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When we’re taking antibiotics, some of the dose is excreted with urine and feces and ends up in our wastewater. The presence of this low dose of antibiotic creates an opportunity for resistant bacteria to evolve. Scientists studying antibiotic resistant bacteria in wastewater at a treatment plant discovered multi-drug resistant strains of bacteria species which are usually not dangerous to healthy people, but which could transmit genes for antibiotic resistance to much more dangerous bacteria like E. coli. 

The scientists then challenged the bacteria with natural compounds which could potentially be included in wastewater treatment to kill off bacteria and fight antibiotic resistance. The most effective were curcumin, which comes from turmeric, and emodin, from rhubarb. 

“Without improved treatment, wastewater could serve as a breeding ground for ‘superbugs’ that may enter water resources such as rivers, lakes, and reservoirs, posing potential risks to public health,” said Dr. Liyuan ‘Joanna’ Hou of Utah State University, senior author of the article in Frontiers in Microbiology. “Our goal was to isolate and characterize multidrug-resistant bacteria, explore the molecular mechanisms of resistance through whole-genome sequencing, and assess the potential of natural compounds as alternative mitigation strategies.” 

Survival of the resistant 

Antibiotic resistance develops when bacteria evolve to be less vulnerable to antibiotics. This is more likely to happen if bacteria are exposed to a dose of vaccine which is too low to kill them all; the survivors develop resistance. Someone infected with these resistant bacteria may then find that their treatment doesn’t work, potentially making routine surgery or illness much more dangerous. 

Some bacteria are resistant to several antibiotics; these infections are often treated with ‘last resort’ drugs like colistin. However, when Hou and her colleagues tested samples of effluent from a wastewater treatment plant in Logan, Utah, they found some colonies of bacteria that were resistant even to colistin. This underlines the urgency of finding ways of preventing and treating bacterial infection which minimize the use of antibiotics. 

The scientists screened their samples using one antibiotic, sulfamethoxazole, to identify nine different antibiotic-resistant strains. These strains of bacteria were then tested against multiple classes of antibiotic to see how many they resisted. Their genomes were also sequenced, which allowed the scientists to identify not just the bacteria themselves but genes which contribute to their antibiotic resistance. One strain, U2, which had the highest number and variety of antibiotic resistance genes, was resistant to all the antibiotics tested. 

The strains represented species of Microbacterium, Chryseobacterium, Lactococcus lactis, and Psychrobacter, which are rarely dangerous to most people – but that doesn’t mean their presence is nothing to be worried about. 

While not traditionally classified as top-priority clinical pathogens, some are opportunistic pathogens associated with infections such as pneumonia in immunocompromised individuals. These bacteria could also act as environmental reservoirs, transferring resistance genes to other bacteria, including clinically relevant pathogens.” 

Dr. Liyuan ‘Joanna’ Hou of Utah State University

Fighting back 

The scientists challenged colonies of these bacteria with different concentrations of 11 natural compounds: berberine, chlorflavonin, chrysin, curcumin, emodin, hesperidin, naringin, quercetin, resveratrol, rutin, and 2′-hydroxyflavone. They then looked at different measurements of the colonies’ health – cell growth, biofilm formation, and how active the bacteria were. 

“We selected a panel of compounds primarily derived from plants, such as curcumin from turmeric, quercetin from onions and apples, and emodin from rhubarb,” said Hou. “These compounds were chosen based on their reported antimicrobial or anti-biofilm properties in previous studies and their natural abundance, making them promising candidates for exploring new, environmentally friendly approaches to mitigate resistance.” 

They found that emodin and curcumin were best at inhibiting cell growth and biofilm formation, while curcumin and a higher dose of emodin reduced cell activity – although a low dose of emodin increased activity for several strains. However, Gram-negative bacteria like Chryseobacterium were resistant to all the compounds. 

