Researchers at the Institute for Biomedical Sciences at Georgia State University have developed a vaccine platform designed to provide protection against a range of influenza virus infections by targeting conserved viral structures and inducing immunity at mucosal surfaces. The study, published in ACS Nano, details how the development of the novel vaccine uses cell-derived extracellular vesicles (EVs) engineered to display multiple influenza hemagglutinins (HAs) in an inverted configuration, which allows the immune system to recognize conserved regions shared across viral strains. In mouse models, the vaccine elicited cross-reactive antibodies, cellular immune responses, and mucosal immunity, providing protection against heterosubtypic H5N1 and H7N9 influenza virus challenges following intranasal administration.
“The influenza virus is smart. They have evolved to evade the immune system by hiding their critical conserved structures, rendering these elements poorly immunogenic,” said senior author Bao-Zhong Wang, PhD, a professor at the Institute for Biomedical Sciences at Georgia State.
The vaccine’s design centers on two key features: the use of extracellular vesicles (EVs) as a delivery platform and the inversion of HA proteins on their surface. EVs are natural nanoparticles involved in cell-to-cell communication and have been researched extensively for therapeutic delivery due to their biocompatibility. In this study, they were engineered to display multiple HA subtypes simultaneously. The HAs were presented in an upside-down orientation, which partially shields the highly variable head domain while exposing the conserved stalk domain. This structural arrangement directs the immune response toward regions less prone to mutation, enabling broader protection across influenza strains.
“These (vaccine responses) highlight that the inverted HA is a smarter strategy for inducing protective immunity to the conserved HA stalk. Meanwhile, cell-origin EVs are a biocompatible platform for mucosal vaccine delivery. Using EVs simultaneously displaying multiple inverted HAs is a powerful approach for developing universal influenza vaccines,” Wang added.
To test their vaccine design the researchers immunized mice intranasally with the EV-based vaccine, allowing researchers to assess mucosal immunity in addition to systemic responses. The data showed that the vaccine induced cross-reactive antibodies targeting HA stalks, virus-specific T cell responses, and a balanced Th1/Th2 immune profile. Importantly, the vaccinated mice were fully protected against lethal infections from reassortant H5N1 and H7N9 viruses.
The new vaccine designed was based on previous research into EV-based vaccine delivery and different strategies to target the HA stalk. Earlier studies had shown that EVs could serve as adjuvants and antigen carriers for intranasal vaccines. In addition, other research seeking to develop a universal influenza vaccine has focused on the conserved HA stalk domain, which evolves more slowly than the immunodominant head. As the researchers noted, “the conserved HA stalk domain has emerged as a promising candidate for a universal influenza vaccine due to its low evolutionary rate and greater tolerance to mutations.” However, previous approaches had used isolated HA stalk constructs, but faced shortcoming related to structural stability and immunogenicity.
By preserving the full HA ectodomain while inverting its orientation, the new design addressed these limitations. “Our findings suggest that utilizing the entire HA ectodomain as an immunogen, while hiding the HA head and increasing exposure of the HA stalk, is an effective strategy to induce robust immune responses targeting conserved HA epitopes,” the researchers wrote, noting that this approach allows the immune system to access structurally intact conserved regions.
If this vaccine design can be shown effective in humans, it could provide a vaccine with broader and longer-lasting protection against influenza, and reduce the need for frequent reformulations. The use of intranasal delivery could also change how vaccines are administered by targeting immune responses at the site of viral entry. “Mucosal vaccination effectively induces local immune responses, protecting against respiratory virus infections at the site of invasion,” the team noted.
Next steps for the team include continued characterization of the immune responses induced by the vaccine, to include the specificity and neutralizing capacity of antibodies, as well as evaluation of anti-EV immunity with repeated dosing. More animal studies, and eventually clinical trials, will be needed to assess safety, scalability, and efficacy in humans.
According to the World Health Organization, an estimated 1.4 billion adults aged 30–79 worldwide had hypertension in 2024, representing around one-third of the global population of that age. Of these, 44% were unaware that they were living with a leading risk factor for premature death and poor health worldwide due to its association with myocardial infarction, stroke, and kidney disease.
Despite the size of the hypertension problem, its diagnosis and treatment pathway has remained largely the same for decades.
A 60-year-old pathway
“The current pathway in hypertension diagnosis and treatment has really not changed in over 60 years,” said Sandosh Padmanabhan, MD, PhD, chair of pharmacogenomics and professor of cardiovascular genomics and therapeutics at the University of Glasgow in Scotland.
He explained that it is based on opportunistic detection of hypertension, which has traditionally been defined as a blood pressure (BP) of 140/90 mmHg in the clinic, although thresholds vary by measurement method and guideline. For example, out-of-office measures typically use lower cut-points (e.g., home/daytime ambulatory averages) of 135/85 mmHg.
Sandosh Padmanabhan, MD, PhD Professor University of Glasgow
Diagnosis typically occurs when a patient visits their primary care physician (PCP) or has a pharmacy BP check. Confirmation follows, ideally with out-of-office BP monitoring to avoid misclassification caused by one-off measurements.
Patients are then stratified by predicted 10-year cardiovascular risk, using risk calculators such as Q-risk or the PREVENT score, and treatment is based on a stepwise algorithm. First, patients are generally given lifestyle advice like reducing salt, alcohol, and caffeine intake, improving sleep, managing stress, and increasing exercise. This may give them a chance to reduce their BP without pharmacologic intervention.
If unsuccessful, depending on local guidelines, patients may be offered an angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker if under 55 years of age. Those over 55 years or of Black African or Caribbean origin are started on a calcium channel blocker. The next steps combine ACE inhibitors and calcium channel blockers, then add a thiazide-like diuretic, followed by spironolactone or other drugs.
However, this approach uses “a population-level logic,” said Padmanabhan. Although age and ethnicity are considered, “these are broad demographic proxies that don’t include any understanding of the individuals’ underlying pathophysiology or the genetic makeup.”
He stresses that, on a public health basis, the system works. There are multiple effective, low-cost antihypertensive drug classes and many generic options available that effectively lower BP. Despite this, control rates are poor. “Fewer than one in four hypertensive adults globally have their BP adequately controlled,” he said.
The measurement problem
Part of the issue lies in how BP is measured. “To give you an idea about the scale of inertia, we diagnose BP using a device that was introduced in the late 19th century,” Padmanabhan noted, referring to the sphygmomanometer invented by Scipione Riva-Rocci in 1896. Not only that, the technique can also be flawed. Variables such as incorrect cuff size, improper positioning, and patient movement can distort readings. Even talking during measurement can increase BP values by 5–9 mmHg or even higher.
