Researchers from the Institute of Food Technology (ITAL) and the University of Campinas (UNICAMP), both in the state of São Paulo, Brazil, in collaboration with scientists from the Fraunhofer IVV Institute in Germany, have developed a food product made from sunflower flour that can be used as a meat substitute.
The ingredient is obtained by extracting oil from the seeds of the plant. In order for it to be consumed by humans, the husks and phenolic compounds from the grains must be removed before processing. These substances give the flour a dark color and reduce its digestibility.
Researchers enriched the product with tomato powder, spices, and a mixture of fat sources made up of sunflower, olive and linseed oils.UnicampThe next step was to prepare two formulations of meat alternatives. The first incorporated flour from roasted grains, and the second used textured sunflower protein. Both were enriched with tomato powder, spices, and a mixture of sunflower, olive and linseed oils.
The patties were shaped into mini-burgers and baked. They then underwent sensory and physicochemical evaluations. The analysis results showed that the textured protein version had superior consistency, as well as high levels of protein and health-boosting fats, such as monounsaturated fatty acids. Additionally, the textured protein option had a significant mineral content, particularly of iron, zinc, magnesium, and manganese at 49%, 68%, 95% and 89% of the recommended daily intake, respectively.
The authors of the study, supported by FAPESP, decided to study sunflower meal because sunflower oil is widely used in Europe and sunflower cultivation is expanding in Brazil. Another advantage of the ingredient is that it is not genetically modified.
Additionally, the plant’s flour is a promising source of protein, which is highly relevant given the growing consumer demand for sustainable, plant-based options.
Maria Teresa Bertoldo Pacheco, a researcher at ITAL’s Center for Food Science and Quality and the last author of an article on the research published in the journal Food Research International, said, “It should also be noted that, after removing the husks and phenolic compounds, the flour has a very neutral taste and aroma, especially compared to the various vegetable proteins on the market.”
Pacheco also points out that the product has a favorable composition of essential amino acids. This is another factor that could lead to its incorporation into the food industry as a meat product substitute from a nutritional point of view.
“From a functional-technological standpoint, processes that build fibrous proteins, such as extrusion, are needed to deliver a product with a more meat-like appearance and texture,” Pacheco said.
“I think the study provided a lot of positive references, both for making full use of the cultivar and for encouraging the consumption and appreciation of the flour. The partnership with German researchers was also very important, thanks to the sharing of working techniques, the exchange of knowledge, and the exchange of students and researchers.”
In the 1920s, the yellow-spored mold Aspergillus flavus gained infamy after members of Howard Carter’s team died not long after opening Tutankhamun’s tomb.
Decades later, a similar fate befell scientists who entered the crypt of Poland’s King Casimir IV. Within weeks, 10 of the 12 researchers succumbed to respiratory illness, and investigators traced the deadly outbreak to dormant A. flavus spores.
Long dismissed as a toxic mold, Aspergillus flavus has revealed a new role: producing compounds that match some of the most trusted cancer therapies for acute myeloid leukemia.
Mold’s molecular treasure map
The breakthrough came from Sherry Gao’s laboratory at the University of Pennsylvania, where researchers hunt for drugs hidden in microbial genomes.
The team focused on ribosomally synthesized and post-translationally modified peptides, or RiPPs – small, ring-shaped molecules known for complex bioactivity. Scientists have cataloged thousands of RiPPs in bacteria, but they’ve found only a handful in fungi.
“Purifying these chemicals is difficult,” explained lead author Qiuyue Nie, a postdoctoral fellow at the University of Pennsylvania. Moreover, scientists can easily overlook the genes that direct their synthesis.
Using a two-pronged strategy, the team first compared the chemical fingerprints of a dozen Aspergillus strains, then zeroed in on gene clusters likely to encode RiPP machinery.
Turning those genes off caused the mysterious chemical peaks to vanish. This confirmed the researchers had found an active RiPP factory inside the tomb-dwelling mold.
From tomb mold to cancer medicine
Isolation and structural analysis revealed four previously unknown molecules sporting an intricate lattice of interlocking rings. The scientists named them asperigimycins in honor of their fungal source.
Two of the four showed notable activity against leukemia cells straight out of the flask, but a chemical tweak proved transformative.
By adding a fatty tail identical to one found in royal jelly – the nutrient-rich substance that turns ordinary bee larvae into queens – the team produced a lipid-capped asperigimycin. It matched cytarabine and daunorubicin, drugs that have anchored leukemia care since the 1970s.
How the drug gets inside
Why did that extra lipid unleash such power? Gao’s group deployed a CRISPR-based screen, knocking out genes in leukemia cells and tracking changes in drug uptake.
One transporter, SLC46A3, emerged as essential. It normally shuttles nutrients out of lysosomes, the cell’s recycling compartments. The researchers learned that the fatty tag let the mold-derived asperigimycins hitch a ride through this portal.
“This gene acts like a gateway,” Nie said. “Knowing that lipids can affect how this gene transports chemicals into cells gives us another tool for drug development.”
