Category: 8. Health

WUHAN, Sept. 5 (Xinhua) — A recent study led by Chinese scientists has identified a key susceptibility gene linked to clubroot disease, often called the “cancer” of cruciferous crops, offering durable resistance resources for cruciferous clubroot disease control and fresh insights into how plants defend against invasive eukaryotic protozoon pathogens.

This study, conducted by a team from the Oil Crops Research Institute of the Chinese Academy of Agricultural Sciences, was published in Nature Genetics on Monday.

Cruciferous crops hold significant economic and nutritional value, providing vegetables, edible oil and protein. However, their production faces a growing threat from clubroot disease, which has spread rapidly across more than 80 countries in recent years, causing global yield losses of 10 to 15 percent annually. In China alone, the disease affects over 20 million mu (about 1.3 million hectares) of farmland each year.

This disease is caused by the protozoon Plasmodiophora brassicae, which exclusively jeopardizes cruciferous species. Traditional breeding methods to control this disease, such as interspecific or intraspecific hybridization, often encounter challenges, including lengthy cycles and rapid loss of resistance.

According to Liu Lijiang, chief scientist of the research team, it took nearly a decade to identify the role of GSL5, a gene that facilitates infection. This gene can easily be hijacked by Plasmodiophora brassicae. This hijacking can result in the reinforcement of immune repression, disabling disease resistance signaling and enabling pathogen proliferation.

After identifying the gene, the researchers performed genome editing to knock out GSL5 in cruciferous plants. The genome-edited plants demonstrated broad-spectrum, high-level resistance to Plasmodiophora brassicae pathotypes with no adverse effects on plant growth or seed yield in the field trials.

This innovation provides a durable, efficient strategy for controlling cruciferous clubroot disease and supports the breeding of high-resistance varieties of cruciferous crops like rapeseed, Chinese cabbage and broccoli, Liu said.  ■

Two molecular targets-human epidermal growth factor 2 (HER2) and cluster of differentiation 24 (CD24)-are highly promising candidates for new nuclear diagnostics and therapeutics for endometrial cancer, according to new research published in The Journal of Nuclear Medicine. PET imaging of these targets could play a significant role in the management of the disease, helping clinicians identify patients who are likely to respond to targeted therapeutics. 

Endometrial cancer is the most common gynecologic malignancy worldwide, and its incidence and mortality rates have increased over the past decade. Although early-stage disease is effectively treated via hysterectomy, a dearth of molecularly targeted therapies means that prognoses are far poorer for those with disseminated or recurrent disease.

“Taken together, these factors clearly indicate that the development of novel approaches to the imaging and therapy of endometrial cancer is an urgent clinical need,” remarked Brian M. Zeglis, PhD, professor of chemistry at Hunter College, City University of New York in New York City. “To address this issue, my colleagues and I explored three biomarkers-HER2, mucin-16 (MUC16), and CD24-as potential radiotheranostic targets for endometrial cancer.” 

In the study, researchers first evaluated the expression of HER2, MUC16, and CD24 antigens in endometrial cancer and healthy uterine and healthy endometrial cell lines as well as in patient-derived endometrial cancer tissues. Next, immunoPET probes targeting each of these antigens-⁸⁹Zr-DFO-trastuzumab (HER2), ⁸⁹Zr-DFO-AR9.6 (MUC16), and ⁸⁹Zr-DFO-ATG-031 (CD24)-were interrogated via PET imaging and biodistribution experiments in cell line and patient-derived murine models of endometrial cancer. 

Researchers found that endometrial cancer cells and tissue samples expressed elevated levels of HER2, MUC16, and CD24 compared with healthy control cells and tissue samples. The three immunoPET probes exhibited significantly different behavior in mice bearing subcutaneous endometrial cancer xenografts: ⁸⁹Zr-DFO-ATG-031 provided the highest tumor uptake and tumor-to-background contrast; ⁸⁹Zr-DFO-trastuzumab produced moderate yet promising results; and ⁸⁹Zr-DFO-AR9.6 yielded substandard images. Subsequent imaging experiments in mice bearing patient-derived xenografts reinforced the potential of the CD24- and HER2-targeted immunoPET probes.

“The clear potential of HER2 and CD24 as molecular targets in endometrial cancer raises the question of how these two targets could be exploited for clinical nuclear medicine,” said Zeglis. “It is our hope that this work leads to the application of new HER2- and CD24-targeted radiotheranostics in endometrial cancer. More broadly, we hope that this investigation spurs increased interest in our field in this understudied disease.”

