The world’s tropical regions are grappling with the rapid spread of mosquito-borne diseases like dengue fever. However, new research from Stanford University reveals an unexpected solution: protecting trees can significantly reduce the risk of these illnesses. A study published in Landscape Ecology found that even small patches of tree cover can keep invasive mosquito species at bay, providing a crucial win-win strategy for conserving biodiversity and public health.

“We already knew that small patches of tree cover support biodiversity for a wide range of plants and animals in this region,” said lead author Johannah Farner. “It turns out to be true for mosquitoes too – and has the upside of keeping out a disease-carrying invasive species.”

The study focused on Costa Rica, where residential areas with low tree cover were more likely to harbor the dengue-spreading Aedes albopictus mosquito. In contrast, forests with high tree density hosted a diverse range of native mosquito species, none of which were the dengue vector. This is because the presence of multiple mosquito species creates competition for resources like food and breeding sites, making it harder for invasive species to thrive.

The findings have significant implications for land use decisions in rural areas worldwide. By preserving trees and natural habitats, communities can reduce the risk of disease transmission while promoting biodiversity conservation. However, researchers caution that tree planting outside of forests should be viewed as a complement – not a replacement – for conserving larger natural areas.

Senior author Erin Mordecai emphasized the need for further research to understand how other vector species respond to increased tree cover and what factors contribute to dengue transmission in rural tropical areas. The Disease Ecology in a Changing World (DECO) program at Stanford is working to address this gap, identifying drivers of rural dengue and other diseases associated with environmental degradation.

Ultimately, the study highlights the importance of forests and tree cover as natural buffers against disease, underscoring the continued need for forest reserves and conservation efforts. By protecting trees and preserving biodiversity, we can reduce the risk of mosquito-borne illnesses and promote a healthier world.

The Broad Institute has made a groundbreaking discovery in treating Huntington’s disease and Friedreich’s ataxia by developing a novel approach to edit the genetic sequences responsible for these conditions. These severe neurological disorders are caused by repeated three-letter stretches of DNA that grow uncontrollably, leading to brain cell death or nerve fiber breakdown. The researchers have successfully disrupted this repeat sequence using base editing, a technique that introduces single-letter changes into the middle of the repeated stretch of DNA.

The study, published in Nature Genetics, was led by David Liu, the Richard Merkin Professor and director of the Merkin Institute of Transformative Technologies in Healthcare at the Broad. The research team included postdoctoral researcher Mandana Arbab, graduate student Zaneta Matuszek, and associate scientist Ricardo Mouro Pinto.

The breakthrough comes from the realization that some individuals with the same disease can inherit different numbers of DNA repeats, with more repeats generally leading to faster symptom progression. However, patients who have naturally occurring single-letter interruptions within these repeats often experience milder symptoms and are less likely to pass their disease along to their children. This observation inspired the researchers to develop a gene-editing therapy that could install an interruption mimicking those that occur naturally.

Using base editing, developed by Liu’s lab in 2016 for making single-letter changes in DNA, the team introduced interruptions into the repeat sequences of patient cells and mouse models of Huntington’s disease and Friedreich’s ataxia. The results showed that the edited DNA tracts stayed the same or even became shorter over time.

The researchers caution that more work is needed to catalog potential side effects of installing these edits in the genome, but the approach could be a valuable tool for understanding diseases caused by repeated three-letter sequences. “A lot more studies would be needed before we can know if disrupting these repeats with a base editor could be a viable therapeutic strategy to treat patients,” said Liu.

The team’s findings suggest that this gene-editing therapy could help treat Huntington’s, Friedreich’s ataxia, and other trinucleotide repeat disorders. “Not only does this study show for the first time that inducing interruptions has a profound stabilizing effect on repeats, but that the base-editing approach we’ve used can also be applied to study any of over a dozen repeat disorders,” said Arbab.

The research was supported by various organizations, including the Chan Zuckerberg Initiative, Lodish Family Foundation, National Institutes of Health, and Howard Hughes Medical Institute. The team is now developing a different approach using prime editing to replace disease-causing repeat tracts with a shorter, stable number of repeats all at once.

Scientists have made a groundbreaking discovery that could revolutionize the way we diagnose and treat gastrointestinal diseases such as gastric cancer, colorectal cancer, and inflammatory bowel disease. Researchers have found a range of “biomarkers” – indicators of specific microorganisms or their byproducts in the gut – that can help improve detection and treatment of these conditions.

Using advanced machine learning and AI-based algorithms to analyze microbiome and metabolome datasets from patients with GC, CRC, and IBD, the research team identified common bacteria and metabolites linked to each disease. The study revealed that certain markers could predict not only one specific disease but also another, suggesting a shared underlying mechanism driving disease progression.

For example, in gastric cancer, researchers found bacteria from the Firmicutes, Bacteroidetes, and Actinobacteria groups were common, along with changes in metabolites like dihydrouracil and taurine. Some of these biomarkers were also relevant for IBD, indicating overlap between the diseases.

Similarly, in colorectal cancer, bacteria such as Fusobacterium and Enterococcus, and metabolites like isoleucine and nicotinamide, were significant, sometimes overlapping with those found in gastric cancer, suggesting possible shared pathways in disease development. In inflammatory bowel disease, bacteria from the Lachnospiraceae family and metabolites like urobilin and glycerate were important, with some of these markers also involved in cancer pathways.

The research team simulated gut microbial growth and metabolite fluxes, revealing significant metabolic differences between healthy and diseased states. This innovative approach could lead to the development of universal diagnostic tools to revolutionize the diagnosis and treatment of gastrointestinal conditions.

Dr Animesh Acharjee, lead co-author from the University of Birmingham, commented: “Current diagnostic methods like endoscopy and biopsies are effective but can be invasive, expensive, and sometimes miss diseases at early stages. Our analysis offers a better understanding of the underlying mechanisms driving disease progression and identifies key biomarkers for targeted therapies.”

The research team now plans to further explore the clinical applications of their findings, including the development of non-invasive diagnostic tests and targeted therapies based on the identified biomarkers. They also aim to validate their models in larger, diverse patient cohorts and investigate these biomarkers’ potential in predicting other related diseases.