The insight may rescue other cyclic peptides that falter in trials because they cannot cross cellular barriers efficiently.
Disarming cancer’s dividing machinery
Microscopy and biochemical assays showed that the modified asperigimycins halt tumor growth by sabotaging microtubules, the protein scaffolds that haul chromosomes apart during mitosis.
Intriguingly, the mold-derived molecules left breast, liver, and lung cancer lines largely untouched, as well as an array of bacteria and yeast.
That selectivity hints at fewer side effects for patients, a perennial challenge for chemotherapy agents that indiscriminately target all fast-dividing cells.
Ancient mold, modern answers
For decades, scientists debated how fungi construct RiPPs, often mistaking them for non-ribosomal peptides. The current study resolves that puzzle by linking chemical signatures to the responsible genes.
“The synthesis of these compounds is complicated, but that’s also what gives them this remarkable bioactivity,” said Nie.
Comparative genomic scans have already flagged similar RiPP gene clusters in dozens of other molds, suggesting a trove of undiscovered molecules with antibiotic, antiviral, or immunomodulatory potential. According to Nie, this is an unexplored region with tremendous potential.
From tomb to trial
The next step is to test asperigimycins in mice to gauge toxicity, dosage, and efficacy in living organisms. Success there could pave the way for human clinical trials. Gao, reflecting on the journey from tomb lore to lab bench, recalls one guiding principle.
“Fungi gave us penicillin. These results show that many more medicines derived from natural products remain to be found,” Gao said.
Nature’s pantry still holds untold remedies waiting to be unlocked. With each advance in genomic mining and synthetic tailoring, the line between microbial menace and medical marvel grows ever thinner.
It’s a testament to evolution’s vast chemical imagination – and to scientists bold enough to mine mold and other microbes for the next life-saving drug.
The study is published in the journal Nature Chemical Biology.
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Patients with rheumatoid arthritis (RA) face a 40% higher risk of being hospitalized for serious dental infections compared with those without RA, underscoring the need to integrate oral health into chronic disease care, according to a national analysis of over 14 million hospitalizations in the US.1
The study, published in Cureus, evaluated data from the National Inpatient Sample to determine whether RA increases the likelihood of hospitalization for cellulitis or abscess of the mouth. While these infections were rare, affecting just 0.07% of nearly 15 million adults hospitalized between 2016 and 2022, their severity and connection to chronic inflammatory disease are increasingly recognized by clinicians and researchers.
Researchers called for multidisciplinary care models to integrate dental services into the routine management of chronic diseases like RA. | Image credit: D Theron/peopleimages.com – stock.adobe.com
Researchers identified 281,142 patients with RA from the sample. After adjusting for confounding variables such as age, race, sex, smoking status, and length of stay, the presence of RA was significantly associated with dental infection–related hospitalization (OR, 1.399; 95% CI, 1.210-1.618; P < .0001).
“This result adds to and validates earlier research highlighting RA patients’ increased susceptibility to infections as a result of immunosuppressive medications and immunological dysregulation,” the authors said.
Black Men Had Highest Odds of Infection
The study also highlighted broader health disparities and modifiable risk factors. Men were significantly more likely to be hospitalized for dental infections than women (OR, 1.79), and Black patients had higher odds than White patients (OR, 1.23). Smokers (OR, 1.33) and patients with longer hospital stays (OR, 1.44) also faced increased risk, and adults 65 and older were less likely to be hospitalized for oral infections than younger adults (OR, 0.25).
“These disparities are reflective of systemic inequities in healthcare access, oral health literacy, and socioeconomic status, which have been well-documented in literature,” the authors said.
They also found the highest infection rates relative to group size among patients aged 18 to 49, suggesting younger adults may delay routine dental care and only seek treatment when conditions become severe.2 Of more than 2 million hospitalizations for oral infections, 3097 (0.11%) adults aged 18 to 34 and 2837 (0.13%) aged 35 to 49 were specifically hospitalized for cellulitis or a mouth abscess.1 Adults aged 65 and older had a notably lower infection rate of 0.03%.
“This finding is unexpected, as younger adults are generally considered to be at lower risk for serious infections,” they said. “However, it may reflect barriers to preventive dental care, including lack of insurance coverage, reduced healthcare-seeking behavior, or limited oral health literacy in this age group.”
Autoimmune Disorders and Dental Care
RA affects about 1.3 million Americans and is known to impair the body’s immune defenses while increasing susceptibility to inflammation throughout the body, including in the oral cavity.3 Taking immunosuppressive therapies like corticosteroids and disease-modifying antirheumatic drugs also reduces the body’s ability to fight off bacterial infections, putting these patients at risk while trying to manage RA.1 According to the authors, the oral cavity is particularly vulnerable to pathogens like Porphyromonas gingivalis, a known trigger of both periodontitis and autoimmunity.
While the analysis benefited from a large, nationally representative sample, the authors acknowledged that the cross-sectional design cannot confirm causality and that relying on administrative coding could have led them to underestimate the true prevalence of infections.
