Category: 8. Health

Millions suffering from myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), a debilitating condition often overlooked due to the lack of diagnostic tools, may be closer to personalized care, according to new research that shows how the disease disrupts interactions between the microbiome, immune system, and metabolism.

The findings-potentially relevant to long COVID due to its similarity with ME/CFS-come from data on 249 individuals analyzed using a new artificial intelligence (AI) platform that identifies disease biomarkers from stool, blood, and other routine lab tests.

“Our study achieved 90% accuracy in distinguishing individuals with chronic fatigue syndrome, which is significant because doctors currently lack reliable biomarkers for diagnosis. Some physicians doubt it as a real disease due to the absence of clear laboratory markers, sometimes attributing it to psychological factors.”

 Dr. Derya Unutmaz, Study Author and Professor, Immunology, The Jackson Laboratory 

The research was led by Dr. Julia Oh, formerly at JAX and now a microbiologist and professor at Duke University, in collaboration with ME/CFS clinicians Lucinda Bateman and Suzanne Vernon of the Bateman Horne Center, and Unutmaz, who directs the JAX ME/CFS Collaborative Research Center. Details appear today in Nature Medicine.

Mapping the invisible

Chronic fatigue syndrome is characterized by severe symptoms that significantly impair physical and mental activities, including persistent fatigue, sleep abnormalities, dizziness, and chronic pain.

Experts often compare ME/CFS to long COVID, as both conditions frequently follow viral infections, such as Epstein-Barr virus. In the United States, ME/CFS affects between 836,000 and 3.3 million individuals- many undiagnosed-and costs the economy $18 to $51 billion annually due to healthcare expenditures and lost productivity, according to the Centers for Disease Control and Prevention.

Prior studies have noted immune disruptions in ME/CFS, Unutmaz said. This new research builds upon those findings by investigating how the gut microbiome, its metabolites, and immune responses interact. The team linked these connections to 12 classes of patient-reported symptoms, which were aggregated from hundreds of datapoints generated by patient health and lifestyle surveys.

These include sleep disturbances, headaches, fatigue, dizziness, and other symptoms the researchers mapped in their entirety from microbiome changes to metabolites, immune responses, and clinical symptoms.

“We integrated clinical symptoms with cutting-edge omics technologies to identify new biomarkers of ME/CFS,” Oh said. “Linking symptoms at this level is crucial, because ME/CFS is highly variable. Patients experience a wide range of symptoms that differ in severity and duration, and current methods can’t fully capture that complexity.” 

To conduct the study, the researchers analyzed comprehensive data collected from the Bateman Horne Center, a leading ME/CFS, Long-Covid, and fibromyalgia research center in Salt Lake City, Utah. Dr. Ruoyun Xiong, also a lead author on the study, developed a deep neural network model called BioMapAI. The tool integrates gut metagenomics, plasma metabolomics, immune cell profiles, blood test data, and clinical symptoms from 153 patients and 96 healthy individuals over four years.

Immune cell analysis proved most accurate in predicting symptom severity, while microbiome data best predicted gastrointestinal, emotional, and sleep disturbances. The model connected thousands of patient data points, reconstructing symptoms such as pain and gastrointestinal issues, among several others. It also revealed that patients who were ill for less than four years had fewer disrupted networks than those who were ill for more than ten years.

“Our data indicate these biological disruptions become more entrenched over time,” Unutmaz said. “That doesn’t mean longer-duration ME/CFS can’t be reversed, but it may be more challenging.”

The study included 96 age- and gender-matched healthy controls, showing balanced microbiome-metabolite-immune interactions, in contrast to significant disruptions in ME/CFS patients linked to fatigue, pain, emotional regulation issues, and sleep disorders.

ME/CFS patients also had lower levels of butyrate, a beneficial fatty acid produced in the gut, along with other nutrients essential for metabolism, inflammation control, and energy. Patients with elevated levels of tryptophan, benzoate, and other markers indicated a microbial imbalance. Heightened inflammatory responses, particularly involving MAIT cells sensitive to gut microbial health, were also observed.

“MAIT cells bridge gut health to broader immune functions, and their disruption alongside butyrate and tryptophan pathways, normally anti-inflammatory, suggests a profound imbalance,” said Unutmaz.

An actionable dataset

Even though the findings require further validation, they significantly advance scientists’ understanding of ME/CFS and provide clearer hypotheses for future research, the authors said.

Since animal models can’t fully reflect the complex neurological, physiological, immune, and other system disruptions seen in ME/CFS, Oh said it will be crucial to study humans directly to identify modifiable factors and develop targeted treatments.

“The microbiome and metabolome are dynamic,”Oh said. “That means we may be able to intervene-through diet, lifestyle, or targeted therapies-in ways that genomic data alone can’t offer.”

BioMapAI also achieved roughly 80% accuracy in external data sets, confirming key biomarkers identified in the original group. This consistency across diverse data was striking, the authors said.

