The Spirit of Giving Shines at PinkDrive’s Christmas in July Fundraiser

Koo Govender, Non-Executive Board Member and CEO of Publicis Groupe

The spirit of Christmas was alive and well at PinkDrive’s annual Christmas in July fundraiser dinner, recently held at the Indaba Hotel in Johannesburg. Twinkling fairy lights, festive décor, generous giving and heartfelt stories created an atmosphere of hope, reminding guests that the greatest gift anyone can give is the chance to save a life.

Supported by long-standing corporate partners, the themed ‘Night of Giving Back’ once again united business, cancer survivors and the community behind PinkDrive’s mission to make early cancer detection accessible to more South Africans.

Each year, this non-profit organisation (NPO) makes a measurable difference to thousands of lives.  Relying on donations, corporate sponsorships and community support, it’s dedicated to the early detection of gender-related cancers in underserved communities. PinkDrives mobile units travel across the country, offering screenings such as mammograms, clinical breast examinations, pap smears, and PSA testing directly to people who might otherwise have limited access to healthcare.

The evening struck a thoughtful balance between festive celebration and meaningful reflection, honouring cancer survivors while remembering those who lost their lives to the disease. One of the most moving moments came through a testimonial video featuring women whose lives were saved thanks to PinkDrive’s mobile screening units. Their stories vividly illustrated the impact of accessible healthcare and reinforced the organisation’s commitment to taking cancer screening to communities where it is needed most.

The message was echoed by guest speaker Nicole Fuller, elite athlete and cancer survivor, who shared her personal journey following an early diagnosis that enabled her to avoid chemotherapy and radiation treatment. Inspired by her own experience, Fuller has since become the first South African to receive specialist training in cancer recovery and rehabilitation. Encouraging guests to prioritise regular screenings, she highlighted how early detection, combined with appropriate rehabilitation and physical activity, can significantly improve both recovery and long-term wellbeing.

An address by Koo Govender, Non-Executive Board Member and CEO of Publicis Groupe, spoke to the strength of PinkDrive’s leadership and the collective expertise steering its mission. Sound governance and committed partnerships, she noted, are what allow the NPO to keep expanding its reach and deepening its impact.

Closing the formal programme, PinkDrive founder and CEO Noelene Kotschan took guests back to where it all began: a single mobile screening unit, and a mission to reach those that healthcare so often overlooks. From that modest start, she traced PinkDrive’s growth into a nationally recognised force in cancer awareness and early detection. She closed with heartfelt thanks to all those whose continued support keeps that mission alive.

The fundraiser’s philanthropic spirit continued throughout the evening with raffle draws and a lively auction at the end.  Guests bid enthusiastically for luxury prizes including diamond earrings and dream holiday experiences, helping to raise significant funds for PinkDrive’s awareness, education and mobile screening programmes.

To add to the Christmas spirit, spot prizes and hampers, generously sponsored by PinkDrive’s corporate partners, sent guests home with some festive spoils too. And as part of its ongoing support, Lee-Chem Laboratories, through its Mandy’s brand, ensured every guest received a generously filled Mandy’s goodie bag, adding another thoughtful touch to an evening centred on generosity, hope and community.

For Lee-Chem, that generosity runs deeper than a gesture on the night.

“You can’t put a price on the moment someone gets the all-clear because they were screened in time. That’s what keeps us partnering with PinkDrive year after year, and why we’re proud to stand with so many others who believe in that same mission,” says Bhavna Sanker, Marketing Manager at Lee-Chem Laboratories.

Because while Christmas may only appear on the calendar once a year, the spirit of giving and the opportunity to change someone’s future are always in season.

Closing the Gap Between Suspecting a Heart Attack and Confirming it

A highly sensitive cardiac test brings traditional lab diagnostics to the field, when it’s most needed

Illustration of a portable cardiac troponin I testing system that wirelessly transmits results to a smartphone.Credit: AI-generated image

A person having a heart attack may be only feet from medical care but miles from the laboratory testing needed to confirm it. That gap matters, especially for rural patients, those in nursing homes, ambulances and other places where access to specialised diagnostics is limited.

In a paper published in Biosensors and Bioelectronics, an international team of researchers details a highly sensitive test designed to bring that molecular evidence closer to the patient.