Crucially, a single measurement provides little insight into cumulative lifetime exposure to high BP and can be skewed by issues like white coat hypertension or masked hypertension. “We look at the BP number, but the patients don’t experience that number. What they experience is a lifelong vascular risk,” Padmanabhan explained. “Treatment is not about a short-term reduction in a number. It’s about long-term sustained risk reduction.”
Yet the current system remains reactive and is not working well enough. “We have to move away from reactive diagnosis to proactive identification,” Padmanabhan said. “The earlier we measure accurately and respond systematically, the fewer surprises we’ll see later.”
Continuous monitoring
The pitfalls of opportunistic, or even planned, BP measurement are driving the emergence of new technologies capable of continuous monitoring.
Josep Solà, PhD CTO and Co-founder Aktiia
Josep Solà, PhD, began working on optical sensing technology in 2004 at the Centre for Electronics and Microtechnology in Switzerland. By analyzing subtle changes in reflected light caused by arterial dilation, it became clear that BP could be measured using these light signals. In 2018, this research was spun out into Aktiia, where Solà is CTO and co-founder. The company has developed and commercialized the Hilo band: a CE-certified wearable medical device designed for continuous, cuffless, BP monitoring that has been clinically validated against traditional ambulatory BP monitoring.
The band tracks BP and heart rate automatically, about 25 times per day, without requiring any action from users. Paired with an app, the device shows users daily, nightly, and long-term BP trends. It is currently available as a certified medical device across Europe, Australia, and Canada, and, following FDA approval in July 2025, the company is preparing for a U.S. launch.
Solà said he and co-founder Mattia Bertschi, PhD, were convinced they could change how hypertension is being managed today. He believes there is no good reason why most people with hypertension cannot control the condition. The medication is cheap and effective; the problem is that there has been no technology that patients can use to properly manage their condition.
“No one wants to use a cuff every day for the next 30 years,” said Solà. “They’re just so inconvenient, and you cannot expect people to proactively measure something they don’t feel.”
The Hilo band gives wearers a feedback loop that has historically been missing from BP measurement. Users can immediately see that reducing their salt or alcohol intake, for example, lowers their BP. “We are empowering people,” said Solà. “We are empowering them to look at the intervention, or combination of interventions, with or without medication, to see what is effective for them, and this reinforces their willingness to continue with the changes they are making.”
Credit: Hilo
Data published by Aktiia has shown that this approach works. A study of 8,950 U.K.-based Hilo users indicated that individuals who monitored their BP continuously showed better control over time. Specifically, users over 50 years of age appeared able to prevent the age-related rise in systolic BP typically seen in the general population, which the researchers say “may reflect greater awareness, stronger treatment adherence, and lifestyle changes prompted by continuous feedback.”
Wearables at scale: Opportunity and caution
Beyond dedicated monitoring devices like the Hilo band, smartwatches and other devices are increasingly capable of detecting physiological signals associated with cardiovascular risk. The Apple Watch can detect potential signs of chronic hypertension by analyzing heart rate sensor data over 30-day periods, the Huawei Watch D provides on-demand and 24-hour ambulatory BP monitoring using an air-filled strap, while the team behind the Oura ring is developing a “Blood Pressure Profile” feature to detect early signs of hypertension.
Although this represents a significant step toward embedding cardiovascular monitoring into everyday life, the increasing use of these devices raises important questions about accuracy, interpretation, and clinical integration, particularly as they often rely on indirect signals rather than direct BP measurement.
Adam Bress, PharmD Researcher University of Utah
As Adam Bress, PharmD, from the Spencer Fox Eccles School of Medicine at the University of Utah, and colleagues have recently shown, translating wearable-derived signals into meaningful clinical information is not straightforward.
They evaluated the hypertension alert feature of the Apple Watch, which has a published sensitivity of 41% and specificity of 92%, meaning that approximately 59% of individuals with undiagnosed hypertension would not receive an alert, while about eight percent of those without hypertension would receive a false alert.
“The problem there, is that this data only tells you how the alert works in a very controlled, limited population,” said Bress. “In order to understand how it’s going to work in the real world, we need to know how the true prevalence of undiagnosed hypertension varies in the population and in subgroups and to what degree.”
Using data from nearly 4,000 adults in the U.S., Bress and colleagues showed that the pretest probability of having hypertension has a significant impact on the reliability of the alert. For example, among adults under 30 years of age, the pretest probability of having hypertension is 14%. A positive alert on the Apple Watch would increase this probability to 47%, whereas no alert reduces the probability to 10%.
However, for adults aged 60 years and older, an alert increases the probability of an individual having hypertension from a pretest level of 45% to 81%, whereas the absence of an alert only lowers it to 34%. This translates to large numbers of false negatives when applied across millions of users.
In Apple’s validation study, the company stresses that the watch is not intended to replace traditional diagnosis methods or to be used as a method of BP surveillance, and that the absence of a notification does not indicate the absence of hypertension.
“The concern is, if you’re not getting an alert, will people interpret that as them not having hypertension,” said Bress. “That’s the worry. … The groups in which the negative alert is the least trustworthy contain the people with the highest risk. We’re most worried about people being falsely reassured.”
At the same time, he is clear that wearables should not be dismissed. “This technology is an important step forward; we need more wearable tech that can screen,” he said.
Unfortunately, access to these devices is not universal. Advanced monitoring technologies are often first adopted by the “worried well”—people who are more affluent and health-conscious—rather than those at highest risk.
“The only thing that can change this is a clear political decision to make awareness of hypertension large scale,” said Solà. Devices like the Hilo band could be used much like the continuous glucose monitors for diabetes. The difference is that if someone with diabetes doesn’t keep their blood glucose levels under control through regular monitoring, they can become ill very quickly. With hypertension, the effects of poor control don’t become apparent for decades.
“We need the policymakers to understand that investing in this technology today will have a return on investment in 10 years from now, not in one year from now,” Solà remarked.
Targeted drug selection
Even when hypertension is detected early and monitored closely, treatment remains largely empirical and can lead to therapeutic inertia, one of the biggest current challenges in hypertension care. “BP is not like diabetes, it doesn’t cause symptoms, and because of that, we don’t escalate treatment often enough,” said Padmanabhan.
At the same time, treatment selection remains largely trial-and-error. Clinicians cycle through medications sequentially, adjusting regimens based on response rather than underlying biology. The issue is that failed attempts risk side effects and can erode trust. That lack of trust can then impact adherence and, therefore, cardiovascular risk.