“Despite diverse data collection methods, common disease signatures emerged in fatty acids, immune markers, and metabolites,” Oh said. “That tells us this is not random. This is real biological dysregulation.”

The researchers intend to share their dataset broadly with BioMapAI, which supports analyses across diverse symptoms and diseases, effectively integrating multi-omics data that are difficult to replicate in animal models.

“Our goal is to build a detailed map of how the immune system interacts with gut bacteria and the chemicals they produce,” Oh said. “By connecting these dots we can start to understand what’s driving the disease and pave the way for genuinely precise medicine that has long been out of reach.” 

The global diabetes epidemic continues its relentless march, with projections suggesting 750 million sufferers by 2045. While current medications help control symptoms, they often come with undesirable side effects and don’t address the root causes of metabolic dysfunction. The search for better solutions has turned scientists toward natural drugs, where traditional remedies may hold untapped potential.

Among these, Nitraria roborowskii Kom – a hardy shrub growing in China’s harsh western regions – has shown intriguing properties in preliminary studies. Its bright red berries, sometimes called “desert cherries,” have sustained local populations for generations, but only now are revealing their scientific secrets. This gap between traditional knowledge and modern understanding prompted researchers to investigate the plant’s therapeutic mechanisms systematically.

Published (DOI: 10.13748/j.cnki.issn1007-7693.20240613) in the April 2025 issue of Chinese Journal of Modern Applied Pharmacy, a collaborative study between Qinghai University and the Northwest Institute of Plateau Biology has yielded compelling evidence. Using rigorous scientific methods, the team demonstrated how a concentrated extract from the desert berry (NRK-C) produced dramatic improvements in diabetic mice.

Over seven weeks of treatment, the natural compound outperformed expectations by simultaneously addressing high blood sugar, poor insulin response, and related metabolic disturbances through a previously underexplored biological pathway.

The research team’s comprehensive investigation yielded striking results, demonstrating NRK-C’s multifaceted therapeutic potential. Over a seven-week treatment period, the desert berry extract produced a remarkable 30-40% reduction in fasting blood glucose levels in diabetic mice, with efficacy increasing in a clear dose-dependent manner. Perhaps most impressively, the natural compound restored insulin sensitivity by approximately 50% compared to untreated diabetic controls, as measured through sophisticated metabolic tests.

Beyond these primary benefits, NRK-C exhibited an unexpected breadth of action, normalizing cholesterol profiles and slashing oxidative stress markers by up to 60% – effects rarely achieved by single pharmaceutical agents. Molecular analysis revealed the extract’s secret lies in its ability to reactivate the PI3K/AKT pathway, essentially rebooting a critical metabolic signaling system that becomes dysfunctional in diabetes.

Microscopic tissue examinations provided visual confirmation of NRK-C’s protective effects, showing preserved liver architecture and pancreatic integrity that starkly contrasted with the damage seen in untreated diabetic mice. These coordinated improvements across multiple physiological systems suggest NRK-C works through a fundamental metabolic reset rather than simply masking symptoms, offering potential advantages over current single-target diabetes medications.

The discovery is particularly noteworthy because it achieves these comprehensive effects through a naturally occurring compound rather than the complex drug cocktails typically required for such broad metabolic benefits.

“These results are exciting because they suggest we might be able to treat diabetes more holistically. Instead of just lowering blood sugar like most medications, this plant extract appears to help the body regain its natural metabolic balance.”

Dr. Yue Huilan, Study Senior Researcher and Associate Professor, Northwest Institute of Plateau Biology

Dr. Huilan added, “The implications could extend beyond diabetes to other conditions involving insulin resistance.” The research team cautions that human trials are needed but believes this could represent a major step toward more natural diabetes management.

The discovery opens several promising avenues for diabetes care. Pharmaceutical companies may explore developing standardized NRK-C extracts as complementary therapies, while nutritionists could investigate incorporating the berries into functional foods. Importantly, the findings validate traditional medicinal knowledge while providing a scientific basis for its effects.

As research continues, scientists are particularly interested in whether NRK-C might help prevent diabetes in high-risk individuals or reduce complications in existing patients. The study also highlights the importance of preserving and studying traditional medicinal plants, which may hold solutions to modern health challenges waiting to be rediscovered.

A potential target for experimental drugs that block PRMT5 – a naturally occurring enzyme some tumors rely more on for survival – has been identified by researchers with the Fralin Biomedical Research Institute’s Cancer Research Center in Washington, D.C.

In a study published this month in Cancer Research, Assistant Professor Kathleen Mulvaney of Virginia Tech’s Fralin Biomedical Research Institute shared research that could help guide development of new therapies for some treatment-resistant lung, brain, and pancreatic cancers.

“Using genetic screening, we found a new drug combination that seemingly works.”