At the same time, they noted that these findings underscore the need for multidisciplinary care models that integrate dental services into the routine management of chronic illnesses like autoimmune diseases; public health efforts should also focus on expanding access to preventive dental care through early screenings, educational outreach, and affordable services for high-risk populations. Together, the authors wrote these strategies could reduce the incidence of preventable oral infections and the serious complications that follow.
“Our findings support the growing consensus that oral diseases do not occur in isolation but rather intersect with broader health trajectories, particularly in immunocompromised populations,” they concluded.
References
Noah GU, Ikwuka OV, Nwadije JC, et al. The burden of dental infections among hospitalized patients with rheumatoid arthritis: a cross-sectional analysis of the national inpatient sample database. Cureus. 2025;17(5):e83568. doi:10.7759/cureus.83568
Nasseh K, Vujicic M. The effect of growing income disparities on U.S. adults’ dental care utilization. J Am Dent Assoc. 2014;145(5):435-442. doi:10.14219/jada.2014.1
Xu Y, Wu Q. Prevalence trend and disparities in rheumatoid arthritis among US adults, 2005-2018. J Clin Med. 2021;10(15):3289. doi:10.3390/jcm10153289
Cases of dengue fever, commonly known as “breakbone fever” for the excruciating joint pain that is the hallmark of the disease, have been rising around the world in recent years. More than half the global population is at risk.
“There’s an urgent need for better prevention and treatment for this global threat. Dengue outbreaks can quickly overwhelm local hospitals,” said lead author Priscila Castanha, Ph.D., MPH, assistant professor of infectious diseases and microbiology at Pitt’s School of Public Health.
The course of the disease varies widely from person to person. Some are asymptomatic; others experience dengue’s painful flu-like symptoms and then recover within days or weeks. “But 5% have serious bleeding, shock and organ failure—they can be critically ill within two days,” said senior author Simon Barratt-Boyes, Ph.D., professor of infectious diseases and microbiology at Pitt Public Health and immunology at Pitt School of Medicine.
For decades, epidemiologic studies have documented a puzzling phenomenon: In countries with ethnically diverse populations—like Brazil, Colombia, Haiti and Cuba—people of African ancestry tend to have milder cases of dengue, while people of European ancestry have more severe disease. But no one could explain why.
In this study, the team used a model they developed with samples of human skin that had been donated by individuals who had undergone elective skin-reduction surgeries after profound weight loss. The participants consented to contributing their tissues to this study.
“We used skin because it is an immunologic organ and the body’s first line of defense against dengue infection,” said Barratt-Boyes. When maintained in culture under proper conditions, the tissue samples used in this model can survive and carry out their normal immune functions for days, providing a unique opportunity for scientific study, he added, “because the skin is where the story begins with all mosquito-borne diseases.”
The study focused on samples from individuals who had self-identified as having European or African ancestry. First, the researchers objectively measured the ancestral geographic origins written into the skin samples’ DNA by analyzing genetic markers known as single nucleotide polymorphisms. The team then injected each sample with dengue virus, observed the samples’ subsequent immune responses over a 24-hour period and compared them.
The team found that the inflammatory response was much greater in skin from people with higher proportions of European ancestry. And unfortunately, in severe dengue, this immune response is prone to “friendly fire.” The virus infects inflammatory cells, actually recruiting them to spread the infection instead of fighting it off. This dynamic is believed to be what is so damaging to blood vessels and organs in severe cases of dengue fever.
In the samples from donors of European ancestry, the team saw this friendly fire in action as myeloid cells mobilized to confront the virus, then themselves became infected. The turncoat cells then moved out of the skin and spread out into the dish—similar to how they would spread within the body, traveling through the bloodstream and into lymph nodes.
The team further showed that the problem was not the skin itself—it was indeed the inflammatory response. In the samples from individuals with higher proportions of African ancestry, the researchers added inflammatory molecules called cytokines, and the friendly fire ensued. Then, when the team blocked the inflammation within those same samples, the virus’s rate of infection in the cells plummeted.
“It makes sense that, in parts of the world where ancient populations were exposed to deadly mosquito-borne viruses—like the one that causes yellow fever, which is related to dengue viruses and has been around for a very long time—those with a limited inflammatory response had an advantage,” said Barratt-Boyes. “They then passed that advantage down to their descendants.” Ancient Europeans’ descendants, however, lack that ancestral exposure and the evolutionary adaptation it made possible.
The authors hope that, eventually, the mechanism they’ve identified could be exploited for precision medicine approaches to things like risk assessment, triage in an outbreak, therapies and vaccines. In future studies, they hope to describe this mechanism in further detail, including which specific gene variants contribute to protection from severe dengue. The current study’s broader analysis of geographic ancestry could be an important first step to that end.
“Ancestry does affect biology. Evolution has made its mark on everyone’s DNA,” said Castanha.