Instead, Padmanabhan believes that we need to move toward mechanistically informed drug selection.
This approach is common in oncology, where targeted therapies have been matched to specific mutations, but the picture is more complex for BP. Genome-wide association studies (GWAS) have identified more than 30 genes associated with monogenic forms of hypertension or hypotension and more than 2,100 single nucleotide polymorphisms linked to BP regulation, underscoring its highly polygenic nature.
This, combined with the strong influence of environmental factors, means that there is no single pathway or biomarker that can be easily targeted to reduce BP.
Padmanabhan’s work on the uromodulin gene (UMOD), however, shows that GWAS data can translate into therapy. His team identified a signal on chromosome 16 linked to uromodulin, a protein that is only expressed in one part of the kidney and plays a role in salt regulation. In a clinical trial comparing people with low BP to those with high BP, they found that people with the UMOD allele that increases protein expression experienced a sustained reduction in BP when treated with the loop diuretic torasemide, whereas the effect was only temporary and followed by rebound in those carrying the UMOD allele that lowers protein expression.
Approximately two-thirds of the population carry the UMOD allele that increases protein expression, meaning that loop diuretics like furosemide or torasemide, which are more commonly used to treat heart failure, could potentially be used in hypertension personalized by the patient’s genotype.
So far, “this is the only clinical trial from a GWAS-identified genetic variant in hypertension,” Padmanabhan noted, highlighting both the promise and challenge of pharmacogenomics in hypertension.
Although clinical translation from GWAS of hypertension has been limited, research has shown that genetic variation in drug-metabolizing enzymes can significantly impact hypertension treatment efficacy and toxicity. For example, variants of CYP2D6 affect metoprolol metabolism whereas those in CYP2C9 influence responses to losartan. Research is needed to determine whether testing for these variants or others could reduce trial-and-error prescription, minimize side effects, and thus increase patient confidence and long-term engagement.
Teresa Castielo, MD Director MIAL Healthcare
On a more fundamental level, biological sex differences remain a significant consideration in cardiovascular medicine. “Biological factors are an integral part of the clinical picture,” noted Teresa Castiello, MD, consultant cardiologist and director of MIAL Healthcare in London. She points out that clinical trials have historically seen a predominance of male participants; as a result, many standard medication dosages are based on data primarily derived from men.
This can lead to challenges with tolerability and a higher incidence of side effects in women as the therapeutic dose required for efficacy often tends to be lower in female patients.
Castiello suggests that this area of management warrants further refinement in clinical practice. She also emphasizes that key aspects of female cardiovascular risk, including reproductive history, menopause, and conditions like polycystic ovary syndrome, are nuances that may not always receive the necessary focus in routine care.
Toward a precise, preventative system
Ultimately, transforming hypertension care will require more than new technologies or therapies. It will require a fundamental change in how care is delivered.
Padmanabhan argues that hypertension should be managed through a “precision prevention service,” that integrates early detection, continuous monitoring, and personalized treatment, and involves more than just PCPs.
This approach recognizes that the disease is not just a clinical condition but a societal one, influenced by factors such as diet, socioeconomic status, work patterns, and access to care. Equity remains another critical issue. “We treat the ideal average patient under ideal circumstances but that’s not reality,” said Padmanabhan.
There also needs to be a cultural shift, said Castiello. “It’s not just the doctor’s responsibility; we also need to take responsibility for our own health.”
Solà shares a similar vision for the future: he would like to see BP measurement to become as routine as brushing your teeth, supported by technologies that empower individuals and reduce the burden on healthcare systems.
If realized, this shift could transform hypertension from a silent, progressive disease into a manageable, preventable condition, saving millions of lives in the process.
Laura Cowen is a freelance medical journalist who has been covering healthcare news for over 10 years. Her main specialties are oncology and diabetes, but she has written about subjects ranging from cardiology to ophthalmology and is particularly interested in infectious diseases and public health.
Laura Cowen interviewed Teresa Castiello, MD, a cardiologist and healthcare prevention advocate, to discuss her insights on hypertension management in the era of precision medicine. Castiello shared her perspectives on the need for a proactive approach to hypertension care, the role of precision medicine and pharmacogenomics, and the potential impact of digital health Hilo in transforming how hypertension is diagnosed, monitored, and treated.
Q: Do you think there needs to be a shift in how hypertension is diagnosed and treated?
Teresa Castiello, MD: Without a doubt. We must move from reactive medicine—treating damage once it has occurred—to proactive medicine. Hypertension is frequently underdiagnosed because it often remains asymptomatic until organ damage is already underway. Furthermore, traditional office readings are often biased by the “white coat” effect, which is why clinical guidelines, including those from the ESC (European Society of Cardiology), are moving away from them. Current monitoring also has limitations; nocturnal readings from standard cuffs often wake the patient, and sporadic readings fail to reflect the true, dynamic daily blood pressure response.
Q: Are there any “uncomfortable truths” about hypertension care that we don’t talk about enough?
Castiello: A significant “uncomfortable truth” is the lingering bias that considers a rising blood pressure to be a normal part of aging. It isn’t. Data from the Yanomami population in the Amazon shows that systolic blood pressure can remain constant at approximately 100 mmHg throughout life. In our Westernized society, blood pressure increases as a response to environmental and stressful “insults” rather than as a physiological necessity. Unfortunately, current clinical practice in the U.K. has not yet fully implemented recent ESC changes. We still see values defined as “normal” when guidelines now identify them as elevated (anything above 120/70 mmHg). Cardiovascular risk actually begins to climb much sooner than most realize, often at systolic levels as low as 110–115 mmHg.
Q: Is there a risk of current treatment strategies controlling blood pressure numbers without addressing underlying mechanisms?
Castiello: Yes. Labeling most cases as “essential hypertension” is essentially admitting we are treating a multifactorial condition of unknown cause. We often fail to assess the individual holistically. Stress, hormonal shifts, poor work-life balance, diet, and physical inactivity are profound drivers of blood pressure increases. While medical therapy is a vital tool, we must not forget that humans are multifaceted and complex. We need a healthcare approach that treats the person, not just the metric.
Q: Is there a need for increased precision medicine in hypertension, e.g., with the use of pharmacogenomics? Could this information redefine high-risk?
Castiello: We are in an era where precision medicine is the only way to deliver effective care. The power of data is enabling us to target prevention and early diagnosis like never before. Pharmacogenomics is a key part of this; by understanding how a patient’s genetic profile influences their metabolism of a drug, we can move away from “trial and error.” This information redefines “high-risk” from a generic population score to an individual biological reality. It allows us to define optimal doses that maximize efficacy while minimizing the toxicity that often leads to treatment non-compliance.