Kathleen Mulvaney, Assistant Professor, Fralin Biomedical Research Institute, Virginia Tech

New therapies are needed. Lung cancer is a leading cause of cancer-related death globally. The five-year survival rate is less than 15 percent for pancreatic cancer patients, and even lower for glioblastoma. 

“With one drug alone, tumors can become resistant really quickly,” said Mulvaney, who is a member of the research institute’s Cancer Research Center in Washington, D.C. Treatment often fails. The findings suggest the PRMT5 inhibitor could be a powerful new approach for certain hard-to-treat cancers. “In all cases, the combination is better at killing than the single agents.”

Many of these solid tumors share a genetic trait: They lack CDKN2A and MTAP, two genes that suppress tumors and help regulate cell growth. Without them, the cancers become dependent on PRMT5 and potentially vulnerable to drugs that block the enzyme.

Mulvaney and colleagues analyzed genetic data from thousands of cancer patients available through the cBioPortal.

They applied CRISPR editing tools to look at biological pathways across a range of samples to determine which genes make cancer cells more vulnerable to PRMT5 inhibitors and which combinations could improve response and long-term outcomes.

An estimated 5 percent of all cancer patients – about 80,000 to 100,000 per year in the U.S. – can benefit from the therapies identified, according to Mulvaney, who also holds an appointment in biomedical sciences and pathobiology in the Virginia-Maryland College of Veterinary Medicine.

Using PRMT5 inhibitors with drugs that block a communication system that tells cancer cells when to grow, divide, or shut down – known as the MAP kinase pathway – scientists identified potential treatments for clinical trials. 

“We also discovered a number of genes that interact with PRMT5 signaling in cancer that were not previously known,” Mulvaney said.

In addition to lung, brain, and pancreatic cancers, the treatment shows promise for some types of melanoma and mesothelioma.

In both animal models and cell cultures derived from patient tissue, lab members saw success after testing potential therapies. 

“In all cases, the combination is better at killing cancer cells than the single agents,” Mulvaney said. “Only the combinations led to complete regressions.”

As artificial intelligence is rapidly developing and becoming a growing presence in healthcare communication, a new study addresses a concern that large language models (LLMs) can reinforce harmful stereotypes by using stigmatizing language.

The study from researchers at Mass General Brigham found that more than 35% of responses in answers related to alcohol- and substance use-related conditions contained stigmatizing language. But the researchers also highlight that targeted prompts can be used to substantially reduce stigmatizing language in the LLMs’ answers. Results are published in The Journal of Addiction Medicine.

“Using patient-centered language can build trust and improve patient engagement and outcomes. It tells patients we care about them and want to help. Stigmatizing language, even through LLMs, may make patients feel judged and could cause a loss of trust in clinicians.”

Wei Zhang, MD, PhD, Study Corresponding Author and Assistant Professor, Division of Gastroenterology, Mass General Hospital

LLM responses are generated from everyday language, which often includes biased or harmful language towards patients. Prompt engineering is a process of strategically crafting input instructions to guide model outputs towards non-stigmatizing language and can be used to train LLMs to employ more inclusive language for patients. This study showed that employing prompt engineering within LLMs reduced the likelihood of stigmatizing language by 88%.

For their study, the authors tested 14 LLMs on 60 generated clinically relevant prompts related to alcohol use disorder (AUD), alcohol-associated liver disease (ALD), and substance use disorder (SUD). Mass General Brigham physicians then assessed the responses for stigmatizing language using guidelines from the National Institute on Drug Abuse and the National Institute on Alcohol Abuse and Alcoholism (both organizations’ official names still contain outdated and stigmatizing terminology).

Their results indicated that 35.4% of responses from LLMs without prompt engineering contained stigmatizing language, in comparison to 6.3% of LLMs with prompt engineering. Additionally, results indicated that longer responses are associated with a higher likelihood of stigmatizing language in comparison to shorter responses. The effect was seen across all 14 models tested, although some models were more likely than others to use stigmatizing terms.

Future directions include developing chatbots that avoid stigmatizing language to improve patient engagement and outcomes. The authors advise clinicians to proofread LLM-generated content to avoid stigmatizing language before using it in patient interactions and to offer alternative, patient-centered language options.

The authors note that future research should involve patients and family members with lived experience to refine definitions and lexicons of stigmatizing language, ensuring LLM outputs align with the needs of those most affected. This study reinforces the need to prioritize language in patient care as LLMs become increasingly used in healthcare communication.

Feeling low or overwhelmed after childbirth? You’re not alone. Many new mothers face emotional challenges after childbirth, and in some cases, these can develop into postnatal depression. Between sleep deprivation, hormonal shifts, and lifestyle changes, it’s easy for mental wellbeing to take a back seat. However, even a small amount of regular physical activity, just 80 minutes a week, can make a real difference. A major study has found that light to moderate exercise can lower the risk of postnatal depression by up to 45%. Whether it’s walking, stretching, or gentle movement, staying active can help support emotional recovery in the weeks and months after delivery.

