Category: 8. Health

  • Outbreaks of ‘life-threatening’ botulism disease found in cattle

    Outbreaks of ‘life-threatening’ botulism disease found in cattle

    Photothek via Getty Images A herd of cattle in a field. A couple of them are looking into the camera. Photothek via Getty Images

    Hundreds of cows are reported to have died or been culled following outbreaks of a “life-threatening” disease among herds of cattle across the country.

    The Food Standards Agency (FSA) and the Animal and Plant Health Agency (APHA) are investigating cases of botulism in Essex, Northamptonshire and Shropshire.

    The governmental departments told the BBC there was no current indication of “any immediate risk to human health”, but safeguarding measures were being implemented.

    Jodie Wild, head of the incidents unit at the FSA, said the outbreak was believed to be linked to contaminated animal feed, which had been withdrawn from sale.

    “We’re working closely with government and local authority partners in response to an outbreak of botulism in cattle thought to be linked to animal feed,” she said.

    “There is currently no indication of any immediate risk to human health.

    “We are taking action to safeguard the food and animal feed supply chain and taking precautionary action to protect both public and animal health and welfare.

    “An animal feed product has been withdrawn from the market on a precautionary basis. We won’t hesitate to take further rapid action to protect animal health.”

    ‘Under investigation’

    According to the NHS, botulism is a “rare but life-threatening condition” caused by toxins which attack the nervous system. It can infect humans as well as livestock, but is not contagious.

    A spokesperson for APHA said: “We are aware of a number of suspected cases of botulism, which are under investigation in various regions including Essex, Shropshire and Northamptonshire.

    “APHA’s Regional Laboratories are involved with on-farm and laboratory investigations into cattle deaths that appear to be linked to the suspected feed contamination.

    “Further information will be provided in due course.”

    Continue Reading

  • FIGO Cancer Report 2025: Advancing global equity, prevention and innovation in gynaecologic oncology

    FIGO Cancer Report 2025: Advancing global equity, prevention and innovation in gynaecologic oncology

    The FIGO Cancer Report 2025, published in the International Journal of Gynecology & Obstetrics (IJGO), marks a significant milestone in the global fight against gynaecologic cancers. This year’s edition highlights urgent calls for equitable cancer care, the transformative potential of technological innovation and the vital role of preventive strategies. 

    Developed by the FIGO Committee on Women’s Cancer in collaboration with leading global partners, including the World Health Organization (WHO), the International Gynecologic Cancer Society (IGCS) and the International Society of Gynecological Pathologists (ISGyP), the report addresses persistent disparities in access to optimal surgical care – particularly for ovarian cancer- in low- and middle-income countries. Recommendations include strengthening health systems, investing in infrastructure and expanding training for multidisciplinary cancer care teams. 

    The report also underscores the impact of modifiable lifestyle and environmental factors on cancer prevention, advocating for integrated public health strategies to reduce risk through healthy diet, physical activity and pollution reduction. 

    A special focus is placed on artificial intelligence as a game-changer in gynaecologic oncology, from AI-powered diagnostics and automated colposcopy to enhanced surgical planning and radiotherapy precision- offering new possibilities, especially in resource-limited settings. 

    With expanded coverage of rare gynaecologic malignancies including cancers of the vulva, vagina, and corpus uteri and updates to staging for gestational trophoblastic neoplasia, we hope this comprehensive and integrative report will serve as a call to action and a blueprint for transformative change in gynaecologic oncology worldwide. 

    – Professor Sarikapan Wilailak, Chair for FIGO Committee on Women’s Cancer 

    Read the FIGO Cancer Report in IJGO.

    Continue Reading

  • Degner, J. F. et al. DNase I sensitivity QTLs are a major determinant of human expression variation. Nature 482, 390–394 (2012).

    Article 
    PubMed 
    PubMed Central 
    CAS 

    Google Scholar 

  • Farh, K. K.-H. et al. Genetic and epigenetic fine mapping of causal autoimmune disease variants. Nature 518, 337–343 (2015).

    Article 
    PubMed 
    CAS 

    Google Scholar 

  • Gaffney, D. J. et al. Dissecting the regulatory architecture of gene expression QTLs. Genome Biol. 13, R7 (2012).

    Article 
    PubMed 
    PubMed Central 
    CAS 

    Google Scholar 

  • Liebhaber, S. A. mRNA stability and the control of gene expression. Nucleic Acids Symp. Ser. 36, 29–32 (1997).

    CAS 

    Google Scholar 

  • Hollams, E. M., Giles, K. M., Thomson, A. M. & Leedman, P. J. MRNA stability and the control of gene expression: implications for human disease. Neurochem. Res. 27, 957–980 (2002).

    Article 
    PubMed 
    CAS 

    Google Scholar 

  • Schwanhäusser, B. et al. Global quantification of mammalian gene expression control. Nature 473, 337–342 (2011).

    Article 
    PubMed 

    Google Scholar 

  • Tani, H. et al. Genome-wide determination of RNA stability reveals hundreds of short-lived noncoding transcripts in mammals. Genome Res. 22, 947–956 (2012).

    Article 
    PubMed 
    PubMed Central 
    CAS 

    Google Scholar 

  • Courel, M. et al. GC content shapes mRNA storage and decay in human cells. eLife 8, e49708 (2019).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar 

  • LaMarre, J., Gingerich, T. J., Feige, J.-J. & LaMarre, J. AU-rich elements and the control of gene expression through regulated mRNA stability. Anim. Health Res. Rev. 5, 49–63 (2004).