Q: Are healthcare systems ready to integrate continuous blood pressure monitoring into routine care?
Castiello: Probably not yet, but they will be forced to be. COVID-19 showed that we can adapt to global interconnection and remote monitoring in a very short time when we have no choice. Prevention is the only way for healthcare systems to survive the rising burden of chronic disease. Philosophically, if we wait until we feel “ready” to take action, we will never act. The time to implement these preventive strategies is now.
Q: In ten years’ time, how do you hope hypertension will be managed differently?
Castiello: I hope every individual has access to a medical-grade wearable—whether a band, ring, or chip—empowered by AI to feed data into a proactive health system. This data will be filtered to flag those requiring care at a pre-pathological stage. We can no longer afford to wait for a crisis to occur before we treat it; global healthcare systems cannot handle that burden. We must prevent what is possible and focus our hospital resources on the conditions that occur despite our best preventive strategies
Researchers at Westlake University in China, lead by Bobo Dang, PhD, and Ting Zhou, PhD, report the development of a high-throughput platform for engineering fast-acting covalent protein therapeutics. The team says their study “A high-throughput selection system for fast-acting covalent protein drugs,” published in Science, opens new avenues for next-generation biologics.
Covalent small-molecule drugs have shown great success in cancer therapy by forming irreversible bonds with their targets. This has inspired efforts to extend covalent strategies to protein therapeutics, especially engineered miniproteins. However, their development is limited by a kinetic mismatch. Miniproteins are rapidly cleared in vivo, while covalent bond formation is typically slow. In addition, high-throughput platforms for systematically optimizing covalent protein reactivity have been lacking.
To address this challenge, the researchers proposed that precise spatial positioning of chemical warheads within protein scaffolds could enable molecular preorganization, thereby accelerating covalent bond formation without increasing intrinsic reactivity (see figure).
The principle for developing fast-acting covalent proteins via comprehensive crosslinker and protein sequence engineering. [Bobo Dang’s Lab at Westlake University]
Based on this concept, the team created a high-throughput platform that combines yeast surface display with chemoselective protein modification to screen diverse crosslinkers and millions of protein variants. The platform enables rapid and irreversible target engagement.
Using this platform, the researchers developed a covalent antagonist targeting PD-L1, termed IB101. Structural analysis revealed that IB101 forms a defined binding pocket that precisely positions the active moiety in a reactive conformation, greatly accelerating covalent bond formation.
Functionally, IB101 effectively blocks the PD-1/PD-L1 immune checkpoint pathway and demonstrates strong antitumor activity in mouse models. Notably, despite its short in vivo half-life, IB101 achieves durable target engagement and tumor suppression, outperforming conventional antibody-based therapies under comparable conditions, according to the scientists.
The platform was further applied to cytokine engineering, leading to the development of a covalent IL-18 variant, IB201. This engineered cytokine rapidly forms a covalent interaction with its receptor, enhancing signaling strength and duration. In vivo studies showed that IB201 induces potent antitumor immune responses without detectable systemic toxicity. These results highlight the potential of covalent engineering to improve the efficacy and safety of cytokine-based therapies.
Beyond immunotherapy targets, the platform was also applied to develop a covalent inhibitor targeting the receptor-binding domain (RBD) of SARS-CoV-2. This molecule showed durable viral neutralization, demonstrating the versatility of the approach across different therapeutic modalities, note the researchers, adding that the study establishes a general strategy for engineering fast-acting covalent protein therapeutics.
By enabling covalent bond formation on timescales compatible with rapid in vivo clearance, the platform overcomes a fundamental limitation in the field, say the scientists. These findings, they continue, provide a new framework for designing biologics with both rapid kinetics and sustained target engagement, with broad implications for cancer immunotherapy, antiviral therapy, and beyond.
Dating back more than a century, biobanks have outgrown their beginnings as small, local collections to become large, global facilities that store and handle millions of samples and serve thousands of researchers at any given time. Over the years, biobanks have transformed from passive repositories into active research infrastructures that are increasingly bridging the gap between medical research and clinical applications.
“Today’s biobanks have evolved far beyond sample storage,” said Yan Zhang, PhD, president of proteomic sciences at Thermo Fisher Scientific. “They are automated, digitally connected systems integrated with hospitals and health networks to ensure appropriate consent, longitudinal clinical context, and the ability to re-engage participants over time.”
Yan Zhang, PhD President Thermo Fisher Scientific
As safeguards of clinical samples, biobanks fulfill a central role in the advancement of precision medicine. Access to the right samples can make or break a research project, with most researchers reporting that they have had to limit their scope of work because of difficulties obtaining the samples they need.
“Robust, population-scale biobanking enables precision medicine to move from isolated findings toward broader clinical relevance,” said Zhang. “Modern biobanks combine genomics, proteomics, and other high-dimensional omics platforms with robust data architecture, high-performance computing, and artificial intelligence (AI)-driven modeling. Dedicated data science teams integrate molecular data, longitudinal health records, and curated public datasets to generate biologically meaningful interpretations.”
Biobanks now provide the infrastructure needed to support population-scale, longitudinal studies that allow scientists to uncover molecular drivers of disease and understand their evolution over time to ultimately identify biomarkers, develop targeted treatments, and inform clinical decisions.
“We’re seeing researchers design studies with scale in mind,” Zhang noted. “They’re combining proteomics, genomics, and clinical data to generate insights that are both statistically powerful and relevant to real-world populations. There’s also a clear shift from searching for a single biomarker to building a more complete, systems-level understanding of disease.”
To navigate today’s rapidly shifting landscape and meet their core purpose of supporting cutting-edge clinical research, biobanks have to keep up with fast-moving targets. Going forward, moving from initial discovery to translation will remain the number one challenge in precision medicine. “Generating discovery insight is no longer the limiting factor,” said Zhang. “Validating, standardizing, and implementing those insights at scale is.”
A matter of scale
Martin K. Rutter, MD Deputy Chief Scientist UK Biobank
One of the most transformative shifts in biobanking over the past decade has been an exponential increase in the scale of data collection and sample storage. At the forefront of this expansion is the UK Biobank, which currently stores around 18 million samples from 500,000 participants, together with imaging and biomarker data, healthcare records, questionnaires, physical measurements, demographics, lifestyle, and environmental data collected over the course of 20 years. This depth of phenotyping is what makes the data so valuable to researchers worldwide, said Martin K. Rutter, MD, professor of cardiometabolic medicine at the University of Manchester and deputy chief scientist at the UK Biobank. “When you link all that together, you can get amazing insights into the biology of disease.”