Struggling with postnatal depression? Light exercise may offer relief

A large-scale analysis published in the British Journal of Sports Medicine found that women who exercise for just over an hour a week after childbirth may reduce their risk of postnatal depression by nearly 45%. This review combined data from 35 studies involving over 4,000 women from 14 countries, making it one of the most comprehensive analyses on the link between exercise and maternal mental health.The findings showed that women who stayed physically active after giving birth had significantly lower odds of developing depressive symptoms commonly referred to as the “baby blues.” These symptoms, such as mood swings, sadness, irritability, and anxiety, can occur in the weeks following childbirth and, if left unaddressed, may progress into clinical postpartum depression. Importantly, exercise was also found to ease existing symptoms in women already experiencing anxiety or low mood during the postpartum period.

Gentle workouts are a safe way to prevent postnatal depression

You don’t need an intense gym routine to benefit. The study found that gentle movements like walking can be a great way for mothers to ease into regular physical activity. As their strength and energy return, women can gradually shift to moderate-intensity exercises such as:

These forms of activity are accessible and can often be done at home or with a baby in tow.

Start early: exercising within 12 weeks may reduce postnatal depression risk

According to the analysis, beginning physical activity within 12 weeks of delivery led to better improvements in mood and a greater reduction in depressive symptoms. However, every mother’s recovery timeline is different. Those recovering from complications or a C-section may need more time and should follow their body’s cues or consult a healthcare provider before starting.

How much exercise helps reduce postnatal depression?

To experience measurable benefits, new mothers are encouraged to engage in at least 80 minutes of moderate exercise per week, ideally across four or more days. This could be as simple as taking a 20-minute walk each morning or doing short bursts of low-impact workouts spread throughout the week.Regular movement helps not only with mood regulation but also improves energy levels, sleep quality, and physical recovery. While staying active is beneficial, it’s equally important to avoid overexertion. If you notice signs like persistent fatigue, discomfort, or slow recovery after a workout, you may be progressing too fast. Rest and gradual increase are key.Additionally, if issues like urinary leakage or pelvic discomfort are present, it’s wise to seek help from a pelvic floor physiotherapist before continuing.

Exercise is a natural and effective way to manage postnatal depression

Postpartum life is filled with emotional highs and lows. Incorporating gentle physical activity into your weekly routine may offer an effective, natural way to lift mood and reduce the risk of postpartum depression. From improved emotional resilience to better physical recovery, the benefits are holistic. And with most activities being baby-friendly, it can even double as bonding time.Getting back into movement might feel daunting in the early days of motherhood, but even small steps can lead to big improvements. Whether it’s a morning walk, light stretching, or dancing around the house, staying active for just over an hour a week may make a significant difference in your postpartum journey.Also Read: 10 Easy home remedies that actually help with arthritis pain

The English philosopher Bertrand Russell once wrote that “the men who do great work in science are happy men, whose happiness is derived primarily from their work.” Indeed, Antonio Pérez and Persis Amrolia are the first to arrive, a little after eight in the morning, to London’s Zayed Centre for Research into Rare Disease in Children, and the last to leave. Over the last year, they have forged an intense professional collaboration as well as a friendship that promises to last the rest of their lives. Both specialize in childhood blood cancers.

Pérez is the director of the CRIS Unit for Advanced Treatments at Madrid’s Hospital Universitario de La Paz, and he is on the brink of finishing a long stint at the Great Ormond Street Hospital, where the Zayed Centre is based. Amrolia, who divides his time between attending children who require transplants and immunotherapy research, is a bone marrow transplant consultant at GOSH.

“Immunotherapy, if you boil it down, is just using the patient’s immune system to fight against cancer. You can use antibodies as treatments for certain cancers, or you can put a chemotherapy attached to the antibody, so that the chemotherapy is targeted to the cancer. In our field, in stem cell transplant, we often use immune cells from the donor to fight against leukemia, and that’s effective in some forms of leukemia, but not in other forms,” Professor Amrolia explains patiently.

The pair received EL PAÍS in their London offices to talk about their year of collaboration and explain their next project. The Fight Kids Cancer initiative, which brings together foundations involved in research of the disease, like the CRIS Cancer Foundation, has decided to support the CARINA Project, which is run by Pérez and Amrolia. The initiative is taking a new and important step towards increasing the efficiency of CAR-T cell therapy, a field in which both professors are pioneers and specialists.

“We’ve been working for some time in a newer form of immunotherapy called CAR-T cell therapy, where we take the patient’s immune cells [T lymphocytes, a type of cell that defends against infections and tumors]. We genetically modify them with a disabled virus, so that they express a new receptor called a chimeric antigen receptor [CAR], which enables them to see the leukemia for the first time. And more than that, those cells, when they see the leukemia, get a signal to proliferate and divide so they can kill thousands and thousands of leukemic cells,” explains Amrolia.

