Researchers from North Carolina State University have found that multiple species of Gardnerella, bacteria sometimes associated with bacterial vaginosis (BV) and pre-term birth, can coexist in the same vaginal microbiome. The findings add to the emerging picture of Gardnerella’s effects on human health.
Gardnerella is a group of anaerobic bacteria that are commonly found in the vaginal microbiome. Higher levels of the bacteria are a signature of BV and associated with higher risk of pre-term birth, but it is also found in women who have no sign of disease.
“We were trying to understand diversity within Gardnerella,” says Ben Callahan, associate professor of population health and pathobiology at NC State and corresponding author of the work. “Scientists have only recently begun to look at individual Gardnerella species, so we don’t know yet whether different species might have different health effects. So our main aim was to explore the ecology of Gardnerella.”
The unique challenge in sequencing the vaginal microbiome is that any samples will be predominantly composed of the host’s DNA, which makes extracting microbial data more expensive and time consuming. The research team’s first job was to establish a methodology that allowed them to identify distinct species of Gardnerella from the microbiome data.
“The available tools to study the vaginal microbiome would consider all Gardnerella as the same species,” says Hanna Berman, postdoctoral research scholar at NC State and lead author of the work. “To even be able to do this work, we had to create our own database of Gardnerella genomes and devise a method to identify the different Gardnerella species. Hopefully this will also allow more researchers to be able to study Gardnerella diversity.”
The research team looked at sequencing data from three cohorts: two random populations of pregnant women, and one population with a history of pre-term birth. They analyzed the metagenomic sequences of Gardnerella from the samples to see if there was a relationship between a particular Gardnerella species and pre-term birth.
While they didn’t find a “smoking gun,” they did make two surprising findings.

First, they identified a potential 14th species of Gardnerella among the samples — prior to this work only 13 species had been identified.
They also saw that in the majority of samples in which Gardnerella was present, multiple species of Gardnerella coexisted in the same microbiome: anywhere from two to as many as all 14 known Gardnerella species were found in single samples.
“Normally if a species of bacteria has colonized an environment, we expect it to exclude close relatives that would occupy the same environmental niche and consume the same resources,” Callahan says. “I often say that with bacteria all things are possible, but this is still unusual. We also saw that when the overall microbial load is higher, Gardnerella is a higher proportion of the microbial load.
“Evidence continues to build that Gardnerella has an association with pre-term birth, but the details of that relationship are complicated. In this work, we didn’t find one bad species of Gardnerella — they may all be bad. This is far from the end of the story.”
The researchers hope to explore questions of species coexistence and microbiome composition further in future work.
“The vaginal microbiome has been understudied,” Callahan says. “For example, it is often dominated by one species of Lactobacillus, which creates an environment that excludes other bacteria. When it isn’t there, Gardnerella is. So how do the bacteria interact?
“Answering these questions may lead to more effective treatments for BV, and for ways to predict and avoid pre-term birth. This work is an important step in that process.”
The research appears in mSystems and is supported by funding from the Eunice Kennedy Shriver National Institute of Child Health and Human Development under Award Numbers 5F31HD104353 and 730 K99HD090290, the National Institutes of Health NIGMS under award R35GM133745, and the March of Dimes. NC State student Megan Anderson, Daniela Aliaga Goltsman of Metagenomi, Inc., and David Relman of Stanford University also contributed to the work.