To keep up with increasing storage needs and researcher requests, the UK Biobank is now getting ready to move more than 10 million samples currently stored in its main laboratory to a new building in central Manchester by the end of the year. The new storage facility is designed to quadruple sample retrieval speed while making the whole infrastructure more energy-efficient and environmentally friendly.
The scale at which facilities like the UK Biobank operate today would have been unthinkable when it was established two decades ago. Such massive growth has been driven by rapid technological advances across genomics, transcriptomics, and proteomics, with costs continuing to fall while coverage, speed, and accuracy keep surging.
Partnerships with the pharmaceutical industry have also been instrumental in nurturing this exponential growth. This can be seen in initiatives like the UK Biobank Pharma Proteomics Project (UKB-PPP), a collaboration between the UK Biobank and 14 biopharmaceutical companies with the goal of analyzing proteomics data from 600,000 samples.
In the long run, scale provides the backbone to enable increasingly ambitious, statistically powerful studies. However, as they grow, biobanks face the challenge of navigating a constantly shifting landscape while making sure the samples and data they collect, store, and maintain are valuable to the entire research community they serve.
“Our job is to make the data available to researchers,” said Rutter. “We are involved now more than ever in connecting with research teams and trying to understand what their needs are.”
Through surveys and consultations, the UK Biobank actively gathers information to design prospective data collection programs that anticipate researcher needs. Next year, the biobank is planning a repeat assessment of its whole cohort, focusing on measurements of aging. The goal is to support researchers looking into causal pathways and mechanisms driving age-related diseases, empowering the development of preventive interventions and new diagnostics and treatments for age-related conditions.
Keeping pace with the evolving demands of researchers, industry, and the broader public is essential for biobanks to secure the funding necessary not only to operate but also to expand such vast enterprises, which remains a major challenge across this resource-intensive field.
Diversity takes the spotlight
Historically, samples collected by biobanks are biased in favor of participants who are white, middle-class, and have a higher education. This creates major disparities in the applicability of clinical research. In fact, studies have shown that patients from non-European ancestry backgrounds have not benefited equally from precision drugs approved by the U.S. Food and Drug Administration (FDA) to treat a range of cancer indications.
Even within biobanks dedicated to sampling the population of a specific region, ethnic minorities, low-income, or elderly people are often underrepresented, skewing results against the real-world populations they strive to serve. As the research community increasingly recognizes the importance of more diverse and representative patient cohorts, demand is rising for resources that address these barriers.
Representation is at the heart of All of Us, a program launched by the National Institutes of Health in 2018 to address the gap present at the time in many biobanks and sample repositories. This precision medicine initiative was designed to enroll participants who reflect the full range of populations found within the U.S., including individuals of varied ancestry backgrounds as well as those living in rural commmunities, which are rarely represented in biorepositories due in part to longstanding barriers to research participation, such as the logistical challenges of collecting samples and data from participants in remote locations.
Joshua C. Denny, MD CEO All of Us
“A lack of diversity impoverishes discovery and applicability of findings for all,” said Joshua C. Denny, MD, CEO of the All of Us Research Program.
For instance, data collected by All of Us has been used to investigate APOL1 gene variants linked to kidney disease, which are more common among people of West African ancestry. This research led to the identification of a novel APOL1 variant that can reduce the risk of kidney disease in individuals carrying high-risk variants.
The program has so far enrolled about 870,000 participants across all U.S. states, with about 80% of them representing communities that have historically been underrepresented in biomedical research. This has been achieved by emphasizing accessibility and flexible participation models; participants can enroll digitally and choose whether to share access to their electronic health records, donate biospecimens, and complete demographics and lifestyle surveys. They may also opt to provide saliva samples, simplifying logistics in rural areas with limited access to blood collection facilities.
“What works in a rural location is different from what works in a big city like New York,” said Denny. Whether it comes to location, age, or language, he emphasized the importance of adapting how the program approaches and engages each population.
Democratizing access to patient data across the research ecosystem is another major biobanking challenge that All of Us is committed to addressing. The program has established a streamlined access model that enables researchers to access the data they need in less than two hours if they belong to one of the 1,300 already approved institutions across the world. Together with central data storage and cloud-based analysis tools, their setup is designed to make the data accessible to researchers lacking the resources and local infrastructure for high-performance computing.
Towards global integration
With precision medicine studies steadily escalating both in size and complexity, researchers increasingly seek to bring together data stored across diverse biobanks to power larger, more ambitious studies with broader scientific and societal impact. However, building the infrastructure needed to enable cross-biobank studies is still a challenge, starting with convening stakeholders to harmonize data collection standards and establish international guidelines.
Anticipating this need, in 2013 the European Union established the Biobanking and Biomolecular Resources Research Infrastructure – European Research Infrastructure Consortium (BBMRI-ERIC), which currently coordinates the activity of about 500 biobanks across 32 countries.
Jens K. Habermann, MD, PhD Director General BBMRI-ERIC
“Precision medicine can only move forward with a strong starting point for research,” said Jens K. Habermann, MD, PhD, professor for translational surgical oncology and biobanking at the University of Lübeck and director general of the BBMRI-ERIC. “It can be very difficult for scientists to get all the information they need in one place, and this is what biobanks can enable.”
Pulling together data from all its members, the BBMRI-ERIC has set up a central catalogue for biobanks, biomolecular resources, and other data and sample collections, which users can employ to identify relevant resources and build virtual cohorts tailored to their research needs. The consortium also works with international committees to set guidelines and support members working towards compliance with international standards.
Despite ongoing progress, there are still obstacles ahead when it comes to harmonizing biobanking practices worldwide, including data collection, annotation, storage, and sharing. Tackling differences in data protection, consent, ethical standards, and regulatory requirements across borders will be another necessary step towards broader standardization. Finally, biobanks will need to invest in cybersecurity to ensure patient data can be shared between institutions safely.
Funding will be key to successfully addressing all these challenges. On this front, biobanks face the difficult task of maintaining their existing infrastructure, staying up to date and relevant to the research community, and investing in cross-biobank initiatives. All this must be balanced with growing financial pressure on research centers, hospitals, and the governments supporting them.
