Category: 8. Health
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IIT Bombay’s chemistry camp makes science accessible for visually impaired students through multi-sensory experiments
Chemistry came alive in a reimagined form at the 75th Yusuf Hamied Chemistry Camp for Visually Challenged Students, hosted at the Indian Institute of Technology (IIT), Bombay.
Whether it’s the vibrant red and green flames of strontium and barium salts during a flame test or the striking ‘golden rain’ formed by the reaction between lead nitrate and potassium iodide, the visual drama of chemical reactions is often what captivates students. The very spectacle that makes chemistry so appealing can also become a significant barrier, shutting visually impaired students out of the full experience while leaving educators grappling with how to make the subject accessible to everyone.
Guided by the belief that chemistry is for everyone, this inclusive education project set out to go beyond the usual high school chemistry experiments. The team redesigned the experiments to engage touch, smell and sound. The result was a rich, multi-sensory experience that allowed 59 visually impaired students from schools in Mumbai, Nasik, Pune and Solapur to explore the wonders of chemistry.
The initiative was supported by the Royal Society of Chemistry (RSC) and Yusuf Hamied, chairman of Cipla.
The camp introduced a new handbook featuring six hands-on experiments developed by Chandramouli Subramanian of IIT Bombay, which were translated into braille. Students were divided into small groups, and each experiment was run by a volunteer from the institute, enabling the students to carry out the activities independently.
‘Science must be accessible to all,’ said Swetavalli Raghavan, head of innovation strategy and government affairs at the RSC. ‘This initiative helps break the myth that chemistry is a visual science. With the right tools and teaching methods, we can open up the world of scientific inquiry to every learner, regardless of ability.’
When light becomes sound
Tactile chemistry kits, featuring textured materials, raised diagrams and braille labels, have helped make science more accessible for students with visual impairments. But Subramaniam pointed out that these kits can be costly for schools. Therefore, his team focused on adapting experiments usually included in the school curriculum.
A school science fair classic, the potato battery experiment shows how a vegetable can power a small electronic device. By inserting two different metals, typically zinc and copper, into a potato, students create a simple electrochemical cell that generates a small voltage that can power low-energy devices, such as LEDs. The team simply replaced the LED with a buzzer.
In designing the activity, the team also aimed to give students a broader understanding of energy conversion. As Subramaniam explained, the experiment became a starting point for a larger conversation – tracing how plants absorb solar energy through photosynthesis, store it as chemical energy in the form of sugars, and how that same energy, now held in a potato or lemon, can be released and transformed into sound through a simple electrochemical reaction.
Experiments involving heat were handled with extra care. These included an esterification, where a carboxylic acid and an alcohol reacted in the presence of an acid catalyst to yield a fruity-scented ester when heated in an oil bath. Unlike other activities where students did most of the work themselves this step required hands-on support from the volunteers.
In addition to pre-measuring the chemicals and carefully supervising each step. ‘One great thing that [the] professor suggested was to put on blindfolds and do your experiments one or two times, so that you’re sensitised to their experiences,’ says Devashish Bhave, a volunteer at the camp. ‘We even tried each other’s experiments with blindfolds on to check if our instructions were clear enough.’ He highlighted that this exercise was a powerful reminder that what might seem simple or obvious with sight becomes much more complex without it.
‘Doing the experiment 72 times might sound repetitive, even boring, but it was one of the best experiences I’ve had in a lab,’ adds Devashish. ‘Each time a student dropped Mentos into the [fizzy drink] bottle and sealed it with the balloon-fitted cap, the balloon began to expand as gas was released. I would ask them to feel the balloon becoming bigger. The joy and excitement that they had on their faces made every single time worth it.’
In conversations with volunteers, several students shared that they had arrived at the camp feeling hesitant, even afraid of the lab, due to past experiences. However, by the end, they felt hopeful about pursuing a career in science.
‘We have chemistry as a subject in school, but the experiments in the syllabus were always taught verbally, we never had the chance to do them ourselves,’ says Saee, one of the workshop participants. ‘This was the first time I experienced chemistry hands-on, and it gave me the confidence to know I’m capable of doing these experiments. Now, I’m excited to explore even more.’
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How to avoid Covid and other viruses this summer
Summer beckons with opportunities for travel, socialising, and sunshine.
But these months can be the ideal conditions for fostering the spread of viruses and bacterial infections.
Prioritising health during these warmer months is crucial.
After all, a positive Covid test or a severe case of food poisoning can swiftly derail holiday plans.