    Article 
    PubMed 

    Google Scholar 

  • Agarwal, V., Bell, G. W., Nam, J.-W. & Bartel, D. P. Predicting effective microRNA target sites in mammalian mRNAs. eLife 4, e05005 (2015).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Wu, Q. et al. Translation affects mRNA stability in a codon-dependent manner in human cells. eLife 8, e45396 (2019).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Pai, A. A. et al. The contribution of RNA decay quantitative trait loci to inter-individual variation in steady-state gene expression levels. PLoS Genet. 8, e1003000 (2012).

    Article 
    PubMed 
    PubMed Central 
    CAS 

    Google Scholar 

  • Alkallas, R., Fish, L., Goodarzi, H. & Najafabadi, H. S. Inference of RNA decay rate from transcriptional profiling highlights the regulatory programs of Alzheimer’s disease. Nat. Commun. 8, 909 (2017).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Li, J.-R., Tang, M., Li, Y., Amos, C. I. & Cheng, C. Genetic variants associated mRNA stability in lung. BMC Genomics 23, 196 (2022).

    Article 
    PubMed 
    PubMed Central 
    CAS 

    Google Scholar 

  • Paulsen, M. T. et al. Coordinated regulation of synthesis and stability of RNA during the acute TNF-induced proinflammatory response. Proc. Natl Acad. Sci. USA 110, 2240–2245 (2013).

    Article 
    PubMed 
    PubMed Central 
    CAS 

    Google Scholar 

  • Bedi, K. et al. Co-transcriptional splicing efficiencies differ within genes and between cell types. RNA 27, 829–840 (2021).

    Article 
    PubMed 
    PubMed Central 
    CAS 

    Google Scholar 

  • The GTEx Consortium et al. The GTEx Consortium atlas of genetic regulatory effects across human tissues. Science 369, 1318–1330 (2020).

    Article 
    PubMed Central 

    Google Scholar 

  • Salton, M. et al. Matrin 3 binds and stabilizes mRNA. PLoS ONE 6, e23882 (2011).

    Article 
    PubMed 
    PubMed Central 
    CAS 

    Google Scholar 

  • Zhang, G. et al. Dynamic FMR1 granule phase switch instructed by m6A modification contributes to maternal RNA decay. Nat. Commun. 13, 859 (2022).

    Article 
    PubMed 
    PubMed Central 
    CAS 

    Google Scholar 

  • Meyer, C. et al. The TIA1 RNA-binding protein family regulates EIF2AK2-mediated stress response and cell cycle progression. Mol. Cell 69, 622–635 (2018).

    Article 
    PubMed 
    PubMed Central 
    CAS 

    Google Scholar 

  • Kim, Y. K. & Maquat, L. E. UPFront and center in RNA decay: UPF1 in nonsense-mediated mRNA decay and beyond. RNA 25, 407–422 (2019).

    Article 
    PubMed 
    PubMed Central 
    CAS 

    Google Scholar 

  • Yang, E.-W. et al. Allele-specific binding of RNA-binding proteins reveals functional genetic variants in the RNA. Nat. Commun. 10, 1338 (2019).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Zhang, J. et al. An integrative ENCODE resource for cancer genomics. Nat. Commun. 11, 3696 (2020).

    Article 
    PubMed 
    PubMed Central 
    CAS 

    Google Scholar 

  • Fabian, M. R., Sonenberg, N. & Filipowicz, W. Regulation of mRNA translation and stability by microRNAs. Annu. Rev. Biochem. 79, 351–379 (2010).

    Article 
    PubMed 
    CAS 

    Google Scholar 

  • Liu, C.-J. et al. miRNASNP-v3: a comprehensive database for SNPs and disease-related variations in miRNAs and miRNA targets. Nucleic Acids Res. 49, D1276–D1281 (2021).

    Article 
    PubMed 
    CAS 

    Google Scholar 

  • Fu, T. et al. Massively parallel screen uncovers many rare 3′ UTR variants regulating mRNA abundance of cancer driver genes. Nat. Commun. 15, 3335 (2024).

    Article 
    PubMed 
    PubMed Central 
    CAS 

    Google Scholar 

  • Griesemer, D. et al. Genome-wide functional screen of 3′ UTR variants uncovers causal variants for human disease and evolution. Cell 184, 5247–5260 (2021).

    Article 
    PubMed 
    PubMed Central 
    CAS 

    Google Scholar 

  • Chen, P. J. et al. Enhanced prime editing systems by manipulating cellular determinants of editing outcomes. Cell 184, 5635–5652 (2021).

    Article 
    PubMed 
    PubMed Central 
    CAS 

    Google Scholar 

  • Bresson, S. & Tollervey, D. Tailing off: PABP and CNOT generate cycles of mRNA deadenylation. Mol. Cell 70, 987–988 (2018).

    Article 
    PubMed 
    CAS 

    Google Scholar 

  • Springer, T. A. Adhesion receptors of the immune system. Nature 346, 425–434 (1990).

    Article 
    PubMed 
    CAS 

    Google Scholar 

  • González-Amaro, R., Diaz-González, F. & Sánchez-Madrid, F. Adhesion molecules in inflammatory diseases. Drugs 56, 977–988 (1998).

