Publisher Health

Vittrup Man was born along the Scandinavian coast before moving to Denmark, where he was later sacrificed, according to a study published February 14, 2024 in the open-access journal PLOS ONE by Anders Fischer of the University of Gothenburg, Sweden and colleagues.
Vittrup Man is the nickname of a Stone Age skeleton recovered from a peat bog in Northwest Denmark, dating to between 3300-3100 BC. The fragmented nature of the remains, including a smashed skull, indicate that he was killed in a ritualistic sacrifice, a common practice in this region at this time. After a DNA study found Vittrup Man’s genetic signature to be distinct from contemporary, local skeletons, Fischer and colleagues were inspired to combine additional evidence to reconstruct the life history of this Stone Age individual at an unprecedented resolution.
Strontium, carbon and oxygen isotopes from Vittrup Man’s tooth enamel indicate a childhood spent along the coast of the Scandinavian Peninsula. Corroborating this, genetic analysis found a close relationship between Vittrup Man and Mesolithic people from Norway and Sweden. Additional isotope and protein analysis of the teeth and bones indicate a shift in diet from coastal food (marine mammals and fish) in early life to farm food (including sheep or goat) in later life, a transition that happened in the later teen years.
These results suggest that Vittrup Man spent his early years in a northern foraging society before relocating to a farming society in Denmark. It isn’t clear why this individual moved, though the authors suggest he might have been a trader or captive who became integrated into local society. Mysteries remain about Vittrup Man, but this detailed understanding of his geographic and dietary life history provides new insights into interactions between Mesolithic and Neolithic societies in Europe.
The authors add: “To our knowledge, this is the first time that research has been able to map a north European inhabitant’s life history in such a high degree of detail and in such high distance of time.”

Since the outbreak of COVID-19, surfaces in public spaces are cleaned more often. While disinfectant solutions eliminate germs, they don’t leave behind a truly bare surface. They deposit a thin film that doesn’t get wiped up, even after giving the surface a good polish. Researchers reporting in ACS ES&T Air show that residues left by commercial cleaning products contain a wider range of compounds that could impact indoor air quality than previously thought.
Residues on indoor surfaces — like those deposited during cooking or cleaning — may contain compounds that are potentially harmful if absorbed through the skin or if they become airborne and are inhaled. To investigate the impact on indoor air quality, scientists study the gunk that builds up with laboratory models of surfaces. In the models, researchers start with the assumption that a thin film exists on any “clean” surface, but the source and actual makeup of these films is unknown. Because the chemical compositions of commercial cleaning products are different from the products used to prep surfaces in the lab, Rachel O’Brien and colleagues hypothesized that commercial sanitizers could be a missing source for the films. So, they decided to characterize films left behind on recently cleaned surfaces.
Using a surface-indoor solvent extractor, the researchers directly collected films from cleaned surfaces in a controlled lab setting and on regularly washed surfaces in university buildings. This method allowed them to pick up and measure a wide array of compounds, including substances that barely evaporate. In contrast, only semivolatile organic compounds (SVOCs) are picked up by wiping a surface film with a solvent-damp cloth, the typical method used to analyze films. The team’s analyses of the residue samples by mass spectrometry found that: Films from commercial cleaning products were different on the model lab surfaces and university building surfaces and more complex than previously thought. While the composition of the films was different, they all contained SVOCs that can become airborne and impact indoor air quality. This method confirmed the presence of lower volatility surfactants, the primary components of soaps, in residues thought to be from the cleaning solutions. However, surfactants’ effects on surface films have not yet been defined.As a result of these findings, the researchers say that more compounds could be deposited on cleaned surfaces than had previously been identified. They add that future indoor film studies should use surfaces prepared with commercial cleaning products to more accurately identify how the residues impact indoor air quality. And given the extent and regularity of cleaning done in public spaces and people’s homes, more research is needed to determine the effects of lower volatility compounds on film growth and behavior.
The authors acknowledge funding from the Alfred P. Sloan Foundation.