Their new project, a revolutionary trial, looks to utilize CAR-T cell therapy for the first time in acute myeloid leukemia, which does not typically respond to treatment and can return, often with devastating effects, after a failed transplant. The trial’s objective is to produce universal cells that can reduce cost, complexity and be used to treat more patients.

“We are working on the next generation of off-the-shelf CAR-T cells, without needing to extract anything from the patient. They come from healthy donors. The complication of these new cells is their manufacturing, because they need more gene editing, which makes them more complex. When we use CAR-T cells from the same patient, there is very low risk of rejection and of targeting different organs. But the advantages are obvious for patients who are unable to travel, who do not have enough T lymphocytes, or their lymphocytes are of very low quality, because they have received previous chemotherapy treatments,” Doctor Pérez says, enthusiastically.

In search of expert critical mass

His time in London has reaffirmed Pérez’s conviction that childhood cancer research does require international cooperation, but also and perhaps most importantly, national cooperation. He sees Spain’s resources are being geographically disperse, which weakens the country’s ability to make advancements.

“The most important thing I’ve learned from them is how they manage the multidisciplinary team, with a lot of people thinking, a lot of gray material concentrated on the patient from different perspectives — immunology, hematology, bone marrow transplant, nurses. They are giving very useful feedback inputs in terms of the cases of very complex patients,” says the Spanish scientist.

“That, to me, is key. You have to concentrate experts in a single facility. In Spain, everything is spread out. There are 52 hospitals that carry out this kind of treatment, but you need to bring genetic specialists, hematologists, immunophenotyping experts, pharmacologists together. When you concentrate things, you learn more quickly and you can carry out better clinical trials. If we were to bring these skills together in five unique facilities (four on the Spanish mainland and one on the Canary Islands) we could begin work on a vast network that would improve response enormously. It’s not possible to have expertise or comprehensive programs everywhere,” he says.

Amrolia is full of praise for Pérez and celebrates the lasting nature of their collaboration. “I am confident that he has learned a little from the way we treat our patients, as we are one of the largest transplant units in Europe, but what he has brought here is knowledge and experience that has allowed us to promote new research protocols over time,” he says.

This, despite Brexit. Because the United Kingdom’s recent era of darkness and uncertainty has certainly had an impact on science. “My observation is that for scientific research, Brexit was a retrograde step. For many years, we were not able to access European grants, which were a great way of setting up collaborations across European countries and pushing forward groundbreaking research. We’re now back in the Horizon Europe funding program, so that’s a good thing. The other thing I have noticed since Brexit is that when we advertise for a postdoctoral post, we get very few, virtually no applicants from Europe. There are so many bright young scientists out there, and it would have been great to work with them,” says Amrolia.

After road traffic accidents, childhood cancer is the primary cause of death among kids under the age of 14 in Europe, at 6,000 annual deaths and with more than 60% of 400,000 survivors spending the rest of their lives dealing with complications. Pérez and Amrolia’s happiness also means being able to pass it on to new patients.

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Bat collection

A total of 460 bats were captured, and blood samples were collected from 368 individuals (Supplementary Table S6), representing seven families: Craseonycteridae (n = 21, 5.7%), Emballonuridae (n = 63, 17.1%), Hipposideridae (n = 153, 41.6%), Megadermatidae (n = 22, 6.0%), Miniopteridae (n = 1, 0.3%), Rhinolophidae (n = 44, 12.0%), and Vespertilionidae (n = 64, 17.4%), encompassing 17 species. The bat species with the maximal number of blood samples was Hipposideros gentilis (n = 120, 32.6%), followed by Taphozous melanopogon (n = 63, 17.2%) and Myotis siligorensis (n = 61, 16.6%). Species from which only a single sample was collected included Hipposideros armiger, Hipposideros larvatus, Miniopterus magnater, Rhinolophus refulgens, and Myotis ricketti. In terms of sampling locations, a majority of the blood samples were obtained from the Phra Cave (PC; n = 209, 56.8%), followed by the Manow Phee Cave (MPC; n = 75, 20.4%) and the Koh Yao Noi Island (KYI; n = 31, 8.5%). The least number of samples was collected at Kaeng Khoi-Cham Phak Phaeo (KCP; n = 0, 0.0%), followed by Pomelo Farm (PF; n = 1, 0.3%) and the Thiwson Resort (TR; n = 2, 0.5%) (Tables 1 and 2).