Other authors on the study are Michelle M. Martí, M.S., Parichat Duangkhae, Ph.D., Jocelyn M. Taddonio, M.S., Kristine L. Cooper, M.S., Megan Wallace, M.S., Gwenddolen Kettenburg, M.S., Geza Erdos, Ph.D., Hasitha Chavva, M.S., Aleena Alex, M.S., Pharm. D., J. Peter Rubin, M.D., Simon C. Watkins, Ph.D., Louis D. Falo, Jr., M.D., Ph.D., and Jeremy J. Martinson, Ph.D., all of Pitt; and Ernesto T. A. Marquesa, M.D., Ph.D., of Pitt and Instituto Aggeu Magalhães.
This research was supported by Pitt, the Institute for Precision Medicine, the Richard K Mellon Foundation for Pediatric Research and the National Cancer Institute (P30CA047904).
/Public Release. This material from the originating organization/author(s) might be of the point-in-time nature, and edited for clarity, style and length. Mirage.News does not take institutional positions or sides, and all views, positions, and conclusions expressed herein are solely those of the author(s).View in full here.
Obstructive sleep apnea (OSA) is known as a chronic and potentially serious disorder in which the upper airway repeatedly collapses during sleep, causing intermittent drops in oxygen levels. It results from a combination of neuromuscular dysfunction during sleep and anatomical predispositions. OSA can affect patients of all genders, ages, ethnicities, and body types including those without obesity, and is estimated to impact 80 million patients in the United States. Despite the sleep disorder’s prevalence, up to 80% of cases remain undiagnosed and untreated.1
Individuals with OSA may experience hundreds of breathing disruptions each night, leading to reduced oxygen levels that impair essential cellular functions. If left untreated, OSA can significantly increase the risk of long-term health issues such as cardiovascular disease, cognitive decline, metabolic disorders, and early death. However, most diagnosed patients either do not initiate, discontinue, or inconsistently use current treatments. Presently, there are no approved pharmacologic therapies that directly target the neuromuscular dysfunction central to the disorder.
The investigational oral therapy AD109 (Apnimed), a combination of aroxybutynin and atomoxetine, is currently being evaluated in the phase 3 LunAIRo study (NCT05811247), a randomized, double-blind, placebo-controlled, 1-year parallel-arm study of patients with mild to severe OSA. The trial, enrolling at least 660 participants aged 18 years and older from 64 clinical centers across the US, is designed to examine the efficacy and safety of the investigational agent compared with placebo.2 The study’s primary end point includes measuring the proportion of participants who experience a reduction in apnea-hypopnea index (AHI) via polysomnography at 6 months and 1 year.
Patrick Strollo, MD, FACP, FCCP, FAASM
If successful, AD109 could become the first medication to address both the nighttime airway obstruction and oxygen deprivation central to OSA, as well as its daytime symptoms, such as fatigue. Taken once nightly at bedtime, this potential first-in-class combination targets neurological pathways involved in activating upper airway dilator muscles to help keep the airway open during sleep. Designed for use across varying levels of disease severity, AD109 offers the promise of a safe, effective, and more user-friendly alternative to current OSA treatments, which are often invasive or difficult for patients to tolerate.
Eligible participants of the trial were adults aged 18 years or older who met specific polysomnography parameters, including an AHI greater than 5, with no more than 25% of events classified as central or mixed apneas and a periodic limb movement arousal index of 15 or less. Individuals also needed to report significant fatigue, as indicated by a PROMIS-Fatigue raw score of at least 17. Additional requirements included intolerance to or refusal of positive airway pressure therapy and a body mass index ranging from 18.5 to 40 kg/m² for men or up to 42 kg/m² for women.
Participants were excluded if they had a diagnosis of narcolepsy, restless leg syndrome, or REM sleep behavior disorder. Those with insomnia marked by difficulty falling or staying asleep, or recent use of medications targeting insomnia symptoms, were also ineligible. Other exclusions included the presence of craniofacial syndromes such as Pierre Robin or Treacher Collins, or grade 3 or higher tonsillar hypertrophy. Individuals with clinically significant heart conditions, such as unstable coronary artery disease or ventricular arrhythmias, were excluded although stable atrial arrhythmia was permitted. Neurological exclusions encompassed neuromuscular disorders, epilepsy, and neurodegenerative diseases such as Parkinson, Alzheimer, or related conditions.
“The LunAIRo study is a complimentary study to SynAIRgy, a 6-month trial looking at safety and efficacy [of AD109]. LunAIRo is looking at safety and efficacy of [AD109] in a fairly similar population of over 600 participants,” Patrick Strollo, MD, FACP, FCCP, FAASM, professor of medicine and clinical translational science at the University of Pittsburgh, told NeurologyLive® in a recent interview. “We’ll get additional insights in terms of safety and efficacy over 1 year with a fairly similar demographic group.”
“We’re also doing some substudies within LunAIRo looking at a more robust analysis of cardiovascular impact. There’s a substudy that we’ve done looking at ambulatory blood pressure. Those data are not fully analyzed. I imagine probably very shortly there will be an announcement of the topline results of LunAIRo, but right now I can’t really speak about results,” Strollo said. “But that’s the difference between LunAIRo versus SynAIRgy, and they should be complementary in terms of helping us understand safety and efficacy and also reassuring the FDA when the company goes to the agency, probably in early 2026.”