The brain is often referred to as a “black box” — one that’s difficult to peer inside and determine what’s happening at any given moment. This is part of the reason why it’s difficult to understand the complex interplay of molecules, cells and genes that underly neurological disorders. But a new CRISPR screen method developed at Scripps Research has the potential to uncover new therapeutic targets and treatments for these conditions.
The method, outlined in a study published in Cell on May 20, 2024, provides a way to rapidly examine the brain cell types linked to key developmental genes at a scale never done before — helping unravel the genetic and cellular drivers of different neurological diseases.
“We know that certain genetic variations in our genome can make us vulnerable or resilient towards different diseases, but which specific cell types are behind a disease? Which brain regions are susceptible to the genome mutations in those cells? These are the kinds of questions we’re trying to answer,” says senior author Xin Jin, PhD, an assistant professor in the Department of Neuroscience at Scripps Research. “With this new technology, we want to build a more dynamic picture across brain region, across cell type, across the timing of disease development, and really start understanding how the disease happened — and how to design interventions.”
Thanks to over a decade’s efforts in human genetics, scientists have had access to long lists of genetic changes that contribute to a range of human illnesses, but knowing how a gene causes a disease is very different than knowing how to treat the illness itself. Every risk gene may impact one or several different cell types. Comprehending how those cell types — and even individual cells — impact a gene and affect disease progression is key to understanding how to ultimately treat that disease.
This is why Jin, along with the study’s first author, Xinhe Zheng, a PhD candidate and the Frank J. Dixon Graduate Fellow at Scripps Research, co-invented the new technique, named in vivo Perturb-seq. This method leverages CRISPR-Cas9 technology and a readout, single-cell transcriptomic analysis, to measure its impact on a cell: one cell at a time. Using CRISPR-Cas9, scientists can make precise changes to the genome during brain development, and then closely study how those changes affect individual cells using single-cell transcriptomic analysis — for tens of thousands of cells in parallel.
“Our new system can measure individual cells’ response after genetic perturbations, meaning that we can paint a picture of whether certain cell types are more susceptible than others and react differently when a particular mutation happens,” Jin says.
Previously, the method for introducing the genetic perturbations into the brain tissue was very slow, often taking days or even weeks, which created suboptimal conditions for studying gene functions related to neurodevelopment. But Jin’s new screening method allows for rapid expression of perturbation agents in living cells within 48 hours — meaning scientists can quickly see how specific genes function in different types of cells in a very short amount of time.
The method also enables a level of scalability that was previously impossible — the research team was able to profile more than 30,000 cells in just one experiment, 10-20 times accelerated from the traditional approaches. In many of the brain regions they examined, such as the cerebellum, they were able to collect tens of thousands of cells that previous labeling methods could not reach.
In a pilot study using this new technology, Jin and her team’s interest was piqued when they saw a genetic perturbation elicit different effects when perturbed in different cell types. This is important because those impacted cell types are the sites of action for particular diseases or genetic variants. “Despite their smaller population representations, some low-abundant cell types may have a stronger impact than others by the genetic perturbation, and when we systematically look at other cell types across multiple genes, we see patterns. That’s why single-cell resolution — being able to study every cell and how each one behaves — can offer us a systematic view,” Jin says.
With her new technology in hand, Jin plans to apply it to better understand neuropsychiatric conditions and how certain cell types correspond with various brain regions. Moving forward, Jin says she’s excited to see this type of technology applied to additional cell types in other organs in the body to better understand a wide range of diseases in terms of tissue, development and aging.

A certain biological pathway, a set of linked reactions in the body, drives the inflammation seen in the skin disease psoriasis, a new study finds. The work could lead to improved therapies for all inflammatory skin diseases, including atopic and allergic dermatitis and a type of boil called hidradenitis suppurativa, say the study authors. Inflammation is the body’s natural response to irritation and infection, but when out of control, it can lead to the reddish, flaky, itchy lesions that come with these skin diseases.
Led by researchers at NYU Langone Health, the new study found that the interleukin-17 (IL-17) pathway, whose activity is blocked by existing anti-inflammatory drugs, activates a protein called hypoxia inducible factor 1-alpha (HIF-1-alpha) in psoriasis. Researchers say that IL-17 has long been known to be active in inflammation, but the role of HIF-1-alpha has until now been unclear.
The research team also found that HIF-1-alpha let inflamed skin cells more actively break down sugar for energy, supporting their metabolism and leading to the production of a waste product called lactate. When consumed by inflammatory T cells, lactate triggered production of IL-17, fueling even more inflammation.
Publishing in the journal Immunityonline May 20, the findings show that in human skin tissue samples from people with psoriasis, measures of gene activity around IL-17 and HIF-1-alpha were similar, suggesting that these factors are interconnected. Experiments in mice treated to develop psoriasis found that subsequent treatment with an experimental drug that blocks the action of HIF-1-alpha, called BAY-87-2243, resolved inflammatory skin lesions.
Further, skin samples from 10 patients successfully treated with anti-inflammatory drug etanercept showed diminished activity for both IL-17 and HIF-1-alpha, suggesting to researchers that when IL-17 is blocked, so is HIF-1-alpha.
“Our study results broadly show that activation of HIF-1-alpha is at the crux of metabolic dysfunction observed in psoriasis and that its action is triggered by IL-17, another key inflammatory-signaling molecule,” said corresponding study author Shruti Naik, PhD, associate professor at NYU Grossman School of Medicine in the Departments of Pathology and Medicine, and the Ronald O. Perelman Department of Dermatology.
Further experiments were performed on skin samples from five patients with psoriasis whose healthy and inflamed skin was separately treated with either BAY-87-2243 or an existing combination of topical drugs (calcipotriene and betamethasone dipropionate). Researchers then compared differences in inflammatory gene activity as a measure of impact and found that the HIF-1-alpha inhibitor had a greater effect than existing topical drugs. Specifically, skin samples that responded to HIF-1-alpha therapy had 2,698 genes that were expressed differently, while standard-of-care-treated samples had 147 differently expressed genes.