    Article 
    PubMed 

    Google Scholar 

  • Ryter, S. W., Cloonan, S. M. & Choi, A. M. K. Autophagy: a critical regulator of cellular metabolism and homeostasis. Mol. Cells 36, 7–16 (2013).

    Article 
    PubMed 
    PubMed Central 
    CAS 

    Google Scholar 

  • Uffelmann, E. et al. Genome-wide association studies. Nat. Rev. Methods Prim. 1, 37–49 (2021).

    Google Scholar 

  • Sollis, E. et al. The NHGRI-EBI GWAS Catalog: knowledgebase and deposition resource. Nucleic Acids Res. 51, D977–D985 (2023).

    Article 
    PubMed 
    CAS 

    Google Scholar 

  • Gusev, A. et al. Integrative approaches for large-scale transcriptome-wide association studies. Nat. Genet. 48, 245–252 (2016).

    Article 
    PubMed 
    PubMed Central 
    CAS 

    Google Scholar 

  • Zhou, M. et al. Inhibition of Fam114A1 protects melanocytes from apoptosis through higher RACK1 expression. Aging 13, 24740–24752 (2021).

    Article 
    PubMed 
    PubMed Central 
    CAS 

    Google Scholar 

  • Subbaiah, K. C. V., Wu, J., Tang, W. H. W. & Yao, P. FAM114A1 influences cardiac pathological remodeling by regulating angiotensin II signaling. JCI Insight 7, e152783 (2022).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Imamachi, N. et al. BRIC-seq: a genome-wide approach for determining RNA stability in mammalian cells. Methods 67, 55–63 (2014).

    Article 
    PubMed 
    CAS 

    Google Scholar 

  • Ghandi, M. et al. Next-generation characterization of the Cancer Cell Line Encyclopedia. Nature 569, 503–508 (2019).

    Article 
    PubMed 
    PubMed Central 
    CAS 

    Google Scholar 

  • Carter, S. L. et al. Absolute quantification of somatic DNA alterations in human cancer. Nat. Biotechnol. 30, 413–421 (2012).

    Article 
    PubMed 
    PubMed Central 
    CAS 

    Google Scholar 

  • Suvakov, M., Panda, A., Diesh, C., Holmes, I. & Abyzov, A. CNVpytor: a tool for copy number variation detection and analysis from read depth and allele imbalance in whole-genome sequencing. Gigascience 10, giab074 (2021).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Abdennur, N. & Mirny, L. A. Cooler: scalable storage for Hi-C data and other genomically labeled arrays. Bioinformatics 36, 311–316 (2020).

    Article 
    PubMed 
    CAS 

    Google Scholar 

  • Wang, X. et al. Genome-wide detection of enhancer-hijacking events from chromatin interaction data in rearranged genomes. Nat. Methods 18, 661–668 (2021).

    Article 
    PubMed 
    PubMed Central 
    CAS 

    Google Scholar 

  • Yan, J. et al. Improving prime editing with an endogenous small RNA-binding protein. Nature 628, 639–647 (2024).

    Article 
    PubMed 
    PubMed Central 
    CAS 

    Google Scholar 

  • Chow, R. D., Chen, J. S., Shen, J. & Chen, S. A web tool for the design of prime-editing guide RNAs. Nat. Biomed. Eng. 5, 190–194 (2021).

    Article 
    PubMed 
    CAS 

    Google Scholar 

  • Nelson, J. W. et al. Engineered pegRNAs improve prime editing efficiency. Nat. Biotechnol. 40, 402–410 (2022).

    Article 
    PubMed 
    CAS 

    Google Scholar 

  • Dobin, A. et al. STAR: ultrafast universal RNA-seq aligner. Bioinformatics 29, 15–21 (2013).

    Article 
    PubMed 
    CAS 

    Google Scholar 

  • Ashuach, T. et al. MPRAnalyze: statistical framework for massively parallel reporter assays. Genome Biol. 20, 183 (2019).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Ormond, C., Ryan, N. M., Corvin, A. & Heron, E. A. Converting single nucleotide variants between genome builds: from cautionary tale to solution. Brief. Bioinform. 22, bbab069 (2021).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Van Nostrand, E. L. et al. A large-scale binding and functional map of human RNA-binding proteins. Nature 583, 711–719 (2020).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Smedley, D. et al. BioMart–biological queries made easy. BMC Genomics 10, 22 (2009).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Sayols, S. rrvgo: a Bioconductor package for interpreting lists of Gene Ontology terms. microPubl. Biol. https://doi.org/10.17912/micropub.biology.000811 (2023).

  • Purcell, S. et al. PLINK: a tool set for whole-genome association and population-based linkage analyses. Am. J. Hum. Genet. 81, 559–575 (2007).

    Article 
    PubMed 
    PubMed Central 
    CAS 

    Google Scholar 

  • Finucane, H. K. et al. Partitioning heritability by functional annotation using genome-wide association summary statistics. Nat. Genet. 47, 1228–1235 (2015).

    Article 
    PubMed 
    PubMed Central 
    CAS 

    Google Scholar 

  • gxiaolab. Gxiaolab/RNAtracker: for publication. Zenodo https://doi.org/10.5281/zenodo.15528784 (2025).