The FTD research landscape is on the verge of major developments. For the first time, a Phase 3 trial has been completed for a potentially disease-modifying treatment for a type of genetic FTD, with results expected in 2025.

As we wait for these Phase 3 trial results, we are taking time to summarize current updates in trials for a type of genetic FTD, as their progress may have impacts for all people impacted by FTD as well as all FTD researchers, healthcare providers, and investors.

Approximately 40% of FTD cases are currently thought to be familial or have genetic underpinnings. These trials all tackle the progranulin hypothesis – the idea that for people with FTD caused by GRN variants, restoring progranulin levels will reduce FTD pathophysiology and symptoms.

There are other major genes that contribute to FTD, such as C9orf72 and MAPT. While there are trials ongoing or emerging which may enroll people with FTD with C9orf72 variants, we focus here on GRN as the genetic target furthest along in trials. There are also trials on other genes and aberrant proteins that are being tested in people with related diseases such as ALS and Alzheimer’s, which may hold promise for genetic and sporadic forms of FTD. While significant drug development progress is being made for specific types of FTD, there will be learnings and progress that will benefit all.

Below are summaries of the status of six active FTD trials as of the time of publication, in alphabetical order by sponsor.   

Important note: AFTD is an informational resource and does not specifically encourage or discourage patient participation any specific clinical trial. 

Sponsor: Alector (with GSK) 

Study: INFRONT-3 (Phase 3) 

Drug: AL001 (Latozinemab) – anti-sortilin monoclonal antibody; intended to block sortilin-mediated progranulin degradation  

Delivery route: Intravenous  

Update: Phase 3 enrollment is complete and results are expected by the end of the 2025 calendar year. Phase 2 updates were previously provided.  

Clinicaltrials.gov: NCT04374136 

Sponsor: AviadoBio 

Study: ASPIRE-FTD (Phase 1/2) 

Drug: AVB-101 – GRN AAV9 gene therapy; intended to increase progranulin levels by delivering a functional GRN gene into the brain  

Delivery route: Intrathalamic infusion  

Update: Dosing is completed of a second cohort  in Phase1/2 and dosing of a third cohort is intended in Q3 2025, with the expectation that early biomarker data will be shared in 2026.  

Clinicaltrials.gov: NCT06064890  

Sponsor: Denali Therapeutics & Takeda Pharmaceuticals 

Study: Phase 1/2 

Drug: TAK-594/DNL593 – recombinant progranulin combined with protein transport vehicle technology;  intended to increase progranulin levels by delivering the progranulin protein across the blood-brain barrier  

Delivery route: Intravenous 

Update: Phase 1 part A data dosing of health volunteers was previously reported and part B dosing of people with GRN-related FTD is ongoing.  

Clinicaltrials.gov: NCT05262023   

Sponsor: Passage Bio 

Study: upliFT-D (Phase 1/2) 

Drug: PBFT02 – GRN AAV1 gene therapy; intended to increase progranulin levels by delivering a functional GRN gene into the brain  

Delivery route: Injection into the cisterna magna  

Update: Interim data has been announced from Dose 1 in people with GRN variants and further interim data from Dose 2, is expected in 2026. Future cohorts are planned to also include participants with FTD-C9orf72.

Clinicaltrials.gov: NCT04747431 

 Sponsor: Prevail Therapeutics, a wholly owned subsidiary of Eli Lilly  

Study: PROCLAIM (Phase 1/2)  

Drug: PR006 – GRN AAV9 gene therapy; intended to increase progranulin levels by delivering a healthy GRN gene into the brain 

Delivery route: Injection into the cisterna magna 

Update:  Interim results for Phase 1/2 were published in 2024 and recruitment is ongoing. 

Clinicaltrials.gov: NCT04408625 

  Sponsor: Vesper Biotechnology  

Study: SORT-IN-2 (phase 1/2) 

Drug: VES001 – small molecule; intended to cross the blood-brain barrier and inhibit sortilin-mediated progranulin degradation
Delivery route: Oral  

Update: Phase 1 data in healthy volunteers was previously reported and Phase 1b/2a has reached enrollment milestones in asymptomatic patients who are carriers of GRN variants, with results expected in the second half of 2025. 

Clinicaltrials.gov: NCT06705192 

For the most up-to-date information on these trials, consider referring patients and families to enroll in the FTD Disorders Registry, which can keep them informed about new and emerging research opportunities; or referring them to AFTD’s HelpLine (info@theaftd.org, 866-507-7222); or referring them to clinicaltrials.gov. Participation in the Registry can also encourage drug development by documenting the numbers of affected people.AFTD has created resources on FTD Genetics and gene therapy, and is committed to enabling and strengthening efficient and informative FTD clinical trials. Visit our For Researchers page for more information about working with us as a researcher. 