“A heart attack doesn’t wait for laboratory results,” said lead author Sayantan Tripathy, assistant research scientist in Texas A&M University’s Optical and Bio-Sensing Laboratory in the College of Engineering. “By reducing the time needed to detect heart muscle damage, we’re helping clinicians move more quickly from uncertainty to action, not only in hospitals, but also in ambulatory and resource-constrained settings where rapid diagnostic tools are often unavailable.”

Clinicians may suspect a heart attack based on symptoms or an electrocardiogram, but confirming heart muscle damage has occurred often requires testing for cardiac troponin I, a protein released into the bloodstream when the heart is injured. The most sensitive versions of those tests typically rely on centralised laboratory equipment, creating a potentially dangerous delay between suspicion and certainty.

“Our goal is for emergency medical technicians in an ambulance to be able to take someone’s fingertip sample – just a small finger prick – put that sample into a cartridge that contains all of our components, plug this cartridge into our device, and then be able to run the test in five minutes,” said Dr Samuel Mabbott, associate professor of biomedical engineering and study co-author.

Faster heart attack diagnosis

Many of today’s troponin tests depend on expensive laboratory instruments and trained personnel. As a result, obtaining the information needed to confirm a heart attack can take time, especially when advanced laboratory resources are not immediately available.

“Our vision is to bring affordable and sensitive advanced molecular diagnostics closer to where care is delivered,” said Dr Gerard Coté, professor of biomedical engineering and director of Texas A&M’s Center for Remote Health Technologies and Systems. “The less distance between the patient and the information clinicians need, the faster critical decisions can be made.”

To create the test, the researchers designed a specific structured DNA molecule that remains inactive until it encounters cardiac troponin I. Once it detects the biomarker, it triggers a series of molecular reactions that amplify the signal, making it easier to detect even very small amounts of heart damage. The amplified signal is then measured using portable optical sensing technology.

The researchers say the technology requires additional development before it could be used in clinical practice. The original work takes approximately two hours to complete, but the current version of the technology has reduced the testing time to less than 25 minutes, and further work is underway to shorten it to under 15 minutes, improving its user applicability.

Still, the study points toward a future in which life-saving diagnostic information is no longer tied to a centralized laboratory and can instead move closer to the patients who need it most.

Source: Texas A&M University

Common Tumours Secrete a Protein That Promotes Lung Metastasis

Confocal image of a lung from a tumour-bearing mouse before cancer cells arrive. Red fluorescent dextran highlights leakage from blood vessels (cyan), while veins are labelled in green, illustrating how tumours prepare distant organs for future metastasis by increasing vascular permeability. Credit: Dr Shani Dror

A protein secreted by common cancer types makes blood vessels leakier to allow metastatic tumours to form in the lungs, according to a study led by investigators at Weill Cornell Medicine and Memorial Sloan Kettering Cancer Center. The discovery could lead to new ways of monitoring and reducing lung metastasis risk in cancer patients.

The researchers, whose findings appear Aug. 5 in Nature Cancer, sought to explain how some tumours enhance their ability to metastasise to the lungs by secreting tiny capsules and particles that carry proteins, DNA and other molecules. These extracellular vesicles and particles (EVPs) are secreted by virtually all cells as a way of signalling to other cells and helping to shape their environments, and tumours have adapted them for their own purposes. In the study, the researchers identified a protein called integrin alpha-5 as the cargo in tumour-derived EVPs that promotes lung blood vessel leakiness and lung metastasis in several types of cancer.

“These findings help us understand one of the mechanisms underlying lung metastasis, so that we can start to think about ways to detect and block it to improve outcomes for patients,” said study senior author Dr David Lyden, Professor in Pediatric Cardiology and a member of the Gale and Ira Drukier Institute for Children’s Health and the Sandra and Edward Meyer Cancer Center at Weill Cornell Medicine.

The recognition that EVPs secreted by tumour cells represent an important layer of cancer biology has come only in the past two decades. As Lyden’s and other labs have shown, tumours use the molecular cargo of EVPs to create a local “pro-tumour” environment and prepare distant organs for metastasis. Tumour EVPs and the molecules they carry are now viewed as promising targets for cancer therapies and for cancer detection and monitoring technologies called liquid biopsies that rely on analysis of blood samples.

In earlier work, Lyden lab researchers found that some tumours’ EVPs have a potent ability to facilitate lung metastasis by inducing a leakiness in blood vessels that allows circulating tumour cells to enter the lungs. In the new study, they looked for the EVP cargo responsible for this effect.