As part of its 10-year roadmap, the BBMRI-ERIC is setting the goal of forming international networks that bring together more diverse biobank types, such as environmental, wildlife, veterinary, and plant biodiversity repositories. The overarching aim is to move towards a One Health approach to biobanking, where samples and data that expand beyond monitoring human populations are brought together to tackle overlapping challenges that simultaneously affect human, animal, and environmental health.
Data-driven horizons
As the field forges ahead, biobanks are undergoing broad transformations in the way they operate. On the technology side, these changes are being propelled by the rise of multi-omics techniques in precision medicine research, as well as by rising demand from the research community for non-invasive patient monitoring data and longitudinal sample collection. All of these will be critical for the development of the next generation of personalized therapies and diagnostics.
“Over the next decade, biobanks are expected to become increasingly integrated into clinical and translational workflows,” said Zhang. “Proteomics, in particular, will play a growing role in helping us understand the dynamic biology of disease, enabling earlier detection, better prediction of recurrence, and more precise therapeutic strategies.”
A key driver of this shift will be AI. No longer just a supporting tool, AI is now becoming an integral part of biobank operations, contributing to real-time sample monitoring, predictive maintenance, risk management, and decision making.
On the data analysis side, Zhang has seen how AI is redirecting the focus from data generation to data interpretation. She said, “Biobanking has already enabled the collection of high-quality biospecimens linked to large-scale molecular and clinical datasets. The challenge now is extracting meaningful biological insight from that complexity.”
Although still in its early days, AI is becoming central to how researchers make use of biobank data, noted Rutter. Drawing from the UK Biobank data, recent studies have developed AI models that can predict a patient’s risk of stroke based on retinal images, calculate the risk of future disease by looking at an individual’s disease history, or spot neurodegenerative diseases like Alzheimer’s and Parkinson’s early using brain scans and physical activity data.
Going forward, Rutter expects to see biobanks moving away from static cohorts and in favor of continuous data collection, enabling more powerful predictions. For example, the UK Biobank is developing a mobile app that can track a participant’s physical activity and monitor their location and sleep patterns, offering an in-depth look at how a variety of factors affect their health with much more accuracy than self-reported surveys.
Over time, all these advances will steer clinical practice from treatment to prevention, allowing healthcare professionals to act early in the patient journey, when interventions are most effective, and eventually, even before disease develops. Ultimately, addressing complex diseases will require coordinated contributions from all stakeholders, including AI innovators, drug developers, clinicians, technology providers, and policymakers.
“The next decade will be incredibly exciting,” said Denny. “It will be all about leveraging the huge scale of resources that are just emerging today.”
Clara Rodríguez Fernández is a science journalist specializing in biotechnology, medicine, deeptech, and startup innovation. She previously worked as a reporter at Sifted and editor at Labiotech, and she holds an MRes degree in bioengineering from Imperial College London.
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The 2027 budget that the Trump administration released on Friday is in many ways a repeat of last year’s proposal: It includes deep cuts to the National Institutes of Health, the elimination of a health research agency, and the creation of a new agency devoted to chronic diseases called the Administration for a Healthy America.
A woman lies on an exam table, holding her partner’s hand tightly with anticipation, as a technician glides an ultrasound probe across her abdomen. On the screen, shifting staticky shadows resolve into a skull, a liver, and the flicker of a beating heart. For many families, this moment brings joy and relief. For others, it’s paralyzing, as doctors detect signs that something is wrong.
A single nucleotide change can cause neurodevelopmental delays and dimorphism, failing livers, and arrhythmia-ridden hearts. For decades, medicine could only identify these conditions, usually after birth. Prenatal screening has made it easier to detect progressive diseases like Duchenne muscular dystrophy, which degenerates and damages muscles before symptoms typically appear in childhood. But treating before birth could preserve tissue prior to the onset of irreversible deterioration.
Once unthinkable, genetic diseases can now be treated before birth. Fetal genetic intervention—including early screening, in utero gene therapy, stem cell transplantation, and even embryo editing—aims not just to diagnose disease but to correct it at its earliest stages. It is a rapidly advancing frontier, defined by technological promise and profound ethical questions.
It starts with detection
Jennifer Hoskovec, vice president of medical affairs at BillionToOne, has spent more than 20 years in prenatal genetics, an era dominated by risk assessment rather than intervention.
Historically, prenatal genetic screening has fallen into two main categories. Aneuploidy testing determines the risk of Down syndrome and other trisomies, sex chromosome abnormalities, and specific microdeletions. Screening is essential for these de novo mutations, which have no U.S. Food and Drug Administration (FDA)-approved genetic interventions. High-risk Down syndrome patients may receive a fetal echocardiogram, closer ultrasound monitoring, or tertiary care delivery with neonatal support. The standard practice is to screen, monitor, and manage.
Jennifer Hoskovec Vice President BillionToOne
The second category involves inherited recessive conditions like cystic fibrosis (CF), spinal muscular atrophy (SMA), and phenylketonuria. If both parents are carriers for the same genetic mutation, then their child has a 25% chance of being affected. Testing typically requires samples from both parents. If both are carriers, chorionic villus sampling (CVS) and amniocentesis can detect fetal abnormalities in the first and second trimesters, respectively. However, getting each partner to follow up is a major hindrance. “When people go through a screening process and are found to be carriers, less than 50% of their partners complete the testing,” Hoskovec told Inside Precision Medicine. “Half of U.S. carriers of these genetic conditions, whether common or rare, don’t know what it means for their pregnancy. That limits their ability to get diagnostic testing because we do not have all the pieces of the puzzle.”
Hoskovec’s team developed a workaround: a single-gene noninvasive prenatal test that analyzes fetal cell-free DNA (cfDNA) circulating in maternal blood. Around nine weeks into pregnancy, fragments of fetal DNA shed from the placenta can be sequenced and quantified. If a mother is a carrier for a condition like CF or sickle cell disease, the test looks for a second variant that is not present in her DNA and forms evidence of paternal contribution.
“For example, if a mother has [the] sickle cell trait, we first sequence the full beta-globin gene in the cfDNA, which contains a mixture of maternal and fetal DNA,” Hoskovec said. “We look for a second variant not present in the mother that would indicate paternal contribution.”
Despite not replacing CVS or amniocentesis, Hoskovec said the result is highly sensitive, identifying 95% of affected pregnancies in the conditions it covers. Crucially, it does not require partner testing. “This is a stepping stone,” Hoskovec explained. “This earlier detection will likely accelerate the field by increasing the number of eligible patients for clinical studies and registries, improving equitable access across ethnic groups, and advancing precision medicine in prenatal care.”