  • Purcell, S. et al. PLINK: a toolset for whole-genome association and population-based linkage analysis. Am. J. Human Genet. 81, 559–575 (2007).

    Article 
    CAS 

    Google Scholar 

  • Quinlan, A. R. & Hall, I. M. BEDTools: a flexible suite of utilities for comparing genomic features. Bioinformatics 26, 841–842 (2010).

    Article 
    PubMed 
    PubMed Central 
    CAS 

    Google Scholar 

  • Li, H. & Durbin, R. Fast and accurate short read alignment with Burrows–Wheeler transform. Bioinformatics 25, 1754–1760 (2009).

    Article 
    PubMed 
    PubMed Central 
    CAS 

    Google Scholar 

  • Yee, T. W. The VGAM package for categorical data analysis. J. Stat. Softw. 32, 1–34 (2010).

    Article 

    Google Scholar 

  • Lex, A., Gehlenborg, N., Strobelt, H., Vuillemot, R. & Pfister, H. UpSet: visualization of intersecting sets. IEEE Trans. Vis. Comput. Graph. 20, 1983–1992 (2014).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar 

  • Gu, Z., Eils, R. & Schlesner, M. Complex heatmaps reveal patterns and correlations in multidimensional genomic data. Bioinformatics 32, 2847–2849 (2016).

    Article 
    PubMed 
    CAS 

    Google Scholar 

  • Gådin, J. R., van’t Hooft, F. M., Eriksson, P. & Folkersen, L. AllelicImbalance: an R/bioconductor package for detecting, managing, and visualizing allele expression imbalance data from RNA sequencing. BMC Bioinformatics 16, 194 (2015).

    Article 
    PubMed 
    PubMed Central 

    Google Scholar 

Continue Reading

  • Mpox Still a Continental Emergency, Africa CDC Advisory Group Recommends – ReliefWeb

    1. Mpox Still a Continental Emergency, Africa CDC Advisory Group Recommends  ReliefWeb
    2. Whatever happened to mpox? Is it still a threat?  NPR
    3. Mpox remains ‘health emergency’ in Africa  TRT Français
    4. Mpox Resurgence Exposes Gaps in Global Health Preparedness  Global Biodefense
    5. Africa’s mpox outbreak claims nearly 2,000 lives since 2024  Latest news from Azerbaijan

    Continue Reading

  • Ultrasound ‘helmet’ could treat Parkinson’s non-invasively, study shows | Medical research

    Ultrasound ‘helmet’ could treat Parkinson’s non-invasively, study shows | Medical research

    An ultrasound “helmet” offers potential new ways for treating neurological conditions without surgery or other invasive procedures, a study has shown.

    The device can target brain regions 1,000 times smaller than ultrasound can, and could replace existing approaches such as deep brain stimulation (DBS) in treating Parkinson’s disease. It also holds potential for conditions such as depression, Tourette syndrome, chronic pain, Alzheimer’s and addiction.

    Unlike DBS, which requires a highly invasive procedure in which electrodes are implanted deep in the brain to deliver electrical pulses, using ultrasound sends mechanical pulses into the brain.

    But no one had managed to create an approach capable of delivering them precisely enough to make a meaningful impact until now.

    A study published in Nature Communications introduces a breakthrough system that can hit brain regions 30 times smaller than previous deep-brain ultrasound devices.

    “It is a head helmet with 256 sources that fits inside an MRI scanner,” said the author and participant Ioana Grigoras, of Oxford University. “It is chunky and claustrophobic putting it on the head at first, but then you get comfortable.”

    Current DBS methods used on Parkinson’s patients use hard metal frames that are screwed into the head to hold them down.

    To test the system, the researchers applied it to seven volunteers, directing ultrasound waves to a tiny region the size of a grain of rice in the lateral geniculate nucleus (LGN), the key pathway for visual information that comes from the eyes to the brain.

    “The waves reached their target with remarkable accuracy,” the senior author Prof Charlotte Stagg of Oxford University said. “That alone was extraordinary, and no one has done it before.”

    Follow-up experiments showed that modulating the LGN produced lasting effects in the visual cortex, reducing its activity. “The equivalent in patients with Parkinson’s would be targeting a motor control region and seeing tremors disappear,” she added.

    An independent expert and neuroscience professor, Elsa Fouragnan, of Plymouth University, said this proof of concept “represents a fundamental neuroscience milestone that opens the way for clinical translation”. Calling it a remarkable achievement, she offered her “heartfelt congratulations to the authors”.

    The work took place over a decade, with interdisciplinary teams from UCL and Oxford University working together to create the helmet and integrate it with the MRI scanner.

    Stagg said: “When we started the project, I was pregnant with my daughter. She is now 12. Hopefully, we will see the first clinical applications before she is at the university.”

    The team is already on the way to test the system on brain areas linked with Parkinson’s, schizophrenia, stroke recovery, pain, depression and other conditions.

    The helmet itself is one of a kind. The core team that built it, the UCL academics Elly Martin and Brad Treeby, emphasise the importance of working with patients to design it to be more comfortable and applicable to many conditions.

    “I created a company to focus specifically on the building of the helmet,” said Treeby. It currently needs an MRI scan to navigate it, but with the help of AI, it could be programmed to work on its own, allowing patients to use it in their own home.

    Martin says further studies are needed, “but our long-term goal is to refine the system into a practical clinical tool – one that could sit alongside or even replace invasive brain implants in the future”.