They confirmed in animal models that for some cancers – melanoma, osteosarcoma, and colorectal, in particular – tumour implantation elsewhere in the body can trigger large increases in lung blood vessel leakiness, doing so via tumour-secreted EVPs. They found that these EVPs have the same effect when injected on their own into healthy, tumour-free mice.

“This effect on lung vessels is surprisingly rapid – we could measure it just an hour or two after injecting the EVPs,” said study first author Dr Shani Dror, a research associate in the Lyden lab.

The researchers expected to find that these EVPs cause vessel leakiness by acting directly on the endothelial cells lining blood vessels. They found instead that the EVPs work indirectly via immune cells called macrophages that reside close to lung blood vessels and exert their effect only when they carry integrin alpha-5. Even a breast tumour model that is not prone to metastasise did so readily when EVPs containing integrin alpha-5 were added. The scientists showed that integrin alpha-5 works on lung macrophages by inducing them to secrete the pro-inflammatory protein IL-6, which then causes nearby endothelial cells to loosen up vessel linings.

To confirm that the results were relevant beyond animal models of cancer, the researchers analysed a large dataset of gene expression in human tumours, finding that high expression of integrin alpha-5 in several tumour types, including colorectal tumours, is associated with poorer overall survival. They also found tumour samples from patients with intermediate to advanced colorectal cancer released EVPs containing integrin alpha-5 and were indeed capable of inducing vessel leakiness.

The results reveal a key metastasis-promoting mechanism in some cancers and have potential clinical implications.

“One possibility is that we could try to detect these integrin alpha-5-containing EVPs during cancer surgery, to assess the risk of metastasis,” said study co-corresponding author Dr Jacqueline Bromberg, a breast oncologist at MSK and an associate professor of medicine at Weill Cornell Medicine. “If we had a good drug for blocking integrin alpha-5, we could give this at the time of surgery to potentially reduce the risk of metastasis.”

Source: Weill Cornell Medicine

Why Doctors and Nurses Keep Leaving

Healthcare leaders say generational differences are making it more difficult to retain doctors and nurses

Source: Pixabay CC0

By Lesley Henton, Texas A&M University Division of Marketing and Communications

Healthcare leaders say retirements, burnout and changing workforce expectations are making it complicated to keep experienced clinicians in place. A new study published in the Joint Commission Journal on Quality and Patient Safety suggests the reasons go beyond staffing shortages. Leaders from four major health systems in one of the United States’ largest metropolitan areas say generational shifts are reshaping who enters healthcare, who stays and why clinicians leave.

“We’ve talked about clinical workforce shortages as a numbers problem involving training and retention,” said study co-author Dr William Sage, founding director of the Texas A&M University Institute for Healthcare Access in Fort Worth. “What these leaders described was something more complicated, as healthcare organisations are struggling to meet growing patient needs while accommodating five distinct generations of clinicians with different needs and perspectives about work, well-being and career longevity.”

Why keeping clinicians is getting harder

Study participants, 17 leaders from four major healthcare systems in the Dallas-Fort Worth metroplex, repeatedly described the departure of clinicians as one of their biggest concerns, whether the higher turnover now common among young physicians or an older physician’s lack of transitional options short of full retirement. Some said replacing a highly experienced physician could require hiring multiple younger clinicians, given the way that the healthcare system measures and rewards productivity.

“When a veteran clinician leaves, healthcare organisations lose more than just a position,” said Keegan Warren, co-author and the institute’s executive director. “They can lose years of institutional knowledge, mentoring relationships and practical experience that are difficult to replace. For physicians in particular, departure carries a high institutional price tag. Treating clinicians as people whose lives and contributions matter is not just the right thing to do; it’s a critical strategy for protecting both continuity of care and the financial health of the system.”

Participants also pointed to burnout and shifting workplace expectations. Younger physicians and nurses are more likely to discuss mental health, work-life balance and scheduling flexibility, and they expect employers to play a major role in addressing those concerns.

Sage said the findings should not be interpreted as a simple clash between generations but as the shifting and mixing of expectations over time, including as the result of discrete events such as the introduction of work hours regulation for medical trainees, the reduction of physician-owned practices in favour of employment by hospitals and other large organisations and the COVID pandemic.

“This isn’t a story about one generation being right and another being wrong,” Sage said. “It’s about how the profession is changing and how healthcare organisations can adapt while continuing to provide excellent patient care.”

