce a neutralizing antibody response,” says Grifoni. “But we’ve shown that T cells are much more stable in the context of viral variants, and that is because T cells look at all the proteins of the virus.”

Using data science to fight COVID-19

Researchers are aware of conserved coronavirus T cell epitopes, including some epitopes on the coronavirus “spike” protein. But it is harder to study which of these epitopes sparks the strongest T cell response, and researchers knew there were other promising epitopes hiding in experimental data.

To find these conserved epitope regions, Grifoni and her team extracted and analyzed data from the Immune Epitope Database (IEDB), a public resource designed and led by LJI scientists. The IEDB provided data on more than 200 coronavirus epitopes uncovered by scientists in labs around the world.

Grifoni worked closely with virologists at the J. Craig Venter Institute (JCVI) to compare the similarities between epitopes from different kinds of coronaviruses. The researchers used a combination of bioinformatic tools, including artificial intelligence (AI) approaches, to look for hidden similarities between the coronaviruses.

Once Grifoni and her colleagues had their results, they compared how T cells recognized different coronavirus epitopes, including epitopes on the viral “spike” protein and those outside the spike protein. Uncovering this T cell activity gives researchers an important guide for how to target coronaviruses via a cross-reactive T cell response.

“The idea is that if a new coronavirus emerges, we might not be able to protect from the infection, but we might be able to protect from hospitalization,” says Grifoni.

Grifoni is thinking about the bigger picture. She says this coronavirus study shows the accuracy and usefulness of a new research pipeline. Researchers could use this same process to pinpoint conserved T cell epitopes across different respiratory viruses (such as paramyxoviruses, including measles and Nipah virus or enteroviruses, including A71 and D68) and even viral species causing hemorrhagic fevers (such as Lassa virus and Junin virus).

“Our laboratory is collaborating with research groups that are interested in many different viral families,” says Grifoni. “We need to fill the knowledge gaps.”

Additional authors of the study, “Highly conserved Betacoronavirus sequences are broadly recognized by human T cells,” include first author Tertuliano Alves Pereira Neto, Christian Zmaseck, Liliana Avalos, John Sidney, Raphael Trevizani, Elizabeth Phillips, Simon Mallal, April Fraizer, Gene S. Tan, Richard H. Scheuermann, and Alessandro Sette.

For patients with amputations affecting the hand, toe transfer surgery provides an alternative to replanting the amputated digits and may lead to greater improvement in hand function and other key outcomes, reports a study in the August issue of Plastic and Reconstructive Surgery^®, the official medical journal of the American Society of Plastic Surgeons (ASPS). The journal is published in the Lippincott portfolio by Wolters Kluwer.

Our study provides the first evidence that toe transfer surgery provides better long-term hand function compared to attempted replantation of the amputated fingers. The findings challenge current approaches to emergency replantation surgery after digital amputations.”

Fu-Chan Wei, MD, of Chang Gung Memorial Hospital, Taipei, Taiwan

Toe transfer versus finger replantation: New data on patient-reported outcomes

Amputations of the fingers and thumb are common injuries, affecting about 45,000 people per year in the United States alone. Digit amputations can leave patients with years of disability, especially if the thumb is lost. Emergency replantation of the amputated digit is the current standard of treatment but is sometimes impossible or unsuccessful.

Toe transfer surgery – using one or more of the patients’ toes to replace the amputated digits – is a potential alternative to replantation. While toe transfer surgery is not a new procedure, few studies have evaluated its impact on hand function and other patient-reported outcomes.

Dr. Wei and coauthor Steven Lo, MD, of Canniesburn Plastic Surgery Unit, Glasgow, Scotland, analyzed long-term outcomes of 126 toe transfer procedures in 75 patients after digital amputation. Hand function and other patient-reported outcomes were compared to those of 96 replantation procedures in 52 patients. All patients were treated at Dr. Wei’s hospital; outcomes were assessed at least five years after surgery.

Data support toe transfer as ‘a viable alternative’ to replantation

On the validated Michigan Hand Questionnaire, hand function was significantly better for patients undergoing toe transfer, compared to replantation. The difference in favor of toe transfer was substantial, with hand function scores about three times higher than the benefit considered clinically important. The more severe the injury, the greater the magnitude of improvement after toe transfer surgery.

Patients in the toe transfer group also had greater improvement in physical health-related quality of life, assessed using the standard SF-36 score. Foot function after toe transfer surgery was comparable to that in the general population.

The researchers performed physical assessments to evaluate the most important factors affecting hand function outcomes. Hand range of motion, tripod pinch (three-finger grip, as in holding a pencil), and moving two-point discrimination (a measure of nerve sensation) were predictors of better hand function after toe transfer. Higher overall physical and mental health scores were also associated with improved hand function.

Previous studies of toe transfer surgery have consistently yielded high surgical success rates. However, these studies have not included validated assessments of hand function. No evidence-based guidelines have been developed to help guide the decision to perform toe transfer versus attempted replantation for patients with amputations of the fingers and/or thumbs.

“These data provide the first evidence for the potential functional superiority of toe transfers over replantation in digital amputation using one of the largest validated outcome datasets of toe transfers to date,” Drs. Wei and Lo write. They believe their findings challenge the assumption that emergency replantation should always be the “gold standard” after digital amputation, and suggest that toe transfer can be considered “a viable alternative” for some patients. Furthermore, this study suggests that integrating toe transfers into national healthcare frameworks has the potential to positively address one of the single largest causes of disability worldwide.