To ensure a healthy and enjoyable sunny season, experts have compiled eight essential tips to help you steer clear of illness.
A positive Covid test can swiftly derail holiday plans 1. Stay hydrated and cool
“Heat-related illnesses are more common than many people realise during the summer, especially when temperatures climb or humidity is high,” says Dr Chun Tang, GP at Pall Mall Medical. “The best line of defence really is prevention, so keep hydrated, wear light, breathable clothing, and avoid strenuous activity during the hottest parts of the day, typically between 11am and 3pm.
“If you start to feel unwell, stop, find somewhere cool to rest, sip water, and use a damp cloth to cool your skin. If symptoms worsen, particularly if you stop sweating or feel confused, don’t delay seeking medical attention.”
2. Stick to cooked foods and bottled water
Summer is prime time for foodborne illness.
“Warm weather and outdoor meals, picnics, barbecues, street food, create ideal conditions for bacteria like salmonella, E. coli, and listeria, especially when food isn’t cooked properly or stored safely,” warns Tang. “To reduce the risk, keep perishable foods cold in a cooler or fridge right up until serving.
“Cook meats thoroughly and don’t leave food out for more than an hour or two in the heat.”
Dr Ireny Salama, GP and aesthetic doctor at London-based wellness and longevity clinic The HVN, agrees and adds: “It’s often the “fresh” things like ice cubes and salads that cause trouble abroad. Stick to bottled water and cooked dishes when you’re unsure about local hygiene standards.”
3. Keep up to date with vaccinations
Summer holidays can increase the risk of exposure to viruses “While COVID-19 doesn’t follow seasonal patterns like the flu, summer holidays and gatherings can increase the risk of exposure, particularly in crowded indoor spaces,” highlights Tang.
“New variants continue to emerge, and immunity from previous infection or vaccination may decrease over time. Keeping up to date with vaccinations, including any boosters, remains one of the most effective ways to protect yourself from Covid.”
4. Build a summer wellness travel kit
“Four essentials: a foldable fan, rehydration sachets, a cooling mist and hand sanitiser, are simple but surprisingly powerful when you need them,” says Salama.
5. Practice good hand hygiene
Practice good hand hygiene before eating COVID-19, food poisoning and gastroenteritis can often be avoided by maintaining proper hand hygiene.
“Practice good hand hygiene before eating,” advises Tang. “Alcohol hand gels are helpful, but soap and water is your best bet when available.”
6. Protect yourself from mosquito-borne illnesses
Mosquito-borne diseases continue to pose a significant risk in tropical and subtropical regions.
“Dengue fever, Zika virus, and malaria are all transmitted via mosquito bites, and with climate change, we’re seeing these illnesses in new regions too,” says Tang. “Protection is key. Use an insect repellent with DEET, sleep under mosquito nets where appropriate, and wear long sleeves and trousers, especially around dawn and dusk when mosquitoes are most active.
“If you’re travelling to a high-risk region, speak with your doctor well in advance about any recommended vaccines or antimalarial medication.”
7. Regularly reapply sunscreen
Even mild sunburn can lead to harm over the years Don’t let your desire for a sun-kissed tan compromise your health.“Sunburn might feel like a short-term nuisance, but over time, repeated exposure to UV radiation can lead to serious skin damage and significantly raise the risk of skin cancer, including melanoma,” warns Tang. “Even mild burns accumulate harm over the years.“To protect your skin, apply a broad-spectrum sunscreen (SPF30 or above) generously, and reapply every two hours, more often if swimming or sweating. If you do get sun burnt, cool the skin with damp cloths or a cool bath, use moisturiser (aloe vera or unscented creams can help), and drink plenty of water.”
8. Adjust sleep schedule ahead of a long-haul flight
Adjusting your sleep schedule several days before your trip will help you start your holiday feeling refreshed and energised.“Long-haul travel can disrupt your internal body clock, causing sleep disturbances, digestive issues and general fatigue,” says Tang. “Travelling east tends to make symptoms worse, and it can take a few days to feel back to normal.“To reduce the impact of jet lag, try adjusting your sleep schedule a few days before travel. Once you arrive, get outside during daylight hours to help reset your rhythm.”
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Electric field treatment restores movement to rats with spinal injuries – Physics World
Electric field treatment restores movement to rats with spinal injuries – Physics World
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TissueTinker’s bioprinted tumors offer new cancer drug testing model
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McGill University’s spinout TissueTinker is exploring a new bioprinting approach that could improve the way cancer drugs are tested in preclinical settings.
