An international group of researchers has uncovered significant insights into pre-industrial aerosol formation processes through a study conducted in a pristine Finnish peatland. The investigation aimed to understand atmospheric particle formation in an environment with minimal human influences, shedding light on historical climate conditions.
The study unveiled that Siikaneva peatland, located in southern Finland, releases highly oxygenated organic molecules at night, leading to aerosol particle formation closely resembling the pre-industrial atmosphere.
The 9000-year-old minerotrophic Siikaneva peatland emits large levels of terpenes dominated e.g., by isoprene and alpha-pinene. The researchers observed the formation of new atmospheric particles initiated by purely natural vapours, a mechanism that could resemble the pre-industrial atmosphere. Previously, the same process could only be verified at the molecular level under laboratory conditions.
“Our results basically mark the first confirmation that pure biogenic new particle formation is possible in ambient conditions,” says Postdoctoral Researcher Wei Huang from the Institute for Atmospheric and Earth System Research INAR at the University of Helsinki.
The results were published in the journal Science Advances in April.
Widespread pure biogenic aerosol formation
The findings underscore the importance of pristine environments, such as present-day Finnish peatland, when studying pre-industrial aerosol production processes.

“These environments with minimal sulphur or nitrogen oxide pollution serve as natural laboratories. Our study is potentially the best current example of pre-industrial aerosol production processes, which shows that truly pristine environments do exist in the present-day atmosphere, largely influenced by human activities. It also demonstrates that pure biogenic aerosol formation could be a widespread and frequent phenomenon in the present day. This will potentially impact the climate of areas dominated by peatlands, as well as other locations with flat topography,” says Professor Federico Bianchi from INAR.
Peatlands cover large areas in the Northern Hemisphere: approximately four million square kilometres north of the 30th parallel and half a million square kilometres north of the 50th parallel. Pure biogenic particles formed from these large areas may have been an important source of cloud condensation nuclei for cloud formation during the pre-industrial era.
Historical aerosols help to understand the future
Understanding pre-industrial aerosol formation is important, as climate change is measured by comparing present-day atmospheric conditions with pre-industrial ones. Aerosol particles cool the atmosphere and climate by scattering incoming radiation and acting as cloud condensation nuclei.The particles control cloud properties, such as the reflection of sunlight back into space. Understanding past conditions helps to estimate how aerosol formation processes have evolved and how they impact the global climate today.
The results may also provide clues for understanding new particle formation in the future, the features of which may revert towards pre-industrial conditions because of air pollution mitigation.
“As air pollution is mitigated, particles will be formed with various species, frequencies, intensities, and chemistry. This can eventually affect cloud formation and the climate (e.g., temperatures) on Earth,” says Bianchi.
The findings also provide valuable model parameterization constraints for future studies simulating pre-industrial peatland aerosol impacts on the climate.

The test that was developed using an existing diagnostic procedure as its basis and has the potential to be applied in clinical trials that target the Epstein Barr Virus
A team of research scientists at Trinity College Dublin have developed a new and unique blood test to measure the immune response to the Epstein Barr Virus (EBV) which is the leading risk factor for developing multiple sclerosis (MS). Their findings are published in the journal Neurology Neuroimmunology and Neuroinflammation and have implications for future basic research in further understanding the biology of EBV in MS, but also has the potential to be applied in clinical trials that target the virus.
MS is a chronic neurological disease with no known cure. It affects approximately three million people worldwide and is the second leading cause of disability in young adults. There is a pressing need for better treatments.
A range of viruses relating to MS have been studied in the past but none have had such compelling evidence as EBV. The question the team considered was why do some people have known MS have a rogue immune response to EBV, a common viral infection that is generally asymptomatic?
To answer this, scientists measured the cellular response of MS patients to EBNA-1, a part of the EBV that can mimic the myelin coating of nerves which are the principal site of attack of the immune system in MS. The team found that the immune response is higher to EBNA-1 in people with MS compared to those with epilepsy, or the healthy control group. The team also showed that this cellular response is impacted by currently approved medications for MS which target the immune system, but not the virus. The immune response to EBNA-1 was found to be lower in people who are taking B cell depleting medications compared to people with MS not taking medication and the level recorded was equivalent to healthy controls.
B cell depleting medications are effective for reducing MS disease activity. It is not known however, how exactly they work. Many people believe that reducing B cells reduces EBV levels, as EBV can lie dormant within B cells. The scientists do not prove this theory, but do show that the immune response to EBV in MS is equal to healthy controls when these medications are used. The team believe that this supports the need for more selective reduction in EBV rather than targeting all B cells. This is of importance as B cells play an important role in fighting infection and an unselective approach can lead to unwanted side effects.
The Trinity researchers are the first team of scientists to capture the immune response to EBNA-1 using whole blood samples carried out exclusively with equipment that is used in the hospital laboratory day to day. This builds on previous research that used extensive pre-processing in research laboratories. We believe this is of importance as it shows the ability for the test to be run elsewhere and at scale without a need for new equipment or personnel.