Clinicians are people first, with lives, families, identities and limits. They’re not just ‘providers’ or FTEs.

Keegan Warren, Executive Director, Texas A&M University Institute for Healthcare Access

Building the healthcare workforce of the future

The researchers say addressing these challenges will require more than simply hiring more clinicians.

The study identifies several approaches that could help strengthen the healthcare workforce:

  • Create more intentional mentorship programs to transfer knowledge from experienced clinicians to younger colleagues.
  • Reduce early career turnover through retention-focused benefits, continuous career development and workplace flexibility.
  • Include multiple generations in leadership and decision-making, ensuring workplace policies reflect different career stages and perspectives.
  • Give human resources leaders a larger role in workforce planning, retention strategies and succession planning.
  • Develop flexible late-career roles for experienced clinicians, allowing them to continue mentoring and contributing even as they reduce clinical workloads.
  • Improve communication across generations to address workplace tensions before they affect morale, retention or patient care.

A stable, capable clinical workforce is foundational to patient access to care, say the researchers, and if healthcare organizations can better support each generation of clinicians throughout their careers, patients will benefit.

“We’re seeing healthcare organizations recognize that retention can no longer be an afterthought,” Warren said.

“Clinicians are people first, with lives, families, identities and limits. They’re not just ‘providers’ or FTEs. When leaders design roles and cultures that honour that humanity, they strengthen commitment, stabilise teams and build a more resilient healthcare system.”

Source: Texas A&M University

Unsafe Food Continues to Be a Global Health Hazard

Escherichia coli. Photo by CDC on Unsplash

If it isn’t safe, it isn’t food – that message sits at the heart of a major new global effort by the World Health Organization (WHO).

University of Waterloo public health researcher Dr. Shannon Majowicz contributed research to the new WHO estimates, which cover the global burden of foodborne disease between 2000 and 2021. 

The estimates, which were released in mid-June alongside peer‑reviewed publications and webinars presenting key findings, represent the most comprehensive updates to date, bringing together global data on the illnesses, deaths and long-term health impacts such as paralysis, cancer and kidney disease associated with unsafe food. 

Foodborne diseases, which are largely preventable, remain a significant public health concern around the world, affecting hundreds of millions of people each year.

By standardising methods and bringing together data from across countries and regions, the new WHO estimates aim to provide governments, public health agencies and researchers with a clearer picture of where risks lie and how they can be reduced.

Waterloo expertise contributing to global effort 

Majowicz and collaborators updated 22 of the 42 WHO estimates, focusing on the global, regional and national burden of both diarrheal and invasive enteric pathogens, which contribute to serious illness, long-term complications such as kidney disease, paralysis, septicaemia, central nervous system infection, as well as death.

“Our aim was to better understand the burden of foodborne illness,” Majowicz says. “How many people are affected? How many develop severe consequences? How many die?”

This research highlights an important reality: Despite general declines over time, diarrhoeal and invasive enteric pathogens transmitted by contaminated food continue to be a substantial cause of illness and death globally.

In the study of diarrhoeal pathogens, Majowicz and colleagues found that in 2021, 14 diarrhoeal pathogens caused 666 million illnesses, with 265 000 deaths, due to contaminated food. The African continent bore the highest disease burden. In the invasive pathogen study, the transmission of eight pathogens by food caused 24 million illnesses, with 106 000 deaths, mostly in Africa and southeast Asia.  

Uneven global health challenge

Moreover, the studies, which are published in the Lancet Global Health (one on foodborne diarrhoeal and the other on foodborne non-diarrhoeal enteric disease hazards), reveal that foodborne disease remains an uneven global health challenge, with unsafe food disproportionately affecting children, populations in lower-income regions and communities with limited access to clean water, sanitation and strong food systems.

For example, children under five make up 9% of the population studied but bear 30% of the disease burden.

The updated estimates provide governments with the evidence they need to justify investing in food safety and foodborne disease prevention measures, Majowicz says. 

“By quantifying illness, death and long-term health impacts, these estimates give governments the data they need to invest in food safety systems, strengthen hygiene and infection prevention measures, improve surveillance and data collection and target interventions where they are needed most. 

“Without it, it can be difficult for policymakers to prioritize food safety alongside other urgent health issues.”