Genetic analysis of skin samples from another 24 psoriatic patients treated with the IL-17A-blocking drug secukinumab showed only decreased, not heightened, gene activity connected to HIF-1-alpha when compared to HIF-1-alpha gene activity in nine healthy patients with no psoriatic disease. Researchers say this indicates HIF-1-alpha’s blocked action was codependent on blockage of IL-17.
Additional experiments in mice showed that blocking sugar (glucose) uptake in the skin slowed psoriatic disease growth by limiting glucose metabolism, or glycolysis. Both the number of immune T cells tied to inflammation and the cell levels of IL-17 also decreased. The researchers found further that levels of lactate, the main byproduct of glycolysis, in psoriatic skin cell cultures dropped once exposed to the glycolysis-inhibiting drug 2-DG.
Directly targeting lactate production in psoriatic mice using a topical skin cream containing lactate dehydrogenase, which breaks down lactate, also slowed disease progression in the skin, with reduced numbers of inflammatory gamma-delta T cells and reduced IL-17 activity. Gamma-delta T cells were shown to take up lactate and use it to produce IL-17.
“Our findings suggest that blocking either HIF-1-alpha’s action or its glycolytic metabolic support mechanisms could be effective therapies for curbing the inflammation,” added Naik, who is also the associate director for NYU Langone’s Judith and Stewart Colton Center for Autoimmunity.
“Evidence of HIF-1-alpha’s depressed action, or downregulation, could also serve as a biomarker, or molecular sign, that other anti-inflammatory therapies are working,” said study co-senior investigator Jose U. Scher, MD, the Steere Abramson Associate Professor of Medicine in the Department of Medicine at NYU Grossman School of Medicine.
Scher, who also serves as director of NYU Langone’s Psoriatic Arthritis Center and the Judith and Stewart Colton Center for Autoimmunity, says the team plans to develop experimental drugs that can block HIF-1-alpha and lactate action in the skin “to end the underlying vicious cycle of IL-17-driven inflammation in skin disease. Our research fundamentally expands the scope of feasible therapeutic options.”
Naik points out that while many available therapies for psoriasis, including steroids and immunosuppressive drugs, reduce inflammation and symptoms, they do not cure the disease. She said further experiments are needed to refine which experimental drug works best, with respect to HIA-1-alpha inhibition, before clinical trials could start. Indeed, Naik and study co-lead investigators Ipsita Subudhi and Piotr Konieczny have a patent application pending (U.S. application number 63/540,794) for inflammatory skin disease therapies derived from their work on HIA-1-alpha inhibition.

More than 8 million Americans and 125 million worldwide are estimated to have psoriatic disease. The condition affects men and women equally.
Funding support for the studies was provided by National Institutes of Health grants P30AR075043, R01AR080436, R01AI168462, UC2AR081029, K22AI135099, K99AR083536, T32AR069515, TL1TR001447, UL1TR001445, and DP2AR079173. Additional funding was provided by the National Psoriasis Foundation, the Judith and Stewart Colton Center for Autoimmunity, the Beatrice Snyder Foundation, the Riley Family Foundation, the American Association of Immunologists, the International Human Frontier Science Program, the Charles H. Revson Foundation, and the Pew-Stewart Scholar Award 00034119, as well as the New York Stem Cell Foundation.
Naik serves on the advisory boards of Seed Inc. and as a consultant for BiomX. She also receives research funding from Takeda Pharmaceuticals. Scher has served as a consultant for Janssen, Pfizer, UCB, and BMS. He also receives research funding from Janssen and Pfizer. All of these arrangements are being managed in accordance with the policies and practices of NYU Langone Health.
Besides Naik, Scher, Subudhi, and Konieczny, other NYU Langone investigators were Aleksandr Prystupa, Rochelle Castillo, Erica Sze-Tu, Yue Xing, Daniel Rosenblum, Ilana Reznikov, Ikjot Sidhu, Cynthia Loomis, Catherine Lu, and Aristotelis Tsirigos. Other study co-investigators were Niroshana Anandasabapathy, at Weill Cornell Medicine; Mayte Suarez-Farinas, at the Icahn School of Medicine at Mount Sinai; and Johann Gudjonsson, at the University of Michigan.