Doctors at UI Health performed the first islet transplant with Lantidra, the only therapy approved by the U.S. Food and Drug Administration to treat brittle type 1 diabetes. A 69-year-old man from Illinois received the therapy on Aug. 26 and subsequently was able to stop taking daily, life-saving insulin injections. Lantidra became available exclusively at UI Health last November.

Pancreatic islet cell therapy is a treatment approved by the FDA only for adults with type 1 diabetes who struggle to control their blood sugar due to frequent episodes of severe low blood sugar and hypoglycemia unawareness, or being unable to detect that blood sugar is dropping. Lantidra is derived from a deceased donor pancreas. To regulate blood glucose, the drug is infused into the patient’s liver where insulin is produced. Lantidra requires a donor match determined by the United Network for Organ Sharing. 

Type 1 diabetes is a chronic autoimmune disease that requires lifelong care. Patients with type 1 diabetes need multiple daily insulin injections or an insulin pump because their own immune system destroys the insulin-producing cells of the pancreas. Even with insulin, they can develop life-threatening complications, including damage to the heart, blood vessels, eyes, nerves and kidneys. The cause of type 1 diabetes is unknown.

This is the first time in the United States that an islet transplant was no longer experimental, rather an FDA-approved medical procedure. I’m proud of the research that was done here at the University of Illinois Chicago to develop Lantidra with our doctors and our faculty.”

Dr. Enrico Benedetti, head of surgery at UI Health

A week after the transplant, the patient, Edward “Ed” Augustin III, of Libertyville, Illinois, was able to stop taking daily, life-saving insulin injections.

“The advantage of islet transplant is that there is no age limit. We would never dream of doing a pancreas transplant on someone Ed’s age, as the risks are too great,” Benedetti said. “With Lantidra, there are no surgical risks, and instead of being in the hospital for up to 12 days following an organ transplant, he was home within 24 hours.”

Augustin called the procedure “life-changing.”

“I can be normal. This is huge. I’m going from shots and reactions to no shots and no reactions. This is just huge for me,” he said. 

Augustin was diagnosed with type 1 diabetes when he was 5 years old, and he regularly experienced severe low blood sugar and hypoglycemia unawareness. In one instance, Augustin recalled, he accidentally walked into a parked ambulance. When paramedics checked his blood sugar, it was at a dangerously low 10.

“When my blood sugar drops, it’s like I’m inebriated. I don’t remember anything,” Augustin added.

This is the third time Augustin has received an islet cell transplant. His first two procedures, in 2011, allowed him to live without insulin injections for 12 years. He relapsed in 2023 and once again required insulin injections daily to manage his diabetes.

Dr. Lorenzo Gallon, medical director of UI Health’s abdominal organ transplant program and director of transplant research and the transplant research laboratory, said the islet transplants have preserved Augustin’s health.

“Pancreatic islet cell therapy not only helps treat hypoglycemic unawareness but may also help prevent kidney damage caused by diabetes if used early, before complications like diabetic nephropathy develop,” he said.

According to the National Institutes of Health, more than 1.4 million people in the United States have type 1 diabetes. Roughly 80,000 people have brittle type 1 diabetes, a more severe form of type 1 diabetes. The disease can lead to blindness, kidney failure, limb amputation, stroke and heart attack.

UI Health partners with individual patients’ health insurance to obtain coverage for Lantidra.

Lantidra was developed through research at the University of Illinois Chicago conducted by Dr. José Oberholzer. The clinical trials that supported Lantidra were conducted at UI Health, UIC’s academic health enterprise. The clinical data was licensed to CellTrans Inc., which Oberholzer founded and serves as the company’s president, to develop the therapy for FDA approval.

Ultra-processed foods don’t just pack on pounds — they change the body in hidden ways.

In a tightly controlled study, young men gained more fat mass on a processed diet even when calorie counts were the same as unprocessed meals. Researchers also found worrying spikes in plastic-derived chemicals, along with drops in testosterone and other key fertility hormones.

Obesity, Diabetes, and Sperm Decline

Over the last 50 years, obesity and type 2 diabetes have climbed dramatically, while sperm quality has steadily declined. One factor that may be fueling these troubling shifts is the growing reliance on ultra-processed foods, which have been tied to numerous health problems. What scientists still debate is whether the harm comes from the industrial ingredients, the processing methods, or simply because these foods make people eat more than they need.