    Continue Reading

  • Penicillin for Syphilis Shown To Be Effective in Single Dose

    Penicillin for Syphilis Shown To Be Effective in Single Dose

    The number of syphilis cases is on the rise, according to a report from the Centers for Disease Control and Prevention. The CDC-recommended treatment for early syphilis is one dose of benzathine penicillin G, but there is debate among clinicians about whether three weekly doses are needed, particularly among persons with HIV. Researchers at the University of Alabama at Birmingham have published a study in the New England Journal of Medicine suggesting one dose of BPG is as effective as the three-injection regimen at treating early syphilis. The National Institutes of Health funded the research.

    “These results will help physicians simplify the treatment of syphilis for patients and reduce the time and inconvenience associated with multiple injections of penicillin administered in the past,” said Edward Hook III, M.D., lead author of the study and a professor of medicine and epidemiology in the UAB Division of Infectious Diseases. 

    Syphilis is an acute and chronic human bacterial sexually transmitted infection (caused by Treponema pallidum) that has been recognized as a threat to human health for centuries. In 2023, the United States reported more than 209,000 cases of syphilis — the greatest number of cases reported since 1950 — and 3,882 cases of congenital syphilis. Without treatment, syphilis can result in neurological and organ damage, as well as adverse pregnancy outcomes and congenital abnormalities. Syphilis can also increase a person’s likelihood of acquiring or transmitting HIV. While BPG has been used as a primary treatment for syphilis for decades, treatment with BPG has been hampered by stock-outs and periodic shortages.

    “We are living in era of unreliable stock of the BPG drug supply to treat syphilis, which has led to the use of alternative therapies that may not be as effective,” said Jodie Dionne, M.D., associate professor of medicine and co-author of the paper. “Now that we know one dose of the drug is just as effective as three doses, this helps extend our local and national drug supply to treat as many people as we can.”

    The study, which was open to anyone with early syphilis, enrolled 249 persons at 10 sites across the United States. Ninety-seven percent of participants were men, 62 percent were Black, and 64 percent were living with HIV infection. According to the study authors, these findings provide substantial evidence that the current treatment guidelines of treating early syphilis with a single dose of penicillin is as effective as the three-injection method.

    Reference: Hook Edward W., Dionne Jodie A., Workowski Kimberly, et al. One Dose versus Three Doses of Benzathine Penicillin G in Early Syphilis. NEJM. 2025;393(9):869-878. doi: 10.1056/NEJMoa2401802

    This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source. Our press release publishing policy can be accessed here.

    Continue Reading

  • How fiber intake shapes your gut microbes’ digestion strategy

    How fiber intake shapes your gut microbes’ digestion strategy

    A new study uncovers how gut bacteria may switch from digesting plant fibers to consuming protective mucus when fiber is scarce, fueling inflammation even in people without gut disease.

    Study: Gut microbiome genes involved in plant and mucin breakdown correlate with diet and gastrointestinal inflammation in healthy US adults. Image credit: Tatjana Baibakova/Shutterstock.com

    In a recent study published in The Journal of Nutrition, researchers investigated the impact of fiber scarcity on the gut’s “carbohydrate-active enzymes” (CAZymes) and their subsequent role in gastrointestinal inflammation amongst healthy United States (US) adults. The study leveraged data from 330 participants and found that a higher ratio of mucin-degrading to plant-degrading enzymes, a novel metric they termed Muc2Plant, was strongly associated with increased gastrointestinal inflammation.

    Study findings highlight that the Muc2Plant ratio was positively correlated with fecal inflammation biomarkers (e.g., calprotectin [p=0.001] and neopterin [p<0.001]), suggesting that imbalances in microbial digestive function (due to low fiber utilization and greater reliance on mucin degradation) can promote a pro-inflammatory state even in healthy individuals, thereby providing insight into potential targets for intervention.

    Background

    While organisms like humans were historically believed to be able to digest much of the food they consume, more recent research has demonstrated that a large portion of the food we consume (e.g., complex carbohydrates) is broken down by the vast enzymatic machinery of the symbiotic gut microbiome.

    Gut microbiotas are known to produce thousands of carbohydrate-active enzymes (CAZymes) that process insoluble plant fibers, releasing beneficial short-chain fatty acids (SCFAs) with validated inflammation-mitigating effects. Unfortunately, recent studies have observed that in the absence of sufficient dietary fiber, some gut microbes can switch to alternative food sources, primarily the mucus layer (made of glycoproteins called mucins) that lines and protects the intestines.

    This degradation of the protective mucin barrier is a hallmark of dysbiosis and has been previously linked to inflammatory bowel disease (IBD). Although the harmful effects of low fiber on gut health are well documented, few studies have directly examined how fiber influences both the gut microbiome’s enzymatic activity (whether microbes choose plant material or mucin as fuel) and gastrointestinal inflammation simultaneously.

    About the study

    The present study aims to systematically investigate the relationship between dietary fiber intake, the gut microbiome’s enzymatic capacity, and subclinical gut inflammation biomarkers in a cohort of healthy American adults. The cross-sectional study leveraged data from the United States Department of Agriculture (USDA) Nutritional Phenotyping Study (participant n = 330 individuals).