Scientists have long thought of the fluid-filled sac around our lungs merely as a cushion from external damage. Turns out, it also houses potent virus-eating cells that rush into the lungs during flu infections.
Not to be confused with phages, which are viruses that infect bacteria, these cells are macrophages, immune cells produced in the body.
“The name macrophage means ‘big eater.’ They gobble up bacteria, viruses, cancer cells, and dying cells. Really, anything that looks foreign, they take it up and destroy it,” said UC Riverside virologist Juliet Morrison, who led the discovery team. “We were surprised to find them in the lungs because nobody has seen this before, that these cells go into the lung when there’s an infection.”
A paper published in the Proceedings of the National Academy of Sciences details how during an influenza infection, macrophages leave the exterior cavity and cross into the lungs where they decrease inflammation and reduce levels of disease.
“This study shows it’s not just what happens in the lung that matters, but also what’s outside of the lung. Cell types not normally connected to the lung can have outsized impacts on lung disease and health,” Morrison said.
There are three main cavities in the body: one around the heart, the abdominal cavity, and the pleural cavity surrounding the lungs. “Because it contains fluid, it prevents the lungs from collapsing. However, people have not thought much about the pleural cavity being a whole organ within itself. This research may change that perception,” Morrison said.
Initially, the researchers set out to understand the more general question of what types of cells are present in the lungs during flu infections. They took existing data on lung-related genes from studies of mice that either died from the flu or survived. They then mined the data using an algorithm to predict cell types that change in the lungs during infections.

“We took big data and broke it down to assign which potential immune cells are in the lung tissues. That’s where I got a hint that maybe we had a previously unknown external source of cells in the lung,” Morrison said.
Next, using a laser-based technique, the team tracked macrophages going into the lungs of mice, and observed what happened if they took these cells out of the equation. “When you take them out of the mouse you see more disease and more lung inflammation,” Morrison said.
Morrison says she hopes this study will encourage other scientists to reevaluate data sets from older studies. “Our approach was to take information already out there and put it to new use, and we were able to see something new,” she said.
Moving forward, the research team is hoping to determine which proteins “tell” the macrophages to move into the lungs. Once the protein signals have been identified, it may be possible to create drugs that boost either the number of macrophages, or their activity.
The strategy of boosting human defenses to infection, rather than developing another antiviral, could offer people a flu treatment that would be more effective for much longer. Morrison became interested in host therapeutics because antibiotic and antiviral resistance to drugs is a growing problem.
This problem occurs when germs like bacteria and fungi develop the ability to defeat the drugs designed to kill them. Misuse and overuse of the drugs is accelerating the problem. According to the Centers for Disease Control and Prevention, more than 2.8 million drug-resistant infections occur each year in the U.S., and more than 35,000 people die as a result.
“If we can boost what resolves infection in us, we probably have a better shot. We’re less likely to have resistance. The immune system is so complicated, but it’s our best bet in the long run to work with what we have rather than chase viruses that continue to escape our therapeutics,” Morrison said.