Avoiding germline editing
David H. Stitelman, MDr Associate Professor Yale-New Haven Children’s Hospital and Yale School of Medicine
As screening opens the door, fetal surgeons and gene therapy researchers are taking their first steps through it. A pediatric surgeon at the Yale School of Medicine, David H. Stitelman, MD, believes prenatal treatment has benefits. The fetus is small, so it can receive higher doses based on weight. As its immune system is still developing and more tolerant, stem cells are growing quickly and organs are still being formed, so problems can be fixed before they become permanent. Because the placenta exchanges oxygen, lung conditions like congenital diaphragmatic hernia can be treated during fetal life. But once a newborn takes a first breath, defective lungs can spell immediate crisis.
Fetal therapy is not new. Specialized centers have performed open fetal surgery for spina bifida and diaphragmatic hernia lung growth, and blood transfusions for fetal anemia dating back to the 1960s. What is new is the molecular toolkit. Stitelman’s lab is investigating gene editing methods that use the cell’s repair machinery to fix one- to three-base-pair DNA errors. Another team, led by pediatric and fetal surgeon Tippi MacKenzie, MD, at the University of California, San Francisco, is using viruses to replace genes for lysosomal storage diseases and fetal stem cells for alpha thalassemia.
Some diseases require only modest correction. In hemophilia, one percent normal clotting factor expression improves outcomes greatly. Increasing the expression of functional CFTR protein to 15% of wild-type levels may cure CF or at least make it manageable. Even a small number of liver cells corrected in hereditary tyrosinemia can boost growth and repopulate the organ. However, some situations, such as congenital cancer syndromes, may require nearly 100% correction. At present, Stitelman’s team achieves single-digit percentage editing in models of CF and beta thalassemia. “We’re in the optimization phase,” Stitelman told Inside Precision Medicine. “We are testing different nanoparticles and generations of editing strategies to incrementally reach therapeutic levels.”
Stitelman draws a clear ethical boundary: this is somatic editing, not germline editing. The aim is to treat the fetus as a patient, not to create heritable genetic changes. Instead of editing embryos in vitro, systemic therapeutic agents are delivered to avoid reproductive cell damage.
Unintended germline modification remains a concern. Editing a target gene could inadvertently disrupt developmental genes and affect future generations. But, Stitelman argues, medicine always carries risk. “In 1950, children with leukemia all died,” said Stitelman. “Today, some forms have a 98% long-term survival rate with chemotherapy. We know chemotherapy can cause germline mutations, yet we accept that risk because it saves lives. With gene editing, the issue is not zero risk but understanding and quantifying the risk. Ideally, there would be no measurable off-target effects. In the places we have examined, we have not seen off-target effects.”
One pregnancy, two patients
In a landmark trial in 2011 known as the Management of Myelomeningocele Study, investigators found that fetal surgery for severe spina bifida (myelomeningocele) achieved better results than postnatal repair. Surgically closing the spinal defect in utero improved motor function and reduced the need for shunting to relieve hydrocephalus. The benefit was so clear that the trial was stopped early and influenced how doctors treat structural birth defects.
Aijun Wang, PhD Professor University of California, Davis
At the University of California, Davis, biomedical engineer Aijun Wang, PhD, is working closely with fetal surgery pioneer Diana L. Farmer, MD, to evolve fetal intervention from heroic surgery to cellular and molecular therapy. Wang and Farmer launched the Cellular Therapy for In Utero Repair of Myelomeningocele (CuRe) trial, combining fetal surgery with stem cell transplantation. The goal is to not only close the spinal defect but also restore neural tissue and improve long-term function.
The lens that Wang has used to focus his research is fetal and maternal safety. “The fetus is the patient, but treatment inevitably carries some risk to the mother,” Wang told Inside Precision Medicine. “Open fetal surgery, in particular, poses significant maternal risk. Genetic treatments introduce additional uncertainties because the long-term effects of DNA modification are not fully understood. Safety must remain the highest priority.”
Genetic medicine delivery is a critical challenge for all life stages, but the stakes are particularly high for a developing fetus. In fetal development, targeting stem cell populations is especially important because these cells are highly active, proliferating, and migrating. If edited successfully at the right developmental window, their progeny will carry the correction. The problem would be if the edit was not just unsuccessful but detrimental.
Wang’s lab focuses on delivery systems, particularly lipid nanoparticles carrying mRNA-encoding gene-editing enzymes. For genetic manipulation and high-throughput screening, Wang’s lab utilizes mouse models. Fetal sheep are used for scaling and dosing, while human organoids are used for human-specific editing and functional outcomes.
“In our clinical work, we have engaged with the FDA and conducted extensive preclinical studies,” said Wang. “Using multiple complementary models is essential. Combining small animal models, large animal translational models, and human organoid systems provides a comprehensive framework for product development, from early screening to human-focused therapeutic design.”
Although the field is highly exciting and progressing rapidly, Wang warns against premature application, which could be dangerous. Safety, developmental biology, ethical considerations, and multidisciplinary collaboration are all essential. “Despite the excitement in the field, we must proceed cautiously,” said Wang. “There is strong potential for correcting specific mutations, especially point mutations, using precise gene editing approaches such as base editing. However, safety evaluation must precede rapid clinical application.”
Effective progress requires a village of physicians, surgeons, researchers, engineers, and ethicists working together. Scientific progress requires caution, responsibility, and thorough evaluation before clinical use.
The earlier, the better
If fetal intervention treats a diagnosed fetus, embryo editing operates even earlier—at the blastocyst stage in in vitro fertilization (IVF). Norbert Gleicher, MD, a fertility specialist known for treating some of the oldest and most difficult IVF patients in the United States, approaches genetic technologies with caution. Due to biological mosaicism, sampling limitations, and his belief that many abnormal embryos self-correct or develop normally, Gleicher opposes preimplantation genetic testing for aneuploidy.
Norbert Gleicher, MD Founder & Medical Director Center for Human Reproduction
But when it comes to single-gene diseases, he sees a different calculus. Couples with recessive mutations may have one-in-four embryos affected, and in dominant or X-linked diseases, half may carry the mutation. For patients who produce few embryos—especially older women—discarding affected embryos can mean losing precious chances at pregnancy. “If you can cure an embryo rather than discard it,” Gleicher told Inside Precision Medicine, “that makes a lot of sense.”