    Data of interest included participants’ socioeconomic demographic information (for statistical model standardization), detailed dietary information (using 24-hour recalls [ASA24] and food frequency questionnaires [FFQ]), and fecal samples (for microbiome characterization, enzymatic estimation, and inflammation biomarker assessment).

    Key study analyses included shotgun metagenomic sequencing to identify all the microbial genes present in the gut, allowing for a detailed profiling of individual-specific CAZyme repertoires. It also included fecal biomarkers to measure markers of gastrointestinal inflammation, including fecal calprotectin, neopterin, and myeloperoxidase (MPO).

    Study findings were used to develop a novel metric (“Muc2Plant”), representing the ratio between the abundance of mucin-degrading CAZyme genes and plant-degrading CAZyme genes. Analyses revealed that a higher Muc2Plant ratio indicates a microbiome better equipped to digest the host’s mucus lining relative to dietary fiber, suggesting reduced fiber utilization and heightened inflammation risk.

    Study findings

    The present study demonstrates a measurable correlation between dietary fiber intake and CAZyme gene recruitment. Habitual intake of total and soluble fiber was positively correlated with a greater abundance and diversity of plant-degrading CAZymes (adjusted R² = 0.015, p = 0.010 for abundance). A lower fecal pH, indicating robust fiber fermentation, was similarly associated with a higher capacity for fiber digestion (adjusted R² = 0.036, p < 0.001).

    The study also validated the utility of the novel Muc2Plant ratio. Higher ratios, indicative of enhanced mucin degradation, significantly and positively correlated with markers of gut inflammation, even in this phenotypically healthy cohort.

    Specifically, a higher Muc2Plant ratio was observed to be associated with higher levels of fecal calprotectin (adjusted R² = 0.038, p = 0.001), a well-established marker of neutrophil infiltration in the gut, and higher levels of fecal neopterin (adjusted R² = 0.071, p < 0.001), a marker of macrophage-driven inflammation.

    At the same time, plant-degrading CAZyme diversity and abundance were negatively associated with fecal myeloperoxidase but positively associated with fecal neopterin, highlighting that different immune pathways may be involved.

    Surprisingly, the study found no link between dietary fiber intake and the Muc2Plant ratio. However, machine learning models identified that a higher intake of white potatoes significantly predicted a lower Muc2Plant ratio, suggesting that certain types of dietary starch may help foster a healthier microbial balance.

    Conclusions

    The present study did not find a direct relationship between dietary fiber intake and inflammation, but did highlight complex associations between dietary fiber intake, microbial enzymatic capacity, and inflammation biomarkers. It provides evidence that the functional capacity of the gut microbiome, specifically its balance of plant-digesting versus mucin-digesting enzymes, is a crucial factor in maintaining gut health.

    The study also introduces and validates the novel Muc2Plant ratio metric, demonstrating the tool’s robust association with subclinical gastrointestinal inflammation, even without overt disease. It emphasizes that these findings are correlative and not causal.

    Download your PDF copy now!

    Journal reference:

    • Blecksmith, S. E., Oliver, A., Alkan, Z., & Lemay, D. G. (2025). Gut microbiome genes involved in plant and mucin breakdown correlate with diet and gastrointestinal inflammation in healthy US adults. The Journal of Nutrition. DOI – 10.1016/j.tjnut.2025.08.027. https://doi.org/10.1016/j.tjnut.2025.08.027  https://www.sciencedirect.com/science/article/pii/S0022316625005334

    Continue Reading

  • WHO at the United Nations General Assembly 2025

    WHO at the United Nations General Assembly 2025

    The World Health Organization and partners will raise global awareness during the 80th United Nations General Assembly (UNGA) on progress to address a range of critical issues impacting people’s health worldwide, and urgent work that needs to be scaled up.

    These will include protecting people from noncommunicable diseases (NCDs) like cardiovascular diseases, cancer, diabetes, and chronic respiratory diseases; advocating for mental health; addressing the common risks caused by tobacco, unhealthy diet, alcohol, physical inactivity and also climate change; and finding solutions to raise resources to finance national health systems. Promoting peace as the best medicine to protect health and end conflicts in various parts of the world will also feature prominently during UNGA.

    On 25 September, the Fourth UNHA High-level Meeting on NCDs and Mental health will be held, providing a status check on efforts to protect people from the world’s leading killers.

    Combined, the four major  NCDs account for 74% of all deaths globally. The WHO Director-General, Dr Tedros Adhanom Ghebreyesus, is expected to address the opening of this event, joined by leadership of the United Nations, Member States and other key partners.

    In addition, strategic events held on 24 September, in collaboration with partners, including the Bloomberg Philanthropies Global Forum, will focus on how pro-health taxes on harmful products such as tobacco can protect people’s health and raise needed resources for national health services. The challenge of the global obesity epidemic will also be a subject of major attention. In addition, WHO will release the Global Hypertension Report during the Assembly, warning that uncontrolled high blood pressure remains one of the world’s leading causes of premature death.

    This year’s General Assembly takes place at a critical time for the multilateral system as it adapts to a range of new realities. WHO has been working closely with fellow UN agencies, through the UN80 Initiative, to improve efficiencies in its operations while remaining committed to deliver on its mission of advancing health for all.

    WHO and partners will also be advocating for action to reduce the threats to health that people face worldwide from the impacts of conflicts, such as those in  Gaza, Sudan and Ukraine, climate change and diseases such as polio.