“While natural compounds like curcumin and emodin show promise in inhibiting Gram-positive multidrug-resistant bacteria, further research is needed,” said Hou. “Future work should include testing these compounds in complex wastewater matrices, exploring synergistic effects with existing treatment processes, and assessing long-term impacts on microbial communities and resistance dynamics. Additionally, scaling up from laboratory studies to pilot-scale trials will be critical for evaluating feasibility and environmental safety.” 

UNAIDS report warns HIV progress at risk as U.S. funding cuts take hold

JOHANNESBURG, South Africa — Decades of progress in the fight against HIV/AIDS are in danger of unraveling, the United Nations Aids Agency (UNAIDS) warned Thursday in its annual report, citing sharp funding cuts from major donors.

The report, launched in South Africa by UNAIDS, says those cuts — especially the sudden withdrawal of U.S. funding — are threatening to reverse gains that have saved millions of lives over the past two decades.

“If the world doesn’t plug this hole,” said Winnie Byanyima, executive director of UNAIDS, “we estimate that an additional six million people will be newly infected in the next four years. We could have four million additional AIDS-related deaths.”

The reports warning comes five months after the Trump administration halted most funding for the President’s Emergency Plan for AIDS Relief (PEPFAR) — the largest single contributor to the global HIV/AIDS response. The decision was made with little warning.

“The sudden withdrawal of the single biggest HIV donor is putting this progress at risk,” Byanyima said during a press briefing in Johannesburg.

Since the start of the epidemic, UNAIDS says 26.9 million lives have been saved through treatment efforts — many of them in sub-Saharan Africa, the region most affected by the virus.

Fallout in South Africa and beyond

South Africa, which has the world’s largest population of people living with HIV, has made major strides. Most of those infected now receive life-saving antiretroviral drugs.

But the fallout is already being felt. At the report’s launch, South Africa’s Health Minister Aaron Motsoaledi called the U.S. cuts “a wake-up call” — and warned of the dangers of depending on a single donor.

“This type of relationship where we depend on one country, and when that country is in some type of negative mood, the whole world collapses — yes, it’s scary,” he said.

Scientific setbacks and a call to action

South African researchers have been at the forefront of global HIV breakthroughs as well as COVID-19 studies. But many trials are now being suspended due to lack of funds.

Dr. Helen Rees, head of the Wits Reproductive Health and HIV Institute in Johannesburg, said the implications are global.

“The research being done for HIV and tuberculosis in South Africa has not only had an impact here, but a huge global impact,” she said.

Rees was recently honored by the World Health Organization for her “outstanding contribution to public health,” but her institute is now facing major U.S. funding cuts.

“Not charity” — a shared fight

Trump has said the shift away from U.S. aid reflects a new emphasis on “trade over charity” in Africa. But UNAIDS’ Byanyima says the sudden withdrawal of U.S. support in February has left UNAIDS with nearly 50% less funding — and no time to prepare for the gap.

“This is not charity,” she said. “This is solving a global problem together. As long as it festers in some parts of the world, it will come back to hit everybody else.”

For longtime HIV activist Nombeko Mpongo in Cape Town, the cuts have felt deeply personal.

“I remember for a few days I felt suffocated, I felt like being choked… It was like a volcano came and took everything away. It felt like a death penalty,” she said.

But after the shock, Mpongo says she rallied.

“I realized — no man, nonsense. Let me fight. Let me reach out to the communities,” she said. “We’ve fought this virus before. We’ll do it again, because hope is what is going to carry us through.”

The time it takes to grow new skin for burns victims could be improved thanks to a new method of cell cultivation using algae, developed by University of Queensland researchers.

Dr. Melanie Oey and her team at UQ’s Institute of Molecular Bioscience combined a new type of Queensland algae, Chlorella BDH-1, with mammalian cells to improve the process of growing tissue cells.

Our work shows muscle cells co-cultivated with the algae grow faster, live longer and require fewer expensive additives.

The algae act like tiny life-support systems that can solve multiple problems at once.”

Dr. Melanie Oey, UQ’s Institute of Molecular Bioscience

The research could benefit tissue engineering and regenerative medicine with accelerated growth of 3D tissues and skin grafts.