A new study provides fresh insight. Researchers found that people put on more weight when eating an ultra-processed diet compared to a diet of minimally processed foods, even though both contained the exact same number of calories. The human trial also revealed that ultra-processed meals exposed participants to higher levels of pollutants already linked to lower sperm quality. The work was published in the journal Cell Metabolism.

Proving the Hidden Harm

“Our results prove that ultra-processed foods harm our reproductive and metabolic health, even if they’re not eaten in excess. This indicates that it is the processed nature of these foods that makes them harmful,” says Jessica Preston, lead author of the study, who carried out the research during her PhD at the University of Copenhagen’s NNF Center for Basic Metabolic Research (CBMR).

Same Calories, Different Outcomes

To get the best possible data, the scientists compared the health impact of unprocessed and ultra-processed diets on the same person. They recruited 43 men aged 20 to 35, who spent three weeks on each of the two diets, with three months ‘washout’ in between. Half started on the ultra-processed and half started on the unprocessed diet. Half of the men also received a high-calorie diet with an extra 500 daily calories, while half received the normal amount of calories for their size, age and physical activity levels. They were not told which diet they were on. Both the unprocessed and ultra-processed diets had the same amount of calories, protein, carbs and fats.

Men gained around 1 kg more of fat mass while on the ultra-processed diet compared to the unprocessed diet, regardless of whether they were on the normal or excess calorie diet. Several other markers of cardiovascular health were also affected.

Ultra-Processed Foods Polluted With Toxins

The scientists also discovered a worrying increase in the level of the hormone-disrupting phthalate cxMINP, a substance used in plastics, in men on the ultra-processed diet. Men on this diet also saw decreases in their levels of testosterone and follicle-stimulating hormone, which are crucial for sperm production.

“We were shocked by how many body functions were disrupted by ultra-processed foods, even in healthy young men. The long-term implications are alarming and highlight the need to revise nutritional guidelines to better protect against chronic disease,” says the study’s senior author Professor Romain Barrès from the University of Copenhagen’s NNF Center for Basic Metabolic Research, and the Université Côte d’Azur.

Reference: “Effect of ultra-processed food consumption on male reproductive and metabolic health” by Jessica M. Preston, Jo Iversen, Antonia Hufnagel, Line Hjort, Jodie Taylor, Clara Sanchez, Victoria George, Ann N. Hansen, Lars Ängquist, Susan Hermann, Jeffrey M. Craig, Signe Torekov, Christian Lindh, Karin S. Hougaard, Marcelo A. Nóbrega, Stephen J. Simpson and Romain Barrès, 28 August 2025, Cell Metabolism.
DOI: 10.1016/j.cmet.2025.08.004

Never miss a breakthrough: Join the SciTechDaily newsletter.

Specialty

Please chooseI’m not a medical professional.Allergy and ImmunologyAnatomyAnesthesiologyBiostatisticsCardiac/Thoracic/Vascular SurgeryCardiologyCritical CareDentistryDermatologyDiabetes and EndocrinologyEmergency MedicineEpidemiology and Public HealthFamily MedicineForensic MedicineGastroenterologyGeneral PracticeGeneticsGeriatricsHealth PolicyHematologyHIV/AIDSHospital-based MedicineI’m not a medical professional.Infectious DiseaseIntegrative/Complementary MedicineInternal MedicineInternal Medicine-PediatricsMedical Education and SimulationMedical PhysicsMedical StudentNephrologyNeurological SurgeryNeurologyNuclear MedicineNutritionObstetrics and GynecologyOccupational HealthOncologyOphthalmologyOptometryOral MedicineOrthopaedicsOsteopathic MedicineOtolaryngologyPain ManagementPalliative CarePathologyPediatricsPediatric SurgeryPharmacologyPhysical Medicine and RehabilitationPlastic SurgeryPodiatryPreventive MedicinePsychiatryPsychologyPulmonologyRadiation OncologyRadiologyRheumatologySubstance Use and AddictionSurgeryTherapeuticsTraumaUrologyMiscellaneous

The pain of gout has been with us for millennia at least, but scientists have gone back much further in time – more than 20 million years – to bring back a gene that could help treat the condition and others like it.

When there’s too much uric acid in the blood, it forms crystals in the joints and the kidneys – which then leads to gout and other problems, including kidney disease and liver damage. This overload is known as hyperuricemia.

A gene called uricase could help, by producing an enzyme that helps reduce levels of uric acid. Unfortunately, our human ancestors lost that gene millions of years ago. So, biologists Lais Balico and Eric Gaucher from Georgia State University in the US wondered whether it could be restored.