    For real time updates on WHO and global health activities during UNGA, follow WHO and the Director-General’s social media accounts:

    X:

    @WHO@DrTedros

    Facebook:

    World Health Organization (WHO) Tedros Adhanom Ghebreyesus

    LinkedIn:

    World Health Organization Tedros Adhanom Ghebreyesus 



    Instagram:

    @who
    @drtedros



    BlueSky:

    @who.int
    @drtedros.who.int



    Threads:

    @who
    @drtedros



    Telegram:

    Tedros Adhanom Ghebreyesus
      


    Continue Reading

  • New Antibiotic for Superbugs May Prevent Recurrence

    New Antibiotic for Superbugs May Prevent Recurrence

    As the effectiveness of antibiotics meant to fight the deadly superbug Clostridioides difficile, or C. diff, wanes, a research team at the University of Houston is seeing positive results of a new antibiotic on the scene — ibezapolstat — which is proving successful in fighting these infectious bacteria in clinical trials.

    C. diff is the nation’s leading cause of death from gastroenteritis causing an estimated 453,000 infections yearly and 29,300 deaths. It causes gastrointestinal illness ranging from diarrhea and abdominal pain to toxic megacolon, sepsis and death.

    Until now the frontline treatments for C. diff have been the antibiotics vancomycin, with a sustained clinical cure of 42% to 71%, and fidaxomicin at 67%.

    And yet, a superbug would not be so deadly if it was not able to outlive the very medicines meant to destroy it.

    “Both vanco and fidaxo are associated with emerging antimicrobial resistance. C. difficile infection recurrence is associated with increased mortality, decreased quality of life and higher healthcare costs. New antibiotics are urgently needed.” said Kevin Garey, Robert L. Boblitt Endowed Professor of Drug Discovery at the University of Houston College of Pharmacy and senior author on recent clinical trial results with ibezapolstat published in Lancet Microbe.

    C. diff infections often return when the natural balance in the gut stays disrupted — good bacteria like Bacillota, Bacteroidota, and Actinomycetota are reduced, while harmful types like Pseudomonadota increase. These changes can weaken the gut’s defenses, causing a loss of the kind of bacteria that helps break down bile acids. When that happens, harmful bacteria can easily take over.

    “Ibezapolstat’s mechanism of action helps restore the healthy microbiota that causes C. diff recurrence” said study lead author Taryn A. Eubank, research assistant professor of Pharmacy Practice and Translational Research at UH.

    Enter ibezapolstat

    Ibezapolstat has a way of working that kills harmful C. difficile bacteria without harming the good bacteria in the gut that protect against C. diff infections.

    “A randomized, double-blind, active-controlled study showed high rates of initial clinical cure in participants treated with ibezapolstat, with no recurrence,” reports Garey.

    “Ibezapolstat was found to be safe, well tolerated, and was associated with the preservation of key health-promoting bacteria responsible for bile acid homoeostasis, a key component in preventing recurrent C. difficile infection.”

    Eubank added, “This helps confirm the important anti-C diff recurrence properties of Ibezapolstat.”

    Ibezapolstat is being developed by Acurx Pharmaceuticals progressing towards phase III clinical trials. The study was conducted at 15 centers, primarily outpatient clinics and hospitals in the United States. Participants were aged 18–90 years, with diarrhea and a confirmed diagnosis of mild or moderate C difficile infection.

    “The findings of our study support further clinical development of ibezapolstat into phase III clinical trials and eventual use in our patients,” said Garey.

    Reference: Eubank TA, Jo J, Alam MJ, et al. Efficacy, safety, pharmacokinetics, and associated microbiome changes of ibezapolstat compared with vancomycin in adults with Clostridioides difficile infection: a phase 2b, randomised, double-blind, active-controlled, multicentre study. Lancet Microbe. 2025;6(8):101126. doi: 10.1016/j.lanmic.2025.101126

    This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source. Our press release publishing policy can be accessed here.

    Continue Reading

  • Gene therapy pioneer Donavon Decker is remembered: ‘Go for it’

    Gene therapy pioneer Donavon Decker is remembered: ‘Go for it’

    On Thanksgiving Day 1998, a geneticist called Donavon Decker and told him the lab had identified the gene that was causing his and his sisters’ muscles to slowly deteriorate. By the way, the geneticist added, this might be a good candidate for gene therapy.

    Decker called back every month until April, when the researcher finally put him in touch with neurologist Jerry Mendell. Mendell said Decker could be of service — but that he couldn’t help Decker. 

    Gene therapy was still new and risky. No muscular dystrophy patient had ever received one. To assure safety, Mendell would only inject a tiny foot muscle. Decker wouldn’t benefit. He could be harmed and might be rendered ineligible for future gene therapies. But if it worked, it could advance the field, including for his four sisters with the disease.

    “He put his foot out,” Mendell recalled, “and said ‘go for it.’”

    Decker died Monday at age 62. There are today still no treatments for his condition, known as limb-girdle muscular dystrophy (LGMD). But Decker’s study paved the way for gene therapy’s resurgence over the past decade, including approval of the first gene therapy for spinal muscular atrophy and Duchenne, the most well-known and fatal form of muscular dystrophy.

    That trial “really set the stage for everything that came afterwards,” said Sharon Hesterlee, a longtime friend of Decker as well as interim head of the Muscular Dystrophy Association (MDA), which sponsored the 1999 study. 