AD109 first demonstrated therapeutic potential in the phase 3 SynAIRgy trial (NCT05813275), which tested the agent across a broad range of patients with mild, moderate, and severe OSA. In the study, the treatment met its primary end point in reducing AHI over a 26-week treatment period. Based on these findings, Apnimed noted that it plans to submit a new drug application (NDA) to the FDA in early 2026 for AD109 as a potential treatment of OSA.1
Considered the largest such drug trial for OSA, SynAIRgy included 646 adults with the disease who were intolerant of or currently refusing continuous positive airway pressure (CPAP). Coming into the study, 34.4% of patients had mild OSA, 42.4% had moderate, and 23.2% had severe. Overall, treatment with AD109 led to a statistically significant change in AHI, the primary end point, over a 26-week period relative to placebo (P = .001).
In SynAIRgy, patients underwent a polysomnogram on treatment at week 4. Overall, treatment with the oral agent led to meaningful improvements in oxygenation, as assessed by hypoxic burden (P <.0001), and oxygen desaturation index (P = .001). Furthermore, 51.2% of treated patients experienced a reduction in OSA disease severity, and 22.3% achieved complete disease control, defined as an AHI of fewer than 5 events per hour.
“Existing data suggests that up to 50% of patients with sleep apnea cannot or will not tolerate CPAP in the long term. There’s a huge unmet need for all of these patients with sleep apnea, and there’s a range of different treatment options being developed. AD109 is one of them that really is targeting neuromuscular function,” study chair Sanjay R. Patel, MD, MS, professor of medicine, epidemiology, & clinical and translational science at University of Pittsburgh, told NeurologyLive® in a recent interview. “There has been exciting data in the phase 2 short term studies and we’ve already very quickly filled enrollment for the phase 3 trial with 660 patients, which I think is just a testament of how many patients out there are interested in a pharmacologic treatment like this. We’re hopeful that we’ll get the results out there in about a year from now and, fingers crossed, there’s some promising results that give patients another treatment option.”
In a previous phase 2 trial, dubbed MARIPOSA (NCT05071612), treatment with AD109 demonstrated statistically significant improvements on both objective and subjective outcomes in patients with OSA. The study featured 211 patients (41% female) with a median age 55 (48-60) years and BMI of 32.2 (28.0-35.2) kg/m2 who were randomized to AD109, atomoxetine, or placebo. All told, AHI4 was reduced from a median of 20.5 to 10.8 events/hour in the AD109 2.5mg/75 mg dose (P <.001 vs placebo).3
Additional data showed that 41% of participants who completed the study achieved an AHI below 10 when treated with AD109, 44% had greater than 50% reduction from baseline, and 15%. Of treated patients had an 80% or greater reduction. Notably, atomoxetine, dosed as a monotherapy, did not improve daytime OSA symptoms, and statistically significantly worsened nighttime sleep subjectively and by the measurement of total sleep time, indicating that atomoxetine alone is an inappropriate therapy for OSA.
AD109-treated patients also demonstrated statistically significant improvements vs placebo in PROMIS-Fatigue, a scale of daytime functioning (P <.05). The investigational agent also showed a trend towards statistically significant on scales measuring other important OSA symptoms such as PROMIS-Sleep Impairment and PROMIS-Sleep Disturbance.
REFERENCES 1. Apnimed Announces Positive Topline Results in the First Landmark Phase 3 Clinical Trial of AD109, an Investigational Once-Daily Oral Pill for Obstructive Sleep Apnea. News Release. Apnimed. Published May 19, 2025. Accessed June 25, 2025. https://apnimed.com/article/ad109phase3toplineresults/ 2. Apnimed Announces Completion of Enrollment in Phase 3 LunAIRo Study of AD109, the Potential First Nighttime Oral Treatment for Obstructive Sleep Apnea. News Release. Apnimed. Published May 9, 2024. Accessed June 25 2025. https://apnimed.com/article/apnimed-announces-completion-of-enrollment-in-phase-3-lunairo-study-of-ad109-the-potential-first-nighttime-oral-treatment-for-obstructive-sleep-apnea/ 3. Apnimed Presented Positive Phase 2b Results on AD109, an Investigational Oral Drug for Obstructive Sleep Apnea, for the First Time at ATS 2023. News release. Apnimed. May 21, 2023. Accessed June 25, 2025. https://apnimed.com/article/apnimed-presented-positive-phase-2b-results-on-ad109-an-investigational-oral-drug-for-obstructive-sleep-apnea-for-the-first-time-at-ats-2023/
Increasing environmental events driven by climate change and human activity exacerbate allergy and asthma conditions, further compounded by exposure to persistent pollutants like per-and polyfluoroalkyl substances and microplastics. | Image Credit: Habibur – stock.adobe.com
Allergy and asthma were linked with environmental events that are increasing in prevalence alongside natural disasters and other extreme weather events, including algal blooms, floods, heat stress, wildfires, and thunderstorms that are coinciding with emissions of per-and polyfluoroalkyl substances (PFAS) and microplastics as downstream outcomes of these environmental events, according to a study published in Current Allergy and Asthma Reports.1
Human activities, primarily the burning of fossil fuels, are largely responsible for the greenhouse gas emissions driving these environmental changes. Weather intensity like droughts and floods have experienced dramatic rises over the past 5 years, based on data from NASA.2 Extreme weather is occurring more frequently, becoming longer-lasting, and more severe.