Researchers at the Icahn School of Medicine at Mount Sinai have designed a regenerative medicine therapy to speed up diabetic wound repair. Using tiny fat particles loaded with genetic instructions to calm down inflammation, the treatment was shown to target problem-causing cells and reduce swelling and harmful molecules in mouse models of damaged skin.
Details on their findings were published in the May 20 online issue of the Proceedings of the National Academy of Sciences (PNAS).
Diabetic wounds, often resistant to conventional treatments, pose serious health risks to millions of people worldwide. Immune cells known as macrophages, which are supposed to help, end up causing inflammation instead. This inflammation harms other cells and makes it harder for the wound to heal properly and quickly.
Using lipid nanoparticles (LNPs) loaded with RNA encoding IL-4, a cell-to-cell signaling protein known as a cytokine, the therapy targeted dysfunctional macrophages while simultaneously reducing inflammation and “reactive oxygen species” (ROS) in diabetic wounds.
ROS molecules are produced naturally in the body during various metabolic processes and play roles in cell signaling and immune responses. However, excessive ROS production can lead to oxidative stress, causing damage to cells, proteins, and DNA. This stress is associated with various diseases and conditions, including inflammation and aging.
“In preclinical models, we basically showed the therapy’s ability to reprogram pro-inflammatory macrophages into reparative ones, leading to improved wound healing outcomes,” says Yizhou Dong, PhD, corresponding author of the study, Professor of Immunology and Immunotherapy, and a member of the Icahn Genomics Institute and the Marc and Jennifer Lipschultz Precision Immunology Institute at Icahn Mount Sinai. “Dysfunctional macrophages drive diabetic non-healing wounds, but we can reprogram them to stop the damage and instead help the healing process. We aim to promote faster and more effective wound closure by reprogramming these cells and modulating the inflammatory environment.”
Earlier this year, in a related study, Dr. Dong and colleagues reported on lipid nanoparticles that enhanced the tissue engineering and regeneration activity of adipose stem cells for treating diabetic wounds (Nature Communications).

While the results of the current study are encouraging, the researchers emphasize the need for a rigorous randomized controlled clinical trial to confirm safety and efficacy in humans.
“Our ultimate goal is to translate these findings into tangible benefits for diabetic patients. With further research and validation, this RNA-LNP therapy could potentially revolutionize diabetic wound management with one easily scalable application of a comparatively inexpensive therapeutic agent,” says Dr. Dong. “The study also suggests the potential for RNA-LNP therapeutics to be more generally designed to reprogram disease-causing macrophages in an organism, as pro-inflammatory macrophages are implicated in a wide range of diseases.”
The remaining authors are Siyu Wang, PhD (Icahn Mount Sinai); Yuebao Zhang, PhD (Ohio State University); Yichen Zhong, BS (Icahn Mount Sinai); Yonger Xue, PhD (Ohio State University, Icahn Mount Sinai); Zhengwei Liu, PhD (Icahn Mount Sinai); Chang Wang, PhD (Icahn Mount Sinai); Diana D. Kang, PhD (Ohio State University, Icahn Mount Sinai); Haoyuan Li, MD (Icahn Mount Sinai); Xucheng Hou, PhD (Icahn Mount Sinai); Meng Tian, PhD (Icahn Mount Sinai); Dinglingge Cao, PhD (Icahn Mount Sinai); Leiming Wang, PhD (Icahn Mount Sinai); Kaiyuan Guo, BS (Icahn Mount Sinai); Binbin Deng, PhD (Ohio State University); David W. McComb, PhD (Ohio State University); Miriam Merad, MD, PhD (Icahn Mount Sinai); and Brian D. Brown, PhD (Icahn Mount Sinai).
The study was funded in part by the National Institute of General Medical Sciences grant R35GM144117.

2 days agoZahra Fatima & Vicky Wong

A quarter of parents report that caffeine is basically part of their teen’s daily life, according to a national poll.
Two in three parents think they know whether their teen’s caffeine intake is appropriate and which products have too much caffeine. Yet a third aren’t able to identify recommended caffeine limits, according to the University of Michigan Health C.S. Mott Children’s Hospital National Poll on Children’s Health.
“Our report suggests parents may not always be aware of how much they should be limiting caffeine consumption for teens,” said poll co-director and Mott pediatrician Susan Woolford, M.D.
“Even for parents who know the recommendations, estimating their teen’s caffeine intake can be challenging.”
Soda is teens’ top caffeinated product of choice, according to the nationally representative report that’s based on responses from 1,095 parents of teens polled in February.
Tea and coffee came in as the second most popular caffeine source while less than a fourth of parents said their teen consumed energy drinks.
“Caffeine is a drug that stimulates the brain and nervous system, and too much of it can contribute to a variety of health problems in young people,” Woolford said.