    He died of complications from an elevator accident, exacerbated by the toll the disease had taken on his lungs.  

    Those in the muscular dystrophy community remembered a fearless and indefatigable advocate who set an example and served as a resource for other parents and patients. “I could cry just talking about him,” said Kelly Brazzo, whose daughter has LGMD. “He moved the gene therapy field forward without ever seeing a benefit himself, just a heroic and selfless act.” 

    The excitement over Decker’s study faded fast. Three days after his injection, he and Mendell appeared on the Jerry Lewis MDA Telethon, where they both spoke about the promise of an imminent cure. Less than two weeks later, 18-year-old Jesse Gelsinger died in a misstep-ridden trial at the University of Pennsylvania. The field, including the LGMD study, shut down overnight.  

    Decker, though, remained a force in the community. In 2001, he testified before Congress to push for the MD Care Act, a bill that dramatically expanded federal investment into muscular dystrophy, and served on the research coordinating committee the law created.

    Mendell, who in 2004 became director of the gene therapy center at Nationwide Children’s Hospital, kept working too, relying in part on data from Decker’s foot. It had been one of the first studies to try to ferry genes into the body with a new, potentially safer group of viruses, called AAVs, than the one Gelsinger received. 

    Although the results weren’t a home run — the dose was infinitesimal — it showed they could safely deliver genes into muscle, Mendell said. Although he never published the data, he said he used it when submitting applications to the Food and Drug Administration.

    In 2013, as the gene therapy field began its modern resurgence, Mendell was ready to start a new trial for Decker’s subtype, called LGMD 2D, this time infusing a full leg, through the blood stream. There are dozens of LGMD subtypes, each tied to a different gene. LGMD 2D, while ultra-rare, had been chosen because it was more common than others, and the gene could fit snugly into viruses.

    Decker volunteered again. But a blood test showed he still had antibodies from the 1999 trial. They would block the gene therapy, which used the same category of virus. “So he asked me if I knew anyone else that would do [it],” Decker recalled at a speech at the MDA’s conference earlier this year, when he was given an MDA Legacy Award for Community Impact in Research. 

    His sister June Burney stepped forward, becoming the first muscular dystrophy patient to receive gene therapy through the new system. She saw some benefit, Decker recalled, but then regressed.

    Mendell moved to dose patients systemically, the approach that would eventually lead to Elevidys, the gene therapy for Duchenne. But that’s where LGMD efforts began sputtering. 

    After promising early results in LGMD 2E, Sarepta Therapeutics bought out a startup spun out of Nationwide to develop one-time treatments for five different subtypes. But it did not move most of those programs forward, including the 2D treatment, for years, spending most of its resources on Duchenne.

    The delays frustrated Decker. Fellow advocates described him as a kind, soft-spoken man, with ample time, support, and wisdom ready, including for those facing a new diagnosis. And he had a humorous streak: He often recounted how, at the end of his hospital stay for Mendell’s trial, he yelped in pain when Mendell poked the site of the injection — the doctor jumped back, terrified the gene therapy had gone horribly awry, only to look up to see Decker laughing. But he could be a fierce advocate when he felt LGMD patients were being left behind.

    LGMD is often described as a less common and less severe form of muscular dystrophy. But he saw the toll the disease could take. In the years since the 1999 trial, he became fully reliant on his wheelchair and had to leave his job as an air traffic control specialist. He lost three sisters to the disease, which slowly sapped strength from their lungs. “They don’t understand the urgency,” he said in a documentary, “In Search of Strength,” about his life that came out this year.

    “Sometimes I feel overwhelmed when I see nothing happening, and I can see how some companies are not working on the research like they say they do,” he said. “That makes me angry at times and sometimes it gets the best of me, but it also makes me a strong advocate.”

    He kept testifying, explaining to the Food and Drug Administration the abilities the disease had taken from him and advocating for the agency for flexibility in ultra-rare diseases.

    And he encouraged other advocates to not leave their full faith in companies. Joe Dion remembered meeting him in 2023, when Sarepta was working on a gene therapy for LGMD 2C, a condition both his children were facing. 

    Decker encouraged Dion to remain skeptical, advice that led him to fund an alternative gene therapy effort. Both of his children have been dosed this year, while Sarepta, facing financial challenges and the death of a patient in another LGMD trial, pulled away from the disease altogether. 

    “If that wasn’t for him” his kids would never have been treated, said Dion. He credits the treatment with giving his 12-year-old son, Peter, who had been declining, the strength to get his student lobster license this summer and pull up traps at 7 a.m. 

    Before Decker died, he was trying to figure out how he could buy Peter’s lobster and have it transported frozen across the country, to his home in Kansas. 

    Decker was also working on his own approach. At one point, he helped another company with interest in LGMD raise nearly $5 million, Hesterlee, the MDA chief, recalled. That company pivoted away, but Decker started his own company, focused on a new non-viral gene therapy approach that might help older patients like himself and his sister June. He recruited top scientific leaders like Hesterlee to advise.

    “And the fact that the company had no money didn’t faze him at all,” said Hesterlee. “You don’t underestimate Donavon ever, that was my advice to anyone. Sure. You know, he sounds like a Midwestern guy. He’s got kind of a low-key, slow way of talking. … Don’t let that make you think that he can’t make things happen, because he really could.”

    Continue Reading