Prevalence of trypanosomes in bats

Of 368 bats, 40 (10.9%) tested positive for Trypanosoma spp., on the basis of at least one positive PCR result of SSU rRNA or gGAPDH, or through microscopic examination. The highest number of Trypanosoma-positive samples was detected at the Phra Cave (PHC; 21/209, 10.1%), followed by the Darwvading Cave (DC; 7/11, 63.7%) and the Manow Phee Cave (MPC; 7/75, 9.4%). In contrast, the lowest number of infections was observed at the Ma Glue Cave (MGC; 3/16, 18.8%), the Koh Yao Noi Island (KYI; 1/31, 3.3%), and the Koh Kham Island (KKI; 1/14, 7.2%). No Trypanosoma infections were detected at the Thiwson Resort (TR), the Pomelo Farm (PF), or Tham Khao Chong (TKC). Among the bat families examined, Rhinolophidae contributed the greatest number of infected individuals (13/44, 29.5%), followed by Megadermatidae (9/22, 41.0%), and Vespertilionidae (7/64, 10.9%). At the species level, the maximal infection prevalence was observed in Rhinolophus pearsonii (7/9, 77.8%), followed by Hipposideros cineraceus (1/2, 50.0%), Megaderma spasma (9/22, 40.9%), and Rhinolophus thomasi (1/3, 33.3%). Conversely, the lowest was recorded in Hipposideros gentilis (4/120, 3.3%), Hipposideros atrox (1/29, 3.4%), Taphozous melanopogon (5/63, 7.9%), Myotis siligorensis (7/61, 11.5%), and Rhinolophus coelophyllus (5/27, 18.5%). No Trypanosoma infections were detected in eight bat species: Craseonycteris thonglongyai (n = 21), Hipposideros armiger (n = 1), H. larvatus (n = 1), Miniopterus magnater (n = 1), Rhinolophus refulgens (n = 1), R. malayanus (n = 4), Myotis muricola (n = 2), and M. ricketti (n = 1) (Tables 1 and 2).

Molecular detection of Trypanosoma DNA in sand flies

In total, 189 female sand fly specimens, representing 14 species from 13 sites across four provinces in Thailand, were examined for Trypanosoma DNA by PCR amplification of SSU rRNA and gGAPDH genes. Among the specimens analyzed, only a single sand fly, identified as Ph. stantoni collected from the entrance of the Tiger Cave (TGC) in Saraburi Province, tested positive for Trypanosoma. This specimen exhibited a successful amplification of the SSU rRNA (895 bp) and gGAPDH (763 bp) genes, resulting in an overall Trypanosoma infection rate of 0.5% (1/189) in phlebotomine sand flies (Table 3). No Trypanosoma DNA was detected in sand fly specimens collected from the remaining 12 locations in Kanchanaburi, Chachoengsao, and Phatthalung provinces (Table 3), suggesting a low prevalence of trypanosomes in sand flies in these regions. However, detecting Trypanosoma DNA only in a single specimen does not confirm the vectorial competency of sand flies, as no attempts were made to culture and observe parasite development from this specimen.

Identification of blood meal source in sand flies

In total, 37 pools (189 specimens) of female sand flies, representing 14 species, were examined for vertebrate blood meal analysis using the mitochondrial COI gene. Among them, 159 (84.1%) were classified as unfed, 29 (15.3%) as gravid, and 1 (0.5%) as engorged. The most commonly identified species were Phlebotomus barguesae (72 individuals, 38.1%), followed by Sergentomyia anodontis (33 individuals, 17.5%) and Sergentomyia spp. 1 (17 individuals, 9.0%). The least frequent were Sergentomyia siamensis and Grassomyia indica, each represented by a single individual (0.5%). A majority of the collected specimens were gravid females, with 11 individuals of Ph. barguesae and 9 for Se. anodontis. However, only one engorged female, Ph. stantoni, was detected. A total of 37 pools, comprising 159 unfed specimens, 29 gravid specimens, and 1 engorged specimen, were analyzed; however, none tested positive for vertebrate blood meals (Table 4).

SSU rRNA and gGAPDH phylogeny of trypanosomes from bats and sand flies

A total of 40 trypanosome SSU rRNA sequences (524–560 bp) from bats and 1 from a sand fly, along with 20 gGAPDH sequences (763 bp) from bats and 1 from a sand fly, were obtained and classified into six distinct clades (Figs. 2 and 3). SSU rRNA analysis revealed that seven T. dionisii isolates from bats clustered with global sequences from Brazil, Japan, Mexico, and Thailand, formed a monophyletic clade. This clade included a human-derived Brazilian sequence (KR905444), supported by high statistical values (BI = 1, ML = 99) (Fig. 2a-b). Similarly, gGAPDH analysis revealed that six bat-derived isolates grouped with reference strains from Australia, Brazil, China, Japan, Thailand, and the UK, confirming broad distribution. The analysis also linked T. dionisii to two human isolates (PP438714 and PP555249) from China (Fig. 3a-b).

The T. noyesi clade included 12 bat SSU rRNA sequences, clustering with reference sequences from bats, sand flies, and tabanid flies in Thailand and Australia. For gGAPDH, four sequences grouped with Thai bat T. noyesi, while one (PV239509) formed a distinct basal clade. Phylogenetic analyses (BI = 1, ML = 100) placed Trypanosoma sp. 1 in a distinct clade with anuran trypanosomes. The SSU rRNA sequence from a sand fly clustered with isolates from sand flies and frogs across Canada, Pakistan, Thailand, and the USA. gGAPDH analysis revealed association with diverse hosts (sand flies, frogs, eels, platypuses, panrays) spanning Africa, Canada, Portugal, Australia, Senegal, and Pakistan, demonstrating wide host range and geographic distribution.