This research is important because a standard blood test that was processed in a hospital laboratory provides important information on the immune system’s response to EBNA-1. This response appears to be at the heart of the pathogenesis of MS. The ability to measure this in a scalable test, that was developed using an existing diagnostic test as its basis, has implications for future basic research in further understanding the biology of EBV in MS. But the test also has the potential to be applied in clinical trials that target the virus. This would mean that there is the potential to directly measure the immune response to any potential antiviral treatments, rather than measuring MS outcome measures alone.
Speaking on the potential benefits of this research, Dr Hugh Kearney, Neurologist, School of Medicine, Trinity College and lead author said:
“In the short term the benefit of this research is likely to be for the research community in MS. We believe the approach adopted in this test that uses whole blood samples on a robust hospital-based platform will facilitate adoption in other centres and also replication of the results with a view towards validation. In the medium term, if validated, then this would be of benefit to researchers involved in clinical trials in MS. Long term benefits will be for people with MS, who live with a chronic neurological illness as new treatments tested in clinical trials have the potential to reduce the burden of this potentially disabling disease.
The next step for our team is to develop a longitudinal study. We aim to do this by recruiting newly diagnosed people with MS and measuring this blood test before treatment has started and then repeating the blood test at an interval to show that B cell depletion directly impacts on the cellular response to EBNA-1 in MS.”

A new study by researchers at the University of Ottawa throws cold water on the idea that fans can effectively cool you down during extremely hot weather events.
With severe heat waves becoming more frequent due to climate change, there’s a growing need for safe and accessible ways to keep people cool, especially vulnerable populations like older adults. Fans are often recommended as cheap and easy solutions, but this study suggests they might not be as helpful as previously thought.
The research was led by post-doctoral fellow Robert Meade and was conducted at the Human and Environmental Physiology Research Unit at the University of Ottawa , a unit led by Dr. Glen Kenny, who is a professor of physiology at the Faculty of Health Sciences.
“Fans do improve sweat evaporation, but this effect is not strong enough to significantly lower your body’s internal temperature when it’s already really hot (above 33-35°C). In older adults, who may have a reduced ability to sweat, fans provide even less cooling benefits,” explains Meade. “In fact, even in younger adults, fans only provide a small fraction of the cooling power of air conditioning.”
The study recommends that health organizations continue to advise against relying on fans during extreme heat events, especially for older adults and other groups at higher risk of heat stroke and other adverse health events during heat waves. Instead, the emphasis should be on providing access to alternative cooling solutions, such as air conditioning, and on exploring ways to make these options more accessible and environmentally friendly.
The research was conducted using “human heat balance” modeling techniques developed in 2015. By extending these models to estimate core temperature under a range of conditions and modeling assumptions, the authors were able to compare the expected effects of fan use under a wide range of scenarios.
“Results from the 116,640 alternative models we produced in sensitivity analyses indicated that fans likely do not significantly reduce core temperature in high heat, or match air conditioning cooling. Comparisons with more advanced modeling techniques and laboratory heat wave simulations supported this conclusion,” adds Meade.
Fans are good at providing air circulation and may work in moderate temperatures but are not as effective in extreme heat. Public health authorities have a role to play.
“Keeping indoor temperature cool is important for vulnerable individuals, but cooling strategies like air conditioning can be costly and harmful to the environment. It is crucial that we improve the accessibility and sustainability of air conditioning and other forms of ambient cooling to protect those in need,” said Meade. “Fans can still have an important role in this, since they can be effective for cooling at lower temperatures, meaning we don’t have to set our air conditioners so low. However, when it gets really hot, a fan alone is not going to cut it.”