The respiratory tract is highly vulnerable to these environmental stressors.1 Asthma, a common chronic disease, affects nearly 25 million Americans and is exacerbated by air pollutants and extreme weather. Similarly, allergic rhinitis, eczema, and food allergies, reported by 1 in 3 adults and 1 in 4 children in the US, are worsened by conditions like high temperatures and thunderstorms. As environmental threats increase respiratory contaminant exposure, continued investigation into these intertwined health outcomes is crucial.
Extreme heat events, or heat waves, are becoming more frequent, intense, and prolonged. This poses a higher risk of premature death from respiratory diseases, especially for vulnerable populations such as children, older adults, pregnant individuals, and those with chronic conditions. Heat stress commonly exacerbates asthma by increasing inflammation, activating sensory fibers, and disrupting epithelial barriers, leading to bronchoconstriction.
High temperatures can also alter cytokine expression and T helper cell ratios, affect mucus production, and disrupt airway structural proteins. The interplay between environmental substances and extreme heat requires further research to understand additive, synergistic, or antagonistic health effects. Additionally, longer pollen seasons are introducing new allergenic species, likely worsening asthma and allergy cases.
Warmer weather, earlier snowmelt, and hotter spring and summer temperatures are escalating the intensity, frequency, and duration of wildfires. These fires release harmful emissions like carbon monoxide, carbon dioxide (CO2), nitric oxide, ozone, particulate matter, volatile organic compounds, and polycyclic aromatic hydrocarbons.
Exposure to wildfire smoke is directly linked to more emergency department visits for respiratory issues, as well as increased respiratory illness and mortality. Perinatal wildfire smoke exposure can lead to earlier use of upper respiratory medications and a higher risk of respiratory birth defects in children. Wildfire smoke also worsens asthma symptoms and increases asthma-related hospitalizations, particularly for young children. Epigenetic changes may contribute to these health outcomes, requiring further research.
The expansion of the wildland-urban interface, where human development meets wildlands, increases the risk of human-ignited wildfires. Fires in these areas are unique because they burn not only biomass but also homes, vehicles, and other synthetic materials, creating a distinct and poorly understood pulmonary toxicity profile. According to the authors, a key goal is to develop effective interventions to prevent adverse wildfire smoke exposure outcomes for communities, especially vulnerable populations like those with asthma and allergic rhinitis.
Changing temperatures, weather patterns, and water acidification from increased CO2 emissions have altered average surface water conditions, which in turn increases the risk of harmful algal blooms by expanding both the geographic range and seasonal growth windows of the different marine and freshwater phytoplankton species that comprise harmful algal blooms. While harmful algal blooms may seem like a niche public health burden, 15% of global asthma cases in coastal regions can be attributed to aerosolized harmful algal blooms toxins. Pulmonary exposure to harmful algal blooms has linked toxins to rapid onset of respiratory irritation symptoms such as cough and congestion, along with increases in hospital admission rates for respiratory diseases. The distance harmful algal blooms aerosols can travel is also unclear, especially as it relates to the size of the at-risk population and the mixtures of aerosolized harmful algal blooms toxins amongst other atmospheric copollutants.
Floods, whether from sea or freshwater, heighten the risk of respiratory diseases, infections, and asthma exacerbations. This is primarily due to mold and microbial growth in flooded buildings. The sensitization to mold and fungi spores creates a proinflammatory environment, triggering conditions like allergic asthma and allergic rhinitis. Further research is needed to understand chronic flood-induced pulmonary issues and identify the specific mold and fungal strains responsible.
Thunderstorm asthma is a global phenomenon characterized by an increase in asthma attacks after thunderstorms. It’s likely caused by a combination of high aeroallergen concentrations like ryegrass pollen, rain, and storm conditions that bring pollen to ground level. During a storm, pollen grains can rupture into smaller, more easily aerosolized subparticles due to physical disturbances. While fungal spores are abundant aeroallergens, their link to asthma exacerbations and thunderstorm asthma is not yet firmly established.
PFAS are pervasive, persistent organic compounds used in consumer goods for their nonstick properties. Their strong carbon-fluorine bonds make them extremely difficult to degrade, posing a significant threat to environmental and human health. Humans are exposed through ingestion, absorption, and inhalation. PFAS exposure can alter inflammasome function in the lung, impacting immune response. Further research is needed to establish comprehensive limits, legislation, and public awareness regarding these chemicals.