“Teens’ brains are still developing, and excessive caffeine consumption can affect their mood, sleep, and school performance, along with other side effects. They can also become dependent over time, as is true for other drugs.”
What drives caffeine consumption among teens
Two in five parents whose teens consume caffeine most or all days of the week say their teen has it because it’s in their favorite product while less than a fourth say it’s because their peers drink it.
Fewer parents believe their teen drinks caffeine to stay awake during the school day, manage an early school start time or help with studying or focus.
“As parents appear to suggest that teens consume caffeine more for the taste than for the stimulant effect, it may be possible for parents to encourage the use of similar tasing options that are caffeine free,” Woolford said. “But parents may not even be aware that kids are drinking several caffeinated drinks a day and how it’s adding up.”
The good news, Woolford notes, is that the most common place teens consume caffeine is at home followed by dining out, making it easier for parents to intervene and help their teens reduce their caffeine intake. Just a third of teens consume caffeine with friends and a quarter consume it while in school, according to the report.

Woolford shares more findings from the poll and her top tips for monitoring caffeine in teens:
Know recommended caffeine limits
For healthy adults, 400 milligrams of caffeine per day is not generally associated with dangerous effects, according to the U.S. Food and Drug Administration. But the FDA has not given guidance for teens due to insufficient evidence, Woolford says.
The American Academy of Pediatrics also discourages caffeine intake by children and adolescents, and other experts suggest a limit of 100 milligrams per day for teens.
However, one in three parents polled thought the recommended daily limit was higher, Woolford says.
Monitor caffeine levels in your teen’s favorite foods and beverages
Sixty percent of parents polled say they’ve heard about the risks of highly caffeinated products but roughly half say they rarely look at caffeine amounts when buying beverages for their teen.
An 8-ounce cup of coffee has about 100 milligrams of caffeine, but the range of sizes and types of coffee drinks include many with excessive caffeine amounts, Woolford notes. Sodas, sports drinks and even certain brands of water can contain substantial amounts of caffeine.
Energy drinks are also consumed by teens, but a single one may contain up to 500 mg of caffeine along with added sugars.
Caffeine is also found in products that parents might not suspect, Woolford points out, such as gum, snack bars, and over-the-counter pain relievers.
“Parents can reduce their child’s risk of becoming caffeine dependent by checking product labels before purchasing any of these items for their family,” Woolford said.
Watch for signs your teen is overconsuming caffeine
People’s reactions to caffeine often depends on weight, gender, and caffeine sensitivity.
Common side effects from overconsumption may include insomnia, headaches, irritability and nervousness. Unfortunately, reducing or eliminating caffeine consumption may induce the same types of symptoms during withdrawal.
The effect of caffeine also wanes over time, Woolford notes, requiring higher amounts to get the same impact and increasing the risk of negative side effects.
“If your teenager regularly consumes caffeine and is having a hard time sleeping or if they appear jittery, you should take a closer look at whether their caffeine intake is too high,” Woolford said.
Model healthy caffeine consumption
Two-thirds of parents polled say they themselves consume caffeine most or all days of the week. A third have tried to cut back on their caffeine intake while 16% say their teen has tried to reduce caffeine consumption.
Many parents who report their teen consumes caffeine 0-3 days per week say that the family does not usually have caffeinated drinks at home or that the teen is trying to be healthy.
“Parents who have reduced their own caffeine consumption can draw on their experiences to help their teen establish a plan to cut back slowly to avoid withdrawal effects,” Woolford said.
Talk to your teen about caffeine
More parents of teens 16-18 years than 13-15 years report their teen has daily caffeine consumption.
The majority of parents think their teen has heard about the risks of too much caffeine from parents or other family members while others think they’ve learned about unhealthy caffeine levels from teachers, coaches, other school staff or a healthcare provider.
But it’s important that parents also have conversations with teens who may select caffeinated beverages from their school vending machines or spend their own money on caffeinated products.
“Parents should consider talking with their teen about the negative impact of excessive caffeine, and then explore non-caffeinated options they can try together at home, at school or when out with friends,” Woolford said. “Parents may also enlist the teen’s healthcare provider in explaining the risks of caffeine and suggesting strategies to cut back.”