Scientists at Cold Spring Harbor Laboratory (CSHL) and the University of California, Davis have reached a new breakthrough in pancreatic cancer research — eight years in the making. It could help slow the disease’s deadly spread.
In 2017, as a postdoc in CSHL’s Tuveson lab, Chang-il Hwang and collaborators from the Vakoc lab uncovered a protein essential for jumpstarting metastasis in pancreatic ductal adenocarcinoma (PDAC). Now an assistant professor at UC Davis, Hwang recently reunited with CSHL Professors David Tuveson and Christopher Vakoc. The trio once again set their sights on PDAC. The disease is known for its aggressiveness. It often spreads to other organs like wildfire, wreaking havoc in its path.
“Metastatic spread is one of the reasons pancreatic cancer is such a deadly disease,” Vakoc says. “Our study led by Dr. Hwang has opened the door to new insights we might one day use to combat aggressive PDAC.”
The team found that late-stage PDAC hijacks a protein called Engrailed-1 (EN-1) to evade the body’s natural cancer defenses. EN-1 is a type of protein known as a transcription factor. These proteins control the timing and duration of gene expression. This particular transcription factor is required to form major areas of the brain.
“EN-1 is known to play a role in neurodevelopment,” Hwang explains. “In the pancreas, it’s not normally expressed. But in the later stages of pancreatic cancer, it gets overly expressed and makes the cancer more metastatic.” That means a faster, deadlier spread. But what if EN-1 could be targeted in cancer? Hwang, Tuveson, and Vakoc sought to find out.
The team used organoids — mini versions of tumors — to identify the role of over-expressed EN-1 in PDAC. They found that higher levels of the aberrant protein blocked genes associated with natural cell death. When EN-1 expression was curtailed, the genes it targets were able to do their job, promoting healthy cell survival.
“Without EN-1, cancer progression slows,” Hwang says. “At the moment, it’s hard to target transcription factors with drugs. But in the future, it may be possible to disrupt the kind of interactions we see with mutated EN-1 in PDAC.”
Pancreatic cancer remains the third-leading cause of cancer-related deaths in the U.S. Hwang plans to continue collaborating with CSHL in hopes that his team’s work may lead to better treatments.
“We know certain types of PDAC are dependent on EN-1,” Hwang says. “If we can develop a way to test for it, we can create more personalized therapeutics and treatment strategies for patients. We’re looking forward to heading in that direction.”

Athletes often suffer injuries to ligaments in their knees, particularly to the anterior cruciate ligament or ACL. While surgery to replace these torn ligaments is becoming increasingly common around the world it often needs to be repeated. That’s because it has proved challenging to anchor fibrous, soft and wet ligament grafting material into hard bone.
Now, McGill University researchers have new information from the eggshell membrane in chicken eggs that could help change this picture thanks to the potential it offers for improvements in tissue engineering and biomaterial grafts.
Their findings also have the potential to reduce losses for commercial egg and poultry producers.
Anchoring soft and wet fibres by “nailing” them in place
The researchers discovered how the hard shell of a bird egg attaches to the underlying wet fibrous membrane of the egg (the thin membranous layer found inside the shell seen when peeling a hard-boiled egg). By using advanced 3D imaging X-ray and electron microscopes together with cryo-preservation methods the research team were able to peer into this interface in three dimensions to visualize and quantify the interlocking phenomenon.
“Until now, no one had considered how this interface between these two very dissimilar substances, one a hard biorock, and the other a soft fibrous membrane, might be secured at the nanoscale,” says Marc McKee, a professor in the Faculty of Dental Medicine and Oral Health Sciences, and in the Department of Anatomy and Cell Biology, and the principal investigator of the study conducted by doctoral student Daniel Buss and published recently in iScience. “What we found about this soft-hard interface is quite remarkable.”
Nanospikes increase the surface area of contact between soft and hard materials and ensure food safety
The McGill team discovered that, at a certain stage in the development of an egg prior to laying, the shell sends mineral nanospikes into the soft and compliant surface fibres of the underlying eggshell membrane. This membrane surrounds the soft contents of the egg interior, being either the egg white and yolk from table eggs, or the developing chick embryo in a fertilized and incubated egg.

This nanospiking attachment process between two highly dissimilar materials substantially increases the surface area of the interface between the soft and wet organic fibres and the hard and largely dry inorganic mineral. Such an attachment importantly anchors and secures this soft-hard interface to prevent slipping and sliding of the fibres within the shell.
Otherwise, detachment of the membrane from the shell can be lethal for the embryonic chick, can weaken the shell, and/or can allow the invasion of pathogens (such as salmonella) into the interior contents of the egg. Food safety of the table egg relies on an intact shell that is well-integrated with its underlying membrane.
Implications for medical procedures and commercial egg production
With this new understanding of the shell-membrane interface as being a characteristic feature of strong, safe and healthy eggs, losses for table egg producers and poultry breeders might be reduced through the establishment of commercial genetic breeding programs that maintain or maximize this interfacial structure.
The findings might also potentially lead to new engineered, hybrid composite material designs, and to new procedures to improve the outcomes of various medical and dental reconstructive surgeries, both of which may require attaching soft wet fibres to hard materials.