Microplastics are expected to increase in the environment and human bodies due to climate change impacts like increased precipitation and melting glaciers. Once released, microplastics do not easily degrade, persisting in environmental media. Inhaled microplastics, with their hydrophobic surfaces, may carry other pollutants and are linked to adverse respiratory outcomes such as irritation, interstitial lung disease, wheezing, and inflammation. More research is needed to understand their biological effects on pulmonary health, exposure routes, internal transport, and overall impact.
“In the future, meta-analyses to quantify the health effects of natural disasters could be an important tool to inform public health measures. It is thus especially relevant for the scientific community also to begin exploring prevention and mitigation techniques in preparation for future disasters,” the authors concluded.
References
Chou CK, Winker R, Rebuli ME, et al. Respiratory health impacts from natural disasters and other extreme weather events: the role of environmental stressors on asthma and allergies. Curr Allergy Asthma Rep. 2025(25);3-19. doi:10.1007/s11882-025-01206-9
Harrabin R. Nasa data reveals dramatic rise in intensity of weather events. The Guardian. June 17, 2025. Accessed June 30, 2025. https://www.theguardian.com/world/2025/jun/17/nasa-data-reveals-dramatic-rise-in-intensity-of-weather-events
Advanced lab-grown tissues help show how special lung cells develop, shedding light on rare ACDMPV disease and suggesting potential ways to repair damage from viral infections such as COVID-19
CINCINNATI, June 30, 2025 /PRNewswire/ — A team of experts at Cincinnati Children’s reports another powerful step forward in organoid medicine: success at making human lung tissue that can produce its own blood vessels.
Their findings, published in the same month as a similar success involving liver organoids, reflect a new wave of advanced lab-grown tissues that can be used immediately in many research applications while moving ever closer to serving as living tissues that can directly repair damaged organs.
Whole-mount staining of embryonic mouse lung alveolar vasculature (white) and epithelium (pink). Source: Yifei Miao and Hill Chang.
Details were posted online June 30, 2025, in the journal Cell.
“Prior to our study, the development of lung organoids with organotypic vasculature had not been achieved,” says co-corresponding author Mingxia Gu, MD, PhD. “Notably, this method also could be applied to other organ systems such as intestine and colon.”
Gu, now at UCLA, was a member of the Center for Stem Cell and Organoid Medicine (CuSTOM) and Division of Pulmonary Biology at Cincinnati Children’s while this research was conducted. Co-first and co-corresponding author Yifei Miao, PhD, (now at the Chinese Academy of Sciences, Beijing) also was with Cincinnati Children’s for this work. Co-corresponding author Minzhe Guo, PhD, remains with Cincinnati Children’s along with several co-authors involved in this study.
Overcoming a major challenge
Researchers have been working for years to grow organoids — sometimes called “organs in a dish.”
Creating organoids involves converting mature human cells (such as blood or tissue cells) back into fetal-like stem cells that can be coaxed into growing a wide range of other tissue types. Unlike disconnected human cells kept alive in a dish, these are growing, developing mini-organs that form into seed-sized spheres that mimic the unique functions of full-sized organs.
Intestines that absorb and secrete. Stomachs that produce digestive acids. Hearts that pulse. Brain tissues with firing nerve cells and so on.
Cincinnati Children’s has been a leader in organoid development since 2010 when experts here produced the world’s first functional intestinal organoid grown from induced pluripotent stem cells (iPSCs).
More recently, the challenge has been learning how to grow organoid tissues that can connect with the rest of the body to integrate nerve connections, blood vessels, bile ducts, immune systems and more. During pregnancy, these differing tissue types naturally find each other as the fetus matures and becomes more complex. Organoid developers seek to re-produce these steps in the laboratory, which eventually may allow people to receive custom-grown tissues that could patch damage or boost disrupted functions.
Simpler forms of organoids have already begun transforming medical research, allowing many scientists to use living human tissue models to study disease while reducing current reliance on animal models to develop new medicines. But without the ability to make internal blood vessels, the tiny seeds lack the ability to grow into larger, more useful tissues.
How the team solved the vascular riddle
The new study thoroughly recounts the results of many experiments the team conducted to demonstrate success at inducing blood vessel formation. The work spanned four years and involved more than 20 people at Cincinnati Children’s plus collaborations with experts at several other organizations.
“The challenge in vascularizing endodermal organs, particularly the lung, stems from different signaling requirements for lung epithelial versus vascular differentiation,” says Miao. “Our success in this endeavor is attributable to our unique differentiation method.”
In essence, the team grew iPSCs from multiple cell types then found the right moment to introduce them to each other. The resulting cell signals helped flip a developmental switch so that progenitor cells that could have become either blood vessels or the outer walls of the lung wound up becoming blood vessels. In achieving this vital step, the team:
Produced lung organoids that include respiratory bronchial epithelial cells (RAS cells), a human cell type not previously reported in conventional lung organoid models.