Co-founded by Benjamin Ringler, Madison Santos, and Isabelle Dummer, the startup recently received a Develop award from the McGill Innovation Fund (MIF) to advance its miniature tumor model platform.
Designed as a human-relevant alternative to 2D cultures and animal testing, the miniature models aim to reduce the 90% failure rate of cancer drugs after preclinical testing by better capturing tumor complexity and improving predictability early on.
“Because the testing environment more readily simulates the human body, researchers can better assess and understand whether or not their drug works before reaching clinical trial stages,” Ringler detailed. “This is key for drug progression and curbing financial waste in the industry.”
McGill Innovation Fund team TissueTinker is reimagining how we test cancer therapies with customizable, human-relevant bioprinted tumor models that replicate human tissue. Photo via McGill University. Miniature models offer customization edge
TissueTinker’s platform centers on bioprinting tumor models at a scale of around 300 µm, a size the team considers optimal for balancing biological relevance with resource efficiency.
Using bioink made from living cells, the models are constructed to include both healthy and cancerous tissue types, positioned with spatial precision. This structure enables the replication of key physiological features, such as hypoxic cores, that influence how tumors grow and respond to treatment.
The platform’s design allows researchers to adjust both the structure and cell composition of each tumor model, depending on the specific biological question being studied. This adaptability makes it possible to replicate a wide range of tumor conditions, offering more targeted insights into how treatments behave under different physiological scenarios.
This approach gains added relevance under updated US Food and Drug Administration (FDA) guidelines, which now allow drug developers to use human-based models in place of animal testing during preclinical research. By offering a method that reflects the complexity of human tumours more accurately, TissueTinker provides a practical option within this shifting regulatory landscape.
Backed by support from the MIF, the team has refined both the technical and strategic dimensions of the platform. In addition to funding, the program provided mentorship that helped the founders focus on long-term development. They are now working to expand their tumor model library and plan to license the platform to pharmaceutical companies and research institutions.
Rethinking drug testing with bioprinted tumors
With cancer responsible for 10 million deaths in 2020 and cases expected to surpass 28 million by 2040 as referenced by McGill, many are seeking more efficient approaches to drug development.
Previously, Edinburgh-based tumor 3D printing specialist Carcinotech and bioprinting firm CELLINK partnered to advance cancer drug development by creating standardized protocols for bioprinted tumor models built from cancer cell lines. These models were designed to replicate the physiological makeup of specific cancer types, incorporating five key cell types in accurate ratios to improve testing relevance.
CELLINK BIO CELLX 3D biodispenser. Photo via CELLINK. Developed for use with CELLINK’s BIO CELLX system, the protocols were expected to enable automated and reproducible 3D cell culture workflows, streamlining drug screening processes. The partnership built on earlier work combining Carcinotech’s expertise in tumor modeling with CELLINK’s bioinks and bioprinting technology to enhance precision in preclinical research.
In 2021, researchers at the University of Stuttgart and Robert Bosch Hospital developed a 3D printed tissue platform designed to improve cancer drug testing while reducing the need for animal experiments.
As part of a €3.8 million initiative funded by the state of Baden-Württemberg, the team used bioprinting and simulation data to create skin-like microfluidic structures that more closely mimic tumor behavior in the human body. Their approach combined ex-vivo, de-novo, and in-silico strategies, producing modular, nutrient-loaded cell structures that can be assembled like “lego bricks” to simulate realistic tumors and better predict drug distribution outcomes.
What 3D printing trends should you watch out for in 2025?
How is the future of 3D printing shaping up?
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Featured image shows McGill Innovation Fund team TissueTinker is reimagining how we test cancer therapies with customizable, human-relevant bioprinted tumor models that replicate human tissue. Photo via McGill University.
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DNA barcodes can make drug discovery screens miss potential medicines | Research
Drug discovery efforts based on DNA-encoded chemical libraries are inadvertently overlooking numerous potential drug candidates, new research shows.
Each molecule in a DNA-encoded chemical library is tagged with a unique DNA sequence that acts like a barcode. Such libraries have revolutionised early drug discovery by allowing researchers to screen millions, if not billions, of compounds simultaneously. And the resulting datasets are often used to train machine learning models that seek out promising drug candidates.