In cell cultures the researchers reported more than 80 per cent increase in cell growth, up to 3 times the number of usable cells and cell cultures that remained viable for longer.

There was also a 50 per cent reduction in the need to use animal cells.

The method also has the potential to benefit other applications such as growing cultivated meat more affordably.

Australia’s food regulator Food Standards Australia New Zealand recently approved the sale of lab-grown or cell-cultured meat – created by growing or multiplying individual animal cells – but cost remains a barrier.

“The growing population requires more protein, but it’s the most expensive macronutrient, and animal farming is also a climate concern,” Dr Oey said.

“But growing meat in the lab is expensive largely due to the nutrients and oxygen the cells need and the waste they produce.

“Our research could make cultivated meat a sustainable, affordable, ethically acceptable alternative protein source.”

Other applications for the use of Chlorella BDH-1 algae in cell culture include:

• Growing organoids (artificially grown masses of cells that resemble an organ) to use in testing drugs and avoiding the need for animal testing.
• Pharmaceutical manufacturing with companies able to grow and test cells more efficiently, with lower overheads and fewer inputs.

Dr Oey said the Chlorella BDH-1 algae was chosen because it does not consume glucose and doesn’t compete with mammalian cells for food.

It naturally produces oxygen and removes waste, creating a more supportive environment for muscle cells to thrive.

“In the human body blood delivers oxygen and removes waste, but in a lab setting you don’t have that system,” she said.

“By adding algae we’re essentially creating a mini-symbiosis or mutually beneficial interaction where the algae provide oxygen and take away waste, helping the cells grow better.

“It’s a simple idea with broad potential.

“By working with nature – using algae to improve the cellular environment – we’ve created a scalable way to support healthier, longer lasting and more efficient cell cultures.”

The research is published in Biotechnology Journal.

New research reveals that while losing weight can rejuvenate aging fat tissue, stubborn immune cells keep a “memory” of obesity, offering fresh targets for lasting metabolic health.

Study: Selective remodelling of the adipose niche in obesity and weight loss. Image Credit: Andrey_Popov / Shutterstock

In a recent study published in the journal Nature, researchers utilized next-generation assays to investigate the regulatory factors, cell types, and molecular events involved in human adipose tissue (AT) remodeling. Their landmark study provides the most detailed view yet into how fat tissue transforms during obesity and weight loss.

Study findings reveal that obesity induces cellular senescence, inflammation, and structural stress within fat, which are only partially reversed by weight loss. Notably, senescence reversal was selective, occurring in metabolic adipocytes, vascular cells, and precursors where p21-positive senescent cells were nearly eliminated, but largely persistent in immune cells. In combination with the 171,247-cell strong atlas, these findings provide a revolutionary understanding of fat tissue plasticity, representing the first step towards novel therapeutic directions that may finally overcome obesity’s notorious capacity to bounce back.

Background

Obesity is a metabolic condition characterized by excessive systemic fat accumulation, with potentially lethal outcomes. Clinically defined as a body mass index (BMI) > 30 kg/m², obesity has been linked to several chronic diseases, including type 2 diabetes (T2D), cardiovascular diseases (CVDs), and even certain cancers.

Alarmingly, more than 1 billion humans live with obesity, with today’s suboptimal lifestyle expected to exacerbate this already grim situation. While pharmacological, behavioral, and surgical interventions have demonstrated promise in achieving weight loss, these benefits are often temporary.

These facts reveal our surface understanding of the association and correlation between weight loss and improved obesity-associated health outcomes, while emphasizing our lack of knowledge of the mechanistic interplay governing fat (adipose tissue [AT]) remodeling.

About the Study

The present study aims to address this knowledge gap and progress our war on obesity by deciphering the cellular, molecular, and spatial changes that occur in human AT during obesity and after weight loss.