A multidisciplinary team of scientists led by University of Helsinki report that a progressive neurodegenerative disease can be triggered by a viral infection. The mechanism relates to mitochondrial roles in antiviral defense mechanisms.
The scientists report that a specific gene variant affecting the mitochondria disturb cellular antiviral defense responses. The results implicate that viral infections can trigger and modify symptoms of neurological diseases in subjects carrying genetic sensitivity.
The article is published in Nature.
Viking-age gene mutation alters viral defense
Why a disease manifests at a certain age, and what kind of triggers may be involved, are still open questions. Recent data indicate that mitochondria, the cellular centers of energy and nutrient metabolism, have new important roles in protecting cells from both internal and external stresses. Importantly, a novel role of mitochondria in strengthening the immune system has been recognized, but the relevance of these functions for human diseases has been unclear.
The current study shows that deficient mitochondrial functions in immune defense is connected to manifestation of brain diseases and sometimes also liver dysfunction. A multidisciplinary team led by academy professor Anu Suomalainen discovered that a genetic variant affecting the function of mitochondrial POLG enzyme delays detection of viral infection, leading to delayed severe inflammatory reaction damaging the brain and liver.
The POLG variant originates from a single individual dating back to Viking times and has spread to populations of European origin. Especially Northern European countries show high carrier frequencies: one in a hundred individuals in Finland and Norway. If a subject inherits the POLG-variant from both parents, a neurological disease, MIRAS (mitochondrial recessive ataxia syndrome), manifests. However, the ages of onset and manifestations of MIRAS are highly variable, raising the question whether the disease is triggered by additional factors.
Using a variable set of model systems, the team shows that the POLG variant leads to a weakened initial immune activation in response to viral infection, followed by a delayed, overactivated inflammation damaging the brain and liver. The scientists suggest that this mechanism explains why some MIRAS patients manifest in teenage with severe epilepsy, while some other patients with the same genetic background show disease signs years or even decades later, as motor coordination defects or Parkinson’s disease.
“Our results indicate that external factors, such as viral infections, can modify manifestation and age-of-onset of neurological diseases,” postdoctoral scientist Yilin Kang comments. “Identification of susceptibility factors and triggering mechanisms are valuable targets for new therapy developments. The current findings indicate the importance of new mitochondrial functions in maintaining brain health.”
The work has been made possible by Jane and Aatos Erkko Foundation, Sigrid Juselius Foundation, Research Council of Finland , European Molecular Biology Organization and PolG foundation.