Women who receive an mRNA-based COVID-19 vaccination or booster during pregnancy can provide their infants with strong protection against symptomatic COVID-19 infection for at least six months after birth, according to a study from the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health. These findings, published in Pediatrics, reinforce the importance of receiving both a COVID-19 vaccine and booster during pregnancy to ensure that infants are born with robust protection that lasts until they are old enough to be vaccinated.
COVID-19 is especially dangerous for newborns and young infants, and even healthy infants are vulnerable to COVID-19 and are at risk for severe disease. No COVID-19 vaccines currently are available for infants under six months old. Earlier results from the Multisite Observational Maternal and Infant COVID-19 Vaccine (MOMI-Vax) study revealed that when pregnant volunteers received both doses of an mRNA COVID-19 vaccine, antibodies induced by the vaccine could be found in their newborns’ cord blood. This suggested that the infants likely had some protection against COVID-19 when they were still too young to receive a vaccine. However, researchers at the NIAID-funded Infectious Diseases Clinical Research Consortium (IDCRC), which conducted the study, did not know how long these antibody levels would last or how well the infants would actually be protected. The research team hoped to gather this information by following the infants through their first six months of life.
In this portion of the study, researchers analyzed data from 475 infants born while their pregnant mothers were enrolled in the MOMI-Vax study. The study took place at nine sites across the United States. It included 271 infants whose mothers had received two doses of an mRNA COVID-19 vaccine during pregnancy. The remaining 204 infants in the study were born to mothers who had received both doses of an mRNA COVID-19 vaccine as well as a COVID-19 booster. To supplement data gathered during pregnancy and at birth, the infants were evaluated during at least one follow-up visit during their first six months after birth. Parents also reported whether their infants had become infected or had demonstrated COVID-19 symptoms.
Based on blood samples from the infants, the researchers found that newborns with high antibody levels at birth also had greater protection from COVID-19 infection during their first six months. While infants of mothers who received two COVID-19 vaccine doses had a robust antibody response at birth, infants whose mothers had received an additional booster dose during pregnancy had both higher levels of antibodies at birth and greater protection from COVID-19 infection at their follow-up visits.
While older children and adults should continue to follow guidance from the Centers for Disease Control and Prevention (CDC) to stay up-to-date on their COVID-19 vaccines and boosters, this study highlights how much maternal vaccination can benefit newborns too young to take advantage of the vaccine: During the course of this study, none of the infants examined required hospitalization for COVID-19. Researchers will continue to evaluate the data from the MOMI-Vax study for further insights concerning COVID-19 protection in infants.

Generative AI techniques, machine learning and simulations give researchers new opportunities to identify environmentally friendly metal-organic framework materials.
Carbon capture is a critical technology in reducing greenhouse gas emissions from power plants and other industrial facilities. But a suitable material for effective carbon capture at low cost has yet to be found. One candidate is metal-organic frameworks, or MOFs. This porous material can selectively absorb carbon dioxide.
MOFs have three kinds of building blocks in their molecules — inorganic nodes, organic nodes and organic linkers. These can be arranged in different relative positions and configurations. As a result, there are countless potential MOF configurations for scientists to design and test.
To speed up the discovery process, researchers from the U.S. Department of Energy’s (DOE) Argonne National Laboratory are following several pathways. One is generative artificial intelligence (AI) to dream up previously unknown building block candidates. Another is a form of AI called machine learning. A third pathway is high-throughput screening of candidate materials. And the last is theory-based simulations using a method called molecular dynamics.
Joining Argonne in this project are researchers from the Beckman Institute for Advanced Science and Technology at the University of Illinois Urbana-Champaign (UIUC), the University of Illinois at Chicago and the University of Chicago.
Designing MOFs with optimal carbon selectivity and capacity is a significant challenge. Until now, MOF design has relied on painstaking experimental and computational work. This can be costly and time-consuming.
By exploring the MOF design space with generative AI, the team was able to quickly assemble, building block by building block, over 120,000 new MOF candidates within 30 minutes. They ran these calculations on the Polaris supercomputer at the Argonne Leadership Computing Facility (ALCF). The ALCF is a DOE Office of Science user facility.