Keen to understand how reliable data linked to DNA-encoded chemical libraries actually is, Raphael Franzini, from the University of Utah in the US, and colleagues investigated a library with over 58,000 compounds designed to target enzymes involved in DNA repair and cancer. When they synthesised and tested 33 molecules that screens had dismissed, they discovered that these compounds were often just as effective as those flagged as promising. In particular, various screens nearly missed compounds that were structurally similar to olaparib, an approved cancer drug.
‘We found that DNA-encoded library data often labels good molecules as bad molecules,’ explains Franzini.
The problem appears to lie with the DNA barcodes themselves. When the team compared molecules with and without these tags, they found that the DNA reduced molecules’ activity. The effect was even more pronounced when molecules were tested against targets they were not originally designed for.
Laura Guasch, a computational chemist at pharmaceutical company Roche, Switzerland, describes the findings as ‘a highly relevant contribution’. She says the study ‘raises crucial awareness regarding how these numerous false negatives can impair the increasingly popular machine learning algorithms used in this domain.’
‘False negatives introduce substantial noise and bias into training datasets, causing machine learning models to learn misleading patterns or ignore valid chemotypes,’ comments Srinivas Chamakuri, an assistant professor at Baylor College of Medicine’s Center for Drug Discovery in the US.
Franzini and colleagues demonstrated that even when machine learning models appeared to perform well, they were actually just recognising recurring structural fragments rather than developing genuine predictive capabilities.
‘A primary implication of this study is the significant risk that current drug discovery programs might be overlooking potential drug candidates due to high rates of false negatives,’ notes Guasch.
The researchers found that removing unreliable data from the training sets and focusing only on confirmed active compounds dramatically improved models’ ability to identify promising drugs. This suggests that current machine learning approaches in drug discovery may need fundamental changes to account for the inherent biases in screening data.
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Hot Dogs, Soda, and a 540,000-Person Warning: Ultra-Processed Foods Shorten Life – SciTechDaily
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Radiation Bridging in CAR T: Where Are We Now?
While the use of radiation bridging therapy (BT) in chimeric antigen receptor (CAR) T-cell therapy for blood cancer is expanding, plenty of unanswered questions remain on topics such as ideal timing and doses, a radiologist cautioned hematologist colleagues.
The lack of guidelines has immediate clinical implications, said John P. Plastaras, MD, PhD, professor of radiation oncology at the Hospital of the University of Pennsylvania, Philadelphia, in a presentation at 18th International Conference on Malignant Lymphoma (ICML) 2025 in Lugano, Switzerland.
“This actually just came up the other day when one of our medical colleagues said, ‘I’m really worried about this patient. They’re ready for CAR T cell, but I think you need to radiate this area. Can you do it a week after [therapy]?’ The answer is, ‘We don’t know.’”
On the other hand, clinicians now have clarity about safety and interaction with CAR T-cell therapy, he noted, and data is coming in rapidly.
Here are some questions and answers about radiation BT:
What is BT in CAR T-cell therapy?
BT refers to treatment that provides a “bridge” for patients between the components of CAR T-cell therapy.
As a 2024 report about BT in hematologic cancer explained, the treatment “is delivered after leukapheresis for CAR T-cells” — the process in which white cells are removed from a patient’s blood, which is then returned to the body — “has been completed and before lymphodepleting chemotherapy and CAR T-cell infusion.”
The report said “patients who receive BT are predominantly those with a higher disease burden and rapidly progressive disease. These patients tend to have worse overall outcomes, likely related to their aggressive underlying disease.”
Where does radiation fit into BT?
According to the 2024 report, “combination chemoimmunotherapy has typically been the form of BT that is used most often.” Targeted therapy is another option, the report said, although data is from “very small sample sizes.”
And then there’s radiation, which the report said is useful “particularly in patients with limited sites of disease or patients who are at risk for structural complications such as airway compromise or renal dysfunction.”
What do we know about radiation’s efficacy?
The first oral report on bridging radiation in CAR T-cell therapy only appeared in 2018, Plastaras said, followed by the first published report in 2019. Despite this fairly short time period, “we are certainly seeing a lot of new data,” Plastaras said.
He highlighted the newly released International Lymphoma Radiation Oncology Group (ILROG) study of radiation BT in conjunction with CAR T-cell therapy for relapsed/refractory B-cell lymphomas. The retrospective study of 172 patients at 10 institutions treated from 2018 to 2020 showed that 1- and 2-year progression-free survival (PFS) rate was 43% (95% CI, 36-51) and overall survival rate was 38% (95% CI, 30-45).
In a multivariable model, comprehensive radiation BT was linked to superior PFS than focal therapy (hazard ratio, 0.38; 95% CI, 0.22-0.63; P < .001).