For about 40% of people diagnosed with colorectal cancer (CRC), the tumor carries a mutation in a gene called KRAS. Many of those mutations have been linked to shorter survival and more aggressive forms of disease. The onset and growth of CRC tumors has also been associated with imbalances in the gut microbiome, but the interplay between these 2 characteristics — gut dysbiosis and KRAS mutations — remains poorly understood.
In a study published this week in Microbiology Spectrum, an open access journal published by the American Society for Microbiology, researchers in China have identified microbiota signatures associated with KRAS mutations in people diagnosed with colorectal cancer. The findings suggest that gut microbes may serve as a kind of non-invasive biomarker for identifying subtypes of CRC and may inform personalized approaches to therapy, said Zigui Huang, a medical student at Guangxi Medical University Cancer Hospital who worked on the study.
The study was led by oncologist Weizhong Tang, M.D., at the same hospital, whose research focuses on harnessing molecular knowledge of CRC for better diagnosis and treatment of the disease. “Our new work contributes to the growing body of evidence highlighting the significance of microbiota-driven mechanisms in cancer pathogenesis,” Tang said.
Nearly 2 million people are diagnosed with colorectal cancer each year worldwide, and more than 900,000 die from the disease, according to the World Health Organization. Globally, it’s the third most common cancer and the second leading cause of cancer-related deaths. Previous studies have connected gut bacterial imbalances to the formation and spread of CRC, suggesting that a closer study of the gut microbial populations in the context of CRC could yield new insights about diagnosis and treatment.
“Understanding the specific associations between different types of KRAS mutations and CRC is vital for several reasons,” Huang said. Those include elucidating the molecular mechanisms that drive the development of CRC and identifying biomarkers for diagnosis and disease progression.
For the new study, the researchers analyzed stool samples from 94 individuals with CRC using 16s rRNA sequencing. Out of the 94, 24 had mutations in the KRAS gene and the rest had the “wild-type,” or non-mutated, form of the gene.
Sequencing revealed 26 different types of gut microbiota that were present in one group but not the other. The genera Fusobacterium, Clostridium and Shewanella were all abundant in the mutant group. Fusobacterium is a Gram-negative microbe found in the GI tract and the oral cavity, and previous studies have connected it to the development of CRC. All 3 of these, the researchers noted, should be considered as non-invasive biomarkers to determine a patient’s KRAS status.
Bifidobacterium and Akkermansia were abundant in the samples from patients without a KRAS mutation. Bifidobacterium is a probiotic, and Akkermansia has shown some probiotic activities in previous studies, including suppression of pro-inflammatory factors in the colon. Based on this finding, the researchers speculate that the presence of these bacteria may reduce a person’s chance of developing a KRAS mutation and, to an extent, slow the progression of CRC.
In the same paper, the researchers introduced a machine learning model that could use this information to guide personalized treatment recommendations based on microbiota signatures. However, Huang said, the model requires data from a larger cohort to improve its efficacy. The group plans to conduct larger studies to validate the findings and better understand the significance of the gut microbiota they’ve identified, in hopes of improving treatment for CRC patients.
“This study aligns with our broader research focus on understanding the intricate interplay between genetic mutations, the tumor microenvironment and gut microbiota in colorectal cancer,” Tang said.

Researchers have made a breakthrough into how two chronic respiratory diseases in childhood affect the immune system, paving the way for better treatments.
The research, led by Murdoch Children’s Research Institute (MCRI) and published in Mucosal Immunology, has found suppurative lung disease and wheezing have the same inflammatory profiles despite their differing symptoms.
MCRI Dr Melanie Neeland said while suppurative lung disease and wheezing were common in children, due to a poor understanding of the underlying mechanisms, treatment options were limited and disease recurrence was common.
The study involved 93 children who had lung fluid and blood samples taken at The Royal Children’s Hospital.
It found, for the first time, two treatable endotypes (disease subtypes) that were similar in frequency and immune signature across both respiratory diseases.
Dr Neeland said the discovery was measurable in a clinical setting, via a lung sample, and if validated in future studies, had the potential to change clinical management.
“The findings provide a significant advance in our understanding of lung inflammation in children with wheeze and suppurative lung disease,” she said.

“We showed that while the clinical presentations of these two diseases are different, identical inflammatory profiles can be found in the lungs and therefore the same anti-inflammatory treatments could be effective against both.
“Importantly, about 50 per cent of children in each disease group showed a hyper-inflammatory response that could potentially be treated with therapies already approved for use in children.
“Targeted anti-inflammatory treatments, such as repurposing asthma biologic medication, could be a new therapeutic approach to treat both diseases.”
Preschool asthma/recurrent wheeze is a leading cause of hospital admissions in children and results in poor lung function which persists for decades. Suppurative lung diseases spans a range of lung diseases characterised by chronic cough, airway obstruction and poor long-term health.
MCRI Dr Shivanthan Shanthikumar said children with chronic respiratory diseases have not benefitted from advances in care as adults with these conditions.
“Currently, management of these conditions in children is lacking, particularly for chronic cough which relies on prolonged antibiotic use despite evidence they’re not very effective,” he said. Recurrent courses of antibiotics for such a highly prevalent condition are of significant concern with antimicrobial resistance being a leading public health threat.
“But we can better manage chronic respiratory diseases if we can identify and target inflammatory profiles which underly these serious health conditions.”
Researchers from the University of Melbourne and The Royal Children’s Hospital also contributed to the findings.