They then turned to the Delta supercomputer at UIUC to carry out time-intensive molecular dynamics simulations, using only the most promising candidates. The goal is to screen them for stability, chemical properties and capacity for carbon capture. Delta is a joint effort of Illinois and its National Center for Supercomputing Applications.
The team’s approach could ultimately allow scientists to synthesize just the very best MOF contenders. ​”People have been thinking about MOFs for at least two decades,” said Argonne computational scientist Eliu Huerta, who helped lead the study. ​”The traditional methods have typically involved experimental synthesis and computational modeling with molecular dynamics simulations. But trying to survey the vast MOF landscape in this way is just impractical.”
Even more advanced computing will soon be available for the team to employ. With the power of the ALCF’s Aurora exascale supercomputer, scientists could survey billions of MOF candidates at once, including many that have never even been proposed before.
What’s more, the team is taking chemical inspiration from past work on molecular design to discover new ways in which the different building blocks of a MOF could fit together.
“We wanted to add new flavors to the MOFs that we were designing,” Huerta said. ​”We needed new ingredients for the AI recipe.” The team’s algorithm can make improvements to MOFs for carbon capture by learning chemistry from biophysics, physiology and physical chemistry experimental datasets that have not been considered for MOF design before.
To Huerta, looking beyond traditional approaches holds the promise of a transformative MOF material — one that could be good at carbon capture, cost-effective and easy to produce.

“We are now connecting generative AI, high-throughput screening, molecular dynamics and Monte Carlo simulations into a standalone workflow,” Huerta said. ​”This workflow incorporates online learning using past experimental and computational research to accelerate and improve the precision of AI to create new MOFs.”
The atom-by-atom approach to MOF design enabled by AI will allow scientists to have what Argonne senior scientist and Data Science and Learning division director Ian Foster called a ​”wider lens” on these kinds of porous structures. ​”Work is being done so that, for the new AI-assembled MOFs that are being predicted, we incorporate insights from autonomous labs to experimentally validate their ability to be synthesized and capacity to capture carbon,” Foster said. ​”With the model fine-tuned, our predictions are just going to get better and better.”
A paper based on the study was authored by Hyun Park, Xiaoli Yan, Ruijie Zhu, Eliu Huerta, Santanu Chaudhuri, Donny Copper, Ian Foster and Emad Tajkhorshid. It appeared in the online issue of Nature Communications Chemistry.
“The study demonstrates the great potential of using AI-based approaches in molecular sciences,” said UIUC’s Tajkhorshid. ​”We hope to extend the scope of the approach to problems such as biomolecular simulations and drug design.”
“This work is a testament to the collaboration between graduate students and early-career scientists from different institutions who came together to work on this important AI for science project,” Huerta said. ​”The future will stay bright as we continue to inspire and be inspired by talented young scientists.”
The work was supported by DOE’s Office of Science, Office of Advanced Scientific Computing Research, laboratory-directed research and development funds, and the National Science Foundation.