For children seeking care at a California urban pediatric health center, extreme heat events were associated with increased asthma hospital visits, according to research published at the ATS 2024 International Conference.
“We found that both daily high heat events and extreme temperatures that lasted several days increased the risk of asthma hospital visits,” said corresponding author Morgan Ye, MPH, research data analyst, Division of Pulmonary and Critical Care Medicine, University of California, San Francisco School of Medicine. “Understanding the impacts of climate-sensitive events such as extreme heat on a vulnerable population is the key to reducing the burden of disease due to climate change.”
Ms. Ye and colleagues looked at 2017-2020 electronic health records from the UCSF Benioff Children’s Hospital Oakland, which included data on asthma hospital visits by patients of the hospital, some of whom are from Benioff Oakland’s Federally Qualified Health Center, and demographics including patients’ zip codes. They used data from the PRISM Climate Group of Oregon State University to determine the timing of daily maximum (daytime heat waves) and minimum (nighttime heat waves) for each zip code. The researchers restricted their analyses to the region’s warm season (June to September). To evaluate the potential range of effects of different heat wave measurements, they used 18 different heat wave definitions, including the 99th, 97.5th and 95th percentile of the total distribution of the study period for one, two or three days.
They designed the study in a way that allowed them to determine the association between each heat wave definition and a hospital visit. They repeated the analysis for Bay Area and Central California zip codes.
The team discovered that daytime heat waves were significantly associated with 19 percent higher odds of children’s asthma hospital visits, and longer duration of heat waves doubled the odds of hospital visits. They did not observe any associations for nighttime heat waves.
According to Ye, “We continue to see global temperatures rise due to human-generated climate change, and we can expect a rise in health-related issues as we observe longer, more frequent and severe heat waves. Our research suggests that higher temperatures and increased duration of these high heat days are associated with increased risk of hospital visits due to asthma. Children and families with lower adaptation capacity will experience most of the burden. Therefore, it is important to obtain a better understanding of these heat-associated health risks and susceptible populations for future surveillance and targeted interventions.”
The authors note that past research has suggested positive associations between extreme heat and asthma, but findings regarding hospitalizations and emergency room visits have been conflicting. Additionally, many other studies have focused on respiratory hospitalizations and not hospitalizations for asthma, specifically, and have not included or had a focus on children. This study is also unique because it investigated the effect of daily high temperatures but also the effects of persistent extreme temperatures.
The San Francisco Bay Area and California overall are unique areas of interest because the state is considered a coastal region with less prevalence of cooling units, such as air conditioners. While temperatures may not reach the extremes experienced in other parts of the country, this study demonstrates that even milder extreme heat temperatures may significantly impact health. These effects are more pronounced in climate-susceptible populations, including children and those who are medically vulnerable, such as those served by the urban pediatric health center in this study. The authors hope these study results will lead to more equitable health outcomes and reduce racial/ethnic disparities observed in climate-sensitive events.
“These results can be used to inform targeted actions and resources for vulnerable children and alleviate health-related stress during heat waves,” they conclude.

University of East Anglia researchers have made a significant breakthrough in ocular device technology with the introduction of a novel resin for 3D printing intraocular devices. This innovation has potential to enhance the manufacture of eye implants universally used in cataract and refractive surgeries.
An artificial intraocular lens (IOL) is primarily required for people with cataracts, a condition where the eye’s natural lens becomes cloudy, obscuring vision.
They can also be also used to correct refractive errors such as myopia (nearsightedness), hyperopia (farsightedness) and presbyopia (when eyes gradually lose the ability to see things clearly up close, as a normal part of aging).
Lead author Dr Aram Saeed, Associate Professor in Healthcare Technologies at UEA’s School of Pharmacy, said: “For the first time, we have developed a resin that can be used to print ocular devices directly.
“While still in the early stages, the ability to 3D print these lenses could significantly enhance eye care for patients by offering unprecedented levels of customisation and design precision, potentially leading to better clinical outcomes.”
Historically, IOLs have been made from a variety of materials, including glass and silicone, although more recently the industry has significantly evolved to predominantly use acrylic materials.
Currently hydrophilic and hydrophobic acrylic are the most commonly used materials due to their excellent optical clarity, flexibility, biocompatibility with the body and for their stability and safety within the eye.

Current methods of making IOLs use lathing and moulding techniques. While these methods offer the production of well-engineered and high-optical quality devices, they also come with inherent limitations, particularly in terms of design complexity and customisation.
Dr Aram Saeed said: “3D printing could significantly enhance the production of ocular devices, not only improving speed and precision in manufacturing but also enabling greater complexity and customisation in design.
“Our proof-of-concept paper is the first in a series that will detail our developments in this area and set the stage for transforming eye care practices globally.
“Our work combines material science with healthcare technology and requires extensive know-how in developing these types of ocular devices.
“As we continue to publish our findings and share our advancements, we aim to be at the forefront of the industry, working with industrial partners and researchers worldwide to refine and enhance the technology.”
Although still in the early stages of development, the innovation could potentially have several advantages: Tailored Lenses: 3D printing could create lenses customised to each patient’s eye shape and vision needs, potentially improving vision correction and comfort.