Study samples (subcutaneous abdominal AT) were obtained from morbidly obese patients (BMI > 35 kg/m²; n = 25; age = 20–70 yrs) and healthy controls (BMI < 26 kg/m²) intra-operatively via laparoscopic bariatric surgery. Follow-up samples were collected five months later for comparative assays. All samples were subjected to single-nucleus RNA sequencing (snRNA-seq) using the Illumina NextSeq2000 platform.

In brief, the study profiled ~100,000 nuclei from fresh biopsies and integrated the resultant sequences with 50,000 additional nuclei from the largest human fat tissue atlas to date. To supplement this single-cell data atlas, the 10x Genomics’ Xenium platform was leveraged to conduct spatial transcriptomics on over 25,000 cells from equivalent cohorts, allowing researchers to observe differences in tissue-specific cell states.

Simultaneously, formalin-fixed paraffin-embedded (FFPE) AT samples were subjected to 5 μm sectioning, 4′,6-diamidino-2-phenylindole (DAPI) staining, and in situ hybridization assays, allowing researchers to both carry out nuclear identification and measure gene activity directly within intact tissue architecture.

Finally, the study used pathway enrichment (MSigDB), differential expression, transcription factor inference, and spatial niche modeling assays to elucidate the movement, activity patterns, and remodellings of metabolic, immune, vascular, and progenitor cell populations.

Study Findings

The present study makes five key findings:

1. Weight loss selectively reverses senescence in metabolic, vascular, and precursor cells

   Metabolic adipocytes, precursor cells, and vascular cells of patients with obesity were found to express senescence-associated secretory phenotype (SASP) genes and other markers of cellular senescence. These cells contribute to fibrosis, immune signaling, and local tissue stress.

   Notably, following weight loss (bariatric surgery), the fraction of “stressed” adipocytes (AD3) was observed to decrease dramatically (from 55% to 14%; P < 0.0001), and p21-positive senescent cells were nearly eliminated in these lineages. However, senescence persisted in immune cells (macrophages), suggesting only partial and cell-type-specific rejuvenation of the adipose niche.

2. Immune cells retain inflammatory programming post-weight loss

   While the infiltration of lipid-associated macrophages (LAMs) was observed to decrease following weight loss, these LAMs retained inflammatory signature (TREM1 and TLR2) expression, indicating transcriptional memory that may predispose to metabolic dysfunction and potentially explain obesity’s frequent reappearance.

3. Adipocyte metabolism globally activates during weight loss but fails to restore lean-state flexibility

   Weight loss enhanced substrate cycling (e.g., triglyceride hydrolysis/resynthesis) and branched-chain amino acid breakdown, but metabolic parameters (e.g., insulin sensitivity) remained suboptimal relative to lean baselines.

4. Weight loss reduces structural tissue stress and fibrosis

   Weight loss was observed to substantially downregulate the expression of genes (e.g., LOX, ACTA2, and VGLL3) involved in fibrosis and cytoskeletal tension, resulting in reduced adipocyte stiffness and inflammation.

5. Spatial mapping reveals stress niches adjacent to immune hotspots

   The study identified five functional tissue niches: adipocyte, vascular, stress, arterial, and stem-like zones. Stressed cells formed distinct “stress niches” adjacent to immune-enriched arterial zones, indicating microenvironments of obesity-caused damage with delayed recovery. Several stress-associated factors (THBS1, NAMPT, AREG) were found to be enriched in obesity and reversed by weight loss (P < 0.05), highlighting them as potential therapeutic targets.