Source: University of Waterloo

Fructose Identified as a Surprise Driver of Metastasis

Photo by Sharon Mccutcheon on Unsplash

A new study from The Wistar Institute has uncovered an unexpected link between fructose and the spread of an aggressive form of ovarian cancer. Published in Nature Aging, the study found that cancer cells not killed by chemotherapy send signals to neighbouring tumour cells, driving metastasis. The researchers identified fructose as a key messenger in this process, revealing a previously unrecognised way that treatment-surviving cancer cells may promote metastasis.

“Some cancer cells that survive chemotherapy aren’t dividing anymore, but they’re still biologically active,” said Aidan Cole, PhD, a postdoctoral fellow in the lab of Katherine Aird, PhD, at The Wistar Institute and first author on the study. “Instead, they continue to release molecules that send signals to nearby cells. Our study is among the first to show that a nutrient – in this case, fructose – can act as one of those signals.”

Ovarian cancer is treated almost universally with platinum-based chemotherapy, and many patients respond well at first. However, the disease recurs in most patients and almost always spreads through the abdominal cavity. That spread, called metastasis, accounts for roughly 90% of deaths from the disease.

Prior research has suggested that cancer cells not killed by chemotherapy play a role in recurrence in part through the ability of these cells to release a complex mix of signalling molecules. Cole and his colleagues began their research by designing a unique experiment: they collected the molecules released by chemotherapy-surviving cells and found these factors alone could significantly increase the spread of cancer cells.

“As far as we know, this is the first time anyone has shown, in a preclinical model rather than just a dish, that it’s the molecules these cells release – not the cells themselves – that drive the cancer’s spread,” said Cole.

That finding sent the team looking for what was being released that caused the cancer cells to spread. Fructose, it turned out, was being made by the surviving cells and sent as the signal for increased spread. Even more interesting, they found that without chemotherapy treatment, consuming the high levels of fructose found in sugary drinks can also signal cancer to spread. The fructose finding is especially compelling because it raises the possibility that simple dietary changes could help shape how cancer progresses. This is particularly important given the prevalence of fructose consumption in the United States, with high fructose corn syrup accounting for ~8-20% of the daily caloric intake in some individuals. Unlike many cancer risk factors outside of patient control, fructose consumption can be modified by dietary choices. While the effectiveness of limiting fructose intake hasn’t yet been tested directly in patients, the study raises the possibility that nutrition could influence cancer progression in previously unrecognised ways.

The researchers next aimed to understand why fructose increases cancer cell spread. Through a variety of large-scale analytical techniques, including the use of a CRISPR screen, they discovered that fructose suppresses cholesterol within the neighbouring cells. Cholesterol is important for cells to stick to each other like a biological glue, so decreased cholesterol allows cells to more easily escape and spread.

The finding that fructose lowers cholesterol production has important clinical implications. Statins, which are taken by 39 million people in the United States, lower cholesterol production. The team found that statins alone decreased the glue between cells to promote escape. The research team is now examining whether these medications could be interfering with the effects of chemotherapy – though they stress this isn’t a reason for patients to stop taking them.

“We haven’t tested this effect in patients yet, but it raises questions about combining cholesterol-lowering drugs with chemotherapy, especially since ovarian cancer is most common in postmenopausal women who are often already on statins,” said Katherine Aird, PhD, professor and co-leader of the Molecular and Cellular Oncogenesis Program in the Ellen and Ronald Caplan Cancer Center at The Wistar Institute, and senior author of the study.

The researchers are also looking into how this mechanism might extend beyond ovarian cancer.

“We think other cancers that spread within the torso – pancreatic, colon, liver – could behave similarly. We can’t call it universal yet, but we think the effects are not just limited to ovarian cancer,” said Aird.

She and Cole have already started designing follow-up experiments to test the reproducibility of their findings in a variety of other cancer types.

Source: The Wistar Institute

Researchers Find Immune Pathway that Keeps Candida in Check

IL-1 pathway prevents a normally harmless fungus developing into a fatal infection

Bacterial-Fungal Clusters in Saliva. An interkingdom assemblage formed by fungi (Candida albicans in blue), bacteria (Streptococcus mutans in green), and bacteria-derived extracellular polymers (α-glucans in red) in human saliva. Credit: Zhi Ren, University of Pennsylvania. NIH support from: National Institute of Dental and Craniofacial Research (NIDCR)

A study from King’s College London provides the first potential clue as to why only certain patients with weakened immune systems, including those undergoing chemotherapy or living with HIV, are at risk of life-threatening Candida albicans infections. Candida albicans is a fungus that normally lives harmlessly in areas such as the mouth and gut but can sometimes spread through the body and cause fatal disease. If the results, published in Nature Microbiology, are confirmed in humans, the results could provide a test to understand who is at risk of developing fatal fungal infections and represent a potential therapeutic target to reduce the risk of developing the disease.