Both SSU rRNA and gGAPDH analyses robustly supported (BI = 1, ML = 100) the placement of bat-derived Trypanosoma sp. 2 with an unidentified Thai bat Trypanosoma sp.—four isolates by SSU rRNA and three by gGAPDH. The phylogenetic analysis of bat Trypanosoma sp. 3 using SSU rRNA showed that 12 isolates clustered with unidentified Trypanosoma sp. from bat and T. noyesi from sand flies in Thailand. While gGAPDH analysis grouped seven Trypanosoma sp. 3 isolates with an unidentified Trypanosoma sp. from a Thai bat. Trypanosoma sp. 3 likely represents a sister lineage to T. noyesi, although this is not fully supported by the topology of the phylogenetic tree. Phylogenetic analysis of Trypanosoma sp. 4 from bats was conducted using SSU rRNA and gGAPDH genes, though data availability varied between the two markers. Five Trypanosoma sp. 4 isolates clustered with an unidentified Thai bat Trypanosoma sp. in SSU rRNA, but amplification with gGAPDH was unsuccessful. In addition, the concatenated ML phylogenetic tree, constructed on the basis of SSU rRNA and gGAPDH genes (provided in Supplementary Fig. S1), supported the results of the individual phylogenetic trees for both genes.

Microscopy of the trypanosomes

According to microscopic examination, three blood films were positive for trypanosomes from Rhinolophus pearsonii (THBAT2173, PCR positive) and Hipposideros gentilis (THBAT2203, PCR negative; THBAT23120, PCR positive). Trypomastigotes in Hipposideros gentilis exhibited a consistent C- or U-shaped morphology with a visible nucleus, kinetoplast, flagellum, and undulating membrane (Fig. 2c). In contrast, the nucleus and kinetoplast were not observed in trypomastigotes from Rhinolophus pearsonii.

TCS haplotype network

The TCS haplotype network was constructed using trypanosome SSU rRNA and gGAPDH sequences, obtained from nine bat and one sand fly species. An analysis of 41 SSU rRNA genes identified 10 genetic variants, while 21 gGAPDH genes revealed 13 genetic variants (details including host species are mentioned in Supplementary Fig. S2) (Fig. 3).

Comparative pairwise distances of trypanosome SSU rRNA and gGAPDH genes

Concerning SSU rRNA and gGAPDH, most clades exhibited low intraspecific genetic distances (≤ 0.01), indicating a high degree of intraspecific genetic similarity. In contrast, interspecific genetic distances ranged from 0.03 to 0.15 for SSU rRNA and from 0.09 to 0.19 for gGAPDH, with clustering patterns revealing evident genetic divergence between clades. Across both genetic markers, the T. dionisii, T. noyesi (T. noyesi subclade-I and II), T. sp. 1, T. sp. 2, and T. sp. 4 clades exhibited minimal intraspecific genetic variation (≤ 0.01), reinforcing a strong genetic similarity level among sequences within each clade. Moreover, T. noyesi exhibits minimal interspecific genetic variation (0.03–0.04 for SSU rRNA and 0.08–0.10 for gGAPDH), with T. sp. 3, strongly supporting that T. sp. 3 likely represents a sister lineage to T. noyesi (Fig. 4). Notably, the T. sp. 1 clade, derived from sand flies, exhibited substantial interspecific genetic diversity (ranging from 0.11 to 0.15 for SSU rRNA and from 0.14 to 0.19 for gGAPDH) when compared with bat-associated Trypanosoma lineages, suggesting the emergence of a distinct evolutionary descent (Fig. 4).

Putative species delimitation of Trypanosoma spp.

Species delimitation identified seven putative Trypanosoma spp. from bats and phlebotomine sand flies in Thailand (Fig. 5). The sand fly Trypanosoma isolate formed a distinct lineage (T. sp. 1) with strong Bayesian support (1.00), positioned peripherally relative to the bat-associated Trypanosoma clades. Such analysis further recognized four, six, and three isolates of T. noyesi, T. dionisii, and T. sp. 2 as separate species, respectively. Notably, six isolates of T. sp. 3 were classified into two putative species (T. sp. 3a and 3b). Interestingly, a single isolate (THBAT23175) was identified as a separate putative species on the basis of bPTP analysis, despite exhibiting complete genetic similarity (0.00 genetic distance) with T. noyesi based on SSU rRNA. Due to a failed gGAPDH amplification, the T. sp. 4 SSU rRNA sequences were excluded from species delimitation.