Related: Huge Study Reveals Where Gout Comes From, And It’s Not What We Thought

“Without uricase, humans are left vulnerable,” says Gaucher. “We wanted to see what would happen if we reactivated the broken gene.”

Evolutionary pressures phased out the uricase gene in several different primate lineages some 20 to 29 million years ago. The thinking is that back then, extra uric acid was beneficial for converting fruit sugar into fat, to help survive food shortages.

That meant it was less advantageous to have uricase, because it limited uric acid. But now that long periods without food aren’t as much of a problem, the uric acid is harming rather than helping the body.

Gaucher and Balico used the CRISPR gene-editing technique to reconstruct the ancient version of the uricase gene, based on the working versions still active in other mammals, and computer models of how the gene may have evolved over time.

They then tested their new gene on engineered human liver cells in the lab, which successfully produced uricase. This had the desired effect, reducing levels of uric acid and the fatty deposits caused by fruit sugar. Similarly positive results were seen in more complex 3D liver spheroids.

“By reactivating uricase in human liver cells, we lowered uric acid and stopped the cells from turning excess fructose into triglycerides – the fats that build up in the liver,” says Gaucher.

This still needs to be demonstrated in animals, but the way that the uricase enzyme found its way into tiny cell compartments called peroxisomes in tests is promising, the team says: it means the uricase is finding its way to the right parts of the cell.

The potential benefits of this kind of treatment go well beyond gout. High uric acid levels have also been linked with different types of cardiovascular disease and high blood pressure, as well as kidney stones.

“Hyperuricemia is a dangerous condition,” says Gaucher. “By lowering uric acid, we could potentially prevent multiple diseases at once.”

However, a lot more research is going to be needed to figure out how to get this uricase gene working safely again in humans – if indeed a tweak like this can be made without interfering with other essential biological processes.

It’s thought that around 1 in 5 people in the US have hyperuricemia, and it can be affected by diet – red meat and alcohol don’t help, for example. While treatments are available, they don’t work for everyone, and sometimes come with unwanted side effects.

“Our genome-editing approach could allow patients to live gout-free lives and potentially prevent fatty liver disease,” says Gaucher.

The research has been published in Scientific Reports.

September 5, 2025

HANOI – Dengue fever cases have surged dramatically across Việt Nam this year, with more than 65,000 infections and 11 deaths recorded so far, according to the Ministry of Health. The number of cases is up by nearly 21 per cent compared to last year, signalling a worrying escalation of the mosquito-borne disease nationwide.

August alone saw 21,640 new cases and six deaths, underscoring the urgent challenge facing health authorities. The southern region, especially Hồ Chí Minh City (including former provinces of Bình Dương and Bà Rịa–Vũng Tàu), has been hit hardest.

Vice director of the city Department of Health Dr Huỳnh Minh Chính revealed that more than 26,000 cases have been reported in the region this year — a staggering increase of over 220 per cent compared to the same period last year.

Other localities have also seen rising numbers, heightening concerns about the spread of the epidemic. In response, the Ministry of Health issued a directive in mid-August urging provincial and city authorities to strictly implement the Prime Minister’s Official Dispatch No 116/CD-TTg dated July 20, aimed at bolstering dengue fever prevention and control measures.

Local governments have been tasked with closely monitoring the epidemic, reviewing the situation regularly, and promptly introducing control measures to halt the spread. Health departments are also required to update their dengue prevention plans, enhance coordination across sectors and strengthen surveillance to quickly identify new cases, especially in areas with previous outbreaks or high risk.

Healthcare facilities are being called on to organise effective patient admission and treatment protocols and to train medical staff at grassroots levels in the diagnosis, care and treatment of dengue fever. Monitoring systems are being reinforced to ensure timely responses and resource allocation to combat the disease.

The ministry emphasised that the most effective way to prevent dengue remains controlling the mosquito population. This includes eliminating mosquito larvae by covering all water containers, sleeping under mosquito nets even during the day, wearing long-sleeved clothing to avoid bites and using repellents such as creams, lamps, or electric mosquito rackets.

Prompt medical attention is critical for anyone exhibiting symptoms. The ministry warned against self-treatment at home, which risks missing early warning signs and can result in complications.

Vaccination is emerging as a new tool in the fight against dengue, with the Ministry highlighting its introduction into national vaccination programmes as a positive step towards reducing infections and fatalities. However, vaccines are not a substitute for traditional prevention measures and must be part of a comprehensive strategy.

As Việt Nam confronts this rising health threat, the Government and health authorities continue to call for community cooperation and vigilance to protect lives and curb the spread of dengue fever.