For single-gene diseases, Gleicher believes genetic editing with CRISPR or other platforms is the most straightforward intervention. He points to the 2025 work at the Children’s Hospital of Philadelphia on Baby KJ as a recent milestone. Even partial correction, which Gleicher believes is likely the case with Baby KJ—though no liver biopsies have been extracted—can transform prognosis. Gleicher said, “Correcting some cells was enough to clinically cure the baby, at least for the time being, from symptoms of a disease that historically kills affected children within a few years. However, we do not know whether the treated baby, who likely still has many affected cells, might become symptomatic again later in life.”
To Gleicher, success in a newborn is all the more reason to apply genetic intervention to fetal stages. “If this can be successful in a full human being, imagine how much easier it would be at the blastocyst stage, or even earlier at the cleavage stage, when the embryo consists of only six to eight cells,” said Gleicher. “If [CRISPR] is applied at that point, correcting those six to eight cells would mean that all their daughter cells would also be corrected. The result would be a normal baby at birth. That is the much stronger argument in this case.”
Just because something is possible, it doesn’t necessarily mean it should be done, and Gleicher establishes a clear ethical boundary. Editing to prevent a devastating single-gene disease is one thing. Editing for traits—eye color, intelligence, polygenic risk scores—is another. Polygenic predictions explain only a fraction of trait variance, and embryo implantation itself is uncertain. To him, offering polygenic selection in IVF is not only scientifically dubious but also ethically troubling. “It is surprising that professionals, particularly in genetics, would suggest such an approach,” said Gleicher. “It is worse than snake oil, because while snake oil may occasionally work by accident, this carries a real risk of causing serious harm.”
A pretty penny
What ultimately restricts fetal genetic intervention is timing. Early screening increases experimental trial eligibility, and early treatment may preserve organ development before irreversible damage. In conditions like CF and SMA, where postnatal gene therapies are expensive and delivered after injury, fetal intervention could change outcomes. Frontline screening can identify high-risk pregnancies at 11 weeks without family history or ethnicity, expanding trial access.
Yet, fetal genetic interventions require specialized teams, advanced delivery systems, counseling, and long-term follow-up. Without careful planning and reimbursement policies, only a few top-tier centers could progress, widening the gap. Ethical scrutiny remains inseparable from progress. Innovation must balance maternal risk, fetal benefit, and future consequences with safety, appropriate use, and clear limits. As prenatal care shifts from prediction to prevention, restraint and evidence will determine its future.
Jonathan D. Grinstein, PhD, North American editor for Inside Precision Medicine, investigates the most recent research and developments in a wide range of human healthcare topics and emerging trends, such as next-generation diagnostics, cell and gene therapy, and AI/ML for drug discovery. He is also the host of the Behind the Breakthroughs podcast, featuring people shaping the future of medicine. Jonathan earned his PhD in biomedical science from the University of California, San Diego, and a BA in neural science from New York University.
ObjectiveTo analyze the prevalence of dyslipidemia and related influencing factors in patients with early-onset schizophrenia (EOS).MethodsWe recruited 289 pediatric and adolescent EOS patients from October 2021 to June 2024 in the Third People’s Hospital of Fuyang. Researchers gathered comprehensive demographic and clinical records. Utilizing the 2023 Chinese Guidelines for Lipid Management, they calculated dyslipidemia prevalence and the incidence of irregularities in total cholesterol, triglycerides, LDL cholesterol, HDL cholesterol, and non-HDL cholesterol. Subsequently, differences in dyslipidemia among different genders, body mass index, and antipsychotic medication groups were analyzed. Finally, independent influencing factors of dyslipidemia in EOS patients were explored.ResultsThe overall prevalence of dyslipidemia was 24.9% (72/289), with abnormal rates of TG, TC, HDL-C, LDL-C, and non-HDL-C being 15.9%, 6.6%, 6.6%, 4.2%, and 7.3%, respectively. Male patients, those who were overweight or obese, and those taking two antipsychotic drugs had significantly higher rates of dyslipidemia. Regression analysis showed that male gender (OR = 2.04, P = 0.016), overweight/obesity (OR = 4.55, P < 0.001), body roundness index (OR = 1.53, P = 0.005), and the use of two antipsychotic drugs (OR = 1.90, P = 0.030) were risk factors for dyslipidemia in EOS patients.ConclusionThe prevalence of dyslipidemia in EOS patients is relatively high. When monitoring lipid levels in clinical practice, particular attention should be paid to male patients, those who are overweight or obese, and those receiving combined drug therapy.
BackgroundEsketamine has a significant and rapid antidepressant effect. Although studies have shown that Neuregulin 1 (NRG1) and it’s signaling pathway are associated with depression, the possible regulatory relationship of esketamine on the NRG1-ErbB4 pathway is not yet clear.MethodsTo induce depressive-like behavior in mice, a Chronic Social Defeat Stress (CSDS) model was established. Behavioral indicators were then employed to assess depression in these mice, categorized into control, susceptible, and resilient groups. Following intraperitoneal injection of a subanesthetic dose of esketamine, behavioral tests were conducted at 30 minutes and 24 hours post-injection to observe any improvements in depressive-like behavior. Additionally, changes in immunofluorescence and protein expression levels of NRG1-ErbB4 and GAD67 in the prefrontal cortex were evaluated.ResultsCompared with the control group, the CSDS susceptible group mice showed decreases in social interaction ratio in the contact area, sucrose preference ratio, NRG1 immunofluorescence protein expression in the prefrontal cortex and NRG1 expression in tissue homogenate; showed significant increases in immobility time; the expression of NRG1 decreased;no significant change in GAD67 and ErbB4 expression level. in After 30 minutes of intraperitoneal injection of esketamine, the expression of NRG1 in the prefrontal cortex of susceptible mice increased significantly. no significant change in GAD67 and ErbB4 expression level. After 30 minutes and 24 hours of intraperitoneal injection of esketamine, the social interaction ratio of susceptible group improved compared to the control group, and the duration of forced swimming immobility was significantly shortened.ConclusionThe subanesthetic dose of esketamine may regulate the NRG1-ErbB4 signaling pathway and improve depressive like behavior in mice.
In a phase 1 basket trial, the small interfering RNA zodasiran, targeting ANGPTL3, lowered triglycerides in patients with severe hypertriglyceridemia and lowered both triglycerides and low-density lipoprotein cholesterol in patients with heterozygous familial hypercholesterolemia.
band: a CE-certified wearable medical device designed for continuous, cuffless, BP monitoring that has been clinically validated against traditional ambulatory BP monitoring.
![The principle for developing fast-acting covalent proteins via comprehensive crosslinker and protein sequence engineering. [Bobo Dang's Lab at Westlake University]](https://www.genengnews.com/wp-content/uploads/2026/04/fast-acting-covalent-p.jpg)