Researchers from the Icahn School of Medicine at Mount Sinai, in collaboration with the Clinical Proteomic Tumor Analysis Consortium of the National Institutes of Health, The University of Texas MD Anderson Cancer Center, Sylvester Comprehensive Cancer Center at the University of Miami Miller School of Medicine, and others, have unveiled a detailed understanding of immune responses in cancer, marking a significant development in the field. The findings were published in the February 14 online issue of Cell.
Utilizing data from more than 1,000 tumors across 10 different cancers, the study is the first to integrate DNA, RNA, and proteomics (the study of proteins), revealing the complex interplay of immune cells in tumors. The data came from the Clinical Proteomic Tumor Analysis Consortium (CPTAC), a program under the National Cancer Institute.
“We aimed to improve our understanding of the mechanisms underlying the functional impairment of immune response in tumors. By closely examining genes and proteins in the tumor tissues, we discovered various patterns in immune activation and suppression,” says Pei Wang, PhD, Professor of Genetics and Genomic Sciences at Icahn Mount Sinai, and the lead-corresponding author on the paper. “Our goal in unraveling these diverse immune subtypes is to help clinicians identify patient groups more responsive to immunotherapy. Revealing the specific pathways and cellular switches for each subtype can also spark new and creative ways to develop treatments.”
“Each type of immune response was linked to changes in gene functions, such as how genes are modified, the messages they send, and the proteins they produce. By providing a comprehensive molecular fingerprint of the immune response in cancer, this study is expected to facilitate the development of future immunotherapy strategies,” says Francesca Petralia, PhD, Assistant Professor of Genetics and Genomic Sciences at Icahn Mount Sinai, and co-corresponding author on the paper.
A key finding was that among seven subtypes identified through advanced statistical models, five included tumors from ten different types of cancer, suggesting shared immune responses across these tumors.
“When we see common immune responses and similar patterns in the way cells behave across various cancers within the same immune group, it hints that certain treatments that boost the immune system could work well for many types of cancer,” says Dr. Wang.
A novel aspect of the research stems from the deep phosphoproteomic data generated for more than 1,000 tumors. This data allows researchers to see how proteins are modified. “With phosphoproteomic profiling of more than 1,000 pan-cancer tumors, we were able to computationally discover a set of key novel drug targets,” says Avi Ma’ayan, PhD, Professor, Pharmacological Sciences, Director of the Mount Sinai Center for Bioinformatics at Icahn Mount Sinai, and a senior author of the paper. “By targeting selected kinases with small molecules or other means, we may be able to convert tumors not responding to immunotherapies into tumors with better immune-therapy response.”
As part of the research, a machine-learning tool applied to digital pathology images also demonstrated correlations between different types of immune responses and the presence of certain immune cells, enhancing understanding of the environment in and around tumors.
Next, the investigators plan to validate their findings further and leverage insights in ongoing clinical studies focused on immunotherapies. This effort aims to streamline the development of biomarker panels for treatment responses and identify enhanced treatment strategies. Collaborative efforts within CPTAC are underway, including a proteogenomic study on molecular mechanisms underlying responses to immune checkpoint treatments in melanoma patients.

For middle-aged women plagued by migraines, or hot flashes and night sweats, another worry may linger in the backs of their minds: whether these experiences have set them up for a heart attack, a stroke or another cardiovascular crisis.
After all, past research suggesting such a link during and after menopause has gotten a lot of attention.
But a pair of new studies in the journal Menopause suggest that most of them don’t need to worry as much, especially if they don’t have both migraines and long-term hot flashes and night sweats.
Instead, they should focus on tackling the other factors that can raise their cardiovascular risk by getting more sleep, exercise and healthy foods, quitting tobacco, and minding their blood pressure, blood sugar, cholesterol and weight.
For women who have experienced both migraines and hot flashes or night sweats over many years, one of the new studies does suggest an extra level of cardiovascular risk. That makes heart disease and stroke prevention even more important in this group, says study leader Catherine Kim, M.D., M.P.H., of the University of Michigan.
And for women currently in their 20s and 30s who experience migraines, the new research suggests that they might be heading for a higher risk of long-term menopause-related symptoms when they get older.
Long-term study yields important insights
Kim and her colleagues at Michigan Medicine, U-M’s academic medical center, published the new pair of studies based on an in-depth analysis of data from a long-term study of more than 1,900 women who volunteered to have regular physical exams and blood tests, and to take yearly health surveys, when they were in their late teens to early 30s.