Fungal infections kill more than 2.5 million people each year, with Candida albicans alone killing almost a million. However, until now we knew little about why fungi escape their natural location in mouths and gut and cause life-threatening disease in around 10% of patients who have a weakened immune system.

The scientists focused on a signal produced by the immune system to trigger symptoms to fight off infection, IL-1. Mice which were genetically modified not to produce IL-1 experienced severe disease when exposed to Candida albicans. The findings suggest that the IL-1 immune pathway is critical in preventing Candida albicans from spreading around the body and causing life-threatening disease.

They investigated this further by injecting IL-1-deficient mice with a drug that removes neutrophils, a type of white blood cell that is among the first to respond to infections and help fight threats such as bacteria and fungi. This allowed the researchers to mimic the weakened immune system seen in some immunocompromised patients. By then introducing Candida albicans to the mouths of those mice, they for the first time observed the fungus spread throughout the body and cause fatal disease, confirming that IL-1 is critical in preventing disease spreading.

While the study focused specifically on Candida albicans, the researchers say the IL-1 immune pathway may be a broader defence mechanism that helps keep fungi normally found in healthy microbiomes from spreading and causing fatal disease, and further research is needed to confirm whether this applies to other fungal species.

Understanding what causes fungi that are naturally present in our microbiomes, such as Candida albicans, to cause life-threatening disease could help spot at-risk patients earlier. The researchers suggest that, if confirmed in humans, the findings could lead to a test that identifies which immunocompromised patients have low levels of IL-1 and so are at risk of Candida albicans escaping their microbiomes and causing disease before it happens.

While drugs such as antibiotics are currently used to treat life-threatening fungal diseases, more targeted therapies are needed that tackle the root cause of infection. The researchers suggest future clinical studies in humans could test whether drugs targeting IL-1 could work as a personalised therapy for preventing life-threatening Candida albicans infection.

Source: King’s College London

Earlier Discharge for Children with Severe Pneumonia After Switching to Oral Antibiotics

Children hospitalised with severe pneumonia can safely switch from injectable to oral antibiotics once they begin to recover, allowing many to return home sooner and complete treatment outside hospital, according to a major clinical trial involving 13 hospitals in Southern Africa.

The new results were published in The Lancet. The trial involved partners across Europe and Africa and was led with researchers at City St George’s, University of London.

Pneumonia remains one of the leading infectious killers of children worldwide, particularly in low- and middle-income countries. Current World Health Organization (WHO) guidelines recommend five days of injectable antibiotics for children hospitalised with severe community-acquired pneumonia, often requiring them to stay in hospital even after they have already substantially improved.

Longer hospital stays are more expensive, placing a higher burden on already pressurised healthcare systems and facilities, whilst increasing the risk of hospital-acquired antibiotic-resistant infections and impacting the wellbeing of the children and their families.

The PediCAP trial is one of the largest studies to assess antibiotic treatment for severe childhood pneumonia in Africa. The study enrolled 1101 children aged two months to six years with community-acquired pneumonia that developed outside hospital but was severe enough to require hospital treatment. Thirteen hospitals across South Africa, Uganda, Zambia, Zimbabwe and Mozambique contributed to the study.

All children in the trial began treatment with a WHO-recommended injectable antibiotic. Some were assigned to switch to either oral amoxicillin or oral amoxicillin-clavulanate when their condition had improved, as confirmed by a healthcare worker. Researchers compared these children to those who received the WHO-recommended injectable treatment for the full five days.

Children who switched to oral antibiotics recovered just as well as those who remained on injectable treatment for five days. Rates of hospital readmission or death within 28 days were similar across all groups – 6% for oral amoxicillin, 7% for oral amoxicillin-clavulanate and 6% for injectable antibiotics – showing that an early switch to oral treatment is a safe and effective strategy.

The standard amoxicillin performed just as well as the broader-spectrum antibiotic amoxicillin-clavulanate, supporting the use of a treatment that is cheaper and widely available.