a, Graphical representation of the primary study cohort (left; single-nucleus analyses in n = 25 obese (OB) people before and after WL and n = 24 lean (LN) people, with spatial analyses in n = 4 people per group) and AT anatomical location (right). b, Clinical characteristics of the primary cohort (n = 24 LN and 25 paired OB–WL donors). Boxplot, median interquartile range minimum and maximum. BMI, body mass index (kg m^–2); F insulin, fasting insulin (mIU L^–1); HbA1c, haemoglobin A1c (%); HDL, high-density lipoprotein cholesterol (mM); DBP, diastolic blood pressure (mm Hg). c, Uniform manifold approximation and projection (UMAP) of 145,452 human AT cells (n = 74 samples of the primary cohort and n = 13 samples of the Emont published cohort¹¹, single nucleus). ASC, adipocyte stem cells; APC, adipocyte progenitor cells; Mono, monocytes; DCs, dendritic cells; ILCs, innate lymphoid cells. d, Cell-type proportions (for the cell types in c) in the combined cohort, mean per group, and for each sample (single nucleus). e, Correlations between cell types and clinical traits (Pearson, LN and OB samples only, single nucleus). Illustration in a created using BioRender (Scott, W., https://BioRender.com/rtmnzaj; 2025).

Conclusions

This study marks a prominent leap in scientific understanding of adipose tissue biology, highlighting that while weight loss can partially and selectively reverse the cellular damage inflicted by obesity (reducing inflammation, senescence in specific lineages, and tissue stress), some immune and metabolic programs retain obesity-associated signatures, potentially explaining the stubborn tendency for weight to return.

The findings highlight fat as a complex, adaptive organ exhibiting cell-type-specific memory, suggesting that future interventions targeting unresolved senescence (e.g., in macrophages) or niche-specific stress signals (e.g., THBS1/NAMPT) may improve long-term outcomes.

More than 75% of children and teenagers experience depression or anxiety, prompting parents to seek effective ways to support their mental health. New research from the University of South Australia suggests that regular exercise may offer a powerful solution.

The study, described as the largest meta-meta-analysis of its kind, examined 375 clinical trials involving more than 38,000 young people. Researchers found that when children participated in structured exercise programs, their symptoms of depression and anxiety improved significantly.

Different exercises target different conditions

The research revealed that specific types of exercise work better for different mental health conditions. Anxiety symptoms improved most through low-intensity, resistance exercises, such as light weights or gentle circuit activities. Depression symptoms showed the greatest improvement through moderate-intensity, mixed-mode, and resistance training, including circuits that combine aerobic and strength programs.

The study found that programs lasting fewer than three months were particularly effective. The biggest improvements in depression symptoms occurred in programs lasting fewer than 12 weeks, suggesting that benefits can emerge relatively quickly, especially for children aged 12 and over.

Interestingly, researchers found no significant differences among the frequency of exercise sessions per week. Children with depression and ADHD showed the greatest improvements from exercise interventions.

Low-cost alternative to traditional treatments

Lead researcher Dr Ben Singh described the findings as presenting parents with a non-invasive, low-cost solution to combat poor mental health in children.

“Depression and anxiety are among the most prevalent mental health issues affecting children and teenagers worldwide,” Singh said. “Evidence-based treatment guidelines often recommend cognitive behaviour therapy and antidepressants as first-line interventions, yet 40 to 60 percent of children don’t receive treatment or fail to gain sufficient benefits, so we clearly need alternatives.”

Singh emphasised that exercise represents a widely accessible strategy that could make a real difference to children’s mental health. He noted that while people generally understand exercise is good for health and wellbeing, little evidence previously showed how exercise works for kids or which types might be more effective than others.

Exercise as core mental health care

Senior researcher Prof Carol Maher highlighted the importance of incorporating exercise into mental health care for children and teenagers.

“Exercise should be a core part of mental health care for children and teens, whether at school, in the community, or clinical settings,” Maher said. “Short, structured programs that include strength training or a mix of activities seem especially promising, but simply exercising, even for short amounts of time will deliver benefits.”

Maher reassured parents that expensive gym memberships or training programs are not necessary. Play-based activities, games, and sport all represent valuable forms of movement that can support mental wellbeing.

“The key message is simple: get active and keep active,” Maher said. “Even short bursts of movement can make a real difference to a child’s mental health and wellbeing – especially for those who are struggling.”

The research demonstrates that exercise offers an effective, accessible lifestyle intervention that can immediately improve mental health issues in children without first defaulting to medicines.