If you thought air pollution just made you cough or ruined your morning jog, think again—scientists at Cambridge University are now warning that it could be messing with your mind, too. And no, we don’t mean just in a “bad vibes” kind of way. We’re talking about a real risk of dementia.Yes, the same toxic air we breathe every day might be doing long-term damage to our brains, not just our lungs.The findings of the study is published in The Lancet Planetary Health.Researchers have found more evidence linking exposure to fine particulate matter (PM2.5)—that super-tiny gunk in the air from traffic, industry, wildfires, and more—with an increased risk of developing dementia later in life. These tiny particles are so small, they can slide past the body’s defenses, sneak into the bloodstream, and even reach the brain. The systematic study of 51 studies looked at data from over 29 million participants who had been exposed to air pollutants for at least a year.So basically, pollution isn’t just getting into your nose—it might be sneaking into your neurons.The scientists behind this research say they’re seeing consistent patterns: the more polluted the environment, the higher the rates of cognitive decline and dementia, especially in older adults. But here’s the kicker, it’s not just seniors who need to worry. The damage appears to start much earlier in life, meaning the longer you live in polluted areas, the greater the risk could be.But air pollution is unique in that it’s invisible, and for the most part, unavoidable—especially if you live in a busy city. Even indoor air isn’t always safe (thanks, cooking fumes and dust mites).Dr Haneen Khreis, the senior author of the study, told The Guardian: “Tackling air pollution can deliver long-term health, social, climate and economic benefits. It can reduce the immense burden on patients, families, and caregivers, while easing pressure on overstretched healthcare systems.”“In this systematic review and meta-analysis, we observed positive and statistically significant associations between incident dementia and previous long-term exposure to PM2·5, NO2, and BC/PM2·5 absorbance, in adults without dementia at baseline. We found no evidence for such an association with NOx, PM10, and annual O3, based on small numbers of studies,” the researchers have said.

How does air pollution cause dementia?

Here’s the gist: tiny particles in polluted air (like PM2.5 from cars, factories, and wildfires) can get breathed deep into your lungs and then slip into your bloodstream. From there, they can actually reach your brain. Once these particles are in your system, scientists believe they trigger inflammation and oxidative stress inside the brain. It’s a bit like your immune system overreacting to an invader, and these constant “mini fires” end up damaging brain cells and blood vessels. Over time, this can lead to memory loss, trouble focusing, and—yes—an increased risk of developing dementia, including Alzheimer’s and vascular dementia.Studies show people exposed to higher levels of air pollution are much more likely to get dementia. In fact, for every 10 micrograms per cubic meter increase in PM2.5, your dementia risk climbs by 17%. And with so many people living in polluted cities, the impact is massive—experts think hundreds of thousands of dementia cases each year may be tied to dirty air.

So what can you do?

Check your local air quality index (AQI) and try to stay indoors or wear a mask on days when pollution levels spike.Ventilate your home when cooking, and consider air purifiers, especially if you live near traffic or industry.Cambridge’s research isn’t the first to sound the alarm, but it adds weight to a growing pile of evidence: air pollution isn’t just a climate or respiratory issue—it’s a neurological one too.

Walking just 7,000 steps a day could be enough to drastically lower the risk of major health conditions, including cancer, dementia, heart disease, and depression, according to a major study published in The Lancet Public Health. Contrary to the popular belief that 10,000 steps is the golden number, researchers found that a more achievable target still delivers powerful health benefits. For many, this revelation could be a motivating and realistic alternative to improve longevity and well-being without the need for intense workouts or gym memberships.

Why 7,000 steps is a game-changer

The 10,000-step goal popularized by fitness trackers originated from a Japanese marketing campaign in the 1960s. However, it wasn’t based on scientific research. The recent global analysis reviewed data from over 160,000 adults and showed that walking 7,000 steps daily reduced the risk of cardiovascular disease by 25%, dementia by 38%, depression by 22%, and cancer by 6%, compared to those who walked just 2,000 steps.Regular walking supports brain health by improving blood flow, reducing inflammation, and promoting the release of mood-boosting endorphins. It also strengthens the heart by helping to control blood pressure, lower cholesterol, and support weight management, which are key factors in reducing the risk of heart disease and stroke.

Why less can be more: the plateau effect

Interestingly, researchers noted that benefits tend to level off beyond 7,000 steps. While walking more can bring additional heart health perks, those who fall short of 10,000 steps should not be discouraged. Even a modest increase in daily steps, from 2,000 to 4,000 or more, offers measurable health improvements.

A realistic goal for everyday life

Unlike structured workouts, walking can be incorporated into daily routines through commuting, running errands, or taking breaks at work. The 7,000-step benchmark is more attainable for older adults, people with busy schedules, or those new to exercise. It also encourages a shift in focus from perfection to consistency.Health experts agree that while step counts are a useful motivator, the real goal is simply to move more. Whether it is 4,000 or 7,000 steps a day, every step counts. For many, aiming for 7,000 could serve as an effective and evidence-based way to improve long-term health outcomes without feeling overwhelmed by unreachable targets.