“Comprehensive radiation was a very strong predictor for improved PFS, but we did not see was a huge dose effect,” said Plastaras, who coauthored the study.
What about toxicity?
Questions about other clinical matters were resolved prior to 2022, he said, when CAR T-cell therapy was used primarily in third line and later settings.
“Does radiation cause excess toxicities?” he asked. “A lot of the single-institution studies answered that, and I think most medical oncologists and hematologists are okay with this idea that radiation isn’t causing a lot of excess toxicities.”
As for whether radiation interferes with the effectiveness of CAR T-cell therapy, “the data to this point have demonstrated that probably not,” he said. “We’ve probably put that one to bed.”
What do we know about treatment timing?
“The timing question is still quite open,” Plastaras said. “How much time should there be between radiation and lympho-depleting chemotherapy? Is it better to put the radiation very close to the CAR T-cell [therapy] so this priming effect might happen, or can that happen weeks in advance? We don’t know the answers to those.”
According to Plastaras, researchers are still trying to understand the role radiation the consolidation period after CAR T-cell therapy. “If we wait for day-30 PET [scan], is that OK? Do we need to wait longer? Are we going to mess up the lymph nodes that have CAR T-cells floating around in them?”
What about doses and imaging?
There’s also a lack of insight into technical questions about radiation dose and fractionation. “The [radiation] volume question is one of key importance. Do we just do gross disease? Do we treat all the other small spots out there, and importantly, do we treat regional nodes or not? We get these questions all the time.”
The role of imaging is also unclear, he said, in terms of timing during and after bridging radiation therapy and after CAR T-cell therapy.
What do we need to learn about now?
Looking forward, Plastaras outlined what he called “version 2.0” questions for the evolving field: Can radiation rebulking decrease CAR-T cell toxicities? Will very low dose “priming” radiation affect outcomes?
He highlighted other questions: Can radiation be part of a combined modality approach in limited stage relapsed/refractory disease? Should central nervous system lymphoma be treated differently?
When will we get new guidelines?
According to Plastaras, Memorial Sloan Kettering Cancer Center Radiology Oncologist Brandon Imber,MD, MA, in New York City, is leading a new ILROG guideline project with the intention of publishing details in the journal Blood. “This is a work in progress,” Plastaras said. “Our target is 2025 to at least get something submitted.”
Plastaras had no disclosures.
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Rare Lung Cells Mitigate Smoke & Virus Damage
A rare cell in the lining of lungs is fundamental to the organwide response necessary to repair damage from toxins like those in wildfire smoke or respiratory viruses, Stanford Medicine researchers and their colleagues have found. A similar process occurs in the pancreas, where the cells, called neuroendocrine cells, initiate a biological cascade that protects insulin-producing pancreatic islet cells from damage.
Treating the airways of mice with an experimental drug that activates the repair pathway protected their airways from damage after infection with influenza or the virus that causes COVID-19. Conversely, animals in which the pathway was blocked experienced much more severe damage to their airways.
Activating the signaling pathway initiated by airway or pancreatic neuroendocrine cells in a similar way in humans might enhance the ability of firefighters and those with respiratory illnesses to avoid permanent lung damage, the researchers believe. They also suspect it could help prevent people with metabolic syndrome from progressing to diabetes.
“This whole signaling cascade both protects and regenerates vulnerable cells in the airway and the pancreas,” said Philip Beachy, PhD, professor of urology and of developmental biology. “If this circuit is disrupted, the damage is much worse — specialized airway cells are lost, and the stem cells can’t divide to repair the damage. We think it’s likely to be important in many other tissues in the body.”
Although the study was conducted in mice, there are tantalizing clues of a similar pathway in humans: People treated with a cancer drug that blocks the pathway are twice as likely as their peers to develop diabetes after their treatment.
“The association is highly significant and gives us early hints that activating this pathway might be protective for people with metabolic syndrome who are beginning to lose beta cell function,” Beachy said.
Beachy, who is the Ernest and Amelia Gallo Professor and a member of the Stanford Stem Cell Institute, is the senior author of the research, which was published online June 9 in Cell. Research scientist William Kong, PhD, is the study’s first author.
Neuroendocrine cells are less than 1% of the total number of cells in the cells that line the airway, which is made up of a type of tissue called epithelium. Some of them cluster together in what are called neuroepithelial bodies and play an important role in sensing oxygen levels and modulating immune responses in the lungs. But others, especially those in the tracheal airway, are solitary, nestled alone among other types of epithelial cells. It’s not been clear until now exactly what function these solitary neuroendocrine cells perform.