Faster Production: Compared to traditional methods, 3D printing has the potential to enable quicker design, testing, and manufacturing of lenses. This speed could reduce the time between diagnosis and surgery, providing faster care to patients. Complex Designs: 3D printing makes it possible to create intricate lens shapes that were previously difficult to manufacture. These designs could better address a wider range of vision problems. Cost Reduction: By using 3D printing, the production cost of custom or high-quality lenses may decrease, making them more affordable for more patients, particularly in economically disadvantaged regions. This could lead to better overall public health outcomes. Compatibility with Imaging: The researchers hope that combining 3D printing with advanced imaging technologies in the future could help produce lenses that fit individual patients’ eyes optimally, reducing the need for adjustments or complications after surgery. The study found that the 3D printed lenses have good optical clarity, can be folded, and implanted into a human capsular bag.
Co-author Michael Wormstone, Emeritus Professor at UEA’s School of Biological Sciences, said: “If successful in further developments, this new technology could transform the industry by enabling portable manufacturing solutions, especially beneficial in remote and economically disadvantaged areas.
“It also has the potential to support the production of premium, customised lenses that could enhance surgical outcomes in more advanced healthcare settings.”
The team’s efforts have been recognised with the awarding of a United States patent, assigned to UEA Enterprise Limited, a business entity of the university focused on fostering innovation and commercialising research.
The UEA researchers continue to work closely with industry partners to refine the technology.
For example, further work has been underway to ensure the process works accurately on a larger scale and to increase the printing resolution to improve the dimensional accuracy.
It is hoped that clinical trials could start in the next few years.
Dr Saeed and Prof Wormstone have a strong partnership with the ophthalmology department at Norwich and Norfolk University Hospital (NNUH), which brings valuable clinical insights and visionary approaches to their work, with both UEA and the hospital members of the pioneering Norwich Research Park.
Mr Anas Injarie, a leading consultant ophthalmologist at NNUH with more than 20 years of experience, said: “This innovation has the potential to enable the production of lenses that match patient specifications in design and optical performance.
“For premium markets, it represents an exciting possibility to provide tailored treatments that could enhance patient satisfaction and surgical success.”
The research was funded by the University of East Anglia through the Innovation Development Fund and Proof-Of-Concept grants; the Humane Research Trust; and the Engineering and Physical Sciences Research Council (EPSRC).
Further funding was provided by UEA’s Impact Acceleration Account (IAA) funding from the Medical Research Council (MRC).
‘Stereolithographic Rapid Prototyping of Clear, Foldable, Non-refractive Intraocular Lens Designs: A Proof-of-Concept Study’ is published in the journal Current Eye Research.

Researchers from the University of Toronto, Canada, and Kyushu University, Japan, have found that increased neuron formation and the subsequent rewiring of neural circuits in the hippocampus through exercise or genetic manipulation helps mice forget traumatic or drug-associated memories. The findings, reported on May 8 in Molecular Psychiatry, could offer a new approach to treating mental health conditions like post-traumatic stress disorder (PTSD) or drug addiction.
PTSD is a mental health condition that can be triggered by experiencing or seeing a traumatic event, such as a natural disaster, serious accident, or attack. Worldwide, around 3.9% of the general population has PTSD, with symptoms including vivid flashbacks and avoidance behaviors, such as staying away from places or pushing away people that remind them of the traumatic event. Currently, PTSD is often treated through therapy or medications such as anti-depressants, but as many people do not respond effectively, researchers are still looking for different treatments.
In this study on mice, Assistant Professor Risako Fujikawa from Kyushu University’s Faculty of Pharmaceutical Sciences, her former supervisor Professor Paul Frankland from the University of Toronto, and their team members including Adam Ramsaran focused on how neurogenesis — the process of forming new neurons — in the hippocampus impacts the ability to forget fear memories. The hippocampus, a brain region important for forming memories linked to specific places and contexts, produces new neurons daily in an area called the dentate gyrus.
“Neurogenesis is important for forming new memories but also for forgetting memories. We think this happens because when new neurons integrate into neural circuits, new connections are forged and older connections are lost, disrupting the ability to recall memories,” explains Fujikawa. “We wanted to see if this process could help mice forget stronger, traumatic memories too.”
The researchers gave mice two strong shocks in different settings. First, the mice were shocked after leaving a brightly-lit, white box and entering a dark, ethanol-scented compartment. After the second shock in another distinct environment, the mice showed PTSD-like behaviors. Over a month later, the mice were still fearful and hesitant to enter the original dark compartment, indicating they couldn’t forget the traumatic memory. This fear extended to other dark compartments, showing generalized fear. Additionally, the mice explored less in open spaces and avoided the center, suggesting anxiety.
The researchers then explored whether these PTSD-like behaviors could be alleviated through exercise, which studies had shown boosted neurogenesis. The double-shocked mice were split into two groups and one group was provided with a running wheel. Four weeks later, these mice showed increased numbers of newly-formed neurons in their hippocampi, and importantly, the PTSD-like behaviors were less severe, compared to the double-shocked mice without wheel access.
Furthermore, when the mice were free to exercise before the second shock, it also prevented some PTSD-like behaviors from developing.