Researchers also compared how well children recovered with different durations of antibiotic treatment, ranging from four to eight days in total. A total antibiotic course of four to five days was as effective as longer courses of seven or eight days, suggesting many children can be treated successfully with substantially less antibiotic exposure than is often used in practice.

Children who switched to oral antibiotics left hospital around one day earlier compared to those who remained on injectable treatment for the full five days.

Co-lead author Dr Michelle Clements, based at UCL Innovative Clinical Trials Unit, said: “PediCAP is the first large-scale study to use an innovative multi-arm trial design, which we developed here at UCL, to evaluate different antibiotics and treatment durations at the same time. Rather than simply comparing one short course with one longer course, this approach allowed us to establish that the shortest studied treatment strategy was effective and safe, while also helping us to understanding the relationship between treatment length and effect.

“By generating robust evidence more efficiently, this trial design has helped answer questions that we hope will support changes to global treatment guidelines and improve care for millions of children with pneumonia worldwide.”

Co-lead author Professor Julia Bielicki, from City St George’s, University of London, said: “Every year millions of children around the world are admitted to hospital with severe pneumonia. Our study shows that once a child is clinically improving, it is safe to switch from injectable to oral antibiotics, and complete treatment at home.

“This simple change could help children get back to their families sooner, reduce pressure on busy hospitals, lower healthcare costs and avoid sometimes catastrophic financial impacts on families from lost caregiver earnings. Because amoxicillin is affordable and widely available, these findings have the potential to change clinical practice and improve care for children around the world.”

The trial was funded by the European Union’s EDCTP2 programme and sponsored by the Penta Foundation.

Source: University of London

Exercise Helps Hip Arthritis Pain, but Perhaps Less than We Thought

Photo by RDNE Stock project


A new Cochrane review finds that exercise may improve pain and function, but the benefits may fall short of what patients would notice in daily life.

Hip osteoarthritis is a condition affecting millions of people worldwide and a leading cause of chronic pain and disability. Exercise is widely recommended as a first-line treatment for managing hip arthritis pain.

Led by researchers from University of Sydney and University of Melbourne, the findings show exercise produces small improvements in pain and physical function for people with hip osteoarthritis, but those improvements may not be large enough to make a meaningful difference to patients.

The review included 18 clinical trials involving 1368 people. Participants were mostly women (63%) and were aged between 53 and 74 years, meaning findings may not apply to younger people. Exercise programmes in the included studies varied widely, lasting between two and 52 weeks and covering a range of types including strengthening, aerobic, and mind-body approaches.

Compared with no treatment or usual care, exercise probably reduces pain by around 7 points on a 100-point scale. However, experts generally consider an improvement of at least 12 points necessary for patients to notice a meaningful difference in daily life. Physical function showed a similar pattern. The authors note, however, that these thresholds were derived largely from knee and mixed osteoarthritis populations, and may not entirely reflect the hip osteoarthritis experience.

Quality of life, arguably the outcome patients care about most, showed little to no improvement with exercise regardless of the comparison used.
 

“Exercise is recommended as a primary treatment for hip osteoarthritis, and this review doesn’t overturn that, but it does suggest we should be honest with patients that the average benefit may be modest, and that we need better-designed trials to understand who benefits most and from which type of exercise.”

— Michelle Hall, co-lead author from the University of Sydney. 


This update analysed results differently from its 2014 predecessor, which pooled all available data together and found high-quality evidence that exercise slightly reduced pain. The new review separated trials according to what exercise was being compared against.

When exercise was tested against a placebo or sham treatment, the evidence for pain relief weakened considerably. And adding exercise on top of another treatment made little difference either. While no single type of exercise came out on top, the authors caution that the evidence to answer that question properly simply isn’t there yet.

Not a recommendation away from exercise

The review stops short of saying exercise is ineffective or should be abandoned as a recommendation. Exercise carries broad health benefits beyond arthritis, is low-cost, and is unlikely to cause harm. 

Most studies included in this review were small and unblinded, which may have influenced outcomes. Because pain and function were largely self-reported, and participants knew whether they were exercising, exercise may appear more effective than it truly is.

The authors call for larger, better-designed trials to give patients and clinicians a clearer picture of what exercise can realistically achieve for hip osteoarthritis specifically.
 

“There just isn’t a huge body of evidence out there. For some people struggling with hip pain, exercise can really be their only hope, but I also don’t want to give patients false hope. It’s important future research is done with larger, better-quality trials, examining what types of exercise work specifically for different people.” 