The hedgehog family
Beachy’s laboratory has focused on the function of a protein family called Hedgehog proteins since Beachy identified the first member in fruit flies in 1992. Members of the family are best known for their critical function in embryo patterning in early development, but they also aid in the rejuvenation of many types of tissue. Desert hedgehog is one of the least studied of the three family members (the others are Sonic hedgehog and Indian hedgehog).
Previous work in Beachy’s lab showed that stem cells in the epithelial lining of the bladder respond to a signal cascade initiated by Sonic hedgehog to regenerate the bladder lining after bacterial infection. They wondered if hedgehog proteins were involved in the repair of damage in other epithelial tissues like the airway.
When Kong used a technique called bulk RNA sequencing to search for genetic messages encoding any of the hedgehog family members in the cells of the trachea, they detected a faint signal for the Desert hedgehog protein, but not for the other two family members. When they engineered mice in a way that caused cells expressing the Desert hedgehog protein to become fluorescent, they saw that the solitary neuroendocrine cells were making the Desert hedgehog protein.
Further research showed that the Desert hedgehog protein leaves the epithelium and travels into the layer of tissue beneath the epithelium, called the mesenchyme. There, it triggers cells to begin producing another protein called Gli1. When the airway cells sense damage, Gli1 induces the expression of a protein called IL-6 that triggers stem cells in the epithelium called basal cells to begin dividing and specializing to repair the damage.
This crosstalk between tissue layers, which the researchers call epithelial-mesenchymal feedback, protects and regenerates specialized cells in the lung epithelium, including multi-ciliated cells that use their feathery arms to sweep particles and viruses out of the lungs and secretory cells that make mucus to trap unwanted invaders. In the absence of these cells, viruses and toxins can penetrate much more deeply into the lungs
Protective process
The entire process happens within hours of toxin exposure in a coordinated cascade that eventually includes even non-Gli1-expressing cells of the airway.
“At each stage, the signal is amplified until the entire trachea is impacted,” Beachy said. “This rapid response not only protects the epithelial cells from dying but it also activates a regenerative response.”
The consequences of impeding this protective message are severe.
“If this signal cascade is disrupted, the damage is much worse. Ciliated and secretory cells are lost, and the basal cells don’t divide. In fact, it’s all they can do to stretch out and try to cover the injured area,” Kong said.
Both Desert hedgehog and Gli1 are critical to the repair process. Mice unable to produce Desert hedgehog or Gli1 were much more sensitive to exposure to sulfur dioxide gas, which is an environmental pollutant and mimics the damage inflicted by other inhaled toxins. While control mice lost 85% of ciliated cells and 41% of secretory cells within 24 hours, mice lacking the protein lost 96% of ciliated cells and 88% of secretory cells during the same time.
Activating the hedgehog signaling pathway with a small molecule dramatically increased cell survival after sulfur dioxide exposure: 66% of ciliated cells and 82% of secretory cells survived in treated animals, versus 9.7% of ciliated cells and 43% of secretory cells in control animals.
Kong next tested the effect of the Desert hedgehog pathway activation on mice infected with influenza and the virus that causes COVID-19. Although no mice unable to make Gli survived more than five days after infection with influenza, all mice treated with the small molecule activator survived at least eight days after infection. Mice infected with the virus that causes COVID-19 that were unable to activate the Desert hedgehog pathway suffered extensive loss of ciliated cells in the airway.
Finally, the researchers turned their attention to the pancreas, which has a similar tissue organization as the airway. They found that the insulin-producing beta cells, which are a type of neuroendocrine cell, also make Desert hedgehog and that the organ exhibits the same epithelial-mesenchymal feedback loop with IL-6 to protect the vulnerable cells.
The researchers are now exploring whether and how the hedgehog pathway could be activated in humans to prevent lung damage in people exposed to airborne toxins or who are at risk for diabetes.
“We have reasons to think it might not be a good idea to activate the hedgehog pathway long term,” Beachy said. “We are considering how to stimulate the pathway in a targeted way, either delivering it to the airway with an aerosol or targeting it to the pancreas. And we have early hints it might be possible.”
Reference: Kong W, Lu WJ, Dubey M, et al. Neuroendocrine cells orchestrate regeneration through Desert hedgehog signaling. Cell. 2025;0(0). doi:10.1016/j.cell.2025.05.012
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