However, since exercise impacts the brain and body in many different ways, it wasn’t clear whether the effect of exercise was due to hippocampal circuit rewiring by neurogenesis, or other factors. The researchers therefore used two different genetic approaches to assess the impact of newborn neuron integration into the hippocampus, exclusively.
Firstly, the researchers used a technique called optogenetics, where they added light-sensitive proteins to newly-formed neurons in the dentate gyrus, allowing the neurons to be activated by light. When they shone blue light on these cells, the new neurons matured faster. After 14 days, the neurons had grown longer, had more branches, and integrated more quickly into the neural circuits of the hippocampus.
In the second approach, the research team used genetic engineering to remove a protein in the newly-formed neurons that slows down neuron growth. This also resulted in the neurons growing faster and increased incorporation into neural circuits.
Both these genetic approaches reduced PTSD-like symptoms in mice after double-shocking and shortened the time taken for the mice to forget the fear memory. However, the researchers found that the effect was weaker than they saw with exercise, and did not reduce the level of the mice’s anxiety.
“It could be that the neurogenesis and the re-modeling of the hippocampus circuits disrupt fear memory, but have less effect on mood or emotions,” suggests Fujikawa. “Exercise also has broader physiological effects, which may contribute to the stronger outcomes seen.”
Finally, the research team explored whether increased neurogenesis and hippocampus re-modeling could also help in other mental disorders where memory plays an important role, such as substance use disorders. For people battling drug dependency, relapse often happens when reminders, like being in a similar environment where the drug was used, trigger powerful cravings.

The researchers placed mice in a cage with two rooms. In one room, the mice were given a saline solution and in the other room, they were given cocaine. Afterward, when given free access to both rooms, the mice spent more time in the room in which they had received cocaine.
However, when the researchers used exercise and genetic methods to boost neurogenesis and hippocampus re-modeling, they found that the mice stopped showing a preference for the room where they had taken cocaine, suggesting the mice had forgotten the link between the room and the drug.
For future research, Risako is planning to find a drug that can boost neurogenesis or hippocampus re-modeling, in the hopes that it could be tested as a potential treatment for PTSD and drug dependence. However, she also stressed the importance of exercise.
“In our experiments, exercise had the most powerful impact on reducing symptoms of PTSD and drug dependence in mice, and clinical studies in humans also show it is effective,” says Risako. “I think this is the most important takeaway.”

In some severe cases of COVID-19, the lungs undergo extreme damage, resulting in a range of life-threatening conditions like pneumonia, inflammation, and acute respiratory distress syndrome. The root cause of those wide-ranging reactions in the lungs has until now remained unclear.
A new study by researchers at Columbia and the Columbia University Irving Medical Center sheds light on this mystery. The study found that ferroptosis, a form of cell death first named and identified at Columbia in 2012, is the major cell death mechanism that underlies COVID-19 lung disease. The finding indicates that deliberately halting ferroptosis with therapeutic drug candidates could improve COVID-19 outcomes.
“This finding adds crucial insight to our understanding of how COVID-19 affects the body that will significantly improve our ability to fight life-threatening cases of the disease,” said professor Brent Stockwell, one of the study’s lead authors.
Ferroptosis was first reported by professor Stockwell in 2012. Ferroptosis is an unusual form of cell death in which certain cells die because their outer fat layers collapse. It differs from the most common kind of cell death, which occurs both in disease contexts and in normal processes like aging and involves cells chopping up the molecules in their interior.
Since proposing the concept of ferroptosis, Stockwell’s lab has demonstrated that it is instrumental to normal bodily processes, but that it can also attack and kill healthy cells in patients with neurodegenerative diseases like Parkinson’s, Alzheimer’s, and Lou Gehrig’s disease.
Though ferroptosis can be destructive, recent studies indicate that it could also be harnessed for good. Intentionally inducing ferroptosis could counteract diseases like cancer where rampant cell growth is dangerously occurring. The ability to inhibit ferroptosis, on the other hand, could offer doctors new ways of combating cell death that should not be occurring, as in the case of COVID-19 lung disease.
“We’re hopeful that these important new findings could improve our ability to confront this pernicious disease, which, in too many cases, still diminishes health outcomes and results in death,” Stockwell said.