— Belinda Lawford, co-lead author from the University of Melbourne. 

Read the review

By Mia Parkinson

Source: Cochrane

Company Successfully Bioprints Kidney and Liver Tissues in Space

Weightlessness of space allows tissues to be bioprinted without collapsing

Bioprinted liver tissue
Bioprinted nerve implant

Auxilium Biotechnologies announced a major milestone in space biomanufacturing with the successful bioprinting of kidney and liver tissues aboard the International Space Station (ISS), marking the first time either tissue type has been manufactured in space. Auxilium’s bioprinted biological tissues and nerve repair implants returned to earth on Mission AXLM-3 that flew on a SpaceX capsule and returned to Earth on June 17th, 2026.

“Successfully bioprinting living liver & kidney tissue aboard the International Space Station marks an important step forward for regenerative medicine.” — Dr. Anthony Atala, MD, Professor & Director of the Wake Forest Institute for Regenerative MedicineShare

During the mission, Auxilium’s AMP-1 orbital bioprinter successfully manufactured kidney, liver, and cartilage tissues while also producing 28 nerve repair implants. The achievement represents the first demonstration of kidney tissue manufacturing in space, the first demonstration of liver tissue manufacturing in space, and the first mission to manufacture three distinct tissue types during a single spaceflight. The production of multiple tissue types and clinically relevant nerve repair implants represents the first demonstration of a scalable, multi-product biomanufacturing platform in space.

Equally important, the mission demonstrated the ability of a single autonomous manufacturing platform to produce both living tissues and implantable medical products during the same flight. The simultaneous production of multiple tissue types alongside 28 nerve repair implants highlights not only the versatility of the platform, but also its scalability and higher-throughput manufacturing in space.

The kidney and liver tissues were manufactured in support of research conducted by the Wake Forest Institute for Regenerative Medicine (WFIRM) using the institute’s cells and tissue designs. Auxilium provided the orbital manufacturing platform that enabled tissue fabrication in microgravity.

“This mission represents a significant milestone for both Auxilium and the future of space biomanufacturing,” said Jacob Koffler, PhD, MBA, CEO of Auxilium. “For the first time, we successfully bioprinted kidney and liver tissues in space, demonstrating that complex biological products can be manufactured in orbit. We also produced cartilage tissue and 28 nerve repair implants during the same mission using the same manufacturing platform. The ability to manufacture multiple tissue types alongside clinically relevant medical products highlights both the versatility and scalability of our technology. These results build on our previous demonstration of large-scale medical device manufacturing in space and represent another step toward establishing practical production capabilities for biomedical products beyond Earth.”

Dr. Anthony Atala, MD, Professor and Director of the Wake Forest Institute for Regenerative Medicine (WFIRM) commented, “Successfully bioprinting living liver and kidney tissue aboard the International Space Station marks an important step forward for regenerative medicine. The uniform cell distribution achieved aboard the space station points to real possibilities for manufacturing medical devices and tissues in space.”

Enabling the Next Generation of Biomedical Research

The successful bioprinting of kidney, liver, and cartilage tissues represents an important step toward enabling advanced biomedical research in space. One particularly promising application is the production of organoids, three-dimensional miniature tissue models that replicate key structural and functional characteristics of human organs. Organoids are increasingly used by researchers and pharmaceutical companies to study disease mechanisms, evaluate drug safety, screen new therapeutics, and predict responses to treatment.

Interest in organoid technologies has accelerated significantly as regulators and researchers seek more human-relevant alternatives to traditional animal testing. The U.S. Food and Drug Administration has identified organoids and other advanced tissue models as important components of its New Approach Methodologies initiative, while the National Institutes of Health has expanded efforts to advance and validate next-generation non-animal research platforms.

Today, organoids used for space-based research are manufactured on Earth and transported to orbit. The ability to manufacture these biological models directly in space could provide researchers with on-demand access to experimental systems while reducing dependence on launch schedules and Earth-based supply chains. As commercial space stations begin supporting larger research programmes, in-space production of organoids will create new opportunities for drug discovery, disease modelling, precision medicine, and human health research in microgravity.

By demonstrating the ability to manufacture multiple tissue types in orbit, Auxilium is helping establish the foundation for future space-based biomedical laboratories capable of producing advanced biological research tools whenever and wherever they are needed.

Source: Businesswire