Those women, now in their 50s and 60s, have provided researchers with a priceless view of what factors shape health in the years leading up to menopause and beyond, through their continued participation in the CARDIA study.
“The anxiety and dread that women with migraines and menopausal symptoms feel about cardiovascular risk is real — but these findings suggest that focusing on prevention, and correcting unhealthy habits and risk factors, could help most women,” said Kim, who is an associate professor of internal medicine at U-M and a primary care physician.
“For the subgroup with both migraines and early persistent hot flashes and night sweats, and for those currently experiencing migraines in their early adulthood, these findings point to an added need to control risks, and address symptoms early,” she adds.
Just over 30% of the middle-aged women in the study reported they had persistent hot flashes and night sweats, which together are called vasomotor symptoms or VMS because they relate to changes in the diameter of blood vessels.
Of them, 23% had reported also having migraines. This was the only group for whom Kim and her colleagues found extra risk of stroke, heart attack or other cardiovascular events that couldn’t be explained by other risk factors that have long been known to be linked to cardiovascular problems.
In addition to those with persistent vasomotor symptoms starting in their 40s or before, 43% of the women in the study had minimal levels of such symptoms in their 50s, and 27% experienced an increase in VMS over time into their 50s and early 60s.

The latter two groups had no excess cardiovascular risk once their other risk factors were taken into account, whether or not they had migraines. Use of hormone-based birth control and estrogen to address medical issues did not affect this risk.
Controlling destiny
In the study of data from the same women in their earlier stages of life, the researchers found that the biggest factors in predicting which ones would go on to have persistent hot flashes and night sweats were having migraines, having depression, and smoking cigarettes, as well as being Black or having less than a high school education.
“These two studies, taken together, underscore that not all women have the same experiences as they grow older, and that many can control the risk factors that might raise their chances of heart disease and stroke later in life,” said Kim. “In other words, women can do a lot to control their destiny when it comes to both menopause symptoms and cardiovascular diseases.”
She notes that the American Heart Association calls these risk factors the “Essential 8” and offers guides for what women, men and even children and teens can do to address them.
Evolving knowledge and treatment
The long-term study that the two new findings come from was specifically designed to look at cardiovascular risks when it launched in the mid-1980s. CARDIA stands for Coronary Artery Risk Development in Young Adults.
Back in the 80s, knowledge about the biology of blood vessels, down to the cellular and molecular level, was nowhere near where it is today. Both vasomotor symptoms in menopause and migraines have to do with blood vessel contraction and dilation.
But decades of research has shown the microscopic impacts on blood vessels of years of smoking, poor sleep, poor eating habits and lack of activity, as well as a person’s genetic inheritance, life experiences and hormonal history.
Newer injectable migraine medications called calcitonin gene-related peptide (CGRP) antagonists have reached the market in recent years.
Using monoclonal antibodies, they target a key receptor on the surface of blood vessel cells to prevent migraines and cluster headaches. But they are expensive and not covered by insurance for all people with migraines.
While the new study is based on data from years before these medications became available, Kim said she recommends them to her patients with persistent migraines, as well as working with them to understand what triggers their migraines and how to use other medications including pain relievers and antiseizure medications to prevent them.
She also notes that the paper on future risk of persistent hot flashes and night sweats echoes the recent trend of using antidepressant medications to try to ease these menopause effects.
Kim also says that evidence has grown about the importance of healthy sleep habits for reducing hot flashes, as well the short-term use of estradiol-based hormone therapy patches, which have not been shown to have a link to cardiovascular risk. And, she notes that research has not shown any over-the-counter supplement or herbal remedy to be effective, and that these are far less regulated than medications.