Mass spectrometry, a technique that can precisely identify the chemical components of a sample, could be used to monitor the health of people who suffer from chronic illnesses. For instance, a mass spectrometer can measure hormone levels in the blood of someone with hypothyroidism.
But mass spectrometers can cost several hundred thousand dollars, so these expensive machines are typically confined to laboratories where blood samples must be sent for testing. This inefficient process can make managing a chronic disease especially challenging.
“Our big vision is to make mass spectrometry local. For someone who has a chronic disease that requires constant monitoring, they could have something the size of a shoebox that they could use to do this test at home. For that to happen, the hardware has to be inexpensive,” says Luis Fernando Velásquez-García, a principal research scientist in MIT’s Microsystems Technology Laboratories (MTL).
He and his collaborators have taken a big step in that direction by 3D printing a low-cost ionizer — a critical component of all mass spectrometers — that performs twice as well as its state-of-the-art counterparts.
Their device, which is only a few centimeters in size, can be manufactured at scale in batches and then incorporated into a mass spectrometer using efficient, pick-and-place robotic assembly methods. Such mass production would make it cheaper than typical ionizers that often require manual labor, need expensive hardware to interface with the mass spectrometer, or must be built in a semiconductor clean room.
By 3D printing the device instead, the researchers were able to precisely control its shape and utilize special materials that helped boost its performance.
“This is a do-it-yourself approach to making an ionizer, but it is not a contraption held together with duct tape or a poor man’s version of the device. At the end of the day, it works better than devices made using expensive processes and specialized instruments, and anyone can be empowered to make it,” says Velásquez-García, senior author of a paper on the ionizer.

He wrote the paper with lead author Alex Kachkine, a mechanical engineering graduate student. The research is published in the Journal of the American Association for Mass Spectrometry.
Low-cost hardware
Mass spectrometers identify the contents of a sample by sorting charged particles, called ions, based on their mass-to-charge ratio. Since molecules in blood don’t have an electric charge, an ionizer is used to give them a charge before they are analyzed.
Most liquid ionizers do this using electrospray, which involves applying a high voltage to a liquid sample and then firing a thin jet of charged particles into the mass spectrometer. The more ionized particles in the spray, the more accurate the measurements will be.
The MIT researchers used 3D printing, along with some clever optimizations, to produce a low-cost electrospray emitter that outperformed state-of-the-art mass spectrometry ionizer versions.
They fabricated the emitter from metal using binder jetting, a 3D printing process in which a blanket of powdered material is showered with a polymer-based glue squirted through tiny nozzles to build an object layer by layer. The finished object is heated in an oven to evaporate the glue and then consolidate the object from a bed of powder that surrounds it.

“The process sounds complicated, but it is one of the original 3D printing methods, and it is highly precise and very effective,” Velásquez-García says.
Then, the printed emitters undergo an electropolishing step that sharpens it. Finally, each device is coated in zinc oxide nanowires which give the emitter a level of porosity that enables it to effectively filter and transport liquids.
Thinking outside the box
One possible problem that impacts electrospray emitters is the evaporation that can occur to the liquid sample during operation. The solvent might vaporize and clog the emitter, so engineers typically design emitters to limit evaporation.
Through modeling confirmed by experiments, the MIT team realized they could use evaporation to their advantage. They designed the emitters as externally-fed solid cones with a specific angle that leverages evaporation to strategically restrict the flow of liquid. In this way, the sample spray contains a higher ratio of charge-carrying molecules.
“We saw that evaporation can actually be a design knob that can help you optimize the performance,” he says.
They also rethought the counter-electrode that applies voltage to the sample. The team optimized its size and shape, using the same binder jetting method, so the electrode prevents arcing. Arcing, which occurs when electrical current jumps a gap between two electrodes, can damage electrodes or cause overheating.
Because their electrode is not prone to arcing, they can safely increase the applied voltage, which results in more ionized molecules and better performance.
They also created a low-cost, printed circuit board with built-in digital microfluidics, which the emitter is soldered to. The addition of digital microfluidics enables the ionizer to efficiently transport droplets of liquid.
Taken together, these optimizations enabled an electrospray emitter that could operate at a voltage 24 percent higher than state-of-the-art versions. This higher voltage enabled their device to more than double the signal-to-noise ratio.
In addition, their batch processing technique could be implemented at scale, which would significantly lower the cost of each emitter and go a long way toward making a point-of-care mass spectrometer an affordable reality.
“Going back to Guttenberg, once people had the ability to print their own things, the world changed completely. In a sense, this could be more of the same. We can give people the power to create the hardware they need in their daily lives,” he says.
Moving forward, the team wants to create a prototype that combines their ionizer with a 3D-printed mass filterthey previously developed. The ionizer and mass filter are the key components of the device. They are also working to perfect 3D-printed vacuum pumps, which remain a major hurdle to printing an entire compact mass spectrometer.
This work was supported by Empiriko Corporation.