Pinned down the developmental moments when a rudimentary gut tube begins to send some cells to form the lungs while sending other cells to form the stomach and intestine. While the basic steps of this transformation have been studied in animals, it had not been possible to study this stage of development in humans without killing fetuses.
Demonstrated that the rare disease ACDMPV occurs when cell signaling “crosstalk” gets disrupted during this early blood vessel formation stage. Within days of birth, infants born with Alveolar Capillary Dysplasia with Misalignment of Pulmonary Veins (ACDMPV) struggle to breathe because their lungs’ air sacs (alveoli) and blood vessels are malformed. Nearly all infants with this condition die within the first month of life, according to the National Organization for Rare Disorders.
Revealed key functional information about the cells involved in gas exchange inside the human lung. Their learnings help explain the damage within tiny blood capillaries that occurs in the lungs in response to injuries. These new clues offer fresh ideas for developing ways to protect and potentially restore affected lung tissues.
What’s Next?
Cincinnati Children’s has filed patent applications related to the methods developed here to produce organoids with blood vessel formation capabilities and the CuSTOM team is moving to further develop this technology.
“We look forward to continuing to learn more about the fundamental biology involved in organ formation and applying those discoveries to improving outcomes across a wide range of difficult human diseases and conditions,” says Aaron Zorn, PhD, co-director of CuSTOM and director of the Division of Developmental Biology.
In addition to publishing these findings in Cell, co-authors plan to present their work at the Keystone conference in Kyoto, Japan (iPSCs: Progress, Opportunities, and Challenges) in January 2026.
About the study
Cincinnati Children’s co-equal first authors were Miao, Nicole Pek, BS, and Cheng Tan, MD.
Contributing co-authors from Cincinnati Children’s were Cheng Jiang, MS, Zhiyun Yu, PhD, Kentaro Iwasawa, MD, PhD, Min Shi, MD, PhD, Daniel Kechele, PhD, Nambirajan Sundaram, PhD, Victor Pastrana-Gomez, MSTP student, Debora Sinner, PhD, Cheng-Lun Na, PhD, Keishi Kishimoto, PhD, Jason Tchieu, PhD, Jeffrey Whitsett, MD, Kyle McCracken, MD, PhD, Michael Helmrath, MD, James Wells, PhD, Takanori Takebe, MD, PhD, and Aaron Zorn, PhD.
Contributing co-authors included experts from Harvard Medical School, Icahn School of Medicine at Mount Sinai, Sophia Children’s Hospital (The Netherlands), Boston University
This research also was supported by the Discover Together Biobank, the Bio-Imaging and Analysis Facility, and the Integrated Pathology Research Core at Cincinnati Children’s and the University of Cincinnati Proteomics Laboratory.
Funding sources for this work included: the National Institutes of Health (R01HL166283, DK128799-01, N01-75N92020C00005 and R01HL095993); an Endowed Scholar Award from the Cincinnati Children’s Research Foundation; the American Heart Association (1013861 and 906513); the Falk Transformational Awards Program; and the Brigham Research Institute.
Learn more about working with CuSTOM
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SOURCE Cincinnati Children’s Hospital Medical Center
June is Men’s Health Awareness Month. In recognition of this event, we spoke with Justin Dubin, MD, a urologist at Memorial Healthcare Systems in South Florida, about the current landscape of care in men’s health.
Dubin acknowledged that while progress has been made in normalizing conversations around issues such as erectile dysfunction, stigma around men’s health conditions remains a large concern in 2025. This has created an opportunity for artificial intelligence (AI) to take off in this space, with many men turning to large language models to find information.
“Men being men, we always want to fix problems ourselves,” Dubin explained. “And instead of going to talk with a provider, they go online. Initially it was social media. It has advanced to things like podcasts and naturally, Dr. Google, Dr.TikTok, and has now progressed to Dr. ChatGPT.”
Dubin touched on both sides of this issue, highlighting both the challenges with AI in health care as well as the potential opportunities for use in the men’s health space.1 One such opportunity is in patient education. Technology such as ChatGPT gives patients the chance to take ownership of their health, allowing them to better understand health concerns, ask informed questions, and feel more confident about seeking care.
For health care professionals, this also means a shift in the way they’re delivering care, with a new focus on making sure that men are using the right tools.
“In general, this is a very interesting time in men’s health. I think a lot of men who [were] always interested in having autonomy over their education and how they learn and autonomy over their bodies, finally have an opportunity to do that in a good way,” Dubin concluded. “You have a lot of information and a lot of opportunity for autonomy at your hands. It’s just really having the appropriate guidance to do so.”
REFERENCE
1. Panken EJ, Patel AU, Schammel J, Dubin J. Man and machine: exploring the intersection of artificial intelligence and men’s health. Curr Opin Urol. 2025;35(3):236-242.
The study focused on samples from individuals who had self-identified as having European or African ancestry. First, the researchers objectively measured the ancestral geographic origins written into the skin samples’ DNA by analyzing genetic markers known as single nucleotide polymorphisms. The team then injected each sample with dengue virus, observed the samples’ subsequent immune responses over a 24-hour period and compared them.