Our lymph nodes are the canaries in the coal mine of our immune system — firing into gear at the first indication of illness, then sending immune cells where they’re needed in the body to fight infection and disease.
For the nearly 20 million patients around the world diagnosed with cancer each year, the lymph nodes are an invaluable early indicator of whether their cancer has metastasized — when cancer cells begin to spread to another organ. Catching metastasis as early as possible means that the patient can be administered the necessary chemotherapy and immune therapies that will vastly improve their prognosis.
Researchers at USC’s Alfred E. Mann Department of Biomedical Engineering have developed a new nanoparticle that can “hitch a ride” on immune cells, or monocytes. Because of its tiny size, the particle can tag along directly into lymph nodes and help metastasis show up on MRIs where it would otherwise be too hard to detect. The results could lead to more advanced contrast agents that can be injected into patients to improve MRI cancer screenings of the lymph nodes.
The work has been published in ACS Nano and was led by Eun Ji Chung, the Dr. Karl Jacob Jr. and Karl Jacob III Early-Career Chair, and Noah Trac, a Ph.D. student in the Chung Lab.
While lymph nodes are an essential factor in cancer detection, screening them via biopsy is painful and invasive, and can lead to unwanted side effects like infection, lymphedema and thrombosis. Imaging tools such as MRI detection are non-invasive. Still, they also have significant shortcomings when it comes to screening lymph nodes,
“MRIs will look at the lymph node’s size, but that does not have a great connection and correlation to the fact that it is metastatic,” Chung said. “Even if you have a cold, your lymph nodes will start inflaming.”
“The major issue with current MRI techniques is not that they don’t detect the immune cells,” Trac said. “A major issue with current contrast agents is that there is no cancer-targeting mechanism, so most lymph nodes are lit up equally, regardless of whether or not there is cancer.”
To address this challenge, Chung, Trac and their co-authors developed a nanoparticle that targets a receptor present on both tumor cells and immune cell monocytes — cells that travel to the lymph nodes and are increasingly prevalent under disease conditions.

“The idea behind this nanoparticle is to try and direct the delivery of the gadolinium contrast agent to lymph nodes that have cancer, so that they show up brighter on the MRI than healthy lymph nodes,” Trac said.
The diagnostic tool would also offer strong clinical value for doctors to not only catch first-time metastasis during an initial cancer diagnosis, but it will also allow clinicians to keep track of cancer recurrence.
“Just say a primary tumor has been removed, but perhaps they didn’t get all of it, or the cancer comes back and it’s metastatic for the second time. Recurrent metastasis is much harder to detect and can lead to worse outcomes for the patient,” Chung said.
Hitching a ride to light up cancer
The nanoparticles work by targeting a protein expressed by cancer cells, known as C-C chemokine receptor 2 (CCR2). The particles “hitchhike” onto the immune cell monocytes that the body produces that also express this same receptor in response to the cancer. The monocytes then give the particles a free ride into the lymph nodes, where the particles can effectively highlight the metastatic cancer cells and enable clearer detection via MRI.
“The reason why this mechanism works, in addition to the targeting elements, is because our particle size is also very unique, and it can reach the lymph nodes,” Chung said. “We found there’s a size cut-off and our particle type is able to pass into the lymph nodes and target cancer cells that have gotten there, along with the monocytes that express this receptor.”
The process offers game-changing benefits for the early detection of cancer metastasis in the lymph nodes. While previously, metastasis could only be assessed by an increase in lymph node size; the new Chung Lab particles could lead to MRI contrast agents that can highlight metastatic cells in lymph nodes that may otherwise appear normal. In experiments using a mouse model, the team demonstrated that the particles increased the signal detected by MRI by up to 50%.

“The particles are amplifying the signal, and we can see that at points where the lymph nodes haven’t yet changed in size, and the metastasis is very early. We’re providing this benefit where, clinically, you wouldn’t be able to see metastasis at all,” Chung said.
The next step for the research team is to get their work closer to clinical applications for MRI contrast agents. The work has been submitted to the Nanoparticle Characterization Laboratory at the National Institutes of Health, where a third party will assess and validate the work to enable it to move closer to human trials.