A new UCLA Health study has found that women who perceive themselves to be lonely exhibited activity in regions of the brain associated with cravings and motivation towards eating especially when shown pictures of high calorie foods such as sugary foods. The same group of women also had unhealthy eating behaviors and poor mental health.
Arpana Gupta, PhD, a researcher and co-director of the UCLA Goodman-Luskin Microbiome Center, wanted to research the negative impacts of loneliness, especially as people continue to be working remotely after the COVID-19 pandemic, and how the brain interplays with social isolation, eating habits, and mental health. While it is established that obesity is linked to depression and anxiety, and that binge-eating is understood to be a coping mechanism against loneliness, Gupta wanted to observe the brain pathways associated with these feelings and behaviors.
“Researching how the brain processes loneliness and how this is related to obesity and health outcomes hasn’t been done,” said Gupta, senior author of the paper, which is published in JAMA Network Open.
The researchers surveyed 93 women about their support system and their feelings of loneliness and isolation, then separated them into two groups: those who scored high on the perceived social isolation scale, and those who scored low. The researchers found that women who had higher levels of social isolation tended to have higher fat mass, lower diet quality, greater cravings, reward-based eating, and uncontrolled eating, and increased levels of anxiety and depression.
The women were then shown pictures of food versus non-food, sweet food versus non-food and savory food versus non-food. MRI scans recorded the participants’ brain activity while they viewed these images.
The researchers found that the group of women who perceived themselves to be lonely experienced increased activation in regions of the brain associated with a greater cravings to eat sugary foods, and decreased activation in the brain region associated with self-control towards eating behaviors.
“These findings are interesting because it provides evidence for what we intuitively know,” Gupta said. “When people are alone or lonely, it impacts more than how they are feeling; they underreport what they eat, their desire to eat, and their cravings especially for unhealthy foods.”
“If you have more cravings, you eat more and may have more anxiety or depression, which may lead you to eat more,” Xiaobei Zhang, postdoctoral researcher and lead author stated, likening this pathway to a “vicious cycle between unhealthy eating and negative mental symptoms.”
The researchers said holistic mind-body interventions may be a solution for breaking out of the cycle. Examples include being aware that you are lonely and, depending on the person, seek connection with others or practice self-compassion. Another suggestion is to make healthier food choices. “Instead of grabbing that highly addictive, sweet, high calorie food that you’re craving, maybe trying to go for healthy foods versus those bad foods,” Gupta said.
Gupta’s future research will focus on looking at other biological markers such as the metabolites, microbiome, and inflammatory signatures associated with loneliness.

A traumatic brain injury (TBI) can quadruple your risk for developing dementia and increase your chances of developing neurodegenerative diseases such as ALS. In a new study published in Cell Stem Cell, USC scientists use lab-grown human brain structures known as organoids to offer insights into why this is the case and how to mitigate the risk.
In the study, former postdoc Jesse Lai and PhD student Joshua Berlind from the USC Stem Cell laboratory of Justin Ichida used human patient-derived stem cells to grow rudimentary brain structures known as organoids in the lab. They then injured these organoids with high-intensity ultrasound waves.
The injured organoids showed some of the same features seen in TBI patients, including nerve cell death and pathological changes in tau proteins, as well as in a protein called TDP-43.
The scientists found that the pathological changes in TDP-43 were more prevalent in organoids derived from patients with ALS or frontotemporal dementia, making their nerve cells more suspectable to dysfunction and death following injury. This suggests that TBI might increase the risk of developing these diseases even more for patients with a genetic predisposition. The worst injuries were sustained by nerve cells that share information — called excitatory neurons — located in the deep layers of the organoids.
In their search for ways to protect these neurons against the effects of TBI, the scientists identified a gene called KCNJ2, which contains instructions for making channels that selectively allow potassium to pass through the cell membrane, helping to enable muscle contraction and relaxation. Inhibiting this gene had a protective effect on organoids derived from patients with and without ALS, as well as on mice, following a TBI.
“Targeting KCNJ2 may reduce the death of nerve cells after TBI,” said Ichida, who is the John Douglas French Alzheimer’s Foundation Associate Professor of Stem Cell Biology and Regenerative Medicine at USC, and a principal investigator at the Eli and Edythe Broad Center for Regenerative Medicine and Stem Cell Research at USC. “This could have potential as either a post-injury treatment or as a prophylactic for athletes and others at high risk for TBI.”
About the authors and the study
Co-corresponding author Ichida is also a co-founder of AcuraStem and Modulo Bio, a Scientific Advisory Board (SAB) member at Spinogenix and Vesalius Therapeutics, and an employee in the Research and Early Development group at BioMarin Pharmaceutical. Co-corresponding author Lai and co-author Violeta Yu were both employees of Amgen during the study, and currently work at Dewpoint Therapeutics. Named companies were not involved in this research project.
First author Berlind is a PhD student in the Ichida Lab. Additional co-authors are Gabriella Fricklas, Cecilia Lie, Jean-Paul Urenda, Kelsey Lam, Naomi Sta Maria, Russell Jacobs, and Zhen Zhao from USC.
Fifty percent of the work was supported by federal funding from the National Institute of Neurological Disorders and Stroke (NINDS) and the National Institute on Aging (grant F31NS117075), NINDS (grant R01 1R01NS097850-01), and the Department of Defense (grant 12907280). The project was also privately funded by an Amgen postdoctoral fellowship, the New York Stem Cell Foundation, the Tau Consortium, the Harrington Discovery Institute, the Alzheimer’s Drug Discovery Foundation, the Association for Frontotemporal Dementia, and the John Douglas French Alzheimer’s Foundation.

Insulinomas are an abnormal tumor, usually benign, that grow in the beta cells of the pancreas. Insulinomas make extra insulin, more than the body can use. They can cause hypoglycemia, or low blood sugar. Low blood sugar can cause confusion, sweating, weakness, confusion, and even coma. Surgery is the only treatment for patients with insulinoma , however, it is usually associated with longer time to recovery and loss of healthy pancreatic tissue can lead to diabetes.
In a new study in the Annals of Surgical Oncology, researchers describe a new technique for the minimally invasive removal of these benign tumors located in the challenging posterior head of the pancreas (right side of abdomen, nestled in the curve of the duodenum (or first part of the small intestine). The technique, called the retro-laparoscopic approach, allows surgeons to safely and effectively remove these tumors without removing healthy pancreatic tissue, thereby preserving organ functionality.
“This finding is important because it offers a less invasive and possibly safer option for the removal of pancreatic tumors, potentially reducing complications and improving patient recovery. Additionally, the technique may lead to less incidence of diabetes and pancreatic insufficiency due to preservation of most of the pancreas tissue,” explains corresponding author Eduardo Vega, MD, assistant professor of surgery at Boston University Chobanian & Avedisian School of Medicine.
Vega, in collaboration with Fernando Rotellar, MD, PhD, from Navarra University Clinic, Pamplona, Spain, performed a laparoscopic retroperitoneal on a 13mm insulinoma located in the posterior head of the pancreasThis involved inserting a camera and specialized instruments through small incisions (10 to 5 mm) in one side of the patient’s abdomen , allowing precise identification and removal of the tumor.
According to the researchers, the technique described in the study may have broader implications for using minimally invasive surgical procedures on other types of pancreatic tumors. “This study suggests exciting possibilities for the future of minimally invasive surgery and its applications in complex anatomical scenarios. It opens the door to further innovations in surgical techniques that could benefit patients with various types of tumors and medical conditions. It may also pave the way for robotic retroperitoneal approaches in the future for pancreatic surgery,” said Vega.